
CARDIOVASCULAR
o Angina pectoris
 Stable – fixed occlusion
 Chest pain results if increased demand
 Unstable – falls under ACS
 Occurs at rest
 Unsteady pattern – increase in frequency and/or severity
 Ischemic symptoms suggestive of ACS with no troponin elevation or ECG changes
 Prinzmetal/atypical/variant
 Coronary vasospasm
 Transient ST elevation
 During rest or early AM that awakens patient
 Cocaine
 Treatment with CCB
o Cardiac arrhythmias/conduction disorders
o Cardiomyopathy
 Dilated
 Etiology
o MC type
o Ischemic CMO is MCC in US
o Increase in cardiac mass with chamber dilatation and systolic dysfunction
o Males
o Weak enlarged heart; thin muscle
o CAD, valvular, HTN, viral, peripartum
o Chemo, ALCOHOL, cocaine, sarcoidosis
 S/S
o CHF, JVD, S3, rales in lungs
 Diagnosis
o Enlarged LV, reduced EF
 Management
o Weight loss
o Diet
o Reduced alcohol
o Smoking cessation
 Hypertrophic
 Etiology
o Genetic frequently
o May develop into HOCM
 S/S
o Diastolic dysfunction
o Myocardial ischemia, syncope, sudden death
o Bulky thick heart, enlargement of septum which can obstruct flow
o Arrhythmias, dyspnea, angina
o S4
o Systolic Crescendo-decrescendo murmur at LLSB
 Decrease intensity with squatting
 Increase intensity with Valsalva and standing
 Diagnosis
o LVH of unknown etiology
o
o
o Systolic anterior motion of mitral valve
 Management
o Beta blockers
o CCB
o Alcohol septal ablation
o Surgical myomectomy
 Restrictive
 Etiology
o Amyloidosis
o Hemochromatosis
o Scleroderma
o Sarcoidosis
 S/S
o Diastolic dysfunctions  poor filing  systolic dysfunction
o Sudden death uncommon
o Presents like RHF
 Diagnosis
o Speckled appearance on echo with normal motion
 Management
o Treat disease
o Systemic amyloidosis is CI for transplant
Hypertensive crisis/emergency
 Etiology
 Elevated BP and acute end organ damage
 Usually > 180/120
 Neuro damage – encephalopathy, hemorrhagic or ischemic stroke, seizure
 Need to perform neuro exam
 Cardiac damage – ACS, dissection, acute HF, pulmonary edema
 ECG, CXR, CKMB, troponin
 Renal damage – ACI, proteinuria, hematuria
 UA, chemistries
 Retinal damage – malignant HTN/Grade IV retinopathy (papilledema) – blurred vision
 Fundoscopic
 Management
 Decrease BP/MAP by no more than 25% within first hour with IV agents
 Neuro – nicardipine or labetalol
 CV
o Dissection – BB (esmolol, labetalol)
o ACS – nitro, BB
o HF – nitro, furosemide
 Renal – fenoldopam
Hypertensive urgency
 Etiology
 Elevated BP with no apparent acute end organ damage
 Management
 Decrease BP/MAP by 25% over 24-48 hours using oral agents
 Drugs
 Clonidine – central acting alpha agonist
o Rebound HTN if DCed abruptly




o
o
o HA, tachycardia, N/V, sedation, fatigue
o Short-term use only
Captopril – ACEI
o Angioedema, AKI
Furosemide – loop
o Electrolyte abnormalities, alkalosis
Labetalol – BB
o CI in COPD, CHF
Nicardipine – CCB
o Reflex tachycardia, HA, nausea
Cardiac arrest
 Etiology
 Cessation of cardiac activity with hemodynamic collapse
 Due to sustained ventricular tachycardia/fibrillation
 MC in structural heart disease and CAD
Cardiac arrhythmias and blocks
 Sick sinus syndrome
 Combination of sinus arrest and alternated atrial tachyarrhythmia and bradyarrhythmia
 Etiology
o Sinoatrial node disease
o Corrective cardiac surgery
 Management
o PPM, may need ICD
 AV blocks – PR interval most helpful
 First degree – constant, prolonged PRI > 0.20 seconds
o QRS follows every P
o Medications, MI, electrolytes, increased vagal tone
o Management – observation
 Second degree
o Mobitz I/Wenckebach – AV node problem
 Progressive PRI lengthening  dropped QRS
 Shortened R-R interval
 Management
 Atropine if symptomatic
 Observation
o Mobitz II – bundle of HIS
 Constant prolonged PRI  dropped QRS
 Management
 Atropine or temporary pacing
 PPI is definitive due to 3rd degree progression
 Third degree – P waves not related to QRS
o Complete dissociation between P waves and QRS  low CO
o Purkinje fibers and bundle branches
o Management – temporary pacing until PPM
 Atrial flutter – flutter “saw tooth” waves
 Rate is usually regular
 Stable – vagal, BB, CCB
 Unstable – cardioversion



 Cardiac ablation
 Needs anti-coagulation
Atrial fibrillation – irregularly irregular rhythm with narrow QRS and no P waves
 MC chronic arrhythmia
 Etiology
o Anything
o Cardiac disease, ischemia, pulmonary, infection, electrolytes, drug, alcohol
o Men>women
o W>AA
 Types
o Paroxysmal – self-terminating within 7 days, recurrent
o Persistent – fails to self-terminate, lasts longer than 7 days
 Requires medical termination
o Long-standing – > 1 year, refractory to cardioversion or CV never tried
o Permanent – decision made to live permanently in afib
o Lone- afib without evidence of HD
 Management
o Rate control
 Beta blockers – metoprolol – caution in reactive airway disease
 CCB – diltiazem
 Digoxin – preferred in CHF patients
o Rhythm control
 CV – need TEE to show no thrombi or anticoag for 4 weeks
 Ibutilide, flecainide, sotalol, amiodarone
o Direct CV if unstable
o Anti-coagulation
PSVT – regular rate > 100 with narrow QRS
 AV nodal reentry tachycardia (AVNRT) – 2 pathways both within AV node – MC
 AV reciprocating tachycardia (AVRT) – 1 pathway within AV node and second accessory
pathway outside node
o WPW
 Orthodromic – MC
o Down the normal AV node first and returns via accessory pathway – narrow
complex
 Antidromic
o Down accessory pathway first and returns via normal pathway – wide complex
o Mimics ventricular tachycardia
 Management
o Narrow/Orthodromic
 Vagal
 Adenosine
 BB, CCB
o Wide/Antidromic
 Amiodarone
 Procainamide of WPW
o Cardiac ablation definitive
Wandering atrial pacemaker & Multifocal atrial tachycardia
 WAP – multiple exotic atrial foci
o ECG with HR < 100 & > 3 P wave morphologies


WPW
 Accessory pathway (Bundle of Kent) pre-excites ventricles
 Slurred wide QRS, delta wave, short PRI
 Management
o Ablation
 PVC
 Premature beat from ventricle
 T wave opposite direction from QRS frequently
 Often a compensatory pause
 Ventricular tachycardia
 > 3 PVCs at a rate > 100
 Evaluate stable vs. unstable
 Sustained is > 30 seconds
 Prolonged QTI predisposes
 Torsades – hypomagnesemia, hypokalemia
o VTach that twists around baseline
 Management
o Stable – amiodarone, lidocaine, procainamide
o Unstable with pulse – cardioversion
o No pulse – defibrillation + CPR
o Torsades – IV Mag
 Ventricular fibrillation
 Management – defibrillation + CPR
 PEA
 Organized rhythm on monitor but no pulse
 Management – CPR + epi + check for shockable rhythm
 Asystole – treat same as PEA
Heart failure
 Etiology
 Inability of heart to pump enough blood to meet metabolic demands
 CAD MC
 Forms
 Left-sided
o MC CAD and HTN
o Valvular disease, cardiomyopathies
 Right-sided
o MC left sided failure
o Pulmonary disease, mitral stenosis
 HFrEF – systolic – MC
o Reduced EF
o S3 gallop
o Post-MI, dilated CM, myocarditis
 HFpEF – diastolic
o Normal to elevated EF
o S4 gallop  forced atrial contraction into a stiff ventricle

o
MAT – ECG with HR > 100 & > 3 P wave morphologies
o Associated with severe COPD
CCB or BB





o Associated with normal cardiac size
o HTN, LVH, elderly
 High-output
o Metabolic demands of body exceed normal cardiac function
o Thyrotoxicosis, wet beriberi, severe anemia, AV shunting, Paget’s of bone
 Low-output
o Inherent problem of myocardial contraction, ischemia, chronic HTN
 Acute
o Largely systolic – HTN crisis, acute MI, papillary muscle rupture
 Chronic
o Dilated cardiomyopathy or valvular disease
NYHA functional class
 Class I – no symptoms or limitations during ordinary activity
 Class II – mild symptoms with activity (dyspnea or angina)
 Class III – symptoms cause marked limitation in activity with minimal exertion.
Comfortably only at rest
 Class IV – symptoms at rest, severe limitations
Left-sided HF S/S – due to increased pulmonary venous pressure from fluid back up into lungs
 Dyspnea MC
o DOE  orthopnea  PND  dyspnea at rest
 Pulmonary congestion and edema
o Rales, rhonchi, chronic nonproductive cough with pink frothy sputum
o CHF MC transudative pleural effusions
 HTN, tachypnea, cyanosis, Cheyne-Stokes breathing
 Increased adrenergic activation – dusky pale skin, diaphoresis, sinus tachycardia, cool
extremities, fatigue, AMS
Right-sided HF S/S – elevated systemic venous pressure  systemic fluid retention
 Peripheral edema – pitting in legs, cyanosis
 JVD – elevated JVP
 GI/hepatic congestion – anorexia, N/V due to edema of GI, HSM, RUQ tenderness
Diagnosis
 Echocardiogram most useful
o EF most important determinant of prognosis
o < 35% - defibrillator
 CXR – CHF
o Cephalization of flow
o Cardiomegaly, pleural effusions/edema
 BNP – cause of dyspnea vs. pneumonia
o Severity and prognosis
Management
 ACEI first line treatment
o Reverse pathology by decreasing renin/sympathetic activation, ventricular
remodeling
o Hypotension, renal insufficiency, hyperkalemia, cough and angioedema
 Beta-blocker – carvedilol, metoprolol
o Decrease mortality by increasing EF and reduce ventricular size
o Added after ACEI/ARB
o May need to stop or decrease dosage during acute exacerbation

o
o
Hydralazine + nitrates combined – good for AA
o Not as good as ACEI
 Diuretics – most effective for treatment of symptoms
o Spironolactone – decreased mortality
 Sympathomimetics – short term use only
o Digoxin can be used long term
 CCB not generally used in systolic HF
 Sacubitril – valsartan – Entresto
o Neprilysin inhibitor – increase BNP levels
o Reduce mortality and hospitalization for Class II-IV
 CHF – decompensated HF
 S/S
o Worsening of baseline symptoms
o Pulmonary congestion
 CXR – congestion, sympathetic activation
o Cephalization
o Kerley B lines
o Butterfly/Batwing pattern
 Management
o diuretics, nitrates, oxygen, upright positioning
Coronary vascular disease
 Etiology
 Atherosclerosis MCC
 Risk factors
o Dyslipidemia
o Tobacco
o HTN
 S/S
 N/V, SOB, diaphoresis, dizziness, palpitations, heavy crushing substernal CHP
 Elderly – dyspnea
 Diagnosis
 12 lead during exercise
 Nuclear stress test
 Cardiac cath gold
 Management
 Control BP, lipids, tobacco, DM
 Modify diet
 Exercise
 Nitrates, beta blockers, CCB, aspirin
Endocarditis
 Etiology
 Infection of heart with vegetation of heart valve
 Left sided MC – mitral valve
 Right sided – IVDU
o Tricuspid valve
 Types
 Acute – infection of noral valves with virulent organism – staph aureus

