CARDIO 15%

ECG Cheat Sheet: Voltage (small square: 1mm or 0.1mV), Time (small square: 1mm or 0.04 sec)
Standardization 10mm = 1mV, 25mm/second
Rhythm R-R Intervals (<0.12 sec) consider regular
Heart Rate Regular Rhythm: 300-150-100-75-60-50, 1500/Small, 300/Large
Irregular Rhythm: R Waves in 6 second strip X 10
Intervals P Wave (0.06-0.10 sec)
PR Interval (0.12-0.20 sec)
QRS Complexe (0.06-0.12 sec)
QT Interval (0.26-0.44 sec)
Axis Deviation Normal I+, aVF+
LAD I+, aVF-
RAD I-, aVF+
AV Block Ps and R are far, Longer longer longer drop, Some Qs don’t get thru, Qs and Ps don’t agree
BBB or Hemiblock RBBB: Wide QRS (>0.12 sec), RsR’ in V1 & V2, Wide S wave in V6
LBBB: Wide QRS (>0.12 sec), Broad slurred R wave in V5 & V6, Deep S wave in V1, ST Elevations in V1-V3
Hypertrophy Right Atrial Enlargement (P-Pulmonale) II, III, aVF (tall peaked >2.5mm), V1 (biphasic p wave larger initial part)
Left Atrial Enlargement (P-Mitrale) I, II (notched m-shaped, >0.12 sec), V1 (terminal part ≥1mm deep and ≥0.04 wide)
RVH: R>S in V1 or R >7mm in V1
LVH: S in V1 + R in V5 or V6 >35mm (men) or >30mm (women)
CAD Look for Q Waves and ST Segment and T Wave Changes. Remember, Not all changes reflect CAD, Know your Ddx

Inferior Leads: II, III, aVF

Anterior Leads: V1-V4
Lateral Leads: I, aVL, V5, V6

Anterior: V1-V4 Left Anterior Descending

Septal: V1 & V2 Proximal Left Anterior Descending
Lateral: I, aVL, V5, V6 Circumflex Artery
Inferior: II, III, aVF Right Coronary Artery
Posterior (ST Depression V1 & V2) Right Coronary Artery & Circumflex Artery

Valves L

1) Harsh/Rumble: Stenosis
Blowing: Regurgitation
2) Increase Venous Return (Supine, Squatting, Leg elevation): Increases intensity of all murmurs except Hypertrophic Cardiomyopathy (decreased) & MVP Click (delayed)
Decrease Venous Return (Standing, Valsalva): Decreases intensity of all murmurs except Hypertrophic Cardiomyopathy (increased) & MVP Click (earlier)
3) Right sided murmurs sound like left sided versions (TR = MR, AS = PS, AR = TR)
How to distinguish? 1) Location, 2) Inspiration increases intensity of right sided murmurs (decreases left sided murmurs)
Aortic: RUSB
Pulmonic: LUSB
Tricuspid: LLSB
Mitral: Apex
4) MR = Axilla
AS = Carotid
5) Systolic: AS, MR
Diastolic: AR, MS

1
CHA2DS2-VASc Score: A-Fib Stroke Risk, Calculates stroke risk for A-Fib patients
≥2: Moderate-High Risk: Chronic Oral Anticoagulation Recommended
1: Low Risk: Based on clinical judgement, Consideration of risk vs benefit and discussion with patient
0: Very Low Risk: No anticoagulation needed
Congestive HF (+1): Signs/symptoms of HF confirmed with objective evidence of cardiac dysfunction
Hypertension (+1) Rest BP >140/90 on ≥2 separate occasions or current antihypertensive meds
Age ≥75 yo (+2)
DM (+1): Fasting glucose >125 or treatment with oral hypoglycemic agent/insulin
Stroke, TIA, or Thromboembolism (+2): Includes any history of cerebral ischemia
Vascular Disease (+1): Prior MI, Peripheral arterial disease, or Aortic plaque
Age 65-74 yo (+1)
Sex (female) (+1): Female is higher risk

SCREENING
Hyperlipidemia: Based on risks: Sex, Age, Smoking, HTN, FamHx CHD (1st degree male with CHD before 55 yo, 1st degree female with CHD before 65yo)
ACC/AHA: Adults 20-39 yo who are free of CVD: Assess their RF Every 4-6 Years to calculate their 10 year CVD risk
Higher Risk (>1 RF): HTN, Smoking, FamHx or 1 Severe RF: Initiate 20-25 yo Males, 30-35 yo Females
Lower Risk: Initiate 35 yo Males, 45 yo Females

CARDIO About Clinical Presentation Diagnostics Treatment

Myocarditis Inflammation of heart muscle
MC young adults
Patho: Myocellular damage -> Myocardial
necrosis & dysfunction -> HF
Etiology
Infectious: Viral MC (esp enteroviruses
– coxsackievirus B), Bacterial
Autoimmune: SLE, RA
Uremia meds (Clozapine, Methyldopa,
ABX, Isoniazid, Cyclophosphamide,
Indomethacin, Phenytoin, Sulfonamides)
Viral Prodrome: Fever, Myalgias,
Malaise for several days, then symptoms
of systolic dysfunction (dilated
cardiomyopathy)
HF Symptoms: Dyspnea, Fatigue,
Exercise intolerance, S3 gallop
Other: Megacolon, Pericarditis
(pericardial friction rub, effusion)
CXR: Cardiomegaly Standard Systolic HF
ACEi, Diuretics, Beta-Blockers
EKG: Non-specific
Sinus tachycardia (MC), Normal, or
Pericarditis (diffuse ST Elevations & PR
Depressions in precordial leads)
Labs: ± +Cardiac enzymes, Increased ESR
ECHO: Ventricular systolic dysfunction
*helpful to rule out other causes
Endomyocardial Biopsy: Gold
Infiltration of lymphocytes with myocardial
tissue necrosis
*usually reserved for severe/refractory

Dilated Systolic dysfunction -> Dilated weak Systolic HF ECHO: DoC Standard Systolic HF
Cardiomyopathy heart Left Sided: Dyspnea, Fatigue Similar findings to systolic HF ACEi, Beta-Blockers (Metoprolol,
Right Sided: Peripheral edema, JVD, Left ventricular dilation (large chamber), Carvedilol), ARB, Spironolactone
MC Cardiomyopathy Hepatomegaly, Ascites, GI symptoms Thin ventricular walls, Decreased EF,
Ventricular hypokinesis Symptom Control
RF: MC Men 20-60 yo Embolic events, Arrhythmias Diuretics, Digoxin
CXR
Etiology PE: S3 Gallop (due to filling of a dilated Cardiomegaly, Pulmonary edema, Pleural EF <30-35%
Idiopathic (MCC) ventricle), Mitral/Tricuspid regurgitation effusion Automated Implantable
Infectious: Viral MC (esp enteroviruses Cardioverter/Defibrillator
– coxsackievirus B, Echovirus) EKG
Postviral, HIV, Lyme, Parvovirus B19, ± Sinus tachycardia or arrhythmias
Chagas
Toxic: EtOH, Cocaine, Anthracyclines
(Doxorubicin), Radiation
2
 Pregnancy, Autoimmune
Metabolic: Thyroid disorders, Vit B1
(thiamine) deficiency
Stress Transient regional systolic dysfunction
(Takotsubo) of LV can imitate MI, but is associated
Cardiomyopathy with the Absence of significant
obstructive CAD or evidence of plaque
rupture
RF: Postmenopausal women exposed to
physical/emotional stress (death of
relative, catastrophic medical diagnoses,
acute medical illness)
Patho: Thought to be multifactorial,
including catecholamine surge during
physical/emotional stress, microvascular
dysfunction, and coronary artery spasm
Hypertrophic Autosomal dominant disorder of
Cardiomyopathy inappropriate LV and/or RV
hypertrophy with diastolic dysfunction
Subaortic outflow obstruction due to
asymmetrical septal hypertrophy and
systolic anterior motion of the MV
Obstruction Worsens
Increased Contractility: Exercise,
Digoxin, Beta-Agonist
Decreased LV Volume: Dehydration,
Decreased venous return, Valsalva
Restrictive Diastolic Dysfunction in a non-dilated
Cardiomyopathy ventricle which impedes ventricular
filling (decreased compliance). Stiff
ventricles fill with great effort
Etiology
Similar to ACS
Substernal chest pain, Dyspnea,
Syncope
May be asymptomatic initially
Dyspnea (MC), Fatigue, Angina, Pre-
syncope, syncope, Dizziness,
Arrhythmias
Sudden cardiac death (esp
adolescent/pre-adolecent, during times of
extreme exertion) usually due to VFib
Right sided HF > Left sided HF
Right Sided: Peripheral edema, JVD,
Hepatomegaly, Ascites, GI symptoms
Left Sided: Dyspnea, Fatigue
EKG
ST Elevation (esp anterior leads) May
have ST Depression
Cardiac Enzymes: Often positive
Coronary Angiography: Absence of acute
plaque rupture or obstructive coronary
disease. On exams this is an all the way
question meaning it is considered in
patients with ACS with no evidence of
obstructive coronary disease on coronary
angiography
ECHO: Transient regional LV systolic
dysfunction (esp apical LV ballooning)
*usually done after ACS ruled out
Murmur
Systolic
Harsh
LSB
Increased: Decreased venous return
(Valsalva, Standing) or Decreased afterload
(amyl nitrate)
Decreased: Increased venous return
(Squatting, Supine, Leg raise) or Increased
afterload (handgrip)
Increased LV volume preserves outflow
± Loud S4, MR, S3, Pulsus bisferiens
ECHO
Asymmetric ventricular wall thickness (esp
septal) ≥15mm, Systolic anterior motion of
MV, Small LV chamber size
EKG
LVH, Anterolateral & Inferior pseudo q
waves, Enlarged atria
ECHO: DoC
Non-dilated ventricles with normal
thickness (may be slightly thick), Diastolic
dysfunction, Marked dilation of both
atria
Systolic function generally preserved early
Initial: Bc it presents similar to ACS, patients
are treated as ACS with ASA, Nitroglycerin,
Beta-Blockers, Heparin, and Coronary
angiography to rule out obstructive coronary
artery disease
Short Term Management
Conservative & Supportive Management (Beta-
Blockers, ACEi for 3-6 months with serial
imaging to access improvement)
Severe LV Dysfunction (EF <30%) or
Thrombus
Anticoagulation
Early detection, Medical management, Surgical
management, ± ICD placement
Medical: 1st: Beta-Blockers
*Alternatives: CCB, Disopyramide
Surgical: Myomectomy (usually younger &
refractory)
*Alternative: EtOH Septal Ablation
Avoid: Dehydration, Extreme exertion,
Exercise
Cautious Use: Digoxin, Nitrates, Diuretics
*digoxin: increases contractility
*nitrates, diuretics: decrease LV volume
No specific treatment
Treat underlying disorder
Chelation for Hemochromatosis
Glucocorticoids for Sarcoidosis
Gentle diuresis for symptoms
3
Infiltrative disease: Amyloidosis (MC),
Sarcoidosis, Hemochromatosis,
Scleroderma, METS, Endomyocardial
fibrosis
Chemo, Radiation
Kussmaul’s Sign: Lack of inspiratory
decline or Increase in JVP with
inspiration
Signs of HF, ± S3, Pulmonary HTN
Bright speckled myocardium in
amyloidosis Vasodilators
CXR: Normal ventricular chamber size,
Enlarged atria, Pulmonary congestion
EKG: Low voltage QRS, Arryhthmias
BNP: Increased
Endomyocardial Biopsy: Definitive
Amyloidosis associated with apple-green
birefringence with congo red staining
4
CARDIO About Symptoms Management
Normal Sinus Every P Wave is followed by a QRS Complex
Rhythm P Waves: Positive: I, II, aVF, Negative: aVR
HR: 60-100 BPM

Sinus Arrhythmia Irregular rhythm, Originating from Sinus node EKG Most cases: None needed
Normal variation for normal sinus rhythm (meets same Normal appearing P Waves *considered normal variant
criteria except rhythm is irregular) Beat to beat variation of P-P Interval (>0.12 sec)
MC seen children, young adults, pt with sinus bradycardia Inspiration: Shorter P-P intervals Symptomatic Bradycardia
Expiration: Longer P-P intervals 1st: Atropine
2nd: Transcutaneous pacing, Epinephrine, Dopamine

Sinus Bradycardia HR <60, Originating from Sinus node EKG Symptomatic/Unstable

Regular, Slow (<60 BPM) 1st: Atropine
Etiology Normal appearing P Wave 2nd: Transcutaneous pacing, Epinephrine
Physiologic: Young athletes, Vasovagal rxn, Increased Every P Wave followed by a QRS Complex
ICP, N/V Asymptomatic
Physiologic: None
Pathologic: Beta-Blockers, CCB, Digoxin, Carotid Pathologic: Observation, Cardiac consult
massage, SA node ischemia, Gram(-) sepsis,
Hypothyroidism

Sinus Tachycardia HR >100, Originating from Sinus node EKG 1st: Treat underlying cause
Regular, Rapid (>100 BPM)
Etiology Normal appearing P Wave Persistent in Acute Coronary Artery Syndrome
Physiologic: Normal response to exercise, Emotional Every P Wave followed by a QRS Complex Beta-Blocker (Metoprolol)
stress, Normal in young children & infants

Pathologic: Fever, Hypovolemia, Hypoxia, Pain,

Infection, Hemorrhage, Hypoglycemia, Anxiety,
Thyrotoxicosis, Shock, Sympathomimetics
(decongestants, cocaine)

Sick Sinus Syndrome Dysfunction of Sinus node -> Combo of sinus arrest
“Brady-Tachy with alternating paroxysms or atrial
Syndrome” tachyarrhythmias & bradyarrhythmias
Etiology
Sinus node fibrosis (MC), Older age, Corrective cardiac
surgery, Meds, Systemic disease that affect the heart
Intermittent bradycardia & tachycardia: Palpitations,
Dizziness, Lightheadedness, Angina, Exertional dyspnea,
Presyncope, Syncope
EKG
Alternating bradycardia (Sinus pause, SA exit block) &
Atrial tachyarrhythmias
Telemetry/Ambulatory EKG Monitoring
*may be needed to document episodes
Stable: May not require urgent therapy as the
symptoms are often transient
Hemodynamically Unstable
1st: Atropine
2nd: Transcutaneous pacing, Epinephrine, Dopamine
Long Term
Permanent Pacemaker: Definitive
Addition of Autonomic Implantable Cardioverter
Defibrillator: If alternating between tachycardia &
bradycardia

5
AV Conduction Blocks
CARDIO About
1st Degree AV R is far from P
Block
AV node dysfunction -> Delayed but
conducted impulses
Etiology
Often a normal variant (high vagal tone
without structural heart disease)
Intrinsic AV node disease, Acute MI
(inferior), Electrolyte disturbances
(hyperkalemia), AV node blocking drugs
(Digoxin, Beta-Blockers, CCB), Myocarditis
due to lyme, Cardiac surgery
2nd Degree AV Not all of the atrial impulses are conducted
Block to the ventricles. Leads to some P Waves
that are not followed by QRS complexes
Mobitz I
(Wenckebach) Mobitz I: Longer longer longer drop
Interruption of impulse at AV node resulting
Mobitz II in occasional non-conducted impulses
Patho: AV node dysfunction (commonly
above bundle of HIS)
Etiology: Often a normal variant (high vagal
tone without structural heart disease), Acute
MI (inferior), AV node blocking drugs
(Digoxin, Beta-Blockers, CCB), Myocarditis
due to lyme, Cardiac surgery
Mobitz II: Some Ps don’t get thru
Interruption of impulse at AV node resulting
in occasional non-conducted impulses
Patho: AV node dysfunction (commonly at
the bundle of HIS)
Etiology: Rarely seen in patients without
structural heart disease (MI, Myocardial
fibrosis, Myocarditis (lyme disease),
Endocarditis. Iatrogenic (AV nodal blockers,
Post catheter ablation, Post cardiac surgery)
Causes
Most asymptomatic
If symptomatic it’s due to bradycardia
related decreased perfusion: Fatigue,
Dizziness, Dyspnea, Chest pain, Syncope
Severe: Hypotension, AMS
Both
Most asymptomatic
Bradycardia related decreased perfusion:
Fatigue, Dizziness, Dyspnea, Chest pain,
Syncope
Severe: Hypotension, AMS
Signs and Symptoms
EKG
All PRI prolonged (>0.20 sec)
All P Waves followed by QRS complex
EKG
Mobitz I: Longer longer longer drop
Progressive lengthening of PRI until
an occasional dropped QRS
Mobitz II: Some Ps don’t get thru
Constant PRI before & after dropped
QRS
If ischemia suspected: Cardiac
biomarkers, CXR, Electrolytes
Diagnose/Management
Asymptomatic: No treatment, Observation
Symptomatic
1st: Atropine
2nd: Epinephrine
Persistently Symptomatic & Severe (>0.30 sec)
Pacemaker: Definitive
Mobitz I: Longer longer longer drop
Asymptomatic: No treatment, Observation
Symptomatic
1st: Atropine
2nd: Epinephrine
Persistent: Pacemaker: Definitive
Mobitz II: Some Ps don’t get thru
Initial: Transcutaneous pacing, Atropine for
symptomatic bradycardia
*these patients often don’t respond to Atropine
Definitive: Permanent Pacemaker
*Required in many patients bc it often
progresses to 3rd degree AV block and in
associated with complications of hypotension
and cardiac arrest
6
 3rd Degree AV Ps and Qs don’t agree
Block
AV Dissociation: No atrial impulses reach
the ventricles so the atrial activity is
independent of the ventricular activity
Leads to an escape rhythm from below the
block
May be asymptomatic
If symptomatic it’s due to bradycardia
related decreased perfusion esp during
exertion: Fatigue, Dizziness, Dyspnea,
Chest pain, Syncope
Severe: Hypotension, AMS
EKG
Regular P-P Intervals & Regular R-R
Intervals but they are not related to
each other
*Patients are often bradycardic
Acute/Symptomatic: Transcutaneous pacing
often followed by permanent pacemaker
placement
Permanent Pacemaker: Definitive

Etiology
MI (inferior), AV node blocking drugs
(Digoxin, Beta-Blockers, CCB),
Endocarditis, Myocarditis due to lyme,
Cardiac surgery
Increased vagal tone, Hypothyroidism,
Hyperkalemia, Myocarditis

Atrial Dysrhythmia

CHA2DS2-VASc Score: A-Fib Stroke Risk, Calculates stroke risk for A-Fib patients
≥2: Moderate-High Risk: Chronic Oral Anticoagulation Recommended
1: Low Risk: Based on clinical judgement, Consideration of risk vs benefit and discussion with patient
0: Very Low Risk: No anticoagulation needed
Congestive HF (+1): Signs/symptoms of HF confirmed with objective evidence of cardiac dysfunction
Hypertension (+1) Rest BP >140/90 on ≥2 separate occasions or current antihypertensive meds
Age ≥75 yo (+2)
DM (+1): Fasting glucose >125 or treatment with oral hypoglycemic agent/insulin
Stroke, TIA, or Thromboembolism (+2): Includes any history of cerebral ischemia
Vascular Disease (+1): Prior MI, Peripheral arterial disease, or Aortic plaque
Age 65-74 yo (+1)
Sex (female) (+1): Female is higher risk

CARDIO About Causes Symptoms Management

Atrial Flutter 1 irritable atrial focus firing at a fast rate
(atrial rate usually ~300/min)
Similar to AFib, there is an increased risk of
atrial thrombus formation that can lead to
cerebral and/or systemic embolization
(stroke)
May occur alone or be an interval rhythm
between sinus tachycardia and AFib
Symptomatic: Palpations, Dizzy, Fatigue,
Dyspnea, Chest pain
Unstable: Due to hypoperfusion:
Refractory chest pain, Hypotension (SBP
double digits), AMS
EKG
Flutter “Sawtooth” waves
*usually 300 BPM
*Identical (1 focus)
No discernable P Waves
Stable: Vagal maneuvers, Rate control with Beta-
Blockers (Metoprolol, Atenolol, Esmolol) or
Non-Dihydropyridine CCB (Diltiazem,
Verapamil)
Unstable: Synchronized Cardioversion
Anticoagulation: Similar criteria (CHA2DS2-
VASc) for nonvalvular AFib in pt at risk for
embolization

Reversion to Normal Sinus Rhythm

Radiofrequency Catheter Ablation: Definitive
Synchronized Cardioversion
IA, IC, or III Antiarrhythmics (Ibutilide)

Atrial Multiple irritable atrial foci fire at fast rates Symptomatic: Palpations, Dizzy, Fatigue, EKG Stable
Fibrillation Dyspnea, Chest pain
(AFib) MC Chronic Arrhythmia
7
Most are asymptomatic
Similar to Atrial flutter, there is an increased
risk of atrial thrombus formation that can
lead to cerebral and/or systemic
embolization (stroke)
Etiology: Cardiac disease, Ischemia,
Pulmonary disease, Infection,
Cardiomyopathies, Electrolyte imbalences,
Idiopathic, Endocrine/Neurologic disorders
(thyroid disorders), Increasing age, Genetics,
Hemodynamic stress, Meds, Drugs, EtOH
Men > Women
White > Black
Types
Paroxysmal: Self-terminating within 7 days
(usually <24 hours) ± Recurrent
Persistent: Fails to self-terminate, Lasts >7
days. Requires termination (medical/electrical)
Permanent: Persistent AFib >1 year (refractory
to cardioversion or cardioversion never tried)
Lone: Paroxysmal, Persistent, or Permanent
without evidence of heart disease
Unstable: Due to hypoperfusion:
Refractory chest pain, Hypotension (SBP
double digits), AMS
Irregularly irregular rhythm
with fibrillatory waves (no
discrete P Waves)
Atrial rate often >250 BPM
AV nodal refractory period
determines the ventricular rate
± Ashman’s Phenomenon:
Occasional aberrantly conducted
beat (Wide QRS) after short R-R
cycles
Rate control: Beta-Blockers (Metoprolol,
Atenolol, Esmolol) or Non-Dihydropyridine
CCB (Diltiazem, Verapamil)
Digoxin: May be used when above C/I (CHF,
Severe hypotension)
Unstable: Synchronized Cardioversion
Long Term
Rate control preferred over Rhythm control
Synchronized/Medical cardioversion
Radiofrequency Catheter Ablation
Anticoagulation: Similar criteria (CHA2DS2-
VASc) for nonvalvular AFib in pt at risk for
embolization
Cardioversion
*Most successful when performed within 7 days
ECHO: Needed prior to cardioversion to ensure
there are no atrial clots
AFib >48 Hours: Undergoing elective
cardioversion, Anticoagulation for ≥3 weeks
before cardioversion or a transesophageal echo
approach with abbreviated anticoagulation
AFib <48 Hours: Undergoing elective
cardioversion, Anticoagulation prior is
recommended
Anticoagulation must be continued for 4 weeks
after cardioversion (stroke risk decreased)
CHA2DS2-VASc ≥2: Chronic oral
Anticoagulation (Warfarin or Novel oral
anticoagulants)
Anticoagulant Agents
NOAC (Non-Vitamin K Antagonist Oral): DTI
(Dabigatran), Factor Xa Inhibitor
(Rivaroxaban, Apixaban, Edoxaban)
Usually now preferred over Warfarin in most cases
due to similar/lower rates of major bleeding as
well as lower risk of ischemic stroke, convenience
of not having to check INR, and Less DDI
Warfarin: May be preferred in some: Severe
chronic kidney disease, C/I to NOAC (HIV on PI,
on CP450 inducing antiepileptic meds
Carbamazepine, Phenytoin), Patients already on
Warfarin who prefer not the change, Cost issues
*Usually bridged with Heparin until Warfarin is
therapeutic
*Monitoring: INR Goal 2-3, PT
8

Premature Frequently the Inciting Event to PSVT
Atrial/Junctional (Paroxysmal Supraventricular Tachycardia)
Contraction
(PAC, PJC) It is going to reset the SA Node
Etiology (anything that irritates the heart)
Normal Variant or enhanced automaticity
Acute Respiratory Failure, COPD, HF, Atrial
Insult, CAD, Myocardial irritation
Early indication for CHF or Atrial Fibrillation
Electrolyte imbalance
Endogenous catecholamine release (pain,
anxiety) Fatigue, Fever, Hypoxia
Medications that prolong refractory period of
SA Node: Procainamide, Quinidine, Digoxin
(toxicity), EtOH, Caffeine, Nicotine
Paroxysmal Any tachycardia originating above the
Supraventricular ventricles (either atrial or atrioventricular
Tachycardia nodal source)
(PSVT)
SVT: Umbrella term when a more specific term
cannot be applied to a tachyarrhythmia
originating above the ventricles
Patho: Reentry circuits
AV Node RE-Entrant Tachycardia: MC
2 pathways (1 normal & 1 accessory
pathway both within the AV node)
AV Reciprocating Tachycardia (AVRT)
2 pathways (1 normal & 1 accessory pathway
outside of the AV node): WPW & LGL
Wandering WAP: Multiple ectopic atrial foci generate
Atrial impulses that are conducted to the ventricles
Pacemaker
(WAP) & MAT: Same as WAP except HR >100
Multifocal Atrial Classically associated with COPD
Tachycardia
(MAT)
Wolff-Parkinson Preexcitation syndrome that is a type of AVRT
White (AV Reciprocating Tachycardia)
(WPW)
Typically asymptomatic, may have
palpitations
Symptomatic: Palpations, Dizziness,
Fatigue, Dyspnea, Chest pain
Unstable: Hypoperfusion can cause
Hypotension (SBP in double digits),
AMS, Refractory chest pain
Most asymptomatic but they are prone to
development of tachyarrhythmias
Dual Antiplatelet Therapy: Aspirin + Clopidogrel
Monotherapy is superior to dual therapy, Dual
reserved for those who cannot be treated with
anticoagulation (for reasons other than bleeding
risk)
EKG Asymptomatic: No treatment, Reassurance
Rhythm: Usually regular except
for the PAC(s) Symptomatic: Avoid known triggers, Beta-
P Wave: “Irregular” P Wave blockers (if not C/I), Catheter ablation
morphology (not coming from
SA Node)
P Wave of ectopic beat occurs
early & differs from Sinus P
Waves Can be flattened or
notched, May be lost in
preceding T Wave (look for
different T waves)
EKG Stable Narrow QRS: Vagal Maneuvers
HR >100 1st: Adenosine (AV nodal blockers)
Rhythm: Usually regular with 2nd: CCB (Diltiazem), Beta-Blocker (Metoprolol),
narrow QRS complexes Digoxin
P Waves: Hard to discern
Stable Wide QRS: Antiarrhythmics (Diltiazem)
Orthodromic (95%) *WPW Suspected: Procainamide
Regular, Narrow complex
tachycardia (no discernable P Unstable: Synchronized Cardioversion
Waves due to rapid rate)
“If you cant tell whether the Definitive: Radiofrequency Catheter Ablation
bump is P or T it must be SVT”
Antidromic (5%)
Regular, Wide complex
tachycardia (mimics ventricular
tachycardia)
EKG MAT: Difficult to treat
WAP: <100 BPM & ≥3 P Wave CCB (Verapamil) or Beta-Blocker if LV function
Morphologies is preserved
MAT: >100 BPM & ≥3 P Wave
Morphologies
EKG Stable (Wide Complex): Antiarrhythmics
Delta Wave (slurred QRS Procainamide: Preferred
upstroke) Amiodarone
9
 Patho: Accessory pathway (Bundle of Kent)
outside the AV node Pre-excites the ventricles
(directly connects the atria and ventricles by
bypassing the AV Node) -> Delta Wave
(Slurred, Wide QRS)
AV Junctional AV node/junction becomes the dominant
Dysrhythmias pacemaker
Etiology: Sinus disease, CAD, MC rhythm seen
with Digitalis toxicity, Myocarditis, May be
seen in pt without structural heart disease
Symptomatic: Palpations, Dizziness,
Fatigue, Dyspnea, Chest pain
Unstable: Hypoperfusion can cause
Hypotension (SBP in double digits),
AMS, Refractory chest pain
Junctional Rhythm: 40-60 BPM
*Reflects intrinsic rate of AV junction
Accelerated Junctional: 60-100 BPM
Junctional Tachycardia: >100 BPM
Shortened PRI *Avoid AV nodal blocking agents ABCD
Wide QRS (>0.12 sec) (Adenosine, Beta-Blockers, CCB, Digoxin) if
Wide QRS, Can lead to preferential conduction
down the Bundle of Kent, worsening the
tachycardia
Unstable: Synchronized Cardioversion
Definitive: Radiofrequency Catheter Ablation
*Electricity destroys the abnormal pathway
*May be indicated if patients experience recurrent,
symptomatic episodes
EKG
Rhythm: Regular
P Waves: Negative (if present)
in leads where they are normally
positive (I, II, aVF) or are not
seen
Classically associated with
Narrow QRS ± Wide
10
Ventricular Dysrhythmias

CARDIO Definition/ Causes Symptoms Diagnosis Management

Premature Premature beat originating from the ventricle -> Unifocal: One Morphology None usually needed
Ventricular Wide, Bizarre QRS occurring earlier than Multifocal: >1 Morphology *common finding on EKG
Complexes expected.
(PVC) Bigeminy: Every other beat Most ventricular arrhythmias
T Wave: Opposite direction of QRS usually Couplet: 2 in a row occur after a PVC

Associated with: Compensatory pause: Overall

rhythm is unchanged (AV node prevents
retrograde conduction)

Ventricular ≥3 Consecutive PVCs at a rate >100 BPM
Tachycardia *usual rate 120-300 BPM
Sustained: ≥30 sec
Non-Sustained: <30 sec
Monomorphic (same QRS morphology)
Polymorphic (different QRS morphology)
Torsades de Pointes: Variant of Polymorphic
Waxing & waning QRS amplitude
Etiology
Underlying Heart Disease: Ischemic heart
disease ie post-MI (MC), Structural defects,
Cardiomyopathies
Prolonged QT Interval, Electrolyte abnormalities
(Hypomagnesium, Hypokalemia,
Hypocalcemia), Digoxin toxicity
Symptomatic: Palpations, Dizziness,
Fatigue, Dyspnea, Chest pain
Unstable: Hypoperfusion can cause
Hypotension (SBP in double
digits), AMS, Refractory chest
pain
EKG
Regular, Wide QRS, Tachycardia
No discernable P Waves
Stable Sustained VT
Antiarrhythmics: Amiodarone,
Lidocaine, Procainamide
Unstable VT With Pulse
Synchronized Cardioversion
VT No Pulse
Defibrillation + CPR
*similar to VFib
Torsades de Pointes
IV Magnesium Sulfate, Correct
electrolyte abnormalities,
Discontinue all QT prolonging drugs

Torsades De Variant of Polymorphic VT Symptomatic: Palpations, Dizziness, EKG 1st: IV Magnesium Sulfate
Pointes Waxing & waning QRS amplitude Fatigue, Dyspnea, Chest pain Polymorphic VT (cyclic alteration of QRS *suppressed early after
amplitude) depolarizations
Patho: Prolonged repolarization and early after *sinusoidal waveform
depolarization and triggered activity Correct electrolyte abnormalities

Etiology Discontinue all QT prolongating

Prolonged QT Interval, Electrolyte abnormalities drugs
(Hypomagnesium, Hypokalemia,
Hypocalcemia), M > F, Congenital long QT Refractory: Isoproterenol,
syndrome Transvenous override pacing
Meds: Digoxin, Class 1A (Quinidine,
Procainamide, Disopyramide), Class III (Sotalol,
Ibutilide), ABX (Macrolides), Antipsychotics,
Antidepressants, Antiemetics

11
Ventricular Type of cardiac death associated with ineffective Unresponsive, Pulseless, Syncope EKG Defibrillation + CPR
Fibrillation ventricular contraction Erratic pattern of electrical impulses
(VFib) No P Waves
Etiology *Coarse or Fine
Underlying Heart Disease: Ischemic heart
disease ie post-MI (MC), Structural defects,
Cardiomyopathies, Sustained VT

Pulseless Organized rhythm seen on a monitor but CPR + Epinephrine

Electrical patient has no palpable pulse
Activity *electrical activity is not coupled with Check for shockable rhythm every
(PEA) mechanical contraction 2 min

Asystole Flatline CPR + Epinephrine

Check for shockable rhythm every

2 min

Early Usually a normal variant EKG

Repolarization May be seen in: Thin healthy males, AA Diffuse Concave ST Elevations >2mm with
Abnormalities Large T Waves (esp precordial)
Tall QRS Voltage
Fishhook (slurring/notching) at J Point

LVH with LV Often seen in patients with LVH who also suffer EKG
Strain from ischemic disease. LVH Criteria
Asymmetric ST Depression & T Wave
Coronary artery supply is strained trying to Inversions in lateral leads (I, aVL, V5, V6)
supply the excess hypertrophic cardiac muscle ST Elevations in right precordial leads (V1-V3)

Brugada EKG
Syndrome RBBB (often incomplete)
ST Elevation V1-V3 (often downsloping pattern)
T Wave Inversion V1 & V2
± S Wave in Lateral leads (I, aVL, V5, V6)

12
Class I – Na Channel Blockers
Class IA
•decreases conduction velocity
•prolongs repolarization
•prolongs refractory period
•prolongs action potential
•increase excitation threshold
moderate depression of phase 0
WORKS ON FAST SODIUM
Class IB
•decreases conduction velocity
•shortens repolarization
•shortens actions potential
*do not affect QRS complex
Class IC
•decreases conduction velocity
•NO effect on action potential
NORMAL repolarization
LONGER depolarization
Class II Drugs - Beta Blockers
-Metoprolol (cardioselevtive)
-Esmolol (IV)
-Atenolol, Carvedilol, Labetlol
Drug About Drug Side Effects/CI/PK/Caution
Quinidine •Potent anticholinergic properties that affect SA and AV nodes -> •Increased ventricular rates with afib or aflutter
increase SA nodal discharge rate and AV nodal conduction è PROLONG QT INTERVAL -> torsades
è Add BBB, CCB, or Digoxin to prevent
*don’t use because of QT prolongation, and rhythm issues •SE: GI, N/V/D
•PK: CYP3A4 inducer or inhibitor
Procainamide •No anticholinergic property •Prolongs QT -> Increases torsades
•LUPUS (SLE) clinical syndrome *MC
•N/V/D, fever
Disopryamide •Potent anticholinergic and negative inotropic effects •Prolongs QT -> Increases torsades
(Norpace) è Use more for HOCM •Precipitation of CHF
•Dry mouth, urinary retention, constipation, blurred vision
•CI: reduced LV EF (<40%)
Lidocaine •Selective to ischemic tissue •SE: CNS, dizziness, disorientation, tremor, agitation, seizure,
•Active fast sodium channel in the bundle of HIS, purkinje fibers, respiratory arrest
*IV form and ventricular myocardium
è Little effect on non-ischemis tissue, atrial myocardium, •Caution: liver failure *stop if Lidocaine level is over 4
SA node
•best for ventricular dysrhythmias with acute MI •PK: hepatic metabolism
Mexiletine •Similar to lidocaine but oral *not used alone •SE: GI, N/V highly, neurologic effects
*can use in combo with class IA and III drugs for refractory - Dizziness, confusion, ataxia, speech disturbances
*oral form ventricular dysrhythmias
Flecainide •Slows conduction velocity in the Purkinje fibers and the AV node •SE: rapid VT resistant to resuscitation
(Tambacor) •Used for afib/aflutter è Lengthen PR interval and QRS duration
- Blurred vision, dizziness, HA, tremor, N/V
•CI: CAD, LV dysfunction, LVH, valvular disease
Propafenone •Slows conduction velocity of purkinje fibers and AV node; mild •SE: same as Flecainide, metallic taste
(Rythmol) non-selective BB effect è May lengthen PR interval and QRS
*similar to Flecainide
•Used for afib/aflutter •CI: CAD, LV dysfunction, LVH, valvular disease
About Indication
Decreased automaticity (lowers resting threshold, takes longer to fire off), prolong Useful in suppressing ventricular dysrhythmias and supraventricular
AV conduction, prolong refractoriness dysrhythmias
à (-) chonotripic and inotropic effects
*beta blockers A à M are cardio selective, N and lower are NOT •CI: bradycardia, 2nd 3rd degree AV block
13
Class III – K Channel Blockers
*use these pretty routinely
Block potassium channels and prolong
repolarization, widening the QRS and
prolonging the QT interval
è Decrease automaticity and
conduction and prolong
refractoriness
è Cant fire neighboring cell as
easily, takes longer
*avoid w/
• QT prolongation drugs
• Anti-psychotic drugs
• Anti-fungals
• -Fluoroquinolones
Drugs About SE/CI/DDI
Amiodarone •Possesses characteristics of all 4 classes SE: *cumulative effects after years, not a one-time dose
(Pacerone) •K+ channel blocks, but also blocks sodium channels, non- •metabolite accumulation of IODINE in numerous organs
selective BB activity, weak CCB properties •Pulmonary Toxicity *pulmonary fibrosis
•Works on all cardiac cells è Stop immediately if occurs
•Minimal to no negative inotropic effects •Thyroid abnormalities (hypo or hyper) due to iodine
*can use in LV dysfunction •Ocular complications (corneal and lens) *rarely effects vision
è Photophobia, halos, blurred
•GI: Nausea (acute), vomit, anorexia, abdominal pain *common
MOST •Neurologic toxicities frequently (warn about)
COMMON è Tremors, ataxia, peripheral neuropathy, fatigue, insomnia
DRUG USE! •Derm: photosensitivity, blue/gray skin IN SUN (warn about)
Monitor:
•CXR and dilated eye exams yearly
•TSH & LFTs every 6 months
•wear sunscreen

DDI: CYP 3A4 inhibitor-Warfarin

*can double serum digoxin concentration

Sotalol •Has non-selective B-adrenergic blocking properties CI: LV dysfunction

(Betapace) •PUT IN HOSPITAL TO START AND MONITOR
è Decrease cardiac contractility SE: QT prolongation; DC if QT >550ms
è Prolongs atrial and ventricular refractoriness *most due to BB properties; do NOT combine with other BB

Dofetilide •Results in prolonged action potential and an increased QT
(Tikosyn) interval
è Effects atria more than ventricles
•No negative inotropic effects *Safe in LV dysfunction
*must have board of pharmacy certification in order to
prescribe because of QT prolongation
SE: development of torsades
*pt in hospital on telemetry with q12h EKGs for first 3 days
DDI: cimetidine, ketoconazole, megestrol, prochlorperazine, Bactrim,
verapamil
PK: Renal excretion (CI if CrCl <20) *regular BMP for CrCl

Dronedarone •Exhibits AA properties of all 4 classes CI: symptomatic CHF, permanent AF, hepatic
(Multaq) è However, does not work as well
SE: CHF exacerbation, QT prolongation, bradycardia, hepatotoxicity,
“safe cousin of Amiodarone” pulmonary toxicity, N/D, pruritis, dyspepsia
*don’t use often & more expensive
Monitor: BUN/CR, EKG q3mo for 1st 6mo tx

Ibutilide •Similar to sotalol, but no beta-blocking activity SE: torsades (QT prolongation)
(Corvert) •Close to a pure potassium channel blocking agent *monitor on telemetry for several hours following IV infusion
•Only in IV form and indicated for afib/flutter
cardioversionto sinus rhythm CI: LV dysfunction and electrolyte abnormalities (low K & Mg)
è Monitor in ICU

14
 Class IV - CCB Drugs About SE/CI/DDI
*Non-dihydropuridines Verapamil •Decreases automaticity and AV conduction CI: LV dysfunction; heart failure (due to negative inotropic)
Diltiazem •Potent negative inotropic effects
SE: peripheral edema, bradycardia, AV blocks

Class V – Other Drugs Drugs About

Digoxin •Predominant AA effects on AV node
-inhibits calcium currents in AV node and activated ACH-
mediated K+ currents in the atrium
-slows conduction through the AV node and prolongs AV
refractory period
-mainly used for slowing ventricular rate in afib/aflutter and
termination reentrant arrhythmias involving AV node
EKG changes: PR prolongation and ST segment depression
PK:
•IV or oral; DOSING IN MICROGRAMS
•Tablets incompletely bioavailable
•Slow distribution to effector sides
*requires loading dose of 0.6-1mg over 24 hours then reduce to maintenance dose
•t ½ of 36 hours
•renal elimination (reduce dose in renal insufficiency)

DDI: amiodarone, quinidine, verapamil, diltiazem, itraconazole, propafenone, flecainide

*decrease clearance, decrease digoxin with these meds

Digoxin Toxicity •Can be precipitated by: S/S: visual disturbances (blurry/tunnel vision), dizziness, weakness, N/V/D, anorexia, any dysrhythmia
-declining renal function
-electrolyte abnormalities Treatment:
-hypoxia or drug interactions •Manage arrhythmias
•IV hydration and electrolyte correction
•Narrow therapeutic index •Digoxin immune Fab (immunoglobin fragment)-> high affinity for digoxin molecules
*can check therapeutic levels

Adenosine •Activates potassium channels and by increasing the outward •Used for converting SVT à sinus rhythm *essentially sinus arrest (stop the heart)
potassium current hyperpolarizes the membrane potential (doesn’t let • t ½ short <10 seconds, so sinus arrest does not last long
*SVT anything in to block it), decreasing spontaneous SA nodal
depolarization
è Inhibits automaticity and conduction in the SA/AV nodes
à SLOWS AV NODE SE: chest discomfort, dyspnea, flushing, HA
*doesn’t really work for atrial fibrillation/atrial flutter *causes vasodilation with a stress test

Atropine •Parasympathetic that enhances both sinus nodal automaticity and •Used in emergent setting of symptomatic bradycardia
AV nodal conduction through direct vagus action •Blocks ACH at parasympathetic neuroeffector sites
è Someone that has a vagal response
SE: tachycardia, paradoxical slowing of HR in patients with Mobitz type II AVB and third degree
INCREASES HEART RATE AVB *never use this drug unless you have a crash cart ready

*Class I and III primarily used for rhythm, class II and IV primarily used for rate control

Goals of dysrhythmia management: prevent sudden death, reduce symptoms, improve QOL, reduce hospitalizations,
- consider costs and risk of therapies, overall patient condition

15
CARDIO About
Coronary Usually due to atherosclerosis
Artery (hardening & narrowing of
Disease coronary arteries)
(CAD)
RF: DM (worst, considered CAD
equivalent), Smoking (most
important modifiable),
Hyperlipidemia, HTN, Men, Men
>45 yo, Women >55 yo, FamHx
CAD (father/brother before 55 yo
or mother/sister before 65 yo)
Angina Complication of CAD leading to sx
Pectoris
Patho: Inadequate tissue perfusion
due to imbalance between increased
demand & decreased coronary
artery blood supply
*Symptoms usually occur with
>70% occlusion
Classes
I: Strenuous activity only, No
limitation
II: Prolonged/Rigorous activity,
Slight limitation
III: Usual daily activity, Marked
limitation
IV: At rest, Often unable to carry
out any physical activity
Angina Substernal chest pain usually
Pectoris brought on my exertion
Complication of CAD leading to sx
Pathophysiology:
•inadequate tissue perfusion due to
decreased blood supply & increased
demand
Classes
•Class I: strenuous activity
•Class II: more prolonged rigorous
activity
•Class III: daily activity
•Class IV: at rest
Clinical Presentation
Chest Pain: Substernal, Poorly localized,
Exertional, Short duration (<30 min but
often resolves within 5 min cessation activity)
May Radiate: Arm, Teeth, Lower jaw, Back,
Epigastrium, Shoulders
Exacerbated: Activity, Stress
Relieved: Rest, Nitroglycerin
Dyspnea, N/V, Diaphoresis, Numbness,
Fatigue
Anginal Equivalent: Instead of chest pain,
develop dyspnea, epigastric/shoulder pain
*esp Women, Elderly, DM, Obese
PE: Usually normal
History:
•Chest pain: poorly localized, substernal
•Radiation: arm, teeth, jaw
•Duration: Short
(1-5 minutes, <30 minutes)
•Alleviating: rest, NTG
•Aggravating: exertion, anxiety
Other SX: diaphoresis, dyspnea, fatigue,
numbness, nausea
Exam: usually normal
Low Dose ASA Prevention:
•considered for primary prevention in patients
40-75 who are not at increased bleeding risk
•NOT for ages >70 for primary
Diagnostics
ALL: EKG and CXR
EKG: WITHIN 10 MINUTES
•ST elevation •ST depression *classic
findings
•+/- T wave inversion, poor R wave
progression
Stress Test *most useful non-invasive tool
•exercise stress test: ST depression,
hypotension/HTN, arrhythmias, sx
•myocardial perfusion (exercise, pharm)
-thallim-201 or 00m-technetium sestamibi
-indication: baseline EKG abnormalities
-pharm agents: Adenosine
-CI: asthmatics
•stress echo: assess global and regional
wall motion abnormalities
Management
Revascularization
•PCI: 1 or 2 vessel disease not of L main
•CABG: L main or 3 vessel of EF <40%
Medical Management
•NTG
-increase supply, O2, decreases demand,
-SE: headache, tachyphylaxis, flushing
•Beta-Blockers
-increases blood supply by prolonging coronary
artery filling times
-reduces demand by reducing HR
•CCB (Diltiazem, Verapamil)
-prolongs diastolic filling increasing supply
-decreased contractility reducing demand
16
 •NOT for anyone with increased risk of -Dobutamine à increases O2 demand
bleeding
•cardiac MRI: dobutamine infusion, assess
perfusion and wall motion abnormalities
Coronary Angiography (GOLD) “Cath”
•Aspirin: does not work with supply/demand, but
prevents progression of by preventing platelet
aggregation
Outpatient: ASA*, BB*, statin, NTG

CAD/ Acute Causes: Pathophysiology: RV infarction triad: elevated JVP, clear •PCI (w/n 90 minutes) or TPA (30 minutes)
Coronary •MCC: atherosclerosis (hardening 1. fatty streak formation: lipid deposits in lungs, (+) Kussmaul sign •MONA: morphine (if NTG fails to relieve pain),
Syndrome and narrowing of the coronary the WBC *no sx *inferior wall MI may be associated with oxygen, NTG, ASA*avoid NTG and morphine in
(ACS) arteries) heart blocks or bradycardia posterior and inferior wall MIs
•Coronary artery vasospasm 2. early plaque formation: LDL enters
à leads to •Aortic stenosis/regurg endothelium in the fatty streak and LDL is STEMI: (+) enzymes, ST elevation >1mm Normal EKG:
MI •Pulmonary HTN oxidixed *total occlusion MONA + serial enzymes and EKG
•HTN NEW LBBB IS STEMI EQUIVALENT
Page 45, 48 •HOCM 3. foam cells: macrophages ingest LDL UA or NSTEMI: MONA, Hepatin, BB
NSTEMI: (+) enzymes, ST depressed •TIMI or HEART assessment
Risks: 4. mature fibrous plaque: proliferating *subtotal occlusion
•DM (biggest risk!) smooth muscle and connective tissue STEMI: MONA, Heparin, BB, reperfusion
•smoking •HLD Unstable: (-) enzymes, ST depressed •ACEI for long term therapy
•HTN •males Symptoms: *subtotal occlusion
•age (>45 men, >55 women) CP: retrosternal, pain at rest, no relief with Location:
•fhx NTG, >30min Enzymes: Anterior: V1-V4 (LAD), V1-V2 (p LAD)
CK/CK-MB: appears in 4-6hr, peak 12- Lateral: V5-6, I, aVL (Circumflex)
24h Inferior: II, III, aVF (RCA)
Troponin I: appears 4-8h, peak 12-24h Posterior: ST dep in V1-V2 (RCA, CFX)
*false elevations in renal failure, HF, PE,
CVA
Vasospastic Triggers: cold weather, exercise, Chest Pain: •EKG: transient ST elevations, resolves •1st line: CCB (Diltiazem, Verapamil, Amlodpine,
(Variant, cocaine, hyperventilation •rest (midnight, mid-morning) with symptom resolution Nicardipine) nightly
Prinzmetal) •not exertional •Angiography: r/o CAD, may rule in •2nd line: NTG
Angina Risks: female, >50, smoker •not relieved by rest vasospasm esp with Ergonovine AVOID BETA BLOCKERS

CARDIO About Pathophys/Clinical Presentation Diagnostics Treatment

Congestive Inability of heart to pump enough blood to meet the Pathophysiology: GOAL: confirm sx & cause Lifestyle modifications:
Heart demands of the body (MCC: CAD) Increased preload and afterload and/or of HF •Wt loss, sodium <2g/d, fluids <2L/d
Failure reduced contractility •Daily weight monitoring, smoking cessation
•Acute: began last few days to weeks Initial Testing
Page 54-58 *systolic à HTN, MI, papillary muscle tear Compensations EKG CI: No-Dihydro CCB( Diltiazem, Verapamil)
1. increased sympathetic
17
•Chronic: sx present for months 2. myocyte hypertrophy/remodel
*typically cardiomyopathy or valve disease 3. RAAS activation à fluid overload,
ventricular remodeling
•High: heart can’t meet demands (supply<demand)
-thyrotoxicosis, anemia; pagets, wet Left: Increased pulmonary venous
beriberi, AV shunting, decreased CO pressure à fluid backing to lungs
-SOB
•Low: insufficiency forward output (low EF) -Rales
-Chronic, non-productive cough with
•Systolic: reduced EF (HFrEF) *MC type, S3 pink frothy sputum
-MI, dilated cardiomyopathy, myocarditis *MCC transudative effusions
-thin ventricles, dilated chamber -increased sympathetic (adrenergic):
sweating, dusky/pale skin, tachycardia,
•Diastolic: preserved EF (HFpEF), S4 cool
-normal or increased EF à forced contraction into a
stiff ventricle Right:Increased venous pressure à
-HTN, LVH, elderly , constrictive pericarditis, systemic fluid retention
restrictive cardiomyopathy -edema
-thick ventricle, small chamber -JVD
-ascites, HSM, RUQ tenderness
•Left: DOE, PND, orthopnea, fatigue
-MCC CAD, HTN Symptoms:
•Chest pain, HTN, Flu-like sx
•Right: JVD, ascities, edema
-MCC LHF, pulmonary, mitral stenosis Physical Exam:
General: tachy, diaphoresis
Narrow pulse pressure: <25
Pulsus Alternans: LV HF
Precordial: lateral displaced PMI
Heart Sounds: S3 & S4
CXR: kerley B, effusion, Pharmacotherapy: **loop, ACEI, BB
congestion, cardiomegaly, Loop Diuretics (Furosemide, Torsemide)
butterfly pattern MOA: inhibits water transport across loop
SE: hypOkalemia, hypOcalcemia, hypOnatremia
Initial Labs:
•CBC, CMP, coagulation Class I: *reduce mortality
studies, glucose, lipids *ACEI (“-pril”)
•BNP -reduce preload and afterload
(>100 likely, >500 very) -reduce aldosterone production (RAAS); vasodilates
-released by ventricles -reduces ventricular remodeling
•cardiac enzymes SE: hypotension, hyperkalemia, cough, angioedema,
renal insuffieiency (CrCl <30)
Echo: GOLD CI: hypotension, pregnant
Normal EF: 55-60%
EF <35% high mortality *Entresto (Sabucitril + Valsartan)
NYHA Class: *BB (Carvedilol, Metoprolol, Bisprolol)
I: normal activity, no sx -reduce mortality (increase EF, reduce ventricular size)
II: stairs, mild sx SE: dizziness, hypotension
III: walking, marked -stop during decompensated HF because EF reduces
limitation initially
IV: conversation/rest -caution: 1st AVB, asthma, bradycardia
*Aldosterone Antagonists (Spironolactone)
-SE: hyperkalemia, gynecomastia
-CI: K+ >5 or GFR <30
*Hydralazine/Nitrate (if black + ACEI/BB)
*safe in pregnancy
MOA: reduces preload and afterload
SE: dizziness, HA, tachyphylaxis
Acute: LMNOP: Lasix, Morphine, O2, Nitrate,
position
18
CARDIO About
Hypertension SBP ≥130 and/or DBP ≥80
≥2 different readings on ≥2
different visits
Etiology
Primary (Essential): MCC
Idiopathic
Associated with: Increased salt
sensitivity, Increased sympathetic
activity, Increased
mineralocorticoid activity
Secondary
Due to underlying correctable cause
Renovascular MCC of secondary
(renal artery stenosis), Endocrine
(Cushing syndrome,
Hyperaldosteronism),
Pheochromocytoma, Coarctation of
aorta, OSA, EtOH, OCP, COX-2
inhibitors
Hypertensive SBP >180 and/or DBP >120
Urgency WITHOUT end-organ damage
Hypertensive SBP >180 and/or DBP >120
Emergency WITH end-organ damage
Clinical Presentation
Complications
CV: CAD, HF, MI, LVH, Aortic
dissection/aneurysm, PVD
Neurologic: TIA, CVA (stroke),
Ruptured aneurysm,
Encephalopathy
Nephropathy: Renal stenosis &
sclerosis, HTN 2nd MCC of ESRD
(after DM)
Optic: Retinal hemorrhage,
Blindness, Retinopathy
HA (MC), Dyspnea, Chest pain,
Focal neurologic deficits, AMS,
Delirium, Seizures, N/V
HA (MC), Dyspnea, Chest pain,
Focal neurologic deficits, AMS,
Delirium, Seizures, N/V
Neurologic: Encephalopathy,
Stroke, Seizures
Cardiac: ACS, Aortic dissection,
Acute HF (pulmonary edema)
Renal: AKI, Proteinuria, Hematuria
Diagnostics
Normal: SBP <120 and DBP <80
Elevated: SBP 120-129 and DBP <80
Stage 1: SBP 130-139 or DBP 80-89
Stage 2: SBP ≥140 or DBP ≥90
*isolated systolic is at GREATER risk for
cardiovascular disease then isolated diastolic
Initial Workup
EKG (document LVH), Fundoscope
(retinopathy), Creatinine, Cholesterol, Urine
Albumin:Creatinine Ratio
Gradual reduction of MAP by no more than
25% over 24-48 hours with oral medications
(Clonidine, Captopril, Labetalol, Nicardipine,
Furosemide)
Treatment Goals: BP ≤160/100
Workup Cardiac: CXR, EKG, Cardiac
enzymes, BNP
IV BP Reduction agents: MAP reduced
gradually by 10-20% in the 1st hour and by an
additional 5-15% over the next 23 hours
3 Main Exceptions
Acute Phase of Ischemic Stroke: BP is usually
not lowered unless it is ≥185/110 in patients
who are candidates for reperfusion treatment
Management
Lifestyle: Salt reduction, Smoking cessation, Exercise,
Diet, Weight reduction
Weight Loss: Achieve BMI 18.5-24.9
Sodium Restriction: ≤2.4g/day
DASH Diet: Increase fruits/veggies, Decrease
saturated/total fats, low sodium
Exercise: ≥30 min/day for most of the week
Limit EtOH: Men (≤2 drinks/day), Women & low BMI
(≤1 drink/day)
Medical Management: Patients who fail diet & exercise
BP Target: ≤140/90 (≤150/90 in ≥60 yo)
Treatment results in: 50% decrease HF, 40% decrease
strokes, 20-25% decrease MI
Clonidine: Short term use only
ADR: HA, Tachycardia, N,V, Sedation, Fatigue, Dry
mouth, Rebound HTN if D/C abruptly
Captopril
ADR: Angioedema, AKI
Furosemide
ADR: Electrolyte abnormalities, Alkalosis
Labetalol
C/I: Severe asthma/COPD, AV block, CHF
Nicardipine
ADR: Reflex tachycardia, HA, Nausea
Neurologic
HTN Encephalopathy: Nicardipine, Clevidipine,
Labetalol, Fenoldopam, Sodium nitroprusside
*Must R/O Stroke
*HTN encephalopathy often presents with confusion, HA,
N/V. Symptoms improve with lowering of BP
ADR Nitroprusside, Nitroglycerin, Hydralazine: May
increase ICP
Hemorrhagic Stroke: Nicardipine, Labetalol
*Benefits vs risks of lowering BP must be weighed
19

Retinal: Malignant HTN, Severe
(grave IV) retinopathy
OR >220/120 in patients who are not candidates
for reperfusion
Acute Aortic Dissection: SBP is rapidly
lowered to a goal of 100-120 within 20 min
Intracerebral HTN: Treatment depends on
different factors
Ischemic Stroke: Nicardipine, Labetalol
*Avoid cerebral hypoperfusion if ischemic
Reduce BP only if BP is: ≥220/120 (not a thrombolytic
candidate), 185/110 (if a thrombolytic candidate)
CV
Aortic Dissection: Esmolol, Labetalol, Sodium
nitroprusside (± added to beta-blocker), Nicardipine,
Clevidipine
*Decreases shearing forces
*Beta-Blocker treatment target: SBP 100-120 & Pulse <60
BPM achieved within 20 minutes
ACS: Nitroglycerin, Esmolol, Metoprolol, Nitroprusside
*Nitroglycerin not used if suspected right MI or
Phosphodiesterase 5 inhibitor use within 24-48 hours
Acute HF: Nitroglycerin, Furosemide, Nitroprusside
*Avoid Hydralazine & Beta-Blockers in CHF
*Only if no evidence of cardiac ischemia
20
HTN PHARM Mechanism of Action Side Effects CI
ACEi Decrease synthesis of Angiotensin II & Aldosterone production Cough & Angioedema (high bradykinin) Pregnancy
“-PRIL” Potentiates other vasodilators: Bradykinin, Prostaglandins, Nitric oxide 1st Dose Hypotension
Captopril, Enalapril, Increases exercise tolerance Azotemia/Renal Insufficiency
Ramipril, Benazepril Improves insulin activity Hyperkalemia
Hyperuricemia
Cardioprotective, Synergistic effect when used with thiazides
Decrease Preload & Afterload

Indication: HTN (esp DM, Nephropathy, CHF, Old MI)

ARB Blocks angiotensin II receptor Hyperkalemia Pregnancy

“-SARTAN” Doesn’t increase bradykinin production (ACE still around)
Losartan, Valsartan,
Irbesartan, Indication: Cant tolerate Beta-Blockers/ACEi or in addition to ACEi
Candesartan

CCB Dihydropyridine: Potent vasodilators HA CHF (esp Non-Dihydropyridine)

Dihydropyridine *Little/No effect on contractility or conduction Dizziness, Lightheaded Non-Dihydropyridine: 2nd/3rd AV Block
Nifedipine Commonly used for HTN Flushing
Amlodipine Peripheral edema
Non-Dihydropyridine
Non-Dihydropyridine Affect cardiac contractility and conduction, Potent vasodilators, Reduce Verapamil: Constipation
Verapamil vascular permeability
Diltiazem

Beta-Blockers Catecholamine inhibitor Fatigue 2nd/3rd AV Block

“-OLOL” Blocks adrenergic renin release Depression Decompensated HF
Impotence
Cardio-Selective (B1) Not usually 1st line unless there is a comorbid condition where they are helpful Non-Selective: Asthma/COPD, May worsen
Atenolol, Metoprolol, Mask hypoglycemia in DM (caution use) PVD, Raynaud’s
Esmolol Caution: Hypotensive or HR <50 BPM

Non-Selective (B1, B2)

Propranolol

Both Alpha & B1, B2

Labetalol, Carvedilol

Alpha-1 Blockers Alpha blockade -> Peripheral arterial dilation 1st Dose Syncope (initiation & increase dose)
Prazosin, Terazosin, Dizziness
Doxazosin Not usually 1st line, may be helpful in pt with HTN + BPH HA
Weakness

Thiazide Diuretics Affect BP by reducing blood volume HYPOnatremia Caution: DM, Gout
HCTZ Prevents kidney Na & H2O reabsorption in DISTAL TUBULE HYPOkalemia
Chlorthalidone Lower urinary calcium excretion
Metolazone HYPERcalcemia
HYPERuricemia
21
 HYPERglycemia

Mild cholesterol elevations

Loop Diuretics Inhibits water transport across loop of Henle Volume depletion Sulfa allergy
Furosemide, Increases excretion: H2O, Na, Cl, K
Bumetanide HYPOnatremia
*Strongest class of diuretics HYPOkalemia
HYPOcalcemia

HYPERuricemia
HYPERglycemia
HYPERlipidemia

Metabolic Alkalosis
Ototoxicity

K+ Sparing Diuretics Inhibits aldosterone-mediated Na+/H2O absorption (spares K+) HYPERkalemia Renal Failure
Spironolactone HYPOnatremia
Amiloride *Weak diuretic, most useful in combo with loop to minimize K+ loss Metabolic Acidosis
Eplerenone
Spironolactone: Gynecomastia

22
CARDIO About
Hyperlipidemia Hypercholesterolemia:
Hypothyroidism, Pregnancy,
Kidney failure
Hypertriglyceridemia: DM, EtOH,
Obese, Steroids, Estrogen
Goals: Weight reduction, Increase
exercise, Dietary restriction of
cholesterol, carbs, trans fatty acids
Goals of lipid lowering agents:
Plaque stabilization, reversal of
endothelial dysfunction,
thrombogenicity reduction,
atherosclerosis regression
Clinical Presentation
•Xanthomas (fatty growths
underneath skin-joints)
•Xanthelasama (lipid plaques on
eyelids)
Pancreatitis may be seen in
hypertriglycerides
Diagnostics Management
Screening: Lifestyle: weight, exercise, dietary changes
Ages 20-79 every 4-6 years
High risk: screening 20-25yo M, 30-35yo F Pharmacotherapy:
Low risk: 35yo M, 45yo F •LDL: Statin, bile acid sequestrants
•Triglycerides: Fibrates, Niacin
Who to Treat: •increase HDL: Niacin, Fibrate
1. DM between 40-75 years old
2. 40-75yo with risk 7.5% and higher High intensity:
3. Age 21+ and LDL 190+ Atorvastatin 40-80 & Rosuvastatin 20-40
4. Clinical ASCVD •Age 40-75yo with DM
•Clinical CAD
•LDL 190+,
•Age 40-75 10 year risk >7.5%
Goals: LDL <100, Cholesterol <200, HDL >60

HLD PHARM Mechanism of Action Side Effects CI

HMG-COA Reductase Inhibits the rate limiting step in hepatic cholesterol synthesis Myositis/Myalgia/Rhabdomyolysis Active hepatic disease, Persistent elevated
Inhibitors (-Statin) Increase LDL receptors, Increase LDL clearance, Reduce triglycerides Hepatitis, Hepatits (MC) LFTs, Pregnancy, Breast feeding
Simva-, Prava-, Lova-, BEST DRUG TO REDUCE LDL GI, DM
Atorva-, Rosuva- *SE rate increased with tetracyclines

Fibrates Inhibits peripheral lipolysis and reduced hepatic triglyceride production Myositis, mylagias CI: hepatobiliary disease or severe renal
Fenofibrate, Gemfibrozil (by decreasing hepatic extraction of fatty acids) Hepatitis disease
Gallstones (blie acide lithogenicity)
BEST DRUG TO REDUCE TRIGLYCERIDES

Niacin (B3) Increased HDL, reduces plasma fibrinogen levels, decreased hepatic Flushing *decrease with ASA before PUD
Nicotinic acid production of LDL and VLDL Headache, Warm sensation High glucose
Pruritis Hepatotoxicity, N/V/D
Hyperuricemia, Hyperglycemia Dry skin

Bile Acid Sequestrates Binds bile acid in intestine blocking liver reabsorption of bile acids GI: N/V/ Bloating, Cramping abdominal pain Severe hypertriglyceridemia, Complete biliary
Cholestyramine, Reduces cholesterol pool, Lowers intrahepatic cholesterol Increased LFTs obstruction
Colestipol, Colesevelam Increased LDL receptors, Decreasing LDL levels Increased TGs
Mild-moderate increases in HDL Long term use: Osteoporosis
Often used with statin
ONLY MEDICATION SAFE IN PREGNANCY DDI: May interfere absorption: ABX, Digoxin,
*Cholestyramine can also be used for pruritis with biliary obstruction Warfarin, Fat-soluble vitamins
*Take these 1 hour before or 4 hours after BAS

Ezetimibe (Zetia) Inhibits intestinal cholesterol absorption HA, Diarrhea, Increased LFTs (esp with statin)
Lowers LDL
*may be used with statins

23
24
CARDIO About
Cardiogenic Primary cardiac/myocardial dysfunction
Shock à inadequate perfusion à low CO and
increased systemic vascular resistance
(SVR) & pulmonary wedge pressure (>15)
Orthostatic Fall in SBP by 20mmHg and/or DBP by
Hypotension 10mmHG
Causes:
•impaired autonomic function
•medications: anti-HTN, diuretics,
narcotics, antipsych, antidep, alcohol
•neuro: parkinsons, DM neuropathy
•hypovolemia
Vasovagal Systemic hypotension associated with
Syncope bradycardia and/or peripheral
vaso/venodilation
MCC of syncope!
CARDIO About
Endocarditis Cause: ORAL (dental, candy, brush)
-others: IVDU, EGD, TURP, cath,
•Localization of the infection is
determined by turbulent blood flow
•Infection of endothelium/valves due to
colonization
•MC bug: S. aureus
•MC on Left side, TV MC in IVDU
•Acute: infection of normal valves
•Subacute: abnormal valve
•IVDU: MRSA, Pseudomonas
•Prosthetic: Staph epidermis
Clinical Presentation
Causes:
Cardiac disease: MI, myocarditis, valve,
congenital, arrhythmia
Cerebral hypoperfusion
•dizziness, lightheadedness
•palpitations
•blurred vision
•darkening of visual fields
•syncope
Prodromal: dizziness, lightheadedness,
epigastric pain, palpitations, blurred
vision
Postdromal: syncope
Clinical Presentation
MC:
•fever (90%), chills, night sweats
•MSK pain (back)
•murmurs (80%)
•CHF (2/3 cases)
Peripheral Manifestations:
•petechia *strep or staph
•splinter hemorrhages *strep, staph
•osler nodes *strep *PAIN (finger)
•Janeway *PAINLESS (palms)
•Roth Spots (eyes on funduscopic)
Diagnostics Treatment
•Oxygen
•Vasoconstriction •Isotonic fluids (NOT AGGRESSIVE) *only
•Hypotension shock where large amounts of fluids are not
•Low CO and increased pulmonary given
capillary wedge pressure
Inotropic support: increase contractility and CO
•Dobutamine, Epinephrine
•blood pressure Conservative:
•tilt table: BP reduction at 60 degrees •increase salt and fluid intake
•labs •gradual position changes
•compression stocking
•discontinue offending meds
Medication
•Fludrocortisone *if fail conservative
Triggers:
•blood
•phobias
•emotiona stress/fear
•trauma
Diagnostics Treatment
3 blood cultures, 1 hour apart Acute Endocarditis: Nafcillin +
EKG, TTE à TEE echo Gentamicin x4-6 weeks
Increased ESR and CRP
Subacute Endocarditis: PCN or
DUKE CRITERIA Ampicillin + Gentamicin
Major criteria
• (+) blood culture (2 are +) Prosthetic valve: Vancomycin +
•endocardial involved on echo (TEE) Gentamicin + Rifampin
•new regurg murmur
Fungal: Amphotericin B
Minor Criteria:
•heart condition or IVDU Prophylaxis: Amoxi 2g 30-60min
•fever (>100.4F) -prosthetic heart valves
•vascular and embolic PNA -prior endocarditis
•immunologic phenomena -cyanotic congenital heart disease
•microbiologic evidence -cardiac transplantation
*1 normal, or 2+ abnormal
Interpretation:
•Definitive: 2 major or
1 major + 3 minor, or 5 minor
25
CARDIO About Clinical Presentation Diagnostics Treatment
Pericarditis Inflammation in pericardium •PLEURITIC CHEST PAIN •Viral titers •FIRST LINE-NSAIDS x7-14d
-worse with inspiration & supine •Cardiac enzymes -Ibuprofen 600-800mg TID or
Causes: -sharp pain, persistent •Echo: assess complications *nml Indomethacin TID for 1-2 weeks
•Idiopathic *MC -relieved with sitting up and leaning •CBC, BMP, ESR/CRP -ASA post MI
•Viral (entero, coxsackie, echo) *MC! forward
•Systemic: thyroid, lupus, RA -radiate to back, neck, shoulder EKG: diffuse ST segment elevation 2nd line: Colchicine
•Neoplasms: lung & breast CA •Fever à pseudonormalization à T wave -use for recurrence
•Drugs: procainamide, INH, hydralazine inversion à normal
•Myocardial Injury Auscultation: -smiley face & diffuse Steroids if sx >48h and refractory
•Pericardial Injury pericardial friction rub *washing -concave V1-V6, PR depressions in leads
-best at end of expiration while upright with ST elevation
and leaning forward *opposite in AVR

Pericardial •Fluid in pericardial space Distant (muffled) heart sounds CXR: cardiomegaly Small/no tamponade: observe and treat
Effusion EKG: low QRS voltage underlying cause
•MCC: pericarditis Echo: increased pericardial fluid
•Others: infection, radiation, cancer,
dialysis, CT disease

Cardiac Effusion causing significant pressure on BECKS TRIAD: Echo: effusion + diastolic collapse of Pericardiocentesis
Tamponade the heart à restricted filling à decreased •JVD cardiac chambers Pericardial window if recurrent
CO •Muffled heart sounds
•hypotension EKG: electric alternans (alternate small and
big QRS complexes)
Exam: Kussmaul & Pulses paradoxus
>10mmHg decrease in SBP with
inspiration
-increased filling of R heart with
inspiration à decreased L filling

Constrictive Thick, fibrotic and calcified heart
Pericarditis à diastolic dysfunction
à increased venous pressure and
decreased stroke volume
MCC=TB *underdeveloped
MC is radiation, surgery, and viral
pericarditis *developed
•Dyspnea (MC sx)
•RHF: JVD, edema, N/V, ascites
Kussmaul sign: increased JVD with
inspiration
Murmur: pericardial knock
-high pitched 3rd heart sound due to
sudden cessation of ventricular filling
from thickened pericardium
Echo: thickening of pericardium, Diuretics for sx improvement
CXR: pericardial calcificiation Definitive: pericardiectomy
-if unresponsive to diuretics
Cardiac CT/MRI: thickening
Cardiac Cath: *CONFIRMATORY
“square root sign”

26
VALVE DISORDERS
AS: Aortic Stenosis

1) Harsh/Rumble: Stenosis
Blowing: Regurgitation
2) Increase Venous Return (Supine, Squatting, Leg elevation): Increases intensity of all murmurs except Hypertrophic Cardiomyopathy (decreased) & MVP Click (delayed)
Decrease Venous Return (Standing, Valsalva): Decreases intensity of all murmurs except Hypertrophic Cardiomyopathy (increased) & MVP Click (earlier)
3) Right sided murmurs sound like left sided versions (TR = MR, AS = PS, AR = TR)
How to distinguish? 1) Location, 2) Inspiration increases intensity of right sided murmurs (decreases left sided murmurs)
Aortic: RUSB
Pulmonic: LUSB
Tricuspid: LLSB
Mitral: Apex
4) MR = Axilla
AS = Carotid
5) Systolic: AS, MR
Diastolic: AR, MS

CARDIO General Features Clinical Presentation Diagnostic Studies Management

Aortic Stenosis MC valvular disease
(AS) Symptoms usually occur when
orifice <1cm²
Patho
LV outflow obstruction ->
Fixed CO, Increased afterload,
LVH -> LLV failure
Etiology
Degenerative: Calcifications,
Wear n tear, Esp >70 yo
Congenital & Bicuspid valve
common in pt >70 yo
Rheumatic Heart Disease: May
be isolated or with AR
Once symptomatic, lifespan dramatically
reduced
Dyspnea, Angina, Syncope, CHF
Weak Delayed carotid pulse, Narrow pulse
pressure
Murmur
Systolic
Crescendo-Decrescendo
RUSB
Radiate: Carotid artery
Increase: Sitting while leaning forward,
Increased venous return (Squatting,
Supine, Leg raise), Expiration
Decrease: Decreased venous return
(Valsalva, Standing), Inspiration,
Handgrip
EKG AV Replacement: ToC
LVH, LAE, AFib
Percutaneous Aortic Valvuloplasty (PAV)
ECHO: Best test Bridge to AVR, Non-surgical candidate, Pediatric
Small aortic orifice, LVH, Thickened/Calcified *50% increase AV orifice area
aortic valve *50% restenosis at 6-12 months
CXR: Non-specific Intraaortic Balloon Pump
Post-aortic dilatation, Aortic valve Bridge to AVR, Temporary stabilization
calcification, Pulmonary congestion
Medical: No treatment truly effective
Cardiac Catherization: Definitive *No exercise restriction with Mild AS
*may be used prior to surgery
Severe AS Prior to Surgery
Avoid: Exertion, Vasodilators (nitrates), Negative
Inotropes (CCB, Beta-blockers)
*Patients are dependent on preload to maintain CO

Aortic Incomplete AV closure -> LV
Regurgitation volume overload with eventual
(AR) LV dilation & HF
Etiology
Acute: Acute MI, Aortic
dissection, Endocarditis. Can
lead to pulmonary edema
Bounding Pulses: Due to increased stroke
volume, Pulsus biferiens can be seen (esp
with combined AS + AR or Severe AR)
Wide Pulse Pressure (only chronic)
Water Hammer Pulse: Swift upstroke &
rapid fall of radial pulse accentuated with
wrsit elevation
ECHO Medical: Afterload reduction improves forward
Regurgitant jet flow (ACEi, ARB, Nifedipine, Hydralazine)
Cardiac Catherization: Definitive Surgery: Definitive
*may be used prior to surgery Indication: Acute/Symptomatic AR, Asymptomatic
AR with LV decompensation (EF <55% - patients
with AR normally have higher than normal EF)

27
Chronic: Aortic dilation:
Marfan, Inflammatory disorders,
Rheumatic fever, Syphilis, HTN
Corrigan’s Pulse: Similar to Water
Hammer but referring to Carotid artery
Hill’s Sign: Popliteal artery SBP >
Brachial artery by 60mmHg (most
sensitive)
Duroziez’s Sign: Gradual pressure over
femoral artery -> Systolic & diastolic
bruits
Traube’s Sound (Pistol Shot): Double
heart sound at femoral artery with partial
compression of femoral artery
De Musset’s Sign: Head bobbing with
each heartbeat (low sensitivity)
Muller’s Sign: Visible systolic pulsations
of the uvula
Quincke’s Pulses: Visible fingernail bed
pulsations with light compression of
fingernail bed
Murmur
Diastolic
Blowing Decrescendo (high pitched)
LUSB
Increase: Sitting while leaning forward,
Increased venous return (Squatting,
Supine, Leg raise), Expiration, Handgrip
Decrease: Decreased venous return
(Valsalva, Standing), Inspiration, Amyl
nitrate
Austin-Flint Murmur
Mid-Late Diastolic
Apex
Secondary to retrograde regurgitant jet
competing with antegrade flo from LA ->
LV
28
CARDIO General Features
Mitral Stenosis Patho: Obstruction of outflow from LA
(MS) to LV, Secondary to narrowed mitral
orifice -> Blood backs up into left
atrium
Etiology
Rheumatic Heart Disease (almost
always the cause, MC in 30s-40s)
Congenital, LA myxoma, Thrombus,
Valvulitis (SLE, Amyloid, Carcinoid)
Mitral Patho: Abnormal, retrograde blood flow
Regurgitation from LV -> LA leading to LA dilation
(MR) & Increased pulmonary pressure
Etiology
Leaflet Abnormality: MVP MCC
USA, Rheumatic fever MCC 3rd world,
Endocarditis, Valvulitis, Annulus
dilation (LV dilation), Marfan
Papillary Muscle Dysfunction: MI,
Cardiomyopathy
Ruptured Chordae Tendinea: Collagen
vascular disease, Dilated
cardiomyopathy
Clinical Presentation Diagnostic Studies Management
Slow progression until symptoms occur, then rapid EKG Percutaneous Balloon Valvuloplasty
Pulmonary: Dyspnea (MC), Pulmonary edema, LAE (P >3mm, Biphasic P in V1 & Best for symptomatic MS in younger with
Hemoptysis, Cough, Frequent bronchitis, V2), AFib, Pulmonary HTN (RVH, non-calcified valves or Refractory to
Pulmonary HTN (if rheumatic sx usually begin RAD) medical therapy
20s-30s)
AFib: Secondary to LAE -> Thromboembolic ECHO: Best test MV Replacement
events (CVA) If Mitral valvuloplasty C/I or with
*Signs of LAE: Dysphagia, Ortner’s Syndrome CXR: Non-specific unfavorable valve morphology
(Recurrent laryngeal nerve palsy -> Hoarseness) LAE, Posterior displacement of
Right Sided HF: Prolonged Pulmonary HTN esophagus, Elevation of left main Medical
Mitral Facies: Ruddy (flushed) cheeks with facial bronchus Diuretics & Na restriction for eddema &
pallor (chronic hypoxia) volume overload
Cardiac Catherization: Definitive Beta-Blockers for AFib rate control
Prominent S1 (closure of MV) *rarely done CCB, Digoxin
Opening Snap (opening of MV)
Loud P2 Anticoagulation (Warfarin)
Patients with AFib
Murmur
Mid-Diastolic
Low Pitched, Rumbling
Apex
Increased: Left lateral decubitus, Isometric
exercise, Increased venous return (Squatting,
Supine, Leg raise), Expiration
Decrease: Decreased venous return (Valsalva,
Standing), Inspiration
Increased Severity: Shorter A2-OS duration,
Prolonged duration
Acute: Pulmonary edema, Hypotension EKG Medical: Symptom control with Afterload
LAE, LVH, AFib reducers (ACEi, ARB, Hydralazine,
Chronic: HF symptoms (Dyspnea MC, Fatigue), Nitrates) or Diuretics (do not reduce
AFib, Hemoptysis, HTN ECHO: Best test progression of disease)
Hyperdynamic LV, Regurgitant jet
Widely split S2 Surgery: Repair preferred over
Laterally displaced PMI CXR: Non-specific Replacement
S3 LAE, LVH, Pulmonary edema Indication: EF ≤60% or Refractory to
Severe: Soft S1 medical
Murmur
Holosystolic
Blowing
Apex
Radiation: Axilla (high pitched)
Increased: Left lateral decubitus, Isometric
exercise, Increased venous return (Squatting,
Supine, Leg raise), Expiration, Handgrip
Decrease: Decreased venous return (Valsalva,
Standing), Inspiration, Amyl nitrate
29
Mitral Valve Leaflets of MV bulge into LA during Most asymptomatic ECHO Most Patients: Reassurance
Prolapse systole Autonomic Dysfunction: Anxiety, Atypical chest Posterior bulging leaflets with tissue *Associated with a good prognosis
(MVP) pain, Panic attacks, Palpations from arrhythmias, redundancy
MCC of MR in USA Syncope, Dizziness, Fatigue Beta-Blockers: Only in pt with autonomic
MC Young women (15-35 yo) dysfunction
Seen in 2-5% population Symptoms Associated with MR Progression:
Dyspnea, Fatigue, CHF MV Repair/Replacement: MVP with
Etiology *not common Severe MR to prevent CHF
Myxomatous degeneration of MV
Connective Tissue Diseases: Marfan, Stroke (rare) Endocarditis Prophylaxis: Not needed
Ehlers-Danlos, Osteogenesis imperfecta
Murmur
Mid-Late Systolic Ejection Click
Apex
May be associated with: Mid-late systolic MR
Earlier & Prolonged Duration: Any maneuver that
makes LV smaller (decreases preload): Valsalva,
Standing
Delayed & Shorter Duration: Any maneuver that
makes LV bigger (increases preload): Squatting,
Supine, Leg raise. Handgrip

CARDIO Causes/ S&S/Physical Exam/Murmur Diagnostics Treatment/Management

Tricuspid Stenosis Blood backs up into RA -> RAE -> Right Murmur Medical: Decrease RA volume overload:
(TS) sided HF Mid-Diastolic Diuretics & Na restriction
Low frequency
LLSB Surgery: Commissurotomy/Replacement if
Increase Intensity: Inspiration, Increased venous Right sided HF or Decreased CO
return (Squatting, Supine, Leg raise)
Opening Snap: Usually occurs later than
opening snap of MS

Tricuspid Carvallo’s Sign: Increased murmur intensity Medical: Diuretics (for volume overload &
Regurgitation with inspiration (due to increased right side congestion). If LV dysfunction: Standard HF
(TR) blood flow during inspiration) Helps to therapy
distinguish TR from MR
Surgical: Repair > Replacement
± Pulsatile liver Suggested for pt with Severe TR despite
medical therapy
Murmur
Holosystolic
High pitch Blowing
Left Mid Sternal Border
Radiation: Little to None
Increase Intensity: Inspiration, Increased venous
return (Squatting, Supine, Leg raise)

30
CARDIO Causes S/S Murmur Management/Treatment
Pulmonic Stenosis RV outflow obstruction of blood across Murmur Balloon Valvuloplasty: Preferred
(PS) PV Mid-Systolic
Harsh, Crescendo-Decrescendo
Almost always congenital Maximal at LUSB
Radiates: Neck
Disease of the young (congenital rubella Increased: Inspiration
syndrome) *longer the duration = Increased stenosis

Systolic Ejection Click: Often buried in S1,

Wide split S2 (delayed P2) ± S4

Pulmonic Etiology Most clinically insignificant Well tolerated: No treatment needed in most
Regurgitation Almost always congenital
(PR) Pulmonary HTN, Tetralogy of Fallot, If symptomatic: Right sided HF symptoms
Endocarditis, Rheumatic heart disease
Graham-Steell Murmur
Patho: Retrograde blood flow from Early Diastolic
pulmonary artery into RV -> Right sided Brief Decrescendo
volume overload LUSB with Full Inspiration
Increased: Inspiration, Increased venous return
(Squatting, Supine, Leg raise)
Decreased: Expiration, Decreased venous return
(Valsalva, Standing)
Increased Velocity: Severe pulmonary HTN

CARDIO About/Risks Clinical Presentation Diagnostics/Screening Management

Abdominal •Dilation of the infrarenal aorta is a Most are asymptomatic! DX: Repair for:
Aortic normal part of aging ~2cm CBC, BMP, PT/INR, PTT -aortic aneurysm larger than 5.5cm
Aneurysm -AAA when >3cm Symptomatic: *more concerning Abdominal US- study of choice -rapid expansion (>0.5cm in 6mo)
(AAA) •UNRUPTURED PAIN *especially if unstable -symptomatic pain & tenderness
Risks: -Mild to severe mid-abdominal
•white male, smoke, age >60 discomfort often radiating to lower back •CT scan w/ IV contrast provide a more >4.5cm: refer to vascular surgery
•Atherosclerosis (MC) -Constant or intermittent reliable assessment of diameter 4-4.5cm: monitor US q6mo
-Exacerbated by gentle pressure -perform when >5cm & surgery 3-4cm: monitor US qyear
Pathophysiology: -Distal embolization is rare -test of choice for THORACIC
Proteolytic degeneration of aortic -pulsatile abdominal mass Beta blockers help reduce shearing forces
wall, connective tissue, and •Angiography: GOLD and decrease expansion
inflammation •RUPTURE PAIN *lethal
-Sudden blood into retroperitoneal space Screening:
Two major groups: -Severe pain, palpable mass, hypotension •One-time screening for:
Fusiform: circumferential -Free rupture into peritoneal cavity is -men 65-75 and have smoked 100
Saccular: outpouching LETHAL *bruising on the back (Flank) cigarettes in a lifetime
*higher risk of rupture

