Cardiovascular System;

Cocaine induced chest pain;

Etiologies; there is coronary vasopasm,

Management; B-blockade is contraindicated in the setting of cocaine use.

ACS;
Anxiety, vomiting, chest diaphoresis ST elevation in 2,3,4, AVF; ACS, acute myocardial
infarctation----severe medications; often administration—ASA, clopedgril, NO, heparin
- MI; ischemia, dependant on oxygen delivery and demand. Both will reduce VR and
decreased preload---reduce MI oxygen demand, NO decreased VR.

Thoracic Aortic Injury:

Patients who present after high speed MVA; CTA is a gold standard for aortic disruption and in
more experienced hands, it is highly sensitive and specific test for aortic dissection;

White Coat HTN; this will have elevated blood pressure in the office but normal blood pressure
in the physician; ambulatory pressure not in the hypertensive range; management is with
regular home monitoring.

Smoking Cessation;
These can be reduced if the patient has a second MI by approximately 50%

Ventricular Arrhythmia;
The most common cause of death within 24 hours of MI is ventricular arrhythmia, it will result
from electrolyte disturbance with ANS inbalance and conduction abnormalities

Ventricular Tachycardia (VT)

Since the patient has been shocked, and there was no response, it is important to adminisiter
amiodarone, however, if there is no response, lidocaine and magnesium are responsible.
Restrictive Cardiomyopathy; this is a result from decreased compliance, that will lead to
impaired ventricular filling, this is caused by idiopathic and autoimmune disorders, diabetes or
infiltrative diseases
- These include amyloidosis, sarcoidosis, and lysosomal storage diseases

B-blockers and Diabetes;

B-blockers are problematic agents for diabetes as they mask the effects of hypoglycemia,
making it hardert to detect hypoglycemic episodes. It can inhibit hepatic gluconeogenesis’s

CHF; this will present with cough and dyspnea and have many comorbidities; this includes HTN,
COPD, and a history of MI
- THe goal of treatment; will be loop diuretics
Endocarditis;
THis will have symptoms of mitral stenosis, this will have dyspnea, pulmonary edema
, this will have elevated LA, increased dyspnea, inceased pulmonary pressures and hoarseness.
Other factors; include oslners nodes, hemorrhages, and IE
+ blood culutres and echo for vaulvar lesions
-

Ruptured Abdominal Aortic Aneurysm

USPSTF, Abdominal US at age 65 reduce risk of aneurysm, there is dyslipidemia, aspirin, b
blockers, and ACE inhibitors. This is a focal dilation > 50%, there will be a crescent shaped ring
in the lumen of the aorta

Risk factors.

Dilated Cardiomyopathy;
DCM; this will be caused by MI, It will also be precipitated by acute events like viral myocarditis,
chronic alcohol use, B1 deficiency and Chagas disease, Cocksackie B, cocaine, danorubicin,
doxorubicin,
-

Restrictive Cardiomyopathy;
This is going to be with carcinoid tumour, this will originate in the GI tract, lungs and the
primary sites, - it can metabolize in the liver.
- There will be flushing and diarrhea that will occur in metastatic carcinoid sundrome.

HOCM;
Overview; this will have characteristic findings of HCM, this will show systolic crescendo and
decrescendo murmurs. There will be increasesd murmur size with valvsalva maneuver, this is
because there is less fluid present

Unstable Angina;
History; angina-----defined by the presence of typical chest pain occurring at rest, at physicial
minimal activity (crescendo), frequency duration. Unstable StEMI, NSTEMI ----ACS, progressive
chest pain

Statin Therapy Initiation;

ACA and AHA, this will recommend treatment with morderate and high intensity statin
DM patients are always high risk, those with moderate intensity statins.
CV disease equiilant, include CHD, Carotid artery disease, PVD and abdominal aortic aneurysm,
and diabetes

ASCVD,
Risk factors > 21, and LDL > 190
4075, diabetics 70-189
Primary prevention, therefore the patient will benefit with a statin

Cardiac Enzymesl
The highest peak represents cardiac troponins, these are serially tested at presentation and are
the most sensitive biomarker, MI will be detected 406 hours