o
Subacute bacterial – indolent infection of abnormal valves with less virulent – strep
viridans
 Endo in IV drug – MRSA, staph
 Prosthetic valve – early vs. late
 Organisms
 Native valve
o Strep viridans (MC in subacute)
o Enterococcus (MC in men 50 with GI/GU procedure)
o Staph MC (IVDU)
o HACEK
 Haemophilus, aggregatibacter, cardiobacterium, eikenenlla, kingella
 Prosthetic
o Within 2 months of surgery – staph
o After 2 months – behaves like native valve
 Presentation
 Acute – septic, bacteremia
 Subacute – FUO with nonspecific symptoms, cough, SOB, arthralgias, abd pain
 PE
o Murmur
o Emboli – spleen and kidney MC
o Peripheral lesions
 Subconjunctival hemorrhages
 Splinter hemorrhages
 Janeway lesions – nontender erythema macules on palms and soles
 Osler nodes – painful nodes
 Diagnosis
 Blood cultures x 3
 Echo is gold – TEE is better than TTE
 CXR
 EKG shows conduction abnormalities
 Elevated ESR
 Treatment
 Nafcillin + gent
 Vanc and ceftriaxone
 Vanc and gent
 Staph
o MSSA – cefazolin
o MRSA – vanc
Hyperlipidemia
 S/S
 Asymptomatic
 Hypertriglyceridemia – pancreatitis
 Xanthomas
 Management
 Lifestyle – weight reduction, exercise, dietary restriction of cholesterol and carbs
 Lipid lowering agents – plaque stabilization, reversal of endothelial dysfunction,
regression
 Screening
o
o
 Low risk – 35 for males, 45 for females
 Higher risk – 20-25 males; 30-25 females
 Drugs
 Low LDL – statins/HMGcoA reductase inhibitors
o Myositis, myalgias
 Lower TRG – fibrates
o Elevated LFTS
o Myositis and myalgias, especially with concomitant statin use
 Increase HDL – niacin
o Flushing, pruritus – take with NSAID
o May precipitate gout, hyperglycemia
Hypertension
 Etiology
 Primary – idiopathic
 Secondary – due to underlying, identified, often correctable cause
o Suspect if refractory to antihypertensives or severely elevated
o Renal – renovascular MC – RAS, fibromuscular dysplasia MC in YA
o Endocrine – 1ary hyperaldosteronism, pheo, Cushing
o Coarctation
 S/S
 Identify risk factors, reveal 2ndary causes, assess for end organ damage
 Fundoscopic exam
o Arterial narrowing
o AV nicking
o Hemorrhages and soft exudates
o Papilledema
 Diagnosis
 Elevated BP > 2 readings on > 2 different visits
 Complications
 CV – CAD, HF, MI, LVH, etc.
 Neuro – TIA, CVA, encephalopathy
 Nephro – stenosis, ESRD (2nd MC)
 Optic – retinal hemorrhage, blindness, retinopathy
 Goals
 < 140/90 gen pop, < 150/90 if > 60
 Drugs
 Caucasian – Thiazide diuretic  ACEI/ARB  BB  CCB
 AA – Thiazide diuretic  CCB
 Diabetics – ACEI
 Heart disease/MI/HF – beta blocker
 Afib – BB or CCB (verapamil or diltiazem)
 Gout – CCB (diuretics increase uric acid)
 Kidney stones – thiazide (reabsorption of Ca from urine)
Myocardial infarction
 etiology
 acute occlusion
 transmural – STEMI
 subendocardial – NSTEMI
o

o
symptoms suggestive of ACS with no ECG changes
S/S
 Similar pain to angina but more severe and unable to relieve by rest or meds
 Chest pain, N/V, weakness, dyspnea
 Diaphoresis, tachycardia
 Diagnosis
 EKG
o Inferior – II, III, aVF
o Anteroseptal – V1, V2
o Anteroapical – V3, V4
o Lateral – I, aVL, V5, V6
o Posterior – V1-V3 depression
 Management
 Morphine, oxygen, nitrates (CI in inferior), aspirin
 Heparin, BB, ACEI, statin
 PCI
 Manage arrythmias
Myocarditis
 Etiology
 Infectious
o Viral – enteroviruses (Coxsackie B) MC
o Bacterial – Rickettsia (Lyme, RMSF)
o Fungal – actinomycosis
o Parasitic – trichinosis, toxo
 Toxic – scorpion envenomation, diphtheria
 Autoimmune – SLE, rheumatic fever, RA
 Systemic – uremia
 Medications – clozapine
 S/S
 Viral prodrome – fever myalgias, malaise  heart failure symptoms
 Heart failure
o Dyspnea at rest, exercise intolerance, syncope, tachypnea, tachycardia,
hepatomegaly
 May have concurrent pericarditis
 Diagnosis
 CXR – dilated cardiomyopathy/cardiomegaly
 ECG – sinus tach
 Cardiac enzymes
o Positive troponin and CKMB
 Echo
o Ventricular dysfunction
 Elevated ESR
 Endomyocardial biopsy definitive gold standard diagnosis
 Management
 Supportive
o Diuretics, ACEI
 Beta blockers – but not in peds
 IVIG
o
o
o
o
Pericarditis
 Etiology
 Idiopathic
 Viral – Coxsackie and Echovirus
 Dressler syndrome – Post-MI pericarditis
 S/S
 Pleuritic chest pain worse with inspiration
 Persistent and postural, worse when supine and relieved by sitting and leaning forward
 Shortness of breath, fever
 Pericardial frication rub heard at end expiration while upright and leaning forward
 Diagnosis
 ECG – diffuse ST elevation in precordial; T wave inversions
 Echo – assess for complications of acute pericarditis
 Management
 NSAIDs
 Steroids
 Colchicine
Pericardial effusion
 Etiology
 Pericarditis
 Malignancy
 Infection
 S/S
 Muffled heart sounds
 Diagnosis
 ECG – low voltage QRS
o Electrical alternans
 Echo – increased pericardial fluid
 Management
 Observation if small
 Pericardiocentesis if tamponade or large
 Window drainage if recurrent
Cardiac tamponade
 Etiology
 Pericardial effusion causing significant pressure on heart
 Restriction of cardiac filling  decreased output
 S/S
 Beck’s triad – muffled heart sounds, hypotension, elevated JVP
 Pulsus paradoxus
 Dyspnea, fatigue, peripheral edema
 Diagnosis
 Echo – effusion + diastolic collapse of cardiac chambers
 Management
 Pericardiocentesis or pericardial window
Rheumatic fever
 Etiology
 Group A strep – usually from strep throat, but can arise from skin infection
 Result of autoimmune reaction, not continued infection
o
 Result of untreated or inadequately treated
 S/S – Jones criteria
 Major manifestations
o Carditis
 Myocarditis, pericarditis
 Confers greater morbidity and mortality
o Polyarthritis – 2 or more joints affected; can be migratory
 Large joints MC affected
 Heat, redness, swelling, severe joint tenderness
o Chorea
 1-8 months after infection
 Sudden involuntary jerky, non-rhythmic movements
 Head and arms
 MC in females
o Erythema marginatum
 Macular erythematous non-pruritic annular rash with rounded, sharply
demarcated borders
 Trunk and extremities
o Subcutaneous nodules
 Joints, scalp, and spinal column
 Minor manifestations
o Arthralgia
o Fever
o Elevated ESR and CRP
o Previous RF or RHD
 Evidence of group A infection
o Positive culture or rapid strep test
o Recent scarlet fever
o Elevated or rising strep Ab titer (ASO)
 Diagnosis
 Requires meeting two major
 One major and two minor
 And evidence of group A infection
 Sequence
 Strep throat  2-3 weeks later acute rheumatic fever  years later rheumatic heart
disease (mitral stenosis)  more years RHD sequalae (infective endocarditis, left atrial
enlargement, afib)
 Management
 Primary prevention of AFR – PCN
 Acute FR
o PCN X 10days
o Bed rest, salicylates, steroids – do not reduce risk of RHD
o Valproic acid for chorea
 RF 2ndary prevention
o Carditis – IM PCN monthly x 10 years or until age 40, whichever is longer
o Without carditis – 5 years
Valvular heart disease
 Systolic
 Aortic stenosis – MC
o


Etiology
 Congenital bicuspid – under 60
 “senile” calcification – over 60
 RHD
o S/S
 Dyspnea, CHF, angina, syncope
o Murmur
 Crescendo-decrescendo at right 2ICS/RUSB
 Radiate to carotids
 May have S4
o Management
 Valve replacement only effective treatment
 Medical treatment is not effective
 Exercise restriction in severe stenosis
 Avoid venodilators (nitrates) and negative inotropes (CCB and BB)
Mitral regurgitation
o Etiology
 Post-MI (acute) ischemic MR
 CHF (chronic)
 Endocarditis (acute)
 MVP
 S/S
o S/S
 asymptomatic
 pulmonary edema due to volume overload
 dyspnea, fatigue
 chronic – afib, progressive dyspnea on exertion, pulmonary HTN, CHF,
fatigue
o Murmur
 Blowing holo/pansystolic murmur at apex (5th ICS at MCL)
 Radiation to axilla
 S3 may be present
o Management
 Repair > replacement
 Vasodilators to decrease afterload
MVP
o Etiology
 Myxomatous degeneration – connective tissue disease
 MC in young women
o S/S
 Asymptomatic
 Autonomic dysfunction
 Anxiety, atypical chest pain
 Panic attacks, palpitations, syncope, dizziness, fatigue
 MR progression – fatigue dyspnea, PND, CHF
o Murmurs
 Mid-late ejection click at apex
o Management
 May use BB for atypical chest pain



Pulmonic stenosis
o Etiology
 Associated with Tetralogy of Fallot
 Pulmonary stenosis
 Overriding aorta
 VSD
 RVH
o S/S
 Asymptomatic initially
 Eventually RCHF
o Murmur
 Crescendo-decrescendo at left 2ICS/LUSB
 Heave on palpation
o Management
 Valve replacement
Tricuspid regurgitation
o Etiology
 Post-MI
 RHF
 Endocarditis
o
S/S
 Asymptomatic
 Symptoms often from underlying cause
 RHF symptoms – right atrial enlargement, RHF
o Murmur
 Holo/pansystolic at LLSB (4th ICS)
 Pulsatile liver, JVD
o Management
 Decrease atrial volume – diuretics and sodium restriction
 Surgical management – RHF or low CO
VSD – MC type of congenital heart defect
o Etiology
 Congenital
 Post-MI
 Perimembranous is MC type – hoel in LV outflow tract
o S/S
 L-R shunt if pulmonary resistance lower than systemic
 CHF
o Murmur
 Holo/pansystolic murmur at LLSB
o Management
 Congenital frequently close on their own
 May need surgical management
o Complications
 Eisenmenger’s
 Blood takes path of least resistance
 Over type pulmonary pressure becomes > systemic pressure
leading to right to left shunt


Asymptomatic at rest but cyanotic with exertion
Diastolic
 Aortic regurgitation
o Etiology
 Valve disease – RHD, endocarditis
 Aortic root disease/dilation – hypertension, Marfan, syphilis, SLE,
dissection
o S/S
 Dyspnea, fatigue, palpitation
o Murmur
 Decrescendo blowing murmur LUSB
 Bounding pulses due to elevated stroke volume
 Water hammer pulse
 Head bobbing with heartbeat
 Visible systolic pulsation of uvula
o Austin flint
 Mid-late diastolic rumble at apex 2ndary to retrograde regurgitant jet
competing with antegrade flow from left atria into ventricle
o Management
 Medical – afterload reduction – vasodilators (ACEI, ARB)
 Surgical is definitive
 Mitral stenosis
o Etiology
 Congenital
 Endocarditis
 RHD – MC
o S/S
 Dyspnea – MC
 Fatigue
 Palpitations – afib due to atrial enlargement
 Pulmonary HTN
o Murmur
 Apex, opening snap – think Dr. Neal and parachutes getting stuck – blow
up and then snap
 Prominent S1
 Early-mid rumble – preceded by OS
 Increased by LLD
o Diagnosis
 ECG – bifid P wave due to atrial enlargement
 CXR – straightening of left heart border
o Management
 Surgical management
 Treatment with anticoagulants – can only use coumadin
 Pulmonic regurgitation
o Etiology – overall rare
 Congenital, endo, PHTN, carcinoid syndrome
o S/S
 Asymptomatic
o Murmur