31
Thoracic Risks: •Most asymptomatic •CXR: widened mediastinum •Repair when 6cm or larger
Aortic •Most due to atherosclerosis *easiest initial tool, do 1st Treatment: endovascular grafting
Aneurysm •Symptoms depend on size and position
•CT disorders: Ehlers-Danlos, Marfan -Substernal back or neck pain •CT scan: modality of choice Involvement of proximal aortic arch:
Syndrome -Hoarseness due to L recurrent laryngeal -open surgery *substantial risk
-aortic regurg due to dilation -may need replacement/repair of AV
•Bicuspid aortic valve -performed by CT surgeon

Aortic •Tear in the innermost part of the
Dissection aorta (intima)
•Locations: Ascending (MC),
descending, aortic arch
*ascending has high mortality
•MC in men over 50
Risks:
•aging, atherosclerosis, HTN
•blunt trauma, Marfans, aortic valve
defect, aortic coarctation, preexisting,
prego
S/S: •EKG: LVH Medical control:
•Chest pain: SUDDEN, severe, ripping, radiating to •CXR: widened mediastinum *initial *descending with no complications
back or neck •Multiplanar CT of chest/ abdomen:
•hypertensive immediate diagnostic study BP Control:
•N/V, sweating •CTA, MRA, TEE: GOLD •lower SBP 100-120 & pulse pressure
•syncope, hemiplegia, paralysis of LE •BB first line! (Lebetolol, Esmolol)
•ischemia (MI) Debakey (Stanford) Classes: -can add CCB or Nitroprusside
•unequal blood pressure in both arms •Type I (A): ascending aorta à aortic arch
-variation >20mmHg b/w R & L arm and possibly beyond Pain: Morphine (pain & vasodilation)
•diastolic murmur •Type II (A): confined to ascending
•acute new-onset aortic regurg with ascending •Type III (B): descending aorta Surgical: acute proximal or acute distal
dissection with complications

32
CARDIO About Clinical Presentation Diagnostics Treatment
PAD Stenosis or occlusion in artery due to atherosclerosis •Atypical leg pain •Pulses: decreased or absent •Lifestyle: smoking cessation
(MC in LE) -rest pain means advanced disease •decreased capillary refill •Exercise therapy
•Blood pressure, carotid bruits
•Coronary artery: angina •Intermittent Claudication (MC!) •Exam legs and feet
•Carotid artery: stroke, TIA -aching, pain, tightness in LE •Skin: COLD, pale, atrophic changes, Pharm: Aspirin or Plavix
•Renovascular: HTN, renal -reproducible thin/shiny hair, hair loss •Cilostazol (Pletal)
•PAD: claudication, limb ischemia -brought on by EXERCISE -ulcers: LATERAL MALLEOLUS -supress cAMP degredation
-relieved with rest within 10 min -reversibly inhibits platelete
•Distal aorta & proximal iliac: smokers -sx are distal to lesion Leg Lift Test: 60 degrees x1min aggregation
-buttock, hip, groin pain (+) if feet turn white when lower down -SE: edema, GI, HA, bleed
-Leriche syndrome: claudication, impotence, •Functional Impairement -CI: HF
decreased femoral pulses -do not have claudication but have Dependent Rubor: seated to supine, assess
•Femoral & popliteal: 60+, minorities rest pain or ulceration blood flow; longer red à severe Others:
-thigh or upper calf •ACEI, statin, glycemic control
•Tibial artery: Diabetics •Limb ischemia: ulcer, gangrene ABI: BEST TOOL (normal 1-1.2)
-lower calf, ankle, foot Abnormal is < 0.90, < 0.50 is severe
-ABI of 0.85 needed to heal ulcer
MC in femoral or popliteal artery -use TBI if non-compressible (>1.40)

Arteriography: GOLD STANDARD

Acute Causes: 5 Ps: •MEDICAL EMERGENCY! Immediate revascularization

Arterial •thrombus: stable atheroma with fibrous cap à •pallor 1. vascular surgery consult
Occlusion of plaque rupture à acute occlusion •pain/ paresthesias (numbness/tingling) •Doppler: little to now flow 2. begin IV Heparin bolus and
a Limb •pulseless •EKG: determine if Afib continuous infusion
•embolus à AFIB MC cause •paralysis (muscles w/ no perfusion) •Labs: CBC, PT/INR, PTT
•polar (cold) •Echo: done LATER if embolic source is •Once stable: Warfarin for at least 3
MEDICAL EMERGENCY! suspected (TEE w/ bubble) months+, goal INR 2-3

Thrombo- NOT ATHEROSCLEROSIS TRIAD: •Aortography: occlusive lesions of TOBACCO CESSATION!

angiitis •Segmental, inflammatory, thrombotic processes in 1. Superficial migratory small/medium vessels with corkscrew
Obliterans small/medium distal arteries thrombophlebitis: large, red, tender collaterals *GOLD -revascularization
(Buerger superficial veins à nodules -amputation frequently required
Disease) •Closely linked to tobacco use •Allen test: abnormal -wound care
•young males <40, smokers 2. Distal ischemia (MC): claudication, -assess patency of radial and ulnar arteries -NSAIDS or opioids for pain
toes to finger ischemia
Pathophysiology: Raynauds: CCB (Nifedipine,
•Vasodysfunction and microthrombi 3. Raynauds Nicardipine, Amlodipine)

•Presents with distal ischemic rest pain

or ischemic ulceration

Atrial •MC cardiac cancer •Dyspnea Diagnostics: Surgical removal

Myxoma •MC in the left atrium •Weight loss •TEE: pedunculated mass with “ball-valve”
•Syncope *due to mitral stenosis obstruction of the mitral valve orifice
•Can cause an obstruction of the mitral orifice •Flu-like symptoms
mimicking mitral stenosis
Exam: similar to mitral stenosis

33
CARDIO About Clinical Presentation Diagnostics Treatment
Deep Vein MC in the calf Unilateral swelling of LE (>3cm), tender D-Dimer: highly sensitive but not Anticoagulant x3 months-First Line
Thrombosis (DVT) specific -LMWH + Warfarin *prego, cancer
Pathophysiology: Exam: *negative d-dimer can eliminate -Heparin + Dabigatran (Pradaxa) or Heparin +
Virchows Triad: •WARM skin & Dusky cyanosis Edoxaban (Savaysa)*1st line
1. Venous stasis •Palpable cord, normal pulses Venous duplex US: 1st line -Rivaroxaban (Xarelto) or Apixaban (Eliquis)
2. Endothelial damage •Homans sign: calf pain with dorsiflexion -noncompressible echogenicity *1st line
3. Hypercoaguability (unreliable)
Venography: GOLD Heparin (antithrombin III): PTT
Wells Criteria: Warfarin (Vitamin K antagonist)
Consequences: PE -extrinsic pathway, monitor PT/INR

IVC Filter: recurrent despite anticoag,

anticoagulation is CI, or RV dysfunction

Varicose Veins •Varicose veins develop in LE
•Dilated, tortuous superficial veins
Increased intraluminal pressure à
reverse venous flow
Hallmark: venous reflux & HTN
•Dull, aching heaviness or feeling of fatigue
in legs brought on by periods of standing,
relieved with elevation
•Itching , palpable
•No diagnostic evaluation
•Imaging needed for surgical
intervention-duplex US
•stockings (20-30mmHg), leg elevation
•Surgical:
-sclerotherapy: inject sclerosing agent
-laser therapy: wavelength
-endovenous ablation -vein stripping

CARDIO About Clinical Presentation Diagnostics Treatment

Chronic Venous •Severe manifestation of venous
Insufficiency hypertension
•Valve leaflets that do not coapt
because thickened and scarred or in a
dilated vein so impaired function
è legs develop venous HTN
and high hydrostatic force
MCC-prior deep venous
thrombophlebitis
Superficial Venous •Inflammation of a vein due to clot in
Thrombophlebitis the superficial vein
-great saphenous vein
Causes: IV catheter, trauma,
pregnancy, varicose veins
•MC pathogen-Staph Aureus
•Burning, aching, heavy leg pain
-worse with standing/sitting
-better with walking & elevation
•Edema, hyperpigmentation,
•Venous ulcers: medial malleolus
•Lipodermatosclerosis
-pigmented, swelling, red, “bowling pin”
•Atrophie Blanche
-star shaped ivory-white depressed atrophic
plaque; red dots within scar
•Corona Phlebectatica
-dilated veins around the ankle
Trousseau’s sign: migratory
thrombophlebitis with malignancy
Local phlebitis: tender, pain, edema,
erythema, induration
•+/- palpable cord •Fever (if septic)
Compression stockings, leg elevation
Regular exercise
lipodermato Ulcer: UNNA boot, wet to dry dressings
atrophic blanche
corona
Trendelenburg test: elevate one leg
at 90 degrees, occlude great
saphenous vein, have patient stand
for 20 sec à slow ankle fillings
suggests competency
•CBC: WBC may be elevated 1st line: supportive therapy
-elevate, warm compression, compression stocking,
•Venous Doppler US: non- NSAIDs
compressible vein with clot
Septic state:
•PCN + Aminoglycoside
•Vanc + Rocephin

34
PULM 12%
TV (tidal volume): Air in and out during normal breathing
RV (residual volume): Air remaining after max expiration
ERV (expiratory reserve volume): Air that can be further exhaled at end of normal expiration
IRV (inspiratory reserve volume): Air that can be further inhaled at end of normal inhalation
VC (vital capacity): Max volume air that can be exhaled following max inspiration: TV + ERV + IRV
TLC (total lung capacity): Volume in lungs at max inspiration: VC + RV
FRC (functional residual capacity): Volume of gas in lungs at normal tidal volume end expiration (ERV + RV).
Air in which gas exchange takes place
Increased: Disorders with hyperinflation (due to loss of elastic recoil, PEEP)
Decreased: Restrictive lung diseases
FEV1 (forced expiratory volume 1 second): Volume of air exhaled at the end of the 1st second of forced expiration
FVC (forced vital capacity): Volume of air that can be expelled from a max inflated lung breathing as hard & fast as possible

Wheezing: High pitched, Whistling, Continuous, Musical. Louder during expiration (compared to inspiration). Produced by narrowed/obstructed airways
Obstructive diseases (Asthma, COPD), Bronchiectasis, Bronchiolitis, Lung cancer, Sleep apnea, CHF, GERD, Anaphylaxis, FB
Rhonchi: Low pitched, Continuous, Rumbling, Rattling, Coarse. Sounds like snoring. May clear with cough/suctioning. Caused by increased secretions or obstruction in bronchial airway
Crackles (Rales): High pitched, Discontinuous, During Inspiration. Usually not cleared by cough/suctioning. Due to popping open of collapsed alveoli and small airways (from fluid, exudates, lack of aeration)
Pneumonia, Atelectasis, Bronchiectasis, Bronchitis, Pulmonary edema, Pulmonary fibrosis
Stridor: Monophonic sound, Usually loudest over anterior neck due to narrowing of larynx or anywhere over trachea. Can be heard throughout respiratory cycle

Normal Ranges
pH: 7.35-7.45
CO2: 35-45
HCO3: 22-26
1st: Look at pH: Acidosis, Alkalosis, or Normal
2nd: Look at PaCO2: Determine whether it's primarily respiratory (ROME)
Primary Relationship to pH and CO2:
For every 10mmHg increase PaCO2, 0.08 decrease in pH Inverse relationship between CO2 and pH
3rd: Look at HCO3: Determine whether its a primary metabolic disorder (ROME) Primary relationship to pH and HCO3
HCO3 increases then pH increases
Direct relationship between HCO3 and pH
4th: Decide whether there is compensation present
pH better than expected: Compensated
pH worse than expected: Mixed respiratory-metabolic disorder

Obstructive: TLC: Normal/Up, FVC: Normal/Down, FEV1: Very Down, FEV1/FVC: Down. Flow loop shifts to left
Asthma, COPD, Bronchiectasis, CF

Restrictive: TLC, FVC, FEV1: Down, FEV1/FVC: Normal/Up. Flow loop same shape, different size
Sarcoidosis, Pneumoconiosis, Idiopathic pulmonary fibrosis

SCREENING
Lung Cancer USPSTF: 55-80 yo + Asymptomatic + 20 pack-year hx + Currently smoke or Quit within 15 years: Annual Low Dose CT
*Discontinue: Once hasn’t smoked for 15 years or Develops health condition that significantly limits life expectancy or ability/willingness to undergo curative therapy
TB Adult: PPD or QuantiFERON Gold: Positive-> CXR (abnormal=active, normal=latent)
>5mm: HIV+, Immunosuppressed, Close contacts with active, CXR consistent with old/healed (calcified granuloma)
≥10mm: High risk settings (prisons, hospitals, homeless shelter), <4 yo, DM, ≤10% underweight, Dialysis, Silicosis, Some malignancies
≥15mm: Healthy ≥4 yo with low likelihood of TB
Suspected Active TB Adult: Obtain: Sputum, AFB Smear, Culture, NAAT
NAAT(+): AFB Smear(+/-) -> TB Likely (initiate therapy pending culture results)
NAAT(-)
35
 AFB Smear(+): TB Not Likely. Non-TB Mycobacterium Possible -> Repeat AFB Smear & NAAT while pending culture
AFB Smear(-): TB Not Likely but Not Fully Excluded: Bacteria burden may be too low to meet the sensitivity threshold. Await culture.

Pneumococcal Vaccines
Pneumovax (PCV) 13: 6 weeks old – 5 years old; 4 dose series: 2, 4, 6, 12-15 months
Pneumococcal (PPSV) 23: ALL ≥65, Younger patients with increased risk of pneumococcal disease
If given prior to 65 yo: Revaccinated at 65 yo unless it was given within 10 years in that case revaccinate 10 years after vaccines
No prior vaccines: PCV, wait 8 weeks, PPSV
Received PPSV in past: PCV one year after PPSV vaccine

PULM About Presentation Diagnostics Treatment

COPD Progressive Irreversible obstruction Chronic Bronchitis is defined by Screening: Annual CT: 55-80 yo + 20 Category A
Loss of elastic recoil of alveoli clinical features (chronic cough) pack-yr hx + Currently smoke or SAMA PRN
Increased airway resistance smoked within past 15yr Or SABA PRN
Emphysema which is defined by Or SAMA + SABA PRN
Risks structural changes (enlarged air CXR
TOB smoking/exposure (>15 pack years) spaces secondary to alveolar CB: Pulmonary HTN: Enlarged right Category B
Alpha-1-antitrypsin (AAT) deficiency destruction) heart border, Vascular markings ADD: LAMA
*only genetic disease linked to COPD <40 yo (particularly at base), Thickened Or LABA
Occupational/environmental exposure, recurrent airway bronchial walls
infections E: Hyperinflation: Flattened Category C
diaphragms, Increased AP diameter, LAMA
Trapped air, Loss of lung markings, Or LAMA + LABA
Bullae Or LABA + ICS

Chronic Productive cough X 3 MONTHS for 2 consecutive Productive chronic cough PFT: Spirometry *Gold Category D
Bronchitis years Dyspnea Airway obstruction: Decreased FEV1, LAMA + LABA
May have prolonged expiration, FEV1/FVC <0.7, FVC (severe) Or LABA + ICS
Blue Bloaters: Secondary to chronic hypoxia Accessory muscle use, Tachypnea Hyperinflation: Increased TLC (esp Persistent: LAMA + LABA + ICS
E)
Chronic inflammation -> Mucus gland hyperplasia Severe V/Q mismatch (normal in Decreased DLCO (E only) Acute Exacerbation (CB)
and goblet cell mucus production, airway narrowing, emphysema), Severe hypoxemia, Macrolide: Azithromycin, Clarithromycin
increased airway resistance à obstruction *infiltration Hypercapnia Pulse Ox: (94-99%) Cephalosporin: Cefuroxime, Cefixime
of neutrophils and CD8 • >90% mild, <90%-needs O2 Augmentin
PE: crackle (rale), rhonchi, wheeze • <88%–supp O2 by medicare Fluoroquinolone
*Increased susceptibility: S. pnuemo & H. flu Cyanotic, obesity, RHF, cor pulm
(enlarged tender liver, JVD, edema)
Emphysema Irreversible enlargement of air spaces distal to Dyspnea (hallmark) ABG: Increased HGB & HCT Other Therapies
terminal bronchioles -> Destruction of alveolar Minimal cough ± sputum (chronic hypoxia), Hypercapnia, Regular physical activity
capillaries and wall destruction Hypoxemia, Respiratory acidosis Pulmonary rehab: Categories B-D
Loss of elastic recoil in acinus, collapse, and increased PE: Hyperinflation (Decreased •mild: low O2, normal CO2 (Outpatient program)
compliance à trapping & obstruction breath sounds, Barrel Chest), •mod/severe: low O2, high CO2 Smoking cessation
Decreased fremitus, Pink PNA & Flu vaccines
Pink Puffer: Destruction of alveolar space complexion, Hyperresonance to
percussion, Thin, no edema O2 Therapy
Areas: Cor pulmonale
Centrilobar (proximal acinar) (MC with smoking) Severe: Tripod, Pursed lips to prevent PaO2 ≤55
Panacinar (diffuse) (MC with AAT deficiency) airway collapse Pulse ox ≤88%
Paraseptal (distal acinar) (can be seen with above or
spontaneous pneumothorax)

36
 Class Drugs
SAMA Anticholinergic (Antimuscarinic). Bronchodilation (M1, M2, M3 receptors)
Ipratropium
Onset: 10 min, Peak: 1-2 hours, Duration: 4-8 hours

ADR: Cough, Bitter taste, Scratchy throat, Anticholinergic (Dry mouth, Thirst,
Blurred vision, Mydriasis, Constipation, Urinary retention, Difficulty swallowing
Caution: Patients with BPH

SABA Central bronchodilator (Beta-2 Agonist). Inhibits vagal mediated

Albuterol bronchoconstriction and nasal mucosal secretions

Onset: Immediate, Peak: 30 min, Duration: 4-8 hours

ADR: Beta-1 Cross Reactivity: Tremor (dose limiting), HR, Restlessness,

Insomnia, Hypokalemia

ICS MOA: reduces inflammation; SE: thrush

Fluticasone
ADR: Oropharyngeal Candidiasis

LABA Central bronchodilator (Beta-2 Agonist). Inhibits vagal mediated

Salmeterol, bronchoconstriction and nasal mucosal secretions
Formoterol
Onset: 15-20 min, Peak: 2-4 hours, Duration: 12-24 hours

NOT TO BE USED ALONE

LAMA Anticholinergic (antimuscarinic). Bronchodilation (M1, M3 receptors)

Tiotropium
Onset: 30 min, Peak: 1.5-3 hours, Duration: 24 hours

ADR: Cough, Bitter taste, Scratchy throat, Anticholinergic (Dry mouth, Thirst,
Blurred vision, Mydriasis, Constipation, Urinary retention, Difficulty swallowing
Caution: Patients with BPH

LABA-ICS Budesonide/Formoterol (Sumbicort)

Combo Fluticasone/Salmeterol (Advair)
GOLD Guidelines Momentasone/Formeterol (Dulera)
GOLD 1: Mild à FEV1 80%+
GOLD 2: Moderate à FEV1 50-70%
LABA- Tiotropium-Olodaterol (Stiolto Respimat)
GOLD 3: Severe à FEV1 30-49%
LAMA -Soft mist inhaler: 2 inhalations once daily
GOLD 4: Very Severe à FEV1 <30%
Combo Umeclidinium-Vilanterol (Anoro Ellipta)
-Dry powder inhaler: 1 inhalation once daily
Gold Stages
Glycopyrrolate-Formoterol (Bevespi)
GOLD A: mMRC 0-1, CAT <10, 0-1 exacerbation
-Metered dose inhaler: 2 inahlations twice daily
GOLD B: mMRC 2+, CAT 10+, 0-1 exacerbation
Triple Trelegy -dry powder inhaler: 1 inhalation once daily
GOLD C: mMRC 0-1, CAT <10, 2+exacerbation or 1+ hospital
GOLD D: mMRC 2+, CAT 10+, 2+ exacerbation or 1+ hospital

37
PULM About
Asthma Airway inflammation,
Hyperresponsiveness, Reversible,
Intermittent, airway Obstruction
Patho
1. Airway hyperactivity: IgE binds to
mast cells
2. Bronchoconstriction: Airway
narrowing due to smooth muscle
contraction, edema, mucus, hypertrophy
à Air trapping
3. Inflammation: Inflammatory
response including increased
leukotrienes
Risks: Atopy (strongest), FHX, air
pollution, obesity, second hand smoke,
male
Atopic Triad: asthma, atopic dermatitis
(eczema), allergic rhinitis
Samters Triad: asthma, ASA allergy,
nasal polyps
Presentation Diagnostics Treatment
Dyspnea Pulmonary Function Test Mild Intermittent: Step 1
Wheezing Spirometry *GOLD ≤2d/wk, ≤2/week med, ≤2x/mo night awake
Cough (worse at night) Reversible No limitation
Chest tightness Low FEV1 (<80%) & FEV1/FVC (<85%) FEV1 >80%, FEV1/FVC normal
Fatigue *Obstruction = Decreased FEV1 therefor
decreased FEV1/FVC
PE Mild Persistent: Step 2
>2d/wk, >2dy/wk (not >1/day) med, 3-4x/mo night awake
Prolonged expiration, Wheezing Bronchodilation
Minor limitation
Hyperresonance percussion After SABA: FEV1 increases by 12% or
Decreased breath sounds 200ml FEV1 ≥80%, FEV1/FVC normal
Tachycardia, Tachypnea
Accessory muscle use Bronchoprovocation: Moderate Persistent: Step 3 & 4
Longstanding dz: Nasal polyp, If you don’t see reversibility then:
daily, daily med, >1x/wk night awake (not nightly)
Atopic dermatitis Methacholine Challenge: ≥20% decrease Some limitation
FEV1
FEV1 60-80%, FEV1/FVC reduced 5%
*don’t do if FEV1 <65%
Severe:
Acute Asthma Exacerbation Severe Persistent: Step 5 & 6
Tripod
Peak Expiratory Flow Rate (PEFR) throughout day, several times day med, awake nightly
Silent chest (no air movement)
Exacerbation severity & response Extreme limitation
AMS
Normal is 400-600 FEV1 <60%, FEV1/FVC reduced 5%
Pulsus paradoxus (inspiratory BP Discharge criteria: >70% predicted or >15%
drop ≥10) initial attempt Treatment
Consult asthma specialist if step ≥4, consider at 3
Pulse Ox Rule of 2's: Yes to any = Step up, maintained step up for 3
SaO2 <90%: Respiratory distress months = Move down
Cough >2 nights/wk, Rescue inhaler >2/wk, Refill >2/yr
ABG 1. SABA PRN
Respiratory alkalosis (tachypnea), 2. + ICS (low)
Pseudonormalization (normal CO2): May 3. + ICS (low) + LABA or ICS (med)
indicate impending respiratory failure 4. + ICS (med) + LABA
5. + ICS (high) + LABA
CXR: Usually normal, may be used to r/o 6. + ICS (high) + LABA + OCS
pneumonia
Admit if: PEFR <50%, ER within past 3 days, Status
Culture: Curschmann’s spirals, Charcot- asthmaticus: O2, Nebulized SABA/SAMA, IV/Oral
Leyden crystals Corticosteroids, IV Magnesium (if not responding)

PULM Drugs Side Effects Routes

SABA Albuterol, Levalbuterol, Terbutaline Tachycardia/arrhythmias, -metered dose: 90mcg two puffs q4-6h
MOA: Agonist B-2 receptors (peripheral), Dilation of the smooth muscles in the bronchioles tremors, CNS stimulation, low -dry powder inhaler: 200mcg, 1 inhalation prn;
2-5min K+ max 4/day

ICS Pulmicort, Flovent, Azmacort, Qvar, Beclomethasone Thrush

MOA: Reduces inflammation

38
LABA Salmeterol, Formoterol, Arformoterol, Indacaterol, Olodaterol BBW: asthma-related death as a -dry powder: one inhalation BID
monotherapy (w/o ICS)

LABA-ICS Budesonide/Formoterol (Sumbicort), Fluticasone/Salmeterol (Advair)

-Momentasone/Formeterol (Dulera)

Mast Cell Cromolyn, Nedocromil SE: throat irritation

MOA: Inhibits mass cell and leukotriene-mediated degranulation

Leukotriene Montelukast (Singulair), Zafrilukast (Accolate), Zileuton (Zyflo) SE: increased LFTs, HA, GI
Modifiers MOA: Blocks leukotriene-mediated neutrophil migration, capillary permeability, smooth mylagias
muscle contraction

Theophylline MOA: bronchodilator that improves respiratory muscle endurance, phosphodiesterance SE: nervous, tachycardia, N/V,
*narrow TI inhibitor which inhibits leukotreiene syntheseis and inflammation anorexia, HA

PULM
Acute Lower respiratory tract infection (bronchi)
Bronchitis without evidence of COPD or pneumonia
Etiology
MCC: Virus:, Parainfluenza, Influenza,
Coronavirus, Coxsackie, Rhinovirus, RSV
Bacterial: S. pneumonia, M. catarrhalis, H.
influenza, Mycoplasma
Cannot differentiate from upper respiratory
tract infection in the first few days
May be preceded by an URI
Cough ± Sputum
≥5 DAYS, Lasts 2-3 Weeks
average 18 DAYS
± Wheezing, Rhonchi (clears with
cough), Chest pain with cough
Diagnosis made by exclusion Self-Limited (1-3 WEEKS)
Normal lung sounds & CXR
exclude pneumonia and confirm Symptomatic: NSAID, Bronchodilators, Cough
acute bronchitis suppressant (Benzonatate, Dextromethorphan)
*ONLY FOR >6 yo
CXR: Usually normal
Only indicated if pneumonia ABX NOT RECOMMENDED
suspected (Tachycardia, RR >24,
Temp >38°C, Rales, Hypoxemia,
AMS, Systemic illness)

PULM
Pneumonia Infection of lung tissue (alveolar infection) Typical: Fever, Productive cough, CXR O2, rest, fluids, antipyretics, analgesics,
Pleuritic chest pain, Dyspnea IVF
Classifications Rigors (severe chills & violent
CAP: Community Acquired shaking)
HAP: Hospital Acquired *classically S. pneumonia Pneumonia: Dull (percussion), Increased
*HCAP: Healthcare Associated fremitus, Bronchial/Egophony breath sounds
VAP: Ventilator Associated Atypical: Fever (low), Dry non-
productive cough, extrapulmonary Pleural Effusion: Dull (percussion), Decreased
Patho symptoms (myalgias, malaise, fremitus, Decreased breath sounds
Normal pulmonary defense mechanisms pharyngitis, N/V/D)
Cough reflex, Mucociliary clearance, Cellular Pneumothorax or Obstructive Lung Disease:
immune response PE: Hyperresonance (percussion), Decreased
Typical: Tachypnea, Tachycardia, fremitus, Decreased breath sounds
Consolidation (bronchial breath
39
 Infection occurs when the defense mechanisms
are compromised or a large infectious load
CAP No hospitalization within 90 DAYS
No medical facility/Dialysis within 14 DAYS
Onset of illness <48 HOURS since admission
Patho: Agents get to lower respiratory tract
Aspiration from Oropharynx (MC)
GI Aspiration: Sleeping, Decreased LoC
Hematogenous/Spread from contagious areas
RF: Advanced age, Alcoholism, Smoking,
Asthma, COPD, Immunosuppression
Etiology: S. pneumonia (MC)
S. pneumonia: Epidemic in crowded area,
COPD, Welder, Alcoholism
Sudden onset chills & rigor, Fever, Productive
cough (blood “rusty” sputum)
H. flu (2nd): Extremes of age (<6, elderly),
Immunocompromised, Asthma, COPD,
Bronchiectasis, Cystic fibrosis, Alcoholism
Often a colonizer of respiratory tract
Legionella: AC, Misting machine, Hyponatremia
due to SIADH, Recent travel
Klebsiella Pneumoniae: Alcoholism, Solid organ
transplant, Liver disease, Dialysis
Mycoplasma Pneumoniae (MCC Atypical
pneumonia): Bullous myringitis
Histoplasmosis: Contaminated bird/bat droppings
Moraxella Catarrhalis: COPD
Hantavirus: Mouse droppings, In the south west
(dry area)
sounds, dullness to percussion,
increased tactile fremitus,
egophony), Inspiratory crackles
(rales)
Atypical: Pulmonary exam often
normal (consolidation usually
absent),
± Crackles (rales)
Elderly/DM/Immunocompromised:
May have minimal symptoms even
with typical
General Chest X-Ray: Confirmatory Outpatient No Comorbidities
Fever, Chills, Sweats, Rigors, Patchy airspace opacities Azithromycin or Doxycycline
Fatigue, Loss of appetite Lobar consolidation (white) with air
bronchograms or diffuse opacities Outpatient Comorbidities/ABX within 3
Respiratory ± Pleural effusions and Cavitation Months:
Cough +/- sputum, Pleuritic chest Takes >6 weeks for CXR to clear after Azithromycin + Augmentin
pain (deep breaths), Hemoptysis successful treatment
Severe/Inpatient
GI: Abdominal pain, N/V Sputum Gram Stain Add Corticosteroids
Urinary Antigen Testing
PE
*S. Pneumonia: Do if you see: Hospital Admission: PSI & CURB-65
General
Leukopenia, Asplenia, Active alcohol use,
Fever/hypothermia, Tachypnea,
Chronic severe liver disease, Pleural effusion, ICU Admission: 1 Major or ≥3 Minor
Tachycardia, Acutely ill
ICU Major: Septic shock with need for
*Legionella: Do if you see: vasopressor support, Respiratory failure
Respiratory
Active alcohol use, Travel within previous 2 with need for mechanical ventilation
Inspiratory crackles (rales)
weeks, Hyponatremia, Pleural effusion, ICU Minor: RR ≥30, Hypoxemia,
*fine short high pitched
Bronchial breath sounds Hypothermia, Hypotension requiring
Dullness to percussion overlying a Flu Rapid Testing: Flu symptoms b4 aggressive fluid resuscitation, AMS,
lobar consolidation or effusion pneumonia Multilobar pulmonary opacities,
(fluid collection around lung) Leukopenia, Thrombocytopenia,
CBC w Diff & CMP: All being admitted for Uremia, Metabolic acidosis, Elevated
CAP lactate3
Blood & Sputum Cultures: ICU before giving
abx (blood from 2 different locations on pt)
40
 Anaerobes: Periodontal disease, Foul smelling
sputum, Absent gag reflex, AMS, Seizure

HAP HAP Can present the same as CAP ABG: Hypoxia or Hypercapnia Begin ABX treatment immediately
≥2 DAYS in hospital in PAST 90 DAYS upon suspicion (do not wait for
VAP >48 HOURS after admission to hospital May also present with non-specific CBC confirmatory tests)
findings with 2/3 findings and
HCAP VAP New/Progressive pulmonary CMP Broad Spectrum ABX (until identified)
>48 HOURS after endotracheal intubation opacity on CXR IV Vancomycin + Zosyn or Cefepime
Fever Blood Cultures Monitor for worsening
HCAP Leukocytosis
Purulent sputum CXR or CT Scan: Might not helpful due to
IV/Wound care/IV chemo in PAST 30 DAYS
Residence in nursing home or other LTCF underlying process
Hospitalization in an acute care hospital for ≥2
DAYS within PAST 90 days Endotracheal Aspiration & Culture: if intubated
Attendance at a hospital or hemodialysis clinic *Tussive sputum cultures are not helpful
within PAST 30 DAYS

HAP & HCAP Etiology

S. Aureus: MSSA & MRSA
Pseudomonas Aeruginosa
Enterococcus
Gram(-) Rods: E. Coli & Klebsiella

VAP: Mechanically ventilated >48 hours after

endotracheal intubation

VAP Etiology
Acinetobacter
Stenotrophomonas maltophilia
Pseudomonas aeruginosa

Anaerobic Aspiration gastric contents or oral/dental Insidious Onset CXR/CT Augmentin

Pneumonia bacteria leads to anaerobic infections
Increased Risk of Aspiration:
Decreased consciousness: Drug/alcohol use,
Seizures, General anesthesia, CNS disease
Impaired swallowing due to esophageal disease or
neurologic disorders, Tracheal/Nasogastric tube
Aspiration -> Pneumonia in dependent lung zones
Posterior Upper Lobes: Lying down
Basilar Lower Lobes: Standing up
Lung Abscess: Thick-walled solitary cavity Amoxicillin + Metronidazole
Fever, Weight loss, Malaise surrounded by consolidation (air-fluid level) Clindamycin
Necrotizing Pneumonia: Multiple areas of
Dentition: Often poor cavitation within an area of consolidation
Cough with expectoration of foul-
smelling purulent sputum
*absence of purulent sputum does not
exclude the diagnosis

Viral Etiology Viral Syndrome Rapid Viral Test or PCR Influenza & Varicella: Antivirals
Pneumonia Influenza (most likely A) Fever, Myalgias, Fatigue, URI-type
RSV symptoms CXR Supportive: Everyone
41
 Parainfluenza
Adenovirus
Fungal Pneumocystis Jirovecii & Histoplasmosis
Pneumonia
Most often: Immunocompromised
P. Jirovecii “PCP
MC opportunistic fungal infection (AIDS
defining illness), Ascomycetous fungi based
organism
Histoplasmosis
Mycelia is naturally infectious form of
Histoplasmosis: Small oval bodies, small enough
to reach the terminal bronchioles & alveoli.
Patho: Shortly after infecting the pt, mycelia
transform into the yeasts that are found inside
macrophages
and other phagocytes, but its not working
Endemic: Ohio & Mississippi River valleys
*Humid and acidic nature of soil
*Soil enriched with bird/bat droppings
Spectrum: Asymptomatic to Life-threatening
Extent and severity depends on: Intensity of
exposure, underlying lung health, immune status
RF: Spelunking, Excavation, Chicken coops,
Demo and remodeling of old buildings, Cutting
dead trees
Respiratory
Increased RR
Diffuse Rales/Wheezes
Non-productive cough (can progress
to cough with pink-frothy sputum in
severe disease)
+/-: Trachea tender from viral
tracheitis, Cervical lymphadenopathy
PCP: Clinical Findings
Abrupt Onset
Fever, Tachypnea, SoB
Usually nonproductive cough
Respiratory findings may be slight
& disproportionate to degree of
illness
+/- Bibasilar Crackles (rales)
Histoplasmosis: Clinical Findings
Symptoms 1-4 weeks post exposure
Flu-like Illness: Fever, Chills,
Sweats, HA, Myalgia, Anorexia,
Cough, Dyspnea, Chest pain
Normal or Patchy areas of consolidation
Bronchial wall thickening
Small pleural effusions
CT Scan
Ground glass opacity
Patchy areas of consolidations
PCP: Diagnostics
CXR
Diffuse interstitial infiltrations
*Ground glass type appearance
*May be perihilar (Batwing appearance)
*5-10% will have normal CXR
ABG: May have hypoxemia with hypocapnia
Histoplasmosis: Diagnostics
CXR
Prominent hilar/mediastinal adenopathy
Pulmonary infiltrates (focal/diffuse)
Histoplasma Antigen Test of Bronchial Lavage
Cytopathology of Bronchial Lavage
NSAID, Cough Suppressants
(Benzonatate, Dextromethorphan),
Proper hydration
Monitor for sepsis or bacterial
secondary infection
PCP: Treatment
Treat underlying immune compromise
1st: Bactrim
PaO2 <70, SpO2 <92%, A-a >35
Corticosteroids
Histoplasmosis: Treatment
Combo: Amphotericin B, Itraconazole
Histoplasmosis: Complications
Affected hilar/mediastinal LN may
undergo necrosis & coalesce
*Forms large mediastinal masses
*Compress great vessels, proximal
airways, esophagus
*Necrotic LN may also rupture and
create fistulas between mediastinal
structures (Bronchoesophageal fistula)
Chronic cavitary histoplasmosis is
seen in smokers who have COPD
*Chronic illness with productive cough,
dyspnea, low grade fever, night sweats,
weight loss
*Chest radiographs usually show upper-
lobe infiltrates, cavitation, pleural
thickening
*Resembles TB
In healed histoplasmosis, calcified
mediastinal nodes or lung
parenchymal nodules may erode
through the walls of the airways
*Causes hemoptysis and expectoration
of calcified material
*Broncholithiasis
Fibrosing mediastinitis is uncommon
but serious
*Fatal in up to 1/3 of cases
*Progressive fibrosis around the hilar
and mediastinal LN
*Major sequelae include SVC
42

PULM
Tuberculosis Mycobacterium tuberculosis (Mtb)
Transmission: Airborne droplets
Patho
Inhalation -> Alveoli -> Incorporated into
macrophages -> Disseminates
RF: Close contact, Immigrants, Crowded
conditions, Healthcare, Immunosuppressed
TB & HIV: 7-10% yearly chance reactivation
Primary TB: Contagious
Initial infection
Chronic (Latent): Not contagious
Caseating granuloma formation (central
necrosis, acidic, low O2 à hard for Mtb)
PPD+ 2-4 weeks after infection
1) PPD+
2) No symptoms of infections
3) No imaging findings active TB
Secondary (Reactivation): Contagious
Reactivation of latent TB (5-10% lifetime,
lowered to 1% with treatment)
Waning immune system
MC: Localized in apex/upper lobes with
cavitary lesions (increased O2 of apices)
Pulmonary: Cough (±sputum),
Hemoptysis, Post tussive apical
rales/crackles (gets worse after
coughing)
Constitutional: Fever, Chills, Night
sweats, Chest pain, Weight loss
Extra-Pulmonary: Potts Disease
(vertebra), Scrofula (cervical LN),
Miliary TB (disseminated), Pericarditis,
Adrenal gland involvement,
Gentiourinary
TB Screening
PPD (purified protein derivative)
Examine 48-72 hours for transverse
induration (redness not considered
positive)
Any positive PPD should be followed
up with Chest X-Ray
Mantoux Test Rules
>5mm: HIV+, Immunosuppressed,
Close contacts with active, CXR
consistent with old/healed (calcified
granuloma)
≥10mm: High risk settings (prisons,
hospitals, homeless shelter), <4 yo,
DM, ≤10% underweight, Dialysis,
Silicosis, Some malignancies
≥15mm: Healthy ≥4 yo with low
likelihood of TB
False Negative: Anergy (HIV,
Sarcoidosis), Faulty application, Acute
TB, Acute non-TB, Malignancy
False Positive: Improper reading,
Cross rxn with an atypical
(mycobacterium avium complex),
Within 2-10 years of BCG vaccination
(usually <10mm)
Chest X-Ray: Initial test
*yearly screening in PPD+ patients
Primary: Middle/Lower lobe
consilidation
Reactivation: Apical (upper lobe)
fibrocavitary disease MC
Miliary: Small millet seed like
nodular lesions (2-4mm)
TB Pleurisy: Pleural effusion caused
by TB
Granuloma: Residual evidence of
healed primary TB. Ghon’s
Complex (calcified primary focus +
LN). Ranke’s Complex (healed
fibrocalcific ghon complex seen)
Sputum Acid Fast Staining:
3 samples on 3 consecutive days
must be negative to rule out TB
*only 1 positive needed to rule in
Sputum Cultures: At least 3 samples
on 3 consecutive days (preferably
early AM)
NAAT: More sensitive than sputum
smears
Interferon Gamma Release Assay
“Quantiferon-TB Gold Assay”:
Blood test with improved
sensitivity, no reader bias, no
booster phenomenon, not affected
by prior BCG vaccination
syndrome, obstruction of pulmonary
vessels, airway obstruction
*Pt may experience: Recurrent
pneumonia, Hemoptysis, Respiratory
failure
Active
RIPE: RIF, INH, PZA, EMB: 2 months then 4
months with RIF, INH (pending sensitivity)
*6 months total
*Streptomycin can be used instead of Ethambutol
Latent Likely INH Sensitive
INH + PZA: Daily 9 Months
*Alternative: RIF: Daily 4 Months
*Alternative: INH + Rifapentine: Weekly 3 Months
*Alternative: INH + RIF: Daily 3 Months
Latent Contact Case INH Resistant
RIF + PZA: 4 Months (consult with ID)
Rifampin (RIF)
MOA: Inhibit RNA synthesis
ADR: Thrombocytopenia, Flu-like symptoms,
Orange colored secretions, GI, Hypersensitivity,
Fever, Hepatitis
CI: PI, NNRTI
Isoniazid (INH)
MOA: Inhibits mycolic acid synthesis
ADR: Hepatitis (esp >35 yo), Peripheral
neuropathy, drug induced lupus, Rash, Abdominal
pain, High AG acidosis, P450 inhibition
Pyridoxine (vitB6): Stop peripheral neuropathy
Baseline LFTs recommended
Pyrazinamide (PZA) “Vitamin B6”
Can be given after 1st trimester
ADR: Hepatatoxicity, Hyperuricemia (gout), GI,
Arthritis, Photosensitive dermatologic rash
Caution: Gout & Liver disease
Ethambutol (EMB)
ADR: Optic neuritis (scotoma, red-green problem,
visual changes), Peripheral neuropathy, GI, Rash
Streptomycin (STM) (aminoglycoside)
ADR: Ototoxicity (CNVIII), Nephrotoxicity
43
 Hx of previous BCG vaccine has no
impact/effect on recommendations for
the screening & treatment of latent TB
in adults

Booster Effect: Infected persons

immune system forgets about TB until
years later when testing reminds it. Next
PPD will be positive bc of initial
infection (years ago) NOT bc recently
converted
*confirmed by 2 step PPD testing

PULM About Presentation Diagnostics Treatment

Sleep Apnea Involuntary cessation of breathing during sleep Snoring, Unrestful sleep (may lead 1st Lab Polysomnography ≥15 Behavioral: Weight loss, Exercise, Avoid
Hypoventilation Complications: Pulmonary HTN, Arrhythmias to chronic daytime sleepiness), events/hour alcohol & sedatives, Non-supine sleep position
Syndrome Nocturnal choking •Alternative: HSAT (home sleep
Risk Factors apnea testing) Mainstay: CPAP
Obesity (strong), Age (MC 60-70s), Males PE: Large neck circumference, Alternative: Oral appliances
Crowded oropharynx, Labs: Polycythemia (chronic
Types: Micrognathia (small lower jaw) hypoxemia) Definitive: Tracheostomy
Central: Reduced CNS respiratory drive -> Alternative: Nasal septoplasty, UPPP
Decreased respiratory effort (Uvulopalatopharyngoplasty)
Obstructive: Physical airway obstruction

1. pharyngeal wall collapse repetitively

2. failure of upper airway dilator muscle
3. sleep-related obstruction and breath cessation

44
PULM About
Bronchial Neuroendocrine tumor
Carcinoid (enterochromaffin cell)
Tumor
Slow growth, Low mets, Usually
well differentiated
MC Mets Site: GI (1st), Lungs (2nd)
Solitary Single small (<3cm) usually well
Pulmonary circumscribed lesion surrounded
Nodule entirely by pulmonary parenchyma
Etiology:
Infectious granuloma (MC) (esp
mycobacteria (TB) & fungi
(Histoplasmosis,
Coccidioidomycosis))
Benign or Malignant (lung cancer,
mets, carcinoid tumors)
*thymoma MC mediastinal tumor
Bronchogenic MCC of cancer related deaths USA
Carcinoma 2nd MC cancer diagnosed USA
METS to: Brain, Bone, Liver, LN,
Adrenals
RF: Cigarettes (MCC): Associated
with 90% exception is lepidic
pattern), Asbestosis (2nd)
Radon exposure, Idiopathic
pulmonary fibrosis, TB, COPD,
Genetics
*Asbestosis & smoking: Synergistic
Two Types:
NSCLC: Adenocarcinoma, Large
cell, Squamous cell, Lepidic pattern
SCLC: Usually mets at time of
presentation
Clinical Presentation
Most: Asymptomatic
Focal wheezing, Cough, Hemoptysis, SIADH,
Cushing’s syndrome, Obstruction
Carcinoid Syndrome (rare but classic): Periodic
Diarrhea (due to serotonin), Flushing,
Tachycardia, Bronchoconstriction (histamine),
Hemolytic instability (hypotension)
Increased Risk: Spiculated nodule, Large
(>2cm), Irregular borders, Asymmetric
calcification, Upper lobe, >40 yo, Smoker,
Enlarging lesions, Abnormal PET
Decreased Risk: Well circumscribed smooth
borders, Small (<1cm), Dense diffuse
calcification, <30 yo, Nonsmoker, No change in
size, Normal CT
Paraneoplastic Syndromes
SVC Syndrome
*MC SCLC & other malignancies
Due to partial/complete extrinsic obstruction of
blood thru SVC: Face/neck swelling, Facial
plethora, HA, Dilated & prominent neck &
chest veins
CXR: Right hilar mass or Widening mediastinum
CT: Better view, Assess degree of obstruction
Lambet-Eaton Syndrome
*MC SCLC, HL, METS, SVC stenosis
Antibodies against presynaptic voltage gated
Ca channels (prevent ACh release) -> Muscle
wasting
Proximal muscle weakness improves with
repeated muscle use (unlike MG). Autonomic:
Dry mouth (MC), Postural hypotension, ED
PE: Hyporeflexia, Sluggish pupillary response,
No muscle atrophy
Voltage gated Ca channel antibody assay
Electrophysiology: Reproducible post exercise
increase in compound muscle activation on
repetitive nerve stimulation test
Diagnostics
Bronchoscopy: Pink-purple well
vascularized central tumor
CT & Octreotide: Tumor Localization
Biopsy: Definitive
Chest X-Ray: Initial test reveals nodule
CT Chest: IoC: Determine likelihood of
malignancy of a nodule found incidentally
PET: May be used to determine metabolic
functioning of nodule
Paraneoplastic Syndromes
Superior Sulcus (Pancoast) Syndrome
*NSCLS >95% (Squamous Cell)
Located in superior sulcus. Dx by
location not histology
Patho: Tumor compress lower brachial
plexus, ulnar nerve, cervical sympathetic
nerve chain
Shoulder & arm pain (MC initial, in C8, T1,
T2 dermatomes) Horner Syndrome:
Ipsilateral ptosis, Miosis, Anhidrosis (may
be preceded by ipsilateral flushing & facial
diaphoresis). Weakness atrophy of hand
and/or arm. Ulnar neuropathy.
Bc tumors are peripheral: Pulmonary
symptoms are uncommon until it advances
CXR: Initial
MRI: etter assess extent infiltration
Needle Biopsy: Definitive
Treatment
Surgical Excision: Definitive
*often resistant to radiation & chemo
Octreotide: May reduce symptoms
*decreases secretion of active hormones
Low: Active surveillance
Intermediate
Central: Bronchoscopy
Peripheral: Transthoracic needle aspiration
High: Resect w/ Biopsy
NSCLC: Surgical Resection
SCLC: Chemo ± Radiation
SVC Syndrome: Supportive Tx: Elevate
head, Endovascular management
Lambet-Eaton Syndrome:
Treat underlying malignancy, Initial:
Pyridostigmine, 3,4-diaminopyridine,
2nd Line: Plasmapheresis, IVIG, PO
immunosuppressants
Superior Sulcus (Pancoast) Syndrome
Induction Chemo/Radiotherapy followed
by Radical Surgical Resection
45

NSCLC Adenocarcinoma: MCC lung
carcinoma
RF: Smoking (strongest), Exposure to
silica, asbestos, radon, heavy metal
Arises from bronchial mucosal
glands
“Lepidic” (formerly
bronchioloalveolar): Describes non-
invasive growth along intact alveolar
septae
Lepidic Pattern: Rare low grade
subtype
Voluminous sputum & interstitial
lung pattern on CXR
Squamous Cell: 2nd MCC of lung
carcinoma
RF: Smoking (strongly associated)
Arises from proximal portions of
tracheobronchial epithelium
*Most are bronchial in origin
SCLC Aggressive, Associated with early
METS
“Oat Cell” 15% of all lung cancers
RF: Cigarette (strongest), Male
*Strongest with SCLC & Squamous
cell (NSCLS)
Mesothelioma Tumor originating from pleura
(MC), Peritoneum (2nd), Tunica
vaginalis, Pericardium
Etiology
80%: Chronic asbestos exposure
Tobacco Most important modifiable RF
Use/Dependence pulmonary, cardiac, cancer deaths
Cessation should be discussed at
every clinicals contact
CT: Assess for underlying malignancy
Adenocarcinoma
Typically peripheral
Signs/Symptoms
Asymptomatic early
Cough, Dyspnea, Hemoptysis, Weight loss
Dx: Histology
Gland formation, Mucin production
Cough, Chest pain, Dyspnea, Hemoptysis,
Wheezing, Weight loss
MC solid tumor to present with Paraneoplastic
Syndromes: SVC syndrome, SIADH
(hyponatremia), Cushing’s syndrome, Lambert-
Eaton syndrome
Pleural:
Pleuritic chest pain, Dyspnea, Fever, Night
sweats, Weight loss, Hemoptysis
Withdrawal
Restless, Anxiety, Irritable, Sleep abnormalities,
HA, Depression, Increased appetite, Weight gain,
Nicotine craving
Squamous Cell Stage 1 &2: Surgical Resection
Typically central
May be associated with widened Stage 3: Chemo then Surgery
mediastinum
Associated with CCCP: Central, Cavitary
Stage 4: Palliative
lesions, Hypercalcemia, Pancoast
syndrome
Dx: May be detected in sputum (bc it’s
commonly central)
Biopsy: Keratinization and/or intracellular
desmosomes (bridges)
CXR: Centrally located Chemo ± Radiation: ToC
CT: Staging *Often METS at presentation
Biopsy: CT guided or Bronchoscopy (if
central)
Histology: Sheets of small dark blue cells
with rosette formation (~2X size of
lymphocytes)
*size of cells differentiates it from NSCLC
Chest X-Ray: Unilateral pleural Chemo & Resection, Radical extrapleural
thickening, Bloody pleural effusions pneumonectomy, Radiation
Pleural Biopsy: Closed, VATS, Open Non-Surgical: Chemo and/or Palliative
thoracotomy radiation
Management Bupropion
Counseling, Support, CBT DA & NOR reuptake inhibitor that reduces
Relapse after abstinence is common cravings and withdrawal
Nicotine Tapering Therapy: Gum, Nasal Begin 1-2 wk prior to quit, continue 4-6
spray, Patches, Inhaler, Lozenges months after quit date
Bupropion: Antidepressant combo w/ NTT
46
Varenicline: Blocks nicotine receptors,
reducing nicotine activity. Partial agonist
(mimics effects, reducing reward,
preventing withdrawal). Begin 1 wk prior
to quit, continue 4 months after quit date.
ADR: HA, Nausea, Insomnia, Increased
Suicidality, Neuropsychiatric conditions
ADR: Seizure, Dry mouth, Insomnia,
Weight loss, HTN, HA, Increased anxiety
& agitation & psychosis risk at high dose
Avoid abrupt withdrawal
Caution: HTN & CV disease
CI: Epilepsy, Dx associated with increased
seizure risk (Bulimia, Anorexia), Pt
undergoing discontinuation of EtOH,
Benzo, Barbiturate, Antiepileptic meds,
Recent MAOi use
47
GI 11%

Rovsing: RLQ pain with palpation of LLQ

Obturator: RLQ pain with internal rotation of hip
Psoas: RLQ pain with hip extension

SCREENING
Hereditary Polyposis Syndromes: >1 family member affected by polyposis syndrome, PMH/FamHx colorectal cancer at <50 yo or >20 polyps: Genetic Counseling
Colorectal Cancer: Until 75 yo
Average Risk ≥45yo: Colonoscopy Every 10 Years, FOBT/FIT Annually, OTHER: Every 1-3 Years (Fecal DNA), Every 5 Years (CT Colonography, Flexible Sigmoidoscopy +/- Biennial FIT
Single 1st Degree Relative with Colorectal Cancer Diagnosed at ≥60 yo, Begin Screening at 40 yo: Colonoscopy Every 10 Years
Single 1st Degree Relative with Colorectal Cancer or Advanced Adenoma, Diagnosed at <60 yo, or TWO 1st degree relatives Diagnosed >60 yo, Begin Screening at 40 yo or at age 10 years younger
than age at diagnosis of the youngest affected relative, whichever is first: Colonoscopy Every 5 Years
Lynch Syndrome: Begin screening at 20-25 yo: Colonoscopy Every 1-2 Years
Familial Adenomatous Polyposis: Begin screening at 10-12 yo: Sigmoidoscopy Annually
HCV: IVDU, Long-term hemodialysis, Chronic liver disease, HIV: HCV Antibody (ELISA) ± HCV RNA (PRC) every 6-12 months
Adults born 1945-1965: HCV Antibody (ELISA) ± HCV RNA (PCR) ONE TIME SCREENING
HCC: Chronic HBV, Cirrhosis due to HBV, HCV, Alcohol: U/S & AFP every 6 months
Gastric Neoplasm: New onset GERD > 50 yo, GERD not relieved by PPI, Progressive dysphagia, Recurrent vomiting, +FOBT, Melena, Hematemesis, Anemia Severe unexplained abdominal pain, Weight
loss,
Anorexia, Famhx gastric malignancy: EGD
Esophageal Varices: At time of cirrhosis diagnosis: EGD
Hepatitis C: IVDU, Long-term hemodialysis, Chronic liver disease, HIV, One Time Screening (Adults born 1945-1965)

SEVERITY
Acute Pancreatitis: Ranson’s Criteria (% Mortality): 0-2: <5%, 3-4: 15%, 5-6: 50%, >6: Few Survivors
Not Due to Gallstones
Admission: >55 yo, WBC >16K, Glucose >200, LDH >350, AST >250
Initial 48 Hours: Hematocrit Fall >10%, BUN Elevation >5, Serum Ca Fall to <8, Base Deficit >4, Estimated Fluid Sequestration >6L, Arterial PO2 <60
Due to Gallstone
Admission: >70 yo, WBC >18K, Glucose >220, LDH >400, AST >250
Initial 48 Hours: Hematocrit Fall >10%, BUN Elevation >2, Serum Ca Fall to <8, Base Deficit >5, Estimated Fluid Sequestration >4L

VACCINE
Hepatitis A: (Inactivated vaccine) Post-exposure prophylaxis in unvaccinated: 1-40 yo: HAV Vaccine, <1 or >40 yo: HAV Vaccine + Immune Globulin (IgG against HAV)
Hepatitis B: Vaccine protection can wane after 20 years, so check titer (IgG, Anti-HBs)
HBV Post-Exposure Prophylaxis in Unvaccinated: HBIG followed by Hep B Vaccine series
Pregnancy: All pregnant women should be tested for HBsAg: Initiate maternal anti-viral treatment in 3rd trimester, C-section + HBIG to Neonate: Reduces risk transmission from HBV+ mother

GI Types Non-Inflammatory Inflammatory Treatment

Acute Increased stool frequency
Diarrhea (>3/DAY) or Loose/watery
stools
Acute: ≤14 days
Persistent: 14-30 days
Chronic: >30 days
Inflammatory:
Bacteria/Toxin invades
mucosal tissues causing
Viral Gastroenteritis: MCC of N/V/D in USA Viral
*Norovirus: MCC stomach flu (ruise ships, daycares, schools) *Cytomegalovirus: Immunocompromised (check for)
*Rotovirus: Infants and young kids (schools, day cares)
Protozoal
Protozoal *Entamoeba Hystolytica: Parasite, untreated water
*Giardia: Untreated water while camping (can spread quickly)
*Cryptosporidium: Untreated water camping (opportunistic) Bacterial Cytotoxin Production
*E. Coli 0157:H5: Undercooked ground beef
Bacterial Onset 2-24 hours
Enterotoxin Preformed (onset faster) With Antibiosis, Massive toxin load can lead to:
Sepsis & Death (dangerous E. coli)
Drink fluids with some carbs &
electrolytes, Large amounts of
sugar can worsen diarrhea
BRAT diet (banana, rice, apple
sauce, toast)
Antidiarrheal Med: Loperamide
*Only Mild-moderate disease
*SE: Risk of Toxic megacolon
& Systemic illness
48
 damage and likely systemic *Staph Aureus: Foods that require hand contact and w/o *Vibrio Parahaemolyticus: Oysters/shellfish
illness further cooking (meat, egg, dairy) Onset 2-24 hours Empiric ABX: Azithromycin 3
Bloody stools, fecal Onset 1-6 hours after digestion *Clostridium Difficile: Opportunistic infection when days or Ciprofloxacin 3-5
leukocytes, fevers N/V/D, Cramping normal colon flora reduced, Recent Antibiotics days: *Consider Only If: Fever,
*Bacillus Cereus: Starchy foods left at room temp too long >6 stools/day, Bloody stools,
Non-Inflammatory: (rice, sauce, soup, gravy, leftovers) Mucosal Invasion Immunocompromised,
Bacteria/Toxin does not Emetic 30 min - 6 hours, Diarrheal 6-15 hours *Shigella: Sandwiches, salads, raw foods in contact Significant clinical dehydration,
invade or lead to Vomiting, Diarrhea with infected person 70 yo or Comorbidities
breakdown of mucosa *Clostridium Perfringes: Protein rich (Beef, poultry, gravy) *Campylobacter Jejuni: Undercooked poultry,
No blood or fecal Onset 6-24 hours (wake up middle of night not immediate) unpasteurized milk, contaminated water Otherwise, wait for labs and
leukocytes in stools Diarrhea, Cramping *Salmonella: Undercooked poultry/eggs, tailor treatment against specific
Enterotoxin Produced (longer onset) unpasteurized milk/juice, cheese, contaminated organism
*E. Coli: Undercook ground beef, Water, Unpasteurized veggies. Also: Reptiles (snakes, turtles, frogs,
milk/juice (why they are pasteurized) lizards), Baby birds
Onset 1-10 days *Yersinia Enterocolitica: Undercooked pork
Diarrhea, Cramping *Listeria: Lunch meats, hotdogs, soft cheeses
*Vibrio Cholerae: Fecal contamination of food and water Fever, Stiff neck, Confusion, Vomiting (not always
Onset 3 hours - 5 days diarrhea, mimics meningitis)
Profuse Watery Diarrhea "rice water stool

Chronic Diarrhea >1 month Osmotic History: Important, usually points in diagnostic Antidiarrheal Agents
Diarrhea Over 4 week period: MCC Malabsorption Syndromes: Carb malabsorption (lactose, direction
Frequency of >3/day, Stool fructose, sorbitol), Laxative abuse, Pancreatic insufficiency Loperamide
weight >200 g/day, *Resolve during fasting periods Establish:
Decreased fecal Malabsorption of carbs is characterized by: Abdominal Onset Codeine & Deodorized
consistency distention, Bloating, Flatulence (increased gas production) Continuous vs Intermittent Tincture of Opium:
*Consider in all postprandial diarrhea Relationship to meals *SE: Dependency, avoid chronic
Fatty or Watery *Ask about diet: Dairy, fruits, artificial sweeteners, alcohol Does it occur at night or during fasting use
*Diagnosis by: Elimination Trial (for 2-3 weeks) or Hydrogen Associated incontinence
Watery: Breath Test (carb malabsorption) Stool appearance may suggest: Malabsorption (greasy Clonidine: Alpha-2-Adrenergic
Osmotic: Increased Stool or malodorous) Inflammatory (blood or purulent Agonist: Inhibits intestinal
Osmotic Gap Secretory material) Secretory (watery) electrolyte secretion
(malabsorption conditions) Increased intestinal secretion or decreased absorption
Secretory: High Volume Results in high volume watery diarrhea with a normal AG Review: History, Medications, Diet, Recent stressors, Octreotide: For Secretory
Stool with Normal Stool *Dehydration & Electrolyte imbalance may develop Travel Diarrhea: Stimulates intestinal
Osmotic Gap Caused by: Endocrine tumors (stimulating intestinal or fluid & electrolyte absorption,
Bloody or Pus: pancreatic secretion), Bile salt malabsorption (stimulating Associated Symptoms: Abdominal pain suggests: IBS Inhibits intestinal fluid secretion
Inflammatory colonic secretion) or Inflammatory disease
Empiric ABX: Only infectious
Common Meds that Cause Systemic Conditions Examine for: Signs of dehydration, malnutrition, etiology suspected and high risk
Watery Diarrhea Hyperthyroidism or DM: Altering motility or intestinal underlying disease, abdominal pain, blood rectal of severe disease
Cholinesterase inhibitors, absorption exam
SSRI, PPI, ARB, NSAID,
Metformin, Allopurinol, Motility Disorders CBC, CMP, TSH, Vitamin A/D, INR, ESR, CRP (C-
Orlistat IBS: MCC in young adults Reactive Protein)
Functional Diarrhea: Abnormal motility and malabsorption IgA Tissue Transglutaminase (IgA-tTG):
w/o pain and no abnormal findings Recommended for signs of malabsorption (Celiac
disease)
Blood or Pus
Inflammatory: Primarily UC & Crohns Stool
Chronic Infection: Persisting bacterial or parasitic infections Cultures
(c. diff, giardia)
49
 Ova & Parasites
Fecal Fat (positive test suggests malabsorption)
Occult Blood
Fecal Leukocytes, Fecal Electrolytes
Fecal Antigen Detection Test (Giardia & E.
Histolytica) and Acid-Fast Staining

Colonoscopy w/ Mucosal Biopsy: Recommended to

rule out IBD and Cancers
EGD: Suspected small intestinal malabsorption
conditions

Traveler’s Diarrhea beginning 2-10
Diarrhea days into travel
Change in climate,
Sanitation standards, Social
conditions
Commonly bacterial
infection: Shigella,
Campylobacter
(inflammatory, bloody
stools), E. Coli
7-10 Stools/day Illness is normally self-limited with resolution in 1-5 Mild
Abdominal cramping days Hydration (maintain)
Nausea +/- Vomiting Bismuth Subsalicylate (pepto
10% symptoms for ≥1 week bismol)
2% symptoms for >1 month *Helps control diarrhea, Slight
antibacterial effect as well,
Majority are benign illness that resolve spontaneously *Helps prevent diarrhea as well
(despite being bacterial) SE: Black/Tarry Stools
Loperamide: Use
symptomatically and judiciously
with strict return precautions
SE: Risk of Toxic megacolon &
Systemic illness

Moderate-Severe (high fever,

bloody stools, worsening pain)
Azithromycin 3 days or
Ciprofloxacin 3-5 days

GI About Associated Sx Diagnostics Treatment

Giardia Lamblia Giardia duodenalis “G. lamblia” “G. intestinalis” Frothy, greasy, foul-smell diarrhea Antigen Assay Rehydration
Protozoan parasite associated with sporadic or (steatorrhea) with No blood/pus, Abdominal
“Beaver Fever” epidemic diarrheal illness cramps, Bloating Stool Exam: ABX: Metronidazole, Tinidazole,
Malabsorption (chronic diarrhea) Trophozoites, Cysts Albendazole, Quinacrine
“Backpackers Etiology: Contaminated water from streams/wells
Diarrhea” Patho: Outbreaks due to contaminated water, food, Children: Furazolidone
fecal-oral transmission
*Beavers are reservoirs

Amebiasis Entamoeba histolytica Most asymptomatic Stool Microscopy O&P Asymptomatic: Paromomycin,
Protozoan parasite MC transmitted by ingestion of *≥3 stools on 3 different Diloxanide, or
cysts from fecally contaminated food and/or water GI: 1-3 week subacute onset: Mild diarrhea days Diiodohydroxyquinoline
to severe dysentery (abdominal pain, diarrhea, Cysts w/ ingested RBC
May also be associated with amebic liver disease bloody stools, mucus in stools, weight loss, Colitis: Metronidazole or Tinidazole
fever) Antigen Testing (ELISA) followed by Paromomycin,
Sensitive, Easy, Rapid Diloxanide, or
Liver Abscess: Fever, RUQ pain, Anorexia Diiodohydroxyquinoline
Stool PCR

50
 Parasitic DNA/RNA in Liver Abscess: Metronidazole or
stool Tinidazole + Paromomycin,
Diloxanide, or
Liver Abscess Diiodohydroxyquinoline followed by
US/CT/MRI Chloroquine
*drainage if no response in 3 days

Diarrhea Drugs MOA CI Adverse Effects

Loperamide (Imodium)
Diphenoxylate (Lomotil)
Schedule V; 1st line
Bismuth
Pepto-Bismol, Maalox, Kaopectate
Ocreotide (Sandostatin)
•Inhibits peristalsis and gut transit
•Opioid receptor agonists (mu receptor gut)
•Reduces secretions, antimicrobial
*can be used in dysentery (fever, bloody)
Inhibits intestinal fluid secretion and stimulates
intestinal absorption*chronic secretory diarrhea
•Bloody or C. diff diarrhea; Pts <2yo
•Loperamide: Acute dysentery or colitis à
toxic megacolon
•Children with viral illness
Caution: DM, thyoid, pancreas, kidney,
liver, arrhythmia
•Constipation, abd cramp, dizzy, CNS
•Serious: paralytic ileus, toxic megacolon
•Black stool, black tongue
•Constipation, Tinnitus
•Cholelthiasis/cholecystitis/biliary tract disease
•Edema, Constipation

Antispasmodics/ Anticholinergics
Hyoscyamine (Levisin)
Dicyclomine (Bentyl)
Phenobarbital, Atropine, Scopalamine
•Relaxes intestinal smooth muscle, inhibits spasms •Toxic megacolon •Ileus, delirium, nervous, palpitations,
and contraction •Inflammatory bowel disease constipation, xerostomia, mydriasis
•anticholingeric à inhibits Ach
*diarrhea associated with IBS (Bentyl)
*can use for bladder spasms (Levsin)

51
GI What is it Causes Symptoms Diagnostic
Constipation Infrequent bowel movements or MCC: Inadequate Fiber/Fluid Intake, Poor Bowel Nausea +/- Vomiting Only if: Considering secondary
Difficult passage of stool Habits Bloated Feeling constipation, Persistent, or RED FLAG
<3 BM/WEEK Intermittent Abdominal Cramping
Primary *"Wave-like" Spasms CBC, CMP, TSH, FIT, FOBT
MC Women No structural abnormalities/systemic disorders Worse Post-Prandial
Frequently idiopathic negatively affecting normal GI track Possible Bowel Incontinence of Water from Colonoscopy: DoC for Red Flags
Primary Slow Colon Transit: Average input-output "Overflow"
Can be serious in extremes of period is 35 hours, can be up to 72 hours Often Flexible Sigmoidoscopy
life (infant, elderly): Aneurysm idiopathic, More commonly in women RED FLAGS
and Encopresis Defecatory Disorders: Impaired coordination of >50 yo with new onset X-Ray Abdomen: Show large stool
musculature during defecation Reports of blood from rectum or in stools burden, doesn't effectively r/o other
Complications Impaired relaxation/paradoxical contraction of anal Weight loss etiologies nor diagnosis
Hemorrhoids sphincter and pelvic floor muscles FamHx Colon Cancer or IBD
Anal fissures CT w/ Contrast: DoC for Undifferentiated
Rectal prolapse Secondary PE abdominal pain w/ constipation
Laxative abuse Complication of another disorder or adverse effect of Mild Abdominal Tenderness
Toxic megacolon a medication Hyperactive bowel sounds progress to Anal Mamometry w/ Balloon Expulsion
Fecal impaction Neurological Disorders hypoactive or absent if constipation Test: Internal pressure & coordination of
May exacerbate cardiac and Myopathies progresses to ileus musculature
cerebral vascular disease Electrolyte Abnormalities +/- Distended abdomen, Palpable mass (often
Medications (Opiates, Anticholinergics, Diuretics, on left side) Rectal Exam Required: Check Defecography: Barium paste put in
CCB, Psychiatric meds) for impacted stool in rectal vault rectum, X-Ray to see shape & position of
Colon Lesions/Cancers: Obstruct passage rectum during poop
RED FLAGS
Signs of systemic disease Radiopaque Markers: Encapsulated
Severe abdominal tenderness, guarding, markers swallowed to determine transit
rebound time by X-Ray
Grossly bloody DRE, +FOBT, or +FIT

Constipation Drugs MOA CI Adverse Effects

Fiber/Bulk Forming Laxatives Fiber promotes intestinal motility by increasing “bulk” of stool Metamucil: Gas & Bloating
1st Line •Draws water into stool (retains water)
Metamucil (psyllium) *problem if not drinking water with fiber then can cause constipation
Citrucil
FiberCon
Benefiber

Stool Softeners Emollient that covers stool and softens it Mineral Oil: Pneumonia if
Ducosate Sodium (colace) Softens stool if straining is required to defecate aspirated
Mineral Oil
Osmotic Laxatives Increases secretion of water into colon via large indigestible molecules in them Lactulose: Cramping, Bloating,
Milk of Magnesia (Mg Hydroxide) Gas
Miralax (Polyethylene Glycol) Effective for chronic constipation
Enulose (Lactulose)
Sorbitol Less bloating than lactulose

52
Stimulant Laxatives Increases ACh regulated GI motility & Alters electrolyte transport in mucosa Cramping
Bisacodyl (Ducolax) Irritates bowels -> Colonic fluid secretion and colon contractions
Senna (Senekot)
Cascara Incomplete response to osmotic laxatives

Rescue or Scheduled intervals, Regular long term use leads to dependency

Onset: 6-12 hours

Enemas In conjunction with digital decompaction

Tap Water
Sodium Phosphate Onset: 5-15 min
Mineral Oil

53
GI
Acute Acinar cell injury -> Intracellular activation Epigastric Pain: Acute Persistent Severe DX: 2/3 Assessment of Severity: Ransons
Pancreatitis of pancreatic enzymes -> Autodigestion Boring, Radiates to back Acute Persistent Severe Epigastric Pain
Worsens: Supine, Eating High Amylase or Lipase Supportive: Rest the Pancreas,
Etiology Alleviates: Sitting, Leaning forward, Fetal pos. Findings on CT/US/MRI NPO, Post-pyloric feeding, High
Gallstone (MCC) volume IV Lactated Ringer’s,
EtOH (2nd MCC, Most severe cause) N/V, Fever All 3 Met = 98% Benign Analgesia
Meds: Thiazides, PI, Estrogen, Didanosine, No Rebound Tenderness *90% recover in 3-7 days
Exenatide, Valproic acid Severe: Shock, Dehydration Normal HCT
Iatrogenic (ERCP), Malignancy, Scorpion Normal Creatinine Gallstone: ERCP
sting, Idiopathic, Trauma, CF, PE: Epigastric tenderness, Tachycardia,
Hypertriglyceridemia, Hypercalcemia, Decreased bowel sounds may be seen secondary Amylase & Lipase: Best initial tests Severe: Broad ABX (Imipenem)
Infection, Mumps (children) to adynamic ileus. *Lipase more specific *not routine
Cullen’s Sign: Periumbilical ecchymosis *Levels do not reflect severity
Grey Turner’s Sign: Flank ecchymosis
ALT
3 fold increase: Suggestive of gallstone

Hypocalcemia, Leukocytosis
Elevated: Glucose, Bilirubin,
Triglycerides

CT: Diagnostic IoC

*alternative: MRI

US
Assess for gallstone, bile duct dilation

X-Ray
Sentinel Loop (localized ileus)
Colon Cut Off (abrupt collapse of colon
near the pancreas)
Severe: Left sided exudative pleural
effusion

MRCP
Stones, Stricture, Tumor

Chronic Chronic inflammation -> Progressive loss of
Pancreatitis endocrine & exocrine function
Etiology
EtOH Abuse (MCC), Idiopathic,
Hypocalcemia, Hyperlipidemia, Islet cell
tumor, Familial, Trauma, Iatrogenic
*gallstones not as significant as acute
Tetrad: Abdominal pain, Weight loss, Amylase & Lipase: Normal (slightly
Steatorrhea, DM elevated)
Calcifications
Epigastric/Back pain may be atypical or absent Pancreatic Function Test
Fecal elastase Most sensitive & specific
X-Ray/CT: Calcification
MRCP/ERCP
EtOH abstinence, Pain control, Low
fat diet small meals, Vitamin
supplementation, PPI/H2RA
Oral Pancreatic Enzyme
Replacement
Refractory: Pancreatectomy

54
Pancreatic Walled off collection of pancreatic fluid
Pseudocyst Typically 4 weeks after infection/trauma
Acute vs Chronic
Acute: Resolves spontaneously in ~4-6
weeks
Chronic: Present for >6 weeks
GI About/Causes
Jaundice Most obvious sign/symptom of liver
dysfunction
Yellowing of skin due to bilirubin
deposition
Scleral Icterus: Yellowing eyes
Dark Skinned: Mucous membranes
(yellowing hard palate, sublingual area)
Livers ability to process bilirubin: Sign
of overall health and functional state
Classify liver dysfunction: Pre-hepatic,
Hepatic, Post-hepatic
Unconjugated: Indirect bilirubin
Conjugated: Direct bilirubin
Total Bilirubin: Direct + Indirect
(increase seen in all forms of jaundice)
Nonalcoholic Extremely common cause of mildly
Fatty Liver abnormal LFT
Disease
(NAFLD) Etiology: Obesity, Hyperlipidemia,
Glucocorticoid use, DM
Early satiety Amylase Surgical Indications
Persistent elevation Complications: Hemorrhage, Leak,
Infection, Persistent symptoms
Surgical Technique
Percutaneous: Aspiration then tube
drainage
Internal: Cystogastrostomy (drain)
Clinical Presentation Diagnostics Treatment
Pre-Hepatic Hepatic Post-Hepatic
Increased unconjugated bilirubin Increased unconjugated & conjugated Increased conjugated bilirubin
bilirubin
More bilirubin being produced than Can uptake & process unconjugated bilirubin but
liver can process Cant conjugate normal levels of bilirubin CANT excrete from body
RBC destruction due to liver dysfunction MC seen in obstructive disorders within biliary system,
Cant process conjugated bilirubin out of also liver dysfunction Blocking bile ducts from
Urobilinogen: Normal/Increased liver due to liver dysfunction excreting conjugated bilirubin into small intestines
Urine: Normal Building up levels of conjugated bilirubin in vascular
Stool: Normal Urobilinogen: Decreased system bc cant get rid of it fast enough
Alk Phos: Normal Urine: Dark
AST/ALT: Normal Stool: Normal Urobilinogen: Decreased/None
Alk Phos: Normal/Increased Urine: Dark
MC Hemolytic anemia AST/ALT: Increased Stool: Pale (acholic)
Hereditary disorders of conjugation Alk Phos: Increased
(Gilbert syndrome) Hepatitis AST/ALT: Increased
Alcoholic Liver Disease
Cirrhosis (liver failure) *Alk phos + ALT/AST increased = Obstructive pattern
Liver mass *Just AST/ALT increased = Damage to liver
MC: Biliary obstruction (choledocholithiasis,
cholangitis, cholecystitis, gallbladder obstruction)
Hepatitis
Biliary Neoplasm/Mass/Disease
Nonalcoholic Fatty Liver (NAFL) AST/ALT: Mildly elevated, Ratio <1 Exclude more serious causes of liver disease
Relatively benign
No: Fibrosis or Malignancy CT: 1st Correct underlying causes
Nonalcoholic Steatohepatitis Biopsy: Most accurate
(NASH) Microvesicular fatty deposits similar to
Associated with inflammation & alcoholic liver disease without history of
fibrosis and the potential to progress heavy alcohol consumption
to cirrhosis, potentially
premalignant
55
GI About/Causes
Hepatitis A Intubation: 30 days
(HAV) HAV: Present in feces 2 weeks
before clinical illness
No chronic carrier state
Low mortality
Transmission: Fecal-Oral
*similar to HEV
RF
Fecally contaminated
food/water, International travel,
Crowding, Poor sanitation
Clinical Presentation
Fever, Fatigue, Loss of appetite
N/V/D/Constipation
RUQ abdominal pain, Muscle aches, Joint
pain
Jaundice (coincides with improvement of
fever)
Distaste for smoking
+/-: White (acholic) stools
PE: Hepatomegaly, Dark urine
Diagnostics
WBC: Normal-Low (±large atypical lymphocytes)
ALT & AST: Markedly elevated early in disease
Bilirubin & ALP: Elevate as disease progresses
Urine: Mild Proteinuria & Bilirubinuria (often precedes
jaundice)
Acute: Anti-HAV IgM, HAV Virus, +/- Anti-HAV IgG
Prior Vaccination/Infection: Anti-HAV IgG
Not Infected/Vaccinated: None
Treatment/Prevention
Supportive: Rest, No hepatotoxins
Encephalopathy/Coagulopathy
Hospitalization ± Liver Transplant
*Indicates acute liver failure and
fulminant disease
Prognosis
Most clinically recover within 3 months
Fulminant Hep A uncommon unless
concurrent chronic Hep C

Hepatitis B Incubation: 6 weeks - 6 months
(HBV) *average 12-14 weeks
1-2% with acute HBV end up
developing chronic HBV
Transmission: Blood, Sex
*Present in blood, saliva, semen,
vaginal secretion
*Mothers to infant in delivery
RF
Sex, IVDU, Healthcare workers
*Half with HBV have been
incarcerated or had another STD
Can present on spectrum: Asymptomatic WBC: Normal to Low Supportive: Rest
to Viral syndrome or Severe systemic
illness AST & ALT: Markedly elevated Encephalopathy/Coagulopathy
*Higher than HAV Hospitalization
Fever, Fatigue, Loss of appetite *Indicates acute liver failure and
Nausea PT (INR): If prolonged associated with increased fulminant disease
RUQ pain mortality
Severe (Elevated INR, Jaundice >4
Jaundice Anti-HBe: Antibody to e-antigen. Differentiates early weeks, Acute LF)
from diminishing or sub-acute infection Tenofovir or Entecavir
PE: Hepatomegaly *Monotherapy is acceptable
Early Acute: HBsAg *D/C once HBsAg negative in 2 tests, 4
Acute: Anti-HBc IgM, HBsAg weeks apart
Resolved Acute: Anti-HBc IgG, Anti-HBs
Chronic: Anti-HBc IgG, HBsAg Prognosis
No Infection, Prior Vaccination: Anti-HBs Most Fully Recover: 3-6 months
No Infection or Vaccination: None Lab abnormalities may linger longer
than clinical symptoms
Elevation of liver enzymes >6 months
indicates transition to chronic hepatitis
*1-2% Healthy Adults and Majority of
Infants or Immunosuppressed

56
Chronic Move From Acute to Chronic
Hepatitis B Elevated AST/ALT: >6 months
HBsAg >6 months
Hepatitis C Incubation: 6-7 weeks
(HCV)
Chronic HCV develops in 85%
with acute infection
Transmission: Blood
IVDU (50% cases), Body
piercings, Tattoos, Hemodialysis,
Incarceration
HIV (30% coinfected with HCV)
Chronic 85% with Acute HCV develop
Hepatitis C Chronic HCV
Increased Risk of Progression to
Cirrhosis:
Men, Heavy EtOH & TOB, Acute
HCV <40 yo, Concurrent steatosis
(fatty liver)
Coffee consumption appears to
slow progression (association)
Hepatitis D Only in association with
(HDV) acute/chronic HBV
HDV & HBV
Have to go together
Chronic HBV + Acute HDV =
Fulminant Hepatitis with rapid
progression to cirrhosis
Often Asymptomatic
+/- Generalized viral syndrome, Jaundice,
Abdominal pain
PR: RUQ tenderness, ± Hepatomegaly
Prognosis: 5 year mortality rate: Sometimes Immediate antiviral therapy,
0-2%: Without cirrhosis but Treatment may be deferred with
14-20%: Compensated cirrhosis careful monitoring
70-86%: Decompensated cirrhosis (cirrhosis with lab
changes, organ dysfunction) Decision based on
Cirrhosis, ALT & HBV levels
Complications
Cirrhosis, Liver failure, HCC (Hepatocellular carcinoma) Pegylated Interferon (PegIFN) or
Entecavir or Tenofovir
ALT & AST: Elevated Genotype Testing of Virus: Antiviral
*CDC Diagnostic Criteria: ALT 7X ULN selection
HCV Ab EIA: Screening Prognosis
*Even if Anti-HCV(+): Not protective (no immunity) >1/2 with Acute HCV will be
*Shows: Current infection or Previous infection (not chronically infected, good success rates
present very early in infection)
Screening
HCV RNA Assay: Confirmatory IVDU, Long-term hemodialysis,
*HCV RNA PCR: If EIA(+) (eliminate false positive) Chronic liver disease, HIV
Recovery from previous HCV infection One Time Screening: Adults born 1945-
(+)HCV Ab and (-)HCV RNA 1965
AST/ALT: Normal 40% cases Genotype Testing of Virus: Antiviral
*Likely mild disease with slow/absent progression selection
HCV Ab EIA: Screening
HCV RNA Assay: Confirmatory
57
 Primarily seen: Immigrants from
Africa, Asia, Eastern Europe,
Brazil
Increased Risk: HCC
(Hepatocellular carcinoma)
Hepatitis E Uncommon in USA
Found in: Asia, ME, North Africa
Transmission: Fecal-Oral
*Similar to HAV
Also: Blood, Perinatal
Self-limited (15-60 days)
GI About/Causes
Cirrhosis Mostly Irreversible liver fibrosis with
nodular regeneration
Patho
Nodules -> Increased portal pressure
Macronodules associated risk HCC
Etiology
Chronic Hep C (MCC)
EtOH, Chronic HBV/HDV, NASH
(obesity, DM, hypertriglyceridemia),
Hemochromatosis autoimmune hepatitis,
Primary biliary cirrhosis, Primary
sclerosing cholangitis, Drug toxicity
Staging Child-Pugh Classification
Cirrhosis Class A: 5-6: 1 yr (100%), 2 yr (85%)
Class B: 7-9: 1 yr (81%), 2 yr (57%)
Class C: ≥10: 1 yr (45%), 2 yr (35%)
Spontaneous Complication of Cirrhosis
Bacterial Infection of ascitic fluid without
Peritonitis perforation of bowel
MCC: E. coli, also s. pneumonia,
anaerobes (rare)
Clinical Presentation
General: Fatigue, Weakness, Weight
loss, Anorexia, Cramps
Insidious Onset
PE: Ascites, Hepatosplenomegaly,
Gynecomastia, Spider angioma,
Telangiectasis, Caput medusa, Muscle
wasting, Bleeding, Palmar erythema,
Jaundice, Dupuytren’s contractures
(pinky & ring stuck flexed)
Hepatic Encephalopathy: Confusion,
Lethargy (elevated ammonia)
PE: Asterixis (flapping tremor w/ wrist
extension), Fetor hepaticus (musky
breath), Esophageal varices
1 Point
Total Bilirubin: <2
Serum Albumin: >3.5
PT INR: <1.7
Ascites: None
Hepatic Encephalopathy: None
Fever, Chills, Abdominal pain,
Increasing abdominal girth, Diarrhea
PE: Ascites (shifting dullness, fluid
wave), Abdominal tenderness
Diagnostics
WNL in compensated cirrhosis
Leukopenia, Thrombocytopenia
AST/ALT: Elevated (normalize
in end stage)
ALP: Increases as nodules begin
to obstruct ducts within liver
GGT: Elevated
Bilirubin: Elevated
Albumin: Decreased
PT/INR: Prolonged Macrocytic
Anemia
Abdominal U/S: Initial
2 Points
Total Bilirubin: 2-3
Serum Albumin: 2.8-3.5
PT INR: 1.71-2.30
Ascites: Mild
Hepatic Encephalopathy: Grade
1-2 or Suppressed with meds
Paracentesis: DoC
*SAAG >1.1: Portal
hypertension
*Cell count ≥250 (determines tx)
Treatment
Liver Transplant: Curative
Treat etiologies/complications, Avoid EtOH &
hepatotoxic meds, Weight reduction, HBV, HAV, Flu,
Pneumococcal
Encephalopathy: Lactulose, Rifaximin, Metronidazole
*Restrict proteins, reduce NH3 producing bacteria
*Lactulose ADR: Diarrhea, Flatulence, Bloating
Ascites: Spironolactone, Furosemide, Paracentesis
*Restrict sodium
Pruritis: Cholestyramine
HCC Surveillance: US Every 6 Months ± AFP
SBP (spontaneous bacterial peritonitis
Complications: ESRD, HCC, Esophageal varices
3 Points
Total Bilirubin: >3
Serum Albumin: <2.8
PT INR: >2.30
Ascites: Moderate-Severe
Hepatic Encephalopathy: Grade 3-4 or Refractory
Cefotaxime or Ceftriaxone
Prophylaxis After Initial Occurrence: Lifelong Bactrim
*frequently occurs: Norfloxacin
58

