CARDIOLOGY

Cardiomyopathy
-A group of diseases of the myocardium associated with mechanical or electrical dysfunction that usually exhibit ventricular hypertrophy or dilation
-Current major society definitions of cardiomyopathies exclude heart disease secondary to CV disorders such as HTN, CAD, or valvular disease
-Etiologies may be genetic, inflammatory, metabolic, toxic, or idiopathic
Type Info Signs & Symptoms Workup Management Prognosis
Dilated Cardiomyopathy: -Common etiologies: viral, -CHF -Treat CHF symptoms
dilation and impaired contraction genetic, alcoholism -Arrhythmias -ICDs
of one or both ventricles -Systolic dysfunction -Sudden death -Eval for transplant
-Exercise intolerance
-Fatigue or weakness
-Dyspnea
Hypertrophic Cardiomyopathy: -Caused by genetic mutations -Varied presentation, may be asymptomatic -Differential: athlete’s -β-blockers to reduce O2 -Annual
disorganized hypertrophy of left -Diastolic dysfunction -CHF heart (physiologic LVH), demand mortality of 1%
ventricle and occasionally right -Usually asymptomatic until -DOE: the most common sx HTN, aortic stenosis -CCB to reduce -May progress
ventricle childhood or adolescence -Orthopnea and PND -Valsalva will increase contractility and improve to dilated
-Athletes with underlying -Exertional chest pain HCM murmur and diastolic relaxation cardiomyopathy
HOCM at greater risk for lethal -Atypical chest pain decrease aortic stenosis -Pacer or AICD
arrhythmia during exertion -Syncope and presyncope murmur -Surgical myectomy,
-May have abnormal SAM -Palpitations -EKG: prominent Q mitral valve surgery, or
movement of mitral valve -Postural hypotension waves, P wave ethanol ablation to
-Fatigue abnormalities, LAD destroy thickened
-Edema -Echo septum
-Arrhythmias -Holter monitor
-Harsh crescendo systolic murmur ± mitral -Exercise stress test
regurg -Screen relatives
-S4
-Displaced apical impulse or thrill
-Sudden death
-Stroke
Restrictive Cardiomyopathy: -Etiologies: scleroderma, -R CHF as pulmonary pressures must increase to -Differential: constrictive
diastolic dysfunction  normal amyloidosis, genetic, HOCM, deliver blood pericarditis
contractility but rigid and stiff DM, chemo, HIV
ventricular walls -Uncommon in US
Arrhythmogenic Right -Genetic cause -Ventricular arrhythmias
Ventricular
Cardiomyopathy/Dysplasia: RV
wall replaced with fibrous tissue
Unclassified Cardiomyopathies -Includes stress-induced
cardiomyopathy and left
ventricular noncompaction

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 Giant Cell Arteritis (Temporal Arteritis)
-Rheumatic disease, most often affects med-large head & neck Signs & symptoms Workup
vessels -Weight loss -Arterial biopsy
-Usually in white patients over 50 -Night sweats -↑ ESR or CRP
-Often co-exists with polymyalgia rheumatica -Fever
-Jaw claudication Management
-Temple tenderness -Immediate steroids while awaiting biopsy results in order to prevent blindness
-Vision loss with pale optic disc -Monitor for thoracic aortic aneurysm (increased risk)
-New headache
-Scalp tenderness

Arrhythmias
Bradyarrhythmias
-Either a delay in impulse formation or conduction Signs & symptoms Management
-Syncope or presyncope -Treat underlying cause
Etiologies -Dyspnea from CHF -Meds
-Hypoxia -Angina pectoris -Pacemaker or transcutaneous pacing
-↑ ICP -Hypotension -Emergent: atropine
-Hypothermia
-Hypothyroid Differential
-Hyperkalemia -Regular rate  sinus brady, complete heart
-Sarcoidosis or amyloidosis block, 2:1 AV block, sinus arrest with escape
-Degenerative disease of conduction system rhythm, “regularized” slow a-fib
-Ischemia -Irregular rate  sick sinus syndrome, 2° AV
-Lyme block (Wenckebach or Mobitz type II), slow a-fib
-Rheumatic heart disease
-Drugs: CCBs, β-blockers, digoxin
Tachyarrhythmias
-Either a result of abnormal impulse formation or Signs & symptoms Workup
abnormal propagation (reentry) -Syncope or presyncope -Labs to exclude underlying exacerbating conditions: BMP, Mg, digoxin levels, TSH
-Risk factors for SVT: hyperthyroid, HTN, mitral -Palpitations
valve disease, COPD, post cardiac surgery -Diaphoresis Management
-Risk factors for VT: prior MI, ischemia, long QT -Chest pain -Cardioversion for any tachyarrhythmias if there is hemodynamic instability; add
syndrome, antiarrhythmics, TCAs, hypoMg, hypo amiodarone if VT is involved
or hyperK Differential -Transcutaneous pacing for torsades
-Narrow complex afib, multifocal atrial -If stable SVT, can try vagal maneuvers, adenosine, beta blockers, CCBs, or digoxin
tachycardia, aflutter, atrial tachycardia, sinus -For stable VT, lidocaine is DOC
tachycardia, WPW, junctional tachycardia, -Atrial fibrillation or flutter: control ventricular response with CCB, beta blockers, or
AVNRT digoxin, and consider anticoagulation with warfarin; can electrically or chemically
-Wide complex  torsades, polymorphic VT, AF cardiovert but afib may recur
with aberrant conduction, VT, SVT -VT: beta blockers if asymptomatic and nonsustained, ICD placement if more severe due to
risk of death
-Torsades: IV magnesium and phenytoin

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 AV Block
Type Signs & Symptoms/Info/Workup Management EKG
First degree -Asymptomatic -Treat reversible
-EKG showing lengthened PR interval causes such as
-Determine site of block using EKG ischemia, increased
findings, atropine, exercise, or vagal vagal tone, or meds
maneuvers -Pacemaker usually not
recommended

Second Wenckebach -Typically asymptomatic -Treat reversible

degree (Mobitz type -EKG shows progressive PR prolongation causes such as
I) for several beats prior to nonconducted P ischemia, increased
wave vagal tone, or meds
-Beats classically occur in ratios of 3:2, 4:3, -Pacemaker if there is
or 5:4 symptomatic
-Can be a result of inferior MI bradycardia

Mobitz type II -May be asymptomatic or have signs of -Treat reversible

hypoperfusion or HF causes such as
-PR interval remains unchanged prior to a ischemia, increased
nonconducted P wave vagal tone, or meds
-Most patients will
require a pacemaker

Third degree -May have dizziness, presyncope, syncope,

v-tach, v-fib, worsening HF, or angina
-P waves don’t correlate to QRS
-Escape rhythm takes over for QRS
(junctional or ventricular)

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 Peripheral Vascular Disease
-Risk factors: smoker, DM, HTN, ↑ lipids, obesity Workup
-Ankle/brachial index: PVD if <0.9, will have intermittent claudication if <0.7, pain at risk if <0.4,
Signs & symptoms impending necrosis if <0.1
-LE disease: claudication (ppt by exercise, relieved by rest) in butt, hip, thigh, calf, or foot;
diminished peripheral pulses; femoral bruits; nighttime pain from ischemia Management
-UE disease: difference in systolic BPs between aroms, arm pain with exertion, dizziness -Smoking cessation
during arm exertion (subclavian steal syndrome) -Walking program
-Cool skin or abnormal skin color -Antiplatelet therapy
-Poor hair growth -Revascularization if necessary via open surgery or stent
-Ulceration or tissue necrosis -BP, lipid, sugar control
-Signs of atherosclerosis elsewhere in the body
Deep Venous Thrombosis
Signs & symptoms
-Palpable cord
-Calf pain
-Ipsilateral edema, warmth,
tenderness, erytema

Workup
-Homan’s is only + 50% of the time
-Determine probability with Well’s
criteria  < 2 indicates unlikely, >
6 highly likely
-Further investigation using D-
dimer
-US for at least moderate Well’s
score

Management
-Immediate anticoagulation with
heparin, LMWH, or fondaparinux
-Lytics or thrombectomy for select
cases
-3 months of anticoagulation for
initial distal DVT or consider IVC
filter if not a good candidate
Aortic Stenosis (Aortic Valve Stenosis)
-Causes obstruction  ↑ LV Signs & symptoms Workup
pressure  LVH  CHF -May have asymptomatic murmur early in disease: harsh systolic < > -EKG for LVH
murmur at RUSB, with radiation to the carotids bilaterally -CXR for cardiomegaly
-Echo is diagnostic
Etiologies -Late: DOE, SOB, angina, syncope, CHF, PND, orthopnea, carotid pulsus
-Age-related calcification parvus et tardus Management
(inflammation + lipids, -Sudden cardiac death -Proven benefit with statins
accelerated with bicuspid -Arrhythmias -Valve replacement if symptomatic
aortic valve) -Endocarditis -Aortic balloon valvotomy as bridge to surgery or for palliation
-Rheumatic fever -Bleeding predisposition
Prognosis
-High risk of sudden death without valve replacement (life expectancy of 2-3 years)
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 Mitral Stenosis
-Causes elevated LA pressure  LA hypertrophy  Signs & symptoms Workup
transmission of high pressures to pulmonary vasculature  -Dyspnea is commonly the only symptom -Echo to stage
pulmonary edema  possible R-sided CHF -A-fib from disruption of electrical conduction in hypertrophied
tissue Management
Etiologies -Fatigue -If asymptomatic, only watchful waiting
-Most commonly due to rheumatic heart disease -Apex murmur: loud S1 with post S2 opening snap, followed by -HTN management
-Congenital malformation low-pitched rumble -Afib management
-Connective tissue disease -RV heave with progression to pulmonary HTN -β-blockers to prevent pulmonary edema
-Pregnancy may bring on symptoms -Anticoagulation for any embolic event
-Follow with echoes every 1-5 years depending on stage
-Mitral valve replacement or balloon valvuloplasty
Hypertension
-95% of cases are essential hypertension Pharmacologic treatment options: single agents only lower by 10-20 mm Hg, may need a 2nd agents
-Secondary cause workup: renal disease, renal stenosis, aortic Thiazides: HCTZ, chlorthalidone -DOC for HTN but can’t use once CrCl < 30
coarctation, hyperaldosteronism from tumor or hyperplasia, -Ca sparing = good for osteoporosis pts
Cushing’s, pheochromocytoma, OSA -Need to check BMP before and after starting
-May hear S4 from forceful atrial contraction -Chlorthalidone has the most evidence but my preceptor thinks
it causes a lot of hypokalemia
JNC- 7 classifications and initial treatment of HTN Loops: furosemide
-Pre-HTN is 120/80 to 139/89  lifestyle changes K-sparing: spironolactone, eplerenone Not very potent
-HTN stage I is 140/90 to 159/99  thiazide (or loop if renal pt)
-HTN stage II is >160/>100  thiazide + 2nd agent ACEIs: benazepril, enalapril, lisinopril -Cough
-Can cause renal failure = need to monitor BMP 1 week and 1
Hypertensive urgency = stable or no end organ damage, no month after starting and periodically after that, STOP if serum
raised ICP Cr ↑ by 30%
-May have SOB, headache, BPs usually > 220/110 -Ok to use in patients with no renal function left
-Tx is to lower BP in clinic slowly over several hours -Pregnancy D
(≤160/100) with labetalol, clonidine, captopril ARBs: irbesartan, losartan, olmesartan, valsartan -Same AEs as ACEIs and also pregnancy D
-Close follow-up CCBs: dihydropyridine (nifedipine, amlodipine) and non- -Useful in the elderly
dihydropyridine (verapamil and diltiazem) -FDA warning about amlodipine, verapamil, and diltiazem use
Hypertensive emergency = rapidly progressing end organ with simvastatin
damage -Contraindicated in heart failure
-Papilledema if malignant Other direct vasodilators: hydralazine, minoxidil
-Chest pain, AMS, weakness, MI, acute CHF, renal failure, α-blockers -Clonidine: only for refractory HTN due to risk of falls
ICH, eclampsia, aortic dissection -Methyldopa: DOC for HTN in pregnancy
-Don’t lower BP by more than 25% original value
β-blockers -Questionable role in the treatment of essential HTN unless
Monitoring HTN: patient also has CHF or MI
-Annual urine microalbumin -Need strict β-1 blockers for asthma/COPD patients so that
-Annual BMP bronchial relaxation is not blocked (atenolol or metoprolol)
-Annual lipids -Propranolol and labetalol block at multiple sites
-Baseline EKG, look for LVH -Can mask signs of hypoglycemia
-Contraindications: heart block

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 Preferred drug classes for initial treatment of HTN with comorbid conditions
Diabetes MI CAD CHF Pregnancy Older patients CKD Recurrent stroke
Thiazide β-blocker Thiazide Thiazide Clonidine CCB ACEI/ARB prevention
β-blocker ACEI β-blocker β-blocker Methyldopa Thiazide
ACEI/ARB AA ACEI ACEI/ARB ACEI
CCB CCB AA
Bacterial Endocarditis
-Mostly affects the elderly Signs & symptoms Workup
-New regurgitant murmur -Blood cultures x 3
Agents -HF -EKG
-Staph aureus is most common -Evidence of embolic events -Echo
-Viridans strep -Peripheral lesions (petechiae, splinter hemorrhages, Roth  Use Duke criteria to determine probability
-Enterococci spots, etc)
-Fever Management
Risk factors: IVDU, prosthetic heart valve, structural heart -Prosthetic valves may need to be replaced
disease, prior endocarditis -Empiric therapy initiated with IV vanco, gentamicin, and either
cefepime or a carbapenem; subsequent AB therapy targeted to
Prevention culture results
-New guidelines from AHA suggest only prophylaxing the -Treat for at least 6 weeks
highest risk groups prior to procedures likely to result in
bacteremia: prosthetic heart valves, h/o endocarditis, unrepaired Prognosis
cyanotic congenital defect, repaired congenital defect with -Complications are common: heart failure, stroke and other embolic
prosthetic material, cardiac valvulopathy in a transplanted heart events, perivalvular abscess, pericarditis, fistulas, aortic valve
-Usual AB is amoxicillin 2 g 30-60 min prior to procedure dissection, meningitis or encephalitis
-In-hospital mortality rate of 18-23%
-6 month mortality rate of 22-27%
Acute Myocardial Infarction
Signs & symptoms Workup Additional STEMI Treatment
-Sudden onset chest -Obtain 12 lead within 10 min of arrival and repeat every 10 minutes if initial EKG is -Antiplatelet and anticoagulant therapy for all patients (in addition to aspirin)
pain, nausea, vomiting, not diagnostic (1st EKG is negative 40% of the time) -Emergent stent if < 3 hours from symptom onset
-Alternative is lytic therapy if not contraindicated, symptoms < 12 hours, and PCI
diaphoresis, SOB -Look for early peaked T waves, ST elevation, Q waves, J point elevation
unavailable within 90-120 minutes
-Jaw, neck, scapular, -NSTEMI does not have EKG changes because the infarction is in an electrically -CABG rarely performed during acute MI
throat, or arm pain silent area
-DOE -Emergent cardiac consult for patients with cardiogenic shock, left heart failure, or Additional NSTEMI Treatment
-Chest pain > 30 min sustained ventricular tachyarrhythmia -Antiplatelet therapy for all patients (in addition to aspirin)
not responsive to NG -Electrolytes, coagulation studies, H/H -Anticoagulant therapy for all patients
-Hypovolemia -Serial troponins: specific cardiac damage marker, including damage from -Invasive intervention based on presence of high risk factors (recurrent angina at rest,
-HTN or hypotension defibrillation, arrhythmias, cardiac procedures, CHF, vasospasms, etc; elevation elevated troponin, ST depression, high risk stress test result, EF < 40%, hemodynamic
instability, sustained VT, recent PCI, prior CABG)
-Tachy or bradycardia begins within 1 hour and remains ↑ for 5-14 days
-S3 or S4 -CK: found in skeletal muscle throughout the body; shows up in 1-6 hours and lasts up Treatment of Cocaine-Related ACS
-Signs of CHF to 1.5 days -Benzos every 15 minutes PRN
-Systolic murmurs -CK-MB: cardiac specific CK; shows up in 2 hours and declines after 24-72 hours -DON’T give β-blockers
-Friction rub if day 2
or later Emergent Management (any ACS) Prognosis
-Remember that -Morphine, oxygen (only if sats < 90% or resp distress), aspirin, NG -33% are fatal
women, the elderly, -Treat HF if present with NG, furosemide -Complications: CHF, RV infarction, ventricular rupture, arrhythmias, mural embolus,
stroke, pericarditis, postinfarction angina
and diabetics may have -Give β-blocker if HF is not present in order to reduce myocardial oxygen demand
-For USA and NSTEMIs, can estimate 14-day risk of death, recurrent MI, or need for urgent
atypical presentations -Begin 80 mg atorvastatin for pts not already on revascularization using TIMI score (Skyscape)

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 Angina Pectoris
Stable Angina Unstable Angina
Signs & symptoms Signs & symptoms
-Gradual onset chest pain due to myocardial ischemia that occurs predictably and reproducibly on -Chest pain refractory to NG treatment or chest pain at rest or nocturnally
exertion -May be associated with SOB, nausea, diaphoresis
-May also have SOB
-Relieved by rest or NG Management
-Usually lasts 2-5 minutes -Treat like other ACS: admission, MOANS, serial troponins, EKGs
-Diffuse discomfort -Stabilize
-Antiplatelet therapy and possible reperfusion for select patients
Management - β-blockers
-Goal is to relieve symptoms and prevent future cardiac events -Statins
-Nitrates and β-blockers are initial DOCs -ACEI with DM, HF, LV EF < 40%, or HTN
-CCB for refractory symptoms -CV risk reduction
-Exercise
-Daily aspirin
-CV risk reduction: BP control, smoking cessation, statins, weight reduction, glycemic control
-Periodic reevaluation with EKGs
-Revascularization therapy an option for select candidates
Acute Rheumatic Fever
-Sequelae of GAS Signs & symptoms Management
pharyngitis 2-4 weeks -Migratory arthritis, carditis, valvulitis -Oral penicillin, cephalexin, or azithromycin
after infection (does not -Syndenham chorea: abrupt involuntary movements, -HF management if present
occur with impetigo) muscle weakness, emotional disturbance -Continuous prophylaxis against GAS (due to increased severity
-Erythema marginatum with subsequent infection) with IM penicillin G after end of
Screening -Subcutaneous nodules over bony surfaces or tendons initial treatment until 18-25 years of age, indefinitely if valvular
-Echo for children and -Fever disease is present, and for one year if reactive arthritis is present
young adults in countries -Elevated acute phase reactants
where rheumatic fever is -Prolonged PR interval
endemic -Mitral regurgitation murmur

Coronary Artery Disease

-Risk factors: age, males, FH, sedentary Chest pain differential Workup Management of new disease or worsening symptoms
lifestyle, tobacco, HTN, DM, ↑ lipids -Atherosclerosis -PE findings: S4, arterial -Referral to cardiology
-Acute MIs are a result of burst plaques  -Vasospasm from cocaine or stimulants bruits, abnormal -ER via ambulance if EKG shows new ischemic changes:
activation of clotting system  infarction -Prinzmetal’s angina: women under 50 funduscopic exam, corneal ST depression or elevation, inverted T waves or there is
-Stable angina will resolve in 2-30 minutes -Coronary artery or aortic dissection arcus, xanthelasma, hemodynamic instability
-Congenital abnormality tendinous xanthoma, CHF,
Classification -Aortic stenosis murmurs Management of stable disease
-Class I = no limitations or symptoms with -HCM -Refer for stress test if pt -LDL goal <100 or <70
normal activity -Coronary thrombus or embolus has low to intermediate -β-blocker (proven mortality benefit), CCB, statin,
-Class II = slight limitations and normal -Non-cardiac: costochondritis (reproducible on probability of CAD clopidogrel, nitrates PRN
activity results in symptoms palpation), intercostal shingles, cervical or thoracic -Refer for cardiac cath if pt -New drug: ranolazine
-Class III = marked limitation and minimal spine disease (reproducible with specific movements of has high probability of -PCP visits every 6 months: annual CBC to check for
activity results in symptoms the head or neck, causes paresthesias), PUD, GERD, CAD anemia, annual lipids, FBG
-Class IV = symptoms persist with minimal cholecystitis, PE, pneumonia, pneumothorax (dyspnea) -Cardiologist every 1-2 years
activity and rest

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 Antithrombotic Therapies
Anticoagulants: for treatment of Vitamin K antagonists Warfarin (Coumadin) -Impairs hepatic synthesis of thrombin, 7, 9, and 10
venous clots or risk of such as factor -Interferes with both clotting and anticoagulation = need to use another med
V Leiden disorder, other clotting for first 5 days of therapy
disorders, post PE, post DVT -Must consume consistent vit K
-Pregnancy X
-Monitor with INR and PT twice weekly until stable, then every 4-6 weeks

Jantoven -Rarely used, usually only if there is a warfarin allergy

Marvan
Waran
Anisindione (Miradon)
Heparin -IV or injection
-Short half-life of 1 hour
-Monitored with aPTT, platelets for HIT
-Protamine antidote
LMWH Ardeparin (Normiflo) -Inhibit factors 10a and thrombin
Dalteparin (Fragmin) -Injections can be done at home
Danaparoid (Orgarin) -Useful as bridge therapy from warfarin prior to surgery
Enoxaparin (Lovenox) -Monitor aPTT and watch platelets initially for HIT, then no monitoring
Tinzaparin (Innohep) needed once goal is reached?
-Safe in pregnancy
Heparinoids Fondaparinux (Arixtra) -Direct 10a inhibitor
Rivaroxaban (Xarelto) -Only anticoagulant that does not affect thrombin
Direct thrombin inhibitors Dabigatran (Pradaxa) -Monitor aPTT
Lepirudin (Refludan)
Bivalirudin (Angiomax)
Antiplatelets: used for arterial clots COX inhibitors Aspirin -Blocks thromboxane A-2 = only 1 platelet pathway blocked = weak
or risk of such as stroke, TIA, antiplatelet
atherosclerosis, CAD, MI, angina, -Only NSAID where antiplatelet activity lasts for days rather than hours
PVD, post PCI, post CABG, a-fib ADP receptor inhibitors Ticlopidine (Ticlid) -No monitoring needed
-May ease migraines
Clopidogrel (Plavix) -Needs monitoring during initiation due to risk of blood count abnormalities
Ticagrelor (Brilinta)
Prasugrel (Effient)
PPD inhibitors Cilostazol (Pletal) -Contraindicated in CHF
-May be useful in PVD as it widens leg arteries
-Pregnancy X
Glycoprotein IIB/IIIA inhibitors Abciximab (ReoPro) -IV only
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
Defibrotide
Adenosine reuptake inhibitors Dipyridamole (Persantine) -Strong treatments for prevention of recurrent stroke
Aggrenox
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 Congestive Heart Failure
-Most often a result of ischemic heart disease Signs & symptoms Other Management
(systolic HF)  myocardial remodeling -R CHF  ascites, + hepatojugular reflex, weight gain, JVD, -Salt restriction, daily weights
-Other causes: bad valves, HTN (diastolic hepatomegaly, edema, abdominal distension, mostly clear lungs with -Avoid NSAIDs, CCBs
HF), myocarditis, pericarditis, alcoholism (R dullness at the bases, ↑ JVP with hepatojugular reflux, tricuspid regurg, -ATP III recommends giving aspirin to reduce prothrombotic state
HF), substance abuse, COPD or other lung peripheral edema -Exercise training program for stable NYHA class II to III
disease (R HF) -L CHF (mostly heart and lung sx)  dyspnea, cough, S3 or S4, crackles, -Devices: AICD, intra-aortic pump, LVAD
-Usually associated with low cardiac output wheezes, dullness at bases, frothy or pink sputum, pulse alternans
but can be high (alternating strong-weak pulse), palpitations, fatigue, diaphoresis,
displaced PMI, mitral regurg, pulmonary edema, orthopnea, PND
Acute/flash pulmonary edema with acute  But research shows there are no hard and fast physical exam
MI, severe illness, PE, HTN, end stage differentiations for R vs L CHF; all of these s/s can overlap!
valvular disease
Workup
Beware acute HF with massive MI, -Referral for echo
tachyarrhythmias, or endocarditis with valve -EKG for LVH
rupture: severe SOB, cool skin, diaphoresis, -Stress test
AMS, pallor, cyanosis -CXR for pulmonary edema (Kerley B lines)
-Labs: BNP, CBC, CMP, fasting glucose, lipids
Decompensated HF with new or worsening -Cardiovascular MRI can help distinguish ischemic heart disease from
sx, new murmur, pt is “cold and wet”, CHF cardiomyopathy
“decision rule” predicts 30 day mortality,
avoid β-blockers

Drugs with proven mortality benefit

-Note that there is only evidence for systolic HF for these drugs; use with diastolic CHF is not yet
substantiated
-ACEI or ARB
-Hydralazine + isosorbide dinitrate: most beneficial for black man as an add on therapy to those already
on β-blocker and ACEI that are still symptomatic
-β-blockers
-Aldosterone antagonists

Prognosis
-Diet and prescription noncompliance are a major cause of hospital readmission for CHF
-Main causes of death are arrhythmia and progressive pump failure

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 PULMONOLOGY
Cor Pulmonale
-A subset of R-sided CHF where diastolic R ventricular failure Signs & symptoms Workup
occurs as a result of pulmonary HTN associated with diseases of -DOE -Concomitant pulmonary HTN workup
the lung, upper airway, or chest wall (most commonly COPD) -Fatigue
-Does NOT include R sided CHF as a result of L sided CHF or -Lethargy Management
congenital heart defect -Exertional syncope or angina -Treat underlying cause
-Usually slow and progressive but may be acute -S4 -Diuretics
-↑ JVP
-Peripheral edema
Pulmonary Hypertension
Etiologies Workup Management
-Arteriolar narrowing in the lungs (idiopathic, familial, scleroderma, portal -Diuretics for fluid retention
HTN, HIV, drugs or toxins, chronic hemolytic anemia) -Anticoagulation therapy if cause is
-Left heart disease familial, drug, or idiopathic
-Lung disease or hypoxia: COPD, interstitial lung disease, OSA, chronic -Supplemental oxygen for resting
high altitude hypoxia
-Chronic thrombotic or embolic disease -CCB
-Splenectomy -Last resort is atrial septostomy or
 May be secondary to multiple “hits” lung transplant
-F/u every 3 months
Signs and symptoms
-Dyspnea, fatigue, chest pain, palpitations, LE edema, dizziness, syncope Prognosis
-Tachypnea and tachycardia -Progressive and fatal if untreated
-Evidence of R heart failure: JVD, ascites, edema -Average time for correct diagnosis is
-Loud P2 from elevated pulmonic pressures slamming valve shut 15 months because symptoms other
-Tricuspid regurgitation murmur because it can’t shut all the way due to the than SOB may not be present and
dilation of muscle there is a lot to rule out
-Pulmonic regurgitation murmur
-Pulsatile liver

