Revalida Reviewer Asmph

Edited & Updated by:
Author: Cuevas, et al. ASMPH Batch 2019, Batch

ASMPH Batch 2018 2020 & Batch 2021
ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 1

FOREWORD
The Grand Osce (along with Revalida) has always been on of the most anticipated and important milestones for any YL6 student in ASMP. The
day of your OSCE brings to an end one of the hardest years in medical school. For many of us who have gone through it, we always look back
fondly at what had transpired leading up to that day – the nerve-wreacking preparation, the hilarious mistakes and answers we said, and the
awkward silence when you can’t find the right answers. Nevertheless, I believe most of us also vividly remember the final bell, seeing everyone
smiling as they went out to the hallways and finally saying to each other, “We made it!”
The OSCE reviewer was written by ASMPH 2018 (Cuevas, et.al) and has been handed down every year. It summaries important information
regarding history taking, physical examination and the most common diagnoses of each subject/specialization. On the Fourth edition, ASMPH
2021 has added two new chapters, Psychiatry and Radiology, updated new information based on recently released guidelines, and added
additional information and diseases.
We hope that this reviewer will help you as much as it helped us, not only during YL6 but also for the next few years to come. We can’t wait to
hear your own batch’s OSCE stories. Our only request is for you to pass this on when the time comes and hopefully this document lives on as
yet another proof that indeed in our school, no Atenean is left behind.
It may not be easy but it will soon be worth it. Study well, study smart!.
“It always seems impossible until it is done”

-Nelson Mandela
TABLE OF CONTENTS
Topic Pages Contributors

1. Public Health 3-5 Ong-Vaño, Pamin, Ruby, Nerva, Tang
2. Clinical Skills 6 - 17 Alcantara, Bitoy, Santos, Mondragon
3. Radiology 18 - 37 Chung, Tang
4. Infectious Disease 38 - 46 Chua, Cruz, Guarin, Mutia, Rivera, Apal, Acosta
Alcantara, Bitoy, Jardin , Mendoza, Pineda, Cotingting,
5. Hematology/ Immunology 47 – 57
Escolano
6. Neurology 58 - 71 Garcia, Tien, Teano, Guzman
7. Head, Ears, Eyes, Neck, Throat Ceballos, Lorena, Paruñgo, Sy, Tenorio, Veneracion, Alcantara,
72 - 93
(HEENT) Besa, Luna
8. Pulmonology 94 - 109 Lok, Young, Go, Sienes, Lumang
9. Cardiology 110 - 128 Basallote, Co, Gaviola, Naval, Rodriguez, Ocat
Chan, Co, Esguerra, Mangaoang, Marcelo, Pabilane, Punsalan,
10. Gastrointestinal 129 -145
Rosario, Javier, Latoga
11. Nephrology 146 - 153 Cabañero, Hernandez, Sy, Velasco, Empedrado, Beltran
12. Endocrinology 154 - 160 Aba, Braga, Cuevas, Salud, Park, Chua, Nepomuceno
13. Pshychiatry 161 - 164 Tan, Zi
14. Orthopedics (MSK) 165 - 172 Carandang, Chua, Punzalan, Rostata, Sapilan, Medalle, Olabre
15. Pediatrics 173 - 179 Gemzon, Ong, Ramirez, Morin, Mirafuentes
16. Dermatology 180 - 187 Davalos, de Dios, Pena, Revillas, Roco, Tantuco, Ledesma
Barlisan, Corpuz, Sy, Gaña, Tan, Ramos, Claveria, Hernandez,
17. Obstetrics/ Gynecology 189 - 202
Estangco, Villanueva, Tagarao
18. Microbiology & Parasitology 203 - 225 Diwa, Salindo, Lagarteja, Lopez
19. Reporting Summary 226 - 234 Juat, Paris, Pine, Oyson
Compilers: Alcantara, Cuevas, Gaviola, Punsalan, Sy

Version 2 Batch 2019 Editors: Andujare, Diwa, Dominguez, Lusica, Mapili, Palma, Ong, Salindo, Turalde
Version 3 Batch 2020 Editors: Alcantara, Apal, Besa, Chua, H., Chua, K., Cotingting, Empedrado, Estangco, Gagelonia,
Javier, Juat, Lagarteja, Lee, Medalle, Morin, Nerva, Paris, Pine, Rodriguez, Santos, Sienes, Sy, Teano, Valdepenas
Version 4 Batch 2021 Editors: Acosta, Beltran, Chung, Escolano, Guzman, Latoga, Ledesma, Lopez, Lumang, Luna,
Mirafuentes, Mondragon, Nepomuceno, Ocat, Olabre, Oyson, Tagarao, Tan Zi., Tang, Villanueva
Cover Page: Ferrer, Sarmiento, icon source: https://www.flaticon.com/free-icon/doctor_822130
Foreword: Lee Revised: Tang

MODULE/TOPIC 1 PUBLIC HEALTH
INTERVIEWING SKILLS
MEDICAL INTERVIEW TYPOLOGY OF ILLNESS
• Gathering information within a trustworthy relationship that takes into account • Nature
BOTH the disease (biomedical) and illness (subjective sense of feeling unwell) o Acute – rapid onset, immediate crisis, little time for adjustment
o Gradual – slow onset, alteration of roles, some time for adjustment
ACTIVE LISTENING SKILLS • Course of illness
• Attending o Constant – stabilizes after initial event
o Use L.O.V.E.R.S. o Progressive – constantly symptomatic, worsens over time
§ Lean forward o Episodic or relapsing
§ Open stance • Outcome
§ Voice of compassion o Fatal – anticipatory grief and separation
§ Eye contact o Non-fatal – must focus on long term adjustments
§ Relax • Incapacitation
§ Sit at 45-degree angle o Severity – mild, moderate, severe
• Bracketing: setting aside biases and ideas, restraining opinion o Type – single, multisystem
• Leading (“Tell me more about that (symptom)”)
• Reflecting PHASES OF CRISIS
o Content: Paraphrasing, Perception checking Phase 1: Triggering of crisis
o Feeling (*look sad*) Phase 2: Mounting tension and disorganization
• Probing Phase 3: Mobilization of resources and reorganization
o Open-ended questions Phase 4: Resolution or maladaptation
CATHARSIS, EDUCATION, ACTION (CEA) STRESSFUL EVENTS, PRECIPITATING CRSIS

• Dealing with the dissatisfaction due to misperception Developmental: life transition events (e.g. graduation from
• Being aware of the hidden emotion college)
• Giving a name to the emotion Existential: inner conflicts and anxieties (e.g. meaningless life)
• Allowing the emotion to be experienced full Environmental: disasters
Catharsis • Realization of what is behind it Medical: diagnosed condition or disability
• Clarifying or defining the problem Psychiatric: syndromes that affect coping, thoughts, or mood
• Steps: Think à Feelà Fear à Summarize Situational: uncommon or situation specific even
• Start with Emotionally Critical Misperception (ECM)
FAMILY ILLNESS TRAJECTORY
• Communicate that you listened and understood
Stage 1: Onset of Illness
• Discuss pathophysiology and pharmacology
Education Stage 2: Impact Phase
o Speak their language
Stage 3: Major Therapeutic Effort
o Dumb it down
Stage 4: Recovery Phase
o Less numbers, statistics
• Diagnose, treatment, follow up
Action • Benefits and risks
Levels of Family Involvement

• Level 1: Minimal emphasis on the family
• Level 2: Information and advice
• Level 3: Feelings and support
• Level 4: Brief focused intervention
• Level 5: Family Therapy
DEALING WITH DIFFICULT PATIENTS

BREAKING THE BAD NEWS
• DESC
SPIKES
o Describe the situation
o Express your feelings • Setting
o Specify the change you want • Perception Check
o Consequences • Invitation
• DISC • Knowledge
o Describe the situation • Empathize
o Indicate problem the behavior is causing • Summary and Strategy
o Specify the change you want ABCDE
o Consequences • Advanced preparation
• HEART • Build a therapeutic environment/ relationship
o Hear them out • Communicate well
o Empathize • Deal with patient and family reactions
o Acknowledge/Apologize • Encourage and validate emotions
o Respond appropriately BREAKS Protocol
o Take responsibility for action/ Thank patient for bearing with inconvenience • Background
• Rapport
GOOD INFORMED CONSENT • Explore
• Disclosure • Announce
• Understanding • Kindling
• Voluntariness • Summarize
• Competence
• Consent

FAMILY ASSESSMENT TOOLS AND STAGES
• The family is the social context in which illnesses occurs and recovery takes place; it is a biological, psychological, and sociocultural unit.
TYPES OF FAMILY
RULES BOUNDARIES ROLES CIRCULAR QUESTIONS
STRUCTURE
Overt: obvious, Clear: negotiable, allows Breadwinner Series questions
Nuclear stated flexibility Caregiver • Explores repetitive behavior
• Parents & children Covert: implied, Rigid: non-negotiable Symptom carrier • When situation A happens, what happens to member
• Two generations not stated Diffuse: over-involvement “Family doctor” 1?
Extended
• Three generations “Who-does-what-and-when”
• Unilaterally (maternal • Explore roles
or paternal) or • When someone gets sick in the family, who do you
bilaterally extended usually go to first?
Single Parent • When that person does not know what to do, who does
• Children (<18 years) he consult?
living with one • When the patient has to be admitted to the hospital,
guardian whose permission must be obtained?
Blended
• Step-children and/or “Closer-farther”
step-parents • Explores emotional closeness and distance
Communal • Who is closest to the patient? Next closest? Farthest
• Groups formed for (emotionally)?
specific
ideological/societal “Who-agrees-with-whom”
purposes • Elicits coalitions
• Bounded by beliefs • Who in the family usually agrees/disagrees with the
patient?

SCREEM
SCREEM Resources Pathology
Assess the family’s ability to cope with crises and
provide health care Family is socially isolated from
Social Evident social interaction
Identifies which resources are helpful or pathologic outside
Relationships of health behavior, practices and utilization Feelings of cultural inferiority or
Cultural Cultural pride
of health services shame
SCREEM Family Resources Survey (SCREEM-RES) Satisfying spiritual
Religion Rigid and limiting dogma or rituals
12-item family resource questionnaire experience
Scoring Able to meet financial
Economic Unable to meet financial demands
3: strongly agree; 2: agree; 1: disagree; 0: strongly demands
disagree Adequate education
Interpretation Education allowing comprehension Unable to comprehend the problem
13-18: adequate family resources of problems
7-12: moderately inadequate
0-6: severely in adequate
Available and accessible
Medical No access or underutilized
medical care
FAMILY APGAR APGAR

• 5-item questionnaire to assess family function Adaptability Share inherent resources
• Measures individual satisfaction with family relationships based Partnership
on five parameters
Scoring: Growth Emotional and physical
0: hardly ever; 1: some of the time; 2: almost always Freedom to change
Interpretation Affection Interaction
8-10: highly functional; 4-7: moderately Emotional interaction
dysfunctional; 0-3: severely dysfunctional Resolve Sharing time with one another
Family Map Family Genogram

Male members to the left
Index patient with arrow or enclosed in the same shape
Always indicate name and age
Always put a legend for diseases
Members of a household are enclosed within a solid line
Include the date the genogram was generated

OTHER ASSESSMENT TOOLS
ECOMAP
Snapshot of the patient within his/her family and social environment at a particular point in time
Draw-a-family test (DRAFT)
Interpretation done by child psychologist
Family Lifeline
Significant events among family members over a period of time in a chronological sequence
Allows exploration of certain family issues
Family Circle
Circles depicting the relationship of the family
FAMILY LIFE CYCLE
Age Freud’s Stages of Psychosexual Development Erickson’s Psychosocial Stages

Infancy (0 – 1.5 years) Oral Basic trust vs Mistrust
Toddler (1.5 – 3 years) Anal Autonomy vs Shame
Preschool (3 – 6 years) Phallic Initiative vs Guilt
School age (6 – 12 years) Latency Industry vs Inferiority
Adolescence (12 – 21 years) Adolescence Identity vs Role Diffusion
Early Adult (21 – 40 years) Early Adult Intimacy vs Isolation
Middle Age (40 – 65 years) Middle Age Generativity vs Stagnation
Old Age (>65 years) Old Age or Senescence Integrity vs Despair
Two levels of order change

First order change (“Need to do”)
Change in the mastery and adaptation in a skill; no change in family structure
Second order change (“Need to be”)
Change in role, his status and meaning; change in role identities; happens between stages
Each stage has an Emotional Process of Transition (EPT) to struggle with
Stage in the Family

EPT Second Order Change Health Issues
Life Cycle
Proper nutrition
Accepting emotional and financial responsibility for Differentiation of self from family origin
1. The Unattached Physical fitness
self Development of intimate peer relationships
Young Adult Safe sex practice
Parent–offspring separation Establishment of self in work
2. The Newly Formation of marital system Pregnancy
Commitment to new system
Married Couple Inclusion of spouse Childbirth
Make space for children and taking on parental roles
Joining childrearing, financial, and household tasks Childhood illnesses
3. The Family with
Accepting new members into the system Inclusion of parenting and grand-parenting roles Focus on immunization
Young Children
Realignment of relationships to include extended families and preventive health
Problem of boundaries
Stress brought about
Shifting of parent–child relationship by gender identity and
4. The Family with Increasing flexibility of family boundaries to include Midlife marital and career issues sexual orientation
Adolescents children’s independence and grandparent’s frailties Caring for elders Peer pressure that may
Vulnerability for the couple lead to drug use and
smoking
Renegotiation of marital system as a dyad
Hypertension, heart
Adult to adult relationships between parent and grown
5. The Launching Accepting a multitude of exits from and entries into diseases, menopause,
child
Family the family system osteoporosis, weight
Inclusion of in-laws and grandchildren in the family
problems, etc.
Disabilities of parents and death of grandparents
Maintaining own and couple function and interest
More central role of middle generation
Chronic illness,
6. The Family in Accepting the shift of generational roles (senior Wisdom and experience of the elderly
degenerative
Later Life citizen) Dealing with loss of spouse, siblings, and other peers;
conditions, debility
preparing for own death
Life review and integration
MOTIVATING BEHAVIOR CHANGE

MOTIVATIONAL COUNSELING
• Both patient-centered and strategic (directive)
• Focuses on “why” change before “how”
THE HEALTH BELIEF MODEL

• Based on the following sequence of events for behavior change to occur:
o The person must believe that his or her health is in jeopardy
o The person must perceive the potential seriousness of the condition
o The person must believe that benefits stemming from the healthy behavior outweigh the costs and are indeed within their grasp
o There must be a “cue to action” or precipitating force that makes the person feel the need to take action
ATTITUDINAL PRINCIPLES IN MOTIVATIONAL COUNSELING

• Express empathy
• Ask about ambivalence
• Avoid argumentation
• Roll of resistance
• Support self-confidence

PUBLIC HEALTH AND RESEARCH
STUDY DESIGN
• Detailed description of how a study is being conducted Descriptive Analytical
• Methodology that is used to investigate a particular health phenomenon, exposure-disease Answers how many, whom Use two groups for
relationship when, & where comparison
• A specific plan or protocol for conducting the study, which allows the investigator to translate Amount of occurrence of Determine whether risk of
the conceptual hypothesis into an operational one disease and its distribution disease is different between
• For identifying variation in exposed and not exposed
CLINICAL RESEARCH disease occurrence Basis of hypothesis testing
• More general term; research conducted involving human subjects Secondary data
• Clinical trials (part of scope of clinical research) Observational studies Intervention studies
o Assigns human subjects to intervention and use of comparison/control groups to • Natural course of events, • Clinical trial, experiment
establish cause-effect relationship (between intervention and outcome) then compare • Investigator controls
• Randomized control clinical trial • Types: allocation of exposure
o Gold standard and is still the best study design with the advantage of establishing
Cross sectional • Most powerful
Case control epidemiologic strategy
causality.
Cohort • Most expensive to conduct
o Placebo is used as a control treatment. It could be No treatment + Placebo or Best
• Strongest evidence for
standard care + Placebo.
testing a hypothesis
• Observational Studies
Cross Sectional Case Control Cohort

“Snapshot”, single point in time; fastest “Backward studies; EXPOSURE à Outcome
OUTCOME à Exposure/s Begins with exposure then outcome.
Begins with outcome, then determine
exposure Types:
Prospective (frequent outcomes)
Exposure has occurred
Retrospective (rare outcomes)
Both exposure and disease have occurred
Quicker, less expensive
Choice for prevalence surveys Choice for multiple exposures, rare Choice for multiple outcomes,
Weakest to prove association diseases or rare outcomes Prospective cohort: for accurate
Use: Hypothesis Generation assessment of exposure and confounding factors
Retrospective cohort: for stability of
exposure status over time (i.e. diet)
TYPES OF ERROR MEASURES OF ASSOCIATION
TRUTH • Calculations used to measure disease frequency relative to other factors

• Cohort study: Relative Risk (RR)
Treatments do
STUDY RESULTS Treatments differ o RR is an estimate of magnitude of association between exposure and disease
not differ
o RR > 1: positive association: exposure is considered as a risk factor for the disease
Correct / True Type 1 error / o RR < 1: negative association, exposure is considered as a protective factor for the
Treatments differ positive False Positive disease
Alpha level o RR =1: no association between exposure and disease
Type 2 error / Correct / True
Treatments do
False negative negative
not differ
Beta level
TYPES OF QUESTIONS
• Case-control study: Odds Ratio (OR)
Background Question Foreground Question • OR > 1: positive association; exposure Is considered as a risk factor for the disease
Asks for basic information or Ask about decisions and • OR <1: negative association; exposure is considered a protective factor for the
general knowledge of actions related to patient care disease
disease, disease process, • OR = 1: no association between exposure and disease
tests, treatment, etc.
Has two components: Has four components

• Root (what, how) • P: Population/ Problem
• Verb (causes, • I: Intervention
prevention) • C: Co-intervention
• O: Outcome
• M: Method


CLINICAL TRIALS: PHASES
Summary of Phases I-IV in Clinical Trials. The duration of each phase increases as you go further, as well as the number of patients. Phase 1 is usually non-
randomized. It is during Phase 3 where it is randomized.
LEVELS OF PREVENTION
Level Tools Objectives

Establish or
Target social and
maintain conditions
Primordial economic policies
to minimize
effecting health
hazards to health
Removal/ reduction Avoiding onset of
Primary
of risk factor disease
Early detection/ Improving
Secondary
Screening prognosis
Treatment of Prevent
Tertiary
existing illness deterioration

MODULE/TOPIC 2 CLINICAL SKILLS
VITAL SIGNS
PROCEDURE
HEART RATE (HR) / PULSE RATE (PR) SIZE AND POSITIONING OF THE CUFF
• Count the heart rate/pulse rate for 1 minute • Cuff size (adults) = 5-inch cuff
• Alternatively, count for 15 or 30 sec then multiply by 4 or 2, respectively • Cuff size (children 2-5 years) = 3-inch cuff
o Use only if there’s time restraint or in patients with no cardiac • Position: Lower edge of cuff is ½ inch (or 2 fingers) above antecubital fossa
problems • Wrap the cuff around the arm (2 fingers under the cuff should be a snug fit)
o HR: Apex beat (Left 5th ICS, 7– 9cm from MSL)
o PR: Radial (most commonly used), brachial, common carotid,
femoral, popliteal, posterior tibial, or dorsalis pedis
Diastolic
Normal (Adult) 60 to 100 bpm JNC 7 2017 Systolic(mmHg)
(mmHg)
Tachycardia > 100 bpm Normal Normal <120 and <80
Bradycardia < 60 bpm Pre-HPN Elevated BP 120-129 and <80
Stage 1 HPN 130-139 or 80-90
RESPIRATORY RATE (RR) Stage 1 HPN Stage 2 HPN 140-180 or 90-120
• Look for rise and fall of their shoulders, for movements of clothes, or for Hypertensive
flaring of nostrils. Crisis and/
Stage 2 HNP >180 >120
o Do not tell your patient that you will count respiratory rate! (consult doctor or
o Observe the rate, rhythm, depth, and effort of breathing immediately)
Normal (adult) 12 to 20 breaths/minute JNC 8 UPDATES

Normal (newborn) 40 breaths/minute • In adults ≥ 60 years, pharmacologic treatment should be initiated when these
thresholds are reached:
BODY TEMPERATURE o Systole ≥ 150 mmHg OR
o Diastole ≥ 90 mmHg
Normal • In adults < 60 years, pharmacologic thresholds are:
Oral 37.0°C (or 98.6°F) o Systole ≥ 140 mmHg OR
Rectal 37.7°C (or 99.6°F)
• In persons ≥ 18 years with CKD or DM, thresholds are:
Aural (Ear) 37.7°C (or 99.6°F)
o Systole ≥ 140 mmHg OR
Axillary (Armpit) 36.3°C (or 97.6°F)
Fever
• In the general, nonblack population (including DM px), first line drugs are:
Low Grade 38-39°C (or 100.4-102.2°F) o Thiazide diuretics (e.g. Hydrochlorothiazide)
Moderate Grade 39-40°C (or 102.2-104.0°F) o CCB (e.g.
High Grade 40-42°C (or 104.0-107.6°F) o ACE inhibitors
Hyperpyrexia >42°C (or >107.6°F) o ARB
• In the general, black population (including DM px), first line drugs are:
BLOOD PRESSURE (BP) o Thiazide diuretic
• Make sure patient is rested and has not smoked or had caffeine 30 o CCB
minutes before the BP is measured • Adults with CKD and HPN:
• Position the arm so that the antecubital crease is at heart level o ACE inhibitor or ARB as initial therapy (moderate evidence that these drugs
• Choose the right cuff and position it on the arm which should be free of improve kidney-related outcomes)
clothing • If target BP (below threshold) is not reached within 1 month:
• Obtain palpatory BP first o Increase dosage of initial drug OR
o Palpate the radial pulse o Add a second drug (do not combine ACE inhibitor with ARB)
o Inflate the cuff until the radial pulse cannot be palpated anymore. o Third drug should be added as necessary
Note the corresponding pressure.
• Deflate the cuff and wait for 15 – 30 seconds SUMMARY OF REPORTING VITAL SIGNS
• Obtain auscultatory BP
o Place the bell of the stethoscope at the brachial artery HR/PR ___ beats per minute
o Inflate the cuff at 20 – 30 mmHg on top of the palpatory BP RR ___ breaths per minute
o Release pressure slowly Temperature ___ °C
• Note the pressure at which the Korotkoff sounds appear (systolic BP ___ /___ mmHg
pressure) and the pressure when it disappears (diastolic pressure)
WEIGHT MEASUREMENT
WEIGHT-HIP RATIO
Formula: Waist Circumference (WC) /Hip Circumference (HC)
IDEAL BODY WEIGHT

BMI
2 Male: 50 kg + 2.3 kg x (height in inches - 60)
BMI = weight (kg)/height (m)
Female: 45.5 kg + 2.3 kg x (height in inches - 60)
INCREASED RISK OF CO-MORBIDITIES – ASIANS
Classification Europe/US Asia Pacific

Measurement Male Female
Underweight <18.5 <18.5
Normal 18.5-24.9 18.5-22.9
Waist Circumference > 35 > 31
Overweight 25-29.9 23-24.9
Obesity Class I 30-34.9 25-29.9
Waist-Hip Ratio > 0.95 > 0.80
Obesity Class III >40

PRESCRIPTION WRITING
PARTS EXAMPLE NOTES
Patient Information Juan dela Cruz
• Name 8 y/o
• Age M
• Sex Pasig City
• Address of the patient April 1, 2011
• Date of visit 26 kg
• Weight (more crucial in pediatric patients)
PARTS EXAMPLE NOTES
Superscription Rx Which means “take thou”
Inscription Paracetamol Drug information
• Name of medicine (Biogesic)
o Generic name 250 mg, 0.5 g
o Brand name Tablet, Suspension, IV, IM
• Strength
• Drug formulation
Subscription Dispense #24 capsules Instructions to the pharmacist:

• Quantity to be dispensed Dispense #3 (three) vials, non-refillable For controlled substances, write in numbers and letters
• Any special compounding instructions
Signa, Signatura, Transcription Sig Instructions for the patient:

• Route of administration Oral (Chew, swallow whole) “Signa”, meaning mark or label
• Number of dosage units per dose Nasal (Spray __ on both nostrils)
• Frequency of dosing Vaginal/ Rectal (Insert __ suppositories in the
• Duration of dosing vaginal area/anus)
• Purpose of medication Topical (Apply in affected area) SAMPLE PRESCRIPTION
• Special instructions Ophthalmic (Instill __ drops/ointment)
o Warnings or adverse effects (if necessary) Inhalational (Take __ puffs)
Take 1 tablet
Give 2 teaspoonful
Every four hours
Twice a day
For 7 days
If needed for pain
For asthma
For pain
Shake well
Refrigerate
Avoid driving after intake because the medicine
may cause sleepiness
Prescriber Information
• Name of prescriber
• Clinic Address
• Contact Information
• Signature
• License Number
• Professional Tax Receipt (PTR) Number
• S2 License Number (if applicable)
Other notes: Always write clearly. Do not use “As directed”. Avoid abbreviations and dangerous dose expressions. Do not make any changes or cross outs! Sign
your name as if it were a legal document. Never pre-sign a blank prescription.
IMAGING MODALITIES
CT (COMPUTED TOMOGRAPHY) MAGNETIC RESONANCE
X-RAY ULTRASOUND
SCAN IMAGING (MRI)
Uses electromagnetic waves with Uses high frequency sound (3-15 Uses a special kind of X-ray + Uses magnetic and radiowaves
-10
shorter wavelength (10 m) that hit mHz) which bounces off tissues computer to form an image emitted by tissues to form images of
radiographic plate internal structures
Radiopaque Hyperdense
Bright Bright Hyperechoic Bright Bright Hyperintense
Opacity or Density Hyperattenuating
Hypodense
Dark Hypoechoic Dark Dark Hypointense
Hypoattenuating
Radiolucent
Dark Similar to
Lucency Isoechoic Similar to Similar to
structure Isodense Isointense
structure structure
Black Anechoic
From most radiolucent to • Safe for pregnant patients • Less expensive than MRI • More expensive than CT
radiopaque: Air – Fat/Liver – • Shorter time to complete than MRI • Longer time to complete
Water/Blood – Bone – • Better bony structure details than • Patients may feel claustrophobic
Contrast/Barium – Heavy MRI • Better soft tissue imaging than
metals/Lead CT
• Safe for pregnant patients
POSITRON EMISSION
FLUOROSCOPY BONE SCAN MAMMOGRAPHY
TOMOGRAPHY (PET) SCAN
Uses electromagnetic waves to Type of nuclear medicine imaging that Uses a radioactive substance to Uses electromagnetic waves to
obtain real-time moving images to uses radioactive tracers diagnose and assess bone metabolism or to take images of the breast from
assess structure and function. determine disease severity. determine if bone metastasis has different angles.
occurred.

PERIPHERAL BLOOD SMEAR
Used to evaluate RBCS, WBS, and platelets, and to determine their relative concentrations in the blood.
SIZE SHAPE COLOR ABNORMAL RBC STRUCTURES
Anisocytosis Variation in Poikilocytosis Variation in RBC Pale, insufficient Nucleated Immature form of RBCs
RBC size shape Hypochromic amount of RBCs
(e.g. anemia) hemoglobin Reticulocytes
Macrocytosis Large RBCs Elliptocytes Elliptical-shaped With greater Iron granules visualized
(e.g. RBCs (e.g. than normal Siderocytes, with Prussian blue dye
Hyperchromic
megaloblastic hereditary concentration of Sideroblasts (e.g. sideroblastic
anemia) elliptocytosis) hemoglobin anemia)
Microcytosis Small RBCs Rouleaux Stack-of-coins Abnormal aggregation of
Basophilic
(e.g. IDA, appearance (e.g. ribosomes
stippling
thalassemia) multiple myeloma)
Sickle Cells Crescent-shaped Large inclusion bodies
(e.g. sickle cell visualized with crystal
Heinz bodies
anemia) violet (e.g. G6PD
deficiency)
Target Cells Usually seen in those Normal color
Normochromic
with inherited
hemoglobinopathies
(e.g. thalassemia) DNA remnants inside
Howell-Jolly
Dacrocytes Teardrop-shaped RBC (e.g. sickle cell
bodies
(e.g. myelofibrosis) anemia)
Spherocytes Sphere-shaped (e.g.
hereditary
spherocytosis)
ELECTOCARDIOGRAM (ECG)
QUICK REVIEW
PHYSIOLOGICAL PACEMAKERS OF THE HEART PRECORDIAL LEADS
Primary pacemaker of the heart; group of cells on V1 – 4th ICS, right parasternum
the wall of the right atrium which spontaneously V2– 4th ICS, left parasternum
Sinoatrial (SA) Node
depolarizes, resulting in contraction at ~60-100bpm V3– midway between V2 and V44
(sinus rhythm) V4– 5th ICS, midclavicular line
Secondary pacemaker of the heart; if the SA node V5– 5th ICS, anterior axillary line
Atrioventricular (AV)
fails to function, the AV node will take over at a rate V6– 5th ICS, mid-axillary line
node
of about 40-60bpm (junctional escape rhythm)
If the impulses above the ventricles
(supraventricular impulses) fail to reach the
Ventricular Cells ventricles, the ventricles may fire at a rate of 15-45
bpm called ventricular escape rhythm (wide QRS
complex).
Normal Values of
Wave Cardiac Events
Intervals
Atrial depolarization <0.12 sec
P wave
(up to 3 boxes wide)
Conduction delay through AV node
PR segment Used as baseline to evaluate ST
segment elevation or depression
Atrial depolarization + conduction 0.12 to 0.20 sec
PR interval
delay through AV node (up to 3-5 boxes wide)
Ventricular depolarization <0.11 to 0.12 sec
QRS (up to 3 small boxes
wide)
Isoelectric, ventricles still
ST segment
depolarized
Ventricular depolarization + 0.35 to 0.45 sec
ventricular repolarization;
QT interval
mechanical contraction of the
ventricles
T wave Ventricular repolarization
PROCEDURE

1. Determine the heart rate (in bpm)
• 1500 method
!"##
o Heart rate =
$%&'() +, -&.// -0%.)(- '(12(($ 3 4(.5-
• R-R method: Rule of 300
o Find a QRS where peak R wave falls on a heavy dark (bold) line.
o Use this as reference then take note where the next QRS falls.
o Starting from the reference point, count 300, 150, 100, 75, 60, 50, 43 for every dark line passed until you reach the next QRS peak.
2. Determine rhythm
• P waves are all uniform • Sinus rhythm
Normal sinus rhythm • P waves appear before every QRS complex Sinus tachycardia • Rate equal to or greater than 100 bpm
• P-P and R-R intervals are equal and regular • Normal sinus P waves and PR interval
• R-R interval is regular • Fast rate
• P wave appears before, after, or within QRS Supraventricular tachycardia • Regular rhythm
Junctional rhythm
complex (SVT) • Absent P wave
• QRS complex is narrow • Narrow QRS complex
• R-R interval is regular • Irregular rhythm
Idioventricular rhythm • P waves are absent Atrial Fibrillation • Absent P wave
• QRS complex is wide • Narrow QRS complex
• R-R interval is regular
• Fast rate
• P waves are absent
Pacemaker rhythm • Regular rhythm
• QRS complex is wide Atrial flutter
(ventricular-type) • Present P wave
• Pacemaker spike precedes the wide QRS
• Narrow QRS complex
complex
3. Measure intervals
• See ECG Waves Forms above
4. Determine axis
• Draw this diagram! From your visual view,
o II, III, aVF are inferior (TO the right is “II the right” of aVF)
o aVR and aVL are superior (aVR is on the Left; aVL is on the Right)
• Look at Lead I from the ECG results and determine if it is positive or negative.
o If it is positive cover the left (your visual left) half of your QRS axis
o If it is negative cover the right (your visual right) half of your QRS axis
• Look at AVF and determine if it is positive or negative.
o If it is positive cover the upper half of your QRS
o If it is negative cover the lower half of your QRS
• Since the prior two steps have determined which quadrant the resulting angle will be in, the next
step would be determining which lead is most biphasic.
o If there’s more than one option that’s biphasic, choose the smaller one.
Using that particular lead find the perpendicular angle which is in the isolated quadrant.
NOTES
ECG IN MYOCARDIAL INFARCTION
NORMAL CARDIAC PARAMETERS
• Locating Infarction in MI
Normal Sinus Rhythm Between 60 and 100 bpm Wall Leads Artery
Left Anterior
Sinus bradycardia Less than 60 bpm Anterior V2 to V4
Descending
Left Anterior
Sinus tachycardia Over 100 bpm Anterolateral I, aVL, V3 to V6
Descending
Left Anterior
RELATIONSHIP OF ECG TO HEART SURFACES Septal V1 to V2
Descending
Inferior II, III and aVF Right Coronary Artery
Lateral I, aVF, V5 to V6 Left Circumflex Artery
Posterior V1 to V2 Right Coronary Artery
STEMI VS NON-STEMI
Non-STEMI (Non ST-

STEMI (ST-segment
segment elevation MI,
elevation MI, transmural MI)
subendocardial MI)
Chest pain, nausea, Chest pain, nausea,
History vomiting, sweating and vomiting, sweating and
breathing difficulty breathing difficulty
Cardiac Troponin I and T, CK are Troponin I and T, CK are
Markers elevated elevated
ST-segment elevation (due ST-segment depression, T-
ECG to a full thickness injury of wave inversion or both
the heart muscle) and later maybe present. This is due
progresses to a pathologic to the partial thickness injury
Q wave. of the heart muscle and
May also have T-wave does not progress to a Q
inversion wave.
Interpretation Angle Examples
Normal -30˚ to +90˚
+270˚ to 330˚ (-90˚ to -
L axis deviation Inferior wall MI
30˚)
R axis deviation +90˚ to +180˚ Antero Lateral wall MI
R axis extreme/ +180˚ to +270 (180 to -
indeterminate axis 90˚)
PHLEBOTOMY, ERYTHROCYTE SEDIMENTATION RATE (ESR), WHITE BLOOD CELL (WBC) COUNT
PHLEBOTOMY
PROCEDURE OTHER NOTES
TIP for OSCE! Memorize steps, explain every step and its rationale while doing the procedure. Hemolysis – breaking of RBC membranes releasing free Hbg into the
circulating blood, leading to inaccurate results
Introduce yourself. Ask for patient’s name. Hemoconcentration – pooling of the blood at the venipuncture site which can
Explain the procedure. Position the patient comfortably. cause falsely elevated results
Assemble equipment and supplies (test tubes, tourniquet,
preparation for cleansing the area and syringes). Wear gloves. To prevent hemolysis of blood
Ask patient to make a fist without pumping the hand. samples:
Choose suitable vein. • Use larger needles (≤ 21 gauge) –
o Preferred: Median cubital and cephalic veins reduce stress and/or turbulence for
Cleanse the site with 70% isopropyl alcohol solution. Begin at the RBCs
puncture site and cleanse outward in circular motion. Air dry. • Avoid trauma and excessive
Apply tourniquet few inches above the site. Never leave it in place probing during venipuncture
for > 1 minute. • Avoid drawing plunger back too
o To prevent hemolysis or hemoconcentration forcefully or too fast as this will
Insert needle, 15°angle, bevel up. cause the vein to collapse
Wait for blood to pool, then begin to aspirate. • Avoid tourniquet time < 1 minute –
Release tourniquet first, withdraw the needle and recap. Apply can constrict blood vessels and
pressure with cotton. cause hemolysis
Ask the volunteer to relax the fist, then apply tape over the wound. • Mix tubes gently at least 6 times
Put blood in the lavender colored-top test tube (with EDTA as
anticoagulant). Thoroughly mix by gently inverting the tube at least 6
times (do not shake), careful not to cause bubbles.
Label: Patient’s complete name, age, date of collection.
Put the test tube in the test tube rack.
Dispose the needle in the “sharps” disposal unit. Dispose the used
cotton, syringe and gloves in a yellow disposal container.
BLOOD COLLECTION TUBES

* Those in bold are the more commonly used tubes
TUBE TOP ADDITIVE MECHANISM USES
Chemistries
Immunology and Serology (HIV, Hepa,
Blood clots. Serum is separated by
Red None antibody testing)
centrifugation.
Blood bank (Crossmatch)
**When you need SERUM
Serum separator tube (SST) contains a Chemistries
Gold None gel at the bottom to separate blood from Immunology and Serology
serum on centrifugation **When you need SERUM
Plasma separating tube Anticoagulates with lithium heparin.
Light Green (PST) with Lithium Plasma is separated with PST gel at the Chemistries
heparin bottom of the tube.
Hematology (CBC)
Blood Bank (Crossmatch)
Purple EDTA Forms calcium salts to remove calcium *Requires full draw – invert 8 times to prevent
clotting
**When you need WHOLE BLOOD
Coagulation tests (PT, PTT)
Light Blue Sodium citrate Forms calcium salts to remove calcium
*Requires full draw
Lithium level – use Sodium heparin
Sodium heparin or
Green Inactivates thrombin and thromboplastin Ammonia level – use Sodium or Lithium
lithium heparin
heparin
Trace element testing (Zn, Cu, Pb, Hg)
Dark Blue EDTA Contains no contaminating metals
Toxicology
Sodium fluoride Antiglycolytic preserves glucose up to 5 GLUCOSE (Fasting, 2 hour glucose)
Light gray
Potassium oxalate days *Requires full draw

HLA tissue typing
Acid-citrate-dextrose
Yellow Complement inactivation Paternity testing
(ACD)
DNA studies
Yellow-Black Broth mixture Preserves viability of microorganisms Microbiology (aerobes, anaerobes, fungi)
ERYTHROCYTE SEDIMENTATION RATE
Sodium citrate
Black Forms calcium salts to remove calcium (ESR)
(buffered)
*Requires full draw
Orange Thrombin Quickly clots blood STAT serum chemistries
Inactivates thrombin and thromboplastin

Light brown Sodium heparin Serum lead determination
No lead
Pink Potassium EDTA Forms calcium salts Immunohematology
Molecular/ PCR
White Potassium EDTA Forms calcium salts
bDNA testing
ERYTHROCYTE SEDIMENTATION RATE (ESR)

PROCEDURE RATIONALE and INTERPRETATION
WESTERGREN METHOD • Reveals inflammatory activity in your body
• Determines rate at which erythrocytes fall to the bottom of a vertical tube of • When anticoagulated whole blood is allowed to stand in a narrow test tube,
anticoagulated blood within a specific period RBCs gradually settle out from the plasma because:
o RBC’s repel each other due to negative charges on the surface
1. Remove cover of lavender colored test tube. o Large surface area-to-volume ratio of normal RBCs resist settling
2. Insert the Westergren tube (vacuette tube) into the test tube touching the • When an inflammatory activity is present
bottom. Avoid bubbles. o RBC’s stick to each other (rouleaux formation) due to high fibrinogen in
3. Place tube in a rack in a vertical position. Note time and room temperature. the blood
4. After one hour, read the level at which cells have settled on the descending o This causes settling to occur faster
scale. • Increased ESR
o Anemia, RF, thyroid malfunction, kidney disease, arthritis, pregnancy,
cancers, body-wide infection
• Decreased ESR
o Hyperviscosity, hypofibrinogenemia, congestive heart failure, sickle cell
anemia, polycythemia, low plasma protein
REPORTING OF RESULTS
Erythrocyte Sedimentation Rate (ESR) = ___ mm per hour
NORMAL VALUES
Males: ESR = 0 – 15 mm/hr
Females: ESR = 0 – 20 mm/hr
WHITE BLOOD CELL DIFFERENTATION COUNT

PROCEDURE RATIONALE and INTERPRETATION
1. Blood smear is examined under a microscope. Count each type of WBC until WBC Differentiation Count
you reach 100. • Assesses the ability of the body to respond to and eliminate infection
2. Determine the percentage of each type.
WBC
NORMAL VALUES • Increased in (Leukocytosis)
o Infectious diseases, inflammatory diseases (e.g. RA, allergy), leukemia,
Neutrophils 40% – 60% severe stress, tissue damage (e.g. burns)
Lymphocytes 20% – 40% • Decreased in (Leukopenia)
Monocytes 2% - 8% o Bone marrow failure, presence of cytotoxic substances, collagen-vascular
Eosinophil 1% - 4% diseases (e.g. lupus), liver or spleen diseases, radiation
Basophil 0.5% - 1%
WBC Description Causes for Increase
Neutrophil • Lightly staining • Bacterial infection
granules • Inflammatory
• Multi-lobed nucleus disease
connected by thin
strands of chromatin
Eosinophil • Large, pink • Allergic disorders,

(acidophilic), course • Inflammation of the
granules skin
• Bilobed connected by • Parasitic infections
a band of nuclear
material
Basophil • Large numerous blue- • Leukemia

purple granules • Chronic
• Granules contain inflammation
heparin and histamine • Hypersensitivity
• Same function as reaction
mast cells in releasing • Radiation therapy
histamine
Lymphocyte • Agranular • Viral infection
• Large, deeply staining • Leukemia
(dark purple) nucleus • Cancer of the bone
• Thin rim of blue marrow
cytoplasm • Radiation therapy

Monocyte • Agranular • Infection of all
• Very large kidney or kinds
bean-shaped nucleus • Inflammatory
• Abundant, light blue disorders
cytoplasm
CLOTTING TIME AND BLEEDING TEST

QUICK REVIEW
Hemostasis: a complex series of processes by which the body stops the loss or COAGULATION TESTS
leakage of blood if an injury should occur while keeping the circulation blood in a • Diagnose coagulopathies
fluid state. • Monitor patients on anticoagulation therapy
• Evaluation of blood clotting status prior to surgery
3 PHASES
1. Vascular platelet phase à Primary Hemostasis MNEMONIC
2. Coagulation cascade à Fibrin Clot Formation PET à PT for Extrinsic Pathway
3. Control Mechanisms à limits clot formation PITT à PTT for Intrinsic Pathway
WEPT àWarfarin acts on extrinsic pathway, prothrombin time
5 STAGES OF COAGULATION PROCESS used to check it.
1. Vasoconstriction Heparin acts on intrinsic pathway, partial thromboplastin time is
2. Platelet plug formation used to check it.
3. Fibrin clot formation
4. Clot retractions
5. Fibrinolysis
CLOTTING FACTORS
I Fibrinogen VIII Antihemophilic factor A

II Prothrombin IX Antihemophilic factor B or
Christmas factor
III Tissue factor X Stuart-Prower factor
IV Calcium XI Plasma thromboplastin
antecedent
V Proaccelerin, Labile factor XII Hageman factor
VI Unassigned – Old name of XIII Fibrin-stabilizing factor
Factor Va
VII Stable factor, proconvertin
Mnemonic: "Foolish People Try Climbing Long Slopes After Christmas, Some
People Have Fallen"
1972: Factors 10, 9, 7 & 2 à Vitamin K dependent
GENERAL STEPS FOR FINGER PRICK
1. Collect supplies.
2. Position the non-dominant hand palm-side up. Choose whichever finger is least calloused, usually the middle or ring finger.
3. Apply intermittent pressure to the finger to help the blood flow.
4. Clean the fingertip with 70% alcohol. Start in the middle and work outward to prevent contaminating the area. Allow the area to dry.
5. Hold the finger and firmly place a new sterile lancet off-center on the fingertip.
6. Firmly press the lancet to puncture the fingertip (approximately 2-3 mm deep).
7. Wipe away the first drop of blood with a sterile gauze pad or cotton ball.
8. Collect the specimen.
9. Apply a gauze pad or cotton ball to the puncture site until the bleeding stops.
CLOTTING TIME
PROCEDURE RATIONALE AND INTERPRETATION
Clotting Time: screening test to measure all stages in the intrinsic coagulation system • Normal: 7-180 seconds
and monitor heparin therapy, measures the time it takes for the coagulation system to form • Prolongation may be indicative of abnormalities
the solid clot.
Whole Blood Clotting Time Measurement
1. Start the stopwatch at the beginning of the bleeding. Do not press on the area so that
blood can freely bleed from the wound.
2. Place two separate large drops (approximately 4-5 mm diameter) of blood on a clean
glass slide.
3. Draw a pin through the center of the first drop at 30-seconds interval.
4. As soon as the pin can pull a fibrin thread, coagulation has taken place.
5. Check with the second drop on the slide to see if coagulation has taken place.
6. Stop the timer. Record the time of coagulation of both the first and the second drops of
blood. Report the time of coagulation of the second drop as the final result if the time is
longer than the first drop.
BLEEDING TIME
Bleeding Time: evaluates the vascular and platelet factors in terms of blood clot formation • Normal: 2-8 minutes
After performing the general method, • Platelet dysfunction: 9-15 minutes
Bleeding Time Measurement • Critical: >15 minutes (test must be discontinued or pressure
1. Start the timer. Blot the blood drop on the finger using a filter paper every 30 seconds. Do must be applied)
not allow the filter paper to touch the wound. • Abnormalities arise when the platelet count is low or platelets are
2. When bleeding ceases, stop the watch and record the bleeding time. dysfunctional àHereditary vs. Acquired

ACTIVATED PARTIAL THROMBOPLASTIN TIME
Activated Partial Thromboplastin Time: measures deficiencies of among the following • The clotting time for the APTT lies between 28-38 seconds
factors: XII, XI, IX, VIII, X, V, II (prothrombin) and I (fibrinogen) as well as prekallikrein • aPTT can be normal with mild deficiencies of these clotting
(PK) and high molecular weight kininogen (HK) factors
Steps • aPTT > 70 seconds à spontaneous bleeding
1. Platelet poor plasma [PPP] is incubated at 37°C
2. Phospholipid (cephalin) and a contact activator (e.g. Kaolin) is added followed by the
calcium (all pre-warmed to 37°C)
3. Addition of calcium initiates clotting and timing begins
4. The APTT is the time taken for a fibrin clot to form
5. Initial incubation times may vary from 2-10 minutes
PROTHROMBIN TIME
Prothrombin Time: evaluates the coagulation factors VII, X, V, II and I (fibrinogen) • Normal range for PT: 10-13 seconds
Steps • Abnormal prothrombin time (PT) alone: Factor VII defects
1. Tissue thromboplastin (animal-derived or recombinant) and patient plasma are incubated
for several minutes
2. The plasma is then recalcified by the addition of 30 mM CaCl2
3. The time required for clot formation is then measured
THROMBIN TIME
Thrombin Time: evaluates the level and function of fibrinogen • The Thrombin time will, in general be prolonged when functional
Steps fibrinogen levels are <1.0 g/L
1. Human thrombin (or bovine thrombin) is added to platelet poor plasma at 37°C and the • Prolonged thrombin time may indicate decreased fibrinogen
time taken for the formation of a fibrin clot recorded. level (hypofibrinogenemia or afibrinogemia) and/or
2. Recalcification of the plasma is not necessary abnormal fibrinogen function (dysfibrinogenemia)
• Normal range for thrombin time: 14-16 seconds
FECAL OCCULT BLOOD TEST

PROCEDURE RATIONALE AND INTEPRETATION
Materials: container with specimen, specimen collection tube (with blue and red Fecal Occult Blood Test
caps), test device • One evaluate and screen GI diseases or malignancies
• Rapid chromatographic immunoassay for the qualitative detection of human
1. Collect feces in a clean, dry specimen collection container. occult blood in feces
2. Unscrew the BLUE cap of the specimen collection tube. Transfer specimen • Principle
from the container by stabbing the specimen collection in at least 3 different o On the test line of the region, the membrane is coated with anti-Hbg
sites (Stab, do not scoop!). antibody
o Stool specimen reacts with the particle coated with the anti-Hbg antibody
o Mixture migrates upward on the membrane chromatographically by
capillary action and reacts with anti-Hbg antibody. A colored line is
generated.
• Limitations
o Indicate presence of fecal occult blood, not necessarily indicate colorectal
bleeding
Should not be a conclusive evidence for GI bleeding/pathology
3. Screw the blue cap of the specimen collection tube. Shake the specimen
collection tube vigorously to mix the specimen and extraction buffer until turbid.
RESULTS
4. Remove the test device from the pouch. Do not touch the membrane of the
strip.
Two distinct colored lines: one line in the control line region
5. Invert and hold the specimen collection tube upright and unscrew the RED cap Positive
(C), and one line in the test line region (T)
of the specimen collection tube.
6. Transfer 2 full drops to the specimen well of the test device. Start the timer. One colored line in the control line region (C). No apparent
Negative
7. Read result in 5 minutes, not beyond 10 minutes. colored line appears in the test line region (T)
8. Discard wastes in proper containers. Invalid No colored line in the control line region (C)
SEMEN (SPERM) ANALYSIS

COLLECTION NORMAL VALUES
Semen Analysis – measures the amount of semen a man produces; determines pH = alkaline
the number and quality of sperm in the semen sample Liquefaction time: 30 mins to 1 hour
Collection is by masturbation maintained at body temperature and brought to the GRADING OF SPERM MOTILITY BASED ON WHO CRITERIA
laboratory within one hour of ejaculation. Time of collection must be reported. If
liquefied, time of liquefaction must also be reported. Grade WHO criteria
4.0 a Rapid, straight-line mobility
1. Describe the specimen – color, odor, viscosity b Slower speed, some lateral
2. Estimate volume. 3.0
movement
3. Estimate and grade the motility. b Slow speed forward
• Place petroleum jelly on two opposite edges of the cover slip 2.0 progression, noticeable lateral
• Put a drop of liquefied semen on center of the cover slip movement
• Turn over cover slip upside down and rest on center of the microscope slide 1.0 c No forward progression
• With HPO, estimate the number of motile sperm per 200 sperms seen using 0 d No movement
this formula: Motility = [Number of motile sperms x 100] / 200
• Using the WHO Criteria, grade the quality of motility of the sperms Parameter Reference Ranges
examined. (Use 2 gradings, e.g. 3.0 / b)
Color Gray-white
4. Sperm count: Draw liquefied semen up to 0.5 mark of WBC pipette
Odor Musty
• Aspirate cold water up to the 11 mark
Viscosity Pours in droplets
• Mix, discard 3-5 drops
Volume 2-5mL/ejaculate
• Charge counting chamber (hemocytometer)
• Count the sperm cells in the 4 corner and center squares of the large center Motility >50% Grade 2.0 after 1 hour
square (RBC counting area) >20 million/mL
Sperm Count
• Calculate the total sperm count using the formula below: >40 million/ejaculate
>14% normal forms (routine)
Morphology
>30% normal forms (strict)

o When using 1:20 dilution and counting 5 RBC squares in large center
square:
§ Sperm concentration/mL = number of sperm counted (5 squares)
x 1,000,000
§ Total sperm count per ejaculate = sperm concentration x
specimen volume
5. Identify sperm morphology
• Make a smear of liquefied semen on a glass slide
• Air dry
• Stain using safranin. Expose the specimen to the stain for two minutes
• Examine 200 sperms under HPO
• Estimate percentage of abnormal forms
ABG ANALYSIS
*Note: for YL6 OSCE, what is important to know is until Step 4 anion gap only
Conditions that decrease RR (hypoventilation), and thus arterial CO is high 2
Expect • Inhibited medullary respiratory center such as in intake of opiates, anesthetics, sedatives, CNS lesions
Respiratory • Muscle weakness (either muscle or nerve dysfunction) as in Myasthenia gravis crisis, GBS, spinal cord
Acidosis in injury
• Upper airway obstruction (acute or chronic) as in aspiration, obstructive sleep apnea, laryngospasm
• Pulmonary Capillary Gas Exchange Disorder such as in ARDS, severe asthma, pneumonia, COPD
Conditions that increase RR (hyperventilation), and thus arterial CO is low

Expect 2
• Hypoxemia such as pneumonia, interstitial fibrosis, emboli, edema, CHF, anemia, high altitude residence
Respiratory
• Direct stimulation of medullary respiratory center as in psychogenic/voluntary hyperventilation, hepatic
Alkalosis in
failure, post-correction of metabolic acidosis, pregnancy, neurologic disorders (pontine tumor,
cerebrovascular accident)
STEP 1: Identify the acid-
base disorder anticipated Conditions that decrease HCO in the body or increase H+ (mnemonic: MUDPILES)
3
-
based from patient's history, • Methanol

identify the possible problems • Uremia
in acid-base balance. Expect Metabolic • Diabetic ketoacidosis
Acidosis in • Paraldehyde
• Isoniazid and other Ingestions
• Lactic acidosis
• Ethylene glycol, Ethanol
• Salicylic acid
Conditions that increase HCO in the body or decrease H+

3
-
Expect Metabolic • GI hydrogen loss such as in vomiting, nasogastric suction, chloride-losing diarrhea, antacid therapy
Alkalosis in • Renal hydrogen loss such as in use of diuretics, mineralocorticoid excess, hypokalemia, refeeding
• Bicarbonate administration
• Contraction alkalosis such as in use of diuretics, gastric losses, sweat losses in cystic fibrosis
• Normal range: 7.37-7.43

STEP 2: Look at the pH, does
o May either mean an absence of any acid-base disorder or indicate a mixed acid-base disorder
it indicate acidemia or
• Acidemia <7.37
alkalemia?
• Alkalemia >7.43
Normal P CO : 36-44 (middle: 40)
a 2
Normal HCO : 22-26 (middle: 24)

3
-
STEP 3: What is the primary

acid-base disorder? Mnemonic: SMOR (Same metabolic, opposite respiratory)
Look at the pH and P CO ; if both go the same direction, then it is metabolic. Conversely, if they go in different directions, it is
a 2
respiratory.
Compute for the expected compensatory response first.
STEP 4: Is it a simple or
mixed acid-base disorder?
What is the anion gap?
Simple: actual value of HCO or P CO is within the computed expected range and the anion gap is not high
3
-
a 2
Mixed: actual level is lower or higher than the computed range of compensation
Reference range for anion gap: 3-11 mEq/L

Anion gap = [Na ] – [Cl ] – [HCO ]
+ -
3
-
A high anion gap always indicates metabolic acidosis
No need to master yet but you can also compute for the delta ratio if there is high anion gap. It just helps identify any underlying
acid-base disorders (i.e. if there is high anion gap with or without metabolic alkalosis or non-anion gap metabolic acidosis).
P O in mmHg= FiO x 713 – (P CO /0.8)
A 2 2 a 2
A-a gradient in mmHg = P O - P O

STEP 5: If hypercapnic, A 2 a 2
Expected A-a gradient for age = (Age/4) + 4

calculate for A-a gradient.
High A-a gradient: consider V/Q mismatch, shunt, alveolar hyperventilation
Normal A-a gradient: consider hypoventilation, low FiO state, chest wall disorder, metabolic alkalosis
2

STEP 6: State your complete
interpretation of the ABG
results, including possible
etiologies of all detected
STEP 7: State your plan of
care
PREGNANCY TEST
PROCEDURE NOTES
Urine Sample Requirements: Early morning urine (more concentrated hCG, Positive • 2 distinct colored lines appear
more accurate), clean-catch midstream, contaminant free or clean container • Any shade of color in the test line (T) should be considered
Steps: positive
1. Collect urine sample. Negative • 1 colored line appears in the control line (C).
2. Remove test kit from sealed pouch and label it with patient’s name. • No colored line appears in the test line region
3. Place test device on a clean and level surface. Invalid Control line (C) fails to appear
4. Hold the dropper vertically and transfer 3 full drops of urine to the specimen
well (S) of the test device, and then start the timer. Avoid trapping air bubbles
in the specimen well.
5. Wait for colored line(s) to appear. The result should be read at 3 minutes.
6. Repeat using the unknown.
RATIONALE SAMPLE RESULTS
BASIS: Detection of Human chorionic gonadotropin (hCG) in urine as produced
by the placenta.
HOME KIT: (what we used)
• Detects limits of about 50 mIU/mL
• Detect elevated urine hCG levels several days afer or shortly after first missed
menses
• Rapid one step visual test for quantitative detection of hCG in urine to aid the
early detection of pregnancy, monitoring of “high-risk” pregnancies, and
a tumor marker for certain cancers.
URINALYSIS
PROCEDURE INTERPRETATION
SAMPLE COLLECTION
Urinalysis ACCEPTABLE SAMPLE
A diagnostic, physical, chemical and microscopic examination of a urine sample • > 10mL of freshly, voided, clean, midstream catch, random urine
(specimen), which is obtained through voiding or catheterization. • Ideal is early morning, when urine is more concentrated
SAMPLE COLLECTION
1. Collect random fresh urine sample. Label with name, date, and time of
collection.
o Stable at room temperature 22-24°C for 1 hour, or refrigerated at 4-6°C for 4
hours.
2. Pour a small sample into a clear test tube, if used for testing.
SPECIMEN EVALUATION
Specimen Evaluation (-) Contamination, sufficient amount, recently
Acceptable
• Look for contamination. Check if urine is red, cloudy or looks unusual. Check voided
unusual odor. Unacceptable (+) Contamination, insufficient amount
PHYSICAL/GROSS EXAMINATION
Physical Examination Components Examples
• Observe color, clarity, and odor. Measure specific gravity by use of urinometer, Color Straw (1), light yellow, yellow, dark yellow,
refractometer or reagent strip. amber (7)
Clarity Clear, hazy, slightly cloudy, cloudy, turbid
Odor Aromatic, ammoniacal
Specific Gravity
CHEMICAL EXAMINATION
A. Reagent Strip Method Components Units
Reagent strips consist of chemical impregnated-absorbent pads attached to a Specific gravity
plastic strip. A color producing chemical reaction takes place when the absorbent pH
pad comes in contact with the urine Leukocytes (Leuko/uL)
Blood/Hemoglobin (Ery/uL)
1. Get one reagent strip. Do not touch reagent pads. Compare color on reagent Nitrite -/+/++
strip to that of normal standard (shown on the canister). Ketones (mg/dL)
2. Dip the reagent strip briefly into urine sample. Remove excess urine by touching
Bilirubin (-/+/++/+++)
the edge of the strip to the container.
Urobilinogen (mg/dL)
3. Compare the color reaction of the strip to the color chart (shown on the canister).
Proteins (mg/dL)
4. Read immediately and record.
Glucose (mg/dL)
B. Glucose Assay: Benedict’s Copper Reduction Test Benedict’s Copper Reduction Test
Glucose and some other sugars reduce copper Negative Clear blue
sulfate (CuSO4) to cuprous oxide (Cu2O) in the Positive
presence of alkali and heat. Trace Green without precipitate
1+ Green, with yellow precipitate
1. Put 2.5 mL of Benedict’s solution in a test 2+ Yellow, with yellow precipitate
tube. 3+ Orange, with yellow precipitate
2. Add 4-5 drops of urine. Mix. 4+ Rust color precipitate
3. Water bath at boiling point for 2 minutes.
C. Protein Assay: Heat and Acetic Acid Test Heat and Acetic Acid Test
Denaturing of proteins by heat. Precipitation occurs and acids augment coagulation Negative No cloudiness
or clumping. Persistent cloudiness indicates the
Positive
presence of protein
1. Put 2.5 mL of urine in test tube. 1+ Diffuse cloud
2. Add few drops of 30% acetic acid. 2+ Granular cloud
3. Heat upper portion of test tube for 2 minutes. 3+ Distinct flocculation
4. If a cloudy precipitate forms, add more drops of acid. Heat again. 4+ Large flocculation
5. Observe if cloudiness persists.
MICROSCOPIC EXAMINATION
MICROSCOPIC EXAMINATION REPORTING
Subdued light is needed to delineate the more translucent formed elements of Blood cells = # per HPF
urine such as cells, casts, and crystals. Casts = # per LPF
Quantity = rare, few, moderate, plenty, TNTC (too numerous to count)
1. Transfer 3mL of urine into a test tube. Centrifuge.
2. Pour off supernatant fluid by quickly inverting tube over sink.
3. Mix sediment by flicking the end of the tube with finger.
4. Place a drop on a microscope slide. Place cover slip.
5. Scan under LPO. Identify and count under HPO.
CRYSTALS
CELLS • May be seen in the urinary sediment of healthy patients but not all the time
• Indicates: Presence of raw materials for the formation of kidney stones
Cells and Images Interpretation Image Morphology
Leukocytes Calcium oxalate dihydrate crystals
• Bipyramidal
Normal Values
• Colorless squares
• Men: >2 WBC/hpf
• In patients with hypercalcemia
• Women: >5 WBC/hpf
and hypercalciuria, in
hyperparathyroidism, diffuse bone
disease, sarcoidosis
Epithelial cells • Normal, but in small amounts
Calcium oxalate monohydrate
Squamous epithelial cells
crystals
• Contamination and poor catch

• Biconcave ovals
• Large, irregularly-shaped; small
• “Dumbbell” form
nucleus, fine granular cytoplasm
• Same as above
Transitional epithelial cells Calcium phosphate
• Normal
• Smaller, rounder; larger nuclei
Renal tubular epithelial cells Triple phosphate (struvite) crystals
• Magnesium, ammonium,
phosphate
• Renal pathology • Rectangular-shaped
• “Coffin lid”
• Infections converting urea to
ammonia
Uric acid crystals

Erythrocytes
• Flat, square plates

• Dysmorphic erythrocytes (grain- • Teardrop-shaped
like shape): Glomerular disease • Red-orange
• Hyperuricemia such as gout,
leukemia
Bacteria
• Gram staining: G (-) rods, Staph,
Ammonium urate (or biurate) crystals
Strep
• Classic diagnostic criterion for
asymptomatic bacteriuria
(compatible with a UTI) = 5
bacteria/hpf represents
roughly100,000 colony-forming
units (CFU) per mL
Mucus thread
Cysteine crystals
• Flat, hexagonal plates

• “Sparkle”
• Lemon-yellow
\

Yeast Cells Tyrosine crystals
CASTS
SUMMARY OF REPORTING OF RESULTS
The predominant cellular elements determine the type of cast
Type of cast Composition Associated Conditions PHYSICAL
Color
Hyaline
• Pyelonephritis Odor
Mucoproteins • Chronic renal disease Transparency
• May be a normal finding Specific Gravity
CHEMICAL
pH
Glucose
Erythrocyte
• Glomerulonephritis Protein
• May be a normal finding MICROSCOPIC
RBC
in patients who play Pus cells
contact sports RBCs
Casts
Epithelial cells
Crystals
Leukocyte • Pyelonephritis
• Glomerulonephritis
WBC • Interstitial nephritis
• Renal inflammatory
processes
• Acute tubular necrosis
• Interstitial nephritis
Epithelial • Eclampsia
• Nephritic syndrome
Renal tubule cells
• Allograft rejection
• Heavy metal ingestion
• Renal disease
Granular
• Advanced renal
Various cell types
disease
Waxy
Various cell types Advanced renal disease
Fatty
Nephritic syndrome
Lipid-laden renal
Renal disease
tubule cells
Hypothyroidism
Broad
Various cell types End-stage renal disease

MODULE/TOPIC 3 RADIOLOGY
HEMATOLOGY
Imaging Patterns Description Pathology
• Diploic space is
markedly widened due
to marrow hyperplasia
Hair on end Thalassemia
and the trabecula is
oriented perpendicularly
to the inner table
(Left) Lateral skull x-ray shows classic hair on end appearance.

(Right) Lateral MRI of the skull.
• Medullary expansion of
the ribs, scapula, and
Rib within a rib Thalassemia
clavicles
• Chest shape is deformed
Chest CT showing rib within a rib sign.
• Triphalangeal thumb
• X-ray anomalies may
Triphalangeal also consist of an absent
thumb and Bifid radius, small ulna, and Fanconi Anemia
Digit an extramedullary digit
• Associated with
horseshoe kidneys
Radiograph of a hand showing the triphalangeal thumb (left) and bifid digit (right)
seen in Fanconi Anemia.
• Numerous well-
circumscribed lytic bone
lesions appear as
Rain Drop Skull Multiple Myeloma
punched-out lucencies
producing a “rain drop
skull”
Lateral skull x-ray showing a “rain drop skull.”

ENDOCRINOLOGY
• Prominent
subendplate densities
at multiple contiguous
vertebral levels
Rugger Jersey • Produce an alternating
Hyperparathyroidism
Sign sclerotic-lucent-
sclerotic appearance,
resembling the
horizontal stripes of a
rugby jersey
Rugger jersey spine on lateral view.
• Multiple tiny well-

defined lucencies in
Salt and Pepper
the calvaria caused by Hyperparathyroidism
Sign
resorption of
trabecular bone
Salt and pepper sign on lateral view of the skull.
NEUROLOGY
• Associated with skull

fractures in 90-95%
• Subperiosteal –
between the skull and
the dura
• Does not cross Epidural Hematoma
sutures (hemorrhage
is limited to its parent
bone)
• Lentiform or
biconvex appearance
Axial CT scan of the brain showing epidural hematoma. Hypodense coloration of

Types of the hematoma on the left denotes acute onset.
Hemorrhages
• Between the dura and

the arachnoid space
• Crosses sutures but
Subdural Hematoma
not dural
attachments
• Crescent-shaped
Axial CT scan of the brain showing subdural hematoma. Hyperdense coloration

denotes a chronic onset.

NEUROLOGY
• Presents with a
thunderclap
headache
• Sulcal/cisternal
hyperdensity
• Most commonly this is
Subarachnoid Hemorrhage
apparent around
the circle of Willis, on
account of the majority
of berry aneurysms
occurring in this
region
Axial CT scan of the brain showing subarachnoid hematoma. Hyperattenuating

material is seen filling the subarachnoid space
• Accumulation of blood
in the parenchyma of
the brain
• Hypertensive
hemorrhages are Intraparenchymal/Intracerebral
usually found in the Hemorrhage
subcortical area of the
putamen, basal
ganglia, and lentiform
nucleus
Axial non-contrast CT scans of hypertensive hemorrhage in the basal ganglia (red
arrows).
• Radiologic sign of
enhanced
demyelinating plaques
Dawson’s
through the corpus Multiple Sclerosis
Fingers
callosum
• Often appears due to
multiple sclerosis
Sagittal MRI showing Dawson’s fingers in demyelinating disease.
• CT
o May have normal
findings
o Hyperdense artery
Coronal CT scan of the brain shows an insular ribbon that is not clearly visible sign – ill-defined
Acute Ischemic Stroke
compared to the left side (yellow arrow)(left) and a dense middle cerebral artery hypodensity
(MCA) due to presence of an acute thrombus (right). indicating a
Hyperdense *as infarcts progress from acute
thrombosed artery
Artery and to chronic, area of infarct
o Loss of insular
Insular Ribbon becomes increasingly
ribbon – due to loss
Sign hypodense, mass effect and
of grey-white matter
edema increases, and sulci
distinction
widens
• MRI
o More sensitive for
hyperacute and
acute infarcts
Axial MRI of the brain reveals a high signal intensity lesion in the right MCA area
(white arrow)(left). Magnetic resonance angiography (MRA) shows total occlusion of
the right MCA (right).
• A region of
hyperdensity can be
seen
Popcorn-like
• Reticulated or Cavernous Angioma
Lesions
heterogeneous signal
with dark hemosiderin
rim (on T2WI)
Axial non-contrast CT (left) and axial MRI of a cavernous angioma.

NEUROLOGY
• Often an incidental
finding
• Medusa-like/stellate
collection of dilated
medullary veins
• “Touch me not” lesion
Medusa-
o Not removed due to
like/Stellate Venous Angioma
adherence of brain
Lesion
parenchyma to
lesion
• Most common brain
vascular
Sagittal MRI of trigonal cavernoma with a developmental venous anomaly. malformation found
at autopsy
• Most common extra-

axial neoplasm in
adults
• Dural-based
Dural Tail Sign Meningioma
enhancing mass with
cortical buckling and
trapped CSF
clefts/cortical vessels
Axial (left) and sagittal (right) MRI of Meningioma.

• Most common
primary brain
neoplasm
• Most malignant
astrocytoma
• Thick, irregular-
enhancing ring of
Butterfly
neoplastic tissue Glioblastoma Multiforme
Glioma
around a necrotic
core
• Irregular, hypointense
at the center with
hyperintense margins
Coronal T1-weighted MRI of glioblastoma. invading the frontal
lobes
HEENT
Imaging Patterns Description Anatomy/Pathology
• Ice cream - head of the

Ice Cream Cone
malleus Normal Ossicles
Configuration
• Cone – body of incus
Axial CT showing the middle ossicular chain.
• Hamburger sign –
appreciated in a normal
cochlea
• If the cochlea appears
Hamburger Sign Normal Cochlea
globular à Mondini
malformation
• If the cochlea is absent
à Michel’s aplasia
Axial CT showing a globular cochlea (left most), hamburger sign (middle) and aplastic
cochlea (rightmost).

HEENT
Imaging Patterns Description Anatomy/Pathology
• Longitudinal
o Line is parallel to the
long axis of the
petrous bone
o Most common
complications:
ossicular injury,
tympanic membrane
Longitudinal rupture,
Longitudinal and
and Transverse hemotympanum with
Transverse Fracture
Fracture conductive hearing
loss
• Transverse
o Line is perpendicular
to the long axis of the
petrous bone
o More common:
sensorineural hearing
loss

Axial CT showing a longitudinal fracture (left) and transverse fracture (left)).
• Hyperdense
cerebellopontine mass
• Usual symptoms:
tinnitus and
sensorineural hearing
Ice Cream Cone
loss Vestibular Schwannoma
Sign
• Hallmark: expansion of
the internal auditory
canal
• Bilateral in
neurofibromatosis 2
Coronal CT of vestibular schwannoma.
CARDIOVASCULAR
• Raised right
ventricular pressures
o Pulmonary arterial
hypertension
o Cor pulmonale
• Lateral bulging of the
• Valvular disease
right heart border
o Tricuspid
Right Atrial • Length of the right
regurgitation
Enlargement heart border exceeds
o Tricuspid stenosis
50% of the mediastinal
o Ebstein’s anomaly
cardiovascular shadow
• Atrial septal defect
• Atrial fibrillation
• Dilated
cardiomyopathy
PA view of the chest on x-ray showing right atrial enlargement.

• Pulmonary valve
stenosis
• Pulmonary arterial
hypertension
• Atrial septal defect
• Ventricular septal
defect
Right Ventricular • Rounding and
• Tricuspid
Enlargement/Boot- upliftment of the
regurgitation
shaped Heart cardiac apex
• Dilated
cardiomyopathy
• Anomalous
pulmonary venous
drainage
PA view of the chest on x-ray showing right ventricular enlargement. • Tetralogy of Fallot

CARDIOVASCULAR
• Mitral stenosis
• Double density sign • Mitral regurgitation
o Left atrium at the • Left ventricular
back enlarges failure
Left Atrial o Cannot enlarge to the • Left atrial myxoma
Enlargement/Double left because of the • Atrial fibrillation
Density Sign pulmonary artery • Ventricular septal
o Goes to the right, defect
resulting to the • Patent ductus
double density sign arteriosi
PA view of the chest on x-ray showing left atrial enlargement
• Pressure overload
• Hoffman-rigler sign
o Hypertension
o Measured 2 cm
o Aortic stenosis
above the
• Volume overload
intersection of the
o Aortic
diaphragm and IVC
Left Ventricular regurgitation
o From the 2 cm point,
Enlargement/Hoffman- o Mitral
draw a line parallel to
Rigler Sign regurgitation
the posterior
• Wall abnormalities
superior borders
o Left ventricular
o (+) if posterior border
aneurysm
extends more than
o Hypertrophic
1.8 cm
cardiomyopathy
PA view (left) and lateral view (right) of the chest on x-ray showing left ventricular
enlargement.
• Left upper area shows Coarctation of the

Figure of 3 Sign
figure of 3 Aorta
Chest x-ray showing coarctation of the aorta.
• Coarctation causes
dilation of collateral
vessels
• Since they pass
through the Coarctation of the
Rib Notching
intercostals, they bump Aorta
into the ribs as they
enlarge causing rib
notching
• Takes time to develop
Chest x-ray showing rib notching.
• Narrow vascular
Egg-on-a-String pedicle Transposition of the
Appearance • Aorta and pulmonary Great Arteries
artery are lined up
Chest x-ray showing transposition of the great arteries.

CARDIOVASCULAR
• Right atrial prominence

• Marked cardiomegaly
Balloon or Box-
• Decreased vascularity Ebstein’s Anomaly
Shaped Heart
• Atrialization of the right
ventricle
Chest x-ray of Ebstein’s anomaly.
• Snowman:
o The snowman’s
head is formed by
the SVC and
pulmonary vein
Total Anomalous
connected to it via
Snowman Appearance Pulmonary Venous
a vertical vein
Return (TAPVR)
o The body is the
heart
• Type II
(Intracardiac/Cardiac):
most common type
Chest x-ray of type II TAPVR showing a snowman.

• Scimitar sign: a vein
can be seen
descending and
impressing upon the
cardiac shadow
• Type III (Infracardiac)
o Connection is
Total Anomalous
below the
Scimitar Sign Pulmonary Venous
diaphragm (portal
Return (TAPVR)
vein, ductus
venosus, or hepatic
vein)
o Pulmonary edema
o Normal sized heart
o Prominence of the
Chest x-ray of type III TAPVR showing scimitar sign.
right atrium
PULMONOLOGY
• Branching radiolucent
columns of air due to
Air consolidation of surrounding
Bronchogram air spaces Bacterial Pneumonia
Sign • Air space disease that
results in opacified alveoli
and lucent bronchioles
Chest x-ray showing air bronchogram sign. Branching lucencies or non-fielled

air spaces are noted by white arrows.
• If two objects of the same

radiographic density touch
each other, then the edge
between them disappears
Silhouette Sign Bacterial Pneumonia
• Useful in localizing
pneumonia and providing
cues to the causative
organism
Chest x-ray showing middle lobe pneumonia. Right cardiac border is not visualized.

PULMONOLOGY
Hilar • Lymph nodes that have

Tuberculosis
Calcifications calcified
Chest x-ray showing hilar calcifications
• Seen on ultrasound
• Artifacts caused by
interaction of air and water
• Criterion: At least 5 B-lines
B-Lines Pulmonary Edema
in the anterior or posterior
chest wall
• Probe is placed along
intercostal spaces
Chest ultrasound showing B-lines.
• Septal lines seen when

interlobular septa become
Kerley Lines prominent Pulmonary Edema
• Normally lines only reach 2/3
of the way of the lungs
Chest x-ray showing Kerley lines.
Cannonball • Different sized lesions

Metastasis
Sign around the lungs
Chest x-ray showing cannon ball sign.
• Composed of a dilated
bronchus and an
accompanying pulmonary
artery branch
Signet Ring
• The bronchus and artery Bronchiectasis
Sign
should be the same size,
whereas in bronchiectasis,
the bronchus is markedly
dilated
Chest CT showing cylindrical bronchiectasis.
• Indicates a significant
Meniscus Sign Pleural Effusion
amount of fluid in the chest
Chest x-ray showing meniscus sign. Left lower zone area is uniformly white, at the
top of this area is a concave surface representing the meniscus sign.

PULMONOLOGY
• Found between visceral and

parietal pleura
Split Pleura
• Fluid occupies the pleural Pleural Effusion
Sign
cavity, causing the two
layers to split
CT with IV contrast shows enhancement of the thickened inner visceral (dashed

arrows) and outer parietal pleura (solid arrows) with separation by pleural fluid.
• Sign
of pneumomediastinum seen
on neonatal chest
radiographs
• It refers to the thymus being
Angel
outlined by air with each
Wing/Spinnaker Pneumomediastinum
lobe displaced laterally and
Sign
appearing like spinnaker
sails.
• Distinct from the sail
sign appearance of the
normal thymus.
Chest x-ray showing the angel wing or spinnaker sign
GASTROINTESTINAL
• A luminal dilatation that

shows a single, dilated,
gas-filled bowel loop
• An important imaging
sign denoting a
possible upper
Single Bubble gastrointestinal tract Hypertrophic pyloric
Sign obstruction, particularly stenosis
in newborns
• Site of obstruction:
beyond the stomach,
possibly pylorus
• Clinical presentation:
non-bilious vomiting
Single bubble sign in AP and lateral view.
• A luminal dilatation that

shows two air filled
loops in the upper
abdomen with little or
Double Bubble no air density
Duodenal Atresia
Sign • Site of obstruction:
beyond or distal to the
duodenum
bilious vomiting
Double bubble sign in AP view. Duodenum (D) and stomach (S).
• Third bubble is seen due

to filling and distension
of jejunum by air
Triple Bubble
• Site of obstruction: Jejunal Atresia
Sign
beyond the duodenum,
at the jejunal tract or
close to the ileum
Tripple bubble sign in AP view. Stars denote distended stomach, duodenum, and
jejunum.

GASTROINTESTINAL
• Abdominal cavity is
outlined by gas from a
perforated viscus
• Soft tissue outlines are
Football Sign Pneumoperitoneum
seen because of the free
air
• Indicative of air in the
peritoneum
Football sign in AP view.

• Walls of twisted bowel
loops with gas-filled
distended areas
• Coffee bean sign arises
from the pelvis and the
apex can extend up to
level of T10
• If it has a lot of air
Coffee Bean Sigmoid or Cecal
proximal to the area of
Sign Volvulus
twisting, it is most likely
sigmoid
• If there is less air or gas
in the ascending,
transverse, descending
colon, and sigmoid,
most likely the twisted
Coffee bean sign in AP view. The white arrow points to the distinct cleft of the coffee
groove is the cecum
bean representing the opposite walls of the bowel.
• Air fluid levels of

different heights but
within the same loop of
bowel
• Requires an upright view
of the abdominal Small Bowel Obstruction
Air Fluid Levels
radiograph for Ileus
differentiation
• While upright, the air
goes superiorly while
fluid goes inferiorly,
creating horizontal lines
Abdominal radiograph shows dilated small bowel loops containing air fluid levels (small
white arrows).
• Combination of wall
thickening and inward
extension Achalasia
Bird’s Beak/Rat • Shows a dilated Scleroderma
Tail Sign segment of the Esophageal Malignancy
esophagus which tapers Esophageal Stricture
off and abruptly
constricts
Bird’s beak sign on radiograph.
• Esophagus appears like

Presence of erosions or
Copula/Dome a dome
disruption in the wall
Sign • Narrowed and irregular
Neoplasms
lumen

GASTROINTESTINAL
Copula sign on radiograph.
• Barium sulfate is used

as contrast
• Parts or segments that
Cobblestone are not opacified are Infections
Sign indicative of an Crohn’s Disease
obstructed lumen
• Can occur in hollow
organs with mucosa
Cobblestone sign on radiograph
• Appears like a stack of

coins due to wall
disruption
• Also called hide-bound
bowel sign
Scleroderma
• Describes the narrow
Coin Stack Sign Sprue
separation between the
Small bowel hematoma
valvulae conniventes
which are of normal
thickness despite
dilatation of bowel
lumen
Coin stack sign on radiograph.
Congenital
• Lumen is dilated or Diaphargmatic Hernia
bulging accompanied • Bochdalek (hernia on
with an area of left hemithorax, defect
Collar Sign
constriction in posterior diapragm)
• Luminal constriction • Morgagni (hernia on
represents the collar right hemithorax, defect
in anterior diaphragm)
Collar sign on radiograph.
• Seen using barium

enema
• Can represent wall
disruption
Coiled Spring • Ring shadows represent
Instussusception
Sign the reflux of contrast
within the luman
between the walls of the
intussusceptum and
intussuscepiens
Coiled spring sign on radiograph.
• The inner and outer

layers of the target sign
represent the mucosa
and the muscularis
propria and/or serosa, Diseases with
Target Sign respectively submucosal edema,
• The high attenuation is a inflammation, or both
consequence of
contrast enhancement
secondary to the
inflammatory process
Target sign on radiograph.

GASTROINTESTINAL
• Persistent narrowing of
a segment caused by
thickening of the bowel Most common cause:
Apple Core Sign wall annular carcinoma of the
• Can occur in any colon
segment of the intestinal
tract
Apple core sign on radiograph.

• Variation of the target
sign
• Formed by the
mesentery, which was
dragged into the
intussusception
Doughnut Sign • Located only on one Intussusception
side of the bowel and
therefore forms a
crescent that is
echogenic
• Also called the
Donut sign seen on ultrasound.
pseudokidney sign
• Infiltration of the
omental fat by material
Caking Sign of soft-tissue density Metastases
• Hypoechoic segment
looks like a cake
Caking sign on ultrasound.
• Halo sign represents

infiltration of the
submucosa with fat Inflammatory Bowel
Halo Sign
• Halo is formed by the fat Disease
that surrounds the
bowel
Halo sign on CT scan (blue arrow).
• Hypervascular
appearance of the
mesentery in active
Crohn’s disease
Comb Sign • Fibrofatty proliferation Crohn’s Disease
and perivascular
inflammatory infiltration
outline the distended
intestinal arcades
Comb sign on MRI. The spine of the comb is the bowel and the teeth of the comb
is the mesentery.

ORTHOPEDIS AND RHEUMATOLOGY
• Periarticular
osteoporosis
Phemister Triad • Gradual joint space TB Arthritis
narrowing
• Bony erosion
Early case of TB arthritis of the knee on AP view.
• Sharply outlined area of

rarefaction or lucency in
metaphysis surrounded
Brodie’s
by irregular dense Osteomyelitis
Abscess
sclerosis
• Thickened overlying
cortex
Brodie’s abscess on lateral view. Further progression of osteomyelitis can lead

to abscess formation.
• Thickened bone with

Sequstrum and wavy sclerotic cortex
Involucrum and lucent areas Chronic Osteomyelitis
Formation • Medullary cavity may not
be apparent
Sequestrum and involucrum formation. Lucent areas represent sequestrum and

opaque areas represent involucrum.
• Pronounced increase in
Wimberger’s
density peripherally at Scurvy
Ring
the epiphysis
Radiographic appearance of scurvy.
• Also known as cortical

infractions or Milkman
lines
• Wide, transverse
lucencies traversing part
way through a bone,
usually at right angles to
Looser’s Zone the involved cortex Osteomalacia
• Pseudofractures and
considered a type
of insufficiency fracture.
• Typically, the fractures
have sclerotic irregular
margins and are often
symmetrical.
Looser’s zone in AP view.
ORTHOPEDICS
Pathology Appearance on Imaging Description
• Blow on top of the head

Jefferson’s Fracture • Splitting of the C1 ring (atlas)
• Usually >1 site of breakage
CT scan showing C1 splitting at 3 points of failure.
• Better prognosis than Jefferson’s fracture

• Hyperextension and distraction
Hangman’s Fracture
• Fracture of the posterior elements of C2
usually with displacement anterior to C3
Lateral view showing fracture of posterior elements of C2 with subsequent

displacement of C3.
• Fracture of the C6 and C7 spinous process

• Seen very well in lateral view
Clay-Shoveler’s Fracture
• Avulsion of the spinous process by
supraspinous ligament
Lateral view showing fracture of the spinous process of C7.
• Due to extreme hyperflexion

• Unstable fracture
• Compressions of a vertebral body
Flexion-Teardrop Fracture
occasionally with subluxation and disruption
of the posterior ligaments
• Associated with spinal cord injury
Lateral view showing an unstable fracture at the anterior portion of C5
• Most common fracture of the lumbar

spine
• Hyperflexion at the waist
Seatbelt Fracture
• Compression of the vertebral body
• Chance fracture – fracture line extends
through the posterior elements

ORTHOPEDICS
Lateral view showing a seatbelt fracture (red arrow) and chance fracture along the
spinous process (yellow arrow).
• Base of the thumb at the carpometacarpal

Bennett’s Fracture
joint
Bennett’s fracture on radiograph.
• Similar to Bennett’s fracture but it’s

comminuted and extends into the articular
Rolando’s Fracture surface
• Needs surgical management because of
extension into articular surface
Rolando’s fracture on radiograph.
• Avulsion injury at the distal phalanx at the

dorsal surface
Mallet Finger
• Caused by a disrupted extensor digitorum
tendon
Mallet finger with avulsion injury at the distal phalanx.
• Avulsion injury of the ulnar collateral

Gamekeeper’s Thumb ligament at the ulnar side of the 1st MCP
joint
Gamekeeper’s thumb on lateral view.
• Fall on an outstretched hand

Colles’ Fracture • Fracture of distal radius with dorsal
angulation
Colles’ fracture on PA and lateral view.
• Fracture of distal radius with volar

Smith’’s Fracture angulation
Smith’s fracture on lateral view.

ORTHOPEDICS
• Ulnar fracture with dislocation of the radial

Monteggia’s Fracture
head
Monteggia’s fracture on AP view.
• Fracture of radius with dislocation of distal

Galeazzi’s Fracture
ulna
Galeazzi’s fracture on AP view.
• Posterolateral humeral head compression

fracture, typically secondary to
recurrent anterior shoulder dislocations, as
Hill-Sach’s Deformity the humeral head comes to rest against the
anteroinferior part of the glenoid
• Indention of the superolateral portion of
the humeral head
Hill-Sach’s deformity on trans-scapular lateral view.
• Frequently seen in association with Hill-

Sach’s deformity
Bankart Deformity
• Bony irregularity or fragment of the inferior
glenoid
Comparison of Hill-Sach’s and Bankart lesions.
• Also called Lisfranc fracture-dislocations

• Most common type of dislocation involving
Lisfranc’s Fracture-
the foot and correspond to the dislocation of
Dislocation
the articulation of the tarsus with the
metatarsal bases
Comparison of normal Lisfranc joint and displaced Lisfranc joint injury.