Hepatorenal Complication of Cirrhosis
Syndrome Azotemia in absence of intrinsic renal
disease
Occurs in 10% with advanced cirrhosis
and ascites
Types
Type 1: Sudden doubling of Cr >2.5
Type 2: Slowly progressive
Patho
Portal Hypertension ->
Congestion of blood in portal vein ->
Blood backs up to GI tract ->
Splanchnic vasodilation (offload) ->
Body thinks that we dont have enough
circulatory volume (bc blood vessel
dilation) ->
Activate RAAS increase blood volume -
>
Body holds onto more sodium -> Ascites
Renal vasoconstriction -> BP up ->
Hepatorenal syndrome
Esophageal Complication of Cirrhosis
Varices
Dilated blood vessels develop from
Liver portal hypertension in attempt to
bypass congestion with collateral blood
flow
RF: Cirrhosis (50% have), Hepatitis,
EtOH
Portal Complication of Cirrhosis
Hypertension
Patho
Liver fibrosis & scarring (cirrhosis) ->
Increased vascular resistance &
intravascular pressure in liver ->
Blood has harder time moving thru the
liver from GI tract ->
Collateral vessel (anastomoses) develops
around liver bypassing the liver's
detoxification function
Kidney injury or Worsening chronic
kidney dysfunction
Precipitated by acute decrease CO
Asymptomatic until they bleed
LE swelling, Abdominal distention,
Jaundice, Easy bruising, Hemorrhoids
PE: Peripheral edema, Ascites,
Splenomegaly, Jaundice, Spider nevi
Sites of Collateral Circulation:
Distal 1/3 esophagus
Umbilical region
Rectum
Retroperitoneal space
Outside surface of liver
Culture: Most accurate test
Gram Stain: Often negative
BUN/C: Increased,
Hyponatremia,
Oliguria
EGD: Diagnostic & treatment
*all cirrhosis patients should get,
screen at diagnosis
Complications:
Portosystemic shunting of blood:
Anastomoses: Caput medusae,
Hemorrhoid, Esophageal
varices
Shunting of blood with toxins
from intestines around liver:
Ammonia: Hepatic
encephalopathy
D/C Diuretics (stop loss of fluids)
IV Albumin Infusion: For volume expansion
*pull extravascular fluid back into blood vessels)
7-14 days Peripheral Vasoconstriction
*Increase blood pressure to help profuse kidneys
Non-Bleeding Esophageal Varices:
Non-Selective Beta-Blocker: Prevent 1st bleed
EVL (endoscopic varicocele ligation)
TIPS (trans venous intrahepatic portosystemic shunts)
Bleeding Esophageal Varices:
Airway Management
Hemorrhage Control: Balloon Tube Tamponade
ABX Prophylaxis: Ceftriaxone
Octreotide or Somatostatin: Reduce blood to liver
Omeprazole: Prevent worsening variceal irritation
Anti-Emetic
Emergent EGD: Definitive Treatment (stabilize first)
59
 Increased pressure in peritoneal
capillaries: Increased hydrostatic
pressure: Ascites

Splenomegaly: Anemia,
Leukopenia,
Thrombocytopenia

GI
Irritable Bowel Chronic, functional idiopathic pain, with NO Abdominal pain with altered Diagnosis of Exclusion 1st: Lifestyle, Diet (Low fat, High fiber,
Syndrome organic cause defecation/bowel habits *After: Colonoscopy, Abdominal CT Unprocessed food), Sleep, Smoking
(IBS) Pain relieved with defecation cessation, Exercise
Onset: MC late teens, early 20s Rome IV Criteria:
MC in women Alarming Recurrent abdominal pain Avoid: Sorbitol, Fructose, Gas producing
GI bleeding: Occult, Anemia ≥1 DAY/WEEK for 3 MONTHS food
Patho Anorexia, Weight loss, Fever, AND 2/3
Abnormal Motility: Chemical imbalance in Nocturnal sx Relieved with defecation Diarrhea: Loperamide, Eluxadoline,
intestine (Serotonin & Ach) -> Abnormal motility FamHx GI cancer Change in stool frequency Rifaximin, Bile acid sequestrants,
& spasm -> Abdominal pain. Altered gut microbe IBD or Celiac Change in stool form (appearance) Alosetron. Anticholinergics (Dicyclomine,
Visceral Hypersensitivity: Lower pain threshold Diarrhea -> Dehydration Hyoscyamine)
to abdominal distention Severe constipation or impaction
Psychosocial: Altered CNS Onset >45 yo Constipation: Prokinetics (Fiber,
Psyllium), Polyethylene glycol (can be
added after fiber), Bulk forming or saline
laxatives.
*Lubiprostone & Linaclotide: Reserved
for those with no response

GI
Acute Gastritis Superficial Inflammation/irritation of stomach MC Asymptomatic EGD w/ Biopsy: DoC Similar to PUD
mucosa Thick, edematous erosion <0.5cm H. pylori Triple Therapy: PPI +
If symptomatic (similar to PUD): Dyspepsia, N/V Clarithromycin + Amoxicillin
Gastropathy: Mucosal injury without evidence H. pylori: Urea breath test, Stool, *test for eradication >4 weeks after
of inflammation Serologic antibodies *symptoms improve 7-14 days
Breath test & Fecal: Require D/C:
Patho PPI 7-14 days, Abx 28 days (False
Imbalance between aggressive & protective negative)
mechanisms of gastric mucosa

Etiology
H pylori (MCC), NSAID & ASA (2nd MCC),
Acute stress in critically ill, Heacy EtOH, Bile
salt reflux, Meds, Radiation, Trauma,
Corrosives, Ischemia, Pernicious anemia,
Portal HTN

Erosive: NSAIDs, alcohol, stress

Non-erosive: H. pylori (MCC), systemic

60
Peptic Ulcer Gastric erosions >0.5cm
Disease MCC of: UGI Bleed
Types
Duodenal (MC): Almost always benign
MC: Duodenal bulb
MC: Younger (30-55 yo)
Damaging: H. pylori, HCl, Pepsin
Better with meals
Worse 2-5 hours after meals
Gastric: 4% gastric adenocarcinoma
MC: Antrum stomach
MC: Older (55-70 yo)
Damaging: NSAID, Decreased mucus, bicarb,
prostaglandins
Worse with meals (esp 1-2 hours after)
Other Etiology
Zollinger-Ellison syndrome: Gastrin producing
tumor (1% PUD)
EtOH, Smoking, Stress, Cancer, Male, Old,
Steroids, Gastric cancer
GI
GERD Reflux of gastric contents into the esophagus
due to incompetent LES
Transient relaxation of LES -> Gastric acid
reflux -> Esophageal mucosal injury
Complications: May present with alarm sx
Esophagitis: Inflammation from acid
Stricture: Narrowing from acidic damage
Barrett’s Esophagitis: Esophageal squamous
epithelium replaced by precancerous
metastatic columnar cells from the cardia of
the stomach
Esophageal Adenocarcinoma: From Barrett’s
Barrett’s Esophageal squamous epithelium replaced
Esophagus by precancerous metastatic columnar cells
from the cardia of the stomach
Complication of longstanding GERD
Esophagitis Etiology
Dyspepsia (burning, gnawing, epigastric pain) EGD w/ Biopsy: DoC *GOLD H Pylori Positive
N/V *all gastric ulcers need repeat EGD H. pylori Triple Therapy: PPI +
to document healing even if Clarithromycin + Amoxicillin
Duodenal: Post-prandial Relief, Nocturnal sx asymptomatic *test for eradication >4 weeks after
*symptoms improve 7-14 days
Gastric: Post-prandial Exacerbation (1-2 hr), H. Pylori
Weight loss EGD w/ Biopsy: DoC *GOLD Bismuth Quadruple Therapy:
Urea breath test, Stool, Serologic Bismuth subsalicylate + Tetracycline
Bleeding: Hematemesis, Melena, Hematochezia antibodies + Metronidazole + PPI
Perforated: Sudden onset severe abdominal pain *Breath test & Fecal: Require D/C: *14 days
(may radiate to shoulder), Peritonitis: Rebound PPI 7-14 days, Abx 28 days (False
tenderness, Guarding, Rigidity negative) Concomitant Therapy:
Clarithromycin + Amoxicillin +
Metronidazole +PPI
*10-14 days
H Pylori Negative
Omeprazole (PPI), Ranitidine (H2
blocker), Misoprostol, Antacids,
Bismuth compound, Sucralfate
Refractory: Parietal cell vagotomy
Bilroth II (associated with Dumping
syndrome)
Typical: Heartburn (pyrosis): Often Dx Typical Lifestyle: Elevate head of bed, Don’t lie down
retrosternal & postprandial Clinical Dx: Hx + Classic sx for 3 hours after eating, Avoid food that delays
Relieves: Antacids 24 Hour Ambulatory pH gastric emptying (fatty, spicy, chocolate,
Worsens: Supine Monitoring: Confirmatory peppermint, caffeine), Smoking cessation,
Regurgitation: Water brash, Sour taste, Esophageal Manometry: Decreased EtOH, Weight loss
Cough, Sore throat Decreased LES pressure
Stage 2 (Intermittent/Mild): <2 episodes/week
Atypical: Hoarseness, Aspiration pneumonia, Dx Malignancy/Alarm/>5 Years PRN Antacids, H2RA
Wheezing, Chest pain EGD
Stage 3 (Moderate-Severe): ≥2 episodes/week
Alarming: Dysphagia, Odynophagia, Weight PPI
loss, Bleeding
Refractory: Nissen Fundoplication
EGD w/ Biopsy Barrett’s No Dysplasia: PPI, Rescope q 3-5 YR
*Metaplasia only
Low Grade Dysplasia: PPI, Rescope q 6-12 MO
High Grade Dysplasia: Ablation w/ EGD,
Photodynamic therapy, Endoscopic mucosal
resection, Radiofrequency ablation
3 Classics EGD: Direct visualization Treat underlying cause
61
 GERD (MCC) Odynophagia (HALLMARK)
Infectious: Candida (MCC), CMV, HSV Dysphagia Candidal: Fluconazole, Voriconazole,
Eosinophilic: Allergic reaction Retrosternal Chest Pain Caspofungin
Pill-Induced: Bisphosphonate, Beta-Blocker, CMV: Gangciclovir, Valgangciclovir, Foscarnet
CCB, NSAID HSV: Acyclovir, Foscarnet
Caustic (Corrosive): Acidic or Basic

Infectious Immunocompromised Odynophagia (HALLMARK) EGD Candida: 1st PO Fluconazole, 2nd Voriconazole
Esophagitis Dysphagia Candida: Linear yellow-white
Candida MCC Retrosternal Chest Pain plaques CMV: 1st Ganciclovir, 2nd Valganciclovir
CMV: Large superficial shallow
ulcers HSV: 1st Acyclovir, 2nd Foscarnet
HSV: Small, deep ulcers

Eosinophilic Allergic, inflammatory eosinophilic
Esophagitis infiltration of the esophageal epithelium
MC: Children, Atopic (Asthma, Eczema)
Odynophagia, Dysphagia (esp solids)
Children: Reflux/Feeding difficulties
EGD
Normal or multiple corrugated
rings, White exudates
Biopsy
Abundance of eosinophils
Remove foods that incite allergic response
PPI: May be needed in some
Inhaled Corticosteroids Without Spacer

Pill-Induced Esophagitis due to prolonged pill contact Odynophagia, Dysphagia EGD Take pills with at least 4 ounces of water
Esophagitis Small, well-defined ulcers of
Meds: NSAID, Bisphosphonates, BB, CCB, varying depths Avoid recumbency at least 30-60 min after
KCl, Iron, Vitamin C

Caustic Ingestion of corrosive alkali or acid Odynophagia, Dysphagia EGD Supportive: Pain meds, IVF
Esophagitis Hematemesis Determine extent & Look for
Dyspnea complications: Perforation,
Stricture, Fistula

Hiatal Herniation of structures thru esophageal hiatus Usually asymptomatic CXR: Possible air fluid level Type I: Manage GERD: PPI, Weight loss
Hernia of diaphragm
± Epigastric/Substernal pain, Early satiety, UGI: Usually definitive Type II-IV: Surgical repair
Type I: Sliding (MC) Postprandial fullness, Retching, Nausea *Linx Device: Prevents GERD
GE junction slides into mediastinum EGD: Normally difficult *Nissen Fundoplication: Cannot vomit
(increased reflux)

Type II-IV: Rolling “Paraesophageal”

Fundus protrudes thru diaphragm with GE
junction remain in place

62
Disease About Clinical Manifestation Physical Exam Diagnosis and Treatment
Colon Polyps Adenomatous: MC neoplastic polyp Hamartomatous Pseudopolyps/Inflammatory Hyperplastic: MC non-neoplastic polyp
10-20 years before they become cancerous Due to IBD (CD/UC) Type of serrated polyps (saw tooth)
(esp >1cm) Juvenile: MC in childhood Not considered cancerous Low risk
Solitary ≠ Increased risk
Tubular Adenoma: Nonpedunculated (MC)
Least risk Juvenile Polyposis Syndrome:
Autosomal dominant
Tubulovillous Adenoma: Mixture. Multiple Hamartomatous polyps
Intermediate risk Increased risk colorectal & gastric CA

Villous Adenoma: Tends to be sessile Peutz-Jeghers

Highest risk Associated with Peutz-Jeghers
syndrome (STK11 mutation). Usually
benign but may undergo malignant
transformation
Usually resected

Colorectal Most arise from Adenomatous polyps Iron Deficiency Anemia: Fatigue, Colonoscopy w/ Biopsy: Diagnostic Localized: Surgical Resection, then
Cancer MCC of large bowel obstruction in adults Weakness Adjuvant Chemo
MCC of occult GI bleeding in adults Barium Enema *radical/endoscopic
Rectal bleeding, Abdominal pain, Apple core lesion (filling defect)
RF Change in bowel habits *needs FU Colonoscopy or CT METS: Palliative Chemo
Age >50 (peaks 65), AA, FamHx
IBD: UC > CD, 8-20 years since diagnosis Advanced: Ascites, Abdominal masses, CBC: IDA
Lifestyle: Diet (low fiber, high red/processed Hepatomegaly
meat, animal fat), Obesity, TOB, EtOH CEA
Proximal (Right Side) Tumor marker used for follow up
Protective Factors Chronic occult bleeding (IDA &
Physical activity, Regular ASA use, NSAID (+)FOBT), Diarrhea

Familial Adenomatous Polyposis Distal (Left Side)

Genetic mutation of APC gene Presents later
Adenomas begin in childhood, almost all will Bowel obstruction, Changes in stool
develop colon CA by 45 yo. diameter
Prophylactic colectomy May develop S. bovis endocarditis

Turcot Syndrome
FAP-like syndrome + CNS tumors

Lynch Syndrome (Hereditary Nonpolyposis

Colorectal Cancer)
Autosomal dominant
Loss of function in DNA mismatch repair
genes (MLH1, MSH2/6, PMS3)
40% risk of colon cancer
*Type 1: Esp on right side
*Type 2: Increased risk of extra-colonic
cancers: Endometrial (esp), Ovarian, Small

63
 intestine, Brain, Skin. Mean age 40s but can
develop in 20s

Peutz-Jeghers Syndrome
Autosomal dominant
Associated with Hamartomatous polyps,
mucocutaneous hyperpigmentation, risk of
breast & pancreatic cancer

GI
Inflammatory Crohn’s & Ulcerative Colitis Extra-Intestinal Manifestations: CD or UC
Bowel Disease Rheumatologic: MSK pain, Arthritis,
(IBD) RF Ankylosing spondylitis, Osteoporosis
Jew (esp Ashkenazi), White
Onset: 15-35 yo. UC M > F, CD F > M Derm: Erythema nodosum, Pyoderma
10-30% have 1st degree relative with IBD gangrenosum
Smoking (CD), may be protective in UC
Western style diet Ocular: Conjunctivitis, Anterior uveitis/iritis
Infections (alterations gut microbes) (ocular pain, HA, blurred vision), Episcleritis
Meds: NSAID, OCP, HRT (mild ocular burning)

Hepatobiliary: Fatty liver, Primary sclerosing

cholangitis

Hematologic: B12 & Fe deficiency (esp CD),

Increased risk thromboembolism

Crohn’s Idiopathic autoimmune inflammatory Ileocolitis (MC) Upper GI Series: Initial DoC Limited Ileocolonic
Disease bowel disease Crampy RLQ abdominal pain String Sign (barium flowing thru narrowed Oral Mesalamine (5-ASA), Oral
Diarrhea (no gross blood) inflamed/scarred areas), Fistula formation Glucocorticoids
Any segment of GI tract (mouth-anus) Weight loss, Fever
MC: Terminal ileum (ileocolitis) EGD Ileal & Proximal Colon
Rectum is often spared Jejunoileitis Segmental “Skip Areas”, Cobblestone, Glucocorticoids (EC
Malabsorption (iron & B12 deficiency) Aphthous ulcerations, Strictures Budesonide, Prednisone)
Transmural Steatorrhea
Nutritional & Electrolyte deficiencies Biopsy Severe/Refractory
Complications Transmural inflammation, Microscopic skip Azathioprine, 6-Mercatopurine,
Perianal: Fistulas, Strictures, Abscesses, Colitis & Perianal areas, Noncaseating granulomas, Creeping fat MTX, Anti-TNF (Adalimumab,
Granulomas Diarrhea, Abscess, Fistula, Fissure, on gross dissection (pathognomonic) Infliximab)
Malabsorption: Fe & B12 Deficiency Obstruction
ASCA (Anti-Saccharomyces Cerevisisae
Antibodies)
Iron & B12 Deficiencies
Severe: Increased ESR & CRP

Ulcerative Limited to colon Bloody diarrhea, Crampy LLQ abdominal Flexible Sigmoidoscopy Mild-Moderate Distal
Colitis Begins in rectum with proximal spread pain, Tenesmus Topical 5-ASA
64
*Rectum always involved
Mucosa & Submucosa only
Smoking decreases risk for UC
Complications
Primary sclerosing cholangitis, Colon
cancer, Toxic megacolon (more common
UC)
Nonspecific: Pseudopolyps, Uniform erythema ± Topical Corticosteroid, Oral 5-
Mild: ≤4 BM/day & Ulceration (friable, mucosa, continuous, ASA
No signs of systemic toxicity circumferential pattern)
± Constipation & Mild abdominal pain Diffuse & Contiguous rectal involvement Mild-Moderate Pancolitis
Topical 5-ASA + Oral 5-ASA +
Moderate: >4 BM/day Biopsy Steroids
Abdominal pain Nonspecific: Crypt abscesses & atrophy,
± Anemic Inflammation, Basal plasmacytosis Severe
Oral Glucocorticoid + Topical
Severe: ≥6 BM/day Barium Enema 5-ASA + Oral 5-ASA (high) +
Severe abdominal pain, Systemic toxicity Stovepipe or Lead Pipe Sign (cylindrical bowel Steroids
(fever, anemia, elevated ESR & CRP) with loss of haustral markings)
± Weight loss Fulminant Colitis
(+)P-ANCA, Increased: ESR, CRP, IV Glucocorticoids, IVF, Broad
Leukocytosis, Anemia of chronic disease ABX
Fecal Lactoferrin & Calprotectin: Sensitive for Some Cases: Surgical Resection
acute inflammation *Curative
65
IBD Pharmacotherapy Indication MOA Side Effects/Adverse Events/ BBW Notes
Aminosalicylates Induction and maintenance therapy Inhibits prostaglandin •N/V, HA, hypersensitivity *must exert effect directly to colon
(5-ASA) of UC and CD production, producing anti- •CI: sulfa or ASA allergy
Sulfasalazine** inflammatory effects
Mesalamine
Corticosteroids Most effective to induce remission *Can use Budesonide (Entrocort) for
(Prednisone in severe flare maint. crohns disease for ~3mo
40-60mg daily) *acute flare -> CD and UC
Immunomodulators/ •Steroid dependent CD and UC Leukopenia, thrompoenia, anemia
Immunosuppressants Remission maintenance in mild- Infection, N/V/D
Azathioprine (Imuran) severe disease Malaise, arthralgia
6-Meracaptopurine Adverse: lymphoma, severe
(Pruinethol) (6-MP)
BBW mutagenic potential, rapid growth, CA

Immunomodulators/ Methotrexate: Cyclosporine: Cyclosprine SE: *must put on folic acid if taking
Immunosuppressants •Mild-moderate active C and •Severe UC/CD refractory to •Multiple serious adverse effects to Methotrexate
Methotrexate maintenance *NOT IN CD steroids
Cycosporine
Antitumor Necrosis TREATMENT OF CHOICE for Inhibits TNF (which promotes •Fever, rigors, N/V, myalgia, urticarial,
Factor Antibodies someone with crohns disease and a inflammation) hypotension
Infliximab (Remicade) fistula
Adalimumab (Humira) •Mod-severe active CD and UC BBW severe infection/sepsis, malignancy
Certolizumab (Cimzia) maintenance

66
GI
Anal Fissure Linear tears in distal anal canal Severe rectal pain & BM PE: Longitudinal tear (not past >80% Resolve spontaneously
MC: Posterior midline Refrain from defecating dentate line) 1st Line: Supportive: Sitz bath,
Bright red blood Chronic: Skin tags Analgesics, Fiber, Increase H2O, Stool
Etiology: Low fiber, Large hard stool, constipation, softeners, Laxatives, Mineral oil
anal trauma
2nd Line: Nitroglycerin (ADR HA,
dizziness), Nifedipine ointment
Botox

Refractory: Lateral Internal

Sphincterotomy

Hemorrhoids Engorged venous plexus
Internal: Proximal to dentate line
Originate from superior hemorrhoid vein
Tend to bleed, Usually painless
1) No prolapse, confined in anal canal
2) Prolapse w/ strain, spontaneously reduce
3) Prolapse w/ strain requires manual
reduction
4) Irreducible may strangulate
External: Distal to dentate line
Originate from inferior hemorrhoid vein
Usually don’t bleed, Tend to be painful
Internal
Intermittent bleeding (MC)
Painless hematochezia
±Rectal itching, fullness, mucus D/C
•Prolapse
Usually not tender/palpable (unless
thrombosed), Rectal pain suggests
complication
External
Perianal pain aggravated w/ BM
±Tender palpable mass, Skin tags
Inspect, DRE, FOBT
Anoscopy (for internal)
*allows direct visualization
Conservative: High fiber, Increase fluids,
Sitz bath, Topical rectal corticosteroids,
Lidocaine (may be used for pruritis,
discomfort, or thrombosis
Fail/Debilitating/Strangulation: Rubber
band ligation (MC), Sclerotherapy,
Infrared coagulation
± Excision of thrombosed external
hemorrhoids
Internal IV/Fail Above/Surgery for
External: Hemorrhoidectomy

RF: Increased Venous Pressure (Strain BM,

Constipation, Pregnant, Obese, Prolonged sitting,
Cirrhosis w/ portal HTN)

67
GI
Cholelithiasis Gallstones in biliary tract (usually GB)
WITHOUT inflammation
Types Gallstones
Cholesterol (MC)
Black: Hemolysis, EtOH cirrhosis
Brown: Asian, Parasitic, Bacterial infection
RF: 5 Fs: Fat, Female, Fertile, Fair, Forty
OCP, Native American, bile stasis, chronic
hemolysis, cirrhosis, infection, rapid weight
loss, IBD, TPN, fibrates, triglycerides
Cholecystitis Inflammation & infection of gallbladder
due to obstruction of cystic duct by
gallstones
Etiology: E. coli (MC), Klebsiella, Other
Gram(-) Enterococci
Chronic:
Fibrosis & thickening due to chronic
inflammatory cell infiltration
*almost always associated with gall stones
Acute Acalculous Necroinflammatory disease of GB NOT
Cholecystitis due to gallstones
10% of acute cholecystitis
Patho: GB stasis & ischemia -> Local
Inflammation rxn -> Conc of bile salts,
distention, infection, perforation, necrosis
RF: Critically ill, Hospitalization
Choledocholithiasis Gallstones in CBD
*can lead to cholestasis
Cholangitis Gallstone lodged & obstruction in CBD ->
Infection
Etiology: Gram(-) enteric ascended from
duodenum, E coli (MC), Klebsiella (2nd),
Enterobacter, B. fragilis.
Anaerobes/Enterococcus
Most Asymptomatic (incidental)
Symptomatic
Biliary colic: Episodic, Abrupt
RUQ/Epigastric pain
Resolves slowly
Lasts 30 min to hours
May be associated: Nausea & Precipitated
by fatty/large meal
*don’t typically see N/V, Fever, Chills
Continuous RUQ/Epigastric pain
Precipitated by fatty/large meal
May be associated with: Nausea &
guarding anorexia
PE: Fever (low), Enlarged gallbladder
+Murphy: Inspiratory pain GB
+Boas: Referred pain to Right
shoulder/subscapular area bc irritation of
phrenic nerve
Fever, Jaundice, Sepsis, Vague
abdominal discomfort
Prolonged biliary colic: RUQ/Epigastric,
N/V
PE: Jaundice, RUQ/Epigastric tenderness
Charcot Triad
RUQ pain + Fever/Chills + Jaundice
Reynolds Pentad
Charcot + Hypotension/Shock + AMS
US: IoC
*may use: CT/MRI
CBC: Leukocytosis (left shift)
CMP: Increased bilirubin, ALP, LFTS
US: IoC: Thick/distended, Sludge,
Stones
*alternative: CT
HIDA Scan: MOST ACCURATE
Positive: No visualization of GB
Labs: leukocytosis
US: IoC: Thick/distended, Sludge,
Without Calcifications
CT Contrast: Uncertain after US
HIDA: Uncertain after CT
CMP: High ALP + GGT (cholestasis)
Also: Increased bilirubin -> AST, ALT
US: Initial test
ERCP: Diagnostic (can be therapeutic)
MRCP: Diagnostic only
CBC: Marked leukocytosis
CMP: High ALP + GGT (cholestasis)
Also: Increased bilirubin -> AST, ALT
US: Initial test
ERCP: Diagnostic (can be therapeutic)
MRCP: Diagnostic only
Asymptomatic: Observation
Symptomatic: Ursodeoxycholic acid
Complications
Choledocholithiasis: CMB
Cholecystitis: Inflammation Cystic
Duct
Cholangitis: CBD + Infection
Supportive: NPO, IVF, ABX
*Ceftriaxone + Metronidazole, then
Lap Cholecystectomy (in 24-72 hr)
Non-Op: Cholecystostomy
Supportive: NPO, IVF, Pain control,
Correct electrolytes, ABX (broad)
ERCP w/ Stone Extraction
*preferred over laparoscopic
choledocholithotomy
IV ABX then CBD Decompression
then ERCP w/ Stone Extraction
*once stable/afebrile 48 hours
ABX: Unasyn, Zosyn, Ceftriaxone +
Metronidazole, Fluoroquinolone +
Metronidazole, Ampicillin +
Gentamicin
68
EENT 8%
SCREENING
Open Angle Glaucoma: AAO: Comprehensive eye examinations by ophthalmologist
With risk factors for glaucoma, every
1-2 years in patients <40 yo
1-3 years in patients 40-54 yo
1-2 years in patients ≥55 yo
Without risk factors, every
5-10 years in patients <40 yo
2-4 years in patients 40-54 yo
1-3 years in patients 55-64 yo
1-2 years in patients ≥65 yo
Amblyopia: AAP, AAFP, USPSTF: Screening All Children <5 yo: Vision risk assessment (all health maintenance visits), Vision screening (at 3, 4, 5 yo)
Any abnormality: Refer to Ophthalmologist
EENT About
Bacterial Etiology
Conjunctivitis S. aureus (MC Adults)
S. pneumoniae, H influenza,
M. catarrhalis, Pseudomonas
N. gonorrhea, C. trachomatis
Viral Etiology: Adenovirus (MC)
Conjunctivitis
MC: Children
Transmission: Direct contact
(highly contagious), Swimming
pool (MC source during
outbreak)
Allergic •Atopic asthma
Conjunctivitis •atopic dermatitis
•allergic rhinitis
Pathophysiology:
Presentation
Purulent (green/yellow) Sticky
discharge, Lid crusting, Eye
stuck shut in morning
Conjunctival erythema with NO:
ciliary injection or visual changes
FB/Gritty sensation, Ocular
erythema & pruritis
Normal vision
Starts unilateral, progressives to
bilateral in 1-2 DAYS
Ipsilateral Preauricular
lymphadenopathy, Copious
WATERY discharge, Tarsal
conjunctiva may have a bumpy
appearance with lid eversion
± Viral symptoms
Conjunctival erythema with
Normal vision
Allergic Symptoms: Nasal
congestion, Sneezing, Marked
Diagnostics
Clinical Dx
Fluorescein Stain: For keratitis or corneal
abrasions
Culture & Gram Stain: Discharge
Slit-Lamp: Punctate staining
PE: Cobblestone mucosa (upper inner
eyelid), Erythema, Watery/Mucoid
discharge, Chemosis (conjunctival
erythema)
Treatment
Erythromycin Ointment, Trimethoprim-Polymyxin B,
FQ (Moxifloxacin, Olfloxacin)
Contacts (cover pseudomonas): Topical Ciprofloxacin
or Ofloxacin
*Alternative: Topical Aminoglycosides (Tobramycin or
Gentamicin)
Supportive (self limited): Warm to cool compress,
Artificial tears
Pruritis & Erythema: Antihistamines (Olopatadine),
Antihistamines + Decongestants (Pheniramine-
Naphazoline)
Symptomatic: Topical Antihistamines (H1 Blocker:
Olopatadine), Antihistamines + Decongestants
(Pheniramine-Naphazoline), Emedastine
Topical NSAID: Ketorolac
69
 •mast cell degranulation and Pruritis (hallmark, distinguishes
release of histamine allergic from viral). Often bilateral

Ophthalmia Neonatal conjunctival infection Day 1: Chemical Conjunctivitis Days 2-5: Gonococcal (most likely cause) Days 5-7: Chlamydia Trachomatis (most likely cause)
Neonatorum contracted by newborns due to silver nitrate Purulent conjunctivitis with exudate & *may occur up to 23 days after birth
during delivery swelling of eyelids
“Neonatal Treatment: Artificial tears may be Treatment: PO Erythromycin
Conjunctivitis” helpful Treatment: IM/IV Ceftriaxone
No effective prophylaxis
Prophylaxis: Erythromycin Ointment
0.5% (given immediately after birth)
*alternatives: Topical Tetracycline 1.0%,
Silver Nitrate, Povidone-Iodine 2.5%

Disease Clinical Presentation Treatment

Papilledema Optic nerve (disk) swelling due to HA, N/V Fundoscopy Acetazolamide: Decreases Aqueous humor
Increased ICP (usually bilateral) Swollen disc & blurry margins & CSF production
Vision often preserved
Etiology: Idiopathic intracranial HTN, MRI/CT first to rule out mass Treat underlying disease
Space-occupying lesions, Increased CSF then LP
production, Cerebral edema, Severe HTN

Disease Bugs/Causes Symptoms Treatment

Pterygium Slow growing thickening of bulbar conjunctiva
RF: Sun (UV), Tropics, Sand, Wind, Dust exposure
Elevated, superficial, fleshy triangular growing
fibrovascular mass
Starts medially, extends laterally (potentially on cornea)
± Irritation, Erythema, FB sensation
Most: Observation, Artificial tears (irritation &
erythema)
Affecting Vision: Removal (advances over cornea,
causes astigmatism, cosmetics)

Pinguecula Slow growing thickening of bulbar conjunctiva Slightly elevated, Yellow nodule No Treatment is Needed
MC on medial side of sclera near the limbal conjunctiva
RF: Often eye is irritated (dry, windy, sunny, trauma) DOES NOT GROW ONTO CORNEA Chronically Inflamed/Cosmetics: Resected

Consists of: Fat, Protein, Calcium

Disease About Clinical Presentation Diagnostics Treatment

Hyphema EMERGENCY Vision loss, Eye pain, N/V,
Blood in anterior chamber due to trauma Photophobia, Decreased visual
acuity, Anisocoria (unequal pupil
size), Iridodialysis (tearing of iris away
from insertion), Increased IOP
Grade Emergent eval by ophthalmologist
Microhyphema: Circulating
RBC on Slit-Lamp exam only Eye shield, Dim light
1: <33% Bed rest, Elevate head of bed
2: 33-50% Control pain: Avoid NSAID (platelet inhibitors)
3: >50% Treat N/V & prevent vomiting
4: 100%

Orbital CT: Suspected Open

Globe

70
Globe Rupture Etiology: High velocity projectile, High impact
blunt trauma, Sharp object
Location: Typically directly behind insertion of
rectus muscles (greatest structural weakness)
Markedly decreased visual acuity, Emergent eval by ophthalmologist
Eccentric/Teardrop pupil,
Increased/Decreased anterior chamber Avoid: Anything that may apply pressure to
depth, Low IOP eyeball (eyelid retraction, IOP measurement)
Leave protruding FB in place

Eye shield, Aggressive pain control, Treat N/V

& prevent vomiting

Disease Bugs/Causes Symptoms Treatment

Bacterial Inflammation/Ulceration of Ocular pain, Photophobia, Erythema, Vision Slit-Lamp Topical FQ (Moxifloxacin, Gatifloxacin)
Keratitis cornea changes, Ocular discharge, Tearing, FB sensation, Increased fluorescein uptake (deeper *after obtaining corneal cultures
May rapidly progress & be Difficulty keeping eye open than abrasion) Same day referral to ophthalmology
“Corneal Ulcer” sight threatening
PE: Limbic injection (ciliary flush), Hazy cornea, DO NOT PATCH EYE
Etiology Hypopyon (severe cases)
S. aureus, S. streptococci, Controversial: Topical Corticosteroids
Pseudomonas (contacts)

RF
Improper contact lens use
(strongest)
Dry ocular, cant close eyes
(Bells Palsy)
Topical steroids or
immunosuppression

Herpes Keratitis Reactivation of HSV in
Trigeminal ganglion
Major cause of blindness
USA
Acute onset
Unilateral Ocular pain, Photophobia, Erythema,
Watery discharge, Blurred vision
PE: Limbic injection (ciliary flush), Hazy cornea,
Prearicular lymphadenopathy
Fluorescein Stain Antiviral: Topical (Trifluridine,
Dendritic corneal ulceration Ganciclovir), PO (Acyclovir)
(hallmark)
Severe: Corneal Transplantation

Disease Clinical Presentation Treatment

Central Retinal Retinal artery thrombus/emboli Sudden, Painless, Monocular Fundoscopy No consensus on optimal treatment
Artery Occlusion MC: 50-80 yo, Atherosclerosis vision loss Retinal ischemia: Pale retina with
(CRAO) ± Preceded by amaurosis fugax, “cherry-red spot” on macula Initial: CO2 Rebreathing, 100% O2,
Etiology Ipsilateral carotid bruit Boxcar appearance of retinal vessels Ocular massage, Decompression of
Emboli from carotid artery (MC) (segmentation of blood flow) anterior chamber (Acetazolamide or
Cardiogenic emboli (2nd overall, MC in Emboli (20%) Chamber paracentesis),
young patients and those without Ophthalmology consult, In-situ
atherosclerosis) fibrinolysis
Vasculitis
Prognosis: Poor ever with treatment

71
Central Retinal Thrombus in central retinal vein -> Fluid Sudden, Painless, Monocular Fundoscopy CONSULTATION
Vein Occlusion back up in retina vision loss Extensive retinal hemorrhage (blood
(CRVO) and thunder appearance) No definitive treatment
RF: HTN, DM, Glaucoma, Smoking, Retinal vein dilation, Macular edema
Hypercoagulable states, Multiple myeloma ± Optic disk swelling

± Marcus-Gunn Pupil (relative afferent

pupillary defect

72
Disease About
Ectropion Eyelid & lashes turned outward (everted), due to
relaxation of orbicularis oculi muscle
RF: MC Elderly (usually bilateral), Congenital,
Infectious, CN VII
Entropion Eyelid & lashes turned inward (inverted)
MC: Elderly
Patho: Spasms of orbicularis oculi muscle
Dacryoadenitis Inflammation of infection within the lacrimal gland;
temporal aspect of upper eyelid
Causes: Sjogrens, mumps (viral), bacterial
Dacryocystitis Inflammation of lacrimal sac, due to obstruction of
nasolacrimal duct
Etiology: S. epidermis, S. aureus, GABHS,
Pseudomonas
Blepharitis Inflammation of eyelid margin
RF: Downs, Atopic dermatitis, Rosacea, Seborrheic
dermatitis
Posterior (MC Type): Meibomian gland dysfunction
*Hyperkeratinization -> S. aureus growth
Anterior: Skin & base of eyelashes
*Infectious (S. aureus, S. epidermis), Viruses
*Seborrheic
Hordeolum Localized abscess of eyelid margin
“Stye” Etiology: S. aureus MC
Increases Risk: Seborrheic dermatitis, Rosacea
External: Infection of eyelash follicle or external
sebaceous gland (gland of Mall/Zeis)
Internal: Inflammation/infection of Meibomian gland
*deep from palpebral margin under eyelid
Chalazion Painless indurated granuloma of Internal
Meibomian sebaceous gland, away from eyelid margin
Symptoms
Irritation, Ocular dryness, Tearing, Sagging eyelid,
Increased sensitivity
Corneal abrasion/Ulceration, Erythema, Tearing, Increased
sensitivity
•Swelling, pain, redness at lacrimal gland
Acute: Tearing & Infection (tenderness, edema, erythema,
warmth to medial canthal (nasal side) of lower lid)
± Purulent discharge
Chronic: Mucopurulent drainage from puncta w/o other
signs of infection
Eyelid: Burning, Erythema, Crusting, Scaling & Red-
rimming (pink/erythematous edges), Flaking on lashes or
lid margins
±Entropion, Ectropion
Focal Abscess: Erythematous, Painful, Warm,
Nodule/Pustule
Non-tender localized eyelid swelling (nodule) on
conjunctival surface of eyelid
± Erythema of affected eyelid
Treatment
Lubricating eye drops & Moisture shields
Surgical Correction: In needed
Lubricating eye drops & Moisture shields
Surgical Correction: In needed
Bacterial: ABX +/- I&D
Viral: supportive care
Acute: Warm compresses + ABX (Clindamycin,
Vancomycin + Ceftriaxone)
Chronic/Severe: Dacryocystorhinostomy
*Topical ABX may be used prior to surgery
Eyelid Hygiene: Warm compress, Eyelid scrubbing,
Lid washing with baby shampoo, Artificial tears
Severe/Refractory: Topical ABX (Azithromycin,
Erythromycin, Bacitracin), Oral ABX, Topical
Glucocorticoids, Topical Cyclosporine
Mainstay: WARM compresses
*most eventually point and drain spontaneously
No Spontaneous Drainage After 48 Hours
I&D
Actively Draining: Topical ABX (Erythromycin,
Bacitracin)
Conservative: Eyelid hygiene & Warm compresses
*small will often resolve without intervention in
days to weeks
73
Patho: Obstruction of Zeis/Meibomian gland
Chalazion vs Hordeolum: Chalazion are usually larger,
firmer, slower growing, and less painful
Refractory: Ophthalmologist referral for injection of
glucocorticoid
Incision & Curettage may be necessary if no
resolution

74
Disease About
Macular MCC permanent legal blindness
Degeneration and vision loss in older adults
Types
Dry (atrophic): MC type
Progressive over decades
Wet (neovascular/exudative)
More aggressive over months
*responsible for most cases of
blindness due to macular
degeneration
Retinal Detachment Separation of retina from
underlying retinal pigment
epithelium
EMERGENCY
RF: Myopia, PSH cataracts,
Advancing age, Trauma
Types
Rhegmatogenous: MC: Full
thickness retinal tear that causes
retinal inner sensory layer
detachment from choroid plexus
Tractional: Adhesions separate
retina from its base (Proliferative
diabetic retinopathy, Sickle cell
disease, Trauma)
Exudative (Serous): Fluid
accumulates beneath retina
causing detachment (HTN,
CRVO, Papilledema)
Diabetic MCC of new permanent vision
Retinopathy loss 20-74 yo
*usually due to maculopathy
Also in
Endocrine
Clinical Presentation
Bilateral, progressive, CENTRAL vision
loss (detail & color)
Central scotomas, Metamorphopsia
(straight lines are bent), Micropsia (objects
seem smaller)
Photopsia (flashing lights) with
detachment, then Floaters (spots), then
Progressive UNILATERAL peripheral
vision loss
*Shadow or “curtain coming down”
initially peripherally then loss of central
vision loss
NO: Ocular pain or redness
Non-Proliferative: Microaneurysms,
Cotton Wool Spots (soft exudates that
resemble grey-white spots due to nerve
layer microinfarctions). Hard Exudates
(yellow spots with sharp margins often
circinate due to lipid/lipoprotein deposits
from leaky blood vessels), Blot & Dot
Hemorrhage (bleeding into deep retinal
layer). Flame-Shaped Hemorrhages
(nerve fiber layer hemorrhage)
Diagnostics
Fundoscopy
Dry (atrophic)
Drusen bodies (small, round, yellow-
white spots on outer retina)
*represent localized deposits of
extracellular material
Wet (neovascular/exudative)
New, abnormal vessels
*can cause retinal hemorrhage & scarring
Fluorescein Angiography
Amsler Grid
Fundoscope
Retinal tear (detached tissue “flapping”
in vitreous humor)
(+)Shafer’s Sign: Clumping of brown-
colored pigment vitreous cells in the
anterior vitreous humor “tobacco dust”
Maculopathy: Macular edema/exudates,
Blurred/Decreased central vision loss
*Can occur at any stage
*Vision loss in non-proliferative often
occurs due to macular edema
Treatment
Dry (atrophic)
Extensive Intermediate Sized Drusen
Zinc & Antioxidant vitamins (C & E)
*may slow progression
Amsler Grid at home (monitor stability)
Wet (neovascular/exudative)
Intravirtreal VEGF Inhibitors:
Bevacizumab, Ranibizumab, Aflibercept
*decrease new abnormal vessels
Laser Photocoagulation
Keep Supine, Head turned TOWARD
side of detachment
*do not use miotic drops
Laser, Cryotherapy, or Ocular Surgery
Non-Proliferative: Glucose control, Laser
Proliferative: VEGF Inhibitors
(Bevacizumab), Glucose control, Laser
photocoagulation
Prevention: Annual eye exams
*to detect diabetic retinopathy
75
 Proliferative: Neovascularization ->
Vitreous hemorrhage

Hypertensive Damage to retinal blood vessels Mild: Moderate: Severe: EMERGENCY

Retinopathy from longstanding HTN Arteriolar arrowing due to vasospasm Hemorrhages (flame or dot) ALL + Papilledema (blurring optic disk)
Abnormal light reflexes on dilated Cotton wool spots (soft exudates)
tortuous arteriole Hard exudates
Copper Wiring: Moderate narrowing Microaneurysms
Silver Wiring: Severe narrowing
AV Nicking: Venous compression at
arterial-venous junction

EENT Presentation Diagnostics Treatment

Corneal Abrasion FB sensation, Tearing, Red & Painful 1st Check visual acuity Antibiotic Drops (Corneal Abrasions & FB)
& eye, Photophobia, Blepharospasms (hard Non-Contact Wearer: Erythromycin Ointment, Bactrim,
Ocular FB to open eye) Fluorescein Stain Sulfacetamide
Corneal abrasion = “Ice rink”/Linear abrasion seen
(esp if the FB is underneath eyelid, evert eyelid to look) Contacts (Pseudomonal): Topical Ciprofloxacin or Ofloxacin
Pain often relieved with instillation of ophthalmologic *Alternative: Tobramycin or Gentamicin
analgesic drops *If Pseudomonas suspected: DO NOT PATCH

FB Removal: Remove with sterile irrigation or moistened sterile

cotton swab

Corneal Abrasions: Patching not indicated for small abrasions, May

patch if >5mm but do not patch for >24 hours. Do not send home
with topical anesthetics (may delay healing and cause corneal
toxicity)

Rust Ring:

24 Hour Ophthalmology FU

ABX containing Corticosteroids are not used: Prolong healing &

increase susceptibility to superinfection

76
Disease Causes
Acute Narrow Increased IOP -> Optic nerve damage
Closed Angle Ophthalmologic Emergency
Glaucoma Need to be seen in under 1 hour
*Leading cause of preventable blindness USA
RF: Preexisting narrow angle or large lens, >60
yo, Hyperropes (far sighted), Female, Asian
Patho
Decreased drainage of aqueous humor via
trabecular meshwork & canal of Schlemm
Precipitants: Mydriasis (dilation, further closes
angle): Dim lights, Sympathomimetics,
Anticholinergics
Primary: Anatomically predisposition
Secondary: Secondary process: Fibrovascular
membrane (grows over the angle to pull it
closed), Neovascular
glaucoma/Mass/Hemorrhage (in posterior
segment of eyeball pushes the angle closed)
Clinical Presentation
Sudden Severe Unilateral Pain
Loss of PERIPHERAL vision “tunnel
vision” & Halos around lights
N/V, HA
PE: Conjunctival erythema, Cloudy
“steamy” cornea, Mid-dilated fixed
pupil (reacts poorly to light), Hard eye on
palpation
Exam Order:
Visual acuity & Visual field test
Pupil evaluation
IOP
Slit lamp exam of anterior segment
Undilated fundoscopic exam
Examination
Fundoscopy: Optic disk
blurring “Cupping optic
nerve” (thinning of outer rim
of optic nerve head)
Tonometry (Slit Lamp)
Increased IOP >21
Gonioscopy: *GOLD
*visualize the angle
Treatment
Prevent or Reverse
Control IOP, Recheck 30-60m
Combo: Topical agents (Timolol,
Apraclonidine, Pilocarpine) with Systemic
Agent (PO/IV Acetazolamide, IV
Mannitol)
Alpha-2 Agonist: Apraclonidine,
Brimonidine
Miotic/Cholinergic: Pilocarpine, Carbachol
Prostaglandins: Latanoprost
Topical Beta-Blocker: Timolol
*Does not affect visual acuity
Definitive: Laser Iridotomy
*also Surgical Iridotomy (not preferred)

Chronic Open Angle between the cornea & iris open which
Angle Glaucoma leads to degeneration & blockage of trabecular
meshwork
RF: African Americans, >40 yo, FamHx, DM
Patho
Open angle: Normal anterior chamber
Increased IOP due to reduced aqueous drainage
thru trabeculum which eventually causes optic
nerve damage
Usually asymptomatic until late
*Vision loss is usually presenting sign
Slow progressive painless bilateral
peripheral vision loss -> Central loss
(compared to rapid painful unilateral in
acute)
Increased IOP (>40mmHg)
Fundoscopy: Cupping of optic 1st Line: Prostaglandins (Latanoprost),
disk, Increased Cup:Disk Beta-Blockers (Timolol), Alpha-2 Agonist
ratio, Notching of disk rim (Brimonidine), Carbonic Anhydrase
Inhibitors (Acetazolamide)
Tonometry (Slit Lamp)
Normal IOP 8-22 Fail: Trabeculoplasty (laser therapy)
IOP >40: Emergent (now)
IOP 30-40: Urgent (24h) Last Line: Surgery
IOP 25-29: (1 week)
IOP 23-24: (repeat/refer)
patients with risk factors for
glaucoma, every: 1-2 years in
patients <40 years
1-3 years in patients age 40 to
54 years
1-2 years in patients aged ≥55
years
patients without risk factors,
every 5-10 years in patients
<40
2-4 years in patients 40 to 54
years 1-3 years in patients 55
to 64 years 1-2 years in
patients ≥65 years

77
Glaucoma Drug s MOA SE CI
Prostaglandinds Selective agonist of prostaglandin receptor; increase the outflow of aqueous •Bonchospam •raynauds
1st LINE *expensive humor -> dropping IOP •irritation, increase lashes, change in pigment •asthma •COPD

Beta-Blockers Reduce IOP by interfering with cyclic adenosine monophosphate (cAMP) which •bradycardia, hypotension •bronchoscpasm •raynauds
is used to produce aqueous humor •burning, stinging on application •asthma •COPD

Alpha-2 Adrenergic Causes iris to dilate (mydriasis) causing decreased congestion in the vessels of •allergic conjunctivitis •MOAIs •tricyclics
Agonists conjunctiva -> decreased IOP by reducing production of aqueous humor •hyperemia •CNS depressants, alcohol, BB,
•ocular pruritis cardiac glycosides,
hypertensives
Cholinergic Agonists •pupil constriction -> contracts trabecular meshwork -> opens schlemm’s canal - •cramping, diarrhea, watery mouth, sweat
> increase outflow of aqueous humor -> decreases IOP •fixed, small pupils; visual

Carbonic Anhydrase Slows the action of the enzyme carbonic anhydrase -> decreased production of •allergy to sulfa
Inhibitors aqueous humor

EENT Causes S/S Diagnostics Treatment

Otitis Externa Inflammation of external auditory
canal
RF
Water “Swimmer’s Ear”: Raises pH
Trauma: Q-tips, Age 7-12, Too
little/Too much ear wax
Etiology
Pseudomonas (MC!)
S. epidermis, S. aureus, GABHS,
Proteus, Anaerobes, Aspergillus fungi
Ear pain/pressure/fullness, Pruritis,
*Pain on traction of canal/tragus
Purulent discharge
Conductive hearing loss
Swollen erythematous canal
TM difficult to visualize
Clinical Dx + Otoscopy
Edema of external auditory
canal with erythema, debris,
discharge
Protect ear from moisture: Drying agents:
Isopropyl alcohol, Acetic acid
Remove debris/cerumen
Topical ABX (pseudomonas & Staphylococcus)
Ciprofloxacin-Dexamethasone, Ofloxacin
± Glucocorticoids (for inflammation)
Aminoglycoside Combo: Neomycin/Poly
B/Hydrocortisone
*NOT used if TM perforation suspected or
cannot be visualized: Aminoglycosides are
ototoxic

Malignant Otitis Invasive infection of external ear
Externa canal and skull base (temporal bone,
soft tissue, cartilage)
“Necrotizing
Otitis Externa” Complication of Otitis externa
Etiology: Pseudomonas >95%
Severe ear pain
*Severe Pain on traction of canal/tragus
*May radiate to TMJ (pain with chewing)
Chronic Otorrhea
CN VIII Palsy: If osteomyelitis occurs
Otoscopy Admission + IV Ciprofloxacin
Edema of external auditory (antipseudomonal)
canal with erythema, discharge, *alternative: Zosyn, Ceftazidime, Cefepime
granulation tissue at bony
cartilaginous junction of ear
canal floor, frank necrosis of ear
canal skin

RF: Immunocompromised: Elderly CT/MRI: Confirmatory

DM (MC), High dose glucocorticoid,
Chemo, Advanced HIV Biopsy: Most accurate

Disease Causes Clinical Findings Diagnosis Treatment

Acute Otitis Media Infection of middle ear Fever, Otalgia, Ear tugging (infants), Clinical Dx Observation in Some
Rapid onset + Signs/Symptoms of inflammation Stuffiness, Conductive hearing loss

78
(AOM) Pneumatic Otoscope >2 Years Old, Dx Certain, Severe
RF: Peaks: 6-18 MONTHS (eustachian tube is TM Rupture Decreased TM mobility (most 1st: Amoxicillin
shorter, narrower, more horizontal), Day care, Rapid pain relief + Otorrhea sensitive) 2nd: Augmentin, Cefuroxime,
Pacifier/Bottle use, Second hand smoke, Not being *usually heals in 1-2 days Cefdinir, Cefpodoxime
breastfed Tympanocentesis: Sample for culture *PCN allergy: Azithromycin,
PE: Bulging & Erythematous TM with *recurrent cases Clarithromycin, Erythromycin-
Etiology: Same organisms seen in acute sinusitis effusion, loss of landmarks Sulfisoxazole, Bactrim
S. pneumonia (MC), H. influenza, M. catarrhalis,
GABHS Severe/Recurrent: Myringotomy
(surgical drainage) +
Patho: MC preceded by Viral URI -> Blockage of Tympanostomy Tube
eustachian tube *may need CT & Fe deficiency
anemia workup

Chronic Otitis Recurrent/Persistent infection of middle ear and/or Perforated TM + Persistent/Recurrent 1st:Removal of Infected Debris +
Media mastoid cell system in the Prescence of TM Purulent otorrhea Topical ABX Drops (Ofloxacin,
perforation >6 WEEKS Often Painless Ciprofloxacin)
Ear fullness
Complication of acute otitis media, trauma, Conductive hearing loss (varies) Severe: Systemic ABX
cholesteatoma ± Primary/Secondary Cholesteatoma
TM Rupture: Avoid Water,
Etiology: Pseudomonas (MC), S. aureus, Gram(-) Moisture, Topical
Rods: Proteus, Anaerobes, Mycoplasma Aminoglycosides

Can become worse after URI or Water entering ear TM Repair or Reconstruction

Serous Otitis Middle ear fluid + No signs/symptoms of acute NO: Fever, Otalgia, Marked erythema, Otoscopy Most Cases: Observation
Media (SOM) inflammation (no fever, no otalgia, no marked Bulging of TM Effusion with Retracted/Flat TM *usually revolves spontaneously
erythema, no bulging of TM) Hypomotility with insufflation
Otitis Media with Persistent/Complicated:
Effusion (OME) May be seen after resolution of acute otitis media or Tympanostomy Tube (for
in patients with eustachian tube dysfunction drainage): Children with hearing
impairment, Developmental
delays, Specific conditions

Parotitis Inflammation of one or both parotid glands Fever, Chills Clinical Dx Based on Lab: IV ABX &
Periauricular/Mandibular Pain & Hydration
Etiology Swelling Culture & Gram Stain: Exudate
Dehydration: Elderly, After surgery Trismus, Dysphagia US: Enlargement, Nodules, Mumps: Contagious for 9 days
Bacterial: S. aureus (MC bacterial) Purulent drainage Increased blood flow from onset of swelling
Viral: Mumps (MC viral), Influenza, Parainfluenza, CT: Extension to surrounding tissue
Adenovirus, Coxsackie, EBV, CMV, HSV, HIV Males: Orchitis CBC: Leukocytosis
Autoimmune: Sjogren’s syndrome, Sarcoidosis Amylase: Rises during first week
Sialolithiasis: Stone blocking parotid duct Viral: No discharge, Prodrome followed without underlying pancreatitis
by swelling lasting 5-10 days IgM against Mumps

79
Disease Causes Clinical Findings Diagnosis Treatment
Cholesteatoma Abnormal keratinized collection of desquamated Painless otorrhea (yellow/brown, Otoscope: Granulation tissue Surgical Excision of debris &
squamous epithelium in middle ear -> Possible strong odor) (cellular debris) ±TM perforation cholesteatoma with ossicle
bony erosion of mastoid ±Vertigo, Tinnitus, Dizziness, CN palsys reconstruction
CHL
Etiology: Chronic middle ear dysfunction or Weber: Lateralization to affected ear
Eustachian tube dysfunction Rinne: BC >AC

TM Perforation Rupture of TM Acute ear pain, Conductive hearing loss Otoscope: Perforated TM Most spontaneously heal, FU
May lead to cholesteatoma Otalgia prior to rupture: Sudden relief *do not perform pneumatic
with bloody otorrhea Topical ABX (Ofloxacin in some)
Etiology: Penetrating /Noise trauma (pars tensa), Tinnitus & Vertigo ±CHL
Otitis media Weber: Lateralization to affected ear Avoid: Water & Aminoglycosides
Rinne: BC >AC

Tinnitus Noise in ear (ringing, buzzing, hissing, whooshing) Continuous: Presbycusis, Long-term MRI Treat the cause
hearing loss Unilateral & Hearing loss: Rule out
Etiology: Acoustic neuroma
Sensorineural Hearing Loss (90%): Loud noise, Episodic Low-Pitched Rumbling: Unilateral, Normal hearing & PE:
Presbycusis, Medications (ASA, ABX, Meniere’s disease Only if it persists >6 months
Aminoglycosides, Loop diuretics, CCB), Meniere's
disease, Acoustic neuroma Pulsatile: Vascular cause
Vascular (5%): Carotid stenosis
Mechanical (5%): Abnormalities: TMJ

Disease Causes Clinical Findings Diagnosis Treatment

Vestibular Neuroma Vestibular Schwannoma: Benign
(CN VIII) tumor involving schwann cells
which produce myelin sheath
Also in
Neuro Arises in cerebellopontine angle
& can compress structures (CN
VIII, VII, V)
Unilateral sensorineural hearing loss Surgery or Focused Radiation Vestibular Neuroma (CN VIII)
*Vestibular neuroma until proven otherwise Therapy
Tinnitus, Vertigo, Ataxia, HA, Facial numbness (CN
V) or Facial paresis (CN VII)
Dx
MRI: IoC
*Alternative: CT

Audiometry: Unilateral sensorineural hearing loss

*Most common

Meniere’s Disease Idiopathic distention of 4 Findings Dx of Exclusion Initial: Avoid salt, caffeine,
endolymphatic compartment of Episodic peripheral vertigo (min-hrs) nicotine, EtOH, chocolate (they
“Idiopathic inner ear due to excess SNHL (fluctuating, unilateral) Caloric Testing: Loss of nystagmus increase endolymphatic pressure)
Endolymphatic endolymph Tinnitus (low tone initially)
Hydrops” Ear fullness Transtympanic Electrocochleography No Relief: (they reduce pressure)
Meniere Syndrome: Identifiable Diuretics: HCTZ
Also in Meniere Disease: Idiopathic Horizontal nystagmus, N/V Audiometry: SNHL Antihistamines: Meclizine,
Neuro Vestibular Test: Affected side Dimenhydrinate,
Prochlorperazine, Promethazine
MRI: Rule out MS, Tumor, Aneurysm Benzo: Diazepam
80
 Anticholinergics: Scopolamine

Labyrinthitis Labyrinthitis: Inflammation of Vestibular (Both) Clinical Dx 1st: Glucocorticoids

& vestibular & cochlear portion of Continuous peripheral vertigo, Dizziness, N/V, Gait
Vestibular Neuritis CN VIII sways toward affected side MRI/CT Brain: Rule out central etiology Symptomatic: Antihistamine
Horizontal & Rotary Nystagmus: Beats away from *MRI preferred (Meclizine), Anticholinergics,
Also in Vestibular Neuronitis affected side *Imaging usually not needed Benzodiazepines
Neuro inflammation of vestibular
portion of CN VIII Cochlear (Labyrinthitis ONLY) Both are self-limited: Usually
Unilateral hearing loss, Tinnitus resolve in weeks even without
Etiology: Idiopathic, Viral/Post- treatment
viral inflammation

Benign Paroxysmal Peripheral Vertigo Recurrent episodes of sudden peripheral vertigo Epley Maneuver Benign Paroxysmal Positional
Positional Vertigo MC due to displaced otolith (lasting ≤1 min) & provoked with specific head Vertigo (BPPV)
(BPPV) particles within semicircular movement Medical therapy usually not needed
canals of inner ear (canalithiasis) ± N/V
Also in Neuro MCC of peripheral vertigo Not associated with: Hearing loss, Tinnitus, Ataxia

Dx: Dix Hallpike

Produces fatigable nystagmus

Disease About Clinical Presentation Treatment

Nasal Polyps Etiology Most Incidental Initial: Intranasal Glucocorticoid
Allergic rhinitis (MCC), If Large: Obstruction, Anosmia
Possible with Cystic fibrosis ±Allergic rhinitis (pale/violaceous, boggy turbinates, Large/Refractory: Surgery
cobblestone mucosa of conjunctiva)

Dx: Direct Visualization

Pale, boggy mass on nasal mucosa

81
EENT About
Epistaxis Anterior
Source: Kiesselbachs Plexus MC
Etiology: Nasal trauma (MC),
Nose picking (MC kids), Low
humidity, Hot temp, Rhinitis,
EtOH, Cocaine, Antiplatelet, FB
*HTN may prolong
Posterior
Source: Sphenopalatine artery
branches & Woodruff’s plexus
(MC) (may cause bleeding in
both nares & posterior pharynx)
RF: HTN, Old, Nasal neoplasm
Clinical Presentation Treatment
Anterior Anterior: Posterior:
Bleeding site visualized 1st Line: Direct Pressure (5-15 min, seated, lean forward) Initial: Balloon Catheters (MC)
Foley cath, Cotton packing
Posterior Adjunct: Topical Vasoconstrictors: Oxymetazoline,
Anterior not visualized Lidocaine w/ Epinephrine, 4% Cocaine
Bleeding from both nares *caution in HTN
Blood into pharynx
Fail & Bleeding Visualized: Electrocautery or Silver nitrate
Fail/Severe: Nasal packing
*Clindamycin or Cephalexin to prevent toxic shock syndrome
Septal hematomas: Loss of cartilage if not removed
Avoid exercise for a few days, Avoid spicy food
Bacitracin, Petroleum gauze, Humidifiers: Moisten mucosa

Disease Clinical Findings/Causes/Bugs Diagnosis Treatment

Acute Acute inflammation of larynx mucosa Hoarseness (hallmark), Aphonia, Usually Clinical Dx Supportive: Hydration, Vocal rest,
Laryngitis Dry, scratchy throat Humidification, Warm saline gargles,
Etiology ±URI (rhinorrhea, cough, sore Anesthetics, Lozenges
Viral URI (MC): Adenovirus, Rhinovirus, throat) *Reassurance that it’s usually self-limited
Influenza, RSV, Parainfluenza
Work Up Needed: ENT FU
Bacterial: M. catarrhalis, Mycoplasma pneumonia

Noninfectious
Vocal strain, Irritants (GERD), Polyp, Cancer

82
Disease Transmission/Causes
Sinusitis Symptomatic inflammation of
nasal cavity & paranasal
sinuses
Etiology
Viral (MC): Rhinovirus,
Influenza, Parainfluenza
Bacterial: S. pneumonia (MC),
M. catarrhalis, H. influenza,
GABSP
Clinical Presentation/Physical Exam Diagnostics
Facial pain/pressure worse with bending over & Clinical Dx (primarily)
leaning forward, HA, Malaise, Purulent nasal
discharge, Fever, Nasal congestion Imaging: Not needed if classic
*Often develops worsening after period of and no complications
improvement CT: IoC if needed
Waters View: Sinus
radiograph
Biopsy/Aspirate: Definitive
*usually not needed
Treatment
Symptomatic: Decongestants, Analgesics,
Antihistamines, Mucolytics, Intranasal
glucocorticoids, Nasal lavage
ABX: Symptoms present >10-14 days with
worsening of symptoms or earlier if severe
Augmentin: DoC
2nd Line: Doxycycline
Resistance: Levofloxacin, Moxifloxacin

RF: MC in setting of viral URI,

Dental infections, Smoking,
Allergies, Cystic fibrosis

Acute: 1-4 weeks

Subacute: 4-12 weeks
Chronic: >12 weeks

Invasive Fungal Invasive fungal infection
Sinusitis Infiltrates sinuses, lungs, CNS
Rapidly dissects nasal canals &
“Mucormycosis” eye into the brain
High mortality
“Zygomycosis”
Etiology: Mucor, Rhizopus,
Absidia, Cunninghamella
RF: MC DM (esp DKA),
Immunocompromised
Rhino-orbital-cerebral infections: Sinusitis (Facial Biopsy & Histopathologic: 1st Line: IV Amphotericin B + Surgical
pain/pressure worse with bending over & leaning Non-septate broad hyphae debridement
forward, HA, Malaise, Purulent nasal discharge, with irregular right angle
Fever, Nasal congestion) progressing to Orbit & branching Posaconazole or Isavuconazole
Brain involvement
PE:
May develop: Erythema, Swelling necrosis, Black
eschar on palate, nasal mucosa, or face

Chronic Sinusitis inflammation of nasal cavity &
paranasal sinuses
Etiology
Bacterial: S. aureus (MC),
Pseudomonas, Anaerobes
Wegener’ Granulomatosis
(necrotic)
Same as acute but for > 12 weeks Biopsy/Histologic: DoC Depends on etiology
Goal: Promote drainage, reduce edema, eliminate
infections
Combo: Nasal irrigation, Topical/PO
Glucocorticoids, ENT FU
Bacterial: ABX, ENT FU

Fungal: Aspergillus (MC),

Mucormycosis (2nd)

83
EENT About
Allergic Rhinitis Types
Allergic MC Type, IgE
mediated (mast cell
release histamine due to
pollen, mold, dust)
Infectious: Rhinovirus MC
infectious cause (common
cold), Streptococcal less
often
Clinical Presentation Diagnostics Treatment
Clear watery rhinorrhea, Sneezing, Nasal Clinical Dx Allergic/Nasal Polyps
congestion, Itching 1st Line: Intranasal Corticosteroids
Eyes, Ears, Nose, Throat: May be involved May also use: Antihistamines, Mast cell stabilizers,
Allergic: ± Bluish discoloration around eyes Short term decongestants
PE Rhinorrhea: Anticholinergics
Allergic: Pale/Violaceous boggy turbinates, Nasal
polyps with Cobblestone mucosa of conjunctiva. Avoidance & Environmental control
Allergic Shiner: Purple discoloration around Exposure reduction
eyes/nasal bridge crease from rubbing

Vasomotor: Nonallergic & Viral: Erythematous turbinates

noninfectious dilation of
blood vessels (temperature
change, strong smells,
humidity)

Disease Clinical Findings/Causes/Bugs Diagnosis Treatment

Acute Etiology Respiratory Virus •clinical •supportive
Pharyngitis Viral (MC overall): Adenovirus, •sore throat, pain •rapid strep to r/o bacterial
Rhinovirus, Enterovirus, EBV, RSV, •Coryzal sx, Fever (RARE) HSV: Acyclovir, Valcyclovir
“Tonsilitis = Influenza, HZV •NO adenopathy or exud
Tonsils”
“Pharyngitis = Bacterial: GABHS (MC bacterial) EBV: white, purple exudate
Throat” HSV: vesicles, shallow ulcer

Streptococcal GABHS Dysphagia, Fever Centor Criteria: Only use if onset ≤3 days 1st Line: PCN VK, Amoxicillin, PCN G
Pharyngitis Rare <3 yo Not usually associated with Fever (+1) *PCN Allergy: Macrolides, Clindamycin,
symptoms of viral infections No Cough (+1) Cephalosporins
“Strep Highest incidence of rheumatic (cough, coryza, conjunctivitis, Tender/Swollen Anterior Cervical LN (+1)
Throat” fever if untreated 5-15 yo hoarseness) Exudate/Swelling Tonsils (+1) Complications
≥3: Further testing Rheumatic fever (preventable with ABX)
Complications: 2-3 weeks PE: Pharyngeal edema/exudate, <3: Unlikely, usually no testing/treatment Acute Glomerulonephritis
•Rhematic fever-antibodies Tonsillar exudate/petechia Peritonsillar Abscess
•Peritonsillar abscess Anterior cervical lymphadenopathy Rapid Antigen: Initial
•Poststreptococcal glomerulonephritis *95% specific, 55-90% sensitive (most useful
positive, if negative throat cultures esp 5-15 yo)

Throat Culture: Definitive *Gold

Disease Clinical Findings Diagnosis Treatment

Peritonsillar Abscess between palatine tonsil and Dysphagia, Severe unilateral Primarily Clinical Dx without need for Secure Airway
Abscess pharyngeal muscle from complication of pharyngitis, Fever (high) imaging/labs if classic Needle Aspiration + ABX
tonsilitis/pharyngitis Muffled “Hot Potato” voice, *can also do I&D
“Quinsy Abscess” MC: Adolescents & 15-30 yo Drooling, Trismus CT: IoC if needed *Oral: Augmentin, Clindamycin
*differentiates abscess vs cellulitis *Parenteral: Unasyn, Clindamycin
Etiology PE

84
 Often Polymicrobial: Predominant (GAS),
S. aureus, Respiratory anaerobes
MC deep neck infection in children &
adolescents
Swollen/Fluctuant tonsil -> Recurrent/Complication/Fail:
Uvula deviation to contralateral Tonsillectomy
side, Bulging of posterior soft
palate, Anterior cervical Prevention: Prompt treatment Strep throat
lymphadenopathy

Retropharyngeal •deep neck space infection posterior to •Neck swelling/mass, pain lateral neck x-ray: increased prevertebral •Airway first
Abscess pharyngeal wall •torticollis (wont move neck) space >50% width
•MC in children 2-4 years old •Spiking fever ABX: IVAmpicillin-Sulbactam (Unasyn)
*complication of •Odynophagia, Dysphagia CT neck with contrast: BEST or Clindamycin
peritonsillar abscess Bugs: *often polymicrobial •ring enhancing lesion
•Strep pyogenes (Group A) Exam: •surgical incision and drainage if large
•Staph aureus •midline or unilat posterior and mature
•Respiratory anaerobes pharyngeal wall edema
•anterior cervical LAD

Disease About Clinical Findings Diagnosis Treatment

Sialolithiasis Stones in salivary gland/duct (no
inflammation)
“Salivary Gland MC in Whartons duct (submandibular
Stones” gland) & Stensens duct (parotid gland)
RF: Decreased salivation (dehydrated,
anticholinergics, diuretics)
Sudden onset pain & swelling with eating or in
anticipation of eating
PE: Stone may be palpated, If gland is compressed
and no saliva flows the stone can be obstructive
Usually Clinical Dx Conservative: 1st Line: Sialagogues
*increase salivary flow
Also: Tart hard candies, Lemon drops,
Increase fluids, Gland massage, Moist heat
Minimal Invasive: Sialoendoscopy, Laser
lithotripsy, Extracorporeal lithotripsy

Fail/Recurrent: Sialoadenectomy

Avoid: Anticholinergics

Acute Bacterial Bacterial infection of parotid or Sudden onset of very firm & tender swelling w/ CT: Assess for ABX + Sialagogues (tart, hard candy)
Sialadenitis submandibular salivary glands purulent discharge (may be able to express pus if associated Dicloxacillin or Nafcillin
massaged), abscess/extent of Metronidazole (can be added for coverage)
“Suppurative Etiology: S. aureus (MC), S. pneumonia, S. Dysphagia, Trismus tissue involvement Clindamycin
Sialadenitis” viridans, H. influenza, Bacteroides
Severe: Fever, Chills
RF: Obstruction (stone), Dehydration, Chronic
illness

Aphthous Ulcers Recurrent disease seen in patients with: IBD, Small, painful round/oval shallow ulcer (yellow, Clinical 1st Line: Glucocorticoids: Clobetasol gel,
HIV, Celiac, SLE, MTX, Neutropenia white, or grey with central exudate) with Dexamethasone elixir, Triamcinolone in
“Canker Sore” Erythematous halo orabase
Etiology: Unknown, possible HHV-6
“Ulcerative MC: Buccal & Labial mucosa (nonkeratinized) Topical Analgesics: 2% Viscous Lidocaine
Stomatitis” Applied QID after meals until healed

85
OBGYN 8%

Gravida: number of times a woman have been pregnant

Parity: Number of pregnancies that led to a birth either at or after 20 weeks
- T (term) à number born at 37 weeks or older
- P (preterm) à born after 20 weeks but before 37 weeks
- A (abortion) à all pregnancy losses prior to 20 weeks
- L (living) à infant who lives beyond 30 days

Nulligravida: woman who currently is not pregnant and never has been pregnant
Primigravida: woman who currently is pregnant and has never been pregnant before
Multigravida: woman who currently is pregnant and who has been pregnant before
Nullipara: woman who has never completed a pregnancy beyond 20 weeks
86
Primipara: woman who has delivered a fetus or fetuses born alive or dead with an estimate length of gestation of >20weeks
Multipara: woman who completed 2+ pregnancies to 20 weeks gestation or mo

Fundal Height: 12 weeks (above pubic symphysis), 16 weeks (midway between pubis & umbilicus), 20 weeks (umbilicus), 38 weeks (2-3cm below xiphoid

SCREENING
Breast Cancer
ACOG: CBE: Every 1-3 years 25-39 yo, Annually ≥40 yo. MMG: Offer 40 yo, Initiate at 40-49, Recommend no later than 50. Annually or Biennially. Continue until 75 yo
USPSTF: CBE: Doesn’t recommend. MMG: Recommend at 50 yo. Biennially. Continue until 75 yo
ACS: CBE:Doesn’t recommend. MMG: Offer 40-45 yo, Recommend at 45 yo. Annually 40-54 yo, Biennially ≥55 yo. Stop when life expectancy is <10 years
NCCN: CBE: Every 1-3 years 25-39 yo, Annually ≥40 yo. MMG: Recommend 40 yo. Annually. Stop when life expectancy is <10 years

Breast CA About Presentation Diagnostics Treatment

Breast Cancer MC non-skin cancer in women
(1/8 lifetime)
2nd MCC cancer death in women
(after lung cancer)
RF:
BRCA 1 & 2: 60-85% lifetime
development (15-40% lifetime
development of ovarian cancer),
BRCA(+) seen in 5-10% of cases of
breast cancer, FamHx
Increasing Age: >50% occur >60 yo
Increased Number of Menstrual
Cycles: Nulliparity, Late first full
term pregnancy, >35 yo, Early onset
menarche (<12 yo), Late menopause,
Never having breastfed
Increased Estrogen Exposure:
Postmenopausal HRT, Prolonged
unopposed estrogen, Obesity, EtOH.
Endometrial CA increases the risk of
Breast CA and vice versa
ER(+): Better prognosis
Types: Mammography (MMG)
Infiltrative Ductal Carcinoma (MC) Initial evaluation breast masses >40 yo
Associated with: Lymphatic mets (esp axillary) Microcalcifications & Spiculated
Ductal Carcinoma In-Situ (DCIS): Doesn’t penetrate masses: Highly suspicious for
basement membrane malignancy
Infiltrative Lobular Carcinoma US
Initial evaluation breast masses <40 yo
Medullary, Mucinous, Tubular, Papillary, Mets Guide FNA with Biopsy
Determine if mass seen on MMG is
Paget Disease of Breast cystic vs solid
Ductal carcinoma: Chronically eczematous itchy scaly
rash on the nipples/areola (may ooze/bleed). Lump is MRI
often present Rapid uptake of contrast: Characteristic
of malignant mass
Inflammatory Breast Cancer
Red, Swollen, Warm, Itchy breast. Often with nipple FNA w/ Biopsy
retraction, Peau d’ Orange (lymphatic obstruction, Advantages: Removes least amount of
associated with a poor prognosis). Usually not tissue
associated with a lump Disadvantages: If positive, doesn’t allow
for receptor testing (E, P, HER2),
Associated with a false negative rate
Premalignant Lesions 10%
Lobular Carcinoma In Situ (LCIS): Not considered
cancer but is associated with an increased risk of invasive Core Biopsy
breast cancer in either breast Advantages: If positive, Allows for
receptor testing (E, P, HER2)
Atypical Ductal Hyperplasia Disadvantages: Greater deformity, May
miss lesion
Based on TMN
*METS workup for ≥ Stage 3
Early Stage Cancer
Lumpectomy + Sentinel Node
Biopsy + Follow Up Radiation
*Breast conservation
*Negative sentinel node eliminates
the need for axillary LN dissection
Diffuse, Large Tumor or
Prior Radiation to Breast or
Radiation Post-Lumpectomy C/I
Modified Radical Mastectomy
Post-Lumpectomy/Mastectomy
Radiation Therapy (External
Beam Radiation, Brachytherapy):
*Destroy residual tumor cells
Pre-menopausal ER(+)
Anti-Estrogen (Tamoxifen)
*ADR: Venous thrombosis &
Endometrial cancer
Post-Menopausal ER(+)
Aromatase Inhibitor (Letrozole,
Anastrozole, Exemestane)
*ADR: Osteoporosis

HER2(+): More aggressive tumors
Follow-Up:
CBE: Every 4 months x 2 years then
Every 6 months x 3 years then
yearly
Mammogram: 6 months after
radiation then yearly
Clinical Presentation Open Biopsy HER2(+) Tumors
Mass MC Upper Outer Quadrant Advantages: Most accurate diagnostic, Anti-HER2 (Trastuzumab)
Allows for frozen section to be done *ADR: Cardiotoxicity
Skin Changes: Asymmetric erythema, Discoloration, followed by immediate resection of the
Ulceration, Skin retraction (dimpling if cooper’s ligament cancer followed by sentinel node biopsy Lesions >1cm or
involved), Changes in breast size & contour, Nipple (+) Axillary Lymphadenopathy or
inversion, Skin thickening Stage 2-4 or
Inoperable (esp ER(-)
Locally Advanced Disease: Axillary lymphadenopathy
87

METS: MC sites: Bone, Lungs, Liver, Brain
Bone: Vertebra, Ribs, Pelvis, Femus
Lungs: Dyspnea, Cough
Liver: Abdominal pain, Nausea, Jaundice
Medication and Usage
SERM •Tamoxifen (Nolvadex)
•Raloxifene (Evista)
•Toremifene (Fareston)
•Used for treatment of breast CA and
chemoprevention of breast CA in some
high-risk women
Aromatase •anastrazole (Arimidex)
Inhibitors •exemestane (Aromasin)
•letrozole (Femara) *induce ovulation
•Used for treatment of breast CA
•May be used alone, in combination with
GnRH blockers, or before/following SERMs
Fulvestrant •used for metastatic breast cancer
(Faslodex) •attaches to and causes destruction of
estrogen receptors
•does not mimic effects of estrogen
OBGYN About
Fibrocystic Noncancerous, Fluid filled cysts due to
Breast Changes exaggerated response to hormones
“Glandular Duct dilation, Breast cysts, Stromal
Hyperplasia” fibrosis
MC benign breast disorder in
reproductive age (30-50 yo)
Often regresses after menopause
MOA
•binds to estrogen receptors
•block estrogen activity in some
•tamoxifen - blocks in breasts;
mimics in uterus, bone
•toremifene - blocks in breasts;
mimics in uterus, bone
•raloxifene - blocks in breasts,
uterus; mimics in bone
•inhibit aromatase (enzyme that
blocks conversion of testosterone to
estrogen)
•GnRH agonists/antagonists
Clinical Presentation
Multiple, Nodular, Mobile, Smooth,
Round/Oval masses of varying sizes that
may increase/decrease in size with
menstrual hormonal changes (often worse
prior to menstruation)
± Pain
Often bilateral
Not usually associated with axillary LN
involvement
MC Upper outer sections of breast
Adjuvant Chemotherapy
(Doxorubicin, Cyclophosphamide,
Fluorouracil, Docetaxel)
*Treat any residual disease
Side Effects DDI
Common •Not for use with other hormone-modulating
hot flashes, nausea, muscle aches and anti-CA therapy
cramps, hair thinning, headache,
paresthesias •SSRIs, cimetidine can reduce efficacy
Benefits: improve bone & lpids •Avoid with QT-prolonging agents
Risks: thrombosis, fatty liver,
endometrial cancer, false thyroid
Common: •Caution when using with, or do not use with,
hot flashes, GI upset, muscle weakness, other hormone-modulating anti-CA therapy
joint pain, headache, worsened
ischemic heart disease •May increase serum concentration of
methadone or L-methadone
Risks:
•Hypercholesterolemia •Do not use with estrogen or immunomodulating
•Insomnia, impaired cognition, fatigue, drugs
mood changes, Thinning hair
CI: pregnancy
•Used to reduce release of GnRH and
FSH/LH
Diagnostics Treatment
US: Initial DoC Supportive: Observation, Supportive bra, Warm/Cool
compresses, Analgesice
FNA
Straw colored or green OCP: Can reduce symptoms
fluid (no blood)
*rarely done FNA Removal of Fluid: Diagnostic & Therapeutic in
complex cases
Mammogram: If lesion is
suspicious or persistent
after drainage
88
Fibroadenoma Benign solid tumor composed of
glandular & fibrous tissue
MC Breast tumor <30 yo
2nd MC benign breast mass (after
fibrocystic disease)
Increased incidence: AA
Usually nontender (may become tender prior Clinical Dx Conservative: Observation, Reassurance, FU
to menstruation) *Most small tumors resorb with time
Gradually grows over time but may enlarge US *Can repeat US in 3-6 Months
in pregnancy Solid, well-circumcised,
Does not change significantly in size with Avascular Enlarging/Large: Excision
menstruation
FNA: Definitive Alternative to Surgery if <4cm: Cryoablation
Firm, Nontender, Solitary, Freely mobile, Fibrous tissue &
Well-circumscribed, Rubbery Lump Collagen arranged in a
*usually 2-3cm & no axillary involvement “swirl”

Gynecomastia Enlargement of glandular breast tissue Palpable mass ≥0.5cm diameter Clinical Dx Stop offending meds
& adipose tissue in males dues to Centrally located (usually under nipple)
increased estrogen or due to decreased Symmetrical Testosterone Levels Early/Physiologic: Observation
androgens Classically Bilateral *if treatment is needed, initiate within 6 months of onset,
Often TTP Mammogram: If breast after 12 months fibrosis may occur
Hormonal: cancer suspected
Infants: High maternal estrogen 1st: Tamoxifen
Puberty (10-14 yo): Lasts 6-24 months
Older Hypogonadism: Androgens

Idiopathic, Persistent pubertal Severe/Refractory/Large/Cosmetic/Fibrosis: Surgery

gynecomastia

Medications: Spironolactone,
Ketoconazole, Cimetidine, 5-a reductase
inhibitors, Digoxin, GnRH agonist
(Leuprolide), Thiazides, Phenothiazines,
Verapamil, Theophylline

Other: Malignacies (NSCLC, Renal,

Hepatic, Testicular, Gastric), Cirrhosis,
Hyperthyroidism, Chronic renal disease,
Klinefelter, Alcoholism

OBGYN About Clinical Presentation Diagnostics Management

Cervical 3rd MC OBGYN cancer Early Stages: Asymptomatic Colposcopy w/ Biopsy Carcinoma in situ (stage 0)
Cancer *(1st = Endometrial, 2nd = Ovarian) Excision (preferred): LEEP, Cold knife
Post-coital bleeding or Spotting conization, Loop
89
 Types
Squamous cell (MC)
Adenocarcinoma
Clear cell (linked with DES)
Spread
Primary nodes: Paracervical (MC),
Parametrial, Obturator, Hypogastric,
External iliac, Sacral
Takes 2-10 years to penetrate
basement membrane
RF
HPV (16, 18, 31, 33, 45, 52, 58)
Early sexual activity, STIs, Lots of
partners
Smoking, DES exposure
Cervical intraepithelial neoplasia
Immunosuppression
Irregular/Heavy bleeding Ablation: Cryotherapy, Laser
Discharge (nonspecific) TAH + BSO
Advanced: Pelvic/Back pain (may radiate to posterior Stage 1A
LE), Bowel/Urinary: Hematuria, Hematochezia, Total Hysterectomy
Vaginal passage of urine/stool Radical Hysterectomy
Conization
PE: Cervical discharge or Ulceration
Stage 1A2, 1B, IIA
External beam radiation + Brachytherapy
Radical hysterectomy + Bilateral pelvic
lymphadenectomy
Locally Advanced (IIB, III, IIVA)
Radiation + Chemo (cisplatin based)
Advanced
Radiation
Systemic Chemo

OBGYN Risks HPV Dysplasia Cancerous

Cervical Risk Factors: HPV & Cervical Dysplasia: CIN I: mild cervical dysplasia Bethesda System
Dysplasia/ Sexual Activity Factors: •HPV present in >80% of all CIN •LOWER 1/3 of epithelial lining
Cancer •multiple sexual partners •HPV 16: 50-70% HPV 18: 7-20% Atypical Squamous Cell (ASC-US/H)
•early onset of sexual activity *cigarettes have a synergistic effect with CIN II: moderate cervical dysplasia •undetermined significance, cannot exclude
•high-risk sexual partner HPV à cancer •LOWER 2/3 of epithelial lining high grade lesion

Infection Factors: High Risk: 16, 18, 31, 33, 35, 39, 45, 51,
•HPV infection (BIG ONE!) 52, 56, 58, 59, 68
•History of sexually transmitted infection
•Immunosuppression (HIV) •High-risk HPV test performed after
abnormal Pap
Others: •Most + do NOT develop CIN or CA
•multiparity
•long term OCP use Vaccines: Gardasil 9
(6, 11, 16, 18, 31, 33, 45, 52, 58)
•female: age 11-26, male: age 11-21
•<15yo: 2 doses, 6 months apart
•>15yo: 0, 2, 6 months
*min interval b/w 1st and 2nd 4 weeks,
b/w 2nd and 3rd is 12 weeks
CIN III: severe cervical dysplasia
•over 2/3 of epithelial lining; FULL
thickness
ALWAYS treat CIN II and III except:
•pregnant woman (wait till postpartum)
•CIN II in adolescents (high chance of
spontaneous regression)
Low-Grade Squamous Intraepithelial
Lesion (LGSIL/LSIL)
à corresponds to CIN-1
High-Grade Squamous Intraepithelial
Lesion (HGSIL/HSIL)
à corresponds to CIN II and III
à excision (LEEP) or ablation
Atypical Glandular Cells (AGC)
Glandular cells: normal components of the
endocervix à secrete mucus
Atypical: dont match normal glandular cells
but are not definitely cancer

Pap Smears Atypical Screening Colposcopy After Colposcopy

<21: NO screening
21-29: Every 3 Years
30-65: Pap + HPV Every 5 Years (preferred)
*Alternative: Pap Every 3 Years
3 options:
1. repeat serial cytology: every 6
months until 2 consecutives normal
-second abnormal à colposcopy
2. High-risk HPV: colposcopy if +
3. Immediate referral to colposcopy
Illuminated low-power magnification
-3-5% aqueous acetic acid solution
-directed biopsies of abnormal areas
-curette or brush of endocervical canal
Indications:
•abnormal cytology or HPV test
CIN I: expectant
•high chance of regression
•2 paps every 2 months or…
Pap + HPV at 6 months
•repeat if abnormal cytology or HPV+
•if all normal, then routine screening
90
 ≥65: NO screening if previous negative
HIGH RISK: HIV
Pap Twice in first year, then Annually
Before repeat, treat the underlying: •clinically abnormal cervix Surgery:
•hormones if atrophic vaginitis •unexplained intermenstrual or postcoital •CIN II/III
•antimicrobials for infections bleed •Invasive Cancer
LSIL, HSIL, ASC-H, AGC à •vulvar or vaginal neoplasia •Otherwise abnormal or unsatisfactory
Colposcopy •history of in utero DES exposure colposcopy

Contraceptive About MOA Side Effects

Male Sterilization MOST EFFECTIVE TIER Snip vas deferens
Vasectomy
20 ejaculations (3 months): Until effective
Safer, Less expensive

Female Sterilization MOST EFFECTIVE TIER Risk of regret!