Mitral Stenosis
Clinical presentation there will be progressive Sob, non-productive cough, rhonchi and diastolic
mumur with mumur suspicious for mitral stenosis; there will be an opening snpa and chest x-
ray showing that the patient has afib

Pathogensis;, streptococcus pyrogenes,

Management; warfarin for afib

Abdominal Aortic Aneurym;

AAA; this is asymptomatic until rupture
Risk factors; atherosclerosis,
Diagnosis; abdominal US will show dilated aorta

IVC Syndrome;
THe patient presents with supne hypotension and peripheral edema, this will manifest with IVC
syndrome,this will reduce preload, and reduce XC and CO.

Acute Pericarditis;
Overview; the patient presents with pleuritic chest pain, viral illness, ECG will demonstrate
diffuse ST elevation. There will be characteristic pericardial friction rub

PVD;
Clinical presentation, this will include pain at rest, there is also going to be interventions such as
lifestyle, pain at rest, nonhealing ulcers and disabiling claudication
Management, usually via graded exercise,

Constrictive Pericarditis;
There will be viral causes, will present post radiation and cardiac surgery
Labs will show calcification and fibrosis, this will limit CO and equalize pressures in the cardiac
chamber
There will be dyspnea, JVD and edema but there will be an absence of S3/S4

Cardiac Tamponade;
Risk factors; there will be linked to HF.
Symptoms will show distant heart sounds and pulsus paradoxis, and electrical alternans,
Diagnosis; we need to do an echocardiogram

Pulmonary System;
Classic triad, wheezing, short breath, symptoms include exercise, cold air, exposure
- There will exercise, cold air, exposure and respiratory infections.
- There will be FEV1, there is FVC and RV, TLC (total volume in inhalation)

Obstructive lung disease; there is difficulty in expiring

Sillicosis;
Overview; the patient has worked in a steel mill and has a 4 week history of clear to yellow
sputum production

Sarcoidosis; there will be worsening dyspnea, cough, fever, fatigue, malaise

- African Americans; 10 x more likely than causasians to have sarcoidosis; this will be
caused by ctivation of IFN-y; there will be managed with prednisone
-

Lung Cancer
There will be a 50 pack year smoking history with presentation to the PCP with dyspnea, cough
and blood tinged sputum with blood tinged sputum with moon like faces- truncal fat
distribution with 2 cm solid central lumen; there will be suspected for SCLC;

Other manifestations; Cushing syndrome; this is not the only paraneoplastic syndrome with
LEMS

Acute Rhinosinusitis;
THis is defiend as lasting < 4 weeks, there will be resolve spontaneously
Pathogenesis viral
Management; this will be with saline irrigation and glucocorticoids.

Sarcoidosis;
Presents with cough, fatigue, and history of arthritis; lymphadenopathy---diffuse pulmonary
infitrates; CXR; lymphoma, TB, and fungal infection; there is with hypercalcemia, and erythema
nodusum---sarcoidosis
- Noncaseating;, would be necessary definitive diagnosis
- T cells; macrophages---African American,
ACE, uveitis, lymphadenopathy, ertyehma nodosum

Adenocarcinoma
This is the most common type of lung cancer, this will be associated with hypertrophic
pulmonary osteoarthropathy
- This wil be characterized by soft and osseus tissue.
- HPOA; this is a common paraneoplastic tumor and can cause proliferation of the soft
and osseus tissue.
- There is synovial effusion effusion of large joints and periostitis.