NEPHROLOGY
• Absence of one or both

kidneys
• Compensatory Renal Agenesis
hypertrophy of the
opposite kidney
• Most common renal fusion

anomaly
• Occurs in inferior poles
more often than superior
Horseshoe-
poles Horseshoe kidney
shaped
• Fusion of both poles is
called Sigmoid Kidneys
• Increased susceptibility of
trauma and urinary stasis
• Normal Variant
Fetal Lobulations • Incomplete fusion of the
developing renal tubules
• Normal Variant
Splenic
• Presence of prominent
Impression/
focal bulge on the lateral
Dromedary Hump
border of the left kidney
• Double collecting system

• Separate moieties
Bifid Ureters • Incomplete fusion of the Ureteral Duplication
upper and lower moieties
of the collecting system
• Upper pole is obstructed

and enlarged which results
to a non-functioning upper
Pelvic and Ureteral
Drooping Lily Sign pole renal mass effect
Duplication
• Lower opacificed calyces
may be displaced by the
large upper pole mass
• Intravesical dilatation of
Cobra Head/
the ureter immediately
Spring Onion Ureterocoele
proximal to its orifice in the
Appearance
bladder

NEPHROLOGY
Champagne Glass • Ureteral dilatation distal to Transitional Cell

Sign a filling defect Carcinoma
• Outpouching of the distal

Outpouching Ureteral Diverticula
ureters
• Renal calculi forming a

Staghorn-shaped cast of the renal pelvis and Staghorn Calculus
calyces
Hyperdensities or
Hyperechoic with
posterior • Stone within the ureter Ureterolithiasis
shadowing in the
ureter
• Ultrasound: Hyperechoic
Star-shaped focus with shadowing
Cystolithiasis
urolith • CT Scan: May appear as
multiple hyperdensities
• Medical emergency
Gas formation • CT scan as best Emphysematous
around the kidney diagnostic modality: Pyelonephritis
Hypodense
• Ultrasound is imaging of
“Pockets of Air”
choice: hypoechoic or of
around the Perirenal Abscess
mixed echogenicity
kidneys
depending on the content

NEPHROLOGY
• Most common renal mass

• Majority are benign
• Can cause obstruction,
Grape-like
pain and hematuria Renal Cystic Disease
Structures
• Modality of choice:
ultrasound, CT Scan and
MRI
Christmas Tree/ • Bladders become eventually

Pine Cone trabeculated. thick-walled Neurogenic Bladder
appearance and reduced in capacity
GYNECOLOGY
• Two separate uterine

bodies, two separate
Didelphys
cervices and two
vaginal canals
Congenital • Most common

Anomalies • Two horns, one cervix Bicornuate
and one vagina
• Two different horns with

Septate
the same cavity
String of Pearls • Ovaries with multiple

Polycystic Ovary
Appearance follicles
• Benign
• Gray specks inside
Lacy Internal hypoechoic cyst, with Hemorrhagic Functional
Appearance blood inside Ovarian Cyst
sudden pain
Calcification • Fluid-fluid layer

with Acoustic • Calcification: bone, Benign Cystic Teratoma
Shadowing teeth and hair
• Malignant
• Silent killer
• Usually has a bad
prognosis
Ovarian Carcinoma
• Predominantly cystic
(Clear Cell Carcinoma)
• Prominent septations of
irregular thickening and
nodularity
• (+) Vascularity

GYNECOLOGY
• Very engorged tortuous
veins that may lead to
infertility
• One of the most
common findings in
Bag of Worms Varicocele
patients complaining of
infertility and pain on
one side
• Dilated serpiginous
veins
• Near-complete
replacement of the
testis
• Homogeneously Seminoma
hypoechoic mass
• Most common testes
pathology seen in adults

MODULE/TOPIC 4 INFECTIOUS DISEASES
DISEASE CLINICAL PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL NOTES

• Characteristic lesion: • Exposure to HSV at • Clinical diagnosis Mucocutaneous and • HSV-1 is the most
multiple vesicular lesions mucosal surfaces or • Tzanck smear – Visceral HSV common cause of
on an erythematous base abraded skin → entry staining scrapings from Infections sporadic
• Vesicles, pustules, or of the virus into the base of the lesions • Acyclovir, encephalitis
painful erythematous epidermal and dermal with Wright’s, Famciclovir, o Present as
ulcers may be cells → viral Giemsa’s, or Valacyclovir altered mental
simultaneously present replication → infection Papanicolau’s stain o MOA: Inhibit viral status, seizures,
of sensory or o Multinucleated replication by and/or aphasia
Oral autonomic nerve giant cells, or interfering with • Viral meningitis
• Gingivostomatits and endings viral nucleic acid
Herpesvirus Cowdry more common with
pharyngitis (most • Latency occurs in the type A inclusion synthesis HSV-2
common manifestation of ganglionic cells in the bodies o Do not eradicate
first episode HSV-1 region of the initial the virus, but
infection; most common infection control and
among children & young shorten the
adults) duration of
• Recurrent herpes labialis symptoms
(most common
manifestation of HSV-1
reactivation)
Genital
• Mostly secondary to HSV-
2 infection
• HSV-1 (rectal and perianal
Herpes infections)
Simplex • Widely-spaced bilateral
lesions
• Fever, headache, malaise,
myalgia
• Pain, itching, dysuria,
vaginal and urethral
discharge
• Tender lymphadenopathy
Eye
• HSV keratitis
• Most common cause of
corneal blindness in the
US
• Acute pain, blurred vision,
chemosis, conjunctivitis,
and characteristic dendritic
lesions on the cornea
HSV encephalitis
Finger
• Herpetic Whitlow –
complication of a primary
oral or genital herpes by
inoculation through a break
in the epidermal surface
• Generally self-limiting • Benign: Types 1, 2, 4, • Biopsy – to determine • Observation – • HPV Vaccine
o Regressing 7 neoplastic changes warts (except (Cervarix and
spontaneously within 6 • High-risk: Types 16, • In situ hybridization or anogenital warts) Gardasil)
months - 2 years 18, 31, 33, 45 polymerase chain may resolve within o 3 shots over 6
• Typical Wart or Verruca o 16 & 18 – major risk reaction – for viral 1 to 2 years months
Vulgaris factors for typing (most sensitive • Non-Genital Warts o Cervarix protects
o Sessile, dome-shaped, squamous cell & specific) o Cryotherapy against types 16
~1cm diameter, carcinoma of the • HPV Test – presence with liquid & 18
hyperkeratotic surface cervix, anus, vulva, of cervical cancer nitrogen (most o Gardasil protects
with small filamentous penis (especially in o Pap smear useful and against types 6,
projections immunocompromis • Colposcope – to convenient) 11, 16, & 18
• Typical Plantar Warts ed individuals) assess vaginal and o Keratolytic • All kids from 11 or
o Endophytic w/ thick • Oncogenic potential is cervical lesions Agents (e.g. 12 can be
keratin cover related to viral genes Salicylic acid vaccinated up until
• Flat Warts or Verruca E6 & E7 – inactivate plasters or 26 y/o
Plana tumor suppressors, solutions) for
Human
o Slightly elevated with activate cyclins, inhibit non-genital
Papilloma
velvety surface apoptosis, and warts
Virus - Warts
o Most common in combat cellular • Genital Warts:
children senescence o Podophyllin
• Filiform Warts o HPV infection alone Solution – in-
o Papillomatous lesions is not sufficient, office
with narrow base must have application;
o Seen on face, neck, skin interaction w/ associated with
folds cigarette smoking, local reactions
• Condyloma Acuminata or other infections, o Topical
Genital Warts dietary deficiencies, Imiquimod –
o Soft, tan, cauliflower-like hormones inducer of
mass, may reach several • Transmission: cytokine release
centimeters in diameter direct contact with Laser Procedures –
o 90% caused by HPV 16 individuals or auto- for recalcitrant warts
& 18 inoculation
o Women: labia,
perineum, perianal skin;

vaginal mucosa, urethra,
anus
• Men: coronal sulcus, shaft
of the penis (most common
if circumcised), scrotum,
perianal skin, urethra
• Benign and self-limited • Epstein-Barr Virus Heterophile Test • Supportive • Most common in
• Sx for 2-4 wks but malaise (EBV), family • (+) in 40% during the Measures early childhood,
and difficulty concentrating Herpesviridae first week of illness o Rest with a second peak
can persist for months • Transmission: Close • (+) in 80-90% during o Analgesia during late
contact, including the third week • Avoid excessive adolescence
Symptoms
saliva, blood, or • Antibodies are not physical activity • Persistence of EBV
• Prodrome of fatigue, venereal transmission detectable in children during first month in a small
malaise, myalgia for 1-2
• Virus infects the <5 y/o, elderly, and to reduce population of
weeks before onset of possibility of latently infected
epithelium of the patients w/ atypical
fever symptoms splenic rupture cells can result in
oropharynx and
• Headache salivary glands; B • Defined as the greatest • Prednisone – 40- late reactivation and
• Abdominal pain, nausea or serum dilution that 60 mg/d for 2-3 B cell proliferation
cells in underlying
vomiting agglutinates sheep days (taper over 1- • Immune system
lymphoid tissues as
• Chills well RBCs 2 weeks) inactivation is the
Signs • Virus binds to CD21 o Prevent airway key to EBV-related
• Lymphadenopathy usually on B cells, which is EBV-specific Antibody obstruction in oncogenenesis:
affecting posterior cervical also the receptor for Test patients with o Burkitt lymphoma
nodes complement C3d • Used in: severe tonsillar o B-cell
• Pharyngitis, most receptor o Patients with hypertrophy lymphomas
common sign, can be o In a minority of suspected acute o Autoimmune o Hodgkin
accompanied by infected B cells, EBV infection who hemolytic lymphoma
enlargement of tonsils with EBV has a lack heterophile anemia o Nasopharyngeal
Infectious
an exudate resembling that productive lytic antibodies o Severe CA
Mononucleosi
of streptococcal infection o Patients with thrombocytopeni
s
pharyngitis o In most cells, it atypical infections a
• Hepatosplenomegaly establishes a latent • Vaccines directed
• Morbilliform rash on the infection that can PCR against the major
arms or trunk induce B cell • Detect EBV DNA in EBV glycoprotein
• Periorbital edema proliferation as CSF of some AIDS reduce the
• Palatal enanthem well as production patients with frequency of the
• Jaundice of non-specific lymphomas infection
antibodies • Monitor amount of EBV
Clinical Findings Per Age DNA in blood of
Grp patients with
• Infants & Young Children lymphoproliferative
o Asymptomatic or mild disease
pharyngitis (with or
without tonsillitis)
• Adolescents
o Incubation period ~4-6
weeks
• Elderly
o Nonspecific symptoms
(prolonged fever,
fatigue, myalgia,
malaise)
• Rash – progresses in • Incubation Period: • Characteristic skin Immunologically • Histologically, the
multiple waves o 10 – 21 days lesions for both Competent lesions appear as a
centrifugally: torso → o Averages 14 – 17 varicella and herpes • Avoiding blister with
head → extremities days zoster are diagnostic complications (i.e. intranuclear
• Affects mucus • Aerosols → for the disease good hygiene, inclusions of
membranes, skin, and hematogenous • History of recent meticulous skin epithelial cells
Acute neurons dissemination exposure for varicella care) • Patients are
Varicella • Low-grade fever, malaise • Infects neurons can strengthen • Symptomatic infectious ~48
Zoster • Hallmark: skin lesions and/or satellite cells suspicion Treatment: hours before onset
Infection o Macropapules, vesicles, in dorsal root • PCR may be o Antipruritic drugs of vesicular rash
(Chickenpox) and scabs in various ganglion conducted to confirm and tepid water • Most common
stages of evolution diagnosis and rule out baths for pruritus infectious
o Severity varies per any possible o Analgesics for complication is
person differentials the neuritis secondary
caused by bacterial
herpes zoster superinfection
o Acyclovir,
• Intense pain, burning, • Sporadic disease that • Occurs at all ages
Valacyclovir, or
itching (due to continuous results from the but incidence rates
Famciclovir to
radiculoneuritis) limited to reactivation of latent are highest from the
limit the extent
an entire dermatome VZV from dorsal root 6th decade
• Unilateral vesicular ganglia onwards
Immunologically
dermatomal eruption, • Recurrent herpes
Compromised zoster is
Latent associated with severe
pain • Low-risk: Oral exceedingly rare
Varicella
Valacycolovir and except in
Zoster o Most common: T3 to L3
Famciclovir immunocompromis
Infection o If ophthalmic branch of
trigeminal nerve is • High-risk: IV ed hosts
(Shingles)
Acyclovir • Most debilitating
involved, zoster
ophthalmicus complication: post-
o If external auditory canal herpetic neuralgia
is affected, Ramsay
Hunt syndrome
o Pain precedes lesions

• Mildest of common viral • Rubella virus, Acquired Rubella • No specific • Causes mild
exanthems Togaviridae • Clinical diagnosis of treatment disease in children
• Self- limiting o Single-stranded rubella is difficult • Symptomatic but serious
RNA, 50 to 70 nm, o Many viral infections treatment for fever congenital disease
Acquired Rubella enveloped produce similar & arthralgia (a ToRCHeS
• Mild generalized • Transmission: symptoms • Prevention: infection)
maculopapular rash on respiratory droplets o Varied clinical o Childhood • Congenital rubella
the face which spreads to presentations immunization findings include
the trunk & limbs (fades Acquired Rubella • Nucleic Acid with rubella “blueberry muffin”
after 3 days) • Initial viral replication Detection vaccine appearance due to
• (+) occipital and post in nasopharynx → o RT- PCR or • IV immune globulin dermal
auricular multiplication in molecular analysis of does not prevent extramedullary
lymphadenopathy, joint cervical lymph nodes throat swabs infection after hematopoiesis
pains, headache, → subsequent viremia • Isolation & exposure
conjunctivitis (day 7-9 until day 13- identification of virus
• Older children: 1-5 day 15 when rash appear) • Serology
Rubella prodrome (fever, malaise, o Hemagglutination
(German upper respiratory Congenital Rubella (standard)
Measles) symptoms) Syndrome o ELISA
• Incubation period: 14 days • Rubella infection o Detection of IgG is
during pregnancy → evidence of
Congenital Rubella infection of placenta & immunity
Syndrome fetus → deranged and
• Classic triad hypoplastic organ Congenital Rubella
o Sensorineural development → Syndrome
deafness (most structural anomalies • Clinical diagnosis is
• Can result in fetal reasonable when infant
common defect)
death & spontaneous presents with the
o Eye abnormalities
abortion classic triad
(cataracts)
o Congenital heart
disease (PDA)
• Thrombocytopenia with
purpura or petechiae
• Low birth weight
• Highly contagious disease • Measles virus, • Clinical diagnosis • Supportive • Host immune
• Prodromal illness: fever, Morbillivirus, • CDC requirements measures – responses to
malaise followed by 3 C’s Paromyxoviridae o Generalized hydration and measles virus are
cough, coryza, o Spherical, maculopapular antipyretics essential for viral
conjunctivitis nonsegmented, rash of at least 3 • Prompt antibiotic clearance, clinical
• Generalized maculopapular single-stranded days treatment if w/ recovery, and the
rash RNA o Fever of at least bacterial infection establishment of
• Headache, abdominal • Transmission: 38.3˚C (101˚F) • Vitamin A reduces long-term immunity
pain, vomiting, diarrhea, respiratory droplets o Cough, coryza, or the rate of
myalgia • Incubation Period: conjunctivitis morbidity and
• Pathognomonic: Koplik’s ~10 days to fever and • Serology – detection mortality
Rubeola spots 14 days to rash onset of measles virus-
o Bluish white dots ~1mm • Virus is deposited on specific IgM in single Prevention
(Measles) • Passive
in diameter surrounded epithelial cells in the specimen of
by erythema mucosa → proliferates serum/oral fluid is immunization –
o Appear first on the in respiratory mucosa diagnostic human
buccal mucosa → draining lymph immunoglobulin
opposite the lower nodes → blood stream given shortly after
molars but rapidly via infected exposure
increase in number to monocytes • Active
involve the entire immunization –
mucosa first vaccination
between 6-15
months
• Zoonotic, almost always • Bullet-shaped • Skin biopsy • Pre-exposure • Survival is rare:

fatal disease Lyssavirus virion o RT-PCR prophylaxis: for <1%
• Prodromal: 2-10 days from family o Immunofluorescen individuals who are • All warm blooded
o Nonspecific symptoms: Rhabdovirus ce staining for viral at high risk for animals are
Malaise, anorexia, • Transmission: bite of antigen rabies exposure susceptible
headache, photophobia, infected animals • Isolation of virus from o 3 doses of rabies • Very high
sore throat, and low • Incubation period: 1- saliva vaccine IM days susceptibility: foxes,
grade fever 3 months, but can o RT-PCR 0, 7, and 21 or wolves, cotton
o Paresthesias radiating range from several • Anti-rabies antibodies 28 rates, coyotes
from site of bite: days to years after in serum or CSF • Post-exposure • High: hamsters,
Tingling, pain, exposure o Immunofluorescen prophylaxis: rabies raccoons, cats,
tenderness, burning, • Virus enters through ce vaccine with or bats, rabbits, cattle
numbness animal bite.Virus o Virus neutralization without rabies IG • Moderate: dogs,
Rabies
• Clinical rabies: Infection multiplies near the site assays • Proper wound care sheep, goats,
can evolve into two forms of inoculation in • Postmortem: (thorough washing horses, nonhuman
(encephalitic or paralytic) muscles and Examining brainstem with soap and primates
o Encephalitic: More connective tissues and neural tissues water) • Low: possums
common • Virus then transports directly
§ Fever, hydrophobia, in a retrograde o Definitive: Negri
pharyngeal spasms direction through PNS bodies (eosinophilic
(due to aerophobia), then to the CNS. neuronal
hyperactivity cytoplasmic
subsiding to paralysis, inclusions)
hypersalivation,
lacrimation, agitation,
coma, and death

o Paralytic rabies
§ Flaccid paralysis,
fasciculations around
bitten limb, nuchal
rigidity, headache,
dense paraplegia,
loss of sphincter tone,
paralysis of muscles
of respiration and
deglutition, death
• Atypical presentation in bat
bites: long incubation
period, paralytic rabies,
choreiform movements of
bitten limb, myoclonus,
seizures sensory or motor
deficits
• Break-bone Fever: fever, • Dengue virus, • Dengue serologic test • Symptomatic & • Four Serotypes
frontal headache, retro- Flaviviridae, Flavivirus (detection of viral supportive o DENV-1 to 4
orbital pain, back pain, • Transmission: antigen NS1) o Bed rest & mild o Type 2 is more
severe myalgia bite of an infected • Complete blood analgesic- dangerous
• Day 1-7: transient mosquito (primarily count: leukopenia, antipyretic
maculopapular rash, Aedes aegypti) thrombocytopenia, o Acetaminophen
lymphadenopathy, palatal • Incubation Period: elevated serum for treatment of
vesicles, scleral injection, 4 – 7 days aminotransferase pain and fever
anorexia, nausea, vomiting • Induces vascular concentrations • Dengue
• Day 3-5: rash spreads permeability and • IgM ELISA or paired Hemorrhagic
trunk → extremities and shock serology during Fever or Dengue
face • Binds to human recovery Shock Syndrome
Dengue • Epistaxis and generalized platelets in the • Antigen-detection o IV blood volume
petechiae in presence of virus- ELISA or RT-PCR replacement
uncomplicated dengue specific antibody and during acute phase o Plasma volume
• Preexisting GI lesions may immune-mediated • Virus isolation in cell expanders
bleed clearance of platelets culture • Prevention
• Second infection with a • Spontaneous o Mosquito control
different serotype leads to aggregation of o Personal
dengue hemorrhagic platelets to vascular protective
fever (HF) with severe endothelial cell pre- measures
shock infected by virus →
aggregation, lysis and
platelet destruction
• Typical Malaria • Protozoan • Peripheral Blood Uncomplicated • Epidemiology

Paroxysm: cold (chills), Plasmodium Smear Malaria o Affects 500
hot (fever spikes), and o P. falciparum, P. o Demonstration of • Chloroquine- million; kills 1
sweating stages vivax, P. ovale, P. parasites sensitive strains: million/year
malariae, and P. o Thin and thick o Chloroquine o 90% of deaths
Based on Species knowlesi smears are o Amodiaquine are from Sub-
• P. vivax, P. ovale, and P. • P. falciparum is the examined • Sensitive P. Saharan Africa
malaria most virulent due to o Preferred stain: falciparum (esp. <5 y/o)
o Low level parasitemia reticulocyte-binding Giemsa at pH 7.2 o Artesunate plus • Host resistance to
o Mild anemia, splenic protein homologue 5 • Dipstick/Card Test Sulfadoxine/ Plasmodium
rupture (rare), and (PfRh5) o Detect P. Pyrimethamine o Inherited
nephrotic syndrome • Vector: Anopheles falciparum- specific, (single dose) alteration of RBC
(rare) mosquito (female) histidine-rich protein (e.g. sickle cell)
• P. falciparum 2 or lactate Prevention • Repeated or
o High level parasitemia Life Cycle dehydrogenase • Personal protection prolonged exposure
o Severe anemia, cerebral • Sporozoite (infective antigen against malaria
symptoms, renal failure, stage) in the • Microtube (avoidance, insect
pulmonary edema, mosquito’s salivary Concentration repellants, bed nets
death gland is released to Methods of Acridine with pyrethroids)
the bloodstream Orange Staining • Chemoprophylaxi
Mild/Non-Life Threatening • Invade liver cells by o Useful for large s
Malaria Malaria binding to hepatocyte numbers of samples • Atovaquone-
• Nonspecific constitutional receptors to be examine Proguanil,
symptoms • They rapidly multiply, rapidly Chloroquine,
• Headache releasing thousands of o Does not quantify Doxycycline,
• Nausea and vomiting merozoites (asexual parasitemia and Hydrochloroquine,
• Classic malaria paroxysms stage) o Requires Primaquine, or
• Anemia o P. vivax and P. fluorescence Mefloquine
• Hepatosplenomegaly ovale form latent microscopy
• Mild jaundice hypnozoites • Laboratory Findings
o Merozoites infect of Severe Malaria
Severe Falciparum Malaria RBCs via sialic o Metabolic acidosis
• High grade fever acid residues o Low glucose,
• Hyperparasitemia • They turn into sodium,
• Cerebral malaria trophozoites (1 bicarbonate,
• Hypoglycemia chromatin mass), then calcium, phosphate,
o <2.2mmol/L (<40mg/dL) into schizonts and albumin
o Due to decreased (multiple chromatin • High lactate, BUN,
gluconeogenesis and masses) creatinine, urate,
increased consumption o Most schizonts turn muscle and liver
by host and parasites into merozoites enzymes, and bilirubin
• Acidosis • Some become
gametocytes that

o Arterial pH <7.25 or infect mosquitoes
plasma bicarbonate taking a blood meal
<15mmol/L
o Respiratory distress
o Due to accumulation of
organic acids
• Non-cardiogenic
pulmonary edema
• Renal impairment
o Renal output: <400mL
(adults) or <12ml/kg
(children)
• Hematologic
abnormalities
o Anemia, slight
coagulation
abnormalities,
thrombocytopenia
• Liver dysfunction
Chronic Complications
• Tropical splenomegaly
• Quartan malarial
nephropathy
• Burkitt lymphoma and EBV
infection
Acute Schistosomiasis • Miracidium infects • Kato-Katz technique Praziquantel 20 • 24 endemic
• Cercarial dermatitis the intermediate host, – most suitable for mg/kg, 3 doses in 1 provinces:
o Swimmer’s itch Oncomelania enumeration of eggs day Sorsogon, Oriental
• Katayama fever hupensis quadrasi, (diagnostic stage) Mindoro, Samar,
o Serum sickness-like where miracidia o S. japonicum eggs Leyte, Bohol, all
syndrome with fever, mature into are ovoid, rounded, provinces in
lymphadenopathy, sporocysts, then into or pear- shaped; Mindanao except
hepatosplenomegaly cercariae curved hook or Misamis Oriental
• RUQ pain • Cercariae (infective spine on the side • Highest among
• 2-8 weeks post-exposure stage) released into near one of the polar children 5-15 y/o
o Fever, lethargy, malaise, water → penetrate ends • Chronic infection
myalgia skin → transform into o S. mansoni (w/ with S.
schistomula → lateral spine) haematobium can
Schisto-
Chronic Schistosomiasis lymphatic vessels or • S. haematobium (w/ lead to squamous
somiasis
• Liver cirrhosis subcutaneous veins → terminal spine) cell carcinoma of
• Portal hypertension lungs → escape into the bladder and
• Ascites, abdominal the pleural cavity and pulmonary
distension into the liver → portal hypertension
• Hematemesis and melena vein → matures into
can occur adult worms →
mesenteric venules of
Pertinent History bowel/rectum (S.
• Travel history (including mansoni/japonicum) or
drinking water sources, venous plexus of
recreational activities, etc.) bladder (S.
haematobium)
Acute Filarial Disease • Abnormal dilated • Identification of • Diethylcarbamazi • World's leading

• Episodes of febrile lymphatics microfilariae by ne (DEC) cause of
adenolymphangitis (ADL) accompanied by microscopic exam o Drug of choice in permanent and
and abnormal lymph flow o Wet smear the Philippines long term disability
dermatoadenolymphangi • Dead or dying worms o Thick blood smear o Safe, effective, • More commonly
tis (DALD) elicit a severe method cheap known as
• Painful, tender, swollen inflammation, o Blood filtration o Taken orally elephantiasis
lymph nodes of different contributing to system o Kills microfilariae • A disfiguring
body parts obstruction o Blood concentration rapidly disease but is
• Usually self-limited • Bacterial infection of • Antigen detection o Side effects typically not the
• May also manifest as skin are partially lost (gold standard) caused by the cause of mortality
epididymo-orchitis in • Lymph node biopsy killing of • One of the
males Life Cycle: • Imaging techniques microfilariae and neglected tropical
• Infective immature o Ultrasonography not the drug diseases (NTDs)
Chronic Filarial Disease forms are introduced o Lymphanography itself
• More commonly into the body by o Lymph node biopsy • Ivermectin
Filariasis encountered female mosquito (Mectizan)
• Increases with age (Anopheles, Culex, o Used in Africa
• Males > females and Aedes) only
• Microfilariae are rarely • Develop into adult • Treatment is mostly
present in blood worms and live in the microfilariacidal (no
• Usually relatively painless lymph vessels/nodes effective treatment
• Lymphedema, • Once fertilized, female against adult filarial
elephantiasis in lower worms continue to worms)
extremities, hydrocele, produce larvae
kidney damage • Released and circulate
in the blood (found
Pertinent History only during the night)
• Exposure to endemic areas • Taken up by another
• Consider superimposed mosquito when it bites
bacterial & fungal infected human
infections

• Caused by Ascaris • Oral-fecal route • Microscopic • Mebendazole 500 • Can live up to 2
lumbricoides and Ascaris • Life cycle identification of eggs in mg tablet single years in the human
suum which are large o Ascaris lives in stool dose body
nematodes lumen of small o Direct wet mount • Albendazole 400
• Most patients are intestine for detecting mg tablet single
asymptomatic o Female produces moderate to heavy dose
• High worm burdens cause about 200,000 eggs infections • Pyrantel pamoate
abdominal pain and a day which is o Kato-katz method 11 mg/kg/day x 3
intestinal obstruction passed in stool and for quantitative days, max of
• Migrating adult worms deposited in soil assessment 1g/day
can cause symptomatic o Embryo becomes • Larvae can be • Side effects: GI
occlusion of biliary tract or infective after 18 identified in sputum or disturbance,
oral expulsion days to several gastic aspirate during nausea, and
• During lung phase of weeks pulmonary migration vomiting
larval migration, cough, o Infective eggs are phase • Contraindications:
dyspnea, hemoptysis, and swallowed and hypersensitivity
eosinophilic pneumonitis larvae infect • Use caution in
may occur intestinal mucosa heavily infected
then carried via patients and
portal to the lungs patients with liver
Ascariasis by systemic disease
circulation
o Larvae mature in
lungs (10-14 days),
penetrate alveolar
walls, ascend to
throat, and
swallowed
o Schistosomes
initially migrate to
peripheral
vasculature and
mature in portal
system
o Paired adult worms
migrate to
mesenteric veins
and lay eggs that
circulate to liver or
stool
In males: Acute Urethritis • Transmission: • Gram Staining of • Ceftriaxone Other Manifestations:

• Incubation of 2-7 days sexually transmitted urethral/cervical (250mg IM, single • Gonococcal
• Scant and mucoid infection of epithelium exudates dose) or vaginitis
discharge • Neisseria gonorrhea o Gram (-) nonmotile, • Cefixime (400mg • Anorectal gonorrhea
• Urethral discomfort, o Gram negative, intracellular PO, single dose) • Pharyngeal
dysuria nonmotile, non- diplococci and • Assume co- gonorrhea
• Possible epididymitis spore forming monococci infection with • Ocular gonorrhea in
organism • Culture in Modified Chlamydia: adults
In females: Gonococcal o Pili – adherence to Thayer-Martin o Azithromycin • Gonorrhea in
Cervicitis cells of mucosal o Small, grayish-white (1g PO, single pregnant women,
• Mucopurulent cervicitis surfaces to colorless mucoid dose) or neonates, and
(most common) o Opa protein – colonies Doxycycline children
• Lower abdominal pain adherence to (100mg PO bid o Ophthalmia
• Cervical friability epithelial cells for 7 days) neonatorum in
• Dysuria (w/o urgency or o Porin – most • Pregnant: give neonates
Gonorrhea frequency) abundant Macrolide instead delivered
• Cervical motion tenderness gonococcal surface vaginally
• Adnexal tenderness/mass protein o Prophylactic eye
• Intermenstrual bleeding o Lipooligo- drops of 1%
• Symptoms develop w/in 10 saccharide – silver nitrate,
days endotoxin erythromycin, or
tetracycline
Pertinent History
• Past history of STDs
• History of sexual assault
• High-risk sexual practices
(e.g. multiple)
• Sexual intercourse with
high-risk individuals
• Type of contraceptive used
• Caused by toxin- • Occurs when spores • Clinical findings • Wound

producing anaerobe of Clostridium tetani • History of antecedent management
Clostridium tetani found in gains access to tetanus-prone injury • Antimicrobial
soil damaged human and inadequate therapy
• Incubation period: tissue immunization o Metronidazole
approximately 8 days but • C. tetani transforms to 500 mg IV every
can be from 3-21 days vegetative rod-shaped 6-8 hours for 7-
Tetanus
o Inoculation in locations bacterium and 10 days
distant from CNS produces o Penicillin G IV 2-
results in longer metalloprotease 4 million units
incubation tetanospasmin every 4-6 hours
• Generalized tetanus: (tetanus toxin) for 7-10 days
most common and severe • Bacteria, via o Alternative:
form retrograde axonal doxycycline 100

o Trismus (lock jaw), transport, reaches mg every 12
autonomic overactivity spinal cord and hours
(irritability, restlessness, brainstem and • Neutralization of
sweating, and secretes tetanus toxin. unbound toxin
tachycardia), tonic • Toxin enters adjacent o Tetanus immune
contraction of skeletal inhibitory interneurons, globulin
muscles, intermittent blocking • Active
intense muscular neurotransmission by immunization
spasms, stiff neck, its cleaving action on o 3 doses in adults
opisthotonus, risus membrane proteins and children >7
sardonicus, rigid producing inactivation years old
abdomen, dysphagia of inhibitory • Benzodiazepine
o In later phases, profuse neurotransmission and other sedatives
sweating, cardiac • Loss of inhibition of (diazepam 10-
arrhythmias, labile anterior horn cells and 30mg IV as
hypertension or autonomic neurons needed) to control
hypotension, and fever results in increased rigidity and spasms
• Local tetanus: tonic and muscle tone, painful • Pancuronium and
spastic muscle spasms, and Vecuronium
contractions in one widespread autonomic (neuromuscular
extremity or region instability blocking agents)
• Cephalic tetanus: • C. tetani will not grow when sedation
dysphagia, trismus, focal in healthy tissues so alone is inadequate
cranial neuropathies, absence of antibodies
cranial nerve deficits plus two or more of:
o Penetrating injury
o Coinfection with
other bacteria
o Devitalized tissue
o Foreign body
o Localized ischemia
• Zoonotic disease caused • Human infection • MAT and culture from • Supportive care • Occurs in both
by spirochetes of occurs from exposure blood and urine (after o Renal temperate and
Leptospira to environmental first week) replacement tropical regions but
• Most cases are mild and sources such as • IgM ELISA or PCR therapy, incidence in the
self-limiting animal urine, • Lab tests may be ventilatory tropics is 10 times
• Incubation period: 2-26 contaminated water or nonspecific support, and higher
days (average 10 days) soil, or infected animal o WBC counts are blood products • Organism infects
• Biphasic: first phase tissue through cuts or generally less than may be required wild and domestic
consist of acute febrile abraded skin, mucous 10,000/μl in severe cases animals especially
bacteremic phase (2-9 membranes, or o Thrombocytopenia • Mild disease: rodents, cattle,
days). Second phase conjunctivae may occur doxycycline swine, dogs,
consists of “immune • Infection in o Hyponatremia and (adults: 100 mg horses, sheep, and
phase” characterized by susceptible host gain elevated creatine twice daily for 7 goats
renewed fever and access to the kinase are common days; children: 2
development of bloodstream through in severe cases mg/kg per day in
complications. lymphatics, resulting o Urinalysis frequently two doses for 7
• Abrupt onset of fever, in spread to organs shows proteinuria, days) or
Leptospirosis
rigors, myalgias, and particularly the liver pyuria, granular azithromycin
headache and the kidney casts, and hematuria o For pregnant
• Conjunctival suffusion • Finding associated women:
(conjunctival redness), with adverse outcomes azithromycin or
nonproductive cough, are oliguria, WBC amoxicillin
nausea, vomiting, and count above • Severe disease:
diarrhea, muscle 12,900/mm3, penicillin (1.5M
tenderness, repolarization units IV every 6
splenomegaly, abnormalities in ECG, hours),
lymphadenopathy, alveolar infiltrates on doxycycline
pharyngitis, jaundice, CXR (100mg IV twice
hematuria, low urine daily), ceftriaxone
output (1-2g IV once
• Less common symptoms daily), or
are arthralgias, bone pain, cefotaxime (1g IV
sore throat, and every 6 hours)
abdominal pain
Early Findings • Salmonella typhii and • Definitive: Isolation of • Prompt antibiotic • Called typhoid fever
• Prolonged Fever (most S. paratyphii serotypes S. typhii or S. therapy leads to because of its
prominent) A, B, and C paratyphii from blood, <1% fatality rate clinical similarity to
o 38.8 – 40.5˚C; up to 4 o Gram (-), non-spore bone marrow, rose (required for those typhus
weeks if untreated forming, facultative spots, stool, or w/ anatomic • Etiologic agents are
• Abdominal Pain – highly anaerobe bacilli intestinal secretion abnormalities & exclusive to humans
variable, due to cytokines • Transmission: • Blood Culture – 40- surgery) • May also be
released by macrophages ingestion of 80% sensitivity, • Ceftriaxone (7-14 transmitted
and epithelial cells contaminated food or reduced by antibiotic days) or sexually (male
Enteric or • Hepatosplenomegaly – water therapy Azithromycin (5 partners) or
Typhoid Fever occurs over time d/t • Bacteria-mediated • Bone Marrow Culture days) nosocomially
recruitment of endocytosis – 55- 90% sensitivity, • Associated with
mononuclear cells & • S. typhii introduces not reduced by poor sanitation and
acquired cell-mediated Salmonella proteins antibiotics lack of access to
response to the bacteria onto epithelial cells • Intestinal Culture – clean drinking water
• Enlargement and (i.e. phagocytic may be positive even if • Risk factors:
Necrosis of the Peyer’s microfold (M) cells others are negative contaminated food
Patches – recruitment of found in Peyer’s and water, flooding,
more leukocytes and patches) street food, lack of
promotion of inflammation hand washing and

& cell death by bacterial • Phagocytosed by toilet access,
secretions macrophages, resist previous
• Rash (“Rose Spots”) – destruction and create Helicobacter pylori
30% of patients; transient, an ideal environment infection
blanchable erythematous for survival &
macules, 2-4mm, usually replication
on trunk • Disseminated around
• Epistaxis the body via the
• Relative bradycardia (aka lymphatics & colonize
Faget sign) at peak of high reticuloendothelial
fever (<50%) cells
Severe Disease (10-15% of
patients)
• GI Bleeding and Intestinal
Perforation – hyperplasia,
ulceration, and necrosis of
the ileocecal Peyer’s
patches at the initial site of
infection
• Neurologic
Manifestations –
meningitis, Guillain-Barre
syndrome, neuritis,
neuropsychiatric
symptoms
• Insidious onset • Mycobacterium leprae • AFB Stain • Sulfones • Humans and
• Incubation period: 2-10 yrs • Transmission: o Scrapings with a (Dapsone) are armadillos are the
• Disease presentation droplets, close and scalpel blade from first-line therapy for only known natural
worsens with a weaker frequent contact with skin or nasal both tuberculoid hosts
immune system untreated cases mucosa or from a and lepromatous • Caused by
• Chronic granulomatous • Tuberculoid leprosy biopsy of earlobe leprosy Mycobacterium
disease affecting skin, o Active cell- skin are smeared on • Rifampicin (RMP) leprae, an acid-fast
peripheral nerves, upper mediated immune a slide and stained or Clofazimine – bacillus that likes
respiratory tract, and eyes response to M. by the Ziehl-Nielssen included in the cool temperatures
leprae technique initial treatment o Infects skin and
RIDLEY JOPLING o Nodules of • Biopsy superficial
regimens
CLASSIFICATION granulomatous o Thickened nerve • Other drugs active nerves—“glove
• Tuberculoid inflammation gives a typical against M. leprae: and stocking”
o Strong cell-mediated o Inflammation injures histologic picture Minocycline, loss of sensation
immunity cutaneous nerves in Clarithromycin,
o Primary lesion: Annular the vicinity; axons, some
plaque Schwann cells, and Fluoroquinolones
o Both borders are sharply myelin are lost, • Several years of
marginated fibrosis of the therapy may be
• Borderline Tuberculoid perineurium and necessary to
o Strong cell-mediated endoneurium adequately treat
immunity; host response • Lepromatous leprosy leprosy
is sufficient for self- o Schwann cells are
cure invaded by the
o Primary lesion: Multiple bacteria
asymmetric plaques and o Segmental
papules demyelination and
o Satellite lesions and remyelination
Leprosy or pseudopods o Thickening of the
Hansen's • Borderline Leprosy perineurial sheaths
Disease o Most unstable occur
o Annular large plaques o Symmetric
with sharply marginated polyneuropathy
interior and exterior affecting the cool
margins with islands of extremities
normal skin o Involves pain fibers,
o Swiss cheese and resulting loss of
appearance sensation
• Borderline Lepromatous contributes to
o Low cell-mediated injury, since the
immunity, sufficient to patient is rendered
induce tissue unaware of injurious
destruction stimuli
o Classic dimorphic
lesion
o Annular with poorly
marginated outer border
with sharply marginated
inner border
o Hypoesthetic or
anesthetic
• Lepromatous Leprosy
o Lack cell-mediated
immunity
o Poorly defined skin
colored nodules
o Widely disseminated
multi-organ disease

• Prolonged febrile illness • Evaluation should have • Empiric therapeutic • Most prevalent
without an established been unrevealing: trials with causes of FUO are
etiology despite intensive o History (travel, antibiotics, infection,
evaluation and diagnostic animal exposure, glucocorticoids, or noninfectious
testing immunosuppression, antituberculous inflammatory
• Fever higher than 38.3C on drug and toxin Hx, agents should be diseases, and
at least 2 occasions and localizing avoided, except malignancy
• Duration of fever for at symptoms), physical when patient’s • Among infections,
least 3 weeks examination, ESR condition is rapidly TB and abscesses
• No known and CRP, platelet deteriorating are most common
immunocompromised count, leukocyte • Antipyretics etiologies
state count, hemoglobin, o However, drugs o Other
• Uncertain diagnosis after 1 electrolytes, with antipyretic considerations:
week of study in hospital creatinine, total effects may osteomyelitis,
protein, ALP, ALT, delay or obscure bacterial
AST, LDH, CK, early symptoms endocarditis
ferritin, ANA & RF, and signs of • Adult Still’s disease
protein specific diseases and giant cell
electrophoresis, • Colchicine (familial arteritis are most
urinalysis, blood and Mediterranean common
urine cultures, CXR, fever), NSAIDs rheumatologic
abdominal (adult-onset Still’s disorders causing
Fever of ultrasound, TST disease), FUO
Unknown • In the absence of glucocorticoids o Other
Origin (FUO) potentially diagnostic (giant cell arteritis considerations:
clues, Hx and PE and polymyalgia polyarteritis
should be repeated rheumatica) nodosa,
regularly o NSAIDs and Takayasu’s
• Scintigraphy, FDH glucocorticoids arteritis
o Abnormalities with must be avoided • Most common
scintigraphic unless infectious malignancies
techniques need to diseases and presenting with
be confirmed with malignant FUO: lymphoma
culture of biopsy lymphoma have (especially non-
specimens been ruled out Hodgkin’s),
• IL-1 and anakinra leukemia, RCC,
HCC
• Other
considerations:
factitious fever,
disordered heat
homeostasis, dental
abscess, fraudulent
fever, exercise-
induced
hyperthermia,
DRESS

MODULE/TOPIC 5 HEMATOLOGY/ IMMUNOLOGY
PART 5A. FOCUSED HISTORY AND PHYSICAL EXAM

This part focuses more on history taking and inspection/palpation for PE J
HISTORY PHYSICAL EXAM
Things to ask on a focused history of the hematologic system: Inspection • Lymph Nodes
• Enlarged nodes: location, duration, number, tenderness o Number
• Constitutional symptoms: fever, chills, night sweats, weight loss, o Size (ideally measured)
anorexia, asthenia (weakness/lack of energy & strength) o Presence of redness
• Anemia: pallor, weakness, fatigue, palpitations o Matted (clumped together) or distinguishable from each other
• Bleeding o Symmetry
o Easy bruising • Visible masses
o Epistaxis/nosebleeds
o Melena, hematochezia Hematology
o Hematuria • General: cachexia, diaphoresis (profuse sweating)
o Hematemesis • Skin: jaundice, pallor (lips, buccal mucosa, conjunctiva, palmar
o Hemorrhagia, prolonged menstrual periods creases), petechiae, ecchymosis
o Postoperative bleeding, bleeding from dental procedures • HEENT: gum hypertrophy, mucosal bleeding, proptosis
• Detailed history of liver disease (affects production of coagulation • Respiratory: signs of infection, pleural effusion,
factors), malabsorption (impaired vitamin K absorption), renal disease tracheobronchial compression
(abnormal platelet function) • Cardiovascular: signs of anemia (hyperdynamic precordium,
• Blood type, previous transfusions bounding pulses, aortic flow murmur)
• History of infection • Abdomen: hepatomegaly, splenomegaly
• Family history • Any signs and sources of infection
Signs of Hematologic Diseases Immunology

• Petechiae, ecchymoses, purpura, hematoma • Skin: macular “rashes”, vesicles, pyoderma, eczema, petechiae,
• Gum hypertrophy alopecia, or telangiectasia may be evident
• Bruises, joint effusion, hemarthrosis, intramuscular bleeds • HEENT: lymph nodes of the head and neck
• Epistaxis Palpation To palpate for lymph nodes, use the pads of the fingers in a
• Jaundice rotatory motion.
• Angular cheilosis (ulceration at the corners of the mouth), glossitis, Lymph nodes
of the head Characteristics
stomatitis, koilonychias (spoon-shaped nails with longitudinal ridging) and neck,
• Pulsatility
axillary,
Things to ask on a focused history of the immunologic system: inguinal • Tenderness – on palpation (suggests inflammation), constant
• History of infection and history of risk factors for infection regions. pain
• Recurrent infections • Shape – oval, round
• Age when recurrent infections began is important. The earlier the age • Mobility – fixed (suggests malignancy), mobile
of onset, the more severe the immunodeficiency. • Size – in cm
• Also important to note how often these are experienced in a year • Consistency – hard (suggests malignancy), soft, firm, rubbery,
• Family history compressible, fluctuant
• Food allergies, atopic dermatitis, asthma, allergic rhinitis • Margins – well-defined margins, irregular margins
• Consanguinity • Number – solitary, multiple
• History of miscarriage/death in infants • Nodularity – lumpy, smooth
• Primary Immune Deficiency in family • Warmth
• History of Autoimmune/Connective Tissue Disorders • Location
• Environment (smoke, allergies)
• Delayed Cord Separation (Leukocyte Adhesion Deficiency) Lymph Nodes (LN)
• HIV risk factors • Axillary LN (lateral, medial, infraclavicular, supraclavicular,
pectoral)
o Drain most of the arm and breast
• Epitrochlear nodes
o Drain ulnar surface of the forearm and hand
• Superficial inguinal nodes and Horizontal (below inguinal
ligament)
o Drains superficial portions of the lower abdomen and
buttock, external genitalia, anal area, lower third of
vagina
• Vertical group (near the great saphenous vein)
o Drains portion of the leg drained by small saphenous
vein
• Head and neck lymph nodes
• Occipital, postauricular, preauricular
• Tonsillar, submandibular, submental, anterior cervical,
superficial cervical, posterior cervical, deep cervical
• Supraclavicular, infraclavicular

PART 5B. HEMATOLOGY – CLINICAL CASES
ADDITIONAL
DISEASE CLINICAL MANIFESTATIONS AND COURSE PATHOGENESIS DIAGNOSIS TREATMENT
NOTES
• Predisposition to African population • Caused by a mutation in the • Characteristic history, physical findings, • On-going continuity of care • Malarial
• Patients with history cerebrovascular accidents are at Beta-globin gene (which peripheral blood smear morphology • Management of painful crises: vigorous resistance is
a higher risk for repeated episodes and may require changes 6th amino acid from • CBC hydration, thorough evaluation for conferred by
partial exchange flow measurements glutamic acid to valine) called ○ Hemoglobin Level: 70-100 g/L underlying causes, and aggressive Sickle cell
HbS (Sickle Hemoglobin) ○ MCV: 80-100 fl analgesia (through standard order or Hemoglobin
• HbS polymerization brought • Hemoglobin electrophoresis patient-controlled analgesia- PCA pump)
about by deoxygenation, which ○ Hb S/A: 100/0 • Morphine (0.1-0.15 mg/kg every 3-4
leads to gelatinous network of ○ Hb F: 2-25% hours) for severe pain or ketorolac (30-60
fibrous polymers that stiffen the • Sickle solubility test measures the degree to mg initial dose, then 15-30 mg every 6-8
RBC membrane, increase which the hemoglobin sample becomes hours) for bone pain
viscosity, and cause dehydration insoluble or gelated as it is deoxygenated • Inhalation of nitrous oxide for short-term
due to potassium leakage and • Genotyping relief
Sickle Cell
calcium influx (these changes • Other lab findings: • Nasal oxygen to protect arterial saturation
Anemia
also responsible for Sickle Cell ○ PTT is prolonged • Blood transfusion for severe cases
shape) ○ PT is normal • Hydroxyurea – mainstay therapy for
• With sickling, microvascular patients with severe symptoms
vaso-occlusion and premature • Other adjuncts:
RBC destruction occur ○ Anti-tumor drug agent 5-
(hemolytic anemia- hemolysis is deoxyazacytidine (decitabine) can
due to abnormal RBC elevate HbF
destruction by the spleen) ○ Bone marrow transplantation
• Clogged capillaries and ○ Gene therapy
venules cause tissue
ischemia, acute pain and
gradual end-organ damage
• β-thalassemia trait blood picture resembles iron • Inherited disorders of α or β • Peripheral blood smear • Patients with β-thalassemia major require • α-thalassemia-2
deficiency and may be misdiagnosed globulin biosynthesis ○ Hypochromic, microcytic intensive transfusion support to survive trait is common
• Persons with α-thalassemia trait may exhibit mild ○ Mutations causing ○ Poikilocytosis and target cells may be • Patients with β-thalassemia intermedia among people of
hypochromia and microcytosis usually without thalassemia can affect any appreciated have a somewhat milder phenotype and African descent
anemia; HbA2 and HbF levels are normal step in the pathway of globin • Childhood: β-thalassemia major is readily can survive without transfusion. • α-thalassemia is
gene expression diagnosed based on severe anemia • Chronic transfusions with RBCs improve most common in
• Beta-thalassemia syndromes: § Most common accompanied by: oxygen delivery, suppress the excessive Asians
• Hypochromia, microcytosis, and minimal anemia mutations: derange ○ Hepatosplenomegaly, profound microcytosis, ineffective erythropoiesis, and prolong life • cis α-thalassemia-
(only for heterogenous states) splicing of mRNA a characteristic blood smear, and elevated ○ Side effects: iron overload fatal by age 1 deletion is
• For homogenous states: formation of toxic precursor or premature levels of HbF and/or HbA2 30 (iron chelation therapy is also almost never seen
inclusion bodies, severe hemolytic anemia, termination of mRNA suggested to prevent this) • α-thalassemia-2
erythroid hyperplasia à producing extramedullary translation • Note: • Splenectomy à required if annual and trans form of
erythropoietic tissues in the liver and spleen • Reduced supply of globulin • Normal values: transfusion rate increases by >50; for α-thalassemia-1
• Massive bone marrow expansion (leading to diminishes production of • HbA 97, Hb 150g/L HbH patients with excessive anemia are very common
“chipmunk facies” (maxillary marrow hyperplasia hemoglobin tetramers, which • Folic acid supplements • HbH and hydrops
and frontal bossing) will cause hypochromia and • Silent thalassemia: • Oxidative drugs should be avoided fetalis are rare
Thalassemia
• Thinning and pathologic fractures of long bones microcytosis • HbA 98-100%, Hb 150g/L • Vaccination with Pneumovax (advised)
• Hepatosplenomegaly, leg ulcers, gallstones and • There’s a continuing normal • Genetic counseling
high-output congestive heart failure (due to rate of synthesis of unaffected • Thalassemia trait: ○ Close monitoring for infection, leg
hemolytic anemia) globins, causing an • HbA 85-95%, Hb 120-130 g/L ulcers, or biliary tract disease
• β-thalassemia major → more severe phenotype unbalanced accumulation of α ○ Early endocrine evaluation is required
• β-thalassemia intermediate → milder phenotype and β subunits • Hemoglobin H disease: for glucose intolerance, thyroid
• β-thalassemia minor → profound microcytosis and ○ In severe homozygous states: • HbA 70-95%, HbH 5-30%, Hb 60-100g/L dysfunction, and delayed onset of
hypochromia with target cells (minimal or mild unbalanced α and β globin puberty or secondary sexual
anemia) accumulation à accumulation • Hydrops fetalis: characteristics
• β thalassemia trait (heterozygotes): hypochromia of highly insoluble unpaired α • HbA 0, Hb 5-10, fatal in utero or at birth • Prevention: antenatal diagnosis of
and microcytosis only chains à form toxic inclusion thalassemia syndromes
bodies à kill developing ○ DNA diagnosis based on PCR
• Alpha-thalassemia syndromes: erythroblasts in the marrow à amplification of fetal DNA (via
• α-thalassemia-2 trait: asymptomatic shortened RBCs’ lives à amniocentesis or chorionic villus
• α-thalassemia-1 trait: resembles severe hemolytic anemia à biopsy followed by hybridization to
β-thalassemia minor stimulate EPO à allele-specific oligonucleotides or
ADDITIONAL
NOTES
• HbH disease: more severe phenotype of α- compensatory erythroid direct DNA sequencing)
thalassemia-1 trait hyperplasia
○ Patients have thalassemia intermedia • Sabotaged marrow response
○ Characterized by moderately severe hemolytic due to ineffective erythropoiesis
anemia but milder ineffective erythropoiesis
• Hydrops fetalis with Hb Barts: tissue hypoxia, • Alpha-thalassemia syndromes
edema, congestive heart failure and death in utero • α-thalassemia-2 trait – four α
globin loci is deleted
• α-thalassemia-1 trait – two
deleted loci
• HbH disease – three deleted loci
• Hydrops fetalis – all four foci
deleted
○ Total absence of α globin
synthesis
○ No physiologically useful
hemoglobin is produced
beyond the embryonic stage
• Signs related to IDA depend on severity and • Begin with negative iron balance • CBC • For pregnant women, growing children, • One of the most
chronicity of anemia where demands for use of iron ○ Decreased Hbg and Hct adolescents, inadequate dietary intake: prevalent forms of
• Usual signs of anemia: fatigue, pallor, and reduced exceeds body ability to absorb ○ Microcytic, hypochromic oral iron therapy malnutrition
exercise capacity iron ○ Low RBC ○ Side effects: GI upset, constipation,
• Signs of advanced tissue ID: cheilosis (fissures at ○ Increased demand for iron: ○ Low corrected reticulocyte count and nausea, vomiting, black stools, metallic
the corner of the mouth) and koilonychias (spooning rapid growth in infancy or reticulocyte production index taste
of the fingernails) adolescence, pregnancy, EPO • Peripheral blood smear ○ Divided doses prior to meals
therapy ○ Hypochromia and microcytosis, and modest • For those who cannot tolerate oral iron:
• Spectrum: ○ Increased iron loss: acute & poikilocytosis parenteral iron therapy with iron
• Ferritin and hemosiderin are adequate chronic blood loss, menses, ○ Low serum iron and ferritin dextran or iron carbohydrate
• Normal Hbg and Hct blood donation • High total plasma iron binding capacity (TIBC) complexes –
• Normal serum iron and transferrin solution ○ Decreased iron intake or (>400ug/dL) • For patients who are symptomatic
• Asymptomatic absorption: inadequate diet, ○ Reduced transferrin saturation (=serum (dizziness, fainting spells, exercise
• Progressive depletion of reserves malabsorption (sprue, Crohn’s iron/TIBC) below 20% intolerance, signs of cardiovascular
Iron Deficiency • Low serum iron and transferrin saturation levels disease), surgery • Serum ferritin <15ug/L collapse): red cell transfusion
Anemia without anemia (gastrectomy, bariatric • No stainable iron in bone marrow: gold ○ 1 mL packed RBC = 1 mg of iron to
• Asymptomatic surgery), acute or chronic standard for diagnosis of IDA body stores
• Increased erythroid activity in the marrow inflammation • Nutritional counselling: breastfeeding,
• Completely depleted iron reserves • IDA in males is GI bleeding iron-rich foods such as meat fish, poultry;
• Low serum iron, ferritin, and transferrin saturation unless proven otherwise increase intake of vitamin C
levels • Treat underlying disorder (e.g. heavy
menses, GI bleeding)
• Note: Ferritin reflects iron stores

• Anorexia, weight loss • Impairment of DNA synthesis • Peripheral blood smear • Key is to differentiate cobalamin (B12) • Common in the
• Diarrhea or constipation which leads to abnormally ○ Oval macrocytes vs. folate as treating for solely folate elderly due to
• Glossitis, angular cheilosis large erythroid precursors and ○ Considerable variation in size can lead to cobalamin neuropathy decreased
• Mild fever, RBCs ○ Abnormally shaped RBCs absorption, and to
Megaloblastic
• Jaundice ○ Hypersegmented neutrophils • Vitamin Supplementation alcoholics
Anemia
• Reversible melanin skin hyperpigmentation • Causes: • Vitamin B12 and folate levels – expensive ○ Cobalamin or hydroxycobalamin 25-
• Thrombocytopenia • Vitamin B12 deficiency or • Bone marrow 100 ug IM/day
• Predisposition to infections abnormalities of cobalamin ○ Hypercellular ○ Folic acid 500 ug to 1 mg/day
• Neurologic deficits present in B12 deficiency only metabolism

ADDITIONAL
NOTES
○ Peripheral neuropathy ○ Vegans ○ Accumulation of primitive cells due to ○ Folinic acid – rescue after
○ Psychotic features ○ Congenital absence of selective death by apoptosis of more mature chemotherapy with methotrexate
intrinsic factor forms
○ Pernicious anemia –
megaloblastic anemia
resulting from lack of intrinsic
factor
○ Total or partial gastrectomy
○ Ileal resection
○ Crohn’s disease, topical
sprue, fish tapeworm
• Folate deficiency
○ Dietary inadequacy
○ Increased demand in
pregnancy and prematurity
• Therapy with anti-folate drugs
(e.g. methotrexate, phenytoin)
• Others / independent of
cobalamin or folate deficiency
(e.g. AML, treatment with
cytosine arabinoside, AZT,
mercaptopurine)
• WHO Classes • Glucose-6-phosphate • Newborn screening • Avoidance of triggers to hemolysis
Magnitude dehydrogenase is an essential • Peripheral smear: Heinz bodies, bite cells ○ Drugs
Severity of
Class Variant of Enzyme enzyme in the pentose § Primaquine, dapsone,
hemolysis
Deficiency phosphate pathway that would sulfamethoxazole, cotrimoxazole,
Harilaou, 2% of Chronic yield NADPH, allowing for nitrofurantoin
Tokyo, normal non- synthesis of glutathione which ○ Infections
I Guadalajara, activity spherocytic protects cells from free radical ○ Fava beans
Glucose-6- Stonybrook, hemolytic damage • Transfusions for patients with acute
Minnesota anemia
Phosphate • In G6PD, because of lack of hemolysis
Mediterranean 3% Intermittent
Deficiency II free radical elimination,
hemolysis
(G6PD) A- 10-60% Intermittent
hemoglobin precipitate out due
hemolysis to the action of peroxide
associated • Sex-linked disorder
III
with
infection or
drugs
B (normal) 100% No
IV
hemolysis
• Clinically indistinguishable • X-linked recessive trait due to • History • Factor replacement therapy: • Most common
• Clinical severity correlates with the level of Factor mutations in F8 gene ○ Easy bruising in early childhood ○ Infusions of recombinant Factor VIII or hereditary
VIII and Factor XI activity (Hemophilia A), F9 gene ○ Spontaneous bleeding into joints, muscles XI or transfusion of cryoprecipitate disease
Clotting (Hemophilia B) and soft tissues (Hemophilia A) and fresh frozen plasma associated with
factor ○ Affects mainly males and • Physical examination (Hemophilia B) life-threatening
Severity Bleeding episodes
level % homozygous female ○ Bruises • Treating bleeds bleeding
activity • 2 types: ○ Hematoma ○ Classify bleeds according to severity:
<1% of Severe Spontaneous ○ Hemophilia A (FVIII) – more ○ No organomegaly § Serious: bleeding to joints, deep
normal bleeding, common • Diagnosis: assay of Factor VIII or Factor IX muscle compartments, mucous
Hemophilia levels predominantly in ○ Hemophilia B (FXI) (<40% of normal) membranes (mouth, gums)
joints and muscles § Life-threatening: intracranial,
• Other lab findings:
1-5% Moderate Occasional neck/throat, gastrointestinal,
○ CBC with normal platelet counts
spontaneous
○ Normal bleeding time severe trauma
bleeding; severe
○ PTT (intrinsic factors) is prolonged and PT ○ Factor replacement therapy
bleeding with
trauma or surgery (extrinsic) is normal ○ Supportive care – Rest, Ice,
6-40% Mild Severe bleeding ○ Mixing studies (mixing 50% of patient plasma Compression, Elevation (RICE)
with major trauma and 50% factor deficient plasma): positive ○ For mucosal bleeds: antifibrinolytic
or surgery therapy (Tranexamic acid or epsilon
aminocaproic acid EACA)
ADDITIONAL
NOTES
• Frequent sites of bleeding correction both immediate and incubated • Vaccine administration: subcutaneous
○ Ankles, knees, elbows / hemarthrosis (70-80%) PT/aPTT tests than IM or intradermal; use smallest
○ Muscles (10-20%) ○ Baseline hepatitis B, C and HIV profile gauge needle possible
• Highly heterogenous: asymptomatic to life- • Quantitative or qualitative • Bleeding time: normal or increased • Desmopressin: treatment of choice for • Most common
threatening bleeding deficiency of von Willebrand • Platelet count: normal mild forms of type 1 and type 2 inherited
• Most common bleeding symptoms: factor (vWF) • PT: normal • Alternatives: plasma virally inactivated bleeding
○ Epistaxis ○ vWF glues platelets to • PTT: sometimes prolonged concentrates of factor VIII and tranexamic disorder
○ Bruising damaged endothelium and • vWF antigen: normal or decreased acid
Von Willebrand
○ Menorrhagia binds and protects Factor VIII • Affect 1-3% of
disease
○ Prolonged bleeding with trauma or surgery • Type 1: most common; population
• Type 1: mucocutaneous bleeding deficiency of vWF
• Type 2 & 3: mucocutaneous, soft tissue, joint • Type 2: abnormal or
bleeding dysfunctional vWF
• Type 3: absent vWF
• Cytopenia dues to leukemic cell marrow infiltration, • Clonal disorder of a primitive • Peripheral blood smear: • Chemotherapy - mainstay • Classification
suppressing normal hematopoiesis hematopoietic stem cell ○ Myeloblasts ○ Induction phase: cytarabine + System: WHO
• Fatigue – frequent first symptom resulting in excess proliferation ○ Auer rods: cytoplasmic inclusions of daunorubicin/idarubicin classification
• Non-specific symptoms: anorexia, weight loss, fever of immature cells and aggregated lysosomes; pathognomonic for § 7+3 regimen: 7 days continuous- • Median age at
• Most common signs and symptoms caused by suppression of normal AML infusion of cytarabine + 3 days of diagnosis: 65
decreased production of normal cells: hematopoiesis • Cytogenetics: for prognostication daunorubicin/idarubicin years old
○ Anemia: pallor, fatigue, and dyspnea • Most cases are idiopathic ○ Consolidation phase: eradicate
○ Thrombocytopenia: petechiae, hematoma, and • Other causes residual leukemic cells to prevent
bleeding (oral, GI) ○ Genetic predisposition relapse and prolong survival
○ Neutropenia: recurrent infections (sepsis, cellulitis, ○ Radiation • Allogeneic stem cell transplant
pneumonia) ○ Chemical/occupational
• Leptomeningeal involvement is more common with exposure
elevated WBC count at diagnosis
○ Headache and altered mental status
Acute Myeloid ○ Cranial nerve palsies – most common sign
Leukemia • Splenomegaly is uncommon
• CBC
○ WBC count
○ Blast count
○ Low hematocrit
○ Low platelet
• Acute onset of symptoms • Dysregulation of expression and • Peripheral blood smear: • Chemotherapy – multiple cycles + • Most common
• Non-specific symptoms: function of transcription factors ○ Lymphoblasts maintenance for at least 2 years malignancy in
○ Fever required from normal B- and T-cell • Flow cytometry • Tyrosine kinase inhibitors (imatinib) – (+) children, but
○ Fatigue development ○ Pre-B cell ALL: CD19 & CD20 t(9;22) occurs in all ages
○ Pallor • Disturbance of differentiation of ○ Pre-T cells ALL: CD3 • B-ALL – typically
Acute ○ Bleeding/bruising lymphoid precursors ○ (+) TdT (terminal deoxynucleotidyl transferase) manifest as
Lymphocytic ○ Infection • Promotion of maturation arrest • CSF analysis for CNS involvement childhood acute
Leukemia ○ LAD • Induction of increased self-renewal • Cytogenetics leukemias
○ Splenomegaly • T-ALL: NOTCH1 mutation (70%) ○ Good prognosis: hyperdiploidy, t(12:21) • T-ALL – presents in
• B-cell types metastasize to CNS and testicles • B-ALL: PAX5, E2A, EBF, t(12:21) ○ Bad prognosis: hypodiploidy adolescent males as
• T-cell type may present as an anterior mediastinal mass ○ T(9;22) thymic lymphomas

ADDITIONAL
NOTES
• Asymptomatic at diagnosis • Arises from B cells • CBC • Chemotherapy: • Median age of
○ Lymphocytosis (25%) • Deletion of ○ Lymphocytosis: ≥ 5000/µL circulating B cells ○ Fludarabine diagnosis: 70 y/o
• Lymphadenopathy ○ 13q14.3 • Peripheral blood smear – small, mature lymphocytes ○ Rituximan, alemtuzumab • Male predominance
• Splenomegaly ○ 11q with smudge cells ○ Chlorambucil, cyclophosphamide • Most common
• Anemia ○ 17p • Proliferation centers in lymph node: pathognomonic ○ Bendamustine leukemia of adults
Chronic • Thrombocytopenia ○ Trisomy 12q • IVIg – for hypogammaglobulinemia and in the Western
Lymphocytic • B symptoms: frequent infection world
Leukemia ○ Fever
○ Weight loss
○ Night sweats
• Richter syndrome (5%) – transformation to aggressive
lymphoma
• Chronic phase • Malignant stem cell disorder • Detection of Philadelphia chromosome • Tyrosine kinase inhibitors • Median age of
○ Asymptomatic elevation of peripheral blood counts characterized by t(9;22) ○ Marrow karyotyping • Allogeneic stem cell transplant diagnosis: 60 years
○ Early satiety (Philadelphia chromosome)that ○ Peripheral blood FISH old
○ Left upper quadrant fullness results in a bcr/abl gene fusion ○ bcr/abl PCR: most sensitive; monitor treatment
○ Fatigue and a constitutively active response
• Slow progression tyrosine kinase causing • Peripheral smear: left shift
Chronic
• Without treatment, median survival is 3 years uncontrolled cell proliferation • CBC
Myeloid and blocked apoptosis 3
• Accelerated phase – increasing anemia, ○ Leukocytosis (>100,000 cells/mm )
Leukemia
thrombocytopenia, basophilia ○ Anemia
• Blast crisis (resembles acute leukemia): ○ Thrombocytosis
○ Fever ○ Eosinophilia/basophilia
○ Night sweats
○ Bone pain
rd th
• Bimodal age distribution (3 and 7 decade) • Malignancy of mature B • Lymph node biopsy • Stage I & II: combination chemotherapy • Majority are curable
• B symptoms lymphocytes ○ Reed-Sternberg Cells (giant “owl eye” cells) followed by radiation • Adverse prognostic
• Asymptomatic enlarged, painless lymph node or mass on • CBC • Stage III & IV: full-course chemotherapy factors:
imaging ○ Leukocytosis • Chemotherapy: ABVD regimen ○ > 45 y/o
○ Common sites: neck and mediastinum ○ Lymphopenia ○ Doxorubicin ○ Male
Hodgkin
• A mediastinal mass in a young person is most often HL ○ Thrombocytosis ○ Bleomycin ○ Stage IV
Lymphoma
• Elevated ESR ○ Vinblastine ○ Abnormal CBC
• CT of chest, abdomen, and pelvis – staging ○ Dacarbazine ○ Albumin < 4g/Dl
○ PET is a useful adjunct • Autologous stem cell transplant – for most ○ Large mediastinal
st
patients who relapse after 1 line treatment mass
• B symptoms • Cancers of mature B, T, and NK cells • Incisional lymph node biopsy preferred over needle • DLBCL: RCHOP chemotherapy • Diffuse large B cell
• May arise from infections: biopsy ○ Rituximab lymphoma – most
○ Epstein-Barr virus – African • CT of chest, abdomen, and pelvis – staging ○ Cyclophosphamide common
Burkitt Lymphoma & AIDS ○ PET is a useful adjunct ○ Doxorubicin • Follicular
nd
related lymphoma • Burkitt lymphoma – starry sky pattern ○ Vincristine lymphoma – 2
○ HTLV-1 – T-cell ○ Prednisone most common
leukemia/lymphoma • Chimeric antigen receptor T cells • Adverse prognostic
• Burkitt lymphoma factors:
Non-Hodgkin ○ Translocation of MYC gene on ○ > 60 y/o
Lymphoma chromosome 8 that lead to ○ Elevated LDH
increased MYC protein synthesis ○ Stage III or IV
○ MYC – regulator of genes for disease
aerobic glycolysis ○ >1 extranodal
• Diffuse large B-cell lymphoma site
○ Usually due to the dysregulation
• Burkitt Lymphoma of BCL6, a DNA-binding zinc-
○ African form: Jaw or facial bone tumor that spreads to finger involved in formation of
extranodal sites normal germinal centers

ADDITIONAL
NOTES
○ Non-endemic form: ascites, renal, and gonadal
involvement
• Diffuse large B-cell lymphoma
○ Elevated LDH
○ Involvement of non-lymph node sites e.g. bone
marrow, testes, etc.
nd
• CRAB • Malignant proliferation of plasma • Asymptomatic/Smoldering form diagnostic criteria: • Not curable; goal is to prolong time to • 2 most common
○ Hypercalcemia cells derived from a single clone ○ Clonal bone marrow plasma cells ≥ 10% or relapse hematologic
○ Renal insufficiency • Possible error in switch ○ Presence of serum and/or urinary monoclonal • Autologous stem cell transplantation malignancy second
○ Anemia recombination-the genetic protein ≥ 3 g/dL • If eligible for transplant: to NHL
○ Bone pain mechanism to change antibody • Active form diagnostic criteria: ○ Bortezomib – proteasome inhibitor • Male predominance
• Bone pain – most common symptom (70%) heavy chain isotype ○ Above criteria with addition of end-organ damage ○ Thalidomide or lenalidomide – • Median age at
• Fracture attributable to the underlying plasma cell immunomodulator diagnosis: 68 y/o
• Renal failure proliferative disorder, specifically the CRAB ○ Steroid (dexamethasone or prednisone)
• Susceptibility to infection criteria: • Ineligible for transplant:
Multiple
• Anemia § Calcium greater than 11.5 g/dL ○ Melphalan + steroid ± bortezomib
Myeloma
• Clotting abnormalities § Renal insufficiency (creatinine greater than • Supportive treatment
• Neurologic symptoms 2 mg/dL) ○ Fractures: bisphosphonate or denosumab
• Hyperviscosity § Anemia (hemoglobin [Hbg] <10 g/100 mL or (anti-RANKL antibody)
2 g/100 mL < normal)
§ Bone disease (osteopenia or lytic lesions)
• Serum β2-microglobulin – most powerful predictor of
survival and can substitute for staging
• Karyotype
• FISH
PART 5C. IMMUNOLOGY - CLINICAL CASES

DISEASE CLINICAL MANIFESTATIONS AND COURSE PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL NOTES
• Can be mild to severe (anaphylaxis) • Failure to develop or breakdown of • History Avoidance of Allergic march:
• Nausea, vomiting, diarrhea, abdominal oral tolerance o Food suspected, quantity of food ingested, interval offending food
pain or cramping o Oral tolerance – suppression of between ingestion and symptoms, symptoms Anti-histamines
• Immediate (IgE mediated): < 1 hour immune response to antigens that • Food diary Emergency
• Tingling in mouth have been previously taken via oral • Skin-prick tests, (+) wheal formation epinephrine (anaphylaxis)
• Swelling of lips, tongue, throat route • IgE antibody blood tests
• Hives, rashes, pruritus • IgE-mediated food allergy • Oral food challenge test: gold standard
• Wheezing o IgE antibody-mediated activation of o 6 hours prior and after food challenge: baseline CBC with
• Itchy, red, watery eyes, periorbital swelling mast cells or basophils followed by differential
• Light-headedness, sneezing rhinorrhea release of histamine & other o Food challenge: 3 equal doses over 30 minutes
Delayed (non-IgE mediated): >24 hours; inflammatory mediators o 4-hour observation before discharge
more chronic; rarely life-threatening o Initial 4-7 hours: Neutrophil & • No specific blood tests or skin tests for non-IgE mediated
• Skin: pruritus, atopic eczema eosinophil infiltration food allergy
Food o Following 24-48 hours: lymphocytic
• GIT: gastroesophageal reflux, loose,
allergy and monocytic infiltration
frequent stool, blood or mucus in stool
Atopic • Non-IgE mediated: other components
dermatitis of immune system apart from IgE (e.g.
vs. food intolerance – non-immunologic (e.g.
enzyme deficiency, sensitivity to food additives food allergen specific T cells)
or chemicals) • Common allergenic food
• Delayed o Children: peanut, milk, egg
• Large amounts required to produce reaction o Adult: peanut, tree nuts, sesame
• Less serious sequelae seed, shellfish
• Common in infancy • Multifactorial Hanifin & Rajka Criteria • Avoid & eliminate exacerbating Allergic march
• Recurring flaky, dry, erythematous, and itchy • IgE dysregulation Major criteria (3 of Minor criteria (3 of the factors
rash o Type 1 hypersensitivity reaction following) following) • Switch soaps
• Defective cutaneous cell mediated • Pruritus • Xerosis • Avoid excessive exposure to sun
immunity • Typical morphology • Icthyosis/palmar hyperlinearity and hot environments)
• Impaired epidermal barrier and distribution - • Elevated serum IgE • Maintain skin hydration
flexural lichenification in • Early age of onset • Use emollients

o Main genetic defect responsible is adult; facial and • Tendency toward cutaneous • Control pruritus
gene encoding filaggrin, a extensor eruptions in infection/impaired cell • Sedating antihistamines
structural protein in stratum infants and children mediated immunity • Topical corticosteroids
corneum • Chronic or relapsing • Tendency toward non-specific • Educate family about triggering
• Phases: dermatitis hand or foot dermatitis factors, prevention, treatment and
o Sensitization phase • Personal or family • Nipple eczema prognosis
§ First exposure to allergen à history of AD • Cheilitis
allergen picked up by dendritic • Recurrent conjunctivitis
cell à presents it to a Th2 cell à • Dennie-Morgan infraorbital
Th2 cell stimulates B cells to fold
produce IgE antibodies • Keratoconus
o Elicitation phase • Anterior subscapular
§ Allergen directly crosslinks to cataracts
specific IgE antibody and trigger • Orbital darkening
mast cell degranulation and • Facial pallor or erythema
release of proinflammatory • Pityriasis alba
cytokines • Anterior neck folds
• Itch when sweating
• Intolerance to wool and lipid
solvents
• Perifollicular accentuation
• Food intolerance
• Course influenced by
environmental and emotional
factors
• White
dermatographism/delayed
blanch
CLINICAL
DISEASE MANIFESTATION AND PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL NOTES
COURSE
• Coughing, wheezing, • Changes in airway following • Philippine Consensus Report on Asthma 2009 classification of • Avoidance of triggers
shortness of breath and/or trigger chronic asthma severity on treatment • GINA-based steps for asthma treatment
chest tightness o Inflammation and swelling
o Muscles of airway constrict
o Excessive mucus
• Common triggers
o Domestic (household mite,
animal dander, insect, mold)
o Pollen
o Food & food additives
o Pollution, cigarette smoke
o Weather changes
• GINA 2018 assessment of asthma control in adults,
Asthma adolescents and children 6-11 years

CLINICAL
COURSE
• Cold-like symptoms: • IgE mediated inflammation • Classification • ARIA guidelines: Recommendations for management of allergic rhinitis
o Rhinorrhea, clear nasal after allergen exposure to the
discharge membranes of the nose
o Swollen nasal
turbinates
o Paroxysms of sneezing
• Often accompanied by
itching of eyes, nose and
palate
o
• Nasal exam: check for
Allergic o Nasal crease
rhinitis o Color of nasal mucosa – pale purple and boggy, not beefy red
o Polyps
o Nasal septal deviation
o Turbinate hypertrophy – cobblestone appearance
o Thin and clear nasal secretions
• Posterior pharynx for postnasal drip
• Frontal and maxillary sinus tenderness
• Allergic shiners – dark puffy lower lids caused by rerouting of
blood flow away from congested nasal mucus membranes
• Dennie-Morgan lines
• Long face syndrome
o Retruded jaw
o High arched palate
o Steep mandibular plane
o Excess in dentoalveolar height
• Urticaria • Binding to antigensà mast cell • History • Identification and elimination of underlying
o Pruritic, generalized degranulation àrelease • Physical exam cause
eruption with histamine, leukotrienes, o Dermatographism: linear wheals • Symptomatic relief: anti-histamines, LTRA &
erythematous cytokines, chemokines o Cholinergic: small wheals surrounded by erythema H2 antagonists (add-on therapy)
circumscribed borders • Acute urticaria: most commonly o Solar/cold: wheals in exposed areas • Phototherapy for dermatographism and
and pale slightly due to infection o Urticarial vasculitis: wheals mainly in lower extremities chronic idiopathic urticaria (CIU)
elevated centers • Chronic urticaria: 70-90% • No specific laboratory tests for acute urticaria • Omalizumab for CIU, cholinergic, solar and
o Fleeting (<24 hours) unknown origin • Chronic urticaria lab test: cold-contact
o Acute urticaria: <6 o Immunologic o Differential blood count
Urticaria weeks § Rheumatic (SLE, JRA) o ESR or CRP
and o Chronic urticaria: >6 § Endocrine
Angioedema weeks (hyper/hypothyroidism)
• Angioedema § Neoplastic
o Sudden swelling of o Non-immunologic:
lower dermis and § Cold contact
subcutis, involvement § Delayed pressure
below mucus § Dermatographism
membranes § Cholinergic
o Resolution up to 72 § Contact
hours
• Hypotension • Potentially life-threatening • History • Cornerstone: patient education to avoid

• Hypoxia systemic allergic reaction • Measurement of elevated serum tryptase allergens
• Upper and/or lower involving one or more organs • Epinephrine
Anaphylaxis respiratory obstruction systems that typically occurs • O2 supplementation
o Laryngeal edema - within seconds to minutes of • Antihistamines
lump in the throat, exposure to trigger (drug, food, • Corticosteroids
hoarseness, stridor hymenoptera sting) • Β-agonists
CLINICAL
COURSE
o Bronchial obstruction – • Type I hypersensitivity reaction
chest tightness, • Mast cells and basophils
wheezing release IgE after allergen
• Cutaneous manifestations exposure
(>90%)
o Urticaria
o Flushing with diffuse
erythema
o Feeling of generalized
warmth
• Systemic: fatigue, • Gene-environment interactions • CBC, platelet count, urinalysis may help diagnose abnormalities • No cure, and complete sustained
malaise, photosensitivity, result in abnormal immune • SLE SLICC 2012 Criteria: ≥4 of these criteria (at least 1 remissions are rare
anorexia and weight loss responses that generate clinical and at least 1 immunologic) OR biopsy-proven lupus • Induce improvement of acute flares and then
autoimmune antibodies and nephritis, well documented, are present at any time in a maintain improvements with strategies that
• Epidemiology immune complexes that patient’s history, the diagnosis is likely to be SLE suppress symptoms to an acceptable level
• Women of childbearing deposit in tissue, activate • Clinical Criteria
age complement, cause o Malar rash (acute cutaneous lupus) • Non-life-threatening SLE
• Multigenic disease inflammation and over time o Discoid rash (chronic cutaneous lupus) • NSAIDS, anti-malarials are mainstays
• People with XXY lead to irreversible organ o Oral or nasal ulcers (palate, buccal, tongue) • Topical glucocorticoids, sunscreens, DHEA,
(Klinefelter’s syndrome) damage o Alopecia hydroxychlorquine, methotrexate
have a significantly o Arthritis (≥2 joints with synovitis, or morning tenderness)
Systemic
increased risk for SLE o Serositis (pleural rub or pericardial pain) • Life-threatening SLE
Lupus
o Renal: PCR of 500mg/24h or RBC casts • Oral glucocorticoids
Erythema-
o Neuro: seizures, psychosis, acute confused state
tosus (SLE)
o Hemolytic anemia
o Leukopenia (<4000/mm3 at least once) or lymphopenia
(<1000/mm3 at least once)
o Thrombocytopenia (<100,000/mm3)
• Immunologic Criteria
o ANA (non-specific)
o Anti-dsDNA (high specificity)
o Anti-Sm
o Antiphospholipid antibody
o Low C3 or C4 complement
o Direct Coombs test
WHO Clinical Staging • Hallmark of HIV disease is a 2 Step Strategy • AIDS is labeled as a “treatable chronic • HIV in the PH:
• Stage I: Asymptomatic profound immunodeficiency • Test 1: ELISA disease” (lifespan of 22+ years) o Started in 1984
• Stage II: Mild symptoms, resulting primarily from a • Enzyme-linked immunoabsorbent assay • Depends on the stage of the disease and any o 50-60% males
minor mucocutaneous progressive quantitative and • Known antigens concomitant opportunistic infections o 25-34 y/o
manifestations and qualitative deficiency of T • Determine viral Ab o 2012: ~3000 cases of
recurrent URTI Helper cells (CD4 molecule on • Reactive: presence of Ab, HIV-infected • HAART (Highly Active Antiretroviral Therapy) HIV, 186 cases of
• Stage III: Advanced its surface) • Non-reactive: absence of Ab, not infected o Principal method for preventing immune positive AIDS, 11 deaths;
symptoms, unexplained • HIV invades macrophages and deterioration 12 new cases a day
chronic diarrhea longer T lymphocytes (also B-cells, NK, • If positive ELISA, confirm with test 2: Western blot – o Multifactorial • RA 8504: Philippine AIDS
than 1 month, severe glial, etc.) determines presence of Ab against specific antigens of a Prevention and Control
bacterial infections and particular organism • Initial regimen: 2 NRTI + 1 NNRTI Act of 1998
HIV/AIDS pulmonary tuberculosis Human Immunodeficiency Virus o 2 nucleoside reverse transcriptase o Education and
• Stage IV/AIDS: Severe (HIV) • If discordant (non-reactive ELISA but with suspicion), retest inhibitors (NRTIs) (e.g. tenofovir disoproxil information: testing,
symptoms, profound • Blood-borne virus after 6 weeks fumarate/emtricitabine) and a non-NRTI screening and
opportunistic infections • Transmitted via sexual (e.g. efavirenz, rilpivirine) counseling about
(toxoplasmosis of brain, intercourse, shared IV drug • Direct methods: measure viral NA or antigens (PCR, Nucleic acid o Started in all adults regardless of WHO discrimination penalties
candidiasis of esophagus, paraphernalia, mother-to- amplification test, etc.) staging o Article VI: Confidentiality
trachea, bronchi or lungs, child (breastfeeding, birth § Section 30:
Kaposi sarcoma) process) FOR TREATMENT PLAN Medical confidentiality
• Components • Plasma Viral Load • History
o Gag: matrix, capsid • Steady state of viral killing vs. viral replication o Unprotected sexual
o Pol: Protease, Reverse • Prognostic value intercourse
o Multiple partners
CLINICAL
COURSE
transcriptase, Integrase • At 6 months, 12 months, then every 12 months o Prior or current STD’s
o Env: gp120, gp41 (Gonorrhea and
FOR RISK ASSESSMENT Chlamydia increase risk
HIV Life cycle • CD4+ T cell count: Reliably reflect current risk of acquiring 7-fold)
• Attachment: Virus Attaches to opportunistic infections o Sharing IV drug
host paraphernalia
• Gp41 (Transmembrane) Bacterial and Viral Coinfection o Received blood
attaches to coreceptor (CCR5 • Increased viremia load transplants (before 1985)
for macrophage or CXCR4 for • EBV, CMV, HSV, HSC, HepB o Mucosal contact w/
T-cell) infected blood
• gp120 (extracellular) attaches to Opportunistic Infection o Needle stick injuries
CD4 receptor of T-cell • Protozoa (Toxoplasma gondii) o Maternal HIV infection
• Penetration: virus enters, • Fungi (C. albicans) (for newborn, infant,
uncoating of capsid • Bacteria (TB) children)
• Reverse Transcription (RT): • PE
o Non-specific
RNA à DNA
o Generalized
• Reverse Transcriptase: lymphadenopathy is
o Transcribe single stranded common
RNA into RNA-DNA double o Weight loss may be
helix apparent
o Copies sense DNA into
antisense DNA to form viral
double stranded helix
o Degrades viral RNA
• Integration
• Integrase: connects viral DNA to
host DNA
LATENCY PERIOD
• Transcription and Translation:
activity of Provirus
• Viral Assembly outside the
nucleus
• Budding: after budding, it
matures
• 2.6-3 days for life cycle
• Up to 10 billion HIV produced
daily during early/infective stage
PART 5D. IMMUNOLOGY – HYPERSENSITIVITY REACTIONS

TYPE IMMUNE MECHANISMS HISTOPATHOLOGIC LESIONS PROTOTYPICAL DISORDERS
Immediate (type I) hypersensitivity Production of IgE → immediate release of vasoactive Vascular dilation, edema, smooth muscle contraction, • Anaphylaxis
amines and other mediators from mast cells; later mucus production, tissue injury, inflammation • Allergies
recruitment of inflammatory cells • Bronchial asthma (atopic forms)
Antibody-mediated (type II) hypersensitivity Production of IgG, IgM → binds to antigen on target cell or Phagocytosis and lysis of cells; inflammation, in some • Autoimmune hemolytic anemia
tissue → phagocytosis or lysis of target cell by activated disease, functional derangements without cell or tissue • Goodpasture syndrome
complement or Fc receptors; recruitment of leukocytes injury
Immune-complex mediated (type III) hypersensitivity Deposition of antigen-antibody complexes → Inflammation, necrotizing vasculitis (fibrinoid necrosis) • Systemic lupus erythematosus
complement activation → recruitment of leukocytes by • Some forms of glomerulonephritis
complement products and Fc receptors → release of • Serum sickness
enzymes and other toxic molecules • Arthus reaction
Cell-mediated (type IV) hypersensitivity Activated T lymphocytes → (1) release of cytokines, Perivascular cellular infiltrates; edema; granuloma • Contact dermatitis
inflammation and macrophage activation; (2) T cell- formation; cell destruction • Multiple sclerosis
mediated cytotoxicity • Type 1 DM
• Tuberculosis

MODULE/TOPIC 6 NEUROLOGY

FOCUSED HISTORY
• Onset ○ Nausea, fainting, vomiting
• Location ○ Seizures
• Duration ▪ How long did it last?
• Characteristic ▪ What were you doing before you lost consciousness?
○ Sensation of tightness, pressure, stabbing throbbing, pulsation ▪ Did the seizure begin in one part before affecting the
• Aggravating and alleviating factors entire body?
• Associated symptoms ○ Weakness, paralysis
○ Blackout (Loss of consciousness) ▪ Left or right side?
HPI ○ Altered mental status ▪ What body parts?
○ Head or neck injury ▪ Was there difficulty in walking or doing activities of daily
○ Headache living?
▪ Stabbing, steady, pulsating, throbbing, or sharp? ○ Numbness, tingling (sensory changes)
○ Dizziness, vertigo ○ Involuntary movements, tremors
○ Visual loss or change, diplopia • Radiation
○ Dysphagia, dysarthria, dysphonia • Timing
○ Tinnitus, hearing loss • Frequency
○ Fever, chills, weight loss • Severity
PMH Stroke, hypertension, diabetes mellitus, alcohol use, drugs (anti-malaria, aminoglycosides)
Social History Withdrawal from alcohol, smoking, or caffeine, occupational, recreational activities, sleep patterns
Family History Migraine, travel sickness, stroke, MI, hypertension, Seizures
GLASGOW COMA SCALE

Eye Response Verbal Response Motor Response
4 Eyes opening simultaneously (Without stimulus) 5 Oriented (Coherent, appropriate answers) 6 Obeys commands
Localizes to pain (Knows where the stimulus
3 Eyes opening to speech (Requires verbal stimuli) 4 Confused (Disoriented, tangential response) 5
is applied and will try to pull away from it)
Eyes opening in response to pain (Bordering on Inappropriate words (Does not combine words Withdraws from the pain (Moves away from
2 3 4
stupor, not coma) into phrases or sentences, incoherent) the stimulus)
1 No eye opening (Comatose) 2 Incomprehensible sounds (e.g. mumbling) 3 Decorticate (Flexion in response to pain)
1 None 2 Decerebrate (Extension to pain)
T If the patient is intubated 1 No motor response
GCS Scoring: Severe: GCS 3-8; Moderate: GCS 9-12; Mild: GCS 13-15
MENTAL STATUS AND HIGHER CORTICAL FUNCTION EXAM

Is the patient normal, hyperactive, agitated, quiet, or immobile?
Appearance and Behavior Is the patient neat and well-groomed?
Do the clothes match the patient’s age, peers, sex and background?
Handedness Is the patient left or right handed?
Quantity (Talkative, spontaneous, expansive, paucity, poverty of speech)
Rate (Fast, slow, normal, pressured)
Volume (Loud, soft, monotonous, weak, strong)
Fluency and rhythm (Slurred, clear, hesitant, dysarthric, aphasic)
Observe for:
• Paraphasic errors – inappropriately substituted words or syllables
Speech /
• Neologisms – non-existent invented words
Stream of Talk
Four Levels of Disturbed Speech Production
• Dysphonia – disturbance In, or lack of, the production of sounds in the larynx
• Dysarthria – disturbance in articulating speech sounds
• Dysprosody – disturbance in the melody and rhythm of speech, accent of syllables, inflections, intonations,
pitch of voice
• Dysphasia – disturbance in the understanding or expression of words as symbols for communication
Mood – internal and sustained state over longer periods of time
Affect – expression of mood and what the patient’s mood appears to be to the clinician
Mood and Affect
• Is the patient’s mood appropriate? Is the patient euphoric, agitated, sad, anxious or angry?
General • Is the patient happy, euthymic, irritable, angry, agitated, flat or emotionally labile?
Describes how thoughts are formulated, organized, and expressed
• Circumstantial – overinclusion of trivial or irrelevant details that impede the sense of getting to the point
• Clang Associations – thoughts are associated by the sound of words rather than by their meaning
• Derailment – breakdown in both the logical connection between ideas and the overall sense of goal
directedness
Thought Process
• Flight of Ideas – succession of multiple associations so that thoughts seem to move abruptly from idea to
idea
• Perseveration – repetition of out of context words, phrases, or ideas
• Tangentiality – when responding to a question, the patient gives a reply that is appropriate to the general
topic without actually answering the question
• Thought Blocking – Sudden disruption of thought or a break in the flow of ideas
Presence of illusions, delusions, hallucinations, misinterpretations, phobias, bodily complaints
• Illusions – false sensory perception based on natural stimulation of sensory receptor (healthy person
recognizes the illusory nature)
Though Content • Hallucinations – false sensory perception not based on natural stimulation
• Delusions – false, fixed ideas that are not shared by others
• Obsessions – unwelcome and repetitive thoughts that intrude into the patient’s consciousness
• Compulsions – repetitive, ritualized behaviors that patients feel compelled to perform to avoid an increase in
anxiety or some dreaded outcome
Note: Remember to ask for the level of education
Intellectual Capacity
• Is the patient bright, average, dull, or mentally retarded?
• Awake – easily aroused
• Drowsy/lethargic – not fully alert, drifts off when not stimulated
Levels of Consciousness • Obtunded – sleeps most of the time and difficult to arouse (loud noise, vigorous shaking or pain as stimulus)
• Stupor – still responds to stimuli but needs persistent loud noise or pain for arousal
• Coma – no response
• Time – Ask for the day, date, month, year, and season
Orientation • Place – Ask where the patient is now, the floor, building, street, city, and country
• Person – Ask who the patient is and what he does, who his companions are, and who you are
• Recite the month
• Spell words forward and backward (W-O-R-L-D; D-L-R-O-W or M-U-N-D-O; O-D-N-U-M)
Attention
• Serial 7s (Subsequent subtraction of 7 from 100) or Serial 3s (Subsequent subtraction of 3 from 20)
• Tapping test (Tapping whenever the physician says the letter A)
Sensorium • Registration (Repeat “Manga, Mesa, Pera immediately after the examiner)
• Immediate (Ask for the 3 words after 3-5 minutes)
Memory • Recent (Ask what they had for breakfast that morning)
• Remote (Ask which elementary school they went to)
• Semantic (Name the presidents backward from the present one)
Fund of Information • Ask about current events in the news
Person’s ability to shift back and forth between general concepts and specific examples
Abstract Reasoning
• Interpretation of a proverb (Time is gold; Kapag may tiyaga, may nilaga)
Insight – person’s understanding of how he or she is feeling, presenting, and functioning
Insight, Judgement, and Judgement – person’s capacity to make good decisions and act on them
Planning • Does the patient have no, partial, or full insight? (Ask about their goals or plans)
• Is the patient’s judgement intact or not? (Give a situation, and listen to what the patient would do)
Calculation • Ask the patient to solve simple calculations (E.g. What is 100-70 or 5 x 6?)
Agraphestesia - Inability to identify letters/numbers traced on the skin
• With the patient’s eyes closed, trace letters or numbers between 1 and 10 on the skin of the palm or
fingertips with any blunt tip. Ask the patient to identify what you traced, then repeat on the other hand
Agnosia
Astereognosis - Inability to identify an object by touch
Inability to understand the meaning, or symbolic
• With the patient’s eyes closed, place an object on their hand (e.g. key, coin, paperclip). Ask the patient to
significance of ordinary sensory stimuli even
identify what you traced, then repeat on the other hand
though the sensory pathways and sensorium
are relatively intact Prosopagnosia - Inability to recognize faces in person or in photos
• Ask the patient to identify a person or a photo
○ In person – the patient can’t recognize the face but immediately recognize him by voice
○ In photo – the patient can see the face and describe the parts but fails to recognize who the person is
Tactile Finger Agnosia
• Assign a name or number to each finger of both hands. With the patient’s eyes closed, randomly touch a
Asomatognosia digit on the right or left hand, and ask the patient to identify the finger by number or name, and whether it is
Inability to identify parts of the body the right or the left hand
Right/Left Disorientation
• Give the patient commands such as, “Touch your right hand to your left ear.”
Starts during history taking.
• Searching for words, pauses, and hesitations
• Substitution for wrong words or phonemes
• Loss of intonation and prosody
• Poverty of speech
Test for:
• Fluency (Ask the patient to write a simple sentence)
Aphasia • Comprehension (Ask the patient to perform a command)
Inability to understand or express words as • Naming (Ask the patient to identify an object shown)
symbols for communication, even though the • Repetition (Ask the patient to repeat “No ifs, ands, or buts” or “Wala nang pero pero pa”)
primary sensorimotor pathways for receiving Dyslexia
and expressing language and mental status are • Agnosia for the meaning of written words despite adequate intelligence and exposure to conventional
relatively intact methods of instruction
Broca’s Aphasia (Motor or non-fluent)
• Good receptive but poor expressive (Difficulty in word finding and naming, failure to make associations,
displays dysprosody, difficulty in writing and repetition)
• Lesion site: Anterior part of the aphasic zone, in the inferoposterior part of the frontal lobe
Wernicke’s Aphasia (Receptive or fluent)
• Good expressive but poor receptive (“Word salad” or production of plentiful but garbled sounds)
• Lesion site: Region around the posterior end of the Sylvian fissure at the parieto-occipito-temporal
confluence in the auditory and visual word association area
Ideomotor - Inability to perform a motor act on command that can be performed spontaneously
• Ask the patient to demonstrate the sequence in how to use a key to lock or unlock a door, or how to use a
match to light a candle
Apraxia Ideational - Defect in the actual handling of common objects or loss of a conceptual knowledge relating to the
Inability to perform a voluntary act: use of tools
• Intact motor system • Ask what a key or hammer is used for
• Intact sensorium Constructional - Inability to put together component parts to form a single shape or figure
• Good comprehension • Ask the patient to copy geometric figures or construct them out of matchsticks
• Previous skills where sufficient to perform the Dressing - Inability to orient the clothes and put them on, and getting the shoes in the right foot
act • Ask the patient to get dressed
• Cause of deficit is an organic cerebral lesion Gait (Bruns)
• Ask the patient to rise and walk
Writing and Speaking
• Aphasia (Discussed above)
Anosognosia • Two techniques
Lack of awareness of any bodily defect ○ Ask the patient whether there is anything wrong with his left or right side. The patient will answer “No”.
Then, ask the patient if he can move his left or right arm. The patient will answer “Yes” despite complete
hemiplegia
○ Stand on the affected side of the patient and place the hemiplegic arm beside the patient. Lay your own
arm (same side as the patient’s hemiplegic arm) across the patient’s waist. If you ask the patient to pick
up his arm, he will pick up yours.
Hemispatial Inattention / Neglect • Patient ignores persons, objects, or any stimuli from the affected side, fails to dress that side, and fails to eat
Failure to attend to the entire other half of space the food from the other half of the plate
• Two techniques
○ Ask the patient to draw a cross or any symmetrical figure. The patient will only draw one half of the
figure accurately and make mistakes in completing the opposite side
○ Draw a straight line 20 cm long across a sheet of paper and ask the patient to make a pencil mark
exactly in the center. The patient makes the mark considerably to one side because of neglect of the
other half of the space
Sensory Inattention • Technique for tactile inattention to simultaneous bilateral stimuli
○ Inform the patient that you may touch one or both sides. With the patient’s eyes closed and using light
pressure, brush one or simultaneously both cheeks randomly with the tips of your index finger or wisps
of cotton. Ask the patient to report what is felt. Test for the dorsum of the hands and the feet as well.
• Technique for tactile inattention to simultaneous unilateral stimuli
○ On one side, simultaneously touch the face and hand several times. Ask the patient to report what is
felt. Do the same for the foot and hand, and face and foot.
Clock Drawing Test - Screening for cognitive impairment and dementia and as a measure of spatial dysfunction
Special Test and neglect
• Ask the patient to draw a clock, with the hour and minute hands on a specific time
Gerstmann’s Syndrome – Caused by lesions in the dominant parietal lobe
• Right-left confusion
Must Know • Agraphia
• Finger Agnosia
• Acalculia
CRANIAL NERVE EXAM

Cranial Nerves: Oh Oh Oh, To Touch And Feel Very Good Velvet, Such Heaven!
Sensory/Motor/Both: Some Say Money Matters But My Brother Says Big Brains Matter Most
• Examine the nostrils for any occlusions present. Ask the patient for nasal congestion.
CN I • Trial 1: With the patient’s eyes closed, compress one nostril, and instruct him to sniff and identify the odor.
(Olfactory) • Trial 2: Do the same test on the other nostril without the stimulus. The absence of stimulus tests the patient’s attentiveness
• Repeat trial 1 on the untested nostril.
• Eye Inspection
○ Symmetry
○ Ptosis – drooping of the upper eyelid
○ Exophthalmos – anterior bulging of the eye
○ Enophthalmos – posterior displacement of the eye
• Visual Acuity
○ Ask if the patient wears corrective lenses
○ With the Jaegger chart held 14 inches away or at arm’s length, or a Snellen chart at 20 feet away, test one eye at a time,
then test with the corrective lenses.
○ For partially blind patients
▪ Count the number of fingers held up at various distances
▪ If they cannot count, see if they can identify hand movements
▪ If hand movements are not visible, check for light perception
• Confrontational Test (Testing of visual fields)
○ Position yourself directly in front of the patient at eye level and test for one eye at a time. Ask the patient to cover one eye
with the palm of the ipsilateral hand
○ Hold a finger equidistant between you and your patient’s eye and start testing from the inferior temporal quadrant
○ Slowly wiggle the finger and move it towards the central field of vision. Ask the patient to say when he is able to see it.
CN II ○ Perform it on all quadrants and on the other eye.
(Optic) ○ To refine the test, you can try asking the patient the number of fingers you are holding up
▪ Use either 1, 2, or 5 fingers, as 3 and 4 fingers are too complicated
• Pupillary Light Reflex
○ Check for the baseline size of the pupil and if they are equal in size. Check for:
▪ Miosis – constricted pupil
▪ Mydriasis – dilated pupil
▪ Anisocoria – one pupil is more constricted than the other
○ Ask the patient to look straight ahead
▪ To check for direct light reflex, starting from the lateral side, move the penlight towards the pupil and observe for
constriction (normal). Do the same on the other eye.
▪ To check for consensual light reflex, do the same technique for testing direct light reflex, but this time, do a crossover
of the penlight to the other eye, passing through the midline. Observe if the other eye is already constricted (normal) or if
it is just starting to constrict (abnormal)
• Swinging Flashlight Test
○ Alternatively swing the light from one eye to the other. Hold on the new eye for 3-5 second intervals. Watch for equal
reactions of both pupils
• Tonometry
○ Palpate the patient’s eyes while he is looking down. It should be firm (firms like the tip of the nose)

CRANIAL NERVE EXAM
• Fundoscopy
○ Turn of the lights and ask the patient to fixate on a specific point straight ahead.
○ Instruct the patient to blink as needed and breathe normally.
○ Remember to hold the ophthalmoscope with your right hand and use your right eye when viewing the right eye of the
patient, to hold the ophthalmoscopy with your left hand, and use your left eye when viewing the patient’s left eye.
○ Start with the ophthalmoscope about 10-15 cm away from your patient’s eye at a 20-45 degree angle temporally.
○ Report the following:
▪ Presence of absence of red-orange reflex (ROR)
▪ Clear or hazy media
▪ Distinct or indistinct optic disc borders
▪ Cup-Disc ratio
▪ Ratio of arteries to veins (AV Ratio of 2:3)
▪ Presence or absence of hemorrhage, exudates, or detachment
▪ Foveal reflex
○ Repeat on the other eye
• Smooth Pursuit
○ Ask the patient to face straight ahead and to keep his head still throughout the exam
○ Hold up your finger about 30 cm away and ask the patient to fixate on it. Move your finger slowly all the way across from the
CN III, IV, & VI
right to the left, and up and down, making an invisible H figure.
(Oculomotor, Trochlear,
▪ Vertical finger – for horizontal eye movements
Abducens)
▪ Horizontal finger – for vertical eye movements
• Accommodation and Convergence
○ Ask the patient to stare at your finger as it is brought closer at the midline. There must be constriction of pupils.
Corneal Reflex
CN V
• Roll a piece of cotton to a fine point. While holding the eyelids in place, touch the patient’s cornea to elicit a blink
(Trigeminal)
○ CN V1 (Ophthalmic Nerve) – afferent component; senses the stimulus
• CN VII – efferent component; elicits the motor response
• V1 – Face and scalp
Light Touch on the Face
above the orbit, to tip of
○ Ask the patient to close his eyes. Using a cotton lightly touch the three sensory divisions of CN V and ask the patient if he
the nose
can feel it. Perform it on both sides of the face and check for symmetry.
• V2 – Below the orbits
Test for the Temporalis and Masseter Muscles
and above the mouth,
• Palpate the temporalis and masseter muscles and check for atrophy. While palpating, ask the patient to bite and check for
including the nasal
bulging of the masseter muscle. The temporalis muscle is difficult to palpate.
cavity, maxillary teeth,
and maxillary sinus
• V3 – Has both sensory Test for Lateral Pterygoid Muscle
and motor components • Ask the patient to move the jaw by protruding it and moving it from side to side. Try to resist the patient’s movements by moving
it back to the center.
Test for Taste (Anterior 2/3 of the tongue)
• Two stimuli will be needed: sugar and salt
• Ask the patient to keep his tongue out while conducting the test so that the stimulus will be kept at one place. Apply the stimulus
to one side of the tongue and ask the patient to identify what he is tasting.
• You can also prepare a piece of paper with different tastes written on it. The patient can then point what he is currently tasting so
he won’t need to pull back his tongue upon answering
• Repeat on the other side
CN VII
Test for Motor Component
(Facial)
• Always observe for facial asymmetry
• Check for the frontalis muscle, orbitalis and orbicularis oculi, buccinators, and platysma through facial expressions
○ Wrinkle forehead and raise eyebrows, Close eyelids forcefully and resist against your attempt to open it. Smile, Whistle/puff
out the cheeks
• Make the patient say “Mi Mi Mi” – Test for difficulty in speaking
Central Facial Nerve Palsy - Presents with “forehead sparing” and affect only the lower part of the face
Peripheral Facial Nerve Palsy - Affects both upper and lower parts of one side of the face
Gross hearing
• Note patient’s ability to hear normal conversational voice, watch ticking, or finger rustling
Rinne’s
• Place the tuning fork on the mastoid process. When the patient no longer hears anything, bring the tuning form to the patient’s
ear and ask if he can still hear a sound
CN VIII Weber’s
(Vestibulocochlear) • Place the tuning fork at the vertex or forehead and ask the patient if there is lateralization
Hearing Loss Rinne Test Weber Test

None AC > BC Midline
Sensorineural AC > BC Normal Ear
Bone Conduction BC > AC Affected Ear
.
Test for Symmetry of Palatal Elevation
• Ask the patient to open his or her mouth and say “Ah”. Look at the palate and the arch, not the uvula. Observe for symmetry of
the tonsillar pillars as they arch upward and medially
CN IX & X • Make the patient say “Ka-Ka-Ka”
(Glossopharyngeal, Vagal)
Test for Gag Reflex
• Warn the patient and instruct him to open his mouth again. Touch the back of the throat lightly on each side using a tongue
depressor. Observe for symmetrical palate elevation
Test for Sternocleidomastoid Muscle
• Hold the palm of your hand against the patient’s cheek, and ask them to turn their head towards the side of resistance. Repeat
CN XI on the other side. Test for neck flexion by having the patient flex the neck against resistance by pushing against his forehead.
(Spinal Accessory)
Test for Trapezius Muscle
• Have the patient shrug the shoulders against resistance by pressing down on his shoulders
Test for Tongue Movement and Tongue Strength
CN XII • Ask the patient to protrude his tongue and move it side to side. Observe for atrophy, fasciculations and deviations.
(Hypoglossal) • Have the patient press his tongue against resistance by pressing on his cheeks
• Make the patient say “La-La-La”