Laparoscopic Bilateral Most based on age
Salpingectomy Laparoscopic bilateral salpingectomy: Decreased ovarian cancer <30 yo: 20%
(preferred), Laparoscopic 66% >30 yo: 6%
bilateral tubal ligation

IUD (Progesterone- MOST EFFECTIVE TIER Endometrial atrophy CI: Pregnancy, uterine anomaly, PID, uterine
Releasing) Thickens cervical mucus infection in last 3 months, uterine/cervical
Mirena, Lietta, Kyleena, Lasts 6 years: Mirena, Liletta Decrease tubal motility neoplasia, uterine bleeding of unknown etiology,
Skyla Lasts 5 Years: Kyleena MAY Inhibit ovulation (Not consistent) untreated acute cervicitis/vaginitis, acute liver
Lasts 3 Years: Skyla *not helpful for cysts or decreasing ovarian disease/tumor, increased susceptibility to pelvic
cancer risk infection, allergy, breast cancer or other
Mirena: Approved for heavy menstrual bleeding (80% stop progestin-sensitive cancer
ovulation within 1 year)

IUD & Implant

Safe & Effective contraception options for nulliparous women,
adolescents, & virgins
*Skyla: Slightly smaller might be better

IUD (Copper) MOST EFFECTIVE TIER Inflammatory response against sperm (Cu) 30%: Increased Cramping & Bleeding
ParaGard Inhospitable endometrium for implantation
Lasts 10 Years CI: Pregnancy, uterine anomaly, PID, uterine
infection in last 3 months, uterine/cervical
Can be used for: Emergency contraception up to 5 days after malignancy, uterine bleeding of unknown
unprotected intercourse etiology, mucopurulent cervicitis, Wilson’s
disease, allergy
No hormones = Doesn't lighten bleeding

IUD & Implant

Safe & Effective contraception options for nulliparous women,
adolescents, & virgins
*Skyla: Slightly smaller might be better

Implant MOST EFFECTIVE TIER Suppress ovulation Irregular bleeding

Nexplanon, Implanon Thicken cervical mucus *Biggest Complaint: Irregular spotting for up to 3
Progestin-containing (etonogestreol) implant Endometrial atrophy years (typically wont normalize)

91
 Lasts 3 Years
Not studied in women who weighed >30% of
Placed sub-dermally in the upper arm IBW (ideal body weight)
*Best to implant during or right after period (when lining is
thinnest) in non dominant arm

IUD & Implant

Safe & Effective contraception options for nulliparous women,
adolescents, & virgins

Injectable VERY EFFECTIVE TIER Thicken cervical mucus Bleeding will get worse before it gets better
Depo-Provera (Depot Thin endometrium (irregular bleeding up to a year)
Medroxyprogesterone 17-Acetoxy-6-Methyl Progesterone 150mg May suppress ovulation
Acetate) IM injection: Every 12 weeks (3 months) Black box 2004: Shouldn't use >2 years
(concerned about bone loss)
Drug Vacations: Not done Restored within 5 years of stopping, Shouldn't
Supplement: Calcium & Vitamin D stop use

Perfect use: 0.3 pregnancies/100 women Weight gain: 18 yo + BMI >30

Typical use: 3 pregnancies/100 women
CI: Pregnancy, Unexplained uterine bleeding,
Liver disease, CV disease, Thromboembolic
disease

92
Contraceptive About About MOA
Oral VERY EFFECTIVE TIER Estrogen + Progesterone (CHC) (COC) Inhibit Ovulation Withdrawal bleed 2-5 days after
Contraceptives Ideal: Begin 1st day of cycle Thicken Cervical Mucus stopping active pills
(OCP) Estrogens Traditional: Begin Sunday following onset Thin Endometrium
CHC, POP Ethanyl Estradiol (MC) menses DDI
Mestradiol Encourage regular routine of taking pills Ways to Take Increase/Decrease efficacy of
Estradiol valerate same time daily 21 Days Active -> 7 Days Placebo Analgesics: Tylenol, opioid
84 Days Active -> 7 Days Placebo Other: warfarin, lamotrigine, benzos,
Progesterones 365 Active corticosteroids, theophylline,
Norethindrone “Mini Pill” Progesterone Only (POP) (Mini Pill) metoprolol
Levonorgesterel Lasts STRICT 24 HOURS Reduce OCP efficacy
Desogestrel 1 pill at the same time each day ABX, Anticonvulsants, Sedatives
Gestodene
Norgestimate CI: Estrogen is the concern
3rd Gen: Desogesterol, Norgestimate *give POP
4th Gen: Drispirenone
CI: Pregnancy, uncontrolled HTN,
DM, CAD, migraines with aura,
DVT/PE, thrombophilias, cardiac
defects/arrhythmias,
breast/endometrial cancer, liver
problems, Smoker >35 yo

Transdermal VERY EFFECTIVE TIER MOA: Similar to OCP Attempt to reattach if comes off C/I: Similar to OCP
Patch
Xulane, Twirla Estrogen & Progesterone Detached <24 hours Women >90kg: Increased risk of
Continue as usual pregnancy
Place 1 patch, Once per week for 3 weeks,
Then remove for 1 week (withdraw bleed) Detached >24 hours Without withdraw bleed: May have
*Can do without withdraw bleed but may Nw patch, backup contraception x1 week irregular spotting
have irregular bleeding

Place anywhere except the breast

Vaginal Ring VERY EFFECTIVE TIER

NuvaRing,
EluRyng Estrogen & Progesterone
Insert for 3 weeks -> Remove for 1 week
Must be refrigerated
Shelf Life: 4 MONTHS
Designed to remain in during sex but can
remove for sex but must replace within 3
hours

Male Condom EFFECTIVE TIER Prevent semen from entering vagina/cervix High failure rate Even higher in
teens!
Must be placed prior to sex every time
Prevents against STDs
*east effective with HPV

Perfect use failure: 2/100

93
 Typical use failure: 18/100

Female Condom EFFECTIVE TIER Prevent semen from reaching the cervix Do not use with a male condom
More expensive, Not convenient
Placed inside the vagina

Cervical Cap & EFFECTIVE TIER

Diaphragm
Placed over cervix
Must be fitted by a healthcare professional
Not commonly used

Spermicide LEAST EFFECTIVE TIER Max duration: 1 hour If used without other forms of
contraception, they are not very
Active Ingredient: Nonoxynol-9, effective
Octoxynol-9
Creams, Gels, Foam, Film Not effective at preventing STDs

Do not use with condoms May increase rate of HIV

transmission
28/100 will get pregnant within 1 year
Do not use with condoms

94
Emergency ParaGard Plan B
Emergency ParaGard: Most Effective Method Plan B: Levonorgestrel (progesterone)
Contraception
ParaGard, UP TO 120 HOURS after unprotected sex Two Dose Method: 0.75mg & 0.75mg
Plan B, Yuzpe 1st dose WITHIN 72 HOURS (possibly up
Method, to 5 days), 2nd dose 12 HOURS AFTER
Ulipristal
Acetate One Dose Method: 1.5mg
Only 1 dose (efficacy similar)
Prevents 75% of Pregnancies
Does not disrupt an existing pregnancy
It is not the abortion pill
No clinical exam is necessary
MOA: Delay/inhibit ovulation, Prevent
implantation
Yuzpe Method
Yuzpe Method: COC
Ethinyl estradiol +
Levonorgestrel/Norgestrel
Dosing pattern is different than use as an
oral contraceptive
2 Doses: 1st dose WITHIN 72 HOURS,
Repeat dose 12 HOURS LATER
100-120mcg Ethinyl estradiol
500-600mcg Levonorgestrel/Norgestrel
MOA: inhibits or delays ovulation
ADR: N/V
*Meclizine 50mg with 1st dose
Ulipristal Acetate
Ulipristal Acetate (UPA) (Ella,
EllaOne, Fibristal)
30mg UP TO 120 HOURS after
unprotected sex
MOA: Antiprogestin (selective
progestin receptor modulator)
Progestin-containing contraceptives:
Should not be used with UPA or for 5
DAYS after because of concerns that
the progestin contraceptive will
interfere with UPA action

ADR: N/V, Cramping

Spontaneous Pregnancy ends before 20 weeks gestation Symptoms Threatened Complete

Abortion *Most occur prior to 12 weeks Crampy abdominal pain POC: Intact POC: All expelled from uterus
Vaginal bleeding Cervical os: Closed Cervical os: Usually closed
Types Supportive: Observation at home, RhoGAM (if indicated)
Threatened Dx Bedrest, Close FU FU with B-hCG
Inevitable US, CBC, Type & Screen, Rh screen, Serial Serial B-hCG: Doubling = Viable
Incomplete B-hCG titers, Progesterone levels Missed
Complete Inevitable POC: Intact
Missed POC: Intact Cervical os: Closed
Septic Cervical os: Dilated <16 Weeks: Dilation & Curettage
*Threatened is the only one that is <16 Weeks: Dilation & Curettage ≥16 Weeks: Dilation & Evacuation
potentially viable ≥16 Weeks: Dilation & Evacuation Medical: Misoprostol
Medical: Misoprostol
Etiology: Chromosomal abnormalities (MC), Expectant Management Septic
Maternal factors (STI, Antiphospholipid POC: Some retained
syndrome, Trauma, Rh isoimmunization, Incomplete Cervical os: Closed
Malnutrition, Anatomic abnormalities POC: Some expelled from uterus *Cervical motion tenderness
Cervical os: Dilated *Foul brown discharge, Fever, Chills
Depends on Expectant: Allow POC to fully pass Dilation & Evacuation + Broad ABX
Products of conception (POC) & Cervical os with serial B-hCG & TVUS to (Levofloxacin + Metronidazole)
*POC = Fetus, Placenta, Any other tissues determine when complete
that may result from a fertilized egg <16 Weeks: Dilation & Curettage
≥16 Weeks: Dilation & Evacuation
All Rh(-) Women: Anti-D Rh Medical: Misoprostol
Immunoglobulin for all abortions

95
Induced Mifepristone then Misoprostol 24-48 hours MTX then Misoprostol 3-7 days later Dilation & Curettage Dilation & Evacuation
(Elective) later *Safe up to 7 weeks *Used during 4-12 weeks gestation >12 weeks gestation
Abortion *Safe up to 10 WEEKS *Less effective
*Return 7-14 days to confirm complete
termination of pregnancy MTX: Folate antagonist

Mifepristone: Progesterone receptor

antagonist (dilation and softening of cervix,
placental separation)

Misoprostol: Prostaglandin E1 analog

(uterine contractions)

96
Menopause Definitions
Menopause Cessation of menses for >1 year due to loss
of ovarian function -> Low E & P
Naturally: Average 51 yo
Prematurely from medical intervention
Perimenopause “menopause transition”
Time around menopause, Most
symptomatic phase for women
Premature Menopause: Occurs <40 yo
Premenstrual PMS (Premenstrual Syndrome): Cluster of
Disorder physical, behavior, mood changes with
cyclical occurrence during luteal phase of
Also in menstrual cycle
OBGYN
PMDD (Premenstrual Dysphoric Disorder):
Severe PMS with functional impairment
where anger, irritability, and internal
tension are predominant (DSMV criteria)
Hormone/HPO Axis Change
Classic
Early: Change menstrual cycle pattern
Vasomotor: Night sweats
Increased: Core body temperature, Skin
blood flow, HR
Intense feeling of heat with reddening of
upper body
Increased: HR peak, Skin blood flow peak,
Sweating
Chills, Shivering
Vulvovaginal: Dyspareunia
Vaginal dryness, Vulvovaginal
irritation/itching, Vaginal atrophy
Other
Sleep disturbances besides night sweats
Cognitive (memory, concentration)
Psychological (depression, anxiety, moody)
Physical: Abdominal bloating & Fatigue
(MC), Breast swelling/pain, Weight gain,
HA, BM changes, Muscle/Joint pain
Emotional: Irritability (MC), Tension,
Depression, Anxiety, Hostility, Libido
changes
Behavioral: Food cravings, Poor
concentration, Noise sensitivity, Loss of
motor sense
Dx: Onset 1-2 WEEKS BEFORE menses
(luteal phase), Relieved within 2-3 days of
menses + ≥7 days symptom free during
follicular phase (period onset to ovulation)
*symptom diary for >2 cycles
Hormones Clinical Presentation
ANDROGRENS HT: Estrogen-alone & estrogen-progestogen
•less production of androstenidone
(primary androgen in women) Estrogen Therapy (ET)
•decreased levels of testosterone Systemically for women who do not have a
*less sex hormone-binding globulin à uterus, Locally in very low doses for any
more active floating around woman with vaginal symptoms
ESTROGEN: *draw estradiol level Estrogen-Progestogen Therapy (EPT):
•reduced endogenous estrogen Progestogen is added to ET to Protect
•greatest decrease in estradiol women with a uterus against endometrial
*primarily secreted from adrenal cancer, which can be caused by estrogen
•estrone levels fall, but not as much alone
*estrone is predominant estrogen after
menopause
PROGESTERONE
•after menopause, no functional follicles
à no CL à low P
•adrenal glands produce remaining
•NO clinical use in diagnosis
GONADOTROPINS *BEST
•FSH and LH RISE (FSH >LH)
•measure FSH, LH, estradiol to help
diagnose menopause
*can measure FSH & LH with estradiol
(FSH and LH increase because no
negative feedback from estrogen and
progesterone)
Lifestyle Modifications: Stress
reduction & Exercise (most
beneficial), Reduce (Salt, Cigarette,
Caffeine, EtOH), NSAID, Vitamin B6
&E
Emotional Symptoms w/ Dysfunction
1st: SSRI: Fluoxetine, Sertraline,
Citalopram
Don’t Want SSRI: OCP (esp
Drospirenone-containing)
No Response SSRI/OCP: GnRH
Agonist with E+P addback therapy
97
 Benefits
HRT Known:
•reduced SX (vasomotor, GU)
*vaginal estrogen is as efficaious as oral
or transderm for GU symptoms
•reduced risk of osteoporosis: improves
density, reduce fracture *benefit from E
Possible
•improved skin collagen & thickness
•reduced UTI
•reduced falls
•reduced cataracts, osteoarthritis, DM
•reduced colon CA (combo therapy)
•reduced CHD (cholesterol clearance)
Lipids
lipids: lower LDL, higher HDL
but can increase TG
Risks
•endometrial CA: hyperplasia within 1yr
-unopposed E à proliferation, hyperplasia,
neoplasia; give Progesterone to decrease
•breast CA: only in COMBO (due to P)
-risks: early menarche, late menopause
•thromboembolic: 2x w/ combo, 33% E only
-lower chance with transdermal
•stroke: increased risk in E only and combo
-lower incidence with transdermal v oral
•gallbladder disease: greater risk with E-only
Other Effects *menstrual cycle symptoms
•other: edema, bloat, mastodynia & breast
enlargement, PMS, HA, lots cervical mucus
CI:
•breast & E-dependent CA *endometrial,
undiagnosed abdominal vaginal bleeding
•thromboembolism, liver, hypersensivity
•pregnancy
Caution: gallbladder, cholestatic jaundice, high TG,
hypothyroid, flui with cardiac/renal, hypocalcemia,
endometriosis, hepatic hemangioma
Main Treatment
1st line: transdermal (decrease SE)
•0.625mg PO conjugated estrogen
•increase dose at 1 month intervals
•must add PROGESTIN if patient has
an intact uterus (no E alone)
-medoxyprogesterone acetate(MPA)
-micronized P: lower risk of breast
cancer and CHD
Regimens:
NOT REC. for >3-4yr
Regimen One: *older method
•Estrogen on days 1-25
•progesterone days 14-25
•withhold both day 26-end of month
•light, painless period each month
Regimen Two: *most common
•daily E & P together w/o stop
•initial bleeding or spotting
•eventually: atrophic endometrium
Only use HRT for vaginal atrophy
and hot flashes
Other Options
Other Forms:
•Progesterone only: *better than SNRI
depot MPA IM or po norethindrone
-more effective than SNRI
•Tissue Selective Estrogen Complex
SERM (Duavee or BZA/BE) + Estrogen
-agonist bone; antagonist endometrium
-neutral on breast
-lower risk breast & endometrial CA
SE: VTE, liver disease
•PO Estrogen + Levonorgestrel IUD
-avoid systemic effects of P but prevent
endometrial hyperplasisa and cancer
•SSRI: Citalopram, Escitalopram
-Paroxetine: caution with Tamoxifen
•SNRI: Venlafaxine, Desvenlafaxine
SE: insomnia
•Anticonvulsant: Gabapentin,
•Clonidine: helpful with comorbid HTN and
menospausal s/s
CAM: black cohosh, isflavones, Vit E,
exercise, weight loss, relaxation
98
OBGYN About
Abnormal Menorrhagia "Heavy"
Uterine “AUB/HMB”
Bleeding (AUB) *Loss ≥80cc per cycle (normal 30-40cc)
*Duration: >7 days
Metrorrhagia "Intermenstrual"
“AUB/IMB”
*Irregular menstrual bleeding
*Bleeding between periods
Polymenorrhea
*Intervals every 21 days or less
Oligomenorrhea
*Less frequently than every 35 days
MCC of AUB: Ovulatory
More common than AUB-O (AUB related
to ovulatory dysfunction)
AUB-O "Anovulatory AUB"
Typically, is the result of: Endocrinopathy
(PCOS)
Mechanism: Unopposed estrogen
Bleeding characteristics: Ranges from
amenorrhea to irregular heavy cycles
(Unpredictable)
Endometrium that develops under these
conditions is fragile, vascular, lacks
stromal support
Causes: Adolescence, Peri-menopause,
Lactation, Pregnancy, Hyperandrogenism
(PCOS), Hypothalamic dysfunction
Dysmenorrhea Painful menstruation that affects normal
activities
Primary: Increased prostaglandins
*Increased uterine wall contractions
*Usually starts 1-2 year after menarche
Secondary: Pelvis/Uterus pathology:
Endometriosis, PID, Adenomyosis,
Leiomyomas
Endometriosis Benign, Endometrial glands & stroma are
present outside the uterine cavity & walls
Amount of disease does not correlate with
the patient's symptoms
Causes Diagnostics Treatment
PALM-COEIN CBC, Platelets, Beta-hCG, AUB-O
Describe different causes of AUB (abnormal PT/PTT/INR Cyclic/Continuous Provera
uterine bleeding) OCP (esp Chronic anovulation, PCOS)
*applies to reproductive aged only HMB since menarche + ONE of NSAID
the following Tranexamic Acid (lysteda)
PALM: Structural *Postpartum hemorrhage Levonorgestrel containing IUD
Polyp: Benign growth from the endometrial layer *Surgery bleeding Surgical: No longer interested in child
Adenomyosis: Cells that line endometrium go into *Bleeding associated with dental Endometrial Ablation: Not 1st line
myometrium procedures therapy and appropriate counseling required
Leiomyomata "Fibroid": Benign, tend to shrink Or TWO of the following Hysterectomy: Failure of medical Tx
with menopause, some contain estrogen receptors *Bruising or epistaxis 1-2x/mo
and may grow, Want to see patient ever 6 months *Frequent gum bleeding
Malignancy/Hyperplasia: Precancerous/Cancerous *FamHx of bleeding symptoms
COEIN: Non-Structural
Coagulopathy: Inherited: von Willebrandt
Disease: vWF antigen, Factor VIII, Ristocetin.
Acquired: Warfarin, heparin, NSAID, clopidogrel,
aspirin, hormonal contraceptives, ginkgo, ginseng,
motherwart
Ovulatory Dysfunction
Endometrial
Iatrogenic
Not Yet Classified
Recurrent, crampy midline lower Labs & Imaging Supportive: Heat compress, Vitamin B, E,
abdominal/pelvic pain 1-2 days before or at Done if pelvic disease suspected Exercise
onset of menses
Gradually diminishes over 12-72 hours 1st: NSAID, OCP
May radiate to lower back & thighs
May be associated with: HA, N/V Unresponsive after 3 cycles Laparoscopy
*Rule out secondary causes
PE Primary: Normal MCC secondary in younger patients: PID,
Endometriosis
Triad Direct Visualization with OCP: DoC
Dysmenorrhea (painful period) Laparoscopy or Laparotomy NSAID
Dyspareunia (painful sex) Mirena IUD
Dyschezia (painful poop) Acceptable to initiate medical Progestin (cant take Estrogen)
treatment if you suspect Danazol: Competitive E&P Receptor
Cyclical: Week before and during period endometriosis ADR: Irreversible deepening of voice
99
 Retrograde Menstruation *FU in ~3-6 months to assess
Implantation theory response
Sampson’s theory *If no response, consider
diagnostic laparoscopy
GnRH Agonists (Depolupron)
ADR: Chemical Menopause
*Short Duration Treatment (6 months)
If patient is satisfied with treatment and her
symptoms are under control, then she may
continue for more than 6 months provided
they are placed on “add-back” therapy (not
during 1st 6 months)
"Add Back" Therapy (E + P)
Lower dose than normal, CV & Bone loss

Surgery If Patient Desires Future Fertility

Laparoscopic or Open Surgery: Destroy
all endometriotic implants & Remove all
adhesive disease
*Large Endometriomas (>3cm): Amenable
only to surgical resection

Surgery If Patient Does Not Desire Future

Fertility
Total Abdominal Hysterectomy (TAH),
Bilateral Salpingo-Oophorectomy (BSO)
Dissection of All Adhesions
*Most comprehensive surgery includes all

Pelvic Ascending infection of upper reproductive Pelvic/Lower abdominal pain, Dysuria, Primarily Clinical Dx Outpatient
Inflammatory tract Dyspareunia, Vaginal discharge/bleeding, N/V Abdominal tenderness + IM Ceftriaxone 250mg Once +
Disease (PID) Chandelier Sign + Doxycycline 100mg BID 14 Days
Etiology: Usually mixed: Chlamydia PE: Lower abdominal tenderness, Fever, Adnexal tenderness + *Often add: Metronidazole 500mg BID 14
trachomatic (MC), Neisseria gonorrhea, Purulent cervical discharge ≥1 of the following: Days
G. vaginalis, M. genitalium, Anaerobes, Chandelier Sign: Cervical motion tenderness *(+)Gram Stain *PCN Allergy: Levofloxacin +
Enteric/Respiratory pathogens *Temperature >38°C Metronidazole
*WBC >10K
RF: Multiple sex partners, Unprotected *Pus on Inpatient
sex, Prior PID, 15-19 yo, Nulliparous, IUD culdocentesis/laparoscopy 2nd Gen Cephalosporin (Cefoxitin,
*Pelvic abnormality on Cefotetan) + IV Doxycycline
US/bimanual exam *PCN Allergy/Pregnancy: Clindamycin +
*Increased ESR/CRP Gentamicin

Work Up
B-hCG: R/O ectopic pregnancy
NAAT: Gonorrhea/Chlamydia
Laparoscopy: Most accurate
*Rarely performed, done if
uncertain, severe, or no
improvement with ABX

Pelvic Organ Types Baden-Walker System "Half Way System" POP-Q System (Pelvic Organ Observation, Kegel exercises
Prolapse Anterior = Cystocele Everything in reference to hymen Prolapse-Quantification) *Kegels/Pelvic Floor Therapy (more likely
Apical = Uterine/Vaginal Vault (apex) Grade 0: Normal position for each site Stage is based on position of to prevent, rather than improve)
Posterior = Enterocoele, Rectocele Grade 1: Descent halfway to the hymen vaginal walls relative to hymen Estrogen (good option if atrophy)
100
 Procidentia = Complete Uterine
Prolapse
RF
Age, Multiparity (esp with injuries
secondary to childbirth), Smoking,
Obesity, Pulmonary disease (chronic
cough), Genetics, Connective tissue
disorders, PSH (hysterectomy)
Colporrhaphy = Vaginal wall repair
Grade 2: Descent to the hymen
Grade 3: Descent halfway past the hymen
Grade 4: Maximal possible descent for each site
Stage 2 is -1 to +1
9 different points that you measure
in reference to the hymen (-1
before, +1 after)
Aa (anterior wall), Ba (anterior
wall), C (cervix/cuff), gh (genital
hiatus), pb (perineal body), tvl
(total vaginal length), Ap (posterior
wall), Bp (posterior wall), D
(posterior fornix)
Pessaries
Surgery Anterior (like hernia)
Anterior Colporrhaphy ± Graft
Paravaginal Defect Repair
Surgery Apical
Sacrocolpopexy (Gold standard)
Attaches surgical mesh from the vagina to
the sacrum (tail bone)
*Takes longer, Mesh graft, Less prolapse
but higher complication rates
Fixation via: Sacrospinous Ligament,
Uterosacral Ligament, or Iliococcygeus
Muscle Fascia
*Doesn't take as long, Less successful

Surgery Posterior
Posterior Colporrhaphy

Cystocele Bladder Heaviness, Pressure, Sensation of: Bulge/Fullness

Prolapse Location: Anterior "Something falling out"
Aggravation: Prolonged standing
Alleviation: Lying down
± Frequency, Urgency, Incontinence, Retention

Apical Prolapse Uterine/Vagina apex (vault) Same as Cystocele

Location: Apical

Enterocele Small intestine Most asymptomatic

Prolapse Location: Posterior Low back/sacral pain, Perineal pressure, Palpable
bulge
Rapid progression typical

Rectocele Rectum Obstructive defecation (digital reduction), Genital

Prolapse Location: Posterior looseness, Perineal pressure, Palpable bulge

101
OBGYN About
Vaginal MCC by: Candida Albicans
Candidiasis (Gram(+) Unicellular Oval-shaped
Diploid Fungus)
“Yeast Infection”
Can be found in vagina of
asymptomatic patients: Commensal
of mouth, rectum, vagina
RF: Immunosuppression, DM,
Pregnancy, Recent broad spectrum
ABX use
No need to treat sexual partners
Bacterial Vaginosis NOT an STD
(BV) Normal Bacteria Overgrowth
Decreased: H2O2 producing
Lactobacilli
Increased: Gardnerella Vaginalis
(Gram(-) Anaerobic Bacillus)
RF: Multiple/New sex partners,
Female partners, Oral sex,
Douching, Smoking, IUD
Trichomoniasis Anaerobic Flagellated Protozoan
"Trich" Parasite: Trichomonas Vaginalis
Most Prevalent Non-Viral STD
Incubation: 3 Days to 4 Weeks
Can Infect: Vagina, Urethra,
Endocervix, Bladder
HSV HSV-1 & HSV-2: 160nm
Enveloped Icosahedral (Spherical)
Double-stranded DNA Virus
Sensory nerve endings ->
Retrograde axonal transport to the
dorsal root ganglion -> Lifelong
latency
Spontaneous reactivation results in
anterograde transport of virus
Clinical Presentation
Pruritus, Burning, Erythema, Edema with
excoriations
Discharge: White Curdy Cottage Cheese
Discharge: Thin White
10% KOH -> Whiff test: “Fishy" Odor
pH >4.5 (normal 3.5-4.5)
Asymptomatic: Up to 50% women
(colonization can last months to years)
Discharge: Foul, Thin, Yellow/Green
± Dysuria, Dyspareunia, Vulvar pruritus,
Vaginal spotting, Lower abdominal pain
"Strawberry Spots" on Cervix
Elevated Vaginal pH (more basic)
Vesicles -> Ulcer -> Crusting (Shedding
mainly occurs during vesicles & ulcers)
Burning, Severe pain, Dysuria, Low grade
fever, HA, Myalgias
Diagnostic
Wet Mount: Normal Saline & 10% KOH
Prep: Yeast buds, Hyphae
Culture: Gold standard
*Only doing if patient not responding,
HIV, DM not controlled
PCR: BD Max Vaginal Panel
*Done in practice
NO culture, NO pap smear
Gram Stain: Gold standard
Amsel’s Criteria: (3 of 4)
Homogenous Thin White Discharge
10% KOH -> Whiff test: “Fishy" Odor
Wet Mount: Clue Cells >20% (fuzzy
without sharp edges)
pH >4.5 (normal 3.5-4.5)
Wet Mount: Trichomonads (protozoa
with flagella)
NAAT: Trichomonal DNA (most
sensitive & specific tests)
Elevated pH
Cell Culture (previous gold standard)
NAAT: Preferred (put probe in the lesion)
Serologic Testing: Only IgG antibody
assays
*Seroconversion following initial
infection takes ~3 weeks
*IgM testing is not recommended (not
great marker for new infection)
Treatment
First Occurrence (No Co-morbidities)
Fluconazole [150mg Once]
Topical Antifungal
*no one agent superior to another
Complicated Candidiasis 10-20%
(Recurrent, Severe, Non-Albicans, DM,
Immunocompromised)
Fluconazole [150mg Q72H, 2-3 Doses]
≥4 Candida Infections in One Year
[10-14 Days] of Topical Agent or Oral
Fluconazole then Fluconazole [150mg
Weekly X 6 Months]
1st: Metronidazole [500mg BID X 7
Days], Metronidazole Gel [0.75% One
Applicator Full (5g) Intravaginally QD X 5
Days], Clindamycin Cream [2% One
Applicator Full (5g) Intravaginally QHS X
7 Days]
Condom use for 3-6 months
No benefit from: Probiotics, Lactobacillus
supplements
1st: Metronidazole [500mg BID X 7 Days]
*Alternative: Tinidazole [2g Once]
*Allergic to Nitromidazoles:
Metronidazole (flagyl) Desensitization
Retest: 3 Weeks to 3 Months
Antiviral
Antipyretic
Pain Medication
Suppressive Therapy
102
 Mean Incubation Period: 1 Week
Gonorrhea Neisseria gonorrhea
Gram(-) Diplococci
Incubation: 2-8 Days
Syphilis Treponema Pallidum: Gram(-)
Micro-aerophilic Spirochete (Long,
Slender, Spiral) Bacterium
Serologic Results Interpretations
[Treponemal, Non-Treponemal, TP-
PA]
[-,-]: Absence or Before conversion
[+,-,+]: Prior treated or Untreated
[+,-,-]: False positive treponemal
[+,+]: Active or Recently treated or
Persistent titers
[-,+]: False positive non-treponemal
Chlamydia Chlamydia trachomatis
MC overall bacterial cause STI
Urethritis & Cervicitis: Discharge, PID,
Epididymitis, Prostatitis
Dissemination: Triad: Dermatitis
(maculopapular, petechial rash),
Polyarthralgia, Tenosynovitis
Often: Fever, Chills, Malaise
Purulent gonococcal septic arthritis (esp
knee)
*in women it occurs more frequently during
menses
Primary
Chancre: Isolated Nontender Ulcer with
Raised Rounded Borders
Secondary
6 weeks-6 months after chancre
Maculopapular rash: Palms, Soles, Mucous
Tertiary
Untreated syphilis that may appear up to 20
years after latency
CV, CNS, MSK
Up to 40% asymptomatic (esp men)
Urethritis: Purulent/Mucopurulent discharge,
Pruritis, Dysuria, Dyspareunia, Hematuria
PID: Abdominal pain, Cervical motion
tenderness
Reactive Arthritis (autoimmune rxn):
Urethritis, Uveitis, Arthritis HLA-B27(+)
Lymphogranuloma Venereum: Genital/Rectal
lesion with softening, suppuration,
lymphadenopathy
NAAT (1st void/catch preferred)
*most sensitive & specific for C.
trachomatis, N. gonorrhea, M. genitalium
*recommended over culture
Gram Stain
UA
Synovial Fluid
Blood Culture
Direct Detection of Spirochetes: Gold
Clinical Assessment + Serologic Testing
*Done in practice
* Seroconversion 3-6 weeks after
exposure (can get false negative even w/
chancre)
Treponemal (ELISA "EIA"): Detect
antibody to: T. Pallidum Proteins
Non-Treponemal (VDRL, RPR): Detect
antibodies to: Lipoidal antigens,
Damaged host cells, Possibly treponemes
*Lupus, Pregnancy, Cancer: Can get false
negative non-treponemal test
Treponema Pallidum Particle
Agglutination (TP-PA): Confirmatory,
Treponemal specific test
NAAT (1st void/catch preferred)
*most sensitive & specific for C.
trachomatis, N. gonorrhea, M. genitalium
Genetic Probe, Culture, Antigen detection
Urethritis & Cervicitis: 1st Line
IM Ceftriaxone 500mg if <150kg or 1g if
>150mg
Gonococcal Arthritis: IV Ceftriaxone 1g
Every 24 Hours
Primary, Secondary, Early Latent (<1
Year)
IM Benzathine PCN G [2.4 Million Once]
*Alternative (PCN Allergy Non-Pregnant):
Doxycycline [100mg BID X 2 Weeks]
*Pregnant: PCN Desensitization
Late Latent (>1 Year), Tertiary, CV
IM Benzathine PCN G [2.4 Million
Weekly X 3 Doses]
*Alternative (PCN Allergy Non-Pregnant):
Doxycycline [100mg BID X 4 Weeks]
*Pregnant: PCN Desensitization
Azithromycin 1g PO Once or
Doxycycline 100mg BID X 7 Days
103
Chancroid Haemophilus Ducreyi (Fastidious
Gram(-) Coccobacillus)
Looks like syphilis but it's tender
Incubation: 3-10 days
Granuloma Klebsiella Granulomatis (Gram(-)
Inguinale Bacillus)
"Donovanosis" Incubation: Days to Weeks
Lymphogranuloma Chlamydia Trachomatis
Venereum "LGV" Serotypes: L1, L2, L3 (Gram(-)
Coccobacillus)
Incubation: 3 Days to 2 Weeks
Soft Irregular Margins, Friable Bases Cell Culture: H. Ducreyi Azithromycin [1g Once]
Tender Inguinal Lymphadenopathy IM Ceftriaxone [250 mg]
NAAT: Now accepted standard for
If Large & Fluctuant: Buboes may suppurate diagnosis
& form fistulas
Many Painless Inflammatory Nodules -> Wright-Giemsa Stain Microscopy: Azithromycin [1g Weekly For At Least 3
Highly Vascular Nontender Ulcers Donovan Bodies "Closed Safety Pin" Weeks]
*Ulcers heal by fibrosis (can result in
scarring resembling keloids)
LN: Usually Uninvolved
Stages Culture, Immunofluorescence, NAAT Doxycycline [100mg BID X 21 Days]
1) Small Painless Papule Genital lesions, Affected LN, Rectum
2) Regional Lymphadenopathy "Groove
Sign" on Nodes
3) Anogenitorectal Fibrosis
104
Pregnancy Signs/Symptoms
Pregnancy Amenorrhea
•cessation of menses in a health
•not reliable until 10d + after menses
•can have “implantation bleeding” for
blastocyst
Vaginal/Cervical Changes
•Chadwick: mucosa appears dark
bluish red & congested
•Goodells sign: cervical softening
•cervical mucus: thick due to P
•uterine change:
•Haegers sign: isthmus soften (6-8)
•Ladin sign: uterus softens (6wk)
Estimate Date of Delivery
•Naegele’s Rule
-LMP + 7days – 3 months
-assumes pregnancy begun
2wk before ovulation
•Ultrasound
à 1st trimester crown rump
is MOST ACCURATE
Breast Changes
•tenderness & paresthesia
•increase in breast & nipple
•thick yellowish fluid à colostrum
•areola becomes deeply pigmented
Skin Changes ~16th wk
•increased pigmentation, linea nigra
•pruritic papules à steroids
•chloasma à “mask”
•striae (stretch marks)
Fetal Movement 16-20 weeks
•Primigravida ~20wk
•Multigravida ~16-18wk
Heart Tones: 10-12 weeks
Prenatal Visit
History
•obstetrical hx: pregnancies,
complications, infertility
•menstrual: interval between menses,
contraceptives
•fhx, shx, medical hx
Physical Exam
•uterine size *bimanual
-small orange ~6wk
-large orange ~8wk
-grapefruit ~12wk
•cervical dilation, length, consistency
*bimanual
•pelvic architecture *bimanual
Diagnostic Tests
Beta human chorionic gonadotropin (B-hCG) Transvaginal US
•produced by syncytiotrophoblasts gestational sac: small anechoic fluid
•blood and urine about 8-9d after ovulation within endometrial cavity
•prevents involution of corpus lutem à first evidence ~4-5wk
•rare false (-): MCC is herephilic antibodies yolk sac: bright echogenic ring with
*urine would be negative anechoic center
•false (+) causes: exogenous hCG, renal failure with à confirms location ~5-6wk
failed hCG clearance, pituitary hCG, tumors fetal pole/embryo: ~6wk
*home pregnancy tests require value of 12.3 to detect crown rump length: used up to 12wk
95% pregnancies à use 1st urination to predict the due date, accurate
within 4d
Lab Tests RhoGam
First Visit MOA: suppresses immune response
•CBC: WBC, Hgb, Hct, Plt of Rh negative individuals to Rh (+)
*monitor anemia & thrombocytopenia RBCs
Blood type and Rh Factor: if Rh (-) mother and Rh (+) Dose: 0.3mg eradicates 15ml of fetal
fetus then receive RhoGam ~28thwk *RhD RBC
•antibody screening
Should be given
rubella serology: infection in 1st semester can cause -bleeding or trauma prior to 28wk
abortion, malformations -postpartum if infant Rh (+)
-invasive diagnostic prenatal test
•pap smear
•gonococcal & chlamydia, syphilis, HIV, hepatitis Keihauer-Betke
•urinalysis •tests amount of fetal RBC in
•urine culture & sensitivity maternal circulation
105
Counseling
Prenatal Vitamin
•400 micrograms of folic acid
*4mg if hx neural tube defect
Employment
•work until labor
Weight Gain
•Maternal weight gain is correlated with
infant weight
*obese women who gain <15lb have the
lowest complication rate
*25-35lbs, underweight: 28-40lbs,
obese: gain around 12-20lbs
Obesity associated risks:
•gestational HTN, DM, preeclampsia
•macrosomia
•C-section
Routine Care
•Every 4 weeks until 28 weeks
•Every 2 weeks until 36 weeks
•Every week unil delivery
Prenatal Surveillance
At each return visit:
•US fetal growth (dating & anatomy)
•maternal BP/weight
•U/A, protein, glucose
•S/S: leak, contractions, N/V, bleed
Diet: additional 100-300kcal/day
- 60-80g protein/day
Seafood
•avoid fish and shellfish contain mercury
•High risk: shark, sword, mackerel, tile fish
•no more than 6oz of white tuna
Lead
Risk factors:
-recent immigrant
-living near lead source
-using lead glazed pottery
-eating nonfood substances
-using imported cosmetics
-remodeling home with lead
-consuming lead water
-living w/ someone with elevated lead
Common Complaints
Nausea/Vomiting “morning sickness”
•common in 1st trimester until 16th wk
TX: small meals, BRAT diet, ginger,
vitamin B6 + Doxylamine, Zofran
•Hyperemesis gravidum: vomiting severe that
dehydration, electrolyte, and acid-base disturbances
and starvation ketosis
•hypokalemic, hypochloremic metabolic alkalosis
Back Pain *low back pain
•increased with gestational age
•Reduce By: squatting rather then bending, avoid
high heels, use a pillow back support, belly band,
PT, Tylenol prn
Seat Belt
three point restraints with lap belt under abdomen
and across upper thigh
Air Travel
can fly up to 36wk, ambulate hourly and wear
TED hose
Dental: no CI including x-rays
Coitus (intercourse): not harmful
Caffeine: >5c can increase abortion, <200mg
(10oz) not associated with issues
Exercise
•do not limit; engage in moderately intense
activity for 30min+/day; *don’t lift >25lb
•avoid: high risk falling or trauma & scuba
Hemorrhoids
•increase in pelvic venous pressure, rectal vein
varicositis occur
•pain and swelling occur
TX: topical applied anestheics, warm soaks, stool
softeners
Varicosities
•femoral venous pressure in pregnant woman
increased 8 à 24mmHg at term
•cosmetic blemished to severe discomfort
TX: rest with leg elevation, elastic stocking
Smoking: person to person counsel
•ask, advise, assess, assist, arrange
Alcohol: MC in white; NO ALCOHOL
Illicit Drugs: less likely to obtain prenatal care
Breastfeeding
•exclusive BF preferred until 6mo
•human milk contains protective immunological
substances à IgA and GF
•protects against rotavirus, decreased atopic
dermatitis and resp infections
CI: street drugs, uncontrolled alcohol, galactosemia,
HIV, TB, medications, breast cancer treatment,
active herpes on breast
Heartburn *very common
•GERD in lower esophagus due to upward
displacement & compression of stomach
TX: antacids, H2 blockers, PPIs
Pica: craving for strange food à iron def.
Sleeping & Fatigue:
•efficiency declines with gestational age, increase
need
TX: Benadryl, daytime naps
Leukorrhea: increase discharge
106
Prenatal Prenatal Diagnosis
Prenatal Chromosomal Abnormalities:
Diagnosis •Risk of fetal trisomy increased with
maternal age, especially after age 35
•Women with fhx or personal history of
aneuploidy should be referred to genetic
counseling
Neural Tube Defects
Birth defects of brain:
•anencephaly
*failure to close neural tube that
becomes cerebrum
•spina bifida
*incompetent closure of embryonic
neural tubule à vertebrae
•cephalocele
•rare spinal fusion abnormalities
•elevated AFP in maternal and fetal
serum and amniotic fluid
•AFP synthesized by fetal yolk sac
Down Syndrome & Trisomy
First Trimester Screening 11-14 weeks
•nuchal translucency: max thickness of the
subcutaneous translucent area b/w the skin and
soft tissue of spine at the back of neck, >3.5 is
abnormal à targeted sonography, chorionic
villous sampling, aminocentesis
•Biochemical screening: beta-hCG, PAPP-A
•Downs: elevated hCG & low PAPP-A
•Trisomy 13 & 18: both low
•ultrasound: heart tones around 10-12week
•Chorionic Villous Sampling: 10-13 weeks
women with increased chromosomal
abnormalities, prior child with chromosomal
abnormalities, materal age >35, abnormal 1st or
2nd T maternal screening tests, abnormal nuchal
translucency, prior pregnancy losses
Risk Factors:
•family history, MTHFR mutation
•aneuploidy, diabetes, hyperthermia
•medications *seizure medications
Screening: mom serum AFP b/w 15-20 wk
AFP can be affected by:
•multifetal gestation
•pilonidal cyst
•chorioangioma of placenta
•placental abruption, preeclampsia
•oligohydramnios, FGR
Second Trimester: 13-27 weeks
Triple test
•hCG, AFP, & unconjugated estriol
•down syndrome:
low AFP & estriol, high hCG
•trisomy 18: all decreased
•spina bifida: high AFP
Quad Screen
•above + inhibin
•Downs: elevated inhibin
Gestational Diabetes: week 24-48
Aminocentesis: same as chorionic
Types of Spina Bifida:
•myelomeningocele (MC): meninges
and spinal cord herniate through gap in
vertebrae
•occulta: no herniation; overlying skin
may be normal or hair; dimling or birth
mark
•meningocele: only meninges herniate
through gap
Combine First & Second Trimester
•enhance aneuploidy detection rates
•combines results from both trimesters
•highest detection of down syndrome
•results after both completed
Third Trimester:
•Gestational Diabetes: 24-28 weeks
à 1 hour glucola testing
•antibody screen in Rh (-): 28wk
*give RHOgam if negative
•CBC repeat: ~28wk, monitor anemia
•UDS repeat if + initial: 28 week
•GBS: vaginal/anal culture 36-37wk
à IV PCN G at labor
*alternative: Clindaycin
Non-Stress Testing:
Baseline fetal HR 120-160bpm
Reactive: 2+ accelerations at rate 15+ bpm
from baseline for at 15 seconds
Nonreactive: no fetal HR accelerations or
<15bpm lasting <15 seconds
•sleeping, immature, compromised
•TX: vibratory stimulation, contraction stress
testing
Contraction Stress Testing:
Negative: no late decelerations
Positive: repetive late decelerations
à hospitalize for fetal monitoring
107
MSK 8%

Muscle Reflex
0: Absent
1: Diminished reflexes 2: Normal
3: Hyperactive without clonus
4: Hyperactive with clonus

Muscle Strength
0: No muscle contraction
1: Muscle contraction but unable to produce joint motion
2: Muscle contraction with full ROM of joint w/o force of gravity
3: Full ROM against gravity but w/o resistance
4: With moderate resistance
5: Full resistance

L1, L2, L3
Reflex: None
Muscle: Iliopsoas (Raise thigh against resistance on thigh), Quadriceps (Extend lower leg against resistance), Hip Adductor (Adducts legs against resistance)
Sensation: Anterior Thigh
L4
Reflex: Patellar tendon
Muscle: Tibialis Anterior (Inversion & Dorsiflexion)
Sensation: Medial Lower Leg
L5
Reflex: None
Muscle: Extensor Hallucis Longus (Great toe extension)
Sensation: Dorsum of Foot
S1
Reflex: Achilles tendon
Muscle: Peroneus Longus & Brevis (Eversion & Plantarflexion), Gastrocnemius-Soleus (Plantarflexion)
Sensation: Lateral Malleolus, Lateral & Plantar Foot
S2, S3, S4
Reflex: Superficial anal reflex, No DTR
Muscle: No isolated testing, Bladder & Bowel function
Sensation: Concentric Anus

Supraspinatus: Jobe's Test "Empty Can Test": 90° Abduction, 30° Forward Flexion, Thumbs pointing down, Patient raises against resistance
Infraspinatus/Teres Minor: Open Book Test: Patient standing, with arm in a neutral position and the elbow flexed to 90°, Apply medial force to the arm while the patient is instructed to resist
Positive if the patient reports pain or weakness when resistance is applied
Subscapularis: Lift Off Test: Patient standing, Places dorsum of hand on the back, Patient lifts the hand away from the back
If patient is able to do then load pushing on hand is done by examiner to check strength Patient with a Subscapularis tear will not be able to do this
ACL: Lachman’s (most specific): Knee bent at 30°, Stabilize femur with opposing hand, Pull smoothly, Anterior Drawer Test: Knee at 90°, Stabilize foot, Pull tibia smoothly
PCL: Posterior Drawer Test: Knee at 90°, Stabilize foot, Push tibia smoothly
MCL: Valgus Stress: Knee bent 30°, Push Knee Inwards
LCL: Varus Stress: Knee bent 30°, Push knee Outwards
De Quervain's Tenosynovitis: Finkelstein’sTest: Grasp thumb in closed fingers and ulnar deviate
Carpal Tunnel: Phalen’s Maneuver: Wrist flexion until symptoms arise, Tinel’s Sign: Tap on the carpal tunnel until symptoms arise
Achilles Tendon: Thompson Test (Integrity of Achilles Tendon): Patient lay with the knee flexed to relax gastrocnemius/soleus, Squeeze calf, Foot actively plantar flexes = Intact. If not = Ruptured
Hip Dysplasia: Barlow Maneuver: Adducting the hip while applying pressure on the knee, direct the force posteriorly, Ortolani Test: Supine, Flex knees & hips 90°,
Galeazzi Test: Flex hips & knees, feet on table, ankles touching buttocks, Uneven height of knees is positive
Hamstring/Sciatic Pain: Straight Leg Raise: Supine, Knee extended, Lift leg (30°-70°), If painful, determine whether pathology is due to problem in sciatic nerve or hamstring tightness
108
 Hamstring pain involves only posterior thigh
Sciatic pain can extend all the way down the leg, At point of pain, lower leg slightly then dorsiflex foot to stretch sciatic nerve
Sjögren's: Schirmer's Test: Filter paper is held inside lower eyelid for 5 min, measured with ruler, <5mm is indicative, Salivary Test: Spits into a test tube every min for 15 minutes, <1.5ml is positive

Schober’s Test
Distraction Test
Patient supine, clinician stabilizes head at chin and occiput Passive traction force applied to cervical spine
Pain or neuro symptoms is relieved

Cervical Compression Test

Patient supine, clinical applies axial traction to top of patient’s head Increases pain and/or neuro symptoms

Spurling’s Test
Tests for cervical radiculopathy
Extension of neck, rotating head with applying axial downward pressure
Positive if creates or intensifies radicular symptoms to side patient’s head is rotated

SCREENING
Osteoporosis: Begin Screening: Women >50 yo, Strong FamHx, Any Fx with low energy mechanism: X-Ray
Indicates bone loss: Central DEXA (T-score: -1.0 or above: Normal, Between -1 and -2.5: Indicates beginning of bone loss (osteopenia), Below -2.5: Indicates osteoporosis
Osteoporosis: ≥65 yo (or anyone with the risk equal to that of a 65 yo Caucasian woman
Starting Biologics: New DMARDs: TNF Inhibitors (Etanercept, Infliximab, Adalimumab, Certolizumab pegol, Golimumab): Screen for TB first
Juvenile Idiopathic Arthritis at Risk for Asymptomatic Uveitis: Routine ophthalmology screening for 4 years from onset, Every 3 months if ANA(+), Every 6 months if ANA(-)

MSK About Presentation Diagnostics Treatment

Ankle Sprain MC lateral ligament: anterior talofibular
and calcaneofibular
•results from inversion (rolling ankle)
Medial liagments: deltoid injuries result in
eversion injury
•pain, swelling, bruising •anterior drawer test
•report a pop •squeeze test: squeeze tib/fib midcalf à (+)
•pain with varus stress and anterior pain
drawer •dorsiflex and external rotation
X-Ray: Ottawa Rules à Ankle
•pain along lateral malleolus
•pain along medial malleolus
•inability to walk >4 steps
•initially: NSAIDs, RICE, protect ankle,
brace if need
•2nd phase: when pt can bear weight without
increase pain or swelling (~2-4wk), use
braces, start exercises
•3rd phase: ~4-6weeks, functional
conditioning and strength, wean off brace

Achilles •inflammation of Achilles tendon •pain/stiffness 2-6cm above the •clinical •RICE, MICE, NSAIDs
Tendinitis •MC in people >30yo posterior calcaneus *burning pain •heel pads
•pain relieved with rest •exercise programs
Risks: run, jump, speed change i •steroids (last resort)
Cause: overuse

Achilles
Rupture MC: Middle aged recreational athletes
Mechanism: mechanical overload from
eccentric contraction of gastrocsoleus
complex
Risks: Fluoroquinalones, steroids
Popping sensation followed by acute
weakness and inability to continue
activity
Palpable defect on distal Achilles
tendon
Thompson Test Immobilization short leg splint
Absence of plantarflexion when squeezing *keeping foot in plantar flexion
calf
Non-weight bearing until seen by ortho
MRI evaluates severity surgeon
Definitive: Surgical

109
Plantar Inflammation & microtears of plantar
Fasciitis fascia due to overuse (esp flat feet, high
arches, heel spurs)
MC in Female, 40-60 yo, Older, Obese
MSK About
Costochondritis Acute inflammation of costal cartilages or
costochondral junctions
Etiology: Often idiopathic can be post-viral
or post-traumatic (excessive coughing)
MC 3rd, 4th, 5th Sternocostal joints
Ganglion Cyst Mucin filled synovial cyst
Most common hand mass (60-70%)
Location is dorsal carpal (70%)
Originate: Herniated tendon sheath fluid
Dorsal DIP Joint (mucous cyst, associated
with Heberden's nodes)
Etiology: Trauma, Mucoid degeneration,
Synovial herniation
Patho: Filled with fluid from tendon sheath
or joint, No true epithelial lining
Associated Conditions If Volar:
Median/Ulnar Nerve Compression, Hand
Ischemia due to Vascular Occlusion
Knee About
Inferior heel pain (often sharp) Mainly Clinical Dx
Worsens: After period of rest (first
few steps in the morning) Radiographs: Not useful for diagnosis
*may show flat foot deformity or heel spur
Decreases throughout the day with
gradual increased activity, walking,
massage, stretching, rest
May worsen towards the end of the
day after prolonged weight bearing
with a return of the pain at night
PE: Local point tenderness
(underside of heel), Pain increases
with dorsiflexion of toes
Clinical Manifestation
Pleuritic chest pain
Worsens: Inspiration, Cough, Movement
PE
Reproducible point chest wall tenderness
Absence of palpable edema (helps distinguish
from loss common Tietze syndrome)
Usually asymptomatic
May cause issues with cosmesis
PE
Transilluminates
Firm and well circumscribed to palpation
Often fixed to deep tissue but not to overlying
skin
Allen's Test: Ensure radial and ulnar artery flow
for volar wrist ganglions
Presentation
Conservative: Rest, Ice, NSAID, Heel/Arch
support (orthotics), PT (plantar stretching)
Refractory: Corticosteroid Injections
Severe/Refractory: Surgery
Diagnostics Management
Diagnosis of Exclusion NSAID
Labs, ECG, X-Ray: Usually normal
X-Ray: Normal 1st Adults: Non-Op
MRI: Not routinely indicated 2nd Adults Dorsal Ganglion:
Aspiration
US: Useful for differentiating cyst from *typically avoided on volar wrist
vascular aneurysm May provide image due to radial artery
localization for aspiration while *higher recurrence rate (50%) than
avoiding artery surgical resection, minimal risk so
reasonable to attempt
Histology: Biopsy not routinely
indicated Bracing: Occasionally help
*mucin-filled synovial cell lined sac
Children: 76% resolve within 1
year
Severe, Neurovascular Symptoms:
Operative Surgical Resection
*Volar ganglions have higher
recurrence after resection than
dorsal ganglions (15-20%
recurrence
Exam and Diagnostics Treatment
110
ACL Tear •MC knee ligament injury
•MC in female athletes
Mechanism:
•noncontact pivoting
•deceleration, change position
•hyperextension, internal rotation
•sudden pain and giving away of the knee •Lachman *MOST SENSITIVE •rest, ice, crutches, PT, compression
•audible “pop” and swelling •anterior drawer *wrost •possible aspiration for effusions
•knee buckling and inability to bear weight •pivot shift test
•possible hemarthrosis Definitive
•segond FX is pathologic for ACL tear x-ray: AP, lateral, tunnel views •ACL reconstruction is best for
young, active pts
Unhappy (O’Donoghue) Triad: MRI: best for confirm •older or less activity à PT
•ACL + MCL + medial meniscus

PCL Tear •strongest ligament in the knee
Mechanism:
•dashboard: anterior force to
proximal tibia with knee flex
•direct blow/fall on flexed knee
•posterior knee pain •posterior drawer •isolated PCL treated nonsurgically
•anterior bruising *most sensitive -rest, ice, ROM exercsies
•effusion
x-ray: AP and lateral surgical reconstruction: fail above
*ACL may rupture first then PCL MRI: confirm

Collateral •outside the joint and stabilize the •minor ambulatory issues (most play on) Varus and valgus stress Grade I (sprain) and II (incomplete)
Ligament Tear knee against valgus (abduction) and •localized swelling, stiffness •LCL: varus stress •conserative: PT, RICE, NSAIDs
(MCL and LCL) varus (adduction) stresses •tenderness along MCL or LCL *medial trauma •early ROM and quad strengthening
•ecchymosis and effusion in 24h •MCL: valgus stress
*lateral trauma Grades III (complete): +/- surgery

Meniscal Tears •fibrocartilaginous pads that
function as shock absorbers
Mechanism:
•degenerative or acute
•axial loading and rotation
•swelling, stiffness after activities
•locking, catching, popping
•patients can ambulate and play sports
•pain on medial/lateral side w/ twist or squat
•tender to medial/lateral joint
•postive McMurrays test
x-ray: AP/lateral, sunrise
MRI: BEST
•RICE, NSAIDs
Surgery: traumatic tears in younger
patients, older patients who do not
respond to conservative

111
 About Signs and Symptoms/PE Tests and Stages Diagnostics and Treatment
Rotator Cuff 4 muscles: SITS •dull ache deep in shoulder Testing: DX:
•supraspinatus *origates here •difficult sleeping on affected shoulder •suprasinpatus: “empty can test” 90% spec •xray
•inraspinatus •difficult reaching overhead, behind back, and -seated, elevated UE to 30-45 degree in plane of •MRI: better
•teres minor even doing normal ADLs scapula with internal rotation thumb down, resist
•subscapularis • “catching” or “grating/grinding” elevation: (+) pain Treatment:
•conservative tx 1st line
Risks: PE: •infraspinatous:“external rotate & lag” -rest, ice, PT, steroids
•repetitive motions *esp overhead •ROM: active motion limited -maintain position of maximal rotation
•increase risk with age •atrophy of infraspinatus if chronic (+) is when lag or angular drop •surgery: arthroscopic, open,
•tears due to direct injury •cant raise the arm (only shrug) if large tendon transfer, shoulder
•cant hold arm in elevated position •subscapularis: Gerbers test/Lift Off replacement
place their hand behind their back, with the palm
facing out à lift hand away

Labrum Tear •soft tissue that connect glenoid and •grinding/catching Impinement Tests:
humeral head •unstable sensation •Hawkins: anterior pain with int. rotation
•limited ROM •Neer test “like empty can but lift arm above
•SLAP tear: superior labrum, their head”
anterior and posterior •Drop arm: pain with slowly lowering arm

Olecranon Superficial extensor side of elbow
Bursitis
Etiology: Trauma, Gout,
Inflammation, Infectious (septic
bursitis): Can occur after penetrating
injury or break in skin S. aureus MC
organism
“Goose egg” Boggy swelling posterior
olecranon process area
Repetitive Trauma or Chronic: Painless or
minimally tender, Associated with full ROM
or mild discomfort with full flexion
Inflammatory or Infectious: Erythema,
Warmth, Tenderness with painful limited
ROM
*Evaluate for skin breaks or overlying
cellulitis if suspected septic bursitis
Clinical Dx Most
Aspiration: Suspected septic bursitis or gout
WBC <500: Noninfectious non-crystalline
WBC >2000: Often septic
Olecranon Bursitis: Avoid further
trauma, Padding to the area,
NSAID (painful/inflammatory),
ACE wrap for compression
Septic Bursitis: Drainage + ABX
(PO Dicloxacillin or
Clindamycin)

Prepatellar Pain with direct pressure on knee (kneel)

Bursitis
Swelling over patella
“Housemaid’s
Knee”

Subacromial
Bursitis

Patellar
Tendinitis

Biceps Tendinitis
Bicep Tendonitis: Tendonitis: •X-rays to r/o other pathology Tendonitis:
Tendinopathy/ •sports, overhead motion or lifting •pain in anterior shoulder over bicipital groove •US may be more helpful •NO NSAIDs & streoids
Tendonitis v. •pain worse with shoulder flexion, forearn •MRI to r/o rotator cuff tears •ice, rest, tapping, PT/OT
Rupture: supination, elbow flexion •surgery if no improvement
112
Bicep Tedon •fall on outstretched hand
Rupture •oversuse, heavy lifting, shoulder Rupture: sudden pain in upper arm / elbow à Rupture:
tears “pop” •Partial: nonsurgical
*involves proximal long head •trouble rotating arm palm down or up •Complete rupture: surgery
• “Popeye” muscle
Overuse Result of repetitive stresses and Tenderness, Stiffness, Tingling Types of overuse injuries NSAID, PT, Ergonomic eval
Syndrome microtrauma outpacing the body's Spondylosis, Metatarsalgia, Plantar fasciitis,
ability to heal Calcanceal bursitis, Achilles bursitis, Stress Fx, Surgery: Rare
“Repetitive De quervains tendinosis, Lateral epicondylitis
Strain Injury” Etiology: Improper technique,
Overuse

113
MSK About
Herniated Disk BACK PAIN
MC L5-S1 or L4-L5
Patho: Sudden movement -> Weakened and
frayed nucleus pulposus prolapse and
protrudes through the annulus where they
impinge on one or more nerve roots and
cause sciatica or radicular pain
Clinical Manifestation
Radicular back pain (Unilateral)
Possible radiation down leg with paresthesia or
numbness along dermatome
Worsens: Sitting, Standing, Walking, Coughing,
Sneezing
PE: SLR(+), limited ROM
L4
Pain: Anterior thigh
Sensory loss: Medial ankle
Weakness: Ankle dorsiflexion
Reflexes: Knee jerk loss, Weak knee extension
Diagnostics
X-Ray
Loss of disk height, Loss of lordosis,
Degenerative changes
MRI: DoC for suspected herniation,
persistent, refractory pain
Management
Initial: NSAID + Continuation of
normal activities as tolerated
± PT, Muscle relaxer, PO steroid
taper
*If doing bed rest, make it brief
Refractory: Corticosteroid Injection
*usually done after MRI confirmation
Persistent, Disabling Pain >6 Weeks
or Evidence of CES: Laminectomy,
Discectomy

L5
Pain: Lateral thigh/leg, hip, groin
Sensory loss: Dorsum (esp bw 1st & 2nd big toe)
Weakness: Big toe extension, walking on heels
Reflexes: Normal ± ankle jerk loss

S1
Pain: Posterior leg/calf, gluteus
Sensory loss: Plantar foot
Weakness: Plantar flexion, Walking on toes
Reflexes: Loss of ankle jerk

Cervical Strain
Lumbosacral MCC Lower back pain Back pain & muscle spasms (activity related) Clinical Dx Initial: NSAID + Continuation of
Sprain/Strain DOESN’T Radiate to the leg normal activities as tolerated
Acute sprain/tear of paraspinal muscles (esp NOT associated with neurological symptoms X-Ray: Not needed unless persistent
after twisting/lifting) ± Stiffness, Difficulty bending or alarming symptoms Moderate Pain: Brief Bed Rest (max
2 days)
PE: Decreased ROM, Paraspinal muscle
tenderness, No neurological changes Some Spasms: Muscle Relaxers

Lumbar Spinal Narrowing of spinal canal with impingement
Stenosis (LSS) of nerve roots
Etiology: Degenerative arthritis or
Spondylolysis MC (esp >60 yo), Post-
surgical, Congenital, Trauma, Inflammatory
Back pain, numbness, paresthesia
± Radiation to buttocks & thighs bilaterally
Worsens: Extension
Relieves: Flexion: Sitting, Leaning forward,
Walking uphill, Cycling (unlike claudication)
*lumbar flexion increases canal volume
MRI: DoC Conservative: Pain control, PT,
Lumbar corticosteroid injections
X-Ray: Nonspecific degenerative (may reduce need for surgery)
changes
Severe/Refractory: Decompression
CT Myelogram laminectomy

Not worsened with Valsalva (unlike herniated

disk)

Vertebral “Burst Fx”: Children jumping/falling Localized back pain with focal midline X-Ray: Loss of vertebral height Ortho & Neurosurgery Consult
Compression Pathologic Fx: Elderly (Osteoporosis), tenderness at Fx level
Fracture Malignancy (MM, Prostate cancer), Conservative: Observation, NSAID,
Systemic illness Bracing, Gradual return to activity
114

Spondylolysis Pars interarticularis defect due to failure
of fusion or stress Fx
MC at L5-S1
MC form of back pain in children &
adolescents
Mechanism: Repetitive hyperextension
trauma, Often the first step to
spondylolisthesis (forward slipping of a
vertebra on another)
Nerve root deficits may be present in the
presence of retropulsed bone fragments in the
spinal canal
Most Asymptomatic
Low back pain with activity
± Hamstring tightness, Sciatica
MRI/CT: Usually not needed,
Indicated if neurologic deficits Severe/Persistent: Kyphoplasty
present
X-Ray Low Grade/Asymptomatic:
Lateral: Radiolucent defect in pars Observation, No activity limitations
Oblique: “scotty dog neck broke”:
Pars interarticularis (neck of dog) has Symptomatic: PT & Activity
a break (looks like a collar around restriction in some
neck)
Failed PT: Bracing
CT
Bone Scan

Spondylolisthesis Forward slipping of vertebra on another:
Bilateral Fx or Defect of pars interarticularis
Mechanism: Complication of spondylolysis
Most Asymptomatic
MC Symptom: Lower back pain
Nerve Compression: Sciatica, Bladder/Bowel
dysfunction, Neurologic symptoms (if severe)
X-Ray: Forward slipping of vertebra Mild: Treated like spondylolysis
Lateral: Measure slip angle & grade
Flexion & Extension: Eval stability Severe: May need Surgery
MRI: Indicated if neurologic
symptoms are present to assess for
stenosis or complications

Cauda Equina Emergency
Syndrome (CES) Constellation of symptoms, result of
terminal spinal nerve compression in
lumbosacral region
Massive central herniation -> Compresses
several nerve roots of the cauda equina
Etiology: Lumbar disk herniation (MC),
Spinal stenosis, Trauma, Tumor, Epidural
abscess, Epidural hematoma, Vertebral Fx
Back pain + ≥1 of the following MRI: DoC Emergent Decompression
Radiculopathy: Bilateral leg radiation of pain
and weakness in multiple root distributions (L3- CT Myelography: If unable to Corticosteroids: Decrease
S1), may be unilateral perform MRI (pacemaker) inflammation
Saddle Anesthesia: Decreased sensation to
buttocks, perineum, inner surfaces of thigh, ED
New Urinary/Bowel Retention/Incontinence
Decreased Anal Sphincter Tone (decreased
anal wink test)

Spinal Cord Emergency Sudden onset focal neurological deficits MRI: DoC Acute Neurologic Symptoms:
Compression Systemic Glucocorticoids
External compression of spinal cord due to Hyperreflexia: Below level of compression
malignancy or infection Not Responsive: Surgical
Decompression

115
MSK About Clinical Manifestation Diagnostics Management
Spinal Pus-filled collection, abscess can expand Triad MRI with Gadolinium: DoC Aspiration, Drainage, ABX:
Epidural compressing brain/spin cord Fever Ring enhancing lesion Decompression laminectomy &
Abscess Often associated with osteomyelitis & discitis Spinal pain (focal & severe) MC symptom Drainage usually indicated if
Neurologic deficits: Radiculopathy, Myelopathy CT: If MRI C/I neurologic deficits, large abscess,
MC type: Posterior (motor, sensory, bowel/bladder dysfunction), Paralysis or spinal instability
(associated with increased risk of irreversibility) X-Ray: Usually normal
Etiology: S. aureus (MC), Gram(-): E. coli, ABX: Vancomycin +
Streptococci, TB ESR & CRP: Increased Cefotaxime/Ceftriaxone
WBC Count: Possible increase *Cefepime/Ceftazidime if
RF: >50 yo, IVDU, Immunodeficiency, pseudomonas suspected
Steroid, Recent spine surgery, Epidural
catheter Control Acute Neurologic Sx:
IV Corticosteroids

Conservative: Systemic ABX

alone may be used in select
patients (no neurologic symptoms,
not a surgical candidate)

About Causes Clinical Presentation/Diagnostics Complications/Treatment

Fibromyalgia Abnormal pain perception of Chronic widespread MSK pain, Extreme Primarily Clinical Dx Conservative: Multidisciplinary approach,
unknown etiology fatigue, Stiffness Normal Labs Patient education, Sleep hygiene, Low
Must be present ≥3 months Sleep & Cognitive disturbances (fibro fog) Sleep Studies: No REM cycle impact aerobic exercise
MC Women 20-55 yo HA Pain present ≥3 MONTHS and
Neurologic symptoms: Numbness Tenderness in 11/18 Trigger Points = Dx Not Responsive: 1st TCA (Amitriptyline)
1 & 2: Low Cervical (C5-C7) SNRI: Duloxetine, Milnacipran
3 & 4: Second Rib (second costochondral) *Alternative Mild-Moderate: Cyclobenzaprine
5 & 6: Greater Trochanter (posterior to
trochanteric prominence) Pregabalin: FDA approved
7 & 8: Knees (medial fat pad proximal to *esp helpful for sleep symptoms
joint line)
9 & 10: Occiput (subocciptal)
11 & 12: Trapezius (mid point of the upper
border)
13 & 14: Supraspinatus (above the
scapular spine near the medial border)
15 & 16: Lateral Epicondyle (2cm distal to
the epicondyles)
17 & 18: Gluteal (upper outer quadrants of
buttocks in the anterior fold of muscle)

116
Arthritis About
Gout Monosodium Urate Crystals
deposition in soft tissues, joints
Typically: Middle aged Male
Etiology
Renal Uric Acid Underexcretion (MC):
Worsened with renal insufficiency, Thiazides,
ASA
Uric Acid Overproduction: Increased cell
turnover (Cancer, Chemo, Hemolysis)
Triggers: Attacks associated with purine-rich
food (EtOH, Red meat, Seafood, Fructose)
Meds: Thiazides, Loop diuretics, ACEi,
Pyrazinamide, Ethambutol, ASA, ARBs
(exception Losartan which decreases uric acid
levels)
Clinical Manifestation
Acute Gouty Arthritis
1st MTP joint great toe MC (podagra) and LE
(knees, feet, ankles)
Monoarticular pain, Swelling
+/- Erythema, Axial load pain, Fever
Initially monarthritis (80-90%): With repeated
attacks ascends from the lower extremity
Untreated attacks last 7-14 days
Acute gout risk of repeat attack ~78% within 2
years
Diagnostics
Arthrocentesis: DoC
*helps differentiate septic arthritis
Negatively birefringent, needle-
shaped crystals
Increased WBC (but <50K),
predominantly neutrophils
X-Ray
Mouse/Rat Bite lesions (punched
out erosions with sclerotic &
overhanging margins)
Soft tissue swelling: Opacities =
Tophi
Normal joint space & ossification
Uric Acid Levels: 40-49% Normal
*only uric acid in joints is what
matters
ESR & WBC: Increased
Leukocytosis: Common
Treatment
Acute Attack
1st: NSAID (Indocin ER, Ibuprofen)
*Avoid ASA
Refractory, C/I NSAID
Corticosteroids (PO/Intraarticular)
Refractory Above: Colchicine
ADR: Diarrhea, Bone marrow suppression
(neutropenia)
Chronic (Prophylaxis)
Lifestyle: Decrease EtOH, Weight loss,
Decrease high purine (meat, seafood)
1st: Allopurinol & Febuxostat (Xanthine
Oxidase Inhibitors)
Decrease uric acid production
*not started during acute attack
*Safe in renal insufficiency

Synovial Fluid: Inflammatory Uricosuric Drugs: Probenecid &

Yellow to Milky Sulfinpyrazone
Cloudy C/I: Renal insufficiency
WBC Count: 20,000
PNM: 70%
Urate Crystals
No Bacteria

Pseudogout CPPD (Calcium Pyrophosphate Dihydrate) Similar to Gout Arthrocentesis: DoC Corticosteroid
deposition in joints & soft tissues Positively birefringent, *Intraarticular if 1 or 2 joints
Rhomboid-shaped crystals *PO if >2 joints
Joints: Knee (MC), Elbow, Wrist, MCP Increased WBC (2-50K),
predominantly neutrophils >2 Joints 1st: NSAID
RF: Hemochromatosis, Hyperparathyroidism, C/I: Renal insufficiency, Active PUD, GI
Hypomagnesemia X-Ray: Linear calcification of bleed, CV, Anticoagulant use
cartilage
Colchicine: Can be used in acute or
Synovial Fluid: Inflammatory prophylaxsis
Yellow *Prophylaxsis if ≥3 attacks annually
Cloudy if acute
WBC Count: 15,000
PNM: 70%
Calcium Pyrophosphate Crystals
No Bacteria

117
Arthritis About
Arthritis Painful inflammation and
stiffness of the joints
Osteoarthritis Chronic disease due to loss of
(OA) articular cartilage & joint
degeneration, minimal/absent
inflammation
MC joint disease
MC in weight bearing joints
(knees, hips, spine, wrists)
Chiefly a disease of aging
RF
Modifiable: Obesity, Trauma,
Heavy labor
Non-Modifiable: Increasing age,
Female, FamHx
Rheumatoid Chronic systemic inflammatory
Arthritis (RA) disease
Symmetric polyarthritis, bone
erosion, cartilage destruction,
joint structure loss
Patho: Hyperplastic synovial
tissue (pannus) -> Joint
destruction (T-cell mediated)
RF: Women, 30-50 yo, Smoking,
HLA-DRB 1 & 4
Clinical Features/Diagnostic Treatment
Disease process that involves the entire joint- Types
subchondral bone, ligaments, capsule, synovial Osteoarthritis
membrane, and periarticular muscles. Ultimately, Rheumatoid Arthritis
the articular cartilage degenerates Gouty Arthritis
Septic Arthritis
Psoriatic Arthritis
Lupus Arthritis
Many more..
Symptoms typically first begin after 40 yo and Diagnosis of Exclusion Lifestyle: Weight management, Moderate exercise,
progress slowly Assistive devices when needed
Lack of Inflammatory Markers
Joint Pain (usage related, worse in late Normal: ESR, CRP, ANA, RF APAP
afternoon & evening), Stiffness, Restriction of
movement X-Ray Topical/PO NSAID
Evening joint stiffness: Worsens throughout Asymmetric joint narrowing *more effective but associated with more ADR in
the day & weather changes Marginal osteophytes elderly (GI bleed, Renal injury)
*if morning stiffness present, it is short duration Subchondral bone sclerosis
(<60 min) compared to RA Bone cysts Duloxetine
PE Synovial Fluid: Non-inflammatory Topical Capsaicin
Hard bony joint, Decreased ROM, Crepitus Yellow, Clear
No inflammatory signs WBC Count: 700 Intraarticular Corticosteroids
PIP (Bouchard Nodes) PMN: 15% *temp relief (4 weeks)
DIP (Heberden Nodes) No Crystals *no more than 3 per year
No Bacteria
Hyaluronic Acid Injections
*No weight bearing activities for 24-48 hrs
*Effectiveness lasts on the order of months
*Can be repeated every 6 months PRN
Joint Replacement
Systemic: Fever, Fatigue, Weight loss, Anorexia RF: Best initial Prompt Initiation: DMARD (MTX, Leflunomide)
+ NSAID
Joint Pain & Stiffness Anti-CCP: Most specific Slows disease and immediate symptom control
Morning stiffness >1 hour after initiating *Glucocorticoids 2nd line for symptom control
movement, Improves later in the day. ESR & CRP: Increased
Decreased ROM
MC Small joints: Wrist, MCP, PIP, MTP, X-Ray
Ankle *often normal early
*Spares DIP Symmetric joint narrowing,
Osteopenia
PE Bone & joint erosions
118
 Joint: Symmetric inflamed joints: Warm, Severe: Joint subluxation (esp C1-
Felty Syndrome Erythematous, Soft “Boggy”. C2)
RA + Splenomegaly + Hand: Ulnar deviation
Neutropenia Swan neck (Flexed PIP, Hyperextended DIP) Treatment: DMARDs + NSAIDS
Boutonniere (Hyperextended PIP, Flexed DIP) •DMARDS: MTX, Leflunomide
Caplan Syndrome Rheumatoid nodules over bony prominences
RA + Pneumoconiosis + Corticosteroids: Prednisone 5-
Pulmonary nodules 10mg qd
•Low dose help with inflammation
and slow the rate of articular
erosion

OA vs RA OA RA
DIP, Thump (CMC) Wrists, MCP, PIP (DIP usually spared)
Heberden’s Nodes (DIP) frequently present Absent Heberden’s Nodes (DIP)
Stiffness: Worse after effort, Evening stiffness, Morning <1 hour Stiffness: Worse after resting, Morning stiffness ≥60 min
X-Ray: Osteophytes, Asymmetric joint narrowing, Subchondral sclerosis X-Ray: Osteopenia, Symmetric joint narrowing
Negative: RF, Anti-CCP, ESR, CRP Positive: RF, Anti-CCP, ESR, CRP

Reactive Inflammatory arthritis, in
Arthritis response to
infection/inflammation in another
“Reiter’s part of the body
Syndrome”
May be seen 1-4 weeks after
Chlamydia trachomatis or GI
infection (salmonella, shigella,
campylobacter, yersinia)
HLA-B27: Associated with
increased incidence
Triad: Arthritis + Ocular (conjunctivitis, uveitis)
+ Genital (urethritis, balanitis, cervicitis)
LE Joints MC Affected (esp knees)
Keratoderma Blennorrhagicum: Hyperkeratotic
lesions on palms & soles
Arthrocentesis: Rule out Septic
arthritis
*Findings similar to other
inflammatory arthritides, Increased
WBC count but <50K,
predominantly neutrophils with
negative cultures (no evidence of
septic arthritis)
Non-specific: Increased ESR &
IgG, Normochromic anemia
1st: NSAID
2nd: Methotrexate or Sulfasalazine
*Also: Intraarticular Glucocorticoid injections
ABX: Do not reverse reactive arethritis once the
joint pain has begun but may be indicated to treat
the underlying cause (Chlamydia trachomatis)