Differential
-Left CHF
-CAD
-Liver disease
-Budd-Chiari syndrome (hepatic or vena cava thrombosis)

-R heart cath showing mean pulm artery pressure > 25 mm Hg at rest is

diagnostic

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 Lung Cancer
-85% of cases occur among smokers Small cell carcinoma Differential
-Other contributing causes include radon -Metastasize rapidly to regional lymph nodes and distant sites -TB
gas, asbestos, and environmental pollutants -Classified as limited or extensive disease -Fungal infection
-2 major groups (small cell and non-small -Very responsive to chemo -Mets to the lung
cell) account for 95% of lung cancers -Remission is common but so is recurrence  overall survival of 5% -Sarcoidosis
-Other lung cancers are rarer and include
primary pulmonary lymphoma, carcinoid Bronchial carcinoid tumor Workup
tumors, bronchoalveolar cancers, and -Previously known as bronchial adenoma -Begin with CXR
mesotheliomas -Rare group of pulmonary neoplasms characterized by neuroendocrine differentiation and -F/u masses with CT
-Overall survival rate of 14% relatively indolent clinical course -Sputum cytology
-Can also arise in the thymus, GI tract, and ovary -Bronchoscopy
Non-small cell carcinoma -Surgical resection is treatment of choice -Transthoracic needle biopsy
-Arises as discrete masses within the lung -Node sampling via transbronchial biopsy,
parenchyma that can spread to regional Signs & symptoms mediastinoscopy, or mediastinotomy
lymph nodes and then metastasize to distant -Lung cancers are more like to cause paraneoplastic syndromes such as hypercalcemia, SIADH,
sites ectopic ACTH secretion, Lambert-Eaton myasthenic syndrome, and hypercoagulable states Management
-Squamous, adeno, and large cell -Nonspecific cough or dyspnea -Assess feasibility of surgical resection and overall
carcinomas -Chest pain patient health/quality of life issues
-Staged by TNM -Hemoptysis -Radiation for advanced disease or nonsurgical
-Limited response to chemo -Anorexia, weight loss, fevers, night sweats candidates
-Surgical resection of limited tumors can be -Hoarseness due to compression of the recurrent laryngeal nerve -Combination chemotherapy for candidates
curative -Facial or UE swelling from SVC syndrome -Monitoring for recurrence
-Bone, brain, liver, or adrenal symptoms
-Axillary or supraclavicular adenopathy
-Digital clubbing
Pulmonary Embolism
Etiologies Signs & symptoms Workup
-Most arise from LE DVT -Onset does not have to be sudden! -D-dimer
-Stasis: surgery, heart failure, chronic venous stasis, immobility -Dyspnea, pleuritic or anginal chest pain, cough, wheezing -ABG
-Blood vessel injury: fractures, surgery -Leg swelling or pain -Troponin
-Hypercoagulability: postpartum, malignancy, OCPs, protein -Hemoptysis -EKG showing nonspecific S1Q3T3
C/S/antithrombin III deficiency, lupus anticoagulant, factor V -Palpitations, syncope -CXR showing edema, cardiomegaly, prominent pulmonary
Leiden, prothrombin gene mutations, hyperhomocysteinemia -Tachycardia and tachypnea, loud P2 from pulmonary HTN vein, left sided pleural effusion
-Diaphoresis -VQ scan or spiral CT (preferred)
Classification -Hypotension
-Massive = sustained hypotension, pulselessness, persistent -Fever Management
bradycardia, or need for inotropic support -Homan’s sign -Give heparin while waiting for imaging results
-Submassive = pt is normotensive with myocardial necrosis -Orthopnea -Continue anticoagulation for at least 3 months
-Minor/nonmassive = normotensive with no myocardial -↓ Breath sounds -IVC filter for repeat clots or poor anticoagulant candidates
necrosis -Consider lytics for massive PE
Differential -Can be managed outpatient for select stable patients with no
-Pneumonia comorbidities
-Infection
-Obstructive lung disease Prognosis
-CHF -30% are fatal without treatment
-Msk disease -Less than 10% mortality if treated by anticoagulation
-Acute MI
-Anxiety
11
 Sarcoidosis
-A rheumatic disease Signs & symptoms Workup
-Cause is unknown -Dyspnea -Myopathies or myositis are uncommon -CXR for staging (I-IV)
-More common in black -Cough -Neurologic: CN palsies, meningitis, brain -Ophtho exam
patients -Chest pain lesions, neuroendocrine dysfunction -PFTs
-Course of disease may -Fatigue -Cardiac: arrhythmias, conduction delays, -UA
be acute and severe or -Eye manifestations pulmonary HTN, CHF, pericarditis -Labs: serum ACE, BMP
mild and chronic -Skin manifestations (with predilection for -GI: abdominal pain, esophageal -CBC
scarred or tattooed areas): lupus pernio or involvement -EKG
Differential erythema nodosum -Liver (90% of pts): jaundice, varices, -TB test
-Leukemia granulomatous hepatitis -Granuloma biopsy
-Multiple myeloma -Endocrine: hypercalcemia, goiter, thyroid  A diagnosis of exclusion
-Amyloidosis nodules
-Diabetes -Renal: calculi, failure, nephritis Management
-Thyroid or parathyroid -GU: epididymitis, AUB -Aimed at site of disease
disease -Pulm  steroids, lung transplant
-IBD -Arthralgias  steroids, NSAIDs, colchicine, biologics
-Hemochromatosis -Polyarthritis in the ankles, knees, wrists, -Steroid sparing agents: methotrexate, cyclosporine, mycophenolate mofetil,
or elbows azathioprine, cyclophosphamide
-Gum hyperplasia
Prognosis
-Acute presentation has a high rate of spontaneous resolution
Pneumonia
Microbial etiology of community-acquired pneumonia in patients Prevention with pneumococcal vaccination Signs & symptoms
who underwent comprehensive testing 23 valent -Adults over 65 -Rigors, sweats, fever or subnormal
(Pneumovax) Persons aged 19-64 years with chronic cardiovascular disease temp, cough ± sputum, dyspnea,
(including CHF and cardiomyopathy), chronic pulmonary disease pleuritic chest pain, fatigue,
(including asthma and COPD), DM, alcoholism, chronic liver myalgias, abdominal pain,
disease (including cirrhosis), CSF leak, cochlear implant, cigarette anorexia, headache, AMS
smoking -PE: pulmonary consolidation,
- Persons aged 19-64 years who are residents of nursing homes or crackles, dullness to percussion, ↓
long-term care facilities breath sounds
-Singe revaccination recommended if adult was < 65 and it was
more than 5 years ago when they got it, and in
immunocompromised 5 years after initial dose

13 valent -Adults who are immunocompromised (should get 23 valent also,

but not at same time)
-Routine for all kids under 5
-Kids 6-18 who have sickle cell disease, HIV or other
immunocompromising conditions, cochlear implant, or CSF leak

7 valent -No longer being used

12
 Outpatient Treatment Inpatient Treatment
Workup Management Workup Management
-CXR: may lag behind PE findings! Segmental -CAP  macrolide -ICU or EtOH or pleural effusion blood -Non ICU  initial therapy with anti-
infiltrates and atelectasis suggest bacterial, diffuse -Underlying comorbidity (higher risk = culture, sputum culture, Legionella & pneumococcal β-lactam (ceftriaxone,
infiltrates and hyperinflation suggest viral need to cover resistant Strep pneumo, pneumococcal antigen testing ertapenem, or ampicillin-sulbactam) +
-Urine test for Legionella enterics, Moraxella, anaerobes)  macrolide, or monotherapy with a FQ
-CBC, BMP antipneumococcal FQ, or macrolide + β- -ICU patients  initial therapy same as non-
lactam (cefpodoxime, cefuroxime, amox ICU, add vanco if suspecting MRSA, add anti-
Disposition HD, ceftriaxone) pseudomonal drug for COPD or frequent
-Use PORT score or CURB-65 to estimate risk steroid or AB users (β-lactam + FQ)
(QX Calculate app) and determine outpatient vs Prognosis -Clinical improvement should occur within 72
inpatient -Fever clears after 2-4 days of treatment hours
-ER if RR > 30, HR > 125, SBP < 90, -CXR clears after 30 days (up to 6 mos if -Switch from IV to orals with clinical
comorbidities elderly) improvement
-F/u CXR for patients over 50 at 7-12 weeks
Tuberculosis
Signs & symptoms Workup Active TB drug regimens Monitoring
-Latent or primary infection: Asymptomatic -If high suspicion, most clinics don’t workup but put a -Initial for 2 months: isoniazid, rifampin, -Sputum smears and cultures
-Active infection: cough, fever, weight loss, mask on and send to ER pyrazinamide, ethambutol throughout treatment
night seats, hemoptysis, fatigue, decreased -CXR: active infection (infiltrates in mid or lower fields, -Continuation for 4-7 months: isoniazid and rifampin -Vision checks and color vision
appetite, chest pain hilar adenopathy, cavitation, emyema) or previous testing with ethambutol
(pulmonary nodules, apical fibrosis, Ghon lesion) Latent TB drug regimens -CMP, CBC, and bili
-TB skin test, AFB smear -9 months of isoniazid or 4 months of rifampin
Bronchiectasis
-Permanent abnormal dilation and destruction of bronchial walls Workup Management
-Caused by an infectious insult + impaired drainage, airway -Abnormal CXR such as linear atelectasis or dilated and -Outpatient acute exacerbation  FQ
obstruction, or a defect in host defense (ex. FB aspiration, thickened airways -Inpatient acute exacerbation  begin 2 IV antipseudomonal
smoking, CF) -Labs: CBC, Ig levels drugs
-An obstructive lung disease -Sputum smear and culture -Chest physiotherapy
-PFTs -Inhaled steroids only for severe wheeze or cough or acute
Signs & symptoms -Chest CT is diagnostic exacerbation
-Cough
-Daily production of mucopurulent sputum for months to years
-Dyspnea, hemoptysis, wheezing, pleuritic chest pain
Pleural Effusion
-Excess fluid accumulation between the two pleural layers (pus, Workup
blood, chyle, or serous fluid) -Upright CXR showing blunting of costophrenic angles (must
be at least 300 mL of fluid to detect)
Signs & symptoms -Lateral decubitus CXR showing air/fluid levels (can detect as
-Decreased movement of the chest on the affected side little as 50 mL)
-Stony dullness to percussion over the fluid, -Thoracentesis with fluid analysis to determine transudative
-Diminished breath sounds on the affected side (HF, renal failure, liver failure) vs exudative effusion (infection,
-Decreased vocal resonance and fremitus cancer, PE)
-Pleural friction rub

13
 COPD
Chronic bronchitis = proximal predominant Management of stable COPD
-“Blue bloaters” = depressed respiratory drive with use of -Goal is to reduce exacerbations requiring hospitalization
accessory muscles  acidosis, productive cough, wheezing, -Get PFTs for diagnosis and classification of disease stage and
rhonchi, hyperinflation of lungs, cor pulmonale to follow course of disease (FEV1/FVC < 70% with FEV1 <
80% are diagnostic criteria)
Emphysema = distal-predominant -Add treatments in a stepwise fashion as needed
-“Pink puffers” = high RR/dyspnea due to damaged vascular -New drug roflumilast (PPD-4 inhibitor) indicated for severe
beds, distant breath sounds, hyperinflation of lungs, low COPD with chronic bronchitis and history of acute
cardiac output exacerbations
-Not recommended: expectorants, antitussives (COPD cough
 Can have both chronic bronchitis and emphysema, and a not centrally mediated), respiratory stimulants
subset of these patients also have asthma -Increased survival when oxygen therapy is used > 18 hours
per day
-Chronic airway inflammation  systemic release of
inflammatory cytokines  CAD, renal insufficiency, Management of acute exacerbations
neuromyopathy, osteoporosis, cachexia, downward spiral -SaβA + inhaled anticholinergic
-Airway obstruction is not fully reversible -10-14 day steroid taper
-Antibiotics if there is increased sputum purulence or vol or
Workup increased dyspnea
-PFTs demonstrating FEV1/FVC ratio < 0.70 -Supplemental oxygen to 90-94% saturation
-NPPV is the preferred form of ventilation if needed

Idiopathic Pulmonary Fibrosis

-A chronic, progressive fibrotic disorder of the lower respiratory Signs & symptoms Management
tract -DOE -No evidence that any treatment improves survival or quality of
-Can be genetic or acquired -Persistent nonproductive cough life
-Usually affects adults over 40 -Crackles or Velcro rales -Supportive care: oxygen, pulmonary rehab
-Risk factors: smoking, environmental pollution, chronic -Digital clubbing -N-acetylcysteine pills
microaspiration -Clinical trial enrollment
Workup -Don’t use steroids as monotherapy
-PFTs -Lung transplant
-Chest CT -Acute exacerbation  broad spectrum antibiotics, high dose
-Lung biopsy or bronchoalveolar lavage steroids, and azathioprine
-Labs: CMP, CBC, CK
-UA
-EKG
14
 ENDOCRINE
Hyperthyroidism
Signs & symptoms: weight loss, hyperphagia, heat intolerance, increased Differential Workup Management
sweating, frequent stools, oily hair or skin, exercise intolerance due to heart -Grave’s disease -Depressed TSH -Referral for endocrine
changes, proximal muscle weakness, nervousness, irritability, sleep -Toxic multinodular goiter with elevated free T4 workup and imaging, possible
disturbance, tremor, palpitations, decreased menstrual flow, onycholysis, -Single toxic nodule (Plummer disease) -↑ LFTs and Ca ablation
exophthalmos, lid lag, goiter, thyroid bruits, brisk DTRs, muscle cramps, -Subacute (de Quervain) thyroiditis: a result of viral -↓ Lipids -Antiadrenergics: propranolol
osteoporosis, pretibial myxedema infection, eventually leads to hypothyroid or diltiazem
-Initial destructive phase of Hashimoto thyroiditis -Antithyroids:
-Postpartum thyroiditis propylthiouracil, methimazole
-Amiodarone-induced thyrotoxicosis
-Rare: gestational trophoblastic disease, increased iodine -Untreated thyrotoxicosis can
intake, thyrotoxicosis factitia (consumption of TH), ovarian progress to a thyroid storm
tumor secreting TH, pituitary tumor secreting TSH, thyroid that can be fatal!
carcinoma

Hypothyroidism
-TSH screen recommended for all elderly with depression and Differential Workup Initial therapy
all elderly entering long-term care -Post-Hashimoto thyroiditis (most common cause) -Elevated TSH -Thyroxine with recheck of TSH in 6 weeks
-Congenital hypothyroidism -↑ LDL, TG, -For patients still having symptoms 2-3 weeks into
Signs & symptoms: cold intolerance, fatigue, heavy menstrual -Post thyroid ablation or neck radiation LFTs, CK therapy, recheck TSH and free T4
bleeding, weight gain, dry skin, constipation, bradycardia, -Transient causes: post-postpartum thyroiditis, post-de
delayed DTRs, hoarseness, coarse hair, hair loss, myalgia, Quervain thyroiditis Maintenance therapy
cognitive impairment, depression, decreased concentration, -Goiterous hypothyroidism: due to impairment of TH -Once TSH reaches reference range, recheck
decreased hearing, periorbital or facial edema, non-pitting synthesis (lack of iodine or genetic) annually
ankle edema, ± goiter -Lithium or other drug therapy -Dose needs to be increased in pregnancy and
-Central hypothyroidism: not enough TSH being made decreased with aging

Hypoparathyroidism
Etiologies Signs & symptoms Differential
-Genetic -Paresthesias in the mouth, hands, and feet -Pseudohypoparathyroidism
-Parathyroidectomy -Muscle cramps in the hands and feet -Vit D deficiency
-Autoimmune -Fatigue -Meds
-Hemochromatosis -Headaches -Kidney disease
-Mg deficiency -Bone pain -Malabsorption
-Insomnia
-Abdominal pain Workup
-Chvostek’s sign -Labs: low Ca, PTH, albumin to correct
-Trosseau’s sign
-Seizures Management
-Arrhythmias -IV Ca gluconate if severe
-Respiratory failure -PTH supplementation

15
 Hyperparathyroidism
Workup

Etiologies
-Primary hyperparathyroidsm: adenoma or other hyperplasia
-Secondary hyperparathyroidism as a response to low Ca levels (vit D deficiency
 impaired abs of Ca, or CKD  failure to activate vit D)

Signs & symptoms

-Incidental hypercalcemia finding on blood test
-Low bone mineral density screen
-Weakness and fatigue, depression, bone pain, myalgias, decreased appetite, n/v,
constipation, polyuria, polydipsia, cognitive impairment, kidney stones and
osteoporosis
-Rickets
-Osteomalacia

Differential
-Malignancy

Management
-Primary hyperparathyroidism  surgical parathyroidectomy if symptomatic,
otherwise monitor Ca and Cr annually and DEXA every 2 years
-Calcium mimics if unable to undergo surgery
Thyroid Neoplasms
Benign Follicular Cell Tumors Malignant Follicular Cell Tumors Medullary Thyroid Carcinoma
Follicular cell adenoma Papillary thyroid cancer -Arises from C-cells of the thyroid
Hurthle cell adenoma -Most common type of thyroid cancer -Age > 40
-Associated with MEN type 2
Follicular thyroid cancer -Regional lymph node involvement with mets to the lung, bone,
-Diagnosis usually occurs during evaluation of a cold thyroid nodule and liver
-Treatment is through radioactive iodine ablation with hormone replacement to suppress TSH -Evaluate serum calcitonin, CEA, Ca, and plasma fractionated
metanephrines
Hurthle cell thyroid cancer

16
 Cushing’s Syndrome
-A general term for hypercortisolism at any level, including adrenal, ectopic, or pituitary Workup
source -Always remember to check for
exogenous glucocorticoid use
Etiologies -Always do labs first before any
-Exogenous steroid use imaging to avoid incidentalomas and
-Excess pituitary ACTH production: includes Cushing’s disease (refers specifically to an false negative scans
ACTH-secreting pituitary adenoma) -Establish presence of cortisol excess:
-Ectopic ACTH production: small cell lung ca, carcinoid tumors, pheochromocytoma, 24 hour urine, dexamethasone
thymoma, pancreatic cell tumors, medullary carcinoma of the thyroid suppression test, or saliva cortisol
-Adrenal hypercortisolism: adrenal adenoma or carcinoma or hyperplasia -Establish ACTH dependence or
independence to pinpoint problem to
Signs and symptoms the adrenals vs the pituitary gland
-Supraclavicular and dorsal fat pads (“buffalo hump”)
-Central obesity Management
-Proximal muscle weakness -Surgical resection is first line
-Thinning of the skin, purple striae, spontaneous ecchymoses, skin hyperpigmentation, -Drugs to block adrenal response:
papular acne somatostatin analogs, adrenal steroid
-Osteopenia synthesis inhibitors
-Hypertension
-Early or delayed puberty
-Growth retardation
-Glucose intolerance
-Decreased libido, infertility, amenorrhea
-Nephrolithiasis or polyuria
-Headaches
Acromegaly
-Caused by GH-secreting pituitary tumor in adulthood Workup Management
-If this occurs before puberty, it is called gigantism -Initial screen is IGF-1 test, will be high -Surgery
-Most sensitive test is ↑ GH after glucose tolerance test -Somatostatin analogs (inhibit GH)
Signs & symptoms -Labs: abnormal glucose, ↑P and PRL -GH receptor agonists
-Enlarged soft tissue of the hands and feet -Pituitary MRI -Radiation
-Teeth splaying, prominent brow -GHRH if MRI is negative
-Hyperhidrosis Prognosis
-Arthralgias -Bony abnormalities usually won’t regress
-Headaches
-Hypogonadal symptoms
-Vision deficits
-Fatigue, weight gain
-Galactorrhea
-CV disease such as HTN, LVH, or cardiomyopathy
-Enlargement of thyroid, liver, kidneys, or prostate

17
 Adrenal Insufficiency
Signs & symptoms Workup
-Chronic fatigue, lack of appetite, unintentional weight loss -Morning cortisol levels: levels > 18 high enough to rule out AI, levels ≤ 3 high enough to rule in
-Joint pain AI
-Abdominal pain, nausea, diarrhea -Synthetic ACTH simulation test
-CV instability, hypoglycemia in times of stress, hyponatremia, hypotension unresponsive to -Lastly check the ACTH levels
fluids or pressors
Management
-If acute crisis, treat with IV dexamethasone and IVF for hypotension
-If chronic, glucocorticoid maintenance therapy is needed
-Primary AI will also need mineralocorticoid replacement
-MedicAlert bracelet and emergency steroid injections
-Stress dose steroids needed for surgeries
Primary Adrenal Insufficiency Secondary Adrenal Insufficiency: Tertiary Adrenal Insufficiency: Adrenal Crisis: acute, life-
(Addison’s Disease): occurs when failure of pituitary to secrete ACTH failure of hypothalamus to secrete threatening low levels of cortisol
adrenal gland does not respond to CRH
ACTH or make adrenal hormones
(including aldosterone) due to damage
Etiologies -Most causes are autoimmune -Pituitary tumor -Usually due to suppression of CRH -Underlying adrenal condition
-Infection -Radiation and ACTH by exogenous cortisol use
-Adrenal hemorrhage -Surgery
-Drugs -Long-term steroid therapy
-Megace (appetite stimulant drug)
-Sarcoidosis
Signs & symptoms -Presentation can be slow or abrupt -Slow onset -Vomiting
-Skin hyperpigmentation -No skin hyperpigmentation (because -Abdominal pain
-Salt craving there is no excess ACTH) -Weakness
-Hyponatremia -Intact RAAS -Fever
-Hyperkalemia -Confusion
-Vitiligo -Syncope
-Pallor
-Autoimmune thyroid disease
Workup -Labs showing hypoglycemia, -Insulin tolerance test -Labs showing low cortisol, low
hyponatremia, hyperkalemia, low -Metyrapone test glucose, hyperkalemia,
aldosterone, and high renin due to hyponatremia, elevated BUN
increased renal sodium losses
Obesity
-Overweight = BMI 25-29.9 Pharmacologic options Bariatric surgery
-Obesity = BMI > 30  greater risk of DM, -Catecholaminergics (phentermine, diethylpropion, mazindol): short-term -NIH recommends limiting to patients with BMI > 40, or > 35 if
stroke, CAD, early death use only obesity complications are present
-Orlistat: inhibits lipase -Results in significant reduction in deaths from obesity

18
 Diabetes Insipidus
Central diabetes insipidus Signs & symptoms Workup
-Lack of ADH production in the hypothalamus or insufficient -5-10 L per day of dilute polyuria -Direct serum ADH measurement is difficult as it is in
release of ADH from the posterior pituitary -Polydipsia extremely low concentration
-Etiologies: idiopathic, familial, panhypopituitarism, infiltrative -Hypernatremia -Pituitary imaging
diseases, metastatic tumor, trauma or surgery, Wolfram -Normal glucose -Water deprivation test: restrict water and check Na, urine
syndrome osmolality, urine output, weight, and orthostatic BPs/HRs every
Differential 1-2 hours  + if body wt ↓ by > 5%, serum Na > 145, or > 2
Nephrogenic diabetes insipidus -Inpatient: mannitol, post-op diuresis, hyperglycemia, diuretics, urine osmolalities differ by < 10%
-Kidney is resistant to ADH overzealous IVF, cured acromegaly -Differentiate central vs nephrogenic by giving desmopressin
-Etiologies: amyloidosis, myeloma, Sjogren’s, sickle cell, -Outpatient: hyperglycemia, psychogenic polydipsia, osmotic (synthetic ADH)  central DI if urine vol ↓ or there is > 50% ↑
hypercalcemia, recovery from ATN, Li, foscarnet, methicillin, load in urine osmolality, nephrogenic if there is < 50% change in
demeclocycline, colchicine urine osmolality
Diabetes Mellitus
Prevention: 7% TBW loss, food journals, and visiting Signs & symptoms: Blurred Prevention of complications Glycemic control
dietician regularly better than starting on metformin vision, fatigue, polyuria, -Diabetic retinopathy, cataracts, -If A1c 6.5-7.5  start on metformin unless
polydipsia, weight loss, glaucoma  annual eye exams contraindicated
Screening hirsutism (DM2), acanthosis -Nephropathy and ESRD  BP and -If A1c is 7.6-9%  start on metformin + additional oral
-ADA says do for all patients who are overweight or who have nigrans (DM2), DKA (more BG control, ACEI, annual urine -If A1c is > 9%  start on insulin if symptomatic or
risk factors, and for all patients over age 45 every 3 years likely DM1) microalbumin (should be < 30) metformin + 1-2 other orals if asymptomatic
-FBG: prediabetes is 100-125, diabetic is 125+ -DM is a cardiac risk equivalent  -Initiate insulin if 3+ orals are needed to control BG or if
-Oral glucose tolerance test: prediabetes is 140-199, diabetes is Other tests cholesterol control (LDL < 100, A1c remains > 8.5 even after dual therapy
200+ -C-peptide: ↓ in DM1, normal HDL > 50, TG < 150), baby aspirin -Rebound (Somogyi) hyperglycemia occurs in response to
-Random glucose test: diabetic if 200+ or hi in DM2 (ADA rec) hypoglycemia
-Hb A1c: diabetic if > 6.5%, want DM to be < 7%, check this -Fructosamine (glycated -Neuropathy is the most common -Dawn phenomenon is morning hyperglycemia as a result
every 3 mo if it is not at goal or 1-2 times per year for patients albumin): gives info about complication: cardiac denervation, glucagon response to waning insulin levels around 3-5 am
at goal short-term BG in last few gastroparesis, neurogenic bladder,  change insulin or move peak to a more physiologic
weeks ED, etc. time
Oral Pharmacologic Treatment: most are not for DM1, they have no insulin to secrete!
Sulfonylureas Biguanides: metformin GLP-1 agonists: exenatide pen, long-acting exenatide,
-1st gen: chlorpropamide, tolazamide, tolbutamide  more -Decrease hepatic glucose output 1st and then increases uptake liraglutide
AEs by fat and muscle -Aid native GLP-1 naturally released by the gut to help insulin
-2nd gen: glipizide, glyburide, glimepiride  don’t work better -May help with weight loss secretion while reducing glucagon
but have less AEs and less drug interactions -Every DM2 should be put on this at time of diagnosis -Only respond when BG is high!
-Hug pancreas all day long = tend to burn out pancreas after 3- -Must monitor creatinine @ baseline and annually to screen for -Need to be paired with a DPP-4 inhibitor like sitagliptin,
5 years of use kidney disease (from the DM, not from the metformin itself), saxagliptin, or linagliptin
-Hypoglycemia risk stop using if Cr > 1.4 in women and 1.5 in men  risk of lactic -Need to decrease sulfonylurea dose to avoid hypoglycemia
-Start on low dose and adjust over 3-4 weeks acidosis -Contraindications: pancreatitis, gastroparesis, GI issues, CrCl <
-Begin combination therapy with another agent when -Contraindicated in kidney or liver disease, elderly, CHF, 30, thyroid cancer
approaching max dose alcohol abuse or binge drinking, IV contrast -Many drug interactions, must take 1 hour prior
Meglitinides: repaglinide, nateglinide Glitazones: pioglitazone, rosiglitazone Amylin agonists: pramlintide α-glucosidase inhibitors: Bile acid Dopamine
-Hug pancreas with one quick squeeze -Increases glucose uptake in fat and muscle -Aid amylin, which is co-secreted with insulin, to acarbose, miglitol sequestrants: agonists:
= take with a meal 1st, then decreases hepatic glucose output suppress glucagon secretion and regulate gastric -↓ Glucose abs in the colesevelam bromocriptine
-Hypoglycemia risk -Current FDA restrictions due to risk of emptying intestine -Only used if patient -Only offer
-May cause weight gain = less bladder ca, fracture risk, CV side effects = try -Can be used in DM1 but at lower doses -Cause farts needs lipid modest
favorable other meds first -Rarely used because it only serves to fine-tune -Contraindicated in bowel management as well as decreases in
-No renal or liver patients -Contraindicated in liver disease, heart failure blood sugar control while doubling the number of disorders, liver or renal DM and can’t tolerate A1c with
-Pregnancy C -Pregnancy C injections needed impairment a statin significant GI
-Contraindicated with GI disorders side effects