SENSORY EXAMINATION
Tract Tested Sensation Modality
With a cotton, apply light pressure on the different dermatomes and ask if the patient can
Light Touch
feel it.
Spinothalamic Pin Prick or Pain With a pointed object, ask the patient is the pain is sharp or dull.
With the shaft of a tuning form or stethoscope as a cold device, and your little finger for
Temperature
warmth, ask if the object touching them is cold or warm.
With a tuning form, place it on any bony prominence, and ask if the patient can feel the
vibration.
Vibration Sense
• Upper extremities - ulnar styloid process or distal radius
• Lower extremities – internal malleolus or shin
Posterior Dorsal Columns Orient the patient what is up and down. Always hold the patient’s finger on the sides and
Joint Position Sense separate the other digits from the one being tested. Move the finger up or down, and ask
the patient what position it is in.
The patient must be able to stand straight with feet together without swaying when eyes
Romberg Test for Propioception
are open. Have the patient close his eyes and observe for swaying.
The patient’s eyes must always be closed
Remember Always compare both sides for equal sensation
Alternate between two stimuli (no light pressure or with light pressure, sharp or dull pain, etc) to see if the patient is attentive.
MOTOR AND DEEP TENDON REFLEXES EXAM

Check for symmetry, muscle bulk (hypertrophy/atrophy), fasciculations, involuntary movements, tremors (resting/postural), and muscle tone (hypertonia/hypotonia)
Always check for laterality and to do the same tests on the contralateral side.
Spasticity
• Increased muscle tone that is rate dependent (tone is greater when passive movement is rapid and less when slow)
• Upper motor neuron or corticospinal tract lesion
Rigidity
• Increased resistance that persists throughout the movement arc, independent of rate of movement (lead pipe rigidity)
• Lesion in basal ganglia system
Flaccidity
• Loss of muscle tone
• Lesion in lower motor neuron system (anterior horn to peripheral nerves
Paratonia or Gegenhalten
• Sudden changes in tone with passive range of motion
• Lesion usually in frontal lobes, both hemispheres
Muscle Grading Check for Subtle Signs of Weakness

5 Full range of motion against • Pronator drift
maximum resistance ○ Supination is weaker than pronation
4 Full range of motion against • Arm rolling
minimum resistance ○ Stronger arm will revolve around the weaker arm
MOTOR
3 Full range of motion against gravity

2 Motion with gravity eliminated (side Upper Extremity Muscle Strength Lower Extremity Muscle Strength
to side) • Shoulder abduction (C5, C6) • Hip flexion (L1, L2); extension (S1)
1 Flicker of contraction • Elbow flexion (C5, C6); extension (C7, C8) • Knee flexion (S1); extension(L3, L4)
0 Complete Paralysis • Wrist flexion (C7, C8, T1); extension (C6, C7, C8) • Foot dorsiflexion (L5); plantarflexion (S1, S2)
Check for motor strength in a sequential, • Finger abduction and adduction (C8, T1) • Foot inversion; eversion (L5)
rostrocaudal manner. • Finger flexion and extension (C7, C8, T1)
Reflex Scoring Deep Reflexes Extensor Toe Sign/Babinski Sign
0 Areflexia • Biceps (C5, C6) • Stroke the lateral aspect of the sole from the heel to
1 Hyporeflexia • Triceps (C7) the ball of the foot, curving medially
DTR
2 Normal • Brachioradialis (C6)

3 Hyperreflexia • Quadriceps (L2-L4)
4 Clonus Present • Triceps Surae (S2)
CEREBELLAR EXAM MENINGEAL IRRITATION EXAM

Test for Dysmetria Kernig Test (K - Knee)
• Finger to nose test • With the patient supine and the knee flexed, flex the limb at the hip. When the thigh
• Heel to knee test reaches the vertical position, gently straighten the knee
• Positive: Patient winces with pain
Test for Dysdiadochokinesia
• Thigh patting or alternating pronation-supination test Brudzinski Test (B - Batok)
• Heel tapping • With the patient supine, flex the patient’s head while the restraining the patient’s
chest from rising
Gait and Balance • Positive: Flexion of the lower extremities
• Observe the patient’s posture, stance and gait
• Observe the patient when he stands from a sitting position
• Ask the patient to stand on one foot, hop on one foot, and to walk
• Additional tests for gait: Heel walking, toe walking, tandem walking

PART 6B. CLINICAL CASES
CLINICAL MANIFESTATIONS AND
DISEASE PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL NOTES
COURSE
Manifestations depend on the Reduction in cerebral perfusion • CT (non-contrast) Goals: Acute ischemic stroke (AIS) is
occluded vessel due to acute occlusion of a ○ Initial test of choice • Prevent/reverse brain injury characterized by the sudden
• Hemiparesis, monoparesis, or cerebral artery secondary to ○ Will present as • Optimize cerebral perfusion in loss of blood circulation to an
quadriparesis thromboembolic disease: hypodense the ischemic penumbra area of the brain, typically in a
• Spasticity, hyperreflexia • Occlusion by an embolus: • Cerebral angiogram • Prevent complications vascular territory, resulting in a
• Aphasia usually affects large vessels ○ Gold standard for corresponding loss of neurologic
• Ataxia such as MCA, PCA atherosclerotic Medical Support function.
• Diplopia • In situ thrombosis: usually in stenosis of cerebral Avoid hypoxemia, hypotension
• Dysarthria smaller arteries (lacunar arteries (therefore also prevent Strokes can be divided into 2
• Facial drooping infarction) • MRI hypovolemia), hypoglycemia, types:
• Visual field deficits • Hypoperfusion due to stenosis ○ Done when hyperglycemia (serum glucose • Hemorrhagic (hyperdense)
• Nystagmus of extracranial or intracranial symptoms are should be maintained at • Ischemic (hypodense)
• Sudden decrease in level of vessels: watershed ischemia hyperacute (~15 <6.1mmol/L), and hyperthermia
consciousness minutes) or if Differentiating Hemorrhagic
• Deficits are maximal at onset Necrotic Pathway affected area is too Thrombolysis with IV rtPA Stroke:
Cellular cytoskeletal breakdown small to be detected (recombinant tissue plasminogen • It is less common
Pertinent History and PE is rapid by CT such as activator) • Deficits worsen after onset
Changes in: due to energy failure of the cell strokes in the Indications: • It commonly presents with
• Cranial nerves • Decrease in cerebral blood posterior fossa • Clinical diagnosis of stroke loss of consciousness, intense
• Motor function flow à decreased oxygen and • Onset of symptoms to time of headache, and vomiting due
• Sensory function glucose à failure to produce drug administration £4.5 hours to increased ICP
• Gait ATP (Time depends on the country) • Common in patients with
• Deep tendon reflexes • Membrane ion pumps stop • CT scan showing no hypertension
• Language (expressive and receptive) functioning à neuron hemorrhage or edema of >1⁄3 of
• Mental status and level of depolarize and intracellular the MCA territory
Acute
consciousness calcium rises • Age ³18years for consent
Ischemic
• Glutamate released from
Stroke
synaptic terminals (also due to Endovascular Revascularization
depolarization) à postsynaptic • Stroke from large vessel
glutamate receptors activated occlusion
à neuronal calcium influx à • May be used in combination
neurotoxicity with rtPA
• Membrane lipid degradation
and mitochondrial dysfunction Antithrombotic Treatment
à free radicals are produced • Aspirin for platelet inhibition
• Free radicals cause catalytic ○ Reduced stroke recurrence
destruction of membranes and risk and mortality if given
damage other functions of within 48 hrs
cells • Anticoagulation: No present
trials that support its use
Apoptotic Pathway
Programmed cell death, which Neuroprotection: Prolongs the
occurs in brain’s tolerance to ischemia by
lesser degrees of ischemia, such decreasing energy consumption of
as in neurons
the area of ischemic penumbra, • Citicoline: Gold standard
in which cell death occurs days
to weeks later Stroke Centers and
Rehabilitation: Improves
neurological outcomes and
reduces mortality

COURSE
• Most are unconscious when first seen • Origin is from a torn dural • CT to see the lesion, OR • Immediate surgical intervention EDH occurs in the potential
• A lucid interval of several minutes vessel, often the middle • MRI to examine the soft • Initial, conservative, close space between the dura and the
to hours before coma supervenes is meningeal artery, which is tissues of the brain clinical observation with cranium, and can also be
characteristics of epidural transected by a fracture of the • Identification of a typical possible delayed evacuation referred to as extradural (outside
hemorrhage, but this is not common squamous portion of the lenticular shape due to • Note that EDHs tend to expand of the dura).
or observed all the time temporal bone the dura tightly attached in volume more rapidly than
• With severe intracranial hypertension, • Extravasation of blood under to the skull subdural hematomas, and EDH results from interruption of
Epidural a Cushing response may occur arterial pressure can cause the patients require very close dural vessels, including branches
Hematoma dura to separate from the inner observation if the conservative of the middle meningeal arteries,
Pertinent History and PE surface of the skull route is taken veins, dural venous sinuses, and
• Glasgow coma scale • The expansion has a smooth skull vessels.
• Level of consciousness, pupillary inner contour that compresses
reactivity and size the brain surface Continued bleeding and growth
• Lateralizing signs (e.g. hemiparesis or can result in intracranial
plegia) hypertension.
Acute Subdural Hematoma • Bleeding is primarily venous • CT Acute Subdural Hematoma In contrast to epidural
• Up to 1/3 of patients have a lucid in origin ○ Crescentic pattern • Small subdural hematomas may hematomas, there is significant
interval lasting minutes to hours ○ Arterial bleeding sites are over the convexity of be asymptomatic and usually do morbidity and mortality
before coma supervenes sometimes found at one or both not require surgical evacuation if associated with acute subdural
• Most are drowsy or comatose from operation hemispheres, most they do not enlarge hematomas that require surgery
the moment of injury ○ Few larger hematomas commonly in the • Emergency craniotomy for
• Signs of larger hematomas: are purely arterial in origin frontotemporal acutely deteriorating patients
○ Stupor or coma • In chronic subdural region
○ Hemiparesis hematoma, the syndrome ○ Initially shows a low- Chronic Subdural Hematoma
○ Unilateral pupillary enlargement occurs days or weeks after density mass, which • Clinical observation with serial
injury becomes isodense imaging for patients with few
Pertinent History and PE compared to symptoms and small chronic
• Glasgow coma scale adjacent brain and subdural collections that do not
• Note level of consciousness, pupillary may be inapparent cause mass effect
reactivity, and size • MRI • Surgical evacuation through burr
• Lateralizing signs (e.g. hemiparesis or ○ Reliably identifies holes is usually successful
plegia) both subacute and • Cranial drain is used
• Unilateral headache chronic hematomas postoperatively
Subdural
Hematoma
Chronic Subdural Hematoma
• Occurs days or weeks after injury
• Headache typically fluctuating in
severity, sometimes with changes in
head position
• Drowsiness, inattentiveness, and
incoherence of thought are generally
more prominent than focal signs such
as hemiparesis
• Slowed thinking, vague change in
personality, seizure or a mild
hemiparesis may appear weeks after
the injury
Pertinent History and PE

• History of trauma may or may not be
elicited in relation to chronic subdural
hematoma

COURSE
○ Injury may have been trivial and
forgotten
• Mental status exam
• Changes in behavior and personality
• Lateralizing signs (e.g. hemiparesis or
plegia)
• Sudden transient loss of • Saccular aneurysms occur • Blood in the CSF – • Early aneurysmal repair and Subarachnoid Hemorrhage is the
consciousness at the bifurcations of large laboratory hallmark correction of increased ICP extravasation of blood into the
• Preceded by a brief moment of arteries at the base of the • HQ non-contrast CT while maintaining adequate subarachnoid space between
excruciating generalized headache brain scan within 72 hours cerebral perfusion pressure (60- the pia and arachnoid
(“worst of my life”, thunderclap ○ As an aneurysm develops, it • If it fails, lumbar 70mmHg)  membranes.
headache) often associated with typically forms a neck with a puncture should be • Correction of hyponatremia and
vomiting and neck stiffness dome done to establish maintenance of euglycemia and It occurs in various clinical
• Delayed neurologic deficits may be ○ The arterial internal elastic presence of euvolemia  contexts, the most common
due to re-rupture, acute lamina disappears at the subarachnoid blood • Blood pressure management  being head trauma.
hydrocephalus, vasospasm, or base of the neck with glucocorticoids may relieve
hyponatremia ○ The media thins and headache and neck stiffness However, the familiar use of the
connective tissue replaces • Short-acting anticonvulsants for term
Subarachnoid
Pertinent History and PE smooth-muscle cells patients with seizures  SAH refers to nontraumatic (or
Hemorrhage
• History of atherosclerosis, ○ At the site of rupture (most • If with significant spontaneous) hemorrhage, which
hypertension, advancing age, often the dome), the wall hydrocephalus, consider usually occurs in the setting of a
smoking, hemodynamic stress, oral thins and the tear allows the ventriculoperitoneal shunt ruptured cerebral aneurysm or
contraceptive use, hormone bleeding insertion arteriovenous
replacement therapy, • The rupture is into the malformation (AVM), most
hypercholesterolemia, engagement in subarachnoid space in the commonly the rupture of
vigorous physical activity basal cisterns and often into saccular aneurysm.
• Fundoscopy: +/- papilledema the parenchyma of the
• Global or focal neurologic activities adjacent brain
• 85% occur in the circle of
Willis.
• Classic triad of fever, headache, • Most common form of • Blood culture • Empiric antibiotic treatment Meningitis is the inflammation
and nuchal rigidity suppurative CNS infection • CSF examination such as Penicillin or Ampiciliin, of the leptomeninges and CSF
• Acute fulminant illness which caused by S. pneumonia • Serology Ceftriaxone + Vancomycin within the subarachnoid space.
progresses rapidly in a few hours which colonizes the • CT/MRT prior to lumbar • Adjunctive treatment to
• Other symptoms: decreased level of nasopharynx and attaches to puncture decrease adverse effects such Bacterial meningitis is an acute
consciousness, nausea and projectile the epithelial cells • Nasopharyngeal swab as Dexamethasone purulent infection within the
vomiting, photophobia, seizures, • Bacteria can reach the subarachnoid space primarily
raised ICP, petechiae intraventricular choroid plexus due to the S. pneumonia and N.
and gain access to the CSF meningitidis
Acute
Persistent History and PE through membrane-bound
Bacterial
• Nuchal rigidity vacuoles, and multiply rapidly
Meningitis due to the absence of effective
• Epidemiologic factors and
predisposing risks host immune defenses
• Exposure to patients or animals with • Its multiplication leads to
similar illness inflammatory response and
• Previous medical treatment and bacterial injury which
existing conditions produces the symptoms.
• Geographic location and travel history • Increase in vessel permeability
• Season and temperature due to cytokine and
chemokine release leads to

COURSE
increased blood-brain
barrier permeability
• Leakage of serum proteins
into the subarachnoid space
obstructs CSF outflow leading
to edema, increased ICP, and
cerebral ischemia and
eventually necrosis
• Classic triad of fever, headache, • Depending on the etiology, it • CSF analysis from • Symptomatic treatment: Viral meningitis is a self-limiting
and nuchal rigidity can be introduced by droplet lumbar puncture – most analgesics, antipyretics, and disease, most commonly caused
• Constitutional signs: mild alteration of inhalation (VZV), direct important antiemetics by Enterovirus.
consciousness, malaise, cough, contact (HSV, EBV, HIV), or • PCR for diagnosing • Fluid and electrolyte therapy
myalgia, anorexia, nausea and mosquito bite (Arbovirus) Enteroviral and HSV • Antiviral Acyclovir for It is more common, but not fatal
vomiting, abdominal pain, and/or • Virus replication occurs at the infections immunocompromised
diarrhea initial organ system and gains • Viral culture • Antiretroviral therapy for HIV
access to the CNS by • Serologic studies for patients
Pertinent History and PE hematogenous or axonal diagnosis of Arbovirus
Acute Viral
• Nuchal Rigidity: Kernig’s or spread and HIV
Meningitis
Brudzinski’s • Transmitted by viremia • Blood tests
• Suggestive of enteroviral infection: (EBV/Arbo), axonal transport • CT/MRI
exanthema (VZV), or
• Symptoms of pericarditis, myocarditis, macrophage/microgial (HSV)
or conjunctivitis
• Syndromes of pleurodynia,
herpangina, and hand-foot-and-mouth
disease
• Acute febrile illness with evidence of • Most common etiology is • CSF analysis should be • Specific antiviral therapy Encephalitis is defined as an
meningeal involvement characteristic Herpesviridae (HSV-1, Herpes performed in all patients should be initiated when inflammation of the brain caused
of meningitis Zoster, EBV) with suspected viral appropriate by infection, usually with a virus,
• Altered level of consciousness • Its pathogenesis is very similar encephalitis unless • Intensive care may be required or from a primary autoimmune
(confusion, behavioral abnormalities) to Viral Meningitis contraindicated by the in initial stages of encephalitis process.
• Hallucinations, agitation, personality presence of severely • Basic management and
change, behavioral disorders, and increased ICP supportive therapy should In contrast to meningitis, the
frankly psychotic state may occur • CSF PCR for diagnosing include careful monitoring of brain
• Focal or generalized seizures CMV< EBV, HHV-6 and ICP, fluid restriction, avoidance parenchyma is also involved in
Viral
• Most commonly encountered focal enteroviruses of hypotonic IV solutions, and encephalitis
Encephalitis
findings are aphasia, ataxia, upper or • Serological studies and suppression of fever
lower motor neuron patterns of antigen detection for • Anticonvulsant regiments, and
weakness, involuntary movements, Arboviruses prophylactic therapy when there
and cranial nerve deficits • MRI/CT/EEG is high frequency of seizures in
• CSF culture is generally severe cases of encephalitis
Pertinent History and PE of limited utility in the • Acyclovir for HSV treatment
• Level of consciousness diagnosis of acute viral
• Changes in behavior and mental state encephalitis
• The clinical syndrome consists of • Incubation from ingestion of Diagnosis is done • Meticulous intensive care Botulism is a neuroparalytic
bilateral cranial-nerve palsies that may contaminated food to onset or clinically and laboratory • Botulinum antitoxin disease
progress to respiratory compromise, a symptoms in food-borne confirmation by specific ○ Should be administered caused by botulinum toxin
Botulism
bilateral descending flaccid paralysis botulism is usually 8-36 hours tests are performed only in empirically as it is most produced by four recognized
of voluntary muscles, and even death but can be as long as 10 days specialized public-health beneficial early in the course species of clostridia: Clostridium
and is dose-dependent laboratories of the clinical illness botulinum, and rare strains of

COURSE
• Patients are afebrile and remain alert • Food-borne botulism is • Demonstration of the ○ The antitoxin can limit the Clostridium argentinense,
and oriented caused by consumption of toxin in clinical progression of the illness as it Clostridium baratii, and
• Cranial nerve deficits may manifest foods contaminated with specimens (serum, neutralizes the toxin in the Clostridium butyricum, which are
as diplopia, dysarthria, dysphonia, botulism toxin stool, gastric aspirate) circulation that are not yet all anaerobic gram-positive
ptosis, ophthalmoplegia, facial • Wound botulism is caused by or samples of ingested bound to nerve endings, spore-forming organisms.
paralysis, impaired gag reflex, toxin produced from food however it cannot reverse
depressed pupillary reflex germinating C. botulism • Isolation of toxigenic existing paralysis Botulinum serotype A produces
• Weakness descending from the spores that contaminate an clostridia from stool the
head to the trunk and extremities abscess or a wound • Wound cultures yielding most severe syndrome, with the
• Cranial never deficits and weakness • Infant botulism is caused by a the organism are highly greatest proportion of patients
can be asymmetric toxin produced in situ by suggestive in requiring mechanical ventilation.
○ Dysarthria, ptosis, and paresis toxigenic clostridia colonizing symptomatic cases
may lead to misdiagnosis of the intestine of children <1 • Because of the toxin’s There is no available
altered mental status year of age extreme potency, serum prophylaxis or
• DTRs may be normal or progressively • Regardless of how exposure toxin concentrations licensed vaccine against
disappear occurs, botulinum neurotoxin below the laboratory botulism.
• Constipation due to paralytic ileus enters the vascular system detection threshold can
• Urinary retention and is transported to cause illness in a patient
• Respiratory failure either due to peripheral cholinergic nerve whose test yields a
paralysis of the diaphragm and terminals, including negative result
accessory breathing muscles or to neuromuscular junctions,
pharyngeal collapse secondary to postganglionic
cranial nerve paralysis parasympathetic nerve
endings, and peripheral
ganglia
• Irritation of the underlying cortex, • Meningioma are • CT Scan (isoattenuating Surgery Meningiomas are usually slow-
which can cause seizures predominantly benign to slightly • Most common treatment for a growing lesions that present
• Compression of the underlying tumors of adults, usually hyperattenuating) meningioma either with vague non-
brain can cause generalized cerebral found along any of the • MRI-enhanced • Periodic imaging to monitor any localizing symptoms or with
dysfunction, focal weakness, external surfaces of the • Cerebral Angiogram recurrence of a tumor focal findings referable to
dysphasia, apathy, somnolence, brain as well as within the ○ A meningioma can compression of underlying
localized or nonspecific headaches ventricular system, where block important Radiation therapy after surgery brain.
• Stereotypic symptoms depending on they arise from the stromal veins that drain • For the most malignant
the specific location of the arachnoid cells of the choroid blood from the brain, meningioma or when the Common sites of involvement
meningioma plexus. it is sometimes neurosurgeon cannot include the parasagittal aspect of
• Narrowing or occluding of cerebral • Prior radiation therapy, important to get an completely remove the the brain convexity, dura over
arteries presenting as transient typically decades earlier, is a angiogram to plan meningioma the lateral convexity, wing of the
ischemic attack-like episodes or risk factor for development of surgery. In addition, • Also used to treat meningioma sphenoid, olfactory groove, sella
Meningioma stroke meningioma. there may be in locations where surgery is not turcica, and foramen magnum
• May also present with obstructive • Other tumors such as abnormal blood safe.
hydrocephalus, panhypopituitarism, metastases, solitary fibrous vessels that feed the
visual field defects, and hematologic tumors, and a range of poorly tumor and these can Observation
disturbances differentiated sarcomas may be seen with the • Small meningioma that does not
also grow as dural-based angiogram cause any significant signs or
Pertinent History and PE masses. symptoms
• Increased ICP: papilledema,
decreased mentation, and brain
herniation
• CN involvement: anosmia, visual field
defects, optic atrophy, diplopia,
decreased facial sensation, facial
paresis, decreased hearing, deviation

COURSE
of the uvula, and hemiatrophy of the
tongue
• Compression: pyramidal signs such
as pronator drift, hyperreflexia,
Babinski sign, Gerstmann syndrome
(dominant parietal lobe), tactile and
visual extinction (nondominant parietal
lobe), homonymous hemianopsia
(occipital lobes)
• Onset may be abrupt or insidious Three types of MS • MRI There are currently no treatment Multiple Sclerosis (MS) is an
• Symptoms may be severe or seem so • Relapsing or bout onset MS ○ Detects increased that promote remyelination or autoimmune disease of the
trivial that a patient may not seek (RMS) vascular neural repair central nervous system
medical attention for months or years – accounts for 90% of MS permeability from characterized by chronic
• Sensory symptoms are varied and cases and is characterized by BBB breakdown as Treatment of acute attacks inflammation, demyelination,
include both paresthesia and discrete attacks of IV gadolinium leaks • Glucocorticoids gliosis (plaques and scarring),
hypesthesia. neurological dysfunction that into the parenchyma ○ Used to manage either first and neuronal loss, with a
• Optic neuritis presents as diminished generally evolve over days to ○ Such leakage occurs attacks or acute relapsing or progressive course.
visual acuity, dimness, or decreased weeks early in the exacerbations
color perception (desaturation) in the • Secondary progressive MS development of an ○ Usually administered as IV Most patients with clinically
central field of vision, and may (SPMS) – always begins as MS lesion and methylprednisolone evident MS ultimately experience
progress to severe visual loss. RMS, before the clinical serves as a useful • Lithium Carbonate progressive neurologic disability.
• Weakness of the limbs may manifest course changes, in which the marker of ○ May help manage emotional
as loss of strength, speed, or patient experiences inflammation lability and insomnia
dexterity, as fatigue, or as disturbance deterioration in function • Evoked Potential associated with
Multiple unassociated with acute
of gait. ○ Assesses function in glucocorticoids
Sclerosis attacks
• Exercise-induced weakness is afferent (visual, • Plasma Exchange
characteristic of MS • Primary progressive MS auditory, and ○ May benefit patients with
• Facial weakness due to a lesion in (PSMS) somatosensory) or fulminant attacks of
the pons may resemble idiopathic – accounts for 10% of cases; efferent (motor) CNS demyelination that are
Bell’s palsy patients do not experience pathways unresponsive to
• Spasticity is commonly associated attacks but rather steadily • CSF glucocorticoids
with spontaneous and movement- decline in function from ○ Typical findings:
induced muscle spasms disease onset Mononuclear cell Treatment with disease-
• Ataxia usually manifests as cerebellar pleocytosis; modifying agents that reduce
tremors, and may involve the head increased level of biologic activity of MS
and trunk, or the voice (dysarthria) intrathecally • More than a dozen
• Vertigo may appear suddenly from a synthesized IgG; immunomodulatory and
brainstem lesion normal or mildly immunosuppressive agents are
elevated protein approved
• May present at any age • Anti-AChR antibodies • As a general rule, a firm • The anticholinesterase drug Myasthenia Gravis (MS) is a
• Symptoms fluctuate throughout the reduce the number of diagnosis is based upon Pyridostigmine (Mestinon) neuromuscular junction (NMJ)
day and are provoked by exertion available acetylcholine ○ A characteristic titrated to assist patient with disorder characterized by
• Eyelids and extraocular muscles are receptors at the NMJ. history and physical functional activities (chewing, weakness and fatigability of
affected causing drooping of one or Postsynaptic folds are examination, and swallowing, strength during skeletal muscles.
Myasthenia both eyelids (ptosis) and double vision flattened, with resulting ○ Two positive exertion)
Gravis (diplopia) inefficient neuromuscular diagnostic tests, • Plasmapheresis or IV immune The underlying defect is a
• In about 15% of people with MG, the transmission. preferably globulin provides temporary decrease in the number of
first symptoms involve face and • During repeated or sustained serological and boost for seriously ill patients, available acetylcholine
throat muscles: muscle contraction, the electrodiagnostic. used to improve conditions receptors (AChRs) at NMJs
○ Altered speaking. decrease in the amount of ACh • Diagnostic before surgery due to an antibody-mediated
○ Difficulty swallowing. released per nerve impulse, investigations of MG

COURSE
○ Problems chewing. combined with disease- should usually include • Thymectomy improves the autoimmune attack.
○ Limited facial expressions specific decrease in both likelihood of long term remission
• Specific muscle weaknesses postsynaptic AChRs, results in ○ Testing for serum in adult patients In comparison to Lambert-
○ In 85%, limb muscles (often pathologic fatigue. anti-AChR Eaton
proximal and asymmetric) are • Thymus is abnormal in 75% of antibodies Myasthenic Syndrome
involved the patients. ○ Repetitive nerve • Clinically characterized by
• Reflex and sensation normal • Other autoimmune diseases stimulation studies weakness improved with
• Complications: aspiration pneumonia, may coexist such as • Tensilon tests activity, fatigability or
respiratory failure, etc. Hashimoto thyroiditis, Graves’ ○ May be readily proximal limb muscles, and
disease, SLE, RA performed at the sparing of extraocular and
bedside bulbar muscles
○ Are not as sensitive, • It is associated with
or specific, as the underlying neoplasms (70%
serological and associated with oat cell
electrophysiological carcinoma of the lung)
studies • Antibodies against tumor
• Single fiber EMG antigens cross-react with
○ Reserved for calcium channels involved in
selected patients in ACh release
whom other tests • Treatment with plasma
have been negative exchange, IVIG, steroids, and
or equivocal. tumor treatment
• Ascending paralysis that may be first Acute inflammatory • CSF protein levels High-dose intravenous immune GBS is the most common and
noticed as rubbery legs demyelinating (elevated or serial globulin (IVIg) best-
• Weakness (hours-days) accompanied polyneuropathy elevation) • Administered as five daily studied type of acute
by dysesthesias in the extremities • Both cellular and humoral • CSF cell count (<10 infusions for a total dose of 2 inflammatory demyelinating
• Legs > arms immune mechanisms mononuclear g/kg body weight polyneuropathy
• Bulbar weakness with difficulty contribute to tissue damage cell/mm3) • Ease of administration
handling secretions and • Cellular elevated levels of • EMG-NCV studies • Good safety record It occurs more frequently among
maintaining an airway (lower cranial cytokines and cytokine • Has anti-idiotypic antibodies patients with lymphoma, HIV-
nerves are affected) receptors in serum and CSF that neutralizes GBS antibodies seropositive individuals, and
• Early GBS: pain in the neck, • Immune responses to non- those with SLE
Guillain-Barre
shoulder, back, or diffusely over the self-antigens that misdirect to Plasmapheresis
Syndrome
spine host nerve tissue through a • ~40–50 mL/kg plasma exchange
• DTRs attenuate or disappear within “mimicry” mechanism (PE) four to five times over a
the first few days of onset • Target: gangliosides → week
• Loss of vasomotor control with wide rendering them susceptible
fluctuation in blood pressure, postural to an antibody-mediated
hypotension, and cardiac attack
dysrhythmias • Pathologic C. jejuni strains
amplifies humoral
autoimmunity

COURSE
• Cardinal features: The hallmark features are: • Imaging of the brain Levodopa Parkinson’s Disease is the
○ Rest tremor • Degeneration of dopamine system with • Mainstay therapy of PD and the second
○ Rigidity (stiffness) dopaminergic neurons in the positron emission gold standard most common age-related
○ Bradykinesia (slowing) substantia nigra pars tomography (PET) or • Routinely administered in neurodegenerative disease,
○ Gait dysfunction with postural compacta single-photon combination with a peripheral exceeded only by Alzheimer’s
instability • Reduced striatal dopamine emission computed decarboxylase inhibitor to Disease
• Additional clinical features include • Intraneuronal proteinaceous tomography (SPECT) prevent its peripheral
freezing of gait, speech difficulty, inclusions known as Lewy ○ Shows reduced and metabolism to dopamine and
swallowing impairment, autonomic bodies and Lewy neurites asymmetric uptake the development of nausea,
disturbances, a series of nonmotor of striatal vomiting and orthostatic
features that include sensory • Dopamine denervation with dopaminergic hypotension
alterations, mood disorders, sleep loss of dopaminergic tone biomarkers,
dysfunction, cognitive impairment, leads to increased firing of particularly in the Dopamine agonists
and dementia neurons in the subthalamic posterior putamen • Act directly on dopamine
nucleus (STN) and globus with relative sparing receptors
pallidus pars interna (GPi), of the caudate • Has shown to be less prone
excessive inhibition of the nucleus than levodopa to induce
thalamus, reduced activation dyskinesia, possibly because it
of cortical motor systems, and is long-acting
the development of
Parkinson’s
parkinsonian features. Monoamine oxidase type B
Disease
(MAO-B)
inhibitor
• Blocks central dopamine
metabolism and increase
synaptic concentrations of the
neurotransmitter
Cathecol-O-methyl transferase
(COMT) inhibitor
• Increase the elimination half-life
of levodopa and enhance its
brain availability
Surgical procedure with deep

brain stimulation (DBS)
• Stimulates the effects of a lesion
without necessitating making a
brain lesion and primarily targets
the STN or the GPi
Focal Onset Seizures • Epileptogenesis – process First goal is to determine • Therapy is individualized and Seizure is the sudden,
• Originate within networks limited to where normal brain undergoes whether the even was almost always multimodal, involuntary, time-limited
one brain region epileptic structural change truly a seizure which includes: alteration in behavior, including a
• Usually associated with structural • Seizures result from a shift in • In-depth History ○ Treatment of underlying change in motor activity,
abnormalities of the brain the normal balance of • Laboratory studies conditions that cause or autonomic function,
Seizures and • Can have motor manifestations (tonic, excitation and inhibition ○ Used to identify the contribute to the seizures consciousness, or sensation,
Epilepsy clonic or myoclonic) or nonmotor within the CNS more common ○ Avoidance of precipitating accompanied by abnormal
manifestations (sensory, autonomic, • Decreased inhibition of the metabolic causes of factors electrical discharge in the brain
or emotional); with or without brain (hyperexcitable brain) seizures such as ○ Suppression of recurrent
impairment of awareness ○ Defective GABA-A and abnormalities in seizures by prophylactic Convulsion is a symptom of a
• May progress to generalized seizures GABA-B inhibition electrolytes, glucose, therapy with antiepileptic seizure
calcium, or medications or surgery

COURSE
Generalized Onset Seizures ○ Defective activation of magnesium, and ○ Addressing psychological or where the muscles contract and
• Arise within and rapidly engage GABA neurons hepatic or renal social issues relax rapidly, resulting in an
networks distributed across both ○ Defective intracellular disease • Antiepileptic drug therapy uncontrolled shaking of the body
cerebral hemispheres buffering of calcium • Electrophysiologic should be started in any
• May result from cellular, • Increased activation of the studies patient with recurrent seizures Epilepsy is a disorder of the
biochemical, or structural excitable channels and ○ All patients who of unknown etiology or a brain
abnormalities receptors have a possible known cause that cannot be characterized by an enduring
• Typical Absence Seizures ○ Increased activation of seizure disorder reversed predisposition to generate
○ Sudden, brief lapses of NMDA receptors should be evaluated seizures and by the
consciousness without loss of ○ Increased synchrony with an EEG as soon neurobiological, cognitive,
postural control usually lasting between neurons as possible. psychological, and social
only for seconds, with sudden ○ Increased synchrony and/or ○ The presence of consequences of this condition
return of consciousness, and no activation due to recurrent electrographic
postictal confusion excitatory collaterals seizure activity Status Epilepticus refers to
• Generalized Tonic-Clonic Seizures during the clinically continuous
○ The initial phase is usually tonic evident event clearly seizures, or repetitive, discrete
contraction of muscles established the seizures with impaired
throughout the body. After 10-20 diagnosis consciousness in the interictal
s, the tonic phase typically evolves ○ The absence of period.
into the clonic phase, produced electrographic
by superimposition of periods of seizure activity does
muscle relaxation on the tonic not exclude a seizure
muscle contraction disorder
○ The post-ictal phase is • Brain Imaging
characterized by ○ Almost all patients
unresponsiveness, muscular with new-onset
flaccidity, and excessive salivation. seizures should have
Bladder or bowed incontinence a brain imaging
may occur at this point study to determine
whether there is an
Epileptic Syndromes underlying structural
• Juvenile Myoclonic Epilepsy abnormality
○ Generalized seizure disorder of responsible for the
unknown cause that appears in seizure
early adolescence ○ MRI has been shown
○ Usually characterized by bilateral to be superior to CT
myoclonic jerks that may be single for the detection of
or repetitive cerebral lesions
• Lennox-Gastaut Syndrome associated with
○ Occurs in children epilepsy
○ Defined by a triad of (1) multiple • Genetic Testing
seizure types, (2) an EEG showing ○ Can provide a
slow (<3 Hz) spike-and-wave definitive diagnosis
discharges, and other ○ Can offer a guide for
abnormalities, and (3) impaired therapeutic options
cognitive function in most cases ○ Presently, being
• Mesial Temporal Lobe Epilepsy done mainly in
Syndrome infants and children
○ Example of epilepsy syndrome with epilepsy
with distinctive clinical, thought to have a
electroencephalographic, and genetic cause
pathologic features

MODULE/TOPIC 7 HEAD, EYES, EARS, NECK, THROAT
PART 7A. FOCUSED HISTORY AND PHYSICAL EXAMINATION

ORGAN BASIC STEPS HOW TO TEST RESULTS PATHOLOGY ADDITIONAL NOTES
General Guidelines Distance Vision Errors of Refraction Acronyms
• Must always be performed first Normal • Emmetropia: condition Oculus Dexter (OD): Right
o You need to establish a baseline VA • Numerator: test distance wherein parallel light rays Oculus Sinister (OS): Left
first except in cases of chemical • Denominator: distance from which a normal eye can fall into a point of focus on Oculus Uterque (OU): Both
burns read the letters in that line the retina
o Other tests may blur visual acuity • VA = 20/20 (at 20 feet, the patient reads a line a normal • Ametropia: condition Sine Correctione (SC):
• Order of testing eye sees at 20 feet) wherein parallel light rays Without Correction
o Uncorrected Abnormal do not fall into a point of Cum Correctione (CC):
o Corrected (with glasses) • Missed <50% of letters in a line: report VA of that line focus on the retina With Correction
o With pinhole if vision is below 20/20 minus the number of mistakes ○ Myopia (near-sighted)
• Test one eye at a time • Missed >50% of letters in a line: report VA as the line § Eyeball longer than Specialized Visual Acuity
o Use an occluder or the palm of the above it plus the number of of correctly identified letters usual or increased Tests
hand but avoid applying pressure • 20/200: legally blind lens refractive index • Infants: (+)/(-) following
• Ensure good lighting ® image focuses in or fixation on light or
• Ask patient not to squint Near Vision front of retina bright moving objects
• Normal: J1 or +1 § Tx: concave lenses • Older Children: hand
Distance Vision ○ Hyperopia (far-sighted) game (imitate hand of
• Snellen Chart Use of Pinhole § Eyeball shorter than examiner) or CF
• Standard test distance: 20 feet or 6 • Refractive error: improvement with pinhole usual ® image • Adults ≥ 40 years old:
meters • Non-refractive error: no improvement focuses behind the near vision testing
retina • Tumbling E: for illiterate
Near Vision Reporting Findings § Tx: convex lenses patients
• Jaeger Chart: arm’s length ○ Astigmatism • Ishihara Color Vision
(approximately 14 inches) § Curvature of the Test: color blindness (21
EYE
Visual Acuity • Ask patient to read until the smallest cornea or the lens is plates)
(Mnemonic:
Determination line visible not the same in • Macular Degeneration:
VAGETF)
• Can be used to estimate VA in bed- different meridians Amsler Grid
ridden patients § Aspherical cornea
§ Parallel light rays
Alternatives for Poor Visual Acuity focus on 2 separate
Poor VA: patient cannot see the largest lines or planes
letter at 20 feet (6 meters). Tests are • Presbyopia: age-related
done sequentially only if the patient is loss of lens
unable to do the previous test/s. accommodation that results
• Reduced Distance in an inability to focus at
○ Bring patient closer in increments of near distances
one foot at a time until he can read (accommodation)
the biggest letter on the first line of
the chart Most Common Causes of
○ Adjust denominator accordingly Decreased Vision
• Counting Fingers (CF) • Cataract
○ Farthest distance that fingers can be ○ Clouding of lens due to
counted correctly denatured lens protein
○ Do until 6 inches away ○ Types: cortical, nuclear
○ Record as: sclerosis, subcapsular
§ VA = CF __ feet ○ “Second sight”: lens
• Hand Motion (HM) becomes thicker causing
○ Wave hand up/down or left/right the patient to become
and ask patient to determine the near-sighted
area of hand direction • Diabetic Retinopathy

§ Gumagalaw ba o hindi? ○ Non-Proliferative:
○ Record as: change in structure and
§ (+) hand movement cellular composition of
§ VA = HM __ feet/inches microvasculature; retinal
• Light Projection hemorrhages
○ Dim room lights ○ Proliferative: infarction
○ Shine a penlight from each of 4 of nerve fiber layer
quadrants (cotton-wool spots);
○ Ask the patient to point in the neovascularization
direction of the light • Age-Related Macular
○ Record as: Degeneration (AMD)
§ VA: (+) L Projection ○ Most common
RUQ/RLQ/LUQ/LLQ irreversible vision loss
○ Drusen: extracellular
• Light Perception deposits
○ Dim room lights ○ Dry Type: minimal
○ Shine a penlight at a distance from bleeding
the patient’s eyes ○ Wet Type: leakage of
○ Ask the patient if he can perceive blood and choroidal fluid
light (choroidal Neovascular
○ Record as: membrane)
§ VA: YES = Good/Fair/Poor
Light Perception
(GLP/FLP/PLP)
§ VA: NO = No Light Perception
(NLP) (total blindness)
General: symmetry, level, Describe lesions as observed (e.g. patient has an elevated, Marcus-Gunn Pupil: Pupillary Light Reflex
sunken/protruded, strabismus hyperpigmented lesion on the R lower eyelid approx. 1 decreased/absent constriction CN II: afferent arm
(exo/esotropia, hypo/hypertropia), mm x 4 mm) in one pupil on both direct CN III: efferent arm
alignment (shine penlight 3 feet away, and consensual PLR (optic
corneal light reflex should fall the center Reporting Findings nerve lesion or severe retinal Gross Visual Field
of both pupils), inflammation disease) Testing: Finger
(erythema/congestion) Confrontation
Blepharitis: inflammation of • Ask patient to fix gaze
Orbital Socket: palpate for fractures the eyelid margin (S. aureus) straight ahead or on the
(elevations/depressions) or tenderness examiner’s nose
Hordeolum (stye/kuliti): • Examiner and patient
Eyebrows and eyelashes: symmetry, infection of eyelid glands both cover the ipsilateral
lesions, pattern of hair distribution (Meibomian gland or gland of eye with their palm
Zeiss) • Present fingers (1, 2, or 5
Gross Ocular
Upper and Lower Eyelids: eyelashes, lid fingers) in each quadrant
Inspection
closure, ecto/entropion, hordeolum Ectropion: eversion of eyelid • Ask patient to identify
margin how many fingers
Conjunctiva: should be smooth and Entropion: inversion of eyelid • Test both eyes
pink margin
Lower palpebral conjunctiva:
pull lower lid down and ask patient to Strabismus: non-alignment of
look up eyes
Upper palpebral conjunctiva:
hold the upper lid up with a cotton Anisocoria: unequal pupil
applicator and ask patient to look down size
Bulbar conjunctiva
Common Causes of Red Eye
Sclera: white, opaque, anicteric • Conjunctivitis: conjunctival
inflammation

Cornea and iris: clear, transparent • Keratitis: corneal
inflammation
Pupils: round, equal and briskly reactive ○ Bacterial (S.
to light (EBRL), anisocoria (unequal pupil pneumoniae, P.
size, pupillary light reflex aeruginosa)
• Direct: pupils constrict by 1-2 mm ○ Fungal (Candida spp.)
upon penlight stimulation ○ Viral (Herpes simplex)
• Consensual: both pupils should • Corneal Abrasion
constrict simultaneously and equally • Acute Angle Closure
upon penlight stimulation of one eye Glaucoma: increased
intraocular pressure
Lens: clear, (+) red-orange reflex (ROR) • Uveitis: anterior eye
(T/N: + dots and patches = cataract) inflammation
• Dry Eye
H Movement • Full EOMs on both duction and version Cranial Nerve Lesions MNEMONIC: LR6/SO4, all
• Sit at a distance in front of the patient, • Full EOM on convergence CN III: ptosis, large pupil, eye the rest CN3
same eye level • (+)/(-) nystagmus down and out • Lateral Rectus: CN VI
• Ask patient to follow the tip of your CN IV: diplopia (double vision) • Superior Oblique: CN IV
finger with his eyes and without Reporting Findings on looking down or in • Other EOMs (MR, IR, SR,
moving his head • 3 lines: cardinal directions of gaze CN VI: diplopia on lateral gaze IO): CN III
Extraocular ○ Bring target to extremes of gaze • Arrowheads: right eye Nystagmus: vertical or lateral
Muscle • Examiner moves finger in an H-pattern • Circles: left eye
Movement ○ Duction: one eye tested, other eye *Indicate until where the movement can reach each
occluded plane
(EOMs)
○ Version: both eyes tested
simultaneously
○ Convergence: bring tip of your
finger to the bridge of the patient’s
nose
*Also take note if with nystagmus
Digital/Finger Palpation Tonometry Normal Hard: increased intraocular Alternative Methods

• Defer if rupture of the globe is • 10-20 mmHg pressure, hypertonic (ex: • Schiotz tonometry:
suspected • Soft, easily indentable, doughy consistency glaucoma) Schiotz tonometer
• Ask patient to look downward without • Firm as the tip of the nose Soft: decreased intraocular Applanation tonometry:
closing his eyes Abnormal pressure, hypotonic Goldman applanation and
Use 2 index fingers on the upper lid to • Ruptured globe (do not palpate!) slit lamp
Tonometry gently press down on the globe • Hard: firm as the forehead
(Intraocular • Soft: soft as the lips
Pressure)
Reporting Findings
Direct Ophthalmoscopy • (+) ROR reflex End-Stage Glaucoma: severe Calibrating the
• Dim room lights and ask patient to fix • Clear media (CM) cupping or big cupped-out Ophthalmoscope
gaze at a distant point • Distinct disc borders (DDB) nerve • Black numbers: positive
Fundoscopy
• Adjust diopter to desired setting, hold • Cup-Disc Ratio (CD): 0.2-0.4 (0.3) • Red numbers: negative
(Retinal Exam)
ophthalmoscope with R hand to R eye • Blood Vessels • Calibrate to your and the
• Direct ophthalmoscope at pupil and ○ A: brighter and narrower patient’s error of
approach ROR temporo-nasally ○ V: darker and wider refraction

• Locate a blood vessel and follow ○ A-V ratio = 2:3
nasally to the optic disc • Hemorrhages
• Move temporally to see the macula • Exudates
Check for: cup-disc ratio, caliber of (+) Foveal reflex (FR)
vessels (A:V ratio)
hemorrhages/bleeding, exudates Reporting Findings
(white/yellow lesions), foveal reflex
(bright light in the middle of the macula)
BASIC
ORGAN HOW TO TEST RESULTS PATHOLOGY ADDITIONAL NOTES
STEPS
Skull: general size, contour, Describe as observed Craniosynostosis: premature
deformities, depressions, lumps closure of sutures causing
Hair: quantity, distribution, texture, abnormal shape of the skull
patterns of loss Parotid gland swelling: may
Scalp: scaling, lumps, nevi, or any be a result of duct
other lesions obstruction, inflammation or
HEAD Inspection
Face: facial expression, contours, neoplasia
asymmetry, involuntary movements, Facial Nerve Palsy (Bell
edema, and masses Palsy): asymmetry of face and
Skin: color, pigmentation, texture, distortion of facial expression
thickness, hair distribution, and any due to injury to the facial
other lesions nerve
• Check for: symmetry, masses, Describe as observed A scar of a past thyroid surgery is often a clue to
scars, visible lymph nodes, tracheal an unsuspected thyroid disease
deviation, fistulous openings, and
any skin lesions
• Also give attention to the position
Inspection and mobility of the head and neck
• Observe swallowing. The thyroid
cartilage, cricoid cartilage and the
thyroid gland should all rise with
swallowing and then fall to their
resting position
Trachea Trachea Tracheal deviation: may be Levels of the Neck and Structures Drained
• Place finger along one side of the • Midline or deviated due to neck masses pushing
trachea and note the space the trachea to one side; may
NECK
between it and the SCM Lymph Nodes also signify problems in the
• Compare with the other side, • Number, size (in cm), tenderness, mobility thorax such as mediastinal
spaces should be symmetric relative to the skin and underlying tissues, mass, atelectasis or a large
Lymph Nodes consistency, laterality, level of the palpable pneumothorax
• Use the pads of your index and lymph node, and their relationship to the
Palpation middle finger with rolling motion surrounding neck structures Lymphadenopathy (enlarged
• Neck should be slightly flexed lymph nodes): infection or
forward to relax the soft tissues Thyroid neoplasm
• Palpate all 6 levels of the neck on • Size, shape and consistency of the gland
both sides: • Identify any nodules or tenderness Thyroiditis: may present with
○ Level 1A: between the anterior a tender thyroid gland
digastric muscles Illustration of findings
Goiter: diffusely enlarged
thyroid gland; may be

○ Level 1B: between the anterior accompanied by signs and
and posterior digastric muscles symptoms of either hyper or IA Submental: lip, tongue, oral cavity
○ Level 2: above the hyoid, from hypothyroidism but can also IB Submandibular: oral cavity, anterior nasal
the posterior belly of the digastric be asymptomatic cavity, soft tissues of the midface, submandibular
anteriorly to the posterior border gland
of the SCM posteriorly; (2A and II Upper Internal Jugular: oropharynx, parotid
2B are separated by the spinal III Middle Internal Jugular: hypopharynx, thyroid
accessory nerve) IV Lower Internal Jugular/Supraclavicular:
○ Level 3: from the inferior border larynx, hypopharynx, thyroid; non-head or neck
of the hyoid superiorly to the sites: lungs, breast, GI or GU
inferior border of the cricoid VA Posterior Triangle Nodes (Superior Half):
inferiorly; from the sternohyoid scalp, lymphoma, nasopharynx
muscle anteriorly to the posterior VB Posterior Triangle Nodes (Inferior Half) :
border of the SCM posteriorly scalp, lymphoma, nasopharynx
○ Level 4: from the inferior border VI Paratracheal: thyroid, larynx
of the cricoid superiorly to the VII Superior Mediastinal: mediastinal area
clavicle inferiorly; from the
sternohyoid anteriorly to the Both sides of the neck along the carotid sinus
posterior border of the SCM should NEVER be deeply palpated at the same
posteriorly time due to risk of developing a carotid sinus
○ Level 5: from the convergence of reflex with bradycardia and vasovagal syncope
the SCM and trapezius superiorly
to the clavicle inferiorly; from the The thyroid gland is usually easier to palpate in
posterior border of the SCM long slender necks. In shorter necks,
anteriorly to the anterior border of hyperextension of the neck may be helpful
the trapezius posteriorly
○ Level 6: from the hyoid bone Note that the thyroid gland may not always be
superiorly to the suprasternal palpable especially when not enlarged
notch inferiorly; bounded laterally
by the common carotid arteries
and the sternohyoid muscles
Thyroid
• Place both thumbs on the side of
the trachea just under the cricoid
cartilage
• Ask the patient to swallow: this will
make the thyroid gland slide under
your thumbs
• If the thyroid gland is enlarged,
auscultate over the lateral lobes to
detect a bruit
ORGAN BASIC STEPS HOW TO TEST RESULTS PATHOLOGY ADDITIONAL NOTES

Use wooden tongue depressor to Describe as observed Marginal Gingivitis: teens and young TIP: To be systematic, inspect oral cavity by
retract, push, or depress structures to adults; red, swollen gingival margins; subsites
facilitate inspection Illustration of findings interdental papillae are blunted,
swollen and red Review of basic anatomy
Lip: color, moisture, lumps, ulcers,
ORAL Inspection
cracking, scaling Pharyngitis: mild to moderate
CAVITY
redness and vascularity of the pillars
Oral Mucosa: color, ulcers, white and uvula; sore or scratchy throat
patches, nodules, report halitosis
Gums and Teeth

• Gums: color, swelling, ulceration, Tonsillar exudates: whitish or
bleeding yellowish substance on tonsils,
• Teeth: number, color, shape, common in Streptococcal pharyngitis
position, missing teeth
Lesions on the floor of the mouth:
Roof of Mouth investigate for possible cancer
• Inspect hard palate (ask patient to
tilt head) Smooth tongue or Atrophic
• Inspect color, architecture, and for Glossitis: riboflavin, niacin, folic acid,
any growths B12, or iron deficiency; chemotherapy
Tongue and Floor of Mouth Varicose Veins: small purplish or

• Stick out tongue upward and then blue-black round swellings
outward
• Note symmetry, color and texture Cranial Nerve Lesions
of dorsum of tongue, sides and • CN X: soft palate fails to rise and 7 subsites of oral cavity
undersurfaces of tongue for uvula deviates to the opposite side • Anterior 2/3 of the tongue
redness, nodules, ulcerations • CN XII: asymmetric tongue • Hard palate
protrusion • Retromolar trigone
Oropharynx • Lips
• When checking the oropharynx, • Buccal mucosa
tongue must be kept inside the • Floor of the mouth
oral cavity to keep it relaxed or ask • Upper and lower alveolar ridge
patient to stick tongue out and say
eh or ah 7 subsites of oropharynx
• Inspect the soft palate, anterior • Base of the tongue
and posterior tonsillar pillars, • Soft palate
uvula, tonsils, and posterior • Anterior and posterior tonsillar pillar
pharynx • Palatine tonsils
• Color, symmetry, exudation, • Vallecula
swelling, ulceration, tonsillar • Lateral pharyngeal walls
enlargement • Posterior pharyngeal walls
• Depress anterior ⅔ of tongue, Visible structures: Lesions in postnasal space (adenoids,
mirror side facing up • Nasal septum tumors of the pharynx, etc.) 3 subsites of the hypopharynx
• Slide the mirror behind the uvula • Inferior and middle concha • Pyriform sinus
• Don’t touch posterior wall: patient • Soft palate • Posterior wall
Posterior • Post-cricoid region
NASO- might gag! • Uvula
Rhinoscopy
PHARYNX • Instruct patient to breathe through
nose to lower soft palate
• Inspect structures of the
nasopharynx and posterior nasal
cavity
• Patient sits upright Vocal cords should move All pathologies present with Take Note:
• Grasp the protruded tongue with a symmetrically: hoarseness Vocal fold = true vocal cords
gauze sponge • Abducted when breathing • Nodules: bilateral Vestibular fold = false vocal cord
• With the head mirror, direct light • Closely apposed (but not tightly) • Polyp: unilateral
toward the uvula during phonation • Vocal cord paralysis: presents
• Advance the mirror beneath the with asymmetric movement of the
Indirect
LARYNX palate to the uvula Illustration of findings vocal folds
Laryngoscopy
• Lift the uvula on the back surface • Laryngitis: boggy, edematous, and
of the mirror, gently push it erythematous vocal folds
backward and upward to visualize
the larynx through the mirror
• Examine the larynx in the
respiratory position (tell the

patient to take a deep breath) and Reflective surface of the mirror should be
in the phonatory position (have warmed to prevent fogging
the patient say “hee”)
• Check for: erythema, inflammation, Touching the base of the tongue or the posterior
edema, scars, masses, growths wall of the pharynx may evoke a gag reflex
Keep in mind that this examination provides an

inverted “mirror” image of the larynx
Direct Laryngoscopy
• Provides direct view into the larynx with the
use of a laryngoscope
• Most commonly performed under general
anesthesia
BASIC
ORGAN HOW TO TEST RESULTS PATHOLOGY ADDITIONAL NOTES
STEPS
• Check for: asymmetry or deformity of Describe as observed Mouth breathing: suspect nasal
the nose, deviated septum, abnormal airway obstruction
creases, and presence of discharge Illustration of findings
or crusting along the nasal vestibule
Inspection
• Apply gentle pressure on the tip of • (+)/(-) tenderness Tenderness of the nasal tip may
the nose with your thumb and check • (+)/(-) airway obstruction suggest local infection (ex:
for any tenderness furuncle)
• Test for airway patency/obstruction:
press on each ali nasi one at a time Mobility or crepitus upon
Palpation
and asking patient to breathe in palpation of the nose may indicate
• Palpate for tenderness on areas fracture of the nasal pyramid if
NOSE AND overlying the frontal and maxillary with history of recent trauma
PARANASAL sinuses
SINSUS
• Ask the patient to lean forward and • Nasal septum: midline Viral Rhinitis: reddened and Nasal speculum
tilt head upward • Nasal turbinates: project into swollen nasal mucosa
• Hold the speculum with left hand nasal passages
when checking for the right nostril • Nasal passages: have sufficient Allergic Rhinitis: bluish, pale, or
and vice versa room red
• Extend index finger and position it on • Mucus membrane: compact and
nasal tip for anchorage red over turbinates and septum Nasal polyps: (can obstruct
Anterior • Insert the speculum in closed position • Small amount of thin secretions airflow) allergic rhinitis, aspirin
Rhinoscopy until the nasal vestibule before may be seen. sensitivity, asthma, cystic fibrosis,
opening gently • Nasal mucosa is normally and chronic sinus infections
○ Inferior turbinate: first structure to somewhat redder than the oral
be seen upon entry of nasal mucosa Fresh blood or crusting (septal
speculum. perforation/ulceration): trauma,
○ Note color, swelling, bleeding, Illustration of findings surgery, and intranasal use of
exudates, ulcers, polyps, septal cocaine or amphetamines
deviation, and patency of nasal
passage

○ If exudate is present: note if it is
clear, mucopurulent, or purulent
• Withdraw speculum gently while still
partially open to avoid hair avulsion
• Inspect the auricle and the Describe as observed

surrounding area
• Check for: symmetry and shape of Crusting or discharge: note if it is
Inspection each ear, swelling, redness, crusting, cerumen, mucus, blood, pus, or
discharge, scars, abnormal growths, CSF
deformities, lumps, and other skin
lesions
• Check for tenderness • (+)/(-) Tug Test Acute Otitis Externa: tenderness
○ Tug Test: move the auricle up and • (+)/(-) mastoid tenderness on Tug Test
down and press on the tragus
Palpation
○ Press firmly just behind the ear (on Acute Otitis Media: tender upon
the area of the mastoid) palpation of the mastoid, non-
tender tug test
• Pull auricle upward, backward, and • (+)/(-) cone of light Cerumen impaction: causes Touching the medial bony portions of the ear
outward (“up and out”) (T/N: for ○ Antero-inferior quarter of the pressure sensation in the ear with canal with the tip of the otoscope is not only
pediatric patients: downward and eardrum concomitant hearing loss; painful, but can easily injure the delicate skin of
backward) ○ Absence of cone of light does presence of yellowish-brown to the canal wall
• Insert the otoscope gently directed not always mean a pathology; black material obstructing the ear
downward and forward with the light it could be the shape of the ear canal Normal findings of the right eardrum on
EAR on just until past the hairy part of the canal or tympanic membrane otoscopy
canal ○ Distortions in cone of light Acute Otitis Externa: main initial
• Optional: anchor the hand holding could be increased inner ear symptom is itching, pain follows;
the otoscope on the patient’s cheek pressure in otitis media presence of crusting and purulent
or pre-auricular area using either the • Cerumen aural discharge; inflammation of
pointer (if using the hammer grip) or ○ Varies in color and the ear canal
the pinky (if using the pen grip) consistency: yellow and flaky,
Otoscopy brown and sticky, and even Acute Otitis Media: severe
○ Inspect the ear canal: discharge,
foreign bodies, erythema or dark and hard earache with opaque, thickened,
swelling ○ May wholly or partly obscure erythematous and sometimes
○ Inspect the tympanic membrane: the view bulging tympanic membrane.
color and contour, Light reflex is either absent or
presence/absence of the cone of Illustration of findings fragmented. Conductive hearing
light, position of the malleus, and loss may be present.
any perforations

Weber Test Normal Conductive Hearing Loss
• Strike tuning fork • Weber Test: vibration is felt • BC > AC: sound is heard
• Press tuning fork firmly on the equally in both ears (no through bone as long as or
patient’s forehead lateralization) longer than it is through air.
• Check lateralization • Rinne Test: AC > BC • Findings: Sound lateralizes to
impaired ear (Weber); BC >
Rinne Test (AC vs BC) • Take note: AC (Rinne)
Hearing • Strike tuning fork ○ Examiner must have normal
EAR • Place tuning fork on mastoid bone, hearing Sensorineural Hearing Loss
Tests
on the level of the ear canal ○ Both tests need to be normal • AC > BC: sound is heard longer
• When the patient can no longer hear for the patient to be considered through air
the sound, remove the fork from the to have normal hearing Findings: Sound lateralizes to
mastoid area good ear (Weber); AC > BC
• Place the fork close to the ear canal (Rinne)
and ascertain whether the sound can
be heard again
PART 7B. CLINICAL CASES: EYE

CHEMICAL BURNS
CLINICAL MANIFESTATIONS PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL NOTES
• ALKALI BURNS • Alkali: lye, “kalburo”, ammonia found in • Clinical • Should be initiated • Consult
• Deep penetration (more severe injury) household cleaners, fertilizers, pesticides immediately ophthalmologist if:
• Pain • Penetrates tissue and have a prolonged • Prolonged copious irrigation o Only one who can
• Reduced visual acuity affect → scarring and/or perforation o Normal saline or Lactated initiate steroid
• Marked edema o More dangerous than acid burns Ringer’s solution (tap water if therapy
• Liquefactive necrosis o Due to saponification of fatty acids unavailable) o May put topical
• Conjunctival inflammation o Interaction of cation with collagen and o Done until pH is within the anesthetic drops
• Limbal ischemia GAGs that increase permeability of physiologic range 7.0-7.6 § Oral is
o Limbus: junction of cornea and sclera where stem the cornea (test with litmus paper) prescribed to the
cells are found • Check and clear fornices of patient because
• Rise in IOP due to corneal collagen shrinkage chemicals anesthetic drops
• Pain control (oral) may be abused by
• Artificial tears (to promote the patient
healing) o Start IOP control if
• Prophylactic topical broad needed
spectrum antibiotics (drops)
• ACID BURNS • Acid: car, battery fluids, vinegar, • Clinical • Similar to treatment of alkali
• Confined to superficial tissue (less severe injury) refrigerants, bleach, toilet bowl cleaner burns but less irrigation time
• Pain (muriatic acid), silver cleaner • Prolonged copious irrigation
• Reduced visual acuity • Exposure to the acid → protein o Normal saline or Lactated
• Mild edema denaturation, precipitation, coagulation Ringer’s solution (tap water if
• Coagulation necrosis o Less severe than alkali burns because unavailable)
coagulated proteins protect the eyes o Done until pH is within the
from further penetration physiologic range 7.0-7.6
(test with litmus paper)
• Pain control (oral)
• Artificial tears (to promote
healing)
• Prophylactic topical broad
spectrum antibiotics (drops)

CENTRAL RETINAL ARTERY OCCLUSION (CRAO)
• Sudden, painless, and severe monocular loss of • Most commonly caused by emboli • Clinical: funduscopy • Golden period: 90 minutes • Only 21-35% recover
vision secondary to an occluded vessel • Cholesterol (carotid) findings • Reduced IOP medically functional vision (when
• Relative afferent pupillary defect (RAPD) • Calcific (atrial/mitral valve) o Pale areas o Carbonic anhydrase detected
• Preceded by amaurosis fugax a few hours or days • Platelet-fibrin clots o Box car appearance inhibitors: Acetazolamide, • early)
o Painless temporary loss of vision • Bacterial/septic valve embolus of ocular vessels Dorzolamide, Brinzolamide
endocarditis o Cherry red spot in the o Beta-adrenergic blocker:
• Tumors center of the macula TImolol
• Fat (long bone fracture) o Visible embolus • Dislodge embolus physically or
• Steroids medically
• Others: amniotic fluid, angiography o Apply firm, direct pressure
contrast, talc with eye closed for 15
• Associated conditions: seconds followed by sudden
• Hypertension release → repeat
• Diabetes • Thrombolytics within 4-6 hours
• Cardiac pathology • Treat underlying cause
• Coagulation abnormality
• Trauma
• Giant Cell Arteritis or Temporal Arteritis
(elderly)
CONJUNCTIVITIS
CLINICAL MANIFESTATIONS PATHOGENESIS TREATMENT IMAGES
FOLLICULAR CONJUNCTIVITIS • More often with viral conjunctivitis
• Constitute lymphoid germinal centers ○ Adenovirus, Herpes Simplex Virus, Enterovirus,
• “Sago-like” appearance Chlamydia
• Coexist with regional lymphadenopathy • Drug Toxicity: Pilocarpine, Timolol
• Vessels surround and can even cross the lesion
but never comes from the center
PAPILLARY CONJUNCTIVITIS • Non -specific inflammatory response (ex:

• Usually on upper tarsal conjunctiva mechanical, allergic)
• Fine, mosaic pattern of telangiectatic blood vessels ○ Vessels arise from the center in a
• Central fibrovascular core with vessel branching in fibrovascular core
spoke-like pattern • More often with bacterial conjunctivitis
• Large papillae with cobblestone appearance
• Connective tissue septa
ADENOVIRAL CONJUNCTIVITIS • Hyperemic and congestive conjunctival reaction • Preventive: rigorous handwashing
• Known as “sore eyes” in the Philippines (or “pink followed by follicular and papillary conjunctivitis with soap
eye”) • Enlargement of lymphoid follicles at the fornix • Treatment: mainly supportive
• Blurry vision • Visualization of lymphoid follicles through slit- • Mild steroids
• Difficulty opening eyes lamp technique (Adenoviral) • Fluorometholone
• Serous, watery discharge • Decongestants like Nafazolin
• Preauricular lymphadenopathy (ipsilateral)
• Conjunctival hemorrhage
• Photophobia
• Severe cases: pseudomembrane formation,
conjunctival scarring

EPIDEMIC CONJUNCTIVITIS • Caused by the host immune response • Steroids (controversial)
• Usually shows that the conjunctiva is no longer • Inflammation of the cornea and conjunctiva o Risk of recurrence once withdrawn
erythematous caused by an untreated or residual adenovirus
o Important to ask during history taking if there was o Serotypes 8,11,19 (most common)
previous redness • “Epidemic” of how the virus spreads
o Close contact
o Non-sterile eye examinations
MEMBRANOUS CONJUNCTIVITIS • Conjunctival scarring can lead to symblepharon •
• Whitish membrane on the palpebral conjunctiva formation
o “True membrane o Collection of inflammatory discharge of fibrin
§ Incorporate epithelium and bleeds on and PMNs coagulate on conjunctival surface
removal
o Pseudomembrane
§ Superficial Fibrin sheet
• Conjunctival scarring can lead to symblepharon
formation
GONOCOCCAL KERATOCONJUNCTIVITIS • Reaches the eyes through infected genital • Systemic IV/IM Ceftriaxone
• Rapid progression (within a few hours) secretions or genital-hand-ocular transmission • Most recommended: 4th gen
• Copious purulent discharge (liquefactive necrosis) • Diffuse epithelial haze → epithelial defects → • Fluoroquinolones
• Chemosis (edema of the orbital conjunctiva) marginal infiltrates → peripheral ulcerative • *Treat sexual partners as well
• Lid edema keratitis→ corneal perforation
• Pre-auricular lymphadenopathy • Complications: endophthalmitis, glaucoma
• Conjunctival membrane formation
• Risk of permanent vision loss
ADULT CHLAMYDIAL KERATOCONJUNCTIVITIS • Chlamydia oculogenitalis • Oral doxycycline

• Most common form of neonatal conjunctivitis and ○ Elementary bodies: infective stage, present in • Topical erythromycin
adult STD conjunctivitis the environment • Cephalosporin
• Associated with: ○ Reticulate bodies: non-infectious, • Sulfacetamide
o Urethritis metabolically active inclusions in the • Azithromycin
o Cervicitis cornea/body *Treat sexual partners as well
o Non-tender pre-auricular lymphadenopathy
o Prominent follicular response
o Punctate epithelial keratitis → marginal infiltrates
and neovascular scars (pannus)
• Neonatal conjunctivitis
o More rapid progression
o No succulent follicles due to underdeveloped
follicular system
o More mucopurulent discharge
o More follicles in tarsal conjunctiva
o More likely to respond to topical medications
ALLERGIC CONJUNCTIVITIS • Type I hypersensitivity reaction (inflammatory Supportive Treatment
• Itching keratoconjunctivitis and atopic dermatitis) • Cold compresses
• Epiphora • Same as bacterial • Topical vasoconstrictors
• Cobblestone papillae: manifestation of an • Cobblestone papillae caused by irritation from • Antihistamines
underlying disease (e.g. asthma, atopic dermatitis) chronic foreign bodies such as contact lenses • Mast cell stabilizers
• Also topical NSAIDs (better than
topical glucocorticoids)

ATOPIC CONJUNCTIVITIS • Type I and IV hypersensitivity reactions • Topical antihistamines
• Pruritus • Mast cell stabilizers
• Photophobia • Corticosteroids
• Watery to mucoid discharge
• Medium-sized papillae on upper and lower tarsal
conjunctiva
• Milky bulbar conjunctival edema
• Severe cases: corneal scarring,
neovascularization, opacification, cataracts
o Scarring leads to symblepharon
GIANT PUPILLARY CONJUNCTIVITIS • Any condition that produces a chronic irritative • Discontinuation of contact lens use
• Seen usually in soft contact lens wearers stimulus → chronic inflammation → hypertrophy of • Topical antihistamine
• Papillary hypertrophy (superior tarsus) superior tarsus • Mast cell stabilizers
• Causes
○ Ocular prosthesis
○ Sutures
○ Filtering blebs
• Contact lens and debris
• Wearing contact lens deprives the cornea of
oxygen → hypoxia → scarring → increase chances
of infection
PTERYGIUM • Associated with chronic exposure to sun, wind, • Surgery: excision with ancillary
• “Pugita/Squid”, “Surfer’s Eye” dust procedure
• Often preceded by pingueculae (yellow spot on • Benign fibrovascular proliferation covered by ○ Conjunctival graft: prevents further
conjunctiva) conjunctival-like epithelium extending into the vessel growth
• Complications peripheral cornea ○ Mitomycin-C: prevents recurrence
o Distortion and/or reduction of central vision • Located within or above the Bowman’s layer
o Redness ○ Scarring occurs if the lesion violates the
o Irritation Bowman’s layer
o Chronic scarring of the conjunctiva and the cornea
PHYLECTENULOSIS • Delayed Type IV hypersensitivity reaction • Topical corticosteroids
• Focal, translucent lymphocytic nodules at the limbus, ○ Seen in patients with history of TB or blepharitis • Antibiotics and steroids can also be
conjunctiva, or cornea • Accompanied by inflammation as neutrophils given as a combination because
enter and result to necrosis steroids alone can increase bacterial
inoculation
EPISCELRITIS • Inflammation and vasodilation of the episclera • Self-limiting

• No significant pain or tenderness • Artificial tears
• Usually monocular and focal • Topical vasoconstrictors and mild
corticosteroids for pain
SUBCONJUNCTIVAL HEMORRHAGE • Extravasation of blood between conjunctiva and • Self-limiting

• Bright red patch with normal surrounding tissue sclera from ruptured vessels
• Painless • Causes
• No visual irritation ○ Idiopathic
○ Valsalva maneuvers
○ Bleeding disorders
○ Drugs: blood thinners, steroids, contraceptives
○ Systemic diseases: dengue, typhoid, malaria

KERATITIS / ULCER
• Severe cases of keratitis (corneal inflammation) can Key predisposing factors: epithelial
result to corneal ulcers defects and injuries
General Characteristics
• Redness
• Pain
• Blurred vision
• Photophobia
• Excessive tearing and discharge
*vary depending on the causative agent
STAPHYLOCCOCUS AUREUS Infection → epithelial defect → corneal • Clinical: corneal • Topical antibiotics (ideally Staphylococcus aureus
• Dense, opaque stromal suppuration perforation (in 4-7 days) opacity or infiltrate in after obtaining cultures)
association with the ○ Fluoroquinolones,
STREPTOCCOCUS PNEUMONIAE • For Pseudomonas infection: characteristic erythromycin
• Most common cause of corneal redness ○ Rapid progression symptoms
• Serpiginous, gray-white stromal infiltrate ○ Stromal necrosis due to proteolytic • Penlight: visualization of
• Sterile hypopyon enzymes ulcers and infiltrates
○ Marked tendency to spread (does not require a slit
PSEUDOMONAS AERUGINOSA ○ Causes keratolysis lamp for identification) Streptococcus pneumoniae
• Tenacious mucopurulent discharge ○ More common in
• Opacification and edma immunocompromised patients and
contact lens wearers with faulty
hygiene
Pseudomonas aeruginosa

ACANTHAMOEBA • Exposure to organism (contaminated • Corneal biopsy • Topical cationic antiseptic
• Blurring of vision water) → infection → corneal trauma o Obtain scrape agents
• Small, patchy subepithelial infiltrates • Risk factors: contact lens wearers, low corneal samples ○ Polyhexanide
• May develop ring infiltrate with stromal opacification levels of anti-Acanthamoeba IgA tears under topical ○ Chlorhexidine
○ Ring ulcer (pathognomonic) anesthesia via slit ○ Brolene
• Perineuritis lamp exam -> culture
on nutrient agar with
E. Coli overlay ->
visualization of cysts
using silver stain
• Use of confocal
microscopy
FUNGAL • Often with history of trauma with plant • Clinical: corneal • Amphotericin B (IV) Fusarium (Filamentous fungi)
• Filamentous fungi material opacity or infiltrate in ○ No approved topical
○ More common in the PH • Etiology association with the antifungals here in the PH
○ Gray-white infiltrate with feathery border ○ Filamentous fungi: Aspergillus, characteristic • Steroids and antibiotic drops
○ “Satellite” infiltrates Fusarium symptoms can worsen the infection
○ Deep lesions with plaques and hypopyon ○ Yeast fungi: Candida • Debridement
• Yeast fungi ○ Reduce fungal load
○ Focal dense suppuration ○ Penetration of
○ Progressive hypopyon medications
HERPES SIMPLEX • Infection by Herpes Simplex Virus • Penlight exam: faint • Topical/systemic acyclovir Dendritic patterm:
• Redness • Lysis and desquamation of infection branching gray opacity • Ganciclovir
• No pain (cornea develops hypoesthesia) cells → ulcer develops in the center of • Fluorescein application: • Debridement
• Foreign body sensation the dendrite → centrifugal spread → best visualization of the • Can resolve on its own since
• Begins as punctate epithelial keratitis geographic ulcer branching opacity the virus stays in the
• Mild stromal edema epithelium only
• Subepithelial infiltrates

Geographic pattern:

CATARACTS
General Characteristics • Clouding of crystalline lens of the eye due • Clinical diagnosis • Phacoemulsification Types of Intraocular Lenses (IOL)
• Lenticular opacity to denaturation of lens protein • Direct ○ Ultrasound probe to • Monofocal
• Gradual, progressive, painless clouding of • Congenital or acquired (aging, DM, UV ophthalmoscopy dissolve nucleus inside the • Multifocal
vision light exposure, or trauma) ○ ROR: darkening, eye and suck out cortical • Accommodative
presence of material • Toric (astigmatism)
NUCLEAR CATARACT • Nuclear sclerosis: opacification of the opacities ○ Insert implant
• Progressively denser central part of lens lens nucleus

• Most common type of cataract • Accumulation of urochrome pigment • Extra-capsular cataract
• Acquired with age, slow progression renders the lens nucleus brown, distorting extraction and lens
• Increasing myopia (“second sight”) patient’s perception of the color blue replacement
CORTICAL OPACITIES/CATARACT • Damaged lens epithelial cells

• Stellate or spoke-like pattern • Ionic imbalance of the lens
• Reduced visual acuity ○ Decreasing: K+
• Water clefts and vacuoles, osmotic in nature ○ Increasing: Na, Cl, Ca
• Problems with glare and light scatter ○ Causes water influx, resulting in
vacuoles, water clefts, and spokes
POSTERIOR SUBCAPSULAR CATARACT • Enlargement of an abnormally-positioned

• Dense patch on the posterior part of the lens epithelium
lens • Migration of the lens epithelium posterior
• Severe glare and early disability to the lens equator
• Typically induced by steroids or radiation
HYPERMATURE CATARACT / PAINLESS • Rare, advanced stage of cortical cataract

PROGRESSIVE BLURRING OF VISION (PPBV) (majority of the lens has already
• Entire lens is opaque “’liquefied”)
• Light projection and color vision preserved
• Lens nucleus floats freely in the capsule bag
(Morgagnian cataract)
CONGENITAL CATARACT • Can be hereditary (Down’s syndrome),

• The younger the patient, the worse the vision infectious (rubella – most common),
loss metabolic (galactosemia), drug exposure
• Leukocoria (abnormal reflection from the (Theophylline)
retina)
• Poor vision
GLAUCOMA
General Characteristics • Chronic increased in intraocular pressure • Fundoscopy • Open Angle Glaucoma What maintains intraocular
• Blind spots results in damage to the optic nerve ○ Increased C:D ○ Medical: prostaglandins, pressure?
• May have preserved visual acuity despite • Loss of retinal ganglion cells in a ratio alpha agonists, beta • Constant production of aqueous
extensive visual field loss characteristic pattern ○ Nerve fiber layer blockers, carbonic humor from the ciliary processes
striations anhydrase inhibitors, behind the iris is balanced by
OPEN ANGLE GLAUCOMA • Structurally-normal: the drainage is • Tonometry pilocarpine continuous drainage of the fluid
• Typically asymptomatic until very late present, but is dysfunctional ○ Increased ○ Laser trabeculoplasty: through the trabecular meshwork
• Minor headaches ○ Peripheral iris physically blocks the intraocular burns on the trabecular • Obstructions to the drainage
• Ocular pain trabecular meshwork pressure meshwork to restore causes the pathology
• Unilateral blurring of vision • Gonioscopy drainage
• Iridescent vision: haloes around lights ○ Determines ○ Treatment cannot reverse
• Nausea and vomiting whether open or nerve damage
closed angle • Closed Angle Glaucoma
CLOSED ANGLE GLAUCOMA • Angle is anatomically closed glaucoma ○ Patent Laster Iridotomy:
• Decreased vision ○ Aqueous humor accumulates behind laser punches a hole in the
• Headache the iris, causing it to bulge forward iris to relieve pressure
• Ocular pain and close the angle
• Nausea and vomiting • Relative pupillary block

AGE-RELATED MACULAR DEGENERATION
• Affects central vision Visual impairment involves neovascular • Amsler Grid • Vitamin A
○ Sharp vision at found at the fovea only and non-neovascular derangements ○ Distinguishes • Laser Treatment
• Dry ARMD: geographic atrophy with loss of RPE • Debris accumulation of yellow between wet and ○ Rarely improved vision,
and photoreceptors, slow progression, spares deposits (Drusen) under the retinal dry ARMD immediate loss of vision
periphery pigment epithelium • Fluorescin • Anti-VEGF (better than laser)
• Wet ARMD: bulging membrane of the retina, rapid angiography (definite ○ Expensive
progression, gray diagnostic exam) ○ Monthly intravitreal
○ Invasive injectionss
○ Detects wet
ARMD

• Macular optical
coherence
tomography
○ Detects wet
ARMD and
monitors its
progression

DIABETIC RETINOPATHY
• Affects central and peripheral vision • Retinal damage due to chronic • Pupillary dilation and • Nonproliferative: blood sugar
• Floaters hyperglycemia direct control
• Usually affects both eyes • Types ophthalmoscopy • Proliferative: anti-VEGF,
○ Nonproliferative: damaged ○ Hemorrhages, photocoagulation, surgery
capillaries leak blood → lipids and
fluid seep into the retina →
microaneurysms,
exudates

hemorrhages and macular edema • Others
○ Proliferative: chronic hypoxia → ○ Fluorescein
angiography
new blood vessel formation with
traction on retina ○ Optical
coherence
tomography
RETINOBLASTOMA
• Most common primary intraocular malignancy in • Occurs in individuals who inherit a • Basis of clinical • Globe sparing
children germline mutation of one RB allele examination • Enucleation
• Most common initial sign: leukocoria (RB1 mutation) • Fundoscopy ○ Large masses will
• Strabismus ○ Creamy white require initial
• Decreased vision mass with chemotherapy to shrink
• Dilated pupil possible vitreous mass
• Age of diagnosis: and/or • Mandatory chemotherapy
○ Unilateral cases (diagnosed at 2 years of age)
○ Bilateral cases (diagnosed at 1 year of age)
calcification
• Ocular

○ Nearly all identified by 3 years old ultrasonography
○ Dome-shaped
mass with internal
calcification
• Histopathology
○ Flexner
Wintersteiner
rosettes
(pathognomonic)

PART 7C. CLINICAL CASES: EARS.
ACUTE OTITIS EXTERNA
• Ear pain • Breakdown of the skin-cerumen barrier • Clinical diagnosis based • First and most important step: Note: if the patient has a
• Pruritus, aural discharge is the first step on history and physical meticulous, repeated perforated tympanic
• Obstruction of the ear canal may produce hearing • Inflammation and edema of the skin examination cleansing and drying of ear membrane, it is likely that
loss leads to pruritus and obstruction canal the primary focus of
• Pruritus prompts further manipulation • Followed by instillation of disease is the middle ear,
Pertinent History and may create further injury antibiotic drops to reduce with secondary
• Vigorous ear cleaning, manipulation or swimming • Excess moisture (e.g. from swimming) swelling (Ciprofloxacin and inflammation of the
(hence, “Swimmer’s ear”) leads to skin maceration and breakdown Ofloxacin preparations) external ear
of the skin-cerumen barrier • Oral antibiotics if infection
Pertinent PE • Trauma and excessive manipulation of appears to have spread beyond
• Tragal tenderness, (+) auricle tug test the ear removes cerumen and creates the ear canal
• Ear canal is erythematous and diameter may be abrasion along the skin of the ear canal, • Pain control with analgesics is
narrowed due to swelling allowing organisms to gain access recommended
• Check for signs of trauma • Usual pathogens:
o Pseudomonas aeruginosa
o Group A Streptococcus
o Staphylococcus aureus
ACUTE OTITIS MEDIA (AOM)

• Initial symptom is severe earache • Infection that ascends to the middle ear • Pneumatic otoscopy • Amoxicillin: liquid suspension In US studies, AOM is
• Fever (first 24 hours) through the Eustachian tube • Tympanocentesis (5-day course) most common among 3 to
• Aural discharge • Majority is triggered by URTI with (aspiration of middle ear • Erythromycin (if allergic to 18-month old babies
• Spontaneous perforation of the tympanic membrane nasopharyngeal involvement contents) only for certain Amoxicillin)
• Infants: irritability, vomiting, diarrhea may be the • Common pathogens: AOM patients (not • NSAIDS/Paracetamol: pain Not contagious, but
dominant features ○ S. pneumonia always done) relief children who have colds
• Older children and adults: Ipsilateral hearing loss ○ H. influenza • Decongestants or irrigations: or other viral infections
and ear stuffiness ○ M. catarrhalis relieving nasal airway may develop ear
• Adenoids are a frequent nidus for middle obstruction infections
Pertinent History ear infections in children
• Onset of symptoms after a previous viral infection of • Complications are rare; most common is
the upper respiratory tract acute mastoiditis
Pertinent PE
• Mastoid moderately tender to pressure
• Opaque, thickened, erythematous, and sometimes
bulging tympanic membrane
• Presence of air fluid level along the tympanic
membrane is indicative of a middle ear effusion
• Conductive hearing loss on affected ear
BAROTRAUMA
Middle ear hemorrhage or • Rapid rise in ambient air pressure • Maneuvers to relieve pressure
presence of fluid ○ When you go high, the pressure ○ When the plane is going up,
Eardrum rupture → pain and outside decreases and the tympanic swallow.
infection discharge membrane bulges outward ○ When the plane is
Hearing loss and tinnitus descending, do Valsalva to
Vertigo and disorientation force open the ET and

Nausea and vomiting ○ When you go low, the pressure deliver pressure into the
outside increases and the tympanic middle ear.
membrane bulges inward
• Mucosa of the Eustachian tube (ET)
collapses → increase in negative
pressure → swelling of the middle ear
mucosa
○ ET: helps maintain equal pressure on
both sides of the eardrum by allowing
outside air to enter the middle ear
OTOMYCOSIS
Ear pruritus • Aspergillus, Candida albicans, Mucor • Hyphal elements seen Antifungal
Ear discharge and dermatophytes in otoscopy solutions (2-4 weeks)
Ear pain (only if superimposed • Warm moist climate is conducive to (pathognomonic) Given after
with otitis externa) fungal infections cleaning
Wet plug ○ More common during the summer Clotrimazole
Predisposing factors months Ketoconazole
Trauma • Complications
Immunocompromised hosts ○ Tympanic membrane perforation
Use of antibiotic/steroid ○ Hearing loss
preparations ○ Invasive temporal bone infection
General diseases such as ○ Fungal otomastoiditis
diabetes mellitus ○ Meningoencephalitis
Relative high percentage of
humidity in the external ear canal
PART 7D. CLINICAL CASES: NOSE AND THROAT.

ACUTE PHARYNGITIS
VIRAL PHARYNGITIS Respiratory viruses are the most • Clinical diagnosis based • Self-limiting Epidemiology:
• Most common cause of sore throat identifiable cause of acute pharyngitis: on history and physical ○ 5-7 days but may persist up to • 85-95% in adults
• Occurs as part of the common cold • Rhinovirus (~20% of cases) examination (important 3 weeks (no longer • 70-80% in children
• Manifestations may overlap with bacterial • Coronavirus (~5% of cases) to rule out GAS contagious)
pharyngitis • Adenovirus pharyngitis) • Symptomatic treatment Coryzal manifestations
• Features that favor a viral etiology: • Parainfluenza virus ○ Antipyretics and NSAIDs including cough are typically
○ Gradual onset • Influenza virus ○ Adequate hydration absent in GAS pharyngitis.
○ Cough • Herpes simplex virus ○ Relief of pain or irritation: Exudates and anterior
○ Nasal congestion • Coxsackievirus A sprays, lozenges, rinses lymphadenopathy (level 1B
○ Conjunctivitis • Cytomegalovirus and 2A) are usually absent.
○ Coryza • Epstein Barr virus
○ Hoarseness • HIV (acute retroviral syndrome)
○ Diarrhea
○ Malaise
○ Viral exanthema

BACTERIAL PHARYNGITIS • Most common pathogenic organism: • Throat swab culture: • Antimicrobial therapy for acute Epidemiology
• Patients involved are usually between 5-15 Group A Beta hemolytic Streptococcus gold standard (sensitivity bacterial tonsillitis 5-15% in adults
years pyogenes (GABHS) and specificity of 90- ○ DOC: Penicillin or 20-30% in
• Features that favor a bacterial etiology: ○ Pathogenic only in humans 95%) Amoxicillin (10 days) children
○ Rapid onset • Other organisms and causes: ○ 24-48 hours ○ Alternative treatment (3-5
○ Exudates and palatal petechiae ○ Sexually-transmitted organisms ○ Sheep agar days)
○ Anterior cervical lymphadenopathy (gonorrhea, syphilis, chlamydia) • Rapid antigen § Cephalosporins
○ Fever ○ Tuberculosis detection test (RADT): § Erythromycin (if allergic
○ Headache ○ Tularemia specificity of 95% and to penicillin)
○ Nausea and vomiting ○ Diphtheria sensitivity of 89.1% (but § Clindamycin
○ Abdominal pain • Associated complications not widely available) § Azithromycin
○ Anterior cervical lymphadenopathy Acute rheumatic fever • Centor & McIsaac • NSAIDs
• Scoring Algorithms and glomerulonephritis Scoring Systems • Tonsillectomy: may be
○ Centor Scoring Rheumatic heart ○ For areas where lab recommended in patients who
§ Absence of cough (1) disease (most feared) tests are not available fulfill the Paradise criteria
§ Swollen and tender anterior cervical Suppurative or too expensive ○ Frequency of sore throat
nodes (1) complications (e.g. peritonsillar episodes
§ Temperature >38°C (1) abscess) § ≥ 7x in the past year
§ Tonsillar exudate or swelling (1) § ≥ 5x in the past 2 years
○ McIsaac Scoring (modified Centor) § ≥ 3x in the past 3 years
§ Age as an additional criterion to the ○ Definition of an episode
ones above § Temperature of >38.3°C
- 3-14 years (1) § Cervical
- 15-44 years (0) lymphadenopathy
- 45 years and older (-1) (tender nodes or >2cm)
○ Score directs additional diagnostics and § (+) GABHS culture
management ○ Treatment
§ Administered in
conventional dosage for
proved or suspected
streptococcal episodes
○ Documentation
§ Each episode and
features are recorded in
a clinical record
§ If not fully documented,
observance from a
clinician in 2 episodes
with patterns of
frequency and clinical
features consistent with
initial history
RHINITIS
General Characteristics Clinical diagnosis based on • Environmental management Usually common colds
• Difficulty in breathing history and physical • Symptomatic treatment resolve within a week
• Sneezing, rhinorrhea examination (decongestants)
• Tearing Allergic rhinitis is usually
INFECTIOUS RHINITIS • Rhinovirus and coronavirus are • Self-limiting (local and systemic confirmed when medical
• “Common cold” responsible for 50% of cases symptoms usually subside in a treatment starts (good
• Most common infectious disease • Transmitted by the airborne route (droplet week) response to anti-histamines)
• Presents with sneezing, congestion and infection) • Supportive treatment
excessive watery nasal discharge • Incubation period: 3-7 days ○ Rest and adequate hydration Itching is the symptom most
• Discharge later becomes more mucoid and • Viruses damage the mucocilliary ○ Decongestants: nasal suggestive of an allergic
viscid transport system → hampers the normal obstruction etiology

• Can also be accompanied by sore throat, clearing of secretions → inflammatory ○ Paracetamol/NSAIDS:
cough or hoarseness changes develop → further damage to the systemic symptoms
• Associated systemic symptoms: fever, nasal epithelium may promote bacterial ○ Antibiotics: bacterial
headache, malaise colonization superinfection or paranasal
• Bacterial superinfection can induce sinus involvement
mucopurulent exudates
Pertinent History
• Ask about the symptoms, including character
and duration
Pertinent PE
• Erythematous and edematous nasal mucosa
• Narrowed nasal cavities
• Enlarged turbinates
• Mucopurulent discharge
• Check the lungs and throat
CHRONIC RHINITIS • Sequela to repeated attacks of acute • Most important step: eliminate
• Obstructed nasal breathing rhinitis the cause
• Mucous nasal discharge • May also be due to anatomic changes (ex: • Supportive measures (ex:
• Frequent throat clearing marked septal deviation, septal spur) or decongestants, nasal irrigation)
• Occasional hoarseness other lesions of the nasal cavity (polyps, are only of temporary benefit
• Eventual development of superimposed tumors) and nasopharynx (adenoids)
bacterial infection • Frequently there is superficial
desquamation and superficial mucosal
ulceration with variable inflammatory
infiltrates that can extend into the sinuses
ALLERGIC RHINITIS • IgE-mediated • Detailed allergy history • Best treatment strategy:
• “Hay fever” • Leukocytic infiltration in which eosinophils • Percutaneous skin test avoidance of allergen
• Affects 20% of individuals predominate) • Allergen-specific IgE • Pharmacologic treatment:
• Classic symptoms: recurrent episodes of • Hypersensitivity reaction to allergens (ex: antibody test ○ Antihistamine
sneezing, pruritus, rhinorrhea, nasal pollen, fungi, animal allergens, and dust ○ Corticosteroids
congestion, and lacrimation that occur after mites) ○ Anticholinergics
exposure to an offending allergen ○ Mast-cell stabilizers
• Ocular symptoms: itching, tearing, and ○ Immunotherapy
conjunctival injection occur frequently
• Associated systemic symptoms may include
general malaise, fatigue, irritability, snoring and
sleep problems
Pertinent History
• Note onset of symptoms and association with
particular triggers
• Family history of allergic diseases (allergic
rhinitis, asthma, atopic dermatitis); if positive,
more likely the nasal symptoms are due to
allergic rhinitis
Pertinent PE
• Inferior turbinates are pale, bluish, and
edematous
• Mucosa is coated with thin, clear secretions

NASAL POLYPS
• Clinical manifestations depend upon extent • Genetic • Rhinoscopic or • Begin with symptomatic
• Obstruct the airway and impair sinus drainage, • Also mainly attributed to chronic endoscopic evaluation of conservative measures
necessitating removal irritation of the mucosa (ex: chronic the nasal cavity (corticosteroid nasal sprays,
• Hyposmia or anosmia (due to obstruction of olfactory rhinitis or sinusitis) (especially lateral nasal systemic anti-histamines)
groove) • Consist of edematous mucosa having wall) • Many require surgical
• Headache (due to impaired ventilation and drainage of a loose stroma, often harboring treatment
sinuses) hyperplastic or cystic mucous glands,
• Frequent throat clearing (due to postnasal drainage) infiltrated with a variety of inflammatory
• Only 0.5% of atopic patients develop polyps cells
SINUSITIS
• Acute <4 weeks • Defective ciliary action • Clinical diagnosis based • Decongestants: symptomatic Kartagener syndrome:
○ Viral < 7 days ○ Diabetics can develop fungal sinusitis on history and physical (conservative) treatment triad of sinusitis,
○ Bacterial > 7 days (ex. mucormycosis) examination • Amoxicillin (10-14 days) bronchiectasis, and situs
○ Children > 10-14 days ○ Impaired sinus drainage (producing • Radiography (CT scan • Surgery may be necessary if inversus due to
• Chronic >12 weeks empyema) and outflow obstruction good choice) acute sinusitis does not congenitally defective
• Nasal drainage and congestion (from the frontal and anterior ethmoid) • Rhinoscopy or respond to conservative ciliary action
• Facial pain or pressure • Non-specific inflammatory reaction endoscopy treatment modalities
• Headache Maxillary sinusitis due to periapical tooth Mucocele: accumulation
• Thick purulent or discolored nasal discharge if infection of mucus secretion in the
bacterial • Offending organisms usually oral absence of bacterial
• Cough, sneezing, fever commensal infection
• Tooth pain (upper molars)
Viral pathogens:
Pertinent PE • Rhinovirus
• Palpate sinuses for tenderness • Parainfluenza virus
• Tap teeth to test for inflamed paranasal sinus • Influenza virus
Bacterial pathogens:
• S. pneumoniae and H. influenzae (50-
60%)
• M. catarrhalis (20%)
• S. aureus

MODULE/TOPIC 8 PULMONOLOGY

INTRODUCTION
• Patient must be properly UNDRESSED, GOWNED and SITTING AT THE END OF AN EXAM TABLE. Examination is always done on SKIN.
• Examination room must be quiet to perform adequate PERCUSSION and AUSCULTATION
• Patient should cross his/her hands in front of the chest towards the shoulder throughout the whole examination
• DO NOT auscultate until the stomach
• Diaphragm is in between 5th and 6th ICS
• PE should be done at the BACK and FRONT
• Always use the diaphragm of the stethoscope when doing the pulmonary examination
Lung Segments and Fissures

• Fissures help determine the location of the upper, middle
and lower lobes
• Oblique fissure: from 4th and 6th ribs; found in BOTH left
and right lungs; starts from T3 posteriorly until the 6th rib
anteriorly
• Horizontal fissure: from the 4th costal cartilage anteriorly
to the 5th rib; found in the RIGHT lung
HISTORY
• Dyspnea • Hemoptysis
® Non-painful, uncomfortable awareness of breathing that is inappropriate ® Coughing up of blood-streaked phlegm or frank blood
to the level of excretion from the lungs
® Shortness of breath, or breathlessness ® Assess the volume of blood produced
® Both a symptom and a sign ® Ask about the related setting and activity, any
® An increase in ventilation in response to abnormalities of gas exchange associated symptoms
and increased work of breathing because of changes in respiratory ® Try to confirm the source of bleeding (hemoptysis vs.
mechanics and/or anxiety hematemesis)
• Cough ® Top 3 causes:
® Sudden, forceful, noisy expulsion of the air from lungs § Tuberculosis
® Stimuli to coughing include exudates in the pharynx or bronchial tree, § Bronchiectasis
irritation of foreign bodies and inflammation § Carcinoma
® 3 stages: • Pleuritic Chest Pain
§ Preliminary inspiration ® Characterized by sudden and intense sharp, stabbing, or
§ Glottal closure and contraction or respiratory muscles burning pain in the chest when inhaling and exhaling
§ Sudden glottal opening to produce the outward blast of air ® Px may feel this anywhere along the front of the body,
between the neck and upper abdomen
® Caused by abnormalities or problems in the pulmonary
vasculature, lung parenchyma or in the pleura and
pleural space

PHYSICAL EXAM
• Observe the patient for general signs of respiratory distress

® Note rate, rhythm, depth, effort of breathing and if expiratory
phase is prolonged
® Note retractions (withdrawn muscles and skin) and use of
accessory muscles in breathing (SCM and abdominals)
• Assess asymmetry, deformity and increased A-P diameter (Barrel
chest in COPD)
• Assess the patient’s color for CYANOSIS and nails for CLUBBING
Inspection
® Cyanosis signals hypoxia
® Clubbing is seen in lung abscesses, malignancy and congenital
heart disease
• Inspect the neck
® Check if there is contraction of accessory muscles (e.g. SCM, scalene muscles) during inspiration, which may signal difficulty
breathing
® Confirm that the trachea is near the midline
® Lateral displacement is seen in pneumothorax, pleural effusion or atelectasis
• Identify any areas of tenderness or deformity by palpating the ribs and sternum
Chest expansion
• Assess expansion and symmetry of the chest by placing your hands on the patient’s
side, thumbs together at the midline and ask them to breathe deeply
® Normal: symmetrical
® Local or lobar impairment in respiratory movement may be due to an underlying
disease (i.e. fluid or atelectasis)
® Unilateral decrease or delay in chest expansion: chronic fibrosis of the underlying
lung or pleura, pleural effusion or lobar pneumonia
Tactile Vocal Fremitus:

Palpation
• Use ulnar side of the hand, by the hypothenar eminence with the
palms facing upwards. Place it at various levels over the back, each
time asking the Px to say “ninety-nine” or “tres-tres”. Note how the
sound is transmitted to the hand
• It is increased over areas of consolidation and decreased or absent
over areas of effusion or collapse
Notes:
Consolidation occurs when the normally air-filled lung parenchyma
becomes engorged with fluid or tissue, most commonly in the setting of pneumonia. If a large enough segment of parenchyma is
involved, It can alter the transmission of air and sound. In the presence of consolidation, fremitus becomes more pronounced.
• Underlying tissues vibrate to produce percussion notes that vary with the density of the organ and the composition overlying the
tissue
• In decreasing density:
flatness → dullness → resonance → hyperresonance → tympani
(order also shows increasing air defining the structure)
® Hyperextend the middle finger of one hand and place the distal
interphalangeal joint firmly against the patient’s chest
® With the end (not the pad) of the opposite middle finger, use a quick
flick of the wrist to strike the first finger
® Categorize percussion sounds as normal, dull or hyperresonant
® Percuss from side to side and top to bottom; omit the areas covered
Percussion by the scapulae
® Compare one side to the other looking for asymmetry
• Note the location and quality of the percussion sounds you hear
Pathologic Examples Example of Location Relative Pitch Intensity Quality of Sound

Large pleural effusion Thigh High Soft Flatness
Tissue consolidation, Water
Lobar pneumonia Liver Medium Medium Dullness
Simple chronic bronchitis Normal lung Low Loud Resonance
Emphysema, Pneumothorax None, normally Lower Very loud Hyperresonance
Large pneumothorax, Gastric air bubble or High Loud Tympany
Air puffed out cheek

Diaphragmatic Excursion:
• Find the level of diaphragmatic dullness of
BOTH sides
• Ask the patient to inspire deeply
• Level of dullness (diaphragmatic excursion
should go down 3-5 cm symmetrically
® Decreased or asymmetric diaphragmatic
excursion may indicate paralysis or
emphysema
Breath Sounds:
• The larger the airway, the louder and higher pitched the sound
• Normal breath sounds: If bronchovesicular or bronchial breath sounds are heard in locations distant from those listed below,
suspect that air-filled lung has been replaced by fluid-filled or solid lung tissue
® Bronchial breath sounds:
§ Heard over large airways, “tubular” quality like sound of air blowing through a cardboard tube
§ Heard at sides close to large airways, on the back between scapulae and axilla (2nd ICS), lung apices and axillae
® Vesicular breath sounds:
§ Heard at a distance from large airways, at the peripheral
§ “Soft” compared to the sound of the wind blowing through leaves of a tree
§ Most common sound heard in the absence of lung disease
Duration of Intensity of Expiratory Pitch of expiratory sound Locations where heard
Sounds sound normally
Vesicular Inspiratory > Soft Relatively low Over most of both lungs
Expiratory
Bronchovesicular Inspiratory = Intermediate Intermediate Often in the 1st & 2nd ICS ant.
Expiratory & bet. scapulae
Bronchial Inspiratory < Loud Relatively high Over manubrium
Expiratory
Tracheal Inspiratory = Very loud Relatively high Over the trachea
Expiratory
* The thickness of the bars indicates intensity; the steeper their incline, the higher the pitch
Adventitious sounds:
Adventitious Description Continuous/ Inspiratory/ Associated
Sound Discontinuous Expiratory conditions
Crackle Coarse, louder, lower in pitch, and last longer than fine Discontinuous Inspiratory Pneumonia,
Auscultation crackles; Congestive heart
Sound like opening a Velcro fastener failure
Wheezes High pitched, whistling sounds; Continuous Expiratory Asthma
Caused by airway narrowing;
Relatively continuous compared to crackles
Rhonchi Lower in pitch than wheezes; have a snoring quality; Continuous Expiratory Bronchitis
Usually clear after coughing;
Caused by airway secretions and airway narrowing
Stridor Low-pitched, grating or creaking sounds; Continuous Inspiratory Epiglottitis, foreign
Caused by inflamed pleural surfaces rubbing together bodies
during respiration;
*Do not confuse with pericardial friction rub (which stops
when breathing stops)
Transmitted voice sounds:

• Bronchophony
® Ask Px to say “ninety-nine” or “tres-tres”
® Auscultate several symmetrical areas over each lung
® Louder and clearer sounds
• Whispered pectoriloquy
® Normal: Ask Px to whisper “ninety-nine” and you should hear faint sounds or nothing at all
® Whispered pectoriloquy if the sounds are heard loudly and distinctively
® Associated with lung consolidation, atelectasis or fibrosis
• Egophony
® Ask Px to say “eeee” continuously
® Auscultate several symmetrical areas over each lung and you should hear a muffled “eeee”
® If you hear “ay”, it is Egophony
® Associated with pleural effusion or consolidation (compressed lungs)
Special • Walk test:

Tests ® Time an 8-foot walk at the patient’s normal pace. Repeat the walk and note the faster time.
® Also observe the rate, effort, and sound of the patient’s breathing.
• Forced expiratory time:
® Assesses the expiratory phase of breathing. Typically slowed in obstructive pulmonary disease.
® Ask the patient to take a deep breath then breathe out as quickly and completely as possible with mouth open. Listen over
the trachea with the diaphragm of a stethoscope and time the audible expiration. Get 3 consistent readings

• Fractured Rib:
® Local pain and tenderness of one or more ribs raise the question of fracture. Anteroposterior compression of the chest can
help distinguish fracture from soft-tissue injury. With on hand on the sternum and the other on the thoracic spine, squeeze
the chest. Locate pain.
Sample of recorded PE findings of the thorax and lungs

Normal findings
Thorax is symmetric with good expansion. Lungs resonant. Breath sounds vesicular; no rales, wheezes, or rhonchi. Diaphragms descend 4 cm
bilaterally.
Abnormal findings
Thorax symmetric with moderate kyphosis and increased anteroposterior (AP) diameter, decreased expansion. Lungs are hyperresonant. Breath
sounds distant with delayed expiratory phase and scattered expiratory wheezes. Fremitus decreased; no bronchophony, egophony, or whispered
pectoriloquy. Diaphragms descend 2 cm bilateral.