PDA

 2nd ICS LUSB
 Brief decrescendo early diastolic
o Management
 Surgical replacement
Tricuspid stenosis
o Etiology
 Congenital, endo, carcinoid, RHD
o S/S
 Fatigue
o Murmur
 Low frequency intensity with opening snap, LLSB 4th ICS
o Management
 Surgical
 Decrease right atrial volume with diuretics and sodium restriction
Etiology
o Congenital
o Normal connection between pulmonary artery and aorta fails to close
 S/S
o Poor feeding, poor growth, SOB
 Murmur
o Continuous, systole and diastole
o Machine-like
o Pulmonic area
 Management
o Indomethacin or prostaglandin antagonists to close
o Surgery
o Bradykinin levels rise – ductus arteriosus closes
 Complications
o Eisenmenger’s syndrome
 PHTN
 Left to right shunt switches and becomes R-L shunt and becomes
cyanotic
 Normal hands and upper extremities
 Cyanotic lower extremities – clubbed and blue
Coarctation
 Etiology
o Congenital
o Many also have bicuspid aortic valve
o More common in males
 S/S
o Secondary hypertension
o Bilateral claudication, DOE, syncope
 Infants – preductal
 Adults – postductal
 Murmur
o Systolic murmur radiating to back, scapula
 Diagnosis
o Elevated BP in upper extremities with delayed/weak femoral pulses
o
o Rib notching
o 3 sign on aorta
o Angiogram is diagnostic
 Management
o Surgical correction with balloon angioplasty and stent
Vascular disease
 Risk factors
 Smoking, hyperlipidemia, HTN, DM
 Arterial
 S/S
o Dull ache with muscle fatigue, craping
o Painful unless neuropathic
o Weak thread pulse
o Skin coldness, pallor, cyanosis
o Thin atrophied skin
o Hair loss
o Skin mottling, tenderness, numbness
 Ulcer
o Toes and dorsum of foot
o Punched out margins
o Destroys deep fascia and may expose tendons
o Poor granulation
 Venous
 Etiology
o Leg edema 2ndary to venous occlusion or incompetency
 S/S
o Chronic ache that worsens as the day goes
o Minimal pain
o Bulging veins
o Aggravated by prolonged standing
o Alleviated by elevation
o Chronic leg edema
o Stasis dermatitis
o Stasis ulcers
 Ulcer
o Above medial malleolus
o Beefy red, shallow, never penetrate deep
o Moist, superficial, diffuse
o Aching and edema
o Mottled brown or black staining
 Diagnosis
 Angiogram, US, ABI
o 0.9-1.30 – normal
o < 0.9 – abnormal
 Management
 Cilostazol
 Revascularization
 Supportive
 Vasculitis


Large vessel
 Giant cell
 Takayasu
o Aorta, aortic arch, pulmonary arties
o Women, Asians, younger
o S/S
 Prodrome
 Vessel stenosis/occlusion/ischemia
 Coronary artery MI
 Carotid or abdominal arterial bruits, diminished pulses
 Asymmetric BP measurements
o Diagnosis
 Angiography
 Helical CT angio or MRA
 Elevated ESR/CRP
o Management
 High dose steroids
 Aortitis
Medium vessel
 Granulomatosis with polyangiitis (Wegener’s)
o Etiology
 Nose, lungs, kidneys
o S/S
 Upper respiratory/nose
 Nasal congestion, saddle-nose deformity
 Epistaxis, otitis media, refractory sinusitis
 Lower respiratory
 Parenchymal involvement
 Cough, dyspnea, hemoptysis, pulmonary hemorrhage,
wheezing, pulmonary infiltrates, cavitation
 Glomerulonephritis
 Rapidly progressing/crescentic
 Hematuria, proteinuria
o Diagnosis
 + ANCA
 CXR – infiltrates, nodules, masses, cavities
o Management
 Steroids, cyclophosphamide
 Buerger’s thromboangiitis obliterans
o Smoking
 Polyarteritis nodosa
o Etiology
 Associated with HBV
o S/S
 Renal – HTN due to elevated renin
 Lungs spared
 Raynaud’s
 Intra-abdominal cavity vessels
 Abdominal pain
o
o


Diagnosis
 Elevated ESR
 Celiac arteriogram
 ANCA negative
Management
 Steroids
Small vessel
 Hypersensitivity vasculitis – HSP/IgA
 Rheumatoid vasculitis
PULMONOLOGY
o Pneumothorax
 Etiology
 Air in the pleural space – increasingly positive pleural pressure causes collapse of the
lung
 Spontaneous – atraumatic and idiopathic
o Bleb rupture
o Primary – no underlying lung disease
 Tall, thin men, smokers
 Family history of PNTX
o Secondary – underling lung disease
 No trauma
 COPD, asthma
 Traumatic
o Iatrogenic – CPR, thoracentesis, PEEP, subclavian line placement
o Car accident, GSW
 Tension
o Any type of PNTX which positive pressure pushes lungs, vessels, and heart to
contralateral side
 Catamenial PNTX – ectopic endometrial tissue in pleura
 S/S
 Chest pain – pleuritic, unilateral, non-exertional, sudden onset
 Dyspnea
 Hyperresonance to percussion, decreased fremitus, decreased breath sounds on
affected side
 Unequal respiratory expansion, tachycardia, tachypnea
 Tension – JVP, pulsus paradoxus, hypotension
 Diagnosis
 CXR with expiratory view
o Decreased peripheral lung markings
 Management
 Observation if small – can’t use CPAP/BIPAP
 Chest tube/thoracostomy if large or severe
 Needle aspiration if TPNTX followed by chest tube
o 2ICS @ MCL or 5ICS @ MAL
o Pulmonary embolism
 Etiology
 95% arise from DVTs in lower extremities above the knee
 Virchow’s triad
o

o
Stasis, endothelial injury, hypercoagulability
S/S
 Dyspnea MC symptom
 Tachypnea MC sign
 Dyspnea, pleuritic chest pain, hemoptysis
 Homan’s sign with DVT
 Diagnosis
 Helical CT for suspected PE
 CTA – gold standard
 VQ – renal impairment and cannot handle contrast
 Doppler US
 CXR
o Westermark’s sign – avascular markings distal to blockage
o Hampton’s hump – wedge-shaped infiltrate
 ECG
o Sinus tach
o S1Q3T3
 D-Dimer
o Helpful only if negative and low-suspicion
 Well’s criteria
o Clinical signs and symptoms – 3
o An alternative diagnosis is less likely – 3
o Tachycardia – 1.5
o Immobilization or surgery within 4 weeks – 1.5
o Previous DVT/PE – 1.5
o Hemoptysis – 1
o Malignancy – 1
o > 4 – likely PE
 Management
 Warfarin or NOAC x 3 months
 Direct factor Xa and thrombin inhibitors
Acute respiratory distress/failure
 Etiology
 Life threatening acute hypoxemic respiratory failure – organ failure from prolonged
hypoxemia
 MC develops in critically ill patients
 Sepsis MC
 Pro-inflammatory cytokines  diffuse alveolar damage  increased permeability of
alveolar capillary barrier  pulmonary edema
 S/S
 Acute dyspnea and hypoxemia
 MSOF
 Diagnosis
 Severe refractory hypoxemia is hallmark
 Bilateral pulmonary infiltrates on CXR – white out pattern
 Absence of cardiogenic pulmonary edema/CHF
o PCWP < 18mmHg
 Not responsive to 100% O2 – refractory hypoxemia

o
o
Management
 Noninvasive or mechanical ventilation and treat the underlying cause
 CPAP with full face mask – attempt to keep O2 above 90%
 PEEP – prevents airway collapse at end expiration
Acute bronchitis
 Etiology and RF
 Viral—adenovirus, parainfluenza, coronavirus
 Bacterial—strep pneumo, HIV, MCat
 Often follows URI
 Patho
 Inflammation of trachea and bronchi
 S/S
 Cough lasting 1-3 weeks which may be productive
 Fever is rare
 Chest discomfort due to coughing
 Diagnosis
 Clinical
 If suspect pneumonia—CXR
 Pro-calcitonin will differentiate pneumonia vs. bronchitis
 Management
 Symptomatic
 No antibiotics
o COPD, immunocompromised, or cough > 10 days without improvement
 Oral steroids only if severe cough with prolonged difficulty sleeping
Asthma
 Etiology and RF
 Samter’s triad—asthma, nasal polyps, ASA/NSAID allergy (associated with atopic
dermatitis)
 Patho
 Airway hyperreactivity due to endogenous and exogenous stimuli
 Bronchoconstriction and airway narrowing  air trapping
 Wall edema, mucus secretion and plugging
 S/S
 Dyspnea, wheezing, night coughing
 Chest tightness, prolonged expiration, fatigue
 Ask about steroid use, previous intubations and hospitalizations
 Tachycardia, tachypnea, accessory muscle use
 Prolonged expiration with wheeze, hyperresonance, decreased breath sounds
 Severe asthma and status asthmaticus
o Unable to speak in full sentences
o AMS, cyanosis, tripoding, silent chest with no air exchange
 Diagnosis
 PFT with reversible obstruction
 Bronchoprovocation
o Methacholine challenge with > 20% decrease in FEV1
o Bronchodilator challenge >12% increase in FEV1 or 200cc
 Peak expiratory flow
o Best and most objective way to assess exacerbation and severity
o
o
o >15% from initial attempt  response to treatment
o Use to monitor
 Admission criteria
 < 50% PEF predicted, 3 days of exacerbation, AMS, status asthmaticus
 Treatment
 Mild—SABA at least 2 days per week but not daily
o Inhaled SABA PRN + low-dose ICS
 Moderate—SABA use daily
o Night-time awakenings at least once per week
o Low dose ICS + LABA or LTRA
o Increase ICS
o Still need SABA
 Severe—SABA use several times per day
o Night-time awakenings nightly
o High dose ICS + LABA + omalizumab (IgE antagonist)
Bronchiectasis
 Etiology
 Recurrent and chronic lung infections
 Cystic fibrosis  pseud
 Hereditary  CF
 Patho
 Irreversible chronic dilation of medium sized bronchi
 Obstruction of airflow and impaired clearance of secretion  lung infections
 S/S
 Daily chronic cough with thick mucopurulent, foul-smelling sputum
 Pleuritic chest pain, hemoptysis (can be massive)
 Persistent crackles at bases
 Diagnosis
 High-res CT
o Airway dilation, tram-track appearance with signet ring sign
 PFT
o Obstructive pattern
 Management
 Antibiotics, mucus management, surgery
Carcinoid tumor
 Etiology and RF
 Younger population
 Patho
 Enterochromaffin neuroendocrine tumor
 Slow growth with low mets
 May secrete serotonin, ACTH, ADH, MSH
 S/S
 Asymptomatic, focal wheezing
 SIADH, Cushing’s, obstruction
 Carcinoid syndrome—excess serotonin
o Diarrhea, flushing, tachycardia, bronchoconstriction
 Diagnosis
 Bronchoscopy—purple/pink well vascularized central tumor

o
o
 Tumor localization on CT
Management
 Octreotide to reduce symptoms
 Surgical excision is definitive
 Resistant to CT/RX
COPD
 Etiology and RF
 Cigarette smoking and exposure—centrilobular emphysema
 Anti-trypsin deficiency—genetic, linked to COPD under 40
o Panlobular emphysema
 Occupational and environmental exposures
 Patho
 Loss of elastic recoil leading to increased airway resistance
 Emphysema—steady decline
o Abnormal, permanent enlargement of terminal airspaces
 Chronic bronchitis—episodic
o Productive cough for > 3 months for 2 consecutive years
o Prone to microbial infections
 Smooth muscle and connective tissue thickening—airway narrowing and fibrosis
 Increase in goblet and mucus glands—more mucus secretion
 Hypercapnia with elevated bicarbonate to compensate for respiratory acidosis
 S/S
 Emphysema—pink puffer
o Cachectic with pursed lip breathing
o Dyspnea MC
o Accessory muscle use, tachypnea, prolonged expiration, mild cough
o Hyperinflation, hyperresonance, decreased fremitus, decreased breath sounds
 Chronic bronchitis—blue bloater
o Obese and cyanotic
o Productive cough MC—white and frothy
o Prolonged expiration
o Severe hypoxemia and hypercapnia
 Diagnosis
 Labs
o Respiratory acidosis
o Elevated Hct and Hgb
 PFT
o FEV1/FVC < 70%
o Hyperinflation—increased lung volumes
 CXR—increased AP diameter, flat diaphragm
 Management
 Smoking cessation
 Bronchodilators—anticholinergics (ipratropium) + beta agonist (albuterol)
 Steroids
 Oxygen –decreases pulmonary hypertension and cor pulmonale
 Need vaccinations
Cor pulmonale

o
Complication of pulmonary hypertension where right ventricular structure and function is
altered
 Pulmonary hypertension induced remodeling of the heart—hypertrophy or dilation
 Leads to impaired function of right ventricle
 Associated with chronic lung disease and/or hypoxemia (Type III)
 Right sided disease due to LHF is not considered CP
 COPD MC
 Acutely – pulmonary embolism and ARDS
 S/S similar to pulmonary hypertension
 Fatigue, tachypnea, exertional dyspnea, cough
 May have split S2
 EKG
 Right axis deviation, Q waves in precordial, increase in P wave amplitude in II, III, aVF
Hypoventilation syndrome
 Patho
 Insufficient ventilation leading to hypercapnia
 Types
 Central alveolar hypoventilation
o Secondary to underlying neurologic disease
o Drugs and CNS disease—CVA, trauma, neoplasms
 Obesity-hypoventilation
o Abnormal central ventilatory drive and obesity
o BMI > 30
o Most have OSA as well
o Hypoventilation is worse during REM
o Daytime somnolence, snoring, fatigue, impaired concentration, PH
 Chest wall deformities
o Kyphoscoliosis, fibrothorax
o Respiratory insufficiency and respiratory failure
 Neuromuscular
o MG, ALS, GBS, muscular dystrophy
o Rapid shallow breathing due to severe muscle weakness or abnormal motor
neuron function
o Central respiratory drive maintained
o Hypoventilation due to muscle weakness
o Nocturnal desaturation during REM sleep
 Diagnosis
o Elevated serum bicarb
o Hypercapnia (>45) with hypoxemia (<70)
o Polycythemia
o PFT
 Restrictive if OHS
o
 Treatment
o Oxygen
o Respiratory stimulants
 Medroxyprogesterone
 OHS and central
 Does not help apnea