19
 Insulin
Formulations Initiating insulin in DM2 Initiating insulin in DM1 Switching from NPH to long-acting insulin: if
-Rapid: aspart, glulisine, lispro  30 minute peak = before each meal -Avg size patient  begin with -Calculate total daily dose, which is 0.5- NPH was once daily, a unit-to-unit change is ok;
-Short (may be purchased without rx): regular  2 hour peak = before each 10 U basal insulin once daily 0.7 U/kg/day in adults if NPH was 2x daily, ↓ total dose by 20% and
meal give it as a once daily dose
-Obese patient  begin with 0.2 -Individual injections of basal and bolus
-Intermediate: NPH (may be purchased without rx)  6-10 hour peak =
before breakfast + supper U/kg basal insulin once daily are best: 50% of TDD should be basal, Rule of 1800: 1800/TDD = how many mg/dL
-Long-acting/basal: detemir, glargine, aspart protamine  no peak = 1-2x -Insulin mixes  begin with 0.6 50% should be bolus (and further divided that 1 U of insulin will change your patient’s BG
daily U/kg total daily dose, 2/3 of this into 3 mealtime doses)
-Mixes: 70% NPH/30% regular, 75% aspart protamine/30% rapid in the am and the remaining 1/3 -Can also use insulin mixes and Rule of 500: 500/TDD = how many g of CHO
in the evening administer as in DM2 for patients who that 1 U of insulin will cover
-Most syringes are U-100 but U-500’s are 5x as concentrated and are are unwilling to do multiple injections
manufactured for patients needing > 200 U of insulin daily per day

Hyperlipidemia
-Most LDLs > 190 have a genetic Labs Cholesterol Goals Management
component -Lipid panel: TC, LDL, HDL, TG (TC and Known LDL goal < 100 1.) With abnormal lipids without CAD or CAD risk
-2° dyslipidemia can be a result of HDL can be measured even if patient was CAD equivalents, set an LDL goal first and initiate
DM, hypothyroid, obstructive liver not fasting) Sometimes < 70 therapeutic lifestyle changes for 3-6 months (unless
disease, chronic renal failure, meds, -Direct LDL: for nonfasting patients or if TG TG > 500, then address this first to prevent
diet, or sedentary lifestyle > 400 Risk MI, stroke, DM, LDL goal < 100 pancreatitis)
-CAD  LDL goal > 100 or sometimes < 70 equivalents carotid artery 2.) If lifestyle changes don’t work, consider meds
-Treating known hyperlipidemia up to -CAD equivalents (MI, stroke, DM, carotid disease, PVD, Sometimes < 70 3.) If meds don’t result in LDL goal being met, add
age 75 results in significant reductions artery disease, PVD, AAA)  LDL goal > AAA a higher dose statin or another med
in morbidity and mortality 100 or sometimes < 70 4.) If TG remain elevated, set another goal for TG
Risk factors Smoking -1 risk factor
-Risks factors (smoking, HTN, HDL < 40, that is LDL goal + 30
HTN makes an LDL
Screening FH premature CAD, men > 55, women > 65)  For CAD or CAD equivalent patients, start meds
HDL < 40 goal < 190
-Once between 2-10 years and q 3-5  one risk factor makes an LDL goal < 190 and lifestyle changes right away
FH premature
years thereafter for pediatric patients while two risk factors makes an LDL goal <
CAD 2 risk factors
with risks (obesity, HTN, FH) 130
Men > 55, makes an LDL
-Every 5 years for patients 20-35 with
Women > 65 goal < 130
risk factors (DM, FH, CV risk)
-Otherwise begin at 35 in men and 45
in women

Drug Class Statins Fibric Acid Bile Acid Niacin Ezetimibe Other
Derivatives Sequestrants Options
Information -Inhibit HMG CoA reductase -Stimulate -Cause liver to break -Blocks VLDL -Inhibits cholesterol -Fish oil: ↓
-First-line medication to reduce LDL transcription factor to down more cholesterol synthesis  shift in absorption at the TG by 20-
-Taken at bedtime, when cholesterol synthesis peaks promote lipid to make new bile LDL from small brush border 50%, minor ↑
-Check baseline LFTs before starting metabolism -Good addition to and dense to larger -Better tolerated LDL and
-FDA recs rechecking LFTs into treatment only if patient is -Contraindicated in statin therapy to and more buoyant than a bile acid HDL,
symptomatic and d/c of therapy if LFTs have increased to 3x severe renal or further ↓ LDL -SE of flushing, sequestrant increased risk
ULN hepatic disease -Contraindicated with prevent with aspirin -Contraindicated in of bleeding
-May also check TSH before starting statin b/c hypothyroidism TG > 400 before liver disease -Red rice
predisposes to myalgias as well as dyslipidemia -Contraindicated yeast: has
-If pt has myalgias, check CK but it isn’t always elevated even with liver disease, natural HMG
with statin-induced myalgias; CK ↑ > 10x ULN is a reason for gout CoA
d/c of statin reductase
20
 -Drug interactions activity
-Contraindicated in chronic liver disease
-Pregnancy category X
Effect on ↓ LDL by 20-60% (doubling dose  additional 6% ↓) ↓ LDL by 5-10% ↓ LDL by 15-30% ↓ LDL by 5-25% ↓ LDL by 15-20%
cholesterol ↓ TG by 7-30% ↓ TG by 20-50% No effect on TG ↓ TG by 20-50% ↓ TG by 5-10%
↑ HDL by 5-15% ↑ HDL by 10-20% ↑ HDL mildly ↑ HDL by 15-30% ↑ HDL mildly
Specific -Atorvastatin: ok to use in CKD -Gemfibrozil -Cholestyramine
Drugs -Lovastatin -Fenofibrate
-Pravastatin: less muscle toxicity, good 2nd choice for pts with ↑
LFTs on other statins
-Fluvastatin: less muscle toxicity, ok to use in CKD
-Rosuvastatin
-Simvastatin: new FDA warning, don’t exceed 20 mg simva with
amiodarone, amlodipine, or ranolazine; don’t exceed 10 mg
simva with diltiazem or verapamil.

ENT
Cataracts
-Opacification of the lens Signs & symptoms
-Gradual loss of vision
Etiologies -Blurred or smoky vision
-Age -Glares
-Steroids -Decreased vision in bright light or at night
-Diabetes
-Electrocution Management
-Congenital anomaly -Surgical removal when it interferes with ADLs with
-Trauma replacement with an artificial lens

21
 Vertigo
Differential -Psych: panic, anxiety
-CV: orthostatic HTN, arrhythmia, CAD -Metabolic: hyperthyroid, menopause
-Neuro: acoustic neuroma, TIA, stroke, Parkinson’s, neuropathy, migraine -Orthopedic: cervical disc disease, lower extremity arthritis
-Anemia -Geriatric: decreased proprioception, off center of balance, polypharmacy
Cause Information Signs & Symptoms Management
Benign -Otolith -Intermittent vertigo lasting < 1 minute
Paroxysmal dislodgement -NO hearing loss
Positional into semicircular -Better with head held still,
Vertigo canals worse with R/L
movements when lying
down
-Vertical or horizontal
nystagmus
+ Dix-Hallpike maneuver:
affected ear will cause
nystagmus when it is
downward

Meniere’s -A result of -Sudden unilateral SNHL, roaring tinnitus, and vertigo for hours -Diuretics
Disease increased -Ear fullness -Low salt diet
endolymphatic -Anti-vertigo meds
fluid
Acute -Infection or -Severe, disabling vertigo for 24-48 hours followed by weeks of -Steroids
Labyrinthitis inflammation of imbalance -PT
& Vestibular the inner ear, -Vomiting
Neuritis usually due to -Pts think they are dying
latent virus
-Neuritis = only
semicircular
canals affected
-Labyrinthitis =
vertigo + hearing
loss
Central -Issue with -Symptoms with gradual onset but are constant
Vertigo balance centers -May have nausea or diaphoresis
of the brain -Vertical nystagmus
-Usually no hearing loss

22
 Glaucoma
Preventative Eye Exams
Age Black Patients White Patients
20-40 Every 2-4 years No guidelines
40-54 Every 1-3 years Every 2-4 years
55-64 Every 1-2 years Every 1-3 years
65+ Every 1-2 years Every 1-2 years
Type Acute/Narrow/Closed Angle Open/Wide Angle
Information -Fluid builds up behind the lens due to malformed iris and trabecular network -Fluid builds up in front of the lens as a result of slowly clogging drain 
contacting each other  sudden blocking of drainage canal sequential damage to optic nerve with progressive loss of visual field

-Most common in Asians and older folks -Most common type of glaucoma
-Most prevalent in blacks over 40 and others over 65  screen with visual field
confrontation
Presentation -Occurs after being in a dark place -Bilateral eyes affected
or after anticholinergic use -Colored halos around lights
-Prior episodes of blurred vision -Progressive peripheral vision loss
-Halos around lights -May be asymptomatic until severe visual field loss
-H/o recent eye surgery or uveitis -Pupil dilation
-Nausea/vomiting
-Eye redness
-Nonreactive pupil
-Hazy cornea
-Shallow depth of anterior
chamber
-Optic disc cupping

Treatment -Give acetazolamide and timolol, apraclonidine, and pilocarpine -Regular aerobic exercise to reduce IOP
-Emergent referral to ophtho, monitoring of IOP q hour until seen -Increase outflow with intraocular prostaglandin analogues
-Suppress production with intraocular β-blockers

23
 Macular Degeneration
-Damage to the retina causes loss of central vision Risk factors
-Age
Forms -Genetics
-Non-exudative (dry): when drusen accumulates between the -Smoking
retina and the choroid  loss of cones; accounts for 90% of -HTN
cases -Micronutrient levels
-Exudative (wet): when blood vessels grow up from the choroid
behind the retina Management
-Smoking cessation
-Vitamins and supplementation with zinc, beta carotene, copper
-Lasering or surgical extraction for neovascularization or
macular translocation
-Antiangiogenesis therapy

Diabetic Retinopathy
-Occurs when hyperglycemia damages the basement membrane Screening Management
of retinal capillaries  loss of pericytes and microaneurysm -Yearly eye exams for diabetics -Nonproliferative  panretinal photocoagulation if severe
formation  leakage of capillaries and macular edema with -Maintain A1c < 7% -Proliferative  panretinal photocoagulation if high risk or severe, early
proliferation of weak blood vessels -HTN control vitrectomy if severe and DM1, intravitreal VEGF inhibitors as therapy adjunct
-Associated with DM1 and DM2 but not gestational diabetes
Signs & symptoms
-Most are asymptomatic

24
 Hearing Loss
-Conductive, sensorineural, or mixed Workup Management
-Office hearing evaluation with Rinne and Weber tests -Standard air conduction hearing aid
Etiologies -Formal audiologic testing if there is no obvious etiology -Bone conduction device for congenital atresia, chronic ear
-Conductive, outer ear: congenital, external otitis, trauma, -Contrasted MRI or CT if there is progressive asymmetric infections, or single-sided deafness
squamous cell carcinoma, exostosis, osteoma, psoriasis, sensorineural hearing loss -Cochlear implant
cerumen -Labs for unexplained sensorineural hearing loss: glucose, CBC,
-Conductive, middle ear: congenital, otitis media, TSH, RPR
cholesteatoma, otosclerosis, tympanic membrane perforation, -Urgent referral to ENT for sudden hearing loss
temporal bone trauma, glomus tumor
-Sensorineural: hereditary, congenital, presbycusis, meningitis,
thyrotoxicosis, viral cochleitis, ototoxic drugs, otologic surgery,
Meniere disease, noise, barotrauma, penetrating trauma,
acoustic neuroma, meningioma, autoimmune disease, multiple
sclerosis, cerebrovascular ischemia
Sialadenitis
-Acute, chronic, or recurrent Signs & symptoms
-Most commonly affects the parotid or submandibular gland -Painful swelling and edema of the cheek, especially with
-Agent is usually Staph aureus meals
-Reddened skin
Risk factors -Malaise
-Decreased salivary flow -Purulent exudate from duct punctum
-Poor oral hygiene
Management
-Antibiotics
-Warm compresses

Prognosis
-Complications: abscess, Ludwig’s angina, cellulitis

Central Retinal Artery Occlusion

-Loss of blood supply to the retina via embolus Signs & symptoms Management
-Risk factors: a-fib, endocarditis, coagulopathies, CAD, -Painless, severe loss of vision in one eye -Emergent ophtho consult with interventions to lower IOP
hypercoagulable states, temporal arteritis -Funduscopic exam shows cherry red spot, pale or swollen optic -Antiplatelets
nerve with splinter hemorrhages, ground-glass retina
Prognosis
Workup -Poor, no treatments proven to improve visual outcomes
-CV exam for bruits and temporal arteritis
-Carotid imaging
-EKG

25
 Central Retinal Vein Occlusion
-When occluded retinal vein backs up and fills the retina with Signs & symptoms Management
blood -Painless loss of vision in one eye -Treat underlying medical disorders
-Risk factors: HTN, mechanical compression, glaucoma, -Aspirin therapy
inflammation of the optic nerve, orbital disease, hyperviscosity -Lasering of ischemic retina
disorders -Treat associated glaucoma and macular edema
Oral Leukoplakia
-An early dysplasia of the squamous epithelium Signs & symptoms Prognosis
-May be malignant or inflammatory -White patches or plaques on the oral mucosa -Between 1-20% of lesions will progress to carcinoma within 10
-Association with HPV years
Workup -Lesions arising in trauma-prone areas of the oral cavity are less
Risk factors -Biopsy likely to be dysplastic
-Smoking

GASTROENTEROLOGY
Esophagitis
Type Etiologies Signs & symptoms Differential Workup Management Prognosis
Medication-induced -Major offenders are -Sudden onset -Only necessary for severe -Most cases
tetracyclines, anti- odynophagia, presentations or atypical heal
inflammatories, KCl, retrosternal pain symptoms without
quinidine, after ingestion of a -Endoscopy or barium intervention
alendronate pill swallow within a
few days
Eosinophilic -Allergic response -Dysphagia -Upper endoscopy with -Allergy referral
-Heartburn biopsy -Elimination diet
unresponsive to -Acid suppression
medications -Topical glucocorticoids (swallowed fluticasone)
-H/o environmental -Esophageal dilation to treat strictures
allergies or atopy -Repeat endoscopies for change in symptoms
-Vomiting
-Abdominal pain
GERD -Transient lower -Heartburn -Infectious -Endoscopy with biopsy for -Lifestyle modification: ↑ HOB, avoid food before sleep,
esophageal sphincter -Regurgitation esophagitis alarm symptoms (dysphagia, avoiding trigger foods, weight loss, smoking cessation
relaxation -Dysphagia -Pill esophagitis odynophagia, weight loss, -Change therapy as needed every 2-4 weeks
-Maintain optimal therapy for 8 weeks
-Hypotensive lower -Chronic cough -Eosinophilic iron deficiency anemia),
-Recurrent symptoms within 3 months suggest disease best
esophageal sphincter -Hoarseness esophagitis symptoms refractory to managed with continuous therapy
-Anatomic disruption -PUD empiric PPI trial, new onset -Acid suppression will reduce the acid but not the reflux!
of the -Non-ulcer symptoms in a patient over -Therapeutic regimens in order of increasing potency: OTC
gastroesophageal dyspepsia 50, or symptoms > 10 years antacids or H2 blockers, rx H2 blockers BID (take 30 min
junction, often with -Biliary tract -Ambulatory pH monitoring to work), PPI for 2 weeks, 20 mg omeprazole daily, 20 mg
hiatal hernia disease for negative endoscopy with omeprazole BID or 40 mg daily
-CAD persistent symptoms -Acid suppression with symptoms worse than mild or
intermittent  PPI recommended over H2 antagonist
-Esophageal -Esophageal manometry for
-EGD every 3 years for patients with known Barrett
motility disorder suspected motility disorder esophagus
Other -HSV: mostly in
immunocompromised
-CMV
-Candida

26
 GI Neoplasms
Colon Cancer
-95% of primary colon cancers are adenocarcinomas Screening Workup
-Adenomatous polyp = pre-malignant  need screens more -Begin assessing risk at age 20 -Colonoscopy for biopsy
frequently for monitoring -Begin screening at 40-45 for AA patients, at 50 for all other -Abdominal/pelvis CT for staging (“apple core” lesions)
-Hyperplastic polyp = not pre-malignant  more frequent patients of average risk; continue until life expectancy is -CXR
screening not needed estimated to be less than 10 years or 85 years at the latest -Labs: CBC, CMP, baseline CEA for f/u
-Risk factors: age, FH (up to 30% have a genetic component), -Begin screening those with FH at least 10 years before the age -PET
DM2, metabolic syndrome, ethnicity, IBD, high red meat or at which the youngest affected family member was diagnosed
processed meat consumption, inactivity, obesity, smoking, -Colonoscopy every 10 years Management
heavy alcohol use -CT colonography or flexible sigmoidoscopy every 5 years -Early stage tumors may be removed endoscopically
-Prevention: diet with plant foods, healthy BMI, limited red -FOBT annually for patients in whom imaging or visualization -Hemicolectomy with lymph node dissection
meats, physical activity is not possible -Local treatment of mets
-Chemo to eradicate micromets
Associated familial syndromes Signs and symptoms -Radiation not typically used to its high toxicity in the gut
-FAP: also incurs risk of thyroid, pancreas, duodenal, and -Rectal bleeding
gastric cancers -Iron deficiency anemia
-HNPCC: associated with endometrial, ovarian, gastric, urinary -Fatigue and weight loss
tract, renal cell, biliary, and gallbladder cancers -Obstruction
-Most occur after age 50 -Change in stool quantity or caliber
-Abdominal mass or pain
-Weakness
-Mets to the liver and lung
Liver Masses
Benign Malignant
Hemangioma Hepatocellular carcinoma
-The most common benign liver tumor -Usually occurs with chronic liver disease or cirrhosis
-Small, asymptomatic -Diagnostic imaging shows multiphasic tumor
-Finding is incidental -Treat by resection or radiofrequency ablation, palliative embolization, or liver transplant

Hepatic adenoma Cholangiocarcinoma

-Associated with long-term estrogen use
-Can rupture and bleed, so it should be resected

Focal nodular hyperplasia

-May be a response to a congenital malformation
-Should be resected

Others
-Hamartoma
-Cysts: simple, infectious, polycystic liver, biliary cystadenoma, Von Meyenburg complex

27
 Esophageal Cancer
-Usually occurs in males 50-70 Workup
-CXR showing mediastinal widening, lung or bony mets
Types -Barium swallow showing many infiltrative or ulcerative lesions and strictures
-Squamous cell carcinoma: occurs in the upper 2/3 of the esophagus, risk factors are alcohol use, -Chest CT
tobacco, achalasia, caustic esophageal injury, head and neck cancers, Plummer-Vinson syndrome, -Endoscopic US for staging
black ethnicity, male
-Adenocarcinoma: occurs in the lower 1/3 of the esophagus, risks are Barrett’s esophagus, white Management
ethnicity, males -Surgical resection with gastric pull-up or colonic interposition
 Recent trend towards adenocarcinoma -Palliative radiation
-Chemo
Signs & symptoms -Palliative stenting
-Progressive solid food dysphagia
-Weight loss Prognosis
-Usually is late stage by time patient is symptomatic -Overall 5-year survival is 17%
Pancreatic Adenocarcinoma
-Typically occurs in ages 70-80 Workup
-Most commonly in the head of the pancreas -Labs: ALP, bili, CA 19-9
-Risk factors: tobacco use, chronic pancreatitis, exposure to dye chemicals, DM2 in nonobese -CT for “double duct sign” = dilation of the common bile and main pancreatic ducts
person arising after age 50, history of partial gastrectomy or cholecystectomy, genetic factors -MRI
including BRCA2 -Tissue diagnosis if imaging is not convincing

Signs & symptoms Management

-Weight loss -Surgical resection + radiation if there is no invasion, lymphatic involvement, or mets
-Jaundice -Locally advanced disease  radiation only
-Courvoisier’s sign (palpable gallbladder due to compression of bile duct) -Chemo, pain control, and palliative stents for metastatic disease
-Trosseau’s sign (hypercoagulable state created by the malignancy  migratory thrombophlebitis
throughout body) Prognosis
-Half of all pancreatic cancers are metastatic by the time of diagnosis, with a life expectancy of 3-
6 months
-Resectable disease survival is < 1.5 years
-Locally advanced disease survival is 6-10 months
Gastric Cancer
-High incidence in Korea, Japan, and China Signs & symptoms Workup
-Usually occurs after age 60 -Early disease is asymptomatic -EGD
-Indigestion, nausea, early satiety, anorexia, and weight loss -Endoscopic US
Etiologies -Advanced: pleural effusions, SBO, bleeding -Barium swallow
-Pickled foods -Palpable stomach -CT/MRI
-Salted foods -Hepatomegaly
-Smoked foods -Pallor Management
-H. pylori -Virchow’s nodes or Sister Mary Joseph nodes -Depends on stage
-Atrophic gastritis -Resection, chemo, radiation, adjuvants if needed
-Polyps
-Radiation Prognosis
-Difficult to cure
-Most will die of recurrent disease even after resection

28
 Esophageal Motility Disorders
Achalasia
-Absence of normal esophageal peristalsis with increased tone of the LES Workup
-Manometry is the gold standard
Etiologies -CXR showing enlarged, fluid-filled esophagus
-Chagas’ disease -Barium swallow showing “bird’s beak” from acute tapering of LES at gastroesophageal
-Others junction
-EGD to look for other cause
Signs & symptoms
-Months to years of symptoms Management
-Gradual, progressive dysphagia of both solids and liquids -Smooth muscle relaxers like CCB, nitrates
-Regurgitation, sometimes nocturnally -Balloon dilation of LES: high perf rate!
-Substernal discomfort or fullness after eating -Surgical myotomy
-Poor esophageal emptying -Botox injection to relax LES

Diffuse Esophageal Spasm

-Simultaneous, nonperistaltic contractions of the esophagus Workup
-Uncommon -Barium swallow showing corkscrew contractions or “rosary bead” appearance
-Manometry shows intermittent, simultaneous contractions of high amplitude not
Signs & symptoms related to swallowing along with periods of normal peristalsis
-Intermittent dysphagia
-Anterior chest pain unrelated to exertion or eating Management
-Provocation by stress, large food boluses, hot or cold liquids -Disease is usually self-limiting

Scleroderma Esophagus
-Atrophy and fibrosis of esophageal smooth muscle  loss of LES competency, decreased Workup
peristalsis, and decreased gastric emptying -Manometry showing diminished peristalsis with low pressures, relaxed LES
-Can also occur with progressive systemic sclerosis, Raynaud’s, or CREST -Barium swallow showing dilated, flaccid esophagus

Signs & symptoms

-Severe acid reflux
-Strictures
-Erosions
-Heartburn
-Dysphagia

29
 Peptic Ulcer Disease
-Causes: H. pylori, chronic NSAIDs, excess acid, cigarette smoking, CMV in transplant pts, Crohn’s Workup
-PUD is the #1 cause of upper GIB -Barium upper GI series films are less sensitive
-Prevent with cox-2 inhibitors vs NSAIDs, PPIs, high dose H2 blockers, misoprostol if must use NSAIDs -EGD with gastric biopsy for definitive diagnosis
-Risk factors: older age, anticoagulation, steroids, NSAIDs, chronic disease -H. pylori test: fecal or urea breath test preferred over antibody test

Signs & symptoms Treatment

-Gnawing, dull, or aching pain localized to the epigastrium that is non-radiating -H. pylori eradication with triple therapy and confirmation via stool or urease breath
-Gastric ulcers are worse after meals test (beware, resistance is on the rise!)
-Duodenal ulcers are better after meals -Bland diet NOT shown to be helpful
-Pain frequently awakens patients from sleep between 2-3 am -Quit smoking as it retards ulcer healing
-May be asymptomatic -H2 blockers block 65% of acid secretion and can heal ulcers in 6-8 weeks
-PPIs block 90% of acid secretion and can heal ulcers in 4-8 weeks, preferred agent
Acute Pancreatitis
-Occurs with inappropriate activation of Signs & symptoms Workup
trypsin within the pancreas  enzymatic -Range of severity from mild illness to severe -↑ Amylase: not specific, can be ↑ in appendicitis, cholecystitis, perf, ectopic pregnancy, or
damage to the pancreas multiorgan failure renal failure; elevated for 24 hours
-Constant epigastric pain radiation to the back -↑ Lipase: more specific for pancreatitis, but can be elevated in renal failure; stays elevated for
Etiologies -Nausea and vomiting 3 days
-Gallstones are the most common cause -Tachycardia secondary to hypovolemia from leaky  Elevated amylase or lipase alone without clinical signs are NOT pancreatitis!
-Alcohol use vessels and 3rd spacing -Bili will be elevated if there is an obstruction blocking it from leaving the liver
-Other obstructions: pancreatic or -Fever -Elevated BUN and hct with vol depletion
ampullary tumors, sphincter of Oddi -Sepsis -US showing large, hypoechoic pancreas
dysfunction, pancreatic malformation -Icterus or jaundice if there is biliary obstruction -CT showing pancreatic enlargement and peripancreatic edema (imaging of choice for
-Meds: diuretics, azathioprine, 6- -Abdominal tenderness with rigidity and guarding pancreatitis)
mercaptopurine, sulfa drugs, ACEIs, HIV -Acute interstitial pancreatitis: mild, with pancreatic -MRCP or ERCP
meds edema
-Infections: mumps, rubella, Coxsackie, -Acute necrotizing pancreatitis: severe, with necrosis of Prognosis
echovirus, EBV, HIV parenchyma and vessels  Gray-Turner’s sign and -Complications: inflammatory cascade can cause ARDS, sepsis, or renal failure; pancreatic
-Metabolic: ↑TG, hyperCa Cullen’s sign necrosis or abscess, pancreatic pseudocyst
-Toxins: methanol, ethanol, scorpion
sting in Trinidad
-Vascular: vasculitis, ischemia
-Abdominal trauma
-Post-ERCP
-Inherited causes