Dyspnea;
Causes
HF, COPD
Infection
Bronchiectasis
Interstitial lung Disease
Egg like calcifications

Lung Cancer Screening; ;

Note that the woman has a 55 year smoking history, lung cancer screenin, 55-80
- Manage with low dose CT

COPD:
Patient is 59 year old and has a history of chronic cough and smoking, she also has low O2
saturation
FEV1 will assess disease severity but will not always correlate with the risk of exasperation
There are different stages
1. Mild COPD; this will cause mild airflow limitation
2. Moderate COPD; with wosening airflow with SOB develops during exertion, the patient
see medical attention
3. There will be worsening airflow with reduced exercise capacity that will impact QOL

Pulmonary Embolism;
The patient presents with dyspnea, pleuritic chest pain and low grade fever, signs and
symptoms
Symptoms began after he got off a plane, the immobility is a risk factor
Manage with anticoagulation, most common agents are LMWH

Sarcoidosis;
Overview this will be associated with bilateral chest infiltration, there will be granular and bony
mets and an elevation of ACE converting enzyme
- This will lead to hypercalcemia, with elevated `1, 25 OH2
A1 blocker receptors;
Baroreceptors in the carotid, they will detect decreased blood flow as the blood pools in the
legs due to gravity, as a result, we see a SNS response which stimulates a1 adrenergic receptors

Small Cell Lung Cancer

Presentation; there will be non-productive cough, unintentional weight loss
Clinical features; HTN, hirsutism, purple striae
Risk factors; smoking history
Management; chemotherapy with cisplatin and etoposide

Asbestos;
The patient will have multiple calcified plaques,
Overview; there wil be interstitial lung disease that will present three decades post initial
exposure, there will be dyspnea on exertion----
Complications; resp failure and cor pulmonale
Bronchogenic carcinoma and malignant mesothelimioma

ARDS;
Presentation; the CXR will show bilateral pulmonary opacities; suggestive of ARDS
THis will occur in the setting of diffuse lung disease---
Diagnosis is made with Berlan definition
- There will be low tidal ventilation,

OSA; this is characterized by excessive daytime sleepiness,

Pathogenesis; there will be collapse of the upper airway
Diagnosis; polysonography,
Management; lifestyle modifications, weight loss, smoking and avoidance of alcohol
However; at the acute level; we will do CPAP

COPD due to a-1 antitrypsin deficiency

There will be associated with fatigue, which will show dyspnea on exertion, FEV: FVC < 0.7
Etiology; the most common cause in a young age is A1AT, this will be in patients homozygous
for the Z allele and will cause panacinar emphysema

There will be inbalence and decreased a1AT actvitiy

Ears/Nose and Throat

Overview; this patient is an avid surfer, he is experiencing ear pain accompanied by discharge,
this is regarded as malignant otitis externa, this is most commonly caused by pseudomonas
aureginosa. This is supported by infection at the external auditory meatus
Dermatology;
Melanoma, has assymetric borders, color variation, diameter and evolutionary changes over
time

Margolin Ulcer
Chronically inflamed ulcers, scars, increased risk for carcinoma, there will be aggressive
malingnancy, there will be a change within a surrounding ulcer.

Paransal Sinusitis;
CT scan is the main diagnosis for the paranasal sinus. We will use a more extended study first.

Endocrinology;
Cushing Syndrome; this will have increased abdominal fat, fatigue, bruising with no obvious
trauma, there will be cushing disease, this is caused by hypercortisolism by excessive adenoma
secretion.

Pathogenesis; increased ACTH from pituitary adenoma leads to hyperstimulation of the adrenal
glands, there will be central obesity . we use dexamethasone to delineate from Cushing
syndrome.

Secondary Parathyroidism;
This will present with severe renal disease, back pain and radiologic findings; increased bone
turnover; with secondary PTHism; there will complex with calciu; leads to hypocalcemia;
- 1,25 dihydroxyitamin D; decreased absorption of calcium

Mechanism of PTH
- Increased osteoclastic resorption; normalize serum calcium this can lead to osteitis
fibrosa cystica; it will develop osteitis fibrosa cystica

Hypoparathyroidism; laryngeal nerve ijury; tingling----hypocalcemia, hypoparathyroidism, if

this removed during thyroidectomy.
Coverstek sign; (tapping of the facial nerve causing contraction of facial muscle )
- Enlarging hands/feet
- Dropping of right upper eyelid, contraction----right pupil (Horner)
- Chyle leak; direct injury;

Papillary Carcinoma of the Thyroid

This will present as a subacute mass with lack of weight change, temperature intolerance; there
will be fibrovascular cores and psammoa bodies with cleaved large nucleoli (orphan annie eyes)