o
o
Acetazolamide
 Causes metabolic acidosis—forces increased ventilation
 Theophylline
 Increases diaphragm muscle strength
 Stimulant, bronchodilator
o Weight loss
o Positive airway pressure—CPAP or BPAP
Idiopathic pulmonary fibrosis
 Etiology and RF
 Men 40-50
 History of Smoking
 Patho
 Chronic progressive interstitial scarring and fibrosis
 Restrictive pattern
 S/S
 Dyspnea and non-productive cough
 Clubbing with cyanosis
 Fine bibasilar inspiratory crackles
 Diagnosis
 CT—diffuse reticular opacities and honeycombing
o Ground glass opacities
 PFT
o Restrictive with decreased lung volume, DLCO
o Normal or elevated FEV1/FVC
 Management
 No effective treatment
 Smoking cessation, oxygen
 Transplant only cure
Pneumoconiosis
 Patho
 Inhalation of mineral dust leads to inflammation and restrictive lung disease
 Silicosis—silica dust inhalation
 Etiology
o Mining, quarry work with granite/slate/quartz, sandblasting
 S/S
o Asymptomatic, DOE, non-productive cough
 Diagnosis
o CXR
 Small round nodules in upper lobes
 Egg shell calcifications in hilar nodes
o Lung biopsy
 Management
o Supportive—bronchodilators, O2, vaccines
 Coal worker’s pneumoconiosis/black lung disease—coal and carbon mines
 Diagnosis
o CXR
 Small upper lobe nodules
 Hyperinflation resembling emphysema

o
Management
o Supportive
 Berylliosis
 Etiology
o Electronics, aerospace, ceramics, tool and dye manufacturing
 S/S
o Dyspnea, cough, arthralgia, weight loss, fever
 Diagnosis
o CXR
 Normal hilar markings in 50%, increased interstitial lung markings
o Positive history, positive beryllium lymphocyte test
 Management
o Steroids, O2, methotrexate
o Increased risk of lung, stomach, and colon cancer
 Byssinosis—cotton exposure
 Worse and beginning of week and improves as week progresses
 Asbestosis
 Etiology
o 15-20 years post exposure
o Destruction and renovation of old buildings
o Insulation, ship building
o Smoking increases the risk
 S/S
o Bronchogenic carcinoma
o Malignant mesothelioma of pleura
 Diagnosis
o CXR
 Pleural plaques with pleural thickening
 Lower lobes primarily
o Biopsy
 Linear asbestos body
 Management—supportive
 Mesothelioma
o Tumor in pleura from asbestos exposure
Pneumonia (viral, bacterial, fungal, human immunodeficiency virus-related)
 Bacteria
 Typical—strep pneumo, HIB, MCat, staph
 Atypical—legionella, mycoplasma, chlamydia, viral
 Strep pneumo—MC CAP
o Rust colored sputum
 HIB—increased incidence with underlying pulmonary disease
o CAP
o Green sputum
 Mycoplasma—MC atypical
o School aged, college
 Legionella—elderly, smokers, immunodeficient
o No person-to-person transmission
o Contaminated water supplies—HVAC, cooling towers
o GI symptoms—N/V/D, hyponatremia






o
Viral



Fungal

o Send urine antigen
Staph—after viral
o Immunocompromised
o Bilateral
o Abscess formation
Kleb—EtOH
o Cavitary lesions
o Currant jelly sputum
Anaerobes—aspiration pneumonia
o RLL with foul smelling sputum
Pseud—IC patients
o CF, bronchiectasis
o Green sputum
RSV and parainfluenza—infants and small children
Influenzas—adults
CMV—transplants and AIDS
PCP—IC
o Pleuritic chest pain with desaturation on ambulation
o AIDS defining disease
o TMP-SMX
 Histo—Mississippi and Ohio River
o Bird and bat droppings
 Coccidiosis—Southwest US
 Treatment
 CAP outpatient
o Macrolide—azithro or clarithro 1st
o Doxy 2nd
o Fluoroquinolones only if comorbid conditions
 CAP inpatient
o Beta-lactam + macrolide or broad spectrum FQ
 HAP
o Anti-pseud beta lactam + FQ
 Aspiration—anaerobes
o Clinda or metronidazole
Pulmonary hypertension
 Patho
 Mean PAP > 25mmHG at rest
 Leads to right heart failure
 Types
 I  idiopathy/primary
 II  due to left heart failure
 III  due to hypoxemia or chronic lung disease
 IV  chronic thromboembolic disease
 Type V caused by other disease or conditions (sarcoid, polycythemia, vasculitis)
 Primary—idiopathic
 MC in young middle-aged women

o
Secondary—due to pulmonary disease
 COPD MC
 S/S
 Dyspnea, chest pain, DOE, cyanosis
 Accentuated S2
 Fixed or paradoxically split S2
 Diagnosis
 CXR
o Enlarged pulm arteries, interstitial alveolar edema, heart failure
 ECG—cor pulmonale, RVH, right axis deviation, RBBB
 Echo
o Large right ventricle, right atrial hypertrophy
 Right heart cath—definitive diagnosis
 CBC—polycythemia
 Management
 Type I/Primary
o Inhaled nitric oxide, IV adenosine, trial of CBB for vasoreactivity
o Prostacyclin, PDE5I
o Oxygen
o Heart-lung transplant definitive
 Type II—treat underlying disease
 Type III—oxygen, treat underlying disease
 Type IV—anticoagulation, treat underlying disease
Pulmonary neoplasm
 Etiology and RF
 Cigarette smoking
 Mets to brain, bone, liver
 NSCLC
 Adeno MC in smokers, women, nonsmokers
o Peripheral
 Squamous
o Centrally located
o Can do sputum cytology
o Hemoptysis
o Can have hypercalcemia
 Large cell—aggressive
 Management
o Surgical resection if localized
 SCLC
 Mets early and often found on presentation
 Central and aggressive
 Management
o Chemo with/out radiation
o Surgery not treatment of choice
 SVC syndrome—SCLC
 Dilated neck veins, facial plethora, prominent chest veins
 Hypercalcemia—squamous
 Due to PTHrP
o
 Treat with bisphosphonates
 SIADH/hyponatremia—SCLC
 Gynecomastia— adeno
 Cushing’s—SCLC
 Ectopic ACTH production
 Lambert-Eaton—SCLC
 Antibodies against calcium gated channels
 Weakness like MG but improves with continued use
 Pancoast syndrome—squamous
 Tumor in superior sulcus
 Shoulder pain, Horner’s, atrophy of hand, arm
 Diagnosis
 CXR/CT
 Sputum and cytology for central lesions
 Bronchoscopy for central lesions
 Transthoracic needle biopsy for peripheral lesions
Sarcoidosis
 Etiology and RF
 Afro-Americans, Northern European females
 Patho
 Multisystem inflammation with granuloma formation
 Granuloma formation due to T cell accumulation
 S/S
 50% asymptomatic
 Pulmonary 50%  dry non-productive cough, dyspnea, chest pain
 Lymphadenopathy  painless intrathoracic (hilar nodes)
 Skin (2nd MC)
o Maculopapular rash MC
o Erythema nodosum—bilateral tender nodules on anterior legs
o Lupus perino—violaceous raised discoloration on nose, ear, cheek
 Visual—need ophtho exams in all patients
o Conjunctivitis
o Anterior uveitis—blurred vision, ocular discomfort, ciliary flush
 Myocardial—arrhythmias, cardiomyopathies
 Diagnosis
 Clinical and radiographic findings, non-caseating granulomas
 Tissue biopsy
 CXR—bilateral hilar lymphadenopathy
o Interstitial lung disease with reticular opacities
o Eggshell nodal calcifications
 PFT—restrictive
 Gallium scan—panda sign with increased uptake in parotid and salivary
 Labs
o Increased ACE, hypercalciuria, hypercalcemia, eosinophilia
 Management
 Observation
 Oral steroids
 Methotrexate

 NSAIDs
o Solitary pulmonary nodule
 nodules < 3cm
 mass > 3cm
 etiologies
 granulomatous—TB MC
 tumors
 inflammation
 mediastinal tumors—thymoma MC
 benign
 round and smooth with slow growth
 malignant
 irregular with speculated borders and rapid growth
 calcifications are speckled
 cavitary with thickened walls
 diagnosis
 observation
 transthoracic needle aspiration or bronchoscopy
 resection
GASTROINTESTINAL/NUTRITIONAL
o Acute and chronic hepatitis
 Alcoholic liver disease
 Histologic
o Early – macro vesicular steatosis
o Progresses to frank fatty liver
 S/S
o Relatively asymptomatic until late in disease
o 4-6 weeks abstinence resolves mild or moderate states
o Jaundice/icterus, anorexia, abdominal pain, N/V
o Tender hepatomegaly, fever, variceal bleeding, ascites, hepatic encephalopathy
 Diagnosis
o Coagulopathy due to elevated INR and prolonged bleeding time
o Elevated LFT – AST:ALT ratio > 2
o Conjugated hyperbilirubinemia
o Elevated GGT
o Leukocytosis, elevated MVC
 Management
o Abstinence
o Prednisone
o Pentoxifylline
 Viral
 HAV
o Etiology
 Fecal-oral transmission
 Contaminated water and food
 Little to no chance of chronic infection
o S/S
 Children usually asymptomatic – MC source for adults

o
o

o
HBV
o
o
o
Immune State
Window period
Acute
Vaccination
Chronic inactive
Chronic active
Resolved
HBsAg
Negative
Positive
negative
Positive
Positive
Positive
Prodromal phase – malaise, arthralgia, fatigue, N/V, anorexia, decreased
smoking
 Spiking fever – only hepatitis associated with fever
 Icteric phase – jaundice
Diagnosis
 + IgM HAV Ab
 Past exposure IgG HAV ab with negative IgM
Management
 Self-limiting with symptomatic treatment
 Post-exposure – HAV immune globulin
 Pre-exposure – HepA vaccine
Can get Hepatitis E
Etiology
 Parenteral, sexual, perinatal, percutaneous
 10% become chronic
S/S
 Acute – 70% subclinical, 30% jaundice
 Chronic – increased risk for HCC; the younger it is acquired (perinatal)
the more likely it is to be chronic
Diagnosis
 Serologic markers
 HBsAg
o Most important test
o Indicates presence of ongoing infection
o If tested too early can be negative
 HBsAb (anti-HBs)
o Indicates active immunity from vaccine or previous
infection
 HBcAb (anti-HBc)
o Not induced by vaccine – infection only
o Appears at time of infection and lasts forever
 HBeAg
o Marker of active viral replication
 HBV DNA
o Surrogate marker for amount of active infection
o Measured via PCR
Anti-HBs/HBsAB
Negative
Negative
Positive
Negative
Negative
Positive
Anti-HBc/HBcAb
IgM
IgM
Negative
IgG
IgG
IgG
HBeAg
Negative
Positive
Negative
Negative
Positive
Negative
HBV DNA
> 10,000
> 20,000
undetectable
< 10,000
> 10,000
Undetectable
o


o
HCV
o
Management
 Acute – supportive
 Chronic – alpha interferon
 Tenofovir
 Need to do serial monitoring of LFTs
 HepB vaccine