SPIROMETRY
Definition of terms: Indications
• Spirometry - Spirometry is a method of assessing lung function by measuring the total volume of air the • Establish baseline lung function
patient can expel from the lungs after a maximal inhalation • Evaluate dyspnea
• FEV1 – Forced expiratory volume in one second • Detect and Evaluate respiratory impairment
o The volume of air expired in the first second of the blow • Monitor effects of therapies used to treat respiratory disease
• FVC – Forced vital capacity • Evaluate operative risk
o The total volume of air that can be forcibly exhaled in 1 breath
• FEV1/FVC ratio – The fraction of air exhaled in the first second relative to the total volume exhaled Contraindications
• Other terms to take note of • Hemoptysis of unknown origin
o Tidal Volume (TV) - the volume of air inspired and expired during normal breathing • Pneumothorax
o Inspiratory Reserve Volume (IRV) – maximum amount of air that can be inhaled after a normal • Unstable angina pectoris
tidal volume • Recent myocardial infarction
o Expiratory Reserve Volume (ERV) – maximum amount of air that can be exhaled • Thoracic, abdominal, cerebral aneurysms
o Residual Volume (RV) – amount of air that’s left in the lungs after exhalation; only volume not • Recent eye, abdominal or thoracic surgical procedures
measured in spirometry • History of syncope associated with forced exhalation
o Vital Capacity (VC) – volume of air that can be expelled after maximum inhalation
• Derived values:
o Inspiratory Capacity (IC) = TV + IRV
o Functional Residual Capacity (FRC) = ERV + RV
o Total Lung Capacity (TLC) =
§ VC + RV
§ IC + FRC
§ IRV + TV + ERV + RV

Spirogram Patterns
• Volume-Time Curves – effectively shows FEV1/FVC ratio
o Red dotted line below represents a normal curve. White solid lines are pathologic
• Flow-Volume Curve - Adds more information than volume time curve; Better at demonstrating mild
airflow obstruction
o Normal Flow Volume Curve
o Pathologic Flow Volume Curves

§ Obstructive lung diseases – presence of scooped-out pattern, called “sagging”
or “scalloping”, which is more pronounced in severe obstructive cases.
§ Restrictive lung diseases – the pattern looks normal; however, the volume (vital
capacity) is decreased (like a “mini” version of a normal flow-volume curve).

§ Flow Volume Curve is also important in identifying upper airway obstructions.
• A. Normal; B. Variable EXTRA-thoracic upper airway obstruction, C.

Variable INTRA-thoracic upper airway obstruction, D. Fixed upper
airway obstruction, E. Small airway obstruction

DISEASE CLINICAL MANIFESTATIONS PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL NOTES
• Non-productive cough à • Primary Disease: Middle and • PPD Test (Mantoux Test) WHO Category I • Remember, TB-DOTS is free
purulent sputum, sometimes Lower Lung Segments • Sputum TB Culture • New smear-positive PTB, New smear- in the health center
with blood streaking • Post Primary Disease: Apical and • TB Polymerase Chain Reaction (TB-PCR) negative PTB w/ extended parenchymal • Other household members
(hemoptysis) Posterior Segments • GeneXpert: rapid test involvement, New cases of extra-PTB should also be screened
• Cough of >2 weeks (high • Etiologic Agent: Mycobacterium (except CNS, Bones or Joints)
index of suspicion) tuberculosis Direct Sputum Smear Microscopy (DSSM) for • Intensive Phase: 2 HRZE Mnemonic: RIPES (drugs) =
• Weight loss • Mode of Transmission: Droplet AFB • Maintenance Phase: 4 HR RPHOON (side effects)
• Night sweats Spread (aerosolized by coughing, • Rifampicin = Red-Orange
• 3 (or at least 2) sputum specimens should be
• Malaise sneezing, or speaking) sent WHO Category Ia Urine, Sweat, Tears
• Unexplained fever and chills ○ The most infectious are those • New cases of extra-PTB including CNS, • Isoniazid = Peripheral
○ 1 : Time of consultation, or as soon as the TB
st
(note: absence of fever does with cavitary pulmonary symptomatic is identified Bones or Joints Neuropathy
not exclude TB) disease and laryngeal TB • Pyrazinamide = Hepatotoxicity
○ 2 : First sputum produced early in the morning
nd
• Intensive Phase: 2 HRZE
• Common hematologic (usually adults)
after waking up • Ethambutol = Ocular
• Maintenance Phase: 10 HR
findings: mild anemia, • Bacteria seeds in the lungs and symptoms (Retrobulbar
○ 3 : When TB symptomatic comes back to
rd
leukocytosis, thrombocytosis forms caseous granulomatous neuritis)

DOTS facility WHO Category II/IIa
with slightly elevated ESR lesions in the alveola • Streptomycin = Ototoxicity,
and/or CRP (Remember: Type 4 • Category II – Retreatment of RIF Nephrotoxicity
Sputum smear Positive (+) susceptible PTB and EPTB (except CNS/
Pulmonary • Hyponatremia may be present Hypersensitivity Reaction)
and may be due to SIADH • At least 2 positives for AFB, w/ or w/o bones or joints)
Tuberculosis Treatment Outcomes
radiographic abnormalities consistent w/ active • Category IIa - Retreatment of RIF
TB, OR • Cured – smear or culture
susceptible CNS, bones or joints
• 1 sputum specimen positive for AFB and w/ negative in the last month of
• UPDATED 2017 GUIDELINES FOR THE treatment and on at least 1
radiographic abnormalities consistent w/ active
TREATMENT OF DRUG-SUSCEPTIBLE previous occasion in the
TB, OR
TB: In patients who require retreatment, continuous phase
• 1 sputum specimen positive for AFB with sodium
the Category II regimen should no • Treatment Completed – a
culture positive for M. tb
longer be prescribed and drug patient who completes
susceptibility testing should be treatment without evidence of
Sputum Smear Negative (-) conducted to inform the treatment of
• At least 3 sputum specimens negative for AFB failure
choice. • Treatment Success – sum of
with radiographic abnormalities consistent w/
active TB, AND “cured” and “completed”
H/INH: Isoniazid • Treatment Failed – a patient
• No response to a course of antibiotics or
• Most active; structurally similar whose sputum smear or
symptomatic medications, AND
to pyridoxine culture is positive at 5
• Decision by a medical officer to treat the patient
• MOA: Inhibits fatty acid months or later during
w/ anti-TB drugs
synthase and mycolic acid treatment, does not show
synthesis (for cell wall)
Chest X-Ray • Adverse reaction: Peripheral clinical improvement anytime
• Recommended for those suspected to have TB Neuropathy, hepatotoxicity, during treatment
whose sputum smears are negative seizures, GI discomfort • Died – patient who dies for
• Note: Initiating treatment based on CXR alone is R: Rifampicin/Rifampin any reason during the course
discouraged • Bactericidal against both IC and of treatment
EC, dividing & non-dividing MTB • Lost to Follow-up – patient
• MOA: Binds to mycobacterial whose treatment was
DNA-dependent RNA interrupted for >= 2
Note right upper lobe
polymerase, blocking RNA consecutive months
infiltrate and a cavity with
synthesis • Not evaluated – patient for
an air-fluid level
• Adverse reaction: Red-orange whom no treatment outcome
color to urine, sweat, tears is assigned; includes patients
transferred to another
Z: Pyrazinamide
treatment facility with
• Bacteriostatic; may be outcome unknown
bactericidal against actively-
replicating organisms
• MOA: Inhibits fatty acid
Note the opacifications
synthetase I (involved in
and infiltrates in the hilar
synthesis of short chain mycolic
area and all throughout
acids)
the chest
• Adverse reaction: most
hepatotoxic; (first to remove)
E: Ethambutol
• Bacteriostatic, provides synergy
w/ other drugs; least potent
• MOA: Inhibits
arabinosyltransferases (cell wall
synthesis)
• Adverse reaction: retrobulbar
neuritis (eyes)
S: Streptomycin
• Low-level early bactericidal
activity against dividing MTB
• MOA: Inhibits protein synthesis
by binding to S12 at 30s of
ribosome
• Adverse reaction: Nephrotoxic,
ototoxic

DIAGNOSTIC ALGORITHM FOR PULMONARY TUBERCULOSIS
Evaluating PTB among smear-negative presumptive TB adults based on laboratory results Evaluating for drug resistant PTB
• Note that Category II/IIa are no longer used
ANTI-TB DRUGS
Drug Description and Mechanism of Action Pharmacokinetics Adverse effects
• Most active drug • Readily absorbed from the GIT; impaired if taken with • Peripheral neuropathy
• Bactericidal for actively growing bacilli (both extracellular and food and with antacids containing aluminum ○ Presents as paresthesia

intracellular organism); bacteriostatic against slowly-dividing ○ Patients are advised to take the drug at least 30 min ○ Due to relative pyridoxine deficiency (Vitamin B6)
organisms before or 2 hours after meals ○ Readily reversed by administration of pyridoxine
• Also indicated for treatment of latent TB • Hepatic clearance (half-life of 1-3 hours) • Hepatitis
H/INH Isoniazid
• Inhibits synthesis of mycolic acids, which are essential ○ most severe side effect
components of mycobacterial cell wall ○ at risk: increasing age, alcoholic drinkers, also taking Rifampicin
• Activated INH inhibits the action of enoyl-acyl carrier protein
reductase (InhA), an important component of FAS II complex
involved in mycolic acid synthesis
• Bactericidal for mycobacteria • Hepatic clearance (half-life 3.5 hours) • Nausea, vomiting, fever
• Binds to the beta-subunit of bacterial DNA dependent RNA • Potent cytochrome P450 inducer • Rash
polymerase, thereby inhibiting RNA synthesis • Adequate CSF concentrations are achieved even in the • Hepatitis
R Rifampicin • Can kill organisms that are poorly accessible to many other drugs, absence of inflammation; can also be used for TB • Red-orange urine, sweat, tears – assure patient that this is
such as intracellular organisms and those sequestered in meningitis harmless
abscesses and lung cavities • Elimination is via the bile into the feces and the urine as
parent drug and metabolite
• Bacteriostatic; may be bactericidal against actively-replicating • Well-absorbed in GIT and widely distributed in body • Most hepatotoxic
organisms tissues, including inflamed meninges • Arthralgia
Z Pyrazinamide • Active in acidic environment and found within phagocytes or • Half-life is 8-11 hours • Nausea, vomiting, fever
granulomas • Parent compound is metabolized by the liver, but • Hyperuricemia – not a reason for discontinuation, just give
• Inhibits the actions of fatty acid synthetase I (FAS I) metabolites are renally cleared analgesics
• Bacteriostatic • Half-life of 4 hours • Retrobulbar neuritis
• Synthetic, water-soluble, heat-stable compound • Accumulates in renal failure ○ Loss of visual acuity
E Ethambutol
• Inhibits mycobacterial arabinosyl transferases • Crosses the blood-brain barrier when meninges are ○ Red-green color blindness
inflamed (higher dose for treatment of TB meningitis) ○ Perform periodic visual acuity testing
• Bactericidal • Renal clearance (half-life 2.6 hours) • Ototoxicity
• Aminoglycoside that interferes with translation of mRNA transcripts ○ Vertigo and hearing loss
in M. tuberculosis ○ Risk increased in elderly
S Streptomycin • Binds to a ribosomal protein (S12) that is a component of the 30s • Nephrotoxicity
subunit of the ribosome complex and inhibits the synthesis of ○ Dose adjusted according to renal function
mycobacterial proteins ○ Limit therapy to not more than 6 months
• Cutaneous hypersensitivity

Classic Triad Symptoms: • Chronic inflammatory disorder of • Spirometry (gold standard) Relievers Goals of Therapy
1. Wheezing the lungs associated with ○ FEV /FVC ratio <0.70
1
• DOC: Short-acting B2 agonists (SABA) • Minimal (ideally no) chronic
2. Dyspnea widespread but variable airflow • Peak Expiratory Flow (PEF) ○ Salbutamol, Procaterol, Terbutaline symptoms
3. Coughing limitation and ○ More important in monitoring than in diagnosis ○ MOA: Stimulate adenylyl cyclase to • Minimal/infrequent
hyperresponsiveness ○ Diurnal variation in PEF >20% increase cAMP (bronchodilation) exacerbations
• Rhonchi and wheezing • Chest X-Ray ○ Rapid onset, best used for symptom • No emergency visits
throughout the chest (but may Inflammatory Cells ○ Usually normal but may show hyperinflation in relief • Minimal (ideally no) use of as-
be normal when asthma is Mast cells, Eosinophils, T 2 cells, severe cases • Others: SAMA (Ipratropium), required B2-agonit
Diagnostic Criteria methylxanthines (theophylline, • No limitations on activities
H
controlled) Basophils, Neutrophils, Platelets

• History of Variable Respiratory Symptoms aminophylline) • PEF circadian variation <20%
Structural cells
• Reversibility ○ Cough – more than one (combination) • (near) normal PEF
Epithelial cells, Smooth muscle
○ Responsive to asthma respiratory symptom Controllers • Minimal (or no) adverse effects
cells, Endothelial cells, Fibroblasts,
therapy ○ Dyspnea – occurs variable over time and • DOC: Inhaled Corticosteroids (ICS) from medicine
Nerves
○ Rapid improvements intensity ○ Beclomethasone, Budesonide,
measured within mins after ○ Wheezing – worse at night or every morning Fluticasone Classification of Severity by
inhalation of a rapid-acting ○ Chest tightness – triggered by exercise, ○ MOA: Reduce inflammatory cells and Level of Control
bronchodilator, or more Mediators allergens, viral infections, laughter eosinophils in airway mucosa Controlled
sustained improvement Histamine, Leukotrienes, • Confirmed Variable Expiratory Airflow • Systemic Steroids (for acute mgt) • No (or 2x or less/week)
over days/weeks after Prostanoids, PAF, Kinins, Limitation ○ Prednisone, Methylprednisolone, daytime symptoms or need
controller treatment Adenosine, Endothelins, Nitric ○ Documented excessive variability in lung hydrocortisone for reliever
oxide, Cytokines, Chemokines, function (see tests below) AND ○ Useful for treatment of acute • No limitation of activities,
• Variability: Growth factors ○ Documented airflow limitation exacerbations nocturnal symptoms,
○ Episodic attacks ○ For both criteria: • Long-acting B2 Agonists (LABA) exacerbation
Bronchial Asthma
○ Precipitation by § At least once during the diagnostic process ○ Formoterol, Salmeterol, Bambuterol • Normal lung function
Effects
allergens/irritants when FEV1 is low, confirm that FEV1/FVC ○ To be given w/ ICS (to lower dosing) –
Bronchospasm, plasma exudate, Partly Controlled
○ Symptoms may be worse is reduced (normal: 0.75-0.80 in adults) Improve asthma control & reduce
mucus secretion, AHR, structural • >2x/week daytime symptoms,
at night and in the early § The greater the variation, the more likely inflammation when added to ICS
changes (fibrosis, angiogenesis) need for reliever
morning the diagnosis of asthma • Leukotriene-Modifying Drugs
• Bronchoconstriction + Edema = • Any limitation of activities,
○ Improvement/ deterioration ○ Montelukast, Zafirlukast, Zileuton
Narrowed airway lumen leading to Tests to document Variable Expiratory Airflow nocturnal symptoms
in symptoms and lung ○ MOA: Block leukotriene receptors or
the triad symptoms Limitation (to meet above criteria) • <80% predicted lung function
function over time inhibit lipoxygenase
• Positive Bronchodilator Reversibility Test • 1 or more exacerbations per
• Cromones
○ Increase in FEV1 or FVC > 12% and absolute year
○ Cromolyn sodium, Nedocromil sodium
improvement of >200mL from baseline; 10- ○ MOA: Inhibit mas cell and sensory Uncontrolled
15 min after albuterol 200-400 mcg or nerve activation • >3 symptoms of partly
equivalent • Anti-IgE controlled asthma in any week
• Excessive Variability in Peak Expiratory Flow ○ Omalizumab • One exacerbation in any week
○ Average daily diurnal PEF variability >10% ○ MOA: Inhibits IgE-mediated reactions
• Increase in lung function after 4-weeks of
anti-inflammatory treatment Non-Pharmacologic: Avoidance of
○ Increase in FEV1>12% and >200mL (or PEF tobacco smoke, occupational sensitizers,
by >20%) from baseline after 4 weeks of house dust mites and cockroaches, animals
treatment with fur, indoor and outdoor pollens, mold,
• Other tests: (+) exercise challenge test, (+) drugs
bronchial challenge test, excessive variation in
lung function between visits (less reliable)

Cardinal Symptoms • Persistent (unlike asthma which • Spirometry (gold standard) Interventions which influence the natural • A common, preventable, and
• Cough is variable) airflow limitation ○ FEV /FVC ratio < 0.70
1
history of COPD treatable disease
• Sputum production • Hallmark: airflow obstruction ○ Differentiated from asthma because this is • Smoking cessation
• Exertional dyspnea that is usually not or minimally reversed by • Oxygen therapy in chronically
progressive and persistent Inflammation: bronchodilators hypoxemic patients (>15hrs/day)
• Chest X-Ray • Lung volume reduction surgery
• Host factors (genetic
○ Low flattened diaphragms • Components of therapy (from GOLD
Risk Factors: components)
○ Hyperlucent lung zones w/ possible bullae COPD 2018 guidelines)
• Smoking (most important!) • Exposure to noxious stimuli
formation and diminished vascular markings • Non-pharmacologic
○ Including 2 and 3 hand
nd rd (smoke, irritants)
○ *Notable changes seen only in severe COPD ○ Assess and monitor disease
○ COPD is unusual in the • Amplifying mechanisms
cases ○ Reduce risk factors, e.g. smoking
absence of smoking or (oxidative stress and increased
• Arterial blood gas cessation
prior history proteinases which leads to
○ Resting or exertional hypoxemia ○ Physical activity recommended
• Genetics: α1-antitrypsin emphysema)
Chronic Obstructive ○ Inc. alveolar-arterial oxygen tension gradient
deficiency contributes to ○ Flu and pneumococcal vaccines
Pulmonary Disorder
proteinase imbalance Encompasses the following • Pharmacologic management for stable
• Other irritant exposures conditions COPD
○ LABAs & LAMAs first line (preferred
• Emphysema – destruction and
over SAMAs & SABAs)
*Mnemonic: ABCCC of COPD enlargement of alveoli (“pink
○ ICS (if no improvement from LAMAs &
1. Age à >40 years puffers”)
LABAs)
2. Breathlessness à • Chronic bronchitis – chronic
○ SAMA/SABAs if LAMA/LABA + ICS
progressive cough and phlegm (“blue
don’t work
3. Cigarette smoke bloaters”), chronic
○ Systemic glucocorticoids for chronic
4. Chronic cough hypersecretion, peribronchial
treatment should be avoided
5. Chronic sputum production inflammation and fibrosis
• Supplemental oxygen
• Small airway diseases/
• Manage exacerbations
bronchiolitis – narrowing of small
bronchioles
Low-Risk CAP • Lower respiratory tract infection • Clinical Evaluation – usually enough for dx • For patients requiring hospitalizations, • Can also be Ventilator-
• Stable vitals involving the pulmonary • Chest X-Ray empiric therapy should be initiated as associated pneumonia and
○ RR < 30/min parenchyma and subsequent ○ Essential in the diagnosis of CAP, assessing soon as possible after a diagnosis of hospital acquired pneumonia
○ PR < 125/min immunologic response mounted severity, differentiating from other conditions CAP is made
by the host and in prognostication • Response to therapy is expected within Other causes:
○ Temp >36 C or <40 C
• Acquired in the community within ○ Best position: Standing PA and lateral views 24-72 hours of initiating treatment • Out-patient
○ BP ≥ 90/60 mmHg 24 hours to < 2 weeks of the chest • Treatment is based on severity and ○ S. pneumonia
• No altered mental state of • Etiologic agent: Streptococcus ○ Cons: Does not predict the likely etiologic presenting symptom
acute onset; no suspected ○ Mycoplasma pneumonia
pneumoniae (most common) agent • Most bacterial pneumonias treatment ○ Chlamydophila pneumonia
aspiration; no or stable co- • Access: duration is 5-7 days
morbid conditions ○ Haemophilus influenza
○ Inhaled ○ Legionella species
• Chest X-ray: (+) localized ○ Hematogenous Phil. CAP guidelines ○ Respiratory viruses
infiltrates, (-) pleural effusion ○ Aspiration from the oropharynx • Low-risk CAP • In-patient (ICU)
(most common) ○ Previously healthy px: Amoxicillin or ○ S. pneumonia
Community-
Moderate-Risk CAP • Causes of invasion: extended macrolides (for atypical ○ S. aureus
Acquired
• RR ≥ 30/min ○ Defect in Host mechanism pathogen) ○ Legionella sp.
Pneumonia
• PR ≥ 125/min ○ Overwhelming inoculum ○ With stable comorbid illness: Beta- ○ Gram–negative bacilli
(CAP) ○ Viral infection that inactivates
• Temp ≤ 36 C or ≥40 C lactamase inhibitor combination (BLIC) ○ H. influenzae
• BP < 90/60 mmHg alveolar macrophage action or second-generation oral
• Altered mental state of acute and mucociliary clearance cephalosporins + extended macrolides
onset • Moderate risk
• Suspected aspiration ○ IV non-antipseudomonal beta-lactam
• Decompensated co-morbids (BLIC, cephalosporin) + extended
(e.g. uncontrolled DM, • Sputum gram stain and Culture macrolide or respiratory
malignancies, CHF FC II-IV, ○ Gram stain: To ensure that sputum sample is
fluoroquinolone
renal failure on dialysis, adequate (>25PMN, <10SEC/LPF)
• High-risk
uncompensated COPD, ○ Culture: to guide specific antibiotic coverage
○ w/o Pseudomonas risk: IV non-
decompensated liver disease, • Invasive procedures (biopsy, bronchoalveolar
antipseudomonal β-lactam (BLIC,
neurologic disease in lavage, brush specimen)
cephalosporin, or carbapenem) + IV
evolution) ○ For non-resolving pneumonia,
extended macrolide or IV respiratory
immunocompromised, patients without
fluoroquinolone

• Chest X-ray: multilobar adequate specimens despite sputum ○ w/ Pseudomonas risk: IV
infiltrates, pleural effusion, induction antipneumococcal, antipseudomonal
abscess β-lactam (BLIC, cephalosporin,
Pneumonia Phases (on histology) carbapenem) + IV extended macrolide
High-Risk CAP 1. Edema: Presence of a proteinaceous exudate + Aminoglycoside OR IV
• Any of the features of and often of bacteria in the alveoli antipneumococcal, antipseudomonal
moderate-risk CAP + any of 2. Red Hepatization β-lactam (BLIC, cephalosporin, or
the following: ○ Erythrocytes in the intraalveolar exudate carbapenem) + IV ciprofloxacin or high
○ Severe sepsis and septic ○ Neutrophil influx is more important from the dose IV levofloxacin
shock, OR standpoint of host defense
○ Need for mechanical ○ Bacteria may be occasionally in the exudate
ventilation 3. Gray Hepatization
○ Cessation of erythrocyte extravasation;
degradation of remaining erythrocytes
○ Neutrophils predominate
○ Fibrin deposition is abundant
○ No bacteria
4. Resolution (final phase)
○ Macrophages predominate
○ Cessation of inflammatory response
• Encompasses Deep Venous Virchow’s Triad – three overarching Deep Venous Thrombosis Anticoagulation
Thrombosis (DVT) and factors that contribute to thrombus • Venous duplex scan – detects vein • Parenteral agents are started over the
Pulmonary Embolism (PE) formation incompressibility (most definite sign of first 5-10 days and are continued as a
• Inflammation thrombosis) transition to long-term oral
Deep Venous Thrombosis • Hypercoagulability • D-dimer – used to rule out DVT anticoagulation
• Cramp in the lower calf – • Endothelial injury • CT Venography • Parenteral Anticoagulants
most frequent symptom o Unfractionated Heparin
• Leg swelling and pain Deep Venous Thrombosis Pulmonary Embolism o Low Molecular Weight Heparin
• Risk factors: older age, • Presence of thrombus in one of • Plasma D-dimer – used to rule out PE if values o Fondaparinux
prolonged immobilization, the deep vein conduits that return are normal • Oral Anticoagulants
paralysis, hyperviscosity blood to the heart • ABG – O2 and PCO2 may be decreased o Warfarin
syndromes, etc. • Most commonly involves the • ECG o Dabigatran
deep veins of the leg or arm, • Cardia Biomarkers – may be increased in RV o Rivaroxaban
Venous Pulmonary Embolism often resulting in potentially life- microinfarction
threatening emboli to the lungs or o Apixaban
Thromboembolism • Unexplained breathlessness – • Chest X-ray:
debilitating valvular dysfunction o Edoxaban
(VTE) most frequent history o Westermark’s sign
and chronic leg swelling o Hampton’s hump
• Dyspnea – most frequent
o Pallar’s sign Fibrinolysis/Thrombolysis
symptom
Pulmonary Embolism • CT Pulmonary Angiography – Method of choice • Only indicated in massive PE
• Tachypnea – most frequent
• Blockage of the main artery of the when PE is highly suspected • Preferred: Recombinant Tissue
sign
lung (or its branches) by a Plasminogen Activator (tPA)
• Presentation depends on size
substance from elsewhere in the
of embolism
body
• Small to moderate PE:
• Increase in pulmonary vascular
pleuritic pain, cough,
resistance from pulmonary
hemoptysis
embolism causes increase in right
• Massive PE: dyspnea, ventricle wall tension leading to
syncope, hypotension, progressive right heart failure
cyanosis (usual cause of death)
Clinical syndrome of: Etiology of ARDS Berlin Definition of ARDS Goal of Treatment •
• Severe dyspnea of rapid • Direct Lung Injury • Oxygenation in ARDS (PaO2/FiO2) • To protect the lung
Acute Respiratory onset ○ Pneumonia ○ Mild - >200 to 300 mmHg; PEEP ≥ 5 cmH2O
Distress Syndrome • Hypoxemia ○ Aspiration of gastric contents ○ Moderate - >100 to 200 mmHg; PEEP ≥ 5 Summary of Treatment Strategies for
(ARDS) • Diffuse pulmonary infiltrates ○ Pulmonary contusion cmH2O ARDS
○ Near-drowning ○ Severe - ≤ 100 mmHg; PEEP ≥ 5 cmH2O • Low tidal volume (best level of evidence)
○ Toxic inhalation injury • Onset • Minimize left atrial filling pressures
• Indirect Lung Injury ○ Within 1 week of known clinical insult or new • Give high positive end-expiratory
○ Sepsis or worsening symptoms pressure (PEEP)
○ Severe trauma (fractures, flail • Chest imaging • Prone position
chest, head trauma, burns) ○ Bilateral opacities not explained by effusions, • Recruitment Maneuvers
○ Multiple transfusions lung collapse, or nodules • Extracorporeal membrane oxygenation
○ Drug overdose • Edema
○ Pancreatitis ○ Respiratory failure not fully explained by
○ Post-cardiopulmonary bypass cardiac failure or fluid overload
Three Phases in the History of

ARDS
1. Exudative Phase (Day 1-7)
○ Alveolar capillary endothelial
cells and type-I pneumocytes
are injured, leading to the loss
of the normally tight alveolar
barrier to fluid and
macromolecules
○ Edema fluid rich in protein
accumulates in the interstitial
and alveolar spaces
2. Proliferative Phase (Day 7-21)
○ Lymphocyte predominant
pulmonary infiltrate
3. Fibrotic Phase
○ While many patients with
ARDS recover lung function 3-
4 weeks after the initial
pulmonary injury, some will
enter a fibrotic phase
APPROACH TO CLASSIFICATION AND MANAGEMENT OF BRONCHIAL ASTHMA

Recommended Options for Initial Controller Treatment in Adults
• Regular daily controllers should be initiated as soon as possible once asthma is diagnosed
• Recommended options for initial controller are listed below
Preferred Initial Controller* Presenting Symptoms
• Symptoms or need for SABA <2x/month; and
• No waking due to asthma in the last month; and
No controller
• No risk factors for exacerbation; and
• No exacerbations in the last year
• Infrequent symptoms, but with ≥ 1 risk factors for exacerbation
Low Dose ICS
• Symptoms or need for SABA 2x/month to 2x/week or wakes due to asthma ≥ 1x/month
(Start with Step 2)
• Symptoms or need for SABA >2x/week
• Troublesome symptoms most days; or
Moderate-High Dose ICS, or Low Dose ICS/LABA
• Waking due to symptoms ≥ 1x/week
(Start with Step 3)
• Especially if with any risk factors for exacerbation
Short-course Oral Corticosteroids and regular controller • Initial presentation is with severely uncontrolled asthma, or
(high-dose ICS or moderate-dose ICS/LABA) • Initial presentation with an acute exacerbation
*After starting initial controller treatment: review response after 2-3 months; step down once good control has been maintained for 3 months
Stepwise Approach to Control Symptoms and Minimize Future Risk
• Asthma treatment is a continuous cycle: assess, adjust treatment, and review response
• Regular controller treatment should be initiated as soon as possible after asthma is diagnosed
• After starting initial controller treatment, review response after 2-3 months, or according to urgency
o Consider stepping up if: uncontrolled symptoms, exacerbations or risks (also assess adherence to medications, correct inhaler technique, and persistent exposure to triggers)
o Consider stepping down if: symptoms controlled for 3 months, low risk for exacerbations
• Find the patient’s lowest treatment that controls both symptoms and exacerbations

Step Preferred Controller Alternative Controller Reliever
None Consider Low Dose ICS for patients at risk of
Step 1
exacerbations
As needed SABA
Low Dose ICS Leukotriene Receptor Antagonist (LTRA)
Step 2
Low Dose Theophylline
Low Dose ICS/LABA Mod-High Dose ICS
Step 3 Low Dose ICS + LTRA
May add Theophylline
Moderate-High Dose ICS/LABA Add tiotropium (as third controller)
As needed SABA or Low Dose
Step 4 High Dose ICS + LTRA
ICS/Formoterol
May add Theophylline
Refer to specialist Add Low Dose OCS
Step 5 Add-on treatment (e.g. tiotropium, anti-IgE, anti-
IL5)
Assessing Asthma Severity
Severity Description
Mild Asthma that is well controlled with Step 1 or Step 2 treatment (e.g., as-needed reliever alone or low-dose ICS)
Moderate Asthma well-controlled with Step 3 treatment (e.g., low-dose ICS/LABA)
Asthma that requires Step 4 or 5 of treatment to prevent it from becoming “uncontrolled” or asthma that
Severe
remains uncontrolled despite treatment (e.g. high-dose ICS/LABA)
GOLD COPD GUIDELINES (2018): APPROACH TO CLASSIFICATION AND MANAGEMENT OF COPD

Classification of COPD Management of COPD – Main goals are to reduce symptoms and reduce future exacerbations
Confirm the Diagnosis of COPD Depending on
Patient Group Essential Recommended
• COPD is considered in patients with dyspnea, chronic cough, and sputum production Non-pharmacologic Local Guidelines
Step 1 with a history of exposure to risk factors (e.g. smoking, burning coal) Management A Smoking cessation Flu vaccination,
• Spirometry is needed to confirm the diagnosis: post-bronchodilator FEV1/FVC < 0.7 of COPD Smoking cessation, Physical activity Pneumococcal
B-D
Pulmonary rehabilitation vaccination
Assess Airflow Limitation • LABAs and LAMAs are preferred over short-acting agents, except for those with
• The classification is based on severity of airflow limitation in COPD using spirometry only occasional dyspnea
(Post-bronchodilator FEV1) • Patients may be started on a single long-acting bronchodilator or dual long-acting
• Spirometry is performed after the administration of an adequate dose of a short-acting bronchodilator therapy
inhaled bronchodilator • Long term monotherapy with ICS is not recommended
Spirometric Spirometry Findings Patient Next Step if No Other Possible
Clinical Findings Preferred Treatment
Classification FEV1/FVC FEV1 Group Improvement Treatment
• Chronic cough and sputum Any bronchodilator Continue, stop, or try
Antioxidant
GOLD 1 production A (either SABA or LABA) alternative class of
≥ 80% predicted mucolytics
Mild • Patient unaware that lung function is bronchodilator
abnormal Start with LABA or LAMA + LABA if no
B Plus SAMA, SABA
• Chronic cough and sputum LAMA improvement
Pharmacologic
production Start with LAMA LAMA + LABA if with further
Step 2 GOLD 2 50 to < 80% Management
• Shortness of breath on exertion C exacerbations Plus SAMA, SABA
Moderate predicted of COPD
• Stage where patients seek medical Alternative: LABA + ICS
Post-
attention LAMA + LABA LAMA + LABA + ICS Plus SAMA, SABA
Bronchodilator Alternative: LABA + ICS Consider PDE-4
• Greater shortness of breath
FEV1/FVC before going to triple therapy inhibitor of FEV1
• Reduced exercise capacity
GOLD 3 < 0.70 30 to < 50% <50% predicted
• Fatigue
Severe predicted D and with chronic
• Repeated exacerbations
bronchitis
• Signs and symptoms of respiratory Consider
failure (PaO2 <60mmHg +/- PaCO2 Macrolide in former
GOLD 4 smokers
>50mmHg) < 30% predicted
Very Severe
• Cor pulmonale

Assess for Symptoms and Risk of Exacerbation
• Prescribe oxygen and titrate to keep SaO2 ≥ 90% in patients with arterial
• ABCD groups below are derived exclusively from the patient’s history of exacerbation Supplemental hypoxemia, defined as:
and symptom assessment Oxygen o PaO2 <55mmHg or SaO2 <88%, or
Exacerbations Symptom Assessment to COPD Patients o PaO2 55-59 mmHg with right heart failure or erythrocytosis
Group
per Year mMRC CAT • Recheck and reassess in 60-90 days
Low symptom severity mMRC 0- CAT <
A ≤ 1 not leading to hospital admission
Low exacerbation risk 1 10
High symptom
mMRC ≥ CAT ≥
B severity ≤ 1 not leading to hospital admission
2 10
Low exacerbation risk
Low symptom severity ≥ 2, or ≥ 1 leading to hospital mMRC 0- CAT <
C
High exacerbation risk admission 1 10
High symptom
≥ 2, or ≥ 1 leading to hospital mMRC ≥ CAT ≥
D severity
admission 2 10
High exacerbation risk
• Classification based on Exacerbations

o Exacerbation of COPD – defined as an acute event characterized by
worsening of the patient’s respiratory symptoms that is beyond normal day-
to-day variations and leads to a change in medication Classification of
Step 3 Overview of Management
Exacerbation
• Modified Medical Research Council (mMRC) Questionnaire for Assessing Severity Management of Mild SABA
of Breathlessness Moderate SABA + Antibiotics +/- Oral corticosteroids
Acute
o Simple measure of breathlessness Requires hospitalization or ER visits
Exacerbations
mMRC Severe Some managed as acute respiratory failure (e.g.
Description
Grade mechanical ventilation)
0 I only get breathless with strenuous exercise
1 I get short of breath when hurrying on level ground or walking up a slight hill
2 On level ground, I walk slower than people of the same age because of
breathlessness, or I have to stop for breath when walking at my own pace on the
level
3 I stop for breath after walking about 100 yards or after a few minutes on level
ground
4 I am too breathless to leave the house or I am breathless when dressing
• COPD Assessment Test (CAT)

o Comprehensive assessment of symptoms
o Consists of 8 items which pertain to symptoms of COPD – patient will give a
score on a5 point rating scale and the points will be added
PNEUMONIA SEVERITY ASSESSMENT

CURB-65 Score for Pneumonia Severity
• The CURB-65 score is a practical method for determining the need for hospitalization in community-acquired pneumonia.
• CURB-65 is more sensitive for determining patients with severe illness, and lacks sensitivity towards other factors dealing with milder cases.
Criteria Management
• Confusion • If the patient meets a criterion, add one point to the CURB-65 score
• Blood Urea Nitrogen > 19mg/dL (>7mmol/L) • The CURB-65 scores range from 0 to 5. Clinical management decisions can be made based on the score,
• Respiratory rate ≥ 30 bpm as described in the validation study below:
• Systolic Blood Pressure < 90mmHg or Diastolic Blood Pressure ≤ 60mmHg o Score 0 or 1 – Outpatient care; 1.5% mortality
• Age ≥ 65 o Score 2 – Short inpatient hospitalization or Closely supervised outpatient treatment; 9.2%
mortality
o Score ≥ 3 - Inpatient admission with consideration for ICU admission especially with score of
4 or 5; 22% mortality

MODULE/TOPIC 9 CARDIOVASCULAR
Part 9A. ARRTHYMIAS

Types of Arrhythmias
Slow rhythms Fast rhythms Arrest rhythms Benign ectopic rhythms
• Sinus bradycardia • Sinus tachycardia • Asystole • Premature atrial contraction
• Sinus pause • Supraventricular tachycardia • Ventricular fibrillation • Premature ventricular contraction
• Junctional rhythms • Atrial fibrillation • Pulseless ventricular tachycardia
• Idioventricular rhythms • Atrial flutter • Pulseless electrical activity
• Heart blocks • Multifocal atrial tachycardia
• Ventricular tachycardia
Algorithms
Slow Rhythms Fast Rhythms
Slow Rhythms (HR<60)

Sinus bradycardia: regularly occurring PQRST
• normal in athletic people, pathologic: early stages
of MI
Sinus pause (sinus arrest): normal PQRST but

there are prolonged pauses between some beats
• Occurs when SA node stops firing during normal
sinus rhythm
• Causes: Acute infections, sick sinus syndrome,
increased vagal tone,
• Cardioactive drugs and cardiac disorders
Atrrioventricular (AV) blocks : represents blocks in the conduction system
First degree AV block: prolonged PR interval.
• Normal P wave and followed by QRST
Second degree AV block: “dropped beats”; the sudden disappearance of QRS complexes
Second degree AV block type I/ Mobitz Type I/
Wenkebach block
• Progressive lengthening of PR intervals until a
dropped beat occurs; then PR interval resets
Second degree AV block type II/ Mobitz Type II

• Fixed PR intervals with intermittent dropped
beats
• More dangerous than Type I. can be
symptomatic. Requires pacemaker
2:1 AV block: 2 P waves for every QRS complex

Third degree (complete) AV block: no relationship
between P waves and QRS complexes (different
rates for P-P intervals and between QRS
complexes)
“one heart beating as two”
High Grade AV block: AV conduction is 3:1 or

higher
Junctional Rhythm: inverted P wave; or P wave

buried within QRS or follows the QRS, narrow QRS
• diseased AV node

Idioventricular Rhythm: absence of normal upright
P wave and associated with QRST complex; wide
QRS
• T wave opposite in direction to QRS

Fast Rhythms (HR>100)
Sinus tachycardia: regularly occurring PQRST

Supraventricular tachycardia: 150-250 beats, no
P waves, narrow QRS

Multifocal atrial tachycardia: at least 3 different P
wave morphologies, narrow QRS

Atrial Flutter: atrial rate is 250-350/ min seen as
atrial flutter. “saw-toothed appearance”

Atrial Fibrillation: no discernible P waves, irregular
PR interval

Atrial fibrillation with controlled ventricular
response: 60-100 bpm

Atrial fibrillation with slow ventricular response:
slow heart rate

Atrial fibrillation with rapid ventricular
response: fast heart rate. Observable P waves,
compared to MAT

Ventricular Tachycardia: 3 or more consecutive
PVCs; wide QRS complexes in a rapid regular
rhythm, may see AV dissociation

Sustained VT: VT lasting longer than 30 secs

Non-sustained VT: VT terminates within 30 secs

Monomorphic: PVCs look the same

Polymorphic: PVCs are different from one another

Torsade de pointes: “twisting of points”. QRS
complexes changes axis and amplitude

Arrest Rhythms
Asystole: flat line
Ventricular Fibrillation: coarse or fine chaotic

undulation of ECG baseline. No P wave and true
QRS complexes
Benign Ectopic Rhythms

Premature Atrial Contraction: prematurely
occurring PQRST complex, P wave different in
configuration from sinus beat
Premature Ventricular Contraction: wide QRS

complexes, usually no preceding P wave. T wave
opposite in deflection to QRS. Complete
compensatory pause follows every premature beat
Deadly Premature Ventricular Contraction

PART 8B. FOCUSED HISTORY AND PE NOTES:
I. Chest Pain Vital Signs
a. Onset When did it start? Suddenly or gradually? • BP, Pulse rate, RR, HR (important in cardio)
b. Location Where exactly is the pain?
• Ischemic: substernal (most common), across mid-thorax, in
Inspection
both arms, shoulder, neck, lower jaw, diffused
• Radial pulse – check at the same time, compare & characterize
• Non-ischemic: left submammary, left chest, can be pointed
• Fingernails – cyanosis, capillary nail refill, Schamroth’s Window test
with one finger
c. Duration How long has the pain been going on? • Lesions – signs of infective endocarditis (Janeway lesions, Osler’s nodes,
d. Character What does it feel like? xanthomata)
• Ischemic: heavy, crushing, tight, constricting, squeezing, • Edema in extremities
rarely burning
Precordium
• Non-ischemic: sharp, stabbing, jabs (pleuritic type)
e. Association Any other symptoms occur with the pain? • Chest shape (normal, pectus carinatum, pectus excavatum, barrel chest)
• Shortness of breath • Visible pulsations
• Palpitations • Apical impulse
• Edema (right-sided heart failure) • Masses, scars, lesions
• Syncope • Signs of trauma and previous surgery
• Dyspnea • Precordial bulge
• Orthopnea • Increase in jugular venous pressure
• Cough
f. Aggravating Does anything make it particularly worse? Notes:
• Patient should be supine, with head elevated 30
o
• Ischemic: exertion (most predictive), emotional, cold
weather, after meals, nicotine, tachycardia • Tangential light is useful
• Non-ischemic: pain after exercise completion, provoked by • Use palpation to confirm the characteristics of the PMI
specific body motion Palpation
g. Relieving Factors Is the pain relieved by rest?
• Typical angina: relieved by rest or sublingual nitroglycerin • Over the 4 auscultation areas
(atherosclerosis) o Heaves – bulging detected by the whole hand (implies involvement of a
• Atypical angina: occurs anytime whether with effort or at large chamber)
rest (coronary artery spasms) o Lifts – bulging in the ICS detected by 2 fingers
h. Radiation Does the pain move anywhere else? o Thrills – fine vibration, palpable murmurs; press the ball of your hand on the
• Most common site: precordial radiates to the left shoulder, chest
neck and inner aspect of the left arm • Apical impulse / Point of maximal impulse
th
i. Time course Does the pain have a patter? (Worse in the o 5 ICS, 1cm medial to the midclavicular line
mornings) o Point with 1 finger
j. Severity Rate the pain on a scale of 0-10? o If you cannot identify this, ask the patient to roll partly to the left side (left
II. Medical History lateral decubitus)
a. Medical Condition
• Heart condition Notes:
• Hypertension • Upon detection of a thrill and to time heart sounds properly, use the carotid
• Diabetes artery
• Stroke o When palpating for S1 and S2, place right hand on the chest wall and left
index and middle fingers on right carotid artery
• Dyslipidemia
o S1: Just before the carotid upstroke
b. Family History of Medical Conditions
o S2: After the carotid upstroke
c. Surgery
• Stent insertion, angiography, etc. Auscultation
d. Medications
• Regular medication – Beta blockers, antihypertensives, 4 auscultation areas
nd
calcium-channel blockers 1. Aortic – 2 ICS, right parasternal border
nd
• Over the counter – NSAID 2. Pulmonic – 2 ICS, left parasternal border
th
• Herbal remedies – St. Johns Wart 3. Tricuspid – 5 ICS, left parasternal border
th
4. Mitral – 5 ICS, left midclavicular line
• Contraceptive pill – increased risk of thromboembolic
disease
• Murmurs, heaves, thrills
• Allergies to medications?
III. Lifestyle • Distinct S1 (louder at apex) and S2 (louder at base) sounds
a. Smoking - How many cigarettes per day? How many years? • Carotid bruits (ask patient to hold breath)
b. Alcohol - How many units a week?
c. Drug use Notes:
d. Obesity • Feel for carotid/radial pulse while auscultating (to check for timing)
e. Diet - High in salt or fat? • Bell – placed lightly, detects low-pitched sounds and murmurs (S3, S4, mitral
f. Exercise level stenosis murmur)
• Diaphragm – pressed firmly, detects high-pitched sounds and murmurs (S1,
S2, murmurs of aortic and mitral regurgitation, pericardial friction rubs)
*Check appendix for interpretation of heart sounds
Percussion (NOT DONE)
Special Tests
Jugular Venous Pressure
• Position: Patient lying supine with the head at 30-45 ,
o
facing left
• Steps:
® Look for the highest point of pulsation on right IJV
® Extend a ruler horizontally from the point of highest
visible pulsation, and another ruler vertically from the sternal angle
® Measure the vertical distance (in cm) where the 2 rulers meet, add 5cm
• Normal: 7-9 cm (elevated in right-sided congestive heart failure)
Hepatojugular Reflux
• Alternate test for measuring JVP
• Distention of neck veins when pressure is applied over the liver

Auscultate Locate Louder at the Stenosis Regurgitation
Aortic 2 R ICS 3 L ICS Systole Diastole
S2 (base)
Pulmonic 2 L ICS 3 L CC Ejection Murmur Decrescendo Murmur
Tricuspid 4 L ICS 4 R ICS Diastole Systole
S1 (apex)
Mitral 5 L ICS 4 L CC Crescendo Murmur Pansystolic Murmur
Heart Sounds Description of some murmurs

Systolic Murmurs
• Aortic stenosis: Crescendo-decrescendo systolic
ejection murmur (ejection click may be present)
Loudest at heart base; radiates to carotids
Most commonly due to age-related calcification in
older patients (> 60 years old) or in younger patients
with early-onset calcification of bicuspid aortic valve
• Mitral regurgitation: Holosystolic, high-pitched
“blowing murmur.”
loudest at apex and radiates toward axilla. MR is
often due to ischemic heart disease (post-MI), MVP,
LV dilatation
• Mitral valve prolapse: A midsystolic or late systolic
murmur with a preceding click.
Most frequent valvular lesion. Best heard over apex.
Loudest just before S2
• Flow murmur: Very common, and does not imply
cardiac disease
Diastolic Murmurs (always abnormal)
• Aortic regurgitation: Most frequent valvular lesion.
Gallops: Best heard over apex. Loudest just before S2
• S3 gallop: Dilated cardiomyopathy (floppy ventricle), mitral valve disease; often normal in younger • Mitral stenosis: Follows opening snap (OS; due to
patients and in high-output states (eg, pregnancy). abrupt halt in leaflet motion in diastole, after
• S4 gallop: Hypertension, diastolic dysfunction (stiff ventricle), aortic stenosis; often normal in rapid opening due to fusion at leaflet tips).
younger patients and in athletes. Delayed rumbling mid-to-late diastolic murmur
(↓interval between S2 and OS correlates with ↑
Splitting severity)
• Wide splitting: delayed RV emptying (eg, pulmonic stenosis, right bundle branch block). • Tricuspid regurgitation: Holosystolic, high-pitched
• Fixed splitting: ASD
“blowing murmur.” loudest at tricuspid area. TR
• Paradoxical splitting: delay aortic valve closure (eg, aortic stenosis, left bundle commonly caused by RV dilatation
branch block) Continuous
• Patent ductus arteriosus: Continuous machine-like
murmur. Loudest at S2. Best heard at left
infraclavicular area

CLINICAL MANIFESTATIONS
Disease/ Definition / PATHOGENESIS DIAGNOSIS TREATMENT ADDITIONAL Notes
PE & HISTORY FININGS
HYPERTENSION
• average of two or more • BP Classification Primary HTN • Heart disease: Most
seated blood pressure (Jameson et al, 2018) • Vast majority (90-95%) of • the average of two or more • BP Goals (JNC 7) common cause of death in
readings during each of two • Normal hypertension is idiopathic seated blood pressure o Uncomplicated HPN: hypertensive patients
or more outpatient visits SBP < 120 and • Genetic factors readings during each of two <140/90mm Hg • Stroke: second most
• Children/adolescentsSBP DBP < 80 • Reduced renal sodium or more outpatient visits o HPN with diabetes, or common cause of death
and/or DBP consistently > • Prehypertension excretion in normal arterial • Basic lab tests for initial renal disease: • Renal injury
95 percentile for age, sex SBP 120-139 or pressure may be a key evaluation (Jameson et al <130/80mmHg • Peripheral artery disease
and height DBP 80-89 initiating event in essential 2018) • Retinopathy
th th
§ BP between 90 to 95 • Stage 1 HTN hypertension. o Renal: microscopic • BP Goals (JNC 8)
percentile: SBP 140-159 or o ↓ sodium excretion à ↑ in urinalysis, albumin o <140/90mm Hg: for pt < Sequelae:
prehypertensive; DBP 90-99 fluid volume à↑ cardiac secretion, serum BUN 60 yrs, or for pt > 18 yrs Hypertensive Heart Disease
indication for lifestyle • Stage 2 HTN output and peripheral and/or creatinine with CKD or diabetes • from increased demands
manifestation SBP ≥ 160 or vasoconstriction à ↑blood o Endocrine: serum sodium, o <150/90mmHg: for pt ≥ 60 placed on the heart by
• Primary (essential/ DBP ≥ 100 pressure potassium, calcium, TSH yrs HTN causing:
idiopathic) Hypertension • Isolated systolic • Factors that induce o Metabolic: fasting blood o pressure overload
o HTN with no identifiable hypertension vasoconstriction or stimuli glucose, total cholesterol, Maintenance medications o ventricular hypertrophy
cause SBP ≥ 140 and that cause structural HDL and LDL cholesterol, • Diuretics: Thiazides, loop • more common in the left
o Risk factors: family history DBP <90 changes in the vessel wall, triglycerides diuretics, potassium sparing heart (as result of systemic
of hypertension or heart • HTN is asymptomatic until can lead to an ↑ in o Other: hematocrit, • Sympathoplegic agents: HTN)
disease, high-sodium diet, complications develop peripheral resistance electrocardiogram o Beta-blockers (-olol)
smoking, obesity, and • Patients should be • Environmental factors: o Alpha 1-blockers (-sozin) Systemic (Left sided) HHD
advanced age evaluated for end-organ stress, obesity, smoking, o Centrally-acting alpha 2 • adaptive response to
• Secondary Hypertension damage to the brain physical inactivity, and agonists (Clonidine, pressure overload
o Secondary to identifiable (stroke, dementia), eye heavy salt consumption Methyldopa) • Early stage
cause (cotton-wool exudates, • Direct vasodilators: o HPN induces LV
o Common causes: primary hemorrhage), heart (LVH), o Ca+ channel blockers (- pressure overload
renal disease, renal artery and kidney (proteinuria, dipine) hypertrophy, initially
stenosis, OCP use, CKD). o Ca + channel blockers without ventricular
pheochromocytoma, • Renal bruits may signify (Non- dihydropiridines; ex. dilation
Conn’s syndrome renal artery stenosis as Diltiazem, Verapamil) • Later stage
(hyperaldosteronism), cause of HTN • RAA inhibitors: o Increased thickness of
coarctation of the aorta • Ask for the following: o ACE Inhibitors (Ex. the LV wall imparts a
• History (Jameson et al Captopril, Enalapril) stiffness that impairs
2018) o Angiotensin II receptor diastolic filling inducing
blockers (Ex. Losartan) LA enlargement
o Direct renin inhibitors (Ex • Morphology:
.Aliskiren; MNEMONIC: • Earliest stage
Alis Ka, REN!) o ↑ transverse diameter of
o Aldosterone receptor myocytes
blockers (Ex. • Advanced stage
Spironolactone) o Variable cellular and
nuclear enlargement
Hypertensive Urgency: o interstitial fibrosis
• Uncontrolled HPN w/o end- • Xray or ECG: Left
organ damage ventricular hyperplasia or
• Use oral agents: general cardiac
o Nifedipine, Captopril, enlargement
Clonidine
Hypertensive Emergency:

• End organ damage • Minimal criteria for the
• Use IV agents: diagnosis of systemic
o Nicardipine – HHD:
dyhydropyridine Ca (1) Left ventricular
channel blocker hypertrophy (concentric
o Hydralazine – direct- thickening of the wall) in
acting vasodilator in the absence of other CV
arteries/arterioles pathology
o Isosorbide dinitrate (2) A history or pathologic
(ISDN) – vasodilation evidence of hypertension in
o Nitroprusside – other organs
vasodilation of arterioles &
venules Pulmonary (Right-sided)
HHD
Non-pharmacologic: Diet, • From right ventricular
lifestyle modification pressure overload
Secondary HTN • Pulmonary venous
• Renovascular hypertension: • same as above o treat underlying etiology hypertension most
renal artery stenosis causes commonly occurs as a
↓ glomerular flow and complication of systemic
pressure in the afferent heart diseases
arteriole of the glomerulus. • Commonly caused by
o Induces renin secretion à diseases of the pulmonary
↑vascular tone and blood parenchyma, especially
volume via the angiotensin- chronic disorders
aldosterone pathway (emphysema)
• Single-gene disorders cause • Characterized by:
severe but rare forms of: ® Right ventricular
o Gene defects affecting hypertrophy
enzymes involved in ® Right ventricular dilation
aldosterone metabolism ® Right-sided heart failure
(e.g., aldosterone
synthase, 11β-hydroxylase,
17α-hydroxylase)
• Primary hyperaldosteronism
• Mutations affecting proteins
that influence sodium
reabsorption.
Morphology
• Hyaline arteriolosclerosis:
• Nephrosclerosis in chronic
hypertension
• Hyperplastic
arteriolosclerosis:
• Necrotizing arteriolitis:
ARTHEROSCLEROSIS
Characterized by intimal • Angina, claudication, but • Hypercholesterolemia • Fasting Lipid Profile (total • Lifestyle modification • Characterized by
lesions called atheromas (also can be asymptomatic promotes accumulation of cholesterol, triglycerides, o Smoking cessation atheromas, or
called atheromatous plaques LDL particles in the intima LDL, HDL) o Proper diet atheromatous or
or atherosclerotic plaques) that Based on the circulatory bed o Fatty streaks – initial • Angiogram o At least 30 mins of atherosclerotic plaques
protrude into vessel lumens affected lesions • Arteriography moderate-intensity • Often form at branching
• Coronary Arteries o Sequestration within the physical activity per day points of arteries (regions
o Angina pectoris intima separates of disturbed blood flow)

o Myocardial infarction lipoproteins from plasma • Tight glycemic control in
• Arteries supplying CNS antioxidants and favors patients with diabetes Risk Factors
o Stroke oxidative modification • Treatment of underlying • Nonmodifiable
o Transient cerebral • Accumulation of leukocytes causes o Age (M >45y/o; F
ischemia (inflammation) o Antihypertensives (ACE >55y/o)
• Peripheral circulation • Mononuclear phagocytes inhibitors, calcium channel o Male gender
o Intermittent claudication ingest lipids and become blockers, thiazide o Family history
o Gangrene foam cells diuretics) o Genetic abnormalities
• Splanchnic circulation • Smooth muscle cells o Lipid-lowering therapy • Modifiable
o Mesenteric ischemia migrate from the media (StatinsL HMG-CoA o Hyperlipidemia
through the internal elastic reductase inhibitors) o Hypertension
Based on development lamina and accumulate • Low-dose aspirin (to prevent o Cigarette smoking
• Acute within expanding intima blood clots) o Diabetes mellitus
® MI, stroke, sudden o Lay down ECM that forms o Lack of exercise
cardiac death the bulk of the lesion • Surgery o Obesity
• Chronic o Coronary angioplasty – to
® Stable, effort-induced Thrombosis provoked by widen coronary arteries
angina pectoris atheroma rupture and o Coronary artery bypass
® Predictable or subsequent healing may graft
reproducible intermittent promote plaque growth o Carotid endarterectomy –
claudication to widen the carotid artery
*Atherosclerotic plaque will

only cause stenosis when it
exceeds ~40% of the internal
elastic lamina
*Other individuals may never
HEART FAILURE
Complex syndrome that results • Cardiac pump dysfunction • Progressive disorder initiated 2 major criteria or 1 major + Acute heart failure LV Remodeling Changes
• Diuretics (1 line) right away • Myocyte hypertrophy
st
from structural or functional à congestion and low after an index event, which 2 minor criteria
impairment of ventricular filling perfusion. produces initial decline in if congested!! • Alterations in contractile
or ejection of blood • Cardinal symptoms: heart’s pumping capacity Major Criteria: Wet and warm: properties of myocyte
dyspnea and fatigue o Most common index • Paroxysmal nocturnal • vascular type: vasodilator + • Progressive loss of
AHA/ ACC guidelines classify • Cardinal signs of HF: events: abrupt MI dyspnea diuretic myocytes
heart failure by clinical edema and rales o Chronic: prolonged • Neck vein distension • cardiac type: diuretic + • B-adrenergic
syndromes uncontrolled • Rales vasodilator + ultrafiltration (if desensitization
Left-sided vs right sided HF hypertension • Radiographic cardiomegaly diuretic resistant • Abnormal myocardial
NYHA Functional Left sided heart failure o Hereditary: hypertrophic • Acute pulmonary edema Wet and cold type: energetics & metabolism
Classification dyspnea predominates obstructive • S3 gallop • SBP < 90 mm Hg • Reorganization of ECM
I: No limitation of activity. • Orthopnea cardiomyopathy • Increased central venous o Isotropic agent
Ordinary physical activity • Paroxysmal nocturnal • Compensatory mechanisms: pressure (>16 cm H2O at o Consider vasopressor if
does not cause symptoms of dyspnea adrenergic nervous system, right atrium) refractory
HF • Pulmonary edema renin-angiotensin- • Hepatojugular reflux o Diuretic (after correcting
II: Slight limitation of physical aldosterone system, cytokine • Weight loss >4.5 kg in 5 perfusion)
activity. Comfortable at rest, Right- sided heart failure system days in response to o Mechanical circulatory
but ordinary physical activity fluid retention predominates • Sustained activation of these treatment support (if no response
results in symptoms of HF • Hepatomegaly systems → secondary end- to drugs)
III: Marked limitation of physical • Jugular venous distension organ damage within the Minor Criteria: • SBP > 90 mm Hg
activity. Comfortable at rest, • Peripheral edema ventricle, with worsening left • Bilateral ankle edema o Vasodilators, diuretics,
but less than ordinary activity ventricular remodeling → • Nocturnal cough inotropic (if refractory)
causes symptoms of HF Systolic vs Diastolic HF cardiac decompensation • Dyspnea on ordinary
IV: Unable to carry on any Systolic heart failure exertion Dry and warm: adjust oral
physical activity without • ↓ EF (<50%) and ↑ LV EDV. • Hepatomegaly therapy
symptoms of HF, or Dry and cold:
• Pleural effusion
symptoms of HF at rest • consider fluid challenge

• caused by ↓ LV contractility • Decrease in vital capacity • consider inotropic agent if still
ACCF/ AHA Stages of HF or ↑ afterload by one third from maximum hypoperfused
A: at high risk for HF but w/o recorded
structural dse or symptoms Diastolic heart failure • Tachycardia (heart rate>120 Chronic heart failure
of HF • ↓ ventricular compliance w/ beats/min.) • First line: ACEI/ ARB
B: w/ structural dse w/o normal systolic function • If still symptomatic and
symptoms of HF (NYHA • ventricle has either Initial labs LVEF≤ 35: ARNI
class I) impaired active relaxation • CBC • If sinus rhythm QRS ≥ 130
C: w/ structural dse w/ or (eg. d/t hypertrophy), or • Urinalysis msec: consider CRT
current symptoms of HF passive filling • Serum electrolytes • if sinus rhythm HR ≥ 70: use
(NYHA class I-IV) • cardiac output and EF • BUN ivabradine
D: Refractory HF requiring usually normal. • Serum creatinine • if still resistant: consider
specialized interventions • Glucose digoxin/ H-ISDN, LVAD or
(NYHA class IV) HFrEF vs HFpEF • Fasting lipid profile transplantation
• HF w/ Reduced Ejection • Liver function tests
Fraction (HFrEF): EF ≤ 40% • TSH
• HF w/ Preserved ejection • ECG
fraction (HFpEF): EF ≥ 50%
o HFpEF, borderline EF 41- Imaging
49 • Chest xray: to detect heart
o HFpEF, improved > 40 size and pulmonary
congestion
• 2D echo w/ Doppler:
ventricular function, size,
wall thickness, wall motion
and valve function
• Pulmonary artery catheter
for patients in respiratory
distress/ impaired systemic
perfusion
CARDIOMYOPATHY
Dilated Cardiomyopathy
• Progressive cardiac dilation • Gradual development of • Most are idiopathic • LV dilation and ↓ EF • Na+ restriction Systolic dysfunction
and contractile (systolic) CHF symptoms • Genetic: mutation in TTN • Echocardiography is • ACE inhibitors,
dysfunction, usually with • Displacement of LV impulse gene coding titin (~20%) of diagnostic • β-blockers
concomitant hypertrophy • Jugular venous distension cases, dystrophin • CXR: enlarged, balloon-like • diuretics
• Most common • S3/S4 gallop • Secondary causes: alcohol heart, and pulmonary • digoxin
cardiomyopathy (90% of • mitral/ tricuspid regurgitation • Myocarditis, Peripartum congestion • ICD
cases) cardiomyopathy, • heart transplant.
• Drugs (doxorubicin,
zidovudine, cocaine),
endocrinopathies (thyroid
dysfunction,
pheochromocytoma),
infection (coxsackievirus,
HIV, Chagas disease), wet
beri-beri
• Most common causes are:
ischemia, and long
standing HTN
• Takotsubo cardiomyopathy
“broken heart syndrome”-
LV apical ballooning

• Likely due to increased
sympathetic stimulation
(stressful situations)
Morgphology:
• Gross: usually enlarged,
heavy (often weighing two
to three
• Times normal), and flabby,
due to dilation of all
chambers
• Eccentric hypertrophy
(sarcomeres added in
series)
Histology: variable myocyte

hypertrophy and interstitial
fibrosis
Hypertrophic Cardiomyopathy
Myocardial hypertrophy Patients are often • Mutations in β-myosin • 2D echo is diagnostic, β blockers: initial therapy for Diastolic dysfunction ensues
Poorly compliant left asymptomatic but may also heavy chain (most shows asymmetrically symptomatic relief; CCB (non-
nd
ventricular myocardium leading present with syncope, common), cardiac TnT, A- thickened septum and DHP) is 2 line
to abnormal diastolic filling, dyspnea, palpitations, angina, tropomyosin, myosin- dynamic obstruction to surgical option for HOCM
and intermittent ventricular or sudden cardiac death binding protein C blood flow avoidance of intense athletic
outflow obstruction systolic ejection crescendo- • Hypertrophic obstructive • ECG: signs of LVH competition and training
decrescendo murmur that ↑ cardiomyopathy (subset)— • CXR: left atrial enlargement
Hypertrophic obstructive with ↓ preload (eg. Valsalva asymmetric septal (LAE) secondary to mitral
cardiomyopathy: most maneuver, standing) and ↓ hypertrophy and systolic regurgitation
common cause of sudden with ↑ preload (eg. passive leg anterior motion of mitral
death in young healthy athletes raise) valve → outflow obstruction
in the US →dyspnea, possible
• Sustained apical impulse syncope.
•
•
S4 gallop
Mitral regurgitation due
•
Gross massive myocardial
hypertrophy, usually
Impaired mitral valve without ventricular dilation
closure • The classic pattern involves
asymmetric septal
hypertrophy “banana-like”
ventricular cavity
Histology: Extreme myocyte

hypertrophy, myocyte disarray,
exaggerated myocyte
branching, interstitial fibrosis
Restrictive Cardiomyopathy
Primary decrease in ventricular • Shows sign of both left- • Caused by infiltrative • 2D echo is is key for Therapeutic options are limited, Diastolic dysfunction ensues.
compliance, resulting in and right-sided heart disease (amyloidosis, diagnosis: rapid early filling generally palliative only Can have low voltage ECG
impaired ventricular filling failure, but symptoms of sarcoidosis, and near normal EF cautious use of diuretics for fluid despite thick myocardium
during diastole right-sided failure usually hemochromatosis) or by • CXR, MRI and cardiac overload and vasodilators to ↓ (especially amyloid).
predominate scarring and fibrosis (2° to catheterization: helpful for filling pressure
radiation) characterization (sarcoid,
amyloidosis)
Other etiologies:

• Loffler syndrome: • ECG: LBBB, low voltage in
endomyocardial amyloidosis
fibrosis with a
prominent
eosinophilic infiltrate
• Endocardial
fibroelastosis (thick
fibroelastic tissue in
endocardium of
young children)
ISCHEMIC HEART DISEASE (aka coronary artery disease or coronary heart disease)
• group of pathophysiologically related syndromes resulting from myocardial ischemia (imbalance between myocardial oxygen supply and demand)
• (>90% of cases) is caused by reduced blood flow due to obstructive atherosclerotic lesions (e.g. plaque/ atheroma)
• Disease manifestations
1) Stable angina pectoris
2) Acute coronary syndrome
Stable angina pectoris
Substernal chest pain 2° to • Retrosternal chest • Inadequate supply of blood • ECG: best initial type for Pharmacologic Treatment • 70% of cases seen in
myocardial ischemia discomfort (heaviness, flow and oxygen to a portion any chest pain • Anti-Ischemic Drugs males; atypical
pressure, squeezing, of the myocardium causing • Stress testing: ST-segment o Nitrates (Isosorbide presentation in women
smothering, or choking) inadequate perfusion of or wall motion changes w/ Dinitrate, Isosorbide • Threshold for development
• Angina crescendo- myocardium supplied by an exercise or pharmacologic Mononitrate): systemic of angina may vary by time
decrescendo involved artery stress (diagnostic of CAD) venodilation, with of day and emotional state
o Lasts 2-5mins • Most common cause: o contraindicated for pt reduction in LV end- • Harbinger/forerunner of MI
o Can radiate to either atherosclerotic disease of w/ abnormal baseline diastolic volume &
shoulder and to both an epicardial coronary artery ECG pressure (MOA); none of Canadian Cardiovascular
arms (esp. ulnar DDx: the long-acting nitrates is Society (CCS) Angina
surfaces of forearm & • GERD as effective as Classification:
hand) but does NOT • MSK/ costochondritis sublingual • Class I: occurs w/
radiate to trapezius • Pneumonia/ pleuritis nitrogyclerin for acute GREATER than ordinary
• Angina caused by exertion • anxiety relief of angina physical activity
or emotion (but may occur o B-blockers (Metoprolol, • Class II: w/ ORDINARY
at rest/while recumbent) and Carvedilol, Atenolol, physical activity
relieved by rest and/or Bisoprolol): inhibit • Class III: with LESS than
sublingual nitroglycerin increases in HR, arterial ordinary physical activity
pressure & myocardial • Class IV: even at REST
Pertinent History contractility (MOA)
• Male >50y/o OR female o Ca channel blockers
>60y/o (Verapamil, Diltiazem,
• Family history of premature Amlodipine,
IHD (<55 yrs in first-degree Felodipine): variable
male relatives, <65 in female and dose-dependent
relatives) & presence of DM, reductions in myocardial
hyperlipidemia, HPN, O2 demand, contractility
cigarette smoking & arterial pressure
(MOA)
PE Findings • Anti-platelet Drugs
• Levine’s sign: Pt places o Aspirin (75-325 mg
hand over sternum, PO/day): irreversible
sometimes with a clenched inhibitor of platelet
fist to indicate squeezing, cyclooxygenase activity
central, substernal o Clopidogrel (300-
discomfort 600mg LD, then
75mg/day): blocks ADP

S4 gallop or mitral receptor-mediated
regurgitation murmur during platelet aggregation
pain • Anti-Dyslipidemic Drugs
o Statins: HMG-CoA
reductase inhibtors
Coronary Intervention
• Percutaneous Coronary
Intervention (PCI): balloon
dilatation usually with
coronary stenting Coronary
Artery Bypass Grafting
ACUTE CORONARY SYNDROME (Jameson, 2018)
commonly classified into:
1. acute myocardial infarction with ST-segment elevation (STEMI)
2. non-ST-segment elevation acute coronary syndrome (NSTE-ACS)
a. non-ST-segment elevation myocardial infarction (NSTEMI), who, by definition, have evidence of myocyte necrosis
b. unstable angina (UA) no myocyte necrosis
Non-ST-segment elevation acute coronary syndrome (NSTE-ACS)
Includes: • At least one of three (1) Disruption of an • based largely on the • Acute symptoms: aspirin, unstable angina: impending
a. non-ST-segment elevation features: unstable coronary plaque due clinical presentation + O2, IV nitroglycerin, IV infarction based on plaque
myocardial infarction (1) occurrence at rest (or to plaque rupture, (most evidence of myocardial morphine stability
(NSTEMI), with minimal exertion), common) necrosis, as reflected in • consider B blockers NSTEMI: impending
b. unstable angina (UA) lasting >10 min; (2) of (2) Coronary arterial abnormally elevated levels • admit to hospital, monitor myocardial infarction
relatively recent onset (i.e., vasoconstriction; of biomarkers (cardiac until acute MI has been
within the prior 2 weeks); (3) Gradual intraluminal troponin I, CK-MB) ruled out by cardiac
and/or (3) a crescendo narrowing; • ECG enzymes
pattern, i.e., distinctly more (4) Increased • • If refractory chest pain: IV
severe, prolonged, or myocardial oxygen demand NSTEMI vs UA heparin, schedule for
frequent than previous (fever, tachycardia, and • UA: (-) cardiac enzyme angiography, possible PCI
episodes thyrotoxicosis) elevations, but may see ST or CABG
• Substernal region and changes on ECG
radiates to the left arm, left SUBENDOCARDIAL (NON- • NSTEMI: diagnosed by
shoulder, and/or superiorly TRANSMURAL) INFARCTION serial elevated cardiac
to the neck and jaw. Subendocardial zone enzymes and ECG
• Anginal equivalents such as • Least perfused region,
dyspnea, epigastric most vulnerable to
discomfort, nausea, or reductions in coronary flow
weakness may occur • Involve: inner third of the
instead of chest discomfort. ventricular wall
• May occur due to coronary
thrombus that becomes
lysed before
• necrosis involves entire
thickness
Prinzmetal’s variant angina
Severe ischemic pain • Generally younger and, • Caused by focal spasm of an • Detection of transient ST- • Nitrates and calcium • May lead to acute MI,
that usually occurs at rest and except for cigarette epicardial coronary artery segment elevation with channel blockers are the ventricular tachycardia or
is associated with transient ST- smoking, have fewer with resultant transmural rest pain main therapeutic agents fibrillation, and sudden
segment elevation coronary risk factors than do ischemia and abnormalities • Coronary angiography statins cardiac death.
patients with NSTE-ACS. in left ventricular function demonstrates transient • Coronary revascularization
• Cardiac examination is • Cause of the spasm is not coronary spasm as the
usually unremarkable in the well defined diagnostic hallmark of
absence of ischemia. • Possibly due to PVA.
However, a minority of hypercontractility of vascular

patients have a generalized smooth muscle d/t
vasospastic disorder adrenergic vasoconstrictors,
associated with migraine leukotrienes, or serotonin.
and/or Raynaud’s
phenomenon
Acute myocardial infarction with ST-segment elevation (STEMI)
• ST segment elevation and • Precipitating factor appears • Typical myocardial infarct • ECG Initial management Sequelae
cardiac enzyme release 2° to be present before caused by occlusion of an o Initial: “tombstone” ST- Prehospital care o Contractile dysfunction
prolonged cardiac ischemia STEMI, such as vigorous epicardial segment elevation (1) recognition of o Arrhythmias
and necrosis physical exercise, vessel in the absence of (total occlusion of symptoms o Myocardial rupture
• Occlusion may lead to: left emotional stress, or a therapeutic intervention coronary artery) (2) rapid deployment of an o Ventricular aneurysm
ventricular damage, medical or surgical illness • Involves full thickness of the o Q waves on the ECG emergency medical team o Pericarditis
intercoronary anastomoses • Often seen in the morning ventricular wall • Serum cardiac biomarkers: (3) transportation of the patient o Infarct expansion
• Little blood flow normally within a few hours of • coronary blood flow Cardiac-specific troponins to a hospital facility o mural thrombus
occurs in coronary arteries awakening decreases abruptly after a T and I (cTnT and cTnI) (4) reperfusion therapy. o progressive heart failure
• May enlarge when coronary thrombotic occlusion of a o Detectable within 2 to
arteries are narrowed over Symptoms coronary artery previously 4 hours, both peaking Emergency Department
time or stimulated by • Substernal chest pain affected by atherosclerosis at 48 hours, and • key medication: aspirin
ischemia (most common) • myocardial damage caused elevated for 7-10 days • O2 nasal prongs or face mask
• Extensive collateralizations o Radiates to neck, left by coronary occlusion o cTnT: peak between for the first 6–12 h after
may lead to paradoxically shoulder, left arm depends on 12-48 hours infarction; if hypoxemia is
distributed sites of infarction o Deep & visceral, heavy, (1) the territory supplied by o cTnI: maximal at 24 present
during occlusion squeezing, crushing the affected vessel, hours MB fraction of
o Occurs at rest, more (2) whether or not the creatine kinase (CK- Control of Discomfort
Cardiac blood supply severe, and lasts longer vessel becomes totally MB) • Sublingual nitroglycerin
• Left anterior descending than in angina pectoris; occluded, o Sensitive but not (↓myocardial oxygen demand
branch of the left coronary does not subside w/ (3) the duration of coronary specific to myocardial and ↑myocardial oxygen
artery: Supplies the apex cessation of activity occlusion, damage supply by vasodilation)
of the heart, anterior 2/3 of • Dyspnea (4) the quantity of blood o Begins to rise within 2- • morphine as analgesic
the ventricular septum, and • Diaphoresis (profuse supplied by collateral 4 hours of the onset of IV β blockers (metoprolol):
anterior wall of the left perspiration) vessels to the affected MI ↓myocardial oxygen demand à
ventricle • Weakness, nausea, tissue o Peaks at about 24 to ↓ ischemia
• Left circumflex branch of vomiting, anxiety, and a (5) the demand for oxygen 48 hours
the left coronary artery: sense of impending doom of the myocardium whose o Returns to normal Interventions
Supplies the lateral wall of blood supply has been within approximately • Fibrinolysis: if no
the left ventricle Signs suddenly limited 72 hours contraindications are present,
• Right coronary artery: • Pallor, pale and cool skin (6) endogenous factors that • Cardiac imaging fibrinolytic therapy
Supplies the entire free wall • Sinus tachycardia can produce early o 2D echo: wall motion o should ideally be initiated
of the right ventricle, • S3 or S4 spontaneous lysis of the abnormalities within 30 min of
posterior 1/3 of the • Quiet precordium; apical occlusive thrombus o High res cardiac MRI: presentation (i.e., door-
ventricular septum, and impulse hard to palpate (7) the adequacy of bright signal areas of toneedle time ≤30 min)
posterobasal wall of the left • Pericardial friction rub myocardial perfusion in the infarction (vs. dark o tissue plasminogen
ventricle (in right-dominant • Carotid pulse decreased in infarct zone when flow is areas of normal activator (tPA),
circulation) volume; temperature restored in the occluded myocardium) streptokinase, tenecteplase
elevations up to 38 C
o epicardial coronary artery. (TNK), and reteplase (rPA)
• Abnormal systolic • Primary Percutaneous
pulsation Coronary
Transient midsystolic or late Intervention: first few hours of
systolic murmur MI; applicable to patients who
have contraindications to
fibrinolytic therapy
o preferred when the
diagnosis is in doubt,
cardiogenic shock is
present, bleeding risk is

increased, or symptoms
have been present for at
least 2–3 h when the clot is
more mature and less easily
lysed by fibrinolytic drugs
Pericardial Disease
Acute Pericarditis • Chest pain: severe, pleuritic • Chest X-ray • Serous pericarditis: • Bed rest
• < 6 weeks (sharp and aggravated by • ECG: diffuse ST-segment produced by noninfectious • Ant-inflammatory treatment
inspiration and coughing); elevation and PR-segment inflammatory diseases w/ aspirin
often mistaken as MI depressions followed by T- • Fibrinous and serofibrinous • NSAID; ibuprofen or
o Intensified by lying wave inversion pericarditis: most indomethacin w/ gastric
supine, and relieved by
• Echocardiogram: pericardial frequent types of protection (e.g. omeprazole).
sitting up and leaning fluid or thickening pericarditis. Acute MI, • Colchicine (enhance
forward Dressler syndrome response to NSAID; ↓ risk
• Pericardial friction rub • Purulent or suppurative recurrent pericarditis)
pericarditis: active infection • Glucocorticoids: suppress
• Hemorrhagic pericarditis: acute pericarditis who failed
malignant neoplasm therapy
• Caseous pericarditis: o Full dose should be given
tuberculous origin for 2-4 days only; then
tapered (can ↑ risk of
recurrence)
• Azathioprine or Anakinra: if
with multiple recurrences
resistant to therapy
• Hospitalize if specific causes
(TB, neoplastic, bacterial
infection) are suspected or
with poor prognosis (fever ˃
38 C, subacute onset or large
pericardial effusion)
Cardiac Tamponade Beck’s triad • Most common causes: • Echocardiogram: right atrial • Aggressive volume expansion
• accumulation of fluid in the • Hypotension o Idiopathic pericarditis and right ventricular diastolic with IV fluids
pericardial space →serious • Soft or absent heart o Pericarditis secondary to collapse. • Urgent pericardiocentesis
obstruction of the inflow of sounds neoplastic disease • CXR: enlarged, globular, (aspirate will be nonclotting
blood into the ventricles • Jugular venous distention o Tuberculosis water-bottle-shaped heart blood).
• may be fatal if it is not with a prominent x (early o Bleeding into the pericardial with a large effusion • Decompensation may warrant
recognized and treated systolic) descent but an space after leakage from • If present on ECG: electrical pericardial window
promptly absent y (early diastolic) an aortic dissection, cardiac alternans is diagnostic of a
descent operation, trauma large pericardial effusion
o Treatment with
• Paradoxical Pulse: anticoagulants
o Greater than normal (10
mmHg) inspiratory decline
in systolic arterial pressure
o May be detected by
palpating weakness or
even disappearance of the
arterial pulse during
inspiration
o Sphygmomanometric
measurement of systolic
pressure during slow
respiration is required

Chronic constrictive • Common: weakness, • Adhesive pericarditis: • ECG: low voltage of the • Definitive treatment: pericardial
pericarditis fatigue, weight gain, plaque-like fibrous QRS complexes; diffuse resection
• healing of an acute fibrinous increased abdominal girth, thickenings of the serosal flattening or inversion of the • should be as complete as
or serofibrinous pericarditis abdominal discomfort, membranes (“soldier’s T waves. Atrial fibrillation is possible
or edema, exertional dyspnea plaque”) • Chest X-ray: • Preoperative preparation:
• resorption of a chronic • anasarca, skeletal muscle o rarely cause impairment o normal or slightly enlarged Dietary sodium restriction and
pericardial effusion followed wasting, cachexia may be of cardiac function heart diuretics preoperative
by obliteration of the present. • Adhesive o pericardial calcification preparation.
pericardial cavity with the • Exertional dyspnea is mediastinopericarditis: (most common in • Preoperative for pt >50 years:
formation of granulation common obliterated pericardial sac, tuberculous pericarditis) coronary arteriography (r/o
tissue. • orthopnea may occur (not and adherence of the • Echocardiogram: pericardial accompanying coronary artery
severe) external parietal layer to thickening, dilation of the disease)
• cervical veins are distended surrounding inferior vena cava and
(may remain after diuretics) structures strain cardiac hepatic veins
• Kussmaul’s sign: venous function
pressure may fail to decline • Constrictive pericarditis:
during inspiration heart encased in a dense,
• Congestive hepatomegaly fibrous or fibrocalcific scar
• Broadbent’s sign: ↓apical o limits diastolic expansion
pulse and may retract in and cardiac output
systole (concretio cordis)
• distant heart sounds and
early third heart sound (i.e.,
a pericardial knock)
Congenital Heart Disease
Acyanotic conditions: left-to-right shunts in which oxygenated blood from the lungs is shunted back into the pulmonary circulation
• 3D’s:
o VSD
o ASD
o PDA
• Eisenmenger’s syndrome: left-to-right shunt leads to pulmonary hypertension and shunt reversal.
o Uncorrected left-to-right shunt (VSD, ASD, PDA) → ↑pulmonary blood flow à pathologic remodeling of vasculature à pulmonary arterial hypertension
o RVH occurs to compensate à shunt becomes right to left.
o Causes late cyanosis, clubbing, and polycythemia.
o Age of onset varies
Ventricular Septal Defect • Small defects: Usually • Opening in the ventricular • Echocardiogram is • Most small VSDs close
• Most common cause of asymptomatic at birth septum diagnostic spontaneously
congenital heart disease o Harsh holosystolic • Allows blood to flow between • ECG: LVH and may show • Asymptomatic patients:
murmur heard best at ventricles both LVH and RVH with monitored via
the lower left sternal larger VSDs echocardiography
border. • CXR: cardiomegaly and ↑ • Antibiotic prophylaxis may be
• Large defects: pulmonary vascular considered during procedures
o Frequent respiratory marking but is indicated only if the
infections, dyspnea, VSD was previously repaired
FTT, and CHF. with prosthetic material.
o If present, holosystolic • Surgical repair:
murmur is softer and o For symptomatic patients
more blowing who fail medical
o Systolic thrill, management
o Crackles o Children < 1 year of age
o Narrow S2 with an ↑ P2 with signs of pulmonary
o Mid-diastolic apical hypertension
rumble reflecting ↑ flow
across the mitral valve

o Older children with large
VSDs that have not ↓ in size
over time.
• Treat existing CHF with
diuretics (initial treatment),
inotropes, and ACEIs
Atrial Septal Defect • Ostium primum defects: • Opening in the atrial septum • Echocardiogram with color • Close to 90% of defects
o Early childhood allows blood to flow between flow doppler reveals blood close spontaneously, and
o Murmur or fatigue with the atria, leading to left-to- flow between the atria most do not require
exertion right shunting (diagnostic), paradoxical treatment.
• Ostium secundum defects • May lead to paradoxical ventricular wall motion, • Surgical or catheter closure:
(more common) emboli (systemic venous and a dilated right ventricle infants with CHF and in
o Tend to present in late emboli use ASD to bypass • ECG: RVH and right atrial patients with more than a
childhood or early lungs and become systemic enlargement. PR 2:1 ratio of pulmonary to
adulthood arterial emboli) prolongation systemic blood flow.
o Symptom onset and • CXR: cardiomegaly and ↓ • Early correction prevents
severity depend on the pulmonary vascular complications (arrhythmias,
size of the defect markings right ventricular dysfunction,
• Easy fatigability, frequent and Eisenmenger’s
respiratory infections, and syndrome)
FTT
• May be observed, but
patients are frequently
asymptomatic
• Right ventricular heave
• Wide and fixed split S2
• Systolic ejection murmur at
the left upper sternal border
(from ↑ flow across the
pulmonary valve)
• There may also be a mid-
diastolic rumble at the left
lower sternal border
Patent Ductus Arteriosus • Typically asymptomatic • Failure of the ductus • color flow Doppler • Give indomethacin unless the
• Large defects may present arteriosus to close in the demonstrating blood flow PDA is needed for survival (eg,
with FTT, recurrent lower first few days of life, leading from the aorta into the transposition of the great
respiratory tract infections, to pulmonary artery vessels, tetralogy of Fallot,
lower extremity clubbing, • Acyanotic left-to-right shunt (diagnostic) hypoplastic left heart) or if
and CHF from the aorta to the • With larger PDAs: indomethacin is
• Continuous “machinery pulmonary artery echocardiography shows contraindicated (eg,
murmur” at the second left left atrial and left intraventricular hemorrhage).
intercostal space at the ventricular enlargement. • If indomethacin fails or if the
sternal border, a loud S2, • ECG may show LVH, and child is > 6–8 months of age,
wide pulse pressure, CXR may reveal surgical closure is required
and bounding peripheral cardiomegaly if lesions are
pulses large
Cyanotic conditions: Have right-to-left shunts in which deoxygenated blood is shunted into the systemic circulation.
• 5T
o Truncus arteriosus
o Transposition of the great vessels
o Tricuspid atresia: absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability
o Tetralogy of Fallot
o Total anomalous pulmonary venous return: pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc); associated with ASD and sometimes PDA to allow for right-to-
left shunting to maintain CO