30
 Chronic Pancreatitis
-Chronic inflammation Signs & symptoms Management
leads to irreversible -Recurrent episodes of epigastric and LUQ pain -Abstinence from alcohol
fibrosis of the pancreas -Steatorrhea -Pancreatic enzyme replacement + PPI + low fat diet
-Fat soluble vitamin deficiency -Insulin
Etiologies -Diabetes -Surgical options
-Chronic alcohol use
-Chronic pancreatic duct Workup
obstruction -Amylase and lipase won’t be elevated because the
-Malnutrition pancreas is burned out by now
-Autoimmune -Secretin stimulation test to see if the pancreas still
-Hereditary works
-Idiopathic -Abdominal x-ray showing pancreatic calcifications
-CT showing calcifications and atrophy
-ERCP showing “chain of lakes” or areas of dilation and stenosis along the pancreatic duct
Diverticular Disease
Diverticulosis
-A 20th century disease associated with Western lifestyle of low fiber, red meat, obesity, and Signs & symptoms
increasing age -Many cases of colonic diverticula are asymptomatic and discovered incidentally
-Diverticula are outpouchings of the mucosa and submucosa through the muscular layer of the -Chronic constipation, abdominal pain, fluctuating bowel habits
colonic wall; they can become perforated and infected with constipation or increased -May have mild LLQ tenderness
intraluminal pressure
Management
-May reduce complications of diverticulosis with fiber supplements
Diverticulitis
Signs & symptoms Management Prognosis
-Mild to severe LLQ or suprapubic pain ± palpable mass -Uncomplicated/simple = empiric treatment with 7- -Complications: lower GIB,
-Acute GIB that is painless and maroon in color 10 days of outpatient antibiotics to cover aerobes intra-abdominal abscess or
-Fever, malaise, constipation, diarrhea, cramping, bloating, and anaerobes (cipro + metronidazole), clear liquids peritonitis secondary to
nausea, vomiting, dysuria, and urinary frequency diet until clinical improvement (2-3 days), surgical perf, fistulas, obstruction
consult if no improvement or worsening of -30-40% of cases will have
Differential: perforated colonic carcinoma, Crohn’s, symptoms in 72 hours episodic abdominal cramps
appendicitis, ischemic colitis, C. diff, ectopic pregnancy, -Refer for colonoscopy, CT colonography, or barium without frank diverticulitis
ovarian cyst, ovarian torsion enema with flex sig 2-6 weeks after recovery to -30% of cases will go on to
evaluate extent of diverticulosis and exclude have a second attack of
Workup malignancy (don’t want to do this right away due to diverticulitis
-CBC shows leukocytosis with left shift risk of causing perforation)
-CT with contrast is imaging of choice to assess severity -Complicated (peritonitis, obstruction, perf, abscess,
-Plain films for free air, ileus, or obstruction or fistula) = hospitalization with IV antibiotics
(ampicillin, gentamicin, and metronidazole), IVF,
pain management, and antiemetics

31
 Toxic Megacolon
-A potentially lethal complication colitis that is Signs & symptoms Management
characterized by total or segmental nonobstructive colonic -Severe bloody diarrhea -Fluid resuscitation
dilation + systemic toxicity -Correction of abnormal labs
Workup -IV vanco and metronidazole
Etiologies -Abdominal plain film showing R colon -Complete bowel rest
-IBD dilation > 6 cm, dilation of transverse -Bowel decompression with NGT
-Infectious colitis colon, absence of normal colonic -Surgical consult for subtotal colectomy with end-ileostomy for
-Ischemic colitis haustral markings, and air-filled pts not improving on medical management
-Volvulus crevices between large pseudopolypoid
-Diverticulitis projections extending into the gut lumen
-Obstructive colon cancer

Ischemic Bowel Disease

-Most cases are acute Signs & symptoms Management
-Risk factors: age, -Diarrhea -Restoration of intestinal blood flow
atherosclerosis, low cardiac -Fever -Hemodynamic support
output, arrhythmias, severe -Hyperactive phase: passage of bloody stool, -Correction of metabolic acidosis
valvular disease, recent MI, severe abdominal pain -Initiation of broad spec AB
intra-abdominal malignancy -Paralytic phase: diffuse abdominal pain, tender -NGT for gastric decompression
abdomen, bloating, no further bloody stools, -Bowel rest
Etiologies absent bowel sounds
-Low blood pressure -Shock phase: fluids leaking through damaged Prognosis
-Clot colon lining  metabolic acidosis, dehydration, -Most patients make a full recovery without sequelae
-Vasoconstriction hypotension, tachycardia, confusion
-Idiopathic Colonic blood supply. Pink - supply from superior mesenteric artery (SMA) and
Workup its branches: middle colic, right colic, ileocolic arteries. Blue - supply from
-Mesenteric angiography is the gold standard inferior mesenteric artery (IMA) and its branches: left colic, sigmoid, superior
-Surgical consult rectal artery. 7 is for so-called Cannon-Böhm point (the border between the
areas of SMA and IMA supplies), which lies at the splenic flexure

32
 Diarrhea
Acute Diarrhea
-Less than 2 weeks’ duration Non-inflammatory Management
-Viral or noninvasive bacteria -Rehydration: ½ tsp salt, 1 tsp baking soda, 8 tsp sugar, 8 oz OJ
Etiologies -Infectious causes: virus, preformed toxin, toxin producing diluted to 1 L with water
-Most common causes are infectious agents, bacterial toxins, or bacteria, protozoa (ETEC, Staph, Bacillus cereus, Clostridium, -Antidiarrheals for mild to moderate illness
drugs viruses, Giardia) -Loperamide (non-systemic opioid) as long as there is no blood,
-Anal sex: Neisseria gonorrhoeae, syphilis, lymphogranuloma -Watery, nonbloody = no fecal leukocytes high fever, or systemic toxicity
venereum, HSV -Diarrhea may be voluminous -Bismuth subsalicylates (Pepto Bismol) good for traveler’s
-Noninfectious: drug reaction, UC, Crohn’s, ischemic colitis, -May have periumbilical cramps, bloating, n/v diarrhea as it is antibacterial and anti-inflammatory
fecal impaction, laxative abuse, radiation colitis, emotional -Prominence of vomiting suggests food poisoning or viral -Empiric antibiotic treatment only for immunocompromised,
stress enteritis significant dehydration, mod-severe fever, tenesmus, bloody
-Typically only eval if persists beyond 7 days or worsens stools, or presence of fecal lactoferrin  cipro, Septra, or
Inflammatory doxycycline
-Invasive or toxin-producing bacteria When to evaluate further -Antibiotics are not recommended in nontyphoid Salmonella,
-Causes: shigellosis, salmonellosis, Campylobacter, Yersinia, C. -Signs of inflammatory diarrhea: fever > 101.3, bloody diarrhea, Campylobacter, EHEC, Aeromonas, or Yersinia
diff, EHEC, Entamoeba histolytica, Neisseria gonorrhoeae, abdominal pain -Antibiotics are recommended in shigellosis, cholera,
Listeria -Passage of > 6 loose stools in 24 hours extraintestinal salmonellosis, traveler’s diarrhea, C. diff,
-Blood, pus, fever = fecal leukocytes usually present -Profuse watery diarrhea and dehydration giardiasis, and amebiasis
-Diarrhea is typically smaller in quantity -Frail older patients -Hospitalization for severe dehydration, severe or worsening
-Associated LLQ cramps, urgency, tenesmus -Immunocompromised patients bloody diarrhea, severe abdominal pain, signs of sepsis, or
-Workup with stool cultures, C. diff, ova, parasites -Hospital-acquired diarrhea worsening diarrhea in patients > 70
 Tests indicated: fecal leukocytes, routine stool culture, C. diff
if recent hospitalization or antibiotics, 3x ova and parasites if >
10 d, travel, community water outbreak, HIV, MSM

Chronic Diarrhea
-Greater than 4 weeks’ duration Workup Management
-Not attributed to viruses or bacteria other than C. diff -Ask if diarrhea occurs at nighttime or while fasting -Loperamide
-Exclude causes of acute diarrhea, lactose intolerance, -Diphenoxylate with atropine
Differential and signs/symptoms IBS, previous gastric surgery, parasitic infections, -Codeine and deodorized tincture
-Osmotic (lactose intolerance or other osmotic agents, factitious Mg overuse or laxative use): stool meds, systemic disease of opium: only for intractable
volume changes with fasting, ↑ stool osmotic gap -Initial tests: CBC, CMP, Ca, P, albumin, TSH, chronic diarrhea
-Secretory (hormonally mediated, factitious, villous adenoma, bile salt malabsorption, meds): > 1L vitamin A, vitamin D, INR, ESR, CRP, IgA for Celiac -Clonidine
stool per day, little change with fasting, normal stool osmotic gap, nonanion gap metabolic acidosis, -Stool studies: ova, parasites, electrolytes, fat stain, -Octreotide: for neuroendocrine
hyponatremia occult blood, leukocytes or lactoferrin tumors and AIDS diarrhea
-Inflammatory (UC, Crohn’s, microscopic colitis, malignancy, radiation): fever, hematochezia, -Consider antigen detection for Giardia and -Cholestyramine
abdominal pain, anemia, hypoalbuminia, ↑ ESR or CRP Entamoeba
-Meds: SSRIs, cholinesterase inhibitors, NSAIDs, PPIs, ARBs, metformin, allopurinol -Consider acid stain for Crypto and Cyclospora
-Malabsorption: weight loss, elevated fecal fat, anemia, hypoalbuminia -Refer for colonoscopy with biopsy
-Motility disorders (IBS): systemic disease or prior abdominal surgery -Further testing: 24 hour fecal fat, neuroendocrine
-Chronic infections (parasites, AIDS-related) tumors

33
 Nutritional Deficiencies
Nutrient Copper Iodine Selenium Zinc Chromium Iron Magnesium Vitamin B12
At risk -X-linked transport -Consumption of -Chinese diet -Low protein intake -Hospitalized patients -Menstruating -ICU -Vegetarians
mutation uniodized salt devoid of selenium -From developing with increased women
-Malabsorption after -TPN without country metabolic demands,
GI surgery or gastric supplementation especially diabetics
bypass -Short bowel
-Ingestion of high syndrome
doses of Zn -Burns
-Trauma
-TPN without
supplementation
Signs & -Anemia -Goiter -Cardiomyopathy -Growth retardation -Impaired glucose -Microcytic -Insulin resistance -Lethargy
symptoms -Ataxia -Hypothyroidism -Skeletal muscle -Hypogonadism tolerance anemia -Constipation -Unwanted weight
-Myeloneuropathy  ↓ growth, dysfunction -Oligospermia -Migraines loss
-Fragile hair development, and -Alopecia -RLS -Mental status
-Skin cognitive function -Impaired taste -Cramping change
depigmentation -Immune dysfunction -HTN -Anxiety
-Edema -Night blindness -Fibromyalgia -Depression
-Osteoporosis -Impaired wound healing -Weakness
- -Skin lesions -Trosseau and
Hepatosplenomegaly Chvostek signs
Cirrhosis
Etiologies Workup
-Alcoholic: average consumption of 8 12 oz beers, 1 L wine, or ½ pint of spirits per day for 20 -High INR and low albumin from decreased ability to make proteins
years -Elevated conj. bili due to inability of liver to process bilirubin, with eventual unconj bili ↑
-Non-alcoholic: a result of chronic inflammation -US to check for ascites and portal vein thrombosis
-Diagnostic paracentesis to determine true ascites vs. bacterial peritonitis (true ascites is a
Signs & symptoms difference between serum albumin and peritoneal fluid albumin > 1.1)
-Portal HTN -Liver biopsy
-Ascites: + fluid wave, shifting dullness -Screen for varices with EGD
-Gastro-esophageal varices
-Splenomegaly  thrombocytopenia Management
-Encephalopathy from lack of toxin clearance -For ascites: salt restriction, diuretics, therapeutic paracentesis, TIPS if refractory, AB for
secondary infection
-For encephalopathy: lactulose to reduce ammonia
-Treatment of viral hepatitis if present
-Alcoholic abstinence
-Hep A and B immunization
-Transplant

Prognosis
-Variable depending on comorbidities and etiology
-Child-Pugh classification estimates 1-year survival rates
-MELD score used for liver transplant evaluation

34
 Hepatitis
Etiologies Signs & symptoms
-Most are due to the hepatitis viruses -Acute: malaise, myalgias and arthralgias, fever, n/v/d, headache, anorexia, dark urine, scleral
-Toxins: alcohol icterus, abdominal pain, tender hepatomegaly, lymphadenopathy, splenomegaly
-Meds -Chronic: malaise, weakness, cirrhosis symptoms if severe
-Industrial organic solvents
-Other infections
-Autoimmune disease
-NASH
Type A B C D E
Source Fecal-oral Blood & assoc fluids, Blood & assoc fluids, Blood & assoc Fecal-oral
parenteral, sex, , dialysis, parenteral, sex, IVDU, fluids
tattoing transfusions
Incubation 28 days 45-180 days 2-26 weeks
Transmission Fecal-oral Percutaneous/mucosal Percutaneous/mucosal Percutaneous or Fecal-oral
Transplacental mucosal
Prevention Immunization, esp Immunization of all Blood donor screening, Immunization Safe drinking water
for travelers, MSM, infants, adolescents and don’t share needles, barrier for HBV
drug users, chronic adults in high risk groups, protection during sex
liver disease perinatal prevention
Presentation ACUTE CHRONIC in 5% unless Usually no acute flare, just CHRONIC ACUTE
RUQ pain, n/v you clear it becomes chronic
Silently progressive
Investigation ↑ ALT/AST + surface Ag with active + AB in present or + AB in present + AB
+ IgM if acute infection previous infection or previous
+ IgG if prior/vacc + surface AB with + RNA in active infection infection
previous infect/vacc + RNA in active
+ core AB with active or infection
prior infect (NOT vacc)
+ E Ag with active viral
replication
+ E AB in chronic infect
w/o replication, + blood
DNA in infection
Treatment IFN, antivirals Type 1  direct antivirals, Benign and self-
Usually clears pegylated IFN, ribavirin limiting
spontaneously Type 2 or 3  pegylated
IFN, ribavirin
Chronic No Yes, especially in kids Yes in 70% Yes No
infection? under 5
Special notes “Infectious “Serum hepatitis” #1 cause for liver Requires Increased severity in
hepatitis” Chronic increases risk for transplant coinfection with pregnant women
Complications of cirrhosis and HCC 6 genotypes, with 1 most hep B Rare in US
fulminant hepatitis, common and hardest to Endemic in India,
cholestatic hepatitis treat Mexico, Iraq, North
Prevalent in Alaska Liver biopsy useful for Africa, etc.
natives, American staging chronic
Indians

35
 GENITOURINARY
Benign Prostatic Hypertrophy
-Risk increases with age, and prostate Workup Pharmacologic MOA Information
undergoes growth spurt after age 40 -DRE +PSA (prostate size will not be correlated to symptoms, Therapy
-Only some men are symptomatic rather you are trying to detect malignant cause) Alpha-1 -Decrease muscle -Do not decrease prostate size
-Abdominal exam for bladder distension blockers tone for rapid -Nonselective (terazosin, doxazosin,
Signs & symptoms -Neuro exam symptom relief prazosin) not recommended with
-Irritative symptoms = bladder storage -Post-void residual/bladder scan concomitant HTN due to risk of first dose
problems like urgency, frequency, -UA to exclude infection or hematuria syncope and orthostatic HTN, take 2-4 weeks
nocturia, urge incontinence, stress -Rule out urethral stricture of bladder neck contracture (no for full effect
incontinence instrumentation, urethritis, or trauma) -Selective (tamsulosin, alfuzosin) have no
-Obstructive symptoms = bladder effect on BP and begin to work in days to 1
emptying problems like hesitancy, poor Management week, slight risk of ejaculatory dysfunction
flow, intermittency, straining, dysuria, -Always based on symptoms (calculate AUA symptom index 5-alpha -Blocks conversion -Finasteride
dribbling, incomplete bladder emptying score) reductase of testosterone  -For those who can’t tolerate alpha- blockers
-Watchful waiting only if pt is not bothered inhibitors dihydrotestosterone -Shrink prostate
-Natural saw palmetto supplement -Take 6-9 months
-Refer to urology for surgical intervention with recurrent -Pregnancy category X
UTIs, recurrent gross hematuria, bladder stones, CKD, urinary -AEs of ED and ejaculatory dysfunction
retention
Saw palmetto -Not shown to be helpful in clinical trials

Pyelonephritis
-Agent is usually uropathic strain of E. coli Workup
-UA with microscopy & culture
Signs & symptoms -Blood cultures if hospitalized
-Same manifestations as lower UTI + fever > 100.4, flank pain, CVA tenderness, n/v, rigors
-Sepsis Management
-Multi-organ dysfunction -If mild with no n/v  outpatient treatment with cipro
-ARF -Mod-severe  inpatient treatment with initial empiric IV ceftriaxone, cipro, or imipenem, f/u
-Alternative presentation of weeks to months of insidious, nonspecific symptoms such as malaise, culture 2 weeks after therapy
fatigue, nausea, or abdominal pain
Genitourinary Neoplasms
Bladder Cancer
-More common in men than omen Workup Management
-Risk factors: smoking, exposure to dyes and solvents -Repeat urine cytologies (low sensitivity) -If superficial, resection ± intravesicular chemo
-Cystoscopy ± transurethral resection -If advanced, combo chem. ± radiation
Signs & symptoms -Staging based on biopsy results and imaging
-Hematuria Prognosis
-Urinary frequency or urgency -Early disease has > 80% survival
-May be asymptomatic
Renal Cell Carcinoma
-More common in men than omen Signs & symptoms Management
-Risk factors: smoking, exposure to dyes and solvents -Hematuria -Nephrectomy
-Flank pain or abdominal mass
-Cough Prognosis
-Bone pain with mets -Good for cancers confined to renal capsule
-Paraneoplastic syndromes -50-60% for tumors extending beyond capsule
-Often found incidentally on other imaging -0-15% for node positive tumors
36
 Prostate Cancer
-Usually adenocarcinoma Signs & symptoms Management
-The most commonly diagnosed male cancer and 2nd leading -Asymptomatic early in disease -Treatment based on life expectancy, general health, tumor
cause of male cancer deaths -Later disease: obstructive urinary symptoms, hematuria, characteristics
-Risk factors: age, black, high fat diet, FH, obesity hematospermia -Treatment is controversial for localize disease
-No association with smoking, sexual activity, prior infections, -Radical prostatectomy
or BPH Workup -Radiation
-Prostate biopsy guided by transurethral US, with scoring by -Hormone therapy for advanced or metastatic disease
Screening Gleason system
-USPSTF grade I for men up to age 75 and grade D after 75 -MRI
-If patient elects, DRE and PSA should be done every 2 years -PET if suspected mets
-PSA will be elevated in cancer, inflammation, or BPH, and will
naturally rise as men age
Testicular Cancer
-Risk factors: cryptorchidism, abnormalities in spermatogenesis, FH Investigation
-Most commonly germ cell tumor, but cana lso be stromal tumor -Scrotal US: distinguishes benign vs malignant and intra vs extratesticular
-Excisional biopsy
Screening -β-hCG levels: will be elevated in some carcinomas and seminomas
-USPSTF grade D in asymptomatic adolescents and adult males -AFP: elevation excludes diagnosis of seminoma
-Chest, abdomen, and pelvis CT
Signs & symptoms
-Firm, painless mass arising from the testis Management
-Scrotal pain -Inguinal orchiectomy with f/u of tumor markers
-Affected area is usually unilateral -May need chemo
-Signs of mets: cough, GI, back pain, neuro signs, supraclavicular lymphadenopathy
Prognosis
-High survival rate if caught early
Acute Kidney Injury (Acute Renal Failure)
• Azotemia: abnormally high levels of Signs & symptoms Workup
nitrogen-containing compounds, such as -Fatigue, loss of appetite, headache, nausea, vomiting -Definition of AKI: acute ↓ in renal function with
urea, creatinine, various body waste -Flank pain from stretching of fibrous capsule surrounding kidney during blockage Cr ↑ of 0.5 (or 50%) above baseline, or CrCl ↓ by
compounds, and other nitrogen-rich -Irregular heartbeat from hyperkalemia 50%
compounds in the blood  can result from -Dehydration -Assess degree of renal dysfunction: estimate
many disorders including renal failure -Decreased UOP  vol overload, peripheral edema, pulmonary edema, pulmonary rales, elevated GFR
• Acute renal failure: an abrupt decrease in JVP, cardiac tamponade, pulsus paradoxus (drop in BP during inspiration) -UA
GFR sufficient to result in azotemia and -Mental status change -Labs: urine Na, urine Cr, compare with serum
perturbation of ECF volume, electrolyte, -Pruritus Na, Cr, and BUN
and acid-base balance = kidney is not -Seizures -Renal US to rule out postrenal causes
removing proteins that should normally be -SOB
removed from the blood -Asterixis and other myoclonus
-Pericardial or pleural friction rub
-Kussmaul respirations from acidosis

37
 Prerenal AKI
-A result of interrupted blood flow to the kidneys  ischemia of the proximal tubular cells Signs & symptoms
-Decreased renal perfusion means renin is released  maximal retention of Na and water in an -Hypotension
effort to ↑ circulating vol -Decreased UOP with concentrated urine

Etiologies Management
-Decreased effective circulating vol: HF, cirrhosis, nephrotic syndrome, excessive diuretic use, -IV NS
vomiting, NGT, diarrhea, burns, DKA, hypercalcemia, Addison’s, shock, pancreatitis, 3rd spacing -Treat underlying illness
-Decreased renal perfusion: severe hypoalbuminemia, sepsis, psychotropic drug overdose, -Stop antihypertensives or diuretics
excessive antihypertensives, NSAIDs, renal artery stenosis or renal vein thrombosis -Octreotide in patients with cirrhosis (helps increase blood flow to kidneys when sick liver is
-Cardiac arrest shutting it down)
-Low BP: anorexia, GIB, cardiac surgery
Intrinsic Renal AKI
Acute Tubular Necrosis Acute Interstitial Nephritis Glomerulonephritis
-The most common cause of AKI where there is abrupt and sustained -Results in abrupt deterioration in renal Focal disease
decline in GFR occurring within minutes to days in response to an acute function with inflammation and edema of the -IgA nephropathy
ischemic or nephrotoxic insult renal interstitium -Membranoproliferative glomerulonephropathy
-SLE
Signs & symptoms Etiologies
-Volume overload -Allergic: cephalosporins, diuretics, NSAIDs, Diffuse disease
-Oliguria or anuria penicillin, rifampin, sulfa -Goodpasture’s disease
-Infectious: hantavirus, HIV, Legionnaire’s, -Churg-Strauss
Workup leptospirosis, pyelonephritis -Cryoglobulinemia
-Rise in Cr and BUN in = proportions -Autoimmune: cryoglobulinemia, Sjogren’s, -Membranoproliferative glomerulonephropathy
-Check urine sodium (should be > 40) to distinguish from volume SLE -SLE
depletion (Na < 20) -Infiltrative: amyloidosis, multiple myeloma, -Vasculitis
-FENa increased at > 2-3% as either excess sodium is lost due to tubular sarcoidosis -Wegener’s
damage, or the damaged glomeruli result in hypervolemia resulting in the -Microscopic polyangiitis
normal response of sodium wasting Workup -Postinfectious glomerulonephritis: usually Strep but can also be TB,
-Will see metabolic acidosis with hyperkalemia -UA showing proteinuria, pyuria, hematuria, HIV, hepatitis, MRSA, or meningococcal infection-induced, with
-UA shows multiple granular and epithelial cell casts with free epithelial renal tubular epithelial cells or casts, onset 1-3 weeks after infection
cells eosinophiluria
-Increased BUN and Cr, hyper or hypokalemia Workup
Management -Hyperchloremic metabolic acidosis -UA showing red cell casts
-Typically conservative -Elevated LFTs
-Consider dialysis if severe
Post-Renal AKI
-A result of obstruction of urine flow

Etiologies
-Enlarged prostate
-Kidney stones
-Bladder tumor or injury
-Obstructed urinary catheter
-GYN cancers
-Retroperitoneal fibrosis
-Neurogenic bladder or spinal cord injury
-Retention secondary to meds: anticholinergics, opioids, amphetamines

38
 Intrinsic Renal Disease
Prerenal Azotemia Postrenal Azotemia Acute Tubular Necrosis Acute Interstitial Nephritis Acute Glomerulonephritis
Serum BUN:Cr Ratio -BUN:Cr ratio > 20:1 -BUN:Cr ratio > 20:1 because -BUN:Cr ratio < 10:1 because there is renal damage causing -BUN:Cr ratio > 20:1 (may
-Rise in BUN out of back-up into the kidney allows reduced reabsorption of BUN not be reliable)
proportion to rise in Cr for increased urea
because decreased flow to reabsorption
kidney means back-up of urea
and Cr in the blood, and while
urea is reabsorbed into the
blood after entering the kidney
(and has greater time to do so
due to the reduced flow) Cr
can’t be and is excreted