Can get hepatitis D
Etiology
 Parenteral – IV, blood transfusions before 1992
 80% become chronic – cirrhosis, ESLD, high risk for HCC
o S/S
 Asymptomatic for long time
 Progressive fatigue and intermittent vague RUQ pain
 Cryoglobulinemia, vasculitis, porphyria
 Progressive portal hypertension
o Diagnosis
 HCV RNA via PCR
 Screening all individuals born between 1945-1965
o Management
 Goal is sustained virologic response – undetectable HCV > 6 months
after treatment
 Need to check for coinfection with HIV and HBV
 Pegylated interferon alpha
 Antivirals specific to genotype
Drug induced liver injury
 Etiology
o PCN
o NSAIDs
o Amiodarone
o Allopurinol
o Methotrexate
o Anti-epileptic
o Isoniazid
 Acetaminophen – class of its own
o Etiology
 Non-intentional OD due to senility/dementia
 Non-intentional OD due to compound medications such as OTC cold
medications
 Intentional OD
 Acutely – 1g/6 hours with max of 4g/24h
 Long term – 3g/day
o Toxicity
 Adult potential – 4-6g
 Truly toxic adult – > 7.5g
 Lethal dose > 15-20g
o S/S
 High index of suspicion required
o
 Typically, > 10g must be ingested in a single ingestion
 Abdominal pain, N/V
 Hepatic encephalopathy, progressive jaundice
 Weakness, malaise
 Rapidly climbing LFTs
o Diagnosis
 Measure acetaminophen levels at presentation and 4-hour level
 Acetaminophen level
o Management
 Single ingestion within 3-4 hours – activated charcoal in ER
 N-acetylcysteine (NAC)
 Dosed PO or IV
 Loading dose followed by 17 consecutive doses every 4 hours
 Once you start, you continue until all doses completed
 Biochemically supports the liver – des not reverse or bind
acetaminophen
 Fulminant hepatic failure
 Etiology
o Raid liver failure + hepatic encephalopathy
o Within 8 weeks of liver injury if healthy prior
o Acetaminophen MC
o Final stage of either severe acute liver failure (DILI, acute hepatitis) or
progression of chronic liver failure to ESLD
o High mortality
 S/S
o Encephalopathy due to high climbing ammonia level
o Deep jaundice and icturia
o Edematous
o AKI due to hepatorenal syndrome
o Elevated PT/INR due to impaired liver functions – prone to bleeding
o Elevated LFTs
o Hypotension
o Hepatomegaly
o Hyperreflexia, asterixis
 Diagnosis
o Elevated ammonia, elevated PT/INR, hypoglycemia, elevated LFTs
 Management
o Lactulose, rifaximin, protein restriction
o Liver transplant
 Reye syndrome
o Fulminant hepatitis MC in children
o Aspirin use during viral infection
o Rash on hands and feet
o Intractable vomiting, liver damage, encephalopathy, dilated pupils, MSOF
Acute/chronic pancreatitis
 Acute
 Etiology
o Gallstones MC, EtOH close 2nd
o Inflammatory response to pancreatic injury

S/S
o
o
o




o
Abdominal pain (band-like), boring, constant, radiating to back
N/V, fever
Grey-turner’s sign – ecchymosis discoloration of flanks from retroperitoneal
bleed – pancreatic necrosis
o Cullen sign – periumbilical discoloration – retroperitoneal bleed
Diagnosis
o Leukocytosis, elevated glucose, bili, triglycerides
o Lipase more specific than amylase
o ALT elevation suggestive of gallstone pancreatitis
o Hypocalcemia – necrotic fat binds calcium
o Abdominal CT
Management
o Rest pancreas
o NPO, IV fluid, analgesia with meperidine (Morphine associated with Oddi
spasm)
o Abx not used frequently
o ERCP if biliary obstruction
Ranson criteria
o Glucose > 200
o Age > 55
o LDH > 350
o AST > 250
o WBC > 16000
Chronic
 Etiology
o Chronic inflammation causing parenchymal destruction, fibrosis
o Loss of exocrine and endocrine function
o EtOH abuse MC
o CF MC in children
 S/S
o Calcifications, steatorrhea, DM
o Weight loss,
 Diagnosis
o Calcified pancreas
o Amylase and lipase usually normal
o MRCP – calcifications and pancreatic duct obstruction
 Management
o Oral pancreatic enzyme replacement
o EtOH abstinence, pain control
Anal fissure/fistula
 Fissure
 Etiology
o Low-fiber diet
o Passage of large, hard stools
o Anal trauma
o Primary – MC, 2ndary to trauma from passage of hard stool, prolonged
diarrhea, anal sex
o Secondary – IBD, malignancy, HIV, TB
o
o



o
Acute – heals within 6 weeks
Chronic – fails conservative management
S/S
o Painful linear tear/crack
o Rectal pain and bowel movements – tearing pain
o Patient tries to refrain from BM due to pain  constipation, BRBPR
o Skin tags in chronic
o Posterior midline MC
Management
o 80% resolve spontaneously
o Warm Sitz baths
o High fiber diet, increased water intake
o Stool softeners
o Topical vasodilators, nitro
o Chronic – lateral internal spincterotomy – risk fecal incontinence
Fistula
 Etiology
o White males
o Obese, hirsute
o Prolonged sitting, local trauma
o Deeper abscesses
o MC etiology is anorectal abscess
 S/S
o Tender abscess with drainage on or near gluteal cleft near midline of coccyx or
sacrum with small midline pits
o Anal discharge and pain
 Diagnosis
o CT or MRI showing air or contrast within fistula
 Management
o I&D
o Excision of pilonidal sinus and tracts recommended if recurrent
 Abscess
 Etiology
o Bacterial infection of anal ducts/glands
o 50% patients with perianal Crohn’s disease
o MC staph aureus
o MC in posterior rectal wall
 S/S
o Anorectal swelling, rectal pain worse with sitting, coughing, defecation
 Diagnosis
o CT or MRI
 Management
o I/D
o Warm-water cleansing, analgesics, sitz bath, high-fiber diet
Cancer of rectum, colon, esophagus, stomach
 Esophagus
 Squamous – proximal esophagus
o MC esophageal CA worldwide
o RF







 Smoking and alcohol
 Diets high in nitrates and low in fruits and veggies
 Red meat
 Previous esophageal disease or injury
o Upper 1/3 of esophagus
o Peaks 50-70
Adeno – Barrett’s
o MC esophageal CA in US
o Near GE junction
o RF
 Smoking, alcohol, GERD
 Obesity, metabolic syndrome
o Barrett’s
 Closer to stomach and GE junction – including 2cm below
 Usually reversible when GERD treated early
 PPI treatment with surveillance
S/S
o Transient sticking of food
o Regurg of food, weight loss
o Progressive solid food dysphagia
o Starts with solid foods  liquids
o Virchow’s node
o Chronic GI blood loss
Diagnosis
o Endoscopy, EUS for staging
o CT and PET
Treatment
o SCC
 Resectable – neoadjuvant followed by surgery
 Inoperable – chemoradiation
o Adeno
 Neoadjuvant chemo then surgery
o Metastatic – palliation
Surveillance
o SCC
 EGD as indicated
 PE every 3-6 months for 1-3 years, then 6 months for 5 years
 Recurrence highest in first year
Complications
o Dysphagia or odynophagia
o Weight loss and malnutrition
o PEG tube
Gastric
 Etiology
o Most present symptomatic and already have advanced incurable disease
o Adenocarcinoma
o Mets to liver
 Risk factors
o H. pylori
o




HCC

Salted, cured, smoked, pickled foods
S/S
o Weight loss, anorexia, nausea
o Mild epigastric abdominal pain, but progresses to severe
o Early satiety, dysphagia, gastric outlet obstruction
o Dysphagia presenting symptom if in proximal stomach at GE junction
o Gastric outlet if distal stomach
o Iron deficiency anemia
Diagnosis
o CT of chest, abdomen, pelvis
o Endoscopic US – linitis plastica – diffuse thickening of stomach wall with leather
bottle appearance
o PET scan
o Serologic markers – CEA, CA 125, CA 19.9
o Non-resection – distant mets, invasion into vascular, disease encasement or
occlusion of hepatic artery
Etiology
o Hepatic malignancies are more common secondary to mets
o Chronic viral hep
o Aflatoxin B exposure – aspergillus
 S/S
o Malaise, weight loss, jaundice, abdominal pain, HSM
 Diagnosis
o US, CT, MRI
o Elevated alpha-fetoprotein
o Do not do needle biopsy—seeding
 Management
o Surgical resection if confined to lobe
Pancreatic
 Etiology
o Adenocarcinoma found in head of pancreas
o Smoking, > 60
 S/S
o Asthenia – abnormal weakness or energy
o Weight loss, anorexia, abdominal epigastric pain
 May radiate to back
o New onset DM
o Painless jaundice, pruritus
o Acholic stools, dark urine
o Trousseau’s sign – migratory phlebitis
o Courvoisier’s sign – palpable, nontender, distended gallbladder associated with
jaundice
 Diagnosis
o Abdominal CT
o ERCP or MRCP
o Tumor markers – CEA, CA 19-9
 Treatment
o Chemo + surgery
o
o Whipple
 Best prognostic factor is nodal status
 Colorectal
 Risk factors
o Hereditary
 Familial adenomatous polyposis
 Screen at age 10
 Surgery
 Lynch syndrome
 Autosomal dominant
 Increase risk of cancer—young age, uterine, etc.
o Aspirin can reduce risk
o IBD – UC increases
o Protective
 Physical activity
 High fiber diet
 Aspirin, HRT< statins, bisphosphates, ANG2I
 Antioxidants
 S/S
o Local tumor
 Hematochezia, melena, rectal bleeding
 Abdominal pain
 Unexplained IDA
 Change in bowel habits
 MC of large bowel obstruction in adults
 Right side – bleeding, diarrhea
 Left – obstruction, later presentation, change in stool diameter
o Metastatic
 Regional LN, liver, lungs
o Unusual
 Perforation, FUO or abscess due to perforation
 Diagnosis
o Colonoscopy, barium enema, CT colonography
o Apple-core lesion
 Labs
o CEA beneficial in follow up
 Get levels pre-op and follow for 5 years
o IDA
 Treatment
o Surgical resection + chemo
o Stage 1-3 – surgical resection
o Stage 3 and metastatic – chemo
 Screening
o Fecal occult blood test annually
o Colonoscopy every 10 years
o Flexible sigmoidoscopy every 5 years with fecal occult every 3
Celiac disease
 Etiology
 Small bowel autoimmune inflammation due to gliadin of gluten



S/S


o
o
Loss of villi and absorption area due to villous atrophy and crypt hyperplasia
Increased incidence in females and European descent
Malabsorption diarrhea, abdominal pain, distention, bloating, steatorrhea
Dermatitis herpetiformis – pruritic, papulovesicular rash on extensor surfaces, neck,
trunk, scalp
 Diagnosis
 Endomysial IgA antibody and transglutaminase antibody (anti-tTG)
o Testing needs to be done on gluten rich diet
o If positive – go for biopsy
 Small bowel biopsy definitive
 Management
 Gluten free diet – avoid wheat, rye, barely
o Can eat oats, rice, and corn
 Vitamin supplementation
 Increased risk for lymphoma
Cholangitis
 Etiology
 Biliary tract infection due to obstruction – malignancy, GS
 Gram negative enteric organisms – E. coli MC, Klebsiella
 S/S
 Charcot’s triad – fever, jaundice, RUQ pain
 Reynold’s pentad – confusion/AMS, hypotension + triad
o Higher morbidity and mortality
 Diagnosis
 Leukocytosis, elevated ALP, GGT, bili
 US, CT
 Cholangiography via ERCP
 Management
 Antibiotics – pip-taz, ceftriaxone + metronidazole
 Biliary decompression if no response to ABX
Cholecystitis
 Etiology
 Acute – GB inflammation 2ndary to stones
 Acalculous – clinically identical to acute but not associated with stones
o Critically ill patients and associated with high M/M
 Chronic – chronic inflammatory cell infiltration
o Acute cholecystitis leading to fibrosis
 Gram negative enteric organisms – E. coli MC, Klebsiella
 S/S
 Fever
 RUQ pain radiating to back or shoulder
o Boas sign
 N/V
 Murphy’s sign positive
 Diagnosis
 US – GB wall thickening (>3mm) or edema, stones, double wall sign
 HIDA – no visualization of GB in cholecystitis
o
o
 Labs – leukocytosis, normal LFT
 Management
 NPO, IV fluids abx
 Cholecystectomy within 72h
 Cholecystostomy if nonoperative
Choledocholithiasis
 Etiology
 GS in common bile duct – ductal dilation
 Primary – formation of stones originating within CBD
o Bile stasis (CF)
 Secondary – passage of GS from GB into the CBD – MC
 S/S
 Asymptomatic – incidental finding
 Biliary colic with RUQ tenderness +/- jaundice
 Diagnosis
 Labs – elevated AST/ALT, elevated ALP, bili
 US – dilation of duct but not reason
 MRI/MRCP best test for dilation and stones
 ERCP – diagnostic and therapeutic
 Management
 Antibiotics
 ERCP
 Cholecystectomy
Cholelithiasis
 Etiology
 Cholesterol – 90%
 Black stones – hemolysis or EtOH cirrhosis
 Brown stones – increased in Asian population, parasitic/bacterial infections
 RF
 Fat, fair, female, forty fertile
 OCP, bile stasis, chronic hemolysis, cirrhosis, infection, rapid weight loss, IBD, TPN,
fibrates, elevated TRG
 S/S
 Symptomatic or asymptomatic
 Biliary colic
o Recurrent attacks of RUQ, epigastric, or CP
o Radiate to back or R shoulder blade
o 1-2 hours after ingestion of fatty meal or large meal
o Resolves slowly
o N/V
 Negative murphy’s
 Diagnosis
 History of biliary colic
 Normal LFT, amylase, lipase, CBC
 US diagnosis
 Can do HIDA to exclude acute
 Treatment
 Without symptoms – no treatment