Transposition of the great • Aorta is connected to the • Critical illness and cyanosis • Echocardiography. • Start IV PGE to maintain or
vessels right ventricle and the typically present within first • CXR: a narrow heart base, open the PDA.
• Most common cyanotic pulmonary few hours after birth. absence of the main • If surgery is not feasible
congenital heart lesion in • Artery to the left ventricle, • Tachypnea, progressive pulmonary artery segment, within the first few days of
the newborn. à parallel pulmonary and hypoxemia, and extreme an “egg-shaped life or if the PDA cannot be
systemic circulations cyanosis silhouette,” and ↑ maintained with
• Incompatible with life • Some patients have signs of pulmonary vascular prostaglandin: perform
without a septal defect CHF markings. balloon atrial septostomy to
(ASD or VSD) and a PDA • Single loud S2 is often create or enlarge an ASD.
• PDA alone is usually not present • Definitive: Surgical
sufficient to allow adequate correction (arterial or atrial
mixing of blood. switch)
Tetralogy of Fallot • Presents in infancy or early 1. Pulmonary stenosis • Echocardiography and • Lesions with severe
• Most common cyanotic childhood with dyspnea 2. Overriding aorta catheterization. pulmonary stenosis or
congenital heart disease in and fatigability. 3. RVH • CXR shows a “boot- atresia require immediate
children • Cyanosis frequently absent 4. VSD shaped” heart with ↓ PGE1 to keep the PDA open
at birth but develops over pulmonary vascular along with urgent surgical
the first 2 years of life • Early cyanosis results from markings. consultation.
• Degree of cyanosis often right-to-left shunting across • ECG shows right-axis • Treat hypercyanotic “tet
reflects the extent of the VSD deviation and RVH spells” with O2, propranolol,
pulmonary stenosis. • As right-sided pressures ↓ phenylephrine, the knee-
• Infants are often in chest position, fluids, and
asymptomatic until 4–6 the weeks after birth, the morphine.
months of age, when CHF shunt direction reverses and • Temporary palliation can be
may develop and manifest cyanosis may ↓ achieved through the
as diaphoresis with feeding o If the degree of creation of an artificial shunt
or tachypnea. pulmonary stenosis is (eg, balloon atrial
• Children often squat for severe: the right-sided septostomy) before definitive
relief during hypoxemic pressures may remain surgical correction (Blalock-
episodes called “tet spells,” high and cyanosis may Taussig shunt)
which ↑ systemic vascular worsen over time
resistance.
• Hypoxemia may lead to
FTT or mental status
changes.
• Systolic ejection murmur at
the left upper sternal border
(right ventricular outflow
obstruction), a right
ventricular heave, and a
single S2
Coarctation of the Aorta • Often presents in childhood • Constriction of a portion of • Echocardiography and o If severe coarctation presents
with asymptomatic the aorta, leading to ↑ flow color flow Doppler are in infancy, the ductus
hypertension (upper proximal to and ↓flow distal diagnostic. arteriosus should be kept
extremity hypertension) to the coarctation • CXR in young children: open with prostaglandin E1
• A murmur may be heard • Occurs just below the left cardiomegaly and (PGE1)
over the back between the subclavian artery in 98% of pulmonary congestion. o Surgical correction or balloon
scapulae patients • Compensatory changes in angioplasty is controversial.
• Lower extremity • In infancy: critical older children may be o Monitor for restenosis,
claudication, syncope, coarctation requires a seen: aneurysm development, and
epistaxis, and headache patent PDA for survival o LVH on ECG aortic dissection
may be present • Such infants may present in o The “3” sign on CXR due
• a systolic BP that is higher the first few weeks of life in to pre- and postdilatation
in the upper extremities; a shocklike state when the of the coarctation
the difference in BP PDA closes

between the left and right • Differential cyanosis may be segment with aortic wall
arm seen with lower O2 indentation;
• Additional findings: weak saturation in the left arm o “Rib notching” due to
femoral pulses, and lower extremities collateral circulation
radiofemoral delay, a short (postductal areas) as through the intercostal
systolic murmur in the left compared to the right arm arteries.
axilla, and a forceful apical (preductal area).
impulse.
RHEUMATIC FEVER (w/ Rheumatic Heart Disease as a sequela)
(Jones Criteria) • Associated with Aschoff • ↑ antistreptolysin O (ASO) Acute Management • 25-40 y/o
consequence of pharyngeal • Carditis – mitral bodies (granuloma with giant titers. • For infection: Penicillin • Females > males
infection with group A β- regurgitation cells), Anitschkow cells • ECG: Prolonged PR • For arthritis/mild carditis:
hemolytic streptococci. • Migratory polyarthritis – (enlarged macrophages with interval Acetylsalicylic acid Duration of Secondary
asymmetric, affecting large ovoid, wavy, rod-like • Elevated ESR or • For moderate-severe carditis: Prophylaxis
joints, highly responsive to nucleus), leukocytosis Prednisone (max of 3 wks) • RF w/o carditis: 5 yrs after
NSAIDS • Immune mediated (type II • Jones Criteria • For severe chorea: last attack or until 21 y/o
• Sydenham’s Chorea – hypersensitivity); not a direct Carbamazepine or valproic (whichever is longer)
involuntary jerking effect of bacteria. acid • RF w/ carditis but no
movements affecting the • Antibodies to M protein residual valvular disease:
head and upper limbs, cross-react with self antigens Prophylaxis 10 yrs after last attack, or
usually resolves in 6wks (molecular mimicry) • Benzathine Penicillin G until 21 y/o (whichever is
• Erythema marginatum – • Penicillin: Erythromycin longer)
pink macular eruption w/
round borders and central RF w/ persistent valvular
clearing on trunk/limbs disease: 10 yrs after last
• Subcutaneous nodules – attack, or 40 y/o; sometimes
painless small lumps on lifelong prophylaxis
extensor surfaces (2-3 wks
after onset)
• Minor manifestations:
Polyarthralgia, fever,
Supporting evidence of
preceding streptococcal
infection within last 45 days
• Late sequelae include

rheumatic heart disease,
• which affects heart valves—
mitral > aortic >> tricuspid
(high-pressure valves
affected most).
• Early lesion is mitral valve
regurgitation; late lesion is
mitral stenosis.
INFECTIVE ENDOCARDITIS
• Infection of the endocardium • Nonspecific symptoms • Prototypic lesion is DUKE CRITERIA • Early empiric IV antibiotic • Classified according to the
• Most commonly affects the • Cardiac manifestations vegetation (mass of • 2 major; or 1 major & 3 treatment for acutely ill temporal evolution of
heart valves, especially the o CHF develops in 30-40% platelets, fibrin, minor; or 5 minor criteria = patients. Vancomycin is an disease, site of infection,
mitral valve of patients (due to microorganisms, scant diagnosis of definite appropriate choice for most cause of infection or a
• Risk factors include valvular dysfunction) inflammatory cells) endocarditis patients. predisposing risk factor
rheumatic, congenital, or o Extension of • Endothelial injury allows • Tailor antibiotics once o Acute endocarditis:
valvular infectionàPerivalvular either direct infection by thecausative agent is known febrile illness that
rapidly damages

heart disease prosthetic abscessesàIntracardiac virulent organisms or the Major Criteria: • Acute valve replacement is cardiac structures,
heart valves; IV drug abuse; fistula with murmurs development of an • Positive blood culture sometimes necessary. hematogenously seeds
and immunosuppression o Murmurs: mitral valve uninfected platelet-fibrin (recovered organisms e.g. • Give antibiotic prophylaxis extracardiac sites,
(mitral regurgitation) is thrombus (aka S. viridans, S. aureus, before dental work in progresses to death
Etiologies more commonly affected nonbacterial thrombotic Enterococcus, HACEK patients with high-risk within weeks if
• S aureus: causative agent than the aortic valve in endocarditis) from cultures drawn >12 valvular disease (eg, those untreated. Can be
in > 80% of cases of acute non–IV drug • Causative organisms enter hrs apart or all of 3 or a with previous endocarditis caused by S. aureus
bacterial endocarditis in users; more right-sided the bloodstream from majority of >4 separate or a prosthetic valve) o Subacute endocarditis:
patients with a history of IV involvement is found in IV mucosal surfaces, skin or blood cultires with first & follows an indolent
drug abuse drug users (tricuspid sites of focal infection à last drawn at least 1hr Antibiotic Treatment course, causes cardiac
• Viridans streptococci: most valve > mitral valve > Proliferate and induce apart) • Streptococci (Penicilln- damage only slowly,
common pathogens for left- aortic valve) platelet deposition and a • Positive sensitive): Penicillin G x rarely metastasizes,
sided subacute bacterial • Noncardiac manifestations procoagulant state at the echocardiographic study 4wks, Ceftriaxone x 4wks, gradually progressive
endocarditis and following o Low-grade fever (rarely site à Fibrin deposition (oscillation intracardiac Vancomycin x 4wks, Pencillin unless complicated. Can
dental procedures in native exceeds 39.4 deg C) combines with platelet mass, abscess, new G or Ceftriaxone x 2wks be caused by Viridans
valves. o Septic embolization in aggregation à Infected dehiscence of prosthetic PLUS Gentamicin x 2wks streptococci, S.
• Coagulase-(-) the skin, spleen, kidneys, vegetation generated valve, new valvular • Streptococci (Penicillin- epidermidis, S. bovis,
Staphylococcus: The most skeletal system and regurgitation) resistant): Penicillin G or fungi
common infecting organism meninges Ceftriaxone x 6wks PLUS • Predisposing conditions
in prosthetic valve o Immune complex Minor Criteria: Gentamicin x 2 wks, have shifted to illicit IV
endocarditis. deposition on GBM • Predisposition Vancomycin x 4wks drug use, degenerative
• Streptococcus bovis: S causes (predisposing heart • Enterococci: Penicillin G valve disease,
bovis endocarditis is glomerulonephritis & condition, injection drug PLUS Gentamicin x 4-6wks, intracardiac devices
associated with coexisting renal dysfunction use) Ampicillin PLUS Gentamicin • Incidence notably
• Fever >38 C
o
GI malignancy. o Mycotic aneurysms: x 4-6wks, Vancomycin PLUS increased among elderly
• Candida and Aspergillus Focal dilations of arteries • Vascular phenomena Gentamicin x 4-6 wks • Risk of prosthetic infection
species: Account for most at points in the artery wall o Janeway lesions – • Staphylococci (Methicillin- greatest during 6-12
cases of fungal endocarditis. that have been non-tender, painless, Sensitive): Nafcillin or months after valve
Predisposing factors include weakened by infection small hemorrhagic Oxacillin x 4-6wks or replacement
long-term indwelling IV nodular lesions on Cefazolin x 4-6wks or
catheters, malignancy, palms/soles Vancomycin x 4-6wks
AIDS, organ transplantation, • immunologic phenomena • Staphylococci (Methicillin-
and IV drug use. o Osler’s nodes: painful, Sensitive): Vancomycin x 4-
red, raised lesions on 6wks
hands & feet • Staphylococci (Prosthetic
o Roth’s spots: retinal Valve): Above PLUS
hemorrhages with pale Gentamicin x 2wks PLUS
centers made of Rifampin x 6-8wks
coagulated fibrin • HACEK Organisms:
• Microbiologic evidence Ceftriaxone x 4wks,
Ampicillin/sulbactam x 4wks
Labs: CBC with leukocytosis
and left shift; ↑ ESR and CRP

MODULE/TOPIC 10 GASTROINTESTINAL
PART 10A. FOCUSED HISTORY AND PE NOTES:

HISTORY
Common Gastrointestinal Symptoms OLDCARTS
o Indigestion  • Onset
o Anorexia  o Gradual, worsens over several hours: progressive
o Nausea, vomiting, or hematemesis (or vomiting of blood) inflammation/infection (e.g. cholecystitis, appendicitis)
o Abdominal pain  o Acute vs. Chronic
§ Location, level of pain, aggravating factors, date of onset, § No strict time period
progression of pain, how and when it occurs, other areas in the § Acute: sudden or recent
body where pain is felt - Implies an inflammatory condition
• Dysphagia and/or odynophagia (pain in swallowing)  § Chronic: continuous or intermittent abdominal discomfort
• Change in bowel function  lasting for at least 6 months
• Constipation or diarrhea  • Location
• Jaundice o Epigastrium (T6-T8): stomach, duodenum, pancreas, liver,
• Other symptoms experienced? Nausea, vomiting, diarrhea biliary tree
o Bowel movement and characteristics of stool o Periumbilical (T9-T10): small intestine, appendix, upper ureters
• Medications taken o Hypogastrium (T11-T12): colon, bladder, lower ureters, uterus
• History for other possible related conditions • Duration
• Dietary family, travel, sexual history o The longer the pain is, the more likely it’s a surgical condition,
o Rule of thumb: more than 6 hours
DIARRHEA • Characteristic
• Stool character o Dull, aching: early appendicitis, hepatitis, pancreatic cancer
o Number per 24 hours o Burning, gnawing: peptic ulcer disease, gastritis,
o Water or bloody gastroesophageal reflux disease, usually upper GI
o Color of stool o Pressure: urinary retention, prostate cancer, feeling of wanting
o Large vs small volume to use the washroom
§ Large – small bowel or proximal colon o Colicky: colon cancer
§ Small – distal colon Sharp, knifelike: splenic abscess, renal tumor
o Change in volume when eating greasy • Aggravating factors, Alleviating factors
§ Fat malabsorption: foul smelling, floating, oily stool o Food aggravates?
• Dietary history (e.g. lactose deficiency), history of IBD, pancreatic § Bowel obstruction, biliary colic, pancreatitis, diverticulitis,
disease, intestinal surgery, DM bowel perforation
• Infection: fever, chills o Food relieves?
• Recent change in medications or antibiotic use § Non-perforated peptic ulcer disease, gastritis
o Worsens with activity
Location and Causes of Referred Pain § Jostles the abdomen
• Right Shoulder § When parietal peritoneum is stimulated
o Liver o Relieves when still
o Gallbladder § Stone problems
o Right Hemidiaphragm • Radiating (other areas of pain)
• Left Shoulder • Timing, frequency
o Heart o Progressive, worsens with time
o Tail of Pancreas o Intermittent
o Spleen o Spasmodic, colicky pain
o Left Hemidiaphragm o When dealing with vomit and pain, always ask which came first:
• Scrotum and Testicles § Pain, then vomit – usually surgical case
o Ureter § Vomit, then pain – usually medical case
• Severity, Other Symptoms
o Visual Analog Scale: On a scale of 1 to 10, how would you rate
your pain?
o Use other analogies such as money (“Kung P100 yung
pinakamasakit…”)

o Always ask for anorexia, nausea, vomiting, hematemesis,
constipation, diarrhea, melena, hematochezia, jaundice

PHYSICAL EXAM
• Position the patient supine with head and knees supported with pillows or linen and the arms are at the sides or folded across chest.
• Undrape the abdomen from the symphysis pubis to just above the xiphoid process.
• Make sure that the patient is covered below the waist.
• Always explain what you will do to the patient before performing it
• Before starting always ask if the patient has already eaten or needs to go to the bathroom (urinate or defecate)
• Note that while you do the Physical Exam in Inspection – Auscultation – Percussion – Palpation, you will still report it as I-Pal-Per-Aus
Visual Inspection
• Scars, Striae (old silver striae or stretch marks are
normal), Dilated veins (hepatic cirrhosis of IVC
obstruction), Rashes and lesions
• Umbilicus: color, location, contour
• Inguinal and Femoral Area
Ventral Hernias:
• Umbilical Hernias (protrusion through a defective
umbilical ring; most common in infants)
• Incisional Hernias (from an operative scar)
• Epigastric Hernias (midline protrusion; linea alba
defect: xiphoid process and umbilicus)
• Diastasis Recti: separation of 2 abnominis
muscles; abdominal contents form a midline ridge
Inspection when the patient raises head and shoulders; pregnancies, obesity and chronic lung disease)
• Lipoma
Contour of abdomen: Flat, Rounded, Protuberant (Fat, Tumor, Gas, Pregnancy), Scaphoid (concave or hollowed)
• Asymmetry of abdomen: Enlarged organ or mass
• Bulging Flanks: Ascites
o Ascitic fluid seeks the lowest point in the abdomen, producing bulging flanks that are dull to percussion. Umbilicus may
protrude. Turn the patient onto one side to detect the shift in the position of the fluid level. (Shifting Dullness)
Movement
• Peristalsis: Observe for several minutes. Visible in thin people. Increased peristalsis is one sign of intestinal obstruction
• Pulsations: Aortic pulsation = epigastrium. Increased pulsation is one sign of aortic aneurysm (high pulse pressure)
Local Bulges, Masses
Differentiating abdominal wall from intra-abdominal masses: Ask the person to raise the head and shoulders or to strain down,
thus tightening the abdominal muscles. Feel for the mass again.
• A mass in the abdominal wall remains palpable.
• An intraabdominal mass is obscured by muscular contraction.
Listen before performing percussion and palpation because these maneuvers may alter the frequency of bowel sounds.
Warm the stethoscope before use

• Listen for 2 minutes before concluding that bowel sounds are absent!
o Normal sounds consist of clicks and and gurgles
o Occasional borborygmic may be heard
o Normoactive bowel sounds: 5 – 34/min
o Hypoactive (<5/min), Hyperactive (>34/min)
BOWEL SOUNDS (Right Lower Quadrant)
• Increased: diarrhea or early intestinal obstruction
• Decreased: adynamic ileus and peritonitis
Auscultation • High pitched tinkling sounds = intestinal fluid and air under tension in
a dilated bowel.
• Rushes of high pitched sounds coinciding with an abdominal
cramp = intestinal obstruction
BRUITS over the ABDOMINAL AORTA, RENAL, ILIAC, FEMORAL
ARTERIES
• Hepatic Bruits: carcinoma of the liver or alcoholic hepatitis
• Arterial Bruits: systolic and diastolic components suggest partial occlusion of the aorta or large arteries (renal).
• Partial occlusion of a Renal Artery: hypertension
FRICTION RUBS over the liver and spleen

• present in hepatoma, gonococcal infection around the liver, splenic infarction, and pancreatic carcinoma
Tympanitic > Dullness: gas in GI but scattered areas of dullness from fluid and feces
Percussion • Large dull areas: mass or enlarged organ: pregnant, ovarian tumor, distended bladder, large liver or spleen
Note where abdominal tympany changes to the dullness of solid posterior structures. Dullness in both flanks = assess for
(Remember ascites.
to Percuss Percuss:
before • Lower anterior chest (between the lungs above and costal margins below)
Palpation!) • Right: dullness of the liver
• Left: tympany that overlies the gastric air bubble and the splenic flexure of the colon. Sinus invertus opposite.

LIVER SPAN
• Percuss span of liver dullness in the MCL. Test for
Hepatomegaly.
o Lower border of dullness: level below umbilicus upward
o Upper border of dullness: Nipple line downwards
• Measure its distance from the costal margin in the MCL.
• Distance increased in hepatomegaly.
• May be missed by starting palpation too high in the RUQ.
SPLEEN
• Percuss the left lower anterior chest wall between lung resonance above
and the costal margin (Traube’s space; N: tympanitic)
• Splenic percussion sign:
o Percuss the lowest interspace in the left anterior axillary line. (N:
Tympanitic)
o Take a deep breath and percuss: N: remain tympanitic
• If dull: splenic enlargement (positive splenic percussion sign)
Ask patient for any areas of tenderness or pain and palpate that last!
• LIGHT PALPATION: Superficial organs, masses, and areas of tenderness or increased resistance (last to palpate)
• DEEP PALPATION: Tenderness, masses, pulsations, palpable bowel loops, rushes or movement.
• Use one hand for light palpation and two hands for deep palpation
LIVER
• Let patient take a deep breath while you are in position.
o Inspiration: palpable 3cm below costal margin at the MCL.
o Cirrhosis: feels like a firm edge
o Not normal: firm/harness, roundness or bluntness and irregularity of contour.
• Hooking technique if patient is obese
SPLEEN
• Spleen is below palpable deep to the left costal margin.
Palpation • Reach over and support the back and press upon the lower left rib cage and
adjacent soft tissues structures. Ask patient to breathe in while palpating
• Normal spleen should not be palpable, non-tender
DECREASE VOLUNTARY MUSCLE GUARDING – Potentially Surgical Abdomen

• Try all relaxing methods: converse with patient
• Feel for relaxation of abdominal muscles that normally accompanies exhalation
• Ask the patent to mouth breathe with the jaw dropped open; breath slowly and deeply
• Flex the thighs and knees
Special REBOUND TENDERNESS – Peritoneal Inflammation

Tests • Press down with your fingers firmly and slowly withdraw them quickly.
• Watch and listen for signs of pain.
• Which hurts more? When I press or let go? Locate.
SHIFTING DULLNESS – Ascites

• Map borders of tympany and dullness.
• Ask patient to turn to one side.

• Percuss and mark the borders again.
• Negative: borders between tympany and dullness usually stay
relatively constant.
• Ascites: Dullness shifts to the more dependent side. Tympany
shifts to the top.
FLUID WAVE TEST – Ascites

• Pressure: stop wave transmission via fat
• Often negative until ascites is obvious. Positive in people
without ascites. Suggest and not prove ascites.
MCBURNEY’S POINT - Appendicitis
• 1/3 distance between RIGHT ASIS & UMBILICUS
• Tenderness suggests Appendicitis
ROVSING’S SIGN TEST – Acute Appendicitis

• Press deeply and evenly in the LLQ. Withdraw – Rebound Tenderness
• (+) Pain in RLQ
OBTURATOR SIGN TEST – Acute Appendicitis

• Flex the patient’s R thigh at the hip, with knee bent and rotate leg internal at the hip. (Stretch
the internal obturator muscle)
• (+) R hypogastric pain = irritation of the obturator muscle = inflamed PELVIC appendix
(determines orientation of appendix)
PSOAS SIGN TEST – Acute Appendicitis

• Two ways to perform
o Hand in patents right knee. Raise thigh vs your hand.
o Turn to left side. Extend right leg at hip to stretch psoas muscle
(+) Pain = irritation of psoas muscle = inflamed RETROPERITONEAL or RETROCECAL

appendix
MURPHY’S SIGN TEST – Acute Cholecystitis

• Hook your thumb under the right costal margin at the edge of rectus muscle
• Pt takes deep breath
• (+) Sharp tenderness and a sudden stop in inspiration
DIGITAL RECTAL EXAM

• Position
o Ask patient to lie sideways on their left side, flex their hip and knee to allow stability and visualization
o Drape the patient appropriately, exposing only the anus and perianal area
• Inspection - Sacrococcygeal and perianal area – lumps, ulcers, inflammation, rashes, or excoriations
• Palpation
o Prepare only one finger to use for the
exam, use non-sterile gloves and lubricate
well
o Ask patient to bear down to relax anal
sphincter. Enter and move into the anal
canal only when the sphincter is relaxed,
always reassure the patient. Insert your
finger from the posterior, pointing towards
the umbilicus, as far as possible
o Palpate for masses, ulcerations, and
tenderness – rotate your finger clockwise,
then counter clockwise
§ Anal sphincter tone – at rest (internal
sphincter) and when contracting
(external sphincter)
§ Prostate gland – size, shape, mobility,
and consistency. Note for any nodules or tenderness
§ Seminal Vesicles – if your finger can reach further above the prostate gland, note for nodules and tenderness

NUTRITION
• Rickets (“sakang”) in growing children Source • 25 hydroxy vitamin D • Calcifediol(Calderol) Excess
• Tetany • Vitamin D2 (Ergocalciferol) blood test [25(OH)D3] • Increased deposition of calcium
• Osteomalacia in adults o Dietary source o Normal: 20ng/mL – • Calcitriol (Rocaltrol) o Increased formation of kidney stones
o Fish oils, salmon, sardines 50ng/mL [1,25(OH)2VitD] o Metastatic calcification of soft tissue
o Fortified milk, breads, cereal o Deficiency = <12ngmL • Ergocalciferol o Bone pain and hypercalcemia
o Animal livers, tuna fish, eggs, (Calciferol)[D2] o Hyperactive nervous stimulation (hyperreflexia)
butter • Cholecalciferol [D3]
• Vitamin D3 (Cholecalciferol)
o Skin by ultraviolet irradiation
Vitamin D
(Calciferol)
Function
Deficiency
• Maintenance of adequate plasma
levels of calcium and phosphorus
• Bone mineralization
• Neuromuscular transmission and
prevention of hypocalcemic
tetany
• Intestinal calcium absorption
• Calcium reabsorption in kidney
• Interaction with PTH
A. Kwashiorkor A. Kwashiorkor • Anthropometrics • Oral nutritional intervention A. Kwashiorkor
• Failure to thrive, edema, moon facies, a swollen • Protein deprivation greater than • BMI (oral supplements) Epidemiology
abdomen (potbelly), and a fatty liver. reduction of total calories • Mini Nutritional • Commonly affect children
• Do not look malnourished due to edema • Loss of protein à decreased Assessment
• Growth failure oncotic pressure à edema • Mini Nutritional Secondary causes of kwashiorkor
• Loss of body fat Assessment Short Form • Chronic diarrhea
• Inadequate growth, loss of motor tissue, • Nutritional Risk Screening o GI enteropathies
hepatomegaly, crazy pavement dermatosis, 2002 – hospital setting o Malabsorption
discolored hair, edema, hypoalbuminemia • Albumin, total • Severe burns
• The skin becomes dark, dry, and then splits open lymphocyte count, CBC, • Nephrotic syndrome
when stretched, revealing pale areas between the creatine, BUN
cracks.
Malnutrition
B. Marasmus B. Marasmus B. Marasmus
• Emaciated with marked loss of subcutaneous fat • Weight falls to 60% percentile of Epidemiology
and muscle wasting. normal sex, height and age • Commonly affect children
• The skin is xerotic, wrinkled, and loose. • ↓ weight = ↓ protein + ↓ carbs + ↓
• Monkey facies secondary to a loss of buccal fat fat
pads is characteristic of this disorder. o clue: marasmus à “marami”
• Depigmentation of hair causes it to be reddish • Decrease supply of amino acids
yellow to white. Curly hair becomes straightened. and nutrients à adaptation:
• Nail plates are thin and soft and may be fissured increased catabolism and
or ridged. Atrophy of the papillae on the tongue, depletion of inherent protein
angular stomatitis, xerophthalmia, and cheilosis storesà growth retardation
can occur.


LIVER
• Asymptomatic • Fecal-oral transmission • IgM anti-HAV – acute Immunoprophylaxis Morphology (NOTE: for all hepatitis)*
• Acute hepatitis w/ or w/o jaundice • Route infection • Epaxal • Acute:
• Flu-like syndrome o Close personal contact • IgG anti-HAV – • Havrix o Diffuse swelling “ballooning degeneration”
• Rarely progress to serious liver disease o Contaminated food, water protective immunity • Avaxim o Cytoplasm looks empty (eosinophilic remnants
• Incubation period: 30 days • Blood exposure of organelles)
Diagnosis Dosage o Bile plugs in canaliculi
Complications Description • Elevated ALT, AST and • Second dose: 6-12 months o Brown pigmentation of hepatocytes
• Fulminant hepatitis • Picornavirus anti-HAV IgM after primary dose o Bridging necrosis
• Cholestatic hepatitis • Icosahedral ssRNA virus o Hypertrophied Kupffer cell
• Relapsing hepatitis • Fecal-oral route Treatment o Inflammatory cells
• No carrier/chronic hepatitis • No specific treatment • Chronic:
Hepatitis A • Supportive treatment for o Finely granular cytoplasm “ground glass
symptoms (diarrhea, hepatocytes”
vomiting, fever) o lymphoid aggregates w/in portal triad (HCV)
• Special care for coagulation o Well preserved liver architecture
factors o Hallmark: Deposition of fibrous tissue
o Hepatocyte apoptosis
o Confluent necrosis of hepatocytes à bridging
necrosis
o Loss of hepatocytes à cirrhosis
Epidemiology
• Common in the Philippines
Acute • Parenteral transmission Antigens and Antibodies Immunoprophylaxis Description
• Symptomatic o Blood (highest concentration) • HBs Ag – active • Hepatitis B Immune • Hepadnavirus
• Flu-like syndrome o Semen, vaginal fluid infection (surface) Globulin (HBIG) • Enveloped dsDNA
• Jaundice, Ascites, Palmar erythema, Spider • Route • HBe Ag – infectivity o Post exposure • Parenteral, sexual or vertical transmission
angiomas, Pedal edema o Perinatal (during delivery) • Anti-HBc • Hepatitis Vaccine • Produce: Asymptomatic carrier, acute hepatitis
• Liver failure o Sexual o Past/ongoing infection o IM: 3 doses (0, 1 and 6
• Hepatocellular carcinoma o Percutaneous (needle stick, • Anti-HBe months) Recovery Stage
• Marked elevated ALT and AST piercings) o Chronic resolving • Euvax, Enegrix and • Acute: Complete recovery, latent infection
o Close person-to-person o Produced when Hepavax • Chronic: (-) HBsAg
Chronic contact (open cuts) HBeAg no longer
• No symptoms • 4-22 weeks incubation period detected Treatment Healthy Carrier State
• Incidental finding of positive HBsAg on check-up • Anti-HBs – immunity, • Goal: Suppression only • (+) HBsAg > 6 mos, (-) HBeAg
Additional Notes: recently vaccinated • Interferons • Serum HBV <105 copies/ml (PCR)
Additional Notes: • Hepatitis C and D – parenteral o peginterferon a-2a • Normal AST and ALT
• Getting virus at birth = chronic infection transmission Diagnosis (new) • Liver biopsy: No inflammation and necrosis
• Adult onset = acute • Hepatitis E – fecal-oral • Serologic testing o Interferon a-2b
• Hepatitis C = needle injections transmission • HBV DNA (Viral load) • Nucleoside Analogs Epidemiology
Hepatitis B • Hepatitis D =only occurs in presence of Hepatitis • Liver enzymes (AST and o Adefovir • Common worldwide
B ALT) o Lamivudine • Hyperendemic in the Philippines
• Hepatitis E = pregnant women • Liver function test o Entecavir, telbivudine
(bilirubin, albumin, and tenofovir Interpretation
protime/INR) • (+) HBsAg, (+) Anti-HBc, (-) Anti-HBs = infected
• Liver ultrasound • (-) HBsAg, (-) Anti-HBc, (+) Anti-HBs = Immune
from vaccination
• (-) HBsAg, Anti-HBc and Anti-HBs = never
infected
• (-) HBsAg, (+) Anti-HBc, (+) Anti-HBs = Resolved
infection w/ immunity development
• (-) HBsAg, (+) Anti-HBc, (-) Anti-HBs = remote
resolved infection/false positive

The range of clinical features of alcoholic liver Pathogenesis of Cirrhosis • ALT and AST • Cessation of alcohol intake A. Hepatic Steatosis
disease varies, from asymptomatic to end-stage • Type I and III collagen deposited • Gamma glutamyl • Microvesicular lipid droplets and macrovesicular
liver disease with portal hypertension, jaundice and in Space of Disse à fibrotic septal transferase globules (chronic alcohol intake) in hepatocytes
encephalopathy. tract formation w/ sinusoids • Fibrosis – perisinusoidal chicken wire fence
capillarization pattern
3 forms of alcoholic liver disease • Hepatocytes regenerate as B. Alcoholic Steatohepatitis
• Hepatic Steatosis spherical nodules (fibrotic nodular Histology
• Alcoholic Steatohepatitis liver and severe compromise of • Hepatocyte swelling and necrosis; Mallory-Denk
Alcoholic Liver • Cirrhosis blood supply) Bodies (eosinophilic cytoplasmic clumps inside
Disease o 3 main characteristics: • Disruption of parenchymal-portal hepatocyte)
§ Bridging Fibrous Septa tract interface à obliteration of C. Cirrhosis
§ Parenchymal Nodules biliary channel à jaundice Chief causes:
§ Disruption of Architecture of Entire Liver • Alcohol abuse, viral hepatitis and non-alcoholic
o Clinical Features: steato-hepatitis (NASH)
§ Anorexia, weight loss and weakness Macroscopically
• Brown, shrunken, non-fatty organ composed of
cirrhotic nodules
• Leannec Cirrhosis
Major complications: • Development of fibrosis to the • Defined • Variceal Hemorrhage: • Hepatorenal syndrome: usually in patents with
• Portal hypertension point that there is architectural histopathologically o Primary prophylaxis à refractory ascites
o Gastroesophageal varices with hemorrhage, distortion with the formation of • Portal hypertension: beta blockers
ascites, and hypersplenism regenerative nodules à activation thrombocytopenia, o Prevent bleeding à
o upper GI bleeding of stellate cells à formation of splenomegaly, ascites, endoscopic variceal
o ascites with peripheral edema increased amounts of collagen encephalopathy, and/or ligation, somatostatin,
o enlarged spleen and other ECM components esophageal varices w/ or octreotide,
• Splenomegaly and hypersplenism • Decrease in hepatocellular mass w/o bleeding sclerotheraphy, variceal
o Enlarged spleen left-sided and left-upper à loss of hepatocellular function o Endoscopy, CT/MRI band ligation,
quadrant abdominal pain à jaundice, coagulation • Splenomegaly and • Ascites:
• Ascites disorders, and hypoalbuminemia Hypersplenism: o Dietary sodium
o Increase in abdominal girth • Alteration of blood flow thrombocytopenia, restriction, large-volume
o Bulging flanks, shifting dullness, fluid wave, • Portal hypertension à leukopenia paracentesis, TIPS
• Spontaneous bacterial peritonitis (SBP) development of ascites and • Ascites: abdominal procedure
Cirrhosis o Fever, altered mental status, elevated WBC, bleeding from esophagogastric imaging, diagnostic • SBP
abdominal pain or discomfort if w/ ascites varices paracentesis o Third gen cephalosporin
• Hepatorenal syndrome • Increased intrahepatic resistance • SBP: absolute neutrophil • Hepatorenal syndrome:
• Hepatic encephalopathy + vasodilation of splanchnic count > 250 / uL o Midodrine + octreotide +
o Altered mental status and cognitive function arterial system + increased • Hepatorenal syndrome: IV albumin, liver
within weeks to months aldosterone à ascites stepwise progressive transplantation
o Brain edema with swelling of gray matter • Bacterial translocation (E. coli, S. increase in creatinine • Hepatic encephalopathy:
• Malnutrition viridans, S. aureus, Enterococcus • Hepatic encephalopathy: o Hydration and correction
• Abnormalities in coagulation sp.) à SBP clinical diagnosis, of electrolyte imbalance
• Bone disease (osteoporosis) • Hypokalemia, infection, increased asterixis o Lactulose
dietary protein load, or electrolyte o Neomycin and
disturbance à hepatic metronidazole
encephalopathy o Rifaximin
o Zinc supplementation


Nonspecific symptoms • Ethanol metabolism forms Laboratory Tests • Cessation of alcohol use: In diagnosis, there should be accurate knowledge
• Vague right upper quadrant abdominal pain reactive oxygen species à • Anemia cornerstone treatment that the patient is continuing to use and abuse
• Fever oxidative damage to hepatocyte • Nutritional deficiencies • Good nutrition alcohol.
• Nausea and vomiting membranes à can result in • Hypersplenism • Glucocorticoids: severe
• Diarrhea Kupffer cell activation • Thrombocytopenia alcoholic hepatitis in Rule out other forms of chronic liver disease
• Anorexia • Formation of protein- (Zieve’s syndrome) absence of infection Liver biopsy may be withheld until alcohol
• Malaise acetaldehyde adducts à • Normal or elevated o For patients with a abstinence has been maintained for at least 6
interferes with microtubular serum total bilirubin discriminant function months to determine nonreversible damage
Symptoms specific for complications of chronic liver formation and hepatic protein • Mildly elevated direct value of >32
disease trafficking bilirubin • Oral pentoxifylline
• Ascites • Production of excess collagen • Prolonged prothrombin • Avoid acetaminophen use
• Edema and ECM à appearance of time w/ no response to
• Upper GI hemorrhage connective tissue in periportal and parenteral vitamin K
Alcoholic Cirrhosis • Jaundice pericentral zones à forms • Depressed serum
• Encephalopathy regenerative nodules sodium (ascites)
• Hepatocyte loss + increased • Elevated ALT, AST
Physical Examination collagen production and
• Hepatosplenomegaly deposition à liver contracts
• Liver edge firm and nodular and shrinks
• Scleral icterus • Process takes from years to
• Palmar erythema decades to occur and requires
• Spider angioma repeated insults
• Parotid gland enlargement
• Digital clubbing
• Muscle wasting
• Edema or ascites
• Fatigue, malaise, vague right upper quadrant • Immune-mediated liver damage • Quantitative HCV RNA • Manage complications Epidemiology
pain, and laboratory abnormalities by HCV testing and analysis for • Antiviral therapy for chronic • 80% of those exposed to hepatitis C virus
o Liver is small and shrunken with HCV genotype hepatitis B develop chronic hepatitis C
characteristic features of mixed • Hepatitis B serologies: o Lamivudine, adefovir, o 20-30% of those will develop cirrhosis over 20-
Cirrhosis due to micro- and macronodular HBsAg, anti-HBs, telbivudine, entecavir, 30 years
chronic viral cirrhosis HBeAg, anti-HBe, and tenofovir o Many have had concomitant alcohol use
hepatitis B or C quantitative HBV DNA • Direct-acting antiviral • 5% of those exposed to HBV develop chronic
levels protocols for 8-12 weeks in hepatitis B
treating cirrhosis due to o 20% of those will develop cirrhosis
hepatitis C
Biliary Cirrhosis Biliary Cirrhosis Primary Biliary Biliary Cirrhosis Biliary Cirrhosis
• Major causes of chronic cholestatic syndromes: • Necroinflammatory lesions, Cholangitis • Extrahepatic: surgical or • Two categories based on anatomic site of
o Primary biliary cholangitis (PBC) congenital or metabolic Laboratory Tests endoscopic biliary tract abnormal bile retention: intrahepatic and
o Autoimmune cholangitis (AIC) processes, or external bile duct • Elevated gamma- decompression extrahepatic
o Primary sclerosing cholangitis (PSC) compression glutamyl transpeptidase
o Idiopathic adulthood ductopenia and ALP Primary Biliary Cholangitis Histopathologic findings
Cirrhosis from Primary Biliary Cholangitis • Mild elevation of ALT • liver transplantation • cholate stasis, copper deposition, xanthomatous
autoimmune Primary Biliary Cholangitis • Portal inflammation and necrosis and AST • (Ursodeoxycholic acid) transformation of hepatocytes, irregular, biliary
hepatitis and • Fatigue out of proportion to severity of the liver of cholangiocytes in small- and • Increased IgM UDCA 13-15 mg/kg per day fibrosis, chronic portal inflammation, interface
nonalcoholic fatty disease or age of patient medium-sized bile ducts à • Hyperbilirubinemia to slow rate of progression activity, chronic lobular inflammation
liver disease • Pruritus increased fibrosis à micronodular • Portal hypertension, • Pruritus: antihistamines,
• Jaundice, hepatosplenomegaly, ascites, and or macronodular cirrhosis hypersplenism: naltrexone, rifampin Primary Biliary Cholangitis
edema Thrombocytopenia, • Plasmapheresis Epidemiology
• Hyperpigmentation: trunk and arms leukopenia, anemia • 100-200 individuals per million
• Xanthelasma, xanthoma • Female preponderance
• Bone pain: osteopenia or osteoporosis • Median age of 50

Primary Sclerosing Cholangitis Primary Sclerosing Cholangitis Primary Biliary Cardiac Cirrhosis Primary Biliary Cholangitis
• Fatigue, pruritus, steatorrhea, deficiencies of fat- • Bile duct proliferation Cholangitis • Manage underlying cardiac Molecular and Histopathologic findings
soluble vitamins • Diffuse inflammation and fibrosis Diagnosis disease • AMA recognize enzymes that relate to pyruvate
• Metabolic bone disease involving the entire biliary tree à • Antimitochondrial dehydrogenase
chronic cholestasis antibodies (AMA) • Earliest lesion: chronic nonsuppurative
Cardiac Cirrhosis • Ductopenia and fibrous • Liver biopsy destructive cholangitis
• Long-standing right-sided congestive heart cholangitis • Cholangiography o Duct destruction of medium and small bile
failure Cardiac Cirrhosis ducts
• Enlarged firm liver • Elevated venous pressure à Primary Sclerosing
dilated and engorged sinusoids à Cholangitis Primary Sclerosing Cholangitis
pericentral fibrosis • Decreased albumin • Over 50% also have ulcerative colitis
levels
Cirrhosis from • Prolonged prothrombin Cardiac Cirrhosis
autoimmune times • Differentiation from Budd-Chiari syndrome (BCS):
hepatitis and • Twofold increase in ALP extravasation of RBCs in BCS, but not in cardiac
nonalcoholic fatty • Cholangiographic hepatopathy
liver disease imaging • Venoocclusive disease seen in those conditioning
(cont.) o MRI with MRCP for bone marrow transplant with radiation and
o ERCP chemotherapy, or iin those ingesting certain
o Multifocal structuring herbal teas and pyrrolizidine alkaloids
and beading involving • Typically seen in Caribbean countries
both intrahepatic and
extrahepatic biliary
tree
o Periductal fibrosis
Cardiac Cirrhosis
• Elevated ALP, AST
• Liver biopsy: fibrosis

Summary of Hepatitis Virus Etiologies
Acute Viral Etiology HAV HBV HCV HDV HEV
Transmission Fecal-oral Percutaneous, Sexual, Perinatal Percutaneous Percutaneous, Sexual, Fecal-oral
Severity mild Moderate mild à severe mild
Chronic x 10% 80-90% Common no
Fulminant x x x 20% superinfection 10-20% pregnant
Prophylaxis Ig vaccine HBIg x x x
Outcome Recovery 6-12 mo Recovery 90% May à cirrhosis
Dx IgM anti HAV HBsAg Anti HCV Anti HDV
IgM Anti HBc
Tx: mainly supportive lamivudine IFN alpha
REMEMBER:
• Vowels (Hep A and E) pass thru your Bowels
• BAkuna Available (Hep B and A)
• Becomes Chronic Din (Hep B, C, and D)

GALLBLADDER
Acute attack • Results from chemical irritation Local signs of inflammation Acute cholecystitis, initial Cholecystitis
• Begins with RUQ or epigastric pain and inflammation of the • Murphy’s sign treatment includes • Is an acute inflammation of the gallbladder,
• Associated with mild fever, anorexia, tachycardia obstructed gallbladder. • RUQ mass/ pain/ • Eliminate oral intake precipitated 90% of the time by obstruction of the
• Sweating • Phospholipases hydrolyzes tenderness • IV hydration neck or cystic duct
• Nausea luminal lecitins to a toxic variant • Correction of electrolyte • It is the primary complication of gallstones and
• Vomiting • Mucus layer of the GB would be Systemic signs abnormalities the most common reason for emergency
disrupted à Exposing mucosal • Fever • Analgesics: NSAIDs, cholecystectomy.
The following may also be reported: epithelium to bile salts à • Elevated CRP opioids
• Peritoneal irritation, pain may radiate to the right Dysmotility develops, distension • Elevated WBC In the absence of medical attention, will subside in
shoulder or scapula of GB and compromise of blood Medical therapy 7-10 days, and frequently within 24 hours.
• Pain frequently begins in the epigastric region flow follows Imaging findings • IV antibiotics for in-hospital Most common presenting symptom is upper
and localizes to the RUQ • Bacterial infection may occur • UTZ: Sonographic stabilization abdominal pain.
• Colicky pain à Constant afterwards Murphy’s sign, o Piperacillin + tazobactam
• Nausea and vomiting are generally present, and thickened and enlarged o Ceftriaxone +
fever may be noted GB, incarcerated GB metronidazole
Cholecystitis o Levofloxacin +
• CT or MRI: Enlarged and
PE may reveal the ff: thickened GB metronidazole
• Fever, tachycardia, and tenderness in the RUQ • Definite Diagnosis: One
or epigastric region, often with guarding or item in A or B are Surgical therapy
rebound positive; C confirms the • Uncomplicated acute
• Palpable gallbladder or fullness of the RUQ (30- diagnosis when cholecystitis: within 48-72
40% of patients) cholecystitis is hours after diagnosis
• Jaundice (~15% of patients) suspected clinically
Charcot’s Cholangitis Triad (infection of the bile

duct)
• Fever
• Jaundice
• RUQ Pain
May be present for decades before symptoms Cholesterol stones formation Lab tests are not necessary The treatment of gallstones Cholesterol stones more pre-dominant in
develop, and 70-80% are asymptomatic involves 4 simultaneous conditions depends upon the stage of developed countries and pigment stones in non-
throughout their lives. 1. Supersaturated bile with Imaging modalities disease, as follows: Western countries due to (bacterial and parasitic
• Conversion rate is 1-4% cholesterol Abdominal radiography • Asymptomatic gallstones – infections)
• Prominent symptom is biliary pain, which tends 2. Hypomotility of the gallbladder (upright and supine) – Used Expectant management
to be excruciating and constant or “colicky” due à nucleation to exclude other causes of • Symptomatic gallstones – Risk factors for pigment stones:
to obstruction. 3. Cholesterol nucleation in the bile abdominal pain (e.g., Usually, definitive surgical • Asians, rural more than urban
is accelerated intestinal obstruction) intervention (eg, • Biliary infection
Cholecystitis in association with stones also 4. Hypersecretion of mucus in the • UTZ – The procedure of cholecystectomy), though • GI disorders
generate pain. GB traps nucleated crystals, choice in suspected medical dissolution may be
• It is the very small stones that are dangerous leads to the stone aggregation gallbladder or biliary considered in some cases Factors for recommendation for cholecystectomy
disease • Presence of symptoms that are frequent enough
Cholelithiasis
Symptomatic gallstones signs include the ff: Medical treatments, used or severe enough to interfere with patient’s
• Sporadic and unpredictable episodes Pigment stones are mixture of individually or in combination, general routine
• Pain that is localized to the epigastrium RUQ, insoluble Ca salts of unconjugated
2+
include the following: • Presence of prior complication of gallstone
sometimes radiating to the right scapular tip bilirubin along with inorganic Ca
2+
• Oral bile salt therapy disease (i.e. history of acute cholecystitis,
• Pain that begins postprandially, typically lasts salts. Due to disorders related to (ursodeoxycholic acid) pancreatitis, gallstone fistula, etc.)
1-5 hours, increases steadily over 10-20 increased levels of unconjugated • Contact dissolution • Presence of underlying condition predisposing
minutes, and then gradually wanes bilirubin in bile (hemolytic • Extracorporeal shockwave the patient to increased risk of gallstone
• Constant pain; not relieved by emesis, antacids, syndromes, bacterial contamination), lithotripsy complications (i.e. calcified or porcelain
defecation, flatus, or positional changes; may be there is an increased risk of stone gallbladder and/or previous attack of acute
accompanied by diaphoresis, nausea, and formation. cholecystitis regardless of current symptomatic
vomiting status)
• Prophylactic: gallstones > 3 cm diameter

APPENDIX
• Pathognomonic: sequence of abdominal • Appendiceal fecalith obstruction: • Moderate leukocytosis • Appendectomy • Most common abdominal surgical emergency
discomfort and anorexia o Accumulation and inspissation (10, 000-18, 000) – • Most useful in excluding GU conditions that may
• Pain: periumbilical region initially, and then of fecal matter around frequent, but absence mimic acute appendicitis – urinalysis
migrating to the RLQ vegetable fibers does not rule out • In pregnancy: most common during second
• Nausea and vomiting – 50-60% of cases o Enlarged lymphoid follicles appendicitis trimester
• Change in bowel habit – little diagnostic value associated with viral infection, • Leukocytosis >20,000 –
• Urinary frequency and dysuria if appendix lies inspissated barium, worms, and perforation
adjacent to the bladder tumors • Radiographs – rarely of
o Yersinia organisms value except when
PE findings o Luminal bacteria opaque fecalith is
• Psoas sign – ask patient to flex right hip against • Invasion of appendicial wall à observed in the RLQ.
resistance; increased abdominal pain indicates a venous engorgement à o Diagnosis may be
Acute Appendicitis subsequent arterial compromise established by
positive psoas sign
• Rovsing’s sign – Do deep palpation on the left à high intraluminal pressure à ultrasonic demo of
lower quadrant. Pain in the RLQ is a positive gangrene à perforation an enlarged and
Rovsing’s sign. thick-walled
• Tenderness to palpation will often occur at appendix.
McBurney’s point • Ultrasound most useful
o 1/3 of the distances between right ASIS to to exclude ovarian cysts,
umbilicus ectopic pregnancy, tubo-
• Temperature – usually normal or slightly elevated ovaran abscess
(37.2-38). T > 38.3 suggests perforation
• Tachycardia is related to elevation of temperature
ESOPHAGUS
History • Esophagitis due to reflux of acid • GI endoscopy Lifestyle Epidemiology
• Heartburn, regurgitation, dysphagia or sour content into lower esophagus • Manometry • Avoidance of foods that • Most frequent cause of esophagitis
brash (“mapakla”) from stomach • 24-hour pH probe test reduce LES pressure • Adults older than 40
• Atypical symptoms: coughing, chest pain and • The reflux occurs when LES • Upper GI series o Fatty foods, alcohol,
wheezing pressure is lower than the spearmint, peppermint, Risk factors
o Severe chest pain mimicking heart attack intragastric pressure coffee and tea • Alcohol and tobacco use, obesity, CNS
• Bile from duodenum may • Avoidance of acidic foods depressants, pregnancy, hiatal hernia, delayed
Consequence exacerbate damage o Citrus fruits, tomato- gastric emptying, increased gastric volume
• Bleeding, stricture development, Barrett • Mechanisms that contribute to based foods
esophagus GERD development: • Adoption of behaviors to Factors that exacerbate reflux
o Decreased lower esophageal minimize reflux and/or • Abdominal obesity, pregnancy, gastric
Gastro-esophageal sphincter resting tone heartburn hypersecretory states, delayed gastric emptying,
reflux disease/ § Transient LES relaxations • Weight reduction disruption of esophageal peristalsis, gluttony
GERD § LES hypotension
§ Anatomic distortion of the Pharmacological Morphology
esophagogastric junction • Antacids • Eosinophils w/ or w/o neutrophils in epithelial
inclusive of hiatus hernia • H2 receptor antagonists layer
o Impaired esophageal acid and H2 blocker therapy • Intraepithelial neutrophils
clearance o Ranitidine, cimetidine, • Basal zone hyperplasia
§ Reduced salivation famotidine, nizatidine • Elongation of lamina propria papillae
§ Impaired peristalsis • Proton pump inhibitors
o Delayed gastric emptying o Omeprazole,
o Impaired tissue resistance iansoprazole,
rabeprazole,
esomeprazole


STOMACH AND INTESTINES
• Profuse watery stools • Most commonly caused by • History and PE • Based on the US CDC • High risk countries: Asia, the Middle East,
• Bloating Enterotoxigenic E.coli (ETEC) • Wet mount, antigen o Main: Antibiotics Africa, Mexico, and Central and South
• Urgent need to have a bowel movement then followed by Campylobacter detection, culture § Ciprofloxacin, levofloxacin, America
jejuni, Shigella spp., and Salmonella Rifaximin • 30 to 70% incidence depending on
• Range from mild cramps and urgent loose spp. o Adjunct to treatment: location
stools to severe abdominal pain, fever, • Produce heat-labile exotoxin § Antimotility: Loperamide • From contaminated food and water
vomiting, and bloody diarrhea o Subunit B binds to brush borders § Fluid and electrolyte
Traveler’s Diarrhea o Bacterial and viral pathogens have an -> Subunit A activates adenylyl treatment (Sports drinks,
(ETEC) incubation period of 6–48 hours. cyclase -> increase cAMP -> oral rehydration salts)
hypersecretion of water and Cl;
• Confined to gut mucosa inhibition of Na resorption
• Alter water & electrolyte balance • Produce heat-stable enterotoxin
o Activation of guanylyl cyclase ->
increase in cAMP -> fluid
secretion
• Rapid onset of vomiting & watery stools (S. • Caused by Staphylococcus aureus, • Same for all except C. perfringes • S. aureus = common cause of food
aureus, B. cereus) Bacillus cereus, Clostridium which needs supportive and poisoning
• Flaccid paralysis of respiratory muscles (C. botulinum, Enterotoxigenic (ETEC), symptomatic treatment
Bacterial non- botulinum) Enteroaggregative (EAEC),
inflammatory • Watery diarrhea (ETEC, EAEC, EPEC) Enteropathogenic (EPEC), Vibrio
Diarrhea/ Bacterial • “Rice water” stool (V. cholerae) cholera (O1 and O139), Clostridium
Gastroenteritis • Self-limited (24 hrs) gastroenteritis perfringes
(C.perfringes) • Enterotoxin production (diarrhea),
• No fever or vomiting (EAEC) Emetic toxin (vomiting)
• Diarrhea to dysentery (blood, mucus, pus in • Cytotoxin production • (+) clear growth on SS • Same as Traveler’s Diarrhea • Most common source is uncooked
stool) o Sloughing off the mucosal agar (Shigella) • Sanitation poultry or in contaminated water and
• Diarrhea, fever, abdominal cramps, leukocytosis surface • Clear on MacConkey unpasteurized milk (C.jejuni & C.coli)
(C.difficile) o Strong inflammatory response agar with sorbitol, PCR, • Commonly found in immunocompromised
Bacterial • Can be brought by organisms such Serology for O157:H7 hosts (Salmonella spp., Shigella,
inflammatory • High number of PMNs and blood in stool as Shigella spp., Enterohemorrhagic (EHEC) Campylobacter)
Diarrhea/ Bacterial • Rectal spasm w/ abdominal pain (Shigella) E.coli (EHEC), Enteroinvasive E.coli • Green colonies on BAP
Gastroenteritis (EIEC), Vibrio parahaemolyticus, and TCBS agar • *Gastroenteritis diarrhea – caused by
Clostridium defficile, Yersinia (V.parahaemolyticus) non-typhoid salmonella; asymptomatic
enterocolitica, Campylobater jejuni, carrier state is possible
Salmonellas spp.
• Rotavirus - major cause of diarrhea for • Infection of cells in the villi of small • Cell culture (very limited) • Rotavirus – Fluids and electrolyte; • *Viruses are the most common causes
infants and children worldwide; acute intestines -> damaged cells • Electron microscopy Oral bovine vaccine of diarrhea in infants and young
vomiting and diarrhea for 3 to 8 days replaced by non-absorbing • PAGE • Astrovirus – acquired immunity children
immature crypt cells -> impaired • Latex agglutination
• Rotavirus – Wheel-like appearance sodium and glucose absorption (rapid test) • *Astrovirus – pediatric gastroenteritis (2-
Viral Diarrhea/
• Astrovirus – star-like appearance • ELISA 10%), school-aged children (70-90%)
Viral
• RT-PCR
Gastroenteritis
• *Take note that many
tests are available but
they are NOT cost-
effective


• Loose feces, stomach pain, and stomach • Most common cause is • Fecal analysis for • Metronidazole for invasive • * Worldwide, approximately 50 million
cramping. Entamoeba histolytica trophozoites amoebiasis cases of invasive E histolytica disease
• Amebic dysentery is a severe form of amebiasis • Ingestion of E histolytica from o Drug of choice for amebic liver occur each year, resulting in as many as
associated with stomach pain, bloody stools environment -> excystation in the abscess 100,000 deaths. Only 10%-20% of
and fever. terminal ileum or colon to form • Luminal agents: iodoquinol, infected individuals become symptomatic.
• Amoebic colitis: 1-2 weeks symptom duration; highly motile trophozoites -> the paromomycin The incidence of amoebiasis is higher in
diarrhea is the most common symptom; trophozoite may encyst and is then o Indicated for eradication of cysts developing countries.
Amoebiasis cramping abdominal pain, watery or bloody excreted in the feces, or it may in colitis or liver abscess, an
diarrhea, and weight loss or anorexia, fever; invade the intestinal mucosal barrier treatment of asymptomatic
rectal bleeding without diarrhea can occur, and gain access to the bloodstream carriers
especially in children -> Excreted cysts reach the
• Chronic amoebic colitis: clinically similar to environment to complete the cycle.
inflammatory bowel disease (IBD); recurrent
episodes of bloody diarrhea and vague
abdominal discomfort
Symptoms: 1. Bacteria passes through • Histologic Endoscopic Treatment aimed at the sequelae and • Usually acquired in childhood and
• Epigastric pain mucous layer and becomes Biopsy not the underlying inflammation persists for decades
• Nausea established at the luminal o Essential for diagnosis • H.pylori: noninvasive, non-spore forming,
• Vomiting surface of the stomach with o H.pylori organisms • Parenteral vitamin B12 s shaped gram negative rod.
• Anorexia adhesins. present (stain with supplementation for pernicious • Highest infection rates in developing
• Early Satiety 2. Interaction of H.pylori with Warthin-Starry, anemia countries
• Weight Loss surface mucosa leads to release Giemsa, or Genta) • 50% of world has H.pylori infection
of IL-8 o Immunohistochemistry H. pylori infection
Cause: 3. Il-8 recruits for H.pylori • Multi-drug treatment:
• H.pylori Infection PMNs→inflammation o PMNs infiltrate lamina clarithromycin, amoxicillin,
4. Activation of transcription propria, glands, metronidazole, tetracycline, and
Course factors (NF-kB, AP-1, CREB-1) surface epithelium, furazolidone
• Chronic and Recurrent → cytokine release and more and foveolar • BMT (bismuth-metronidazole-
• Can progress as an asymptomatic inflammation epithelium tetracycline) most effective
• Development of complications such as: 5. H.pylori strains with vacuolating o Longer duration of Gastric Acid Secretion
o Peptic Ulcer Disease (10% of infected) Toxin A leads to more gastric disease- loss of • PPIs (Omeprazole, etc.)
o Gastric Adenocarcinoma (1-3% lifetime risk) mucosal injury → peptic ulcer glands and intestinal Triple therapy (1 PPI + antibiotics) is
o MALT Lymphoma (0.1% of infected) metaplasia first line
Chronic Gastritis • Progresses to 2 patterns • Urease neutralizes ammonia → • Fecal Bacterial Urea • OCA (Omeprazole, Clarithromycin,
o Antral predominant gastritis –characterized elevated gastric pH Breath Test Amoxicillin)
by inflammation and is mostly limited to the o Ammonia by bacterial • OCM (Omeprazole , Clarithromycin,
antrum; individuals with peptic ulcers usually urease Metronidazole)
demonstrate this pattern • Rapid Urease Test Long-term Monitoring
• Bacterial Culture • Evaluate after 4 weeks of start of
Multifocal atrophic gastritis –characterized by • Bacterial DNA in PCR medications
involvement of the corpus and gastric antrum with
progressive development of gastric atrophy (loss
of the gastric glands) and partial replacement of
gastric glands by an intestinal-type epithelium
(intestinal metaplasia); individuals who develop
gastric carcinoma and gastric ulcers usually
demonstrate this pattern.
PE/Histo
• Previous H.pylori infection
• Epigastric tenderness
• With Gastric Ulcers- fecal occult blood loss

• Bacterial Overgrowth-Bad Breath (halitosis),
Abdominal pain, with bloating
Symptoms • NSAID and H.pylori: disrupt Endoscopy Treat H.pylori infection • 4:1 incidence duodenum:stomach
• Epigastric burning or aching pain mucosal permeability barrier --> • Upper GI endoscopy • See chronic gastritis • Common in gastric antrum and first
• Pain 1-3 hours post-prandial; relieved by food • vulnerable to mucosal injury preferred diagnostic test portion of duodenum
or antacid • Elevated Gastric and Duodenal • Discrete mucosal lesions NSAID management • Tend to be solitary
• Iron Deficiency Anemia Acidity: epithelial cell injury with punched-out smooth • Avoid unnecessary use • Diagnosed with middle-aged and older
• Hemorrhage ulcer base • Appropriate course of PPIs adults
• Perforation Causes Radiography • If NSAID is still needed switch to a • Present in 85 to 100% of patients with
• Severe cases: • H.pylori Chronic Gastritis and • Upper GI contrast study: COX-2 inhibitor duodenal ulcers; 65% with gastric
o Dark or black stool NSAID Use: primary underlying extravasation of contrast ulcers
o Hematemesis cause indicates gastric Bleeding Peptic Ulcers
o Weight loss • Smoking perforation • Endoscopic therapy
• High-dose steroid Serum Gastrin Level • Acid suppression with PPIs
History • Zollinger-Ellison Syndrome • To screen for Zollinger-
• H. Pylori infection (Uncontrolled release of gastrin) ellison syndrome Diet
• NSAID use • Stress Lab • Avoid foods that aggravate
• Smoking Course • CBC and Iron count to symptoms
• Epigastric pain 1-3 hours post prandial relieved • Chronic and recurrent check for anemia
by food or antacid • Rarely develops into cancer • H.pylori tests (see Long-term monitoring
Peptic Ulcer • Experience nightly pain chronic gastritis) • Maintenance with antisecretory
Disease • Fullness and bloating with nausea and emesis medications
• Family history of ulcer or GI cancer
• Anemia Acid-Suppressing drugs
• Perforated PUD: sudden onset of severe • Antacids: Mylanta, Maalox, Tums,
sharp abdominal pain Gaviscon
• H2 receptor antagonists:
PE cimetidine, ranitidine, famotidine,
• Epigastric tenderness, rebound tenderness, nizatidine
guarding, and rigidity • PPIs: omeprazole, lansoprazole,
• RUQ tenderness rabeprazole, pantoprazole,
• Occult blood loss esomeprazole, dexlansoprazole
• Melena
• Succusion splash in complete gastric outlet Mucosal protective agents
obstruction • Sucralfate
• Symptoms of septic shock: tachycardia, • Prostaglandin analogue:
hypotension, and anuria. misoprostol
• Bismuth-containing compounds:
bismuth subsalicylate (BSS)
Symptoms Genetic Pathway Upper GI Endoscopy • Gastrectomy Most Common Malignancy of the
• Early: • Germline mutations in CDH1à • Main Test to find cancer o Subtotal gastrectomy: treatment stomach
o Dyspepsia Loss in E-cadherin • Most common area of choice for distal carcinomas • >90%
o Dysphagia • E-cadherin decreased in gastric involved is antrum o Total or near-total gastrectomy: • Higher incidence in Japan, Chile,
o Nausea CA Biopsy for more proximal tumors Costa Rica, Eastern Europe
• Late Complications • Absence of E-cadherin denotes • Main Diagnostic Test • Extended lymph node dissection • Mean age: 55 years old
Gastric o Weight Loss cancer • Presence of • Radiation: only for palliation of pain • 2:1 M to F ratio
Adenocarcinoma o Anorexia Adenocarcinoma cells • Cytotoxic drugs: • Intestinal type
o Alternating constipation and diarrhea H. pylori o Intestinal: columnar, o cisplatin + epirubicin or • Forms bulky tumors
o Anemia • Chronic Superficial Gastritis à gland-forming cells docetaxel • Irregular ulcer crater with mucosal pile
o Hemorrhage Chronic Atrophic Gastritis à infiltrating desmoplastic o infusional 5-FU or capecitabine up
Outcome Diffuse Type Adenocarcinoma stroma o irinotecan or oxaliplatin • Loss of rugal folds
• The 5-year survival rate for a curative surgical • Chronic Superficial Gastritis à o Diffuse: Signet-ring cells, • Predominates in high-risk areas
resection ranges from 60-90% for patients with Chronic Atrophic Gastritis à infiltrating neoplastic

stage I, 30-50% for patients with stage II Intestinal Metaplasia à Dysplasia cells with marked • Diffuse type
disease, and 10-25% for patients with stage III à Intestinal Type pleomorphism • Leather bottle appearance
disease Adenocarcinoma o Immunohistochemistry:
• High likelihood of local and systemic relapse HER-2 (+) Prognosis:
• Most powerful prognostic indicator: depth of GERD • CT-guided needle biopsy • 5-year survival rate:
invasion and extent of nodal and distal • Reflux Esophagitis→ Intestinal o 25-35% who underwent complete
metastasis Metaplasia→ Dysplasia→ • Endoscopic Ultrasound resection: ~20% (distal tumors), <10%
Intestinal Type Adenocarcinoma • Precise preoperative (proximal tumors)
assessment of tumor stage o Recurrences for at least 8 years after
History Causes/Risks: • CT Scan surgery
• H.pylori infection • Chronic H.pylori infection • Preferred imaging
• GERD o Strongest risk factor • MRI
• Gastric Ulcers o 1-3% chance in infected • PET Scan
• Complaints of indigestion, nausea or vomiting, • GERD
dysphagia, postprandial fullness, loss of • Smoking
appetite, melena, hematemesis, anemia, and • Diet
weight loss o pickled vegetables, salted fish,
• Familial Cancer salt, and smoked meats
• Genetics
• Environmental
PE
• Palpable enlarged stomach with succussion
splash
• Hepatomegaly
• Sister Mary Joseph Nodule
• Enlarged lymph nodes; Virchow Nodes
• Blumer shelf
SMALL BOWEL OBSTRUCTION SIMPLE MECHANICAL obstruction: • Supine and upright • Nasogastric suction • Most common causes of obstruction:
• Abdominal cramps around umbilicus or blockage without vascular abdominal x-rays – • IV fluids adhesions, hernias, and tumors; a small-
in epigastrium compromise adequate to diagnose • IV antibiotics if bowel ischemia bowel obstruction in the absence of prior
• Vomiting • Ingested fluid and food, digestive • Only laparotomy can suspected surgery or hernias is often caused by a
• Obstipation (in complete obstruction) secretions, and gas accumulate definitively diagnose • Surgical repair tumor
• Diarrhea (in partial obstruction) above the obstruction strangulation • Vomiting and third spacing of fluid cause
• Shock and oliguria: late simple obstruction or • Proximal bowel distends, distal • Elevated WBCs and volume depletion
strangulation segment collapses acidosis: strangulation has • Prolonged obstruction à bowel
• Severe steady pain: strangulation • Normal secretory and absorptive already occurred - but ischemia, infarction, and perforation
• No strangulation: non-tender abdomen functions of mucosa are depressed these may be absent if • Use nasogastric suction and IV fluids
• Hyperactive, high-pitched peristalsis with • Bowel wall: edematous and venous outflow from the prior to surgical repair
rushes coinciding with cramps congested strangulated loop of bowel • Consider a trial of nasogastric suction
• Palpable dilated bowel loops • Severe intestinal distention: is decreased rather than immediate surgery for
• With infarction: tender, minimal or silent progressive, intensifying peristaltic patients with recurrent obstruction due
abdomen and secretory derangements, to adhesions
Intestinal increasing risks of dehydration and
Obstruction progression to strangulation
LARGE BOWEL OBSTRUCTION
• Milder and more gradual progression of STRANGULATING obstruction:
symptoms compromised blood flow
• Increasing constipation à obstipation and • Nearly 25% of patients with small-
distention bowel obstruction
• Vomiting is rare • Associated with hernia, volvulus,
• Lower abdominal cramps unproductive of feces intussusception
occur • Venous obstruction occurs first,
• Systemic symptoms relatively mild followed by arterial occlusion à
• Fluid and electrolyte deficits are uncommon rapid ischemia of the bowel wall
• Distended abdomen with loud borborygmi • Ischemic bowel à edematous and
• No tenderness, and the rectum is usually empty infarcts à to gangrene and
• Mass corresponding to the site of an perforation
obstructing tumor may be palpable

VOLVULUS • Large-bowel obstruction:
• Abrupt onset strangulation is rare except with
• Pain is continuous sometimes colicky volvulus
Perforation may occur in an ischemic
segment or when marked dilation
occurs.

Relapsing and remitting condition, chronic Inflammation: from cell-mediated CROHN’S: • Supportive care • IBD affects people of all ages but usually
inflammation at various sites in the GI tract immune response in GI mucosa • Barium x-rays • 5-Aminosalicylic acid begins before age 30, with peak
resulting in diarrhea and abdominal pain. • Precise etiology is unknown • Abdominal CT • Corticosteroids incidence from 14 to 24
• Evidence suggests that normal • Magnetic resonance • Immunomodulating drugs • IBD may have a second smaller peak
CROHN’S: intestinal flora trigger an abnormal (MR) enterography, • Anticytokine drugs between ages 50 and 70; however, this
• Chronic diarrhea with abdominal pain, fever, immune reaction in patients with a upper endoscopy, • Sometimes antibiotics (e.g., later peak may include some cases of
anorexia, and weight loss multifactorial genetic predisposition and/or colonoscopy metronidazole, ciprofloxacin) and ischemic colitis.
• Abdomen is tender, and a mass or fullness may • UTZ probiotics
be palpable The immune reaction involves release UC:
of inflammatory mediators, including • Stool cultures and
ULCERATIVE COLITIS: cytokines, interleukins, and TNF microscopy
• Extensive UC, symptoms include malaise, fever, • Sigmoidoscopy with
anemia, anorexia, and weight loss biopsy
• Bloody diarrhea of varied intensity and duration
Inflammatory is interspersed with asymptomatic intervals. • All patients should have
Bowel Disease Usually an attack begins insidiously, with their bone mineral
increased urgency to defecate, mild lower density monitored.
abdominal cramps, and blood and mucus in the
stools. Some cases develop after an infection Lab Tests
(eg, amebiasis, bacillary dysentery). • Screen for: anemia,
hypoalbuminemia, and
electrolyte abnormalities
• Elevated alkaline
phosphatase and γ–
glutamyl transpeptidase
levels in patients with
major colonic
involvement: possible
primary sclerosing
cholangitis
• Usually asymptomatic • Abnormal cell proliferation and • CBC • Colonoscopy
• Polyps >1 cm: usually rectal bleeding, apoptosis. • Iron Studies • NSAIDS may be prophylactic
abdominal pain, and a change in bowel habits. • In villous adenomas, mesenchymal • Fecal Occult Blood Test • Surgical resection
• Occult/overt bleeding with microcytic anemia proliferation à longer, larger • Genetic studies
o Family history of polyps and colon cancer. polyps. • Double contrast barium
o Nonspecific symptoms include diarrhea, • Molecular genetic studies also enema
constipation, and flatulence describe an adenoma-to-carcinoma • CT colonography
o Change in stool caliber sequence thru accumulation of • Upper GI series
lesions in a variety of genes • Video Capsule
Colonic adenoma • K-ras oncogene activation endoscopy
• Inactivation of tumor suppressor
genes on arms 5q, 18q, and 17p
• APC gene, on 5q, has an important
role in adenoma formation
• Mutations in the APC gene occur
early in adenoma development
• Mutation on the TP53 gene, on 17p,
results in malignant transformation
of adenomas

• Loss of TP53
• Loss of normal DCC (deleted in
colon cancer) gene, on 18q is
important in the transition from an
intermediate adenoma to a late
adenoma.

PANCREAS
• Symptoms • Gallstones: leading cause of acute • Diagnosis established • Most important: safe, aggressive • occurs in 5-10% of patients following
o Severe acute pain in the abdomen or back pancreatitis in most series (30-60%) by two of the following: intravenous fluid resuscitation endoscopic retrograde
o Nausea • Alcohol: second most common o Typical abdominal (lactated Ringer’s or normal saline) cholangiopancreatography (ERCP)
o Emesis cause (15-30% of cases in the US) pain in the • Gallstone pancreatitis: undergo • Hypertriglyceridemia: 1.3-3.8% of cases;
o Fever • Autodigestion: currently accepted epigastrium that may ERCP within i4-8 hours of serum triglyceride levels are usually
o Tachycardia pathogenic theory radiate to the back admission >1000 mg/dL
• Two phases of acute pancreatitis o Proteolytic enzymes (e.g. o Threefold or greater • Hypertriglyceridemia: insulin, • Differential diagnosis should include
o Early (<2 weeks) trypsinogen, chymotrypsinogen, elevation in serum heparin, or plasmapheresis o Perforated viscus, especially peptic
§ Lasts 1-2 weeks, severity is defined by proelastase, lipolytic enzymes) lipase and/or amylase • Nutritional therapy: low-fat solid ulcer
clinical parameters are activated in the pancreas o Confirmatory findings diet o Acute cholecystitis and biliary colic
§ Most patients exhibit SIRS and may acinar cell rather than in the of acute pancreatitis • Necrosis: start broad-spectrum o Acute intestinal obstruction
predispose to organ failure intestinal lumen on cross-sectional antibiotics in septic patients o Mesenteric vascular occlusion
§ Assess for organ failure: • Disease that evolves in three abdominal imaging o Renal colic
- Score for 2 or more for one of these phases • Serum lipase and o Inferior myocardial infarction
three organ systems using the o Initial phase: intrapancreatic serum amylase o Dissecting aortic aneurysms
modified Marshall scoring system digestive enzyme activation (e.g. o Threefold or more o Connective tissue disorders with
(respiratory, cardiovascular, and trypsin activation) and acinar cell above normal values vasculitis
renal) injury o Serum lipase is more o Pneumonia
§ Persistent organ failure (>48h): most o Second phase: activation, specific and is o Diabetic ketoacidosis
important clinical finding in regard to chemoattraction, and preferred • Interstitial pancreatitis: blood supply
severity of the acute pancreatitis episode sequestration of leukocytes and o No correlation with maintained; usually self-limited
o Late (>2 weeks) macrophages in the pancreas, severity of pancreatitis • Necrotizing pancreatitis: blood supply
§ Protracted course of illness resulting in an intrapancreatic • Leukocytosis interrupted; extent of necrosis may
Acute Pancreatitis
§ May require imaging inflammatory reaction • Hemoconcentration, correlate with the severity of the attack
§ Persistent organ failure also the most o Third phase: active enzymes Hematocrit >44% and its complications
important clinical parameter of severity and cytokines digest cellular o Harbinger o more • Genetic variants associated with
§ May require supportive measures (renal membranes and cause severe disease susceptibility to pancreatitis
dialysis, ventilator support, supplemental proteolysis, edema, interstitial • Prerenal azotemia, BUN o Cationic trypsinogen gene (PRSS1)
nutrition) hemorrhage, vascular damage, > 22mg/dL o Pancreatic secretory trypsin inhibitor
• Severity classification coagulation necrosis, fat o Significant risk factor (SPINK1)
o Mild acute pancreatitis necrosis, and parenchymal cell for mortality o Cystic fibrosis transmembrane
§ Without local complications or organ failure necrosis • Hyperglycemia conductance regulator gene (CFTR)
§ Self-limited and subsides spontaneously, • Hypocalcemia o Chymotrypsin C gene (CTRC)
usually within 3-7 days after treatment is • Hyperbilirubinemia o Calcium-sensing receptor (CASR)
instituted • Hypertriglyceridemia
o Moderately severe acute pancreatitis • Hypoxemia
§ Transient organ failure (resolves in <48h) or • Abdominal ultrasound:
local or systemic complications in the recommended initial
absence of persistent organ failure diagnostic imaging
§ May or may not have necrosis modality
o Severe acute pancreatitis • CT scan
§ Persistent organ failure (>48h), single or
multiple
§ CT scan or MRI should be obtained to
assess for necrosis and/or complications

MODULE/TOPIC 11 NEPHROLOGY

HISTORY
Some signs and symptoms pointing to a renal disease Hematuria
• Edema • Blood in the urine
• Flank pain • May be gross or microscopic hematuria
• Hematuria, Proteinuria (bubbly urine) • In women, be sure to distinguish menstrual blood from hematuria
• Hypertension, esp. in young individuals • Also ask about medications that might discolor the urine (e.g. Rifampicin)
• Test with urine dipstick and microscopic examination before diagnosing
Suprapubic pain hematuria
• Pain in the lower abdomen, typically dull and pressure-like
• Sudden bladder distention: agonizing pain Kidney or Flank Pain
• Chronic bladder distention: painless • Pain at or below the posterior costal margin near the costovertebral angle
• Visceral pain produced by the distention of the renal capsule
Dysuria • Typically, dull, aching and steady
• Painful urination usually felt as a burning sensation
• May also mean difficulty voiding Ureteral Pain
• Possibly from infection or irritation of either bladder or urethra • Pain that is usually severe and colicky
• In women, described as pressure or external burning from the flow of urine • Originating at the costovertebral angle and radiating around the trunk into
across irritated or inflamed labia the lower abdomen
• In men, typically felt as a burning sensation proximal to the glans penis • Results from sudden distention of the ureter and associated distention of
the renal pelvis from renal or urinary stones or blood clots
Urgency
• Unusually intense and immediate desire to void Specific for Older Men
• Sometimes leading to involuntary voiding (urge incontinence) Probe for possible benign prostatic hyperplasia
FUNWISE (FUN = irritative symptoms, WISE = obstructive symptoms) or
Frequency WINSURF
• Abnormal frequent voiding Frequency, Urgency, Nocturia, Weak stream, Intermittency, Straining,
Emptying incomplete/Retention
Polyuria
• Excessive production/passage of urine Weak stream, Intermittency, Nocturia, Straining, Urgency, Retention or
• Significant increase in 24-hr urine volume, exceeding 3L incomplete voiding, Frequency
Nocturia Terms and definitions

• Needing to wake up at night to urinate • Azotemia: Elevation of blood urea nitrogen (BUN) and serum creatinine
• Urinary frequency at night levels, reduction in GFR
• Need to differentiate if it is physiologic (e.g. does the patient drink a lot • Prehn’s sign: Pain relief with testicular elevation
before sleeping?) or not o Found in epididymitis
• Priapism: abnormally prolonged, painful penile erection
Urinary Incontinence • Uremia: accumulation of urea in the blood
• Involuntary loss of urine
• May become socially embarrassing or cause problems with hygiene
• Stress incontinence: involuntary leakage on effort/exertion, sneezing,
coughing, or giggling
• Urge incontinence: Involuntary loss of urine following an urge to void
• Flow incontinence: limited bladder emptying due to neurologic disorder or
anatomic obstruction
• Functional incontinence: from impaired cognition, musculoskeletal
problems or immobility
PHYSICAL EXAM
Normal: kidneys are retroperitoneal and not usually palpable Inspection
Left Kidney • Inspect the skin of the penis and around its base for
• Move to patient’s L side. excoriations or inflammation
• Place R hand behind the patient, below and parallel to • Inspect the prepuce and, if present, retract it (or ask the
12 rib, fingertips just reaching the costovertebral angle.
th
patient to retract it)
• Lift, trying to displace the kidney anteriorly. o Check for chancres, carcinomas, and smegma (cheesy,
• Place left hand in the LUQ. Ask the patient to take a whitish debris)
deep breath. • Inspect the glans for ulcers, scars, nodules, signs of
• At the peak of inspiration, press L hand firmly and inflammation
deeply into LUQ, capturing the kidney between your two • Check the pubic hairs for nits or lice
Kidney hands. Penis • Note the location of the urethral meatus (hypospadias,
• Ask the patient to breathe out and slowly release the epispadias)
pressure of your L hand, still feeling for the kidney • Compress the glans between your index finger above and
returning to its expiratory position. your thumb below to check for discharge
Right Kidney o Normally there is no discharge
• Return to patient’s R side
• Use L hand to lift from the back, and R hand to feel Palpation
deep in the RUQ • Palpate any abnormalities and note any tenderness or
• Proceed as before induration
Palpate the shaft between your thumb and first two fingers
and note for any induration

• Note: Normal R kidney may be palpable, especially Inspection
when the patient is thin and the abdominal muscles are • Inspect the skin, including the posterior surface
relaxed. It may be slightly tender. The lower pole is • Check the scrota contours for any swelling, lumps, or veins
rounded.
Palpation
• Palpate each testis and epididymis between your thumb
and first two fingers
• Epididymis: located at the superior posterior surface of
Scrotum each testicle
o Feels nodular and cordlike
• Note size, shape, consistency, and tenderness
• Palpate each spermatic cord
• Note any nodules or swellings
Transillumination of the scrotum can be done to assess any

swelling.
Inspection
Causes of kidney enlargement: hydronephrosis, cysts, • Inspect the inguinal regions and genitalia for bulging and
tumors asymmetry
Bilateral enlargement suggests polycystic kidney disease. • Ask the patient to strain and bear down (Valsalva
maneuver)
Kidney enlargement vs Splenomegaly o It is a hernia if the bulge appears with straining
• Preserved normal tympany in LUQ (no obliteration of
Traube’s space) Palpation
• Ability to probe with your fingers between the mass and • Done while facing the standing patient
costal margin • Right inguinal hernias: place the tip of your right index
(Perform if there is tenderness of the abdomen) finger close to the inferior margin of the scrotal sac then
move upward along the inguinal canal
Fist Percussion • Follow the spermatic cord to the inguinal ligament
• Place the ball of one hand in • Palpate the external inguinal ring (triangular slitlike
the costovertebral angle. opening) above and lateral to the pubic tubercle
• Strike it with the ulnar o Ask the patient to bear down and check for any bulges or
surface of your fist. Use Hernias
masses
enough force to cause a o (+) bulge suggests a direct inguinal hernia
perceptible but painless jar • From the external ring, palpate obliquely along the inguinal
or thud. canal toward the internal inguinal ring
o Ask the patient to bear down and check for any bulges
Pain with fist percussion o (+) bulge suggests an indirect inguinal hernia
suggests pyelonephritis but may • Left inguinal hernias: same as above, but use the left
also have musculoskeletal cause. index finger
• Femoral hernias: Place your fingers on the anterior thigh
at the femoral canal and ask the patient to strain or cough.
Note any swelling or tenderness.
Further evaluation
• Ask the patien to lie down
• If the mass returns to the abdomen by itself, it is a hernia
• Auscultate the mass for bowel sounds
Normal: bladder cannot be examined unless it is distended • Digital Rectal Exam: to check for prostate enlargement
above the symphysis pubis o Identify the prostate gland’s lateral lobes and median
sulcus
Distended bladder: o Note the size, shape, and consistency of the prostate
• The dome of the distended bladder feels smooth and o Identify any nodules or tenderness (normally rubbery
round. and nontender)
• Check for tenderness. • Cremasteric Reflex
• Suprapubic tenderness is common in bladder infection. Some o Stroking of the inner thigh causes the contraction of
Bladder • Check for dullness. Special the cremaster muscle, which pulls the ipsilateral
• Determine how high the bladder rises above the symphysis Tests testicle upward
pubis. o Absence may suggest testicular torsion
• Bladder volume must be 400 to 600 mL before dullness • Anal Wink/Anocutaneous Reflex
appears. o Contraction of the anal sphincter in response to
stroking the perineum with a pin
Bladder distention causes: urethral stricture, prostatic o Evidence of normal S4-S5 function
hyperplasia, stroke, multiple sclerosis o Absence may suggest a nervous defect

URINARY TRACT INFECTION
PERTINENT HISTORY AND PE
PATHOGENESIS DIAGNOSIS
FINDINGS
This is an infection, so it is important that you know UTI can be cystitis or pyelonephritis. By convention, there are 3 easy
the common etiologic agents: diagnostics used in UTI: (1) urinalysis, (2)
E. coli (most common), S. saprophyticus, Klebsiella Cystitis, or the inflammation of the urine dipstick test, and (3) urine gram
pneumoniae, Proteus mirabilis, N. gonorrhoeae urinary bladder, manifests with stain.
common urinary symptoms: dysuria,
Most UTIs are due to ascending infection urinary frequency, urgency, nocturia, Urinalysis will tell you if there is possible
Think about it, where else would the bacteria come hesitancy, suprapubic discomfort and bacterial infection because of the presence
from but from outside to inside (via entrance through gross hematuria. There is NO vaginal of WBCs in urine. The same goes for urine
the external meatus of the urethra). These bacteria can discharge in uncomplicated cystitis. dipstick. Note, however, that urinalysis and
propagate and ascend from the urethra, to the urine dipstick are not solely for detecting
bladder, to the ureters, and eventually to the kidneys. Pyelonephritis, or the inflammation of infections. For example, hemoglobin or
the ureters and/or kidneys, manifests blood in urine can also be detected through
This is also why women are more prone to UTI than with systemic symptoms. In mild this test. Urine gram stain confirms the
men – they have a shorter urethra and their urethral cases, it may manifest with low-grade presence and characterizes basic
meatus and anus are close to each other (thus, some fever or costovertebral pain while in morphology of bacteria.
women need to be advised that wiping after severe cases, it manifests with high
defecation should be upwards or away from the vagina fever, rigors, nausea, vomiting and Review the positive results for the three of
and urethra). flank/loin pain. them:
Conversely, if it is common in women, then it shouldn't Additionally, probe if the patient has Urinalysis
be common in men because of their longer urethras. the ff risk factors: Normal value: 0-5 WBC/HPF
Hence, when men get UTI, they are almost always • Sexually active: 3x more likely to
automatically categorized as complicated. Unless: 1 st
catch UTI Urine dipstick test

episode of symptomatic lower UTI in the young (15-40) • Use of diaphragm and Positive: >10WBC/mm3
and healthy man. spermicides: alter the pH of the
vagina and
Nosocomial UTI • History of UTI: 5x more likely
Remember, urethral catheterization puts patients at Urine gram stain
risk for UTI because you are "invading" with a possibly Positive: 1/OIF =100,000 bacteria/ml
infected "foreign body"
• Extraluminal ascension- microorganisms in the You can also do urine culture and
urethral meatus are introduced directly into the sensitivity test to identify bacteria causing
bladder when the catheter is inserted the infection and guide you in your
• Intraluminal contamination- infecting organisms antibiotics.
migrate along the internal lumen if the catheter is
contaminated Note that you don't always have to do all
the test for UTI
CLINICAL ADDITIONAL
TYPE DIAGNOSIS TREATMENT
PRESENTATION NOTES
• Dysuria • CLINICAL diagnosis Empiric antibiotic treatment TMP-SMX has
• Frequency • NO NEED FOR been removed
1st line:
• Urgency URINALYSIS if any of the as 1st line
• Nitrofurantoin
• Gross hematuria listed symptoms on the left treatment d/t
monohydrate/macrocrystals 100
• No conditions defining are present resistance,
mg BID for 5 days PO
complicated UTI • Pre-treatment urine culture TMP-SMX may
Acute • Fosfomycin trometamol 3 g single
• NO vaginal discharge and sensitivity is NOT be given ONLY
uncomplicated dose PO
• More common in women recommended
cystitis if with proven
(but should not be • Urine microscopy and Alternatives:
susceptibility
pregnant) dipstick leukocyte esterase • Pivmecillinam, fluoroquinolones,
are not needed for treatment amoxicillin-clavulanate,
cephalosporins (cefuroxime,
cefaclor, cefixime, cefpodoxime,
ceftibuten)
• Otherwise healthy • Urinalysis (positive for 1st line: • TMP-SMX
women, without evidence pyuria, ≥5 WBC/HPF) • Ciprofloxacin 500 mg BID 7-10 may be given
of anatomic or functional • Gram stain days PO ONLY if with
urologic abnormalities • Urine culture (≥10,000 CFU • Levofloxacin 250 mg OD for 7-10 proven
• Fever (≥38°C) of uropathogen/ mL) days susceptibility
• Chills • Sensitivity test • Ofloxacin 400 mg BID for 14 days
• Flank pain Indications for
Acute • Costovertebral angle NOT recommended: Alternatives: admission
uncomplicated tenderness • Blood cultures, unless septic • Cefixime: 400 OD for 14 days PO • Inability to
pyelonephritis • Nausea (temp. >38°C or < 36°C, • Ceftibuten 400 mg OD for 14 days maintain oral
• Vomiting leukopenia or leukocytosis, • Cefuroxime axetil 500 mg BID for hydration or
• With or without signs and tachycardia, tachypnea, 14 days PO take
symptoms of lower hypotension) • Co-amoxiclav 625 mg TID for 14 medication
urinary tract infection days PO • Concerns
regarding
Antibiotics should be adjusted once compliance
culture and sensitivity results are • Presence of
obtained possible

complicating
If the patient is admitted: conditions
Give IV antibiotics until the patient is • Severe illness
afebrile, then switch to oral with high
antibiotics. fever, severe
• Ceftriaxone 1-2 q 24 hours pain, marked
• Ciprofloxacin 400 mg q 12 hours debility, and
• Levofloxacin 250-750 mg q 24 signs of sepsis
hours
• Ofloxacin 200-400 mg q 12 hours
• Amikacin 15 mg/kg BW q 24 hours
• Gentamicin +/- ampicillin 3-5 mg/kg
BW q 24 hours
• No symptoms of UTI • Asymptomatic bacteriuria • Cephalexin BID for 7 days (FDA B) • Asymptomatic
with • Cefuroxime axetil BID for 7 days (B) bacteriuria,
o >100,000 CFU/mL of the • Fosfomycin trometamol 3 g single unlike in non-
same uropathogen in two dose (B) pregnant
consecutive midstream • Amoxicillin-clavulanate BID for 7 women,
urine specimens; OR days (B) should be
o ≥100 CFU/mL of a single • Nitrofurantoin macrocrystal QID for treated in
uropathogen in one 7 days (B) pregnant
catheterized urine o May be given on the second tri women to
specimen until 32 weeks AOG, use in the decrease the
• Test of choice: urine culture first trimester of pregnancy is chance of fetal
Asymptomatic of clean-catch midstream appropriate when no other compromise
bacteriuria in • Urinalysis is not suitable alternatives are available and infection
pregnancy recommended as an initial • Trimethoprim-sulfamethoxazole
screening test, as well as 160/800 mg BID for 7 days (C)
urine dipsticks for leukocyte (avoid in 1st and 3 trimesters)
rd
esterase and/or nitrites

• If no urine culture, gram
stain of uncentrifuged urine
is recommended
• Dipslide culture technique is
an alternative
• Screen all pregnant women
between 9 -17 week AOG,
th th
preferably 16 wkth
• Dysuria Prior to treatment Treatment should be instituted Compared to

• Frequency • Urine culture and sensitivity immediately to prevent pyelonephritis acute
• Urgency test of a midstream clean • Cephalexin 500 mg QID for 7 days uncomplicated
• Gross hematuria catch urine specimen PO cystitis in non-
• Bacteriuria without fever • If culture is unavailable, • Fosfomycin 3 g single dose PO pregnant
and costovertebral angle o Significant pyuria on • Nitrofurantoin 100 mg QID for 7 patients, more
tenderness urinalysis days PO tests are done in
§ ≥8 pus cells/mm of 3
pregnant
uncentrifuged urine, OR Unless the patient is not improving or patients, and the
Acute
§ ≥ 5 pus cells/HPF of when there is worsening of signs and medications
uncomplicated differ, as well.
centrifuged urine symptoms, there is no need to adjust
cystitis in
o AND positive leukocyte antibiotic therapy based on culture
pregnancy
esterase and nitrite test results
on dipstick
Post-treatment follow-up tests

are done 1-2 wks after
completion of therapy to
confirm the eradication of
bacteriuria and resolution of
infection
• Fever (≥38°C) Routinely recommended Give IV medications first until patient Indications for
• Chills pretreatment is afebrile for 48 hours, then give oral admission
• Flank pain • Urinalysis (positive for medications. • Inability to
• Costovertebral angle pyuria, ≥5 WBC/HPF) maintain oral
IV medications:
tenderness • Gram stain hydration or
• Ceftriaxone 1-2 g IV q 24 hrs
• Nausea • Urine culture (≥10,000 CFU take
• Cefotaxime 1-2 g IV q 8 hrs medication
• Vomiting of uropathogen/ mL)
Acute • Ceftazidime 2 g IV q 8 hrs
• With or without signs and • Sensitivity test • Concerns
uncomplicated
symptoms of lower Oral medications: regarding
pyelonephritis
urinary tract infection NOT routine: • Cephalexin 500 mg QID for 14 days compliance
in pregnancy
• Blood cultures: done if • Cefadroxil 1 g BID for 14 days • With possible
septic • Cefuroxime axetil 500 mg BID for co-morbidities
• Renal ultrasound: only for 14 days • Severe illness
women who fail to respond with high
to initial treatment fever, severe
pain, marked
Post-treatment debility

• Urine culture after • Signs of
completion of antibiotics + preterm labor
follow up for symptoms + • Signs of
monthly urine cultures until sepsis
delivery
Significant bacteriuria Routinely recommended For mild to moderate illness (fever + Indications for
(>100,000 CFU/mL) plus pretreatment UTI, without urosepsis, circulatory admission
clinical symptoms in a • Urine gram stain failure, and/or organ • Marked
setting of: • Urine culture and sensitivity dysfunction/failure): debility and
• Functional or anatomic • Ciprofloxacin 500-750 mg BID for signs of sepsis
Additional ancillary tests 7-14 days
abnormalities of the • Uncertainty in
• Imaging of the urinary tract if • Norfloxacin 400 mg BID for 7-14 diagnosis
urinary tract or kidneys;
suspecting anatomic or
or days • Inability to
structural abnormalities
• Presence of an • Ofloxacin 200 mg BID for 10-14 maintain oral
• CT-Scan of urinary tract is days hydration or
underlying disease that
preferred over KUB • Levofloxacin 500-750 mg OD for 7- take
interferes with host
ultrasound 14 days medication
defense mechanisms; or
Any condition • Amoxicillin/ clavulanic acid 500 • Concerns
Post-treatment regarding
that increases the risk of mg/125 mg for 7-14 days
• Urine culture 1-2 weeks after compliance
acquiring persistent
completion of antibiotics For severely ill patients:
infection and/or treatment
• Referral to specialists if • Broad-spectrum parenteral
Complicated failure
significant bacteriuria persists antibiotics
UTI Iatrogenic
post-treatment • Fluoroquinolones are not
conditions (presence of in-
recommended as empiric
dwelling catheter)
antibiotics due to high rates of
Pathogen-
resistance locally
related complication
factors (antibiotic resistant
IV medications
organisms)
• Amikacin 15 mg/kg q24h
Others
• Gentamicin 3-5 mg/kg/day q24h
UTI in males
• Doripenem 500 mg q8h
except in young males
• Ertapenem 1 gm q24h
presenting exclusively with
lower UTI • Imipenem-cilastin 250-500 mg q6-
8h
Chemical or
radiation injuries of • Meropenem 1 gm q8h
uroepithelium • Piperacillin-Tazobactam 2.25-4.5 g
Urosepsis or q6-8h
severe pyelonephritis
NEPHROLITHIASIS
OVERALL PATHOPHYSIOLOGY DIAGNOSIS PERTINENT HISTORY AND FINDINGS
• CBC: leukocytosis
• Blood chemistry: serum creatinine,
• Acute renal colic: Sudden onset of severe
electrolytes
flank pain, begins in the lateral upper-
Results from increased concentration of • Urinalysis: hematuria, bacteriuria, crystals,
midback over the costovertebral angle, and
stone constituents, changes in urinary pH, urinary pH
radiating inferiorly and anteriorly
decreased urine volume, bacterial infection, • Gold Standard: Helical CT scan
• Microscopic hematuria, painless groin
loss of inhibitors of crystal formation (citrate, • X-ray: Plain KUB (except for uric acid
hematuria
pyrophosphate, glycosaminoglycans, stones, which do not appear on X-ray)
• Pyuria
osteopontin, nephrocalcin) • Abdominal ultrasound
• Pain radiating to the lumbar or groin area
• Urologic imaging (intravenous pyelography,
• UTI
plain renal tomography, retrograde
• Hydronephrosis (rare)
pyelography)
TYPES COMMON ETIOLOGIES URINE CRYSTAL TREATMENT

Calcium oxalate • Hypercalciuria, hypocitraturia, dietary Dumbbell shaped • Increase water intake to at least 2 L/day
stones (most hyperoxaluria, low urine volume and pH (monohydrate) or • Low-sodium, low-protein diet
common, 75%) • Medullary sponge kidney envelope shaped • Low-oxalate (for hyperoxaluria)
(dihyrdate) • Thiazide diuretics (for idiopathic
hypercalciuria)
• Alkali supplements (for hypocitraturia,
hypouricosuria)
• Allopurinol (for hyperuricosuria)
Calcium • High urine pH • Increase water intake
phosphate stones • Avoid unnecessary urine alkalization
(15%)
Uric acid stones • Low urine pH Rhomboid/parallelograms • Alkali supplements to raise urine pH to 6.5
(8%) • Low urine volume • Increase water intake to 2-3 L/day
• Hyperuricosuria • Low purine diet
• Allopurinol if daily urine uric acid > 1000mg
Cystine stones • Hereditary cystinuria Hexagonal • Large amount of fluids to produce a urine
(1%) output of at least 4 L/day
• Alkalinize urine to pH 7.5

• D-penicillamine if needed
Struvite stones: • Infection from Proteus, Klebsiella, Coffin lid • Complete stone removal
magnesium, Providencia, Morganella, Pseudomonas • Prophylactic antibiotics post-op
ammonium, which convert urea to ammonia, • Urease inhibitors, if with recurrent upper UTI
phosphate; can generates alkali urine which precipitates
form staghorn struvite stone formation
calculi (5%)
• Risk Factors: previous UTI, catheters,
neurogenic bladder
NEPHRITIC VS. NEPHROTIC SYNDROME

NEPHRITIC SYNDROME NEPHROTIC SYNDROME
Pathophysiology Glomerular inflammation Derangement in glomerular capillary walls, leading to
Numerous cells in the glomeruli increased permeability to plasma proteins (including
albumin, globulin, lipoproteins, immunoglobulins,
antithrombin III)
Symptoms • Hematuria • Massive proteinuria (≥3.5 g of protein; mostly albumin)
• Red cell casts in urine o Highly selective proteinuria: loss low molecular weight
• Azotemia proteins
• Oliguria due to low GFR o Poorly selective proteinuria: loss of higher molecular
• Mild to moderate hypertension due to lack of filtration weight globulins and albumin
• Proteinuria are relatively less severe • Hypoalbuminemia (plasma albumin < 3 g/dL)
• Pyuria • Generalized edema
o Soft and pitting edema
o Periorbital regions and dependent portions of the
body
o Can lead to pleural effusions and ascites
• Hyperlipidemia, lipiduria
• Hypercoagulable state
• Increased vulnerability to infections
Diseases • Acute Proliferative GN, Post-infectious GN, Post-
streptococcal GN
• Rapidly Progressive GN • Minimal Change Disease
• IgA Nephropathy (Berger Disease) • Focal Segmental Glomerulosclerosis
• Hereditary Nephritides: Alport Syndrome, Thin • Membranous Nephropathy
Basement Membrane Lesion • Membranoproliferative Glomerulonephritis
• Chronic Glomerulonephritis
• Lupus Nephritis
GLOMERULAR DISEASES
Nomenclature:
Focal vs Diffuse
Focal (<50% of glomeruli involved)
Diffuse (>50% of glomeruli involved)
Global vs Segmental
Global = the whole glomerulus is involved
Segmental = only a part of the glomerulus is involved
DISEASE PATHOGENESIS HISTOPATHOLOGY NOTES