Disease About Clinical Presentation

119
Systemic Lupus Chronic systemic multi-organ
Erythematosus autoimmune disorder of connective
(SLE) tissues
Primarily a Type III hypersensitivity
reaction (Ag-Ab immune complexes)
RF: Young females (onset 20-40s), AA,
Hispanic, Native American women,
Genetic, Environmental, Sun exposure,
Infections, Estrogen
Osteoporosis About
Triad ANA: Screening of choice
Joint pain *most sensitive but not specific
Fever
Malar “butterfly” Rash Anti-Double Stranded DNA & Anti-Smith
*fixed erythematous rash on cheeks or bridge *Pathognomonic & Specific (not sensitive)
of nose sparing nasolabial folds *During flares, dsDNA antibodides rise &
complement (C3, C4) decrease
Constitutional *dsDNA used in monitoring
Fever, Chills, Fatigue, Night sweats
Antiphospholipid Antibodies
Discoid Lupus *Includes: Anti-cardiolipin antibodies &
Annular, Erythematous patches on the face & Lupus anticoagulant
scalp that heal with scarring Increased risk of arterial & venous
thrombosis
Systemic
CNS (HA, Stroke, Seizures) Pancytopenia: Anemia of chronic disease
CV (more common), Hemolytic anemia,
Glomerulonephritis Leukopenia, Lymphopenia,
Retinitis Thrombocytopenia
Oral ulcers
Alopecia Decreased Complements (C3, C4)
Serositis (Pericarditis, Pleuritis)
DX: ≥4 of the following 11
“ANA SMITH was stranded on an island &
developed a RASH when the RAIN made
way for the SUN”
Rash: Malar, Discoid, Oral ulcers,
Photosensitivity (each count as 1)
Arthritis
Serositis: Pericarditis, Pleuritis, Peritonitis
Hematologic: Hemolytic anemia,
Leukopenia, Leukocytosis,
Thrombocytopenia
Renal Disease: Glomerulonephritis,
Proteinuria
Anti-Nuclear antibodies
Immunologic disorders: Anti-Double
Stranded DNA, Anti-Smith, False positive
syphilis(RPR, VDRL) with a negative FTA
Neurologic: Seizures or Psychosis in
absence of any other cause
Findings Diagnostics
Sunscreen, Avoidance of prolonged
sun exposure
Mild (skin, joint, mucosal)
Hydroxychloroquine ± NSAID
and/or Glucocorticoids (low)
*in very mild cases NSAID only
possible
Moderate (significant but not life
threatening)
Hydroxychloroquine/Chloroquine +
Short term Glucocorticoid
Severe (life/organ threatening)
Glucocorticoid (high) or Intermittent
IV pulses of Methylprednisone with
other immunosuppressive agents
(Cyclophosphamide, Mycophenolate,
Rituximab)
Belimumab: Monoclonal antibody
that inhibits B-lymphocyte stimulator
binding to B-cells which inhibits B-
cell survival. It was designed for SLE
and it usually reserved for active
cutaneous/MSK disease unresponsive
to glucocorticoids or other
immunosuppressive agents
Treatment
120
Osteoporosis Loss of bone density (mineral &
matrix) over time due to imbalance of
increased bone resorption >
Formation of new bone.
Osteopenia: Precursor
Primary
Postmenopausal & Senile
RF: Caucasians > Asian > AA, Low
BMI (thin), Corticosteroid use,
Smoking, Chronic kidney disease,
EtOH, Low calcium & vitamin D
intake, Inactivity
Secondary
Chronic disease or Medications,
Hypogonadism, High cortisol states
(Glucocorticoid use, Cushing’s
syndrome), Hyperthyroid states, DM,
Low estrogen, Malignancy, Heparin,
Phenytoin, Lithium, Levothyroxine
Usually asymptomatic
Bone Fx: May develop pathologic Fx
(Vertebra MC, Hip, Distal radius), Back
pain, Deformity
Spin Compression: Lumbar & Thoracic
Loss of vertebral height, Kyphosis
(hunchback), Dowager's Hump (severely
rounded upper back), Back pain, Loss of
height
Often diagnosed through low impact or
spontaneous fractures
Fall from standing/low energy mechanism =
Fragility Fx
X-Ray: Can indicate bone loss and then
investigate further
DEXA Scan: Best diagnostic
Z-Score: Compared to peers
T-Score: Compared to young woman
T-Score ≥1.0: Normal
T-Score -1.0 to -2.5: Osteopenia
T-Score ≤-2.5: Osteoporosis
CBC: Anemia, Infection (WBC)
CMP: Serum Calcium, LFT, Vitamin D
TSH (thyroid function)
Sex Hormone: Testosterone/Progesterone
PTH (rule out hyperparathyroidism)
Work Up
Low energy fractures require work up
Start with getting normal Calcium and Vitamin
D levels
Postmenopausal woman start on
bisphosphonates (typically alendronate or
risedronate)
Severe disease may require anabolic agents
(Teriparatide (forteo), Abaloparatide = PTH
Hormones)
These are very expensive and have not yet
proven to be completely effective
Lifestyle: Breakfast Vitamin D (200-
800) + Calcium Carbonate (1200),
Weightbearing exercises, Smoking
cessation, Fall prevention
1st Management & Prevention
Bisphosphonates
PO: Alendronate, Risedronate,
Ibandronate (vertebra only)
IV (postmenopausal): Zoledronic
acid, Ibandronate (IV increase BMD,
PO decrease vertebral Fx)
Inhibit osteoclastic activity and are
potent antiresorptive agents
*PO must be taken with a full glass of
water
*30-60 minute wait is required before
reclining or consuming other
medications, beverages, or food to
lower the risk of upper GI ADR
(esophagitis, ulcers)
C/I PO: Esophageal disorders, Gastric
disorders, Inability to remain upright for
30 minutes after taking the medication
Chronic kidney disease, Intolerance
*Duration of treatment is unknown
*Treatment is 3-5 years, Drug holiday
for 1 year to prevent fragility fracture,
Then resume: Biphosphonate Fx: Thick
but not strong, Hypertrophic
Calcitonin Nasal Spray
Antiresorptive agent
Decrease occurrence: Vertebral
Compression Fractures Not: Non-
vertebral or Hip fractures
Use: Postmenopausal osteoporosis
Not 1st line for osteoporosis because
more effective medications are available
Teriparatide (forteo)
Recombinant human parathyroid
hormone with potent bone anabolic
activity
Decreases: Vertebral & Non-vertebral
Fx
Some evidence that it may actually help
to rebuild bone
ADR: Increased risk osteosarcoma
121
NEURO 6%

SCREENING
Cerebral Aneurysm: FamHx two 1st degree relatives: CTA/MRA Head starting in 20s then every 5-10 years
Dementia: ≥70 yo: Repeat 3 simple nouns, Clock test, Recall 3 simple nouns
Any deficit quick screen -> Full MMSE (Mini Mental State Exam)
Any deficit MMSE -> Full Neuropsychiatric Evaluation
Dementia: Screen for Depression

Disease Causes Clinical Findings

Vertigo False sense of motions Peripheral
Horizontal Nystagmus: Beats AWAY from affected
Types side
Peripheral: Labyrinth or Vestibular nerve Fatigable
BPPV: Episodic vertigo, NO hearing loss Sudden onset of tinnitus & hearing loss can occur
Meniere’s: Episodic vertigo, Hearing loss
Vestibular Neuritis: Continuous vertigo, NO hearing loss Central
Labyrinthitis: Continuous vertigo, Hearing loss Vertical Nystagmus
Cholesteatoma Non-fatigable (continuous)
Gradual onset
Central: Brainstem or Cerebellar Gait Issues more severe
Vestibular Neuroma Positive CNS Signs
Migraine
MS
Cerebral Vascular Disease
Cerebellopontine Tumor

Benign Peripheral Vertigo Recurrent episodes of sudden peripheral vertigo Epley Maneuver
Paroxysmal MC due to displaced otolith particles within semicircular canals (lasting ≤1 min) & provoked with specific head
Positional of inner ear (canalithiasis) movement Medical therapy usually not needed
Vertigo MCC of peripheral vertigo ± N/V
(BPPV) Not associated with: Hearing loss, Tinnitus, Ataxia

Dx: Dix Hallpike

Produces fatigable nystagmus

Meniere’s Idiopathic distention of endolymphatic compartment of inner 4 Findings Initial: Avoid salt, caffeine, nicotine, EtOH, chocolate
Disease ear due to excess endolymph Episodic peripheral vertigo (min-hrs) (they increase endolymphatic pressure)
SNHL (fluctuating, unilateral)
“Idiopathic Meniere Syndrome: Identifiable Meniere Disease: Idiopathic Tinnitus (low tone initially) No Relief: (they reduce pressure)
Endolymphatic Ear fullness Diuretics: HCTZ
Hydrops” Antihistamines: Meclizine, Dimenhydrinate,
Horizontal nystagmus, N/V Prochlorperazine, Promethazine
Also in Benzo: Diazepam
EENT Dx of Exclusion Anticholinergics: Scopolamine

Caloric Testing: Loss of nystagmus

Transtympanic Electrocochleography

Audiometry: SNHL
122
 Vestibular Test: Affected side

MRI: Rule out MS, Tumor, Aneurysm

Labyrinthitis Labyrinthitis: Inflammation of vestibular & cochlear portion of Vestibular (Both) 1st: Glucocorticoids
& CN VIII Continuous peripheral vertigo, Dizziness, N/V, Gait
Vestibular sways toward affected side Symptomatic: Antihistamine (Meclizine),
Neuritis Vestibular Neuronitis Horizontal & Rotary Nystagmus: Beats away from Anticholinergics, Benzodiazepines
inflammation of vestibular portion of CN VIII affected side
Also in Both are self-limited: Usually resolve in weeks even
EENT Etiology: Idiopathic, Viral/Post-viral inflammation Cochlear (Labyrinthitis ONLY) without treatment
Unilateral hearing loss, Tinnitus

Clinical Dx

MRI/CT Brain: Rule out central etiology

*MRI preferred
*Imaging usually not needed

Vestibular Vestibular Schwannoma: Benign tumor involving schwann cells Unilateral sensorineural hearing loss Surgery or Focused Radiation Therapy
Neuroma (CN which produce myelin sheath *Vestibular neuroma until proven otherwise
VIII)
Arises in cerebellopontine angle & can compress structures (CN Tinnitus, Vertigo, Ataxia, HA, Facial numbness (CN
VIII, VII, V) V) or Facial paresis (CN VII)

Dx
MRI: IoC
*Alternative: CT

Audiometry: Unilateral sensorineural hearing loss

*Most common

Management of N/V mediated by: GABA, ACh, Histamine, Dopamine, Serotonin
N/V in those Antiemetics: Block these
with Vertigo
1st Line Vertigo (N/V), Motion sickness
Antihistamines/Anticholinergics
Meclizine, Scopolamine, Dimenhydrinate, Diphenhydramine
MoA: Acts on brain’s control center for N/V
ADR: Anticholinergic: Dry mouth, Blurred vision (dilated),
Urinary retention, Constipation, Dry skin, Flushing, Tachycardia,
Fever, Delerium
CI/Caution: Acute narrow angle glaucoma, BPH w/ urinary
retention
N/V, Motion sickness
Dopamine Blockers
Prochlorperazine, Promethazine, Metoclopramide
MoA: Blocks CNS dopamine receptors (D1, D2) in
brain’s vomiting center
ADR: QT prolongation, Sedation, Constipation
EPS: Rigidity, Bradykinesia, Tremor, Restlessness
Dystonic reactions, Tardive dyskinesia, Parkinsonism
Refractory
Benzodiazepines
Lorazepam, Diazepam
MoA: Potentiates GABA
Serotonin Antagonists
Ondansetron, Granisetron, Dolasetron
MoA: Blocks serotonin receptors (5-HT3) both
peripherally & centrally in the chemoreceptor trigger
zone of the medulla (suppressing vomiting center)
ADR: Neurologic (HA, Fatigue), GI (Nausea,
Constipation), Cardiac (Prolonged QT, Arrhythmias)

NEURO
Parkinson’s Movement disorder due to idiopathic loss of Triad: Resting tremor, Rigidity, Bradykinesia Clinical Dx Selective MAOB Inhibitors: Rasagiline,
Disease dopaminergic neurons in the substantia nigra Normal DTR, Usually no muscle weakness Must have: Selegiline
Bradykinesia + Inhibits breakdown of dopamine
MC onset 45-65 yo Resting Tremor: Often 1st symptom Rigidity or Tremor *May slow disease progression, so typically
“Pill roll” of hand started early in disease or in young patients
123
 Patho: Loss of dopaminergic neurons -> Failure
of ACh inhibition in the basal ganglia
Affects dopamine’s ability to initiate movement
*ACh = Excitatory, Dopamine = Inhibitory
Worsens: Rest, Emotional stress
Alleviates: Voluntary activity, Sleep
Usually confined to one side/limb for years
until it becomes generalized
Rigidity
Increased resistance to passive movement
“Cogwheel” “Lead Pipe”
Festination: Speed up while walking
Bradykinesia
Slowness of voluntary movement & decreased
autonomic movements (Lack of swinging
arms, Shuffling gait)
Facial
Immobile face, Widened palpebral fissure
Myerson’s Sign: Tapping the glabella causes a
repetitively causes a sustained blink
Decreased blinking, Seborrhea of skin
Postural Instability: Late finding
Pull Test: Standing behind the patient and
pulling the shoulders causes the patient to fall
or take steps backwards
Dementia: Late finding
Many develop depression
Post-Mortem Histology
Lewy Bodies (cytoplasmic
inclusions) & Loss of
pigment cells seen in the
substantia nigra
Amantadine
May increase dopamine release or block
dopamine reuptake.
*Improves all clinical features. Improves
dyskinesias from chronic levodopa therapy
Dopamine Agonists: Pramipexole,
Ropinirole
*Similar mild side effects as Levodopa
*Use prior to starting Levodopa or with
Carbidopa-Levodopa.
*Effective in early to advanced Parkinson’s
Levodopa: Most effective treatment
Converts to dopamine after BBB
*Improves all clinical features
*DOESN'T stop progression
*Long term use = Wearing off effect
*Significant dose related SE: N/V,
Hypotension, Cardiac arrhythmias,
Dyskinesias (chorea, dystonia, tics,
myoclonus)
C/I: Psychosis, Glaucoma, MAOI use
Carbidopa
Limits extra-cerebral (pre blood brain barrier)
breakdown of Levodopa
*Limits N/V, hypotension, cardiac
arrhythmias from chronic Levodopa therapy

Carbidopa-Levodopa (sinemet)

NEURO About Cardiac/Other Neuro Diagnostics and Treatment

Reflex Syncope Transient LOC due to
abnormal reflex
Causes vasodilation and/or
bradycardia
Leads in systemic hypotension
and cerebral hypo perfusion
resulting in syncope
Reflex Syncope
Vasovagal (MC)
Self limited systemic
hypotension characterized by
bradycardia and/or peripheral
vasodilation Acute, self limited
postural hypotension (blood
donation)
Vasovagal Syncope
"Common Faint"
Triggered by emotional/orthostatic stress:
Venipuncture, painful/noxious stimuli, fear,
prolonged standing, heat exposure, exertion
Lightheadedness
Feeling of being warm/cold
Sweating
Palpations
Nausea or non-specific abdominal discomfort
Visual "blurring" occasionally proceeding to
temporary darkening or "white-out" of vision
Diminution of hearing and/or occurrence of
unusual sounds (especially whooshing noise)
Pallor reported by others
Upright Tilt Table Test
Recommended for pt with:
Unexplained single syncopal episodes in high
risk settings, Recurrent episodes without
organic heart disease, or after cardiac cause has
been excluded, Clinical value of knowing the
susceptibility to reflex syncope, Questionable
reflex versus orthostatic hypotension syncope
Diagnostic
Reflex hypotension/bradycardia induced WITH
reproduction of spontaneous syncope
Suggestive
Reflex hypotension/bradycardia induced
WITHOUT reproduction of syncope
Acute: Supine position with legs raised
Recurrent Vasovagal Syncope
Restriction of activities while symptomatic
Education regarding nature, risks, prognosis
Supine position teaching
Avoid triggers
Discontinue med associated w/ hypotension
Physical Counterpressure: Tensing the arms
with clenched fists, legs pumping, and leg
crossing
*May abort a syncopal episode or at least
delay it to assume the supine position
124
Common, does not usually Supine positioning restores adequate blood Holter Monitor: For one month if symptoms
recur or require treatment flow to the brain, patient may feel fatigued occur frequently (cardiac cause)
Commonly young and
otherwise healthy ILR (Implantable Loop Recorder): SubQ
monitoring device for the detection of cardiac
Situational arrhythmias placed in the left pectoral region
Post-micturition, Post-tussive,
Straining, Squatting Treat by
avoiding the triggers if possible

125
NEURO About
Epidural Between Skull & Dura
Hematoma
MC rupture Middle Meningeal
Artery often associated with
temporal bone Fx
May lead to hemorrhagic
stroke & brain herniation
Subdural Between Dura & Arachnoid
Hematoma
MC rupture Cortical Bridging
Veins after blunt trauma
RF: Elderly & Alcoholics,
Anticoagulant, Shaken baby,
Child abuse
Subarachnoid Between Arachnoid & Pia
Hemorrhage
MC ruptured berry aneurysm
at anterior communicating
artery (circle of willis)
Arteriovenous malformation,
Stroke, Trauma
RF: Smoking & HTN (most
important), Polycystic kidney
disease, Atherosclerotic
disease, Excessive EtOH,
Ehlers-Danlos, Marfan, FamHx
Intracerebral Intraparenchymal
Hemorrhage May compress the brain,
ventricles, sulci
RF
Trauma, Old age, High EtOH,
Coagulopathy
HTN (MC overall cause of
spontaneous ICH)
Clinical Presentation
3 Phases
Brief LoC
Lucid interval
Neurologic deterioration (HA, Vomiting,
Aphasia, Hemiparesis, Seizures)
Uncal Herniation: CN III Palsy (fixed dilated
blown pupil) on ipsilateral side (tentorial
herniation compressing CN III). Cushing
reflex (HTN, Bradycardia, Respiratory
irregularity)
Venous bleeding: Can develop over a longer
time compared to epidural
Varies: Usually gradual increase in
generalized neurologic symptoms (HA,
Dizzy, N/V) or Focal neurologic symptoms
± LoC
Sudden Intense “Thunderclap” HA
*Unilateral & Occipital area
“Worst HA of my life”
May be associated with: Delirium, Seizures,
N/V, Meningeal symptoms (photophobia,
neck stiffness, fever)
± LoC initially
May have: Sentinel Leak (prior milder HA)
PE: ± Meningeal signs (nuchal rigidity, (+)
Brudzinski & Kernig signs)
Usually not associated with focal neurologic
deficits but may have CN III Palsy
Terson Syndrome: Retinal hemorrhages
Neurologic symptoms increase within minutes
to hours
HA, N/V, Syncope, Focal neurologic
symptoms (hemiplegia, hemiparesis, seizures),
AMS (lethargy, obtundation)
PE
May have focal motor & sensory deficits
Diagnostics
CT w/o Contrast
Biconvex (lens), DOESN’T cross suture lines
*usually in temporal area
CT w/o Contrast
Concave (crescent), DOES cross suture lines
*may be negative right after, need serial
Severe: Midline shift due to increased ICP
CT w/o Contrast
Subarachnoid bleeding
LP: CT Negative + No papilledema/focal signs
Xanthochromia: Yellow-Pink CSF
4 Vessel Angiography: Usually performed after
confirmed SAH to identify source
CT w/o Contrast
DO NOT PERFORM LP (herniation)
Treatment
Hematoma evacuation or Craniotomy
Prevent irreversible brain injury & death
Small & Good Condition: Observed with
serial imaging
Increased ICP: Head elevation, Short term
hyperventilation, Hyperosmolar therapy
(IV Mannitol or Hypertonic saline)
Non-Op: If Stable with small hematoma, No
CT signs of brain herniation (midline shift
<5mm), No signs of increased ICP
≥5mm Midline Shift: Burr hole
trephination, Craniotomy, Decompressive
craniectomy
Supportive: Bed rest, Stool softeners, Lower
ICP
Nimodipine: Reduces cerebral vasospasms
improving neurologic outcomes
Lowering BP may decrease the risk of
rebleeding but may also increase the risk of
infarction, if needed: Labetalol,
Nicardipine, Enalapril are preferred
antihypertensives
Associated with Hydrocephalus:
Ventriculostomy
Prevention of Rebleeding: Coiling/Clipping
of aneurysm or AVM
*Coiling preferred over clipping
Supportive: Gradual BP reduction
Prevention of Increased ICP
Raise head of bed, Limiting IVF, BP
management, Analgesia, Sedation
Reduction of Increased ICP if present
IV Mannitol, Temporary hyperventilation
BP Reduction
IV Labetalol, Nicardipine, Esmolol,
Hydralazine, Nitroprusside, Nitroglycerin
126
 Cerebral Amyloid
Angiopathy (MCC of
nontraumatic ICH in elderly)
Arteriovenous Malformation
(MCC in children)
NEURO
Delirium Acute abrupt TRANSIENT reversible confused state Rapid onset
Fluctuating mental status changes
Etiology: Identifiable cause
Meds, Infections, Electrolyte abnormalities, CNS injury, Disturbance of Consciousness: "Isn't
Uremia, Organ failure, Drug intoxication, Withdrawal acting quite right"
Distractibility (hallmark): Tangential
Common in hospitalized elderly or disorganized speech, Drowsy,
Drugs, Dehydration, Infection (UTI) Lethargic, Semi-Comatose
Change in Cognition: Decrease in level
of functioning (need previous level)
Dementia can impair cognitive ability
and frequently underlies delirium
Perceptual Disturbances:
Misidentifying people/objects in the
room, Can be associated with vague
delusions of harm, Hallucinations:
Visual, auditory, somatosensory
(usually with lack of insight)
Language Difficulties: May lose ability
to write/speak a second language
Dementia Progressive decline intellectual function severe enough to Short Term Memory Loss
compromise social/occupational functioning Hippocampus
Repeating questions/stories
No disturbance in consciousness (compared to delirium) Diminished ability to recall recent
conversations/events
Insidious onset, Gradual progression
Word Finding Difficulty
Typically no precipitating event Tempoparietal junction of left
Usually acquired from: Neurodegenerative disease hemisphere
Stroke Difficulty recalling names of people,
places, objects
“Mild cognitive impairment” Cognitive decline but no Uses many pronouns &
change in level of function (NOT Dementia) circumlocutions
Difficulty w articulation, fluency,
comprehension, meaning is a different
location (broca/wernicke)
Visuospatial Dysfunction
Right Parietal lobe
Poor navigation, getting lost in familiar
places Impaired recognition of familiar
people/places
*Aggressive reduction only if
SBP >200
MAP >150
CBC, UA, Urine culture Treat underlying cause
CMP
Tox screen, Drug levels Prognosis
ABG Usual full recovery within 1 week
TSH/T4
Vitamin B12 Delirium: Wernicke Encephalopathy
CT Head Thiamine Deficiency: Alcoholism
MRI (MCC), Also: Malabsorption,
LP: Mandatory if unknown (esp if dialysis, bariatric surgery, anorexia,
febrile) AIDS, hyperemesis of pregnancy
Confusion (MC), Ataxia,
Ophthalmoplegia (horizontal
Delirium vs Dementia nystagmus)
Delirium: Acute reversible 500mg IV Thiamine tid for 3 days
syndrome caused by a medical (or 500mg IV/IM daily for 5 days)
condition
Dementia: Long term irreversible Korsakoff Syndrome
impaired memory disease Wernicke encephalopathy +
(Alzheimer’s) Antegrade and retrograde amnesia
w/ confabulation Thiamine
Cholinesterase Inhibitors: First line
(but not very effective)
Donezepil, Rivastigmine,
Galatamine
Alzheimer & Lewy body
Can prolong capacity for
independence
Do not prevent disease progression
C/I in FTD: Worsen behavioral
symptoms
Memantine (Namenda): Alzheimer
Disease and possibly Lewy body
Dementia
C/I in FTD
Dementia: Behavioral
Pharmacotherapy
SSRIs: Depression: Also can use
Bupropion (wellbutrin), Venlafaxine
(effexor
127
 Avoid Paroxetine (paxil):
Executive Dysfunction Anticholinergic effects Trazodone
Frontal lobes or Subcortical areas (oleptro): Insomnia
(white matter, basal ganglia) Avoid: Antihistamines,
Distractibility, Impulsivity Benzodiazepines, Zolpidem: Can
Mental inflexibility, Concrete thought cause delirium Methylphenidate
Slowed processing speed, Poor (ritalin): Apathy. Selected pt only,
planning/organization can cause agitation
Impaired judgement

Apathy
Frontal lobes or Subcortical areas
(white matter, basal ganglia)

Alzheimer’s MC type of dementia Short-term memory loss (often 1st Clinical Dx: No specific test ACH Inhibitors: Donepezil,
Disease RF: Age (MC >65 yo), Genetics, FamHx sign) Progresses to Long-term memory Tacrine, Rivastimine, Galantamine
loss & Cognitive deficits: MRI: Cortex atrophy Improve memory & symptom relief
Patho: Unknown (3 hypotheses) Disorientation, Behavioral/Personality Medial temporal lobe atrophy, *Does not slow disease progression
Amyloid: Extracellular amyloid-beta protein changes, Language difficulties, Loss of Reduced hippocampal volume,
deposition (senile plaques) in brain are neurotoxic motor skills White matter lesions NMDA Antagonist: Memantine
Tau: Neurofibrillary tangles (hyperphosphorylated tau Adjunct or monotherapy in
proteins) are neurotoxic Usually gradual progression Histology: Amyloid-beta protein moderate-severe.
Cholinergic: ACH deficiency -> Memory, Language, deposition (senile plaques) in Slows Ca influx & nerve damage
Visuospatial Loss PE: Abnormal clock drawing test brain. Neurofibrillary tangles:
Intracellular aggregations of tau
proteins

R/U other causes: MRI, CBC,

Renal/Liver tests, VDRL/RPR
(syphilis), B12, Thyroid function

Vascular Due to ischemia & multiple infarction (lacunar infarcts) Sudden decline in functions with a Clinical Dx Prevention
Dementia stepwise progression (random infarct - Work up similar to Alzheimer, Strict BP control
RF: HTN (most important), DM, CVA, AFib > Decline -> Stable -> Another infarct rule out other causes: B12, Folate,
-> Decline) RPR

Cortical: Depends on area affected MRI

Medial Frontal: Executive dysfunction, White matter lesions
Apathy, Abulia Cortical/Subcortical Infarcts
Left Parietal: Apraxia aphasia or
Agnosia CT: May show lacunar infarcts
Right Parietal: Hemineglect,
Confusion, Visuospatial abnormalities

Subcortical: Focal motor deficits, Gait

abnormalities, Urinary difficulties,
Personality changes

Frontotemporal Localized brain degeneration of the frontotemporal Early Histology

Dementia (Picks lobes Changes in social behavior, Picks bodies: Round/Oval
Disease) May progress globally personality, language (aphasia) aggregates of tau protein

128
 Eventually
Executive & memory dysfunction
*Onset of dementia is earlier than
Alzheimer’s

Behavioral Changes: Disinhibition,

Socially inappropriate behavior,
Apathy, Hyperorality (binge eat,
change in food preferences)

PE: Preserved visuospatial.

Advanced: ± Positive primitive
reflexes (palmomental, palmar grasp)
May have parkinsonism

Dementia with Progressive dementia characterized by the diffuse Early Histology Treatment of parkinsonian symptoms
Lewy Bodies presence of Lewy Bodies (parkinsons is localized, not Visual hallucinations, Episodic Cortical Lewy Bodies may worsen the neuropsychiatric
diffuse) delirium (cognitive fluctuations), symptoms and vice versa
Parkinsonism, REM sleep disorder

Late
Dementia

Delusions, Sensitivity to antipsychotic

drugs, Autonomic dysfunction
(orthostatic hypotension)

129
NEURO
CVA A sudden onset of neurologic deficit
resulting from a loss of blood flow to a
“Stroke” part of the brain
*cell death and irreparable damage to
brain tissue w/n 5min
Types:
Ischemia: thrombotic, emboli
*MCC is atrial fibrillation
Hemorrhagic: intracerebral (HTN),
subarachnoid (aneurysm, AVM)
Lacunar •small vessel disease of the penetrating
Infarction branches of the cerebral arteries in the
pons & basal ganglia
Risks: HTN, DM
Transient •transient episode of neurologic
Ischemic dysfunction caused by cerebral acute
Attack (TIA) infarction (blood supply temporarily
blocked à lack of O2
-embolic, thrombotic, or lacunar
-most resolve within 1-2 hours
*body immediately breaks it down and
so symptoms are short
Carotid •Most severe within 2cm of the
Artery bifurcation of the common carotid artery
Stenosis
•HX of stroke-like sx or benign
•hemi/mono/quadriparesis •Oxygen Saturation
•hemisensory deficit •Finger stick blood glucose
•visual loss; one or both eyes, diplopia
•dysarthria, facial droop, ataxia, vertigo •CT brain w/o contrast
•aphasia (Brocas or Wernickes) -GOAL: w/n 25min of arrival
•decrease in LOC
Other Immediate Studies:
Exam: •CBC, BMP, PT/PTT, troponin
•ABCs and vitals •EKG/cardiac monitoring
•Skin: petechial, janeway, osler, livedo Additional Work-Up:
reticularis, purpura •CTA, MRA, MRI
•carotid duplpex •Echo
•HEENT: trauma, funcoscope, mouth
•Cardio: rhythm, M/R/G, bruit Additional Labs: *based on pt
•Respiratory: breath sounds •toxicology, blood alcohol, LP, ABG,
hCG, CXR, EEG, UA/Cx
•Neuro: CNs, NIHSS scale
0: no sx, 1-4: minor, 5-15: mod
16-20: mod-severe, 21+ severe
Pure Motor (MC): hemiparesis or hemiplegia Sensorimotor: weakness & numb of
in absence of sensory/cortical signs (aphasia, face, arm, leg on onse side
agnosia, apraxia)
Dysarthria “clumsy hand”: dysarthria,
Ataxic Hemiparesis: ipsilateral weakness and facial weakness, dyaphgia, clumsy
clumsiness legs >arm hand
Sensory: numb face, arm, leg on onse side
•Assessing severity of symptoms (look for 1. Order US of carotids (CAD)
persistent neurologic deficits) 2. EKG, Echo (emboli)
3. MRA/CTA (vessel disease)
•Neurologic deficits <24 hours
*most last a few minutes with complete ABCD2 Score: 3+ admitted
resolution in 1 hour •Age 60+
•BP >140 or >90
•clinical SX
•duration: >10 min (+1), >60 (+2)
•diabetes
•Symptoms due to reduced blood flow and/or Imaging:
superimposed thrombus formation 1. Carotid Duplex US
2. Order MRA or CTA to see true
Physical Exam: stenosis of the vessels
•carotid bruit or palpable sclerosis 3. Cerebral angiography
*GOLD* but not used b/c invasive
•Keep NPO à IVF
•elevate head 30 degrees, supine
•Hypoglycemia: dextrose
•Blood pressure: Labetolol
•Cerebral edema: Mannitol
•Seizure: Lorazepam
Ischemic: SBP < 185 + DBP < 110
•TPA (Altepase): maintain BP <180/105 for
24 hours after
*within 3 HOURS
*do not treat BP if not elgible for TPA, only
if BP >220/120
•CI: BP >185/110, recent bleed, bleeding
disorder, recent trauma
•>3-4.5 hours: ASA
Intracerebral : lower BP w/n 1hr to 140
•ASA
•Control risk factors
Pharm:
•Plavix, ASA, Agrenox *antiplatelet
•Control BP, Statin
•TPA if neuro deficit potentially disabling
Asymptomatic: antiplatelet agents
Symptomatic: endarectomy or stenting
Stenosis 60-99%: vascular surgery for
carotid endarcectomy
• <60 and >99 then do nothing
130
NEURO About
Seizure Episode of abnormal neurologic
Disorder function cause by inappropriate
electrical discharge of neurons
Seizure: One-time event
Disorder (Epilepsy): Multiple
•DX requires at least 2
“unprovoked” seizures
Non-Epileptic Seizure
•Triggered (“provoked”) by a
disorder, event, or other condition
within 7 days
Status Epilepticus:
•seizure activity for 5+ minutes or
2+ seizures without regaining
consciousness
Refractory: persists despite IV of 2
antiepileptics
Risk Factors:
•age (MC child, adults >60)
•brain infections, tumor, injury
•family history
•inadequate O2 supply to brain
•cerebral edema, dementia
•vascular disease
•prescription drugs
Focal Abnormal neuronal discharge from
(Partial) one discrete section of one
Seizure hemisphere
Simple: Retained awareness
Complex: Impaired awareness
Absence Generalized seizure (both
Seizure hemispheres)
“Petit Mal” MC Childhood, Onset: 4-10 yo
(often ceases by early puberty or 20
yo in most patients)
Types
Type I: Focal (Partial) Seizures-ONE AREA
-simple: no LOC; discongitive: LOC
Type II: Generalized-ALL AREAS, no aura
1. Absence (Petit Mal) Seizures (CHILD!)
•staring à normal when seizure ends
2. Myoclonic Seizures *no LOC
•sudden brief jerks/twitches
(+) sx =contractions, (-) sx=relaxations
3. Atonic (Astatic) Seizure “Drop”
•slumping or nodding >1 second
4. Tonic: muscles (arms, legs, back) tighten
5. Clonic Seizures: convulsive movements à
rhythmic, jerking, muscle movements
6. Tonic-Clonic (Grand-Mal)
•LOC, shaking, body stiffening, bladder/bowel
Symptoms and Diagnostics
1. PRE-ICTAL/Aura *simple
Frontal: wave sensation, smell
Parietal: numb or tingling, taste
Occipital: visual
Temporal: déjà vu, hearing
2. ICTAL *during seizure
3. POST-ICTAL: body relaxes
•Todd’s paralysis: transient focal deficit
after a simple or complex focal zeisure
Diagnostics: HISTORY IMPORTANT
Labs:
•HX: glucose, drug levels, Hcg
•NO HX: “ + BMP, Mg, toxicology
•CT scan of head without contrast
•MRI *progressive or new in pt >20yo
•LP
EEG: *BEST TEST
•electrodes à sense & record activity
•prep: wash hair, no caffeine, take med
Rule Out Reversible Causes
CBC, Electrolytes, Liver/Renal function,
RPR
MRI: Rule out focal mass
EEG
Simple Partial: Focal discharge at onset
Complex Partial: Interictal spikes or with
slow waves in the temporal or
frontotemporal area
EEG
Bilateral symmetric 3 Hz Spike & Wave
activity
Treatment
Emergency Room:
•turn on side, 2 IV large bore access
•Lorazepam x2 DOSES
•Diazepam, Midazolam
•2nd line: Fosphenytoin, Phenytoin
*phenytoin incompatible with benzos
AED Drugs: * after 2+ unprovoked
-Benzos, Barbituates, Clonazepam, Gaba,
Phenobarbital, Valproic Acid,
***Phenytoin, Carbamazepine
AED SE:
•drowsiness, dizziness, diplopia,
imbalance, N/V, teratogenic
•gingival hyperplasia (Phenytoin)
AED Monitoring:
•CBC, CMP, albumin, depression
Discontinuing AED:
•after at least 2-year seizure free
•slow rates of AED taper (6 months)
1st: Ethosuximide
2nd: Valproic acid
Lamotrigine
Carbamazepine or Gabapentin: Can
exacerbate absence seizures
131
Generalized Simultaneous neuronal discharge of Rule Out Reversible Causes Treat underlying cause
Seizure both hemispheres (diffuse) CBC, Electrolytes, Liver/Renal function,
RPR Long Term Options
“Grand Generalized Tonic-Clonic (Grand Levetiracetam, Phenytoin, Valproic acid,
Mal” Mal) MC MRI: Rule out focal mass Carbamazepine, Lamotrigine,
Phenobarbital, Topiramate
Increased Prolactin & Lactic Acid: *Levetiracetam & Lamotrigine: Safest in
Immediately after seizures pregnancy
*Rule out pseudo seizures

EEG: Generalized high amplitude rapid

spiking during active episodes of tonic-
clonic seizures

Status Emergency
Epilepticus
Single continuous epileptic seizure
lasting ≥5 min or ≥1 seizures
within a 5 min period without
recovery in between episodes
Etiology: Structural abnormalities,
Infections (meningitis,
encephalitis), Metabolic
abnormalities, Meds, Toxins
Complications Neuroimaging: Once stabilized to determine 1st: IV Benzo (Lorazepam)
Hypoxia, Aspiration, Respiratory failure, if intracranial mass/hemorrhage present Rapid control of seizure
Arrhythmias *Additional doses can be given
*Midazolam can be used IM if cant access
IV site
2nd: Phenytoin or Fosphenytoin
*can be used to prevent recurrence
*Alternative: Valproate & Levetiracetam
3rd: Phenobarbital

General Anesthesia: Midazolam, Propofol

NEURO About Clinical Presentation Management

Bell Palsy Idiopathic Unilateral CN VII Palsy
Hemifacial weakness/paralysis due to
inflammation/compression
Lower motor neuron disorder
Causes: Idiopathic, HSV reactivation
RF: DM, Prego (3rd T), Post-URI, Dental nerve block
Sudden onset
Ipsilateral hyperacusis (reduced tolerance to sound) 24-48
hours then Hemifacial weakness & paralysis involving
forehead (upper and lower affected, unlike stroke)
*unable to lift affected eyebrow, wrinkle forehead, loss of
nasolabial fold, drooping corner of mouth
Taste disturbance (anterior 2/3)
Bite cheek, Eye irritation (inability to fully close eyelid)
Bell Phenomenon: Affected side’s eye moves laterally &
superiorly when eye closure attempted
ONLY AFFECTS THE FACE
No treatment needed (85% resolve 1 month)
Supportive: Artificial tears
Severe: Eye patches at night (corneal ulceration)
Prednisone (esp 72 hours of onset)
Reduces time to recover and likelihood of complete
recuperation
Severe: Acyclovir + Prednisone
Do not use steroids if lyme disease is suspected
EMG: If paresis fials to resolve within 10 days
Surgical Decompression: Progression/Deterioration

132
NEURO
Headache Primary (90%)
Migraine, Tension, Cluster
*Migraine & Tension MC Women

Secondary: Suspect if
acute/progression
Meningnitis, SAH, Intracranial
hypertension, Hypertensive crisis,
Acute glaucoma

Migraine HA MC Women Prodrome Dx Move to a quiet, dark room

FamHx 80% 24-48 hours prior to onset
Euphoria, Depression, Irritability, Food cravings,
Types Constipation, Neck stiffness, Increased yawning
Migraine w/o Aura (MC)
Migraine w/ Aura (classic) Aura
Develops gradually, lasts 5-60 minutes (right
before development of pain)
Positive symptoms: Visual: Bright lines, Shapes,
Objects Auditory: Tinnitus, Noises, Music
Somatosensory: Burning, Pain, Paresthesias
Negative symptoms: Loss: Vision, Hearing,
Feeling, Ability to move a part of the body
HA
Pulsatile Throbbing in Unilateral distribution
N/V, Photophobia, Phonophobia
4-72 hours
Worsens: Routine physical activity, Stress,
Lack/Excessive sleep, EtOH, Specific foods,
Hormonal, Dehydration
Postdrome
Mild continued pain, Feel drained, Exhausted
≥5 attacks
Lasts 4-72 hours
≥2 of the following
Unilateral location
Pulsating quality
Moderate/Severe pain causing
Aggravation/Avoidance of routine
physical activity
During ≥1 of the following
Nausea, Vomiting, or both
Photophobia & Phonophobia
Not better accounted for by another
diagnosis
To add "with aura"
≥2 attacks
≥1 of the following fully reversible
aura symptoms:
Visual, Sensory, Speech and/or
Language, Motor, Brainstem, Retinal
≥3 of the following
≥1 aura symptom spreads gradually
over ≥5 mins
≥2 symptoms occur in succession
Each aura symptom lasts 5-60 mins
≥1 aura symptom is unilateral
≥1 aura symptom is positive
Aura accompanied, or followed within
60 minutes, by HA
Take 1st dose at onset of HA or warning
Simple analgesics: APAP, NSAID
Triptans
Sumatriptan: (SubQ most efficacious)
Zolmitriptan: (ODT good for N/V)
Rizatriptan: (ODT good for N/V)
Naproxen-Triptan Combination
With Nausea & Vomiting
SubQ Sumatriptan
PLUS
IV Metoclopramide or Prochlorperazine
PLUS
IV Diphenhydramine: To prevent dystonic
reactions (from reglan/compazine)
Can add IV/IM Dexamethasone: To reduce
the risk of early HA reoccurrence
Preventive Therapy: Consider:
>4 times per month
Last >12 hours
Associated with significant disability
Topiramate, Valproic acid, Gabapentin,
Candesartan, Propranolol, Timolol,
Verapamil, Amitriptyline
May slowly taper off medication once the
HA are well managed
OTHERS: Avoid/Manage triggers, Botox
Magnesium, Acupuncture, Transcutaneous
supraorbital nerve stimulation Occipital
nerve block/Decompression, Biofeedback

Not better accounted for by another

ICHD-3 diagnosis

133
Tension HA MC overall cause of primary HA HA: Bilateral Pressing Tightening “Band-Like” Diagnosis of Exclusion 1st: NSAID, APAP, ASA, Local heat
Mean onset: 30 yo Non-Throbbing (non-pulsatile) steady/aching *no specific tests
*often worsens throughout the day Anti-Migraine medications
RF: Mental stress, Sleep deprivation, Worsens: Stress, Fatigue, Noise, Glare
Eye strain Not Worsened: Routine activity (unlike migraine)

Not associated with: N/V, Photophobia,

Phonophobia, Focal neurological sz (auras)

PE: Usually normal but may have peri-cranial

muscle tenderness (head, neck, shoulders)

Cluster HA Young & Middle aged Men
*10X more common than women
Associated with: Multiple frequent
HA with high intensity & brief
duration
Triggers: Worse at night, EtOH,
Stress, Specific foods
HA: Severe Unilateral Periorbital/Temporal
Pain (sharp, lancinating)
*Lasts <2 hours with spontaneous remission
*Bouts occur several times a day, may have 1 or 2
cluster periods per year (each lasting weeks to
months)
PE: Ipsilateral: Horner’s syndrome (ptosis,
miosis, anhidrosis), Nasal congestion,
Rhinorrhea, Conjunctivitis, Lacrimation
Clinical Dx Acute: 100% O2 (6-10L)
During Attack: Anti-Migraine Meds (SQ
Sumatriptan or Ergotamines
(vasoconstriction)
Prophylaxis: Verapamil, Corticosteroids,
Ergotamines, Valproic acid, Lithium

Intracranial Syndrome of increased ICP w/o a
Tumor space occupying lesion
“Pseudotumor •excessive CSF, defective absorption,
Cerebri” venous sinus pressure
•HA that are typically worse w/
awakening or lying down
•May awaken person at night
•New onset HA age >40
•Fever, Night sweats
•throbbing headache *worse with straining
•transient visual obstructions
•photopsia à flashing lights
•Immunocompromised/ malignancy hx
Exam: papilledema, visual field, CN VI palsy,
high ICP
DX: MRI •Repetitive LPs/CSF volume removal until
target pressure of 10-20cm H2) à 1ml CSF
Lumbar puncture lowers pressure by 1cm H2O
•high opening pressure >250
•CSF is normal Combo: Oral acetazolamide, Furosemide,
Steroid, Topiramate
New dx: admission
Previous dx: discuss with neuro

Risks:
•obese women of childbearing age
•vitamin A toxicity

134
Disease Mechanism of Action Drugs CI/BBW Caution Education
Triptans •Agonistics effect on serotonin of •Sumatriptan (Imirex) *ER CI: •medications for HTN •pain at site & tingling 30min
meningeal arteries (5-HT1B) and -SC, onset 10-15minutes •CAD, PVD, IHD •SSRIs or SNRIs •don’t use if MOA w/n 14d
trigeminal nerve (5-HT1D) •Zolmitriptan (Zomig) •don’t use within 72h of •wait 2 hours after taking one before
-nasal spray *pt for home •stroke or risks (HTN, DM, Ketoconazole taking another
•inhibit proinflammatory •Treximet (Imitrex+Naproxen) HLD, TIA, obese) •will only tx HA once it has begun
neuropeptide release *tablet Pregnancy Cat C (not prophylaxis)
•prinzmetal angina •may breastfeed 12h after •do not use <18yo or >65yo
Rest are oral; end in “-triptan” dose, but discard milk within •may impair think/reactions
•ergot compound meds the 12h span *driving caution

Ergotamine •Agonist, binding to several different •Cafergot (Ergotamine w/ BBW: peripheral ischemia with •Elderly SE:
receptors, producing peripheral caffeine) CYP3A4 inhibitors and •Cardiac disease risk HTN, coronary vasospasms,
*cant give vasoconstriction and decreased blood •Migergot with caffeine marcolides •Valvular heart disease peripheral ischemia, dependency,
right away flow •Dihydroergotamine (DHE) HA exacerbatib, valvulopathy, N/V,
CI: PVD, CAD, HTN, renal abd pain, leg weaknes, myalgia,
•However, may be a vasodilator in impairment, hepatic, sepsis, numbness, int claudication,
large amounts pregnancy (cat X), photosensitivity
•Similar to Epi & serotonin breastfeeding
Preventative •Alteration of central •botox •Topiramate (Toapamx) •CCB •TCA (Amitriptyline)
neurotransmission •acupuncture •Valproic Acid (Depakote) •Candesartion •Venlafaxine *EVIL!
*continue for months if helps •Propranaol •Guanfacine (Intuniv) •Riboflavin

NEURO
Essential Autosomal dominant Intentional Tremor: Postural bilateral action Dx of Exclusion Mild/Situational: Propranolol
Tremor Etiology: Unknown tremor FamHx, Hx, PE *can add Primidone if not working
Incidence: Increase with age MC: UE, Head (neck, voice)
Worsened: Intentional move, Stress, Anxiety ET vs Parkinson 3rd Line: Alprazolam
Defined by: Improved: EtOH ET: affects head & voice,
•enhanced by emotional stress Worse with movement, Refractory: Thalamotomy
•decreased with ETOH NO tremor at rest Relieved with EtOH &
•fhx common (dominant) Propranolol, Bilateral &
•no other abnormal findings PE: Finger to Nose (tremor increase at end) symmetrical
Parkinson: Resting tremor,
Worse at rest, Relieved with
voluntary movement,
intentional movement, sleep,
Usually starts on one side of
body

NEURO About Clinical Presentation Diagnostics Management

Concussion Mild TBI -> AMS ± LoC
*may result after blunt force or
acceleration/deceleration injury
HA, Dizzy, Psychological, Cognitive impairment
Confusion: Blank expression, Blunted affect
Amnesia: Pretraumatic (retrograde) or
Posttraumatic (antegrade) amnesia. Duration of
retrograde amnesia is brief. HA, Dizzy, Visual
disturbances: Blurred/Diplopia
CT w/o Contrast: Acute head injury
MRI: Symptoms >7-14 Days or
Worsening not explained by concussion
syndrome
CT Angiography: If vascular injury
suspected
Cognitive & Physical Rest
Observation (min 24 hours)
*inpatient or outpatient
Resume strenuous activity after
resolution of symptoms & recovery of
memory as well as cognitive functions

Delayed responses & Emotional instability

135
 Neurosurgical/Neurologic Consult: If
Signs of increased ICP: Persistent vomiting, CT shows Mass effect, Substantial
Worsening HA, Increasing disorientation, hematomas, SAH, Pneumocephalus,
Changing levels of consciousness Depressed skull Fx, Cerebral. edema

136
DERM 5%

Non-Palpable: Macule (flat <10mm) Patch (flat >10mm)

Palpable: Papule (solid <5mm), Nodule (solid >5mm)

Fitzpatrick's Skin Phototypes

I. Pale White: Always burns, Never tans
II. White: Always burns, Then tans
III. White: Sometimes burns, Can tan without prior burn
IV. White to Light Brown: Usually does not burn, Tans easily & deeply
V. Brown (Moderately Pigmented): Rarely burns, Tans easily
VI. Dark Brown to Black (Darkly Pigmented): Burns only with very high UV doses, Tans

DERM About Clinical Presentation Diagnosis Treatment

Hidradenitis Chronic inflammatory skin Deep seated inflammatory nodules & Clinical Dx Lifestyle: Diet (avoid high glycemic foods),
Suppurativa condition abscesses, draining tracts, fibrotic Smoking cessation, Local skin care, Eliminate
hypertrophic scars irritants, Reduce skin friction
“Acne Sites: Axilla (MC), Inguinal, Recurrent
Inversa” Anogenital Pea-Marble sized Mild: 1st Line: Topical Clindamycin
Small Cysts: Intralesional Triamcinolone
RF: Obese, Female, Smoking, Hx
acne, FamHx, Mechanical friction, Systemic ABX: Tetracycline, Clindamycin +
Meds Rifampin

Deep, Recurrent: Punch debridement

Painful Abscess: I&D

Epidermal Benign encapsulated subepidermal Skin colored dermal, freely mobile, Usually Clinical Dx Not Infected/Inflamed: No treatment
Cyst nodules filled with fibrous & compressible cyst/nodule
keratinous (cottage cheese) tissue Often: Central punctum (dark comedone) Histology: Cyst wall stratified Not Infected But Inflamed: Intralesional Kenalog
“Epidermal squamous epithelium
Inclusion, MC: 30-40s (rare before puberty) Ruptured Infected: Fluctuant, painful, larger, Recurrent/Cosmetic: Complete surgical excision
Epidermoid, M:F, 2:1 erythematous ± Foul smelling yellowish with cell wall intact
Pilar, cheese-like discharge *ideally once inflammation has gone down
Sebaceous” Patho: Cysts from plugging of
follicular orifices Infected: I&D

Sebaceous Cyst: Misnomer

Lipoma Benign subcutaneous tumors of
adipocytes in thin fibrous capsule
MC: Benign soft tissue neoplasm
Soft, painless, subcutaneous nodules (1-10cm) No treatment needed
Oval, Non-tender, Easily mobile,
Rubbery/Doughy, Slow growing Painful/Cosmetic/Rapidly Growing: Excision
MC Location: Trunk, Neck, Forearm, Proximal
extremities

137
Acanthosis Common benign disorder
Nigricans Velvety hyperpigmented plaques
MC Obese, associated with DM,
Insulin resistance, PCOS
Asymmetric darkening of skin pigmentation Diagnostics Treat underlying cause
Velvety with skin lines accentuated Rule out DM if negative:
Skin biopsy Topical Keratolytic/Retinoids
Typical: Skin folds (Neck, Forehead, Groin,
Naval, Axilla)
138
DERM About
Pemphigus •Autoimmune disorder of mucous membranes
Vulgaris and skin
•type II hypersensitivity reaction à IgG
against desmoglein (component of desmosome)
à acantholysis (separation)
Risks:
•patients 30-40yo, middle eastern
•meds: Penicillamine, Captopril,
Cephalopsorins, Phenobarbital
MC areas:
•scalp, face, chest, axillae, groin, umbilicus
Bullous Bullous autoimmune disease usually seen in
Pemphigoid geriatric patients (60-80 yo)
Patho: Blistering skin disorder caused by linear
deposition of autoantibodies (IgG) against
hemidesmosomes in the epidermal-dermal
junction
Less severe than pemphigus vulgaris
Does not affect mucous membranes
Negative Nikolsky sign
About/Causes
Lichen Planus Acute/Chronic inflammatory
dermatitis (cell mediated
immune response)
MC: Middle age adult (F:M, 3:2)
Increased Incidence: Hep C,
Drug (sulfonamides, tetracycline,
quinidine), Graft vs host,
Malignant lymphoma
Lichen Simplex Skin thickening in patients with
Chronicus atopic dermatitis secondary to
“Neurodermatitis” repetitive rubbing & scratching
“Itch-scratch” cycle
Clinical Presentation
1. painful erosion/ulceration of
mucous membrane (intraoral)
2. painful, flaccid skin bullae *easily
rupture & bleed
•spares palms and soles
Exam:
•(+) Nikolsky: superficial
detachment of skin under
pressure/trauma
Pruritic, papular, and/or
urticarial lesions with large tense
bullae and erosive mucosal lesions
PE: Nikolsky Sign (-): No
epidermal detachment
Clinical Presentation
Pruritic rash MC extremities (esp volar wrist,
ankle) ± mouth, scalp, genitals, nails, mucous
membrane
6 Ps: Purple, Polygonal, Planar, Pruritic,
Papules, Plaques with fine scales & irregular
borders ± Whickham striae (white lines)
Koebners Phenomenon: New lesions at site of
trauma (also seen in psoriasis)
Nail Dystrophy: May cause scarring alopecia
Scaly, well-demarcated, rough hyperkeratotic
plaques with exaggerated skin lines
Diagnostics
Skin Biopsy:
•intraepithelial splitting with
acantholysis
Direct Immunofluorescence:
•IgG throughout epidermis
•basal keratinocytes
ELISA: anti-desmoglein or anti-
epithelial autoantibodies
Biopsy
Linear IgG deposits along the
basement membrane zone
Circulating anti basement
membrane IgG antibodies
Types/DDX/DX
Primarily Clinical Dx
Biopsy & Immunofluorescence: Confirmatory
Saw-tooth lymphocyte infiltrate at the dermal
epidermal junction
Clinical Dx
Treatment
•Prednisone 2-3mg/kg + local wound care
*continue steroids until cessation of new blister
formation and disappearance of (+) Nikolsky
Wound Care: wet compression, routine bathing,
anticipate infection
•Concomitant Immunosuppresive
-1st line: Azathioprine or MEthotrexate
Complications: fluid, electrolytes, secondary
bacterial, osteoporosis
Corticosteroids
IV Immunoglobulin
Methotrexate
Treatment
1st Line: Topical Corticosteroids with
occlusion dressing
Pruritis: Hydroxyzine 25mg PO Q6H
2nd Line: PO/Intralesional Corticosteroid,
Topical Tretinoin, Photosensitizing
Psoralen + UV therapy
Prognosis: Usually resolves spontaneously
in 8-12 months
Avoid scratching
Topical Corticosteroids (high),
Antihistamines, Occlusive dressings
139
 About
Seborrheic MC benign epidermal skin tumor
Keratosis
MC fair skinned elderly with
prolonged sun exposure
Patho: Benign proliferation of
immature keratinocytes
Clinical Presentation
Well demarcated, Round/Oval Velvety Warty
Lesions with a Greasy or “Stuck on” appearance
Varied colors: Flesh, Grey, Brown, Black
Diagnostics Treatment
Usually Clinical Dx No treatment needed: Benign
*Not premalignant
Biopsy: Performed if uncertain
Well-demarcated proliferation of keratinocytes Cosmetic/Symptomatic
with small keratin-filled cysts Cryotherapy (MC), Curettage,
Electrodestruction, Laser

Actinic MC Pre-Malignant Skin
Keratosis Condition *can lead to SCC
“Solar Patho
Keratosis” Proliferation of atypical
epidermal keratinocytes
RF: Prolonged sun exposure,
Lighter skin, Increase age, Male
Dry rough macules/papules
“Sandpaper” feel (feel before see)
Often: Transparent, yellow scaling, Can range
from skin colored to erythematous or
hyperpigmented plaques
± Cutaneous horn (projection on skin)
MC Areas: Face, Forehead, Nose, Cheeks,
Temples, Ears, Neck, Forearms, Hands, Legs
CLINICAL DIAGNOSIS Avoid sun exposure, Use sunscreen
Punch/Shave Biopsy: Atypical epidermal Localized
keratinocytes, hyperchromatic pleomorphic nuclei Cryosurgery liquid nitrogen
from basal layer upwards (no invasion into Curettage & Electrodesiccation,
dermis) Dermabrasion
Differentiates from SCC
Multiple
Biopsy if: >1cm, indurated, ulcerated, rapid Topical: 5-FU, Imiquimod
growth, fail to respond to therapy

DDX: SCC (lips and ears MC)

About Clinical Presentation Diagnostic Treatment

Common •benign overgrowth of skin cells •asymptomatic without •dermatoscopy •none if diagnosis is confirmed
Melanocytic change -will not appreciate
Nevi Types: •symmetric neoplastic changes Indications for excision:
•congenital (CMN): develop defect in melanoblasts •sharp borders •locations: scalp, anogenital, mucosa
à increased risk of melanoma development if large •uniform color •rapid change
•irregular borders
•Acquired (MN): develops early in childhood •erosions
à often regresses by age 6 •persistent itching, pain, bleeding
Dysplastic •pigmented lesion from proliferation of atypical •asympatomatic •clinical diagnosis & confirmed •observe with dermoscopy +/- digital
Melanocytic melanocytes •irregular shape w/ histopathology
Nevi (DN) •MC onset in late childhood-early adulthood •sharp and ill-defined •surgical excision w/ biopsy-r/o melanoma
•precursor to superficial spreading melanoma (SSM) bordered Education: -indications: changing, cant observe
-one lesions increase risk by 2x •varigated color •monthly self-exams
-10+ lesions increase risk by 12x •maculopapular •sun protection •routine exams q3-12mo
•family member skin checks -3 if fhx of DN or melanoma, 6-12 if
sporadic DN

140
 About
SCC •Malignancy of cutaneous
epithelial cells (keratinocytes) on
sun-exposed areas
•Greater risk of mets on the lip
and oral mucosa
MC Areas & people:
•face and dorsal hands
•MC skin cancer in AA
Risks:
•sun exposure, fair skin
•fhx skin cancer, increased age
•scarring processes
•radiation, immunosuppression
•HPV, tattoos, piercing, burn
Kaposi Vascular cancer
Sarcoma Associated with HHV-8
MC Seen: Immunosuppressed
(HIV <100 CD4, Transplant)
Sporadic: Old Mediterranean men
Endemic: East & South Africa
About
Melanoma Cancer from melanocytes
MC affecting skin
MCC skin cancer related death
*Aggressive with high
malignant potential (3% skin
cancers, 65% deaths)
MC METS to: Regional LN,
Skin, Liver, Lung, Brain
MC on sun exposed areas but can
occur anywhere
RF
UV radiation, Blistering
sunburns, FamHx, >3 burns
before 20 yo, Tanning, Large
number of nevi
Caucasians, Light hair/eye,
Xeroderma pigmentosum
Clinical Presentation
Differentiated:
•Hard, firm papule, plaque, nodule with a
thick adherent keratotic scale
•Erythematous, yellow, skin colored
•LAN with mets
Undifferentiated: *large, irregular border
•soft, fleshy, erosive papule/nodule
•papillomatous, cauliflower, bleeds easy
•found on less sun exposed areas
Squamous in situ (SCCIS): BOWENS
•confined to epidermis
•more frequent & aggressive in immunosuppres
•organ transplant and HIV/AIDS
Painless non-pruritic macular, papular,
nodular plaque-like brown, pink, red, or
violaceous lesions
Sites: Skin, Lung, Lymph nodes, GI tract
Cutaneous KS MC: LE, Face, Oral mucosa,
Genitalia
Types
Superficial Spreading (MC)
May arise de novo or from preexisting nevi
MC trunk in men, legs in women
Nodular (2nd)
Rapid vertical growth
Lentigo Maligna
MC on face
Acral Lentiginous (MC found on dark skin)
May be seen: Palms, Soles, Nail beds
Desmoplastic
Most aggressive type
Diagnostic Treatment
Tumor Subtypes: •excision w/ margins (3-5mm) & Mohs
•bowen diseae (SCCIS) *TREATMENT OF CHOICE
•acantholytic, adenoid, psuedoglandular -6mm margin in high risk
•well v poorly differentiated
Non-surgical Candidates
Biopsy BEST TEST Superficial: electrodessication, curettage (x3)
•atypical keratinocytes & malignant cells, with margins of 3-4mm, radiation
pleomorphic and hyperchromatic SCC with
variable nuclear size Others: Imuquimob, 5-FU, IF-alpha,
•loss of full-thick epidermal maturation electrochemotherapy, Intralesional
-CAN NOT USE PICATO
Biopsy: Angiogenesis, inflammation, Chemotherapy
proliferation (whorls of spindle-shaped cells
with leukocytic infiltration & Indolent Superficial Lesions: Radiation,
neovascularization) Cryotherapy, Electrocoagulation, Excision,
Electron beam
Immunohistologic Staining
HIV: HAART *AIDS defining cancer
Clinical Presentation Diagnostics and Treatment
ABCDE Complete Wide Surgical Excision +
Asymmetric Sentinel LN Biopsy
Borders irregular >1-2mm Thick = 2cm marginal tissue
Color variation 2-4mm Thick (T3) = 2cm marginal tissue
Diameter >6mm
Evolution (recent/rapid change) Some High Risk: Adjuvant Therapy:
Interferon-alfa, Immune therapy (Nivolumab,
Lesions on: Upper back, Upper arm, Neck, Ipilimumab) or Radiotherapy
Scalp: Decrease likelihood of survival
Dx
Full Thickness Wide Excisional Biopsy + LN
Biopsy
*Shave biopsy discouraged
141
 About
Basal Cell MC SKIN CANCER USA
Carcinoma MC cancer in humans
Neoplasm of basal keratinocytes
(BCC)
Slow growing: Locally invasive, but
very low incidence of mets
MC Locations:
Face, Nose, Neck, Trunk
RF:
Light skin, Prolonged sun exposure,
Xeroderma pigmentosum
Flat Firm area with Small Raised
Translucent Pearly or Waxy Papule
with Raised Rolled Borders &
Central Ulceration with overlying
Telangiectasia Vessels. Often Friable
(bleeds easily)
Clinical Presentation Diagnostics Treatment
Nodular (MC!) Superficial Multicentric Good prognosis w/ tx
Translucent “pearly” papule/nodule *can rub alcohol pad over it Likely recurrence in 5 years
Well defined borders (rolled-edge) Thin plaque/patch, pink/red
Smooth, firm, telangiectasias ± Scaling Education:
Avoid sun exposure
Treatment
Mohs Micrographic Surgery
Facial involvement, Difficult cases,
High risk cases, Recurrent
Ulcerating
Best long term cure rates & spare tissue
Translucent, pearly, smooth, firm, Pigmented
Telangiectasia with a central ulcer Firm papule/nodule ± umbilications
Electrodisection & Curettage
± Elevated border (rodent ulcer) Smooth pearly surface Non-facial & low risk recurrance
Generally pigmented or stippled globules
Surgical Excision
Either low or high risk of recurrence
Cryosurgery
Sclerosing
Plaque, scar like lesion Imiquimod or Fluorouracil
Pink/white in color, telangiectasia
Ill-defined borders Diagnosis:
Punch/Shave Biopsy: Clusters of basaloid cells
w/ palisade arrangement of nuclei at periphery
Excisional Biopsy: May also be done

DERM About Clinical Presentation Risks/Diagnostics Diagnostics/Management

Impetigo Highly contagious superficial
vesiculopustular skin infection
MC bacterial skin infection in
children (highest incidence 2-6 yo)
RF: Poor hygiene, poverty,
crowding, warm/humid weather, skin
trauma
Etiology: S. aureus (MCC),
GABHS (2nd)
Non-Bullous Type: MC form
Papules, vesicles, pustules with weeping then
“honey colored gold crust”
*Usually at site of superficial skin trauma
Associated with regional lymphadenopathy
Bullous Type
Vesicles form large bullae (rapidly) with thin
”varnish-like crusts”
Fever, Diarrhea
Rare: Usually newborns or young kids
Ecthyma: Ulcerative pyoderma caused by
GABHS (heals with scarring). Not common
Usually Clinical Dx
Gram stain & Culture
Mild: Topical Mupirocin (DoC): TID 10 days
Bacitracin, Retapamulin, Wash area gently with
soap & water, Good skin hygiene
Extensive/Systemic: Cephalexin, Dicloxacillin,
Macrolides
Community Acquired MRSA: Doxycycline,
Clindamycin, Bactrim
Complications: Cellulitis (MC 10%), Acute
glomerulonephritis (1-5%)

Molluscum Benign infection Firm, Dome-shaped, Flesh-Pearly White Waxy Usually Clinical Dx Most Cases No Treatment Needed
Contagiosum Molluscipoxvirus (Poxviridae Papule w/ Central Umbilication (2-5mm) *Spontaneous resolution 3-6 months
family) Single/Multiple Histology
Curd-like material may be expressed if squeezed 1st When Indicated: Curettage
142
 Transmission: Highly contagious Palms & Soles: Spared Henderson-Paterson bodies *Others: Cryotherapy, Podophyllotoxin,
Direct contact (MC), Fomites (keratinocytes with Electrodesiccation, Imiquimod
eosinophilic inclusion
MC: Children, Sexually active, HIV bodies) Severe: Topical Retinoids

DERM About Clinical Manifestation Diagnostics Diagnostics and Management

Atopic Defective skin barrier susceptible to drying Pruritis (required for dx) Clinical dx Acute
Dermatitis -> Pruritis & Inflammation Erythematous, ill-defined blisters, 1st line: Topical Corticosteroids
(Eczema) “Itch that rashes” papules, pustules. Increased IgE: Supports dx Alternative: Tacrolimus, Pimecrolimus *no atrophy
Later: Dry, crust, scale Type I hypersensitivity reaction Wet Dressings
Atopic Triad ABX: Secondary infection
Atopic dermatitis, Allergic rhinitis, Asthma Location Itching: Benadryl, Hydroxazine, Cetirizine,
MC: Flexor creases in older Fexofenadine, Loratadine
Patho children & adults
Disruption of skin barrier (filaggrin gene Systemic
mutation) and disordered immune response. Infantile: Face, Extensor extremities Phototherapy (UVA, UVB), Cyclosporine,
Most manifest infancy, almost always <5 yo Azathioprine, Mycophenolate mofetil, MTX,
Nummular Dupilumab
Environmental Triggers Sharply defined Discoid/coin-
Heat, Perspiration, Allergens, Contact irritants shaped lesions Chronic
(wool, nickel, food, synthetic fabrics) Dorsum, Feet, Extensor surfaces Skin Hydration: BID 3 min after lukewarm shower
(knees, elbows) Avoid Triggers (heat, low humidity, irritants)

Dyshidrotic Recurrent pruritic vesicular rash affecting Pruritic small tense vesicles Clinical dx Topical Corticosteroid Ointments: Triamcinolone
Eczema palms and/or soles “Tapioca Pudding” (medium potency), usually spontaneously resolves
“Acute MC Onset <40 yo Palms, soles, fingers over several weeks
Palmoplantar Later: Desquamation, papules,
Eczema” Triggers: Sweat, stress, warm/humid, metals scaling, lichenification, ± erosions Severe: Oral Corticosteroids
“Pompholyx” Severe: ± Bullae
Frequent/Refractory: Topical Psoralen + UVA

General: Cold compress, Burrows solution, Avoid

triggers, Lukewarm water and soap free cleansers

Contact Inflammation of dermis and epidermis from
Dermatitis direct contact. Irritant or Allergic
Irritant: MC form: 1 exposure (immediate)
Chemical, alcohols, creams
Diaper: May develop candida infection
Allergic: Delayed type IV; 24-48h
Nickle MCC
Poison ivy, oak, sumac
Detergents, cleaners, fragrances, hair dyes,
acids, prolonged water
Acute: Well Demarcated
Erythematous papules/vesicles
(linear/geometric),
Localized pruritis, stinging,
burning
May ooze, develop edema and
progress to blisters/bullae
Chronic: Lichenification, fissures,
scales
Clinical Dx (usually)
Patch Testing: Identify allergens
Histology (rarely done): Spongiosis
(intrcellular edema in epidermis)
Identification & Avoidance of irritants
1st: Topical Corticosteroids
*oral if severe/extensive reactions
Alternative: Topical Calcineurin Inhibitors
Tacrolimus, Pimecrolimus

143
Seborrheic Patho: Not fully understood Erythematous plaques with fine Usually Clinical Dx Mild: Topical Selenium sulfide, Sodium
Dermatitis Increased sebaceous gland activity + white scales & greasy appearance sulfacetamine, Zinc pyrithione, Ketoconazole,
Hypersensitivity rxn to Malassezia furfur ± Burning & Pruritis Cicopirox, Corticosteroids (low)

More Severe: Neurologic (Parkinson), HIV Common in areas of high sebaceous Calcineurin Inhibitors: Pimecrolimus, Tacrolimus
M>F gland secretion: Scalp (dandruff), *do not cause facial atrophy
Worsen: Fall & winter (UV helpful), Stress Eyelids, Beard, Mustache,
Nasolabial folds, Chest, Groin Severe/Resistant: Oral Itraconazole, Fluconazole,
Ketoconazole, Terbinafine
Infantile Patho: Not fully understood Erythematous plaques with fine Usually Clinical Dx Observation
Seborrheic Circulating maternal hormones in infancy may white scales & greasy appearance
Dermatitis lead to sebaceous gland overactivity + Emollient to Scalp: Mineral oil, Vegetable oil, Baby
“Cradle Cap” Hypersensitivity rxn to Malassezia furfur oil, White petrolatum overnight or 15 min prior to
shampooing with baby shampoo or removal of scales
Benign with a soft brush
Self-limited
Usually resolve by 1 yo Extensive/Persistent: Ketoconazole

Perioral MC: Young women (20-45 yo) Erythematous grouped Eliminate topical corticosteroids & irritants
Dermatitis papulopustular may turn into (cosmetics)
RF plaques with scales
Hx Topical Corticosteroid *Spares Vermillion Border 1st Line: Topical: Pimecrolimus, Metronidazole,
Fluoride toothpaste Uncommon: Affect periorbital & Erythromycin, Topical Azelaic acid
paranasal skin
Extensive/Refractory: Oral Tetracycline

144
 About
Pityriasis Self-limited inflammatory skin
Rosea disorder. Potentially related to a
viral infection (herpes)
Psoriasis Chronic immune mediated
multisystemic disease with genetic
predisposition
Environmental Triggers
Skin trauma, Bacterial infections,
Weather changes, Stress,
Medications (indomethacin, lithium,
antimalarials)
Patho: Keratin hyperplasia &
proliferating cells in the stratum
basale + Stratum spinosum due to
T Cell activation & Cytokine
release -> Greater epidermal
thickness & Accelerated
epidermis turnover
Locations
Extensor surfaces (elbows, knees),
Scalp (MC initially), Nape of neck
Usually Pruritic
Koebner Phenomenon: New
isomorphic lesions at the sites of
trauma
Auspitz Sign: Punctate bleeding
with removal of plaque or scale
*Also seen in Actinic Keratosis
Clinical Presentation
Single herald plaque develops, Usually on trunk
Often with centrally-adhered peeling skin
1-2 weeks later a generalized pruritic hyper-
/hypo-pigmented, erythematous eruption
develops in "Christmas Tree" distribution
Plaque-Type: MC
Pruritic, Erythematous/Hypopigmented,
Sharply demarcated Plaques with silvery scales
Extensor surfaces
± Pitting Nails
Present for months-years
Eruptive/Guttate
Pruritic, Smaller, Round Plaques
Pink Small Teardrop Papules with Fine Scales
Often after bacterial infection (strep throat)
Spares Palms & Soles
Greater tendency toward spontaneous resolution
Generalized Pustular “Von Zumbusch”
Abrupt widespread, painful
erythematous patches or thin plaques,
Rapidly become studded with numerous
pinhead-sized sterile pustules
“Lakes of Pus”: Coalescence of pustules
Pustules resolve within several days,
leaving erythema and extensive scaling
Erythroderma may occur
Fever, Leukocytosis may be seen
Inverse
Erythematous (lacks scale)
MC body folds
Erythrodermic
Involving entire skin
Can be life threatening (worst type)
Treatment
Treatment: Unnecessary unless the patient is
uncomfortable
Pruritus: Oral Antihistamines and/or Topical
Antipruritic lotions
Short course of Systemic Glucocorticoids:
Best option to speed resolution
May be improved by UV phototherapy or
natural sunlight exposure if begun in 1st
week
Mild-Moderate
1st: Topical Corticosteroid (Clobetasol)
(high dose)
Vitamin D analogs (Calcipotriene)
Topical Coal Tar
Topical Retinoids/Vitamin A Analogs
(Tazarotene)
Calcineurin Inhibitors (Pimecrolimus &
Tacrolimus) can be used on delicate areas
(face, penis)
Moderate-Severe
Phototherapy (UVB, PUVA)
Severe
Systemic: Cyclosporine, Retinoids
(Acitretin), Biologics (TNF inhibitors:
Etanercept, Adalimumab, Infliximab)
Last Resort: Methotrexate
*Except in psoriatic arthritis where it is 1st
line of severe
145
Vitamin D MOA Indication and Application SE/CI Vehicle
Calcipotreine •binds to vitamin D receptors and regulated Indication: psoriasis SE: burn, itching, irritation, •solution, ointment
(Dovonex, cell growth photosensitive, high Ca+ cream, foam
Calcitrene) -inhibits proliferation of keratinocytes Directions: thin layer to rea BID à avoid apply to •Solution best for scalp
-inhibits proinflammatory cytokines <40% body surface area-max 100g/wk CI: hypersensitivity
0.005%

Calcitriol •binds to vitamin D receptors and regulates Indication: psoriasis SE: hypercalcemia, photosensitivity
cell growth
0.0003% -inhibits proliferation of keratinocytes Directions: apply thin layer to affected area BID 20g/wk CI: none
ointment -inhibits proinflammatory cytokines max

146
DERM Risks
Adverse Drug Med induced changes in skin &
Reactions mucous membranes
Most are hypersensitivity rxn
Most are self-limited if offending
agent removed
About
Exanthematous Type IV (delayed)
Drug Eruption Causes: Any drug but MC with
PCN, Sulfa, NSAID, Allopurinol
Angioedema Self-limited, localized
subcutaneous swelling resulting
from extravasation of fluid
Types:
Mast Cell (histamine) Mediated
Allergic rxn
Bradykinin Mediated
ACEi, Hereditary (C1 esterase
inhibitor deficiency)
Fixed Drug Eruption
Other Types •Solitary erythematous
patch/plaque that will recur at
same site if re-exposure
Lesion:
Risks
RF: Antigen from food, Insect bites,
Drugs, Environmental, Exercise
induced, Infections
Presentation
Maculopapular
Generalized distribution of bright
red macules & papules, coalesce to
form plaques
MC: Trunk, Proximal extremities
MC: 5-14 days after drug initiation
or 1-2 days in previously sensitized
Systemic: Low grade fever, Pruritis
Mast Cell Mediated
With other allergic symptoms:
Urticaria, Flushing, Generalized
pruritis, Bronchospasm, Stridor,
Throat tightness, Hypotension
Bradykinin Mediated
NO allergic symptoms
Management *remove agent
•non-eroded: steroid ointment
•eroded: topical ABX (Bactroban or
Mupiciron)
•SX: antihistamines for pruritis
Immediate vs Delayed
Immediate
<1 hour
Urticaria, Angioedema, Anaphylaxis
Delayed
After 1 hour, usually before 6 hours, occasionally
weeks-months
Exanthematous eruptions vs Fixed drug eruptions vs
Systemic reactions
Information
High: PCN, carbamazepine, allopurinol, gold
Medium: sulfonamides, NSAIDS, isoniazid,
chloramphenicol, erythromycin, streptomycin
Low: barbituates, BZDs, phenothiazines,
tetracyclines
Affects: Mucosal tissues of face, Lips, Tongue,
Larynx, Hands, Feet, Genitalia
Onset: Minutes to Hours
Spontaneous Resolution: Hours to Few days
If there is no other info to suggest an external cause
and the patient has isolated angioedema (without
pruritis or urticaria): C4 levels & C1 inhibitor
antigenic levels
Pustular Drug Eruption
•An acute febrile eruption
Clinical Findings:
•sterile pustules on an erythematous base, often
start in the intertriginous fold and/or face
Types
Type I: IgE Mediated ”Immediate”
Urticaria, Angioedema, Anaphylaxis
Type II: Cytotoxic Antibody Mediated
Drugs in combo with cytotoxic antibodies
Type III: Immune Antibody-Antigen
Complex
Drug mediated vasculitis, Serum sickness
Type IV: Cell Mediated “delayed”
Erythema multiforme
Non-Immunologic: Cutaneous drug rxn
due to genetic incapability to detoxify
certain meds
Anticonvulsants, Sulfonamides
Treatment
Prompt withdrawal offending agent
*most are self-limited once D/C
Symptomatic Treatment: Oral 2nd Gen
(Cetirizine, Loratadine, Fexofenadine),
1st Gen (Benadryl, Hydroxyzine,
Chlorpheniramine)
Severe: Oral Corticosteroid (short course)
Immediate assessment, Airway
protection, Epinephrine (severe)
Mast Cell Mediated
Epinephrine (severe), Glucocorticoids,
Antihistamine
Bradykinin Mediated
C1 inhibitor concentrate, Ecallantide,
Icatibant, FFP (if other therapies not
available)
Long Term Management Hereditary:
Danazol (lowest dose)
Labs: leukocytosis
Course/Prognosis:
•pustules resolve over 2 weeks then
desquamation for 2 weeks
147
 •sharply marginated macule liquid compound for oral lesions •fever
•erythema; dusky-red color
•edematous & bullous à erode

DERM About Clinical Presentation Diagnostics Treatment

Urticaria Histamine related increase vascular permeability
Type I IgE Mediated -> Superficial localized
edema & erythema of dermis, mucous
membranes, subcutaneous tissues
Patho
Mast cells & Basophils release vasodilators
(histamine, bradykinin, kallikrein, prostaglandin)
-> Extravasation of fluid
Triggers: Food, meds, head/cold, stress, insect
bites, environment, infection
Chronic (>6 months): Usually idiopathic
Sudden onset Clinical Dx Eliminate Known Precipitants
Circumscribed hives/wheals
Blanchable, raised, erythematous skin or mucous 2nd Gen H1 Blockers: Cetirizine, Loratadine,
membranes may coalesce Fexofenadine
Intense Pruritis *preferred due to less anticholinergic SE
Usually Transient (disappear in 24h)
± Dermographism H2 Blocker: Ranitidine
*may be added if no response to above
Severe/Recurrent/Persistent: Glucocorticoid
Concern for Airway Compromise: Epinephrine

About Clinical Presentation Diagnostics Treatment

Melasma Hypermelanosis (Hyperpigmentation) Mask-like hypermelanotic (brownish) Clinical Dx Sun Protection (during & after treatment)
of sun exposed areas symmetrical macules
“Chloasma” MC face & neck Woods Lamp Triple Therapy: Tri-Luma (Fluocinolone 0.01%,
RF: Dermal melasma: Unchanged Hydroquinone 4%, Tretinoin 0.05%)
Increased estrogen (prego, OCP) Dermal melasma (deeper): bluish-grey Epidermal melasma: Enhanced
“Mask of Pregnancy” Topical Bleachers: Hydroquinone, Azelaic acid
Sun exposure, Phototoxic drugs Histology: Increased melanin all
FamHx, Darker complexion layers of epidermis Topical retinoids

Chemical peels

Dermal Melasma: Laser therapy

Vitiligo Acquired skin disorder, Skin
depigmentation
Patho: Not fully understood
Autoimmune destruction of
melanocytes -> Skin depigmentation
Possibly associated with other
autoimmune diseases
Generalized (MC): Symmetrical
Lip-Tip: Mouth, fingers, toes, nipples,
genitalia
Segmental: One side/part of body
Localized: 1-3 macules in single location
Vitiligo Universalis: Confluence
Irregular discrete white macules &
patches (total depigmentation)
Painless, Without pruritus
Locations: Dorsum, Axilla, Face, Fingers,
Body folds, Genitalia
Koebner Phenomenon: New macules in
areas of recent trauma
Clinical Dx Cosmetic camo, Sunscreen
Wood’s Lamp Localized: Topical Corticosteroids
Fluorescence
Facial: Topical Calcineurin Inhibitors
Skin Biopsy (rarely needed)
Loss of epidermal melanocytes Disseminated: Systemic phototherapy (Narrow band
UVB) + Topical/PO Corticosteroids
Autoimmune: TSH, T4, fasting
glucose, ANA, CBC ACTH Limited Areas: Laser, Grafts, Cultured epidermal
stimulation suspensions
*may be effective

148
DERM About Stages Treatment
Pressure Breakdown of the skin and underlying tissue I III Wound care with moist wound environment
Injury resulting from unrelieved soft tissue pressure Superficial Full thickness of skin Pain control
between bony prominence and external Non-blanchable redness that May extend to subcutaneous
“Decubitus surface doesn’t dissipate after pressure relieved layer Necrotic Tissue: Debridement, Negative
Ulcer” pressure wound therapy, Optimize nutrition
RF: Elderly, Immobile, Incontinent II IV (protein & caloric intake esp if III or IV
Epidermal damage extends into dermis Deepest
Location: Bony prominences (sacrum, calcaneus, Resembles blister or abrasion Extends beyond fascia into Pressure Redistribution: Positon and reposition
ischium) muscle, tendon, bone using support surfaces (air-fluidized beds,
powered mattresses)
Patho: Pressure impairs oxygen and nutrient Unstageable
delivery & waste removal. Moisture causes skin Tissue loss obscured by slough I: Transparent film (for protection)
maceration -> Skin breakdown or eschar, Slough/Eschar must be
removed to determine III vs IV II: Dressing that maintains a moist environment.
*If no infection: Transparent films or Occlusive
dressings (hydrocolloids, hydrogels)

III & IV: Debridement of necrotic tissue

(mechanical, surgical, enzymatic)
*Extensive necrosis or Thick eschars: Surgical
debridement

149
DERM About Clinical Presentation Diagnostics Treatment
Verrucae Cutaneous warts Common & Plantar Clinical Dx Most resolve within 2 years
HPV-1: Commonly affects soles, Firm, hyperkeratotic papules 1-10mm *If immunocompetent
associated with Plantar Red-brown punctations (thrombosed Serologies
capillaries are pathognomonic) Topical: OTC Salicylic acid & Plasters.
Types Borders: Rounded/Irregular Immunofluorescence Podophyllin, 5-Fluorouracil
Verruca Vulgaris: Common Common on hands
Verruca Plantaris: Plantar Histology Cryotherapy, Electrocautery, Imiquimod
Verruca Plana: Flat Flat Koilocytotic squamous cells with
Sharply defined, Numerous, small, hyperplastic hyperkeratosis Others Fail: Intralesional Interferon or
Patho: HPV infects keratinized skin -> discrete, flesh-color papules 1-5mm Bleomycin
Excessive proliferation & retention of Typically: Face, hands, shins
the stratum corneum Excision is associated with recurrence

Condyloma HPV 6, 11 (90%), also: 16, 18, 31, 33, 35 Painless papules à Soft, fleshy Clinical dx Cryotherapy, TCA
Acuminatum MC in sexually active YA cauliflower-like lesions Electrocauterization, Excision: Scar
Skin colored/pink/red/tan/brown Acetic Acid: Whitening of lesion Imiquimod, Podofilox (not for anogenital)
“Genital warts” Transmission Clusters genital regions & oropharynx
Invasion of the basal cells of epidermis by Persist for months, may spontaneously Histology: Koilocytotic Vaccine: Gardasil 9
“Condyloma microabrasion, active lesions NOT resolve (80%), remain unchanged, or grow squamous cells with hyperplastic <15 yo: 2 doses 6 months apart
Acuminata” required for transmission hyperkeratosis >15 yo or Immunocompromised: 3 doses (0, 2,
Complications: SCC (cervix, anal, penile, 6 month)
vaginal, vulvar cancers) CI: Pregnant or Lactating

PHARM MOA Application SE/CI Education

Imiquimob 5% •Induces immune systems response to Apply small amount at night 3x/week and rub until gone •SE: localized reaction •Avoid sexual contact during
Not in SCC recognize and destroy lesions -wash off in morning with mild soap (6-10h) -If too severe, can take a application times
holiday then resume

Podofilox •Prevents cell division and causes •apply q12h for 3 days then off 4 days, then repeat MC: mild-severe irritation •Apply initial tx in office to
tissue necrosis •apply to normal skin between lesions; avoid open wounds MC systemic SE: HA educate on proper application
•wash medication off after 1-4 hours •Avoid sexual activity
•tx area <10cm AND total volume <0.5ml/d CI: pregnancy