Anaplastic carcinoma; this will present with progressive mass effect symptoms such as
hoarseness and difficulty breathing.
Follicular carcinoma; this will show a solid, trabecular or follicular growth

Familal Hypercalcuric Hypercalcemia;

THis is an autosomal dominant disorder caused by a CsR leading to hypercalcemia, hypocalcuria

and mild hypermagnesemia; heterozygotes typically have beningn hypercalcemia

Parathyroid Adenomas;
There will be recurrent nephrolithiasis with flank pain, there will demonsrate an elevated PTH,
leading tp PTH adenoma.
Management; surgical intervention

Struma Ovariae; this will present with weight loss, loose stools, fatigue, anixiety, and high T3
and low TSSH, with a normal thyroid gland and the absence of exogenous

Struma ovarii; this is a thyroid tissue within the ovarian gland most likely a teratoma.

HHS; this will have hyperglycemia with hyponatremia; this will be linked to type II DM, this will
dilutee the serum osm.

Malinngering;
Patient has insulin dependant diabetes, and the patient has been stressed
- This means that factitious hyperglycemia, leads to hypglycemmia,
- THis will cause confusion, fatigue, anxiety swearing and tingling.
- There is decreased c peptide and elevated inslin

Graves Disease During Pregnancy

Hyperthyroidism
This will have TSH secreting antibodies that will cause graves disease
- This is seen in both pregnan women and non pregnant women,
- Risk factors; will cause spontaneous abortion, premature labor, preeclampsia, and
maternal HF
- Management, PTU; this will prevent thyroperoxidase.

DKA; there will be increased thirt, frequent urination, abdomianal pain, there is also cataracts,
- There will be macrovascular complications including CAD, PAD and gastroporesis

Gastrointestinal System:
The patient is experienced intermittent positive diffuse esophageal spasm
DES; is characterized by spontaneous, uncoordinated (non-influenza)----chronic presentation, of
DES is characterized by spontaneous, uncoordinated contractions of the esophagus with normal
lower esophageal with normal lower Es pressure
- Fatigue, progressive dysphagia---retrosternal chest pain, there is not always dysphagia
 - Globus; or feeling food is very common

Esophageal cancer; less likely, there is decreased appetite, hoarsness, will relax smooth muscle

Osler Weber Rendu; Fatigue easily; signs and symptoms-----multiple telangectasia

Pathogenesis; AD—hemorrhagic, AVMs and aneurysms
Bleeding in GI tract

Ectopic ACTH from Cushings

Overview; there is fatigue, weight gain and fat deposition in the back; resulting from ectopic
ACTH production from SCLC, there will br excess cortisol, other findings are fatigue, weight gain,
polydipsia

- Should not respond to high and low dose dexamethasone

Carcinoid Syndrome
Risk factors; flushing and wheezing, will show elevated 5HIAA, this will result from hormone
producing tumours through the neural crest cells.
Location; bronchi, ileo jejunum and rectum, there will produce an inactive form in the liver.
Labs; include electron dense neurosecretory granules

Diabetes
Associations with obesity and clearly elevated level of Hba1c, there will be risk for DM and will
show urine microalbumin indicating peripheral neuropathy

Primary Adrenal Insufficiency

There will be weight loss, dizziness, anorexia, weakness, and increased skin pigmentation
Diagnosis; measure the serum cortisol level. And we can delineate primary, secondary and
teritiary.

Primary Adrena Insufficency

Overview there will be generalized weakness, hypotension, and hyperpigmentation
There will be hyperpigmentation in the gingiva and oral mucosa

Diagnosis; there will be measuring of the morning cortisol level.