Urinary Indices -UA will be normal or near-

normal
Urine Na < 20 Variable > 20 Variable < 20
FENa -FENa will be < 1% (salt Variable, usually normal if > 1% if oliguric < 1% -Variable
conserving, indicating a injury is acute and there is still
functioning kidney with tubular functioning
normal physiologic response
to volume depletion)
Urine Osmolality > 500 < 400 250-300 Variable Variable
Urinary Sediment -Benign or hyaline casts -Usually normal -Muddy brown casts, renal -White cells, white cell casts, -Red cells, dysmorphic red
-May see RBCs, WBCs, or tubular casts ± eosinophils cells and red cell casts
crystals
Chronic Kidney Disease
-Defined as GFR < 60 for at least 3 months or presence of Signs & symptoms Management
kidney damage irrespective of GFR -Salt and water imbalance  fluid accumulation, HTN, -BP control using ACEIs
-Blacks have 3.8x greater risk, native Americans have 2x peripheral edema, hypo or hypernatremia, neuro effects -Smoking cessation
-Lipid management
greater risk, and Latinos have 1.5x greater risk -Cardiac conduction errors due to potassium imbalance
-Tight control of A1c in diabetics
-Imbalance of Ca and P affects bone metabolism and cell -Avoid nephrotoxins: contrast, NSAIDs
Stages membrane activity  loss of bone Ca with metastatic -Monitor for anemia and treat with folate, B12, or Fe if needed, then
-Stage I = GFR > 90 with kidney damage but asymptomatic deposition, osteoporosis, fx consider EPO
-Stage II = GFR 60-89 and kidney damage but asymptomatic -Acid/base imbalance affects functioning of cells and enzymes -Check GFR 1-2 times per year
-Stage III = GFR 30-59, mild anemia, ↑ BUN and Cr, but -Buildup of uremic toxins  nausea, anorexia, abnormal -Every 3 months monitor PTH, P, Ca, bicarb, and vitamin D if stage 3
asymptomatic metallic taste in mouth, insomnia, seizures, coma, bleeding, or above
-Stage IV = GFR 15-29, symptoms of fatigue, electrolyte immune dysfunction, arrhythmias, accelerated atherosclerosis, -Diet: good Ca intake, minimize P, low salt, fluid restriction to 2 L
-Phosphate binders if needed: Ca acetate, sevelamer, lanthanum
imbalance, acidosis, anemia cardiomyopathy, pruritus
-Treat hyperkalemia: usually avoided as long as GFR > 10, prevent by
-Stage 5 = GFR < 15 or dialysis-dependent -No erythropoietin  anemia avoiding K-sparing diuretics and cautious use of ACEI in ESRD
-No activation of vit D  hyperparathyroidism, renal -Treat hypokalemia
Screening osteodystrophy, fx -Treat vol overload: thiazides for stages 1-2, loop for stages 4-5 (greater
-Regularly screen those with risk factors for DM, glomerular diseases, -Heart disease: CAD lesions, CHF, acute MI (most patients will diuresis)
vascular diseases, cystic diseases, transplant complications, FH of die of a cardiac-related cause before ESRD develops) -Daily baby aspirin
severe kidney disease, CV disease, etc, as early diagnosis can add 2+ -Refer to nephrologist when GFR < 30
ESRD-free years to a patient’s lifespan
-Use spot urine:creatinine test in diabetics
-Use spot test or urine dipstick in all other populations
39
 Polycystic Kidney Disease
-Common after age 50 Signs & symptoms Workup
-Usually asymptomatic -UA for hematuria or proteinuria
Etiologies -If inherited form, may have abdominal or flank pain, -Renal US: diagnosis depends on age and # of cysts present
-Genetic form characterized by multiple cysts in both kidneys, hematuria, history of UTIs, history of stones, HTN, abdominal
with increased risk of UTIs, renal cell carcinoma, ESRD mass Management
-Usually requires kidney transplant
Hyponatremia
Management of hyponatremia
-Treat to magic number 125
-Don’t exceed replacement of sodium by more than 12 mEq/L due to risk of causing a demyelination syndrome
-Definitive treatment is based on underlying cause of impaired renal water excretion
Isotonic Hyponatremia: low Hypertonic Hyponatremia: low Hypotonic Hyponatremia: occurs when ↑ ADH  water and Na loss in urine  low serum osmolality
serum Na with normal ECF serum Na with high ECF osmolality
osmolality (total solutes) and and tonicity
tonicity (no oncotic pressure
generated)
-A kind of pseudohyponatremia -A kind of pseudohyponatremia -True hyponatremia
-Probably due to high levels of TG -Caused by a highly osmotic -Further characterized based on volume status
or proteins (multiple myeloma) that molecule with glucose or mannitol
push Na intracellularly to prevent in the ECF, which draws water out Hypervolemic hypotonic hyponatremia
increased serum osmolality of cells and dilutes the Na -3rd spacing of fluids  reduced circulating vol (even though TBW will be hypervolemic)  activation of ADH 
-No treatment needed concentration serum that is hypotonic because too much Na is retained in the urine
-Treat with NS until -Occurs in CHF, liver failure, nephrotic syndrome, and ESRD
hemodynamically stable, then ½ NS -Management is water and Na restriction, treat underlying cause of 3rd spacing

Euvolemic hypotonic hyponatremia

-Due to excessive ADH release
-Occurs in SIADH & paraneoplastic syndromes, postoperative hyponatremia, hypothyroidism, psychogenic polydipsia,
excess beer drinking
-Management is water restriction with hypertonic NaCl infusion

Hypovolemic hypotonic hyponatremia

-Occurs when water loss causes salt loss
-An extrarenal cause when kidneys are attempting to resuscitate volume by saving Na and water, such as dehydration,
diarrhea, or vomiting
-A renal cause when kidneys allow high Na losses despite ↓ circulating vol, such as diuretics, ACEIs, nephropathies, and
mineralocorticoid deficiencies
-Manage with NS

40
 Hypernatremia
Signs & symptoms
-Lethargy
-Weakness from brain cell shrinkage
-Irritability
-Twitching
-Seizures
-Coma
-Focal intracerebral and subarachnoid hemorrhages
Hypovolemic Hypernatremia Euvolemic Hypernatremia Hypervolemic Hypernatremia Chronic Hypernatremia
-Non-renal causes: excess water loss from skin -Non-renal causes: excessive sweating from -Non-renal causes: treatment of previous -Must correct especially slowly to prevent
or diarrhea  concentrated urine with low Na skin or respiratory system water loss hypotonic fluid loss with higher sodium fluids, cerebral edema
-Renal causes: osmotic diuresis due to -Renal cause: due to diabetes insipidus sea water ingestion, or overuse of NaHCO3 in -Calculate water deficiency and accomplish
mannitol, glycosuria, or diuretics  salt as (inadequate ADH or kidney nonresponse to CPR correction over 36-72 hours (normal TBW =
well as free water loss  high urine Na with ADH) -Management is to give D5W to reduce present TBW x (present serum Na/140)
normal urine osmolarity -Management is to increase PO water or use IV hyperosmolality, may need dialysis if pt has
D5W renal failure
Hypokalemia
Etiologies Signs and symptoms Management
-Decreased K+ intake -Mild hypokalemia can be treated orally with KCl supplements
-Increased K+ entry into cells: alkaline pH, insulin, stress, Workup -IV supplementation if severe
epinephrine, β-agonists, ↑ RBC production, hypothermia, -EKG may show U wave -K sparing diuretic if resistant
chloroquine toxicity
-Increase GI losses: vomiting, diarrhea, tube drainage, laxative
abuse
-Increased urinary losses: diuretics, mineralocorticoid excess,
loss of gastric secretions, non-reabsorbable anions, metabolic
acidosis (causes intracellular K+ shift and increased urinary
excretion of HCO3- coupled to K+), hypomagnesemia,
amphotericin B, salt-wasting nephropathies, polyuria
-Increased sweat losses
-Dialysis
-Plasmapheresis
-Blood tube metabolism of K+
Hyperkalemia
Etiologies Signs & symptoms Management
-Renal insufficiency -Malaise -Depends on EKG findings; if there is a change treat using “BIG
-Meds: ACEI, ARBS, K-sparing diuretics, NSAIDS -Palpitations & arrhythmias K” mnemonic:
-Mineralocorticoid deficiency -Muscle weakness -Bicarb IV
-Excessive release from cells: rhabdo, burns, tumor lysis, blood -Insulin to increase K+ cellular uptake
transfusion, hemolysis, acidosis, low insulin, β-blockers Workup -Ca gluconate or Ca chloride IV to stabilize the myocardium
-Excess intake: salt substitute, KCl infusion -EKG showing peaked T waves (give first!)
-Lysis from cells after blood draw -K+ binder (Kayexalate)
-Dialysis

41
 Hypocalcemia
Etiologies Signs & symptoms Workup
-If PTH is low  hypoparathyroidism -Acute: AMS, hallucinations, psychosis, Chvostek’s and -Check Mg level, phosphate, vitamin D
-If PTH is high  vit D deficiency, chronic renal failure, Trousseau’s signs, paresthesias, seizures, laryngospasm,
inadequate production of PTH or resistance, CKD, hepatic bronchospasm, prolonged QT, hypotension, HF, arrhythmia, Management
disease, osteoblastic mets, hypomagnesemia, large blood papilledema -If severe or symptomatic, give Ca gluconate or CaCl3, treat
transfusion, acute pancreatitis, severe sepsis or illness, meds, low Mg if present
pseudohypocalcemia (gadolinium interference with assay) -If asymptomatic, give oral Ca
-If due to vit D deficiency, give calcitriol (active vit D)
-Can add Ca to dialysis fluid if on HD
Hypercalcemia
Etiologies
-Increased bone resorption: malignancy/paraneoplastic effects, hyperparathyroidism, CKD, thyrotoxicosis, immobilization,
Paget’s disease of bone
-Increased Ca absorption: increased intake, lots of milk & Tums, elevated vit D, genetic, meds, pheochromocytoma,
adrenal insufficiency, rhabdo, ARF

Signs & symptoms

-“Stones, bones, groans, and psychiatric overtones”
-Anxiety, depression, lethargy, confusion, psychosis, coma
-Constipation, anorexia, pancreatitis, PUD, abdominal pain, n/v
-EKG changes: prolonged PR and QRS, AV block, cardiac arrest
-Volume depletion, renal insufficiency, nephrolithiasis, nephrogenic diabetes insipidus, distal RTA
-Muscle weakness, fatigue, bone pain, fractures

Management
-Treat if symptomatic or serum Ca is > 14
-IVF as pts tend to be volume depleted
-Calcitonin if severe
-Bisphosphonates
-Steroids
-Dialysis is last resort

Hypomagnesemia
Etiologies Signs & symptoms Management
-GI loss: diarrhea, short gut syndrome, TPN -Secondary electrolyte disturbances like hypoK, hypoCa, vit D -Oral replacement with MgO2
-Alcoholics deficiency
-Renal loss: diuretics, EtOH, nephrotoxic drugs, primary -Weakness, anorexia, tetany, convulsions
aldosteronism, post ATN -Widened QRS, peaked or inverted T waves, QT or PR
-Pancreatitis prolongation, VT, torsades
-DM
-Hypercalcemia or hypophosphatemia
-Hungry bone syndrome
42
 Metabolic Alkalosis
-Primary problem is that there is too much bicarb (no H+ left to react with)
-Body will eventually compensate by hypoventilation to ↑ CO2, and kidneys can compensate by increasing bicarb excretion
Chloride-Responsive (urine Cl < 10 mEq/L) Chloride-Resistant (urine Cl > 20 mEq/L)
Vomiting Hyperaldosteronism
-Occurs when vomiting/NGT  loss of HCl and vol depletion -Occurs when adrenals make too much aldosterone  ↑↑ Na and bicarb reabsorption with urinary
-Vol depletion stimulates renin & aldosterone  ↑ Na reabsorption with loss of K+ and H+ loss of K+/H+ (countertransporter pumps)
(countertransporters)  low urine Na, serum hypokalemia, and alkalosis
Other etiologies
Loop or thiazide diuretics -Bicarb retention
-Cause loss of Cl- with retention of bicarb -Hypokalemia  H+ shift into cells
-Excess administration of antacids
-Weird syndromes
Metabolic Acidosis
-Initially kidney ramps up production of bicarb but then the Winter’s formula: Expected PCO2 = (1.5 x bicarb) + 8 ± 2 Urine anion gap
primary problem is that bicarb is used up or there is not enough -If pt’s PCO2 corresponds, they are compensating adequately via -Only calculated in NAGMA
to offset the increased acid respiration changes -Main anion is Cl-, unmeasured anions are bicarb, PO42-, SO43-,
-There is respiratory compensation by talking rapid, deep -If measured PCO2 is higher than expected, there is also a lactate
breaths (Kussmaul respirations); check to see if the pt is primary respiratory acidosis -Main cations are Na+ and K+, unmeasured cations are Li, Ca,
adequately compensating using Winter’s formula -If the measured PCO2 is lower than expected, there is also a Mg, and NH4+
primary respiratory alkalosis -Normally urine is electrically neutral (UAG = 0) or slightly
Etiologies positive/acidic
-Most common cause is decreased tissue perfusion/ischemia Serum anion gap = diff bet + and – ions = Na+ – (Cl- + bicarb) UCl- + UA = UNa+ + UK+ + + UC
(exercise, sepsis, shock, seizures, neuroleptic malignant -Normally 8-12 (UA –UC) = UNa+ + UK - UCl-
syndrome)  production of lactic acid from anaerobic -Used to estimate NH4+ levels if you don’t have a direct test
metabolism Types of Metabolic Acidosis -Decreased UAG (abnormally negative) when there is loss of
-Ketone bodies 1.) Normal anion gap (hyperchloremic anion gap) bicarb via the bowel and kidneys respond by increasing
-Decreased renal excretion of H+ -Occurs when Cl- replaces lost bicarb as the H+ buffer excretion of NH4+ (= high amounts of an unmeasured anion),
-Bicarb loss from kidney -Causes (HARDUP): hyperalimentation or hyperventilation, or after eating a protein-rich meal
-Diarrhea  loss of bicarb acetazolamide, RTA (loss of bicarb from kidneys), diarrhea, -Increased UAG (higher than normal positive) when there is a
uretosigmoidostomy (loss of bicarb through colon), pancreatic renal cause blocking urinary acid excretion such as RTA
fistula (loss of bicarb through colon) because kidney is not getting rid of enough NH4+
2.) Increased anion gap
-Occurs when anion replacing bicarb is not one that is routinely Management
measured, such as albumin, PO42-, SO43-, lactate -Give NaHCO3-
-Causes (MUDPILES): methanol, uremia, DKA, paraldehyde, -Intubate for respiratory distress/can’t keep up with breathing
iron ingestion/INH, lactic acidosis, ethanol (makes acetic acid), quickly
salicylates
Respiratory Acidosis
-Primary problem is that there is ↑ CO2 due to hypoventilation
-Kidneys respond by secreting H+, generating new bicarb and other H+ buffers, and excreting NH4+  acidic urine
Respiratory Alkalosis
-Primary problem is that there is ↓ CO2 due to hyperventilation
-Kidneys compensate by increasing bicarb excretion in urine and decreased NH4+ excretion in urine  alkaline urine

43
 Nephrotic Syndrome
-Occurs when kidney damage causing pores in the podocytes Signs & symptoms Workup
allows large amounts of protein leakage, but not large enough -Generalized edema: periorbital, pitting edema of the legs, -Proteinuria ≥ 3.5 g/day
for RBCs to pass pleural effusions, ascites -Hypoalbuminemia
-Anemia due to transferrin loss -Hyperlipidemia
Etiologies -Foamy urine -Granular or fatty urine casts with oval fat bodies and Maltese
-DM cross crystals
-Focal glomerulosclerosis -Must get biopsy
-Membranous nephropathy
-Amyloidosis
-Minimal change disease
-SLE
-HIV, hep B or C

MUSCULOSKELETAL
Ankylosing Spondylitis
-Strong association with HLA-B27 Workup Management
-Spine film showing syndesmophytes (bony growth within spinal -Can use BASDAI questionnaire to assess level of disease
Signs & symptoms ligament)  bridging and fusion of vertebral bodies  “bamboo spine” activity
-Inflammatory back pain > 3 months’ duration that is -Pelvis film showing erosions -Initial therapy with NSAID like indomethacin with trial
improved by exercise and worsened with rest and sclerosis at the SI joints for at least 4 weeks
-Bilateral sacroiliitis -Augment with other non-opioid and low potency opioid
-May also have involvement of hips, shoulders, and joints analgesics as needed
of the LEs, as well as extra-articular manifestations in the -Exercise program or PT
eye and heart -Joint injections for persistent peripheral joint
-Schober’s test shows loss of lumbar flexion involvement, enthesitis, or sacroiliitis pain
-Nonbiologic DMARDs are ineffective for axial disease,
need to use anti-TNF agent if nonresponse to NSAIDs
-For peripheral disease, can use sulfasalazine or
methotrexate
-Surgical intervention for severe cases: joint replacement,
wedge osteotomy

Prognosis
-Poor prognostic indicators are severe hip disease, early
age of onset, persistent elevation of ESR

44
 Osteopenia & Osteoporosis
Risk factors Workup
-Meds associated with bone loss: glucocorticoids, anticoagulants, anticonvulsants, -Osteoporosis is diagnosed if the bone mineral density is 2.5 SD below (T score = -2.5) the young normal mean
aromatase inhibitors, cyclosporine, tacrolimus, GnRH agonists, barbiturates, Li, at the hip or spine
Depo-Provera, chemo, TPN -Osteopenia is diagnosed if the BMD is 1.0-2.5 SD below the young normal mean
-Previous fracture
-Parental history of hip fracture Management of low T score
-Low body weight -Treat all postmenopausal women with established osteoporosis, fragility fracture, and select postmenopausal
-Current cigarette smoking women with osteopenia with pharmacologic therapy
-Excessive alcohol consumption -First-line therapy is oral bisphosphonates, 2nd line is raloxifene
-Rheumatoid arthritis -Re-check DEXA after 2 years
-Hypogonadism, premature menopause, malabsorption, chronic liver disease, or
IBD Bisphosphonates
-MOA: inhibit bone resorption
Prevention -Alendronate, resideronate, ibandronate, zoledronic acid
-Ca and vit D supplementation recommended for all patients with inadequate intake -Must take on empty stomach and wait 30-60 minutes before eating and drinking while sitting upright (causes
-Ca carbonate: Tums, Caltrate, Os-Cal, Viactiv  should be 500-600 mg BID acid reflux)
-Ca citrate: Citracal  should 215 mg QID -AEs: hypocalcemia, dysphagia, esophageal inflammation, gastric ulcer, visual d
-Vit D supplements: should be 800-1000 IU daily isturbance, arthralgia, HA, myalgia, fever after first dose, possible atypical femoral fx = take a break every 5
-Exercise, smoking cessation, counseling on fall prevention, avoidance of heavy years, a-fib?, possible osteonecrosis of the jaw in cancer pts receiving IV treatment
alcohol use -Contraindications: inability to sit upright for 30 min, esophageal strictures, hypocalcemia
 Also recommended for all postmenopausal women with osteoporosis
PTH Antagonists
Screening -Calcitonin: comes in a nasal spray
-DEXA preferred over peripheral measurements -Teriparatide: costs $950 per month, AEs
-Screen women of average risk > 65 with DEXA
-Screen women younger than 65 who have risk factors Hormonal
-Screening for men generally not recommended unless there is evidence of -Raloxifene: black box warning for risk of DVT and fatal stroke with women with CHD
radiographic osteopenia, h/o trauma fx, loss of > 1.5 in in height, taking risky meds, -AEs: DVTs, hot flashes, edema, arthralgia, flu syndrome, MI, breast cancer, stroke
androgen deprivation therapy for prostate cancer, hypogonadism, hyperthyroidism,
etc. Monoclonal AB
-Women with initally good DEXA results need not be screened again for 10-15 -Prevent osteoclast formation
years -Costs $825/injection
-Women with osteopenia on their initial DEXA should be re-screened anywhere -Lots of AEs
from 1-5 years later, depending on how low their T-score was
Polymyositis
-A persistent inflammatory muscle disease that causes proximal Signs & symptoms Workup
weakness of the skeletal muscles -Insidious onset with nonspecific symptoms -Elevated CK, LDH, aldolase, and LFTs
-Caused by killer T-cells attacking muscle cells expressing -Proximal muscle weakness (can’t get up from chair, can’t raise -Autoantibodies (anti-Jo) and + ANA
MHC class I (slow fibers)  muscle fiber necrosis, arms above head) -EMG alteration
degeneration, and inflammatory cell infiltration -Muscle atrophy if long-standing -Positive muscle biopsy
-Related to dermatomyositis and inclusion body myositis -Dysphagia, nasal regurgitation, aspiration
-May be triggered by certain cancers -Sclerodactyly Management
-Low-grade fever -High dose steroid taper
-Peripheral lymphadenopathy -DMARDS for patients unresponsive to steroids
-Interstitial lung disease
-Frequent co-occurrence with other systemic autoimmune
diseases, another connective tissue disease, or bacterial or viral
infection
45
 Gout
-Monosodium urate deposition  arthritis and inflammation Signs & symptoms Management
-Peak incidence in males ages 40-50 -First attack is usually podagra (sudden inflammation of the 1st -Do not treat asymptomatic hyperuricemia!
-Risk factors: infection, trauma, weight loss, hospitalization, MTP) -Acute attack  continue taking any gout prophylaxis meds,
dyslipidemia -Warmth, swelling, dusky red appearance just like a septic joint treat arthritis first with NSAIDs, consider giving colchicine for
-Usually manifests at night due to fluid shifts continued symptoms, then treat the hyperuricemia 24 hours after
Etiologies -Systemic signs may be present resolution of attack (allopurinol ± probenecid, pegloticase,
-Usually a result of decreased renal clearance of uric acid -Maximum severity in 12-24 hours febuxostat)
(alcohol, CKD, low urine vol, HTN, diuretics, aspirin, -If chronic: tophi in articular structures, tendons, bursae, or bone -Oral or injectable steroids only for suboptimal response to
vasopressin, lactic acidosis, myxedema, respiratory acidosis, NSAIDs & colchicine
preeclampsia, MI, renal insufficiency) Differential -Consider pharmacologic prophylaxis with uric acid lowering
-Sometimes due to increased renal production of uric acid -Septic arthritis agents (and colchicine bridge if needed to avoid ppt attack) if >
(purine consumption, alcohol use, myeloproliferative disorders, -Trauma 2 attacks per year, x-ray erosions, nephrolithiasis or uric acid
polycythemia, leukemia, EBV, psoriasis, drugs) -CPPD/pseudogout nephropathy, or chronic polyarticular gout (wait at least 4-6
-Also influenced by body type, diet, insulin resistance, CHF, -Other inflammatory arthritis weeks after most recent attack and treat for 3-12 months until
and organ transplantation uric acid goal is reached then d/c)
Workup
Stages of gout -Joint aspiration with Gram stain, culture, and microscopy is
1.) Hyperuricemia: typically asymptomatic mandatory if possible for all new cases of monoarticular Prognosis
2.) Acute gout: development may take decades after onset of inflammation, will see urate crystals in joint fluid -Without urate-lowering treatment there is greater risk of tophus
hyperuricemia -Otherwise can diagnose clinically using Rome, New York, or formation, development of chronic gouty arthritis,
3.) Intercritical gout: period between attacks ACR diagnostic criteria nephrolithiasis, and chronic urate nephropathy
4.) Chronic tophaceous gout: caused by repeated attacks  -Plain films will show well-defined erosions in random
resembles RA with chronic symmetric polyarthritis and distribution with overhanging edges a well as tophi
tophaceous deposits, less sudden attacks that take longer to -MRI only used to detect early changes
resolve
Systemic Lupus Erythematosus
-A result of abnormalities in apoptotic Signs & symptoms Workup
cell clearance  generation of -Relapsing and remitting symptoms -Findings accumulate over time, dx may take years
autoantibodies to nuclear antigens, -Fatigue, low-grade fevers -ACR has SLE classification criteria for dx
phospholipids, and other cell surface -Malar rash, discoid rash (differentiate from tinea corporis -CBC, Cr, ESR, CRP, ANA, anti-dsDNA, anti-Sm, anti-RNP, antiphospholipid, anti-Ro, anti-
proteins by its non-fluorescence), psoriasis-like rash La
-A type III hypersensitivity -Skin photosensitivity -X-rays demonstration Jaccoud’s arthropathy (ulnar deviation, MCP subluxation, swan-neck
-Hereditary predisposition based on -Painless oral or nasal ulcers deformities, and diffuse soft-tissue swelling as a result of tendon laxity rather than RA-type
MCH II polymorphisms (HLA-DR2 -Inflammatory arthritis, arthralgias, tenosynovitis, tendon bony destruction)
or HLA-DRR3) or complement rupture, osteonecrosis, myositis, myalgias -Head CT may show unidentified bright objects of unknown clinical significance
deficiencies  can be triggered by an -Vasculitis -UA may show proteinuria and RBC casts if there is lupus nephritis
exposure (infection, UV light, drugs, -Serositis around the heart or lung
stress) in a genetically susceptible -Glomerulonephritis Management
individual -CNS lupus: seizures, psychosis, transverse myelitis, -Always hydroxychloroquine, which is “lupus life insurance”
-Most common in nonwhite women depression, peripheral neuropathy, optic neuritis -Sunscreen
15-40 -Autoimmune hemolytic anemia -NSAIDs for msk complaints, fever, HA, and mild serositis
-Pneumonitis, pulmonary hemorrhage, pulmonary HTN, -Systemic steroids for patients with renal, CNS, or other significant organ involvement
shrinking lung syndrome -Immunosuppressives (methotrexate, cyclophosphamide, azathioprine, mycophenolate,
-Myocarditis, CAD rituximab, etc) for patients with significant organ involvement and inadequate response to
-IBD, pancreatitis, liver disease, lupoid hepatitis steroids
-Lymphadenopathy -CV risk reduction
-For resistant disease, consider high dose chemo followed by autologous stem cell transplant