Tricholoracetic •Burns, cauterizes, erodes •Apply Vaseline around lesion to create barrier then apply VERY EFFECTIVE
Acid medication to area with cotton top applicator x6-10weeks

5-FU •Blocks DNA synthesis: apoptosis and •BID to affected region x2-4wk •localized skin reaction Education: success is parallel to
selective cell death -Alt: daily for face & anterior scalp only àburn, itch, erythema, erosion, compliance
•D/C once erythema, erosion, crusting, and necrosis have crusting, ulceration
occurred •F/U in 2 weeks

Ingenol Mebutate 1. disrupt cell membrane & •0.015% gel: face/scalp once daily x3days •Localized skin irritation; AK ONLY
(Picato) DNAàcell necrosis •0.05% gel: trunk/extremities, apply nightly x2d erosions
2. Neutrophil-mediated cytotoxic •Plant derivative
•Caution: risk of SCC?
Diclofenac •COX-2/prostglandin inhibit •3% Gel-Apply to treatment area BID x60-90d •Localized skin reaction

150
DERM About Clinical Presentation Diagnostics Treatment
Pediculosis Etiology: Pediculus humanus corporis Pruritis (rxn to louse saliva), Excoriations Clinical Dx: Identification of Hygiene Improvement: Bathe thorough
Capitis Papular urticaria near lice bites louse or nits (more commonly Infested clothing/bedding heat washed, dry
Transmission: Close contact, Person to seen) in clothing (esp seams) cleaned, or discarded
“Head Lice” person, Fomites (hats, headsets, clothing, Maculae Cerulean: blue grey macules Iron seams to destroy lice
bedding) *pathognomonic for lice Nits: Ovoid greyish-white eggs
fixed to base of hair shafts. Heavy Infestation: Permethrin Shampoo
Outbreaks: 3-12 yo, Warm/humid weather Each adult lays 3-5 eggs/day *10 min application then fine tooth comb
Girls > Boys *nits outnumber lice and are not a *safe in kids ≥2 months old
Less common in AA marker of infestation severity Reapplication in 7-10 days recommended
Sex partners treated simultaneously

Alternative: Malathion (8-12 hour period), Benzyl

EtOH, Spinosad (no need to comb), Topical
Ivermectin, Lindane (ADR neurotoxic avoid in
kids), Oral Ivermectin (refractory cases)

Pediculosis Etiology: Pediculus humanus corporis
Corporis
Transmission: Usually sex
“Body Lice” Strongly related to poor body hygiene
(homeless, prison, crowded unsanitary,
natural disasters, refugees)
Patho: Unlike head & pubic lice, body lice
do not live on skin. Body lice they their
eggs in seams of clothes/bedding and move
to skin only to feed
Pruritis (rxn to louse saliva), Excoriations
Maculae Cerulean: blue grey macules
*pathognomonic for lice
Clinical Dx: Identification of
louse or nits (more commonly
seen) in clothing (esp seams)
Nits: Ovoid greyish-white eggs
fixed to base of hair shafts.
Each adult lays 3-5 eggs/day
*nits outnumber lice and are not a
marker of infestation severity
Hygiene Improvement: Bathe thorough
Infested clothing/bedding heat washed, dry
cleaned, or discarded
Iron seams to destroy lice
Heavy Infestation: Permethrin 5% Cream
8-10 hour application
*safe in kids ≥2 months old
Reapplication in 7-10 days recommended
Sex partners treated simultaneously

Disease: Body lice can be a vector for

disease (relapsing fever, epidemic typhus,
trench fever)

Pediculosis Etiology: Phtirus pubis Pruritis (rxn to louse saliva), Excoriations Clinical Dx: Identification of Hygiene Improvement: Bathe thorough
Pubis louse or nits (more commonly Infested clothing/bedding heat washed, dry
Transmission: Usually sex (esp teenagers Maculae Cerulean: blue grey macules seen) in clothing (esp seams) cleaned, or discarded
“Phthirissis and young adults) *pathognomonic for lice Iron seams to destroy lice
Pubis” Nits: Ovoid greyish-white eggs
fixed to base of hair shafts. Heavy Infestation: Permethrin 5% Cream
“Pubic Lice” Each adult lays 3-5 eggs/day 8-10 hour application
*nits outnumber lice and are not a *safe in kids ≥2 months old
“Crabs” marker of infestation severity Reapplication in 7-10 days recommended
Sex partners treated simultaneously

Scabies Highly contagious skin infection due to the Intense pruritis (esp at night) Clinical Dx All clothing, bedding, etc should be placed in a
mite Sarcoptes scabiei Infected patients may remain without plastic bag for at least 72 hours, then washed &
symptoms for 4-6 weeks Skin Scraping dried using heat
Patho: Female mites burrow into the Mites, eggs, feces on
stratum corneum of the epidermis to lay PE magnification All close contacts should be treated
eggs, feed, and defecate -> Multiple, small erythematous papules, simultaneously
Hypersensitivity reaction to scybala (fecal excoriations Dermoscopy
particles) Topical Permethrin: DoC
151
Linear burrows (pathognomonic) MC in
intertriginous zones (scalp & web spaces)
Usually spares face and neck
Red, itchy papules/nodules on scrotum,
glans/penile shaft, body folds
Delta Wing Sign: Dark Triangle =
Head of mite within burrow
Applied topically from neck down for 8-14 hours
before showering (overnight)
Repeat application after 1 week
*Safe in pregnancy & lactation
Lindane: Cheaper
*Do not use after bath/shower (causes seizures)
C/I: Teratogenic, Not usually used in lactating
women and children <2 yo
Pregnant, Children <2 yo: 6-10% Sulfur in
petroleum jelly
Extensive: Ivermectin
152
DERM
Tinea Capitis Superficial fungal infection of Scalp
“Ring worm”
Etiology: MC fungus Trichophyton
RF: Poor hygiene, Direct contact,
Preadolescents, More common AA
Tinea Barbae Dermatophyte infection Beard Hair follicles
Tinea Corporis Superficial Fungal infection on Body
Not: Feet, Hands, Groin, Nails, Scalp
Etiology: Fungus of Trichophyton &
Microsporum genera, T. rubrum MC
Transmission: Direct contact (MC in
preadolescents), Animals, Another part of
body
Tinea Cruris Superficial Fungal infection on Groin or
Inner thighs
“Jock Itch”
Etiology: Fungus of Trichophyton genera, T.
rubrum MC or Epidermophyton floccosum
RF: Male, Copious sweating,
Immunocompromised
Tinea pedis may be the source
Tinea Pedis MC dermatophyte infection: T. rubrum, T.
interdigitale, Epidermophyton floccosum
“Athletes Foot”
MC Adolescents & Young men
Transmission: Direct contact
Patches of Alopecia w/ Black Dots Clinical Dx 1st: PO Griseofulvin
Multiple black dots due to the broken hair shafts *6-12 Weeks
due to endothrix infection KOH: MC initial test *Better absorbed with fatty food
Fungal element inside/surrounding ADR: Hepatitis, GI, HA, Disulfiram
Scaly Patches w/ Alopecia base of hair rxn
Single/Multiple patches with hair loss
± Erythema & Pruritis Woods Lamp 2nd: Terbinafine (Lamasil)
Trichophyton spp: No fluorescence *Less Common: Itraconazole,
Kerion: Severe Microsporum: Fluorescence Fluconazole
Inflammatory plaque w/ pustules & thick crusting
Often painful Culture: Definitive Lifestyle: Use of antifungals by all
house members, Avoid sharing hats,
Favus: Less common form clippers, combs
Cup-like shaped yellow crusts composed of dried
scalp secretions, fungi cells, inflammatory cells
Oral Antifungal
Single/Multiple Pruritic, Erythematous, Scaly, KOH: Segmented hyphae 1st: Topical Clotrimazole,
Circular/Oval Plaques/Patches with Central Ketoconazole, Butenafine,
clearing and well-defined raised borders that Culture: Definitive Terbinafine, Naftifine, Ciclopirox,
spread outwardly *slower method Tolnaftate
± Pustules *Usually 1-2 weeks
Ineffective/Extensive: PO
Terbinafine, Itraconazole
2nd: Griseofulvin, Fluconazole
Pruritis (hallmark) Clinical Dx Desiccant powder, Avoidance of
Annular patches/plaques, Diffuse erythema with tight fitting clothes and noncotton
sharply demarcated raised border that may have KOH: Best initial test underwear, Putting on socks before
tiny vesicles Segmented hyphae underwear
Often spares: Scrotum & mucose
Culture: Definitive 1st: Topical Clotrimazole,
Butenafine, Terbinafine,
Ketoconazole
Topical Ineffective/Extensive
PO Terbinafine or Griseofulvin
Interdigital (MC): Pruritis, Erythematous Clinical Dx Clean shoes with antifungal spray,
erosions or scales between the toes Keep cool/dry
MC between 3rd & 4th digital interspaces KOH: MC initial test
Segmented hyphae 1st: Topical Antifungal (Butenafine,
Hyperkeratotic: Diffuse hyperkeratotic rash Tolnaftate, Ciclopirox, Azoles)
involving soles, lateral, medial surfaces of feet Woods Lamp *4 weeks
with “moccasin” pattern Trichophyton spp: No fluorescence Terbinafine 1% cream X 1 week
Microsporum: Fluorescence Hyperkeratotic: Burrow’s solution
153

Tinea Versicolor NOT caused by dermatophytes
Overgrowth of the yeast Malassezia furfur
MC Adolescents & Young adults
RF: Hot & Humid (tropical), Excessive
sweating, Oily skin
Candidiasis Candida albicans part of normal GI & GU
Cutaneous flora but MC opportunistic pathogen
MC Neonates & >65 yo
RF: Warm moist environment,
Immunocompromised (DM), Obese
DERM Cause/Incubation/Tran
Hand Foot and Coxsackie Virus (esp type A)
Mouth Disease Enterovirus, Piconavirus family
MC: <5 yo
Transmission: Oral-Oral/Fecal
MC: Summer & Early Fall
Rubeola Rubeola Virus
“Measles” Paramyxovirus family
Incubation: 6-21 days
Transmission: Respiratory
droplets, Person to person,
Airborne
Vesiculobullous: Pruritic vesicular or bullous Culture: Definitive Topical Ineffective: PO Terbinafine,
eruption with underlying erythema Fluconazole, Itraconazole,
Esp medial foot Griseofulvin
May be painful
Hyper or Hypopigmented, Well-demarcated, KOH 1st: Topical Selenium sulfide,
Round/Oval Macules with Fine Scaling Hyphae & Spores “Spaghetti & Sodium sulfacetamide, Zinc
Often coalesce into patches Meatballs” pyrithione, & -Azoles
MC on upper trunk & proximal extremities (less Woods Lamp Systemic Therapy
often face & intertriginous areas) Yellow-green fluorescence Adults, Widespread, Failed Topical:
Itraconazole, Fluaconazole
Involved skin fails to tan with sun exposure *Ketoconazole & Fluconazole can be
used but associated with
hepatotoxicity. With Fluconazole,
patients must not shower for a few
hours after oral administration
Intertrigo: Cutaneous infection Clinical Dx Keep area dry
Pruritic rash beefy red erythema with distinct
scalloped borders & satellite lesions KOH: skin scrapping Mild-Moderate
Budding yeast +/-pseudohyphae Topical Clotrimazole
Severe: Oral Fluconazole
Contagious Presentation Diagnostics/Treatment
Very contagious 1st week Mild fever URI, Decreased appetite: 3-5 days after exposure Supportive: Antipyretics (APAP,
Oral Enanthem: Erythematous Macules -> Painful oral vesicles Ibuprofen), Hydration, Topical Lidocaine
surrounded by thin halo of erythema (buccal, tongue) then
Exanthem: Bilateral Grey-yellow vesicular, macular, Complication: Aseptic meningitis, GBS
maculopapular lesions on distal extremities (often including
palms & soles). Usually not painful or pruritic
Clinical Dx
Koplik Spots: Precede URI Prodrome: Malaise, Anorexia, High fever (>104°F) + 3Cs Supportive: APAP/NSAID, PO hydration
rash by 48 hours (cough, coryza, conjunctivitis) then Koplik Spots (1-3mm pale
white/blue papules w/ erythematous base on buccal mucosa Vitamin A: Reduces mortality & morbidity
Exanthem: Usually lasts opposite 2nd molars)
~7 days Exposed High Risk (pregnant, infants)
Exanthem: Maculopapular brick-red rash begins at hair line, Immunoglobulin
Patients must isolate for spreads cephalocaudally and centrifugally that darkens and
1 week after onset of rash coalesces Vaccine MMR (2): 12-15 mo, 4-6 yo
Lymphadenopathy, Pharyngitis Complication: Diarrhea (MC), Otitis
media, Conjunctivitis, Encephalitis
MCC Death: Pneumonia
154
Rubella Rubella Virus •10d before rash à Prodrome: Low grade fever, Cough, Anorexia, Lymphadenopathy Supportive: APAP/NSAID, PO hydration
“German Measles” Togavirus family 1-2 weeks after gone (posterior crevicular, posterior auricular)
Prognosis: Generally not associated with
Incubation: 2-3 weeks Exanthem: Becomes Exanthem: Pink/Light Red Non-confluent Maculopapular rash complications in children (esp kids)
Transmission: Respiratory generalized within 24 Starts on face, spreads to trunk & extremities
droplets hours, Lasts 3 days Compared to Rubeola: Spread quicker, no coalesce or darken Teratogenic (esp 1st trimester)
(CRS congenital rubella syndrome)
Forchheimer Spots: Small red macules/petechiae on soft palate Deafness, Cataracts, TTP, Mental
*may also be seen with scarlet fever retardation

Transient Photosensitivity & Arthralgia (esp young women &

adolescents)

Erythema Parovirus B19 Nonspecific Viral Symptoms: Fever, Coryza, Malaise then Supportive
Infectiosum MC: <10 yo Symmetrical Erythematous Malar rash with “slapped cheek” Anti-inflammatory: APAP, NSAID
appearance and Circumoral Pallor for 2-4 days then, Lacy,
“Fifth Disease” Respiratory droplets Reticular Maculopapular rash on Extremities (esp upper, Self-limited disease
Incubation: 4-14 days usually spares palms & soles) resolving in 2-3 weeks
Rash: Does not extend over bridge of nose or around mouth
Associated with: Increased fetal
loss during pregnancy Older Children & Adults: Arthropathy/Aralgias

Sickle Cell or G6PD Deficiency: DX: Usually clinical

May cause aplastic crisis

Roseola MCC: HHV-6, sometimes 7 Fever: 3-5 days, Resolves Fever Prodrome: High fever (may >104°F) & Lyphadenopathy Supportive: APAP/NSAID, PO hydration
90%: <2 yo abruptly before onset of Appears well & alert during febrile phase Self-limited
“Sixth Disease” rash
Incubation: 10 days Rash: Rosey-pink macular/maculopapular blanchable rash Adequate handwashing: Prevent spread
Transmission: Respiratory Rash: Lasts hours-2 days Begins trunk & neck then spreads to face
droplets *Only viral exanthem that begins on trunk Complication: 15% Febrile seizures

Nagayama Spots: Erythematous papules on soft palate & uvula

Erythematous TM, Respiratory symptoms, Anorexia

About Symptoms Causes, Risks, Complic. Treatment

Onychomycosis Nail infection caused by fungi
Etiology
Dermatophytes: Trichophyton &
Epidermophyton genera (T. rubrum MC)
Candida albicans (more likely fingernails),
Non-dermatophyte molds
RF
Increasing age, Tinea pedis, Psoriasis,
Occlusive shoes, Immunodeficiency
Thick, Opaque, Discolor ± Cracked
Subungual Hyperkeratinization
3 Variants: Distal lateral, Superficial
white, Proximal
MC: Great toe
Bc only 50% of dystrophic
nails are due to fungal
infections, Confirmation of
fungal infection before Tx
Fungal Culture + KOH
KOH wet prep: Only 60%
sensitive
Periodic Acid-Schiff Test:
Most sensitive
Perform on nail plate clippings
Management initiated if KOH(+) while waiting for cultures
Most Effective: Systemic Antifungals
1st Dermatophytes: Terbinafine
Dermatophytes & Candida: Itraconazole
ADR: Hepatotoxicity, DDI
C/I: EtOH & Hepatitis
Oral C/I or Not Desired: Topical Antifungals
Efinaconazole, Tavaborole

155

Paronychia Infection of lateral & proximal nail folds
<6 WEEKS
Etiology
S. aureus (MC, esp if rapid), GABHS
Oral Flora: Associated w/ nail biting
Candida: Associated w/ chronic disease
Patho: MC occurs after penetrating skin
trauma (dishwashing, nail biting, cuticle
damage in manicure, ingrown nail)
Fungal Cultures: Very specific,
not sensitive, takes weeks
Painful, Red, Swollen around the Mild Without Abscess: Warm water or Antiseptic swabs
proximal/lateral nail folds at the (10-15 min) followed by Topical ABX (Mupirocin)
cuticle
± Purulent discharge Moderate Without Abscess: PO Cephalexin/Dicloxacillin
Nail Biting Without Abscess: Augmentin or Clindamycin
MRSA: Bactrim, Clindamycin, Doxycycline
With Abscess: I&D
156
DERM About
Erysipelas Variant of cellulitis involving Upper
Dermis & Cutaneous Lymphatics
Etiology: GABHS (MC), S. aureus
Cellulitis Acute bacterial infection of Deeper
Dermis & Subcutaneous Tissue
Etiology: GABHS (MC), S. aureus
Pilonidal Disease Chronic gland infection in the
depths of the gluteal cleft
“Jeep Seat
Disease” Patient: Young, Hisrute with pain,
swelling, and drainage
Hidradenitis Suppurative: Most
frequent condition stimulating PD
Patho: Follicles in midline gluteal
cleft become blocked, infected, and
then drains pus leaving open midline
pits. Hair accumulates in the pits
acting as a nidus of infection causing
drainage to persist
About
Alopecia Nonscarring autoimmune hair loss
Areata targeting anagen hair follicles (scalp MC)
Associated with other autoimmune (thyroid,
Addison, SLE)
Onset usually <30 yo
Male = Female
FamHx predisposition
Clinical Presentation Risks/Diagnostics Diagnostics/Management
Intensely Erythematous Raised area with Clinical Dx Oral: PCN G, Amoxicillin, Cephalexin
Sharply Demarcated borders. Tender & Warm PCN allergy: Clindamycin, Bactrim, Linezolid
MC: LE, Face, Skin (impaired lymphatics) If Underlying Abscess
Milian Sign: Ear involved US + Gram stain + Culture IV: Cefazolin, Ceftriaxone
CBC: WBC Increased May need if systemic symptoms: Flucloxacillin
Unlike Cellulitis: Often has systemic symptoms CRP/ESR: Increased
Fever, Chills, Leukocytosis Antistreptolysin Titer O MRSA: IV Vancomycin
Localized macular erythema (flat margins not Primarily clinical dx Oral: Cephalexin, Dicloxacillin
sharply demarcated) Culture: taken and followed PCN allergy: Clindamycin, Erythromycin
Pain, Swelling, Warmth, Tenderness up within 48 hours
IV: Cefazolin, Unasyn, Ceftriaxone, Clindamycin
Systemic (not common): Fever, Chills,
Lymphadenopathy, Myalgias, Vesicles, Bullae, Cat Bite: Augmentin
Hemorrhage, Necrosis, Lymphangitis (streaking) PCN allergy:Doxycycline
Human/Dog Bite: Augmentin. Clindamycin +
Ciprofloxacin/Bactrim
MRSA
Oral: Clindamycin, Doxycycline, Bactrim
IV: Vancomycin or Linezolid
Acute Abscess Acute Abscess: I&D ± ABX
Chronic Draining Pits *Incise 1cm off midline
Complex, Recurrent Disease Post Surgery
Chronic Draining Pits: Shave gluteal skin, Remove
Location: Superior gluteal cleft over sacrum hair from pits
*Repeat every 1-2 weeks
*If persists for 2-3 months, refer for surgery
Complex, Recurrent Disease: Flap Surgery
removing all tissue from midline
Clinical Presentation Diagnostics Presentation
Smooth, discrete, circular patches of Clinical Diagnosis May spontaneously resolve or progress to
complete hair loss Punch biopsy: Definitive alopecia totalis (complete scalp loss) or
Develop over weeks alopecia universalis (complete loss scalp
Painless not pruritic and body)
Relapse is common
Nails: Pitting, Fissure, Trachyonychia (rough)
Mild Local: May be observed
Exam: Local: Intralesional Steroids
•Black dots: no scaring Extensive: Topical Corticosteroids
157
 Patho •Dermoscope: hair breaks before surface Peribulbar lymphocytic inflammatory
Damage to hair follicle in anagen stage, •Exclamation point hairs: blunt distal end infiltrates surrounding follicles
transform to catagen & telogen and taper proximally near scalp at margins
NO SCARRING of patches

Androgenetic Genetically predetermined progressive loss Gradual onset, usually occurs after puberty Usually clinical dx Topical
Alopecia of terminal hairs on scalp in characteristic Minoxidil (Rogaine)
pattern Hair thinning & Non-scarring hair loss Dermatoscope: Miniaturized hair and brown Widens blood vessels to allow oxygen
perihilar casts and nutrients promotes anagen phase
MC: Type of hair loss in men and women Men: Bitemporal thinning of frontal scalp then Best used with recent onset, requires 4-6
involves the vertex month trial must be used indefinitely
Patho: ADR: Pruritis, Local irritation, Flaking
Dihydrotestosterone (DHT) key androgen Women: Hair between frontal and vertex
Activation of androgen receptor shortens the without affecting frontal hairline Oral
anagen (growth) phase Finasteride
Decreased Anagen:Telogen Ratio MEN ONLY (cat X)
Inhibits T conversion to DHT
Anagen (growth) ADR: Decreased libido, sex/ejaculatory
Catagen (involution) dysfunction. Increased risk high grade
Telogen (death) prostate cancer

Hair Transplant: Effective

158
DERM About Clinical Presentation Diagnostics Treatment
SJS & TEN Severe mucocutaneous rxn, Prodrome (1-7 days): Fever & URI symptoms then Clinical Dx D/C offending agent
Detachment of epidermis & extensive Widespread flaccid bullae beginning on trunk & face Supportive
necrosis (palms/soles rarely involved) Biopsy: Full thickness necrosis *treat like severe burn
Erythematous macules with pruritic centers or Diffuse
RF: Meds (MCC): Sulfa, Lamotrigine, erythema with involvement of ≥1 mucous membrane + Epidermal Medical Emergency Burn unit, Pain control, Fluid &
Anticonvulsant, Allopurinol, NSAID, detachment Electrolyte repletion, Wound
Antipsychotic, ABX SJS: <10% BSA care
Infections (less common): Mycoplasma Skin: TTP SJS/TEN: 10-30% BSA
pneumonia, HIV, HSV Eyes (common): Corneal ulceration, Uveitis TEN: >30% BSA
Malignancy, Idiopathic Pulmonary: Bronchitis, Pneumonitis

PE: Nikolsky(+)

Erythema Type IV hypersensitivity rxn of skin
Multiforme Often following infection/med exposure
MC: Young adults (20-40 yo)
RF: HSV (MC)
Mycoplasma (esp kids), S. pneumonia
Drugs: Sulfa, Beta-lactams, Phenytoin,
Phenobarbital, Allopurinol
Malignancy, Autoimmune, Idiopathic
Target Lesions: dusky central area/blister, dark red inflammatory Usually Clinical Dx Symptomatic: D/C offending
zone surrounded by pale ring & erythematous halo on extreme agent, Antihistamines,
periphery Biopsy: If unclear Analgesics, Skin care
MC: Extremities & Trunk
Oral: Corticosteroid and
Minor: Distributed acrally, no mucosal membrane involvement Lidocaine + Benadryl
Major: Target lesions acrally progressing centrally + Mucosal mouthwash
membrane involvement, No epidermal detachment
Severe: Systemic Corticosteroid
PE: Nikolsky(-), Often Febrile
Mycoplasma: ABX

HSV: Oral Acyclovir

About Clinical Presentation Diagnostics Treatment

Rosacea Chronic acneiform skin condition
Erythema of the central face that
persists for months
Becomes a chronic, waxing and
waning skin disorder (flares often
initiated by triggers)
MC Women 30-50 yo, Fair skin
Often mistaken as acne, but it does
not have comedones (blackheads)
Etiology: Unclear
Persistent vasomotor instability,
Capillary vasodilation, Abnormal
pilosebaceous activity
Triggers: Sunlight, Exercise,
Hot/Cold weather, Emotional stress,
Topical steroids, Alcohol (wine)
Gradual onset Clinical Dx Avoid triggers, Wear sunscreen
Facial redness, flushing, Papulopustules "pimples" on central
face and possibly periorbital areas Biopsy: Definitive Mild-Moderate
Central face stinging or burning sensations *rarely done 1st Papulopustules: Topical Metronidazole,
Azelaic acid, Ivermectin cream, Sulfacetamide,
Sensitivity to skin care products that previously caused no Anti-acne topical meds
problems DDX
Sun damage Moderate-Severe
PE: Convex Areas of nose, cheeks, chin, forehead Acne: Rosacea has no PO ABX (Tetracyclines), Laser therapy
Telangiectasis, Papulopustules comedones
+/- Nodules, Rhinophyma (red enlarged nose) SLE: SLE has no Papules, Refractory: Oral Isotretinoin
NO comedones Pustules, SLE the malar
rash spares the nasolabial Facial Erythema: Topical Brimonidine, Laser
Types folds
Erythematotelangiectatic (MC): Persistent erythema of central
face, telangiectasia, sting Prognosis: Long term disorder but symptoms
Papulopustular: Papules, pustules, edema can be controlled with medications and
Phymatous: enlarged cobblestones, nose avoiding triggers
Ocular rosacea: blepharitis, conjunctivitis, hyrpemia

159
160
DERM About
Folliculitis Superficial hair follicle
infection/inflammation
RF: Men, Prolonged ABX, Topical
corticosteroids
Etiology: S. aureus (MC), other
gram(-) and (+), Fungi,
Pseudomonas aeruginosa (MCC hot
tub folliculitis)
Clinical Presentation Diagnostics/Management Management
Singular or clusters of perifollicular papules •clinical Mild: Topical Mupirocin, BPO
and/or pustules with surrounding erythema on Clindamycin, Erythromycin
hair bearing skin •gram stain, C/S
Often Pruritic •KOH if fungal Severe/Refractory: Oral ABX
Usually not painful *KOH dissolves the skin so you see the Cephalexin or Dicloxacillin
actual fungus
MRSA: Bactrim, Clindamycin,
Doxycycline
Gram(-):Daily Acetic acid or Topical
BPO *Usually resolves w/o treatment

Hot Tub: Oral Fluoroquinolone

General: Gentle cleansing with

antibacterial soap and Mild compress

DERM About Clinical Presentation Diagnosis Treatment

Brown Brown recluse (Loxosceles reclusa)
Recluse have violin pattern on anterior
Bite cephalothorax
MC Southwest & Midwest
Patho: Venom is cytotoxic & hemolytic
Local symptoms can be necrotic and
associated with lack of severe systemic
symptoms
Most wounds heal spontaneously in
days to weeks
Local Effects
Burning & Erythema at bite for 3-4 hours
Blanching of area (vasoconstriction)
“Red Halo”: Erythematous around ischemic center for 24-72 Hr
Hemorrhagic bulla that undergoes eschar formation
10% develop skin necrosis
Systemic Effects
± Fever, Chills, N/V, Morbilliform rash
Clinical Dx Local wound care & Pain control (NSAID or Opioids)
Spider Local Wound Care: Clean the affected area with soap &
collection & water, Apply cold packs to the site (avoid freezing the
identification tissue). If possible elevate or keep in neutral position
Tetanus Prophylaxis: If needed
Dermal Necrosis: Debridement (if needed)
*Delayed until the lesion is demarcated and clinically
stable, In some cases, it may lead to better wound healing
*Dapsone: Has been used in the past

ABX: Only if a secondary infection develops

*Treat like cellulitis

Black Black widow (Latrodectus Hesperus) Latrodectism Mild: Wound care & Pain control (NSAID, Opioid)
Widow has a red hourglass shape on underside Local Symptoms: Pain at bite *Gently clean the area with mild soap & water
Bite of belly Onset of systemic & neurologic symptoms in 30-120 min:
Produces a neurotoxin Muscle pain (most prominent, affects extremities, back, Moderate-Severe: Muscle relaxant (Benzo, Methocarbamol)
abdomen), Spasms, Rigidity
RF: Outdoors, Gardening, Sleeping Not Responsive: Antivenom
outside PE: Blanched circular patch with surrounding red perimeter *Not always readily available
& central punctum (target lesion)
Usually self-limited: Resolve 1-3 days

161
162
 About
Acne Inflammatory skin condition
Vulgaris associated with papules &
pustules involving pilosebaceous
units
Women > Men bc hormones
Begins around puberty due to
androgens stimulation
pilosebaceous unit changing
keratinzation at follicular orifice
Patho
Follicular hyperkeratinzation
Increased sebum (oil)
Propionibacterium acnes
overgrowth
Inflammation
Clinical Presentation
Comedone: Small non-inflammatory bumps
Open comedone (blackhead): Incomplete
Closed comedone (whitehead): Complete
Rosacea: Does not have comedones
Inflammatory Acne: Papules & Pustules
Nodular (>5mm) & Cystic Acne: Can cause
scarring, including pitted or hypertrophic scar
Areas with increased sebaceous glands: Face,
Back Chest, Upper arms
Causes/Location
COMEDONES MUST BE PRESENT!
•Definitive-skin biopsy
•Itchy back, shoulder, scalp à scrap for
potassium hydroxide (KOH) for Pityrosporum
folliculitis à fungal shampoo
Clinical Presentation
Often resolves after teen years
Nodulocystic acne: Aggressive treatment
Consistent, regular care over months
Mild: Topical: Retinoids, BPO, Azelaic aicd,
Salicylic acid, ABX (Clindamycin,
Erythromycin)
Moderate: + Oral ABX (Minocycline,
Doxycyline). Spironolactone
Severe: Oral Isotretinoin
Most effective medication
ADR: Dry lips & skin, Teratogenic,
Increased triglycerides & cholesterol
Neonatal Acne: Ketoconazole 2% Cream
newborn-8 wks, limited to face

Class Drugs Indication/About MOA SE/CI

Topical Tretinoin, Tazarotene •1st line for comedonal & inflam decreases cohesion and increases turnover of Side effect: dryness, photosensitivity
Retinoids Adapalene Gel •every 3rd night à nightly epidermal cells *speed up exofiliation CI: pregnancy

Benzoyl •Start with lowest concentration •no baceterial resistance à Release free- SE: skin irritation, bleaching of hair/clothing
Peroxide (2.5%) than increase as tolerable radical oxygen oxidized protein
(BPO)

Topical Clindamycin (BID, foam qd) •Mild-moderate inflammatory acne •reduces number of P. acne in pilosebaceous SE: skin irritation
Antibiotics Erythromycin (BID) (papulopustular) unit
* use with BPO
Oral ABX Doxycyline or minocycline Moderate acne with inflammatory •Inhibits P, acnea SE: upset stomach, photosensitivitiy, lupus
*add 100mg BID papules or deeper-seated lesions •Quickers results than topicals

Tetracyclines *1st line •Anti-inflammatory and ABX CI: pregnancy and young children
SE: photosensitivity, teeth staining in children

Macrolides Erythro &Azithromycin *1st Increased resistance Pregnancy category B

Bactrim *2nd line •Severe acne unresponsive to others SE: SJS, TEN; CI: Avoid in pregnancy

Oral Isotretinoin •Severe resistance nodular/cystic •Decrease in P. acnes SE: dryness of skin and mucous membranes,
Retinoids (Claracis or Acutane) •Inhibition of sebaceous gland headaches, suicide & depression, teratogenic
*monotherapy •2 contraceptives *can decrease athletic performance •increased TG and cholesterol
*after FAILED oral •2(-) pregnancy tests & monthly test
•no blood donation Labs: CBC, LFT, lipids monthly CI: tetracycline; pregnancy à birth defects

163
ENDO 5%
ADRENAL GLAND: GFR-ACE (superficial to deep): Glomerulosa-Aldosterone, Fasciculata-Cortisol, Reticularis-Androgens
Hypothalamus (CRH) -> Anterior Pituitary Gland (ACTH) -> Adrenal Gland -> Cortisol
Primary Disorders: Labs in the opposite direction = Problem is the target organ
Secondary & Tertiary Disorders: Labs in the same direction

TSH: Best initial thyroid functioning test, Used to follow patients on thyroid disease therapy. Low TSH -> Increase Levothyroxine, High TSH -> Decrease Levothyroxine. Used with T4 to manage Graves
Free T4: Metabolically active hormone. Ordered when TSH Abnormal to determine thyroid hypo/hyperfunction
Free T3: Used to diagnose hyperthyroidism when TSH Low & T4 Normal
Thyroid Antibodies
Graves = TRab & Anti-TSI (thyroid stimulating immunoglobulins, TSH receptor antibodies)
Hashimoto & Other Autoimmune Disease = Anti-TG & Anti-TPO
Primary (Thyroid): TSH High & T4 Low (labs in opposite direction)
Secondary (Pituitary): TSH Low & T4 Low (labs in same direction)
Tertiary (Hypothalamus): TRH Low
Radioactive Iodine Test (RAIU)
Graves, TSH-Secreting Adenoma: Diffuse Uptake
Thyroiditis (Hashimoto’s, Postpartum, DeQuervian): Decreased Uptake
Toxic Adenoma: Hot Nodule
Toxic Multinodular Goiter: Multiple Nodules
Rule Out Malignancy: Cold Nodules

SCREENING
Diabetes: ADA: All Adults ≥45 yo OR Any Adult BMI ≥25 & 1 additional RF, USPSTF: Any Overweight/Obese 40-70 yo: Every 3 years
Diabetic Retinopathy: Time of diagnosis & Annual: Dilated & Comprehensive Eye Exam
Diabetic Nephropathy: Annual Albumin, BUN, Creatinine, GFR
Diabetic Neuropathy: Time of diagnosis & Annual: Sensory function in feet and ankle reflexes
MEN-2: Genetic Screening for Children
Asymptomatic Thyroid Screen (USPSTF NO to Asymptomatic Screening): PMH autoimmune disease, neck radiation, thyroid surgery, FamHx thyroid disease, Radiologic abnormality: Screening TSH ± T4
AAFP: Older women: Periodic assessment
ATA & AACE: At risk of hypothyroidism (PMH T1DM, autoimmune disease, neck radiation, thyroid surgery, FamHx thyroid disease
Patients >60 yo: Consider TSH
Asymptomatic Hypogonadism Population screening NOT cost effective and NOT recommended

Disease Causes/Types Presentation/Labs & Testing Work-Up Treatment/Management

164
Primary Hyper- Bilateral idiopathic TRIAD: HTN + HYPOKALEMIA + BMP: High NA+ and bicarb,low K+ Unilateral Adrenal Adenoma “ Conn”
aldosteronism adrenal hyperplasia METABOLIC ALKALOSIS •surgical excision + Spironolocation
*increased urinary hydrogen excretion Plasma Renin & Aldosterone
Primary: *in the morning in seated position Bilateral Adrenal Hyperplasia (MC)
•Renin-independent •Refractory hypertension (young age w/o risk •aldosterone:renin ratio (ARR):>20:1 •Medical management
•idiopathic(MC) factors) *high aldosterone, low plasma renin •Low Na+ diet
•conn syndrome •K+ spare diuretics:
“unilateral adenoma” Hypokalemia: CT Scan-Adrenal Spironolactone or Eplerenone
•proximal muscle weakness <4-Conn, >4- carcinoma •HTN: ACEI, CCB, ARB
Secondary: •polyuria, constipation •thickening-hyperplasia
•increased renin à •decreased DTR •negative CT à adrenal vein sampling Adrenal Carcinoma: Oncology referral
increased aldosterone in •hypomag
RAAS Adrenal Vein Sampling Referrals: Endo, Cardio
*perform if negative CT scan
•assess aldosterone in blood Monitor: HTN and electrolytes

Confirmatory:
•sodium loading test (oral preferred)
-high urine aldosterone >12 à primary
*If no oral, then IV over 4 hours while
seated, >10 is confirmatory

Pheo- Catecholamine secreting Triad: Plasma Free Metanephrines Management: resection of tumor after 1-2 weeks of
chromocytoma adrenal tumor à NE and episodic palpitations, HA, diaphoresis •sit 15min; elevated à assess urine hypertensive therapy
*Adrenal Gland E •Anxiety, pallor, syncope, tachycardia
•Paroxysms <1hr 24h Urine Metanephrine and Creatinine Awaiting Surgery: Maintain BP < 160/90
Rule of 10s: • (+) if >2.2mcg/mg of creatinine •Alpha-Adrenergic Blockers:
•10% bilateral *triad + HTN is HIGHLY suggestive Cardura, Minipress, Hytrin
•10% extra-adrenal Imaging: CT/MRI with contrast
•10% malignant Diet-high salt and water intake

Adrenal Nonfunctional (MC) Nonfunctional: Asymptomatic •Detailed HP Surgery referral

Adenoma/ Benign, does NOT •Labs based upon suspected adrenal zone
Carcinoma secrete steroids Functional: *related to cellular involvement affected
•Glomerulosa-hyperaldosteronism
LOW ACTH Functional: •Fasiculata-cushings •Fine Needle Aspiration
•Benign >1cm •Reticularis-hyperandrogenism *only to r/o metastasis in patient with
•Secrete steroids ind. •Medulla-pheochromocytoma known malignancy
ACTH/ RAAS *must r/o Pheochromocytoma

165
ENDO
Adrenocortical Disorder where the adrenal gland
Insufficiency doesn’t produce enough
hormones
Secondary: Pituitary failure of
ACTH secretion (lack of
cortisol only). MCC of
secondary & overall
insufficiency. *Aldosterone
intact bc RAAS
Etiology: Hx of exogenous
glucocorticoid use (esp without
tapering), Hypopituitarism
Primary: “Addison Disease”:
Adrenal gland destruction
(lack of cortisol & aldosterone)
Etiology: Autoimmune MCC
USA, Infection MCC 3rd world:
TB, HIV, Vascular:
Thrombosis/Hemorrhage in
adrenal gland (Waterhouse-
Friderichsen Syndrome). Others:
Trauma, Mets, Meds
(Ketoconazole, Rifampin,
Phenytoin, Barbiturates)
Due to Lack of Cortisol
Weakness, Myalgias, Fatigue. Non-Specific
GI: Weight/Appetite loss, Anorexia, N/V/D,
Abdominal pain. HA, Sweating, Abnormal
menstruation, Mild hyponatremia, Salt
craving, Hypotension.
*Hypoglycemia more common in secondary
Primary “Addison’s Disease”
Due to Lack of Sex hormones & Aldosterone
Hyperpigmentation (increased ACTH
stimulates MSH secretion), Orthostatic
hypotension
*Women may have: Loss of libido,
Amenorrhea, Loss of axillary pubic hair
Baseline Labs Glucocorticoid Replacement
8AM ACTH, Cortisol, Renin 1st Line: Hydrocortisone
*Increased Renin esp with primary Also: Dexamethasone
ACTH Primary “Addison’s” ONLY
Addison’s: Elevated Mineralocorticoid Replacement
Secondary: Decreased Fludrocortisone
Addison’s: Hypoglycemia, Hyponatremia,
Hyperkalemia, Non-AG metabolic acidosis (due to Patient Education
increased aldosterone) Must be treated with IV
Glucocorticoids & IV Isotonic
Screening Tests Fluids before & after surgical
High Dose ACTH (Cosyntropin) Stimulation Test procedures
Insufficient Rise in Serum Cortisol (<18) = Adrenal *mimicking body’s natural response
insufficiency
*normal response = Rise in serum cortisol During Illness/Surgery/High Fever
Oral dosing needs to be adjusted to
recreate the normal adrenal response
to stress: 3X3 Rule (triple the
normal dose for three days)
Everyone should carry a medical alert
tag as well as an injectable form of
cortisol for emergencies

Acute Adrenal •Sudden worsening of adrenal •Hypovolemic Shock (MC!) BMP •IVF: normal saline (D5NS if
Insufficiency insufficiency due to “stressful” •Hypotension, Hypovolemia •hypoglycemia hypoglycemia)
event •Abdominal pain, N/V •hyponatermia
“Addisonian •Fever, Weakness, lethargy, confusion •hyperkalemia •IV HIGH dose Hydrocortisone
Crisis” *normal response is a 3x increase
Triggers: abrupt steroid withdrawal, surgery, Confirm: cortisol and aldosterone •Reversal of electrolytes
trauma, volume loss, hypothermia, MI, fever, •Fludricortisone
sepsis, hypoglycemia

Cushing’s Cushing’s Syndrome: Signs &
Disease symptoms related to cortisol
excess
Exogenous: MC overall: Long
term high dose glucocorticoid
therapy
Endogenous: Cushing’s Disease
MC endogenous cause:
Pituitary gland ACTH
overproduction (hyperplasia or
adenoma)
Ectopic ACTH Producing
Proximal muscle weakness, Weight gain, HA,
Oligomenorrhea, ED, Polyuria, Osteoporosis,
Mental disturbances (mild-psychosis)
PE:
Fat Redistribution: Truncal obesity, Moon
facies, Buffalo hump, Supraclvicular fat
pads, Thin extremities
Skin: Thin skin (atrophy), Striae, Easy
bruising, Decreased wound healing,
Hyperpigmentation (if increased ACTH)
Acanthosis Nigricans
Androgen Excess: Hirsutism, Oily skin, Acne
HTN
Screening Tests
24 Hour Urinary Free Cortisol: Most specific
Nighttime (11PM) Salivary Cortisol
Low Dose (1mg) Overnight Dexamethasone
Suppression Test
*Elevated cortisol or No suppression = Cushing’s
Syndrome
Differentiating Tests
Baseline ACTH + High Dose Dexamethasone
Suppression Test: Helps distinguish Cushing’s
Disease (pituitary)
Cushing’s Disease: Increased ACTH + Suppression
of Cortisol on High Dose
Taper Off Corticosteroid Use
(to prevent Addisonian crisis)
Cushing’s Disease: Transsphenoidal
Resection
*Inoperable: Radiation, Pasireotide,
Mifepristone
Adrenal Tumor: Tumor Excision
Ectopic ACTH Producing Tumor:
Resection
*Inoperable: Ketoconazole,
Metyrapone
166
Tumor: SCLC, Medullary
thyroid cancer)
Adrenal Tumor (adenoma):
Secretion of excess cortisol
*only one that suppresses with high dose
Ectopic ACTH Producing Tumor: Increased
ACTH + NO suppression of Cortisol on High Dose
Adrenal Tumor & Steroids: Decreased ACTH +
NO suppression of Cortisol on High Dose
Work Up After Labs
Cushing’s Disease: Pituitary MRI, if negative
sample petrosal sinus
Ectopic ACTH Producing Tumor: Chest imaging
Adrenal Tumor & Steroids: CT Abdomen
Dyslipidemia
CBC: Leukocytosis
CMP: Hyperglycemia, Hypokalemia, Metabolic
acidosis
167
ENDO
Type I DM Insulin deficiency (pancreatic beta cell destruction) Hyperglycemia w/o Fasting Blood Glucose: *Gold Intensive Diabetes Therapy: Coordination of
Require exogenous insulin Acidosis (MC initial Impaired: 110-125 meals/diet and activity with insulin replacement
“T1DM” Onset: <30 yo (3/4 dx childhood) Peaks: 4-6 yo then presentation): 3 Ps: DM: ≥126 Frequent Monitoring: At least 4 times daily or
10-14 yo Polyuria, Polydipsia, *fasting ≥8 hours, 2 occasions Continuous glucose monitoring
Not associated with obesity Polyphagia
Glycemic Targets
Type IA (MC): Autoimmune: Often triggered by 2 Hour Glucose Tolerance (GGT) Standard: A1c <7% as a standard
Weight loss, Lethargy
environmental (infection) 3 Hour GGT: *GOLD gestational DM Older/Comorbidities/Limited Life: A1c <8 %
*Increased with HLA DR3-DQ2 & DR4 genes Impaired Glucose: ≥140-199 Pregnancy: A1c <6%
DKA (2nd MC initial
DM: ≥200
presentation) (more
Type IB: Non-autoimmune Young w/ T1DM: Seen every 3 months (minimum)
common in T1DM)
Hgb A1c *Review blood glucose levels
Impaired: 5.7-6.4% *Assess A1C level
Silent (asymptomatic) *Watch for hypoglycemia when blood glucose
incidental discovery DM: ≥6.5%
concentration is lowered to near normal
*average blood sugar 10-12 wk prior
*Ensure that the patient's family is well equipped
to deal with symptomatic hypoglycemia
Random Plasma Blood Glucose *Glucagon available for emergency use
DM: ≥200 *Watch weight gain due to insulin
*in patient with classic DM symptoms
or complications

Type II DM Combo: Insulin insufficiency (resistance) & Classic: Polyuria, Fasting Blood Glucose: *Gold Initial: Diet + Exercise + Lifestyle
Relative impairment of insulin secretion Polydipsia, Polyphagia Impaired: 110-125 *Carbs: 50-60%, Protein: 15-20%, Unsaturated
“T2DM” *increased insulin early, may diminish with Poor wound healing, DM: ≥126 fats: 10%
progression Increased infections. *fasting ≥8 hours, 2 occasions
MC >40 yo HHS Not Controlled: Oral Antihyperglycemic Meds
*Metformin (biguanide) (initial therapy in most)
RF: Genetic & Environmental. Obesity (greatest), 2 Hour Glucose Tolerance (GGT) Others:
Decreased physical activity. 90% are overweight. 3 Hour GGT: *GOLD gestational DM Sulfonylureas: 1st Gen: “-MIDE“ 2nd Gen: “GL-“
Hx impaired glucose tolerance, FamHx, 1st degree Impaired Glucose: ≥140-199 Meglitinides “-NIDE”
relative, Hispanic, AA, Pacific islander, HTN, DM: ≥200 Thiazolidinediones: “-GLITAZONE”
Dyslipidemia, Delivery of baby >9lbs, Syndrome X, Alpha-Glucosidase Inhibitors
Insulin resistance Hgb A1c GLP-1 Agonist: “-TIDE”,
CHAOS: Chronic HTN, Atherosclerosis, Obesity Impaired: 5.7-6.4% DDP-4 Inhibitors: “-GLIPTIN”
(central), Stroke DM: ≥6.5% SGLT-2 Inhibitors: “-FLOZIN”
*average blood sugar 10-12 wk prior
Insulin functions: glucose transport; stops protein & Insulin may be needed if uncontrolled with others
TG breakdown, and gluconeogenesis Random Plasma Blood Glucose
DM: ≥200
Incretin: hormone that stimulates the release of insulin *in patient with classic DM symptoms
and decrease blood glucose or complications

Diabetic Consequence of: Insulin deficiency & Polyuria, Polydipsia, Plasma Glucose >250 Goals: Closing AG determines complete
Ketoacidosis Counterregulatory hormone excess Nocturia, Weakness, *usually not >600 management
MC seen with T1DM Fatigue, AMS, N/V, Bicarb level more important than glucose levels
“DKA” Chest pain, Abdominal Decreased Arterial pH <7.30 & Bicarb in determining severity of DKA
Excessive counter hormones pain <22
•↓ Bicarbonate b/c depleted by ketoacids *due to high AG acidosis
168
 •↓ Insulin, ↑Glucagon
-↑ hepatic gluconeogenesis and glycogenolysis
-↑ free FA release -> ↑ ketones
*triggered during increased physiologic need
Mild: Glucose (>250), Arterial pH (<7.30), Bicarb
(15-18), Ketones (Positive), Serum Osmolarity
(Variable)
Moderate: Glucose (>250), Arterial pH (7.0-7.24),
Bicarb (10-<15), Ketones (Positive), Serum
Osmolarity (Variable)
Severe: Glucose (>250), Arterial pH (<7), Bicarb
(<10), Ketones (Positive), Serum Osmolarity
(Variable)
PE: Tachycardia, *Bicarb replacement only in severe cases bc
Tachypnea, Hypotension, Increased Serum Osmolarity complication (overcorrection, increased cerebral
Decreased skin turgor, edema
Fruity (acetone) breath, Positive Ketones (urine & blood)
Kussmaul respirations SIPS: Saline, Insulin, Potassium, Search for
(deep continuous) cause
IVF: Critical initial step: 0.9% NS (isotonic) until
hypotension & orthostasis resolves. Then switch to
0.45% NS. When glucose get ≤250 use D5 version
of current NS (prevent hypoglycemia from insulin
therapy)
Regular Insulin: Lowers serum glucose &
switches body from catabolic to anabolic state
(reduces ketones & fatty acid production, decreases
gluconeogenesis)

Potassium Repletion: Despite K levels, pt are

always in total body K deficit. Correction of DKA
will cause hypokalemia. Unless Serum K is >5.3,
Repletion is recommended.
*3.3-5.3: IV KCl (20-30mEq/L) added to each L of
IFV
*<3.3: IV KCl (20-40mEq/L) should be given
*>5.3: Delay replacement until K ≤5.3. Check
Hourly

Hyperglycemia Consequence of: Insulin deficiency & Hyperglycemia: Increased: SIPS: Saline, Insulin, Potassium, Search for
Hyperosmolar Counterregulatory hormone excess Polydipsia, Polyuria, Osmolarity >320 cause
State MC seen with T2DM, Older pt Nocturia, Weakness, Serum Glucose >600 *Saline most important component
Associated with: More severe dehydration & higher Fatigue, Confusion, N/V, *Regular insulin
“HHS” mortality compared to DKA AMS Absence of significant acidosis
(arterial pH >7.30 & serum bicarb HHS: Glucose (>600, Arterial pH (>7.30), Bicarb
Etiology: Response to stressful triggers: PE: Tachycardia, >15) (>15), Ketones (Small), Serum Osmolarity (>320)
MCC: Infection (UTI, Pneumonia), Undiagnosed Tachypnea, Hypotension,
DM, MI, CVA, Pancreatitis Decreased skin turgor,
Dry mouth, Increased
Patho: Illness -> Reduced fluid intake -> Profound capillary refill time
dehydration, Increased osmolarity, hyperglycemia,
total body K deficit
Not usually associated with severe ketosis or
acidosis (they make enough insulin to prevent
ketogenesis)

Drug MOA Advantages Disadvantages Contraindications

Binguanide Decreases glucose production (inhibiting No hypoglycemia GI (MC): Diarrhea, Nausea, Abdominal Severe renal/hepatic
Metformin gluconeogenesis) No weight gain, Weight loss discomfort, Anorexia, Metallic taste impairment, Cr >1.5, HF,
*FIRST LINE T2DM Increases insulin utilization peripherally Vit B12 Deficiency (decreased absorption) Excessive EtOH
Decreases intestinal glucose absorption Decreases: A1c by 1.5% & Glucose *Macrocytic anemia
concentrations by 20%, Triglycerides, CV
No effect on beta cells risk, Possible decreased cancer risk
169
 Lactic Acidosis: Tends to happen in those Stop 24 hours before iodinated
predisposed to hypoxemia, hypoperfusion, HF, contrast, can resume 48 hours
severe renal/hepatic impairment after
*monitor Creatinine
Thiazolidinediones Increase insulin sensitivity peripherally No hypoglycemia Peripheral edema & Fluid retention, CHF, HF (symptomatic, Class III
“-GLITAZONE” (adipose, muscle, liver) -> Increased glucose Increased Fx (female) or IV), Hx bladder cancer,
Pioglitazone utilization & Decreased glucose production Decreases: A1c at most 2% (monotherapy) Hepatotoxicity: Monitor LFTs Active liver disease, High risk
Rosiglitazone for Fx, Pregnancy, T1DM
No effect on beta cells Pioglitazone: Bladder cancer
Rosiglitazone: Higher incidence CV events &
atherogenic lipid levels

Sulfonylureas Stimulates beta cell insulin release (insulin Initial therapy in those CI to Metformin or Hypoglycemia (MC): Esp long acting 1st gen:
1st Gen “-MIDE”: secretagogue, non-glucose dependent via Adjunct to Metformin bc insulin release is non glucose dependent
Tolbutamide, mimicking the action of glucose -> Closure *Similar glycemic efficacy to Metformin GI upset (take with food to reduce)
Chlorpropamide of K-ATP channel of SUR1 receptor) Dermatitis: Photosensitivity, Pruritis, Erythema,
2nd Gen “GL-“: Short Acting Glimepiride/Glipizide: Safer Rash, Urticaria
Glimepiride 2nd Gen Preferred: Less ADR & Shorter in patients with chronic renal disease Sulfonamide allergies, Cardiac arrythmias,
Glipizide, Glyburide duration of action Weight Gain (Glipizide & Glimepiride lower)
DDI: CP450 Inducer

Chlorpropamide: Hyponatremia (increased

ADH), Disulfiram rxn (flushing rxn after
EtOH ingestion by inhibiting metabolism of
acetaldehyde)
Meglitinides Stimulates beta cell insulin release (insulin May use monotherapy in those with CI to Hypoglycemia (lower incidence than Nateglinide: Should not be
“-NIDE” secretagogue that is more glucose dependent Metformin or Adjunct to Metformin Sulfonylureas) used with chronic renal/liver
Repaglinide -> Postprandial insulin release) *Often administered with meals to decrease disease (metabolized by liver
Nateglinide Similar benefits to Sulfonylureas without postprandial hyperglycemia with active metabolites renally
sulfa allergy concern Weight gain excreted)

Repaglinide: Safer with chronic renal

disease (primarily metabolized by liver)

Alpha Glucosidase Delays intestinal glucose absorption No hypoglycemia GI: Flatulence, Diarrhea, Abdominal pain, Caution Use: Gastroparesis,
Inhibitors (inhibits pancreatic alpha amylase & Hepatitis (Increased LTFs) IBD, Bile acid resins
Acarbose, Miglitol intestinal alpha-glucosidase hydrolase) Can be used with renal insufficiency

Less potent than Metformin & Sulfonylureas

No effect on beta cells

SGLT-2 Inhibitors Lowers renal glucose threshold -> Increased No hypoglycemia Transient N/V, Thirst, Abdominal pain, AKI, T1DM, T2DM w/ GFR <60
“-FLOZIN” urinary glucose excretion Most often used with: Metformin, Bone Fx
Empagliflozin, Pioglitazone, Sitagliptin, Insulin Canagliflozin: May be
Canagliflozin, SGLT = Na-Glucose Transport UTI & Yeast infections (increased urinary associated with increased risk
Dapagliflozin CV Risk Reduction: Improved CV glucose) of amputation
SGLT-2 is expressed in the proximal tubule outcomes & decreases risk of HF (esp
& mediates reabsorption of ~90% of the Empagliflozin) ±Hypotension (in pt taking hypertensive meds, Caution: With other meds that
filtered glucose load (relatively weak glucose due to osmotic diuresis) cause dehydration (NSAID,
lowering agents) BP reduction & Weight loss ACEi, ARB, Diuretics) and
Low bone mineral density
170
GLP-1 Agonists Mimics incretin -> Increased insulin No weight gain, Weight loss Low risk hypoglycemia Hx: Gastroparesis or
“-TIDE” secretion (Increased glucose dependent), Reduction of CV events (esp Liraglutide) Pancreatitis
Liraglutide, Exenatide, Decreased glucagon secretion, Delayed GI: N/V/D
Dulaglutide gastric emptying Medullary thyroid
carcinoma or MEN2
Injection syndrome

DDP-4 Inhibitors Decreased degradation of GLP-1,
“-GLIPTIN” Increasing GLP-1 levels -> Increased
Sitagliptin, Linagliptin, insulin release & uptake of glucose
Saxagliptin peripherally, Decreased glucagon & hepatic
glucose production
Monotherapy or Adjunct Low risk hypoglycemia
HA, Pancreatitis, Hepatitis, Skin changes,
Joint pain, Renal dysfunction

Amylin Analogs Synthetic amylin (hormone) Delays gastric emptying, Decreases Risk of hypoglycemia which can be difficult to
Pramalintide Impersonates the effects of amylin glucagon release, Decreases appetite correct to delay in gastric emptying

Injection Decreases A1c: 0.5% N/V, Anorexia

Approved for T1DM & T2DM

Insulin Drugs Onset Insulin Coverage

Rapid Lispro (Humalog) Onset: 5-15 min Time of meal
Aspart (Novolog) Peak: 45-75 minutes *often used with intermediate or long acting
Glulisine (Apidra) Duration: 2-4 hours

Short Regular Insulin Onset: 30 min 30-60 minutes prior to meal

Peak: 2-4 hours *often used with intermediate or long acting
Duration: 5-8 hours

Intermediate NPH Onset: 2 hours Half day or Overnight

Lente Peak: 4-12 hours *often combined with rapid or short acting
Duration: 8-18 hours *NPH often given at bedtime

Long Detemir (Levemir) Onset: 2 hours 1 full day, Detemir 6-24 hours
Glargine (Lantus) Peak: 3-9 hours (Detemir), No peak (Glargine) *Glargine: Fewer hypoglycemia episodes than NPH
Duration: 6-24 hours dose dependent (Detemir), 20-24 hours (Glargine) *Should not be mixed with other insulin in same syringe

Pre-Mixed Humulin 70/30 (NPH/Regular) Generally given BID before mealtime

Humulin 50/50 (NPH/Regular)
Novolin 70/30 (NPH/Regular)
Novolog 70/30 (NPH/Aspart)

Complication DM About Characteristics Treatment

Somogyi Phenomenon Nocturnal hypoglycemia then rebound if 3am dose is lOw (hypOglycemia) then it is sOmOgyi Prevent Hypoglycemia (with any)
hyperglycemia Decreasing nighttime NPH dose
171

Patho: Hyperglycemia occurs due to surge in GH after
early AM hypoglycemia
Dawn Phenomenon Normal glucose until rise in serum glucose levels
between 2-8AM
Patho: Results from decreased insulin sensitivity &
nightly surge of counterregulatory hormones
(during nighttime fasting)
Insulin Waning Progressive rise in glucose from bed to morning. Seen
when NPH evening dose is administered before
dinner
Due to ineffective dosing of NPH insulin
Hypoglycemia Blood glucose ≤70
Usually due to: Too much insulin, Too little food,
Excess exercise
Diabetic Retinopathy MCC of new permanent vision loss 20-74 yo
*usually due to maculopathy
Also in
EENT Non-Proliferative: Microaneurysms, Cotton Wool
Spots (soft exudates that resemble grey-white spots
due to nerve layer microinfarctions). Hard Exudates
(yellow spots with sharp margins often circinate due
to lipid/lipoprotein deposits from leaky blood
vessels), Blot & Dot Hemorrhage (bleeding into
deep retinal layer). Flame-Shaped Hemorrhages
(nerve fiber layer hemorrhage)
Proliferative: Neovascularization -> Vitreous
hemorrhage
Diabetic Nephropathy DM MCC of ESRD
Patho: Progressive kidney deterioration ->
Microalbuminuria (1st sign diabetic nephropathy)
*can lead to nephrotic syndrome with massive
proteinuria, edema, HLD, hypoalbuminemia
Move the evening NPH dose earlier
Give a bedtime snack
If it rises with the sun at 3AM, it is Dawn Phenomenon Reduce Early AM Hypoglycemia (with any)
Bedtime injection of NPH (blunts AM
hyperglycemia)
Increase NPH dose
Avoiding carb snack late at night
Insulin pump use early in AM
Move NPH dose to bedtime or Increase
evening dose
Autonomic: Sweating, Tremors, Palpitations, Nervous, Mild-Moderate: 15-20g fast-acting carbs,
Tachycardia, Cool, Pallor, Clammy fruit juice, hard candies
CNS: HA, Lightheaded, Confusion, Slurred speech, Dizzy, *recheck in 10-15 min
Irritable, Difficulty concentrating, Blurred vision, Nausea,
Syncope Severe/Unconscious (<40): IV Bolus D50 or
IV Glucagon (glucagon SC/IM if no IV)
Unknown Cause: Order C-Peptide, Plasma
insulin levels, Anti-insulin antibodies.
Elevated C-Peptide seen in endogenous
insulin production
*C-Peptide is normal with exogenous insulin
Maculopathy: Macular edema/exudates, Blurred/Decreased Non-Proliferative: Glucose control, Laser
central vision loss
*Can occur at any stage Proliferative: VEGF Inhibitors
*Vision loss in non-proliferative often occurs due to macular (Bevacizumab), Glucose control, Laser
edema photocoagulation
Prevention: Annual eye exams
*to detect diabetic retinopathy
Urine Dipstick: (+)dipstick for protinuira = 24 hour urine protein ACEi/ARB: Reduces protein leakage &
loss between 30-300mg slows progression via efferent arteriole
24 Hour Urine: For albuminuria dilation
±Anemia & Acidosis
Histology: Kimmel-Wilson lesion (pink hyaline material) Screening: Annual Microalbuminuria,
around the glomerular capillaries from protein leakage BUN, Creatinine
172
Peripheral Neuropathy Many Forms Glucose Control
Symmetric Polyneuropathy: MC type. Progressive
distal sensory loss “stocking glove” pattern (distal FDA Approved: Pregabalin, Duloxetine,
LE first, progressing to hands): Loss of vibratory, Amitriptyline, Gabapentin
proprioception, light touch, temperature. Decreased
ankle reflexes, Gait abnormalities, Motor dysfunction, 2nd Line: Venlafaxine, Topical Capsaicin,
Can lead to foot ulcer formation Lidocaine patches, Alpha-lipoic acid, TENS

Autonomic: Orthostatic hypotension, Gastroparesis Screening: After initial screening, All

(after many years), Enteropathy diabetics screened annually by examining
(constipation/diarrhea) sensory function in feet and assessing
ankle reflexes
Cranial Mononeuropathy: MC EOM: CN3 Palsy:
Diplopia & Ptosis w/ sparing of pupils (unlike other
CN 3 palsies), CN4, CN6, CN7 palsies

Peripheral Neuropathy: Median neuropathy MC

(carpal tunnel syndrome), Ulnar neuropathy

Diabetic Gastroparesis
Cardiovascular
Decreased GI motility & delayed gastric emptying
due to Decreased ability of the gut to sense the stretch
of the bowel walls in the absence of a mechanical
obstruction
Patho: Impaired neural control of gastric function
(diabetic neuropathy)
Atherosclerosis: DM is considered CAD equivalent
PAD
Stroke: 2-4X greater than general population
CHF
HTN
N/V, Bloating, Early satiety, Upper abdominal discomfort & Initial: Glycemic control & Diet (small,
constipation in the setting of longstanding DM (years) frequent, soluble fiber, low in fat)
PE: Gastric distention with a succussion splash Prokinetics: Metoclopramide,
*no rigidity/guarding Erythromycin, Domperidone (they increase
GI motility)
Dx: EGD (initially), Nuclear Gastric Emptying Scintigraphy:
Delayed gastric emptying in the absence of structural obstruction Avoid meds that delay gastric emptying:
GLP-1 agonist Exenatide & DPP-4 inhibitors
CV Risk Reduction
ASA regularly >30 yo
Statin: LDL goal <100
Reduce other cardiac risks
A1c: <7.0%
BP goals: <140/90
BP ≥140/90 or Urine(+) for Microalbuminuria: ACEi/ARB

Skin Candida: Below breasts, axilla, between fingers, Vulvovaginitis

Cutaneous Xanthomas (due to severe hypertriglyceridemia)
Shin Spots: Brown, painless, no treatment
Acanthosis Nigricans: Hyperpigmented, velvety plaques
*Hyperkeratosis with normal melanocyte count

ENDO Etiology Clinical Presentation Complications/Management

Subacute Patho: Unknown, Often follows Painful thyroid, Aggravated with head movements ESR High + Negative thyroid antibodies Supportive: Reassurance, Self-
Thyroiditis antecedent viral respiratory tract & swallowing) limiting
infection or post-viral inflammation *Starts lower neck & radiates to jaw & ear Primary Hyperthyroid Profile Early: *95% return to euthyroid state
“Granulomatous, *NOT autoimmune TSH Low, T4 High
DeQuervian” Usually present hyperthyroid phase due to: Acute *may present in euthyroid or hypothyroid Pain/Inflammation: ASA,
Initially hyperthyroidism then neck pain state later NSAID
HYPER -> euthyroidism then hypothyroidism then
NORMAL -> URI: Fever, Myalgias, Malaise, Fatigue Adjunctive Fail/Severe: Prednisone
173
HYPO resolution & restoration of normal thyroid
function
Suppurative Bacterial infection of thyroid by
Thyroiditis Gram(+) S. aureus MC or Gram (-),
Pneumocystis, Mycobacterial
Rare, Usually occurs in children
*only two causes of painful thyroids are
subacute and suppurative thyroiditis
Riedel Rare chronic autoimmune thyroiditis
Thyroiditis Dense fibrosis that invades thyroid &
adjacent neck structures
Part of the IgG4 related systemic disease
Euthyroid Sick Abnormal thyroid function tests in pt
Syndrome with normal thyroid function
MC seen with severe non-thyroidal
illness
*Sepsis, Cardiac, Malignancies
Patho: Severe illness decrease peripheral
conversion of T4 -> T3
PE: Diffusely tender goiter
Sudden onset thyroid pain & tenderness
*worse with hyperextension
*improve slightly with flexion
May: Radiate to mandible, ears, posteriorly
May have overlapping erythema to skin
Fever, Chills, Pharyngitis, Dysphagia, Dysphonia,
Hoarseness
Present similar to malignancy: Rock hard
nontender rapidly growing fixed goiter (moves
poorly with swallowing)
*Rock hard = Anaplastic thyroid cancer or Riedel
thyroiditis
Compression: Neck tightness/pressure, Hoarseness,
Dysphagia, Choking, Coughing, Increased RR
NO Cervical Lymphadenopathy
RAIU: Diffuse, Decreased uptake
*similar to Hashimoto & Postpartum
thyroiditis
Biopsy: Granulomatous inflammation
with multinucleated giant cells
*rarely done
Leukocytosis & ESR Increased ABX
FNA w/ Gram Stain & Culture Fluctuant: Surgical drainage
Thyroid US
IgG4 Serum Levels, Euthyroid or Surgery: Reduce compression
Hypothyroid (30%)
Open Thyroid Biopsy: Dense Fibrosis
*FNA insufficient test if suspected
*Rules out malignancy
Low T3 Syndrome Treat underlying illness
T3 Low, Reverse T3 High
Thyroid Replacement: Usually
Severe Disease: T4 Normal/Decreased not needed
TSH Normal/Low/High
*usually low in severe, high in recovery
174
ENDO
Hyperthyroidism Etiology:
Graves Disease (MCC)
Toxic Adenoma
Toxic Multinodular Goiter
TSH Secreting Pituitary Adenoma
Thyroiditis: Postpartum, deQuervain, Silent
(lymphocytic) earlier stage
Iatrogenic Thyrotoxicosis
Amiodarone
Excess Intake T3, T4
Grave’s Disease MCC of hyperthyroidism USA
Highest incidence: Women 20-40 yo
Patho
Autoimmune: TSH-receptor autoantibodies
target & stimulate TSH receptor on
thyroid -> Increased thyroid hormone
production, Thyroid gland enlargement,
Hyperthyroidism
Ophthalmopathy: TSH receptors antibodies
activate retro-ocular fibroblasts & adipocytes
-> orbitopathy
*specific to Grave’s
Calorigenic: Increased Metabolic Rate:
All metabolic processes are increased,
except for menstrual flow which is
decreased (Oligomenorrhea). Heat
intolerance, Weight loss despite increased
appetite
Skin: Warm, Moist, Soft fine hair,
Alopecia, Easy bruising
CNS: Hyperactivity: Anxiety,
Nervousness, Fatigue, Weakness, Increased
sympathetic output (Tachycardia,
Palpations, AFib, Fine tremor),
GI: Diarrhea, Hyper-defecation
CVS: Tachycardia, Palpations, High output
HF
Hyperthyroidism: Palpations, Heat
intolerance, Tremors, Weight loss, AFib
Specific to Grave’s: Ophthalmopathy:
Proptosis, Exophthalmos, Lid lag,
Diplopia, Vision changes. Pretibial
Myxedema: Swollen red/brown patches on
legs with non-pitting edema
PE: Diffusely enlarged nontender goiter,
Thyroid bruit
Primary Hyperthyroid Profile
TSH Low, T4/T3 High
TRab (TSH receptor antibodies): Anti-TSI
*hallmark
RAUI: Diffuse Increased Uptake
Radioactive Iodine: MC therapy
*ablates thyroid within 6-18 weeks
ADR: May exacerbate
ophthalmopathy initially
CI: Pregnant & Lactating
Thioamides: Methimazole or PTU
Prevents thyroid hormone synthesis,
will often achieve euthyroid state
within 3-8 weeks. May use in older
and CV patients. May be used prior
to more definitive treatment. PTU
also prevents peripheral conversion
of T4 -> T3
ADR: Agranulocytosis, Aplastic
anemia, Fulminant hepatitis.
Methimazole generally preferred
(less ADR but teratogenic in 1st
trimester)
PTU: Preferred in 1st trimester &
Thyroid storm
Beta-Blockers: Propranolol
*rapidly ameliorate symptoms
(tremor, HTN, AFib, tachycardia)
Ophthalmopathy: Glucocorticoids:
Best initial therapy. Usually given
before radioactive iodine
*Alternatives: Decompressive
therapy & Orbital radiotherapy
Definitive: Thyroidectomy,
Radioactive iodine
175
Toxic Adenoma Single/Multiple hyperfunctioning
autonomous nodule(s)
Nontoxic usually asymptomatic
Toxic = Symptoms of thyrotoxicosis
TSH Secreting Benign pituitary adenoma, Secretes TSH
Pituitary
Adenoma Rare cause of hyperthyroidism (<1%)
Iatrogenic Often due to the treatment of
Hypothyroidism hyperthyroidism with Radioactive Iodine or
Surgery (Total/Subtotal Thyroidectomy)
without subsequent thyroid hormone
replacement
Thyroid Storm Rare, Potentially fatal complication of
untreated thyrotoxicosis usually after
“Thyrotoxic precipitating event (surgery, trauma,
Crisis” infection, illness, pregnancy)
Only 1-2% with hyperthyroidism present
with thyroid storm (75% mortality)
Hyperthyroidism: Anxiety, Heat
intolerance, Weight loss despite increased
appetite, Fatigue, Weakness, Increased
sympathetic output (tachycardia, palpations,
AFib, fine tremor), Diarrhea, Increased
metabolic rate, High output HF,
Oligomenorrhea
Obstructive (due to enlarged goiter):
Dyspnea, Dysphagia, Stridor, Hoarseness
(if goiter presses on recurrent laryngeal
nerve)
Diffuse goiter (95%)
Hyperthyroidism
Compression: Bitemporal hemianopsia
(bilateral loss of outer visual fields bc
compression of optic chiasm), HA, Mental
disturbances
Amiodarone: Contains iodine and may
induce hypothyroidism (by Wolff-Chaikoff
effect) or Hyperthyroidism (by Jod-
Basedow effect) depending on underlying
state of patient
Hyperthyroidism + Hypermetabolic state
CV Dysfunction: Palpations,
Tachycardia, AFib, CHF
High Fever (104-106), N/V, Tremors
CNS Dysfunction: Agitation, Delirium,
Psychosis, Stupor, Coma. May later
progress to Come & Hypotension
± Signs of Hyperthyroidism: Warm/Moist
skin, Hand tremor, Ophthalmopathy
Primary Hyperthyroid Profile
TSH Low, T4/T3 High
RAIU: Single/Multiple areas of increased
iodine uptake “hot nodules”, with decreased
uptake in surrounding tissues
US
Secondary Hyperthyroid Profile
TSH High, T4 High
RAIU: Diffuse Increased Uptake
*same as graves
Pituitary MRI: To detect adenoma
Increased Alpha Subunit: Distinguishes it
from TSH resistance syndrome
Alpha-Interferon: By stimulating the immune
system in patients with baseline thyroid
autoimmune predisposition (patient with Anti-
TPO or Anti-TG antibodies)
Primary Hyperthyroid Profile: MC pattern
TSH Low, T4/T3 High
*may be so low it’s undetectable
± Hyperglycemia
RAI Ablation or Surgery
*usually preferred over long term
antithyroid meds (PTU,
Methimazole)
Compressive: Surgery
Definitive: Transsphenoidal
Surgery
Somatostatin Analogs: May be used
prior to surgery to restore
euthyroidism
Lithium: Mechanism that causes
hypothyroidism is poorly understood
(may affect colloid)
IVF + Propranolol +
Propylthiouracil + IV
Glucocorticoids
Beta-Blockers: Reduces tachycardia
& decreases adrenergic symptoms
Antithyroid Meds (Propylthiouracil):
Block synthesis of new T3 & T4.
Propylthiouracil preferred over
Methimazole bc PTU also reduces
peripheral conversion of T4 -> T3
Glucocorticoid: Reduce peripheral
conversion of T4 -> T3
THEN: Oral/IV Sodium Iodide (1
hour after PTU)
*blocks release of thyroid hormone
176
 Antipyretics: Avoid ASA bc it can
displace thyroid hormones off of
carrier proteins.

Cooling Blankets

Hypothyroidism Etiology: Calorigenic: Decreased Metabolic Rate:

Iodine Deficiency (dietary, cretinism)
Hashimoto’s Thyroiditis MCC
Thyroiditis: Postpartum, deQuervain, Silent
(lymphocytic) later stage
Pituitary Hypothyroidism
Hypothalamic Hypothyroidism
Riedel’s Thyroiditis
Medication: Amiodarone, Lithium, Alpha-
Interferon
All metabolic processes are decreased,
except for menstrual flow which is
decreased (Menorrhagia). Cold intolerance,
Weight gain despite decreased appetite
Skin: Dry Thickened Rough Skin, Loss of
outer 1/3 of eyebrow, Goiter, Nonpitting
edema (myxedema)
CNS: Hypoactivity: Fatigue, Sluggish,
Memory loss, Depression, Decreased DTR,
Hoarseness
GI: Constipation, Anorexia
CVS: Bradycardia, Decreased CO,
Pericardial effusion

Hashimoto’s MCC of hypothyroidism USA Hypothyroidism Primary Hypothyroid Profile Levothyroxine

Thyroiditis
Patho: Autoimmune thyroid destruction
due to Anti-TPO & Anti-TG
Goiter Symptoms: Hoarseness & Dyspnea
Women may have Galactorrhea (due to
increased prolactin)
PE: Thyroid may be atrophic, normal, or
enlarged (goiter). Bradycardia, Decreased
DTR, Loss of outer 1/3 of eyebrows.
Myxedema: Nonpitting edema (periorbital,
peripheral)
TSH High, T4/T3 Low
Positive: Anti-TPO and/or Anti-TG
RAIU: Diffuse Decreased Uptake
Biopsy: Lymphocytic infiltration with germinal
centers & Hurthle cells (enlarged epithelial cells
with abundant eosinophilic granular cytoplasm)
*rarely done

Cretinism Untreated congenital hypothyroidism
HYPO Etiology: Dysgenesis of thyroid gland or
defect in enzymes (1st world), Lack of
maternal iodine (3rd world), May be
acquired if maternal TSH receptor blocking
antibodies passed into fetal circulation via
placenta
Mental development delays, Short stature Primary Hypothyroid Profile: Levothyroxine
TSH High, T4/T3 Low
Symptoms of Hypothyroidism: Decreased
metabolic rate, Cold intolerance, Dry thick
rough skin, Constipation, Weight gain
despite decreased intake, Menorrhea,
Myxedema (eyelid & facial edema),
Weakness, Lethargy

Goiter Symptoms (older children):

Myxedema Rare, Extreme form of hypothyroidism
Coma with high mortality rate (>40%)
MC in elderly women with longstanding
hypothyroidism in the winter
Hoarseness & Dyspnea (trachea
compression)
Severe Signs of Hypothyroidism: Primary Hypothyroid Profile (MC) IV Levothyroxine + Supportive
Bradycardia, Obtundation (coma), TSH High, T4 Low
Hypothermia, Hypoventilation, *may be so low that it’s undetectable ICU Admission
Hypotension, Hypoglycemia, Passive Warming (not rapid)
Hyponatremia Serum Cortisol IV NS
IV Glucocorticoids (often given)
177
Patho: Usually an acute precipitating factor
(infection, CVA, CHF, Sedative/Narcotic
use) in a patient with longstanding
hypothyroidism,
Discontinuation/Noncompliance with
Levothyroxine therapy, Failure to start
Levothyroxine after treatment for
hyperthyroidism

178
Disease Signs/Symptoms
Thyroid >90% of nodules are benign
Nodules and Follicular adenoma MC benign
Goiters
Risks:
•exteme ages
•history head/neck radiation
Symptoms:
•most are asymptomatic
•compressive symptoms (large
multinodular goiters)
Exam:
•benign: varies
•malignant: rapid, fixed, no movement
with swallowing
Thyroid Cancer papillary thyroid carcinoma *MC
•single thyroid nodule, painless
•MC after radiation exposure
•least aggressive, slow, confined
Follicular Thyroid Carcinoma
•metastasize (distant MC)
• ↑ iodine uptake
Medullary Thyroid Carcinoma
•Secrete calcitonin, prostaglandins,
5HT, ACTH, CRH, other chemicals
•Local mets, NO good iodine uptake
Anaplastic Thyroid Carcinoma
•Most aggressive, worst survival
•Rapidly enlarging mass in MNG
•Does not have good iodine uptake
•hard rock thyroid mass
Labs Imaging Results
Order TSH *FIRST TEST Multinodular Goiter
•if normal or high à FNA biopsy •Multiple hyperechoic nodules
•Enlargement of isthmus and thyroid
Thyroid US: *usually after labs lobes
•determines if FNA is needed
•concerning-irregular margins, hypoechoic, Thyroid nodule
central vascularity, growth, >1cm •Single nodule, color flow Doppler
FNA Biopsy *BEST TEST Solitary Thyroid nodule
•nodules >1.5cm with normal TSH or highly •Discrete hypoechoic nodule
suspicious nodules
Multinodular Goiter
RAI Uptake *hyperfunctioning tissue •SVC compression
•hypofunction=cold, high cancer risk •Tracheal deviation
•hyperfunction=hot, low cancer risk
•Palpable, firm, nontender nodule/mass Serum Tg
•↑-metastatic papillary and follicular
Symptoms:
•Anaplastic-s/s of metastasis Serum Calcitonin
•Medullary-flushing, diarrhea •↑-medullary thyroid carcinoma
*Medullary can be associated with Men IIa and b
Serum CEA
MC Met Sites: lung, lymph, bone •↑-medullary thyroid carcinoma
Thyroid US *size, location of mass
RAI Scan *use after thyroidectomy
•reveal metastatic tissue
High uptake: follicular
CT or MRI: Distant metastases
CA: COLD & LOW uptake
Management
•Follow-up with regular palpation and •US
every 6mo
•LT4 suppression for nodule >2cm and
normal or high TSH
*reduces emergence of new nodules
•Ethanol Injection *shrink benign nodules
Toxic Multinodular Goiter:
•Methimazole +/- BB
•Surgery
Cancer, Hyperfunction, Toxic: Surgery
Toxic adenoma, Tosic MNG, Graves
•RAI therapy *shrinks nodules by ~60%
Surgery-First Line
>1cm cancer: total
<1cm cancer: lobectomy
<4cm inderterminate: lobectomy
>4cm indeterminate: total
RAI therapy
CI-prego, nursing
*low iodine diet for 2wkbefore
Chemo: aggressive CA
179
PSYCH 5%

SCREENING
Depression: PHQ-2 (little intrest/pleasure in doing things?, feeling, down, depressed, or hopeless?): If positive -> PHQ-9. Another one that’s self reported: Zung Self-Rated Depression Scale
GAD: GAD-7 (89% sensitive, 82% specific)
PTSD: PC-PTSD-5 (primary care), CAPS-5 (clinician administered)
Autism: American Academy of Pediatrics: All kids at 18-24 months old, >24 months only if there are concerns for ASD
1st year of life: Reduced response to name & Reduced frequency of looking at faces
2nd year of life: Difficulties sharing experiences, interests, or attention with others
16-30 mo: M-CHAT-R/F (Modified Checklist for Autism in Toddlers, Revised with Follow Up) (yes/no parent report questionnaire, Healthcare professional driven questions of care takers)
4-11 yo: AQ-Child (Autism Spectrum Quotient-Child
7-16 yo: ASSQ (Autism Spectrum Screening Questionnaire)
Anorexia & Bulimia: SCOFF (make urself sick, lost control, one stone in 3 months, fat, food dominates, ≥2 yes: 100% specificity & sensitivity for anorexia & bulimia, Eating Disorder Screen for Primary
Care
Somatic Symptom Disorder: PQH-15 (Patient Health Questionnaire 15 item)
Adult EtOH: AUDIT-C, CAGE
Adult Opioid: Rapid Opioid Dependence Screen
Adolescent Substance Use Disorder: Starting at 11 yo: CRAFFT annually ( ≥2 positives = positive screen)
Domestic Violence “Does the person you love…” (NOT: Why don’t you leave, what did you do to make him angry, why do you keep going back)
• Track" all of your time?
• Constantly accuse you of being unfaithful?
• Discourage your relationships with family & friends?
• Prevent you from working or attending school?
• Criticize you for little things?
• Anger easily when drinking or using other drugs?
• Control all finances and force you to account in detail for what you spend?
• Humiliate you in front of others?
• Destroy personal property or sentimental items?
• Hit, punch, slap, kick or bite you or the children?
• Use or threaten to use a weapon against you?
• Threaten to hurt you or the children? Force you to have sex against your will?