Nephritic Syndrome;
There is respiratory infection, edema and HTN; there is hematuria and proteinuria----igA
nephropathy; this is the most common gross hematuria ----IgA levels

Primary Adrenal Insufficiency;

There will be deficiency in hormone production, glucocorticoids and mineralocorticoids
 - There will be signs and symptoms such as asthenia, skin, pigmentation and eight loss
- Management; consyntropin stimulation test

Dextrose 50,
There will likely going to allievate the symptoms
Sulfonylureas, are mild secretogauges

Allergy and Immunology

Overview; this is a three year old boy with reddish/purplish rash on the buttocks, there is pain
in the legs (this is the classical tetrad of HSP)
It is associated with intussusception.
- There are high antistreptolysin O titers; this is with post infectious
- glomerulonephritis, oligura, edema, and HTN

Hyperthyroidism;
Clinical presentation, fatigue, weight loss, tachycardia and tremors
This is suggestive of hyperthyroidism, the labs revela normal T4/T3, this is subclinical
hyperthyroidism,
Most patients are asymptomatic or exhibit hyperthyroid symptoms.

Medullary Cancer of the Thyroid;

Clinical picture, solitary firm thyroid mass, there will be amyloid deposition
Presentation, medullary cancer of the thyroid
THis is associated with Men2a, this will have medullary cancer of the thyooid, hyperPTHism,
pheochromocytoma
- To prevent pheochromocytoma, will need to check urinary metanephrines

Renal and Electrolytes;

Patient presents with generalized edema, this is due to nephrotic syndrome, membranous
nephropathy is the most common cause with white adults and is idiopathic. There is association
with anti-phospholipase A2, Management is controversial for this

Pseudohyperkalemia; this will cause peaked t waves, the management for psuedohyperkalemia
should be considered. The next best step is to have another sample for K+ drawn

Poor phlebotomy technique; traumatic venipuncture, prolonged touriniqut time

Way to remember causes for hyperkalemia
Machine Drummer (Medications, acidosis, cellular destruction, hemolysis, acidosis,
hyperaldosteronism, nephrons, excretion impaired, reflexes,
Pyelonephritis;
Clinical presentation; dysuria, flank pain, fever, and CVA
Pathogenesis; ascending UTI
Risk factors; UTI, anatomical abnormality, immunosuppression, AKI and HAP

Nephrotic Syndrome
Type II DM, this can cause nephrotic syndrome---edema, HTN and Sob, there will also be
deceased in homoral immunity
Risk factors; DM, others include minimal change disease, FSGS, amyloidosis,

Hyperkalemia;

CHF; this will cause weakness and fatigue, this will be associated with spironolactone----
furosmide can help to excrete it

Causes for hyperkalemia

MACHINE DRUMMER

MACHINE: Medications (ACE inhibitors, NSAIDs, spironolactone); Acidosis; Cellular

destruction (burns, traumatic injury); Hemolysis, hypoaldosteronism; I - excessive Intake;
Nephrons, renal failure; Excretion impaired

DRUMmER: Decreased cardiac contractility; Respiratory distress; Urinary abnormalities

(oliguria, anuria); Muscle weakness/cramps; ECG changes; Reflexes (hyperreflexia or areflexia)

Nephrogenic Diabetes Insipidus

Nephrogenic DI; this will be caused by lithium, this will prevent water resorption, this will
present with dilute urine, it will cause a urine gravity < 1.010.

VUR; (Vesiculoterine reflux)

This is associated with renal scarring,
There will be associated with bodys born with posterior urethral valves.
Pathogenesis; this will havescarring, HTN, ESRD

Primary Hyperaldosteronism
Presentation; there will be elevated aldosterone, this will act on Na+/K_ channels, this will
cause hypernatremia, alkalosis and hypokalemia
Management; can do surgery or if unable to do that will use spironolactone

Cystinuria;
There will be episodes of nephrolithiasis, there will be management with KHCO3
Pathogenesis; this is a defect in the tubular amino acid transport system

Acute Cystitis
Overview; this is a young woman who is sexually active and presents with urinary tract infection
Differential diagnosis; should include STDs, the labs will show a urinary tract infection making
this the most likely diagnosis

Clinical presentation, dysuria, hesitancy, urgency and frequency, this is the hallmark of the
urinary tract infection----manage with TMP SMX

Acute Bacterial Prostatitis;

Patient presents with dysuria, fatigue, back pain, UA will show positive leukocyte esterase