46
 Osteomyelitis
Agents Signs & symptoms Management
-GAS or GBS -Onset can be insidious or chronic -IV AB for 4-6 weeks
-Staph aureus -Pain, swelling, tenderness, warmth, overlying cellulitis, fever, -MSSA  nafcillin, oxacillin, or cefazolin
-Polymicrobial in IVDU chills, n/v -MRSA or Staph epidermidis  vanco
-H/o direct trauma  Staph or Pseudomonas -Progression of diabetic foot ulcer -Surgical draining and debridement
-Salmonella in sickle cell patients -Gram negs  cipro, levo, ceftazidime, cefepime
Workup -Empiric  vanco + Zosyn
Etiologies -Gold standard is bone biopsy with culture
-Hematogenous seeding (usually monomicrobial) -Can also treat based on + blood cultures
-Contiguous spread from adjacent soft tissue or joint -CBC showing leukocytosis
(polymicrobial) -X-rays only good for chronic osteomyelitis
-Direct inoculation of bone from trauma or surgery -MRI best modality for obtaining details of bone marrow and
(polymicrobial) soft tissue inflammation
Rheumatoid Arthritis
-Genetic role with strong association Signs & symptoms Workup
with HLA-DR1 and HLA-DR4 -Slow, insidious onset with duration of symptoms over weeks to months -Bilateral radiographs of hands, wrists, and feet  imaging
-Risk factors: nulliparity, older age, -Waxing and waning of symptoms shows bony erosion with preservation of joint space
FH, female, cigs, certain infections -Usually > 5 joints involved, with small bones of hands and feet usually the first to be involved, -Rheum labs: ESR and CRP, RF, ANA, anti-CCP
-Protective factors: estrogen, tea, with later progression to larger joints -Arthrocentesis if diagnosis is uncertain
high vit D, breastfeeding -Morning stiffness for at least 1 hour -Diagnostic criteria: inflammatory arthritis of 3+ joints,
-Aggravated by prolonged periods of rest in the same position +RF or +anti-CCP, ↑CRP or ESR, symptoms > 6 weeks,
Pathophysiology -Fatigue, malaise, low-grade fever, weight loss exclusion of other diseases on differential (however, it is
-Triggering incident  -Chronic swelling and joint warmth (but usually no erythema), decreased ROM possible to have seronegative RA)
proliferation of macrophages and -Hands: boutonniere or swan neck deformities of the fingers, ulnar deviation of the fingers
fibroblasts -Feet: subluxation of MTPs  calluses on bottom of feet Management
-Lymphocytic invasion of the -Wrists: synovial proliferation  median nerve compression, extensor tendon rupture -Goals are to prevent further joint damage, prevent loss of
-TMJ syndrome function, decrease pain, control systemic complications,
perivascular space
-Manifestations in the atlantoaxial joint  UE paresis with head movements, pain radiation to and maximize quantity of life
-Local blood vessels become occiput -NSAIDs should not be used alone as they don’t alter
occluded  outpouching of -Less common manifestations: palindromic rheumatism, monoarthritis of large joint, extra- disease course
synovial membrane (“pannus”) articular manifestations (skin, CV, pulm, eye, neuro, heme, renal, bone) -Glucocorticoids are usually used long-term
that eventually invades cartilage -DMARDS should be started within 3 months of diagnosis
and bone  release of cytokines, Differential -PT/OT
proteases, and IL  further joint -Post-infectious sequelae -Survey for infections, malignancy, osteoporosis, and
destruction by T-cells and -Other systemic rheumatic disease: SLE depression
macrophages -Lyme arthritis
-Fibromyalgia Prognosis
-Psoriatic arthritis -Disease will be lifelong with 3-5 year reduction in life
-IBD-associated arthritis expectancy
-CPPD -Spontaneous remission can occur
-Polyarticular gout -Complications: infection with unusual pathogens from tx,
Felty’s syndrome, Bakers cysts, risk of malignancy

47
 DMARDs
Agent & MOA Methotrexate: inhibits Hydroxychloroquine: interferes Sulfasalazine: impairs Leflunomide: inhibits Biologics
difolate reductase in WBCs with Ag presentation lymphocyte transformation synthesis in WBCs
and suppresses NK cells
Info -First-line DMARD -The best-tolerated DMARD, -Good for mild disease -Can be used alone or with -Anti-TNFs
-Best for moderate-severe best for mild disease -Takes 1-3 months to work methotrexate -Costly
disease -Takes 1-6 weeks to work -Slows radiographic -Used in combination
-Slows radiographic damage -Does not slow radiographic progression with other DMARDs
and may reduce mortality damage so should not be used
alone
Risks & AEs -AEs: n/v/d, anorexia, -AEs: n/v/d, myopathy, HA, -AEs: HA, photosensitivity, -AEs: diarrhea, weight loss, -AEs: HA, infusion
alopecia, rash, retinopathy, agranulocytosis, rash, n/v/d, anorexia, HTN, alopecia, rash, elevated reaction, abd pain,
myelosuppression, liver or skin pigmentation  monitor myelosuppression, liver and LFTs  monitor LFTs, Cr, vomiting
renal failure, hyperuricemia, with eye exams, CBC, neuro kidney failure, oligospermia CBC, signs of infection,
oral ulcers, cough, SOB  exam  monitor CBC, LFTs, BMP pregnancy tests
need to monitor LFTs, CBC, -Interactions with thiazides -Pregnancy X and elimination
Cr, CXR, liver biopsy every and warfarin can take up to 2 years so
1.5 g couples wishing to conceive
-Pregnancy X must undergo a cholestyramine
-Interactions with NSAIDs, washout
penicillins -Contraindicated in hepatitis or
h/o alcohol abuse b/c it’s
metabolized in the liver
Polyarteritis Nodosa
-Rheumatic vasculitis of medium-sized arteries with occasional Signs & symptoms Workup
involvement of small muscular arteries -Systemic presentation: fever, fatigue, weakness, loss of -CBC showing leukocytosis
appetite, weight loss -↑ESR or CRP
Etiology -Infarctions manifest as renal failure, HTN, edema, oliguria, -CMP
-Most cases are idiopathic uremia, skin lesions, arthralgias, myalgias, peripheral -Rheum workup tailored to differential
-Hep B or hep C or hairy cell leukemia are linked to some cases neuropathies, MI, CHF, pericarditis, and GI tract issues, but -Confirmatory diagnosis should be made by biopsying clinically
typically spares the lungs affected organ
-Skin manifestations include tender erythematous nodules, -Alternative for dx is arteriography or cross-sectional imaging
purpura, livedo reticularis, ulcers, bullous or vesicular eruptions
(may be focal or diffuse and can progress to infarction and
gangrene)
-Limb edema
Polymyalgia Rheumatica
-Seen mostly in white female patients over age 50 Differential Workup
-Seronegative RA -Elevated ESR/CRP
Signs & symptoms -Bursitis or tendonitis
-Pain and stiffness of neck or torso, shoulders or proximal -Spondyloarthropathy Management
regions of the arms, and hips or proximal aspects of the thighs -CPPD -Prednisone
for at least 1 month -Hypothyroid
-Most severe in the morning and lasts at least 30 min -Fibromyalgia
-Decreased ROM of the shoulders, neck, and hips -Malignancy
-No weakness or decrease in muscle strength -Infective endocarditis
-Often co-exists with giant cell arteritis -Dermatomyositis or polymyositis
-Vasculitides

48
 NEUROLOGY
Dementia
-The most common cause of dementia is Alzheimer’s disease Signs & symptoms Management
-Other major types are Lewy body dementia, frontotemporal -Insidious appearance and progression of cognitive deficits, -Cholinesterase inhibitor for mild to moderate dementia (MMSE
dementia, vascular dementia, and Parkinson-associated usually beginning with language function and visuospatial skills 10-26): donepezil, rivastigmine, galantamine
dementia -Pt will not usually report memory loss but family members will -Vitamin E 1000 IU BID if no CV disease
-Dementia is characterized by memory impairment and -Later deficits in executive function and behavior -Add memantine for mod-advanced dementia (MMSE < 17)
impairment in one other cognitive domain (aphasia, apraxia, -Noncognitive neurologic deficits in late-stage disease: -D/c treatment when MMSE < 10 unless pt worsens
agnosia, executive function) pyramidal and extrapyramidal motor signs, myoclonus, and significantly when off of them
seizures -For behavioral issues, first r/o superimposed delirium
Screening -Atypical presentations: visual variant, primary progressive -Agitation and aggression are best managed by behavioral
-USPSTF grade I aphasia intervention rather than antipsychotics like haloperidol
(evidence for aromatherapy exists as well as exercise, music, pet
DSM-IV criteria Differential therapy, and massage)
-History and MMSE indicate major impairment in learning and -Delirium -Depression: SSRIs may help, better choice for the elderly is
memory as well as at least one of the following: -Depression citalopram
• handling complex tasks -Brain disease -Sleep disorders: small quantities of trazodone if needed
• reasoning ability -Normal age-related cognitive decline: mild changes in -Wandering
• spatial ability and orientation memory and rate of info processing that are NOT progressive -Sexually inappropriate behavior: antidepressants,
• impaired language and don’t affect daily function antipsychotics, cholinesterase inhibitors, other agents
-Cognitive symptoms must significantly interfere with work -Delusions and hallucinations: atypical neuroleptics incur
performance, usual social activities, or relationships with others Workup increased risk of mortality but may be necessary
-This must represent a significant decline from previous -Full neuro exam
functioning -MMSE: scores < 24 suggestive of dementia or delirium Prognosis
-The disturbances are of insidious onset and are progressive, -Clock drawing test appears to correlate with MMSE -Average life expectancy of 3-8 years
based on evidence from the history or serial MMSEs -Labs: B-12, TSH
-Not accounted for by delirium, other major psychiatric -Depression screen
diagnosis, systemic disease, or another brain disease -Noncontrast head CT or MRI

Huntington’s Disease
-Abnormal CAG repeats on chromosome 4  loss of caudate Signs and symptoms Management
and squared-off lateral ventricles -Usually begins with a psychiatric disorder -Symptomatic
-Onset will occur between ages 20-40, which can be affected by -Subcortical dementia, chorea, dystonia, motor impersistence, -Give dopamine-R blockers for chorea (like a DA-excess state)
anticipation incoordination, gait instability, depression, anxiety, impulsivity, such as haloperidol or risperidone
apathy, OCD, athetosis -SSRIs for depression and anxiety

Workup Prognosis
-Diagnosis is clinical -Death within 10-15 years of onset of symptoms
-CT or MRI will show cerebral atrophy and loss of caudate

49
 Seizure Disorders
-Epilepsy = documented h/o at least 2 seizures Differential Workup Management
not related to a metabolic or febrile cause -Hyperventilation -EEG to determine seizure -When to treat after a single seizure: patients with structural lesion, abnormal EEG, focal
-Risk factors: head trauma, CNS infections, -Migraine type seizure
cerebrovascular disease, alcohol, drug -Panic attack -Electrolytes, glucose, -When NOT to treat after a single seizure: EtOH, drug abuse, provoked seizure, head
overdose or withdrawal, metabolic disorders, -Pseudoseizure anticonvulsant levels, alcohol injury with no structural abnormality
genetics, malignancy -Syncope and tox screen, ABG -Drugs are selected based on type of seizure, AEs, toxicity, cost, and childbearing
-Common provoking factors: sleep deprivation, -Transient global -LP to r/o meningitis potential
excessive stimulants, withdrawal from ischemia -Head CT or MRI -Begin with monotherapy
sedatives or alcohol, substance abuse, high -TIA -Consider 2nd agent if inadequate trial of 2 different single agents
fever, hypoxia, hypoglycemia, electrolyte -Sleepwalking
disturbance, estrogen (= more seizures during -Meningitis Prognosis
ovulation and menses) -Most epileptics who go into remission do so within 3 years after their first seizure
-Poor prognostic factors for remission: FH of epilepsy, psychiatric comorbidity, h/o
febrile seizures, > 20 seizure history, adult age, failed monotherapy
Partial Seizures
Simple Partial Seizures Complex Partial Seizures Management
-No LOC -The most common kind of seizure -1st line: carbamazepine,
-Alternation contraction and relaxation of muscle groups -Can occur after head trauma and many of these pts will have phenytoin, lamotrigine,
-Eye movements and turning of head to the same side abnormal tissue or lesions in their temporal lobe valproate, or oxcarbazepine
-Speech arrest or vocalization -Involves alteration of consciousness -2nd line: gabapentin,
-May see flashes of light or color or have hallucinations -Automatisms such as lip smacking, picking, patting, chewing, or topiramate, levetiracetam,
-May hear humming, buzzing, or hissing swallowing zonisamide, tiagabine,
-May experience unpleasant tastes or odors -Inability to carry out simple commands or execute willful phenobarbital, felbamate
-Dizziness movement
-Autonomic symptoms: flushing, incontinence, nausea, vomiting, goose bumps, pupillary -Lack of awareness of surrounding and events
dilation, sweating, tachycardia -Can become generalized tonic-clonic seizure
-Psychiatric symptoms: detachment, memory distortion, time distortion, unprovoked emotion
-Can turn into a complex partial seizure or manifest in a continuous form (epilepsia partialis
continue)
Generalized Seizures
Absence (Petit Mal) Seizures Tonic-Clonic (Grand Mal) Seizures Myoclonic Seizures Other Seizures
-5-10 recurrent episodes of staring -Tonic phase begins with LOC, tensing -Caused by metabolic abnormalities such Tonic seizures
-May have minor motor automatisms of muscles, and often a loud yell or moan as hepatic or renal failure -Relatively rare to occur alone
-Pts have no memory of incident but are completely -Clonic phase commences with -Brief major motor seizure with quick, -Involve stiffening of the body, upward deviation of
normal afterwards convulsions, eyes rolling back, strong lightning-like jerking movements of the the eyes, dilation of the pupils, and altered
-Can be triggered by hyperventilation jaw contractions trunk or extremities respiratory patterns
-May have aura -May occur throughout body or limited to
Workup -Lasts 5-20 minutes certain muscle groups Atonic seizures
-EEG abnormality will be present even when not -May have incontinence -Onset may be so sudden that pt falls to -Sudden loss of muscle tone that may cause a fall
seizing -May have unconsciousness after seizure the ground but can also be so brief that -Last 1-4 secondes but without LOC
followed by post-ictal state consciousness is not lost -May affect one part of body to all body tone
Management
-1st-line: valproate, ethosuximide Management Management Management
-2nd line: lamotrigine, levetiracetam -1st line: phenytoin, carbamazepine, -1st line: clonazepam, valproate -1st line: valproate
valproate -2nd: lamotrigine, levetiracetam, -2nd line: lamotrigine, topiramate, zonisamide
nd
Prognosis -2 line: lamotrigine, levetiracetam, topiramate, felbamate, zonisamide
-Most cases resolve spontaneously topiramate, phenobarbital, primidone,
oxcarbazepine
50
 Anticonvulsants
Agent & MOA Info Risks & AEs
Carbamazepine: inhibits -Also for treating bipolar disorder, trigeminal neuralgia, and -AEs: diplopia, dizziness, drowsiness, nausea, Stevens-Johnson (don’t use in Asians), hypoCa, hypoNa,
voltage-gated Na channels glossopharyngeal neuralgia SIADH, hematologic, hepatitis  monitor CBC, LFTs, mental status, bone density, levels
-Decreases effectiveness of OCPs and warfarin
-Pregnancy D
Oxcarbazepine: blocks voltage- -For partial seizures -AEs: sedation, dizziness, ataxia, nausea, Stevens-Johnson, hypoNa  monitor Na
gated Na channels, modulates Ca -Decreases effectiveness of OCPs and phenytoin
channels, increases K -Pregnancy C
conductance
Clonazepam: modulates GABA -Not a first-line choice
transmission in the brain -Frequently added as a 2nd agent with levetiracetam
Ethosuximide: increases seizure -For absence seizure -AEs: ataxia, drowsiness, GI, unsteadiness, hiccups, Stevens-Johnson, hematologic, SLE
threshold, depresses nerve -Interactions with carbamazepine and valoproate
transmission in the motor cortex -Pregnancy C
Felbamate: glycine-R agonist -For partial and generalized seizures -AEs: anorexia, n.v, insomnia, HA, Stevens-Johnson, aplastic anemia, hepatic failure = weekly LFTs &
last resort drug!
-Must sign informed consent
-Interacts with many other seizure meds
-Pregnancy C
Gabapentin or pregabalin: -Add-on therapy for seizures -Renal dosing needed
modulate Ca channels -Also for neuropathic pain -AEs: dizziness, fatigue, ataxia, nystagmus, tremor, HA, peripheral edema, Stevens-Johnson
-Pregnancy C
Lamotrigine: blocks voltage- -Also for bipolar disorder -AEs: nausea, diplopia, dizziness, unsteadiness, HA, rash, Stevens-Johnson, hematologic, liver failure
gated Na channels and inhibits -Interaction with valproate
glutamate release -Pregnancy C
Levetiracetam: inhibits Ca -For partial, tonic-clonic, and myoclonic seizure -AEs: sedation, suicidal ideation, pancytopenia, liver failure
channels, facilitates GABA, -Pregnancy C
reduces K currents, modulates
NT release
Phenobarbital: decreases post- -Indicated for seizure and sedation -AEs: ataxia, hyperactivity, HA, unsteadiness, sedation, nausea, cognitive impairment, blood dyscrasia, S-
synaptic excitation J, hepatic injury, osteopenia
-Many drug interactions
-Pregnancy D
Phenytoin: stabilizes neuronal -May be given as fosphenytoin for faster effect -AEs: ataxia, nystagmus, behavior, dizziness, HA, sedation, lethargy, incoordination, blood dyscrasias,
membranes by altering Na efflux -For generalized and complex partial seizures rash, hirsutism, peripheral neuropathy
Tiagabine: inhibits GABA -Adjunct therapy for partial seizures -Pregnancy C
reuptake
Topiramate: modulates Na -For partial or generalized seizures -AEs: difficulty concentrating, psychomotor retardation (“dopamax”), speech or language problems,
channels, enhances GABA, -Also indicated for migraine prevention fatigue, HA, metabolic acidosis, kidney stones  monitor BMP
antagonizes glutamate-R -Interacts with OCPs
-Pregnancy C
Valproate: increases GABA -For absence, complex partial, or mixed-type seizures -AEs: GI upset, sedation, unsteadiness, tremor, thrombocytopenia, palpitations, immune hypersensitivity,
-Also for bipolar disorder or migraine prophylaxis ototoxicity  monitor CBC and LFTs
-Many drug interactions
-Pregnancy D
Vigabatrin: irreversibly inhibits -For refractory complex partial seizures or complex generalized seizures -AEs: permanent visual loss, psychiatric disturbances = in a restricted dist program
GABA transaminase
Zonisamide: MOA unknown -Adjunct for partial seizure -AEs: sedation, dizziness, cognitive impairment, nausea, kidney stones, S-J, schizophreniform disorder
-Pregnancy C

51
 Myasthenia Gravis
Etiology Differential Workup
-Production of ABs against Ach receptors -Botulism -Tensilon test: acts as an Ach converting enzyme inhibitor to temporarily overcome
-Many cases are associated with a thymoma -ALS neuromuscular jcn Ach deficit
-Dermatomyositis or polymyositis -Labs: anti-Ach-R AB, MuSK AB
Signs & symptoms -Lambert-Eaton myasthenic syndrome -Repetitive nerve stimulation test
-Ocular: Ptosis, blurred vision, diplopia -MS -Single fiber EMG is the most sensitive test for myasthenia gravis
-Bulbar/facial: difficulty chewing or swallowing, dysarthria, tired -MI -Chest CT to rule out thymoma
facial appearance, difficulty smiling or whistling, difficulty keeping -PE
food in mouth -Sarcoidosis Management
-Asymmetric proximal or distal extremity weakness -Neuropathy -Thymectomy
-SOB -Thyroid disease -Meds: Ach converting enzyme inhibitors like pyridostigmine, immunosuppressants
-Muscle weakness with repetitive use -Intubation if needed (don’t use depolarizing or non-depolarizing agents)
-Plasmapheresis to remove pathologic AB
-Exacerbation can be precipitated by infection, surgery, pregnancy, or certain meds
= avoid aminoglycosides, azithromycin, quinolones, botox, CCB, Mg, IV contrast
Transient Ischemic Attack
-An acute focal neurologic deficit as a result of Workup Management Prognosis
ischemia that resolves within 24 hours -CBC, BMP to r/o metabolic causes -Risk reduction: smoking cessation, statins, BP -Incurs greater risk of stroke in the future, can
-Can be caused by brain, spinal cord, or retinal -Lipids control use ABCD2 criteria (age, BP, clinical features,
ischemia -Brain imaging to r/o hemorrhage or cerebral -Antiplatelet therapy indicated for duration of sx, DM) to estimate risk
tumor noncardioembolic attacks: aspirin or
Differential -Neurovascular imaging: carotid US, CTA if clopidogrel (only marginally better than ASA)
-Seizure needed -Anticoagulant therapy indicated for pts with
-Migraine with aura -Cardiac eval: EKG, echo if there is suspected concurrent afib
-Syncope endocarditis -Carotid endarterectomy for select patients
-Hypoglycemia
-Encephalopathy
-Multiple sclerosis

52
 Stroke
-An acute neurological deficit of vascular etiology with symptoms lasting > 24 hours Differential: transverse myelitis, Bell’s palsy, Gullain-Barre, myasthenia gravis, TIA
-More prevalent in the “stroke belt” in SE US
Types of Stroke
Hemorrhagic Ischemic
Accounts for 15-20% of strokes -Accounts for 80-85% of strokes

Parenchymal ICH Atheroembolic

-Occlusion of artery supplying the brain due to CAD, stenosis, or cholesterol embolus
-Bleeding within the brain itself
-The most common kind of stroke
-Primary if due to spontaneous rupture of -There will be warning signs with a stepwise progression to full stroke, such as transient language
small vessels damaged by chronic HTN or disturbances and weakness
amyloid angiopathy -Ophthalmic artery occlusion  amaurosis fugax
-Secondary if due to trauma, vascular -ACA occlusion  weakness and sensory loss in contralateral leg, may have mild weakness of the arm
abnormalities, tumors, impaired coagulation, -MCA occlusion  contralateral hemiplegia, hemisensory loss, homonymous hemianopia with eyes deviating
or vasculitis towards affected side, global aphasia if in dominant hemisphere,
-Presentation will be severe HTN, bad HA, -Lacunar stroke: a kind of atheroembolic stroke where one of the penetrating arteries providing blood to the
brain’s deep structures is occluded  can appear as pure motor strokes, pure sensory strokes, ataxic
n/v, focal neuro deficits
hemiparesis, or dysarthria + clumsy hand
-If in thalamus or basal ganglia  -Dilated pupils with vertebrobasilar stroke
contralateral motor and sensory deficit,
aphasia, language or spatial neglect, depressed LOC due to Cardioembolic
mass effect, intraventricular extension  hydrocephalus -Embolus thrown from the heart goes to the brain; can then break up into many clots and travel to multiple
-If in the cerebellum  ipsilateral ataxia, depressed LOC vascular territories
-If in the pons  vertigo, diplopia, crossed signs, depressed -Can also cause a hemorrhagic infarction as the ischemic blood vessels die and split open (will want to
LOC differentiate this from primary ICH, because if it’s primary you can’t give blood thinners or lytics ever again
but if the hemorrhage is secondary to blood clot you want to put the pt on blood thinners to prevent future
embolic strokes)
Subarachnoid hemorrhage -Sources: afib, cardiomyopathy, acute MI, valvular heart disease
-Bleeding outside the brain -Most commonly lodges in the middle cerebral artery
-Most common cause is a ruptured aneurysm, usually of the
anterior communicating artery, but can also occur at the Workup
bifurcation of the carotid, PCCM, MCA, basilar tip artery, or -Head CT: warning! will look normal until several hours into stroke
PICA
-Less common causes are vasculitis, infection, neoplasms, or Management
-Start TPA if within 4.5 hours of symptom onset (this is the cutoff point for prevention of disability) after
blood coagulopathies
cleared by head CT
-Risk factors: heavy alcohol, smoking, HTN, genetics -TPA relative contraindications, within 3 hours of symptom onset: recent head trauma or stroke, prior ICH,
-Presentation will be with an abrupt, severe headache, recent arterial puncture, active bleeding or acute trauma, on oral anticoags with hi INR, low platelets,
meningismus, may have rapid LOC hypoglycemia, HTN > 185/110, CT with hypodensity in > 1/3 of cerebral hemisphere, rapidly improving
-Neuro exam will be nonfocal because it is outside of the symptoms, seizure with postictal impairment, recent MI, recent major surgery
brain -TPA further contraindications if > 3 hours after symptom onset: age over 80, oral anticoags, h/o prior stroke
+ DM
Workup -Consider endovascular repair or clot removal if TPA is not an option, and give aspirin instead
-Avoid D5W as glucose crosses into the brain and is quickly metabolized  edema
-CT will show white in area of bleed
-Only lower BP if > 220/120, and only by 15-20% the first day, otherwise avoid treating HTN for at least 2
weeks to avoid further cerebral ischemia
Management -Hypothermia induction therapy?
-Parenchymal ICH is managed supportively, with surgical consult if there is mass effect -Antithrombotic agents
-Subarachnoid hemorrhage typically requires surgical intervention -Later PT, OT, speech therapy

Prognosis
-Everyone improves to some degree after a stroke
-Fastest period of recovery is the first 30-60 days afterwards

53
 Parkinson’s Disease
-Degeneration of CNS due to death of DA- Signs & symptoms Workup
generating cells in the substantia nigra and -Most symptoms are unilateral (if bilateral the cause is more like to be an exposure) -Diagnosis is usually clinical
accumulation of Lewy bodies in neurons -Pill-rolling resting tremor, cogwheel rigidity, shuffling steps, difficulty initiating movements with -Head MRI to rule out brain lesions
-Risk factors: age, exposure to synthetic heroin festinating gait (unwanted acceleration after walking commences) -Genetic testing is available but should
byproduct MPTP, manganese exposure, flu -Bradykinesia, fatigue, stooped posture, masked facies only be performed after careful
epidemic -Memory loss consideration due to inconclusive testing
-Small, cramped handwriting results and lack of specific treatment for
Etiology the disease
-Most cases are idiopathic Differential
-5% of cases are hereditary -Lewy body dementia and other neurodegenerative disorders Management
-Essential tremor -Treatment should begin when patient
-Secondary parkinsonsism (usually a drug reaction) experiences functional impairment
Pharmacologic Therapy
Synthetic DA: DA precursor that can cross the BBB to DA Agonists: act directly on DA-R in COMT Inhibitors: prevent MAO-B Inhibitors: inhibit Others
replace deficit the corpus striatum breakdown of levodopa by another metabolism of dopamine
pathway

-Levodopa -Bromocriptine, pramipexole, -Entacapone, tolcapone -Selegiline, rasagiline -Amantadine:

-Must also give carbidopa to prevent peripheral conversion ropinirole, apomorphine -Allows for decreased levodopa -Can help delay need for antiviral that
-Can be given to help diagnose Parkinson’s -First-line therapy for younger patients dosage levodopa increases DA release
-First-line therapy in older patients (> 65) as effectiveness ↓ with milder disease -AEs: dyskinesias, nausea, -AEs: insomnia, nausea from nerve terminals
over time -Can delay need for levodopa dizziness, hallucinations, abd pain, -Anticholinergics:
-Won’t help with postural instability, dementia, autonomic -Can be add-on to levodopa therapy diarrhea, orthostasis, somnolence, block Ach
dysfunction, or “freezing” -AEs: cardiac valve fibrosis, dizziness, HA -Vit E
-Won’t stop disease progression HA, insomnia or somnolence, fonusion, supplementation not
-AEs: n/v, anorexia, postural hypotension, arrhythmias, hallucinations, hypotension, syncope, shown to be
mental disturbance, dyskinesias, overactivity, agitation impulsivity beneficial