o
o
o
Symptoms – elective surgery
Atypical symptoms and stones – rule out other causes (PUD, GERD)
Typical symptoms but no stones – rule out other causes and consider repeat US vs HIDA
Cirrhosis
 Etiology
 Irreversible liver fibrosis with nodular regeneration due to chronic liver dease
 EtOH MC in US
 Viral hepatis
 NAFLD
 Hemochromatosis
 S/S
 General symptoms – fatigue, wakens, weight loss
 Ascites, gynecomastia due to inability to metabolize estrogen
 Spider angioma, bleeding, HSM, janduice
 Hepatic encephalopathy due to ammonia
 Asterixis – flapping tremor
 Spontaneous bacterial peritonitis – >250 WBC from peritoneal fluid
 Diagnosis
 US, biopsy
 Management
 Encephalopathy – lactulose
 Ascites – sodium restriction, diuretics, paracentesis
 Pruritus – cholestyramine – bile acid sequestrant
Diverticular disease
 Etiology
 Diverticulum – sac-like protrusion
 Diverticulosis – presence of diverticula
 Diverticulitis – inflammation/infection of diverticula
 Western – left sided disease
o Sigmoid
 Everyone else has right sided disease
 Low fiber diet, increases with age, family history
 S/S
 Diverticulitis – fever, LLQ abdominal pain, N/V, diarrhea, constipation, change in bowel
habits
o Can have perforation, fistula, abscess
 Diverticulosis – MC cause of lower GI bleed, otherwise generally asymptomatic
 Diagnosis
 CT
 Elevated WBC, guaiac positive
 Management
 Diverticulosis – high fiber diet, fiber supplements
 Diverticulitis – bowel rest – clear liquid diet, ABX – cipro + metronidazole, pip-taz
 After resolution of acute episode, need colonoscopy to establish extent of disease
Esophageal strictures
 Strictures – prolonged GERD/reflux
 Webs – upper 1/3
 Thin membrane


o
o
Asymptomatic or intermittent dysphagia
Plummer Vinson syndrome
o Dysphagia, webs, IDA
 Rings – GEJ
 Schatzki ring
 Sliding hiatal hernia
 Intermittent dysphagia to solids
 Chest discomfort – steak house syndrome
 Diagnosis
 Barium swallow
 EGD
 Management
 dilation
 PPI following dilation to decrease risk of recurrence
Esophageal varices
 Etiology
 Swollen vessels due to obstructed portal flow due to portal vein HTN
 Cirrhotic patients need to undergo screening
 S/S
 Upper GI bleed – hematemesis, melena, hematochezia
 Diagnosis
 EGD – enlarged veins with red wale markings and cherry red spots – increased risk of
bleeding
 Management
 Endoscopic ligation
 Octreotide – somatostatin analog
 Beta blockers – propranolol, nadalol
o Reduces portal venous pressure
o Not used in acute settings
o Isosorbide – long acting nitrate to reduce esophageal variceal pressure
 Withdraw alcohol
Esophagitis
 Etiology
 GERD/reflux
 Eosinophilic
o Young male, history of food/environmental allergies, asthma
o Rings/strictures and peak eosinophil count
 Candida
o HIV patients
o Odynophagia
o Linear yellow-white plaques
 Infectious
o HSV – small deep ulcers
o CMV – large superficial shallow ulcers
 Medication
o Tetracyclines, NSAIDs, bisphosphonates, iron, KCl
 Diagnosis
 Barium swallow


o
o
o
pH monitoring
EGD
o Reflux
o Pill – discrete ulcer with normal surrounding mucosa
o Eosinophilic – esophageal rings or feline esophagus
 Biopsy shows increased number of eosinophils
 Management
 Reflux – lifestyle changes; H2 blocker, PPI
 Eosinophilic – PPI, inhaled steroids without spacer, diet/allergy testing
 Infectious – treat infection
o HSV – acyclovir
o Candida – fluconazole
o CMV – ganciclovir
 Medication – alternate drug, large glass of water, stand/sit for 30 minutes after taking
Gastritis
 Etiology
 Inflammation associated mucosal injury to stomach lining
 Secondary to infectious or autoimmune
 Drugs, hypersensitivity reactions, or extreme stress
 H. pylori, NSAID, alcohol, autoimmune, stress, bile reflux
 S/S
 Epigastric pain, bloating, anorexia
 Fullness after eating
 N/V, hematemesis, anemia
 Management
 Withdraw the causative agent
 Medications to reduce acid
 H. pylori treatment
o Clarithromycin, amoxicillin, Prilosec
o Metronidazole if PCN allergic
Gastroenteritis
 Etiology
 Norovirus MC in adults
 Rotavirus MC in children
 Management
 Rehydration (PO or IV) – mainstay of treatment
 Diet – bland low-residue diet
 Anti-motility agents
o Patients <65 with moderate to severe signs of volume depletion
o CI in invasive diarrhea
Gastroesophageal reflux disease
 Etiology
 Transient relaxation/incompetency of LES leads to gastric acid reflux and esophageal
mucosal injury
 S/S
 Heartburn, water brash, sour taste, dysphagia, cough at night, hoarseness, noncardiac
chest pain
 Alarm symptoms – dysphagia, odynophagia, weight loss, bleeding

o
o
Diagnosis
 Clinical
 Endoscopy most often used
 24h ambulatory pH monitoring GS
 Management
 Lifestyle modifications
 PRN pharm therapy
 PPI
Hemorrhoid
 Etiology
 Engorgement of venous plexus
o Superior hemorrhoid vein (internal) proximal to dentate line
o Inferior hemorrhoid veins (external) distal to dentate line
 RF
o Increased venous pressure
o Straining during poo, constipation, pregnancy, obesity, prolonged sitting,
cirrhosis with portal HTN
 S/S
 Internal
o Intermittent rectal bleeding
o Hematochezia seen on TP, coating the stool, or dispersed in water
o Rectal itching and fullness, mucus discharge
o Rectal pain with internal suggest complication
o Uncomplicated should not be tender nor palpable
 External
o Perianal pain, aggravated with defecation
o Tender palpable mass
o Thrombosis may have precipitated by cough, heavy lifting
 Diagnosis
 Visual inspection, DRE, fecal occult blood test
 Proctosigmoidoscopy
 Management
 Conservative – high-fiber diet, increased fluids
 Topical rectal corticosteroids
 Rubber band ligation, sclerotherapy
 Hemorrhoidectomy
Hernia
 Inguinal
 Indirect
o Protrudes at internal inguinal ring
o Lateral to inferior epigastric artery
o Congential due to persistent patent process vaginalis
o Intestines may follow through the ring into the canal and into the scrotum
o MC in young children and young adults
o MC overall type of hernia
o Right side more common
o Scrotal swelling
 Direct—acquired
o Protrude medial to the inferior epigastric vessels within Hesselbach’s triangle
o
o Weakness in floor of inguinal canal
o Does not reach scrotum
 Incarcerated – painful, enlargement of irreducible hernia
o N/V if bowel obstruction
 Strangulated – ischemic, systemic toxicity due to compromised blood supply
o Severe painful BM – they try and refrain from defecation
 Often require surgical repair – strangulated are emergent
 Femoral
 Abdominal contents through femoral canal below inguinal ligament
 MC in women
 More complications
 Surgical repair done due to frequent incarceration or strangulation
 Hiatal
 Type 1 – sliding
o Displacement of GE junction above diaphragm
o Stomach remains in usual longitudinal alignment and fundus remains below GE
junction
 Type II-IV – paraoesophageal
o True hernia with hernia sac
o Upward dislocation of gastric fundus through defect in phrenoesophageal
membrane
o Abnormal laxity of gastrosplenic and gastrocolic ligaments
o Greater curvature of stomach rolls up into thorax
o Stomach gixed at GE junction – herniated stomach rotates around longitudinal
axis – organoaxial volvulus
 S/S
o Sliding – GERD
o Paraoesophageal
 Epigastric pain, postprandial fullness, nausea, retching
 Complications
o Paraoesophageal
 Gastric volvulus, bleeding, respiratory
 Diagnosis
o EGD
 Management
o Sliding – symptomatic with PPI
o Paraoesophageal – if symptoms or volvulus surgery
Irritable bowel syndrome
 Etiology
 Chronic function idiopathic GI disorder with no organic cause
 WOMEN
 S/S
 Abdominal pain associated with altered bowel habits – diarrhea, constipation, both
 Pain relieved with defecation
 Rome criteria – recurrent pain at least 3 days/ month in the last 3 months with 2 of the
following
o Improvement with defecation
o Onset associated with a change in frequency of stool
o Onset associated with a change in form of stool
o
 Visceral hypersensitivity – lowered pain thresholds to intestinal distention
 Psychosocial interactions and altered CNS processing
 Diagnosis
 Exclusion
 Alarm symptoms – rectal bleeding, nocturnal or progressive abdominal pain, weight
loss, lab abnormalities
o Imaging or colonoscopy warranted
 Without alarming symptoms or FH
o Limited work-up
o Consider TSK, stool studies, celiac panel
 Management
 Fiber/bulking agents
 Anti-spasmodic – bentyl, levsin
 Anti-diarrheal
 Pro-motility agents – lactulose, miralax, linzess
 Anti-depressants
 Stress reduction
Inflammatory bowel disease
 Etiology
 Genetic predisposition
 Crohn’s
 Area affected
o Any segment of GI tract – mouth to anus
o MC in terminal ileum
 Depth – transmural
 S/S
o Abdominal pain – RLQ, crampy
o Weight loss more common
o Diarrhea with no visible blood
 Complications
o Perianal disease – fistulas, strictures, abscesses, granulomas
o Malabsorption – IDA, B12
 Colonoscopy
o Skip lesions – normal areas interspersed between inflamed areas
o Cobblestone appearance
 Barium
o String sign – barium flow through narrowed inflamed/scarred area due to
transmural strictures
 Labs – +ASCA
 Diagnosis
o Upper GI series with small bowel follow through
 Surgery – noncurative
 Ulcerative colitis
 Area affected
o Limited to colon – rectum with contiguous spread proximally
 Depth – mucosa and submucosa only
 S/S
o Abdominal pain – LLQ MC, colicky
o
o
o Tenesmus, urgency
o Bloody diarrhea, mucus pus, hematochezia
 Complications
o Primary sclerosing cholangitis
o Colon CA
o Toxic megacolon
o Smoking decreases risk for UC
 Colonoscopy
o Uniform inflammation and ulceration in rectum/colon
o Pseudo-polyps
 Barium
o Stovepipe sign – loss of haustral markings
 Labs – + P-ANCA
 Diagnosis
o Flex sigmoidoscopy in acute
o Endoscopic biopsy
 Surgery – curative
 Management
 5-Aminosalicylic Acid – sulfasalazine, mesalamine
o Flares and remission
 Steroids – acute flares only
 Immune modifying agents
 Anti-TNF agents
 Erythema nodosum
 MC cutaneous finding in IBD
 Red/violet SQ nodules on pretibial area
 Painful
 Treat underlying IBD
 Pyoderma gangrenosum
 Inflammatory papule, pustule, vesicle that breaks down to form erosion/ulcer
Mallory-Weiss tear
 Etiology
 Longitudinal mucosal laceration in distal esophagus and proximal stomach
 Bleeding from submucosal arteries
 Forceful retching, straining, coughing, hiccups, heavy lifting
 RF
 Hiatal hernia, alcoholism, age
 S/S
 Hematemesis after vomiting, melena, hematochezia, syncope, abdominal pain
 Hydrophobia
 Diagnosis
 EGD shows superficial longitudinal mucosal erosions
 Management
 Supportive
 Acid suppression to promote healing
 Severe bleeding – epi injection
Pancreatitis
 Etiology