Clinical picture, abrupt onset of fever, chills and malaise, and other constitutional symptoms,
Labs will show urine culture and gram stain

Primary HTN Due to Primary Hyperaldosteronism;

There will be hyperaldosteronism and undetectable renin levels there will also be hypokalemia
and metabolic alkalosis.
There will be BAH,

Gastroenterology

Gastroparesisis; there will be postprandial nausea and vomiting along with lightheadedness,
this is suggestive of gastroparesis, this will result in autonomic neuropathy. There will be GI and
GU abnormalities
- Pathophsyiology; the postprandial glucose will damage the nerves controlling gastric
function
- Management; smaller more frequent meals, there will be slowing of gastric emptying.
Discontinue pramlintide, others that can be used are metacopramide

Crohns Disease;
There will be appropriate therapy such as infliximab,
Overview; this is a chimeric IgG monoclonal antibody against TNF a, as a result, tuberculin skin
test or IFNy test can be done.,

Esophageal Cancer
CLinicl presentation, difficulty swallowing, age > 55, history of dysphagia, alcohol and tobacco
use.
- Endoscopic imaging with biopsy, with suspicious lesion, obtaining tissue tissue is the
best way to establish the diagnosis
Liver Failure;
Patient obtained liver transplant; this will raise risk for opportunistic infections
Management; TMP/SMX, this is for 6-12 months

Hepatic Adenoma
This will present with RUQ pain and nausea, there is also a solitary hepatic mass with transient
h omogenious enhacement

DDx; HCC, focal nodular hyperplasia, and hepatocelula radenoma

Celiac Disease;
The physician will present with fatigue, abdominal cramping, and foul smelling chronic diarrhea.
Histology will show diffuse villous atrophy, and positive igA endomysial testing

Other associations; there wil be dermatitis, herpatiformis, tere will be be papulovasular lesions.

Celiac Disease; there will be passage of bulky and foul smelling stools and poor weight gain;
This will also be known as a gluten sensitive enteropathy; there will be failure to thrive,
malabsorption associated with ingestion, weight loss with gluten products

Pathophysiology; HLA-DQ2, DQ8

Colorectal Cancer Screening;

The patient is > 52m with no associated medical or family history who has never obtained CRC
screening. Patient should be screened for CRC between ages of 50-75

Sigmoidoscopy 5 years or FOBT, 3 years FIT; every year

Colorectal Cancer;
Presentation, there will be bright red blood per rectum, signs of anemia and dyspnea
- The type II DM will be because insulin is a stimulant, colonic tumor cells.
- There is a hypothesis; insulin and IGF1, will promote colon cancer cells,

CHro

Barretts Esophagus
There will be dyspepsia and dysphagia as well as cough with a bitter taste in the throat
There will be transition to columnar epithelium
Infectious Disease;
Tetanus Exposure;
This should be administered as soon as possible, for dirty and large wounds administer tetanus
specific immunoglobulin and tetanus.

Viral Rhinosinusitis vs Bacterial sinusitis;

This will be caused by streptococcus pneumonia, haemophilius influenza and Moraxella
catarrhalis

HIV Infection; HIV viral load no matter the level must be started on HAART therapy, there will
be reduction of HIV transfmission; early ART ca improve the symptoms

Spontaneous Bacterial Peritonitis;

Clinical presentation, abdominal pain, fever, hypotension, AMS and rancid breath
SBP, this will be an intraabdominal etiology, it will cause advanced liver cirrhosis. Most
commonly caused by chronic alcohol use.

SBP > 250, there is portal HTn,

SAAG; > 1,1m ut is trasudative
SAAG < 1.1, this will be caused by infarction, serositis, and nephrotic syndrome.

Eiknella;
There will be a fight bite, it will cause clenched fist when striking tooth.
- There will be oral flora with eiknella, will be susceptible to antibiotics.