PSYCHIATRY
Generalized Anxiety Disorder
Etiology Workup Management
-Likely a combination of genetic factors and environment -DSM-IV criteria: -First-line is CBT or an SSRI or SNRI with a 6-8 week trial, treat for at
1. Excessive anxiety and worry about lots of things least a year
Screening out of proportion to the likelihood or impact of -Second-line:
-GAD-7 has been validated as a primary care tool feared events, occurring more days than not for at • buspirone: reduced abuse potential, less weight gain and sexual
least 6 mo AEs
Signs & symptoms 2. Worry is pervasive and difficult to control • benzos
-Common comorbidity is major depression 3. Anxiety and worry are associated with 3+ of these • TCA such as imipramine: limited use due to AEs
sx: restlessness or on edge, easily fatigued, -Third-line:
Differential difficulty concentrating, irritability, muscle tension, • hydroxyzine: use limited by sedation and lack of efficacy in
-Adjustment disorder with anxious mood: fits pts who sleep disturbance comorbid diseases
have had sx < 6 mo that are associated with a particular 4. Anxiety, worry, or physical symptoms cause • pregabalin
stressor or event within 3 months of onset of sxs significant stress or impairment socially, at work, • quetiapine
-CV problem or in other areas of life -For remaining insomnia, add on a non-benzo hypnotic, benzo,
-Excess caffeine or MSG intake or other stimulants -Labs to consider: CBC, BMP, TSH, UA with tox screen, trazodone, mirtazapine, or sedating hypnotic
-Vitamin deficiency EKG in pts over 40 with associated chest pain or palps -For inadequate response, switch antidepressants or add atypical
-Anemia, adrenal disease, or secreting tumor antipsychotic, benzo, antihistamine, or buspirone
54
 Depressive Disorders
-Episodes are classified as mild, moderate, or severe Screening Workup Management
-Half of cases are missed by PCPs -USPSTF grade B for nonpregnant -MMSE -Referral to psychiatry indicated for pts
-First episode most common in ages 30-40, with smaller adults as long as there are supports in -TSH, CMP and Ca to r/o metabolic disturbance, with severe depression, depression
peak at 50-60 place for effective treatment RPR, CBC to r/o systemic infection, folate, vit D, unresponsive to initial treatment,
-PHQ-2 or PHQ-9 vit B12, drug screen psychotic depression, depression with
Subtypes -Geriatric depression scale -DSMI-IV diagnostic criteria: 5+ of the following other psychiatric diagnosis
-Melancholic depression: loss of pleasure in most symptoms present nearly every day for a minimum -Psychotherapy recommended in
activities, nonreaction to pleasurable stimuli, worsening of Differential of 2 weeks (at least 1 symptom must be depressed combination with pharmacotherapy for
sx in early morning hours, psychomotor retardation, -Dysthymia: a chronic, milder mood mood or loss of interest or pleasure) patients with severe chronic or
excessive weight loss or guilt disturbance that has been present for at • Depressed mood recurrent depression
-Atypical depression: mood reactivity, weight gain, least 2 years • Loss of interest or pleasure in most or all -Exercise
excessive sleep, heavy sensation, significant social -Adjustment disorder with depressed activities -Electroconvulsive therapy is last resort
impairment mood: occurs when identifiable • Insomnia or hypersomnia -Melancholic subtype responds best to
-Catatonic depression: rare form involving disturbances of psychosocial stressor(s) that has • Change in appetite or weight gain TCAs or MAOIs
motor behavior occurred within the last 3 months can • Psychomotor retardation or agitation -Atypical subtype responds best to
-Postpartum depression: intense, sustained depression be attributed to depressed mood, and • Low energy SSRIs or SNRIs
experienced within 1 month of giving birth depressed mood resolves within 6 • Poor concentration -For refractory depression, confirm dx
-Seasonal affective disorder: resolves in spring months after the stressor has ended and medication adherence and r/o
• Thoughts of worthlessness or guilt
-Major depression with psychotic features: delusions or (BUT if pt meets criteria for MDD this organic causes of depression, switch to
• Recurrent thoughts about death or
hallucinations are present diagnosis will supersede dx of another antidepressant or augment, and
suicide
adjustment disorder) consider less common regimens such as
Etiology -Minor depressive disorder: pt meets tranylcypromine or venlafaxine +
-Multifactorial, involving biologic, psychologic, and social criteria for 2-4 of MDD criteria mirtazapine
factors -Bipolar disorder
-Dementia
Pharmacologic Management
-Effectiveness of SSRIs, SNRIs, bupropion, TCAs, and MAOIs is generally comparable
-Begin dose at lowest effective dose and increase incrementally until patient achieves remission
-Switch after 8 weeks of therapy if no response
-If partial response at 8 weeks, can switch or augment therapy with bupropion or buspirone
-May need to use doses higher than what is FDA approved
-Duration of treatment should be continued until 4-9 months after remission of symptoms for 1st episode, an additional year after that for 2nd episode, and possibly continue treatment indefinitely for
3rd episode or more
Class & MOA Agents Info Risks & AEs
SSRIs: inhibit reuptake -Fluoxetine: longest half-life, many drug -AEs: GI, CNS, sexual, sedation, fatigue, dry mouth, hypotension, withdrawal if
of serotonin as well as interactions, lowest weight gain = good for d/c abruptly, prolonged QT, rash, insomnia, asthenia, seizure, tremor,
slight effects on eating disorders, highest risk for serotonin somnolence, mania, suicidal ideation, worsened depression
histamine-R, α1-R, and syndrome
muscarinic-R -Citalopram and escitalopram: low risk of
sexual AEs
-Fluvoxamine
-Sertraline: few drug interactions
-Paroxetine: shortest half-life, most sedating,
greatest weight gain, greatest sexual AEs,
greatest anticholinergic activity

55
SNRIs: inhibits -Venlafaxine: ER available -Equally effective as SSRIs for -AEs: GI, HTN, CNS, permanent sexual?, diaphoresis, dizziness, fatigue,
reuptake of both -Duloxetine: less AEs than venlafaxine treating major depression insomnia, blurred vision, suicidal ideation, dysuria, worsened depression
serotonin and -Desvenlafaxine -May be more effective in the -Fewer drug interactions
norepinephrine setting of diabetic neuropathy,
fibromyalgia, msk pain, stress
incontinence, sedation, fatigue, and
patients with comorbid anxiety
Atypical Bupropion -May increase sexual function -AEs: lower seizure threshold, insomnia, nervousness, agitation, anxiety, tremor,
Antidepressants -Has stimulant effects = good for comorbid arrhythmias, HTN, tachycardia, S-J, weight loss, GI, arthralgia or myalgia,
ADHD but don’t use if comorbid anxiety confusion, dizziness, HA, psychosis, suicidal ideation
Mirtazapine -Less nausea and sexual AEs -AEs: the most sedating antidepressant, weight gain, orthostatic hypotension,
-Overdose is generally safe dizziness, dry mouth
Nefazodone
Trazodone -AEs: arrhythmia, hyper or hypotension, diaphoresis, GI, hemolytic anemia,
leukocytosis, dizziness, HA, insomnia, lethargy, memory impairment, seizure,
somnolence, priapism, weight gain
Tricyclic -Amitriptyline -AEs: anticholinergic, CV, CNS, weight gain, sexual dysfunction, decreased
Antidepressants: -Clomipramine seizure threshold
inhibits reuptake of both -Desipramine -Overdose can be lethal
serotonin and -Doxepin
norepinephrine -Imipramine
-Nortriptyline
MAOIs: block -Phenelzine: irreversible -MAO-A acts on norepinephrine -AEs: anticholinergic, lower seizure threshold, weight gain, rash, orthostasis,
destruction of -Tranylcypromine: irreversible and serotonin sexual dysfunction, insomnia or somnolence, HA, HTN crisis in presence of
monoamines centrally -Selegiline: reversible -MAO-B acts on phenylethylamine monoamines,
and peripherally and DA -Overdose is lethal
-2 week washout period of other antidepressants needed before starting in order
to prevent serotonin syndrome
Alcohol Dependence
-Strong genetic risk factors, with heritability similar to DM or Withdrawal Management
HTN -Triggered by abrupt cessation or reduction of intake in -Inpatient management needed for possible withdrawal if there
-Associated health risks include HTN, a-fib, cardiomyopathy, dependent individuals is h/o seizures, delirium, mental instability, suicidal or
esophagitis, gastritis, upper GIB, pancreatitis, hepatitis, cirrhosis -S/S: tremor, tachycardia, HTN, sweating, insomnia, nausea, homicidal ideation, psychosis, unstable environment, or no
-Related illnesses include pneumonia, TB, and cancers of the vomiting, photophobia, hallucinations, hyperreflexia, irritability, support or transportation available
breast, liver, throat, and esophagus alcohol craving, seizures -Can consider outpatient management if there are no risk factors
-Onset in 12-24 hours after last drink, with peak intensity at 24- -Thiamine supplementation
48 hours
-Lasts 4-7 days
-Mortality is 10-15%

56
 Tobacco Dependence
Screening Withdrawal symptoms Nonpharmacologic management
-Readiness assessment: 5 A’s (ask -Onset of symptoms 2-3 hours after last tobacco use -STAR: set quit date 2 weeks out, tell family and friends, anticipate challenges, remove tobacco
about smoking status, give clear with peak in 2-3 days, resolution in 1 month after products from environment
personalized advice, assess readiness quitting -Assess dependence level and suggest dosing using Fagerstrom questionnaire
to quit and barriers, assist with quit -Increased symptoms if > 25 cigs per day, first cig -Nonpharmacologic methods: cold turkey, unassisted tapering, assisted tapering (QuitKey), formal
resources, arrange for quit date and within 30 min of waking, discomfort if forced to cessation programs, aversion therapy, acupuncture, hypnotherapy, massage therapy
f/u refrain from smoking -Electronic cigarette: recent safety issues with battery igniting, not FDA approved

Prognosis
-Tobacco smoke increases risk of certain cancers: lung, laryngeal, oral cavity, esophagus, bladder,
kidney, pancreas, uterus, and cervix
Pharmacologic Management
-Good combination therapy: nicotine patch + lozenge or gum, nicotine patch + nicotine inhaler, nicotine patch + bupropion SR
Nicotine Replacement Therapy
-Increases likelihood of successful quit by 2-3x
-Low abuse potential
-Pt must not use any tobacco products while using
-Most formulations are available OTC although minors need a Rx
-Cautions: underlying CV disease (as nicotine causes ↑HR and BP), recent MI, serious arrhythmias, serious or worsening angina, pregnancy, lactation
Transdermal patch Nicotine gum Lozenge Inhaler Nasal spray
-Nicoderm -Nicorette, generics -Commit, Nicorette -Nicotrol -Nicotrol NS
-Avoids first pass metabolism -Need to chew n’ tuck -Can’t chew, need to let large -Rx only -Rx only
-Can’t cut patches as this causes -Can’t eat or drink for 15 before lozenge dissolve over 30 min -Benefit of hand-to-mouth behavior -Benefit of nicotine bolus that mimics
nicotine evaporation and ↓ and after (although new mini lozenge will -Not meant to be inhaled all the way burst from cigs  fast reduction of
effectiveness -Helps with acute ravings dissolve faster) into lungs cravings but ↑ abuse potential
-Must remove patches before MRI -AEs: n/v, abd pain, hiccups, -Dose based on time to first -Open cartridge only potent for 24 hours -AEs: local nasopharyngeal irritation,
to avoid burns mouth irritation, sore jaw, cigarette -AEs: mouth and throat irritation, cough runny nose, sneezing, cough, throat and
-Not for relief of acute cravings unpleasant taste -Helps with acute craving relief -Caution with severe reactive airway eye irritation, HA
-AEs: skin irritation, insomnia, -Contraindicated with TMJ, poor -AEs: mouth irritation or ulcers, disease -Caution with severe reactive airway
nightmares or vivid dreams dentition, dentures abd pain, n/v/d, HA, palps disease
Other Pharmacologic Management
Bupropion Varenicline (Chantix) Other 2nd line therapies:
-1-2 daily doses, starting 1 week prior to quit date to allow time -Blocks nicotine from cigs from binding -Nortriptyline
for accumulation of norepinephrine and DA in the body -Begin 7 days before quit date, with differing doses throughout -Clonidine
-Try at least 7 weeks before d/c treatment
-Best option for patients with CV disease -AEs: insomnia, nausea, abnormal dreams, impaired driving or
-AEs: insomnia, dry mouth, suicidality operating machinery, suicide risk (accounts for most cases of
-Contraindications: pt with seizure disorder, pt with h/o suicide attempt while undergoing smoking cessation), CV risk
anorexia or bulimia, pts undergoing abrupt d/c of ethanol or
sedatives

57
 Somatoform Disorder
-Not all patients with somatization have a true disorder, but it is more Conversion disorder Hypochondriasis
likely to be a psychiatric illness if there are many organ systems -The presence of symptoms or deficits that affect -Preoccupation with the fear of having a serious disease based upon
involved in symptoms, if symptoms fluctuate, if there is comorbid voluntary motor or sensory function in a way that misinterpretation of body symptoms or normal functions
anxiety or depression, if symptoms lead to psychological or suggest neurologic condition but is medically -Disturbance must last at least 6 months and persists despite appropriate
emotional gain, if symptoms are chronic, or if there is idiosyncratic unexplainable medical evaluation and reassurance
response to meds -The most common somatoform disorder
-Preceded by psychological distress, can have Differential
Somatization disorder relapses -Factitious disorder = intentionally faking symptoms in order to assume
-Physical symptoms due to psychologic stress that can’t be explained -Typically there is onset of a dramatic but the sick role, without gain of external incentives (frequently present with
by another general medical condition physiologically impossible condition such as wound healing problems, excoriations, infection, bleeding,
-Diagnostic criteria: paralysis, aphonia, blindness, deafness, or hypoglycemia, and GI ailments)
• physical complaints must begin before age 30 and occur pseudoseizures -Malingering = intentionally faking or grossly exaggerating symptoms
over several years -Focus is on one symptom rather than multiple in for an obvious incentive such as avoiding work or criminal prosecution,
• 4 pain symptoms, 2 non-pain GI symptoms, 1 sexual somatization disorder obtaining financial compensation, or obtaining medications
symptom, 1 pseudoneurologic symptom -Depression
• all symptoms must be investigated Body dysmorphic disorder -Panic disorder
• symptoms are neither intentionally produced nor feigned -Preoccupation with an imagined or exaggerated -Substance abuse
defect in physical appearance
Undifferentiated somatoform disorder Management of somatoform disorders
-“Somatoform light” Somatoform pain disorder -Investigate all symptoms
-For patients not fitting existing category criteria -Pain in one or more sites associated with -Don’t try to reason away symptoms as they are not a conscious process
-Diagnostic criteria: 1+ medically unexplained physical complaints psychological factors that have an important role -Focus on care rather than cure: provide reassurance and schedule brief,
persisting for more than 6 months in the onset, severity, exacerbation, or regular visits that don’t coincide with symptoms
maintenance of the pain -Treat comorbid psychiatric conditions
-Symptom is not intentionally produced or feigned -Minimize polypharmacy

DERMATOLOGY
Classic Drug Eruptions
Type Information Photo
Common Offenders
Drug-Induced -The most common drug eruption
Exanthem -Thought to be a delayed type IV hypersensitivity reaction
-Common offenders are antibiotics, especially sulfa
-Described as morbilliform, macular, or papular eruptions
-Eruptions begin in dependent areas (= lower than the heart) and then generalize
-Onset is usually within 2-3 weeks of beginning new drug or within days if there was prior exposure
-May have mucous membrane erythema, pruritus, low grade fever
-Can progress to more serious reactions such as S-J, toxic epidermal necrolysis, hypersensitivity
syndrome, or serum sickness
-D/c of offending drug usually results in resolution of rash in 7-14 days
-Drugs causing a morbilliform eruption should only be continued when there is no alternative therapy
available

58
 Urticaria & -Mechanism can be type I hypersensitivity, or via a non-IgE mechanism  = can be immediate,
Angioedema accelerated (hours later), or delayed (days later)
-Urticaria is mediated by mast cells in the superficial dermis
-Angioedema is swelling of the deeper dermis and subcutaneous tissues that can be mediated by mast cells
(although not always) and can coexist with urticaria
-Common offenders causing type I hypersensitivity are antibiotics, especially penicillins, cephalosporins,
and sulfonamides
-Common offenders causing a non-IgE type hypersensitivity are morphine and codeine (“red man
syndrome”)
-Described as intensely pruritic , circumscribed, raised, and erythematous eruption with central pallor
-Lesions may coalesce
-Typically disappear over a few hours, although urticaria can manifest in a chronic form (present > 6
weeks) which is usually due to autoimmunity or chronic disease
-Can be treated with H1 or H2 blockers, doxepin, glucocorticoids if acute, epinephrine, or around-the-
clock antihistamines if chronic
Anaphylaxis -A type I hypersensitivity that affects multiple organs, including pruritus, urticaria, angioedema, laryngeal
edema, wheezing, nausea, vomiting, tachycardia, sense of impending doom, and occasionally shock

Hypersensitivity -AKA drug-induced vasculitis, leukocytoclastic vasculitis, serum sickness, serum sickness-like reaction,
Vasculitis or allergic vasculitis
-Symptoms usually begin 7-10 days after exposure
-ACR criteria: age > 16, use of a possible offending drug in temporal relation to the symptoms, palpable
purpura, maculopapular rash, skin biopsy showing neutrophils around an arteriole or venule
-Other S/S include fever, urticaria, arthralgias, lymphadenopathy, low serum complement levels, and
elevated ESR
-Common offenders include penicillins, cephalosporins, sulfonamides (including loop and thiazide
diuretics), phenytoin, and allopurinol
-Resolves after days to weeks, NSAIDS or steroids may be needed for more severe cases
Exfoliative -Begins with generalized eczema or morbilliform erythema that progresses into chronic erythema and
Dermatitis scale involving > 50% of the body surface area
(Erythroderma) -Can be caused by drugs as well as atopic dermatitis, malignancy, or psoriasis
-Common offenders include penicillins, barbiturates, gold salts, arsenic, and mercury

59
 Stevens-Johnsons -Severe mucocutaneous eruptions characterized by epidermal necrosis and sloughing of mucous
Syndrome & Toxic membranes and skin
Epidermal -Whether it is S-J or TEN depends on % of body surface involved, if > 10% it is S-J, if > 30% it is TEN
Necrolysis

Erythema -A different condition than S-J

Multiforme -An acute eruption with distinctive target skin lesions that tend to affect the distal extremities including the
palms and soles
-Often caused by infections such as HSV or Mycoplasma pneumoniae, but it has had some reports with
medication use

Hypersensitivity -AKA drug reaction with eosinophilia and systemic symptoms (DRESS) or drug-induced hypersensitivity
Syndrome syndrome (DIHS)
-Infection with HHV-6 may play a role
-Reaction typically occurs 2-6 weeks after drug is first used
-Usually begins with morbilliform or erythrodermic eruption with possible erythematous follicular
papules, pustules, bullae, or purpura, as well as fever, hepatitis, arthralgias, lymphadenopathy,
hematologic abnormalities, pneumonitis, renal failure, myocarditis, thyroiditis, and neurologic symptoms
-Severity is dependent on length of time drug is continued
-Can be life-threatening no some cases
-Common offenders include phenytoin, carbamazepine, phenobarbital, sulfonamides, lamotrigine,
valproate, allopurinol, minocycline, antidepressants, NSAIDs, ACEIs, beta blockers

Fixed Drug -A distinctive reaction characterized acutely by erythematous and edematous plaques with a grayish center
Eruption or bullae, dark postinflammatory pigmentation
-Usually occurs on the lips, tongue, genitalia, face, and acral areas
-Common offenders are laxatives, tetracyclines, barbiturates, sulfonamides, NSAIDs, and salicylates

60
Symmetrical Drug- -AKA baboon syndrome
Related -Rare
Intertriginous and -Occurs hours to days after administration of offending drug
Flexural Exanthem -Sharply demarcated V-shaped erythema in the gluteal, perianal, inguinal, or perigenital areas, often with
involvement of at least one other flexural or intertriginous fold
-Common offenders are amoxicillin, ceftriaxone, penicillin, clindamycin, erythromycin, iodinate contrast,
pseudoephedrine, valacyclovir
-Treat with topical or systemic steroids

Photosensitivity -Phototoxic variety: result of direct tissue or cellular damage following UV irradiation of a phototoxic
agent that has been ingested or applied to the skin (tetracyclines, thiazides, sulfonamides,
fluoroquinolones, NSAIDs, phenothiazines, griseofulvin, voriconazole, retinoids, St. John’s wort)
-Photoallergenic variety: a delayed-type hypersensitivity reaction to an allergen whose antigenicity has
changed after UV exposure (sunscreens, antimicrobials, NSAIDs, fragrances, griseofulvin, quinolones,
sulfonamides, ketoprofen, piroxicam)

Melanoma
-Flat, raised, nodular, or ulcerated
-Variable color
-Consider in any new mole or a mole changing shape, size, or color

Workup
-Lymph node palpation.
Punch or incisional biopsy
Picture Picture
Type of Melanoma Info Type of Melanoma Info
Lentigo maligna (melanoma Melanoma restricted to Acral lentiginous Primarily on hands, feet,
in situ) epidermis. melanoma nails. Most common type of
melanoma in blacks and
Asians. Common in males.

Superficial spreading Most common type of Amelanotic melanoma Innocent-appearing pink to

melanoma melanoma. Asymmetric, flat red colored papules that
lesions > 6 mm. Vary in enlarge to plaques and
color. Lateral spread. nodules. Scary.

61
Nodular melanoma Rapid growth vertically from
and through skin. Most
common on extremities.

Cellulitis
-Risk factors: skin trauma, inflammation (eczema or radiation), Signs & symptoms Management
pre-existing impetigo or tinea pedis, edema -Skin erythema, edema, and warmth -Can usually be treated with oral antibiotics
-Indolent onset with development of symptoms over days -Careful, erysipelas must be covered with IV therapy for initial
Agents -May have purulent drainage or exudate management
-Most commonly GAS or GBS -IV AB for systemic toxicity or rapid progression
-Staph aureus Differential -Empiric therapy for nonpurulent cellulitis to cover Strep and
-Gram negs -Necrotizing fasciitis MSSA  oral dicloxacillin (or cephalexin or clindamycin), IV
-H. flu -Gas gangrene cefazolin (or oxacillin, nafcillin, or clindamycin)
-Clostridium -TSS -If risk factors for MRSA (recent hosp, LTC resident, recent
-Pseudomonas -Bursitis AB, HIV, MSM, IVDU, HD, incarceration, military, DM) with
-Osteomyelitis nonpurulent cellulitis oral clindamycin (or amoxicillin +
Differential -Herpes zoster Septa or doxy, or linezolid)
-Erysipelas: more acute onset that involves the upper dermis and -Erythema migrans -Purulent cellulitis ( = risk for MRSA)  clindamycin, Septra,
superficial lymphatics while cellulitis involves the deeper doxy, or linezolid
dermis and subcutaneous fat; lesions will be raised above Workup -May need suppressive therapy for recurrent cellulitis
surrounding skin with clear demarcation between involved and -Diagnosis is clinical
uninvolved tissue -Cultures if there is systemic toxicity, extensive skin
-If it involves the ear, it’s erysipelas! (no deep tissue here) involvement, underlying comorbidities, unusual exposures like
animal bites or water-associated injury, or recurrent or persistent
cellulitis
Varicella Zoster Infection - Primary
-Will be contagious for 1 week Management
-Oral acyclovir for adults with uncomplicated varicella
Signs & symptoms -IV acyclovir for immunosuppressed host or with disseminated disease such as pneumonia or
-Intensely pruritic lesions that come in crops over 3-4 days  see lesions in all different stages encephalitis
-Acute neuritis with rash most commonly presenting in the thoracic and lumbar dermatomes -Acetaminophen for fever
-Disseminated lesions in immunocompromised host -Antihistamines for pruritus

Prognosis
-Can be fatal in adolescents and adults
Varicella Zoster –Secondary (Shingles)
-Primary infection is varicella, secondary is zoster Treatment Complications
-High dose acyclovir within 72 hours of onset -Post-herpetic neuralgia
Prevention -Prednisone if over age 50 -Ophthalmic complications
-Zostavax vaccine indicated after age 60 -Analgesics -Hemiplegia

62
 Psoriasis
-A hyperproliferation of the Signs & symptoms Differential Management
epidermis with altered -Red scaling papules that coalesce into round-oval plaques with a -Atopic dermatitis (eczema) -Initial treatment with topical
differentiation  inflammation of silvery white adherent scale -Contact dermatitis corticosteroids and emollients for mild
the epidermis and dermis with -Pustules may border lesions -Nummular eczema to moderate plaque psoriasis
accumulation of T-cells and -Lesions are most commonly on -Tinea -Alternatives: tar, topical retinoids,
cytokines the scalp, elbows, legs, knees, -Candidiasis topical vitamin D, topical tacrolimus or
-Can be flared by strep infections, arms, trunk, lower body, palms, -Intertrigo pimecrolimus
injury, trauma, drugs, low humidity, and soles, and occur at sites of -Seborrheic dermatitis -Localized phototherapy
emotional stress, and overtreatment trauma -Pityriasis rosea -Systemic therapy for refractory cases:
-Variable pruritus -Secondary syphilis methotrexate, cyclosporine, biologics
-Extracutaneous manifestations: -Onychomycosis -Treating coexisting depression can
onycholysis, geographic tongue, -Cutaneous features of reactive arthritis also help the psoriasis
destructive polyarthritis, -Cutaneous T-cell lymphoma
ankylosing spondylitis, DIP arthritis, CV disease, depression, -Lichen simplex chronocus
lymphoma

Chronic Plaque Psoriasis Erythrodermic Psoriasis Pustular Psoriasis Guttate Psoriasis Intertriginous (Inverse)
Psoriasis
-Sharply defined erythematous scaling -Generalized erythema with scaling and exfoliation -Individual or coalescing -Multiple small papules of short -Presentation involves the
plaques in symmetric distribution -Accounts for 10% of cases non-infectious pustules 1- duration inguinal, perineal, genital,
-The most common type of psoriasis -Patients are very sick, with hypo or hyperthermia, 10 mm that are -Associated with recent strep intergluteal, axillary, and
-Lasts months to years protein loss, dehydration, renal and cardiac failure generalized or localized infection inframammary regions
-May have nail involvement -May need a punch biopsy to differentiate from contact -Can also see typical plaque
dermatitis lesions on the knees and elbows

Onychomycosis
Tinea unguium -3 forms: distal subungual, proximal subungual, and -1st line is oral terbinafine
(onychomycosis) white superficial -2nd line is oral azole or ciclopirox topical lacquer
-Most pts will also have tinea pedis -3rd line is repeat therapy or nail removal
-Infection may be yeast or nail dystrophy = must to
KOH scrape to be sure before starting therapy as
terbinafine won’t cover candidiasis