o Peptic ulcer disease
 Etiology
 H. pylori MC
 NSAIDs 2nd MC
 ZE
 Suspect GI malignancy in nonhealing ulcer
 GU – decrease mucosal protective factors
 DU – increase damaging factors like acid and pepsin
 S/S
 Dyspepsia – hunger -pain or burning pain
o Can be food provoked
 Epigastric discomfort, fullness, early satiety, N/V
 DU – relief with food, antacids, worse before meals or 2-5 hours after meals, nocturnal
symptoms
o MC
 GU – pain 1-2 hours after meals, weight loss
 Diagnosis
 EGD
o Need biopsy to rule out malignancy if GU present
 Upper GI series
 H. pylori testing
o EGD with rapid urease test
o Urea breath test – diagnosis and eradication
o Stool antigen – diagnosis and eradication
o Serologic – only confirming infection not eradication
 Management
 H. pylori
o Triple therapy – clarithromycin, amoxicillin, PPI
o Quad therapy – PPI, bismuth, tetracycline, metronidazole
 H. pylori negative
o PPI, H2 blocker, misoprostol, antacids, bismuth, sucralfate
ORTHOPEDICS/RHEUMATOLOGY
o Fibromyalgia
 Etiology
 Women
 Increase in pain perception
 Autoimmune disorders like RA, SLE
 S/S
 Chronic widespread muscular pain
 Fatigue, muscle tenderness, HA, poor sleep/memory problems
 Diffuse pain in the AM, stiffness, painful tender joints
 Sleep disturbance
 Diagnosis
 Diffuse pain in 11/18 trigger points > 3 months
 Muscle biopsy shows moth eaten appearance of type I muscle fibers
 Management
 Exercise – swimming


o
o
o
Gout

TCAs, SSNRI, SSRI
Pregabalin
Etiology
 Uric acid deposition in soft tissue, bone, joint
 Underexcretion of uric acid
 Attacks secondary to purine-rich roods – alcohol, red meat, liver, seafood, yeast
 Meds – thiazide and loop diuretics, ACEI, ethambutol, ARB (except losartan),
pyrazinamide
 Men and post-menopausal women
 S/S
 Severe joint pain, erythema, swelling, stiffness
 Podagra – 1st MTP joint
 Tophi deposition – collection of solid uric acid in soft tissue
o 10-20 years of chronic hyperuricemia
 Uric acid stones – low urine volume and acidic pH
o May lead to renal failure
 Diagnosis
 Arthrocentesis – negatively birefringent needle-shaped urate crystals
 Radiographs – mouse/rat bite punched out erosions with overhanging margins
 Elevated ESR and WBC during attacks
 Serum uric acid levels do not reflect joint involvement – normal is 7
 Management
 Acute
o NSAIDs – avoid aspirin
o Colchicine 2nd
o Steroids for renal disease or no response to other choices
 Chronic
o Allopurinol – reduces uric acid production by inhibiting xanthine oxidase
 Take with meals to prevent gastric irritation
 Can cause SJS
o Colchicine
Pseudogout
 Etiology
 Calcium pyrophosphate deposition in joints/soft tissue
 Elderly females
 S/S
 Asymptomatic
 Red, swollen tender joint
 MC in knee
 Chondrocalcinosis – linear radiodensities on radiographs
 Diagnosis
 Arthrocentesis – positive birefringent rhomboid shaped CPPD crystals
 Management
 Intraarticular steroid, NSAIDs
 Colchicine
Polymyalgia rheumatica
 Etiology


o
o
o
Associated with GCA
S/S
 Aching and morning stiffness in shoulders, hip girdle, neck
 Upper arms, posterior neck, pelvic girdle, lumbar region
 Pains in groins and lateral aspects of hips
 Severe morning stiffness and gelling
 Bilateral
 Diagnosis
 Limited ROM but normal muscle strength
 Elevated ESR
 Management
 Low-dose steroids
Polymyositis
 Etiology
 Inflammatory disease of muscle
 S/S
 Proximal muscle weakness with no rash
 Diagnosis
 Clinical
 Elevated CPK, aldolase
 EMG abnormalities – on dominant side
 Muscle biopsy – non dominant side
 + Anti-Jo1 Ab
 + Anti-SRP Ab
 Need pulmonary work-up, prone to interstitial fibrosis
 Treatment
 Steroids
Dermatomyositis
 Etiology
 Inflammatory disease of muscle
 S/S
 Proximal painless weakness
 Symmetrical
 Heliotrope rash – purple blue discoloration of upper eyelid
 Gottron’s papules – raised violaceous scaly knuckle eruptions
 Shawl sign – rash on back and shoulders
 Poikiloderma – photosensitive erythematous rash on face, neck and anterior chest
 Diagnosis
 Muscle enzymes, aldolase
 Higher incidence of malignancy
 + Anti-Mi-2 Ab
 EMG on dominant side
 Muscle biopsy on non-dominant
 Need pulmonary work-up, prone to interstitial fibrosis
 Management
 High dose steroids
Reactive arthritis
 Etiology




o
Autoimmune response to infection in another part of body
MC 20-40y males
1-4w after Chlamydia MC, gonorrhea, salmonella, shigella, CJ, yersinia
S/S
 Arthritis – asymmetric inflammation
 Conjunctivitis/uveitis
 Urethritis/cervicitis
 Sausage toes/fingers
 Keratoderma blennorrhagicum – hyperkeratotic lesions on palms/soles
 Diagnosis
 + HLA-B27
 Elevated CBC, ESR, IgG
 Synovial fluid is aseptic
 Management
 NSAIDs
 No response  methotrexate
Rheumatoid arthritis
 Etiology
 Chronic inflammatory disease with symmetric polyarthritis, bone erosion, cartilage
destruction, and joint structure loss
 Due to destruction by pannus – granulation tissue that erodes into cartilage and bone
 T-cell mediated
 Females, smoking, family history
 S/S
 Prodrome – fever, fatigue, weight loss, anorexia, decreased ROM
 Small joint stiffness – MCP, wrist, POP, knee, MTP, shoulder ankle
o Worse with rest
o DIPs are spared
 Swelling, redness, warmth, pain, stiffness
 Morning stiffness > 60 minutes after initiating movement, improves later in day
 Symmetric arthritis – swollen, tender erythematous boggy joint
o Boutonniere deformity
o Swan neck deformity
 Ulnar deviation at MCP
 Rheumatoid nodules
 Extra-articular manifestations
o Cardiac – pericarditis, atherosclerosis, vasculitis
o Lung – pleural effusions, interstitial lung disease, nodules
o Skin – nodules, vasculitis
o Neuro – entrapment neuropathy, neuropathy
o Heme – anemia, thrombocytosis
o Bone – osteopenia
o Eye – sicca, scleritis
o Kidney – amyloidosis
 Diagnosis
 + RA factor – best initial test, sensitive but not specific
 Elevated CRP, ESR – can be used to monitor treatment and disease activity
 + anti-CCP antibodies most specific for RA


o
o
Arthritis > 3 joints, morning stiffness, disease duration > 6 weeks
Radiologic
o Narrowed joint space, subluxation
 Management
 DMARDs
o Methotrexate
o Hydroxychloroquine – retinal toxicity
 Eye exam 2x per year
 NSAIDs for pain control
 Does into remission during pregnancy
Sjögren syndrome
 Etiology
 Autoimmune disorder attacking the exocrine glands – B cell mediated
 Primary – occurs alone
 Secondary – associated with other autoimmune disorders like SLE and RA
 High incidence of non-Hodgkin lymphoma, interstitial nephritis, pneumonitis
 S/S
 Salivary glands – xerostomia (dry mouth)
 Lacrimal glands – dry eyes (keratoconjunctivitis sicca)
 Parotid enlargement
 Thyroid gland dysfunction
 Difficult dentition with dental caries
 Genital dryness, dryness in ear canal
 Diagnosis
 ANA
 antiSS-A (Ro)
 antiSS-B (La)
 + RF
 + Schirmer test – decreased tear production
 Management
 Artificial tears
 Pilocarpine for xerostomia
o Diaphoresis, flushing, sweating, bradycardia, diarrhea, N/V, incontinence,
blurred vision
 Cevimeline – stimulates muscarinic cholinergic receptors
Systemic lupus erythematosus
 Etiology
 Young women of ethnic descent
 B cell mediated antigen – antibody and complement
 Drugs – procainamide, hydralazine, INH, quinidine
 S/S
 Malar rash
 Discoid rash
 Photosensitivity
 Oral ulcers
 Alopecia
 Serositis –pericarditis, pleuritis
 Renal disease

 Neurologic disorder
 Hematologic disorder
 Immunologic disorder
 Antibody findings
 Any 4/11 and positive ANA  75% specific
 6/11 are 95%
 Negative ANA rules out SLE
 Diagnosis
 ANA positive 100% of time
 Negative ANA rules out SLE
 Antiphospholipid syndrome
o Increased risk of thrombosis
 Anti-DS-DNA
 Management
 CBC, CMP, antibody panel, complement levels
 Need to watch for renal disease, cardiac
 NSAIDs
 Hydroxychloroquine – good for skin limited lupus
 Methotrexate – inflammatory
 Cyclophosphamide – renal SLE
o Systemic sclerosis (scleroderma)
 Systemic
 Rapid onset
 Raynaud’s tendon friction rubs – moving arms feels like leather
 Rapidly ascends
 Internal organ involvement
 Trunk and proximal extremities
 Diagnosis
o SCL-70
 Treatment
o Supportive – not inflammatory
 Limited cutaneous – CREST
 Calcinosis, Raynaud’s, esophageal dysmotility, sclerodactyly, telangiectasias
o Face, neck, distal to elbows and knees
o Pulmonary HTN
 Lower internal organ involvement
 Diagnosis
o Anti-centromere ANA
 Treatment
o Sildenafil, vasodilators
o Symptomatic care
ENDOCRINOLOGY
o Acromegaly
 Etiology
 GH excess
o Acromegaly in adults
o Gigantism in children
 Patho



o
Benign pituitary adenoma stimulates GH release
GH stimulates IGF-1
S/S
 Enlargement of hands, feet, jaw, and internal organs
 No effect on long bones
 Doughy, moist hands, macroglossia, carpal tunnel, deep voice, OSA
 Cardiomegaly, weight gain, insulin resistance
 Acanthosis nigricans, HA, spinal stenosis, decreased libido
 Diagnosis
 Elevated ILG-1
 Oral glucose suppression test—elevated GH
o Normal is low
 MRI imaging modality of choice
 Treatment
 Somatostatin analogs—octreotide/lanreotide
 Dopamine agonists—cabergoline/bromocriptine
 Transsphenoidal surgery
 Pegvisomant—GH receptor antagonist
Addison’s disease
 Primary—adrenal gland destruction—lack of cortisol and aldosterone
 Autoimmune – MC in industrialized countries – adrenal atrophy
 Infection – MC worldwide – TB, HIV, fungal – adrenal calcification
 Vascular – thrombosis or hemorrhage in adrenal gland – Waterhouse-Friderichsen,
trauma
 Metastatic disease, medications: ketoconazole, rifampin, phenytoin, barbiturates
 Secondary – pituitary failure of ACTH secretion – lack of cortisol (aldosterone intact
 Exogenous steroid use MC
o Abrupt cessation—patients unable to increase cortisol levels during times of
stress
 Tertiary – hypopituitarism
 S/S
 Primary—lack aldosterone, sex hormones, increase ACTH
o Hyperpigmentation—increased ACTH
o Orthostatic hypotension (syncope, dizziness)
o Hyponatremia, hyperkalemia, non-anion gap metabolic acidosis, hypoglycemia
o Low sex hormones in women – loss of libido, amenorrhea, loss of axillary and
pubic hair
 1ry, 2ndary, 3ry—symptoms due to lack of cortisol
o Weakness, muscle ache, myalgias, fatigue, non-specific GI
o Weight and appetite loss
o Anorexia, N/V/D, abdominal pain
o Headache, sweating, abnormal periods, salt craving
o Hypoglycemia
 Diagnosis
 Baseline 8am ACTH, cortisol, renin levels
o Elevated renin in primary
 High dose ACTH stimulation –screening
o Measured at 30 and 60m
o
o
o Normal response—rise in blood and urine cortisol
o Insufficiency  little to no increase in cortisol levels < 20
 CRH (corticotropin releasing hormone) stimulation – differentiate between primary and
2ndary
o Primary – elevated ACTH with low cortisol
o Secondary – low ACTH with low cortisol
 Management
 Hormone replacement
o Glucocorticoids + mineralocorticoids
o Hydrocortisone, prednisone, dexamethasone
 Prednisone and dexa will not interfere with screening
o Fludrocortisone for salt balance
o Need two daily doses—larger dose in AM
 20-25 AM with 10-12 PM
 Need to be treated with IV steroids and fluids before and after surgeries and stressful
events
 During illness, surgery, high fever, oral dosing needs to be adjusted
 Salt foods liberally, do not fast, high carbs and proteins, emergency kit
Adrenal crisis (Addisonian)
 Sudden worsening of adrenal insufficiency due to stressful event
 Etiology
 Abrupt withdrawal of steroids
 Previously undiagnosed patient
 Exacerbation of previous diagnosis
 Bilateral adrenal infarction—hemorrhage
 S/S
 Shock—low blood pressure, hypovolemia
 Abdominal pain, N/V/D, fever, weakness, lethargy, coma
 AMS
 Diagnosis
 BMP – hyponatremia, hyperkalemia, hypoglycemia
 Cortisol levels, ACTH, CBC
 Management
 Fluids – NS, D5NS if hypoglycemic
 IV hydrocortisone (dexamethasone if undiagnosed)
 May give vasopressors
 Fludrocortisone
Cushing disease
 Etiology and RF
 Syndrome  effects of excess cortisol on the body
 Disease  caused by ACTH secreting tumor
 Overall more common in females
 Exogenous  iatrogenic MC
o Long-term high dose steroid therapy
 Endogenous
o Cushing’s disease – benign pituitary adenoma or hyperplasia secreting ACTH
o Ectopic ACTH – SCLC, medullary thyroid cancer
o Adrenal tumor – adrenal adenoma secreting cortisol