Disorder About Presentation Findings Treatment

Anorexia Failure to maintain a normal weight Behaviors targeted at maintaining a low weight or body Hypokalemia Medical Stabilization:
Nervosa Fear & preoccupation with weight, body image, image: Excess water intake, Food related obsessions *GI loss from vomiting/laxative Hospitalization for <75%
being thin (hoarding, collecting) expected body weight or
MC: Teenage girls (14-18 yo): 90% are women Increased BUN Medical complications:
Frequently seen in: Athletes, Dancers Ego-Syntonic: Their behaviors are acceptable to them and in Dehydration, Electrolyte
*dehydration
harmony with their self-image goals abnormalities may lead to
cardiac arrhythmias
60% incidence of depression Hyperchloremic Metabolic
Highest mortality rate of all psych diseases, due Restrictive Type: Strict, reduced calorie intake, diet, fasting, Acidosis
excessive exercise, diet pills Nutritional Rehab: MC
to arrhythmias: 5-18% *vomiting Complication: Refeeding
syndrome (increased insulin -
Binge Eating/Purging Type: Primarily engages in self- Hypogonadotropic > hypophosphosphatemia &
induced vomiting as well as laxative, diuretic, or enema abuse Hypogonadism cardiac complications)
*low estrogen
PE: Emaciation, Hypotension, Bradycardia, Skin/Hair changes
Psychotherapy: CBT,
(lanugo), Dry skin, Salivary gland hypertrophy, Amenorrhea,
Hypothyroidism Supervised meals, Weight
Arrhythmias, Osteopenia
monitoring
Russel’s Sign: Callouses on dorsum of hand from self-induced
vomiting
If Depressed: SSRI (may also
BMI ≤17.5 or Body Weight <85% of IBW
help with weight gain),
180
 Atypical Antipsychotics (may
also help with weight gain)

Bulimia Eating disorder PE: Hypokalemia, Hypomagnesemia Most Effective:

Nervosa Frequent binge eating + Compensatory Teeth pitting or Enamel erosion (vomiting) *Electrolyte imbalance may lead Psychotherapy + Fluoxetine
behaviors to prevent weight gain Russel’s Sign: Callouses on dorsum of hand from self-induced to cardiac arrhythmias
vomiting Psychotherapy: CBT, Group
Unlike Anorexia, patients with Bulimia usually Parotid gland hypertrophy Metabolic alkalosis therapy, Interpersonal therapy
maintain a normal weight (or overweight) & *vomiting
their compensatory behaviors are ego-dystonic Recurrent Episode of Binge Eating Pharmacotherapy: Fluoxetine
(troublesome to patient) Increased Amylase
Eating within a 2 HOUR period more than people would *salivary gland hypertrophy & *only FDA approved med,
in a similar period with lack of control during an overeating has been shown to reduce the
vomiting
F:M, 10:1 episode. Occurs AT LEAST WEEKLY FOR 3 MONTHS binge-purge cycle
Onset: Late teens or Early adulthood *may be triggered by stress/mood changes ADR: CV effects, esp if
electrolyte abnormalities
Perception of self-worth is excessively influenced Compensatory Behaviors present
by shape & body weight Purging Type: Primarily engages in self-induced vomiting,
diuretic, laxative, diet pills
Non-Purging Type: Reduced calorie intake, dieting,
fasting, excessive exercise, diet pills

Disorder About Criteria Treatment

Intimate 1/4 women, 1/7 men: Experience physical violence by partner lifetime Clues to Violence Screening, Assessing, Referring
Partner 1/3 women, 1/6 men: Experience sexual violence lifetime Contusions to chest ,breast, abdomen, face, neck
Abuse Women who leaves abusive partner has 70% increased risk of being MSK & “Accidental injuries” Once Suspected: Address patients
killed, compared to staying Multiple injuries in various stages of healing directly with non-threatening
Pregnancy abuse can make up 10% pregnancy hospital admissions Non-specific general symptoms: Fatigue, HA questions
Barriers to Screening: Lack of privacy, Low self-esteem, Fear, Sensitive
nature It Occurred: Alternatives discussed
with Referral
*patient can refuse

Sexual Abuse 1/4 - 1/3 female children: Experienced sexual abuse before 18 yo Clues to Violence
Common ages 9-12 yo Children with sexual knowledge
MC Perpetrators: Males, Relatives/Known by child (access) Initiate sex acts with peers or show knowledge
33% sexual offenders: Were once victims themselves of sexual abuse Genital/Anal: Bruises, Pain, Pruritis
Evidence of STI

Child Abuser often female and primary caregiver Signs

Physical Cigarette burns, Burns in stocking glove pattern
Abuse Laceration, Healed Fx, Subdural hematoma, Multiple bruises
Retinal hemorrhages

Shaken Baby Syndrome: Hyphema or Retinal hemorrhages

Child Neglect Failure to provide basic needs of a child Signs

*supervision, food, shelter, affection, education Malnutrition, Failure to thrive, Withdrawal, Poor hygiene

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182
Disorder About & Criteria Symptoms Treatment
General F>M ≥3 Symptoms Most Effective: SSRI + CBT
Anxiety Onset: Early 20s Fatigue, Restless, Difficulty concentrating, Muscle tension,
Disorder Sleep disturbances, Irritability, Shakiness, HA 1st Line: SSRI (Fluoxetine, Paroxetine,
Excessive Anxiety/Worry on majority of days for ≥6 Escitalopram), SNRI (Venlafaxine)
(GAD) months NOT: Episodic, Situational, Focal *Adjunct: Buspirone (no sedation)
*Anxiety is usually out of proportion to the event
Significant Social/Occupational Dysfunction CBT & Psychotherapy

Not due to: Substance use, Medical condition Benzos: Can be used for short term use
only, until long term therapy takes effect
*watch for dependence/abuse

Beta-Blocker, TCA

Panic Attacks Sudden abrupt discrete episode of intense fear or
discomfort, usually peaks within 10min, Most 20-30 min
*rarely lasts ≥1 hour,
May feel anxious hours after attack
Panic attacks are a feature of many different anxiety
disorders but is not a disorder in and of itself
Hallmark: Sense of impending doom/dread 1st Line: Alprazolam, Lorazepam,
Diazepam
≥4 Symptoms of Sympathetic Overdrive *watch for dependence/abuse
Dizziness, Trembling, Choking feeling, Paresthesia, Sweating, SoB,
Chest pain/discomfort, Chills/Hot flashes, Fear of losing control, Rule Out Potentially Life Threatening
Fear of dying, Palpations/Increased HR, Nausea/Abdominal distress, Conditions (MI, Thyrotoxicosis)
Depersonalization/Derealization *even in those with panic disorder

Panic Disorder Average onset: Early-Mid 20s Recurrent Unexpected Panic Attacks (≥2) ± Trigger Most Effective: SSRI + CBT
Greater risk: 1st degree family ≥1 of the following must occur for ≥1 month
>60% also MDD Panic attacks often followed by persistent concern about future attacks Long Term: 1st Line: SSRI (Sertraline,
F>M Persistent worry about the implication of the attacks (losing control) Citalopram, Fluoxetine)
Significant maladaptive behavior related to the attacks *may initiate therapy with: SSRI + Benzo
then taper and D/C Benzo.
Not due to: Substance use, Medical condition, Other mental disorder *other options: SNRI & TCA

Adjunct: CBT: Relaxation,

Desensitization, Examine behavior
Psychotherapy: May be used as initial
therapy in mild cases

Acute Panic Attacks: Alprazolam,

Clonazepam
*watch for dependence/abuse

Phobic Persistent ≥6 Months Intense Fear/Anxiety of Specific
Disorder Situation (heights, flying), Object (pigeons, snakes, blood),
or Place (hospital)
Exposure to the situation triggers immediate response
Fear is out of proportion to any real danger Exposure & Desensitization: ToC
Situation is actively avoided/endured with intense fear/anxiety Short Term: Benzos or Beta-Blockers
*can be used in some
Everyday activities must be impaired by distress/avoidance

Subtypes: Animal, Situational, Natural environment, Blood- Not due to: Substance use, Medical condition, Other mental disorder
Injection

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Social Anxiety MC type of phobia (public speaking) Exposure to social situations: Almost always provokes anxiety & 1st Line: Psychotherapy: CBT
Disorder Causes expected panic attacks (desensitization), Relaxation, Insight
Disabling ≥6 MONTHS Intense Fear of oriented therapy
Formerly: Social/Performance situation where you can be May realize that feelings are excessive & Out of proportion to any
Social Phobia scrutinized for fear of embarrassment (public speaking, actual threat/danger. May avoid those situations Pharmacotherapy: SSRI (Fluoxetine,
meeting new people, eating/drinking in front of people, Sertraline), SNRI (Venlafaxine)
public restrooms) *adjunct: Benzo (can be used until full
effect of SSRI for patients with need of
faster relief)

Moderate-Severe: Psychotherapy +
Pharmacotherapy

Situational: Beta-Blocker (Propranolol,

Atenolol)
*30-60 min before performance

Agoraphobia Intense Fear of going into places/situations where escape Symptoms ≥6 Months Most Effective: SSRI + CBT
or obtaining help may be difficult *similar to Panic Disorder
Significant Social/Occupational Dysfunction
Commonly seen with panic disorder, it is now seen as a
separate entity Not explained by another disorder

Triggering situation causes fear/anxiety out of

proportion to the potential danger of the situation

RF: Strong genetic factor & may follow a traumatic event

Post- Traumatic event occurred ANYTIME in the past Exposure to Actual/Threatened: 1st Line: SSRI, TCA, MAOi
Traumatic Death, Serious injury, or Sexual Violence via: *may augment: Atypical Antipsychotics
Stress 1) Direct experience of traumatic event
Disorder 2) Witnessing event in person CBT: Psychotherapy, Individual/Group
3) Learning event happened to someone close counseling, Relaxation
(PTSD) 4) Experiencing extreme/repeated exposure to aversive details of
PTSD vs Acute Stress Disorder: Same symptoms the traumatic event (1st responders collecting human remains, Insomnia: Trazodone
*difference is time of event & duration of symptoms War, Rape, Natural disasters)
Nightmares & Hypervigilance: Prazosin
PTSD ≥1 of the following intrusive symptoms after the event may lead to
Trauma occurred at any time in the past significant distress/impairment in function
Symptoms >1 month
Re-Experiencing: >1 Month Leading to Physiologic distress and/or
Acute Stress Disorder Physiologic reactions
Trauma occurred <1 month ago Repetitive Recollections (distressing dreams)
Symptoms <1 month Dissociative Reactions (flashbacks)

Avoidance of stimuli associated with event

≥2 Negative Alterations in Cognition & Mood:

Inability to remember an important aspect of the event
Dissociative amnesia
Negative feelings of self, world, or others
Anhedonia
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 Negative emotions (horror, guilt, anger, shame)
Detachment or Inability to experience positive emotions

≥2 Arousal & Reactivity Symptoms

Angry outbursts
Irritable behavior
Reckless/Self destructive behaviors
Hypervigilance
Sleep disturbances
Concentration issues
Exaggerated startle response

Acute Stress Similar to PTSD EXCEPT: Symptoms 1st Line: Counseling & Psychotherapy
Disorder Traumatic event occurred <1 MONTH AGO & Intrusive symptoms *bc by definition the symptoms will
Symptoms last <1 MONTH Avoidance revolve in 1 month
Increased arousal *symptoms >1 month: Treat as PTSD
Negative alterations in thought & mood

Adjustment Maladaptive Emotional/Behavioral Reaction to an
Disorder Identifiable Stressor (job loss, physical illness, leaving
home, divorce) or Non life threatening event that causes a
disproportionate response than would normally be
expected WITHIN 3 MONTHS of the stressor (doesn’t
include bereavement) & Usually resolves WITHIN 6
MONTHS of the stressor removal
≥1 of the following
Marked distress out of proportion to the severity of stressor
Significant impairment in areas of functioning (occupation, social, etc)
May manifest as: Depressed mood, Anxiety, Disturbance of conduct
Initial ToC: Psychotherapy: Individual &
Group therapy
Mediations may be used in select cases but
they are not the preferred treatment
Patients may self-medicate w/ drugs/EtOH

Disorder About Criteria Treatment

Bipolar I RF: FamHx (1st degree): Strongest (10X more likely)
1% of population, M =F
Onset: 20-30 yo (new onset rare >50yo)
Earlier onset = More likely psychotic features & poorer prognosis
≥1 Manic or Mixed episode (only requirement) 1st Line: Mood Stabilizer: Lithium
Manic episodes often cycle with occasional depressive *acute mania & long term
episodes but major depressive episodes are not required for *reduces suicide risk
diagnosis
Rapid Cycling/Mixed Features: Valproic acid,
Mania: Abnormal & persistently elevated, expansive, or
Carbamazepine
irritable mood ≥1 WEEK (less if hospitalized) with Marked
impairment of social/occupational function. ≥3 symptoms
Mood: Euphoria, Irritable, Labile, Dysphoric Monotherapy/Adjunct: 2nd Gen Antipsychotics:
Thinking: Racing, Flight of ideas, Disorganized, Easily Risperidone, Quetiapine, Olanzapine,
distracted, Expansive/Grandiose thoughts, Impaired Ziprasidone
judgement.
Behavior: Physical hyperactivity, Pressured speech, Faster & More Effective: Lithium + 2nd Gen
Decreased need for sleep (may go days w/o), Increased Antipsychotics
impulsivity, Excessive involvement in pleasurable activities
(risk taking, hypersexuality, disinhibition, increased goal Psychotherapy: Cognitive, Behavioral,
directed activity) Interpersonal, Good sleep hygiene
Psychotic Symptoms (may be seen): Paranoia, Delusions,
Hallucinations Bipolar Depression: Lithium, Quetiapine,
Lurasidone, Lamotrigine
Symptoms not due to medical condition/substance abuse
Antidepressants may be used as adjunct to mood
stabilizers for severe depression, but
185
 monotherapy may precipitate mania or
hypomania

Acute Mania: Most Effective: Antipsychotics:

Risperidone or Olanzapine > Haloperidol or
Mood Stabilizers (Lithium, Valproic acid)

Acute Psychosis/Agitation: Antipsychotics or

Benzos

Refractory/Life Threatening Acute Mania or

Depression: Electroconvulsive Therapy
*also best treatment for pregnant with manic
episodes

Bipolar II Recurrent major depression episodes with hypomania Hx ≥1 major depressive episode + ≥1 hypomanic episode Management: Same as Bipolar I
*any current/previous manic episode makes the dx bipolar I

Hypomania: Abnormal & persistently elevated,

expansive, or irritable mood <1 week. Does not require
hospitalization. Not associated with marked impairment of
social/occupational function & not associated with psychotic
features. ≥3 symptoms affecting: Mood, Thinking, or
Behavior (symptoms otherwise similar to manic episodes)

Bipolar I vs Mania/Mixed Major Depression

Bipolar II vs Bipolar I: YES Bipolar I: Typical but NOT REQUIRED
Cyclothymia Bipolar II: HYPOmania ONLY (no mania) Bipolar II: YES
vs MDD vs Cyclothymia: NO (may have periods of mood elevation) Cyclothymia: NO (associated with relatively mild depressive episodes)
Dysthymia MDD: NO MDD: YES
Dysthymia: NO Dysthymia: Usually mild but can meet criteria in some cases

Cyclothymic Similar to Bipolar II but less severe ≥2 YEARS of Prolonged, Milder elevations & depressions Similar to Bipolar I
Disorder ~1/3 will develop Bipolar in mood that do not meet the criteria for full hypomanic
M=F episodes or major depressive episodes Mood Stabilizers (Lithium) or 2nd Gen
May coexist with Borderline Personality Disorder *≥1 YEAR in children Antipsychotics (Risperidone, Olanzapine,
Quetiapine, Ziprasidone)
Symptom free periods DON’T LAST >2 MONTHS at a
time for those 2 YEARS

Major depressive, Manic, Mixed episodes DO NOT occur

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 Drug MOA Indication Side effects DDI CI
Benzodiazepines Enhance GABA at •Anxiety, panic •Drowsiness •ETOH •Pregnancy
Short: receptor •insomnia, •dizziness •Opioids •Allergy
-Midazolam •ETOH withdrawal •decreased motor coordination •CNS depressants •Myasthenia gravis
-Triazolam •agitation •decreased libido •Anticonvulsants •Glaucoma
Long: •seizure •disinhibition •antidepressants
-Diazepam •procedural sedation •rebound anxiety, SI •antifungal
-Flurazepame
-Chlordiazepoxide Rare: respiratory depression

Buspirone •5HT-1a receptor Anxiety •Dizziness, headache •Other Psych meds Allergy
agonist •Drowsiness, nausea, HA •CNS depressants
•dopamine *NO SEDATION •Serotonin Syndrome
receptors

Hydroxyzine Histamine receptor •Anxiety •Drowsiness •Potassium Allergy

(Vistaril, Atarax) antagonist •muscle relax •dizziness •MAOIs 1st trimester prego
•antihistamine •dry mouth •CNS depressants *only use po route
•antiemetic •rash
•insomnia •respiratory depression

•Antidepressants take about 4-6 weeks to reach efficacy

•Duloxetine first line if depression + neuropathic pain

Serotonin Syndrome: increased serotonergic activity in the CNS due with initiation or change in srotonergic drugs (SSRI, SNRI, TCA, MAOI, Buspirone, triptans or combo)
- AMS, agitation, confusion, hyperthermia, tachycardia, diarrhea, N/V, spontaneous/inducible conus, hypertonia (increased DTR), tremor, mydriasis (dilated pupil)
- TX: discontinue medication, supportive care; NO antipyretics for hyperthermia

187
Disorder About Criteria Treatment
Major RF: Famfx, Female:Male, 2:1 ≥2 Distinct episodes of Psychotherapy: CBT, Interpersonal
Depressive Peak onset: 20s ≥5 symptoms for most days of the week for therapy, Supportive therapy
Disorder ≥2 WEEKS
Patho: Alteration in neurotransmitters (serotonin, epinephrine, *MUST have one of these two: Depressive mood or Anhedonia 1st: SSRI: 4 Weeks if not affects after 4
(MDD) norepinephrine, dopamine, acetylcholine, histamine), Gentics Fatigue (almost all day) weeks then adjust
Neuroendocrine Dysfunction: Adrenal, Thyroid, GH dysfunction Insomnia or Hypersomnia
“Unipolar Guilt or Worthlessness 2nd: SNRI (Duloxetine, Venlafaxine),
Depression” 15% commit suicide (esp male 25-30 & female 40-50 yo) Thought of Death or Suicide NDRI (Bupropion)
*higher rates in those with detailed plan, white males >45 yo, and Psychomotor Agitation (restlessness) or Retardation (slowness)
concurrent substance abuse Significant weight change (Gain or Loss) Others: TCA, Tetracycline, MAOi
Decreased or Increased Appetite
Screen: Decreased Concentration or Indecisiveness Electroconvulsive Therapy: Rapid
PHQ-2 if (+) -> PHQ-9 response in patients unresponsive to
Zung Self-Rated Depression Scale Not associated with Mania or Hypomania medical therapy, unable to tolerate medical
therapy, or rapid reduction in symptoms
Subtypes “course specifiers” of MDD Must cause significant distress/impairment
Seasonal Affective Disorder: Symptoms at same time each year
Not due to substance use, bereavement, medical condition
Atypical Depression: Shares many of the typical symptoms of Seasonal Affective Disorder: SSRI,
MDD but patients experience mood reactivity (improved mood in Bupropion, Light therapy
response to positive events)
Symptoms: Significant weight gain, Increased appetite, Atypical Depression: MAOi
Hypersomnia, Heavy feelings in arms/legs, Oversensitivity to
interpersonal rejection Melancholia:

Melancholia Catatonic Depression:

Symptoms: Anhedonia, Lack of mood reactivity, Depression,
Severe weight loss, Loss of appetite, Excessive guilt,
Psychomotor agitation/retardation, Sleep disturbances
(increased REM, decreased sleep) *sleep disturbances may ->
Early morning awakening, Mood that is worse in the morning

Catatonic Depression
Symptoms: Motor immobility, Stupor, Extreme withdrawal

Persistent DSV5 combined dysthymia & chronic major depressive disorder Chronic depressed mood for Psychotherapy + Pharmacotherapy
Depressive into persistent depressive disorder ≥2 years (adults) *more effective than either alone
Disorder ≥1 year (kids/adolescents)
MC women That last for most of the day, more days than not Psychotherapy: Interpersonal, Cognitive,
(Dysthymia) Onset: Childhood, Adolescence, Early adulthood In this period, NOT symptom free for >2 MONTHS at a time Insight-oriented
≥2 MUST be present: Insomnia, Hypersomnia, Fatigue, Low self
No: Manic (not bipolar 1) esteem, Decreased appetite, Overeating, Hopelessness, Poor Pharmacotherapy: SSRI, SNRI, TCA,
No: Hypomanic (not cyclothymic disorder) concentration, Indecisiveness MAOi

May have major depressive episodes or meet the criteria for

MDD continuously

Must never have had

Manic episode (rules out bipolar 1)
Hypomanic episode (rules out cyclothymic disorder)
188
Grief Reaction Altered emotional state in response to major loss Abnormal Grief Psychotherapy
Only persistent complex bereavement disorder is considered a Severe symptoms, Symptoms >1 YEAR, or Suicidal ideation,
mental disorder Psychosis, Illusions, Hallucinations (patient perceives are real) Insomnia (some patients): Benzos (short
course)
5 Stages: Denial, Anger, Bargain, Depression, Acceptance Persistent Complex Bereavement Complex
Severe grief reactions persist >1 YEAR (6 months in kids) after
Normal Grief: Usually resolves in 6-12 MONTHS, Peaks within the death of the bereaved
the first couple MONTHS.
Symptoms: Intense emotions, Appetite, Sleep disturbances
± Illusions, Hallucinations of the deceased (patient understands
this is not real)
Patients are usually able to function

Premenstrual PMS (Premenstrual Syndrome): Cluster of physical, behavior, Physical: Abdominal bloating & Fatigue (MC), Breast Lifestyle Modifications: Stress reduction
Disorder mood changes with cyclical occurrence during luteal phase of swelling/pain, Weight gain, HA, BM changes, Muscle/Joint pain & Exercise (most beneficial), Reduce
menstrual cycle (Salt, Cigarette, Caffeine, EtOH), NSAID,
Also in Emotional: Irritability (MC), Tension, Depression, Anxiety, Vitamin B6 & E
OBGYN PMDD (Premenstrual Dysphoric Disorder): Severe PMS with Hostility, Libido changes
functional impairment where anger, irritability, and internal Emotional Symptoms w/ Dysfunction
tension are predominant (DSMV criteria) Behavioral: Food cravings, Poor concentration, Noise sensitivity, 1st: SSRI: Fluoxetine, Sertraline,
Loss of motor sense Citalopram

Dx: Onset 1-2 WEEKS BEFORE menses (luteal phase), Don’t Want SSRI: OCP (esp
Relieved within 2-3 days of menses + ≥7 days symptom free Drospirenone-containing)
during follicular phase (period onset to ovulation)
*symptom diary for >2 cycles No Response SSRI/OCP: GnRH Agonist
with E+P addback therapy

Suicide RF: SADPERONS Assuring the patient’s safety to prevent the

Plan: Previous attempt (strongest). Organized > Not organized Sex: Male patient from committing suicide
Access to firearms Age: <19 or >45
Gender: F (more attempt), M (more successful) Depression/Hopelessness Admission & Psych Evaluation
Age: Increases with age, Elderly white males (highest risk USA) Previous attempt/Psychiatric care
Race: White > Black Excessive alcohol/drug use Once safety established, treatment is
Psychiatric Disorders: Majority who attempt/commit have Rational thinking loss aimed at diagnosing & treating any
Substance Abuse: Increased risk Social support lacking underlying mental disorder, including
Marital Status: Alone > Never married > Widowed > Organized plan psychotherapy
Separated/Divorced > Married w/o Kids > Married w/ Kids No spouse (alone)
Others: +FamHx, Hx of impulsivity, Chronic illness, Sickness Low risk: Indicates remorse, shame or
*among highly skilled workers, physicians are at increased risk embarrassment at suicide attempt
*Marriage is protective 0-2: Send home with FU
3-4: Close FU, Consider hospitalization High risk: Sits quietly, engages poorly
5-6: Strongly consider hospitalization, depending on confidence in with physician, voices regret for surviving
the FU arrangement •require hospital admission to psych
7-10: Hospitalize or Commit service or medical with psych consult

189
Insomnia Difficulty initiating, maintaining, or non-restorative sleep
despite adequate opportunity & circumstances for sleep
Most of the time the patient will tell you they have insomnia
Episodic: 1-3 MONTHS
Persistent: >3 MONTHS
Recurrent: ≥2 EPISODES in 1 YEAR
Acute (MC) (FEW DAYS/WEEK) or Chronic (3 MONTHS)
Prevalence increases with age
F:M, 5:1
Insomnia (acute & chronic) 5-35% of the population
*10-15% associated with daytime impairment
Chronic insomnia: 10% middle aged adults, 1/3 of people > 65 yo
Acute
Stress/excitement/bereavement, Shift work, Medical illness, High
altitude
Chronic
Medical (GERD, sleep apnea, chronic pain), Psychiatric (mood,
anxiety, psychotic disorders), Primary sleep disorder, Circadian
rhythm disorder, Environmental (light, noise, movement),
Behavioral (poor sleep hygiene, adjustment sleep disorder),
Substance induced, Medications
Diagnostics: None usually, Consider:
Polysomnography (sleep study)
TSH
Urine Toxicology
PSQI (Pittsburgh Sleep Quality Index)
Sleep Problems Questionnaire
DSM-5
Dissatisfaction with sleep quantity/quality, associated with ≥1 of
the following
Difficulty initiating sleep
Difficulty maintaining sleep
Early-morning awakening with inability to return to sleep
Causes clinically significant distress or impairment in social,
occupational, educational, academic, behavioral, or other important
areas of functioning
Occurs ≥3 NIGHTS/WEEK
Present for ≥3 MONTHS
Occurs despite adequate opportunity for sleep
Not better explained by and does not occur exclusively during the
course of another sleep-wake disorder
Coexisting mental disorders and medical conditions do not
adequately explain the predominant complaint of insomnia
Not attributable to the physiological effects of a substance
Build strong relationship with patient,
Counsel patient, Practice consistent sleep
hygiene:
Fixed wake-up times and bedtime, Go to
bed only when sleepy, Avoid naps, Sleep
in a cool dark quiet environment, No
activities or stimuli in the bedroom
associated with anything but sex/sleep, 30
minute wind down time before sleep, If
unable to sleep within 20 mins move to
another environment and engage in quiet
activity until sleepy, Limit caffeine intake
to mornings, No alcohol after 4PM, Fixed
eating times, Avoid medications that
interfere with sleep, Regular moderate
exercise
Treat underlying disorders
CBT (especially if medications fail)
Pharmacotherapy: Short term use only
(Benzodiazepine hypnotics,
Nonbenzodiazepine hypnotics) all have
abuse potential except Ramelteon
(Rozerem)
Zaleplon, Zolpidem, Eszopiclone,
Triazolam, Temazepam, Estazolam,
Flurazepam Antidepressants: Doxepine
(only antidepressant FDA approval for
insomnia)
Trazodone, Mirtazapine, Amitriptyline

Keep a sleep log, Exercise (more effective

than medications avoid 4 hours prior to
sleep), Melatonin, Valerian and
Acupuncture (not useful), Counsel not to
use OTC antihistamines

Depression MOA CI Side effects Differences

SSRIs Selectively decreased action of •Allergy •N/D, anorexia •Sertraline: diarrhea, less QT, drowsy
FIRST LINE 5-HT reuptake •MOAI w/n 2 weeks •Sleep changes, HA, anxiety, dizziness •Citalopram/Escitalopram: more QT, least liver
*Fluoxetine 5wks •Decreased libido, anorgasmia, ED •Fluvoxamine: shorted t ½ and CYP
•Prolonged QT, WT gain, bleeding •Fluoxetine: long t ½ and don’t use with Tamoxifen
•Serotonin syndrome, increased SI •Paroxetine: anticholingeric SE, CYP, don’t use with Tamoxifen
*panic disorders 1st line

190
SNRIs Block reuptake of 5-HT and •Allergy •N/D/V, constipation, dry mouth •Venlafaxine: high SE, elevated BP
2nd line if cant NE (Milnacipran and •MOAI w/n 2 weeks •Sleep changes, HA, anxiety, dizziness •Desvenlafaxine: less HTN
tolerate SSRIs Levomilnacipran greater) •Angle closure glaucoma •Decreased libido, anorgasmia, ED •Cymbalata: least associated with BP
•Diaphoresis, HTN, SS syndrome •Milnacipran/Levomilnacipran: anticholinergic SE
•LESS SEX and NO WEIGHT GAIN!

Atypicals Buproprion: •Buproprion:, seizure, Buproprion: *NO WT GAIN OR SEX

Buproprion dopamine and NE reuptake anoremia, MAOI 2 weeks •dry mouth, insomnia, nausea
Remeron inhibitor •seizures, tobacco cessation
•Remeron: MAOI 2 wks
Remeron: antagonizes alpha- Remeron:
2 and 5-HT2/3 •dry mouth, drowsiness, sex dysfunction
•wt gain, increased appetite

Serotonin Nefazadone/Trazadone:
Modulators Antagonize 5-HT
Vilazadone/ Vortioxetine:
Partial agonist 5-HT
•Allergy HA, N/D, SI risk, serotonin syndrome •Nefazadone: BBW-hepatotoxicity
•MOAI w/n 2 weeks • Drowsiness, xerostomia, hypotension
*with initiation and increase in dose •Trazadone: SEDATION, dry mouth, WT NEUTRAL
• Rare: priapism, cardiac arrhythmia
•Vialazdone/Vortioxetine: N/V/C/D, sex dysfunction
• Faster onset and less sexual dysfunction

MAOIs MAOa: Break down serotonin •Allergy *MANY DDI INTERACTIONS Selegiline (Eldepryl): low doses for Parkinsons
Parnate and NE •Serotonin w/n 2 weeks •hypotension • Less CI than other MAOIs
Nardil •Cardiovascular •GI, urinary hesitancy • Less hypertensive crisis with transdermal
Marplan MAOb: •Pehochromocytoma •HA, myoclonic jerks
Eldepryl Break down dopamine •Hepatic/renal •edema
•Hypertensive crisis-foods with tyramine

TCAs Inhibits reuatake of •Allergy •Anticholinergic, drowsiness, sweating Nortiptyline and Desipramine: highest tolerability
5-HT and NE •MOAI w/n 2 weeks •sexual dysfunction, wt gain & appetite
•Acute recovery of MI •tremor, OD fatality Tertiary(5-HT): Amitriptyline, Doxepin, Imipramine
•Cardiotoxicity (QT) Secondary (NE): Nortrip, Despiramine, Protriptyline

TeCAs •Ludiomil: •Less anticholinergic and more antihistaminic *have extra cyclic ring
block NE & 5-HT than TCAs *last resort, don’t ever really prescribe
Ludiomil •SI risk
Asendin •Asendin: blocks NE,
dopamine

191
 Bipolar Labs/Indication Side effects DDI CI
Lithium Indication: Acute: GI, tremor, thirst, polyuria, weight gain, loose •Diuretics •CKD, dehydration, sodium
•Acute mania/hypomania or stools •NSAIDS depletion
maintenance •ACEIs •cardiovascular disease
Long term: LITH-PA •Tetracyclines •pregnancy
•Antidepressant *several wk onset •Leukocytosis, insipidus (renal), tremor, •Metronidazole •Ebstein’s anaomly
•Reduced SI risk & relapse risk hypothyroidism, parathyroid, arrhythmia •theophylline •increased lithium toxicity

Valproate •Bipolar I/II N/V, HA, hair loss, bruising, weight gain, tremor, •TCAs •Allergy
*Depakote enteric dizziness •anticonvulsants •Liver
coated Labs: •Mitochondrial
*increase GABA •Serum drug. LFT Rare: hepatotoxic, pancreatitis, low platelets •Pregnancy

Lamotrigine •Bipolar I/II Nausea, rash, pruritis, drowsiness, MANY Allergy

*inhibit glutamate *safest for pregnancy
Labs: Serum drug, LFT, renal Rare: multiorgan hypersensitivity. SJS, TEN

Carbamazepine •Bipolar I/II Nausea, rash, pruritis, hyponatremia, fluid MANY •Allergy
retention, leukopenia •TCAs
Labs: •MAOI w/n 2 weeks
•Serum drug levels Rare: bone marrow suppression, aplastic anemia, SJS, •Bone marrow suppression
•LFTs, CBC, sodium TEN •Pregnancy

Substance About Intoxication Withdrawal Treatment

Alcohol Dependence
Alcohol abuse becomes dependence when
withdrawal symptoms develop or tolerance
CAGE Screening (≥2 considered positive)
Cutdown (felt need to cut down)
Annoyed (people told you theyre annoyed)
Guilt (guilty about drinking)
Eye opener (needed to start day)
Treatment
Supportive: Psychotherapy (AA), Inpatient,
Residential rehab
Disulfiram (Antabuse): Deterrent
Inhibits aldehyde dehydrogenase -> Increased
acetaldehyde when coupled with alcohol
intake -> Hypotension, Palpations, Flushing,
Hyperventilation, Dizziness, N/V, HA,
Metallic taste
C/I: CV disease, DM, Hypothyroidism,
Epilepsy, Kidney/Liver disease
Naltrexone: Opioid antagonist
Reduces alcohol craving & alcohol induced
euphoria
Intoxication
Disinhibition
Depression: Slurred speech, Impaired
judgement, Somnolence
Ataxia
Labile Mood: Erratic behavior, Aggression
Prolonged reaction time, Muscular
incoordination, Facial flushing
Chronic
Wernicke’s Encephalopathy: Triad
Ataxia, Confusion, Oculomotor palsy
Due to thiamine/B1 deficiency
Korsakoff Syndrome: Amnesia (both
retrograde & antegrade)
Hepatomegaly, Palmar erythema, Cirrhosis,
Dupuytren's contractures, Gynecomastia,
Testicular atrophy
Increased mean corpuscular volume
Uncomplicated: 6-36 hours after last drink
No seizures, hallucinosis, delirium tremens
Increased CNS activity: Tremors, Anxiety,
Irritability, Diaphoresis, Palpations, Hypertension,
Insomnia, GI (N/V/D)
Withdrawal Seizure: 6-48 hours after last drink
Usually generalized tonic-clonic type
MC occurs as a single brief episode
Alcoholic Hallucinosis: 12-48 hours after drink
Visual auditory and/or tactile Hallucinations with
normal vital signs
Patient has clear sensorium
Delirium Tremens: 2-5 days after last drink
Delirium (altered sensorium), Hallucinations,
Agitation, Abnormal vital signs (Tachycardia,
Hypertension, Fever)
Patients often diaphoretic
Withdrawal
Requires medical treatment &
hospitalization: Can be fatal
IV Benzo: Diazepam,
Lorazepam, Chlordiazepoxide,
Oxazepam
Potentiates GABA-mediated CNS
inhibition, alcohol mimics GABA
at the receptor sites, so alcohol
withdrawal causes CNS activity.
*Titrated until the patient is
slightly somnolent and then
gradually tapered
*Lorazepam or Oxazepam
preferred in patients with advanced
cirrhosis or alcoholic hepatitis
(Chlordiazepoxide may cause over
titration in these patients)
IVF, IV Thiamine (B1),
Magnesium, Multivitamins (B12
& Folate), Electrolyte repletion
192
 Gabapentin, Topiramate

Alcohol Chronic Use

Drug MOA Side Effects CI/DDI
Thiamine (B1) •Low BP
•Effect glucose metabolism

Naltrexone Blocks dopamine release, antagonizes mu receptor BBW: hepatocellular CI: opioid dependency
1st LINE à decreases craving and reward •N/V/D/C, abd pain DDI: opioids
•dizzy, HA, anxiety, fatigue
Acamprosate Restores glutamate •Diarrhea, nausea, abd pain CI: renal (Cr <30)
(Campral) è Stops withdrawal S/S •fatigue, HA, amnesia, mood
1st LINE
Disulfiram Inhibits enzyme aldehyde dehydrogenase à •Metallic taste CI: heart or CAD, ethanol
(Antabuse) increases acetaldehyde à Fs you up •Effects of drug à sweating, HA, dyspnea, low BP, DI: “WAM”-warfarin, amitriptyline, metronidazole
2nd Line flushing, palp

Substance Intoxication Withdrawal Treatment

Marijuana Mechanism: Binds to CB1 & CB2 cannabinoid receptors Withdrawal Intoxication
Irritability, Insomnia, Depression, Restlessness, Usually not needed, Symptomatic: If needed
Intoxication Diaphoresis, Diarrhea, Twitching
Euphoria, Giddiness, Anxiety, Disinhibition, Intensification of Hyperemesis Syndrome: Chronic severe emesis in
sensory experiences, Cotton mouth, Increased appetite, Motor chronic users: Cessation of use, Antiemetics
impairment (Ondansetron & Metoclopramide)
Some: Fear, Depression

Psychosis may occur

Chronic use: Cognitive performance issues

Psychosis in some cases

PE: Conjunctivitis, Tachycardia, Hypotension

Hallucinogen Phencyclidine (PCP): NMDA glutamate receptor antagonist Intoxication Intoxication

PCP Dissociative, anesthetic, hallucinogenic
Also activates dopaminergic neurons
Can cause CNS stimulant or depressive symptoms
Short onset, brief duration (1-4 hours)
Impulsiveness, Fear, Homicidally, Rage, Supportive: ABCs, Low stimulant environment
Psychosis, Delirium, Psychomotor agitation,
Hallucinations, Multidirectional nystagmus, Agitated/Hyperthermic/HTN/Seizure: 1st: Benzo
Ataxia, Tachycardia, Erythematous & dry skin
Severe Agitation: Restraints may be required
Severe: Hyperthermia, Seizures
Psychotic: Antipsychotics (Haloperidol)

Opioid MOA: mu receptor agonist Withdrawal Intoxication

Heroin, Lacrimation, Hypertension, Pruritis, Tachycardia, Acute/OD: 1st: Naltrexone
Oxycodone, Intoxication N/V, Abdominal cramps, Diarrhea, Sweating, Opioid antagonist
Hydrocodone, Euphoria, Sedation: Drowsiness, Impaired social function, Yawning, Piloerections, Pupil dilation MC used in those with Respiratory depression
Morphine, Impaired memory, Slow/slurred speech *Onset: 2 min (IV), 5 min (IM)

193
Methadone, ± N/V, Seizures, Coma
Meperidine,
Codeine PE: Pupil constriction (miotics), AMS, Respiratory
depression, Bradycardia, Hypotension, N/V, Flushing
± Biot’s Breathing (quick shallow inspirations ->
regular/irregular periods of apnea)
Long term: Constipation, Hypothermia
Stimulants Intoxication: Stimulant effect via inhibition of reuptake of
Cocaine dopamine, norepinephrine, epinephrine in synaptic cleft
Elevated/Euphoric Mood, Psychomotor agitation, Pressured
speech
May progress to: N/V, Seizures
PE: Sympathetic hyperactivity: Increased motor activity,
Tremor, Flushing, Hyperthermia, Cold sweats, Pupillary
dilation
Severe: Respiratory depression, Arrhythmias, Hypertension,
Seizures, Repetitive behaviors, Agitation, Aggression,
Hallucinations, Paranoia
Deadly Complications: MI, Stroke, ICH
(mydriasis), Flu-like symptoms: Rhinorrhea,
Joint pains, Myalgias
Unpleasant but not life-threatening
Withdrawal
Craving with resultant Dysphoria, Post-
intoxication depression, Anhedonia,
Hypersomnia, Increased appetite, Constricted
pupils
May develop: Nightmares, Suicide ideation, HA,
Increased irritability
*Duration of action: 30-60 min
Withdrawal
Symptomatic: Clonidine (decreases sympathetic
symptoms), Loperamide (diarrhea), Dicyclomine
(abdominal cramps), NSAID (joint pain, muscle aches)
*Benzo: May be helpful in some mild cases
Severe: Detox with Methadone or Suboxone
Long Term Dependence: Methadone, Suboxone,
Naltrexone
Opioid Dependence
Methadone: Long acting opioid receptor agonist, Can be
used in pregnant ADR: Prolonged QT
Buprenorphine: Partial opioid receptor agonist
Naltrexone: Competitive opioid antagonist, Precipitates
withdrawal if used within 7 days of heroin use
Intoxication
Mild: Benzo & Reassurance
Severe/Psychosis: Antipsychotics (Haloperidol),
Treatment of arrhythmias, Do not place in restraints (may
lead to rhabdomyolysis)
CV Effects: 1st Benzos: Bc most of the CV effects are
centerally mediated via the sympathetic system.
*Phentolamine can reduce BP but may cause tachycardia
*May be used: Nitroglycerin or Nitroprusside
*If Beta blocker is used, a mixed alpha-1/beta blocker
(Labetalol) is preferred
Hyperthermia: Cooling blankets, Possibly ice baths
Withdrawal: Bupropion
194
195
GU 5%-balanitis
GI
Indirect Inguinal Indirect: Tip of Finger
Hernia MC hernia both sexes (more common in
men), young children, young adults
Protrudes: LATERAL inferior epigastric a.
Patho: Patent process vaginalis, increase in
abdominal pressure may force intestines thru
internal ring into inguinal canal (may follow
testicle into scrotum)
Hesselbach’s Triangle
• Medial: Rectus Abdominis
• Lateral: Inferior Epigastric
• Inferior: Inguinal Ligament
Direct Inguinal Direct: Side of Finger
Hernia
Protrudes: MEDIAL inferior epigastric a.
*MC Right side
Patho: Weakness in floor of inguinal canal,
increase in abdominal pressure may force
intestines thru internal ring into inguinal
canal (may follow testicle into scrotum)
Hesselbach’s Triangle
• Medial: Rectus Abdominis
• Lateral: Inferior Epigastric
• Inferior: Inguinal Ligament
Femoral Hernia Protrusion of the contents through the femoral
canal
Umbilical Hernia Hernia thru umbilical fibromuscular ring,
Congenital (failure of umbilical ring closure)
Usually due to: Loosening of tissue around
the ring in adults
Incisional Hernia Hernia thru weakness in abdominal wall
“Ventral Hernia” MC in: Ventral incisions & Obese
Obturator Hernia Rare
Hernia thru pelvic floor where contents
protrude thru obturator foramen
Asymptomatic: Swelling/Fullness at Clinical Dx Often Require: Surgical Repair
hernia site. Enlarges with increased
intraabdominal pressure/standing Groin US: Often initial IoC of Surgical Emergencies: Strangulated
± Scrotal swelling occult uncomplicated inguinal
hernia
Incarcerated: Painful, Enlargement of *alternatives: CT/MRI
irreducible hernia
*if bowel obstruction: N/V
Strangulated: Ischemic incarcerated
hernias with systemic toxicity. Severe
painful bowel movement (may refrain
defecation)
Asymptomatic: Swelling/Fullness at Clinical Dx Often Require: Surgical Repair
hernia site. Enlarges with increased
intraabdominal pressure/standing Groin US: Often initial IoC of Surgical Emergencies: Strangulated
± Scrotal swelling occult uncomplicated inguinal
hernia
Incarcerated: Painful, Enlargement of *alternatives: CT/MRI
irreducible hernia
*if bowel obstruction: N/V
Strangulated: Ischemic incarcerated
hernias with systemic toxicity. Severe
painful bowel movement (may refrain
defecation)
•below the inguinal ligament •often become incarcerate or
•MC in women strangualted b/c small ring
Observation: Usually resolve by 2yo
Persist ≥5 yo: Surgical Repair
*to avoid strangulation/incarceration
MC in women (esp multiparous) or
women with significant weight loss
196
GU
Nephritic NephrITIC (NephrITIS) “Glomerulonephritis” NephrOTIC Syndrome (NephrOSIS)
Vs INFLAMMATORY NON-INFLAMMATORY
Nephrotic Immune-mediated glomerular inflammation -> Glomerular damage ->
Glomerular damage -> Increased urinary protein loss
Increase urinary protein & RBC loss
HALLMARKS: Proteinuria: >3.5 g/day,
HALLMARKS: Hematuria (RBC casts), Hypoalbuminemia <3, Hyperlipidemia,
Proteinuria <3.5g/day, HTN, Oliguria <400ml/day, Edema (peripheral, periorbital, esp kids)
Azotemia (elevated BUN & Cr) ± Bland urine “maltese cross”
Smokey colored urine Hypercoagulability: Loss of antithrombin
Decreased GFR Increase Risk Infections: Lose complement & IG
Fever, Abdominal/Flank pain Osteomalacia: Loss of Vit D-binding proteins
Edema (not as much as nephrOTIC) Dyspnea, Transudative pleural effusion
Biopsy: Hypercellular (increased WBC, Mesangial ± Increased BUN, Cr (varies)
cells), Immune complex deposition Biopsy: Hypocellular
*Crescent shaped = RPGN

Acute Immunologic inflammation of glomeruli -> Protein Hematuria (hallmark) UA: Hematuria (RBC casts), Dysmorphic IgA Nephropathy or Proteinuria
Glomerulonephritis & RBC leak into urine *Cola/Tea urine RBC, Proteinuria (usually <3 but can be in ACEi ± Corticosteroids
nephrotic range), High SG >1.020 osm
IgA Nephropathy (Berger’s): MCC Edema (facial, Edema/Hypovolemia/HTN
Young males 1-2 Days after URI/GI infection peripheral, & CMP: Increased BUN & Creatinine Loop diuretic, Beta-blocker, CCB
IgA overproduction periorbital)
Renal Biopsy: *GOLD (not needed most cases) Post-Streptococcal
Post-Infectious AKI: Fever, Malaise, Berger’s: IgA Mesangial Deposits Supportive ± ABX
MC after Group A Strep Abdominal/Flank pain, Post-Streptococcal: Hypercellularity, Increased
2-14 yo Boy up to 3 weeks after strep/impetigo with Oliguria monocytes & lymphocytes, Immune humps of Lupus Nephritis
Facial edema, Scanty Cola/Dark urine (hematuria & IgG, IgM, C3 Steroids or Cyclophosphamide
oliguria) HTN GoodPasture: Linear IgG deposits in GBM
Increased ASO Titers, Decreased C3 RPGN/Severe
Corticosteroid +
Membranoproliferative Cyclophosphamide
SLE, HCV, HBV, Hypocomplementemia,
Cryoglobulinemia
Usually presents as Mixed Nephritic-Nephrotic Require Plasmapheresis
(hematuria & proteinuria >3.5) NephrITIS
Membranoproliferative Type 1
Rapidly Progressive (RPGN) Membranoproliferative Type 2
Poor prognosis (ESRD weeks-months) GoodPasture
Crescent formation on biopsy (fibrin & plasma Pauci-Immune Necrotizing
protein deposition collapsing crescent shape of
Bowman’s capsule NephrOSIS
Henoch-Schonlein Purpura
Any cause of AGN can present with RPGN Focal Segmental Glomerulosclerosis
Next two can ONLY present with RPGN

GoodPasture “Anti-GBM”
Anti-GBM antibodies (antibodies against type IV
collagen of GBM in kidney & lung alveoli)
Acute glomerulonephritis + Hemoptysis
197
Vasculitis
Lack immune deposits & (+) ANCA antibodies
Microscopic Polyangitis (Vasculitis Small Vessels)
“Pauci-Immune Necrotizing”
*(+)P-ANCA
Granulomatosis with Polyangitis (Wegener’s)
*(+)C-ANCA

198
Masses About/ Causes Signs/ Symptoms Diagnosis Treatment
Testicular MC solid tumor 15-35 yo Painless mass (MC) Scrotal US: Initial ToC Low Grade Non-Seminoma (limited to testes)
Cancer Non-Seminoma: Cystic, Non-homogenous Radical Orchiectomy w/ Retroperitoneal LN
RF: Cryptorchidism (strongest, 4- Dull pain, Testicular heaviness Seminoma: Hypoechoic Dissection
10X risk), White, Klinefelters,
Hypospadias Secondary hydrocele (10%) Tumor Markers Low Grade Seminoma
Non-seminoma: Increased AFP & B-hCG Radical Orchiectomy (may need Radiation to
Types: PE: Hard, Firm, Fixed Mass that *increased B-hCG esp in Choriocarcinoma paraaortic LN or Platinum based chemo)
Germ Cell (MC 97%) DOESN’T Transilluminate Seminoma: Increased B-hCG (25%)
Non-Seminoma (2/3) High Grade Seminoma
*Increased Serum AFP & B-hCG & Staging: CT Abdomen, Pelvis, Chest Debulking Chemo then Orchiectomy &
Resistant to Radiotherapy Radiation
• Embryonal cell carcinoma
• Yolk sac (MC in ≤10 yo)
• Choriocarcinoma (worst px) Prognosis: Excellent
• Mixed (seminomatous + 5-year survival: >95%
non-seminomatous): Treated
like non-seminomas
Seminoma (1/3)
4 Ss of seminoma
• Simple (lack AFP)
• Sensitive (to radiation)
• Slower growing
• Stepwise spread

Non-Germ Cell (3%)

Leydig: May be benign, May secrete
hormones (androgens/estrogens which
may lead to precocious puberty,
gynecomastia, loss of libido)
Sertoli: Often benign, May secrete
hormones (androgens/estrogens)
Gonadoblastoma
Testicular Lymphoma

Disease Causes/Risks Signs/Symptoms Labs/Imaging Treatment

Benign Nonmalignant Periurethral/Transitional zone
Prostatic hyperplasia -> Bladder outlet obstruction
Hyperplasia Hyperplasia is part of normal aging process,
hormonally dependent on increased DHT
(BPH) production
Develops: As early as 30s, Strongest growth
50-70, >70 stabilizes/shrinks
Common older men (discrete nodules in
periurethral zone)
Normal: Walnut shape, ~4-20g
Irritative: Frequency, Urgency, Nocturia
Obstructive: Hesitancy, Weak stream,
Incomplete emptying, Dribbling
Sympathomimetics (pseudoephedrine) may
worsen
DRE: Uniformly enlarged, firm,
nontender, rubbery
PSA: Correlates with risk of symptom
progression (elevated in 30-50%)
*normal = <4
UA: Look for hematuria/other causes
Urine Cytology: If increased risk of
bladder cancer (TOB, irritative
symptoms, hematuria)
Mild: Observation + Annual Monitoring
Best Initial Therapy Symptomatic
Alpha Blockers: Tamsulosin, Terazosin,
Doxazosin
*relieve symptoms, do not change size
*Tamsulosin is 1a (less SE)
ADR MC: Hypotension
5 Alpha Reductase Inhibitors:
Finasteride, Dutasteride
*reduce size over time (6-12 months)
199

Drug Class Drugs in class
SELECTIVE Prazosin (Minipress)
Alpha-1-blockade Doxazosin (Cardura)
“-osin” Terazosin (Hytrin)
*doxazosin and Terazon more
effective but more SE
NON-SELECTIVE Sildosin (Rapaflo)
Alpha-1a-blockade Tamsulosin (Flomax)
“-osin” Alfuzosin (Uroxatral)
5-alpha-reductaste Finasteride
inhibitors Dutasteride *more efficacious
Jalyn (combo of dutasteride and
tamsulosin)
PDE 5 Inhibitors Tadalafil (Cialis)
Phytotherapy Saw Palmetto
*approved in Europe
GU About
Nephrolithiasis Kidney stones
M > F, White > AA
Urolithiasis Peaks: 40-60 yo
• Calcium Oxalate (MC)
• Uric Acid: Protein, Gout,
Chemo (tumor lysis
syndrome)
• Struvite: Magnesium
Ammonium Phosphate
“Staghorn renal pelvis” bc
urea splitting organisms
(proteus, klebsiella,
Persistent/Progressive/Refractory: Surgical
TURP (Transurethral Resection of
Prostate): Removes excess tissue relieving
obstruction. ADR: Sex problems, Urinary
incontinence
Others: TUIP (Transurethral Incision)
*smaller & concerned about ejaculation loss
Prostatectomy
Minimally Invasive
Laser: TULIP, PVP, ILT, HoLEP
TUNA (Transurethral Needle Ablation)
TUEP (Transurethral Electro-vaporization)
Prostatic Urethra Lift
MOA SE Notes
Help with •Orthostatic hypotension, dizziness, tiredness, combo of alpha blocker and 5-alpha reductase is first
symptoms retrograde ejaculation, rhinitis, HA line
•Intraoperative floppy iris syndrome
DDI: Antihypertensives & PDE-5 inhibitors
*drop BP when taken with alpha blockers
reduces size of •Decreased libido •Don’t work overnight and may take up to 6 months to see
prostate gland •Erectile or ejaculatory dysfunction treatment
*more effective for very large prostates because reduce
PSA by 50% and size by ~20%
BPH + ED •Not covered well by insurance
•If doesn’t want to take meds- try this
Clinical Presentation Diagnostics Treatment
Sudden Severe Colicky Flank pain UA: Hematuria Conservative: Stone <9mm & Stable
over CVA Radiating to pH <5.5: Uric acid & Cystine PO/IV Hydration, IV Ketorolac ± Opioid,
groin/anteriorly pH >6.5: Struvite & Calcium Metoclopramide
Difficult to get comfortable KUB: Good for follow-up Medical Expulsion: Tamsulosin, Terazosin,
Calcium & Struvite: Radiopaque Doxazosin, Nifedipine (CCB): If Alpha Blockers
N/V, Frequency, Urgency, Hematuria Uric acid & Cystine: Radiolucent cause hypotension (can also use both classes)
Usually afebrile *4-6 weeks
Renal US: Good initial alternative in
•<5mm pass spontaneously ER, Indicated if pregnant Uncomplicated UTI: Ciprofloxacin, Levofloxacin,
•10mm+ do NOT pass *cannot detect small stones (3mm) or Cefpodoxime (culture pending)
*stone size does NOT correlate with Distal/Lower ureter stones
severity ± Prednisone 10mg QD 5-10 Days
200
 pseudomonas, serratia,
enterobacter): Women UTI
• Cystine (rare): Indinavir
(HIV med), Congenital defect
in reabsorption of AA
cysteine
RF: Male, Smoking, HTN, Gout,
Gallstones, DM, Bowel surgery,
Recurrent UTIs, hyper/hypo-PTH,
Hypercalciuria, Hyperoxaluria,
Hyperuricosuria, Hypocitraturia,
Animal protein, Foods high in oxalate
(veggies), High sodium intake, Sucrose
and fructose, Low water consumption,
Outdoors occupations, Limiting
hydration/restrooms breaks, Meds (loop
diuretics, zonisamide, topiramate,
decongestants, indinavir, laxatives),
Genetics (cystinuria, distal RTA),
Hyperparathyroidism: Increased PTH
& Ca: Primary hyperparathyroidism,
Hypoparathyroidism: Decreased PTH
& Ca: Look for Cancer
Decrease Risk: Hydration, Coffee, Tea,
Beer, Wine, Supplemental Ca & Vit D
(if deficient)
About
Acute Cystitis Infection of lower GU, Usually ascending
infection from urethra
F > M (60% F have one in lifetime, 10% yearly)
Etiology
Gram(-): E. coli (MC), Klebsiella, Proteus
Gram(+): S. aureus (2nd), Group B Strep
Other Gram(-):, Enterobacter, Pseudomonas
Kids: E. coli, S. saprophyticus, Enterococcus
Culture Grows ≥2: Lactobacilli, Enterococci
RF
Women: Sex, Diaphragm w/ Spermicidal,
Pregnancy, Hygiene, Cystoceles
Postmenopausal: Sex, Urinary incontinence
Children: Vesicourethral reflux, Diapers
DM, AKI, CKD, Med (anticholinergics), Urinary
stones/tumors, Overweight, Catheters,
Immunocompromised
KUB & US will diagnose ~80%
Non-Contrast CT: Gold & Diagnostic
All stones are visible by CT except
PI stones (Indinavir)
*recent passage of stone: Perinephric
stranding (inflammation, infection)
*assess for hydronephrosis
Presentation Diagnosis
Dysuria (burn), Frequency, Urgency, UA: Pyuria, Hematuria, Leukocyte
Malodorous urine, Hematuria esterase, Nitrates, Bacteriuria,
Increased pH (with proteus)
Mild suprapubic tenderness
Urine Culture (CCMS): Definitive
NO CVAT, FEVER, CHILLS >5-10 WBC
Pediatric: Fever unknown origin,
Enuresis, Vague abdominal pain, Loss of
appetite, N/V/D
Elderly: ± AMS
Urine Strainer (catch stone for analysis)
Return/Report to ED if symptoms worsen 48-72 hours
FU with PCP 1-2 weeks (KUB, labs, 24-hr urine)
Follow Up: Ca, P, Uric acid, Bicarbonate, PTH,
Albumin, Alk phos, 24-hour urine, Stone analysis
Stone does not pass >4 weeks: Refer to Urology
Stone 6-10mm: ESWL (Etracorporeal shockwave
lithotripsy), Ureteroscopic basket extraction, or
Both
Stone >10mm: Percutaneous Nephrolithotomy,
Ureterolithotomy
Admission: Complicated w/ Urosepsis, AKI,
Obstruction ± hydronephrosis, Intractable pain/NV,
Solitary kidney, Renal transplant, Staghorn stone
IV Hydration, Metoclopramide, IV Ketorolac
30mg, Hydromorphone (if renal compromise),
Infection (urine culture guides treatment): IV
Gentamycin, Tobramycin + Ampicillin, Zosyn,
Cefepime, Timentin, Ciprofloxacin, Consult Urology
Discharge: Once stable
Treatment
Nitrofurantoin 100mg BID 5 Days,
Bactrim DS BID 3 Days, Fosfomycin 3g
Once
Recurrent: Nitrofurantoin, Bactrim SS,
Cephalexin 250mg QHS
*monitor for yeast infections
Honeymoon: Bactrim SS, Ciprofloxacin
250mg
Analgesics: Phenazopyridine 200mg TID
2 Days ADR: Not to be used >48 hours bc
will turn tears/contacts/urine orange),
Hyoscyamine, AZO (mask symptoms
does not treat infection ADR:
discoloration of urine)
Adjunct: Increase H2O, Void after sex,
Hot sitz bath
201
 FU: 48-72 Hours if worsens will call if
abnormal results

Pregnancy: Amoxicillin, Augmentin,

Cephalexin, Fosfomycin
AVOID: Bactrim 1st trimester,
Aminoglycosides, FQ, Doxycycline

Child >2 Years

E. coli: Cephalosporin (1st, 2nd, 3rd)
Enterococcal: Amoxicillin, Augmentin,
Ampicillin
*afebrile 5 Days, febrile 7-10 days

Child 2-24 Months

Toxic/Dehydrated: Admit, IVF, ABX
Nontoxic/Hydrated: Wait on culture

Child <2 Months: Hospitalize

Urethritis Infection/Inflammation of Urethra Pruritis, Dysuria NAAT (1st void/catch preferred) Nongonococcal: Azithromycin 1g PO
*most sensitive & specific for C. Once or Doxycycline 100mg BID X 7
Nongonococcal urethritis (NGU): Chlamydia Discharge trachomatis, N. gonorrhea, M. Days
trachomatis (MCC NGU urethritis), T. Nongonococcal: Thin genitalium
vaginalis, M. genitalium, Viral Gonococcal: Thick/Mucoid *preferred over culture Gonococcal: IM Ceftriaxone 500mg if
Incubation: 5-8 Days <150kg or 1g if >150mg
Asymptomatic: up to 42% UA: >10
Treatment Failure (consider):
Gonococcal Urethritis Gram Stain Moxifloxacin 400mg BID
Incubation: 4-7 Days *for M. genitalium
Asymptomatic: 5-10% Wet Prep
NS: For Trichomonas/clue cells Follow Up: 72 hours if worsens, otherwise
KOH: For Candida) 3 months to test for re-infection
RF: STI, Multiple sex partners, Unprotected sex, *get results in few hours
MSM, AA > White Referral to Urology: Persistent/Recurrent
Culture w/ Thayer-Martin (chocolate
agar w/ Abx for everything but No sex for 7 DAYS after initiating
gonorrhea) treatment AND their symptoms have
resolved AND their partner(s) were treated
Other: Syphilis, HIV, HBV, HCV *Need to treat the partner(s) if sexually
active within 6 MONTHS of infection

Pyelonephritis Infection of upper GU, Usually ascending Fever, Chills, Flank pain, N/V/D, UA: Pyuria, Hematuria, Leukocyte Outpatient
infection from lower GU Dysuria, Urgency, Frequency, esterase, Nitrates, Bacteriuria, WBC Levofloxacin 750mg 5-7 Days or
Progression to AMS Casts (hallmark), Increased pH Ciprofloxacin 500mg BID
Etiology: E. coli (MC) (with proteus) *cant take FQ: Ertapenem Daily
Other Gram(-): Klebsiella, Proteus, Enterobacter, PE: CVAT, Tachycardia MDR: Add Ertapenem 1g IV/IM Once
Pseudomonas Urine Culture *LTCF, Had ABX, Endemic travel
Enterococci (with catheter) Refer/Admit: No improvement in 48
CBC: Leukocytosis w/ left shift Hours

202
 RF: DM, Recurrent UTI/Kidney stones,
Pregnancy, GU malformations
Prostatitis Infection/Inflammation of Prostate
MC urinary tract problem in men <50 yo
Bacterial: Acute or Chronic
Nonbacterial: Inflammatory or Non-inflammatory
Acute Not common, Bacterial infection
Bacterial Pain, Pyuria, Bacteremia
Prostatitis
RF: Any GU infection, Structural abnormalities,
Instrumentation (catheter, biopsy)
Patho: Ascending infection, Instrumentation,
Biopsy (Staph), Hematogenous/Lymphatic (rare)
Etiology:
Gram(-): E. coli, Klebsiella, Proteus,
Enterobacter, P. aeruginosa
I-Acute Bacterial
Not common, Bacterial infection
Pain, Pyuria, Bacteremia
II-Chronic Bacterial
Uncommon, Recurrent UTI
± Pain, Pyuria, Bacteremia
Acutely Ill: Fever, Chills, N/V, Malaise,
Myalgias
Frequency, Urgency, Dysuria, Nocturia,
Urge incontinence, Urinary retention
(dribbling, hesitancy or weak stream),
Painful ejaculation
Pelvic/Perineal/Low back pain
PE: Febrile, Tachycardia, Discharge
(maybe only urine), LN, Scrotum
KUB: Initially
Non-Contrast CT: Diagnostic
III-Chronic Non-Bacterial
IIIa-Inflammatory: MC
"Chronic Prostatitis"
Pain >3 MO, Pyuria, NO Bacteremia
IIIb-Non-Inflammatory
"Chronic Pelvic Pain Syndrome"
Pain, NO Pyuria, NO Bacteremia
UA
Culture & Sensitivity
Gram Stain
CBC w/ Diff
ESR
CRP
Blood Cultures
PSA: Not indicated for acute
Inpatient
Ceftriaxone 1g Daily or Zosyn Q6H
MDR: Zosyn or Imi/Mero/Dori-penem
Critical: Carbapenem + Vancomycin
Discharge: Fever free and stable for 24
hours (start on PO ABX), FU with PCP,
Return to ED if worsens within 72 hours
Pregnancy
Mild-Moderate: Ceftriaxone 1g QD or
Cefepime 1g BID or Aztreonam or
Ampicillin 1-2g Q6H + Gentamycin
1.5mg/kg Q8H
Severe: Zosyn, Meropenem, Ertapenem,
Doripenem
Avoid: FQ, Aminoglycoside, Tetracycline
Fever/Symptoms >48 hours: Workup
Discharge: Fever free and stable for 24
hours (start on PO ABX 10-14 days), FU
with PCP, Return to ED if worsens within
72 hours
Preventing Recurrence: Recommend low
dose antimicrobial therapy for remainder
of pregnancy: Antibiotic to the susceptible
pathogen or Nitrofurantoin 50-100mg
QHS or Cephalexin 250-500mg QHS
Declines Prophylaxis: Follow up with
monthly urine C&S
IV- Asymptomatic Inflammatory
Incidental, Probably BPH, no Tx needed
NO Pain, NO Pyuria, NO Bacteremia
Outpatient
Gram(-): Bactrim DS BID 4 Weeks or
Ciprofloxacin or Levofloxacin 500mg
BID 4 Weeks
Gram(+): Amoxicillin, Ampicillin,
Dicloxacillin, Cephalexin
Suspect STI: IM Ceftriaxone 500mg or
1g Once + Doxycycline 100mg BID 2
Weeks
Education: Increase fluids, Bedrest,
Analgesics, Stool softeners
203
 Gram(+): S. aureus, Streptococci, Enterococci
STI: N. gonorrhea, C. trachomatis
Chronic Uncommon, Recurrent UTI
Bacterial ± Pain, Pyuria, Bacteremia
Prostatitis
Milder form of acute bacterial prostatitis
RF: Failed treatment of acute prostatitis, Prostate
stones, Instrumentation, TOB, DM, BPH
Patho/Etiology: Same as acute prostatitis
Chronic IIIa: Inflammatory "Chronic Prostatitis" "CP"
Non-Bacterial MC of the prostatitis syndromes
Prostatitis Pain (>3 months), Pyuria, No Bacteriuria
*Chronic Pelvic Pain ≥3 months in the absence of
identifiable causes (DOE)
Clinical syndrome defined by pelvic pain ±
urinary symptoms
Etiology: Unknown
IIIb: Non-Inflammatory "Chronic Pelvic Pain
Syndrome" “CPPS” “Prostatodynia”
Pain, NO Pyuria, NO Bacteremia
Misnomer because prostate is normal
Normally affecting young and middle-aged men
Etiology: Voiding or Pelvic floor muscles
dysfunction; psycho-social component
Epididymitis Inflammation/Infection of Epididymis
MCC scrotal pain in adult male: ~600K
cases/year
Bacterial
<14 No Sex: Reflux of urine: E. Coli
<35: STIs: GC, Chlamydia
Gentle DRE: Painful, Firm, Indurated,
Edematous/Boggy
*NO prostatic massage
Gradual onset over 3 MONTHS
Painful ejaculation, Trouble starting
stream, Recurrent UTIs, Nocturia,
Urinary retention
+/-: Fever, Frequency, Urgency, Dysuria,
Pain (genitalia, groin, lower abdomen and
back)
DRE: Varies (Normal, Enlarged, Tender,
Boggy, Nodular, or Edematous)
*unlike acute
Pain & Sexual dysfunction same as
bacterial prostatitis
IIIa: Inflammatory "Chronic Prostatitis"
"CP"
Prostate (± tenderness, spasms,
myofascial tenderness to perineum/pelvic
floor/area)
IIIb: Non-Inflammatory "Chronic Pelvic
Pain Syndrome" “CPPS” “Prostatodynia”
Hx: Admit to lifelong of difficulty
voiding and pelvic pain
PE: Unremarkable, Except increased
anal sphincter tone
Acute (sex, lifting, trauma) or Gradual
(infection): Onset, Unilateral (Rt > Lt)
Scrotal: Pain, Swelling, Induration
High Fever, Chills, Rigors
UA: Usually normal unless
concurrent infection occurring
NAAT: If patient is sexually active
Two (or Four) Glass Urine Method
*Pee in cup, Prostate massage, Pee
in cup: Higher levels of leukocytes
or bacteria in the expressed
prostatic secretions compared to the
urine, suggests chronic prostatitis
IIIa: Inflammatory "Chronic
Prostatitis" "CP"
UA, Culture & Sensitivity, Gram
stain (normal), STI (negative), DRE
(+/- tender)
± Trans Rectal US (TRUS): Can
look at the size of the prostate
IIIb: Non-Inflammatory "Chronic
Pelvic Pain Syndrome" “CPPS”
“Prostatodynia”
UA & Cultures: Normal
Scrotal US: Best Initial
Enlarged, Increased blood flow
UA: Pyuria, Bacteriuria
NAAT (1st void/catch preferred)
FU: RTC 72 hours if symptoms worsen, If
responding to ABX, repeat urine culture in
7 days (if still positive, switch antibiotics),
Follow-up 4-6 weeks to repeat labs and
urine culture
Inpatient
IV Levofloxacin or Cipro ± Gentamycin
or Tobramycin
*switch to oral meds when: Fever-free,
Symptom improvement, Tolerate oral
meds, FU as above
Ciprofloxacin or Levofloxacin 500mg
BID or Bactrim DS 4-6 Weeks
If C. Trachomatis: Doxycycline or
Azithromycin
Concurrent BPH: Alpha-Blockers:
Terazosin, Doxazosin, Tamsulosin,
Alfuzosin
Prognosis: Difficult to cure, but ABX can
decrease recurrent infections & symptoms
Refer to Urology: Symptoms persist
IIIa: Inflammatory "Chronic Prostatitis"
"CP"
Trial of ABX 4-6 Weeks
IIIb: Non-Inflammatory "Chronic Pelvic
Pain Syndrome" “CPPS” “Prostatodynia”
Initially Try ABX
<14
Bactrim 6-12mg/kg Q12H or Cephalexin
25-50mg/kg Q6-8H 7-10 Days
<35 or Suspect STI
IM Ceftriaxone 500mg or 1g +
Doxycycline 100mg BID 10 Days
204
 >35: UTIs, Prostatitis: E. Coli, Klebsiella, STI
>65: BPH, Prostate cancer, Strictures: E. Coli
Patho: Retrograde infection spread from the
urethra or bladder
RF: Unprotected sex, Strenuous activity,
Bicycle/Motorcycle riding, Prolonged sitting,
Recent UTI, Structural abnormalities, Meds
(Amiodarone)
Orchitis Inflammation/Infection Testes
Associated with: Epididymitis
Can lead to: Infertility & Testicular atrophy
Viral MCC: Mumps (MC viral cause),
Echovirius, Coxsackie, Rubella
*orchitis is the MC complication of mumps
Balanitis Balanitis: Inflammation of glans penis
Posthitis: Inflammation of foreskin
Posthitis Balanoposthitis: Inflammation of glans &
foreskin (DM)
Balanoposthitis
Etiology: Inadequate hygiene, Candida, Staph,
Strep (usually a mixture): Uncircumcised males,
Uncontrolled DM
RF: DM, Obesity, Immunosuppressed, Meds
(oral corticosteroids, HRT, oral BCP, ABX)
Gonorrhea Neisseria gonorrhea
Gram(-) Diplococci
Also in Incubation: 2-8 Days
OBGYN
Chlamydia Chlamydia trachomatis
Cremasteric Reflex: Stroke ipsilateral
inner thigh Testicle elevates (positive):
supports diagnosis of epididymitis,
Testicle does not elevate (negative):
suggestive of torsion
Prehn Sign: Elevating testicles Relieves
Pain (Positive): supports diagnosis of
ePididymitis Does Not relieve pain
(Negative), suggestive of torsioN
Scrotal: Pain (abrupt unilateral), Swelling,
Tenderness
PE: Parotiditis, Fever, Chills
Itching, Burning, Swelling, Rash/Lesions
Superficial denuded, beefy-red areas ±
Satellite lesions
Whitish curd-like concretions on mucous
membrane
Urethritis & Cervicitis: Discharge, PID,
Epididymitis, Prostatitis
Dissemination: Triad: Dermatitis
(maculopapular, petechial rash),
Polyarthralgia, Tenosynovitis
Often: Fever, Chills, Malaise
Purulent gonococcal septic arthritis
(esp knee)
*in women it occurs more frequently
during menses
Up to 40% asymptomatic (esp men)
*most sensitive & specific for C.
trachomatis, N. gonorrhea, M.
genitalium
Same as epididymitis
10% KOH Wet Mount
Clusters budding yeast & pseudo-
hyphae
Culture: Confirms
NAAT (1st void/catch preferred)
*most sensitive & specific for C.
trachomatis, N. gonorrhea, M.
genitalium
*recommended over culture
Gram Stain
UA
Synovial Fluid
Blood Culture
NAAT (1st void/catch preferred)
*alternative: Azithromycin (1g PO)
*no FQ
>35 or Low Risk for STI:
Levofloxacin 500mg or Ofloxacin 300mg
BID 10 Days
*alternative: Bactrim DS BID 10 Days
MSM
Ceftriaxone 500mg or 1g + Levaquin
500mg QD 10 Days
Scrotal Support: Ice, Scrotal elevation,
Pain, No heavy lifting/straining, Rest
Return to clinic 48-72 hours if worsens
FU after treatment to repeat urine & C&S
Viral: NSAID, Bed rest, Scrotal support,
Cool
Bacterial: Same as epididymitis
Clean & Dry, Air, D/C offending med
Mild: Topical Nystatin or Clotrimazole
Itching/Burning: Dilute Aluminum
Acetate (15 min)
Severe: Clindamycin 300mg TID 7 Days
or Metronidazole 500mg BID 7 Days
and Fluconazole 150mg Once
Complications: Phimosis (refer urology)
Urethritis & Cervicitis: 1st Line
IV Ceftriaxone
Gonococcal Arthritis: IM Ceftriaxone
250mg + Doxycycline/Azithromycin
Azithromycin 1g PO Once or
205
 MC overall bacterial cause STI *most sensitive & specific for C. Doxycycline 100mg PO BID 10 Days
Also in Urethritis: Purulent/Mucopurulent trachomatis, N. gonorrhea, M. *re-test in 3 weeks
OBGYN discharge, Pruritis, Dysuria, Dyspareunia, genitalium
Hematuria
Genetic Probe, Culture, Antigen
PID: Abdominal pain, Cervical motion detection
tenderness

Reactive Arthritis (autoimmune rxn):

Urethritis, Uveitis, Arthritis HLA-
B27(+)

Lymphogranuloma Venereum:
Genital/Rectal lesion with softening,
suppuration, lymphadenopathy

HEME 4%

SCREENING
Sideroblastic Anemia of Lead Poisoning: Children: Lead levels

HEME
Microcytic All: Hypochromic, Microcytic Anemia Decreased Iron Availability Decreased Heme Production Decreased Globin Production
Anemia *Severe iron deficiency *Lead poisoning *Thalassemia & Hemoglobinopathies
Etiology *Anemia of chronic disease *Sideroblastic anemia (sickle cell, Hgb SC)
Iron Deficiency *Copper disease
Alpha/Beta Thalassemia
Early Anemia of Chronic Disease (ACD)

Iron MCC anemia worldwide •Fatigue, weakness, dyspnea, exercise •High TIBC, RDW Ferrous Sulfate
Deficiency intolerance •Low iron, ferritin, transferrin *take with Vitamin C
Etiology •hair thinning •Low MCV, low MCH, nml MCHC
Chronic blood loss (MCC USA): •pallor, pica, cheilitis *microcytic, hypochromic
Menstruation, Occult GI (colon cancer), •koilycia, plummer vinson syndrome
Decreased Absorption: Diet (MCC Bone marrow: absent iron stores
Worldwide), Celiac, Bariatric, H pylori *DEFINTIIVE

Patho: Decreased RBC production due to

lack of iron & decreased ferritin (iron
stores). Ferritin in bone marrow, liver, spleen

RF: Increased metabolic requirements (kids,

pregnant, lactating), Cow milk ingestion in
young kids (cow milk <1 yo, toddlers large
volumes)

Lead Patho: Enzymes cause cell death -> Neuro: ataxia, fatigue, learning disabilities, Serum lead: >10 •removal of the source of lead
Poisoning Shortening life span of RBC & inhibits difficulty concentrating Capillary initial à venous best
Anemia enzymes needed for synthesis -> Acquired •wrist or foot drop <44mcg: outpatient follow-up and
sideroblastic anemia Smear: microcytic hypochromic anemia lifestyle modfications
“Plumbism” with basophilic stippling
206
 RF: MC in kids (esp <6 yo) due to increased
permeability of BBB as well as iron
deficiency (may increase lead absorption)
Sources: Primary: Ingestion/Inhalation of
environmental lead (paint, dust), Lead in
gas, Industralized use of land
GI: abdominal pain, vomit, constipation, •ringed sideroblasts inmarrow 45-69mcg: succimer
loss of appetite
X-rays: lead lines
Butrons lines: thin, blue-black line at base
of the gums near the teeth

Alpha •Decreased alpha-globin •¼-silent •microcytic hypochromic •Moderate: folate, avoid oxidative
Thalassemia •MC in S.E. Asians •2/4- minor (trait) •normal/increased iron, ferritin stress, avoid iron supplementation
•¾- HbH (Heinz bodies)
Microcytic -Symptomatic at birth Smear: target cells •Severe: transfusions, splenectomy iron
-HSM, pigmented gallstones chelation (IV Deferoxamine),
-Frontal bossing Electrophoresis: all equal
•4/4- hydrops fetalis •HbH with ¾ deletion

Beta •Decreased beta-globin •½: Minor (trait)-asymptomatic electrophoresis: Minor: no treatment

Thalassemia •MC in Mediterranean •2/2: major (cooleys) •increased HbA2 and HbF,
-symptomatic around 6 months Major:
Microcytic HbF=2a2y -HSM, Frontal bossing & maxillary smear: target cells, nucleated cells •blood transfusions
HbA=2a2b, HbA2=2a2d growth, osteoporosis, cardiac (high •folate & vitamin C supplements
output HF) X-ray: crew-cut skull appearance •iron chelating (Deferoxamine)
“hair on end” appearance from
extramedullary hemtopoieses Definitive=bone marrow transplant

207
 HEME/ONC
Folate Pathophysiology: •fatigue, exercise intolerance, pallor Labs: Folate supplement
Deficiency •folate required for DNA synthesis •Glossitis, cheilosis •high MCV and homocysteine
Macrocytic •deficiency causes abnormal synthesis of •NO NEUROPATHY •normal MMA
DNA, nucleis acis, metabolism
Smear: hypersegmented neutrophils,
Causes: macro-ovalocytes
•MCC=diet à leafy greens, alcoholic
•increased requirements (prego, infant,
malignancy)
•impaired absorption
•impaired metabolism: MTX, Trimethoprim
•loss from dialysis
B12 Source: animal meat, eggs, dairy •fatigue, exercise intolerance, pallor Labs: B12 (Cobalamin) Injections weekly
Deficiency •glossitis, diarrhea, malabsorption •high MCV until corrected à monthly
Macrocytic Pathophysioogy: •dereased B12
•intrinsic factor is released by the stomach •NEUROPATHY (symmetric), loss of •high homocysteine & MMA •can switch to oral therapy after
parietal cells which allows B12 absorption in vibratory, sensory, and proprioception symptoms resolve
ileum •decreased DTRS Smear: hypersegmented, macro- •if pernicious, then need lifelong IM
•B12 deficiency causes abnormal synthesis of ovalocytes, basophilic stippling therapy
DNA, nucleic acids, and metabolism. B12 is
needed to convert homocysteine to MMA

Causes:
•decreased absorption: pernicious anemia à
damaged parietal cells à lack of intrinsic
factor
•diet (vegans)

HEME/ONC
Anemia of MCC of normocytic anemia •fatigue, exercise intolerance, pallor Labs: EPO if renal disease or low EPO
Chronic •normocytic normochromic anemia
Disease Pathophysiology: •increased hepcidin
Normocytic •increased hepcidin and decreased EPO •Increased ferritin
à not able to produce heme •Low iron and TIBC
•decreased RBC production

Caauses
•MCC: Chronic Kidney Disease (CKD)

Hemolytic Anemia: increased RBC destruction > bone marrow replacement

- Intrinsic (sickle cell, thalassemia, G6PD, spherocytosis); Extrinsic (autoimmune, DIC, TTP, HUS, PNH, hypersplenism)
- Labs: increased reticulocytes, increased INDIRECT bilirubin, low haptoglobin

208
HEME/ONC
Hereditary •autosomal dominant •varying degrees, may go undetected, Labs: All: folic acid (1mg daily)
Spherocytosis may present acute after infection •high reticulocytes
autoimmune Pathophysiology: •normal MCV, high MCHC Definitive: splenectomy
abnormally shaped RBC due to proteins in •anemia, jaundice, splenomegaly •(+) osmotic fragility, (-) coombs *could be partial
cytoskeleton à sphere instead of flexible and •pigmented gallstones *delay until 5+yo or puberty
biconcave à destroyed by spleen Smear: hyperchromic
microspherocytes -pneumococcal vaccine
-transfusions of EPO if severe
EMA binding: PREFERRED
•flow cytometry analysis
Sick Cell Anemia •Autosomal resessive •trait usually asymptomatic Electrophresis: •PCN at 2mo, folic acid at 1yr
Normocytic •MC in African Americans •trait: HbA and HbS •supportive: folic acid, vaccines
Disease: *begin as early as 6mo •disease: HbS
Types: •dactylitis-inflammation of finger/toe •Hydroxyurea
•trait (heterozygous-AS) joints Smear: Howell-Jolly, target cells, MOA: increases production of HbF,
•disease (homozygous-SS) •osteomyelitis (Salmonella) sickled RBC reduces RBC sickling
•aplastic crisis with parovirus B19 SE: myelosuppression, GI
Pathophysiology: •Jaundice, HSM, cardiomegaly Labs: increased reticulocytes
•Valine substitutes for glutamic acid on B •Ill appearing, poor healing, retinopathy, Acute Crisis :
chain à HbS has decreased solubility under stroke, tibia skin ulcers Splenic Sequestration: HOP: hydration, oxygen, pain
hypoxia à abnormal shape à vaso-occlusive •reticulocytosis
episodes à spleen Splenic Sequestration Crisus: *differentiates from aplastic crisis Definitive: allogenic stem cell
•acute splenomegaly •drop in hemoglobin
Triggers: SHITAE: stress, hypoxemia, •rapid decrease in hemoglobin •thrombocytopenia
infection, temperature changes, acidosis,
exercise Vaso-Occlusive Crisis:
•acute chest syndrome
•back, abdominal, bone pain
•priapism

G6PD •X-linked recessive; MC in AA males •EPISODIC hemolytic anemia Smear: Prevent: avoid oxidative drugs, triggers
Normocytic •Jaundice, dark urine •Bite & Blister cells; Heinz Bodies
•Deficit in G6PD enzyme •Malaise, weakness, pain •Folic acid supplementation
Labs:
•RBC is vulnerable to oxidative state à hgb Triggers: •Low hgb & hct
denatures à forms Heinz bodies à damages infection, food (fava beans), ABX •High reticulocytes & High MCH
membrane à spleen destroys •G6PD assay
Autoimmune •antibody forms against RBC (IgG) •abrupt, life-threatening Smear: Prednisone 1-2mg/kg/day orally
Hemolytic •fatigue, exercise intolerance, pallor •microspherocytosis *esp warm
Anemia Pathophysiology: •polychromataphils Severe: splenectomy
*autoimmune Warm:IgG, Cold:IgM for complement •hemolysis: hemoglobinuria, jaundice
• macrophages remove membrane à •splenomegaly Labs: Comorbitities: treat underlying
spherocytes à destroyed by spleen •low hgb, hct, RBC
•complement can tag Kupffer cells •high reticulocytes Transfusion: required
•high indirect bilirubin *give without type/cross matching
Causes:
•warm: idiopathic, meds, autoimmune DIAGNOSTIC: COOMBS (+)
•cold: infection (mycoplasma, EBV)