Clostridium Difficile;
Overview; the patient presents with sudden onset crampy pain, there will be multiple episodes
of watery diarrhea, this is most likely C. Diff, this is a gram positive obligate aneorbe, this is
associated with treatment with clinda, cephalosporine and floroquinolone.
- Clindamycin, floroquinolone, cephalosporins, penicillins and macrolides

Tinea Capitis; this is caused by trichophyton tonsurans, this will be a gray patch, the condition
doesn’t respond with topical antifungals

Cellulitis;
This will manifest with recent injury to the left leg while fishing, he has redness
Given the exposure to saltwater; this will be caused by vibrio parahemolyticis this will emerge
in the warm summer months however, it can be acquired

Keratoconjuctivitis Sicca;
Infectious keratoconjunctivitis; secondary to HSV virus infection, photophobia, foreign body
sensation, and constricted pupil, ----fluoroscein stating, will be with HSV keratitis.
Managemet; acyclovir

Haemophilus Influenza;
Chancroid; caused by painful lesion with exudates---multiple lesions, hemophilis; painful lesions
with exudate
HSV/syphilis,-----treatment is with a single gram dose of azithromycin (orally---chancroid is a
single dose 250 IM

Molluscum Contageiousum;
THis will be caused by DNA poxvirus; this will be very unusual for an adult; this will be found in
the perigenital and perianal areas;

HAART therapy;
THe patient was most likely affected by HIV during blood transfusion, there will be risk of
developing thrush.
Prevention; HAART

TB;
Silocosis; this will show hilar lymphadenopathy, small opacities. This is diagnosis with small
rounded opacities.
Risk; Tb, radiographich findings will show hilar infiltrates.

Acute Silicosis;
Sandblaster is suspicious----sign of cor pulmonale, loud second heart sound. Pulmonary atery
HTN, and the prominent A wave, acute silicosis,

Mycoplasma TB:
Clinical presentation there will be going to be Tb, focal infiltration, mycosis and other organism.
- There will be hilar enlargement

Fever of Unknown Origin

 38.3 C, there will be caused by neoplasm, infection, tissue damange and miscellaneous
causes
 CXR will be an initial screening tool for FUO

Lyme Disease Management/Prevention

The patient presents with characteristics of secondary lyme disease, this can manifest months
to years post tick bite
- Manage with ceftriaxone, cefotaxime if cannot use doxy
Hematology-Oncology
B12 deficiency; this will have a two month history fo generalized weakness and symmetric
numbness, this will also associate with pale conjunctiva, the colalbumin deficiency is secondary
to the Crohns disease,

Role of B12; this will be critical for thymidylate synthase, and without we can see impairment in
synthesis
- There will be hypersegmented neutrophils and macrocytic anemia

Burkett Lymphoma, there is severe onset of abdominal pain, there will also be linked to
intussusception
- There are three times of BL, endemic (Africa) sporadic nonendemic, and
immunodeficiency and there will be abdominal associated
11:14, Mantle Cell Lymphoma
11: 22, Ewing Sarcoma
9:22, CML

Multiple Myeloma;
This is a malignancy in which the plasma cells fill the bone marrow ad other cell lines; there will
lead to osteolytic lesions and osteopenia that can manifest as bone pain; it will manifest in the
appendicular skeleton
- MM this will require organ or tissue impairment and bone marrow biopsy revealing
plasma cells

Sickle Cell Trait;

Hemoglobin electrophoresis; will show sickle cell trait
Pathogenesis, this will be a point mutation in the B chain, valine to glutamate, there will be only
sickle in the renal medulla.

ITP; this will present with isolated thrombocytopaenia, nosebleeds consistant with ITP; there
will be a generation of antiplatelet antibodies; this will follow viral prodrome
- There will be mucocutaneous bleeding and thrombocytopaenia
- > 30000, observe, with < 27000, must use IVIG

Amyloidosis
Roloux Formation is associated with impaired kidney function, there will be light chains, this is
in association with multiple myeloma. Other associations include increased risk for infection.
- There will be widespread changes with amyloidosis including HF, edema, macroglossia

Rheumatology and Orthopaedics;

Summary; there will be back pain, kyphosis, and dexa scan < -2.5,
USPSTF, we need to measure for women 65 or older, there will be compared to BMP of a 20-30
year old
Risk factors, advanced age, glucocorticoid therapy, low body weight, cigarette smoke, alcohol in
excess, RA, DM, and IBD