LM: Diffuse proliferation of
Immune complex
glomerular cells + neutrophil influx • Nephritic syndrome
deposition 1-4 weeks
Post-Streptococcal (hypercellular) • Frequent in children
after Group A β-
Glomerulonephritis IF: granular IgG, IgM, and C3 • Tx: sodium restriction, glucocorticoids, and
hemolytic streptococcal
along GBM and mesangium antihypertensives
infection
EM: subepithelial humps
LM: segmental proliferation, focal
May be genetic or
or diffuse GN
secondary to liver or • Nephritic syndrome
IgA Nephropathy (Berger IF: Mesangial deposition of IgA
intestinal disease, e.g. • May maintain renal function, but slowly
Disease) with C3
gluten enteropathy progress to chronic renal failure
EM: electron-dense deposits in
(celiac disease)
mesangium
Immune dysfunction LM: Normal
causes loss of IF: Normal • Most common cause of nephrotic syndrome
Minimal Change Disease polyanions, producing a EM: Effacement of foot in children
cytokine response that processes/ podocytes (melted • Tx: corticosteroids
damages the podocytes Hershey’s Kisses)
LM: focal and segmental sclerosis
Focal Segmental Various causes, e.g. HIV,
and hyalinosis • Most common nephrotic syndrome in adults
Glomerulosclerosis idiopathic, etc.
IF: Focal IgM + C3

EM: Diffuse effacement of foot
processes and denudation of
GBM
Capillary BM thickening
Diffuse mesangial sclerosis
Kimmelstiel-Wilson lesions:
Hyperglycemia causes
nodular glomerulosclerosis with
Diabetic glomerulopathy an increase in GFR à • Most common cause chronic kidney disease
hyaline in the capillary or
glomerulosclerosis
Bowman’s capsule, and with
nodules in the periphery of the
glomerulus
Deposition of circulating
immune complexes and “Full house” because all types of • Class IV: Diffuse proliferative is the most
Lupus Nephritis
in situ immune complex deposition can be present common and most severe pattern
formation
• Poor prognosis, rapid deterioration of renal function
Rapidly Progressive • Type I: Anti-GBM antibody induced (e.g. Goodpasture Syndrome)
(crescentic) GN • Type II: Immune complex-mediated (e.g. PSGN, lupus nephritis)
• Type III: Pauci-immune (e.g. Granulomatosis with polyangiitis)
• Wire looping of capillaries in light microscopy
Diffuse proliferative GN
• A common cause of death in SLE
• Genetic: X-linked mutation in type IV collagen
Alport syndrome • Presents with eye problems, GN, and sensorineural deafness
• (can't see, can't pee, can't hear a bee)
• "Tram track" or “double contour” appearance on PAS stain
Membranoproliferative GN • Type 1: can be caused by Hepatitis B and C
• Type 2: Dense-deposit disease
Membranous nephropathy • Spike and dome appearance with subepithelial deposits
(membranous GN) • Most common cause of nephrotic syndrome in Caucasian adults
• Nephrotic syndrome that does not respond to steroid therapy
Amyloidosis • Congo red stain shows apple-green birefringence
ACUTE KIDNEY INJURY

What is AKI? Sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products
What causes • Prerenal causes: Hypovolemia, decreased cardiac output, decreased effective circulating volume (e.g. CHF, liver failure),
AKI? impaired renal autoregulation (NSAIDs, ACEi, ARB, Cyclosporine)
• Intrinsic causes
o Glomerular: Acute glomerulonephritis
o Tubules and interstitium
§ Ischemia
§ Sepsis/Infection
§ Nephrotoxins (endogenous and exogenous)
• Postrenal causes: bladder outlet obstruction (e.g. nephrolithiasis), bilateral pelvoureteral obstruction (or unilateral if there is
only one kidney)
How to tell if Signs and Oliguria
it is AKI? symptoms Flank pain
Volume overload
Other signs and symptoms specific to the cause of the AKI
KDIGO • Increase in SCr by ≥ 0.3 mg/dl (≥ 36.5 µmol/L) within 48 hours, or
Definition • Increase in Scr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7
days, or
• Urine volume < 0.5 mL/kg/h for 6 hours
Other helpful • Urinalysis: check for proteinuria, casts, crystals
lab tests • CBC: Anemia, eosinophilia
• Blood chemistry: hyperkalemia is the most common electrolyte disturbance in AKI
• Other Renal Failure Indices: BUN/ Crea Ratio (BCR), Fractional Excretion of Sodium (FENa), Urine
Osmolality
• Imaging (Xray, MRI, vascular imaging)
• Kidney biopsy
• Novel biomarkers: KIM-1, NGAL, IL-8
How to treat • Monitor the patient
of AKI? • Identify and treat the cause
• Supportive care: optimize hemodynamics, correct electrolyte imbalances, discontinue nephrotoxic medications, dialysis*,
dose adjustment of administered medications
*Dialysis Indications:
• Failure of medical management
• Toxic ingestions
• Severe complications of uremia

CHRONIC KIDNEY DISEASE
CKD Abnormalities of kidney structure or function, present for > 3 months, with implications for health
KDIGO Criteria for CKD (either of the following, present for > 3 months): kidney damage (one or more of those listed below), decreased
definition GFR (GFR categories G3a-G5)
• Albuminuria
• Urine sediment abnormalities
• Electrolyte and other abnormalities due to tubular disorders
• Abnormalities detected by histology
• Structural abnormalities detected by imaging
• History of kidney transplantation
PROGNOSIS
CLINICAL FINDINGS TREATMENT
Early signs: • Hemodialysis

• Polyuria (frequency • Peritoneal dialysis
and nocturia) • Transplant
• General signs such as
anorexia, nausea, Other goals of management:
vomiting, weight loss • Treatment of reversible causes
• Bone marrow of renal failure
depression > altered • Preventing or slowing the
blood chemistry (e.g. progression of renal disease
anemia) • Treatment of the complications
• High blood pressure of renal failure
• Adjusting drug doses when
Late signs (uremic appropriate for the level of
stage) estimated glomerular filtration
• Oliguria rate (eGFR)
• Dry, pruritic, • Identification and adequate
hyperpigmented skin preparation of the patient in
• Easy bruising whom renal replacement
• Bone, heart, brain and therapy will be required
nerve dysfunction • Proper diet and exercise
• Impotence
PART 12C. SKILLS

GFR CALCULATION
FORMULA USE
Creatinine Clearance (CrCl) from Cockcroft-Gault
140 − *+, × #,*. /012 3,4+ℎ6 4. 7+

!"!# = Measures creatinine clearance instead of estimated GFR (eGFR)
72 ×:,";< =",*64.4., 4. <+/1?
If female, multiple the result by 0.85

CKD-EPI • Preferred method for measuring eGFR
• Validated in the Filipino population
• Not validated for children and pregnant patients
Revised Bedside Schwartz • For ages 1-17
• Normal GFR = 90 mL/min/1.73 m or higher; ~125 mL/min/1.73 m in young adults
3 3
o The best way to calculate for GFR is by calculating the clearance of inulin; however, this is difficult to do. Usually, eGFR is calculated from
the serum creatinine.
• Downloading the eGFR calculator app by the National Kidney Foundation is recommended

MODULE/TOPIC 12 ENDOCRINOLOGY

SYMPTOMS OF ENDOCRINE Hirsutism Skin: Hirsutism, striae, foot ulcers
DISEASE Loss of Libido Face: Facial edema, moon facies, coarse facial features, prognathism, exophthalmos,
Galactorrhea Diabetes/Thyroid s/sx leonine facies
Amenorrhea Visual disturbances: bitemporal Body Habitus: Central obesity, supraclavicular fat pad, buffalo hump, large hands and feet
Gynecomastia hemianopsia Neck: Masses, nodules
DISEASE-SPECIFIC HISTORY DIABETIC FOOT EXAMINATION
Inspection
• Hyperglycemia Shoes, Skin status (color, thickness, drying, cracking), sweating, infection (check
• Keep in mind the classifications: Type 1, Type 2, between toes), ulceration, calluses/blistering, texture of nails, presence of hair,
gestational
deformities (hammer toes, Charcot foot or rocker-bottom deformity, hallux valgus)
• 3Ps: Polyuria, Polyphagia, Polydipsia
• Unintentional weight loss Ulceration and Infection: consider infected if they have purulence and/or at least 2 of the
• Ask about glycemic control following: pain, warmth, erythema, edema, lymphangitis, loss of function
• Medications: Insulin, glucose lowering agents,
Palpation
ACE-I, lipid-lowering agents
Differences in temperature between right and left limbs
• Social History: Smoking, diet, exercise
• Investigate possible complications: BEAN
Pulses (4): dorsalis pedis, posterior tibial, femoral pulse, popliteal pulse
(Bugs, Eyes, Arteries, Nephropathy, Nerves)
Graded from 0 to 3+ (3+ bounding; 2+ brisk, expected, normal; 1+ diminished, weaker
o Bugs: PMHx of infections
than expected; 0 absent)
o Eyes: retinopathy, cataracts, glaucoma
DIABETES o Arteries: HTN, ischemic heart disease, Special Tests
MELLITUS peripheral vascular disease, stroke/transient • Monofilament sensation (Protective Sensation):
ischemic attack test 10 pedal sites (if cannot feel at least 7 of 10
o Nerves: altered proprioception, pedal sites = absent protective threshold, risk for
mononeuropathies (CNs III, IV, VI), peripheral ulceration)
neuropathy, autonomic neuropathy (postural • Vibration sense: 128 Hz tuning fork to tip of hallux
hypotension, gastroparesis) and bony prominences (on first MTP)
Criteria for diagnosis: • Pinprick sensation: distinguish if sharp or dull
• FBS ≥ 7.0mmol/L (126mg/dL) • Ankle reflex: absence associated with increased
• HbA1c ≥ 6.5% risk of foot ulceration
• 2-hr plasma glucose after OGTT ≥ 11.1mmol/L • Ankle-brachial index: vascular insufficiency in
(200mg/dL) lower limbs
• Random plasma glucose > 11.1mmol/L Fundoscopy: findings of diabetic
(200mg/dL) + classic symptoms or retinopathy
hyperglycemic crisis Dot and flame hemorrhage, cotton-wool exudate, neovascularization, thinned
blood column
HPI THYROID PE
• Chief complaint Inspection
• Symptoms of hyper or hypothyroidism General Survey: Outfit (appropriate for temperature?), Mood (expressionless [hypo] or
• Anatomic abnormalities: palpable masses, agitated [hyper]), With or without ophthalmopathy
enlargement, obstructive symptoms, neck pain
• Onset, previous and present treatment (e.g. neck Inspect the thyroid gland at rest and when swallowing
radiation, surgery, thyroid hormones) • Neck extended (head tilted back), tangential lighting
• Accompanying s/sx (See common s/sx below) • Landmarks
o Temperature intolerance: o First bump or Adam’s apple: thyroid cartilage; Second bump: cricoid cartilage
Preference for hot or cold weather? Dressing o Thyroid is in region between cricoid and substernal notch
more or less warmly than others? Palpation
o Perspiration/sweating Palpate for tracheal deviation
o Palpitations
o Changes in weight: loss (hyper) or gain • Palpate thyroid (Posterior Approach): From
(hypo) behind the patient, palpate the thyroid gland,
o Menstrual changes: amenorrhea (hyper) or including the isthmus and the lateral lobes (at
menorrhagia (hypo) rest and when swallowing)
o Bowel movement: more frequent (hyper) or • Ask for permission, hands are clean and warm,
constipation (hypo) use four fingers to palpate
o Changes in mood: nervousness, • Neck flexed
restlessness (hyper) or extreme fatigue, • Palpate for levels of the neck (See levels and
THYROID lethargy (hypo) boundaries below)
DISEASE • Report: Size (12-20g), consistency, nodularity, tenderness, lymphadenopathy in
PMHx cervical and supraclavicular areas
• 3As: Arrhythmia, Amiodarone, Attack (Heart)
• Arrhythmia • Possible abnormal findings: goiter, nodules, tenderness of thyroiditis
• Amiodarone intake: anti-arrhythmic, high • Diffuse enlargement: Graves’ disease (hyperthyroidism), Hashimoto’s thyroidism
content of iodine, may cause hypo or hyper (autoimmune hypothyroidism), endemic goiter (iodine deficiency), or sporadic goiter
• Previous MI, CHF (adjust dosage of treatment) • Multinodular goiter: enlargement with ≥2 identifiable nodules
o Hyperglycemia • Single nodule: cyst, benign tumor, cancer, or palpable nodule in clinically unrecognized
o Asthma, liver, or kidney disease multinodular goiter
o Medications for hyperthyroidism (beta
Auscultation
blockers) may aggravate asthma
Check for BRUITS in hyperthyroidism (bell, ask Pt to hold his/her breath listen over lateral
o To determine metabolism of medication (liver
lobes if thyroid enlarged; due to hyperdynamic circulation)
function)
o Allergies: to address possible drug reactions Special Tests
o OB-GYNE: miscarriage, infertility, menstrual • Deep Tendon Reflexes
changes o Delayed in hypothyroidism (slow relaxation
phase)
FAMILY HISTORY: history of thyroid disorders o Hyperreflexia in hyperthyroidism
• Pemberton’s Maneuver (Superior Vena Cava
syndrome: symptoms due to obstruction)
SOCIAL
Diet (iodine deficiency) o Substernal goiter (goiter in thoracic inlet)
o Ask patient to lift both arms up until they touch
Smoking
the sides of the face
o Positive: facial congestion and cyanosis

COMMON SYMPTOMS OF THYROID DISEASE COMMON SIGNS OF THYROID DISEASE
PRIMARY PRIMARY
HYPERTHYROIDISM HYPOTHYROIDISM HYPERTHYROIDISM HYPOTHYROIDISM
High T4/T3; Low TSH Low T4/T3; High TSH
• Nervousness • Fatigue, lethargy • Warm, smooth moist skin • Dry, coarse skin
• Weight loss despite • Modest weight gain with • Increased systolic and • Cool peripheral extremities
increased appetite poor appetite decreased diastolic BP • Puffy face, hands, feet
• Excessive sweating and • Dry, coarse skin and cold • Tachycardia (myxedema)
heat intolerance intolerance • Hyperdynamic cardiac • Diffuse alopecia
• Palpitations • Swelling of face, hands, pulsations with • Bradycardia
• Frequent bowel and legs accentuated S1 • Peripheral edema
movements • Constipation • Tremor and proximal • Delayed tendon reflexes
• Muscle weakness of • Muscle cramps, arthralgias muscle weakness • Carpal tunnel syndrome
proximal muscles and • Changes in memory and • Graves: ophthalmopathy • Serous cavity effusions
tremors hearing (exophthalmos, lid lag,
stare) and thyroid
dermopathy or pretibial
myxedema (swelling)
LYMPH NODE LEVELS OF THE NECK

Boundaries of the Triangles of the Neck
Level Superior Inferior Anterior Posterior
IA – Submental Symphysis of mandible Body of hyoid Anterior belly of contralateral Anterior belly of ipsilateral
digastric muscle digastric muscle
IB- Submandibular Body of mandible Posterior belly of muscle Anterior belly of digastric Stylohyoid muscle
muscle
IIA Skull base Inferior body of the hyoid bone Stylohyoid muscle Spinal accessory nerve
IIB Skull base Inferior body of the hyoid bone Spinal accessory nerve Lateral border of the SCM
III Inferior body of hyoid Inferior border of the cricoid Lateral border of the Lateral border of the SCM
cartilage sternohyoid muscle
IV Inferior border of the cricoid Clavicle Lateral border of the Lateral border of the SCM
cartilage sternohyoid muscle
VA Apex of the convergence of the Lower border of the cricoid Posterior border of the SCM Anterior border of the trapezius
SCM and trapezius muscles cartilage muscle
VB Lower border of the cricoid Clavicle Posterior border of the SCM Anterior border of the trapezius
cartilage muscle
VI Hyoid bone Suprasternal notch Common carotid artery Common carotid artery

DISEASE PATHOGENESIS DIAGNOSIS TREATMENT
COURSE
THYROID DISEASE
• Increase in BMR: flushing, heat • Graves’ Disease: most common • Serum TSH assay: most useful single Anti-Thyroid Drugs
intolerance, weight loss despite cause of endogenous screening test for hyperthyroidism • Thioamides
increased appetite hyperthyroidism; autoimmune, genetic o Normal rules out thyroid pathology o Inhibits thyroid-peroxidase, thereby
• Cardiac manifestations are the susceptibilities, results to production of • FT4 used to confirm diagnosis blocking iodination and coupling steps
earliest and most consistent feature multiple circulating antibodies • Radioiodine uptake (I-131): measures (deprives thyroglobulin of iodine, stops
(tachycardia, palpitations) o 20-40yo, females thyroid gland activity synthesis of thyroid hormones;
• Overactivity of sympathetic o Triad: hyperthyroidism • Thyroid ultrasound: monitoring nodule incapable of reducing goiter size)
nervous system: tremor, (hyperfunctioning, diffuse thyroid size, guide for FNAB o Methimazole/thiamazole (MMI)
hyperactivity, emotional lability, enlargement), infiltrative § DOC for hyperthyroidism except
anxiety, inability to concentrate, ophthalmopathy with exophthalmos, Findings: in: pregnancy, methimazole
diarrhea, staring gaze, lid lag pretibial myxedema (localized, Hyperthyroidism intolerance, thyroid storm
• Proximal muscle weakness, infiltrative dermopathy) • Primary hyperthyroidism: low TSH, § Methimazole is 10x more active
decreased muscle mass o Symmetrical enlargement high FT4 and has a longer half-life
• Osteoporotic lesions: increased • Toxic multinodular goiter • Graves: homogenously increased tracer o Propylthiouracil (PTU)
bone resorption o Irregular enlargement due to uptake § PTU has an additional MOA:
• Thyroid storm: abrupt onset of recurrent episodes of hyperplasia • Toxic Adenoma: presents with a hot inhibits peripheral conversion of
severe hyperthyroidism (common in and colloid involution nodule, focal areas of increased uptake T4 to T3 by inhibiting deiodinase
Graves) due to acute elevation in o When hyperfunctioning, causes • Toxic Multinodular goiter: multiple enzyme
catecholamines à febrile, Plummer syndrome areas of increased/decreased uptake § Used for thyroid storm due to
tachycardia, medical emergency (hyperthyroidism without additional MOA and faster onset
Hyperthyroidism • Goiter and mass effects: airway ophthalmopathy and dermopathy) Hypothyroidism § Less placental transfer than MMI
obstruction, dysphagia, neck-vein o Mass effects • FT4 levels decreased in hypothyroid of o ADRs: urticaria (most common),
enlargement • Toxic adenoma any origin agranulocytosis (rare, most
o Benign tumor that produces thyroid • Primary: TSH increased dangerous)
hormones and causes thyrotoxicosis • Secondary (hypothalamus, pituitary): • High dose iodides: iodinated contrast
TSH normal o Wolff-Chaikoff effect: excess iodide
transiently inhibits organification of
iodine
• Non-selective beta-blockers:
propranolol preferred
o Inhibit peripheral conversion of T4
(deiodination)
o For patient with tremors, palpitations,
diarrhea
o Contraindicated in asthma
• Corticosteroids: inhibit peripheral
conversion of T4, immunosuppression of
antibodies in Graves
DEFINITIVE: Radioactive iodine therapy
and Surgery
o Disadvantage: hypothyroidism
• Cretinism: hypothyroidism in • Endemic (Iodine Deficiency): most • Replacement of deficient hormone
infancy or early childhood common cause worldwide • Synthetic levothyroxine (T4): DOC
o Impaired skeletal system and • Hashimoto’s Thyroiditis: most because of stability, uniform content, low
CNS: severe mental retardation, common cause in iodine-sufficient cost, long half-life (7 days), and
short stature, coarse facial countries conversion to T3
Hypothyroidism
features, protruding tongue, o Autoimmune destruction of the o T4 is less active so less side effects
umbilical hernia gland leading to thyroid failures compared to giving T3
• Myxedema aka Gull disease: § Cytotoxic T cell and cytokines
older children o CTLA4, PTPN22 mutations
o Breakdown in self-tolerance

o Fatigue, sluggishness, decreased
sympathetic stimulation,
shortness of breath, increased
total cholesterol

COURSE
DIABETES MELLITUS
• Hyperglycemia: usually manifests • Dysfunction in regulatory T cells leading • Criteria for diagnosis of type 1 & 2 • Treatment depends on severity
during childhood and adolescence, to breakdown in self-tolerance to islet diabetes: Any of the ff • Lifelong insulin therapy
but can now manifest at any age auto-antigens o Fasting plasma glucose (FPG): o Short acting: regular human insulin
• Polyphagia, polyuria, polydipsia o Autoimmune disorder (autoreactive § Pre-diabetic: 100 – 125 mg/dL o Rapid acting: insulin analogs (lispro,
• Weight loss T cells) § Diabetic: 126 mg/dL or higher (7.0 glulisine, aspart)
• More common sequelae: (without o Pancreatic beta cell destruction mmol/L) o Intermediate acting: NPH
insulin) Diabetic ketoacidosis o Absolute insulin deficiency o 2-hr plasma glucose after OGTT: o Long acting: glargine, detemir
• Insulitis (inflammatory infiltrate of T • Genetic factors: Multiple genetic § Pre-diabetic: 140 – 199 mg/dL o Ultra long acting: degludec, glargine
cells and macrophages) susceptibility loci § Diabetic: 200 mg/dL or higher (11.1 U-300
Type 1 o β-cell depletion, islet atrophy o Chromosome 6p21: HLA-DR3 or mmol/L) • Self-monitoring of glucose levels
Diabetes Mellitus o Progressive decrease in insulin HLA-DR4 haplotype o HbA1c: • Diet management
levels • Environmental Factors § Pre-diabetic: 5.7-6.4% o Timing, size, frequency and
o Viral infections trigger islet cell § Diabetic: > 6.5% composition of meals
Physical Examination destruction o Random plasma glucose: o To avoid hypoglycemia / post prandial
• Labored breathing (Kussmaul • Associated with mumps, rubella, § > 200mg/dL WITH classic hyperglycemia
respiration) in diabetic coxsackie B, CMV symptoms of hyperglycemia or o Managing chronic hyperglycemia
ketoacidosis hyperglycemic crisis • Exercising regularly is necessary
• Hemorrhage, exudates, retinopathy o Systemic effects on blood glucose
on fundoscopy level
• Lower extremity paresthesia
• Hyperglycemia • Insulin resistance and abnormal • Multiple targets: Glycemia, lipids, blood
• Usually adult onset; increasing insulin secretion pressure
incidence in childhood and o Failure of target tissues (liver, skeletal • Most common cause of mortality:
adolescence; lifestyle disease muscle, adipose tissue) to respond Macrovascular and microvascular
o Many afflicted (80%) are obese normally to insulin complications
• Often asymptomatic o Inadequate secretory response by o Control of glycemia and blood
• If symptomatic: polyphagia, beta cells pressure
polyuria, polydipsia, and weight • Relative insulin deficiency § Limiting eye and kidney
loss • Environment: sedentary lifestyle and complications (micro)
• Acanthosis nigricans, PCOS (“Westernized”) dietary habits § Neurologic risk reduction
• More common sequelae: o Obesity: most important § Appropriate self-monitoring of blood
Hyperglycemic hyperosmolar environmental factor glucose
Type 2 Diabetes state • Genetic Factors: first-degree relative o Lipid control, hypertension, smoking
Mellitus • No insulitis; amyloid deposition in with T2DM confers 5-10x risk cessation, aspirin therapy
islets • Multiple obesity-associated factors § Limiting coronary, cerebrovascular,
o Mild β-cell depletion (circulating non-esterified fatty acids, peripheral vascular complications
inflammatory mediators, (macro)
Physical Examination adipocytokines) linked to pathogenesis o All of these include dietary and
• Blood pressure measurement will of insulin resistance exercise (lifestyle) modifications
most probably disclose • Symptomatic treatment
hypertension • Glycemia: Oral anti-diabetic agents
• Orthostatic vital signs may be o Metformin (Biguanide)
useful in suggesting presence of § Decreases hepatic gluconeogenesis
autonomic neuropathy production and improves peripheral
• Retinopathy often worse due to glucose uptake/utilization
delayed diagnosis § Generally low side effects

o Capillary microaneurysms, retinal • Hypertension: ACE inhibitors, ARBs
ischemia (cotton wool spots), o Because of proven renal protection
hemorrhages, neovascularization • Dyslipidemia:
o Diet & exercise
o Carvedilol (Beta blocker)

COURSE
OTHER ENDOCRINE DISORDERS
• Early hypertension and weight gain • Exogenous/Iatrogenic: most common • Increased 24h urine free-cortisol Exogenous: gradual withdrawal of steroid
• Truncal obesity, moon facies, cause; due to administration of concentration (rapid removal may precipitate adrenal
buffalo hump glucocorticoids • Loss of normal diurnal pattern of cortisol insufficiency)
• Decreased muscle mass and o Bilateral cortical atrophy due to secretion
weakness of proximal limbs lack of stimulation of zona • Dexamethasone suppression test Endogenous: Surgical resection of
• Skin is thin, fragile, and easily fasciculata and reticularis by causative tumor
bruised; red/purple abdominal endogenous ACTH Imaging Studies
striae; poor wound healing • Endogenous (ACTH-dependent) • (after biochemical evaluation) Agents that inhibit steroidogenesis:
• Osteoporosis, backaches, o High ACTH, high cortisol • Abdominal CT recommended if primary Mitotane, Ketoconazole, Metyrapone,
fractures o Mostly caused by ACTH-producing adrenal problem is suspected Aminoglutethimide, Trilostane, Etomidate
Cushing’s Syndrome • Increased risk of infections due to pituitary adenoma (Cushing’s • Contrast-enhanced MRI study of
Hypercortisolism immune suppression of disease) pituitary gland if pituitary adenoma is
glucocorticoids o Ectopic corticotrophin secretion suspected
• Mental abnormalities (mood (e.g., SCC of the lung) • Chest and abdominal CT: ectopic
swings, depression, frank o Both causes will result in bilateral ACTH production
psychosis) cortical hyperplasia
• Hirsutism, menstrual irregularity • Endogenous (ACTH-independent)
• Secondary diabetes o High cortisol, low ACTH
(hyperglycemia, glucosuria, o Primary adrenal neoplasms
polydipsia) (adenoma, carcinoma)
o Macronodular hyperplasia
Pertinent Hx: Steroid use
Women: amenorrhea, infertility, Hyperprolactinemia due to secretion by • PRL > 100 ug/L Mainly MEDICAL treatment through oral
galactorrhea functional pituitary adenoma • Negative pregnancy test dopamine agonists: suppress PRL
Men: impotence, loss of libido, CNS • Prolactinoma is the most common • TSH abnormal secretion
compression, headache functional pituitary tumor • Pituitary MRI: suprasellar mass with • Bromocriptine: short-acting; rapidly
• Female:Male ratio is 20:1 for compression of the optic chiasm lowers PRL levels
microprolactinoma (<1cm) and 1:1 Other causes: o Tumor size generally correlates with o Preferred drug when pregnancy is
for macroadenomas (>1cm) • Physiologic hyperprolactinemia: PRL concentrations desired
• Men present with larger tumors pregnancy (peaks at delivery); nipple o Decreases tumor size and restores
than women stimulation; stress gonadal function
• Pathologic hyperprolactinemia: o Most common problem is intolerance
Prolactinoma
Compressive Effects lactotroph hyperplasia, interference (nausea, vomiting, hypotension)
Hyperprolactinemia
• Headache with dopamine inhibition (damage to • Cabergoline: long-acting dopamine
(due to functional
• Visual field defects if tumor dopaminergic neurons of pituitary stalk, agonist
pituitary adenoma)
extends outside the sella drug intake, mass in suprasellar o Suppresses PRL for >14 days after a
(bitemporal hemianopsia) compartment) single dose
• Drug-induced (dopamine antagonists) o Normalizes gonadal function,
• Estrogen, renal failure, hypothyroidism improves or resolves galactorrhea,
induces prolactinoma shrinkage
Indications for Surgery (transsphenoidal)

• Persistent intolerance or tumor
resistance to dopamine agonists
• Pituitary apoplexy

• Tumor growth during medical therapy
• CSF leakage due to invasive tumors
Primary Hyperparathyroidism • Primary: autonomous overproduction • Blood test: comparing PTH to serum Primary
• Often asymptomatic of PTH calcium • Parathyroidectomy: reduces mortality
o Clinically silent hypercalcemia o Parathyroid adenoma: most o Primary: High PTH with high calcium and morbidity
is the most common common cause indicates a parathyroid problem o Indicated even for asymptomatic
manifestation § Sporadic: MEN1, Cyclin D1 o Secondary: High PTH and low patients with:
o Inappropriate elevation of PTH mutations calcium indicates pathology § Ca >1.0mg/dL
2+
for level of serum calcium, § Familial: MEN1 and MEN2 elsewhere § Creatinine clearance <40mL/min
hypophosphatemia, increased o Primary hyperplasia o Normal PTH: 10-55 ng/mL § <50yo
urinary excretion of calcium o Parathyroid carcinoma • Parathyroid adenoma § Bone density more than 2.5 SDs
Hyperparathyroidism and phosphate • Secondary: compensatory PTH o Tc99 sestamibi scan below average
hypersecretion in response to o UTZ and FNAB • Bisphosphonates: inhibits osteoclasts
prolonged hypocalcemia, usually due • Estrogen replacement if post-
to chronic renal failure menopausal
• Tertiary: persistent PTH oversecretion
despite normal calcium levels, usually Secondary
after renal transplant or long-term • Address underlying cause of
dialysis hypocalcemia
• Supplement with Vitamin D (calcitriol)
and phosphate binders

COURSE
OTHER ENDOCRINE ORGANS
• Symptomatic hypercalcemia:
usually due to malignancy
o PAINFUL BONES (bone
problems, fractures due to
osteoporosis)
o KIDNEY STONES (pain and
obstructive uropathy)
o ABDOMINAL GROANS
(constipation, nausea, peptic
ulcer, pancreatitis)
o PSYCHIC MOANS
Hyperparathyroidism
(depression, lethargy, seizures)
(continued)
Secondary Hyperparathyroidism
• Excessive PTH secretion in
response to hypocalcemia
(tetany, neuromuscular irritability)
• Decreased phosphate excretion
resulting to hyperphosphatemia
• Symptoms are dominated by renal
failure
• Calciphylaxis: vascular
calcification
METABOLIC SYNDROME
Major features IDF Definition (2005): • Weight reduction is the primary
• Insulin resistance
Metabolic Syndrome • Central adiposity • Central obesity defined by waist approach
o Normal concentration of insulin
(syndrome X, insulin • Hypertriglyceridemia circumference o Caloric restriction, increased physical
produces less than normal biological
resistance syndrome) • Low HDL o South Asians: >90 cm (males) or activity (60-90 mins/day)
response
• Hyperglycemia >80 cm (females) • Pharmacologic agents

• Hypertension o Onset is heralded by postprandial o Americans: ≥102 cm (40 in) in men or o Appetite suppressants: Phentermine
hyperinsulinemia, followed by fasting ≥88 cm (35 in) in women o Absorption inhibitors: Orlistat
Typically asymptomatic but the ff hyperinsulinemia, and ultimately by • PLUS any TWO of the following: o LDL lowering drugs: Statins,
may be seen on physical exam: hyperglycemia o Raised triglycerides Ezetimibe, Cholestyramine, Fibrates,
• Expanded waist circumference o Overabundance of circulating fatty § >150 mmol/L Nicotinic acid
• Elevated blood pressure acids § (or specific treatment for this lipid o Antihypertensive drugs: ACE
• Lipoatrophy § Insulin mediates both anti-lipolysis abnormality) inhibitors or ARBs
• Acanthosis nigricans, hirsutism, and the stimulation of lipoprotein o Reduced HDL o For blood sugar
menstrual irregularities lipase in adipose tissue § <40 mg/dL (males) control/improvement of insulin
• Peripheral neuropathy, retinopathy § When insulin resistance develops, § <50 mg/dL (females) resistance: Metformin,
• Chest pain or shortness of breath increased lipolysis produces more § (or specific treatment for this lipid Thiazolidinediones
(CV complications) fatty acids, which further decrease abnormality)
• Xanthomas, xanthelasmas (severe the anti-lipolytic effect of insulin o Raised blood pressure
dyslipidemia) • Leptin resistance § Systolic >135 mmHg or diastolic
• Oxidative stress hypothesis >85 mmHg
§ (or treatment for hypertension)
o Raised fasting plasma glucose
§ >100 mg/dL
§ (or previously diagnosed T2DM)

MODULE/TOPIC 13 PSYCHIATRY

This part focuses more on history taking and inspection/palpation for PE J
HISTORY
Some concepts: Developmental and Social History / Anamnesis
• Transference – patient unconsciously projects or displays onto the • Early childhood (Birth to 3 years old)
physician his or her feelings from persons from his or her past o Prenatal history and mother’s pregnancy and delivery
• Countertransference - physician unconsciously displaces onto the patient o Feeding habits
patterns of behaviors or emotional reactions as if he or she were a o Early development
significant figure from earlier in the physician’s life § Language and Motor development
§ Sleep pattern
HPI § Stranger and Separation anxiety
• Onset and duration of current episode § Object constancy
• Other symptoms o Toilet training
• Stressors o Symptoms of behavioral problems
• Alleviating/Exacerbating symptoms § Thumb sucking
• Severity § Temper tantrums
o Changes in functionality (interest, interpersonal relationships, personal § Sleep pattern
habits, physical health) § Stranger and Separation anxiety
• Why seek help now? § Object constancy
• Rule out other psychiatric conditions o Toilet training
o Mood, Anxiety, Psychosis, Substance Abuse Disorders, etc o Personality and temperament as a child
• Middle childhood (3-11)
Past Psychiatric History o Early school history
• Past symptoms/episodes • Late childhood (prepuberty through adolescence)
• Past treatments (medications and their side effects) o Peer relationships
• Past diagnosis o School history
o Cognitive and motor development
Substance Use, Abuse, Addictions o Particular adolescent emotional or physical problems
• CAGE questionnaire § Nightmares
o C – Have you ever felt the need to cut down on your alcohol drinking? § Phobias
o A – Have you ever been annoyed when somebody criticizes you about § Masturbation
your drinking? § Bed-wetting
o G – Have you ever felt guilty because of your drinking? § Running away and delinquency
o E – Have you ever felt that in the morning you have to drink just to get § Smoking, drug or alcohol use,
through the day (eye-opener)? § Weight problems
§ Feeling of inferiority
o Psychosexual history
Past Medical History
o Religious background
• Important to know patient’s medical illnesses because they can precipitate
• Adulthood
or mimic a psychiatric disorder and may influence the choice of
o Occupational history
treatment
o Social activity
o Adult sexuality
Family History
o Military history
• A lot of psychiatric illnesses are familial
o Value systems
MENTAL STATUS EXAMINATION

• Psychiatric equivalent of physical examination
• Must not be confused with MMSE in neurological exam
o Tests for cognitive impairment
• Must not be confused with MMSE in neurological exam
Appearance and • General description of how patient acts during interview

Behavior • Appears of stated age? Appropriateness of attire, grooming, hygiene
Motor Activity • Normal, slowed, or agitated
• Gait, limitations in movements, posturing
• Tics, mannerisms, stereotypies
Speech • Fluency
• Production
• Rate
• Tone and volume
Mood and Affect • Mood – refers to the patient’s internal and sustained emotional state
• Affect – refers to the expression of the mood/what the mood of the patient appears to be to the clinician
Thought Content • Obsessions - unwelcome and repetitive thought that intrude into the patient’s consciousness
• Delusions -fixed, false beliefs that are not shared by others
o Eratomanic, Grandiose, Persecutory, Jealous
• Suicidality or homicidality
Thought Process • Normal – linear, goal-directed, organized
• Circumstantiality - overinclusion of trivial or irrelevant details that impede the sense of getting to the point
• Clang associations – thoughts are associated by sounds of words rather than by their meaning
• Flight of ideas – succession of multiple associations so that thoughts seem to move abruptly from idea to idea
• Neologisms – invention of new words or phrases or use of conventional words in idiosyncratic ways
• Thought blocking – sudden disruption of thought or a break in the flow of ideas
• Perseveration – repetition out of context words, phrases or ideas
• Tangentiality – giving a reply that that is appropriate to the topic without actually answering the question
• Derailment / Looseness of Association – breakdown in both the logical connection between ideas and the overall sense of goal-
directedness
• Word salad – confused, often repetitious, language with no apparent
Perceptual Disturbances • Hallucinations – perception in the absence of stimuli
o Auditory – most common
• Illusions – misperceptions of stimuli
• Derealization and Depersonalization
Cognition • Level of consciousness, orientation, concentration, memory, calculation, fund of knowledge
Abstract Reasoning • Ability to shift back and forth between general concepts and specific examples

• Identifying similarities, interpreting proverbs, educational factors and limitations
Judgement • Capacity to make good decisions and act on them
• Test judgment and social judgment
Insights • Degree of personal awareness and understanding of disease
• Grading:
o 1 – complete denial
o 2 – slight awareness but still denying
o 3 – blames others
o 4 – intellectual insight
o 5 – true emotional insight

PART 13B. PSYCHIATRY ILLNESS
DISEASE SYMPTOMS PATHOGENESIS/ETIOLOGY TREATMENT
• Sad mood or loss of pleasure in usual activities • Biological causes • Medication along with psychotherapy
• At least five symptoms experienced nearly every day, ○ Biochemical imbalance • Pharmacological
most of the day at least two weeks (Mnemonic: SPACE ○ Genetic ○ SSRIs
WD) ○ Sleep abnormalities § Fluoxetine, Sertraline, Paroxetine, Fluvoxamine, Escitalopram
○ Sleeping too much or too little ○ Neuroanatomical abnormalities ○ SNRIs
○ Psychomotor retardation or agitation ○ Neurological and medical causes § Venlafaxine, Duloxetine
○ Change in Appetite or weight loss ○ Pharmacological ○ NaSSA
○ Difficulty Concentrating • Psychological Causes § Mirtazapine
Major Depressive Disorder
○ Loss of Energy ○ Internalizing stress ○ Tricyclic Antidepressants
○ Feelings of Worthlessness or excessive guilt ○ Psychosocial triggers § Imipramine, Amitriptyline, Clomipramine, Trimipramine
○ Recurring thoughts of Death or suicide ○ Transitional states ○ Monoamine Oxidase Inhibitors
○ Learned helplessness • Psychological
○ Personality types ○ Psychoanalytic
§ Dependent and Obsessive-compulsive personality ○ Cognitive therapy
types are prone to depression ○ Interpersonal
○ Family therapy
• Manic symptoms – defining feature • Biological causes • Pharmacological
○ Excessively “high”, overly good, euphoric mood ○ Biochemical imbalance in neurotransmitters (serotonin ○ Mood stabilizers
○ Extreme irritability and dopamine) § Lithium, Divalproex, Carbamazepine, Lamotrigine, Topiramate
○ Inflated self-esteem or grandiosity ○ Decreased sleep time ○ Atypical antipsychotics
○ Decreased need for sleep, without fatigue ○ Kindling § Olanzapine, Quetiapine, Aripiprazole, Risperidone
○ More talkative than usual or pressured speech ○ Genetic • Psychosocial Therapy
○ Racing thoughts • Psychosocial causes ○ Psychotherapy
○ Distractibility ○ Life events and environmental stress ○ Cognitive Behavioral Therapy
○ Physical agitation ○ Psychological (defense against depression, strict ○ Psychoeducation
○ Poor judgment about activities superego, ego overwhelmed by impulses ○ Family Therapy
Bipolar Mood Disorder • Mania – state if intense elation or irritability accompanied ○ Interpersonal / Social Theory
by other symptoms shown in the diagnostic criteria
• Hypomania – less extreme form of mania
• Bipolar I – Includes a single episode of mania during the
course of a person’s life
• Bipolar II – includes experiencing at least one major
depressive episode and at least one episode of hypomania
• Cyclothymia - has frequent but mild symptoms of
depression, alternating with mild symptoms of mania
present for at least 2 years
• Psychosis – state in which the person’s thoughts, affective • Biological causes • Goal is to reduce suffering from mental disorders, reduce symptoms
response, ability to recognize reality, and ability to ○ Genetic – single largest risk factor and improve functioning and quality of life
communicate and relate to others are sufficiently ○ Dopamine hypothersis • Biological Therapy
impaired ○ Glutamatergic hypothesis ○ Typical Antipsychotics – Chlorpromazine, Haloperidol,
• Common characteristics of psychosis: • Neuropathology Levomepromazine, Fluphenazine
○ Hallucinations – false sensory perception without any ○ Neurochemical abnormalities in limbic system, basal ○ Atypical Antipsychotics – Olanzapine, Clozapine, Risperidone,
stimuli ganglia, cerebral cortex, thalamus and brainstem Quetiapine, Amisulpride, Aripiprazole, Ziprasidone, Asenapine,
§ Auditory – most common in psychiatric • Psychoanalytic causes Paliperidone
disorders ○ Resulted from early developmental fixations (Freud) • Psychotherapies
○ Delusions ○ Distortions in reciprocal relationship between infant and • Social Interventions
Schizophrenia ○ Disorganized thinking (Speech) – disturbance in the flow mother (Mahler)
of thoughts or in the content of thoughts ○ Disturbance in interpersonal relatedness (Sullivan)
○ (Gross) Disorganized behavior – abnormal motor • Learning Theories
behavior • Family Theories
• Negative symptoms
○ Diminished emotional expression
○ Avolition
○ Alogia
○ Anhedonia
○ Asociality

DISEASE SYMPTOMS PATHOGENESIS/ETIOLOGY TREATMENT
• Panic Attack – abrupt onset of an episode of intense fear • Biological causes • Pharmacological Therapy
of discomfort which peaks in approximately 10-15 minutes ○ Genetics ○ SSRIs
• Includes at least four of these symptoms: • Neuropathology § Escitalopram, Fluoxetine, Sertraline, Citalopram, Paroxetine
○ Feeling of imminent danger or doom ○ Neurotransmitter imbalances (Norepinephrine, GABA, ○ Buspirone
○ Need to escape serotonin) ○ Benzodiazepines
○ Palpitations • Life circumstances § Alprazolam, Diazepam
○ Sweating • Personality factors • Behavioral and Cognitive Therapy
○ Trembling ○ With low self-esteem and poor coping skills ○ Teaches patients to react differently
○ Shortness of breath or a smothering feeling • Medical Causes ○ Breathing exercises
Panic Disorder ○ Feeling of choking ○ Hyperthyroidism, Vit B12 deficiency, Hypoxia, ○ Desensitization for Phobias
○ Chest pain/discomfort Neurological disorders, Cardiovascular disease, Anemia, ○ Alternative treatments
○ Dizziness/lightheadedness Pheochromocytoma, Hypoglycemia § Acupuncture, Aromatherapy, Exercise, Meditation, Diet and
○ Sense of things being unreal, depersonalization • Substances which induce anxiety Nutrition, Vitamins
○ Fear of losing control ○ Caffeine
○ Fear of dying ○ Amphetamines
○ Tingling sensations ○ Alcohol and sedative withdrawal
○ Chills or hot flushes
○ Rash

MODULE/TOPIC 14 ORTHOPEDICS (MSK)

HISTORY
• If patient complains of pain, ask patient to locate/point to the afflicted area (b) Common relieving factors
• If there is a history of trauma, ask the patient to describe the mechanism of (i) Pain killers (specify)
injury (ii) Rest
• Determine if complaint is: (iii) Ice
o Acute vs. Chronic (6 weeks) (iv) Compression
o Articular vs Non-articular (v) Elevation
o Inflammatory vs. Non-inflammatory • Determine if there’s inflammation
• Assess: o Cardinal signs
o Location § Pain
o Timing § Redness
o Inflammation § Swelling
o Swelling or stiffness § Heat
o Systemic manifestations § Loss of function
• Common locations of pain: o Ask for any history of infections (fever, chills)
§ Joints • Determine if there are associated systemic manifestations
- Assess if single or multiple joints are affected • Also inquire about the following:
(a) If multiple, ask for pattern of involvement (all at the same time, o Exercise
migratory) o Nutrition/Diet
- Assess if unilateral or bilateral o Weight
- Ask for associated pain (extra-articular) o Age
(a) Myalgia – muscles o If female: ask if already in menopause
(b) Arthralgia – pain with no evidence of arthritis (inflammation)
(c) Bursitis, tendinitis, tenosynovitis (tendon sheath), sprains Take note of the following risk factors for Osteoporosis:
§ Neck o Postmenopausal status of women
- Radiation to arms or legs o Age older than 50
- Weakness or paresthesia o Weight less than 70kg
§ Lower back o Family history of fracture in a first-degree relative
- Assess if pain is midline, over the vertebrae, or off-midline o History of fracture
- Ask for associating numbness or paresthesia on lower o High intake of alcohol
extremities o Women with delayed menarche or early menopause
- Associated bladder or bowel dysfunction o Current smokers
• Assess the timing of the pain o Low levels of 25-hydroxyvitamin D
o Progression o Use of corticosteroids for more than 2 months
§ Rapid or slow development o Inflammatory disorders
§ Fluctuation in pain severity
§ Particular timing (in the morning, as the day progresses, at night) *Tip: Make sure to remember the proper name of major joints in the body
o Aggravating or relieving factors
(a) Common aggravating factors
(i) Walking
(ii) Side stepping
(iii) Bearing weight (standing, jumping)
(iv) Flexion or extension
PHYSICAL EXAMINATION
A. INSPECTION III. Spine
I. General Inspection Note for:
• Mood • Scoliosis – abnormal sideward curvature of the spine
• Signs of pain or discomfort • Kyphosis – abnormal outward curvature of the upper thoracic vertebra
• Functional Impairments (“humpback” or “round back”)
• Evidence of malingering (Waddell Signs) • Lordosis – abnormal inward curvature of the lumbar spine
o Physical signs indicating non-organic or physiologic component of pain B. PALPATION
II. Limbs • Palpate over the muscular groups overlying each joint area
• Symmetry • Joints and soft tissues should be assessed for the following:
• Circumference o Effusion
• Contour o Warmth
• In persons with amputation, assess the residual limb for the following: o Masses
o Level o Tight muscle bands
o Length o Tone
o Shape o Crepitus
• Depending on the clinical situation, assess for the following: C. RANGE OF MOTION
o Muscle atrophy • Determine what type of joint (hinge, ball and socket, etc.) and actively move
o Masses the joint through its range of motion
o Edema D. MUSCLE TONE
o Scars, skin breakdown, and fasciculations E. MUSCLE STRENGTH (Grading):
• Identify and assess the following: Grade 5: The muscle can move the joint crossing through a full range of motion,
o Shoulder: shoulder girdle and clavicle; scapulae against gravity, and against full resistance applied by the examiner.
o Elbow: contours of the elbow including extensor surface of the ulna and Grade 4: The muscle can move the joint crossing through a full range of motion
the olecranon process against moderate resistance.
o Wrist: observe hand in motion, must be smooth and natural Grade 3: The muscle can move the joint crossing though a full range of motion
o Fingers: slightly flexed and aligned and almost parallel, check for Bouchard’s against gravity, but without any resistance.
and Heberden’s nodules Grade 2: The muscle can move the joint crossing through a full range of motion
o Hip: observe gait; lumbar portion of the spine only if gravitational force is eliminated.
o Knee: in normal gait, knee should be extended at heel strike and flexed at Grade 2: Muscle contraction is seen or identified with palpation, but it is
other phases; knee joint should normally have hollows around it, absence insufficient to produce joint motion even with elimination of gravity.
indicates swelling Grade 1: No muscle contraction is seen or identified with palpation; paralysis.
o Ankle and Foot: observe surface of the ankle F. SPECIAL TESTS (SEE NEXT SECTION)

SPECIAL TESTS AND COMMON MUSCULOSKELETAL INJRUIES
Must-know for YL6 OSCE!
Shoulders Rotator Cuff Tear Empty can/ Supraspinatus A positive test is pain or weakness in the
test ipsilateral shoulder with resisted abduction of the
Mechanism of injury shoulder, which is in internal rotation, with the
o Commonly degeneration (age), thumb pointing toward the floor, and a forward
impingement, or overload angulation of 30 degrees.
o High frequency of tears seen in
activities requiring overhead
activity (throwing, volleyball,
badminton, etc.)
Drop arm test A positive test is noted if the patient is unable to

return the arm to the side slowly or has severe
pain after the examiner abducts the patient’s
shoulder to 90 degrees and then asks the patient
to slowly lower the arm to the side.
Wrist and Carpal Tunnel Syndrome Carpal compression test This test consists of gentle, sustained, firm
Hands pressure to the median nerve of each hand
Mechanism of Injury simultaneously. Within a short time (15 seconds
o Increased pressure in the intracarpal to 2 minutes) the patient will complain of
canal reproduction of pain, paresthesia, and/or
o Occupational factors numbness in the symptomatic wrist(s).
§ Repetitive or forceful hand or wrist
use
§ Sustained wrist or palm pressure
Phalen test (wrist flexion) This test is positive if there is numbness and
paresthesia in the fingers. The patient is asked
to hold the forearms vertically and to allow both
hands to drop into flexion at the wrist for
approximately 1 minute.

Wrist extension test The patient is asked to keep both wrists in
(reverse Phalen test) complete dorsal extension for 1 minute. If
numbness and tingling were produced or
exaggerated in the median nerve distribution of
the hand within 60 seconds, the test is judged to
be positive.
Tinel’s sign This test is positive if there is numbness and

paresthesia in the fingers. It is done by
extending the wrist and tapping in a proximal to
distal direction over the median nerve as it
passes through the carpal tunnel, from the area
of the distal wrist crease, 2 to 3 cm toward the
area between the thenar and hypothenar
eminences.
De Quervain Tenosynovitis Finkelstein test This test is positive if there is pain at the styloid
process of the radius as the patient places the
Mechanism of Injury thumb within the hand, which is held tightly by
o Inflammation of the tendon sheath, the fingers, followed by ulnar deviation of the
usually of the APL and APB d/t hand.
repetitive motion or strain
Adam forward bend test Ask the patient to reach for their toes (not
Scoliosis necessarily touch) Do this with the feet together,
knees straight, arms hanging freely. Check for
the symmetry of the back and for rib
prominences
Spine
Anterior Cruciate Ligament Tear Anterior drawer test The patient is supine, hip flexed to 45 degrees
with the knee flexed to 90 degrees. The
Mechanism of Injury examiner sits on the patient’s foot, with hands
o ACL injuries are sustained by behind the proximal tibia and thumbs on the
§ High-energy (e.g. collisions) tibial plateau. Anterior force is applied to the
§ Low-energy (e.g. quick proximal tibia. Hamstring tendons are palpated
Knee deceleration, hyperextension, or with index fingers to ensure relaxation.
rotational injury) Increased tibial displacement compared with the
opposite side is indicative of an anterior cruciate
ligament tear.

Lachman test The patient lies supine. The knee is held
between full extension and 15 degrees of
flexion. The femur is stabilized with one hand
while firm pressure is applied to the posterior
aspect of the proximal tibia in an attempt to
translate it anteriorly.
Anterior drawer test The patient is supine, hip flexed to 45 degrees

with the knee flexed to 90 degrees. The
examiner sits on the patient’s foot, with hands
behind the proximal tibia and thumbs on the
tibial plateau. Anterior force is applied to the
proximal tibia. Hamstring tendons are palpated
with index fingers to ensure relaxation.
Increased tibial displacement compared with the
opposite side is indicative of an anterior cruciate
ligament tear.
Posterior Cruciate Ligament Tear Posterior sag sign The patient lies supine with the hip flexed to 45
degrees and the knee flexed to 90 degrees. In
this position, the tibia “rocks back,” or sags back,
on the femur if the posterior cruciate ligament is
torn. Normally, the medial tibial plateau extends
1 cm anteriorly beyond the femoral condyle
when the knee is flexed 90 degrees.
Posterior drawer sign The patient is supine with the test hip flexed to
45 degrees, knee flexed to 90 degrees, and foot
in neutral position. The examiner sits on the
patient’s foot with both hands behind the
patient’s proximal tibia and thumbs on the tibial
plateau. Posterior force is applied to the
proximal tibia. Increased posterior tibial
displacement as compared with the uninvolved
side is indicative of a partial or complete tear of
the posterior cruciate ligament.
Patellofemoral Injury Patellar grind test The patient is supine with the knees extended.
The examiner stands next to the involved side
and places the web space of the thumb on the
superior border of the patella. The patient is
asked to contract the quadriceps muscle while
the examiner applies downward and inferior
pressure on the patella. Pain with movement of
the patella or an inability to complete the test is
indicative of patellofemoral dysfunction.

Meniscal Injury McMurray test With the patient lying flat, the knee is first fully
flexed; the foot is held by grasping the heel. The
leg is rotated on the thigh with the knee still in
full flexion. By altering the position of flexion, the
whole of the posterior segment of the cartilages
can be examined from the middle to the
posterior attachment. The leg is brought from its
position of acute flexion to a right angle while the
foot is retained first in full internal rotation and
then in full external rotation. When the click
occurs (in association with a torn meniscus), the
patient is able to state that the sensation is the
same as experienced when the knee gave way
previously.
Apley grind test With the patient prone, the examiner grasps one
foot in each hand and externally rotates as far as
possible, then flexes both knees together to their
limit. The feet are then rotated inward and knees
extended. The examiner’s left knee is then
applied to the back of the patient’s thigh. The
foot is grasped in both hands, the knee is bent
to a right angle, and powerful external rotation is
applied. Next, the patient’s leg is strongly pulled
up, with the femur being prevented from rising
off the couch. In this position of distraction,
external rotation is repeated. The examiner
leans over the patient and compresses the tibia
downward. Again, the examiner rotates
powerfully and if addition of compression
produces an increase of pain, this grinding test
is positive and meniscal damage is diagnosed.
Patellar injury Patellar mobility Test Position the knee in a fully extended position.
Vertically divide the patella into four equal
• Mechanism of injury segment. Visualize where the midline, the
o Direct trauma medial, and the lateral edge of trochlea are.
o Valgus, varus, hyperextension, and Measure the percentage of the patella
twisting motions positioned beyond the midline. Displace the
patella and determine how much can be
displaced past the medial and lateral edge.
Displacement of less than a quarter signifies a
tight retinaculum. Displacement of three-
quarters signifies a hypermobile patella
Achilles Tendon Rupture Tests Thompson test The patient lies in a prone position with the foot
extending over the end of the table. The calf
muscles are squeezed in the middle one third
below the place of the widest girth. Passive
plantar movement of the foot is seen in a normal
reaction. A positive reaction is seen when there
Ankle is no plantar movement of the foot and indicates
rupture of the Achilles tendon.

Palpation test The examiner gently palpates the course of the
tendon. A gap indicates an Achilles tendon
rupture.
Ankle Stability Anterior drawer test With the patient relaxed, the knee is flexed and
the ankle at right angles, the ankle is grasped on
the tibial side by one hand, and the index finger
is placed on the posteromedial part of the talus
and the middle finger lies on the posterior tibial
malleolus. The heel of this hand braces the
anterior distal leg. On pulling the heel forward
with the other hand, relative anteroposterior
motion between the two fingers (and thus
between talus and tibia) is easily palpated and is
also visible to both the patient and examiner.
PART 14B. CLINCIAL CASES:

Common Diseases Clinical Manifestations and Course Pathogenesis Diagnosis Treatment Additional Notes
• Localized pain and swelling, • Majority of mutations are in RB1 and • X-ray: destructive lesion with a moth-eaten • Standard management: • Spindle cell neoplasm that
typically months duration. TP53 genes. appearance, sunburst appearance (spiculated preoperative chemotherapy + produces osteoid or bone
• Palpable soft tissue mass, tender • Can also be seen in the elderly especially periosteal reaction), Codman's triangle (cuff of limb-sparing surgery + • 60% occur in children and
on palpation in those with Paget’s Disease of the periosteal new bone formation at the margin of postoperative chemotherapy adolescents in the second
• Bimodal distribution bone, radiation exposure and bone the mass) • Therapeutic: methotrexate + decade, 10% in the third
• Predilection for metaphyses of long infarction • CT scan: defining bone destruction and doxorubicin + cisplatin regimen decade
bones: distal femur, proximal tibia, calcification pattern (America, Osteosarcoma Study • Predilection for the
Osteosarcoma
proximal humerus, middle and • MRI: intramedullary and soft tissue extension Group). metaphyseal region of the long
proximal femur • Core needle biopsy or open biopsy: carried out • Administer chemotherapy for 10 bones
by orthopedic surgeon, preferably by the same weeks prior to surgery and • Male predilection
surgeon who will perform the definitive surgery. continued for 29 weeks
postoperative.
• Radiation therapy has NO role
(not sensitive to radiation)
• History of vertebral and hip • Results from bone loss due to age, and • Lab: CBC, serum and 24-h urine calcium, renal • For fractures • Reduction in the strength of
fractures imbalance between bone absorption and and hepatic function • Analgesics, NSAIDs, bone that leads to an
• Significant loss of height, lordosis, resorption • Bone biopsy: tetracycline labeling of the acetaminophen, narcotics increased risk of fractures
and kyphosis • Primary osteoporosis skeleton (codeine or oxycodone), internal • Occurs more frequently with
o Height loss >2.5-3.8 cm (>1- o Senile osteoporosis • Biochemical markers: to measure bone or external fixation, increasing age and bone
1.5in) § Decreased osteoblastic and formation or bone resorption arthroplasties, rehabilitation tissue loss
o Post-menopausal kyphosis or osteoprogenitor activity • Bone mineral density (by WHO definition of • For underlying disease: • Menopause precipitates rapid
back pain § Diminished capacity to make bone osteoporosis) by DXA • Risk factor reduction (decrease bone loss
Osteoporosis • Predisposes person to vertebral o Postmenopausal osteoporosis smoking/alcohol intake),
fractures, femoral neck and pelvic § Due to decrease in serum estrogen: calcium, vitamin D
fractures trigger release of cytokines (eg. • Pharmacologic:
TNF) that activate osteoclasts • Bisphosphonates (alendronate,
risedronate), calcitonin, PTH,
§ Increased osteoclastic activity: BMD T-Score Diagnosis estrogen, progestin, selective
increased bone destruction estrogen response modulators
• Secondary osteoporosis T-score ≥ -1 Normal (tamoxifen, raloxifene)
• Due to endocrinopathies, neoplasia,

drugs
-1 > T-score > -2.5 Low bone mass
T-score ≤-2.5
Osteoporosis
T-score ≤-2.5, with

existing fracture Severe osteoporosis
• Commonly affected joints: cervical • Hyaline articular cartilage loss present in • Physical exam • Supportive MOST COMMON type of
and lumbosacral spine, hip, knee, a focal and initially nonuniform manner • X-Ray: Features narrowed joint space, bone o Avoid activities that arthritis
first MTP, distal and proximal • Increasing thickness and sclerosis of the sclerosis, cortical thickening, osteophytes precipitate pain
interphalangeal joints of the hand, subchondral bony plate, outgrowth of • MRI: meniscal tears in cartilage and bone o Exercise
base of the thumb osteophytes at the joint margin, stretching lesions o Correction of misalignment
• Heberden’s (DIP) and of the articular capsule, mild synovitis, • Pharmacotherapy
Bouchard’s nodes (PIP) muscle weakness, meniscal degeneration o Acetaminophen, NSAIDs,
• Pain presents either during or just COX-2 inhibitors
Osteoarthritis after joint use and then gradually • Risk factors o Intra-articular injections:
resolves • Age: >50% over age 70 glucocorticoids and
• Initially: episodic pain triggered by • Genetics: polymorphism within growth hyaluronic acid
overactive use of diseased joint differentiation factor 5 gene (GDF5) • Surgery
• As disease progresses: continuous • Geno varus/valgus • Cartilage regeneration
pain that is bothersome at night • Obesity
• Prominent stiffness of affected joint • Repeated joint use
• Morning stiffness is brief (<30 min)
• Knee buckling, catching or locking
• Early morning stiffness (1hr), • Genetic predisposition • Classification Criteria • NSAIDs • Increased incidence among
easing with physical activity • Environmental factors • Score of ≥6 fulfilling the requirements for definite • Glucocorticoids 25-55 years old, plateaus until
• Symmetric distribution • APCs activating CD4+ T cells à CD4+ RA • Disease-modifying anti- 75 years old, then decreases
• Hallmark: flexor tendon Th cells activating B cells à Some B cells • Based on joint involvement, serology, acute- rheumatic drugs (DMARDs) -
tenosynovitis (“trigger fingers”) differentiate into autoantibody-producing phase reactants (CRP and ESR), and duration include hydroxychloroquine,
• “Swan-neck deformity” - plasma cells of symptoms sulfasalazine, methotrexate,
hyperextension of the PIP joint with • Rheumatoid factors (RFs) and anti–cyclic • Laboratory Features and leflunomide
flexion of the DIP joint citrullinated peptides (anti-CCP) • Serum IgM • Anti-TNF agents
• “Boutonniere deformity” - flexion antibodies, may form inside the joint, • Serum anti-CCP antibodies - most value for • Anakinra - IL-1 receptor
of the PIP joint with hyperextension activating the complement pathway and predicting worse outcomes antagonist
of the DIP joint amplifying inflammation • Synovial Fluid Analysis • Abatacept - CTLA4 linked with
• “Z-line deformity” - subluxation of • Imaging human IgG
the first MCP joint with • Plain Radiograph • Rituximab
Rheumatoid Arthritis
hyperextension of the first o Soft tissue swelling • Tocilizumab
interphalangeal (IP) joint o Symmetric joint space loss
• Constitutional symptoms o Subchondral erosions most frequently in the
• Rheumatoid nodules wrists, hands, and feet
o Firm, non-tender • MRI
o Developing in areas of the o Greatest sensitivity for detecting synovitis and
skeleton subject to repeated joint effusions, and early bone and bone
trauma or irritation such as the marrow changes
forearm, sacral prominences, • Ultrasound
and the Achilles tendon • Able to detect more erosions than plain
o Typically benign radiography, especially in easily accessible
• 10% of patients with RA have joints
secondary Sjogren’s Syndrome
• Gout flare is typically • Transient attacks of acute arthritis • Needle aspiration of synovial fluid: needle- and Acute gouty arthritis • Four clinical phases
monoarticular and intensely initiated by crystallization rod-shaped monosodium urate crystals • NSAIDs, colchicine, o Asymptomatic
inflammatory. • Crystals begin to precipitate within the (strong negative birefringent under polarized glucocorticoids Hyperuricemia
Gout • Often involves the MTPJ of the first joint space, due to: LM) Hypouricemic therapy o Acute Gouty Arthritis
toe § Increase urate input • Urinalysis, serum creatinine, hemoglobin, WBC • Control body weight, low purine o Intercritical Gout
• Also involves tarsal joints, ankles, § Increased in dietary sources, count, liver function tests, serum lipids diet, increase liquid intake, limit o Chronic Tophaceous Gout
endogenous biopsy and purine ethanol/fructose rich food and
knees, Heberden or Bouchard nucleotide degradation • X-ray: cystic changes, erosions with sclerotic beverages, avoid diuretics
nodes in elderly o Problems with excretion margins (overhanging bone edges), soft tissue • Uricosuric agents (probenecid,
• First episode of acute gout: begins • Secondary to a systemic disease masses benzbromarone for renal failure,
at night with dramatic joint pain o X-linked Lesch-Nyhan Syndrome losartan, amlodipine)
and swelling § Deficiency in HGRPT (Hypoxantine- • Xanthine oxidase inhibitor
• Joints rapidly become warm, red, guanine phosphoribosyl transferase) (allopurinol): MOST COMMON,
tender • Purine metabolites, which are not BEST
• Attacks subside within 3-10 days recycled, are degraded to uric acid
with no residual symptoms crystals
• Chronic gouty arthritis: manifest as
periarticular tophaceous deposits
without synovitis
Main Manifestations May be: • Physical Examination - mostly inspection and • Bone is unique in its ability to Degree
• Swelling • Traumatic - bone cannot withstand an looking out for main manifestations of fractures repair itself. It does so through • Complete: complete loss of
• Unbearable or intense pain, outside force • Imaging overlapping stages with bony continuity
especially on movement • Non-traumatic (pathologic fractures) o For a better assessment and image of the particular molecular, • Incomplete: bone has not
• Inability to move the affected bone Common Causes (traumatic): injury biochemical, and histologic completely loss continuity.
or joint • Fall from a height o X-ray features. • Closed (simple): Bone is still
Other Manifestations • Traffic accidents o CT-scan within the skin.
• An out-of-shape limb or joint that is • Direct blow to the bone o MRI Conservative Treatment: • Open: (compound): Bone has
visible to the eye • Repetitive force as in running (stress o Bone scan • Pain Management already pierced through the
• Bruising fractures) • Clinical: (+) trauma, deformities, tenderness, • Immobilization - may be done skin.
• Muscle spasms Other Fractures swelling through casts, metal plates and Location:
• Feeling of numbness or a tingling • Avulsion Fractures: Fragment of bone screws, intramedullary nails, • Anatomic Orientation:
sensation pulled away at the site of ligament or and external fixators. Proximal, Distal, Distal third
• Skin discoloration around the tendon attachment. AKA “Chip Fractures” • PT (Physiothearapy) - restores • Segment (long bones):
affected area • Stress Fracture: Seen in bones with muscle strength and mobility epiphysis, diaphysis or
• In some cases, the broken bone normal mineralization but with exposure metaphysis
can be seen protruding out of the to repetitive prolonged stress AND Non-Conservative Treatment: Type
skin surface muscular action to bones that have not • Surgery - when conservative • Spiral: the break spirals
• Bleeding in case of open fracture accommodated to such actions. Normal treatments failed or resulted into around the bone. (<45
Common Sites Xray in 90% of cases but abnormality sets poor functional outcome. May degrees) Common in twisting
Fractures
• Most common site of fractures are in 10-20 days. involve bone grafts and metal injuries
the hips, ankles and wrists. • Pathologic fractures: implants. • Oblique: diagonal break across
• Most common sites of osteoporotic o Altered by a disease process the bone. (>45 degrees)
fractures are the wrist, spine, o Abnormal mineralization Complications • Transverse: the break is in a
shoulder and hips. o Normal to minimal stress • Deformity straight line across the bone
• Most common sites for stress o Usually abnormal from the start • Delayed union/nonunion • Comminuted: bone injury that
fractures are the weight-bearing o Fractures happening to bones • Pseudoarthrosis - false joints results in more than 2 separate
bones of the lower extremities, o With abnormal mineralization • Infection bone components
most especially the lower leg and • Even with normal to even minimal stress • Impacted: one whose ends are
the foot. driven into each other.
Position and Alignment
• Relation of distal to proximal
segment
• Anterior
• Posterior
• Medial
• Lateral angulation (Give the
degree)
Apposition: Proportion to
proximal shaft; say if overlapping
Rotation: Internal or External
Three Stages of Fractures:
• Hematoma (minutes to days): Rupture of blood that fills the gap; Fibrin mesh (seal site; influx of inflammatory cells, fibroblasts, capillaries)
• Soft callus/procallus (1 week): Cytokines and GF activate osteoprogenitor cells to stimulate osteoblasts and osteoclasts; Anchorage but no rigidity for weight bearing
• Hard/Bony callus (several weeks): Deposition subperiosteal trabeculae of woven bone within the medullary cavity; Mesenchymal cells differentiate into chondroblasts that make cartilage; Cartilage undergoes
endrochondral ossification à bridging the fractured ends with a bony callus; Mineralizes à stiffness and strength of the callus increases (weight tolerated)

MODULE/TOPIC 15 PEDIATRICS
IMPORTANT CONSIDERATIONS IN THE PEDIATRIC HISTORY AND PHYSICAL EXAMINATIONS
• Tailor observations on the child’s age and individual context
o Order of examination depends on the child’s comfort
• Preferred location of child (infancy to pre-school years): parent’s lap
• Avoid or learn to interact with a struggling or crying child and distraught parent
HISTORY
HEADSSS Assessment
GENERAL OUTLINE
Population: Adolescents (12 – 18 years of age)
• Rapport – greet patient (parent and child), introduce
Preparation for adolescent psychosocial assessment
self, ask properly what they are consulting about, ask if
they have questions • Ask parent to leave and assure confidentiality of the adolescent
o Establish rapport with the child and the parents • Use open-ended questions
• Identifying data – name, sex, age, nationality, religion;
Home
relation of informant to patient
• Reason for Consult/Chief Complaint • How well does the family get along with each other?
• Past Medical History • Who lives with the young person? Where?
o Prenatal History • Do they have their own room?
§ Age of mother at delivery • What are relationships like at home?
§ OB score GP (TPAL) upon patient’s delivery • What do parents and relatives do for a living?
§ Complications, pre-natal exams, diagnostics, and • Ever institutionalized? Incarcerated?
medications given • Recent moves? Running away?
o Birth and Neonatal History • New people in home environment?
§ Birth attendant, place of birth
§ Duration of labor and pregnancy Education and Employment
§ Duration of ruptured membranes • How do you like school and your teachers?
§ Maternal treatment with medications and their • School/grade performance—any recent changes? Any dramatic past changes?
timing (antibiotic and anesthetic agents) • Favorite subjects—worst subjects? (include grades)
§ Presentation (vertex vs. breech) • Any years repeated/classes failed
§ Method of delivery (including forceps or vacuum
• Suspension, termination, dropping out?
extraction)
• Future education/employment plans?
§ Birth weight
• Any current or past employment?
§ APGAR scores
• Relations with teachers, employers--school, work attendance?
§ Interventions in the delivery room, length of stay in
the hospital after birth, and need for ICU care Activities
§ Diagnosis of hypoglycemia, hypothermia, anemia,
• On his/her own, with peers (what do you do for fun? where? when?), with family?
convulsions, respiratory distress, jaundice, birth
• Sports – regular exercise?
injuries
• Church attendance, clubs, projects?
§ First month of life is extremely important
• Hobbies – other activities?
o Feeding History
§ Initial feeding by breast or bottle (including • Reading for fun – what type of readings do they enjoy?
frequency and duration/quantity), quality of • TV--how much weekly--favorite shows?
latching and suck • Favorite music?
§ Introduction of solids (including quality and • Does young person have car, use seat belts?
quantity of solids, any adverse reactions to foods) • History of arrests--acting out--crime?
§ Nutritional supplementation • Social media – Any accounts? How often do you use? Who do you add?
§ Nutritional balance, meal frequency, fluid intake Drugs
(including milk, juice, water, sports drinks, etc.)
o Past illnesses: pneumonia, allergies, asthma, • Use by peers? Use by young person? (include tobacco, alcohol)
gastroenteritis, congenital diseases (*see section on • Use by family members? (include tobacco, alcohol)
Congenital Defects), Allergies • Amounts, frequency, patterns of use/abuse, and car use while intoxicated?
o Prior hospitalizations and/or surgeries • Source--how paid for?
• Family History
Sexuality
o At least two generations
o Childhood diseases or adult diseases with childhood • Orientation? Degree and types of sexual experience and acts? Number of partners?
onset Masturbation?
o History of consanguinity • History of pregnancy/abortion?
• Immunizations: BCG, DPT, HepB, OPV, Measles, • Sexually transmitted diseases- knowledge and prevention?
MMR • Contraception? Frequency of use?
o See section on immunization • Comfort with sexual activity, enjoyment/pleasure obtained? History of sexual/physical abuse?
• Developmental/Behavioral History: Gross Motor, Fine
Motor, Language, Personal, Social Suicide/Depression
o See section on developmental milestones
• Sleep disorders (usually induction problems, also early/frequent waking or greatly increased
• Social/ Environmental History
o If adolescent, use HEADSSS sleep and complaints of increasing fatigue)
Ø Important to conduct a separate interview for • Appetite/eating behavior changes, Feelings of 'boredom', Emotional outbursts and highly
adolescents (without the parents)* impulsive behavior, History of withdrawal/isolation, Hopeless/helpless feelings
o Who lives at home with the patient including • History of past suicide attempts, depression, psychological counseling; suicide attempts in
extended family members and family friends family or peers; History of recurrent serious 'accidents'
o Occupation of patient and/or parents • Psychosomatic symptomology
o Educational attainment • Suicidal ideation (including significant current and past losses)
o Smoking and alcohol consumption; Illicit drug use • Decreased affect on interview, avoidance of eye contact--depression posturing
o Sexual history • Preoccupation with death (clothing, media, music, art)
o Reproductive history
Safety
o Parent-child and parent-doctor interaction
• Stakeholder’s Analysis • Seatbelt and helmet use, conflict resolution skills, substance use

(Focus on Anthropometrics, Primitive Reflexes, and Other Specific Topics)

ANTHROPOMETRICS
Z-Scores
(Length-for-age, height-for-age, weight-for-height etc.)
Z-Score Interpretation
< -3 Severe undernutrition
≤ -2 Low LFA, HFA,WFH; Moderate undernutrition
> -2 Normal
-1 to +1 Ideal
< +2 Normal
≥ +2 High LFA, HFA, WFH; Overweight
Shortcuts in absence of growth charts
ABDOMINAL
WEIGHT LENGTH HEAD CIRCUMFERENCE CHEST CIRCUMFERENCE
CIRCUMFERECE
• Birth to 6th month: age in • In first year of life, child • Measure until 3 years • Preferably measured • Approximately the same
months x 600 + birth will grow a total of 25 cm old mid inspiration as the chest
weight (9-8-5-3) • Landmarks: anterior and • Landmark: Level of the circumference
• 7-12 months: age in o 0-3 months: 9 cm posterior fontanelle, nipples • Landmarks: Above the
months x 500 + birth o 3-6 months: 8 cm glabella, occipital • <5 years: Lying down level of the umbilicus
weight o 6-9 months: 5 cm protuberance • >5 years: Standing
• > 1 year old: (2 x years) + o 9-12 months: 3 cm position
8
Expected vital signs of pediatric patients (Nelsons Textbook of Pediatrics 17th Edition)
• Note: Heart rate and respiratory rate decreases while blood pressure increases with age
Neonates
Neonatal Classification
Gestational Age* Birthweight*
Preterm < 34 weeks (wks) Extremely low birthweight < 1,000 grams (g)
Late preterm 34 – 36 wks Very low birthweight ≤ 1,500 g
Term 37 – 42 wks Low birthweight ≤ 2,500 g
Postterm > 42 wks Normal birthweight > 2,500 g
*Based from Bates’ Guide to Physical Examination and History-Taking, 11E
Neonatal Classification based on WHO Asian growth charts
Category Abbreviation Percentile
th
Small for gestational age SGA < 10
th
Appropriate for gestational age AGA 10 – 90
th
Large for gestational age LGA > 90
Infants and Young Children
• Infancy (≤ 1Y) and young children (1 – 10Y)
• Note: compare length, weight, and height against WHO Asian growth charts
Length Weight Head Circumference
• Children < 2Y • Children < 1Y: use infant scales • Children < 2Y
o Measure supine/recumbent length • Children who can stand: use standing scales • Indirect measure of brain development
o Extend hips and knees • BMI: use age- and country-appropriate • Measure from glabella to occipital protuberance
• Children > 2Y charts
o Measure upright o DO NOT USE ADULT BMI STANDARDS

Primitive Reflexes
(Based from Bates’ Guide to Physical Examination and History-Taking, 11E)
Reflexes Timing Stimuli Response Pathology Illustration
Place fingers in baby’s Persistence > 4 mos:

Birth to 3 – 4 months Flexion of baby’s
Palmar Grasp Reflex hands and press pyramidal tract
(mos) fingers
palmar surface disease
Persistence > 8 mos:

Plantar Grasp Reflex Birth to 6 – 8 mos Touch sole at toe bases Flexion of toes pyramidal tract
disease
1. Mouth open Absence: severe

Stroke baby’s skin at 2. Head will turn to generalized or central
Rooting Reflex Birth to 3 – 4 mos
mouth corners stimulated side nervous system
3. Suck disease

possible neurologic
disease
1. Hold baby supine 1. Arms abduct and
2. Support head, extend
Moro Reflex strongly suggestive
Birth to 4 mos back, legs 2. Hands open
(Startle Reflex) of neurologic disease
3. Suddenly lower 3. Legs flex
Asymmetric response:
baby 4. Crying may occur
clavicular or humeral
fracture; brachial
plexus injury
1. Hold baby supine 1. Ipsilateral arm and asymmetric central
Asymmetric Tonic
2. Turn head to one leg extend nervous system
Neck Reflex Birth to 2 mos
side 2. Contralateral arm development;
(Fencing Reflex)
3. Jaw over shoulder and leg flex possibly predictive of
cerebral palsy
Hold baby prone on one 1. Head will lift up Persistence: delayed

Landau Reflex Birth to 6 mos
hand 2. Spine straightens development
Delayed onset:
Hold baby prone on one Arms and legs will possibly predictive of
Parachute Reflex Persistent after 8 mos
hand extended (protective) voluntary motor
function delay
Areflexia: possible
1. Hips, knees, ankles
hypotonia, flaccidity
1. Hold baby upright at extend
Scissoring (fixed
Positive Support around trunk 2. Partial weight-
Birth – 2 mos to 6 mos extension, adduction):
Reflex 2. Lower until feet bearing
neurologic spastic
touch the floor 3. Sags after 20 – 30
disease (example:
seconds
cerebral palsy)
1. Hold baby upright

1. Ipsilateral hip, knee Absence: possible
Birth (strongest 4 days (similar positive
Placing and Stepping flex paralysis
from labor) to variable support reflex)
Reflex 2. Contralateral foot Breech delivery:
age 2. One sole touches
step forward possibly absent
floor

Tanner Staging (Female: Breast and Pubic Hair)
Tanner
Breasts Description Illustration Pubic Hair Description Illustration
Stage
Preadolescent—no pubic hair
Preadolescent. Elevation of except for the fine body hair
I
nipple only (vellus hair) similar to that on the
abdomen
Breast bud stage. Elevation of Sparse growth of long, slightly

breast and nipple as a small pigmented, downy hair, straight
II
mound; enlargement of areolar or only slightly curled, chiefly
diameter along the labia
Further enlargement of elevation Darker, coarser, curlier hair,

III of breast and areola, with no spreading sparsely over the
separation of their contours pubic symphysis
Coarse and curly hair as in

adults; area covered greater
Projection of areola and nipple to
than in stage 3 but not as great
IV form a secondary mound
as in the adult and not yet
above the level of breast
including the thighs
Mature stage; projection of

nipple only. Areola has receded Hair adult in quantity and quality,
to general contour of the breast spread on the medial surfaces of
V
(although in some normal the thighs but not up over the
individuals, the areola continues abdomen
to form a secondary mound).

Tanner Staging (Male: Genitals and Pubic Hair)
Tanner Stage Pubic Hair Description Penis Description Testes and Scrotum Description Illustration
Preadolescent—no pubic hair
except for the fine body hair Preadolescent—same size and Preadolescent—same size and
I
(vellus hair) similar to that on the proportions as in childhood proportions as in childhood
abdomen
Sparse growth of long, slightly

Testes larger; scrotum larger,
pigmented, downy hair, straight
II Slight or no enlargement somewhat reddened, and altered
or only slightly curled, chiefly at
in texture
the base of the penis
Darker, coarser, curlier hair

III spreading sparsely over the Larger, especially in length Further enlarged
pubic symphysis
Coarse and curly hair, as in the

adult; area covered greater than Further enlarged in length and
Further enlarged; scrotal skin
IV in stage 3 but not as great as in breadth, with development of the
darkened
the adult and not yet including glans
the thighs
Hair adult in quantity and quality,

spread to the medial surfaces of
V Adult in size and shape Adult in size and shape
the thighs but not up over the
abdomen

DEVELOPMENTAL SCREENING AND SURVEILLANCE
• In absence of established risk factors or parental/provider concerns: general developmental screen is recommended at 9th, 18th, and 30th month visits
• Autism screening at 18 months
Primitive Reflexes Disappear
3 months Moro
4 months Rooting
6 months Palmar
12 months Babinski
Developmental Milestones (First 2 Years of Life)
Milestone Average Age of Attainment (Months) Developmental Implications
Gross Motor
Holds head steady while sitting 2 Allows more visual interactions
Pulls to sit, with no head lag 3 Muscle tone
Brings hands together in midline 3 Self-discovery of hands
Asymmetric tonic neck reflex gone 4 Can inspect hands in midline
Sits with support 6 Increasing exploration
Rolls back to stomach 6.5 Truncal flexion, risk of falls
Walks alone 12 Exploration, control of proximity to parents
Runs 16 Supervision more difficult
Fine Motor
Grasps rattle 3.5 Object use
Reaches for objects 4 Visuomotor coordination
Palmar grasp gone 4 Voluntary release
Transfers objects hand to hand 5.5 Comparison of objects
Thumb-finger grasp 8 Able to explore small objects
Turns pages of book 12 Increasing autonomy during book time
Scribbles 13 Visuomotor coordination
Builds tower of 2 cubes 15 Uses objects in combination
Builds tower of 6 cubes 22 Requires visual, gross and fine motor coordination
Communication and Language
Smiles in response to face, voice 1.5 More active social participant
Monosyllabic babble 6 Experimentation with sound, tactile sense
Inhibits to “no” 7 Response to tone (nonverbal)
Follows one-step command with gesture 7 Nonverbal communication
Follows one-step command without gesture 10 Verbal receptive language (e.g., “Give it to me”)
Says “mama” or “dada” 10 Expressive language
Points to objects 10 Interactive communication
Speaks first real word 12 Beginning of labeling
Speaks 4-6 words 15 Acquisition of object and personal names
Speaks 10-15 words 18 Acquisition of object and personal names
Beginning grammaticization, corresponds with 50
Speaks 2-word sentences (e.g. “Mommy shoe”) 19
word vocabulary
Cognitive
Stares momentarily at spot where object Lack of object permanence (out of sight, out of
2
disappeared mind [e.g. yarn ball dropped])
Stares at own hand 4 Self-discovery, cause and effect
Bangs 2 cubes 8 Active comparison of objects
Uncovers toy (after seeing it hidden) 8 Object permanence
Egocentric symbolic play (e.g. pretends to drink
12 Beginning symbolic thought
from cup)
Uses stick to reach toy 17 Able to link actions to solve problems
Pretend play with doll (e.g. gives doll bottle) 17 Symbolic thought
ASSESSMENT FOR DEVELOPMENTAL DELAY (UPPER RANGE)

Age (months) Gross Motor Fine Motor Social Skills Language
3 Supports weight of forearms Opens hands spontaneously Smiles appropriately Coos, laughs
6 Sits momentarily Transfers objects Shows likes and dislikes Babbles
Plays pat-a-cake, peek-a-
9 Pulls to stand Pincer grasp Imitates sounds
boo
Releases an object on
12 Walks with one hand held Comes when called 1-2 meaningful words
command
Walks upstairs with
18 Feeds from a spoon Mimics action of others At least 6 words
assistance
24 Runs Builds a tower of 6 blocks Plays with others 2 to 3-word sentences

chedule
ation Schedule
ion Schedule presents recommendations for immunization for children and adolescents based on updated literature review, experience and premises current at the time of publication. The PPS,
al circumstances may warrant a decision differing from the recommendations given here. Physicians must regularly update their knowledge about specific vaccines and their use because inform
ecommendations relative to their administration continue to develop after a vaccine is licensed.
pine National Immunization Program (NIP) The following vaccines are in the 2018 NIP:
p B, Pentavalent vaccine (DTwP-Hib-HepB), bivalent OPV, IPV, PCV, MMR, MR, Td and HPV
es
included in the NIP which are recommended by the Philippines Pediatric Society (PPS), Pediatric Infectious Disease Society of the Philippines (PIDSP) and the Philippine Foundation for Vaccina
ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018

VACCINATIONS FROM 7-18 YEARS OLD
Range of Dose(s) Schedule of Route of Precautions &
Vaccine
Recommended Age Needed Immunization Administration Contradiction
• Severe allergic reaction to
Unvaccinated
Hep B Vaccine 3 0,1,6 months IM vaccine component
7-18 yrs. old
• Moderate to severe illness
2nd dose given
at least 6
Hep A Vaccine Unvaccinated 7-18 yrs. old 2 IM vaccine component
months from the
1st dose
4 weeks interval between • Severe allergic reaction to
Unvaccinated 7-18 yrs. old 2
doses vaccine component
• Pregnancy
MMR Incompletely vaccinated 7-18 yrs.
2nd dose given anytime SC • Immunosuppression
1 but at least 4 weeks from • Recent receipt of blood
old
1st dose products
Minimum interval between
doses is 3 months
Minimum interval
vaccine component
Unvaccinated ≥ 13 yrs. old 2 between doses is one
• Pregnancy
month
Varicella SC • Immunosuppression
Given anytime 7-12 yrs.
• Recent receipt of blood
old at least 3 mos. from
Incompletely vaccinated 7-18 yrs. products
1 the 1st dose,13 yrs.old at
old • Moderate to severe illness
least 1 month from the
1st dose
vaccine component
Give annually beginning • Moderate to severe illness
Influenza Vaccine 9-18 yrs. old 1 IM/SC
February • History of Guillain-Barre
syndrome following a
previous dose
0,1 and 6 months Tdap
preferably as the 1st dose
then Td for the remaining
Td/Tdap IM
doses • Severe allergic reaction to
Incompletely vaccinated 7-18 yrs. One dose Tdap then Td vaccine component,
1-2
old for remaining dose • Moderate to severe illness
Fully vaccinated
7-18 yrs. old
(Fully vaccinated defined as 5
1 dose Tdap then Td
doses of 1
every 10 years
DTaP or 4 doses of DTap if the 4th
dose was administered on or after
the 4th birthday)
HPV: vaccine component
Bivalent HPV Females: 15-18 yrs. old 3 0,1,6 months IM • Moderate to severe illness
(2vHPV) • If found to be pregnant
after starting immunization,
Quadrivalent HPV Females: delay remaining doses until
(4vHPV)/Nonvalent 15-18 yrs. old 3 0,2 and 6 months completion of
HPV (9vHPV) Males: 15-18 yrs.old pregnancy
For Females: • Severe allergic reaction to
(2vHPV)/ vaccine component
Quadrivalent HPV • Moderate to severe illness
(4vHPV/)/ • If found to be pregnant
9-14 yrs. old 2 0,6-12 months IM
Nonvalent HPV after starting immunization,
(9vHPV) delay remaining doses until
For Males: completion of
4vHPV/9vHPV pregnancy

MODULE/TOPIC 16 DERMATOLOGY
• History-taking must include: GENERAL
o Exact description of onset • Appropriate Dress: Patient should be gowned, and examined completely in
o Careful description of first lesions sections or quadrants. If the patient is a pregnant woman, you ask them to wear
o Details of development and extension of lesions jeans to allow inspection of the abdomen.
o Note: Skin has important social functionà also • Level of Consciousness of the Patient: Is the patient awake, alert, and responsive
ask for anxieties, insecurities, and experiences of to you and others in the environment? Also note the posture, gait, motor activity and
the patient regarding the lesion facial expressions
• Inspect the entire skin surface in good light. View entire skin to evaluate distribution
• Information taken during a medical history: and configuration. Use magnifying lens to examine individual lesions. Palpate
o Chief complaint lesions for firmness and fluctuations. You may rub to elucidate the nature of scales
o History of present illness (Darier’s sign). You may also scrape ro reveal nature of lesions’ base (Auzpits sign)
§ Investigate chief complaint using the PQRST • Correlate findings with observations of the mucous membranes, especially when
(Precipitating/provoking, Quality, Radiation, assessing skin color, because diseases may appear in both areas
Relieving, Severity, Timing) or OLDCARTS
(Onset, Location, Duration, Character, Go gross first, from head to toe and on both sides
Aggravating factors, Relieving factors, Timing, • Face (look for lesions)
Severity) or ABCDE (Appearance, Border, • Mucous membrane
Color, Diameter, Evolution) • Trunk (anterior and posterior portions)
- Begin by asking open-ended questions • Hands and feet
- Progress to focused questions • Intertriginous skin - areas of skin prone to rubbing and touching each other
- Minimize interrupting patient
- Ask questions using simple terms SKIN:
- Do not forget to clarify • Skin color: look for increased pigmentation (brownness), loss of pigmentation,
§ The following questions may be asked: redness, pallor, cyanosis, yellowing of the skin
- When and where did the lesions start? • Moisture: look for dryness, sweating and oiliness
- Do the lesions itch, burn or hurt? • Temperature: use backs of your fingers to make this assessment; identify
- How did the lesions spread? generalized warmth or coolness and note temperature of any red areas
- Are they transient or consistently there? • Texture: look for roughness or smoothness
- Are there any other similar lesions in the Inspection • Mobility and Turgor: Lift a fold of skin and note the ease with which it lifts up
past? and (mobility) and the speed with which it returns to place (turgor)
- Is there any change in appearance? Palpation • Lesions: observe any lesions noting their characteristics
- Are there any aggravating lesions? • Anatomic location and distribution: generalized or localized?
- Do you apply any topical medications or o Arrangement: linear, clustered, annular, arciform, dermatomal?
take in any medications? o Number: multiple or singular?
o Past Medical/Dermatological illness o Shape
§ Presence of other illnesses, asthma, allergic o Type: macules, papules, vesicles, nevi?
rhinitis or eczema, previous operations and o Color
hospitalizations, allergies to food or drugs, o Surface characteristics: smooth, shiny, rough, dull, waxy, verrucuous
intake of alcohol or drugs, smoking o Others: borders, blanching
o Family and personal history
§ Family members that have asthma, allergic, NAILS: Inspect and palpate fingernails and toenails. Note color and shape and any
rhinitis or eczema, similar skin lesions, history lesions; look for paronychia, clubbing of the fingers, onycholysis, check for terry’s
of urticaria, keloids, allergy, SLE, diabetes, nails (ground glass appearance, distal band of reddish brown, obliteration of the
thyroid problems, tuberculosis in the family lunula), white spots, transverse white bands, transverse linear depressions, pitting
o Social history • Psoriasis: pitting, ridging, onycholysis, nail loss (no effective treatment)
§ Occupation, related-sun exposure, exposure • Atopic eczema: pitting, transverse ridging
to chemicals, detergents or rubbing alcohols, • Alopecia areata: fine pitting may occur in severe cases
recent travels and sleeping arrangements with • Lichen planus: longitudinal ridging, thinning of nail plate
family members • Darier’s disease: notching of free edge of nail
o Gynecological history if patient is female • Beau’s lines: transverse grooves on all nails caused by cessation of nail growth
o Review of systems before you go to your initial during severe acute illness
impression • Dermatomyositis: nail fold telangiectasia, ragged cuticles
§ Do it from head to toe • Yellow nail syndrome: associated with hypoplasia of the lymphatic system;
§ Having symptoms such as headache, blurring presents with nail discoloration, pleural effusion and peripheral edema
of vision, hearing loss, chest pain, difficulty of
breathing, abdominal pain, changes in bowel HAIR:
movement, dysuria, hematuria, edema, • Note quantity, distribution and texture (coarse or fine)
cyanosis or any joint pain. • Presence/absence of: Alopecia (diffuse, patchy or total), infestations, masses,
scaling, pigmentation, infection
• Diagnostic Details To test for nail clubbing: Schamroth’s Sign
o Distribution: • Have the patient place both forefinger nails together and look between them
§ Flexors: Atopic eczema (antecubital and • If you can see a small diamond space between them (Schamroth's window) then
popliteal) the nails are not clubbed
§ Extensors: Severe scaling indicate psoriasis
§ Seborrheic: Seborrheic dermatitis
- Common in Nasolabial areas, chest,
grow area
§ Sun exposed sites would be indicative of light
sensitive disorder Special
o Evolution - How lesion started or how it clear or Tests
persisted
o Involution
o Grouping - Patterns give clue to diagnosis
o Configuration
o Color
o Consistency - Soft or hard

DISTRIBUTION PATTERNS
Pattern Description Picture
• Like scratch marks

Linear
• Ex. Scratches, striae
• Complete circle
Annular • Central clearing
• Ex. Tinea corporis, leprosy
• Wandering or twisting like a

Serpiginous
snake
• Like the umbilicus
• On the surface, there is a dent
Umbilicated
in the middle
• Ex. Molluscum contagiosum
• Tight clustering of lesions,

heaped on top of one another
Herpetiform
• Ex. Herpes zoster, herpes
simplex
PRIMARY LESIONS
Lesion Description Picture
• Soft or firm, movable, or fixed
• Flat lesion < 1 cm
Tumor masses generally > 2 cm
• No elevations when viewed
• Bigger than a nodule
from the side
• May be of various colors.
Macule • When there is a confluence of
macules, you can have skin
lesions such as freckles
(brown) or tinea versicolor • Edematous, transitory
(white). plaque which lasts less than
24 hours
• Note its evanescent nature: it
Wheal
• Flat lesions > 1 cm comes and goes within the
• Large macule day
• May be several macules • From 2018 Trans: Could
Patch grouped or combined signify allergic reactions
together
• It can be brown, black, blue,
any color even white. • Small, superficial cavity
containing clear fluid
• Can become a lesion of
herpes simplex
Vesicle
• Any lesion that is superficial • Another example is that of
and raised above the Milliary pustulosa (sterile
surface ( Size < 1 cm) pustules independent of
Papule follicles)
• E.g. Molluscum
contagiosum with multiple
papules that are umbilicated.
• Blisters containing fluid ( Size

> 1 cm)
Bullae
• Contain clear fluid
• Superficial, raised lesion
• Can be seen in Chicken pox
where the diameter is
Plaque greater than the thickness
> 1 cm
• Conglomeration of papules
• < 1 cm, vesicle containing

pus
Pustule • yellow fluid, creamy colored,
• Size > 1 cm raised lesion with content within the lesion
• Firm, and round surface • Seen in Herpes zoster
Nodule • Deeper Involvement
• You can feel something
underneath
• Extravasated red blood cells

• Flat lesion that contains
blood vessels
Purpura
• Larger than petechiae (>3
mm)
• May or may not be palpable

• Superficial pinhead sized
usually 1-2 mm in size • Collection of new connective
tissue
Petechiae • Non-blanchable Scar
• Implies dermoepidermal
• Round hemorrhagic macules
damage
• Associated with dengue
• Bruises or “black and blue

marks” • Diminution of some or all
Ecchymoses • Deeper and more extensive layers of the skin
Atrophy
hemorrhage • Superficial loss of skin at
• Non-blanchable epidermis
SECONDARY LESIONS
• Symptoms of stress where a
Lesion Description Picture patient would constantly pick
or scratch a lesion, and the
lesion becomes elevated
• Dry or greasy laminated Lichenification with scratch markings
masses of keratin • Opposite of atrophy
Scale • Dead skin cells that don’t • Secondary to severe
contain nuclei scratching or itchiness
• Desquamated • Increase in linear markings
• Dried serum, blood, or

purulent exudate
Crust
• E.g. Honey-colored crust of
impetigo
• Punctate or linear abrasion

produced by mechanical
Excoriation
means
• Scratch marks
• Linear cleft through the

epidermis or dermis
Fissure • The cut is deeper than an
excoriation
• E.g. Cracks on the heels
• Loss of all or portions of the

epidermis
Erosion • Still superficial but a large
portion is lostà no to minimal
involvement of the dermis
• Complete loss of epidermal

Ulcer layer plus some portions of
the dermal layer

• A chronic skin disease involving blockage or • Acne vulgaris develops from four 1. Mostly a clinical diagnosis • Treatment includes addressing
inflammation of pilosebaceous glands different factors: based from history and PE of each of the pathogenic factors
• Mostly affects the face, but can also present o Follicular epidermal the patient that cause the symptoms
in the back and chest hyperproliferation/ 2. Findings can be classified • Treatment is also based on
• Usually characterized by open of closed hyperkeratinization causing into: severity and grade of the acne
comedones, inflammatory papules, pustules plugging of the follicle 1. Comedonal acne: presence of open and • Pharmacotherapy:
• Local symptoms include pain, tenderness, or o Excess sebum production closed comedones but no inflammatory 1. Antibioticsà erythromycin,
erythema o Presence and follicular lesions yet clindamycin, tetracycline,
• In severe cases, may progress to: colonization of the 2. Mild acne: presence of comedones and a few sulfamethoxazole
1. Acne conglobataà highly inflammatory commensal bacteria papulopustules 2. Retinoidl agentsà isotretinoin,
nodulocystic acne with interconnected Cutibacterium acnes 3. Moderate acne: presence of comedones, tazarotene
Acne
abscess (formerly Propionibacterium inflammatory papules, and pustules but in 3. Acne productsà benzoyl
Vulgaris
1. Acne fulminansà has systemic symtoms acnes) greater number compared to milder version peroxide, salicylic acid
such as fever, joint pain, and general o Inflammation through the 4. Nodulocystic acne: Presence of comedones, 4. Selective aldosterone
malaise release of inflammatory inflammatory lesions, and large nodules antagonistsà spironolactone
mediators into the skin greater than 5mm in diameter; scarring is also 5. Hormonesà
usually present estrogen/progestin OCP
• May sometimes merit laboratory examinations • Non-pharmacologic:
when work-up for Polycystic Ovarian Syndrome 1. Manual extraction/ evacuation
and cases refractory to antibiotic treatment are of the comedones
needed 2. Intralesional Steroid injections
3. Light and laser therapy
• Characterized by widespread erythema, • Not fully understood but hypotheses • Mostly a clinical diagnosis • Treatment is mainly supportive
necrosis, and bullous detachment of the include: • Classification system based on extent of until epithelium layer recovers:
epidermis and mucous membranes 1. Hypersensitivity reaction epidermal detachment: 1. Fluid resuscitation when
• Most commonly drug induced: 2. Keratinocyte apoptosisà through è TEN with spots: defined as widespread, needed
Examples: fas ligand activation leading to irregularly shaped erythematous or purpuric 2. Regular cleaning and
è Sulfonamides death receptor-mediated macules with blistering and affects more debridement of the lesion
è Chloramphenicol apoptosis than 30% of the body surface area 3. Withdraw inciting agent
Toxic è Macrolides 3. Overproduction of T-cell and è TEN without spots: no discrete lesions and
Epidermal è Penicillins macrophage-derived cytokines affects more than 10% of the body surface
Necrolysis è Quinolones 4. Drug-induced secretion of area
(TEN) è Phenobarbital granulysin from CTLs, natural killer è SJS-TEN overlap: widespread, irregularly
è Phenytoin cells, and natural killer T cells shaped erythematous or purpuric macules
è Carbamazepine with blistering
è Valproic acid
è Lamotrigine
è Indomethacin
è Ibuprofen
• a.k.a erythroderma is characterized by • Increased skin turnover • Based on skin findings and not on the underlying • Treatment is mainly supportive
generalized edema with scaling or • Number of cells in the germinative etiology and depends on the severity of
desquamation affecting at least 90% of the layer and their mitotic rate is • Usually a clinical diagnosis, but some cases may symptoms:
body surface area increased require the need for a skin biopsy • Fluid resuscitation
• Systemic derangements with it may include • The transit time of cells through the • To assess the patient and get baseline values, lab • Correction of electrolyte and
peripheral edema, increased insensible fluid epidermis is shortened tests that may be ordered include: thermoregulatory disturbances
losses, poor nutritional status, disturbed • This results in incompletely 1. Complete blood count to check for anemia or • Initiation of antihistamines if there
Exfoliative
thermoregulation, and high-output failure keratinized exfoliated scales eosinophilia is pruritus
dermatitis
• Common etiology include (however generally • Another process that may cause this 2. ESR to assess inflammation • Use of corticosteroids to lessen
cause is variable): psoriasis, drug reactions, condition includes an increased 3. Chemistry panel to check if there are inflammation should be done with
atopic dermatitis, cutaneous T-cell lymphoma amount of blood flow to the skin, electrolyte imbalances that needs to be monitoring since the use of these
• Idiopathic in nature impaired skin barrier function immediately addressed drugs can make the patient
causing fluid loss through susceptible to infection
transpiration a.