63
 Vasculitis
-The vasculitides are characterized by inflammatory Signs & symptoms Workup
leukocytes in vessel walls with reactive damage to -Systemic symptoms in combination with evidence of single or -Ascertain type of vasculitis: CMP, CK, ESR, hepatitis serologies, UA,
mural structures multiorgan dysfunction CXR, echo; may need CSF, CNS imaging, PFTs, blood or tissue culture
-Nonspecific: fatigue, weakness, fever, arthralgias, abdominal pain,
-Can be a primary or secondary process -More specific tests: ANA, complement (deficiency in lupus and mixed
HTN, renal failure, neurologic dysfunction
-May case bleeding and compromise of lumen  -Specific: mononeuritis multiplex, palpable purpura, combined cryoglobulinemia), ANCA (Wegener’s)
downstream tissue ischemia and necrosis pulmonary and renal involvement -EMG if neuromuscular symptoms are present
-Affected vessels vary in size, type, and location -Tissue biopsy of affected organ is essential for diagnosis
Differential -Arteriogram if suspecting vasculitis of large and medium arteries to look
Types -Fibromuscular dysplasia for aneurysms, occlusions, and vascular wall irregularities
-Large vessel: Takayasu arteritis, giant cell arteritis -Cholesterol emboli
-Medium vessel: polyarteritis nodosa, Kawasaki -Infective endocarditis Management
disease, primary CNS vasculitis -Malignancy -Depends on severity and type of vasculitis
-Mycotic aneurysm with embolization
-Small vessel: Churg-Strauss, granulomatosis with -Stop offending drugs
-Bacteremia
polyangiitis (Wegener’s), microscopic polyarteritis, -Rickettsial infection -Antihistamines, NSAIDs, or steroid course for inflammation
Henoch-Schonlein purpura, essential cryoglobulinemic -Thrombocytopenia -Monitoring with US
vasculitis, hypersensitivity vasculitis, vasculitis -Radiation fibrosis
secondary to connective tissue disease, vasculitis -Neurofibromatosis Prognosis
secondary to viral infection -Congenital coarctation of the aorta -60-80% 5 year survival with polyarteritis nodosa
 Criteria for classification of the major forms of -Amyloidosis -60% survival with Churg-Strauss
vasculitis have been established but only include -Livedo reticularis -75% survival with Wegener’s
-Cocaine abuse
characteristics that help distinguish one disorder from -85% + survival with hypersensitivity vasculitis, Henoch-Schonlein
-Hereditary disorders: Marfan, Ehlers-Danlos, etc.
other vasculitides = good for research but not very -Atherosclerosis purpura, giant cell arteritis, Takayasu arteritis
helpful clinically -Vasospasm
Acanthosis Nigricans
-19% of primary care patients will have this, with rates up to 47% in Native Signs and symptoms Management
Americans -Velvety, hyperpigmented plaques that most -Treat underlying disorder
frequently occur on the neck and axillae but -Weight loss, metformin or rosiglitazone
Etiologies can appear on other skin sites or mucosal -D/c offending meds
-Acquired or inherited surfaces -Topical retinoids, vitamin D analogs, and keratolytics
-Most commonly a result of obesity or endocrine or metabolic disorders, but can also -Rapid onset if associated with malignancy
be associated with genetic syndromes, familial acanthosis nigricans, malignancy, or
drug reactions
Decubitus Ulcers
-Infections of these are typically polymicrobial, including staph and strep, enterococci, Differential Management
Enterobacter, Proteus, and anaerobes -Diabetic neuropathy ulcer -Comprehensive analysis of patient’s general medical condition and evaluation of the wound
-Arterial or venous -Daily monitoring using healing and staging scales
Risk factors insufficiency ulcer -Adequate pain control
-Shearing forces, friction, moisture, immobility, incontinence, poor nutrition, decreased skin -Nutritional supplementation if needed
perfusion Workup -Repositioning every 2 hours
-MRI is best for evaluation -Dressing choice depends on wound characteristics: wet to dry, semiocclusive, occlusive, sterile
Staging of osteomyelitis maggots, etc.
-Stage 1 = intact skin but with non-blanchable redness for > 1 hour after relief of pressure -Wound cultures: gold -Stage 1 ulcers need transparent film dressing
-Stage II = blister or other break in the dermis ± infection standard sample is of a -Stage 2 ulcers need a moist wound dressing
-Stage III = full thickness tissue loss, may see subcutaneous fat, destruction extends into deep tissue specimen from -Stage 3 and 4 ulcers need infection treatment, debridement, and other special dressings
muscle ±infection, may have undermining or tunneling a surgically cleaned and -For superficial infections, topical antibiotics such as sulfadiazine are used to reduce bacterial
-Stage IV = full thickness skin loss with involvement of bone, tendon, or joint ± infection, debrided ulcer; superficial counts
often with undermining or tunneling cultures tend to represent -For deeper infections or complicated infections, systemic therapy is needed
-Unstageable = full thickness tissue loss in which ulcer base is covered by slough or eschar colonization rather than
-Suspected deep tissue injury = purple or maroon localized ara of discolored intact skin or true wound infection Prognosis
blood-filled blister due to damage of underlying tissue from pressure or shear -Complications: bacteremia, sepsis, death

64
 Leg Ulcers
Risk factors
-Poor circulation, venous insufficiency, disorders of clotting, diabetes, sickle cell, neuropathy, renal failure, HTN, lymphedema, inflammatory skin diseases, smoking, genetics, malignancy, meds
Diabetic (Neurotrophic) Ulcers Venous Insufficiency Ulcers Arterial (Ischemic) Ulcers
Screening -Classified by CEAP system, which helps distinguish initial disease severity as well Signs and symptoms
-Recommended annually with as changes over time -PAD symptoms: pain and claudication with
visual examination and -Varicose veins in the absence of skin changes are NOT chronic venous walking that is relieved by rest (however may
monofilament test (checks most insufficiency! have more pain with leg elevation in severe
common sites of ulceration) disease)
Risk factors -Ulcers are usually on the feet at points of
-Advancing age, FH, increased BMI, friction and appear punched-out
smoking, h/o LE trauma, prior DVT, -Feet will turn red when dangled and pale white
pregnancy or yellow when elevated

Signs & symptoms

-C/o tired, heavy legs, leg pain, or leg
swelling
-Telangiectasias, reticular veins, and varicose
veins
-Edema, inflammation, pruritic dermatitis
-Ulcers with irregularly shaped borders along the medial ankle or saphenous veins
Signs & symptoms that are tender, shallow, exudative, and have a base of granulation tissue
-Ulcers with punched-out borders with calloused -Skin discoloration or redness, may appear shiny or tight
surrounding skin -20% of symptomatic patients will have no visible clinical signs
-Underlying neuropathy
Management
Workup -Leg elevation, exercises, and graduated compression stockings
-Ankle-brachial index with symptoms of PAD -SCDs for patients refractory to stockings
-Horse chestnut seed extract for patients who can’t tolerate or are noncompliant with
Management compression therapy
-Comprehensive assessment of ulcer and patient’s overall -Skin moisturizers
medical condition -Wound debridement PRN
-Classification of wound at each follow-up -Barrier creams to protect adjacent skin
-Debridement, local wound care, pressure relief, infection -Selection of proper wound dressing
control, and proper dressing selection -NOT effective: topical antibiotics, debriding enzymes, growth factors, or honey
-Negative pressure wound therapy following debridement -Compression bandages for severe edema, weeping, eczema, or ulceration
after infection, necrosis, or amputation -Aspirin therapy accelerates healing
-Revascularization for critical wound ischemia -Referral to subspecialty for slowly healing ulcers, persistent dermatitis, or recurrent
cellulitis

65
 HEMATOLOGY
Aplastic Anemia
-A result of bone marrow failure due to injury or suppression Signs & symptoms Management
-Abrupt onset of fatigue, weakness, dyspnea, excess bleeding & -Based on severity of disease
Etiologies bruising, petechiae, purpura, pallor, and infections -None if mild
-Idiopathic -BMT or immunosuppression if severe
-Drugs: phenytoin, sulfas, chemo, radiation, chemicals Workup
-Viruses -Labs show pancytopenia, severe normocytic anemia, ↓ retics,
-Pregnancy reduced cells in BM with fat replacement
-Hereditary (Fanconi’s anemia)
Hemolytic Anemia
Etiologies Workup
-Hereditary spherocytosis: intrinsic inherited defective spectrins in RBC membrane  weak, -Increased hemolysis markers: LDH
deformed spherical RBCs prone to rupture in blood vessels or spleen -Reduced or absent serum haptoglobin (since it binds free Hb, which is abundant during
-Hereditary elliptocytosis hemolysis)
-G6PD deficiency: results in oxidation-prone RBCs  intracellular ppt of oxidized Hb into Heinz -May have + Coomb’s test (DAT)
bodies  bite cells and hemolysis after journey through the spleen -Increased retic % or retic # as BM responds to anemia
-Sickle cell disorders -Abnormalities on peripheral smear
-Acquired disorders: TTP, HUS, giant hemangioma, artificial heart valves, sepsis, DIC,
autoimmune hemolytic anemia, hemolytic disease of the newborn Management
-Treat underlying cause
Signs & symptoms
-Rapid onset of pallor and anemia
-Jaundice with ↑ unconjugated bili
-Bilirubin gallstones
-Splenomegaly
Coagulation Disorders
Thrombocytopenias
*Remember to distinguish from pseudothrombocytopenia in patients that are “EDTA clumpers” or in patients on aspirin, clopidogrel, prasugrel, NSAIDs, or other antiplatelets
Acute Thrombocytopenia Immune Heparin-Induced Thrombotic Hemolytic Uremic Disseminated Other Causes
Thrombocytopenic Thrombocytopenias Thrombocytopenic Syndrome Intravascular Coagulation
Purpura Purpura
-Sudden ↓ in platelets from -Due to anti-platelet Abs -HIT type I is non-immune, -Caused by Ab to -Classically caused by E. -A pathological activation of -Liver disease low
destruction, less production, -Can be from viral infection transient, and improves upon ADAMSTS13  extensive coli damage to endothelia coagulation that is always thrombopoietin (tx with
or sequestration in kids that is self-limiting d/c of heparin microthromboses throughout and renal arterioles and associated with an FPP)
-S/s: dried blood in nose, -In adults tends to be chronic -HIT type II is due to IgG body inactivation of underlying disease such as -Vit K deficiency due to abx
wet purpura in the mouth, with no prior infection, but against PF4 formation of -Assoc with certain meds ADAMSTS13  plt sepsis, burns, cancer, head killing vit K synthesizing gut
splenomegaly, petechiae can also occur after valve immune complexes that -S/s: AMS, fevers, chest activation  trauma, snake bite, or bacteria, malnutrition, or
-Plt will be < 150k replacement, cardiac cath, activate platelets to form pain, dyspnea, not urinating, thrombocytopenia, uremia vasculitis biliary tract disease (tx with
drugs microthromboses in small similar to acute -Very similar to TTP, -W/u: ↓ plt, schistocytes, + vit K supp + FFP)
-S/s: neurologic symptoms, vessels throughout body thrombocytopenia or ITP distinguish it by renal D-dimer, ↓ fibrinogen (all
fever, ± renal failure -S/s: MAHA, limb necrosis, -W/u: plt ~20k, normal dysfunction vs neuro used up), prolonged PTT/PT
-W/u: normal PT/PTT, pulseless extremities PT/PTT, schistocytes impairments (factors all used up)
normal cell lines, normal -W/u: plt ~50k, normal -Tx: plasmapheresis to -Tx: supportive, volume -Tx: treat underlying
marrow, normal spleen = dx PT/PTT, PF4 Ab, remove Ab, steroids repletion, pressors, plasma disease, replace blood
of exclusion schistocytes on peripheral exchange; only give pRBCs products PRN, may need
-Tx: steroids, immune smear with severe anemia; NO abx LMWH to inhibit further
modulation with IV Ig or -Tx: stop heparin, use direct as it will worsen HUS, NO clotting
splenectomy, thrombin inhibitors, and plt as this will worsen
plasmapheresis, EPO begin warfarin after plt MAHA
-90% fatal without treatment normalize
66
 Thrombopathies
-Characterized by prolonged bleeding time despite normal platelet counts
Von Willebrand Disease Glanzmann’s Thrombasthenia Bernard-Soulier Syndrome Hemophilia Other Thrombopathies
-The most common hereditary -Rare genetic disease where platelets lack -Rare genetic disease that causes a -Hemophilia A is factor 8 deficiency -Decreased factor 8 due to autoimmunity
coagulation abnormality glycoprotein IIb/IIIa = no fibrinogen or deficiency of the receptor for vWF -Hemophilia B is factor 9 deficiency (differentiate from hemophilia by doing a
-A result of a functional or quantitative vWF bridging can occur -Giant platelets dominate = functional -S/s: hemarthroses, muscle bleeds, other mixing study, it won’t correct)
deficiency of vWF -W/u: platelet agg studies are the opposite thrombocytopenia abnormal bleeding -Acquired thrombopathy from drugs,
-A spectrum of disease of Von Willebrand disease -W/u: giant platelets on peripheral smear, -W/u: prolonged PTT, decreased factor 8 infection, renal disease, hepatic disease,
-W/u: electrophoresis shows decreased platelet agg studies are the opposite of or 9 AIDS, NSAIDs
vWF multimers (the opposite of TTP), Von Willebrand disease -Tx: factor concentrates
hyperagglutination with ristocetin,
prolonged closure time for collagen and
ADP
-Tx: only treat severe cases with vWF &
factor 8 concentrates, or desmopressin for
quick release of vWF from endothelial
stores
Hypercoagulable States
Hereditary Acquired
Factor V Leiden Virchow’s triad
-Hereditary resistance to factor 5 inactivation by protein -Vascular damage, hypercoagulability, vascular stasis = after surgical procedures
-PTT may be shortened and does not correct
-Definitive PCR test Anti-PL syndrome
-Recurrent spontaneous abortions
Prothrombin G20120A -Livedo reticularis
-Inherited mutation that causes increased prothrombin levels -Treat indefinitely with warfarin
-Definitive DNA test
Others
Protein C or protein S deficiency -Hormones: pregnancy, OCPs
-Deficiency of natural vitamin K-dependent anticoagulants -Malignancy
-Smoking
Antithrombin III deficiency -Immobilization
-Reduced inhibition of the conversion of fibrinogen to fibrin -Surgery
-Fatal if homozygous
Acute Lymphoblastic Leukemia
-Cancer of the lymphoid progenitor, affecting B or T cell Signs & symptoms Workup
lineage -Illness over days to weeks -CBC with differential showing 1-2 cytopenias
-Incidence peaks @ 2-5 years and drops @ 8-10 years = more -Fever, pallor, petechiae, ecchymoses, lethargy, malaise, -Confirmatory blood smear or bone marrow aspirate showing
common in children anorexia, bone or joint pain, meningitis, weight loss, blasts
lymphadenopathy, splenomegaly, dyspnea -LP to eval for CNS involvement

Differential Management
-Infection -3-4 agent induction therapy
-Aplastic anemia -Radiation if CNS disease is present
-Juvenile RA -Continuous therapy for 2-3 years
-Other malignancy
Prognosis
-Overall cure rate 20-40% for adults

67
 Acute Myeloid Leukemia
-Cancer of the myeloid progenitor (gives rise to all WBCs other Signs & symptoms Workup
than B/T and NK cells), where cells do not mature and do not -From cell deficiencies: pallor, fatigue, dyspnea, -Differentiate from ALL by peripheral smear showing Auer
die and take up the bone marrow space of other needed cells thrombocytopenia, petechiae, hematomas, bleeding, neutropenia rods
-Most common in first 2 years at life, peaks again in with sepsis, cellulitis, pneumonia
adolescence -From hyperleukocytosis: obstruction of capillaries and small Management
arteries with high numbers of blasts -Aggressive chemo
-From CNS involvement: HA, AMS, CN issues
-Leukemia cutis lesions Prognosis
-DIC -Overall survival of 30%
-Tumor lysis syndrome
Chronic Lymphocytic Leukemia
-Clonal proliferation and accumulation of mature-appear B cells Signs & symptoms Management
-The most commonly occurring leukemia -Fatigue, night sweats, weight loss, persistent infections, -Observation
-Mostly occurs in those > 50, and more common in males lymphadenopathy, hepatomegaly, splenomegaly -Chemo with tumor lysis prophylaxis
-RAI system for staging -BMT
Workup -Radiation for lymphadenopathy
-CBC showing lymphocytosis with WBCS > 20k with
concomitant anemia and peripheral smear showing mature small Prognosis
lymphocytes and cobblestone-appearing smudge cells -Typically slow-growing, but has potential for Richter’s
-Coexpression of CD19 and CD5 transformation to aggressive disease
-High IgG -Worse prognosis with deletion of chromosome 17
-Average 5 year survival rate of 50%
Chronic Myelogenous Leukemia
-Excess proliferation of the myeloblast or its progeny with no Signs & symptoms Management
negative feedback -Fever, bone pain, LUQ pain with splenomegaly, weakness, -Chemo
-Usually occurs in young to middle age adults night seats, bleeding & bruising, petechiae -BMT

Categories Workup Prognosis

1.) Chronic: < 15% blast component of bone marrow or blood -Detection of Philadelphia chromosome via FISH or RT-PCR -Average survival is 6 years with treatment
2.) Accelerated: peripheral blood > 15% blasts or > 30% blasts -CBC showing leukocytosis and thrombocytopenia
+ promyelocytes, or > 20% basophils
3.) Acute: when blasts comprise > 30% of BM

Multiple Myeloma
-Malignancy of plasma cells where replacement of Signs & symptoms Workup Management
bone marrow leads to failure -Forms lytic lesions on bone  bone -Bone marrow biopsy shows > 5% plasma cells -Chemotherapy
-Etiology is unknown, but there is increased incidence pain, pathologic fx, and -Lytic lesions on metastatic bone survey x-ray series -Local radiation for pain control
with h/o pesticides, paper production, lather tanning, hypercalcemia -Spikes in M protein in protein electrophoresis (differentiate -Autologous BMT
nuclear radiation exposure, and abnormalities of -Renal failure from excretion of from MGUS, where M protein level will still be WNL) -Bisphosphonates for
chromosome 13 proteins -IgG and IgA spikes on electrophoresis hypercalcemia
-Multi-hit hypothesis that development of MM -Fatigue -Peripheral smear showing rouleaux formations (poker chips)
requires 2 oncologic events: MGUS (a common, age- -Recurrent infections -Urine has Bence-Jones proteins (produced by malignant Prognosis
related medical condition characterized by -Spinal cord compression plasma cells) -Average survival with chemo is
accumulation of monoclonal plasma cells in the BM -Hyperviscosity syndrome from high -Hypercalcemia 3 years, 7 years for BMT
 moderate IgG spike on electrophoresis) + 2nd hit circulating Ig of all kinds -Anemia
causing transition of MGUS to severe MM
68
 Lymphoma
Hodgkin Lymphoma Non-Hodgkin Lymphoma
-A group of cancers characterized by orderly spread of disease from one lymph node to another -A diverse group of blood cancers that include any kind of lymphoma except Hodgkin (includes
and by the development of systemic symptoms with advanced disease CLL, Waldenstrom’s, and multiple myeloma)
-Extranodal presentation in the lung, liver, or BM in some cases -Associated with congenital or acquired immunodeficiency
-Peaks in adolescence and young adulthood, and in ages 50+ -Single or multiple areas of involvement
-Association with EBV -Low, intermediate, and high grades
-Incidence increases with age
Signs & symptoms
-Painless, firm lymphadenopathy (often supraclavicular and cervical areas), mediastinal mass Signs & symptoms
causing cough or SOB, fever, weight loss -Lymphadenopathy  hydronephrosis, bowel obstruction, jaundice, wasting, SVC syndrome
-Abdominal pain
Workup -Fever, weight loss, night sweats
-Peripheral smear showing Reed-Sternberg cells -Edema
-CT scans of chest, abdomen, and pelvis
-PET scan Workup
-BM biopsy -CBC and smear are usually normal
-Lymph node biopsy -Lymph node biopsy
-CT scans of chest, abdomen, and pelvis
Management
-Chemo Management
-Low dose radiation -Systemic chemo

Prognosis Prognosis
-Overall survival 90% but there are 3 separate risk groups -70-90% survival rate

INFECTIOUS DISEASE
Cryptococcosis
-Cryptococcus neoformans Signs & symptoms Workup
-Invasive fungal infection that is becoming increasingly -Pulmonary infections  solitary, non-calcified nodules -Must culture organism from CSF for definitive dx of
prevalent in the immunocompromised population (AIDS, -Meningoencephalitis: seen in HIV, sx occur over 1-2 weeks, meningitis but can presumptively ID with CSF Ag testing
prolonged steroids, organ transplant, malignancy, sarcoidosis)
-Associated with soil frequented by birds and with rotting Treatment
vegetation -Amphotericin B and flucytosine for meningitis
-Worldwide distribution
Pulmonary Histoplasmosis
-Histoplasma capsulatum Signs & symptoms Differential
-The most prevalent endemic mycosis in the US -Symptoms begin weeks to months following exposure -Sarcoidosis
-Associated with bird and bat droppings, chicken coops, farm -Pneumonia with mediastinal or hilar lymphadenopathy -TB
-Malignancy
buildings, abandoning buildings, caves, wood lots -Mediastinal or hilar masses
-Most infections will be asymptomatic or self-limiting -Pulmonary nodule Workup
-Cavitary lung disease -CXR looks just like sarcoid
-Pericarditis with mediastinal lymphadenopathy -Histo serologies
-Arthritis or arthralgia + erythema nodosum -Special stains on biopsy specimens
-Dysphagia from esophageal narrowing -EIA: urine, blood, or BAL
-SVC syndrome
-With dissemination: fever, fatigue, weight loss, GI, CNS, Management
-Itraconazole for moderate infection, amphotericin B for severe
adrenal manifestations
69
 HIV
-Progresses from primary infection with seroconversion  Signs & symptoms Workup
clinical latency  early symptomatic disease  AIDs -Only lymphadenopathy during asymptomatic disease -Serologies are + 3-7 weeks after infection
-Transmission is mostly heterosexual in developing countries -May have mononucleosis-like syndrome during primary -Drug resistance testing
while both MSM and heterosexual in the US infection -Definition of AIDS is when CD4 count drops to < 200
-Patients are most infectious during primary infection -Febrile illness
-Aseptic meningitis Management
-Large debate about aggressive treatment of primary infection
vs waiting until disease is symptomatic
Lyme Disease
-Borrelia burgdorferi with a tick vector Workup
-Transmission usually does not occur until 72 hours after attachment -Dx can be clinical if erythema migrans is present (serologies will be neg)
-Serologies will be + during early disseminated disease
Signs & symptoms
-Early localized disease: erythema migrans ~1 mo after exposure, nonspecific viral syndrome Management
-Disseminated disease: acute neurologic or cardiac involvement weeks to months after tick bite -Treat with doxycycline, amoxicillin, or cefuroxime, for 10-21 days for erythema migrans, 14-21
(AV blocks days for facial nerve palsy, 28 days for meningitis or arthritis
-Late disease: years after disease; arthritis, subtle encephalopathy or polyneuropathy -IV antibiotics needed for patients with cardiac symptoms or late neurologic disease
-HA, fatigue, arthralgias may persist for months after treatment but don’t represent active -No evidence for extended-course antibiotics for presumed chronic Lyme
disease -Can give single dose doxycycline for prophylaxis if attached tick is identified, estimated to be
present > 36 hours, local tick Borrelia infection rate > 20%
Cholera
-Vibrio cholerae Signs & symptoms Workup
-US cases are only acquired overseas or via consumption of -Severe, watery diarrhea -Stool Gram stain for curved Gram neg rods
contaminated seafood -Vomiting -PCR for toxinogenic strains

Prevention Management
-Dukoral vaccine available -Begin treatment before definitive diagnosis!
-Rehydration
-Antibiotics: doxycycline, FQ if resistant
Mycobacterial Disease
-Mycobacterium tuberculosis Signs & symptoms Workup
-Mycobacterium leprae -MAC: pulmonary disease with cough, fatigue, malaise, -Sputum or BAL culture
-Non-tuberculous mycobacteria: MAC, Mycobacterium weakness, dyspnea, chest discomfort, occasional hemoptysis
kansasii, Mycobacterium abscessus -M. kansasii presents as lung disease that is very similar to TB Management
-Superficial lymphadenitis -3 drug regimen for 12 months+
-Disseminated disease in the immunocompromised
-Skin and soft tissue infection from direct inoculation
Amebiasis
-Entamoeba histolytica Workup
-Serology or Ag testing along with parasitic stool exam
Signs and symptoms
-Intestinal amebiasis has a subacute onset of 1-3 weeks with mild diarrhea or dysentery, Management
abdominal pain, bloody stools, can have fulminant colitis with bowel necrosis  perf and -Treat with metronidazole, then paromomycin to kill the cysts
peritonitis or toxic megacolon
-Extraintestinal manifestations present as liver abscesses or pulmonary, cardiac, or brain
involvement

70
 Toxoplasmosis
-Toxoplasma gondii Signs & symptoms Workup
-Acquired via ingestion of contaminated meat or cat poop, -Majority of adult infections are asymptomatic -Serology (IgM will be + within 1 week and may persist for
through vertical transmission, or via blood transfusion or organ -Fevers, chills, sweats years, IgG persists for lifetime)
transplantation -Cervical lymphadenopathy -Brain MRI for HIV patients showing ring-enhancing lesions
-High amount of seroprevalence in US as 30-40% of household -Can have reactivation illness during times of
cats are infected immunosuppression Management
-In HIV can have encephalitis -Pyrimethamine + sulfadiazine for cerebral toxoplasmosis
Prevention -With vertical transmission there is congenital toxo syndrome
-AIDS pts should be given prophylaxis
Syphilis
-Treponema pallidum Signs & symptoms Workup
-Most cases are MSM -Primary/acute infection lasts 5-6 weeks: contagious chancre, -Remember that negative tests do not exclude a diagnosis of
painless rubbery regional lymphadenopathy, followed by syphilis
generalized lymphadenopathy -Darkfield microscopy of chancre sample
-Secondary infection 6 weeks-6 months after exposure (not all -LP for neurosyphilis
pts will develop this): fever, malaise, HA, arthralgias, bilateral -Direct fluorescent antibody testing
papulosquamous rash on the palms and soles, alopecia, denuded -Serology: RPR (has a 3-6 week latency period)
tongue, condyloma lata -HIV test recommended as syphilis facilitates this infection
-Tertiary infection occurs in disease > 4 years’ duration: end
organ manifestations, CV symptoms, gummas, neurosyphilis Management
-Latent infection has no clinical manifestations but serology will -Mandatory reporting within 24 hours
be reactive -Penicillin G
-Recheck serologies at 6 and 12 months after treatment to look
for fourfold reduction in titer
Cytomegalovirus
-Transmission may be sexual, close contact, or blood and tissue Signs & symptoms Workup
exposure -Generally asymptomatic or nonspecific in immunocompetent -CBC shows lymphocytosis
-HIV patients and transplant patients are at increased risk of host -PCR test
reactivation disease -Can have CMV mononucleosis with fever (distinguish from -Serologies
EBV by absence of lymphadenopathy and pharyngitis) -Viral culture
-Rare associations with colitis, encephalitis, myocarditis
-Can have reactivation in critically ill patients Management
-Antivirals only for immunocompromised with severe
manifestations

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