Management; first line will be alendronate and risendronate

Multiple Myeloma;
Deep venous; malignancy, hypercoagulability disorders (factor V leiden, DVT)
Risk factors; DVT, full anticoagulation therapy-----antithrombin and PE
IV heparin, low molecular weight heparin

Spinal Stenosis;
Clinical presentation, there will be pain in the the lower back which worsens with lumbar
flexion and there is decreased sensation over the distal aspect of the lower extremities.
- This is a classical description of neuroclaudication (Spinal stenosis)

Rheumatoid Arthritis;
Clinical picture; there will be worsening pain, swelling and stiffness of the hands and fingers.,
the treatment wll be directed towards controlling the synovitis,
- There will be started on the DMARDS (methotrexate, hydroxychloroquine, sulfasalazine
and lefolonmide)

AML: there will be fatigue and easy bruising, there will also be pallor, bony tenderness, and the
lab will show leukocytosis, anemia and thrombocytopaenia.
- Tihis will e due to Auer rods
- Auer rods are pathonomonic, they will be associated with DIC leading to increased
bleeding, widespread ischemia, infarction and dysfunction
- Epidemiology; there will be associated with peroxidase

Ankylosing Spondylitis;
Presents with lower back and gluteus muscles----increasing in severity of several months.
AS; chronic inflammatory, axial skeleton most common 20-30,
HLA-B27;
- AS, chronic inflammatory back disease- 3 months,
- Associated with uveitis, dactylitis, good response---bamboo spine
- One of the most common things is unilateral eye pain, blurred vision, and photophobia.

Giant Cell Arteritis;

It will present in people over 50, there will be unilateral and bilateral in association. There is
also pain in the temporal region.
Histology; will show subacute granulomatous inflammation
Key associations; polymyalgia rheumatic will cause weight loss, myalgia and arthralgia
Management; high dose steroids.

Paget Disease;
There will be history of hearing loss, and dull aching pain,
Pathogenesis; there is increase osteoclast activity
Labs; show elevated ALP and normal electrlytes
Complications; osteogenic sarcoma

Granulomatosis with Polyangitis;

Presentation, there will be sinusitis, hemoptysis and fatigue as well as bibasilar crackles and
granulomatous inflammation
- There will be infiltration o of the medium sized arteries.
- There will be progressive crecentric glomerulonephritis.

Polyarteritis Nodosa;
Presentation, fatigue, purpuric skin rash, and AKI with mild proteinuria , there will be a medium
vessel vasculitis,
MR angiogram will show aneurysm.

In sum, PAN is a necrotizing vasculitis thatwill affect the medium vessels of the kin and vessels.
This will be associated with neural lesions, and purpura.

HLA B27;
There will be chronic back pain and this is worst in the morning,
There will be improved during the day and post exercise
Key associations; there will be linked to HLA-B27, this will linked to low back pain,
Other associations, with achillis tendonitis and planter fasciitis.

Imaging; will show fibrotic and abnormally fused spine

Epidemiology
This study involves folks who are exposed to a risk factor and a control group, there will
determine a relationship between sun exposure and skin cancer.

Reative risk; risk of comparing disease in an exposed population to the disease in the general
population,

Male Reproductive System;

This will present with lower urinary tract symptoms, including increased weakened stream
This is suggestive of BPH
Managememtn, a-1 antagonists (Tamsulosin, and terazosin) first line, second line, finasteride
Social Sciences;
THe patient while having signed for the procedure, she is allowed to change her mind, we
should wait until the anesthetic wears off and then assess the patients desires

Error Disclosure
Physicians are obligated to disclosure to patients and documents errors made in their care. The
error is harmless because the patient discovered the mistake---taking the wrong medication.

Elder Abuse; The patient has dementia and is brought to the ED by caregiver; because of the
inconsistent history; the patient presents with signs of elder abuse
- Major risk factor; dementia, motor impairment, blindness and deafness; for any
suspicion of child or elder abuse, we must report it to authorities; such as adult
protective services