209
 HEME/ONC
Polycythemia Acquire disorder causing
Vera OVERPRODUCTION of ALL 3
hematopoietic cell lines
Pathophysiology: JAK2 gene mutation
Causes: radiation, toxins, men, 50-60yo
MCC of death=thrombosis
Primary v. Secondary Erythrocytosis:
Primary: low EPO, high WBC & plt
Secondary: high EPO, normal other
Aplastic Anemia Failure of hematopoietic bone marrow due
to suppression or injury of stem cells from T
cell attack
MC: idiopathic autoimmune Diseases,
toxins, medications, infections (hepatitis
Pathophysiology:
Hypoplasia of hematopoietic bone marrow
à decrease WBC, RBC plts
Primary Hemostatis:
Platelets form a plug at the site of vascular injury à platelet adhesion, activation, and aggregation
Platelets send out ADP and Thromboxane A à more platelets à platelet plug
- Diseases: ITP, TTP, HUS, DIC, vWF deficiency
- Labs: affects bleeding time, but NOT PT or PTT
- Classic Presentation: petechiae, mucocutaneous bleeding
Secondary Hemostasis:
Clotting factors respond in a cascade to form fibrin strains to strengthen platelet plug
Extrinsic pathways (1, 2, 5, 7, 10): prolongs PT *DIC, warfarin therapy, vitamin K deficiency, Intrinsic Pathway (1, 2, 5, 8, 9, 11, 12): prolongs PTT *heparin overdose
- Diseases: hemophilia, DIC, vWF
- Presentation: deep delayed bleeding (hemarthrosis), delayed bleeding after surgery
•Fatigue, HA, dizziness, vertigo
•Generalizes pruritus due to histamine
release
*worse in a warm shower/bath
•Bleeding-engorged vessels from plts
•Hypercoaguability
*increased blood viscosity and platelet
dysfunction
•abdominal pain, discomfort à ulcers
due to increased histamine,
hepatosplenomegaly
•Engorged conjunctival & retinal
vessels à vision changes
•Plethora-reddish uneven complexion to
the face, palms, nail beds, mucosa
•Decreased WBC-infection
•Decreased RBC-anemia, fatigue, pallor
•Decreased platelets-bruising, bleed
Exam:
•pallor, purpura, petechial “3 Ps”
*no hepatomegaly, splenomegaly, bone
tenderness, lymphadenopathy
CBC:
•Elevated RBC, WBC, plt
•HCT> 54%males, 51% females
CMP: liver and renal
Peripheral Smear: normal
•Low EPO
•Genetic mutation: (+) JAK2
•Iron studies due to blood loss
Criteria:
3 major or 2 major + 1 minor
•Major: increased RBC mass
(hgb/hct), + BM biopsy, JAK2
•Minor: decreased EPO, increased
ALP, iron deficiency
Labs:
•low WBC, RBC, platelets
•normal MCV, MCH
Bone marrow biopsy: BEST
•hypocellular fatty aspirate
•low/no hematopeitic precurosors
Management: Refer to Hematology,
educate
Treatment:
Phlebotomy
•1unit decreased Hct by 3%
•Remove 1 units weekly until <45%
•ASA 81mg daily
•alternative=hydroxyurea
Myelosuppressive chemo if:
•Frequent phlebotomy
•High risk or mod/severe thrombosis
•Pruritis
Supportive: RBC & PLT transfusion
Mild: bone marrow growth factors
•erythropoietic (EPO), myeloid
MOA: recombinant DNA
SE: HTN, thrombosis
BBW: vascular, heart issues, tumor
CI: uncontrolled HTN, aplasia
Severe: stem cell transplant
210
HEME About Clinical Presentation Diagnostics Treatment
Immune Thrombo- •antibodies against antigens on platelets •Bleeding, petechiae, bruising ISOLATED thrombocytopenia •Steroids
cytopenic Purpura surface à destruction by spleen •mucosal bleeding <100,000
•2nd line: IVIG, splenectomy
Causes: •NO splenomegaly •normal PT. PTT, INR
•primary: MC after URTI
•secondary: HIV, HCV, SLE, Marrow: megakaryocytes
antiphospholipid syndrome

Thrombotic platelets into thrombi in vessel à shearing of FATRN: Fever, anemia, Tests: Plasmapheresis with FFP
Thrombocytopenic erythrocytes thrombocytopenia, renal, neuro •vWF LOTS, ADAMTS13 low •removes antibodies, adds
Purpura (TTP) •LOW Hgb & platlets ADAMTS13 to serum
Pathophysiology: •Acute/subacute onset of neurologic •HIGH fibrinogen, bilirubin
Adults •low ADAMTS13 symptoms, anemia, or 2nd line: steroids,
Brain, Fever, vWF •high vWF thrombocytopenia Direct Coombs: negative (-) immunosuppression
*antibodies against ADAMTS13 •Fever 50% pts Smear: mod/severe schistocytosis
•Hemoglobinuria, splenomegaly 3rd line: splenectomy

Hemolytic-Uremic •Renal failure with microangiopathic •Prodromal gastritis Labs: Typical:

Syndrome (HUS) hemolytic anemia and thrombocytopenia à (Fever, blood diarrhea for 2-7d before •BMP: elevated BUN/CR Supportive care
damages endothelial cells onset of renal failure) •CBC: severe anemia, varying
Kids •Irritability, lethargy, Seizure thrombocytopenia Atypical:
Kidney Typical: Shigella toxin, E. coli O157:H7 •Acute renal failure, Anuria Plasma exchange ASAP
NO fever •diarrhea in 2-3yo, acute renal failure •HTN Smear: schistocytes (helmet cells)
Diarrhea •Edema *Antibiotics and anti-motility agents
Atypical: non-STx, sporadic or familial •Pallor (due to anemia) •stool for E. coli and Shigella are avoided

Heparin Induced Pathophysiology: •Venous thrombosis: legs, cardiac, skin •new thrombocytopenia •anticoagulation: Argatroban
Thrombo-cytopenia •Antibody to hapten of heparin and +PF4 à necrosis, gangrene •platelet drop >50% *direct thrombin inhibitor
(HIT) forms neoantigen on platelet à antibodies à •can be hypercoaguable because •venous or arterial thrombosis
clearance à low destroyed platlets release granules •GOLD: 14-C-serotonin release assay
•onset 5-7d post therapy

211
HEME About Clinical Presentation Diagnostics Treatment
DIC Pathologic activation of coagulation system à •Widespread hemorrhage & thrombosis Labs: •Treat underlying cause
widespread microthrombi à consumes clotting factors •bleeding from venipuncture sites, •Increased PTT, PT/INR •FFP if severe bleeding
à thrombocytopenia and diffuse bleeding catheters, drains •Decreased fibrinogen •platelets if <20,000
*MC at venipuncture sites •Increased D-dimer
Causes: •gangrene or multi-organ failure •Thrombocytopenia
•infections (gram – sepsis)
•malignancies, obstetric (pre-eclampsia) Smear: fragmented RBC, shistocytes

vWF Disease •Autosomal Dominant •recurrent nose bleeds, heavy periods, •Decreased vWF, decreased VIII •DDAVP
•MC inheritable bleeding disorder prolonged wound bleeding •prolonged PTT and bleeding time •recombinant vWF or Factor
•ineffective plt adhesion due to low vWF •family history •normal PT/INR VIII
•use Celebrex for anti-
vWF function: promotes plt adhesion by crosslinking GOLD: Ristocetin-induced platelet inflammatory
GP1b receptor on plts with exposed collagen on aggregation *helps determine type
damaged epithelium
•factor VIII degradation

Hemophilia •X-linked recessive; MC in children & males •hemarthrosis (joints, MC ankle) •prolong PTT & bleeding time • A: Factor VIII or DDAVP
•A: factor VII deficiency (MC) •hemorrhage due to trauma •normal platelets • B: Factor IX
•B: Factor IX deficiency *christmas tree •possible purpura/petechiae • C: Factor XI
•C: factor XI deficiency *ashkenazi jews

HEME
Factor V Leiden •MCC inherited thrombophilia (hypercoag) •DVT, PE, Clotting •normal PT, PTT Anticoagulant indefinitely

Pathophysiology: Factor V: activated by thrombin and helps Activated protein C resistance

•Mutation of Factor V à does not respond to protein C convert prothrombin to thrombin assay
à does not turn off and keeps clotting à confirm with DNA test

Protein C/S •Autosomal dominant •DVT, PE •Protein C and S assay Indefinite anticoagulant
Deficiency •Vitamin K dependent anticoagulant proteins •purpura fulminans in newborns: red purpuric •plasma antigen levels
lesion at pressure points à eschar Necrosis: IV vit K, heparin,
•Protein C: risk warfarin induced necrosis protein C, FFP, Heparin

Anti-thrombin III •Autosomal dominant •Venous thrombosis, DVT, PE •antithrombin III assay Thrombosis: high-dose IV
deficiency Normal: inactivated thrombin, IIa, IXa, Xa •MC in deep veins and mesenteric veins heparin à oral

Antiphospholipid •Acquired hypercoaguable condition Cardiac: Libman-Sacks, endocarditis, Antibodies anticoagulation

Syndrome •antibody (aPL) in plasmsa pulmonary HTN, thrombotic events
•necrosis of hip
HX: pregnancy complications •Livdeo reticularis, adrenal insufficiency

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ONC
Hodgkins •Germinal B cells undergo
transformation
•2 peaks: 20s, 50s
Risks: EBV, smoking,
immunosuppressed
Types:
•nodular: MC, females
•mixed: EBV
•lymphocyte rich: MC in males
•lymphocyte poor: MC >60yo
Non-Hodgkins •Accumulate in lymph tissue (spleen,
nodes, thymus)
•malignant overgrowth of
lymphocytes; MC: B cells
Risks: increased age, radaiation, fhx,
immunosuppressed, infections (EBV,
HIV, HHV-8), autoimmune
•PAINLESS cervical/supraclavicular LAD •Staging: Ann Arbor Stage I-II: Combo Chemo +
*alcohol may cause pain radiation
•lymph spread in contiguous fashion •CBC normal, elevated ESR
(cervical MC) •CT/PET for staging Stage III-IV: combo
•Mediastinal mass, fatigue, wt loss ABVD: Adiramycin,
Biopsy: Reed Sternberg cells: large cells with Bleomycin, Vinblastine,
•B SX: wt loss >10%, T >38C, sweats bi/multi-lobed nuclei (owl-eye appearance) & Dacarbazine
*indicate advanced disease inclusions
MOPP: Mustine,
Exam: HSM, nephrotic syndrome, hyercalcemia Oncovorin/Vincristine,
PRocarbazine, Prednisolone
•PAINLESS lymphadenopathy •viral serology Asymptomatic: no tx
*non-contiguous •CXR à CT of chest
•Cough, dyspnea, edema Stage I: Chemo
•Mediastinal mass, RLQ mass tissue biopsy: DIAGNOSTIC
•extranodal (GI MC) Intermediate/Aggressive:
•bone marrow RCHOP: Rituximab,
Types: Cyclophasphamide,
•Diffuse large B-Cell: MC, aggressive Doxorubicin, Hydrochloride,
•Folicular: slow growing, hard to cure ONcovorin, Prednisolone
•Lymphoblastic: TT “teen, T-cells”
•Burkitt: BBBB: boy, B-cells, belly,
chromosome B *EBV
•Large Cells: B and T cell
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ONC
ALL •MC malignancy in children •Fever, weakness, fatigue CBC: ANC <1000, WBC 5-100,000 Combination chemo
•Bone pain, pallor, anemia Smear: lymphoblasts (~25%) (anthracyclines, Vincristine,
•Leukemic BLASTS replace marrow (immature •Petechia, purpura, infection steroids)
cells) •Marrow FNA & biopsy DEFINTIVE
Exam: HSM, weight loss, lymphadenopathy, maintenance: 6-MP, MTX
abdominal pain

AML •MC acute leukemia in adults •Fatigue(MC), infection, nodules, HSM CBC: low WBC & plt, normocytic Combo chemo
•accumulation of BLASTS •pantocytopenia normochromic anemia
Smear: auer rod Leukostasis:
Types: Leukostasis reaction: MC w/ AML & CML •leukapheresis
•acute promyelocytic (APL): MC associated with •increased viscosity à plug microvasculature Bone Marrow Biopsy: GOLD
DIC, myeloperoxidase (+), auer rods •SOB, hypoxic, HA, dizzy, vision change •>20% myeloblasts, auer rods
•acute megakaryoblastic: MC in children <5yo •WBC >100,000
and downs •tre
•acute monocytic: infiltration in gums (gingival
hyperplasia)
CLL •MC LEUKEMIA IN US! •Slow onset! Usually found incidentally •pantocytopenia, WBC > 20,000 Low stage: observe
•mature B cell malignancy •lymphadenopathy (MC!) •Isolated lymphocytes (>5,000)
•recurrent infections (PNA, HSV, HZV) *small, well-differentiated, normal appearing High stage/SX:
Risks: old age, men with “smudge cells” chemotherapy (Fludarabine,
•hepatosplenomegaly Rituximab,
Complications: *upper abdominal discomfort/fullness FLOW CYTOMETRY: CONFIRMS Cyclophasphamide,
•obstructive lymphadenopathy •anemia/thrombocytopenia Confirms abnormal B-lymphocytes Chlorambucil)
•transformation into aggressive large cell
lymphoma (Richter syndrome) BM Aspiration/Biopsy: small lymphocytes *not •stem cell transplant is
required curative

CML •uncontrolled production of maturegranulocytes •Fatigue! *often first symptom CBC: WBC 100-150,00 w/ left (neutrophilia, Chronic:
•Single specific genetic mutation (translocation) of •Low-grade fever, night sweats, wt loss basophilia, eosinophilia) Tyrosine kinase inhibitor
gene 9:22 •abdominal fullness, bone tenderness (Imatinib, Nilotinib,
•PHILADELPHIA on PCR •pruritis, flushing Alk Phos: low Dasatinib) “-tinib”
•GI ulcers with elevated basophils due to
First (Chronic): MC à mature cells histamine Smear: Accelerated: blast cells, promyelocytes Accelerate or Blast:
Second (Accelerated): cytogenic TKI + multidrug chemo
Third (Terminal Blast): immature PE: HSM, LAD BM Aspiration/Biopsy: hypercellular with *possible stem cell
increased granulocytes and progenitors

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ID 4%

SCREENING
Routine HIV: 4th Gen Antigen/Antibody Combination HIV-1/2 Immunoassay (screening)
If Negative: No HIV, No further testing
If Positive: Confirmatory HIV-1/2 Antibody Differentiation Immunoassay
If Indeterminate/Negative: Plasma HIV RNA
If Positive: Plasma HIV RNA (evaluate for acute infection)

VACCINE
Influenza:
Inactivated: Annual for all ≥6 Months (including pregnancy). High-Dose in >65 yo
Live Attenuated (Intranasal): Can be used 2-49 yo
Timing: Annually, Ideally before the onset of flu season (by the end of October)
ADR: Injection site rxn, Fever, Myalgia, Irritability, Allergic rxn, Anaphylaxis (rare), Nasal Spray (upper & lower respiratory tract symptoms)
C/I: Both (Anaphylaxis, GBS within 6 weeks of a previous influenza vaccination, High fever, Infants <6 months)
*egg allergy of any severity, can safely receive the egg-based inactivated flu vaccine in a medical setting
C/I Live Attenuated: Immunocompromised, Pregnant, ≥50 yo, Taken flu antiviral within past 48 hours, Close contacts & caregivers of immunocompromised who require a protected environment

PENICILLINS
Bactericidal: Inhibition of cell wall synthesis (via beta-lactam ring)
PCN G Benzathine-Procaine, PCN VK
Gram(-) (Most potent), Covers N. meningitidis & Treponema pallidum
Strep pharyngitis, Oral/Dental infections, Syphilis
Nafcillin, Oxacillin, Dicloxacillin
Gram(+) (esp beta-lactamase producing S. aureus). NOT: Enterococcus, MRSA, Gram(-)
Amoxicillin, Ampicillin
Gram(-) Gram(+), Including: H. influenza, E. coli, Listeria, Proteus, Salmonella
UTI in pregnancy, Listeria monocytogenes, Acute otitis media, Lyme disease, Dental infection, Enterococcal infections
Augmentin, Ampicillin-Sulbactam (Unasyn)
Gram(+), Gram(-), Anaerobe
Acute otitis media, Acute sinusitis, Animal/Human bites, Dental infections, Skin & Soft tissue infections
Piperacillin-Tazobactam (Zosyn), Ticarcillin-Clavulanate, Carbenicillin
Pseudomonas
ADR: Hypersensitivity (MC drug class), GI (N/V/D), Neurotoxicity (seizures at higher doses), Acute interstitial nephritis, Hematologic (Thrombocytopenia, Neutropenia, Methmoglobinemia)

CEPHALOSPORIN
Similar to penicillins but interisically effective against beta-lactamase producing bacteria
Increasing level of Gram(-) activity & loss of Gram(+) as you go from 1st gen to 4th gen
In general: Not effective against: Enterococci, MRSA, L. monocytogenes, C. difficile
1st: Cephalexin, Cefazolin, Cefadroxil
Gram(+), Anaerobes, Gram(-) Rods: E. coli, H. influenza, Proteus, Klebsiella
Skin & Soft tissue infections (staph, strep), Surgical prophylaxsis
2nd: Cefaclor, Cefuroxime, Cefoxitin, Cefotetan
Broader Gram(-): Neisseria, M. catarrhalis, Weaker Gram(+). Excellent coverage Bacteroides fragilis
Skin, Respiratory/ENT, UTI
Cefotetan & Cefoxitin for Anaerobic infections (abdominal)
Inpatient PID: IV Doxycycline + Cefoxitin/Cefotetan
3rd: Ceftriaxone, Ceftazidime, Ceftibuten, Cefotaxime, Cefixime
Broader Gram(-): Serratia, Enteric. Good CNS penetration (esp Ceftriaxone)
Bacterial meningitis, Gonorrhea, CAP (combined with macrolides), Lyme disease (involving heart/brain), Ceftazidime (pseudomonas)
4th: Cefepime
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 Gram(-): Pseudomonas. Gram(+): Only Methicillin-Susceptible
5th: Ceftaroline
Gram(+): MRSA, Gram(-). Doesn’t cover Pseudomonas or Anaerobes
ADR: Allergic reactions: 5-15% cross reactivity with PCN (shouldn’t be used in anyone who had an anaphylactic reaction to PCN, 1-2% hypersensitivity reaction in those without PCN allergy.
Cefotetan (2nd) & Cefoxitin (2nd): Increase bleeding risk
Cefotetan (2nd): Disulfiram like reaction
Ceftriaxone (3rd): Inadequate biliary metabolism esp in neonates (Cefotaxime preferred over Ceftriaxone in neonates)

ID-Bacterial
Typhoid Diarrheal illness
(Enteric) Fever Gram(-) Rod: Salmonella typhi & paratyphi
Incubation: 5-21 Days
MC in Children, Young adults
Transmission: Fecal-oral, Contaminated
food/water, Travel to area of poor sanitation
Patho: Crosses intestinal epithelium through M
cells overlying the lymphoid follicles of Peyer’s
patches
*may colonize gallbladder in chronic carriers
HA, Intractable fever, Chills, Abdominal Culture of Stool/Blood PO Rehydration & Electrolyte
pain, Constipation initially followed by non- replacement
bloody diarrhea “Pea-Soup” Green, Malaise,
Anorexia ABX (often given): FQ (Ciprofloxacin,
Ofloxacin), Macrolides, Ceftriaxone
PE
Fever with bradycardia
Rose spots (faint pink/salmon macular rash
spreads from trunk to extremities)
*occurs in the 2nd week
Abdominal tenderness
Later: Hepatosplenomegaly, GI bleeding,
Dehydration, Delirium

Non-Typhoidal Diarrheal illness N/V, Fever, Abdominal cramp, Malaise, HA Culture Stool PO Rehydration & Electrolyte
Salmonella Salmonella enteriditis, S. tymphimurium replacement
Diarrhea “Pea-Soup” Brown-Green ± bloody *usually self-limited
Incubation: 8-72 Hours
ABX (if severe): FQ
One of the MCC of foodborne illness in USA

Sources: Poultry, Eggs, Milk products, Fresh

produce, Contact with reptiles (turtles)

Shigellosis Diarrheal illness
Gram(-) Rod: Shigella sonnei (MC), S. flexneri,
S. dysenteriae (produces most toxin)
Incubation: 1-7 Days, HIGHLY virulent
Highest Risk: Children <5 yo in daycare
Transmission: Fecal-oral, Contaminated
food/water
Lower abdominal pain, Abdominal cramp,
High fever, Tenesmus, Explosive watery
diarrhea progresses to mucoid & bloody
diarrhea
Neurologic (esp young kids): Febrile seizure
Complications: Reactive arthritis, Hemolytic
uremic syndrome (esp kids), Toxic megacolon
Culture Stool
Positive Fecal WBC & RBC
CBC
Leukemoid rxn: WBC >50K
Sigmoidoscopy
Punctate areas of ulceration
PO Rehydration & Electrolyte
replacement
Avoid: Anti-Motility Drugs
*can worsen due to retained toxins
Severe: ABX: FQ, 3rd Gen
Cephalosporins, Azithromycin,
Bactrim

216
Spirochete
Lyme Borrelia burgdorferi Gram(-) spirochete
Disease MC Spread Deer Tick (Ixodes Scapularis)
MC in Spring & Summer (nymphs feed)
MC Source White-tailed deer & White-
footed moose
MC in Northeast, Midwest, Midatlantic
Highest likelihood of transmission:
attached 72 hours, minimum 24 hours
needed
Early, Localized (within 1 week) Clinical Dx Early
Erythema migrans: Bulls eye/Target (expanding warm Doxycycline BID
annular erythematous rash with central clearing Serology *Localized: 10-21 Days
*often seronegative at this point ELISA then Western blot (if *Disseminated: 14-28 Days
Flu-like: HA, Fever, Myalgia, Fatigue, Arthalgias ELISA +) *Alternative: Amoxicillin,
Use in patients if all 3: Cefuroxime
Early Disseminated (1-12 weeks) Reside/Travel endemic area *Pregnant: Amoxicillin
Neurologic: CN palsies (CN VII Palsy MC), HA, RF for exposure to ticks
Meningitis, Weakness, Neuropathy Symptoms Early disseminated/Late Late/Severe
Cardiac: AV Block (MC), Pericarditis, Arrhythmias Not in: IV Ceftriaxone: If 2nd/3rd AV block,
Multiple erythema migrans lesions Pateints with erythema migrans Syncope, Dyspnea, Chest pain, CNS
Screening asymptomatic disease other than CN VII palsy
Late (months-years) Non-specific symptoms only (meningitis)
Intermittent/Persistent Arthritis (MC) (esp large
joints, Knee MC) False Positive ELISA Prophylaxis
Persistent neurological symptoms: Subtle cognitive Other spirochetal disease: Syphilis, Doxycycline 200mg Once
changes, Distal paresthesias, Spinal radicular pain, Yaws, Viral/Bacterial disease, Other *given within 72 hours of tick
Subacute encephalitis Borrelial species removal if the tick was present ≥36
hours and there are >20% of infected
ticks where the bite occurred
*if Doxycycline C/I: No prophylaxis
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Viral About Contagious Presentation Diagnostics/Treatment
Infectious EBV (HHV-4) Fever, Lymphadenopathy (esp posterior cervical, Heterophile Antibody (Monospot): DoC Supportive: Rest, Analgesics,
Mononucleosis 80% adults seropositive can be generalized) Positive within 4 weeks Antipyretics
Tonsilar pharyngitis (may be exudative, may have *Symptoms may last for months
Patho: EBV infects B-Cells petechiae on hard palate) Rapid Viral Capsid Antigen Test
May be aassociated with: Fatigue, HA, Malaise, Increased LFTs Corticosteroids: Only if airway
Transmission: Saliva Splenomegaly, Hepatomegaly obstruction due to lymphadenopathy,
(kissing disease) (esp 15- Peripheral Smear hemolytic anemia, or severe
25 yo) Rash 5% (esp if given Ampicillin) Lymphocytosis >50% with 10% Atypical thrombocytopenia
lymphocytes *Strep & EBV can coexist

AVOID TRAUMA & CONTACT

SPORTS x3-4 WEEKS IF
SPLENOMEGALY

Complications
Hodgkin lymphoma, Burkitt lymphoma,
CNS lymphoma, Nasopharyngeal
carcinoma, Gastric carcinoma

Viral
Influenza Influenza A more severe outbreaks than B
Transmission: Airborne respiratory (sneezing,
coughing, talking, breathing), Contaminated
objects
Increased Risk: >65 yo, Pregnant,
Immunocompromised
Children are important vectors for the disease
Highest rates of infection: Children
Highest risk of complications: Elderly
Complications: Pneumonia, Respiratory
failure, Death, Meningitis, Myocarditis,
Encephalitis, Rhabdomyolysis, Kidney failure
Abrupt Onset
HA, Fever, Chills, Malaise, URI
symptoms, Pharyngitis, Pneumonia
Myalgias (MC legs & lumbosacral)
Rapid Influenza Nasal Swab
Viral Culture
Mild & Healthy: Supportive (APAP/ASA,
Rest, Fluids)
Hospitalized, High Risk Complications: >65
yo, CV (except isolated HTN), Pulmonary
disease, Immunosuppression, Chronic liver
disease, Hemoglobinopathies: Antivirals
Neuraminidase Inhibitors: Oseltamivir
*Best if initiated within 48 hours
*Works against A & B
ADR: Skin rxn, N/V, Transient
neuropsychiatric events
Alternatives: Zanamivir, Peramivir
*Zanamivir C/I: Egg allergy
Adamantane Derivatives: Amantadine &
Rimantadine
*Effective against A only (not recommended
for prophylaxis against A)

Chemoprophylaxis
Oseltamivir: High risk groups, ≥1 yo
During outbreaks in LTCF, all residents
should receive chemoprophylaxis
regardless of immunization status

218
*General population, only individuals who did
not receive the annual vaccine

219
Viral About
HIV Retrovirus: Changes RNA Acute Seroconversion Early HIV HAART Regimens: All HIV Patients
into DNA via reverse *During this stage, Highly infectious Viral RNA: Usually high (>100K, often millions)
transcriptase *10-60% with early HIV do not have sx CD4+: Can drop transiently (lower than CD8) NNRTI + 2 NRTI
HIV-1 (MC), HIV-2 Flu/Mononucleosis-like illness (acute retroviral syndrome) CBC: Mild anemia, Thrombocytopenia,
Leukocyte & Lymphocytes: Vary PI + 2 NRTI
*usually within 2-4 weeks of infection
Transmission: Sex, IVDU, Liver Enzymes: Elevated
Fever, Fatigue, Myalgias (MC symptoms) INSTI + 2 NRTI
Mother, Blood contact Nontender generalized lymphadenopathy (cervical, axillary, Dx Suspected Early HIV
occipital) Antigen/Antibody Immunoassay (screening) + NNRTI: Non-Nucleoside Reverse
AIDS: CD4 <200 Sore throat (usually w/o tonsillar exudates/enlargement) HIV Viral Load Testing (RT-PCR) Transcriptase Inhibitor
Painful mucocutaneous ulceration
Arthalgia Both negative, high suspicion, repeat in 1-2 weeks NRTI: Nucleoside Reverse
Diarrhea Transcriptase Inhibitor
Weight loss (-)Screening Immunoassay & (+)Virologic Test
Suggests Early PI: Protease Inhibitor
HA
2nd (+) Virologic suggests HIV
Malaise INSTI: Integrase Strand Transfer
Generalized rash (+)Screening Immunoassay & (+)Virologic Test Inhibitor
Early/Established infection
Opportunistic Infection Confirm with a 2nd test (repeat HIV RNA or
Oral & Esophageal Candidiasis (MC) Serologic test) Several weeks later.
CMV (proctitis, colitis, hepatitis) (+)Screening Immunoassay: 2nd Antibody only
immunoassay (preferably the HIV-1/2
PCP pneumonia
differentiation immunoassay
Cryptosporidiosis
HIV RNA Viral Load
Can be positive in the window period
(-)Screening Immunoassay or (+)Combination
Antibody/Antigen Immunoassay with a (-
)Antibody Only Immunoassay
*Also used to monitor infectivity & treatment
effectiveness in patients diagnosed with HIV

Viral Drugs MOA Adverse Effects

NRTI Zidovudine Abacavir Inhibits viral replication by interfering with HIV viral RNA-dependent DNA polymerase Zidovudine: Bone marrow suppression, Peripheral
Lamivudine Emtricitabine Truvada (Emtricitabine/Tenofovir) neuropathy, Pancreatitis
Tenofovir Stavudine Abacavir: C/I if (+)HLA-B*5701: Increased risk of
Didanosine hypersensitivity reaction

NNRTI Efavirenz Nevirapine Inhibits viral replication by interfering with HIV viral RNA-dependent DNA polymerase Rash
Delavirdine Rilpivirine Efavirenz: Vivid dreams
Etravirine

PI Atazanavir Indinavir Inhibits HIV protease leading to production of noninfectious, immature HIV particles Lipodystrophy, Hyperlipidemia
Darunavir Ritonavir N/V/D
“-VIR” Nelfinavir Saquinavir

220
 INTI Raltegravir Dolutegravir Prevents insertion of DNA copy into host Hyperlipidemia
GI symptoms

Fusion Enfuvirtide Disrupts the virus from fusing with healthy T-cells Hyperlipidemia
Inhibitors GI symptoms

CCR5 Maraviroc Blocks viral entry into WBC

Antagonist

OPPERTUNISTIC INFECTIONS
CD4 COUNT DISEASE 1ST PROPHYLAXIS 2ND PROPHYLAXIS
700-1500 Normal
>500 TB INH (if latent) Rifampin
Kaposi sarcoma, Thrush, Lymphoma, Zoster
≤200 Pneumocystis Bactrim Dapsone, Atovaquone, Pentamidine (aerosolized)
≤150 Histoplasmosis Itraconazole Amphotericin B
≤100 Toxoplasmosis Bactrim Dapsone + Pyrimethamine + Folinic acid
Cryptococcus Fluconazole Amphotericin B
≤50 MAC Azithromycin or Clarithromycin Rifabutin (must obtain CXR prior to rule out active TB)
CMV Retinitis Valganciclovir Ganciclovir + Foscarnet

221
NEURO About
Encephalitis Infection of brain parenchyma
Etiology: HSV-1 (MCC), VZV, EBV,
Measles, Mumps, Rubella, HIV, St. Louis
Virus
Bacterial Infection & inflammation involving the
Meningitis meninges and subarachnoid spaces
Types
Bacterial
Aseptic (non-bacterial)
Etiology
S. pneumonia
MCC Adults & Children 3mo-10yr
N. meningitidis “Meningococcus”
MC Older Children (10-19 yo)
2nd MC Adults
Petechial rash on trunk, legs, conjunctiva
Crowded conditions: Dorms/barracks
GBS
MC Neonate <1mo & Infants <3mo
Listeria monocytogenes
Neonates, >50 yo, Immunocompromised
Neonates
GBS, E. coli, Gram(-) Rods, Listeria
monocytogenes, H. influenza
Findings
Meningeal Symptoms: HA, Neck stiffness,
Photosensitivity, Fever, Chills, N/V,
Seizures
Presence of: AMS, Changes in
Personality, Speech, Movement
*distinguishes encephalitis from aseptic
meningitis
PE
Focal neurologic deficits: Hemiparesis,
Sensory deficits, CN palsies
Meningeal Symptoms: HA, Neck stiffness,
Photosensitivity, Fever, Chills, N/V
May develop: AMS, Seizures
PE
Meningeal Signs: Nuchal rigidity,
(+)Brudzinski (neck flexion produces knee
and/or hip flexion)
(+)Kernig (Inability to extend the knee/leg
with hip flexion)
Focal neurologic findings
Diagnostics
CT: Rule out space occupying lesion
*often have AMS, requiring imaging
before LP
LP: After CT
Normal Glucose
Increased Lymphocytes
*similar to aseptic meningitis
MRI
Temporal involvement of HSV
PCR Testing of CSF Fluid: Most
accurate test for herpes encephalitis
CT: Prior to LP only if you need to
rule out mass effect if any of these are
present: Papilledema, Seizures,
Confusion, Focal neurologic findings,
>60 yo, Immunocompromised, Hx
CNS disease
LP + CSF: Definitive
Decreased Glucose <45
Increased: Neutrophils, Proteins,
Increased: Pressure
Treatment
Early Empiric Treatment HSV Encephalitis
IV Acyclovir
*initiated ASAP if the patient has encephalitis
with no obvious cause
Supportive
ABX + Dexamethasone (when indicated)
Start ASAP: After LP, If LP C/I, or Prior
to CT if CT is to be performed prior to LP
*ASAP after blood cultures are obtained
*Dexamethasone in adults: reduce mortality
of S. pneumonia, H. influenza, N.
meningitidis
*Dexamethasone in children: reduce incidence
of CN VIII related hearing loss if H. influenza
suspected
Empiric >1 Month to 50 yo
Vancomycin + Ceftriaxone (or Cefotaxime)
Empiric >50 yo
Vancomycin + Ceftriaxone + Ampicillin
*for Listeria
Empiric Neonates (up to 1 month)
Ampicillin + Gentamicin and/or
Cefotaxime
Droplet Precautions: Should be continued for
24 hours after the initiation of ABX with
suspected/confirmed N. meningitis
Post-Exposure Prophylaxis
PO Ciprofloxacin 500mg Once or
PO Rifampin 600mg Q12H 2 Days
*Only needed for close contacts with
prolonged exposure (>8 hours) or direct
exposure to respiratory secretions
222
 *NOT recommended for healthcare workers
who have had direct exposure to respiratory
secretions

Aseptic Clinical & lab evidence of meningitis with
Meningitis negative routine bacterial cultures
Etiology
Enteroviruses MCC (Coxsackievirus &
Echovirus)
Other Viruses, Mycobacteria, Fungi,
Spirochetes, Meds, Malignancies
Classic symptoms, but may be milder Diagnosis of Exclusion Supportive: IVF, Analgesics, Antipyretics
*after ruling out bacterial meningitis
Meningeal Symptoms: HA, Neck stiffness, Most have a self-limited course with
Photosensitivity, Fever, Chills, N/V LP + CSF: Most accurate -mass effect resolution even without specific therapy
Normal Glucose
PE Lymphocyte Predominance
Meningeal Signs: Nuchal rigidity, Protein Count usually <200
(+)Brudzinski (neck flexion produces knee
and/or hip flexion)
(+)Kernig (Inability to extend the knee/leg
with hip flexion)
No Focal neurologic deficits
*helps differentiate it from encephalitis

CSF Exam
NORMAL BACTERIAL ASEPTIC (VIRAL) ASEPTIC
(FUNGAL/TB)
Opening 5-20cm Increased Normal/Mildly Increased Normal/Mildly
Pressure Increased
Appearance Normal Turbid Clear Fibrin Web
Protein 0.18-0.45 Increased Normal/Mildly Increased Increased
Glucose 50-80 Decreased (<45) Normal Decreased
WBC Count 0-5 (NO RBC) 100-100K 10-300 10-200
>80% Neutrophils (PNMs) Lymphocytes Lymphocytes
Gram Stain Normal 60-90% Positive Normal

223
URGENT CARE 4%

Heat Illness Heat Edema Heat Syncope Heat Cramps

Wasp, Bee, •stinging results in envenomation
Ants causing one of 3 presentation
-localized reaction
-systemic reactions
-anaphylaxis
Clinical Presentation:
•localized bee sting: MC reactions
-small pruritis, painful,
erythematous, edematous
lesion at sthe sting site
-occasionalyl >5cm
Fire Ant Sting Labs: Wound Management:
•sterile pustule evolves of 6-24h •ONLY FOR SYSTEMIC and ANPHYLACTIC •do not delay tx of systemic reaction to
•may results in necrosis and scarring sx care for wound
•directed at complications: •remove stinger w/ scraping technique
Systemic/Toxic (nona-allergic) -CBC, CMP, caogs, CK •wash wound
•more common with >50 stings •ice and elevated
•N/V/D with irticarial lesions distant from site Management: •tetanus update
of string Anaphylaxis
•symptoms usually subside within 48h •intubation if needed Disposition:
•severe acses may lead to complications •Epinephrine 1:1000 (adults 0.3-0.5) •local: discharge home
-rhabdo, liver failure, hemolysis, •IV Methylprednisolone •systemic
thrombocytopenia, DIC •IV Diphenhydramien (Benadryl) -admit child, elderly, comorbid,
•IV Famotidine (Pepcid) 50+ stings, or prolonged reactions
Anaphylactic Reactions: allergic rxn •Nebulized albuterol
•occurs within 6hr (most within 15 min) -otherwise can send home:
•itchy eyes, urticarial, cough, resp failure, CV Localized reactions only: observe for 6 hours in the ED to
collapse •Benadryl make sure not rebound sx, repeat
•oral pain control: NSAIDS, Tlenol labs before discharge, RX
•systemic: IV methylpred, Benadryl, famotidine EpiPen, f/u with allergist
•complications: may require blood, dialysis, and
extensive hostpital care

Abortion Presentation Management

Scorpion •most scorpions produce localized •sting is painful without initial •most pateints can be managed symptomatically •antivenin (anascorp) indicated in severe
reactions erythema/swelling -oral or IV pain medication systemic toxicity
•exquisite pain with light percussion known as -Benzo for motor control
•bark scorpion “tap sign”
-only systemic toxic scorpion •neuromuscular excitation
-infants & child high risk -spasms, CN dysfunction, roving eye
-southwestern US movement, diplopia, dysphagia

Snake Bites •large triable shaped head with a
(Pit Vipers) heat sensitive depression “pit”
between their eyes
•venom is cytotoxic
•copperhead, rattlesnake
•fang marks wit hpain, edema, hemorrhage
and necrosis around bite & extending distant
from bite if severe
-usually within 30 minutes but may be
delayed up to 12h
-if no s/s after 12h: dry bite
Systemic:
•hemolysis, thrombocytopenia, coagulopathy
•vomiting
•respiratory failure with CV and collape
•consult poison control
•cardiac monitoring and IV access
-administer fluids and resp support
Labs: CBC, CMP, coags, CK, urine myoglobin,
type and crossmatch
•Immobilize biten extremity
-EMS may apply contrisction band
-not effective from EBM
•serial (30 mintes) wound evaluation
-measure affected limb above and
below bite and mark border
-assess sx of compartment syndrome
Antivenin (CroFab)
•approved for bites from rattlesnackes,
copperheads and cottonmouths/water
moccasins
•compare severity of envenomation to SE
of antivenin
-hypersensitvity reaction in 5-19%
-recurrent coagulopathy in 50%
•td upate
Disposition
•observe in ER for 8 hours, DC if no
progression, ICU if severe

224
 Physical Exam
Poisoned •mental status, vital signs, pupillary
Patient examination help classify excitation or
depression
Excitation:
•CNS stimulation, mydriasis
•tachy, increased BP, RR, temperature
•anticholinergics, sympathomimetic,
serotonin syndrome, hallucinogens
Depression:
•depressed mental status, miosis
•low BP, RR, temperature
•sedative-hynoptic agents, opiates,
cholinergic agents
Exam
•vital signs
•mental status
•general appearance: agitation, confused
Poison Enhanced Elimination
TX Multi-Dose Activated Charcoal
indications: ingestion of toxic levels of
carbamazepine, dapsone, phenobarbital,
quinine, theophylline
CI: uprotected airway, absent BS
•caution in ingestions resulting in reduced
GI motility
Urinary Alkalinization
•skin (full exposure): cyanosis, flushing,
diaphoresis or dry, injury, ulcer, bullae…
•Eyes
-mydriasis: anticholinergics, sympatho
-miosis: cholinergics, opioids
-nystagmus: ethanol, phenytoin,
ketamine, PCP
-lacrimation: cholinergic
•mucous membranes
-hypersalivation: cholinergic
-dryness: anticholinergics
•heart
•lungs: bronchorrhea (cholinergic), wheeze
•abdomen:
-diminished: anticholinergic, opiate
-enlarged bladder; anticholinergic
-tender/rigid: ASA, anticholinergic
•neuro:
-tone, tremor: cholinergic, serotonin
-assess cogitation, CN, DTRs, strength,
coordination, gait
Urinary Alkalinization
•ionizes acidotic toxins preventing
resorption across the renal tubule
•indications: moderate-severe salicylate
toxicity
•cautions: hypokalemia
•Procedure:
-IV sodium bicarb +/- KCL
-monitor K+ and bicarb q2-4h
•maintain K+ between 4-4.5
-pH q15-20min with goal 7.5-8.5
Diagnostics
Abdominal X-ray:
•suspected body packer
•Bezoar formation: small stony
concentration form in stomach or
intestines (ASA, salicylates)
CXR: pulmonary edema
Toxicology:
•UNNECESSARY if non-intentional
ingestion, asympatomatic, or have
clinical findings consistent with
medical history
•individual screen for lithium and
digoxin may be needed
Common Coigestatnts:
•APAP, ethanol, salicylate
*ALWAYS in unknown ingestion
UA: calcium oxalate crystals with
ethylene glycol (antifreeze)
Hemodialysis/Hemoperfusion
•hemodialysis: more effective at clearing
highly protein-bound drugs and lipid-
soluble drugs
•hemoperfusion: clear water-soluble low
molecular weight
•both require critical care setting and are
expensive and invasive
à complications
Gastric Decontamination
activated charcoal *BEST!
•indicated if ingestion of toxic
substance within 1 hour prior to arrival
*can used after 1hr
if antichol or salicylates
•AC is not able to bind to metals, corosives,
alcohols
•CI: cant protect air à aspirate
Gastric Lavage
•removes non-absorbed toxins
•indication: <1hour, no antidote to toxin,
poor response to supportive care
•high risk of aspiration
Procedure
•insert 36-40F orogastric tube
•lie LLD w/ head of bed tilted down
•200ml warm tap water in stomach
Whole Bowel Irrigation
•indications: ingestion of chemicals poorly
absorbed to charcoal (lithium, iron, lead)
and ingestion of drug-filled packets
•GoLYTELY to flush out
-administer NG tube 1-2L/ht
-continue until clear (2-5h)
CI: absent BS, ileus, obstruction
Decontamination/Contamination
Decontamination: Inhaled
•administer oxygen
•water aerosol inhalation à dilute irritants
•delayed upper airway obstruction or pulmonary
edema
Decontamination: Eyes
•irrigate with plain water or NS
•assess pH after 2L irrigation
Contaminated Skin
•avoid direct self-exposure
•wash skin with water and dilute soap
•hydrofluoric acid burns are particularly penetrating
& corrosive10% Ca gluconate gel
225
Poison MOA and Examples Presentation Management
Opioid •heroin, morphine, methadone, meperidine, “physiologically depressed” •ventilation
hydrocodone, oxycodone •MC: CNS and respiratory depression, decreased BS, miosis •Naloxone
•hypothermia, bradycardia, orthostatic hypotension, bronchospasm,
pulmonary edema, seizures
Sympthato- Mimic the effects of endogenous agonists of •physiologic excitation •External cooling, sedation with benzos, hydration
mimetic the sympathetic nervous system (epi, norepi, •MC: psychomotor agitation, diaphoresis, HTN, hyperthermia,
dopamine) mydriasis, tachycardia •CI: Beta Blockers
•seizures, rhabdomyolysis, MI
EX: cocaine, caffeine, amphetamines,
cathinones (bath salts)
Cholinergic Blocks acetylcholinesterase, leading to MC: salivation, lacrimation, diaphoresis, bronchorrhea, urination & •airway protection and ventilation
excessive Ach defecation, N/V, muscle fasiculations, weakness •Atropine: blocks Ach receptors
•bradycardia/tachycardia, rales, miosis/mydriasis, seizures, respiratory •Pralidoxine: Antidote
EX: organophosphate insecticides, carbamate failure, paralysis •Diazepam: seizure, muscle fasiculations
insecticides

Anti-cholinergic Block the acetylcholine muscanaric
receptors à inhibits parsympathetic nerve
impulses
Examples: Scopolamine, Atropine,
Antihistamines, TCAs, Antiparkinson,
Antispasmodics/
muscle relaxants
MC symptoms: •activated charcoal to decrease drug absorption
•hot as hades: hyperthermia •address complications
•fast as a hare: tachycardia -wide QRS: sodium bicarb
•dry as a bone: no secretions or sweat -agitation: benzos
•mad as a hatter: AMS -fluids: rabdo
•full as a tick: urinary retention
•blind as a bat: mydriasis supportive: treat hyperthermia with external
•red as a beet: flushed skin cooling methods

Disposition: •decreased/absent BS, dysrhythmias, rhabdo, hypotension/HTN •Physostimine: cholinesterase inhibitors increases
•discharge home if resolve in 6h concentration of Ach
•admit with more significant symptoms or -if conventional therapies fail
those receiving physostigimine

Sedative/ 3 classes: •MC: slurred sppech, lethargy, CNS depression, respiratory depression, Supportive
Hyponotic •benzos confusion •venilation/intubation, 2 large bore IV
•carisoprodol/alcohol.hypnotics •bradycardia, hypotension, hypothermia, bradypnea, hyporeflexia •IV fluids bolus for hypotension
•barbituates -dopamine or norepi if fails
•activated charcoal
Disposition •barbituates that don’t response
•admit if sx after 6 hours •benzos: confirmed benzo OD with respiratory
•consult psych for intentional OD depression
-Flumazenil *get toxicity back 1st

Serotonin •increased serotonergic activity •altered mental status, seizures, tremors/increased muscle tone •veniality support
Syndrome •hyperthermia, tachycardia, HTN, tachypnea •benzos for agitation, tremors, seizures
EX: MAOI, SSRI, Meperidine, •discontinue serotonergic drug
Dextromethorphan, TCAs, L-tryphtophan Labs: UA/CK, ABG *ADMIT ALL PATIENTS •Crypoheptadine if above fails

Hallucinogenic •LSD, PCP, muschroom, dextromethorphan, •disorientation, hallucination, anxiety, seizures, agitation, muscle tension, •Benzo: agitation, hyperthermia, tachy, HTN
ketamine N/V, HTN, tachycardia, tachypnea, hyperthermia, mydriasis •Nitropruss, phentolamine: refractory HTN
•aggressive IV fluids if rhabdo concern

226
Poison About Presentation Diagnostics Management
Salycilate EX: ASA, pepto bismol, liniments, Chronic salicylate level: >30 is toxic •ABCs
flavoring agents •fever, hyperventilation, AMS, volume -peak concentration may not •correct volume depletion
depletion, acidosis, hypokalemia occur for 4-6 hours
•ASA hydrolyzed to salicylic acid à -repeat every 1-2hr until peak •GI decontamination: activated charcoal single
acid environment Acute then every 4-6 hours dose
•<150mg: tinnitus, hearing loss, dizziness,
•higher mortality with chronic N/V •CMP and magnesium •reduce salicylate burden
•risk for bezoar formation -systemic/urinary alkalinization
•150-300: high RR, hyperpyrexia, •ABG: mixed acid/base disturbance with sodium bicarb
diaphoresis, ataxia, anxiety -alkalemia w/ resp alkalosis and -FIRST LINE in mod-severe
metabolic acidosis
•>300: AMS, seizure, heart/lung/renal, shock
•assess for coingestants Hemodialysis:
-APAP, toxicology severe not responding to above

•CXR and EKG for end-organ

•ABD image if bezoar suspected

-suspect is salicylate level
continue to rise despite tx with
gastric lavage or charcoal

Poison About Presentation Diagnostics Management

Tylenol Risks:
•chronic alcohol, AIDS
•anticonvulstants and anti-TB
Suggested When:
6 years old and older:
•ingests >10g (200mg/kg) over as
single ingestion or over 24hr
•>6g/day (150mg/kg) x2 consecutive
days
Children <6 years old
•200mg/kg as single ingestion or
over 8hours
•150mg/kg per day x2consecutive
days
Stage 1 (day 1 after ingestion) serum APAP level •Activated charcoal
•anorexia, N/V, malaise, hypokalemia •assess levels in asymptomatic patients
too due to delay •Acetylcysteine: oral or IV
Stage 2 (days 2-3 after ingestion) •peak serum concentration 30-120min -prevents metabolite from
•improvement in stage 1 sx after acute ingestion binding to hepatic cells (if within
•RUQ abd pain, elevated LFTs and bilirubin, 8hr) & diminished necrosis
prolonged PT •Rumach-Mathhew nomogram
-determine clinical outcome •Extra-corporal excretion
Stage 3 (Days 3-4 after ingestion) -only after one acute ingestion -patient with severe intoxication
•fulminant liver failure, metabolic acidosis, between 4-24 hours post who present too late to remove drug
coagulopathy, renal failure, encephalopathy, -hepatic encephalopathy
pancreatitis, recurrent GI symptoms
Disposition:
Stage 4 (Day 5 and beyond) •admit all patients requires acetylcysteine
•survival: improvement & recovery •discharge after 4-6h of observation if
•continued deterioration to multi-organ failure and acetylcysteine is not needed
death

227
DERM About Clinical Presentation Diagnostics Managment
Thermal Causes: scalding, direct thermal, flame burns Descriptions: •lab evaluation: assess complications Management:
Burn *based on % of BSA •ABG, CBC, CK, CMP •supplemental O2 & intubation if needed
Depth •rule of 9s •UA, carboxyhemoglobin •vitals: pulse ox may be falsely high by CO
•old: 1st, 2nd, 3rd, 4th degree •lund and broder •assess & treat trauma, inhalation, CO
•new systemic: superficial partial thickness, deep •palmar method: palm=1% Complications •IV opiates for pain control
partial thickness, full thickness •inhalation injury •urinary cath: measure I&Os
•carbon monoxide
•1st degree (sunburn): •bacterial super infection IV Fluids:
erythema, skin blanches with pressure •sepsis •IV LR: 2 bore needle in unburned area
•multiorgan failure •Parkland formula to determine fluid
•2nd degree (partial): red and blistered *½ over first 8 hours, ½ over 16 hours
-adults: 4ml x wt (kg) x %BSA
•3rd degree (full): tough, lethargy, non-tender -children: 3ml x wt (kg) x %BSA

•4th degree: bone and muscle Minor: clean with soap and water
Large Bullae >2cm: drain, debride, 1% silver
Moderate/Severe: dry sterile sheet & admit

Disease Bugs/Causes Symptoms Diagnostics Treatment

Orbital •Infection of the orbit-fat and ocular muscle •inflammatory proptosis present (buldging) •clinical ADMIT and IV ABX
(Septal) •POSTERIOR to the orbital septum •ocular pain with EYE MOVEMENT •high-resolution CT •Vancomycin + 1 of the below:
Cellulitis •MC in children 7-12 years old •diplopia scan to confirm -Ceftriaxone
•eyelid edema nd erythema -Cefotaxime
Bugs: S. aureus, GABHS, H. flu -Zosyn
Triad: -Unasyn
Causes: MC secondary to sinus infection, •ptosis -Clindamycin
blepharitis, trauma, surgery, dental infections •chemosis
•limited EOM (opthalmoplegia)

Periorbital Bacterial infection superficial/ANTERIOR to the •eyelid swelling, erythema •clinical Outpatient is >1 yo and mild
(Preseptal) orbital septum •inflammatory proptosis •high-resolution CT
Cellulitis NOT present scan to confirm MRSA: Clindamycin oral
•spread of infection arising within the eyelid •NO limitation of
è hordeolum, wound, animal bite extraocular movement Others: Bactrim + Amoxicillin, Augmentin, or
•NO pain with EOMs Cefpodoxime

228
 About Signs and Symptoms/PE Tests and Stages Diagnostics and Treatment
Shoulder •most common joint to dislocate •visible or palpable deformity X-Ray: scalpular Y & Axillary views Treatment:
Dislocation •MC is ANTERIOR •swell, ecchymosis, pain, decreased ROM •Anterior: head anterior & inferior •reduction & immobilization
•hold affected limb close w/ elbow flexed •Hill Sach Lesion: groove fracture
Risks: young males •numb & weakness (neck & muscle spasm) •Bankart lesion: glenoid rim fracture 1st time anterior dislocations:
•AP: “light bulb sign” appearance of humeral head •reduced then immobilized in
Most Common Causes Anterior: abduction and external rotation à posterior neutral rotation for 3 weeks
•sports: football, hockey, volleyball Posterior: adduction and internal rotation followed by PT
•trauma: during MVA, falls Complications: *focus on supraspinatous
•seizures: POSTERIOR dislocation •axillary nerve (MC) à anterior

AC Joint •MCC: fall on tip of shoulder •pain over AC joint Type I: AC joint partially, CC intact Type I & II: non-surgical
Dislocation •scapula moves downward due to weight •pain w/ lifting arm (esp abduction) Type II: AC torn, CC intact, partial clavicle •ice, sling & analgesia
of arm à bump or bulge above the •deformity with type III – VI Type III: AC and CC complete, clavicle separated •full return within 4 weeks
shoulder •support arm in an adducted position from acromium
•clavicle prominence-esp with type II Type IV: clavicle posterior displaced Type III: nonsurgical
Type V: AC, CC, DT disruption
Type VI: inferior displacement or clavicle Type IV+: surgery

Arm About Presentation & Exam Diagnostics Treatment

Elbow •MC dislocation in children •extreme pain, swelling •AP and lateral x-ray Stable: REDUCE: steady, downward
Dislocation •>80% posterior •flexed elbow traction of forearm
•inability to bend elbow (extend) •posterior splint at 90 degrees flexion
Mehcanism: FOOSH •marked olecranon prominence •NSAIDS

•associated with ulnar collateral Physical Exam Unstale: ORIF

ligament disruption and fx of radial •extreme tenderness over elbow
head or medial epicondyle •deformity Refer: cant reduce, instability >3wk,
neurovascular injury

Radial Head •Subluxation of the radial head due to •child avoiding using the arm •X-rays are typically normal •Reduction
Subluxation sudden pulling force on the child’s -Usually not ordered unless - Flex elbow w/ forearm in supination
(Nursemaids) arm Physical Exam there is a hx of fall or trauma or the OR:
•Pain over the radial head & arm slightly child continue not to use arm -Extension w/ forearm in pronation
Mechanism: lift, swing, pull flexed

Medial •inflammation of the pronator teres- •pain w/ wrist flexion & forearm pronation •AP and lateral radiographs •activity modification, RICE. NSAIDS
Epicondylitis flexor carpui radialis •tenderness over medial epicondyle •MRI is helpful in confirming •surgery if refractory (4-6 weeks)
“Golf Elbow” •pain worse with pulling activities *not necessary
Causes: repetivite overuse, excessive
wrist extension

Lateral •inflammation at tendon insertion of •pain in the lateral elbow and forearm with
Epicondylitis extensor carpi radialis brevis activities involving wrist extension
“Tennis muscle •more severe & occur at rest or with
Elbow” minimal activity (holding a cup)

229
 About Clinical Presentation Diagnostics Treatment
Humeral Mechanisms: •pain, swelling, bruising, decreased ROM AP & axillary lateral views •minimally displaced < 1 cm
Fracture •FOOSH •arm held in adducted position •initial test -sling, analgesics, PT
•direct trauma
Physical Exam •2 part fx greater tuberosity > 0.5cm
Risks: young or elderly patient •if forearm & hand appear pale à r/o axillary *proximal humerus/humeral head is -surgery
artery injury common site for metastatic fx in breast CA
•the most common 2 part •RULE OUT RADIAL INJURY in humeral Operative: ORIF for open, vascular or nerve
fracture occurs at neck hsaft pfracture injury

Clavicle •most common bony injury
Fracture Causes: FOOSH, sports, MVAs
Groups:
I: midshaft (middle 1/3) (MC)
II: lateral (distal) third
III: proximal (medial) third
•pain increases with shoulder ROM AP and 10 degree cephalic tilt views
•swelling, tenderness, bruising, bulging confirm diagnosis
•grinding or crackling w/ ROM
•sagging of the arm downward and forward Complications:
•skin may appear tented •pneumothorax, hemothorax
•CC ligmanet disruption
•nerve injuries
non-surgically: figure 8 splint / sling
Proximal 1/3: ortho consult
•surgical repair for open, shortened or
fractures associated with neurovascular
compromise

Arm About Presentation & Exam Diagnostics Treatment

Distal Humeral Mechanism: FOOSH •swelling, echhymosis, deformity AP and lateral xray: FAT PADS Stable, nondisplaced:
Fracture •pain around the elbow •lateral fat pad: bleeding in joint •long arm posterior splinting x10days
“Supracondylar Patterns: •worsens with flexion of elbow •posterior fat pad: always pathologic
Humerus •complex •anterior fat pads: nml “sail sign: Displaced fractures: ORIF
Fracture” •communiuted Types:
•intra-articular A: fracture is non-articular Refer: displaced, neurovascular, patients
B: fracture is partially articular small part that fail to regain motion
remains in continuity with shaft
C: fractures are articular and no fragment Complcations: medial & brachial nerve
remains in continuity *Y and T injury à Volkmann ischemia (claw)
•radial nerve injury

Radial Head Mechanism: FOOSH
Fracture
Types:
Type I: Nondisplaced/minimal
Type II: Partial fractures with
displacement >2 mm
Type III: Comminuted fractures
Type IV: fracture of radial head w/
dislocation of elbow joint
•Pain & swelling of the lateral aspect of the AP and lateral Radiographs Type I and II: long arm 90 degrees
elbow •FAT PADS: posterior or displaced
•May be concomitant with an elbow anterior Type III: ORIF
dislocation Type IV: closed reduction
•Crepitus with passive forearm rotation
Referral
•Type II or greater
•Failure of conservative TX or persistent
pain with limited ROM

Fracture •Easily fractured and occurs with a
Olecranon direct blow to the elbow
Mechanism: direct blow
•Pain worse on flexion AP & Lateral x-ray
•May see ulnar nerve compression
•swelling of the entire elbow joint Non Displaced:
•Tenderness of Olecranon Process •Posterior long arm splint with elbow in
90o flexion for 4-6 weeks
•F/u xray in 7-10
•Protected ROM in ~2-3 weeks
Nondisplaced: posterior long arm splint w/
in 90 degree flexion x4-6wk
Displaced Fractures: ORIF
Referral
•displaced, open, malunion, neurovasc

230
Hand Exam and Diagnostics Treatment Bennett Fracture Rolando Fracture
Fracture of The most frequently occurring fracture •Acute pain, tenderness, AP & lateral xray: forearm and wrist Stable: closed reduction
Distal Radius in adults swelling, and deformity *may want to due an xray of the elbow •sugar tong splint x2-3 weeks
(Colles and •pain worse with passive •Colles: dorsally displaced or angulated
Smith) Mechanism: FOOSH motion •Smith: ventrally displaced or angulated Unstable/comminuted: ORIF

Colles: distal fragment dorsal (back) Physical Exam Colles Complications:

•deformity and bruising •extensor pollicus longus tendon rupture
Smith: distal fragment ventral (front) • “Silver Fork Deformity” (MC)
-fx of ulnar styloid Process •malunion or nonunion, median nerve
•Garden Spade (smith fx) colles smith

Lunate •lunate does not articulate with both the •swelling, pain of wrist AP view: lunate appears triangular Emergent closed reduction and splint à
Dislocation capitate and the radius • “peice of pie” sign ORIF *EMERGENCY
and Fracture Fracutre:
*near pinky Mechanism: high energy while wrist is •most serious carpal fracture due Lateral View: volar displacement and tilt Fracture: immobilization
extended and ularly deviated to avascular necrosis • “spilled tea cup” sign

Fractures of •metacarpal fracture of base of thumb •pain with thumb movement AP and lateral x-ray Thumb splica splint
Base of •tenderness, swelling over the •Bennet: fragment articulating with trapezium
Thumb (1st) Mechanism: CMC joint •Rolando: Y sign Bennet: immobilization
Bennet and •axial force to flexed thumb
Rolando Rolando: ORIF, esternal fication, closed
Bennet: 2 pieces, oblique, non- reduction w/ pinning
comminuted
Rolando: Y-shape intra-articular Rolando-
fracture; comminuted
Bennet

Fracture of •MC carpal bone fracture •pain worse ulnar deviation Ulnar Deviation PA/olique view •thumb spica splint
Scaphoid •MC in young adult males •Marked tenderness of the •may ne normal for 2 weeks •referred to orthopedic surgery
(Navicular) anatomical snuffbox (radial *if there is snuffbox pain then treat likfe FX
*near thumb Mechanism: FOOSH surface of wrist)
•Decreased ROM & strength
Complications: nonunion, avascular
necrosis (radial artery

Boxers •Fracture of the 5th metacarpal neck •pain along 5th metacarpal •x-rays •ulner gutter splint 60 degree flexion
Fracture •MC in distal phalanx •swelling, ecchymosis •reductoin first if FX >25-30 degree
•distal fragment rotated angulation
Mechanism: direct trauma against a
closed wrist (boxers) >40 degree angulation: ORIF

Gamekeeper •tear of ulnar collateral ligament – •Pain and weakness of pinch •clinical, xray •thumb splica splint and referral
(Skiers) instability at MCP joint grasp (valgus stress)
Thumb •Pain, swelling, ecchymosis Complete rupture: surgery
Mechanism: forced abduction around thenar eminence

231
Pelvis Overview Clinical Presentation Diagnostics Adverse Outcomes and Treatment
Hip •occurs when femoral head is •severe pain in the hip/groin X-Ray: AP of pelvis, AP & lateral femur •EMERGENCY
Dislocation displaced from the acetabulum •unable to move LE •normal: femoral head and joint equal •reduction ASAP: closed reduction
•MC is posterior •other MSK injuries with it •posterior: head smaller & superior -rule out femoral head FX and intra-
•anterior: head larger, inferior, medial articular loose bodies before reducing
Cause: Physical Exam: •post-reduction xray/CT
•trauma (MVA, fall) •posterior: shortened, hip flexed, Complications: •neurovascular assessment
adduction, internal rotation •osteonecrosis is MC early complication
Mechanisms: - sciatic nerve palsies -may not appear for 2-3 years Post-Reduction:
•Posterior (MC): axial loading on •sciatic nerve injury (posterior) •abduction exercises, use walking aid in the
adducted femur •anterior: mild flexion, abduction, •femoral nerve injury (anterior) OPPOSITE hand until walk without limp
•Anterior: axial load on abducted external rotation •DVT
& externally rotated - femoral nerve palsy •bleed

Fracture of •fracture of the pelvic ring and •pain in the groin, lateral hip, or •AP xray of pelvis and oblique views A and B: conservative management
the Pelvis acetabulum buttock with attempts at weight C/severe: traction and/or fixation (ORIF)
bearing or inability Stable: involve one side
Mechanism: High energy: surgery
•high impact injuries (MVA) Low energy Unstable: disrupt ring at two sites as well as Low Energy: Stable, anlagesics
•low imapc injuries •pain with attempted ROM and involvement of the symphysis or SI structure
•fall straight leg raise, antalgic gait, stance Adverse Outcomes:
shortened •Grade A: stable, minimal displacement •GU injuries
Type: open book •Grade B: rotational unstable, vertical stable •distal neurologic injuries
High energy •Grade C: all unstable •chronic pain
•pain, swelling, deformity,
ecchymosis (perineal)

Femur Overview Presentation and Diagnostics Treatment

Fracture of •MC in elderly and osteoporosis pts •limb externally rotated, abducted, short xrays: AP of pelvis and cross-table •ORIF
Proximal •pain with attemting to rotate •MRI if xray normal •surgery ASAP, delay no more
Femur Mechanism: •unable to SLR than 48h
“hip fracture” •minor/indirect trauma elderly Proximal femur fractures can be associated
•high impact in younger patients Femoral Neck with thromboembolic event, PNA, •type of repaire depends on
•INTRASCAPULAR decubitus ulcers, UTIs location
3 main types: •disruption of blood supply causing nonunion •thromboembolic prophylaxis
•femoral neck: above trochanters FX or osteonecrosis
*associated with avascular necrosis Femoral Shaft:
•intertrochanteric: between greater and Intertrochanteric/Subtrochanteric: •surgical treatment (open
lesser trochanter EXTRASCALPULAR reduction internal fixation
•subtrochanteric: below trochanters •does NOT disrupt blood supply
•more extensive repair

Femoral Mechanisms: •pain, swelling Complications: •immediate ortho consult

Condyle •axial loading •inability to bear weight •peroneal nerve injury: foot drop and •ORIF
Fractures •direct blow to the femur decreased sensation in web spaces
•popliteal artery injury

232
Knee About Presentation Diagnostics Treatment
Tibia •lower leg comprised of tibia and fibula •swelling, pain, inability to bear weight X-ray: AP/lateral •urgent refer to ortho (1-2d)
(Pilon) FX •tibia and fibula usually fractured together •OPEN FX MOST COMMON Displaced: intramedullary nailing
•MC long bone fracture: tibial shaft emergent if: open, NV injury, Nondisplaced: long leg cast x4-6wk
Compartment SX: increase and unrelenting compartment syndrome,
pain, tense swelling, pain with passive dislocation
flexion/extension of toes

Fibula FX •fibula is non-weight bearing •deformity, shortening or angulation X-ray: AP/lateral Distal FX: short leg cast
•stabilizer of ankle against eversion *however, usually normal Proximal FX: long leg cast
•twisting injury or direct blow •tenderness, swelling, bruising
Displaced/angulate, spiral, comminuted:
urgent ortho referral

F/A About Presentation Diagnostics Treatment

Fracture of •due to trauma with a twisting
Metatarsals or rotational force, or blunt
trauma (drop something on
foot)
•swelling, pain on weight bearing
•ecchymosis and tenderness
X-ray: AP, lateral, oblique of foot
Ottawa Rules à Foot
•navicular bone (midfoot) pain
•5th metatarsal pain
•inability to walk >4 steps
nondisplaced metatarsal neck and shaft:
-short leg cast or fracture brace
•multiple fx, displacement, angulation, avulsion:
-surgery w/ open or closed reduction & fixation

Stress •fracture due to overuse or •localized aching pain, swelling, X-rays: usually negative •rest, avoid high-impact activities
(March) high-impact activities tenderness •ice, splint
Fracture •worse with activity
•3rd metatarsal is the MC •loaclized bone tenderness

Lisfranc 1+ metatarsal bones are •midfoot pain, swelling “Fleck Sign” avulsion fracture of medial REFER TO ORTHO
Injury displaced from the tarus •trouble bearing weight cuneiform or second metatarsal
•tenderness of TMT joints -FX to proximal metatarsal

Jones •transverse fracture through •pain over 5th metatarsal and x-ray: transverse fracture involving the •short leg cast x6-8 weeks
Fracture diaphysis of 5th metatarsal at lateral border of foot metaphyseal-diaphyseal junction
the metaphyseal-diaphyseal
junction

Pseudojones •fracture through base •transverse abulsion fracture •walking cast x2-3 weeks
Fracture (tuberosity) of 5th metatarsal •ORIF id displaced
due to plantar flexion
Fractures of •involves proximal phalanx •pain, swelling, ecchymosis X-ray: AP radiographs •buddy taping the fractured toe to the adjacent toe
Phalanges and is a result of direct trauma •limited ROM of toe •gauze pad placed between toes to absorb moisture
*5th toe MC

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MSK About Presentation Diagnostics Treatment
Ankle Includes: •ankle pain with weight bearing Weber Classification: •minimally displaced fractures may not show
Fracture •lateral malleolus (distal fibula) •palpable gap A: below syndesmosis on x-ray, if you are suspicious then treat as fx
•medial malleolus (distal tibia) •tenderness over fractured site B: level of syndesmosis
•posterior tibia (malleolus) C: above syndesmosis Stable: short or long leg cast
•collateral ligament of talar dome
Unstable/open: ORIF
stable: one side of joint
unstable: both sides of ankle

Calcaneous/ Cause: severe trauma (MVA, fall) •severe pain, inability to bear weight X-ray: 3-view ankle xrays •posterior splint toe to upper calf
Talus FX •most involve articular surface and are •swelling and tenderness •CT •urgent referral
unstable compression of lumbar spine •most require ORIF

Maisonneuve •spiral fracture of proximal third of the •associated with distal medial •proximal x-rays
Frature fibula malleolar fracture or rupture of deep
deltoid ligament

Peds Fracture About Clinical Presentation Diagnostics Treatment

Greenstick •incomplete fracture with
Fracture angular deformity and
corticol disruption
•result of rotational force
•due to bone softness, there is a fracture
on one side of the bone and a buckle on
the other
•fracture line does not extend completely
through bone width
X-Ray: bowing •cast to prevent further movement are further
fracturing of the bone à stays on 4-6 weeks
•Tylebol

Torus (Buckle) •Incomplete fracture of •distal metaphysis where the bone is more • stable and do not require surgical intervention
Fracture one cortex spongy •can apply simple splinting for ~3-4weeks
•peds patients •may be very subtle so multiple xray •NSAIDs/analgesia
•MC site: distal dorsal views are needed
radius

Salter-Harris •fracture that involves the S: slipped à type I straight across •goal is for anatomic reduction
Fracture epiphyseal growth plate A: above à type II •fractures heal rapidly usually within 4-6 weeks
(physis) L: lower à Type III
TE: through everythingà Type IV •Type I/II: closed reduction & cast
•females 12-14yo, males R: rammed à Type V Slipped(I) Above(II) •Type III/IV: open reduction & fix (surgery)
14-16yo
If the fracture is 7+ days post injury, reduction
should be AVOIDED in children <13yo because
of risk of growth plate re-injury and growth arrest

Lower (III)

Through everything(IV) Rammed (V)

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GI
Intussusception Telescoping of an intestinal segment into adjoining distal TRIAD: Ultrasound: BEST INTIAL •Barium enema with
intestinal lumen •vomiting •donut or target sign pneumatic air or
•MCC of obstruction first 2 years of life •abdominal pain à draw legs up hydrostatic (saline)
•6-12 months of age MC • bloody stool: “currant jelly” stools Abdominal x-ray: lack of gas
•fluid and electrolyte
Risks: idiopathic, meckels, enlarged lymph nodes, tumors, FB, Exam: sausage shaped mass in RUQ Air or contrast enema: replacement à NG
hamartomas Emptiness in RLQ (Dance’s sign) DIAGNOSTIC AND decompression
THERAPEUTIC
Hirschprung Congenital megacolon due to absence of ganglion cells à •meconium ileus (failure of meconium to Contrast enema: transition zone Resection of affected
Disease functional obstruction *MC in distal colon & rectum pass in >48h) bowel
•bilious vomiting Anorectal manometry: increased anal
Risks: male, downs, Chagas, MEN II •abdominal distention sphincter pressure and lack of
•enterocolitis: vomit, diarrhea, toxic relaxation
Pathophysiology:
•failure of complete neural crest à absence of enteric Rectal biopsy: DEFINITIVE
ganglion cells (auerbach plexus) *rectal suction biopsy

Meckels’ (Ileal) Persistent portion of embryonic vitelline duct (yolk stalk, •usually asymptomatic Meckel Scan: Surgical excision
Diverticulum omphalomesenteric duct) in the small intestine •painless rectal bleeding or ulceration •look for ectopic gastric tissue in ileal
area
Rule of 2s: Complications:
•2% population, 2% symptomatic •intussuception Mesenteric arteriography or
•w/n 2 feet of ileocecal valve, 2in length •volvus abdominal exploration
•2 tissues, 2 years old, 2x MC in males •obstruction

Tissues: gastric (MC), pancreatic

GI
Paralytic Ileus Loss of peristalsis of the intestine (STOP)
without structural obstruction
Causes: surgery (abdominal and pelvic),
peritonitis, meds(opiates), illness, infection,
metabolic (low K, high Ca)
•N/V obstipation (severe const.) Labs: CBC, CMP •Complete bowel rest
•Abdominal distention with tympany è IV fluids/TPN, NG tube
Abd X-ray: dilated loops of bowel •Slowly advance diet *gas=good
Exam:Diminished/absent BSs with no transition zone •Activity
•Remove drugs that reduce intestinal
motility

Volvulus •Torsion bowel à bowel obstruction
Location: Sigmoid (MC!), cecum
•crampy abdominal pain, distention X-ray: “bent inner tube” •Endoscopic decompression
•N/V, constipation “coffeebean sign” (proctosignmoidoscopy) à elective
•tympanitic abdomen à U shaped appearance of the air- surgery
•fever, tachycardia, peritonitis filled closed loop of colon, loss of •IV Fluids
hausta
Neonates: bilous vomiting, colicky pain
GI series & CT: “birds beak”

Splenic Rupture Spleen is MC organ injured with trauma •abdominal pain, hypotension, shock FAST abdominal exam Incomplete rupture: endovascular
or Laceration embolization
Causes: L sided rib fracture, blunt abdominal •Kehr sign: referred left shoulder pain due to
trauma, infectious mono irritation of diaphragm and phrenic nerve Complete: splenectomy

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GI
Toxic Total/segmental non-obstructive colonic dilatation •colitis present for at least 1wk prior XRAY (best!): •Complete bowel rest
Megacolon (>6cm) + toxicity to onset •Transverse or R colon is dilated, •bowel decompression: NG tube
•Profound bloody diarrhea 6-15cm supine •fluid and electrolyte replacement
Causes: •abdominal pain, distention, N/V •broad ABX: Ceftriaxone +
•Complication of IBD (ulcerative colitis) •toxicity: fever, AMS, tachycardic, 3+ of following: Metronidazole
•infectious or ischemic colitis hypotension, dehydration •fever >38C
•volvulus •pulse >120
•diverticulitis PE: FAT BAT •neutrophil leukocytosis >10,500 •DC all antimotility agents (opiates,
•Fever, AMS, Toxic •anemia anticholinergics)
•BP low, abd pain, tachycardia
AND 1+ of following:
•hypotension
•altered mental status (AMS)
•dehydration
•electrolyte abnormalities

Chronic Ischemic bowel disaese due to mesenteric •chronic, dull abdominal pain that is Angiography: DEFINITIVE Revascularization
Mesenteric atherosclerosis à decreased supply during worse AFTER MEALS (Angioplasty with stenting or bypass)
Ischemia increased demand (eating) •anorexia (aversion to eating)
•weight loss
Risk: Atherosclerosis

Acute •Abrupt onset of small intestine hypoperfusion •Crampy, abdominal pain Labs: leukocytosis, lactic acidosis, •NPO, rest, fluids
Mesenteric *MC in superior mesenteric artery •Bloody diarrhea increased hematocrit, increased •SURGERY-revascularization or
Ischemia •N/V/D amylase resection
Causes: emboli (A-Fib), thrombus, shock, cocain, •Pain control, anti-emetics
vasopressors •HALLMARK: pain out of DX:
proportion •CT angiogram (initial)
•Arteriography: DEFINITIVE

Ischemia Colitis Decreased colonic perfusion à inflammation •LLQ pain, crampy CT Abdomen: 1st test •Restore perfusion
•Bloody diarrhea •”thumbprinting” à segmental •bowel rest
MCC: hypotension or atherosclerosis •abdominal tenderness bowel wall thickening •IV Fluids
*superior and inferior mesenteric arteries •observe for perforation
*MC splenic fixture & rectosigmoid junction Colonoscopy
•segmental ischemic changes in areas
Risks: elderly, DM, cardiac cath, MI, sontipcation of low perfusion
inducing medications

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GI
Small Bowel Partial/complete mechanical blockage of SI “CAVO” WBC: Leukocytosis Non-Strangulated: NPO, IVF
Obstruction Crampy abdominal pain Severe: Bowel decompression (NG
Etiology: Post-surgical adhesions (MC), Abdominal distention Abdominal X-Ray: Multiple air tube)
Incarcerated hernia (2nd), Crohn, Vomiting fluid levels in a “step-ladder”
Intussusception, Malignancy (MCC large Obstipation (late) appearance, dilated loops Strangulated: Surgery
bowel)
PE: Distention, High-pitched tinkles CT: Transition zone (dilated loops
Types: Visible peristalsis (early) with contrast to no contrast)
Closed vs Open: closed - Occluded at 2 points Hypoactive (late)
Partial vs Complete: complete - Obstipation
Distal vs Parietal: distal - More distention less
vomiting

Appendicitis Obstruction of lumen of appendix à
inflammation and bacterial overgrowth
MCC of: Acute abdomen 12-18 yo
Etiologies
Fecalith & Lymphoid hyperplasia (MC),
Inflammation, Malignancy, FB
MCC Children: Lymphoid hyperplasia due to
infection
Anorexia & Periumbilical/Epigastric pain then CBC, UA, B-hCG Appendectomy
RLQ pain (12-18 hours), N/V (vomit after pain) *laparoscopic preferred
Appendiceal Inflammation: Stimulates nerves CT Scan: IoC
around T8-10 -> Vague periumbilical pain. Once
the parietal peritoneum becomes irritated it US/MRI: Pregnant, Kids
radiates to RLQ
Retrocecal Appendix: Atypical (Diarrhea),
+Rectal/Gyn exam *appendix may be pelvic

PE: Rebound tenderness, Rigidity, Guarding

McBurney’s Point Tenderness: RLQ pain
*1/3 rt anterior superior iliac spine & umbilicus
Rovsing: RLQ pain w/ LLQ palpation
Psoas: RLQ pain w/ rt hip flex/extension (SLR)
Obturator: RLQ pain w/ internal/external
rotation of hip with flexed knee

Small Bowel 24-40% adenocarcinomas in the duodenum •Abdominal pain: intermittent & crampy Diagnosis usually delayed à poor •Surgery
Carcinoma •N/V, wt loss, jaundice outcomes •Chemo if (+) lymph nodes
Risks: hereditary, CF, Crohns, alcohol, sugar, •Anemia
red meat, salt-cured, smoked foods •CT scan
• (+) CEA •Wireless capsule endoscopy

PULM About Presentation Diagnostics Treatment

Pneumo- spontaneous:
thorax •primary: no lung disease, atraumatic
-rupture of subpleural apical bleb
-tall, thin males 20-40yo
•secondary: underlying lung disease
traumatic: penetrating or blunt,
iatrogranic ((+) pressure, CPR)
tension (EMERGENT)
•Sudden chest pain CLINICALLY Tension Pneumothorax:
-pleuritic, unilateral, non-exertion •Needle aspiration (14-16G) à chest tube
•Dyspnea CXR: expiratory view upright -2nd ICS at midclavicular line
•decreased peripheral markings •Oxygen 2-4L nasal cannula
Physical Exam: •companion lines (visceral pleural line
•diminished breath sounds & TF running parallel to ribs) Small Primary (<3cm):
•hyperresonance to percussion •deep sulcus sign •observation and oxygen; repeat CXR in 6hr
•mild tachypnea
•pneumothorax under tension Chest CT, bedside US: large or unstable Large Primary (>3 cm):
-increased JVP •needle or catheter aspiration v. chest tube
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•air entering pleural sac -systemic hypotension
•MCC: cardiopulm, (+) pressure -pulsus paradoxus Stable Secondary: chest tube + hospital

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PULM
Pulmonary Obstruction of pulmonary blood flow due to a blood clot Symptoms: EKG: tachycardia, S1Q3T3 Oxygen, IV Fluids if needed
Embolism (thromboembolism) •Dyspnea (sudden onset)
•Pleuritic chest pain CXR: Stable
Risks (Virchows Triad): •Hemoptysis (pulm infarction) •normal is MC Anticoagulation
•venous stasis: immbolization, sitting > 4 hours, surgery •Cough, wheeze •atelectasis •Heparin or LMWH + Warfarin
•intimal damage: trauma, infection, inflammation •Hamptoms Hump: wedge shaped •Dabigatran, Rivaroxaban, Apixaban,
•hypercoagulability: medications, protein C or S PE: infiltrate due to infarction Edoxaban
deficiency, Factor V Leiden, antithrombin III deficiency, •tachypnea, tachycardia •Westmark Sign: avascular
OCP use, pregnancy, malignancy •hypoxemia; rales markings distal to PE IVC Filters
•hypotension and syncope •if anticoagulation is CI or
•JVD & S3 and S4 sounds ABG: respiratory alkalosis and unsuccessful or RV dysfunction seen
•(+) homans: calf pain w/ dorsiflex hypoxemia à acidosis on echo

PERC (PE rule out criteria) D-dimer: if low suspicion Unstable:

•age <50 years old BP <90, acute RB dysfunction
•HR <100 VQ Scan: •Thrombolytics
•O2 95% or greater *pregnant, increased creatinine •Thromboembolectomy (if TPA is
•no hemoptysis •poor perfusion, good ventilation contraindicated)
•no estrogen use
•no prior DVT or PE Helical (Spiral) CT: BEST
•no unilateral leg swelling Pulmonary angiography: GOLD
•no surgery/trauma requiring
hospitalization 4 weeks prior Wells Score >6: high, 2-6: mod
+3: DVT, alt dx not likely
+1.5: HR >100, VTE hx,
immobilization for 4 weeks
+1: malignancy, hemoptysis

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PULM About Presentation Diagnostics Treatment
Acute MC form non-cardiogenic •rapid onset of profound DYSPNEA CXR: •Non-invasive or mechanical ventilation
Respiratory pulmonary edema within 12-48h af •bilateral pulm infiltrates -CPAP-full face ≥ 5 (mild disease)
Distress •SOB, tachypnea, intercostal •AIR BRONCHOGRAMS -PEEP ≥ 5 (mild, mod, or severe disease)
Pathophysiology: retractions, crackles •spares costophrenic angles •Treat underlying cause
•diffuse alveolar damage and •hypoxemia (no response to O2)
surfactant ABG: severe hypoxemia refractory to PEEP ((+) end-expiratory pressure)
•increased permeability of the •multiple organ failure: kidney, liver, supplemental O2 -prevents alveolar collapse
capillary-alveolar barrier CV, CNS •Mild: PaO2/FiO2 201-300 -give at lowest effective levels
•acute hypoxemic without •Mod: PaO2/FIO2 101-200 -does not improve mortality
hypercarbia HALLMARK: diffuse alveolar •Severe: PaO2/FIO2 <100 -risks: barotrauma, pneumothorax, auto-peep
damage
Risks: Absence of cardio pulmonary edema
•critically ill (gram - sepsis) •pulmonary wedge <18mmHg
•trauma, aspiration
FB Aspiration Common items: food (MC peanuts), SUDDEN onset of choking, cough, CXR: air trapping Rigid Broncoscopy to remove FB
coins, toys, balloons dyspnea, wheezing, assymetric breath
sounds Rigid bronchoscopy: MC on the R side (wider, vertical, shorter main
MC age is 2 years old DEFINITIVE DIAGNOSIS bronchus)

OBGYN About/Rsiks Presentation Diagnostics Management

Placental Separation of the placenta either partially or totally •Sudden onset of abdominal •DIAGNOSIS OF EXCLUSION •fluids and blood if needed
Abruption from its implantation site before delivery PAIN •CBC, CMP, PT/PTT/INR, blood type •emergenct OBGYN consult
•vaginal bleeding -possibly emergent C-section
Cause: hemorrhage into decidua basalis •uterine tenderness •transabdominal US à TVUS
Complications:
Risks: MCC bleeding in THIRD •May be associated with elevated AFP •hypovolemic shock
•maternal HTN TRIMESTER •DIC
•trauma, uterine fibroids, lupus Speculum and digital pelvic exam CI unltil •AKI (hypovolemia)
•increasing maternal age, past abortion Exam: US r/o placenta previa •Couvelair uterus: extravasation of
•Preeclampsia, smoking, cocaine •tender, rigid hypertonic blood into uterine musculature &
uterus beneath serosa
•NO PELVIC EXAM -myometrium “blue-purple” tone

Placenta Placenta that is implanted either over or near •PAINLESS vaginal bleeding
Previa internal cervical os usually after the second C-Section performed in complete,
trimester (28 wks) major degrees, and fetal distress
Classifications:
•Placental previa: os covered partial or complete *uterine body is remodeling to
•Low-lying: implantation in lower uterine segment form the lower uterine
•partial: partial coverage segment à internal os dilates
•marginal: adjacent to internal os (<2cm away) à bleeding occurs

Risks: maternal age, mult. gestations, C-section,

smoking, high MSAFP, preveious previa

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