• Usually asymptomatic • Most important predisposing factors Early recognition of changes in pigmented lesions • Surgical excision (especially Most deadly of all skin
• Changes in pigmented lesions (ABCD) are inherited genes and sun (ABCD) during radial growth phase) cancers
o Asymmetry exposure • Complete physical examination of the entire o 5-mm margin of uninvolved • Aggressive malignancy of
o Irregular, notched border • UV solar radiation à genetic cutaneous surface and regional lymph nodes tissue should be obtained with melanocytes, the pigment
o Variegated color changes in skin à impairs • Favorable Prognostic Factors after Biopsy in situ melanoma producing cells
o Over 6mm in diameter cutaneous immune function à o Tumor depth / Breslow Thickness (<1.7mm) – best o 1-cm margin with a tumor • Predominantly a disease of the
• Bleeding, itching, or pain increase production of growth prognostic indicator thickness of 1-mm or less white skinned (98%)
• Hutchinson’s sign: pigmentation of proximal factors and ROS that affect o Number of mitoses (none) o 2-cm margin may be § 1.3:1 (men: women)
nail fold keratinocytes and melanocytes à o Evidence of tumor regression (absence) considered with tumor • Cutaneous melanomas in
accumulation of DNA damage in o Presence and number of tumor infiltrating thickness greater than 1-mm or Blacks, East Asians, and other
lymphocytes (TILs) (brisk response) with Clark level IV or greater
Radial Growth: horizontal spread of melanoma these cells dark skinned are often
o Gender (female)
within the epidermis and superficial dermis, no • Together with other mutations, with any thickness diagnosed at higher stages
o Anatomic location (extremity)
capacity to metastasize promote cell proliferation and o Ulceration (absence)
• Sentinel Lymph Node Biopsy • Most common sites for lesions
• Superficial spreading: most common, sun inhibit normal apoptosis • Clark Classification System of Microstaging: • Continuous surveillance are the back for men, and the
exposed skin o E.g. Mutation in cyclin-dependent o Level I: Confined to the epidermis (in situ) back and lower leg for women
• Lentigo maligna: indolent lesion on the face of kinase inhibitor 2A (CDKN2A) o Level II: Invasion into the papillary dermis
Melanoma older men, may remain like this for decades o Level III: Penetration to the papillary-reticular Risk Factors: sun exposure,
• Acral/mucosal lentigionous: unrelated to sun interface increasing intermittent exposure
exposure; palm, sole, nail bed, mucous o Level IV: invasion into the reticular dermis to UV-rays, occupational vs.
membrane o Level V: Penetration into subcutaneous fat Recreational, sun tan as a symbol
• Sentinel Lymph Node Biopsy, CT Scan or PET for wealth and health
Vertical Growth: after a period of time, tumor Scan to assess metastasis
cells invade deeper dermal layers • Molecular analysis
• Nodular: emergence of clone of cells with • Staging: 2009 AJCC based on thickness,
metastatic potential ulceration, nodal involvement
Clinical Warning Signs

• Enlargement of a pre-existing mole
• Itching or pain in a pre-existing mole
• Development of a new pigmented lesion
during adult life
• Irregularity of borders of a pigmented lesion
• Variegation of color with a pigment lesion
• Also known as hives • No underlying cause can be Histology • Avoidance of triggers, although
• Pruritic, erythematous, edematous, often identified in majority (around 50%) of • Superficial dermal edema, manifested by spaces these can be identified in only 10-
circular plaques are characteristic cases (Chronic Idiopathic Urticaria) between collagen bundles, and dilated lymphatic 20%of patients with chronic
• Blanch with pressure • Associated with localized mast cell and blood-filled vascular spaces urticaria
• Individual lesions develop and fade within degranulation and resultant dermal • Epithelium is normal • First-line pharmacotherapy for
hours (<24 hours) microvascular hyperpermeability acute and chronic urticaria:
• Acute <6 weeks; chronic >6 weeks History nonsedating second-generation
• Persistent episodes of urticaria may herald an 1. IgE-dependent urticaria (most) • Ask about activities/exposures during, antihistamines (histamine
underlying disease (collagen vascular Antigen-induced release of immediately before, or within past 24h H blockers)
1
disorders, Hodgkin lymphoma) vasoactive mediators from mast • Specifically ask about recent exercise, exposure • Adjunctive
cell granules through sensitization to allergens/animals, new detergents/soap, recent o First-generation antihistamines
Urticaria
with specific IgE antibodies infection, recent stressful life events, drug intake o Histamine H blockers
2
2. IgE-independent urticaria • Important associated symptoms: pruritus, o Leukotriene receptor

Directly incite the degranulation of rhinorrhea, swelling of face and tongue, dyspnea, antagonists
mast cells angioedema o Brief corticosteroid bursts
Suppress prostaglandin synthesis • More than half of patients with
from arachidonic acid chronic urticaria will have
3. Complement-mediated urticaria resolution/ improvement w/in 1
Inherited deficiency of C1 inhibitor year
à uncontrolled activation of the
complement system and
production of vasoactive mediators
• Reaction pattern with various causes • In the beginning, the epidermis is Histology • Remove offending agents Types:
• Another name is dermatitis thinned out, there are more • Characterized by spongiosis (spongiotic • Emolients • Atopic Dermatitis (most
Eczema
• Caused by abnormal function of immune infiltrates dermatitis) • Topical steroids may be used to common)
system block inflammatory response
• Characterized by red, papulovesicular, oozing • As the lesions progress, the • Edema seeps into the intercellular spaces of the o Major Criteria: severe
and crusted lesions that, if persistent, develop epidermis thickens and there are epidermis, splaying apart keratinocytes pruritus, typical morphology
into raised, scaling plaques less inflammatory infiltrates. • Ingested drug is marked by lymphocytic infiltrate and distribution, personal
• There may be thickening of skin in the • Persistent lesions develop into with eosinophils around, and/or family history of
popliteal and antecubital areas. raised, scaling plaques due to • Contact allergens tends to produce an atopy
reactive acanthosis and inflammatory reaction o Minor Critera: dry skin,
Acute spongiotic dermatitis: hyperkeratosis. palmar hyperlinearity,
• Formation of vesicles/blisters caused by hand/foot dermatitis, nipple
severe spongiosis enough to sever the eczema, susceptibility to
desmosomes cutaneous infections, orbital
darkening due to chronic
Chronic: scratching underneath the
• Involves lichen simplex chronicus eye, infraorbital folds
• Increased skin markings on the area with (Dennie-Morgan folds), food
hyperkeratosis or epidermal hyperplasia allergy, white
dermatographism,
keratoconus / cataract
• Seborrheic Dermatitis
o Papulosquamous disorder
patterned on the sebum-rich
areas of the scalp, face and
trunk
o aka dandruff in the scalp
• Nummular Dermatitis
• Dyshidrotic Eczema
o Chronic relapsing vesicular
palmoplantar dermatitis
o Also known as pompholyx
• Contact Dermatitis
o Irritant Contact Dermatitis
o Allergic Contact Dermatitis
• An array of several “multiform” lesions: • Hypersensitivity reaction to certain Histology • Immediate withdrawal of agents Two extreme variants:
macules, papules, vesicles, and bullae infections (herpes simplex, • Interface dermatitis: dermal edema and and drugs causing EM 1. Steven-Johnson Syndrome:
• Symmetric involvement of the extremities mycoplasma, histoplasmosis, accumulation of lymphocytes along the • Antivirals for EM caused by herpes 10% of body surface involved;
• Characteristic target lesion has 3 zones of coccidioidomycosis, typhoid, and dermoepidermal junction, where they are simplex erosions ad hemorrhagic
color change (Peripheral rim of erythema, leprosy), drugs (sulfonamides, intimately associated with degenerating and • Antihistamines to control itching crusts involve the mucosal
Inner rim of relative pallor, Central penicillin, barbiturates, salicylates, necrotic keratinocytes (pink cells) • Over-the-counter medications areas (lips, oral mucosa,
erythematous macule, papule, or vesicle ) hydantoins, and antimalarials ), (such as acetaminophen) to conjunctiva, urethra, perianal
• Symmetric involvement of extremities malignancy (carcinomas and reduce fever and discomfort and genital areas)
• Uncommon, self-limited disorder lymphomas), collagen vascular • Supportive care for the patient 2. Toxic Epidermal Necrolysis:
• Affects individuals of any age diseases (lupus erythematosus, while removal of drug or offending >30% of body surface area
Erythema dermatomyositis, and polyarteritis agent is critical. involved; diffuse necrosis and
Multiforme nodosa) sloughing off of cutaneous and
• If extreme, may present with mucosal epithelial surfaces
erythema multiforme (10% of body analogous to an extensive burn
surface area) or toxic epidermal
necrolysis (>30% of body surface
area)
• Immunologically mediated epidermal
cell injury
o Epithelial cells are killed by skin-
homing (CLA+) CD8+ cytotoxic T
lymphocytes
• Sharply demarcated, erythematous plaques • Seems to be multifactorial with • Diagnosis of psoriasis is clinical • Avoid excess drying or irritation of One of the world’s most common
with mica like scale; predominantly elbows, contributions from genetic and • Laboratory studies and findings skin dermatologic diseases, affecting
knees and scalp, atypical forms may localize environmental factors; strong o Negative rheumatoid factor (RF) • Midpotency topical up to 1% of the world’s
Psoriasis
to intertriginous areas; eruptive forms may be association between psoriasis and o Erythrocyte sedimentation rate (ESR) is usually glucocorticoids for plaque-type, population
associated with infection HLA-C, particularly with HLA normal Oral glucocorticoids should be
Cw*0602 allele avoided Types:

Clinical History • T cell homing to the skin may create o Uric acid level may be elevated in psoriasis o MOA: anti-inflammatory 1. Plaque-type: stable, slowly
• Worsening of long-term erythematous scaly an abnormal microenvironment by (especially in pustular psoriasis), causing o Long term use: loss of enlarging plaques, elbows,
area inducing the secretion of cytokines confusion with gout in psoriatic arthritis. effectiveness and atrophy of the knees, gluteal cleft and scalp;
• Sudden onset of many areas of scaly redness and growth factors that induce o Fluid from pustules is sterile with neutrophilic skin symmetric involvement
• Recent streptococcal infection, viral infection, keratinocyte proliferation, resulting in infiltrate. • Topical vitamin D analogue,
immunization, use of anti-malarials characteristic lesions o Perform fungal studies (important in cases of calcipotriene + retinoid, tazarotene 2. Inverse: intertriginous regions;
• Family history of similar rash • Interactions between CD4+, hand and foot psoriasis that seem to be o MOA of Calci: binding to individual lesions are sharply
• Pain CD8+, dendritic cells and keratinocytes worsening with the use of topical steroids.) Vitamin D receptor modulates T demarcated plaques, may be
• Pruritus give rise to “cytokine soup” dominated • In difficult cases, dermatologic biopsy can be cell gene transcription) moist and without scale
• Fever/afebrile by IL-12, interferon-Y, TNF, and IL-17 used o MOA of Taza: blocks induction 3. Guttate (eruptive): most
• Long term rash with recent presentation of o May reveal basal cell hyperplasia, proliferation of mouse epidermal ornithine common in children and young
joint pain (Psoriatic arthritis) of subepidermal vasculature, absence of normal decarboxylase (ODC) activity adults; small erythematous,
cell maturation, and keratinization. A large and suppresses expression of scaling papules, frequently
Signs/Symptoms number of activated T cells are present in the MRP8 after URTI with beta hemolytic
• Nails- pitting, onycholysis, nail thickening, epidermis. • UV light therapy for patients with strep
subungual hyperkeratosis • Radiographs to differentiate from other types of widespread psoriasis 4. Pustular: may have disease
• Scalp: silvery scales especially along the hair arthritis • Methotrexate for psoriatic arthritis localized to palms or soles or
line o Joint x-rays for diagnosis of psoriatic arthritis o MOA: inhibition of T cell may be generalized; if
• Koebner’s phenomenon: psoriatic lesions o Bone scans can identify joint involvement early activation and ICAM expression generalized, may be
are induced by local trauma of T cells characterized by fever lasting
• Sausage digits • Acitretin: binds to CRABP a several days, an accompanying
• Auspitz sign: when the scales are removed, protein present in psoriatic eruption of sterile pustules, and
small droplets of blood appear within a few plaques, Teratogenic a background of intense
seconds. • Cyclosporine and erythema
immunosuppressive agents
o T-cell modulators: Alefacept,
Efaluzimab
o TNF alpha inhibitors:
Etanercept, Adalimumab,
Infliximab
o Cytokine inhibitor: Ustekinumab
• Superficial bacterial infection of epidermis, • Usually caused by S. aureus • Diagnosis mainly based on history and PE • Topical antibiotic or a combination Streptococcal infections:
usually involves exposed skin, particularly o S. aureus – golden crusting • Evolution: single erythematous macule à of systemic and topical agents • Erysipelas: infect superficial
that of the face and hands lesions or bullous impetigo vesicles/bullae à rupture with seropurulent • Topical: dermins; rapidly spreading
• Often seen in the nasal area of child (nose is o S. pyogenes – reddish dischard à golden-yellow colored crust with o Mupirocin – bactericidal against cutaneous erythema and
commonly colonized by S. aureus) maculopapular eruptions central healing à crusts removed to leave a MRSA and Streptococcus; edema with sharp borders
• Highly contagious • Bacterial species in the epidermis smooth, red, moist surface à lesions spread inhibits bacterical RNA and • Cellulitis: infect deeper layers
• 2 Forms (differ by size of pustule): evoke an innate immune response peripherally and fuse to form gyrate protein synthesis of the skin such as the dermis
o Impetigo contagiosa that causes epidermal injury, leading patterns/plaques o Retapamulin (Medscape) and subcutaneous fat
Impetigo o Impetigo bullosa to local serous exudate and • Satellite lesions may occur by autoinoculation • Systemic: • Impetigo: rapidly spreading
“mamaso” • Erythematous macules forming pustules formation of a scale crust (scab) o Oxacillin/Cloxacillin erythema with vesicular or
associated with honey-colored crusts • Blister formation: bacterial Histology: denuded areas and salmon-
• No dermal involvement à lesions heal without production of a toxin (exfoliative • Characteristic microscopic feature: subcorneal colored crust
scarring toxin - Harrisons) that specifically pustule (contains serum proteins and inflammatory • Culture of wound or blood
• Pharyngitis is absent but mild regional cleaves desmoglein 1, the protein cells) grows group A beta hemolytic
lymphadenopathy may be present responsible for cell-to-cell adhesion streptococci
within the uppermost epidermal • Complication:
layers glomerulonephritis
• A superficial mycosis • Malassezia furfur complex (M. • Most are diagnosed clinically Topical creams and lotions for 2 • 25.34%
• Usually on the upper trunk globosa): lipophilic indigenous • KOH test - mixture of budding yeasts and short weeks • Benign and self-limited,
• Also on neck, upper arms, scalp, face human flora found in the stratum septate cigar butt hyphae; spaghetti & meatballs • Selenium sulfide shampoo: although recurrences are the
• Macules of various sizes and colors (hypo- or corneum of the back, chest, scalp, • ± Calcoflour white / parker ink cytostatic/antimitotic effect on rule
Tinea /
hyperpigmented) with a fine peripheral scale and face—areas rich in sebaceous • Wood’s lamp: coppery-orange fluorescence epithelium, results in decreased • Common in moist & humid
pityriasis
• Usually asymptomatic but can be pruritic glands • Culture if disseminated infection is suspected, add corneocyte adhesion and allows areas
versicolor
• Scalp lesions are termed cradle cap in babies • Dimorphic: lives on the skin in the sterile olive oil to medium shedding of the fungus • Can be mistaken for vitiligo,
and dandruff in adults yeast phase but transforms to the o 30-37.5 °C for 5 days (fast growing) • Ketoconazole shampoo or cream: which is NOT scaly
mold phase as it causes disease o Raised, smooth, creamy yellow to brown imidazole broad-spectrum • Part of normal flora thus is not
colonies antifungal agent; inhibits synthesis a contagious disease

o Turn darker as it grows older of ergosterol, causing cellular
• Family history = (+) higher rate of recurrence and components to leak, resulting in
long duration of disease fungal cell death
• Terbinafine cream: inhibits
squalene epoxidase, which
decreases ergosterol synthesis,
causing fungal cell death
• Ciclopirox cream: interferes with
synthesis of DNA, RNA, and
protein by inhibiting the transport
of essential elements
Tinea Corporis • Superficial fungal infections of the • KOH smear from advancing edge: fungal elements • Keep affected area dry • 22.63%
• Expanding, annular, pruritic, slightly skin: confined to the stratum • Wood’s lamp: mainly for capitis, yellow to green • (especially for tinea cruris) • Dermatophytosis of the body
erythematous plaque with an elevated scaling corneum (caused primarily by fluorescence surface
border that undergoes central clearing dermatophytes) • Culture: if clinical suspicion is high yet KOH result Topicals • Common
• Inflammation can cause scale, crust, papules, o In contrast with deep fungal is negative; outbreaks; not responsive to treatment • Imidazoles (Miconazole, • Affects all ages, particularly
vesicles, and even bullae to develop, infections of the skin: dermis or o Saboraud’s agar Ketoconazole, Clotrimazole): children
especially in the advancing border subcutis primarily involved o 25 °C Inhibits ergosterol synthesis by • Can be seen in adults caring
• Can manifest as folliculitis with pustule • Dermatophytes grow in the soil and o Slow-growing, 2 weeks blocking lanosterol 14-alpha- for children with T. capitis
formation on animals and produce a number of demethylase • Should be differentiated from
diverse and characteristic clinical Tinea Corporis • Allylamines (Naftifine, contact dermatitis, eczema,
Tinea cruris: inguinal areas; risk factors: heat, lesions • Predisposing factors: excessive heat & humidity, Terbinafine): Inhibits sterol and psoriasis
friction, maceration, obesity o Dermatophyte infections occur exposure to infected animals, chronic synthesis by blocking squalene • Relapses of tinea cruris and
Tinea pedis (athlete’s foot) more commonly in male than in dermatophytosis of the feet or nails epoxidase tinea pedis are common and
Cutaneous Tinea capitis: scalp dermatophytosis female patients, and progesterone • History of contact sports, military enrolment, • Benzylamines (Butenafine): should be treated early with
Mycoses Tinea barbae: beard infection has been shown to inhibit contact with similar lesions (for Tinea in general) Inhibits sterol synthesis by topical creams to avoid
dermatophyte growth blocking squalene epoxidase development of more extensive
• Ring shape lesions is due to • Ciclopirox olamine disease.
outward centrifugal growth in the (Hydroxypyridone shampoo):
stratum corneum interferes with macromolecules
• Symptoms are caused by the membrane transport, disrupts
inflammatory reaction elicited by membrane integrity, and inhibits
fungal antigens and not by tissue respiratory enzymes
invasion
MaTE(ing) is Ha SiN
• Microsporum: hair, skin
• Trichophyton: hair, skin, nails (Tri =
all 3)
• Epidermophyton: skin, nails
Leprosy
(see
Infectious
Diseases
section)

HISTORY
MODULE/TOPIC 17 OBSTETRICS AND GYNECOLOGY
GYNECOLOGIC HISTORY OBSTETRIC HISTORY

• Menarche • OB Scoring
• Menstrual cycle o Gravidity – number of pregnancies irrespective of outcome
o LMP (Last Menstrual Period) – the first day of the patient’s last § Nulligravida – no history of pregnancy
menstrual period § Primigravida – first pregnancy
o PMP (Previous Menstrual Period) – the first day of the patient’s § Multigravida – history of ≥ 2 previous pregnancies
menstrual period before LMP o Parity – number of pregnancies reaching 20 weeks AOG
o Interval (28 ± 7 days) § Nullipara – no pregnancy reaching 20 weeks
§ Regular or irregular? § Primipara – first fetus delivered at ≥ 20 weeks
§ Does the patient have her period monthly? § Multipara – history of ≥ 2 previous fetal deliveries at ≥ 20 weeks
o Duration (4 ± 2 days) § Twins and other multifetal pregnancies are counted as 1 pregnancy
§ How many days does the patient usually have her period? § Not decreased by stillbirths
o Amount o T-P-A-L – count the number of infants (not pregnancies) that
§ How many pads/tampons does the patient use per day? correspond to each criterion
§ Are the pads/tampons soaked? § Term – 37-42 weeks
• Menstrual symptoms § Preterm – 20-37 weeks
o Dysmenorrhea – pain with menses, often with bearing down; aching or § Abortion/Miscarriage – < 20 weeks, or < 500 grams
cramping sensation in the lower abdomen or pelvis • Early abortion – < 12 weeks AOG
o Premenstrual syndrome (PMS) – a cluster of emotional, behavioral, • Late abortion – 12 weeks, but < 20 weeks
and physical symptoms occurring 5 days before menses for 3 § Live – currently living children
consecutive cycles • Trimesters
o Amenorrhea – absence of menstrual bleeding, can be primary (never o 1st Trimester – 0-14 weeks
occurring) or secondary (cessation some time after initiation) o 2nd Trimester – 15-28 weeks
o Abnormal uterine bleeding o 3rd Trimester – 29-42 weeks
§ Polymenorrhea - < 21-day intervals between menses • Pregnancy history
§ Oligomenorrhea – infrequent, scanty bleeding o Preterm – < 37 weeks
§ Menorrhagia – excessive bleeding § Early preterm – < 34 weeks
§ Metrorrhagia – intermenstrual bleeding § Late preterm – 34-36 weeks
§ Hypomenorrhea – regular, decreased bleeding o Term – 40 weeks
o Headaches, dizziness, light-headedness § Early term – 37 weeks – 38 6/7 weeks
o Vaginal discharge – amount, color, consistency, odor § Full term – 39 weeks – 40 6/7 weeks
o Pruritus § Late term – 41 weeks – 41 6/7 weeks
o Pelvic pain o Post-term – ≥ 42 weeks
• Menopause
• Sexual history Date of Type of Place of
Gravida AOG Sex Weight Complications
o Age at first coitus Delivery Delivery Delivery
o Sexual orientation and gender identity 38 Pre-

G1 1/15/93 SVD Hospital F 5.9 kg
wks. eclampsia
o Number of sexual partners
40 Shoulder
o Contraceptive use G2 7/3/94 CS
wks.
Home M 6.5 kg
dystocia
o Sexually transmitted diseases Naegele’s Rule
§ Active lesions, discharge o Expected Date of Delivery (EDD) = LMP +7 days, -3 months, +1 year
o Other symptoms
§ Post-coital bleeding
Month Day Year
§ Pain during intercourse (dyspareunia)
LMP 7 03 2018
• History taking for the breast
o Lumps/mass Naegele’s Rule -3 +7 +1
§ 50% of women have palpable lumps or nodularity EDD 4 10 2019
§ Premenstrual enlargement and tenderness are common T/N: In this example, the mother’s LMP is on July 3, 2018. Using the
§ Location, duration, mobility, changes in size, variation within the Naegele’s Rule, the EDD is on April 10, 2019.
menstrual cycle
§ Make sure to ask at what point during their menstrual cycle they felt • Prenatal Care
the mass/lump
o Changes in breast contour (i.e. dimpling, swelling, puckering of skin Age of Gestation Recommended Prenatal Visits
over the breasts) < 28 weeks (1 to 2 trimesters)
st nd
Monthly
o Discomfort 28-36 weeks Every 2 weeks
o Pain (Mastalgia) > 36 weeks Every week
§ Breast pain alone is a risk for breast cancer
§ Identify if pain is diffuse or focal, cyclic or non-cyclic, related to SIGNS AND SYMPTOMS OF PREGNANCY
medications Morning sickness 6-18 weeks – Peak of hCG at 8-10 weeks, plateau at 16 weeks
o Identify family history of breast cancer, and other related illnesses Fatigue ---
• Past medical history 1st trimester
Urinary frequency
o Previously diagnosed diseases and comorbidities 3rd trimester – due to bulkiness of uterus
§ Diabetes Primigravid – 18-20 weeks AOG
Quickening
§ Hypertension Multigravid – 16-18 weeks AOG
§ Cardiovascular diseases Cessation of
Not reliable until 10 days or more after expected menses
§ Obesity menses
Beading cervical 6 weeks – poor crystallization or beading is due to
§ Thyroid diseases
mucus progesterone
§ Renal diseases
Breast changes 6-8 weeks – breast engorgement begins
§ Hematologic diseases (e.g. anemia) Melasma – mask of pregnancy; due to increased MSH
§ Psychiatric illnesses Linea nigra – darkening of the linea alba; due to increased MSH
Skin changes
§ Malignancies Striae gravidarum – due to collagen breakdown
o Current medications, previous hospitalizations, surgical procedures, Spider telangiectasia – due to increased estrogen
recent laboratory or imaging tests done Increased
6 weeks – due to increased progesterone
• Personal and social history temperature
Abdominal
o Educational attainment 6 weeks – abdominal enlargement begins
changes
o Nutritional history
Thyroid changes Enlargement is normal
o Occupation, stressors in life 6 weeks – vaginal mucosa becomes dark-bluish red and
o Physical activity Chadwick’s sign
congested (violaceous) due to increased blood flow
o Alcohol intake, smoking, usage of illicit drugs 6-8 weeks – softening of the uterine isthmus;
Hegar’s sign
firm cervix now contrasts with softer fundus and isthmus
Goodell’s sign 6-8 weeks – Softening of the cervix due to edema
T/N: Hey Good Chad! Hegar – isthmus, Goodell – cervix, Chadwick – vagina

APPROACH TO BLEEDING HISTORY-TAKING FOR ERECTILE DYSFUNCTION
• Sexual History
o Rate your level of sexual desire. Rate your partner’s level of sexual
desire.
§ [Mulq 1-10]* Paano niyo po ire-rate ang gana ninyo sa pagtatalik?
Ang gana naman po ng inyong partner?
o How many times each week do you have sexual intercourse?
§ Ilang beses sa isang linggo kayo nakikipagtalik?
o How many times each week do you masturbate?
§ Ilang beses sa isang linggo kayo nagsasalsal?
o Do you ejaculate during sexual intercourse? Into your partner’s
vagina?
§ Nilalabasan po ba kayo tuwing nakikipagtalik kayo? Sa puwerta po
ba ng partner ninyo?
o Do you ejaculate prior to penetration?
§ Nilalabasan po ba kayo bago po kayo makapasok?
o How many minutes does intercourse last before you ejaculate?
§ Ilang minuto po/gaano po katagal bago kayo labasan?
• Erectile History
REPORTING o How long have you had problems with your erections?
§ Gaano na po katagal kayo nagkakaproblema sa pagtayo ng inyong
Patient (initials), a (age)-year-old G__P__, currently at ___ weeks AOG ari?
consulting for (chief complaint). o When was the last time you had normal erections?
§ Kailan po kayo huling nagkaroon ng normal na pagtayo ng ari?
Patient has a history of (comorbidities, previously diagnosed diseases), and is o Do you experience having firm erections?
currently taking (medications). She has had a history of (hospitalizations, § Ngayon po ba nakakaranas kayo ng sapat na paninigas sa pagtayo
surgeries) for (reasons). ng inyong ari?
o Describe the quality of your erections with intercourse and with
Patient is a non-smoker and an occasional alcoholic beverage drinker. She masturbation.
denies use of illicit drugs. She is a (educational attainment) and is currently § Maaari niyo po bang ilarawan ang kalidad ng pagtayo ng inyong ari
employed as a (occupation). kapag nakikipagtalik po kayo? Kapag nagsasalsal? May pagkakaiba
po ba?
The patient had her menarche at (age). Her menstrual cycles have a (regular o Are your erections straight or curved?
or irregular) interval, usually occurring every (number of days, 28 ± 7 days) § Ang pagtayo po ba ng ari niyo, diretso po ba? O nakabaluktot po?
and lasting for (duration, 4 ± 2 days). The patient uses (average number) of o Does the duration or quality vary at times?
pads/tampons per day, (soaked vs. non-soaked). Patient usually experiences § Nagbabago po ba sa tagal at kalidad ng pagtayo ng inyong ari?
(specify symptoms) during her period. LMP was on (date), PMP was on (date). o Do you obtain erections easily?
§ Madali po ba kayo tigasan o tayuan?
The patient had her first coitus at (age) years old, and she has a history of o Do you often have erections in the morning?
(number) sexual partners. She has/has no history of contraceptive use, and § Sa umaga po ba nagkakaroon po ba ng pagtayo ng ari?
STD’s.
Author’s suggestion on rating:
The patient is a G__P__, currently on her (e.g. 2 ) pregnancy.
nd
T/N: Having erections is not enough! The patient should sustain it enoug
Her previous pregnancy was last (year), delivered via (mode of delivery,
include indication), at (place of delivery) by a (attendant of delivery). Live baby
(sex), (birthweight, AGA/SGA/LGA), with/without complications.
T/N: AGA – appropriate for gestational age, SGA – small for gestational age, LGA – large
for gestational age
OR
Her previous pregnancy resulted in spontaneous abortion at ___ weeks AOG;

dilatation and curettage done at (place of procedure).
IMPORTANT SIGNS AND SYMPTOMS OF THE MALE REPRODUCTIVE

SYSTEM
• Penile discharge, genital sores – evaluate for STI’s
• Scrotal swelling or pain
• Sexual dysfunction
• BPH: WINSURF
o Weak stream
o Intermittency
o Nocturia
o Straining
o Urgency
o Retention
o Frequency
o FUN – irritative symptoms usually caused by detrusor muscle
hypertrophy
o WISR – obstructive symptoms
• Prostate Cancer
o Nocturia
o Urgency
o Hesitancy
o Weak stream
o Painful or burning urination
o Erectile dysfunction
o Decrease in ejaculate
o Painful ejaculation
o Hematuria or blood in semen
o Rectal pressure or pain
o Pain or stiffness in the lower back, hips, pelvis, thighs

BREAST EXAMINATION
Ensure full exposure of the chest. Inspect the breasts and nipples with the patient in sitting position and disrobed to the waist.
Arms at sides
• Note appearance of the skin – color, thickening of the skin and unusually prominent pores (lymphatic obstruction), lesions, scarring
• Size and symmetry of the breasts – some differences in size and areolae are common and normal
Inspection
• Contour of the breasts – visible masses, dimpling, flattening (breast CA); compare one side with the other, peau d’ orange
• Characteristics of the nipples – size, shape, direction, rashes and ulcerations, discharge; note nipple retraction and deviation
Arms over head, hands pressed against hips, leaning forward
• Important in observing otherwise invisible dimpling or retractions (contracts the pectoral muscles)
Best performed when the breast tissue is flattened. Patient should be supine with her arm raised and place under her head. Examine both breasts.
• Palpate rectangular area: clavicle to inframammary fold (bra line), midsternal line to posterior axillary line, axilla (tail of the breast)
• Use pads of the 2nd, 3rd, and 4th fingers
• Be systematic – use vertical strip pattern (lateral to medial, or vice versa) or concentric circles (from areola outward, or inward toward areola)
• Be sure to cover all areas of the breast!
• Examine for: consistency of tissues, breast tenderness, nodules
• Note the following characteristics of breast nodules: location (by quadrant/clock, cm from nipple), size (in cm), shape (round or cystic, disc-like, irregular), consistency
Palpation (soft, firm, hard), delimitation (well-circumscribed or not), tenderness, mobility
• Carefully palpate and pinch the areola. Note any discharged expressed.
Sample Reporting:
There is a 2x2 cm, well-circumscribed, firm, round, movable, non-tender mass on the 12 o-clock aspect of the left breast. The mass is 2 cm from the nipple. No discharge.
Do not forget to palpate for lymph nodes!

Supraclavicular, infraclavicular, axillary
SPECIAL TESTS
Fundal Height Fetal Heart Tone
Ideally, patient’s bladder must be drained first (important!). The fundal height is Doppler
measured if the fundus is above the level of the umbilicus (~20 weeks AOG) • Heard as early as 8 weeks AOG
• Measure from the top of the pubic symphysis to the maximum height of the fundus • Almost 100% by 10 weeks AOG
using a tape measure Stethoscope
• Done to determine if the fetus is growing adequately • Heard as early as 16 weeks AOG
• Compute for the AOG before getting fundal height, and compare • 80% at 20 weeks
• If the pregnancy is between 20-34 weeks, the age of gestation (in weeks) closely • 100% at 22 weeks
correlates to the fundal height (in cm) à 34 weeks = 34 cm Note the following
• 4 cm greater than expected – consider multiple gestation, a large fetus, extra • Location – midline of abdomen (10-18 weeks), depending on fetal position (>18 weeks)
amniotic fluid or uterine leiomyoma • Rate – 110-160 bpm à fetal heart rate same as the maternal heart rate may indicate a
• 4 cm smaller than expected – consider low-level amniotic fluid, missed abortion, dead fetus
intrauterine growth retardation or fetal anomaly • Rhythm – rate should vary 10-15 bpm from second to second; after 32-34 weeks, rate
should become more variable and increased with fetal activity
LEOPOLD’S MANEUVER
Used to determine the fetal position in the maternal abdomen beginning in the 2nd
trimester, with the greatest accuracy during the 36th week of gestation.
ALWAYS STAY ON THE RIGHT SIDE OF THE PATIENT.

LM1 (Fundic Grip)
• Identifies which fetal pole occupies the fundus, presentation, and lie
• Palpate the uppermost part of the gravid uterus gently with the fingertips together
• Cephalic presentation: irregular, nodular (feet)
• Breech presentation: hard, round, ballotable, mobile (head)
• Fetal lie: longitudinal, transverse (fundus feels empty), oblique
LM2 (Umbilical Grip)
• Palpation of the fetal back
• Palms are placed on the anterolateral aspect of the abdomen, and gentle but deep
pressure is applied
• Fetal back: linear, convex, bony ridge (where fetal heart tone is best heard)
• Soft parts: numerous nodulations
LM3 (Pawlick’s Grip)
• Determines the lower fetal pole, and which fetal part lies above the pelvic inlet
• Place palmar surfaces of the fingertips on the fetal pole just above the pubic symphysis
• Palpate the presenting fetal part for texture and firmness to distinguish the head from
the buttock
• Judge the descent or engagement of the presenting part into the maternal pelvis
• Head engaged – feel shoulder, fixed, knob-like
• Head not engaged – feel round, ballotable mass
LM4 (Pelvic Grip)
• Determines the laterality of cephalic prominence, assesses the flexion or extension of
the fetal head
• Position hands on either side of the gravid uterus, Identify the fetal front and back sides
• Using one hand at a time, slide fingers down each side of the fetal body until the
cephalic prominence is reached
• Engaged – hands are parallel and do not meet
• Not engaged – hands converge
PELVIC EXAMINATION
• Wash hands
• Counsel patient regarding the examination, making sure to explain the procedures that will be happening
• Check that the instruments and supplies are available
Preparation
• Properly drape and position the patient on the bed
• Turn on the droplight
• Wear gloves properly
Inspection Palpation
• Seat yourself comfortably • Palpate for any lesions or masses
• Warn the patient that you will be touching her genital area • Bartholin’s Glands – insert index finger into the vagina near the posterior
• Inspect the mons pubis, labia, perineum introitus and place thumb outside the posterior part of the labia majora; with the
External
• Separate the labia and inspect the following: labia minora, clitoris, urethral index finger and thumb, palpate each side in turn, approximately at the “4
Examination
meatus, vaginal opening or introitus o’clock” and “8 o’clock” positions à note swelling or tenderness; note and
• Note any inflammation, ulceration, discharge, swelling or nodules culture any discharge
• Skene’s Glands – with the index finger, gently palpate and milk Skene’s glands;
note any discharge which should be cultured
Pap Smear
Speculum Exam
• The patient should not be menstruating, and she should have voided her bladder
• Select speculum with appropriate size and shape, moisten with warm water
• The patient should also avoid intercourse and use of douches, tampons,
• Inform the patient you are about to insert the speculum
Internal contraceptive foams and creams, and vaginal suppositories for 48 hours before
• With the index finger of the unoccupied hand, apply downward pressure on the
Examination examination
introitus to widen the opening
+ Pap Smear • Carefully collect specimen from ectocervix and endocervix using a cervical
• Insert the closed speculum at a 45° angle, slide inward along a downward slope,
broom/scrape or endocervical brush
and slowly open the speculum blades
• Properly apply specimen to a previously labeled slide
• At full insertion, the speculum should be in a horizontal position, and the blades
• Fix specimen with 95% ethanol
should be opened adequately to visualize the cervix
• Inform the patient that the speculum will be removed

• Unlock the speculum and slowly withdraw while closing the blades
• The speculum should be removed with its blades fully closed and at a more
vertical position
• Inspect the vaginal canal, note any discharge and lesions (this can be done as
the speculum is being inserted into the canal)
• Inspect the cervix and the cervical os; note color, position, smoothness,
discharge, masses
• Fix the speculum; both hands should be free to obtain the pap smear
• Inform the patient that you will be conducting the bimanual examination
• Lubricate index and middle finger of one of your gloved hands
• From a standing position, insert lubricated fingers into the vagina
• The thumb should be abducted and the ring and little finger should be flexed into the palm
• Note nodularity and tenderness in the vaginal wall, including region of urethra and bladder anteriorly
• Palpate cervix – note position, shape, consistency, regularity, mobility, tenderness
• Use other hand as the abdominal hand, and press down on the abdomen; try to grasp the uterus and adnexae between the two hands
• Palpate uterus – note size, shape, consistency, mobility; identify tenderness or masses
• Palpate ovaries – note size, shape, consistency, mobility, tenderness; palpate both ovaries
Bimanual
Examination
• Inform the patient that you will be conducting the rectovaginal examination
• Slowly insert the middle examination finger into the rectum
Rectovaginal
• Check for masses and tenderness in the cul-de-sac and parametria
Examination
• Check for patency of the rectovaginal septum, sphincter tone
• Check for rectal bleeding
MALE GU PHYSICAL EXAMINATION
• Observe lie of the testicles within the scrotum – left is often lower than the right
Inspection • Transilluminate – negative in tumor or hernia
• Inspect for excoriations, rashes, ulcerations, etc.
Auscultation • Using the diaphragm, auscultate for masses and bowel sounds for hernia
Palpation • Palpate testicles, epididymis, spermatic cords – note size, shape, contour, consistency
Digital Rectal Examination
• Examine the anus and rectum
• Lubricate gloved finger
• Explain the procedure to the patient and inform him that it might trigger an urge for bowel movement but that this will not occur
• Ask the patient to bear down; inspect the anus and note any lesions
• Place the pad of the gloved and lubricated index finger over the anus; as the sphincter relaxes, gently insert your fingertip into the anal canal in the direction pointing
toward the umbilicus
• If the sphincter tightens, pause and reassure the patient; when the sphincter relaxes, proceed
• Note sphincter tone, tenderness, induration, irregularities and nodules
• Palpate rectal surface; rotate your hand clockwise and then counterclockwise
• Palpate prostate gland; rotate your hand further counterclockwise – tell the patient that examination of the prostate gland may prompt an urge to urinate
• Note size, shape, mobility, and consistency of the prostate; identify any nodules or tenderness
Special Tests

COMMON DISEASES OF THE BREAST
PERTINENT
CLINICAL
DISEASE PATHOGENESIS DIAGNOSIS HISTORY AND PE TREATMENT ADDITIONAL NOTES
MANIFESTATIONS
FINDINGS
LCIS Genetics • Biopsy of a • Family history of In-situ: wide • ER+, PR+,
• Always • BRCA1 and nodule detected breast cancer (both excision with HER2/NEU- with
incidental BRCA2 (tumor by mammogram father and mother breast radiation better prognosis
biopsy finding suppressor genes) or self-palpation side) therapy (treatment • BRCA mutations
(not associated mutations • A mass in pre- • Lump felt upon self- of choice); adjuvant increase risk of
with Tumor Markers menopausal palpation tamoxifen further ovarian cancer,
calcifications) • Estrogen women that • Tumor/calcification reduces the risk of pancreatic cancer
• 20-40% receptor (ER) and persists found upon recurrence • BRCA2: increased
bilateral, progesterone throughout her mammography/MRI Invasive type: risk in men
occurring 80- receptor (PR): cycle and any • (+) for tumor Operable: Fibroadenoma:
90% before testing for mass in markers modified radical possible differential for
menopause effectiveness of postmenopausal mastectomy or breast masses; most
• Morphology: hormone therapy women needs to lumpectomy common benign
consist of such as tamoxifen be aspirated followed by breast neoplasm in breast
dyscohesive • Human epidermal • If cyst reveals radiation therapy • Biopsy to determine
cells with oval or growth factor residual mass or • Sentinel node if malignant
round nuclei and receptor 2 bloody fluid, biopsy • Large lobulated
small nucleoli (HER2): present in patient needs • Tumors <1cm, popcorn
• Cells lack E- large amounts in mammogram; negative axillary calcifications in
Lobular cadherin (cell 20-25% of breast if solid, proceed nodes require no mammography
Carcinoma adhesion protein) cancers; to excisional additional
(in-situ and resulting in the determines if biopsy therapy
invasive) cells appearing trastuzumab • Screening by • Adjuvant
rounded without treatment is mammogram chemotherapy
attachment to effective starts at 40 y/o for 6 months
adjacent cells • Cancer antigen • Women with benefits both
• Mucin-positive 15-3 (CA15-3), familial breast positive for
signet-ring calls cancer antigen cancer usually lymph node
are commonly 27.29 (CA27.29) have negative involvement and
present and mammography, no lymph node
Invasive Lobular carcinoembryonic so MRI is better involvement
Carcinoma antigen (CEA): for this group • Estrogen
• Presents as a used to monitor positive tumors
palpable mass early recurrence that are >1cm
or after tumor (with or without
mammographic excision lymph node
density with • Urokinase involvement) can
irregular borders plasminogen be treated with
• In about ¼ of the activator (uPA) aromatase
cases the tumor and plasminogen inhibitor
infiltrates activator inhibitor • Women with
• “Indian filing” (PAI-1): higher HER2 tumors
DCIS levels mean a show better
• Most common more aggressive prognosis with
calcification cancer trastuzumab
found in • Tamoxifen
mammography (20mg/day for
• Malignant clonal 5years) for
population of patients with
cells limited to poor prognostic
ducts and features
lobules by the Locally advanced:
basement Neoadjuvant
membrane combination
• 5 subtypes: therapy (CAF:
comedo- cyclophosphamide,
carcinoma, solid, doxorubicin, and 5-
cribriform, fluorouracil, IV)
Ductal
papillary, and followed by surgery
Carcinoma (in-
micropapillary and radiation
situ and
(majority of DCIS therapy
invasive)
are in mixtures of Metastatic: No
these types) therapy is known to
Invasive cure patients with
• Majority of metastatic breast
carcinomas (70- cancer
80%), firm to • Conventional
hard and have an treatment:
irregular border aromatase
inhibitors
(letrozole or
anastrozole) for
ER+ and
combination
chemotherapy
for ER- patients

COMMON DISEASES OF THE FEMALE GENITOURINARY TRACT
PERTINENT
CLINICAL ADDITIONAL
DISEASE PATHOGENESIS DIAGNOSIS HISTORY AND TREATMENT
MANIFESTATIONS NOTES
PE FINDINGS
• Discharge: Yellowish • Caused by • Nucleic acid • Recent sexual • Metronidazole • Men usually
green or gray, possibly Trichomonas amplification test contact 2g orally single appear
frothy; often profuse vaginalis, a (NAAT), current • Vestibule and dose, OR asymptomatic, if
and pooled in the protozoan often, gold standard, 3- labia minora Tinidazole 2g female is
vaginal fornix; may be but not always 5x more sensitive may be orally single diagnosed, male
malodorous. (Primary acquired sexually compared to wet erythematous, dose should be
symptom) à destruction of mount vaginal • Alternative treated as well
• Pruritus epithelial cells by • Scan saline wet mucosa may regimen: • Many women
• Dysuria (from skin direct contact and mount for motile be diffusely Metronidazole are symptom
inflammation or cytotoxicity trichomonads reddened, with 500 mg orally free
urethritis) (poor sensitivity) small, red BID for 7 days • 7-35% of
• Dyspareunia granular spots • Note: women in STD
or petechiae in Metronidazole clinic
the posterior is safe in all • T. vaginalis is
fornix trimesters of unicellular and
Trichomoniasis
• In mild cases, pregnancy, fusiform in
the mucosa whereas shape
looks normal Tinidazole is in • Patients are
• Vulvar skin Category C rescreened in 3
involvement is months with
limited to the NAAT due to
vestibule and high reinfection
labia minora, rates
distinguishing
it from the
more extensive
vulvar
involvement in
Candida
vulvovaginitis
• Discharge: Gray or • Bacterial Amsel’s Criteria for • Risk factors: Symptomatic • Most common
white, thin, overgrowth Bacterial Vaginosis new or multiple patients, cause of adult
homogeneous and probably from (at least ¾) sexual pregnant vaginitis
malodorous; usually anaerobic • Scan saline wet partners, patients (start at • It is isolated in
not profuse, may be bacteria; often mount for >20% women who 3 trimester)
rd
80% of urethras
minimal transmitted clue cells (epithelial have sex with • Metronidazole of male sexual
• Most frequent sexually cells with stippled women, 500mg PO bid x partners of
symptom: Unpleasant • Alteration of borders) lesbian 7 days OR, women with BV
fishy or musty genital vaginal flora • “Whiff test”: sniff couples who • Metronidazole
odor, often stronger resulting in for fishy odor after share sex toys 0.75%, one full
Bacterial after intercourse decreased applying KOH without applicator
vaginosis • The vulva and vaginal lactobacilli à • Test vaginal cleaning, intravaginally,
mucosa appear normal overgrowth of secretions for pH > douching daily for 5 days
• Rare to have pruritus Gardnerella 4.5 OR,
or vulvar irritation vaginalis, • Thin, watery • Clindamycin
anaerobes, and discharge 2% cream 5g
Mycoplasma intravaginal,
hominis nightly x 7 days
for mild
infection
• Discharge: White and • When the • Scan KOH • Sexual contact • Symptomatic
curdy, may be thin but ecosystem of the preparation for the • 3 most treatment:
typically thick; not as vagina is branching hyphae important 100-mg
profuse as in disturbed, or spores of factors that miconazole
trichomonal infection; Candida albicans Candida alter the vaginal
not malodorous (cause of candida vaginal suppository or a
• Pruritus (predominant vaginitis in 90% ecosystem: 2%
symptom) of patients) hormonal butoconazole,
• Vaginal soreness becomes an factors, 1% clotrimazole,
• Dysuria opportunistic depressed 2% miconazole,
• Dyspareunia infection cell-mediated or 0.4%
• The filamentous immunity, and terconazole
forms of C. antibiotic use cream, any of
albicans are able • Vulva and which is used
to penetrate the surrounding daily for 7 days
Candida vaginal mucosa skin are often • Shorter, 3-day
vaginitis and intertwine inflamed and regimen: daily
with host cells, sometimes 2% clotrimazole,
resulting in swollen 4% miconazole,
hyperemia and • Vaginal or 0.8%
tissue lysis near mucosa is tioconazole
site of infection. often cream, or daily
reddened, with 200-mg
white miconazole or
tenacious 80-mg
patches of terconazole
discharge suppository
• Mucosa may
bleed when
these patches
are scraped
off; in mild

cases, the
mucosa looks
normal
• Most women are • Sexually active • Pap Smear • Smoking • HPV • It is the second
symptomatic women are Screening (age 21 (higher risk of vaccination most common
• First symptom is exposed to HPV: years old or within 3 dysplasia with program for and most lethal
usually post-coital infects the years of onset of HPV infection), HPV 6, 11, 16 malignancy in
vaginal bleeding epithelium near sexual activity) oral and 18 women
• Metastasis include the transformation • Histologically, contraceptives, (quadrivalent) or worldwide
extrapelvic lymph zone of the cervix SCCA presents as high parity, HPV 16 and 18 • Squamous cell
node, liver, lung and • High risk type of nest and tongues altered (bivalent) giving carcinoma
bone HPV (HPV 16 and of malignant immune status, 5 years accounts for
18) encode E6 squamous gene protection from 80% of cases of
and E7 which are epithelium, either alteration, the vaccine cervical
effective in keratinizing or non- history of • Surgical carcinoma. This
inhibiting normal keratinizing invading venereal removal of is followed by
cell cycle the cervical stroma disease, early invasive adenocarcinoma
checkpoint • HPV DNA testing age of first cancers (such (15%)
functions of the (age 30 and above) intercourse as in
regulatory • Colposcopic • HIV is hysterectomy) Staging
proteins leading examination of the associated with adjunctive • Stage 0:
to immortalization cervix and vagina to with higher radiation and carcinoma in
but not full see delineate the rate of high- chemotherapy situ
transformation of extent of lesion and grade • CIN I: Pap • Stage 1:
the cervical to target areas to be dysplasia and smear follow up carcinoma
epithelium biopsied shorter latency • CIN II or III: confined to
Cervical
• If not cleared, between cryotherapy, cervix
cancer
some women infection and laser loop • Stage 2:
develop high- invasive electrical carcinoma
grade dysplasia disease excision extends beyond
• Low-grade procedure and the cervix but
squamous core biopsy not onto the
intraepithelial • Microinvasive pelvic wall; it
lesion with no carcinoma: involves vagina
significant core biopsy but not the
disruption or • Invasive lower third
alteration of host carcinoma: • Stage 3: Cancer
cell cycle à high- hysterectomy has extended to
grade squamous with lymph the pelvic wall; it
intraepithelial node dissection involves lower
lesion with and radiation for third of vagina
increased advanced lesion • Stage 4: It has
proliferation, extended
decreased beyond the true
epithelial pelvis or has
maturation, and involved the
lower rate of viral mucosa of the
replication à bladder or the
invasive rectum
carcinoma
Leiomyoma • Benign tumor of • Intramural: tumor • Gross: Firm, white • Abnormal • Most uterine • Most common
smooth muscle cells located at the appearance on bleeding fibroids are tumor in
• Distinction from myometrium sectioning (submucosal) harmless, do humans (in
leiomyosarcomas is (within the • Histology: Well- • Urinary not cause women
based on the following: muscular layer) differentiated, frequency symptoms, and especially)
(1) Absence of atypia • Submucosal: regular, spindle- • Sudden pain shrink with • Most common
(2) Increased tumor is seen shaped smooth (disruption of menopause indication for
mitotic index in under the mucosa muscle cells blood supply) • Surgical fibroid hysterectomy
leiomyosarcoma of endometrium associated with • Impaired removal • Leiomyomas
(3) Zonal necrosis • Subserosal: hyalinization fertility (myomectomy): may undergo
(4) Presence of tumor underneath • Can be (especially treatment to enlargement
10+ the serosa, the differentiated from when the increase chance during the
mitoses/10HPF’s outermost layer of the myometrium by myoma is of conception reproductive
indicates the uterus, the presence of a located in the • May consider years, then
malignancy, projecting to the capsule surrounding uterine cavity hysterectomy regress after
particularly if peritoneal cavity the lobule due to • To shrink a menopause
accompanied by • Leiomyosarcomas difficulty in fibroid for a • Larger
cytologic atypia arise de novo pregnancy) short time, leiomyomas
and/or necrosis from the hormone may have
myometrium or therapy with a central softening
endometrial gonadotropin- with
stromal precursor releasing hemorrhage
cells hormone
analogue
(GnRH-a) puts
the body in a
state
like menopause

OBSTETRIC COMPLICATIONS
PERTINENT
CLINICAL ADDITIONAL
DISEASE MANIFESTATIONS
PATHOGENESIS DIAGNOSIS HISTORY AND PE TREATMENT
NOTES
FINDINGS
Vaginal bleeding in • Abnormal Decrease in Hgb and • Pelvic and Medical Philippines: 1.7 in
the 1st half of implantation of Hct abdominal pain Systemic methotrexate 100 pregnancies
pregnancy the blastocyst Serum B-hCG assay (most frequent, (IM) (POGS)
other than in the ≥ 1,500-2000 mIU/mL 95%), usually • Indications: AOG < 6
Locations endometrial without evidence of accompanied by weeks, tubal mass < Risk factors
• Ampullar (most lining of the intrauterine pregnancy in amenorrhea 3.5 mm, dead fetus, • HIGHEST RISK:
freq, 70%) uterine cavity ultrasound • Vaginal bleeding/ serum b-HCG <10- surgeries for a
• Isthmic (12%) – • Transit of fertilized Serum progesterone spotting (60-80%) 15,000 prior tubal
outcome is ovum blocked • > 25 ng/mL – probable • Exquisite • Contraindications: pregnancy, for
rupture • Fertilized ovum normal pregnancy tenderness on breastfeeding, fertility
• Infundibular burrows through • < 5 ng/mL – cervical motion immunodeficiency, restoration, or
(11%) tubal mucosa to intrauterine dead fetus • Uterus may be alcoholism, liver/renal for sterilization
• Interstitial (2- muscular wall or ectopic pregnancy pushed to one disease, etc. • Prior sexually
3%) – most • The periphery of Ultrasound side or slightly Direct injection into transmitted
bloody zygote is a • Transabdominal: enlarged ectopic mass disease or other
capsule of rapidly cannot recognize • Vital signs: Oral methotrexate tubal infection
proliferating uterine pregnancy until normal Intramuscular • Peritubal
trophoblasts that 5-6 weeks; fetal heart (unruptured) or adhesions
Ectopic invade and erode action outside uterus hypotension Surgical • Repeated
pregnancy the subjacent provides evidence of (ruptured) Conservative supratherapeutic
(Tubal muscularis layer ectopic • Pelvic mass on • Salpingostomy – ingestions of
pregnancy) • Maternal blood • Transvaginal: bimanual incision left open to contraceptives
vessels are imaging method of examination heal by itself; for • Failed
opened, and choice for early • Hemoperitoneum small pregnancies (< contraception
blood pours into pregnancy; EP may (ruptured) 2 cm) at distal 1/3 of • Assisted
spaces within the manifest as adnexal identified via fallopian tube reproductive
trophoblast or mass; Sensitivity for culdocentesis • Salpingotomy – technology
between it and the diagnosing EP: 20- same procedure with
adjacent tissue 80%; presence of fluid salpingostomy Other types of EP
• Expanding in cul-de-sac increases except that incision is • Tubal (95-.96%)
conceptus leads likelihood of EP closed with suture • Heterotopic /
to rupture of Laparoscopy – gold Radical simultaneous
muscle wall standard for diagnosis • Salpingectomy – • Cervical (<1%)
Laparotomy (open excision of tubes • Ovarian (3%)
surgery) – when patient from uterine • Abdominal (1%)
is hemodynamically attachment • Cesarean Scar
unstable or when • Segmental resection
laparoscopy is not with or without
feasible anastomosis
Painless vaginal • Placenta is • Physical exam • Most • If fetus is immature Risk factors
bleeding in the implanted in the • Speculum exam + characteristic and active bleeding • Previous
3rd trimester lower uterine diagnostic ultrasound event: painless subsides, observe. If placenta previa
segment (LUS) (avoid internal exam) vaginal bleeding bleeding ceased for • Grand
Types/Grading ahead of the • Monitor contractions (bright red) in the 2 days and fetus is multiparity
I – low lying (less leading fetal pole • CBC, platelet count, 3rd trimester judged to be • Multiple
than 2 cm from • Inflammatory or blood typing o Bleeding healthy, patient can gestation
internal cervical os) atrophic change • TVS –confirmatory; usually starts be discharged and • Increased
II – placenta previa • Defective decidual reported as the actual without instructed a pelvic maternal age
marginalis (covers vascularization distance from the os warning and rest • Uterine scar
margin of cervical • Supra-cervical from 18 weeks à without pain or Delivery: (previous LSCS,
os) adherence overlap of 2cm in the contractions • Vaginal delivery: if therapeutic
III – placenta • 3rd trimester LUS 3rd trimester is o May recur at placental edge lies abortion,
previa partialis bleeding predictive of CS unpredictable >2 cm from internal myomectomy)
(partially covers • Thrombin • MRI – rule out intervals cervical os
cervical os) promotes placenta accrete o Almost entirely • CS indications Morbidly adherent
IV – placenta contractions external (marginalis, partialis, placentas are a
Placenta
previa totalis • Placental o Bleeding stops totalis): any degree of frequent and
previa
(entire placenta migration spontaneously overlap >35 weeks serious
covers cervical os) o Recurs with • Most placenta previa complication
labor cases undergo CS associated with
• Abnormally delivery and a vertical placenta previa
implanted skin incision is
placenta recommended by
many surgeons.
Others
• Prevention and
treatment of anemia,
• Screening for
infections
• Thromboprophylaxis
for at risk groups
• Regional (epidural)
superior to general
anesthesia
Profuse vaginal Caused by the Sonographic criteria • Usually no • Preterm delivery Predisposing
bleeding during partial or complete • Loss of normal symptoms may be necessary. factors
placental absence of the hypoechoic during • Preoperative • Placenta previa
separation decidua basalis à retroplacental zone pregnancy prophylactic • History of
Placenta
adherence of the (<2 mm) • May have catheterization – to previous CS
accreta
Depth of invasion placental villous • Multiple and massive bleeding in the mitigate blood loss • Advances
• Accreta (75%): tissue directly to placental lakes (new 3rd trimester and enhance maternal age
villi are the myometrium à vascular formation) (Mayo Clinic) surgical visibility, but • Multiparity
failure of placental

attached to the separation (blood • Disruption of the • Usually, vaginal may cause • Submucous
myometrium vessels and placenta serosa-bladder bleeding is thrombosis myoma
• Increta (15%) – grow too deeply into complex (<1 mm) profuse during • CS delivery • Asherman’s
villi invade the uterine wall) • Large interplacental manual • Hysterectomy – syndrome
myometrium • Imperfect lacunae separation of confirmation of
• Percreta (5%): development of • Focal echogenic the placenta percreta or increta Possible outcomes
penetrates the fibrinoid layer mass-like elevation after delivery of almost always • Maternal: DIC,
through the • Trophoblast beyond uterine serosa the fetus mandates this. hemorrhage,
myometrium breaks barrier and • Bleeding may be visceral injury,
and to or invades the minimal or ACOG acute respi
through the myometrium, absent but the recommendations distress
serosa, serosa and organs placenta is not • Patient counseling syndrome, renal
Cotyledon • Uteroplacental delivered within on the likelihood of failure, sepsis,
involvement: neovascularization 30 minutes after transfusion and death
total, partial, or delivery of the hysterectomy • Fetal: preterm,
focal fetus • Blood products and restricted fetal
clotting factors growth
ensured available
• Consideration of
location and timing
of delivery
• Access to surgery
personnel/equip
• Preoperative
anesthesia
assessment
Vaginal bleeding • Premature Diagnosis generally • Placental • Stabilize the mother; Risk factors
in the 2nd half of separation of a obvious with severe abruption is most prompt and intensive • Higher maternal
pregnancy normally- placental abruption, but likely to occur in resuscitation with age
implanted mostly it is a diagnosis of the last trimester blood and crystalloid • Previous
Type placenta (distant exclusion of pregnancy • Detect coagulation placental
• Revealed – part from cervical os, derangement abruption
of placenta unlike in previa) Ultrasound Classic S/Sx • Emergency CS • Most frequent
pulls away from • Rupture of the • Check for blood • Vaginal bleeding delivery when fetus is associated
uterus; blood decidual spiral underneath placenta • Sudden onset of viable size condition:
may leak out of artery, resulting in • Negative scan does abdominal pain • Sonographic Hypertension,
cervix retroplacental not rule out! • Back pain confirmation of fetal preeclampsia
• Concealed – hematoma • Acute: hyperechoic to • Uterine heart activity is • Trauma
blood collects • Expansion of isoechoic placenta tenderness important when • PROM
between uterus hematoma to • Hypoechoic in 1 week • Fetal distress evaluating fetal • Cigarette
and placenta; disrupt more • Sonolucent in 2 weeks • Rapid uterine status smoke, cocaine
enlarged vessels and contractions, • CS delivery: best use
bleeding inside extend placental MRI – considered to be often coming one type of delivery for a • Folate
cervix without separation. the most sensitive for right after another compromised fetus deficiency
symptoms may • If there is no identifying placental • Vaginal Delivery: best • Chorioamnionitis
lead to fetal further abruption type of delivery for a • Advanced
death separation, the dead fetus maternal age
Extent abruption is EFM tracing: Recurrent and parity
• Total discovered on late deceleration, severe • Severe IUGR
Abruptio
• Partial examination of variable deceleration, Acute causes:
placentae
freshly delivered reduced variability, shearing forces
placenta. bradycardia, sinusoidal from trauma,
• With continued pattern sudden uterine
bleeding, blood decompression
can escape Clot Observation Test: from membrane
through the sample of blood -> test rupture with
cervix to cause tube, (+) coagulation hydramnios, acute
external defect if: 1) clot does not vasoconstriction
hemorrhage. form within 6 mins, OR 2)
clot forms and lyses Utereplacental
within 30 mins insufficiency
plays a role
Serum levels of alpha-
fetoprotein >280 μg/L Majority involve a
have a positive chronic process
predictive value of (from 1st trimester)
placental abruption
Biopsies – lack of
adequate
trophoblastic
invasion, thrombin
within the
hemorrhages
Gestational Maternal Aspect • Hypertension – at • Rales in the Prevention Pregnancy-
Hypertension • Predisposition to least 140 mmHg SBP spaces of the • Antiplatelet therapy Induced
• at least 140 cardiovascular or at least 90 mmHg lungs (high risk (low dose aspirin 60- Hypertension
mmHg SBP or disease à DBP for pre- 80mg – start • Most common
at least 90 physiological • Preeclampsia: eclampsia) treatment in second medical
Eclampsia mmHg DBP changes in presence of • MAP-2 semester, only in complication
and after 20 weeks pregnancy à proteinuria or >90mmHg or high risk patients) encountered in
Pre- in previously manifests as pre- evidence of MAP-3 • High dose calcium pregnancy
eclampsia normotensive eclampsia multiorgan >105mmHg = • Nitric oxide donors • 2nd most
women involvement increased (endothelium-derived common cause
Fetal Aspect ○ Proteinuria – 300 pregnancy- relaxing factor) of maternal
Preeclampsia • Impaired mg/L per 24 hour induced Treatment mortality and an
• Development of trophoblastic collection of urine; hypertension and • Anticonvulsants important cause
hypertension invasion of persistent 1+ on perinatal deaths (MgSO4) of perinatal

plus proteinuria maternal spiral dipstick, or urine (MAP-2 is mean • Antihypertensives mortality and
(after 20th week
th
arteries protein: creatinine arterial pressure o Labetolol is 1st morbidity
of gestation) (abnormal ratio ≥ 0.3 in 2nd trimester; choice
• HELPP placentation) à ○ Multiorgan MAP-3 is in 3rd o Hydralazine is 2nd
Syndrome placental hypoxia involvement may trimester)* choice
(hemolysis, and inflammatory include • Absence of mid- o Calcium blockers:
elevated liver factor release à thrombocytopenia, trimester drop in Nifedipine is 3rd
enzymes, low
endothelial cell renal insufficiency, BP may predict choice
platelet count:
activation à hepatocellular future pregnancy- o Alpha adrenergic
<100,000/mm ) 3
systemic vascular necrosis (elevated induced blockers

Eclampsia dysfunction, liver enzymes), hypertension (Clonidine)
• Occurrence of capillary leak, pulmonary edema (absence of o Low dose
convulsions in a and vasospasm • Severe pre- arteriolar diazoxide
woman previously à manifests as eclampsia vasodilation) o Nitroprusside
fulfilling criteria pre-eclampsia indications: SBP ≥ • Roll-Over test o ACE inhibitors
for preeclampsia (hypertension, 160mmHg, DBP ≥110 • Delivery
• Cerebro- proteinuria, mmHg, proteinuria > Severe Pre- • Neonatal support
vascular coagulation 4g/day or >2+ on eclampsia
complication of abnormalities and dipstick • Severe headache
pre-eclampsia cerebral edema) • Doppler Ultrasound: or visual
• 2 competing problematic when the disturbance
factors (in normal ratio of the systolic (cerebral edema)
pregnancy, there peak to the diastolic • Pulmonary
is equilibrium trough is more than 3 edema or
between these): • Doppler velocimetry – cyanosis
○ Pro- increased uterine • Intrauterine
angiogenic artery velocimetry in growth restriction
factors: the first two • RUQ or epigastric
placental GF trimesters may serve pain
and VEGF as predictive test for
○ Anti- preeclampsia
angiogenic • Placental volume –
factors: sFlt-1 placenta of
and endoglin; preeclamptic women
if there is a are smaller relative ro
shift towards non-preeclamptic
this, there patients
will be • Maternal serum
development markers: VEGF, PlGF,
of pre- sFlt-1, PAPP-A, PP13,
eclampsia AFP, HCG, UE3,
• Loss of balance inhibin, endoglin
between these
factors lead to
endothelial
dysfunction
Abnormalities of the Powers (uterine • Maternal effects: • Difficult labor;
contractility and maternal expulsive efforts) uterine rupture, abnormally slow
• Hypertonic dysfunction lacerations, amniotic progress of labor
• Hypotonic dysfunction fluid embolism, uterine • Normal rate of
Management
• Tachysystole: short periods of muscle atony cervical dilation
• Hypertonic dysfunction: Sedation
relaxation affect oxygenation of the fetus • Fetal effects: o Nullipara:
• Hypotonic dysfunction: Administer oxytocin
• Causes of precipitous labor and delivery: inappropriate blood 1.2cm/hour
low resistance of the soft parts of the flow, intracranial o Multipara:
birth canal, strong uterine and abdominal trauma, injury, Erb- 1.5cm/hour
contractions, absence of painful Duchenne palsy
sensations
Abnormalities in the Passenger (fetus) • Maternal • Leopold’s Management
• Presentation: cephalic, breech, face, consequences: Maneuver • Apply suprapubic pressure with downward
brow hemorrhage, traction of fetal head (Rubin’s maneuver)
Dystocia • Position: usually occiput rotates to lacerations, infections • McRoberts maneuver – sharply flex thigh
anterior position (occiput directly beneath • Fetal consequences: to abdomen
the symphysis) brachial plexus palsy, • Woods Corkscrew – delivery of posterior
• Development: hydrocephalus or fractures shoulder
enlargement of the abdomen • Hibbar maneuver – pressure applied to
• Size: shoulder dystocia may occur fetal jaw and neck
• Zavanelli maneuver – cephalic replacement
into pelvis and then CS
• Symphisiotomy
• Cleidotomy
Abnormalities of the Passage (pelvis)
• Inlet Contraction: diagonal conjugate of less than 11.5cm (normally sacral promontory should not be felt)
• Midpelvic Contraction: ischial spines are prominent (interischial diameter < 10cm), sidewalls convergent, shallow sacral concavity, narrow
sacro-sciatic notch
• Outlet Contraction: fist should be able to fit between the two ischial tuberosities

• Abnormal Complete H-Mole Sonologic Pictures SSx Management • Most common
growth of cells • Endoreduplication: Complete HMole Complete HMole • Surgical evacuation gestational
inside a uterus most common; • Snowstorm pattern • Vaginal and close HCG trophoblastic
characterized sperm enters an • Heterogeneous bleeding monitoring disease
by proliferation empty ovum and appearance with cystic • Uterine size • Suction curettage or • Highest
of placental doubles its spaces greater than for hysterectomy prevalence
tissue that does genetic Partial HMole AOG • Avoid: hysterotomy among Asian
not develop information to • Focal cystic changes • Presence of (removal of countries,
from the cells form 46XX in placenta theca lutein vesicles) and use of particularly SEA
of the uterus. • Dispermy: two • Presence of a rowth- cysts oxytocin and • 2.4/1000
sperms penetrate retarded fetus with • Hyperemesis prostaglandin pregnancies in
• Vaginal the empty ovum to multiple congenital gravidarum • Chemoprophylaxis the Philippines
bleeding – form 46XX or 46 anomalies attached to • Pre-eclampsia • Methotrexate
most common XY a hydropic placenta • Hyperthyroidism • HCG monitoring for a Risk Factors
reason for • Fertilization by a • Ratio of transverse to • Respiratory year after molar • Maternal age –
patient diploid sperm antero-posterior failure evacuation higher in older
consultation; (sperm that dimensions of the Partial • Pregnancy may be and very young
with color and contains 2 sets of gestational sac > 1.5 • Similar to allowed after 6 women (>50yo –
consistency of chromosomes) complete HMole, months of normal 200-400 fold
prune juice penetrates ovum B-HCG titer: Elevated but more HCG serum levels increased risk)
Hydati- and produces XX HCG >100,000U/L subdued • Paternal age –
diform or XY H-mole higher risk with
Mole Histopathology advancing age
Partial H-Mole • Complete H-Mole: no • Previous molar
• Fertilization of embryo parts, pregnancy
normal egg with trophoblastic • Diet (deficiency
two sperms à proliferation, large in Vitamin A
triploid partial avascular hydropic villi, derivatives and
moles cistern formation; protein)
• Maternal gross: grape-like • OCPs
contribution translucent vesicles • Race
allows fetal • Partial: admixture of
components. normal villi and large
• Dispermy is the edematous villi, lesser
most common trophoblastic
mechanism proliferation,
scalloping of
structures, presence of
fetal elements and
blood vessels; gross:
less bulky placental
tissue with variable
proportion of vesicles
• Maternal/Fetal Biochemical markers Methods of • Corticosteroids: for • Philippines
Presenting HPA Axis • Fetal fibronectin Prediction fetal lung maturity ranks #7 in
symptoms Activation: stress • Salivary estradiol • OB history o 24-34 weeks countries with
(subjective): à increase in • Metalloproteinases (previous preterm gestations greatest
• Painful or corticotrophin • Cytokines delivery) anticipated to number of pre-
painless uterine releasing • Interleukins • Digital have premature term births
contractions hormone Ultrasonography examination of delivery
• Menstrual-like ® ↑ maternal • Cervical length (risk the cervix (Betamethasone
cramps and fetal increases as length Behavior of is preferred)
• Lower back pain adrenal decreases) - <25mm at uterine • Oxytocin receptor

cortisol à ↑ 16-24 weeks has contraction antagonist (e.g.
Preterm: before prostaglandin increased risk; <20mm • Biochemical Atosiban)
37 completed
à ↑ for multifetal markers • Magnesium sulfate:
weeks myometrial pregnancy has • Ultrasound criteria include AOG
contraction increased risk evaluation of the ≤ 31 6/7 weeks AND
® ↑ DHEAS à • Assess during 22-24 cervix singleton or
↑ placental weeks multifetal risk for
estrogen à • Dilatation of the delivery within the
early loss of internal os (>5mm at next 30 min to 24
uterine 30 weeks is 33% risk) hours
quiescence – shape of internal os • Progesterone: role in
• Proteases or fetal from closed to open: T maintenance of
Preterm
fibronectin from àYàVàU pregnancy
Labor
the amniochorion • Cerclage: leads in
à cervical increased cervical
weakness length
• Uretonins • Pessary: rotates the
produced by cervix posteriorly
chorion and and corrects the
decidua à cervical angle
uterine • Tocolytics (B-
contractions adrenergic receptor
• Intra-amniotic agonists,
infection and fetal magnesium sulfate,
inflammatory calcium channel
response blockers, COX
syndrome (FIRS) inhibitors, NO
– role of donors, oxytocin-
interleukins receptor
IL1,6,8 and antagonists)
cytokines TNF,
CSF, FasLà
breakdown of
fetal membrane
and cervix

• More than 80% • Death is • Patients with General Management
of abortions accompanied by spontaneous abortion • Early abortion (<12 weeks) – do curettage
occur in the hemorrhage into usually present with • Late abortion (>12 weeks) – expectant management; formed bony
first 12 weeks the decidua delayed menses, spicules can lacerate the uterus if curettage is done
of pregnancy. basalis. vaginal bleeding,
• At least half of • This is followed and lower abdominal T/N: See table below for the different classifications of spontaneous
all miscarriages by necrosis of pain abortion, and their respective management.
have tissues adjacent • Physical examination
chromosomal to the bleeding, should focus on
anomalies. that stimulates determining the
• After the first uterine source of bleeding
trimester, contractions and • Differential
abortion rate expulsion. diagnosis for
and incidence • An intact bleeding or pain in
of gestational sac is early pregnancy:
chromosomal usually filled with o Physiologic (i.e.
anomalies fluid and may or related to
decrease. may not contain implantation)
• Increased risk an embryo or o Ectopic pregnancy
of spontaneous fetus. o Gestational
abortion is • First-trimester trophoblastic
associated loss: death of the disease (GTD)
with: maternal embryo or fetus o Cervical, vaginal or
Sponta- age (>35 precedes uterine pathology
neous years), previous spontaneous o Subchorionic
abortion treatment of expulsion hematoma
mother with • Late pregnancy • Findings on
abdominopelvic loss: fetus transvaginal
radiotherapy or usually does not ultrasound according
chemotherapy, die before to the CPG on
increasing expulsion Abortion, 2015
paternal age, o Crown-rump length
conceives > 7 mm and no
within 3 months cardiac activity
following term o Mean gestation sac
birth, parity diameter > 25 mm
without embryo
o Absence of embryo
with cardiac activity
> 2 weeks after a
prior scan that
found a GS without
a yolk sac.
o Absence of embryo
with cardiac activity
> 11 days after a
prior scan that
found a GS with a
yolk sac
SPONTANEOUS ABORTION
CONTRAC- CERVICAL UTERUS BAG OF
CATEGORIES FEATURES TIONS
BLEEDING
DILATATION & AOG WATERS
OTHERS MANAGEMENT
• Bloody vaginal discharge ++ +/- Closed = Intact (+) FHT • Observation
or bleeding appears • Acetaminophen-based
through a closed analgesia will help relieve
cervical os during the discomfort from
first 20 weeks. cramping.
• Bleeding occurs first. • No evidence to support
• Cramping abdominal bed rest,
pain follows from a few progestrogens and
hours to several days vitamin
later. supplementation as
• Vital signs within advantageous in the
Threatened
normal limits (unless prevention of
Abortion
with infection or miscarriage
hypovolemia due to • Progesterone – may be
bleeding) beneficial in women who
• Bloody vaginal have had 3 or more
discharge with/without miscarriages
hypogastric pain, low
back pain
• Soft and non-tender
abdomen
• Bimanual examination
unremarkable
• Gross rupture of +++ ++ Open = Ruptured (+) FHT • If sudden discharge of
membranes à leaking fluid in early pregnancy
amniotic fluid occurs before any pain,
• Sudden discharge of fever, or bleeding:
amniotic fluid followed woman may be put to
Inevitable by heavy vaginal bed and observed
Abortion bleeding • After 48 hours, if no
• (+) Abdominal pain and additional amniotic
cramping fluid has escaped, and
• In the presence of there is no bleeding,
cervical dilatation, it is pain, or fever: resume
nearly always followed her usual activities

by uterine contractions except for any form of
or infection vaginal penetration
• Termination is typical in • If gush of fluid is
spontaneous rupture in accompanied or
the first trimester. followed by bleeding,
pain, or fever: abortion
should be considered
inevitable and the uterus
emptied
• Fetus or placenta may +/- ++ Open ≠ Ruptured Passage • Surgical evacuation is
remain entirely in utero or of meaty the
or may partially extrude unappreci tissue standard treatment
through the dilated os. able • Expectant management
• Before 10 weeks AOG: is also an acceptable
fetus and placenta are alternative but it carries
frequently expelled higher risk of incomplete
together miscarriage and bleeding,
• After 10 weeks AOG: and subsequent need for
they deliver separately surgical emptying of the
• Uterus is smaller for uterus
AOG. • Manual vacuum
• Vaginal bleeding may be aspiration
intense and (MVA) and sharp
accompanied by curettage
Incomplete
abdominal pain. have comparable
Abortion
advantages
• Antibiotics are to be
used when indicated
• Hysterotomy is
performed in situations
where:
(1) myometrium is too thin
(2) cervix is blocked by a
fibroid or other uterine
anomalies
• In the Philippines,
misoprostol is not
approved for
therapeutic
use in miscarriage.
• Complete detachment of - +/- Closed ≠ Unappreci Absent • If an expelled complete
the placenta from the able signs of gestational sac is not
uterus and expulsion of pregnanc identified, transvaginal
the conceptus followed y sonography is performed
by closure of the internal to differentiate a
cervical os complete abortion from
• Bleeding and pain have threatened abortion or
subsided or minimal, but ectopic pregnancy
Complete history of heavy bleeding, • Characteristic findings
Abortion cramping, and passage of include a thickened
tissue is typical endometrium without
• History of expulsion of gestational sac
products of conception
• Cervix is closed
• Uterus should be
contracted or small for
AOG
• Uterus softer than normal
• Uterus retains dead - Spotting Closed ≠ Unappreci (-) FHT • Expectant management
products of conception able by awaiting spontaneous
behind a closed cervical expulsion
os for days or even • Cervical preparation
weeks decreases
• Prolonged retention of a the length of the uterine
dead fetus carries a risk evacuation process
of serious coagulation • Adjuncts to surgical
defects procedures consisting of
• Vital signs are within laminaria and other
normal limits dilators, intraoperative
• Uterus usually small for real time ultrasound and
AOG intracervical vasopressin
Missed
are acceptable
Abortion practices.
• The use of uterotonics
in the form of oxytocin
has been well
established as standards
in the pharmacologic
management of missed
miscarriage
• In the Philippines,
misoprostol is not
approved for
therapeutic
use in miscarriage.
Bacteria gain uterine entry and colonize dead conception products à Organisms may invade myometrial • Uterine evacuation
Septic Abortion tissues and extend to cause parametritis, peritonitis, septicemia and rarely endocarditis (worrisome are severe • Intensive broad-
necrotizing infections and toxic shock syndrome caused by S. pyogenes and C. perfringens) spectrum antibiotic

therapy (i.e. clindamycin
+ gentamicin, w/ or w/o
ampicillin)
ASSISTED VAGINAL BIRTH

VACUUM DELIVERY
A Address Consent
Anesthesia Pain relief
Assistance Neonatal support
B Bladder Empty bladder
C Cervix Fully dilated, effaced and membranes ruptured
Contractions Adequate
D Determine Position, station, clinical pelvimetry
E Equipment Inspect vacuum cup, pump, tubing, check pressure
F Fontanelle Position cup over flexion point, clear maternal tissue, start at 100 mmHg
G Gentle traction Increase pressure to 600 mmHg as contraction begins, encourage continuous expulsive efforts, pull with contraction
H Halt • If there is no progress after 3 traction-aided contractions
• If vacuum pops off three times
• Should not exceed 20 minutes total application time
I Incision Consider episiotomy
J Jaw Removal of vacuum if jaw is reachable or delivery assured
FORCEPS DELIVERY
A Address Consent
Anesthesia Pain relief
Assistance Neonatal support
B Bladder Empty bladder
C Cervix Fully dilated, effaced and membranes ruptured
Contractions Adequate
D Determine Position, station, clinical pelvimetry
E Equipment Check equipment if functional and appropriate
F Forceps Start with phantom application
Insert left blade: left blade, left hand, maternal left, pencil grip, vertical insertion, right thumb directs
Insert right blade: right blade, right hand, maternal right, pencil grip, vertical insertion, left thumb directs
Lock blade and support
Posterior fontanelle 1 cm above plane of shanks
Fenestration not >1 finger-breadth
Sagittal suture perpendicular to plane with occipital sutures 1 cm above blades
G Gentle traction Encourage continuous expulsive efforts, pull with contractions only
H Handle elevated Traction in birth canal axis, do not elevate handle too early
I Incision Consider episiotomy
J Jaw Removal of forceps if jaw is reachable or delivery assured
SHOULDER DYSTOCIA
DEFINITION RISK FACTORS COMPLICATIONS DIAGNOSIS MANAGEMENT
After the Antepartum Fetal/Neonatal • “Turtle sign” – head DO NOT
delivery of the Factors • Hypoxia/asphyxia recoils against • Pull
head, there is • Suspected fetal • Birth injuries: perineum • Push
impaction of macrosomia fractures, brachial • Spontaneous • Panic
the anterior • Gestational age plexus injury restitution • Pivot
shoulder on > 42 weeks Maternal • Failure of delivery with ALARMER
the pubic • Multiparity • Post-partum maternal expulsive Ask for help
symphysis in • Previous hemorrhage efforts and usual • Assure availability of appropriate equipment and personnel
the AP shoulder • Serious perineal, maneuvers • Get cooperation of stakeholders
diameter. dystocia, cervical, and • Wait for the next contraction
macrosomia uterine lacerations Lift or hyperflex the legs
• Obesity, • Uterine rupture • Flatten the head of the bed
excessive weight • McRobert’s maneuver – Remove legs from stirrups and
gain sharply flex the thighs to the abdomen.
Intrapartum Anterior shoulder disimpaction
Factors • Mazzanti maneuver (abdominal approach) – apply
• Prolonged labor suprapubic pressure with the heel of clasped hands from the
• Operative vaginal posterior aspect of the anterior shoulder
delivery • Rubin maneuver (vaginal approach) – shoulder is pushed
• Induction of forward the chest or pressure is applied to the scapula of the
labor anterior shoulder
• Epidural Rotation of posterior shoulder
anesthesia • Wood’s Corkscrew maneuver – Place hand behind the
posterior shoulder of the fetus. The shoulder is then rotated in
a corkscrew manner so that the impacted anterior shoulder is
released.
Manual removal of posterior arm
• Flex posterior arm by applying pressure on the antecubital
fossa; the hand is grasped and swept across the chest to be
delivered
Episiotomy
Roll over to “all-fours” position
• Gaskin maneuver – position the mother on all-fours to alter
pelvic dimensions
Other maneuvers
• Cleidotomy – deliberate clavicular fracture
• Symhysiotomy
• Zavanelli maneuver – reverse the cardinal movements of
labor and replace head into the uterus for CS delivery

BREECH PRESENTATION AND DELIVERY
DEFINTION DIAGNOSIS MANAGEMENT
Buttocks of the • Leopold’s External Cephalic Version
fetus enters the maneuver • Fetus is turned in-utero from a non-cephalic to a cephalic presentation by external manipulation
maternal pelvis • Vaginal exam • Dislodge buttocks from the pelvis, pushing upwards and laterally
before the head • Ultrasound • Grasp the head and direct it downwards
• Rotate by pushing the baby upward and to the side of the fetal back with 1 hand holding the buttocks
• Maneuver head over the pelvic inlet
• Timing: 34-36 weeks, NOT before
• Contraindications: contraindications to labor (previa, active HSV, etc.), antepartum hemorrhage, major fetal
anomalies, multiple gestation, ruptured membranes
• Risks: abruption, ruptured membranes and cord prolapse, labor, FHR abnormalities, hemorrhage
• Optional adjunct procedures: tocolytics, anesthesia, moxibustion, postural management
Caesarian Delivery
• Factors favoring CS: large fetus (>3,800 - 4,000 grams), healthy and viable preterm fetus either with active labor
or with indicated delivery, severe fetal-growth restriction, fetal anomaly incompatible with vaginal delivery, prior
perinatal death, incomplete or footling breech presentation, hyperextended head, pelvic contraction or
unfavorable pelvic shape, prior CS
Vaginal Breech Delivery
• May be attempted if fetal and maternal conditions permit
• Encourage mother to have expulsive forces
• Fetal traction should be avoided; manipulation must be done after delivery at the umbilicus level (spontaneous
delivery until umbilicus)
• Pinard’s maneuver – deliver each leg by applying pressure on the popliteal fossa and sweeping the lower
extremities outward
• Spontaneously deliver until level of the scapula
• Loveset maneuver – rotate baby to position shoulders across AP diameter; vaginal hand reaches into the sacral
hollow; deliver posterior arm by applying pressure on the antecubital fossa and sweeping arms across chest
• Fetal head may deliver spontaneously with suprapubic pressure, Mauriceau maneuver, or Piper forceps

MODULE/TOPIC 18 LABORATORY DIAGNOSIS
PART 1: MICROBIOLOGY
I. SPECIMEN COLLECTION GUIDELINES
GENERAL GUIDELINES
• Observe aseptic technique always
• Specimen should be transported within 2 hours from the time of
collection
Specimen Container Preparation/ Instruction
• Disinfect venipuncture site with 70%
alcohol and Povidone iodine
Blood
Blood or • Draw blood at the time of febrile
culture
Bone Marrow episode
bottles
• Draw 2 sets ACID FAST STAIN (AFB STAIN)
• Draw >20 ml/set
• RATIONALE: To differentiate organisms by acid fast staining. Mycolic
• Disinfect skin before aspirating
acid absorbs the primary stain (carbolfuchsin) causing acid-fastness of
• Transport to laboratory within 15
Sterile bacteria
Cerebrospinal minutes
Screw Cap • PROCEDURE/ INTERPRETATION
Fluid • Inoculate in Chocolate Agar
Tube o Kinyoun Method—cold method
• If 3 specimens were collected, send
2 specimen to Microbiology
nd o Ziehl- Neelsen Method—hot method of AFB
Clean, • Clean catch as much as possible Non- Acid-
Acid-Fast
Stool Culture leak-proof • Specimen must not be contaminated STEPS Fast
Organism
container with urine Organism
Cervical / 1. Primary staining with
• Do not use lubricant for speculum Red Red
Vaginal Swab carbolfuchsin
• Do not allow the swab to get dry
Specimen 2. Heat steam (will serve as
Red Red
• Midstream clean catch urine mordant)
• Clean the area prior to specimen 3. Decolorize with acid alcohol Red None
collection 4. Counterstain with methylene
Screw- Red Green
Urine • Do not acquire specimen from Foley blue
Cap Tube
Catheters
• Disinfect skin prior to suprapubic • REPORTING OF AFB RESULTS
aspiration Number of AFB seen per 1000x
Report
magnification
BIOSAFETY LEVELS 0 AFB per field No AFB Seen
Biosafety 1-2 AFB per 300 fields Doubtful
Risk Sample Organism
Level 1-9 AFB per 100 fields 1+
I No risk M. gordonae, B. subtilis, C. albicans 1-9 AFB per 10 fields 2+
Staphylococcus aureus, Bacillus anthracis, 1-9 per field 3+
Bordetella pertussis, C. diphtheria, N. >9 per field 4+
Moderate
II gonorrhea, Proteus, Klebsiella, Proteus,
Risk
Streptococcus pyogenes, Rabies virus, III. SPECIMEN CULTURE
Hepatitis A-C, most parasitic agents
High risk but Mycobacterium tuberculosis, Brucella, CRITERIA AND CHARACTERISTICS FOR MICROBIAL CLASSIFICATION
III with Francisella, Yersinia pestis, Pasteurella, Phenotypic
Principle
treatment HIV, Yellow Fever virus, prions, mold Criteria
High risk Characteristics of microbial growth patterns on
IV and no Ebola virus, Marburg virus, Lassa virus artificial media as observed when inspected with
Macroscopic
treatment the unaided eye. Examples of such characteristics
Morphology
include the size, texture, and pigmentation of
bacterial colonies.
II. STAINING
Size, shape, intracellular inclusions, cellular
Microscopic appendages, and arrangement of cells when
GRAM’S STAIN observed with the aid of microscopic
Morphology
• RATIONALE: To differentiate organisms by gram activity of bacteria. The magnification.
presence of peptidoglycan layer in gram positive cells will prevent Ability of an organism to reproducibly stain a
decolorization and coloring of cells with secondary stain (safranin) particular color with the application of specific
• PROCEDURE/ INTERPRETATION dyes and reagents. Staining is used in conjunction
Staining
Gram- with microscopic morphology for bacterial
Gram-Positive Characteristics
Steps Purpose Negative identification. For example, the Gram stain for
Reaction
Reaction bacteria is a critical criterion for differential
1. Heat Fixate the identification.
Fixation bacteria on NONE NONE Ability of an organism to grow at various
slide Environmental temperatures, in the presence of oxygen and
2. Add Crystal Primary stain Requirements other gases, at various pH levels, or in the
VIOLET VIOLET
Violet (1 min) presence of other ions and salts, such as NaCl.
3. Add Lugol’s Mordant / fixes Ability of an organism to utilize various carbon
VIOLET VIOLET
Iodine (1 min) primary stain Nutritional and nitrogen sources as nutritional substrates
4. Add Alcohol Decolorizer Requirements when grown under specific environmental
(until no color VIOLET COLORLESS conditions.
drops) Exhibition of a characteristic inherent resistance to
Resistance
5. Apply Counterstain specific antibiotics, heavy metals, or toxins by
VIOLET PINK Profiles
Safranin (1 min) certain microorganisms.
Establishment of profiles of microorganisms by
• COLONY MORPHOLOGIES Antigenic various serologic and immunologic methods for
Properties determining the relatedness among various
microbial groups.
Establishment of the molecular constituents of the
cell that are typical of a particular axon, or
Subcellular organism group, by various analytic methods.
Properties Some examples include cell wall components,
components of the cell membrane, and
enzymatic content of the microbial cell.
Haemophilus Non-hemolytic, opaque, non-creamy to gray
TYPES OF CULTURE MEDIA influenzae colonies (Blood Agar shows no growth)
Type of Media Example
Allows growth for
General all organisms as Blood Agar Plate (BAP),
Purpose Media long as not Nutrient Agar
fastidious
Allows growth for Chocolate Agar Plate,
Enriched Media
fastidious Buffered Charcoal Yeast
organisms Extract (BCYE)
Allows
Blood Agar Plate (BAP)
differentiation of
MacConkey (MAC), Eosin
Differential organisms by Eosin Methylene Blue (EMB)
Methylene Blue (EMB),
Media differentiation of Purpose Selective and differential media for Salmonella and
Xylose Lysine Deoxycholate
biochemical Shigella spp. (isolation of fecal coliforms)
(XLD)
reactions Components • Peptone
Thiosulfate Citrate Bile Salt • Lactose & Sucrose – provides differentiation of the
Inhibits growth of
(TCBS), Salmonella-Shigella different coliforms
Selective Media some and allow
Agar (SS), Thayer-Martin • Eosin Y & Methylene Blue – inhibit growth of gram
growth of some
Agar (TMA), Campy Blood (+) organisms
organisms
Agar (CBA) o Green metallic sheen – indicator of the vigorous
Inhibitory Agents: lactose and/or sucrose fermentation typical of
• Dyes, Bile salts, Vancomycin (TMA) – inhibits gram-positive fecal coliforms
• Trimethoprim (TMA) – inhibits gram-negative Positive Result Growth in agar
• Nystatin (TMA) – inhibits fungi • Greenish metallic sheen – suggestive of E. coli
• Pink – lactose fermenter
• Colorless – non-lactose fermenter
Blood Agar Plate (BAP)
Used as general purpose media for isolation and
Purpose
growth of bacteria
Components 5% sheep’s blood in nutrient agar base
Growth in agar with distinct hemolytic patterns
• ALPHA hemolysis – green
Uninoculated Lactose Lactose Non-lactose
Positive Result • BETA hemolysis – clearing/yellowing of agar
fermenter w/ fermenter fermenter (at 6
• GAMMA hemolysis – no hemolysis
greenish and 9 o’clock)
Medusa head colonies – Bacillus anthracis
metallic sheen
Negative Result No growth
Mannitol Salt Agar (MSA)
Used for isolation and differentiation of pathogenic
Purpose
staphylococci, principally Staphylococcus aureus
• Phenol Red – indicator
Components • 7.5% NaCl – selective for Staphylococcus aureus
• Mannitol – CHO Source
Growth in agar
Alpha Hemolysis Beta Hemolysis Gamma hemolysis
Positive Result • Yellow – S. aureus
• Colorless/ Pink other Staphylococcus spp.
MacConkey Agar (MAC)
Negative
Used to isolate and differentiate members of the No growth
Result
Purpose Enterobacteriaceae based on the ability to ferment
lactose
• Lactose – CHO source
• Neutral Red – indicator
Components
• Bile Salt – inhibits growth of gram (+) organisms
• Crystal Violet – inhibits growth of gram (+) species
Growth in agar with distinct patterns
Positive
• Pink – Lactose fermenter Yellow colonies – S. aureus
Result
• Colorless – Non-lactose fermenter Pink colonies – other Staphylococci
Negative
No growth
Result Mueller Hinton Agar
Media used for bacterial susceptibility testing using Kirby
Purpose
Bauer (Disk Diffusion) Method
Thymidine and thymine levels are monitored and kept low
Component
to prevent false inhibition of TMP and SXT
Bacterial Susceptibility patterns (Sensitive, Intermediate,
Results Resistant) based on growth pattern around each bacterial
disk
Non-Lactose
Uninoculated Lactose Fermenter
Fermenter
Chocolate Agar (CHOC)

Used to isolate fastidious organisms that requires
Purpose Factors X and V for growth, and are usually
capnophilic
Blood is heated to lyse RBC, releasing Factors X & V
from hemoglobin
Components • Factor X – Hemin
• Factor V – NAD (Nicotinamide adenine
dinucleotide)
Positive Result Growth in agar
Negative Result No growth
Growth Characteristics
Growth on agar is grayish, non-hemolytic, round,
Neisseria
convex, smooth, moist, glistening colonies with a
meningitidis
clearly defined edge
Neisseria Colonies are pinkish-brown and translucent, exhibit
gonorrhoeae smooth consistency and defined margins
E-Test Strip • Mineral salt solution
Uses the principle of a predefined antibiotic gradient on a • Glycerol & Pyruvate
plastic strip to generate a Minimal Inhibitory Concentration o If with glycerol: favors M. tuberculosis growth
Purpose o If without glycerol but with pyruvate: favors M.
(MIC) value. It is processed in the same way as the disk
diffusion. bovis growth
Individual antibiotic strips are placed on an inoculated agar Positive Result Growth on medium
surface. After incubation, the MIC is read where the Negative Result No growth
Principle
growth/inhibition edge intersects the strip graduated with an
MIC scale
Results MIC on Intersection
Left—uninoculated; Right—with growth
Modified Thayer Martin Agar

Selective medium used for the isolation of
Purpose gonococci (Neisseria gonorrheae) from specimen
Thiosulfate Citrate Bile Salt Sucrose (TCBS) Agar containing a mixed flora of bacteria and/or fungi
Purpose Undefined, selective, and differential medium used for Contains antimicrobials which inhibit the growth of
the primary isolation of Vibrio species organisms other than N. gonorrhoeae
Components • Alkaline pH (pH 8.6) – supports growth of Vibrio spp. • Vancomycin inhibits gram-positive bacteria,
• Oxgall and sodium cholate – inhibit the growth of Components • Colistin inhibits gram-negative bacteria including
Gram-positive bacteria the commensal Neisseria spp.,
• Sucrose – carbohydrate source • Trimethoprim inhibits swarming of Proteus spp.,
• Bromothymol blue – pH indicator • Nystatin is an antifungal agent
• Sodium thiosulfate – electron acceptor for sulfur Positive Result Growth
reduction Negative Result No Growth
• Ferric ammonium citrate – H2S indicator
Positive Growth in agar
Result • Yellow colonies – sucrose fermenter
• Black colonies – H2S producer
Negative No growth
Result
OTHER PLATING MEDIA FOR ROUTINE BACTERIOLOGY

Medium Primary Purpose
Differential: Group D Streptococci and
Bile Esculin Agar (BEA)
Enterococci
Bordet Gengou Agar;
Isolation of Bordetella pertussis
Uninoculated Non-Sucrose Sucrose Fermenter Regan Lowe Agar
Fermenter Buffered Charcoal Yeast
Enrichment of Legionella sp.
Extract (BCYE)
Salmonella-Shigella Agar (SSA) Campy Blood Agar (CBA);
Selective for Campylobacter spp.
Used for the isolation, cultivation and differentiation Skirrow agar
of gram-negative enteric microorganisms. This medium Columbia Colistin-Nalidixic
Selective for gram-positive cocci
Purpose is not recommended for the primary isolation of Acid (CNA) Agar
Shigella as some of Shigella strains may not grow on SS Cystine-tellurite blood agar Isolation of C. diphtheriae
agar due to relatively high level of selectivity Selection and differentiation of E. coli
MacConkey Sorbitol Agar
• Lactose: fermentable carbohydrate; allows 0157:H7
differentiation of enteric organism Selective for N. gonorrhoeae and N.
Thayer-Martin agar
• Beef extract, proteose peptone: provides the meningitidis
nitrogen, vitamins, and amino acids in SS Agar Enrichment broth used for subculturing
Trypticase soy broth
• Sodium thiosulfate & sodium citrate: selective various bacteria from primary agar plates
agents, providing an alkaline pH to inhibit Gram- Isolation and differentiation of Salmonella
Xylose lysine
Components and Shigella spp. from other gram-
positive organisms and suppress coliforms desoxycholate (XLD) agar
negative enteric bacilli
• Ferric citrate: acts with sodium thiosulfate as an
indicator to detect hydrogen sulfide production
COMMON COLONY MORPHOLOGIES
• Bile salts: The bile salts inhibit growth of gram-
positive microorganisms Mucoid Colonies
• Brilliant Green/Neutral Red: pH indicator Encapsulated organisms:
Colorless colonies with black Streptococcus pneumoniae
Salmonella enterica Streptococcus agalactiae
centers
Shigella flexneri Colorless colonies Haemophilus influenza
Result Meningiococcus
Pink to rose red colonies with
Escherichia coli Klebsiella pneumoniae
precipitate
Salmonella
Entercoccus faecalis Inhibited
Swarming
Usually seen in Proteus spp.
Lactose Fermenter H S producer

2
Non-Lactose
Fermenter
Red colonies
Lowenstein-Jensen Agar Indicative of Serratia marcescens
Nutrient and differential medium for the growth of
Purpose
Mycobacterium species.
• Malachite green
Components
• Whole, inspissated eggs
Blue-Green or Green Colonies
Indicative of Pseudomonas spp.
Yellow colonies
Micrococcus spp.
IV. BIOCHEMICAL TESTING OF MICROORGANISMS

Left—resistant; Right—sensitive
Catalase Test
Purpose Used to differentiate Streptococcus from Staphylococcus cAMP Test
The CAMP test (an acronym of the developers of the
Principle test—Christie, Atkins, and Munch-Peterson) is used to
Purpose
differentiate Group B Streptococcus agalactiae (+) from
other Streptococcus species (-)
Bubbling of organism upon contact with hydrogen
Group B Streptococcus agalactiae produces the
Positive peroxide
CAMP factor that acts synergistically with S. aureus.
Staphylococcus spp Principle
When streaked perpendicularly with each other, it
Negative Streptococcus spp
produces arrowhead hemolysis
Left: Positive Right: Negative
Coagulase Test
Purpose The coagulase test is typically used to differentiate
Staphylococcus aureus from other Gram-positive cocci
Principle Agglutination of the cells on the slide within one to two
minutes indicates the presence of bound coagulase Optochin Test
Components Citrated Plasma or Rabbit’s Plasma Purpose • Used to presumptively differentiate Streptococcus
Positive Coagulation (if slide: Clumping) pneumoniae from other alpha-hemolytic
Negative No coagulation streptococci
• Chemical name of optochin: Ethyl hydrocupreine
hydrochloride (Taxo P)
Positive S. pneumoniae
Negative S. pyogenes
Tube coagulase Slide Coagulase

Positive - Top, Negative - Bottom
Bacitracin Susceptibility
Used to differentiate and presumptively identify beta-
hemolytic group A streptococci (Streptococcus
Purpose
pyogenes-susceptible) from other beta-hemolytic
Streptococci (resistant)
Positive Susceptible – S. pyogenes
(Sensitive) Zone of inhibition seen Oxidase Test
Negative Purpose Used to identify bacteria containing the respiratory
Other beta hemolytic Streptococci
(Resistant) enzyme cytochrome c oxidase
Positive Purple color
Pseudomonas spp.
Negative Other members of Enterobacteriaceae
Left: Negative; Right: Positive
Negative—Top; Positive—Bottom Indole Test

Purpose Used to identify organisms that produce the enzyme
Novobiocin Test tryptophanase (hydrolyzes tryptophan to indole)
• Used to differentiate coagulase negative Principle Kovac’s reagent (dimethylamine-benzaldehyde and
Staphylococci hydrochloride), when added to the broth culture, reacts
Purpose • Most frequently used to presumptively identify with the indole, producing a red color.
the novobiocin-resistant Staphylococcus Components Indole Reagent
saprophyticus Positive Pink
Positive (Sensitive) S. epidermidis Negative No color change
Negative (Resistant) S. saprophyticus

Triple Sugar Iron (TSI) Agar
Left - Positive; Right - Negative
Urease Test
Purpose Used to determine an organism’s ability to produce the
enzyme urease, which hydrolyzes urea. Proteus sp.
may be presumptively identified by the ability to rapidly
hydrolyze urea. Left to Right: K/A; K/NC; uninoculated control; K/A+; A/AG
Common Results
Principle Hydrolysis of urea produces ammonia and CO2. The
Organism Slant Butt Gas H2S
formation of ammonia alkalinizes the medium, and the
pH shift is detected by the color change of phenol red Escherichia
from light orange to magenta/pink Klebsiella A A + -
Components Urea Enterobacter
Phenol Red - Indicator Seratia
K A - -
Positive Pink Shigella
Negative No color change Salmonella
K A + +
Proteus
Pseudomonas K K - -
Lysine Iron Agar (LIA)

Used to differentiate enterics based on their ability to
decarboxylate or deaminate lysine and produce
Purpose hydrogen sulfide (H2S). LIA also is used in
combination with Triple Sugar Iron Agar to identify
members of Salmonella and Shigella.
/ Above the slash - Slant
Below the slash - Butt
K (slant) Lysine deaminase negative
Triple Sugar Iron (TSI) Agar Symbols
K (butt) Lysine decarboxylase positive
Used to differentiate members of Enterobacteriaceae R Lysine deaminase positive
Purpose and to distinguish them from other Gram-Negative Sulfur Reduction
HS
bacilli such as Pseudomonas or Alcaligenes 2
Lysine- to determine lysine decarboxylation or

/ Above the slash - Slant
Components deamination
Below the slash - Butt Ferric ammonium citrate- sulfur anaerobic reduction
A Acid accumulation and fermentation
Result Interpretation Symbol
Symbols K Alkaline accumulation
Lysine deaminase
NC No change Purple Slant/
negative; Lysine K/A
H2S/ + Sulfur reduction Purple Butt
decarboxylase positive
G or Å Gas production Lysine deaminase
Result Interpretation Symbol negative; Lysine
Purple Slant/
Glucose and lactose decarboxylase K/K
Yellow Yellow Butt
fermentation with acid Results and negative; Glucose
Slant/ A/A
accumulation in slant and Interpretation fermentation
Yellow Butt
butt Lysine deaminase
Glucose fermentation positive; Lysine
Red Slant/
with acid production. decarboxylase R/A
Yellow Butt
Red slant/ Proteins catabolized negative; Glucose
K/A
Yellow Butt aerobically (in the slant) fermentation
with alkaline products Black Sulfur reduction
HS
(reversion) Precipitate 2
No fermentation.
Peptone catabolized
Red Slant/ aerobically and
K/K
Red Butt anaerobically with
alkaline products. Not
from Enterobacteriaceae
Results and No fermentation.
Interpretation Red Slant/ Peptone catabolized
no change aerobically with alkaline K/NC
in Butt products. Not from
Enterobacteriaceae
No change
Organism is growing
in slant/ No
slowly or not at all. Not NC/NC
change in
from Enterobacteriaceae
butt
Sulfur reduction. (An
acid condition, from
Black fermentation of glucose
precipitate or lactose, exists in the H2S
in Agar butt even if the yellow
color is obscured by the
black precipitate. Sulfur Indole Motility (SIM) Medium
Cracks/ Purpose Part of biochemical testing for Gram- Negative Organisms
Lifting of Gas production G/ Å
Principle Sulfur Determines ability to utilize iron as source
Agar of energy

Indole Identifies bacteria capable of producing
indole using the enzyme tryptophanase Citrate Agar
using the Kovac’s Reagent Used to determine the ability of an organism to use citrate as
Motility Determines motility of organism its sole source of carbon. Citrate utilization is one part of a
Results test series referred to as the IMViC (Indole, Methyl Red,
Purpose
Sulfur • (+): blackening of medium along line of inoculation Voges-Proskauer and Citrate tests) that distinguishes between
• (-): no blackening members of the family Enterobacteriaceae and differentiates
Indole • (+): pink to red bank at the top of medium them from other Gram-negative rods.
• (-) yellow band at the top of medium Simmons Citrate Agar is a defined medium that contains
Motility • (+): diffuse zone of growth flaring from line of sodium citrate as the sole carbon source and ammonium
inoculation phosphate as the sole nitrogen source. Bromthymol blue
• (-): growth is confined to stab line dye, which is green at pH 6.9 and blue at pH 7.6, is added as
an indicator. Bacteria that survive in the medium and utilize
Principle the citrate also convert the ammonium phosphate to
ammonia (NH3) and ammonium hydroxide (NH4OH), both
of which tend to alkalinize the agar. As the pH goes up, the
medium changes from green to blue (Figure 7-23). Thus,
conversion of the medium to blue is a positive citrate test
result.
Citrate Agar
Positive Blue
Negative Green
A B C D E
Sulfur - - + - +
Indole + - - - +
Motility + - + + +
Sample E. S. Salmonell Enterobacter Proteus
Organism coli aureus a aerogenes Vulgaris
COMMON MOTILITY PATTERNS
Tumbling motility Listeria
Gliding motility Mycoplasma
Darting motility Vibrio cholerae, Campylobacter
jejuni
Swarming motility Proteus, spp, Clostridium tetani
Corkscrew motility Spirochetes
ALGORITHM FOR GRAM POSITIVE BACTERIA

ALGORITHM FOR GRAM NEGATIVE BACTERIA
COMMON MICROBIOLOGY ORGANISMS
GRAM POSITIVE COCCI

Organism Virulence Factor Clinical Treatment Culture/ Biochemical Characteristics
Protective proteins: Exotoxin-dependent: • Penicillinase- Gram’s Stain Gram positive cocci in clusters
• Protein A: binds IgG, • Gastroenteritis (food resistant penicillin Culture BAP: Alpha- Hemolytic colonies
prevents opsonization poisoning) • Clindamycin Characteristics MSA: Yellow colonies on MSA
and phagocytosis • Toxic shock syndrome • If methicillin- Biochemical Catalase (+)
• Coagulase: allows fibrin o High fever resistant, treat with Characteristics Coagulase (+)
clot formation around o Nausea and intravenous
organisms vomiting vancomycin
• Hemolysin o Watery diarrhea • If vancomycin-
• Leukocidin • Erythematous rash resistant, use
• Catalase • Hypotension linezolid
• Pencillinase • Desquamation
Staphylococcus • Scalded skin
aureus Tissue-Destroying Proteins syndrome
• Hyaluronidase: spreading
factor Direct invasion:
• Staphylokinase: lyses • Pneumonia
formed clots • Meningitis
• Lipase • Osteomyelitis
• Acute bacterial
Toxins endocarditis
• Enterotoxin: food • Septic arthritis
poisoning • Skin infection:
• Toxic shock syndrome folliculitis, furuncle,
toxin carbuncle, impetigo
Gram’s Stain Gram (+) cocci single/ in clusters
Culture BAP: Non-hemolytic colonies
• Nosocomial infections Characteristics MSA: Pink colonies
o Prosthetic joints Catalase (+)
Biochemical
• Polysaccharide capsule o Prosthetic heart Coagulase (-)
Characteristics
(glycocalyx): adheres to valves Novobiocin SENSITIVE
a variety of prosthetic o Ventriculoperitoneal
Staphylococcus • Vancomycin
device shunt
epidermidis
• Highly resistant to o IV line sepsis
antibiotics o UTI
• Frequent skin
contaminant in blood
cultures
Gram’s Stain Gram (+) cocci single/ in clusters

Culture BAP: gamma hemolysis
• 2nd most common
• Penicillin Characteristics MSA: pink colonies
Staphylococcus urinary tract infections
• TMP-SMX Catalase (+)
saprophyticus in sexually active
• Quinolones Biochemical  Coagulase (-)
women
characteristics Nitrate (-)
Novobiocin RESISTANT

GRAM POSITIVE COCCI
Organism Virulence Factor Clinical Treatment Culture/ Biochemical Characteristics
• Penicillin G (DOC) Gram’s Stain Gram (+) cocci in chains

• Penicillin V Culture
Beta- hemolytic colonies on BAP
• Erythromycin Characteristics
Direct Invasion: • Following rheumatic Catalase (-)
• Pharyngitis fever Biochemical Bacitracin SENSITIVE
Virulent proteins:
• Skin infection: o Penicillin characteristics CAMP (-)
• M Protein
folliculitis, furuncle, prophylaxis to  Na hippurate (-)
• Lipoteichoic acid
carbuncle, impetigo, prevent repeat
• Streptokinase
erysipelas, necrotizing strep throat
• Hyaluronidase
fasciitis infections that
• Beta-hemolytic
could potentially
Toxigenic: lead to a
Streptococcus Toxins:
• Scarlet fever rheumatic heart
pyogenes • Erythrogenic toxin or
• Toxic shock syndrome disease
pyrogenic toxin: for
o If permanent heart
scarlet fever
Antibody-mediated valve damage has
• Toxic shock syndrome
(long-term): occurred,
toxin (pyogenic exotoxin
• Rheumatic fever antibiotics are
A)
• Acute post- required when
• Streptolysin-O: O labile
2
streptococcal certain
• Streptolysin-S: O stable
2
glomerulonephritis procedures are
performed due to
high risk of
bacterial
endocarditis
Gram’s Stain Gram (+) cocci in chains
Culture
• Neonatal meningitides BAP: beta hemolytic colonies
Characteristics
Streptococcus • Neonatal pneumonia • Penicillin G
Catalase (-) 
agalactiae • Neonatal sepsis
Biochemical Bacitracin RESISTANT
characteristics CAMP (+) 
Na hippurate (+)
Gram’s Stain Gram (+) cocci in chains
Culture
Alpha hemolytic colonies on BAP
Characteristics
Optochin RESISTANT
• Subacute bacterial Biochemical
 Alpha Hemolytic on Blood Agar
endocarditis characteristics
• Glycocalyx: enhances Catalase (-)
Streptococcus • Dental caries (S. • Penicillin G
adhesion to damaged
viridans mutans)
heart valves
• Brain or liver abscess
Gram (+), diplococci, lancet-

Gram’s Stain
shaped
Culture
Alpha hemolytic colonies on BAP
Characteristics
Optochin SENSITIVE
• Pneumonia (most  Alpha hemolytic under aerobic
• Penicillin G
common cause of
• Capsule (83 serotypes) • Erythromycin Biochemical conditions 
CAP)
Streptococcus • Pneumolysin: binds to • Ceftriaxone characteristics Bile soluble (+) 
• Meningitis Catalase (-)
pneumoniae cholesterol in host-cell • Vaccine: against the
• Sepsis Quellung (+)
membranes 23 common capsular
• Otitis media
antigens
GRAM POSITIVE BACILLI

Organism Characteristics & Virulence Clinical Treatment Diagnostics
• Triad: Gram’s Stain: Club-shaped bacilli showing
• Endospores (heat-resistant)
o Symmetric terminal spores (tennis racket-shaped)
• Anaerobic
descending pattern of
Clostridium • Motile (flagella) • Antitoxin
flaccid paralysis with
botulinum • Fresh honey: associated with • Penicillin
prominent bulbar
infant botulism • Hyperbaric oxygen
involvement
• Neurotoxin: inhibits release
o Absence of fever
of Ach from peripheral nerves
o Intact sensorium
• Endospores • Lockjaw • Tetanus toxoid
Clostridium
• Anaerobic • Opisthotonos o Antitoxin (Ig) at
tetani
• Found in soil • Trismus wound site

GRAM POSITIVE BACILLI
• Tetanospasmin: inhibits • Penicillin or
release of GABA and glycine metronidazole
resulting to spasms • Vaccine: DPT
• Gas gangrene
• Double hemolysis on blood
o Pain Gas gangrene:
agar
o Edema • Wound debridement
• Nonmotile but with rapidly
o Cellulitis with • Penicillin G
Clostridium spreading growth on culture
crepitation
perfringens media
• Food Poisoning Food poisoning:
• Alpha toxin: lecithinase that
o Watery diarrhea with • Supportive
cleaves cell membranes
cramps management
• Enterotoxin
o Little vomiting
• Pseudomembranous
colitis
• Exotoxin • Withdraw causative
o Nonbloody diarrhea
• Transmitted by fecal-oral antibiotic
Clostridium o Pseudomembranes
route • Oral metronidazole or
difficile (yellow-white plaques)
• Hands of hospital personnel – vancomycin
on colonic mucosa
important intermediaries • Replace fluids
o Toxic megacolon can
occur
Gram (+), rod, V-shaped
Gram’s Stain clusters, palisades  or
Chinese letters  
• Small, grayish
colonies with a
granular appearance  
• Mostly translucent,
Diphtheria but with opaque
• Mild sore throat with fever centers, convex, with
Culture
• Exotoxin initially  continuous borders  
Characteristics
o A subunit – blocks protein • Pseudomembrane forms • Antitoxin • Potassium Tellurite
synthesis by inactivating on pharynx • Penicillin G or agar shows dark
Corynebacterium black colonies
EF2 erythromycin
diphtheriae • Loeffler’s medium
o B subunit – provides entry Diphtheria complications • DPT vaccine for
into cardiac and neural • Myocarditis (10%) prevention shows Babes- Ernst
tissue • Neural involvement granules
o Peripheral nerve palsies Catalase (+)
Biochemical
o GBS-like syndrome Urease (+)
Characteristics
Nitrate (+)
• Gram (+) bacilli with

centrally located
spore (beads on a
Gram’s Stain string/ Pearl necklace
appearance)
Cutaneous anthrax • Sometimes, box car-
• Ciprofloxacin like appearance
• Unique protein capsule that is Anthrax
antiphagocytic (polymer of • Cutaneous (95%) - • White, dry texture  
Pulmonary & GI anthrax • Flat and irregular
gamma-D glutamic acid) painless black vesicles
• Ciprofloxacin + 1 or Culture colony borders w/
Bacillus • Non- motile • Pulmonary (woolsorter’s
2 antibiotics Characteristics lobate margins
anthracis • Exotoxin disease)
(rifampcin, (medusa head
o Protective Antigen (PA) • GI: bloody diarrhea,
vancomycin, colonies)
o Edema Factor (EF) abdominal pain, vomiting
penicillin, imipenem,
o Lethal Factor (LF)
clindamycin,
clarithromycin)
Food poisoning
• Exotoxin • Emetic (caused by heat
• Symptomatic
Bacillus cereus o Heat labile stable exotoxin) Gram (+) spore-forming rod
treatment
o Heat stable • Diarrheal (caused by heat
labile exotoxin)
GRAM NEGATIVE COCCI

Organism Characteristics &
Clinical Treatment Diagnostics
Virulence
• Asymptomatic carriage in the • Vaccine against
• Capsule
nasopharynx capsular antigen A,
• Serotypes A, B, & C are
• Meningitis: C, Y and W-135 only • Gram-stain
associated with epidemics
o Fever not B • Culture:
Neisseria • IgA1 protease
o Nuchal rigidity • Antibiotics o Chocolate agar
meningitidis • Pili: for adherence
o Headache o Penicillin G (DOC) o Thayer-Martin
• Endotoxin:
o Photophobia o Ceftriaxone (or • Ferments glucose and maltose
lipopolysaccharide
• Meningococcemia (septicemia) other 3rd gen)
• Complication: Waterhouse-Friderichsen
Neisseria • Humans only • Third generation • Gram’s Stain: Gram Negative
• Men: urethritis
gonorrhea • Facultative anaerobe cephalosporin intracellular diplococci
GRAM NEGATIVE COCCI
Organism Characteristics &
Clinical Treatment Diagnostics
Virulence
• Ferments only glucose • Women: cervicitis which can progress to (ceftriaxone) +
• Pili: adherence to PID doxycycline (for
epithelial cells • Complications: chlamydia coverage)
• IgA protease o Sterility • Fluoroquinolones
• Lipooligosaccharide o Ectopic pregnancy • Ophthalmia
• Septic arthritis neonatorum:
• Ophthalmia neonatorum erythromycin eye • Culture:
drops immediately o Chocolate agar
after birth o Thayer-Martin
• Ferments glucose only
• Acid-fast stain of specimen
• Rapid culture (Bactec)
• Chest xray
• Primary tuberculosis (may be First line drugs: • GeneXpert PCR
asymptomatic) • Isoniazid (Abbrev. • PPD: measure cone of induration
• Mycolic acids cell wall • Reactivation or secondary tuberculosis INH) o >10mm or >5mm in an
Mycobacterium • Aerobic o Pulmonary • Rifampin immunocompromised host
tuberculosis • Slow growth rate (6-8 o Extrapulmonary • Pyrazinamide
weeks) o CNS, joints, bones (advanced • Ethambutol
• No exotoxin nor endotoxin extrapulmonary)
o Pott’s disease (spine) Second-line drugs:
o Miliary Tb (disseminated) • Streptomycin (IM)
GRAM NEGATIVE BACILLI

Transmission
• Fecal/oral route
• Newborn meningitis
• Migration up the urethra • Gram-stain
• Urinary tract infection Meningitis & sepsis
• Culture (specimen may be
• Diarrhea • Cephalosporin (3rd
Virulence: urine, sputum, CSF or blood)
o Non-invasive strain gen)
• Fimbriae (pili): colonization factor • Pathogenic strain may be
(enterotoxigenic) releases LT
• Capsule (K-antigen) isolated from the stool
and ST toxins; traveler’s UTI
Escherichia • Flagella (H-antigen) o *E.coli ferments lactose so
diarrhea • TMP-SMX
coli • Endotoxin (O-antigen) colonies has a metallic
o Enterohemorrhagic: bloody
sheen on EMB and pink-
diarrhea; no fever, no pus in Others
Enterotoxins: purple on MacConkey agar
the stool • Aminoglycoside
• LT (heat labile): inc cAMP o Urease negative
o Enteroinvasive: bloody diarrhea • Fluoroquinolones
• HT (heat stable): dec cAMP o TSI: A/A
(with pus in the stool); secretes
• Shiga-like toxin (verotoxin):
Shiga-like toxin; aka EIEC
inhibits protein synthesis by
inactivating the 60s ribosome
• Gram stain of urethral pus
• Pneumonia with significant lung • Third generation • Mucoid colonies on MAC
necrosis and bloody sputum cephalosporin: • Urease (+)
Klebsiella • Large polysaccharide capsule (“currant jelly” appearance) ceftriaxone
pneumoniae • Non-motile o Most common in alcoholics • Ciprofloxacin
• Hospital acquired urinary tract
infections and sepsis
• Found only in humans

• Zoonotic
• Enteric fever (typhoid fever):
• Found in uncooked eggs • Culture: blood, urine, stool that
fever, abdominal pain, • Ceftriaxone: crosses
• Produces H2S (black) may contain S. typhi (not part
hepatosplenomegaly, rose spots blood-brain barrier
Salmonella • Does not ferment lactose of normal flora)
• Chronic carrier state • Azithromycin
typhi • Black colony on SSA
• Gastroenteritis • TMP-SMX
Virulence • (+) selenite broth
• Sepsis • Ciprofloxacin
• Motile (H-antigen) • TSI: K/A + H2S
• Osteomyelitis: sickle cell patients
• Capsule (Vi antigen): protects
from intracellular killing
• Human pathogen
• Stool culture (Shigella is never
• Fecal-oral transmission
• Bloody diarrhea with mucus and a part of the intestinal normal
• No H2S production
pus (similar to EIEC) • Fluoroquinolones flora)
Shigella • Invades submucosa of intestinal
(for severe cases) • Colorless on SSA
dysenteriae tract (not l. propria)
Complications: Reiter syndrome, • TMP-SMX • Non-lactose fermenting
• Non-motile
Hemolytic Uremic Syndrome (HUS) • TSI: K/A
• Shiga toxin: inactivates 60s
ribosome
• Phase contrast microscopy of
• Fecal-oral transmission • Replace fluids
the stool
• Motile (H-antigen) • Doxycycline
• Cholera: severe diarrhea with rice o Comma-shape
• Mucinase: digests mucous layer • Fluoroquinolone
Vibrio cholerae water stools; no pus in the stool o Shooting star motility
• Choleragen (enterotoxin) • Tetracycline or
• Serotypes: Classical and El Tor • Oxidase (+)
increases levels of cAMP, azithromycin
• TCBS agar: grow as flat yellow
causing electrolyte secretion shortens duration
colonies
Transmission: • Microscopy: curved (seagull
• Secretory or bloody diarrhea
• Zoonotic wing-shaped), motile (darting
o Most common cause of • Symptomatic
• Present in uncooked meat motility), gram-negative rods
bacterial gastroenteritis treatment
Campylobacter • Optimum temperature at 42°C
• Animal abortion • Fluoroquinolone
jejuni Virulence: • Microaerophilic
• Erythromycin (for
• Enterotoxin similar to cholera • Media: Butzler, Skirrow,
Complications: severe disease)
toxin and LT of E. coli CBAP agar (selective media
• Guillain-Barre syndrome
• Cytotoxin with antibiotics)
GRAM NEGATIVE BACILLI
• Reactive arthritis (Reiter
syndrome)
• Erythema nodosum
• OCA (Omeprazole, • Curved rod with a tuft of polar
Clarithromycin, flagella
• Duodenal ulcers (peptic ulcer
Helicobacter Amoxicillin) • Highly motile
• No toxin disease)
pylori • OCM (Omeprazole, • Microaerophilic
• Chronic gastritis
Clarithromycin, • Urease-positive (survives
Metronidazole) stomach acidity)
• Obligate aerobe • Culture: greenish-metallic
• #1 opportunistic infection • Cefepime
• Non-lactose fermenter appearing colonies on blood
• Pneumonia (especially in cystic • Ceftazidime
• Motile (polar flagellum) agar, with a fruity (grape) smell
fibrosis patients) • Extended spectrum
• Exotoxin A (similar to C. o Produces pigment when
• Burn wound infections (ecthyma beta lactams
Pseudomonas diphtheria toxin): inhibits protein cultured (pyocyan and
gangrenosum) (Ticarcillin,
aeruginosa synthesis by blocking EF2 pyoverdin)
• Malignant otitis externa Piperacillin)
• Pyocyanin: damages cilia & • TSI: K/K
(swimmer’s ear) • Aztreonam,
mucosal cells • Grows on MAC and BAP
• UTI, Sepsis, corneal infections, Imipinem
• Verdoglobin: hemoglobin • Growth: 42°C
osteomyelitis • Ciprofloxacin
breakdown • Metabolically inert
• Gram stain: coccobacillary
• 2nd or 3rd gen • Culture on blood agar heated
• Meningitis (type b) in infants 3-36
• Obligate human parasite cephalosporin to 80°C for 15 mins (called
months of age; complications
• Transmitted via respiratory route • Hib vaccine: H. chocolate agar); need for
include mental retardation,
influenza hematin (X factor) and NAD (V
deafness, death
Haemophilus Virulence polysaccharide factor); placed in a high CO2
o Acute epiglottitis
influenzae • Capsule: 6 types (a-f, where b is capsule of type b environment
o Sepsis in asplenic patients
the most virulent) strain is conjugated • Fluorescent labeled ab (ELISA,
o Pneumonia
• Attachment pili to diphtheria toxoid latex agglutination)
• Non-encapsulated type: otitis
• IgA1 protease o Given at 6, 10, 14 • (+) Quellung test
media, sinusitis
months of age • Satellite phenomenon around
S. aureus
• TMP-SMX • Gram (-) rods
Proteus • Urease: hydrolyzes urea to form • Complicated UTI • Ampicillin • Non-lactose fermenting
mirabilis ammonia, making urine alkaline o Staghorn calculus • Surgery for larger • Urease (+)
stones • Swarming motility
Trachoma
• Corneal scarring & blindness
• Serotype A, B & C
• Classically grown in chick yolk
• Obligate intracellular parasite
sac
• Gram-negative without Genitourinary diseases
Genital and eye • Scrapings can show inclusion
peptidoglycan and muramic acid • Caused by serotypes D-K
infection bodies
• Direct contact transmission • Urethritis
• Doxycycline (adults) • Immunofluorescent slide test:
• Prevents phagolysosome fusion • Pelvic inflammatory disease
Chlamydia • Erythromycin (infants test for genital secretions
• Non-motile, no pili, no exotoxin o Complication when giving
trachomatis and pregnant • Serologic titers
birth: neonatal conjunctivitis
women) • McCoy agar – can be used as
Forms
• Azithromycin medium for growth
• Elementary body: infects the cell Lymphogranuloma venereum
• Giemsa stain: shows
• Reticulate body: non-infective, • Caused by serotypes L1-3
cytoplasmic inclusion
reproductive • Buboes
Important complication:
• Fitz-Hugh-Curtis syndrome
Whooping cough:
• Erythromycin
• Transmitted via respiratory route • 1. Catarrhal phase: highly
• Vaccine: DPT • Bordet-Gengou media:
• Obligate aerobe contagious (1-2 weeks)
o Never vaccine: potatoes, blood and glycerol,
• Capsule o Antibiotic susceptibility
acellular pertussis with penicillin added
Bordetella • Filamentous hemagglutinin: a o Low grade fever, runny nose
toxin, FHA, o *Note: collect specimen
pertussis pili rod that extends from the and mild cough
pertactin, and using throat swab
surface and enables binding to • 2. Paroxysmal phase (2-4 weeks)
fimbrial antigens • ELISA
epithelial cells of the bronchi o Whoop (non-productive cough
• Treat household • Direct fluorescein-labeled
• Pertussis toxin: activates G – paroxysmal)
contacts with antibodies
protein, increases cAMP o Antibiotics ineffective
Erythromycin
• 3. Convalescent stage
SPIROCHETES
Spirochetes Characteristics & Virulence Clinical Treatment Diagnostics
• Aerobic Mild
• Zoonotic (dogs, rats, cats) • First phase: organisms in blood and • Doxycycline
• First week: culture blood or
• Direct contact with infected CSF causes high grade fever and • Ampicillin
CSF
urine, animal tissue; bacteria myalgia (calf tenderness) • Amoxicillin
Leptospira • Second week to months:
penetrates intact mucous • Second phase: emergence of IgM Severe
interrogans culture urine
membranes and often with meningismus • Ampicillin
• Dark field microscopy
• Immune complex-mediated • Weil’s disease: severe case with • Ceftriaxone/Cefotaxime
(Shepherd’s crook)
meningitis and hemorrhage • Addition of renal
glomerulonephritis support (dopamine)
Syphilis • Dark field microscopy
• Penicillin G
• Primary: painless chancre examination of skin lesions
• Erythromycin
• Secondary: rash on palms and soles, • ELISA, silver stain
• Strict human pathogen • Doxycycline
condyloma lata (painless, wartlike) • Non-specific treponemal
Treponema • Obligate intracellular • Jarisch–Herxheimer
• Latent: (-) serology tests: VDRL, RPR
pallidum • Corkscrew motility reaction: acute
• Tertiary: Gummas of skin and bone, • Specific treponemal tests:
• Motile worsening of symptoms
neurosyphilis FTA-AB, MHA-TP
after antibiotics are
• Congenital: Hutchinson teeth, • Cannot grow on agar
started
deafness, keratitis medium

PART 2: VIROLOGY
SUMMARY OF MORPHOLOGICAL CHARACTERISTICS OF MEDICALLY IMPORTANT VIRUSES

Strand of Nucleic Specific Pathogenic Viruses or Disease
Nucleic Acid Symmetry Envelope Sense Family
Acid Caused
Poliovirus
Coxsackie A and B
Echovirus
Picornaviridae
SS Non- Hepatitis A virus
+
Naked Segmented Rhinovirus
New enteroviruses
Norwalk virus
Caliciviridae
Hepatitis E virus
Icosahedral
DS Segmented Reoviridae Rotavirus
Mosquito-borne encephalitis
Togaviridae
Rubivirus (rubella)
Yellow Fever virus
SS Non-
Enveloped + Dengue virus
Segmented
Flaviviridae St. Louis Encephalitis
Japanese Encephalitis
RNA Hepatitis C virus
SS Non-
+ Coronaviridae Respiratory illness (cold)
segmented
Rift valley fever virus
Bunyaviridae
Hantavirus
SS Segmented - Orthomyxoviridae Influenza virus
Marburg virus
Helical Enveloped Filoviridae
Ebola virus
Parainfluenza virus
RSV
SS Non- Paramyxoviridae
- Measles
Segmented
Mumps
Rhabdoviridae Rabies virus
Complex HIV
SS Diploid + Retroviridae
Coated HTLV
Erythema infectiosum
SS Linear Parvoviridae
Transient aplastic anemia crisis
HPV
Naked DS Circular Papovaviridae BK Polyomavirus
JC Polyomavirus
Childhood respiratory illness
DS Linear Adenoviridae
Icosahedral Epidemic keratoconjunctivitis
DNA
HSV 1 and 2
(mnemonic:
VZV
HAPPPy)
DS Linear Herpesviridae CMV
Enveloped
EBV
HHV-6
DS Circular Hepadnaviridae Hepatitis B virus
Smallpox
Complex
Complex DS Linear Poxviridae Vaccinia
envelope
Molluscum contagiosum
NON-ENVELOPED (NAKED) DNA VIRUSES

Important
Viral family Characteristics Transmission Diseases Other Notes
genera
• Exanthema in children (Erythema
infectiosum / Fifth disease)
• Single stranded DNA • Respiratory o Slapped cheeks
Human
Parvoviridae • Icosahedral symmetry droplets o Fever, coryza, sore throat
parvovirus B-19
• One serotype • Transplacental • Hemolytic crisis in people with
sickle cell disease, thalassemia
or spherocytosis
• Respiratory infections in humans
(cold)
• Histopathology:
• Double stranded DNA • Gastrointestinal (Infantile
• Aerosol droplet Cowdry type B
• Icosahedral symmetry diarrhea)
Adenoviridae Adenovirus • Fecal-oral route intranuclear
• Only virus with fiber • Eye infections
• Direct contact inclusions
(penton fiber) (keratoconjunctivitis)
• Has vaccine
• Genitourinary (hemorrhagic
cystitis)
• Treatment
o Genital warts:
podophyllin
• HPV 1-4: skin and plantar warts
• Double stranded circular • Direct contact o Skin warts: liquid
Human • HPV 6 & 11: genital warts
DNA • Sexual contact nitrogen
Papillomavirus • HPV 16 & 18: cervical, penile,
• Icosahedral nucleocapsid for genital warts o Plantar warts:
and anal carcinoma
salicylic acid
• Vaccine for HPV 6,
Papovaviridae 11, 16 & 18
• Progressive multifocal
leukoencephalopathy
• Double stranded circular
o Demyelinating disease
JC Polyoma virus DNA
affecting oligodendrocytes
• Icosahedral nucleocapsid
o Deficits in speech,
• Only causes disease in
coordination, and memory
immunocompromised host
BK Polyoma • Hemorrhagic cystitis &
virus nephropathy

o Patients with solid organ
(kidney) and bone marrow
transplants
ENVELOPED DNA VIRUSES

Important
genera
• Acute Gingivostomatitis • Site of latency is on the
• Herpes labialis (cold sore) trigeminal ganglia
• Skin infection • Tzanck smear:
• Herpetic Keratitis multinucleated giant
Herpes Simplex
• Saliva • Herpes Encephalitis (temporal cells
Virus – 1 (HSV-1
• Direct contact lobe) • Cowdry type A
/ HHV-1)
• Neonatal herpes (during passage inclusions
through birth canal) • Acyclovir shortens
• Herpetic whitlow (fingers) duration & reduces
• Herpetic gladiatorum (trunk) extent of shedding
• Site of latency is on the
lumbosacral ganglia
• Tzanck smear:
• Genital herpes multinucleated giant
Herpes Simplex
• Neonatal herpes (virus crosses cells
Virus – 2 (HSV-2 • Sexual contact
placental barrier) • Cowdry type A
/ HHV-2)
• Aseptic meningitis inclusions
• Acyclovir shortens
duration & reduces
extent of shedding
• Varicella (chickenpox)
o Vesicular centrifuge rash
(dewdrop on rose petal)
o Complications: • Tzanck smear:
§ Encephalitis multinucleated giant
Varicella-Zoster
• Respiratory § Pneumonia cells
Virus (VZV /
droplets § Reye's syndrome. • Acyclovir shortens
HHV-3)
§ Neonatal varicella duration & reduces
• Zoster (shingles) extent of shedding
• Linear double o Vesicular rash along the
stranded DNA affected cutaneous sensory
Herpesviridae
• Icosahedral nerves
nucleocapsid • Infectious mononucleosis
o Fever
o Sore throat
o Swollen lymph nodes
Epstein-Barr • Saliva (kissing)
o Of rare death is rupture of
virus (EBV / • Rarely through •
enlarged spleen
HHV-4) blood transfusion
• Malignancies:
o Burkitt lymphoma
o B-cell lymphoma
o Nasopharyngeal carcinoma
• CNS abnormalities: microcephaly,
mental retardation
o Most common cause of
congenital abnormalities
• Utero, perinatally, o When mother is infected in 1st
or postnatally. trimester (part of TORCH
• Sexual diseases)
Cytomegalovirus • DOC: Ganciclovir
transmission • Eye: optic atrophy
(CMV / HHV-5) o Resistant to acyclovir
• Blood and blood • Ear: deafness
products • Liver: hepatosplenomegaly and
• Organ transplant jaundice (due to hepatitis)
• Lung: pneumonitis
• Heart: myocarditis
• Thrombocytopenic purpura,
hemolytic anaemia
• Kaposi Sarcoma
o Malignancy of vascular
Human Herpes • Seen in patients • Treatment: surgical
endothelial cells
Virus – 8 (HHV-8) with AIDS incision, radiation
o Dark purple, flat to nodular
lesions
• Smallpox
o Only disease that has been • Histopathology:
• Largest virus
eradicated Guarnieri bodies
Orthopoxvirus / • Brick-shaped • Aerosol
Poxviridae o Prodome: fever & malaise o Intracytoplasmic
Variola virus • Linear double • Direct contact
o Centrifugal rash eosinophilic
stranded DNA
• Cowpox inclusions
• Monkeypox
• Histopathology:
Henderson-Peterson
• Brick-shaped • Molluscum contagiosum bodies
Molluscipoxvirus • Linear double • Direct contact o Pinkish, popular skin lesions o Intracytoplasmic
stranded DNA with umbilicated center eosinophilic
inclusions
• Treatment: cidofovir
• Incomplete circular • Hepatitis B • Hep B vaccine
Hepadnavirus • Blood
Hepadnaviridae double stranded o Fever, anorexia, jaundice o Given at 0, 1, and 6
(Hepatitis B virus) • Body fluids
DNA • Hepatocellular carcinoma month schedule

NAKED RNA VIRUSES
Important
genera
Poliovirus
• Poliomyelitis & meningitis
spectrum
o Inapparent, asymptomatic
infection
o Abortive poliomyelitis
§ Most common clinical form
§ Mild febrile illness with
headache, sore throat,
nausea & vomiting
o Nonparalytic poliomyelitis
§ Aseptic meningitis
o Paralytic poliomyelitis
§ Flaccid paralysis
§ Permanent motor nerve
damage
Poliovirus
Coxsackie virus • Histopathology:
• Herpangina Cowdry type B
Enterovirus • Hand-foot-and-mouth disease • Vaccine
• Hemorrhagic conjunctivitis o Killed (Salk IPV)
Picornaviridae • Pleurodynia o Live, attenuated
• Myocarditis and pericarditis (Sabin OPV)
• Aseptic meningitis
aseptic meningitis
• Single stranded RNA Echovirus
• Oro-fecal route
• Linear (+) sense • Enteric Cytopathic Human
Oprhan
• Aseptic meningitis
• URTI
• Febrile illness with and without
rash
• Infantile diarrhea
• Hemorrhagic cystitis
Rhinovirus
• Common cold
• Hepatitis A
Hepatovirus o Children most frequently
(Hepatitis A virus) infected
o Self-limited
• Hepatitis E
o No chronic carrier state
o No cirrhosis / hepatocellular
Hepatitis E virus
CA
o High mortality in pregnant
women
Caliciviridae
• Viral gastroenteritis
nonbacterial diarrhea in adults
Norovirus
o Sudden onset of vomiting and
diarrhea accompanied by fever
and abdominal cramping
• Naked double layered • Viral gastroenteritis
Reoviridae Rotavirus capsid • Oro-fecal route o Most common cause of
• Double stranded RNA childhood diarrhea
ENVELOPED RNA VIRUSES

Important
genera
Virulence factors
• Influenza
• Helical nucleocapsid • Hemagglutinin
o A: causes pandemics
• Segmented, single- • Respiratory • Neuraminidase
Orthomyxoviridae Influenzavirus o B: causes major outbreaks
stranded, negative sense droplets
o C: mild infections; does not
RNA [ss (-) RNA] • Prevent with yearly
cause outbreaks
vaccine
Laryngotracheobronchitis (Croup)
• Caused by parainfluenza virus 1
• Respiratory &2
Respirovirus
droplets • Inspiratory stridor, cough &
hoarseness
• Steeple sign on xray
• Histopathology:
• Helical nucleocapsid Warthin-Finkeldey
• Single-stranded, Measles bodies
Paramyxoviridae
negative sense RNA [ss • 3Cs: cough, coryza, o Multinucleated giant
(-) RNA] conjunctivitis cells
• Pathognomonic Koplik spots • Live, attenuated vaccine
Morbillivirus • Aerosol
• Maculopapular rash o Can be conjugated
o Spreads cranio-caudally with mumps and
• Complication: subacute rubella (MMR)
sclerosing panencephalitis o Should not be given
to
immunocompromised
patients or pregnant
women
• Live, attenuated vaccine
o Conjugated with
Mumps
measles and rubella
• Tender swelling of parotid
(MMR)
• Respiratory glands (parotitis)
Rubulavirus o Should not be given
droplets • Resolves in 1 week
to
• Complications: orchitis,
immunocompromised
meningitis
women
Rabies
• Prodomal period
o Paresthesia
• Rod or bullet-shaped o Fasciculations around the
• Helical nucleocapsid bite • Pre-exposure: vaccine
Rhabdoviridae Lyssavirus • Single-stranded, • Animal bite • Encephalitic phase • Post-exposure: vaccine
negative sense RNA [ss o Excessive motor activity, and immunoglobulin
(-) RNA] excitation & agitation
o Prominent brainstem
dysfunction
• Coma/death
• Single-stranded, non- • Direct contact
• Ebola
Filoviridae Filovirus segmented, negative- with blood or
• Marburg
sense RNA [ss (-) RNA] body fluids
• Co-infection or
• Single stranded, circular, • Prevented by
superinfection
(unclassified) Deltavirus negative-sense RNA [ss • Hepatitis D vaccinating with
with Hepatitis
(-) RNA] Hepatitis B
B
Rubella / German measles
• Known as 3-day measles
• Prevented by live,
• Maculopapular rash that
attenuated vaccine
spreads cranio-caudally
o Conjugated with
• (+) Posterior auricular
measles and mumps
lymphadenopathy
• Icosahedral nucleocapsid o Confers lifelong
• Respiratory
Togaviridae Rubivirus • Single stranded, positive- immunity
droplet Congenital Rubella
sense RNA [ss (+) RNA] o Should not be given
• Classic triad
to
o Cataract
immunocompromised
o Cardiac abnormalities
o Deafness
women
• Infection during 1st trimester
(part of TORCH)
Dengue / Breakbone fever
• Influenza-like syndrome
• Maculopapular rash (Herman
• Icosahedral nucleocapsid • Mosquito bite
rash)
Flaviviridae Flavivirus • Single stranded, positive- (Aedes
• Severe muscle and joint pain
sense RNA [ss (+) RNA] aegypti)
Dengue Hemorrhagic Fever
• Severe form of dengue
HIV Infection
• Sexual contact
• Symptoms are nonspecific
• Parenteral
o Fatigue, rash, headache,
exposure • Uses reverse
nausea, night sweats
• Single-stranded, linear, through transcriptase to
positive sense RNA [ss contaminated produce DNA from viral
AIDS
Retroviridae Lentivirus (+) RNA] blood genome
• Pronounced
• Cylindrical nucleoid in a products • Treatment: HAART
immunosuppression
mature virion • Vertical o 2 NNRTI + 1 INSTI
• Development of a wide variety
transmission (dolutegravir)
of sever opportunistic
(mother to
infections or unusual
child)
neoplasms

PART 3: PARASITOLOGY
PROCEDURES IN PARASITOLOGY
FECAL SMEAR THICK AND THIN BLOOD SMEAR

DIRECT FECAL MODIFIED KATO • Use the Fourth Non-dominant hand
SMEAR THICK o Less calloused- easier for the needle to penetrate and greater yield of
Amount 2 mg 40-60 mg blood drop
Cellophane covered with o Less nerve endings so subject to less pain
Fixation 0.85% Saline 50% glycerine and o Distance between skin, nail bed, and bone is thicker, thereby
malachite green preventing iatrogenic injury and possible contamination and infection
Stages of Trophozoite, cyst, Best for helminth of puncture site
parasite viewed oocyst infection, eggs, larva
Eggs Thick Smear Thin Smear
Parasites that Protozoans
Cestode More sensitive due to Less sensitive but more
can be Eggs of Nematodes,
Nematode Sensitivity greater blood volume specific for identifying
visualized Cestodes
Trematode used spp. of Plasmodium used
Liquid/ watery stools Well-formed stools • Can help assess
Stool Specimen Live/ motile parasites More sensitive because response to treatment
• Can detect mild
can be seen it has more sample • Other RBC/ Blood
parasitemia
Advantage abnormalities can be
• Determine presence
FORMALIN-ETHER CONCENTRATION TECHNIQUE appreciated
of Plasmodium
• Widely used sedimentation technique for diagnosis of intestinal protozoa • Can quantify
in preserved stool sample parasitemia
• Uses 1.0-1.5 grams of stool sample • Difficult to • Not sensitive enough
• Lacks sensitivity for diagnosis of helminths differentiate specific for low parasitemia
o Diagnostic accuracy is inferior to Kato-Katz technique Plasmodium species • More tedious to
Disadvantage
• Distorted appearance perform due to
of parasite technical skill required
• Risk of false (+) to do thin smear
PROTOZOANS
Parasite Immature Stage Mature Stage Biology & Pathogenesis Disease and Treatment
• Pseudopod-forming, • Amebic colitis
nonflagellated o Dysentery without fever
• Most invasive among Entamoeba o Flask-shaped colon
spp. ulcers
• Transmission: oro-fecal route o Tx: iodoquinol
Entamoeba
• Amebic liver abscess
histolytica
Virulence Factors o Most common
• Lectin: mediates adherence extraintestinal form
*infective stage • Amebapores: penetration o Anchovy sauce-like
• Cysteine protease: cytopathic aspirate
effect o Tx: metronidazole
Entamoeba
• Harmless inhabitant of the colon
coli
Cyst Trophozoite
Iodamoeba Cyst
One nucleus in mature cysts • Commensal amoeba
buetschlii
usually eccentrically placed.
Chromatoid bodies are not
Trophozoite
present. Glycogen is present
as a compact well defined
mass staining dark brown with
iodine.
• Balantidial dysentery
• Transmission: oro-fecal route o Diarrhea with bloody
• Tissue invader and mucoid stools
Balantidium
• Trophozoites are characterized • Hyaluronidase: lytic enzyme o Indistinguishable from
coli
by their large size, the presence causing ulceration amebic dysentery
of cilia on the cell surface, a • Intermediate host: pork o Round-based, wide-
cytostome, and a bean shaped necked intestinal ulcers
Cysts – infective stage
macronucleus which is often
visible and a smaller, less
conspicuous micronucleus
• Acute infection
• Habitat: duodenum, jejunum & o Abdominal pain
upper ileum o Diarrhea
Giardia • Falling leaf motility o Excessive flatus
lamblia • Transmission: oro-fecal route smelling like rotten
• Adhesive disc & lectin: facilitate eggs
attachment to avoid peristalsis • Chronic infection
Cyst – infective stage Trophozoite
o Constipation

PROTOZOANS
Parasite Immature Stage Mature Stage Biology & Pathogenesis Disease and Treatment
o Weight loss
o Steatorrhea
• Treatment: metronidazole
• Mononucleosis – seen in
immunocompetent hosts
• Encephalitis with ring
enhancing lesions – seen
• Definitive host: domestic cat
in immunocompromised
o Humans & other mammals are
hosts
Toxoplasma intermediate hosts
• Congenital toxoplasmosis
gondii • Transmission: ingestion of cysts
o Intracranial calcification
in raw meat; transplacental
o Chorioretinitis
Oocyst – infective stage Tachyzoites transfer
o Part of TORCH
diseases
• Treatment: sulfadiazine +
pyrimethamine
PLASMODIUM SPP
Plasmodium falciparum Plasmodium vivax

• In P. falciparum infections, red blood cells (RBCs) are normal in size • In P. vivax infections, RBCs can be normal to enlarged (up to 1 1/2× to
• Typically only rings and gametocytes are seen unless the blood sat 2×) in size and may be distorted
before the smears were prepared • Under optimal conditions, Schüffner's dots may be seen in Giemsa-
stained slides
RING FORMS
• Delicate cytoplasm and one or two small chromatin dots RINGS
• RBCs that are infected are not enlarged • Large chromatin dots
• Multiple infection of RBCs is more common in P. falciparum than in other • Cytoplasm can become ameboid as they develop
species
• Occasional appliqué forms (rings appearing on the periphery of the rbc)
can be present
TROPHOZOITES
• Amoeboid cytoplasm, large chromatin dots, and have fine, yellowish-
brown pigment
• Schüffner's dots may appear more fine in comparison to those seen in P.
ovale
GAMETOCYTES
• Crescent or sausage shaped
• Chromatin is in a single mass (macrogamete) or diffuse (microgamete)
GAMETOCYTES
• Round to oval with scattered brown pigment and may almost fill RBC
• Schüffner's dots may appear more fine in comparison to those seen in
SCHIZONTS P. ovale
• Seldom seen in peripheral blood
• Mature schizonts have 8 to 24 small merozoites
• Dark pigment, clumped in one mass
SCHIZONTS
• Large, have 12 to 24 merozoites, yellowish-brown, coalesced pigment,
and may fill the RBC
TROPHOZOITES
• Older, ring stage parasites
• Ctoplasm of mature trophozoites tends to be more dense than in
younger rings
Plasmodium ovale
• In P. ovale infections, RBCs can be normal or slightly enlarged (up to 1
1/4×) in size, may be round to oval, and are sometimes fimbriated
RINGS
• Sturdy cytoplasm and large chromatin dots
TROPHOZOITE
• Sturdy cytoplasm, large chromatin dots, and can be compact to slightly GAMETOCYTE
irregular • Round to oval with scattered brown pigment; they may almost fill the
infected RBC
GAMETOCYTE
• Round to oval and may almost fill the RBC
• Pigment is brown and more coarse in comparison to P. vivax
SCHIZONT
• Have 6 to 14 merozoites with large nuclei, clustered around a mass of
dark-brown pigment
Plasmodium malariae
• In P. malariae infections, RBCs are normal or smaller than normal (3/4×)
in size
RINGS
• Sturdy cytoplasm and a large chromatin dot
TROPHOZOITE
• Compact cytoplasm and a large chromatin dot
• Occasional band forms and/or basket forms with coarse, dark-brown
pigment can be seen
SCHIZONT
• Have 6 to 12 merozoites with large nuclei, clustered around a mass of
coarse, dark-brown pigment
• Merozoites can occasionally be arranged as a rosette pattern

SUMMARY

NEMATODES (ROUND WORMS)
Parasite Adult Transmission & Risk Factors Treatment &
Egg
Prevention
Ascaris
lumbricoides,
fertilized • Soil transmitted helminth Albendazole
• Ingestion of embryonated eggs • Mebendazole
• Risk factors • WASH
o Open defecation o Water
o Poor hygiene o Sanitation
A. lumbricoides o Lack of access to clean water o Hygiene
infertile
• Albendazole
• Soil transmitted helminth • Mebendazole
Trichuris • Ingestion of embryonated eggs • WASH
trichiura • Same risk factor as Ascaris o Water
o Sanitation
o Hygiene
Hookworm
• Skin penetration • Albendazole
(Ancylostoma
• Risk factors • Mebendazole
duodenale,
o Walking barefoot on soil • Footwear use
Necator
o Open defecation • Sanitation
americanus)
Ancylostoma duodenale (L)
Necator americanus (R)
• Ingestion of embryonated eggs
(self-infection occurs when hand
• Albendazole
contacts mouth after scratching
• Mebendazole
perianal area)
Enterobius • Pyrantel pamoate
• Handling of contaminated
vermicularis • Treat household
clothes or linen
contacts
• Reinfection may occur
• Hygiene
• Crowding and poor hygiene are
risk factors
• Albendazole
Capillaria • Ingestion of raw or undercooked
• Mebendazole
philippinensis fish
• Thorough cooking
Cestodes (Segmented Worms)

Parasite Adult Proglottids Transmission & Risk Factors Treatment &
Egg
Prevention
Taenia solium
(pork tapeworm) • Ingestion of raw or undercooked
• Praziquantel
infected meat
• Niclosamide
Taenia saginata • Risk factor – occupation (working at
(beef tapeworm) abbatoirs, working with cattle, etc.)
• Ingestion of cysticercoid-infected • Praziquantel

Hymenolepis
arthropods, contaminated food or • Niclosamide
nana
water • Nitazoxanide
• Praziquantel
Diphyllobothrium • Ingestion of raw or undercooked
• Niclosamide
latum infected fish
Trematodes (Flukes)
Parasite Egg Adult Transmission & Risk Factors Treatment & Prevention
• Skin penetration by free-swimming
• Praziquantel
cercariae in freshwater
• Protective equipment when
Schistosoma • Occupational risks – farmers &
exposed to water
japonicum fishermen
• Stop open defecation in
• Only intermediate host is Oncomelania
freshwater
hupensis quadrasi snail

• Ingestion of undercooked crustaceans
Paragonimus containing metacercariae • Praziquantel
westermani (Sundathelphusa crab) • Thorough cooking
Opisthorchis • Ingestion of freshwater fish infected with

• Praziquantel
viverrini and metacercariae
• Albendazole
Clonorchis • Koi pla in northern Thailand (raw fish
sinensis dish)
Opisthorchis viverrini (above)
Clonorchis sinensis (below)
Fasciola
hepatica and • Triclabendazole
• Ingestion of water plants infested with
Fasciolopsis • Strict control of water plant
metacercariae
buski growth
Fasciola hepatica
PART 4: MYCOLOGY
SUPERFICIAL MYCOSES
Organism Reservoir Diagnosis and Morphology Clinical Manifestations Treatment
Pytriasis versicolor
• KOH smear: spaghetti and meatballs
• Hypo or hyperpigmented patches on the
appearance
skin
o Surrounding skin darkens with sunlight
while patches remain white • Dandruff shampoo
Malassezia (containing selenium
furfur sulfide)
• Topical imidazole
• Wood’s lamp: yellow-green

fluorescence
Tinea Nigra
• Brown- pigmented branched, septate • Dark brown to black patches on the soles
hyphae and budding yeast cells of hands and feet
Exophiala • Dandruff shampoo
werneckii • Topical imidazole
• KOH: branched hyphae

• Wood’s Lamp: Green fluorescence
• Microsporum gypseum showing
ellipsoidal/ spincdle-shaped, multi-
celled macroconidia
Microsporum Dermatophytosis
species • Depends • Tinea corporis (body) – ringworm
• Topical imidazole
on • Tinea cruris (groin) – jock itch
• Oral griseofulvin for
Trichophyton species • Tinea pedis (feet) – athlete’s foot
tinea unguium and tinea
species • Soil • Tinea capitis (scalp)
capitis
• Animals • Epidermophyton floccosum shows • Tinea unguium (nail) – onychomycosis
• Oral terbinafine
Epidermophyton • Human club-shaped macoconidia • Tinea manum (hand)
floccosum • Tinea barbae (beard)
Sporotrichosis
• Subcutaneous nodule gradually appears
the site of thorn prick
• Nodule becomes necrotic and ulcerates
Dimorphic Fungi o Ulcer heals but new nodules pop up
• Found nearby along the lymphatic tracts • Oral potassium iodide
Sporothrix • Culture at 25 C will grow branching
on rose • Amphotericin B
schenckii hyphae
thorns • Itraconazole
• Culture at 37 C will show yeast cells
Phialophora Chromoblastomycosis
verrucosa • Following a puncture wound, a small violet
• Rotting • KOH smear: copper-colored cells called wart-like lesion develops (originates in • Itraconazole
Cladosporium wood sclerotic bodies subcutaneous area) • Local excision
carrionii • With time, clusters of this skin lesions can
develop (resembling cauliflower)

SUPERFICIAL MYCOSES
Fonsacaea
species
• Phialophora verrucosa: flash-shaped

phialides
SYSTEMIC MYCOSES
• Mycelial forms with spores at 25 C
Coccidioidomycosis
• Yeast forms at 37 C
• Asymptomatic in most persons
• With 90 degree branching and thick walled,
• Desert area of • Pneumonia
barrel-shaped arthroconidia with empty cells
southwestern • Disseminated: can affect the
• Amphotericin B
Coccidioides US and lungs, skin, bones, and meninges
• Itraconazole
immitis Northern • Erythema nodosum – painful
• Fluconazole
Mexico erythematous nodular lesions
• Soils, rodents • Common opportunistic infection
in AIDS patients from southwest
United States
• Mycelial forms with spores at 25 C
• Yeast forms at 37 C
• Mississippi Histoplasmosis
• No capsule
Valley • Pneumonia—lesions calcify which • Itraconazole
Histoplasma • Bird and Bat may be seen on CXR (look similar • Amphotericin B (in
capsulatum droppings to tuberculosis) immunocompromised
• Respiratory • Can survive intracellularly within patients)
transmission macrophages
• Yeast form: Broad-based buds
• Mississippi Blastomycosis
River valley • Pneumonia—lesions rarely calcify
• Itraconazole
Blastomyces • Resides in soil • Disseminated infection—present
• Conidia: lollipop -shaped • Ketoconazole
dermatitidis or rotten wood with weight loss, night sweats,
• Amphotericin B
• Respiratory lung involvement, and skin ulcers
transmission • Cutaneous—skin ulcers
OPPORTUNISTIC MYCOSES
• Polysaccharide capsule surrounds
yeast
• Yeast form only
• Found in • Seen using india ink stain Cryptococcosis
• Amphotericin B and
pigeon • Subacute or chronic meningitis
Cryptococcus Flucytosine
droppings • Encephalitis
neoformans • Fluconazole
• Respiratory • Pneumonia – usually self-limited
(chemoprophylaxis)
transmission • Skin lesions – look like acne
Candidiasis in a normal host

• Oral thrush
• Pseudohyphae • Vulvovaginal candidiasis (curd-like discharge)
• Oval yeast with single bud • Cutaneous
• Normal
• Form germ tubes in serum o Diaper rash
inhabitant of • Choice of antifungal
o Rash in the skin folds of obese individuals
the skin, agent depends on
Candida (satellite lesions)
mouth, and the type of candida
albicans o Onychomycosis
GI tract infection and
• Not found in severity
Candidiasis in an immunocompromised host
blood
• Thrush, vaginitis and/or cutaneous plus
o Esophageal
o Disseminated candidiasis
o Chronic mucocutaneous candidiasis
• Branching (V-shaped) septated Aspergillosis
hyphae • Allergic bronchopulmonary aspergillosis (IgE
• Everywhere mediated) – asthma type reaction with
• Aspiration of shortness of breath and high fever
Aspergillus • Amphotericin B and
aspergillus • Aspergilloma (fungus ball) – associated with
spp surgery
causes hemoptysis
asthma • Invasive aspergillosis – necrotizing pneumonia
• Aflatoxin consumption can cause liver damage
and liver cancer

OPPORTUNISTIC MYCOSES
Mucormycosis
Rhizopus • Rhino-orbital-cerebral infections (associated
• Saprophytic • Hyphae: broad, non-septated, without • Amphotericin B and
Rhizomucor with diabetes)—stays on nasal mucosa and
molds walls, and branches at right angles surgery
Mucor invades the sinus and orbit
• Pulmonary mucormycosis

MODULE/TOPIC 19 PE AND REPORTING SUMMARY

CARDIOVASCULAR PHYSICAL EXAMINATION
START
• Introduce yourself
• Ask for patient’s identity
• Briefly explain the procedure
• Ask for consent
The patient is alert, awake, coherent, dressed appropriately, and not in respiratory
distress
INSPECTION
• Adequate exposure of anterior, posterior, and lateral chest areas HR is ___
• Check for vital signs RR is ___
BP is ___
No shortness of breath
No retractions
No use of respiratory accessory muscles
Face No malar flush or any discoloration on the face
• Malar flush/ Plum red discoloration of cheeks: mitral stenosis
Eyes Conjuctiva is pink
• Pallor conjunctiva: anemia No corneal arcus
• Corneal arcus/ Yellow/grey ring surrounding iris: hypercholesterolemia No xanthelasma
• Xanthelasma/ Yellow raised lesions around eyes: hypercholesterolemia Anicteric sclerae
• Icteric sclerae: jaundice
Mouth No central cyanosis
• Central cyanosis/ bluish discoloration of lips/underneath tongue: IDA No angular stomatitis
• Angular stomatitis/ inflammation of the corner of the mouth: IDA Palate is
• High arched palate – Marfan syndrome (increased risk of aortic aneurysm/ No masses, bleeding, signs of inflammation in the oral cavity
dissection Describe dental carries*
• Dental hygiene (e.g. carries)
Chest No lesions, masses, scars, asymmetry, chest deformities observed

Hands The hands are non-erythematous, warm, and not sweaty/clammy.
• Note color, temperature, if sweaty/clammy No clubbing
• Finger clubbing No edema
• Edema/ swelling No xanthomata
• Xanthomata/ raised yellow lesions: hyperlipidemia No Janeway lesions
• Janeway lesions/ non-tender maculopapular erythematous palm pulp lesions No Osler’s nodes
• Osler’s nodes/ tender red nodules on finger pulps/thenar eminence No tar staining
• Tar staining: smoking No splinter hemorrhages
• Splinter hemorrhage/ reddish brown streaks on nail bed Capillary refill is less than 2 seconds.
• Capillary refill time
o Normal: <2 seconds
Legs No scars
No visible masses
No edema
No missing limbs/ toes
PALPATION
Pulses No radio-radial delay
• Rate, rhythm No collapsing pulse
• Radio-radial delay
• Collapsing pulse: aortic regurgitation
Assessment of JVP JVP measures __cm
• Ensure patient is positioned at 45 degrees
• Ask patient to turn their head away from you Upon evaluation of hepatojugular reflux, JVP is not sustained, and measurement is
• Observe neck for JVP (inline with SCM) still less than 4cm.
• Measure JVP (cm from sternal angle to upper border of pulsations)
• Normal: 3-4 cm
• Raised JVP: fluid overload/ RV failure/ tricuspid regurgitation
• Hepatojugular reflux
o Apply pressure to the liver
o Observe JVP rise
o Normal: 1-2 s then falls
o If JVP is sustained and > 4cm: right sided heart failure/ tricuspid regurgitation
Apex beat PMI is palpated at the 5 Left ICS midclavicular line.
th
• Located at the 5th intercostal space / midclavicular line

• Palpate the apex beat with your fingers (placed horizontally across the chest)
• Lateral displacement: cardiomegaly
Heaves: heel of the hand No heaves
• A parasternal heave is a precordial impulse that can be palpated
• Place the heel of your hand parallel to the left sternal edge (fingers vertical) to
palpate for heaves

• If heaves are present you should feel the heel of your hand being lifted with each
systole
• Positive: right ventricular hypertrophy
Thrills: palm/ball of the hand No thrills
• A thrill is a palpable vibration caused by turbulent blood flow through a heart valve
(the thrill is a palpable murmur)
• You should assess for a thrill across each of the heart valves in turn
• To do this place your hand horizontally across the chest wall, with the flats of your
fingers and palm over the valve to be assessed
AUSCULTATION
Heart valves The precordium is adynamic.
• Palpate the carotid pulse to determine the first heart sound. The heart has regular rate and sinus rhythm.
• Auscultate ‘upwards’ through the valve areas using the diaphragm of the At the apex, S1 was louder than S2.
stethoscope:
o Mitral valve – 5th intercostal space – midclavicular line (apex beat)
o Tricuspid valve – 4th or 5th intercostal space – lower left sternal edge
o Pulmonary valve – 2nd intercostal space – left sternal edge
o Aortic valve – 2nd intercostal space – right sternal edge
• Repeat auscultation across the four valves with the bell of the stethoscope
o Note:
o M1TS
§ Mitral & Tricuspid CLOSE during SYSTOLE: ventricular ejection
o 2PAD
§ Aortic & Pulmonic CLOSE during DIASTOLE: ventricular filling
Murmurs No murmurs or extra heart sounds heard.
• SYSTOLIC - MRAS
o MR, TR: holosystolic
o AS, PS: mid-systolic
o MVP: late systolic
• DIASTOLIC - MSARdines
o MS, TS: mid-diastolic
o AR, PR: early diastolic
• OTHER
o PDA: continuous
Accentuation maneuvers
• For aortic stenosis murmur
o Auscultate the carotid arteries with the patient holding their breath to check
for radiation
• Aortic regurgitation
o Sit the patient forwards and auscultate over the aortic area during expiration
to listen for the murmur
• Mitral murmur (regurgitation/stenosis)
o Roll the patient onto their left side and listen over the mitral area with the bell
during expiration
Bruits No bruits
Auscultate the carotid arteries
END
Thank the patient
PULMONARY PHYSICAL EXAMINATION

START
• Ask for consent
distress
INSPECTION
• Adequate exposure of anterior, posterior, and lateral chest areas HR
• Observes respiratory rate (patient should not be aware you are checking RR
respiratory rate); counts the number of breaths in 30 secs to 1 minute No difficulty of breathing
• Checks rhythm, depth & effort of breathing; note whether the expiratory phase is No signs of respiratory distress
prolonged No tachypnea or dyspnea observed
• Checks for retractions & use of accessory muscles (sternocleidomastoids, No retractions and use of accessory muscles when breathing
abdominals). Expiratory phase is not prolonged
• Checks for asymmetry, deformity, ↑anterior-posterior (AP) diameter No signs of pallor
• Checks for scars, masses etc at the anterior & posterior, and lateral chest wall No signs of cyanosis
• Confirm that the trachea is near the midline Trachea is at the midline, no deviation
No lesions, masses, scars, asymmetry, chest deformities observed
AP diameter not increased
No presence of clubbing
No signs of edema

PALPATION
• Performs the procedure on skin and not over clothes or gown No palpable masses
• Let the patient know that you will be placing your hands on their chest wall identify No tenderness
any areas of tenderness or deformity by palpating the ribs & sternum Symmetrical chest expansion, no chest lag
• Chest lag – assess expansion & symmetry of the chest by placing your hands on
the patient's side, thumbs together at the midline, & ask them to breathe deeply
Assessment of tactile fremiti Symmetrical tactile fremiti on all lung fields
• Performs the procedure on skin and not over clothes or gown
• Ask patient to grab his shoulders to move scapula laterally;
• Compare both sides of the chest, using the palmar base of your hand or ulnar side
to the interspaces; asking patient to say “99” every time you reposition hands,
moving from top to bottom, and sides (at least 3 areas posteriorly & one area
laterally)
PERCUSSION
• Ask patient to grab his shoulders to move scapula laterally; Upon percussion, resonant in all lung fields and symmetrical
• Performs the procedure on skin and not over clothes or gown
• Hyperextend the middle finger of one hand & place the distal inter-phalangeal joint
firmly against the patient's chest
• With the end (not the pad) of the opposite middle finger, use a quick flick of the
wrist to strike finger
• Percuss from side to side & top to bottom. Omit the areas covered by the
scapulae
• Compare one side to the other as you go from top to bottom looking for
asymmetry
• Percussion sounds must be audible categorize percussion sounds as flat, dull,
resonant, hyperresonant, or tympanitic
Diaphragmatic Excursion Diaphragm descends __ bilaterally and symmetrically
• Find the level of the diaphragmatic dullness during quiet respiration on both sides
• Holding the pleximeter finger above and parallel to the expected level of dullness,
percuss downward in progressive steps until dullness clearly replaces resonance
Normal: 3 – 5.5cm, symmetrical
AUSCULTATION
• Ask patient to grab his shoulders to move scapula laterally Breath sounds vesicular over most of both lungs (I > E)
• Performs the procedure on skin and not over clothes or gown Bronchial breath sounds heard best over the manubrium (E > I)
• Uses the diaphragm of stethoscope Tracheal breath sounds heard best over trachea and neck (I = E)
• Ask the patient to inhale and exhale normally with mouth open Bronchovesicular breath sounds heard best in the 1 and 2 ICS anteriorly and
st nd
• Listen to at least one full breath (include inhalation & exhalation) in each location between scapula especially on the right side (I = E)**
• Auscultate from side to side & from top to bottom Omit the areas covered by the
scapulae
• Compare one side to the other looking for asymmetry
• Note if equal, decreased or absent breath sounds
• Note the location & quality of the breath sounds (tracheal, bronchial,
bronchovesicular, vesicular)
Adventitious sounds No crackles, rhonchi, wheezing, stridor, pleural friction rub
• Note the presence or absence of adventitious breath sounds (crackles, rhonchi,
wheezing, stridor)
Trasmitted voice sounds Negative for bronchophony, whispered pectoriloquy, and egophony
• Theoretically, if there are abnormally located breath sounds, we would auscultate
for transmitted voice sounds
o Bronchophony
§ ‘Tres tres’ (+ if louder)
o Whispered pectoriloquy
§ Whisper ‘tres tres’ (+ if louder and clearer)
o Egophony
§ ‘Eeee’ (+ if ee sounds like A)
END
Thank the patient
ABDOMINAL PHYSICAL EXAMINATION

START
• Ask for consent
• Make sure patient has empty bladder
• Position the patient in supine position
• Put pillows under the head and the feet
• Ask the patient to relax and lie flat back
• Drape:
o Below nipple line, just above xiphoid process
o Symphysis pubis
• Ask patient to point any areas of pain

The patient is alert, awake, coherent, dressed appropriately, and not in respiratory distress
INSPECTION
Skin: The skin is warm
• Temperature No bruises, erythema, or jaundice
• Color
• Scars No scars
• Striae Old silver striae / stretch marks on ___*
o Pink-purple striae: Cushing syndrome
• Dilated veins Small visible veins on ___*
o Dilated veins: portal hypertension from cirrhosis/ IVC
obstruction No rashes
• Rashes No ecchymoses
• Ecchymoses
Umbilicus: The umbilicus has no discoloration
• Color Color is same as the skin
o Cullen’s sign – Bluish purple: Intraabdominal bleeding Negative for Cullen’s sign
• Location Umbilicus is at the midline
• Contour No enlargement
o If protruded, not > 0.5 cm No herniation
• Eversion – intraabdominal bleeding or umbilical hernia Umbilicus is ____ (recessed or inverted)*
Abdomen:
• Symmetry
The abdomen is symmetrical and ___ (flat/ rounded/ protuberant/ scaphoid)*
o Asymmetry: hernia, organ enlargement, mass, diastasis recti,
bowel obstruction
Peristalsis
• Not seen normally
No visible peristalsis
o But usually seen in thin individuals
• Increased peristaltic waves: intestinal obstruction
Pulsations No visible pulsations or
• Increased pulsations: AAA or increased pulse pressure No increased pulsations. There is slight aortic pulsation in the epigastrium
Masses
• Theoretically, if a mass is present, it can be determined as an
abdominal wall mass rather than an intra-abdominal wall mass if it No visible masses
becomes more prominent with tense abdominal muscles upon
palpation
AUSCULTATION
Bowel sounds
• Warm diaphragm of your stethoscope
• Normal
o 5-34/ minute
o Intermittent, low-pitched, chuckling sounds
• If it is hypoactive or absent, listen to all quadrants before saying that Normoactive bowel sounds, specifically ___ bowel sounds/minute.
there is decreased bowel sounds (1 min/each) before labeling the
patient with ileus or hypoactive bowel sounds  
o Quiet: ileus
o Hyperactive: enteritis and early ischemic intestine  
o High-pitched “tinkling” sounds, usually associated with pain:
mechanical bowel obstruction
o Far away, “echoing” sounds - significant luminal distention
No bruits over the abdominal aorta, renal arteries, and iliac arteries.
Abdominal Bruits & Friction Rub
No hepatic and splenic friction rubs.
• Aortic, renal, iliac, femoral
PERCUSSION
Abdomen Upon percussion, all quadrants are tympanitic.
• 4 quadrants
Liver span
Liver span is ___, which falls under the normal range.
• Normal: 6-12 cm Right MCL, 4-8 cm MSL
Tympanitic over the spleen.
Spleen span
• Traube’s space
o Boundaries: left anterior axillary line, 6 rib and costal margin
th
• Castell’s sign Still tympanitic over the spleen; thus, negative for Castell’s sign
o Lowest left intercostal in left anterior axillary line (8 or 9 ICS) on
th th
 
full inspiration
Shifting dullness
Negative for shifting dullness
• Negative: no sign of ascites
PALPATION
Light palpation No tenderness, muscular resistance, superficial organs, palpable masses
Deep palpation No tenderness, muscular resistance, superficial organs, palpable masses
Rebound tenderness No tenderness, and no sign of possible peritoneal irritation
Edge of the liver Liver edge is smooth, soft, and has regular border surface.

The spleen is not palpable.
Spleen
No palpable mass over the spleen.
Fluid wave Negative for fluid wave
Murphy’s Sign
Negative for Murphy’s sign
• Negative: no sign of acute cholecystitis
McBurney’s Point
Ne tenderness over McBurney’s point
• Negative: no sign of appendicitis
Rovsing’s Sign
Negative for Rovsing’s sign
• Negative: no sign of appendicitis
Obturator Sign
Negative for Obturator sign
• Negative: no sign of pelvic appendicitis
Psoas Sign
Negative for Psoas sign
• Negative: no sign of retroperitoneal or retrocecal appendicitis
CVA Tenderness No CVA tenderness upon kidney punch
Digital Rectal Examination Good sphincter tone, no masses or lesions palpated
END
Thank the patient
HEENT PHYSICAL EXAMINATION

HEAD PHYSICAL EXAMINATION
START
• Ask for consent
• Position the patient seated comfortably
distress
INSPECTION
• Skull: general size, contour, deformities, depressions, lumps
• Hair: quantity, distribution, texture, patterns of loss No cranial abnormalities
• Scalp: scaling, lumps, nevi, or any other lesions Hair is abundant, evenly distributed, with no patterns of hair loss
• Face: facial expression, contours, asymmetry, involuntary movements, edema, No lesions or masses on the scalp
and masses Facial features appear symmetrical
• Skin: color, pigmentation, texture, thickness, hair distribution, and any other Skin is
lesions
OPHTHALMOLOGICAL PHYSICAL EXAMINATION

START
• Ask for consent
distress
Remember!
VAGETF = Visual Acuity, Gross inspection, EOMs, Tonometry, Fundoscopy
VISUAL ACUITY
Using a Snellen chart with the patient 20 ft away
*Jaeger chart at arm’s length
Test one eye at a time
If patient cannot see the largest text:

• Allow the patient to move closer Visual acuity of 20/20 on both eyes (numerator: distance a normal person would see,
• Counting fingers denominator: distance the patient can see)
• Hand motion No visual field deficits
• Light projection
• Light perception
Test for visual fields with visual confrontation on all four quadrants (point to moving
finger)
GROSS INSPECTION
• Inspect from external to internal No visible masses or lesions observed
o Use of eyeglasses No orbital fractures
o General eye position and symmetry- strabismus, protrusion Eyebrows appear symmetric
o Orbit socket: palpate for depressions and elevations Lashes were distributed evenly and directed outwards
o Lids- ptosis, styes, masses, entro/ectropion Anicteric sclerae
o Lashes- loss of lashes, clumping, crusts, infestation Pink conjunctiva
o Conjuctiva and sclera- redness, pterygium No cataract
o Iris and pupils- anisocoria, color/discoloration, asymmetry, pupillary light reflex Pupils are round, equal, and briskly reactive to light

o Lens – ROR, cataract Direct and consensual pupillary reflexes were intact
Accommodation reflex was intact
Lenses are clear, (+) ROR
EXTRAOCULAR MOVEMENTS
• H movement – both eyes open, follow the tip of the finger or pen
o Remind patient to not move his/her head Equal, full-range, and smooth eye motion towards all directions on duction and
o (Duction: One eye; Version: both eyes) version with convergence
• Test for convergence by bringing finger towards the bridge of the patient’s nose: No nystagmus present
note pupillary dilatation and moth eyes looking medially
TONOMETRY
• Using your two index fingers and with the patient looking down (w/o closing the
Globe is not ruptured
eyes) press down on the lid
Firm
• Soft: lips; Firm: tip of the nose; Hard: forehead
FUNDOSCOPY/RETINAL EXAM
• Darken room
• Set diopter appropriately Use the right hand when testing the patient Right eye ROR was intact
and vice versa Media is clear
• Approach from temporal area Optic disc was visualized with a 0.3 cup-to-disc ratio, 2:3 A-V ratio
• Locate the vessel and follow to optic disc No hemorrhage or exudates noted
• Look for cup to disc ratio (N 0.2-04), disc swelling, blood vessels (N A-V ratio: 2:3), Positive foveal reflex
hemorrages, pallor, exudates, foveal reflex
EARS PHYSICAL EXAMINATION

START
• Ask for consent
INSPECTION
• Symmetry
Both ears are symmetrical
• Shape of each ear
Ears show no visible masses, lesions, discoloration, and erythema
• Swelling, redness, crusting, discharge, scars, abnormal growths,
No discharge was noted
deformities, lumps, and other skin lesions
PALPATION
Tug test was negative
• Check for tenderness
No tragal tenderness on both ears
○ Tug Test: move the auricle up and down and press on the tragus
No mastoid tenderness on both ears
○ Press firmly just behind the ear (on the area of the mastoid)
OTOSCOPY
• Pull auricle upward, backward, and outward (“up and out”) (for
Ear canal was clear, with no discharge, erythema, or swelling
pediatric patients: downward and backward)
Cerumen is yellow brown and sticky, partly obscuring the view
• Ear canal: discharge, foreign bodies, erythema or swelling
Intact and translucent tympanic membrane with cone of light in the antero-inferior quadrant of the
• Tympanic membrane: color and contour, presence/absence of the
right/left ear
cone of light, position of the malleus, and any perforations
HEARING TESTS
Weber Test
• On the patient’s forehead
• Check lateralization Weber – Vibration is felt equally in both ears, no lateralization
Rinne Test (AC vs BC)
• On mastoid bone, on the level of the ear canal Rinne – Air conduction is greater than bone conduction
• Place the fork close to the ear canal and ascertain whether the sound
can be heard again
ORAL CAVITY PHYSICAL EXAMINATION

START
• Ask for consent
INSPECTION
• Lip: color, moisture, lumps, ulcers, cracking, scaling Lips are pink, no lumps or ulcers noted
• Oral Mucosa: color, ulcers, white patches, nodules, report halitosis Oral mucosa appears moist with structures intact, uvula and tongue midline, with no visible lesions
• Gums and Teeth or
○ Gums: color, swelling and ulceration ulcerations, no halitosis
○ Teeth: number, color, shape, position, missing teeth No erythema, discharges, masses, or swelling
• Roof of Mouth Tonsils are not enlarged

○ Inspect color, architecture, and for any growths
• Tongue and Floor of Mouth
○ Symmetry, color and texture of dorsum of tongue, sides and
undersurfaces of tongue for redness, nodules, ulcerations
• Pharynx
○ Soft palate, anterior and posterior tonsillar pillars, uvula, tonsils,
and posterior pharynx
○ Color, symmetry, exudation, swelling, ulceration, tonsillar
enlargement
NECK PHYSICAL EXAMINATION

START
• Ask for consent
General appearance The patient is alert, awake, coherent, dressed appropriately, and not in respiratory distress
INSPECTION
Inspect with the neck slightly extended, use tangential lighting
No visible masses or lesions
The thyroid is normally between the cricoid and the sternal notch
Negative anterior neck mass
• Masses
Trachea is in midline position
• Discoloration
PALPATION
Palpate for lymph nodes on all levels of the neck No lymphadenopathies
Palpate for the thyroid Trachea is observed to be midline
• Position the neck in slight flexion Thyroid is not enlarged, non-tender, no nodules or masses noted
• Use thumb if from in front or the pads of the 2-4 fingers if from behind
th
• Ask the patient to swallow If mass is present: Size, consistency, nodularity, tenderness
Check if trachea is midline 1 cm solitary soft, movable, non-tender mass on the anterior neck
AUSCULTATION
Using the bell of a stethoscope auscultate for bruits over the enlarged
No bruits noted
thyroid
END
Thank the patient
*if thyroid disease is suspected, a more comprehensive physical examination should be done
NOSE AND PARANASAL SINUSES PHYSICAL EXAMINATION

START
• Ask for consent
General appearance The patient is alert, awake, coherent, dressed appropriately, and not in respiratory distress
INSPECTION
• Asymmetry or deformity of the nose, deviated septum, abnormal Nares are symmetrical
creases, and presence of discharge or crusting along the nasal There are no deformities, septum is not deviated
vestibule No present discharges, lesions, or masses
PALPATION
• Airway obstruction: press on each ali nasi one at a time and asking
patient to breathe in No tenderness on the frontal and maxillary sinuses
• Palpate for tenderness on areas overlying the frontal and maxillary No airway obstruction
sinuses
ANTERIOR RHINISCOPY
• Inferior turbinate: first structure to be seen upon entry of nasal
speculum. Both inferior turbinates can be observed
• Note color, swelling, bleeding, exudates, ulcers, polyps, septal Nasal canal is pink, with no discharge, exudates, ulcers, or polyps
deviation, and patency of nasal passage Air passage is patent
• If exudate is present: note if it is clear, mucopurulent, or purulent
NEUROLOGY PHYSICAL EXAMINATION

START
• Ask for consent

MENTAL STATUS EXAMINATION
• General Appearance and behavior
o Normal, hyperactive, agitated, quiet, immobile, well-groomed
• Mood and affect
o euphoric, agitated, giggling, silent, weeping, angry
• Content of thought
o presence of illusion, delusions, hallucinations, misinterpretations,
phobias, bodily complaints
• Intellectual capacity
o bright, average, dull, mentally retarded
• Sensorium
o aware, oriented, attentive
• Level of consciousness
o awake, lethargic, obtunded, stupor, coma
• Orientation to person, place, and time
• Attention
o Recite the months or spell words forward and backward (“L-U-N-
E-S, S-E-N-U-L”, WORLD)
o Serial 7s (subsequent subtraction of 7 starting from 100), Serial
3s (subtract from 20)
o Tapping test (tapping whenever physician says letter A)
• Memory Patient is alert, awake, dressed appropriately and well-groomed, cooperative
o Immediate (repeat “mangga, mesa, pera” immediately and after Language is fluent and appropriate, patient is able to comprehend, name, read, write, and repeat as
the entire exam) tested
o Recent (what they had for breakfast) Oriented to time, person, and place
o Remote (which elementary school did they go to) Intact: attention, memory, insight, judgement, and planning (may report specific findings of tests
o Semantic (name the presidents backward from the present one) done)
• Fund of Information Negative apraxia
o Ask about current events in the news
• Insight, Judgment, and Planning
o Ask about their goals and plans
o Give a situation and listen to what the patient would do
o Calculation Serial 7
• Apraxia
o Ideomotor apraxia (demonstrate how to unlock a door, use
scissors, etc)
o Ideational apraxia (ask what a key is used for and how to use it,
etc)
o Constructional apraxia (copy a geometric figure)
o Dressing apraxia
o Gait apraxia
o Writing and speaking apraxia
• Aphasia
o Fluency, understanding, naming, repetition
• Visual Spatial Function
• Gerstmann’s Syndrome:
o Finger agnosia (identify pointed finger), Right left confusion,
agraphia (writing), acalculia (arithmetic)
CRANIAL NERVES
CN 1: Olfaction (one nostril at a time, pt should close eyes)
CN 2: Visual acuity, visual fields, PLR, fundoscopy
CN 3: Eye motion, PLF All cranial nerve functions intact
CN 4: Eye motion Ideally it should be reported per cranial nerve based on what was tested
CN 5: Sensation of the face (test V1,2,3 territories, light touch, pinprick • Olfaction intact, visual acuity ___, no visual field cuts, full range smooth eye motion, no
and temp), strength of muscles of mastication, corneal reflex strabismus, equally and briskly reactive pupils, intact ____ sensation on the face, strong muscles
CN 6: Eye motion of mastication, intact corneal reflex, no facial asymmetry, good and equal strength of facial
CN 7: Facial expression, taste of anterior tongue, conreal reflex, muscles, intact taste on anterior tongue, no lateralization on weber, AC>BC, negative nystagmus
CN 8: Hearing, Rinne/Weber, Vestibular function (nystagmus, balance) on provocative testing, intact gag reflex, symmetric palatal elevation, intact phonation of labial,
CN 9 &10: Gag reflex, palatal phonation (“ka ka”, palatal elevation, lingual and palatal sounds, no hoarseness or dysphagia, good strength of traps and SCM, no
hoarseness, dysphagia, taste of posterior tongue tongue deviation, and good tongue strength and motion.
CN 11: strength test of the traps and SCM
CN 12: tongue deviation, or atrophy, tongue strength and motion
MOTOR EXAMINATION
Check for symmetry, muscle bulk (hypertrophy/atrophy), fasciculations,
involuntary movements, tremors (resting/postural), muscle tone
Symmetric on upper and lower extremities, no atrophy or fasciculations noted, tremors absent
(hypertonia/hypotonia), and spasticity
(*note that a resting tremor is normal).
Test of range of motion
Normotonic, without spasticity
Test for muscle strength on all major muscle groups individually on both
Full range of motion of joints
the upper and lower extremities, include pronator drift, always compare
No weakness, 5/5 strength on (all muscles tested)
right and left
Muscle Strength Grading:

• 5: Full range of motion against maximum resistance

• 4: Full range of motion against minimum resistance
• 3: Full range of motion against gravity
• 2: Motion with gravity eliminated (side to side)
• 1: Flicker of contraction only
REFLEXES
Test for Deep tendon reflexes on triceps, biceps, brachioradialis, patella,
Normoreflexive, brisk reflexes (+2)
and ankle
Negative babisnki, absent grasp and rooting reflex
May check cutaneous reflexes and frontal release signs
SENSORY EXAMINATION
• Light-touch, pain, temperature
o Compare right and left, proximal and distal, if cord injury is
suspected test for dermatomes (to determine level) Intact (type of sensation) sensation on (areas tested)
• Vibration and proprioception Intact vibratory sense, proprioception on both upper and lower extremities
o Tests vibration on the ring finger on a bony prominence/nail Intact stereognosis and graphesthesia on both hands
o Be wary of handling during proprioception 2-pt discrimination (result, test distance) on (test site) *each area of the body will have a different
• Two-point discrimination, stereognosis, graphestesia normal value
All tests dons with eyes closed

CEREBELLAR TESTING
• Check for passive movements, posture when walking and resting,
stance
• Check for nystagmus
• Finger-to-nose test, finger-to-finger or heel-to-shin test (dysmetria)
• Alternating pronation-supination test (dysdiadochokinesia) Normotonic
• Rebound test Negative nystagmus
• Gait and balance No dysmetria or dysdiadochokinesia
o Check for cadence, if pt walks with a wide base, shuffling gait or Pt has good balance when walking and turning, pt is able to perform toe-to-toe, tip-toe and heel
other gait deviations, listing to one side, loss of balance walking with good balance (describe the other gait parameters as needed)
o Check turning, toe-to-toe walking, tip-toe walking, and heel
walking
• Rhomberg tests (to rule our proprioception deficits as a cause of
balance problems, not that it is a test for proprioception)
END
Thank the patient


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Edited & Updated by:

Author: Cuevas, et al. ASMPH Batch 2019, Batch

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 1

“It always seems impossible until it is done”

Topic Pages Contributors

Compilers: Alcantara, Cuevas, Gaviola, Punsalan, Sy

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 2

CATHARSIS, EDUCATION, ACTION (CEA) STRESSFUL EVENTS, PRECIPITATING CRSIS

Levels of Family Involvement

DEALING WITH DIFFICULT PATIENTS

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 1

FAMILY APGAR APGAR

Family Map Family Genogram

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 2

FAMILY LIFE CYCLE

Age Freud’s Stages of Psychosexual Development Erickson’s Psychosocial Stages

Two levels of order change

Stage in the Family

MOTIVATING BEHAVIOR CHANGE

THE HEALTH BELIEF MODEL

ATTITUDINAL PRINCIPLES IN MOTIVATIONAL COUNSELING

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 3

Cross Sectional Case Control Cohort

TYPES OF ERROR MEASURES OF ASSOCIATION

TRUTH • Calculations used to measure disease frequency relative to other factors

Has two components: Has four components

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 4

Level Tools Objectives

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 5

Normal (adult) 12 to 20 breaths/minute JNC 8 UPDATES

IDEAL BODY WEIGHT

INCREASED RISK OF CO-MORBIDITIES – ASIANS

Classification Europe/US Asia Pacific

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 6

Subscription Dispense #24 capsules Instructions to the pharmacist:

Signa, Signatura, Transcription Sig Instructions for the patient:

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 7

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 8

Non-STEMI (Non ST-

BLOOD COLLECTION TUBES

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 10

Inactivates thrombin and thromboplastin

Pink Potassium EDTA Forms calcium salts Immunohematology

ERYTHROCYTE SEDIMENTATION RATE (ESR)

WHITE BLOOD CELL DIFFERENTATION COUNT

Eosinophil • Large, pink • Allergic disorders,

Basophil • Large numerous blue- • Leukemia

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 11

CLOTTING TIME AND BLEEDING TEST

I Fibrinogen VIII Antihemophilic factor A

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 12

FECAL OCCULT BLOOD TEST

SEMEN (SPERM) ANALYSIS

ASMPH YL6 OSCE/REVALIDA REVIEWER / BATCH 2018 13

Conditions that increase RR (hyperventilation), and thus arterial CO is low

based from patient's history, • Methanol

Conditions that increase HCO in the body or decrease H+

• Normal range: 7.37-7.43

Normal HCO : 22-26 (middle: 24)

STEP 3: What is the primary

Reference range for anion gap: 3-11 mEq/L

A high anion gap always indicates metabolic acidosis

A-a gradient in mmHg = P O - P O

Expected A-a gradient for age = (Age/4) + 4