S/S



Redistribution of fat  central obesity, moon facies, buffalo hump, supraclavicular fat
pads
 Thirst, polyuria, with/out glycosuria
 Catabolism/breakdown of proteins
o Wasting of extremities/thin extremities
o Proximal muscle weakness
o Skin atrophy with easy bruising and striae
o Impaired wound healing
o Increased infections – especially fungal
o Hyperpigmentation with elevated ACTH
 Hypertension, weight gain, osteoporosis, hypokalemia, acanthosis nigricans
 Mental – depression, mania, psychosis
 Androgen excess  hirsutism, oily skin, acneiform rash, elevated libido, virilization,
amenorrhea
 Decreased immune response
o Prone to infection
o Decrease resistance to stress
o Death usually from infection
o Low WBC, lymphs, eosin
Diagnosis
 Labs
o Hypokalemia, metabolic alkalosis
o Hyperglycemia, hypernatremia (maybe), hyperchloremic (maybe)
 Screening
o Low-dose dexamethasone suppression
 Normal is suppression
 No suppression—Cushing’s syndrome
o 24-hour urinary free cortisol levels
 Elevated urinary cortisol – Cushing’s syndrome
o Salivary cortisol levels—performed in PM
 Elevated in Cushing’s syndrome
 Differentiating
o High-dose dexamethasone suppression
 ACTH from disease only partially resistant
 Adrenal tumors and ectopic tumors independent
 Suppression – Cushing’s disease
 No suppression – adrenal or ectopic ACTH
o ACTH levels
 Decreased ACTH  adrenal tumors
 Produce high levels of cortisol suppressing ACTH levels
 Can also be seen in exogenous steroid use
 Normal/increased ACTH – Cushing’s disease or ectopic ACTH tumor
 Imaging
o MRI is preferred in pituitary tumors
o CT may show adrenal
Management
 Disease—transsphenoidal surgical removal
o Radiation if unresectable

o
o
Ectopic ACTH tumor or adrenal tumor
o Tumor r emoval
o Ketoconazole may be used if inoperable
 Iatrogenic steroid therapy
o Gradual steroid taper
Diabetes insipidus
 Etiology
 Central – lack of production
o Idiopathic, tumor, brain surgery, head trauma
 Nephrogenic – absent or abnormal receptors
o Lithium, hypercalcemia, hypokalemia, tubulointerstitial disease
 S/S
 Polydipsia, polyuria, dehydration (hypotension, tachycardia)
 Hypernatremia
 Diagnosis
 Dilute urine
 High serum osmolality, low urine osmolality
 BUN may be low
 Can try vasopressin challenge
 Management
 Central
o Mild – increase water intake
o Severe – hormone replacement with desmopressin
 Nephrogenic
o Fluid replacement
o Sulfonylureas to increase renal response
o Thiazide diuretics – cause proximal salt and water retention
o Amiloride
o NSAIDs – indomethacin
Diabetes mellitus (type I & type II)
 Etiology
 Disorded metabolism and inappropriate hyperglycemia
 Hyperglycemia due to either/both inabilities to produce insulin or insulin resistance
 Type 1—pancreatic beta cell destruction – no longer able to produce insulin
o Children and young adults
o 1A—autoimmune destruction
o 1B—nonautoimmune destruction
 Type 2 – combo of insulin resistance and relative impairment of insulin secretion
o Genetic and environmental factors – weight gain and decreased activity
o 90% are overweight
o RF
 Family history, Hispanic, AA, HTN, hyperlipidemia, delivery of baby >
9lb, central obesity
 Typically, older population, but starting to present younger
 Gestational diabetes – during pregnancy
 Prediabetes
o Above normal BG without meeting criteria for diagnosis
o 35% over 20 and 50% over 65 meet criteria
o A1C between 5.7-6.4%



Metabolic syndrome
 Predispose to DM, CAD, and stroke
 Low HDL, HTN, elevated TRG, impaired fasting glucose, waist circumference above 35
(female) or 40 (male)
Presentation
 Most are asymptomatic, may be incidental
 DM1
o Polydipsia, polyuria, nocturia, rapid weight loss
o Weakness, pruritus, vulvovaginitis, blurred vision
o DKA
 DM2
o Polyuria, polydipsia
o Fatigue, blurred vision, chronic skin infections due to poor wound healing
 DKA and HHS
Complications
 Neuropathy – MC complication
o Sensorimotor – paresthesias, abnormal gait, low proprioception, stocking glove
pattern, pain, decreased DTR
 Impaired fine hand coordination, foot flapping, toe scuffing, frequent
tripping
o Autonomic – orthostatic hypotension, gastroparesis, N/V/D, constipation,
impotence, incontinence
o CNIII palsy
o Treatment
 Pregabalin – lyrica
 Gabapentin
 Foot exam with monofilament
 Retinopathy – #1 cause of new blindness in 25-74
o Floaters, distortion, blurred vision
o Non-proliferative – microaneurysms earliest change
 Hard exudates
 Famle hemorrhages
 Cotton wool spots
o Proliferative – neovascularization
o Maculopathy – macular eema, blurred vision, central vision loss
o Treatment
 Control BS, laser photocoagulation
 Nephropathy – #1 cause of CKD
o Progressive kidney deterioration
o Microalbuminuria is first sign
o Persistent albuminuria > 300mg confirmed on 2 occasions 3-6m apart
o Progressive decline in GFR
o Screening
 Check urin albumin in DM1 after 5 years
 DM2—at diagnosis and annually
 Measure Cr annually
o HTN accelerates decline
o Nodular glomerulosclerosis with pink hyaline materal
o Manage with ACEI to reduce protein leakage


 Macrovascular – atherosclerosis, CAD, PVD, CVA
Diagnosis
 2 fasting (8h) plasma glucose > 126
 2-hour glucose tolerance > 200
o Gestational diabetes
 HgbA1c > 6.5%
 Random > 200
Management and goals
 Insulin in DM1 and gestational
 Drugs
o Metformin
 First choice
 Lactic acidosis
 Cannot be given in renal or hepatic impairment
 GI complaints MC
 Need B12 supplementation
o Sulfonylureas—glyburide, glipizide
 Whip pancreas
 Hypoglycemia, weight gain
 Sulfa allergy reaction
o Thiazolidinediones—pioglitazone, rosiglitazone
 Sensitize peripheral tissue to insulin
 CI in CHF and liver disease
 Increase fracture risk
o Alpha-glucosidase inhibitors—acarbose, miglitol
 Delay dietary carbohydrate absorption
 Decrease postprandial glucose levels
 GI SE
o GLP1 – exenatide, liraglutide
 Injections
 Stimulate pancreatic insulin response to glucose
 Delays gastric emptying
 Weight loss
 SE pancreatitis
 CI in gastroparesis, thyroid cancer
o DDP4 inhibitor – linagliptin, saxagliptin
 Prolong endogenous GLP1
 Dosed orally
 Pancreatitis, urticaria, angioedema
o SGTL2—canagliflozin, dapagliflozin, empagliflozin
 Lowers renal glucose threshold –increase urinary excretion
 Thirst, nausea, abd pain, UTIs
o Pramlintide
 Delays gastric emptying
 Injectable
 Approved for patients on insulin therapy—DM1
 Somogyi effect
o Nocturnal hypoglycemia followed by rebound hyperglycemia due to GH surge
o Prevent hypoglycemia by decreasing nightly insulin or give PM snack

o
o
Dawn phenomenon
o Normal glucose until rise in glucose levels between 2 and 8am
DKA/HHS
 Insulin deficiency and counterregulatory hormonal excess as response to stressful event
 Infection, infarction, noncompliance, new diagnosis
 S/S
 Hyperglycemia
o Thirst, polyuria, polydipsia, nocturia, weakness, fatigue, confusion, N/V, chest
pain, abdominal pain (DKA), AMS (HHS)
 PE
o Tachycardia, tachypnea, hypotension, fever if infection, decreased skin turgor
o DKA
 Ketotic breath from acetone
 Kussumaul respiration – deep continuous respirations – attempt to blow
off excess CO2 to reduce acidosis
 Diagnosis
 HHS
o Severely elevated glucose
o Normal pH (normally)
o Normal bicarb
o Small amount of ketones
o Elevated serum osmolarity > 320
 DKA
o Elevated glucose
o pH < 7.30
o bicarb < 15
o ketones positive
o serum osmolarity variable
o elevated BUN-Cr ration
 management
 massive fluid transfusion
o when glucose reaches 250, switch to D5NS
 insulin – regular
o do not begin insulin until potassium > 5.5
 potassium
o correct hypokalemia
 treatment goal
o normal AG in DKA
o normal mental status in HHS
hypoglycemia
 etiology
 endocrine—Addison, myxedema
 liver malfunction, acute alcoholism, ESRD
 too much insulin, too little food, excess exercise
 insulin, sulfonylureas, EtOH, insulinoma, adrenal insufficiency
 fasting—haven’t eaten
 reactive—medication or insulin related
 s/s
 autonomic—sweating, tremors, palpitations, nervousness, tachycardia, hunger


o
o
o
CNS—HA, lightheadedness, confusion, slurred speech, dizziness, anxiety
Whipple triad
o History of hypoglycemic symptoms
o Fasting BG of 45
o Immediate recovery on administration of glucose
 Blood sugar between 50-60
 Symptoms @ 60
 Dysfunction @ 50
 Treatment
 < 60  fast acting carb, fruit juice, candy, recheck in 15m
 < 40  IV bolus of D50 or glucagon SQ injection
Hypercalcemia
 Etiology
 Cancer—lung
 Hyperthyroidism
 Iatrogenic
 Myeloma
 Primary hyperparathyroidism
 Sarcoidosis
 S/S
 Serum levels need to exceed 12 to be symptomatic
 Polyuria nephrolithiasis
 Anorexia, vomiting, constipation, rarely pancreatitis
 Weakness, fatigue, confusion, stupor, coma
 Osteopenia, fractures
 Stones, bones, moans, groans
 Treatment
 Fluids!
 Loop diuretics
 IV bisphosphonates
 Calcitonin
 Glucocorticoids
Hypernatremia
 Some degree hypovolemic/dehydration
 Insufficient water intake/excess water loss
 Diabetes insipidus
 S/S
 Lethargy, irritability, AMS/encephalopathy, seizures, coma and death
 Concentrated urine
 Treatment
 Correct volume deficit to euvolemia first with NS
 Then switch to more dilute IVF
Hyperparathyroidism
 Etiology
 Primary  excess PTH production
o Parathyroid adenoma MC
o Hyperplasia/enlargement
o Lithium



S/S

o
o MEN syndromes
Secondary  elevated PTH due to hypocalcemia or vitamin D deficiency
o CKD MC
o Severe calcium deficiency, severe VD deficiency – Osteomalacia and Rickets
 Elevated PTH due to hypocalcemia
Tertiary  prolonged PTH stimulation after 2ndary  autonomous production
o Post-transplant patients
Primary
o Hypercalcemia
 Kidney stones
 Painful bones and fractures—osteopenia, osteoporosis, pathologic
fractures
 Ileus, constipation
 Weakness, fatigue, AMS, decreased DTR, depression
 Shortened QT
 secondary
o hypocalcemia
 diagnosis
 primary—hypercalcemia, elevated intact PTH, low phosphate, elevated urine calcium
o osteopenia on bone scan
o adjusted serum calcium level > 10.5 and phosphate < 2.5 with PTH > 55
 secondary
o elevated serum calcium with low PTH
 all patients need to be screened for familial benign hypocalciuric hypercalcemia—24hour urine for calcium and creatinine
 management
 primary
o surgery—parathyroidectomy
 symptomatic—proximal muscle weakness, gait disturbance, atrophy,
hyperreflexia
 adjusted calcium > 1 above upper limit
 history of life-threatening hypercalcemia
 urinary calcium > 400
 creatinine clearance < 60
 osteoporosis
 nephrolithiasis
 pregnancy
 parathyroid carcinoma
o IV saline, furosemide
 Avoid HCTZ
o Bisphosphonates for bone absorption
 Secondary
o Vitamin D supplementation
Hyperthyroidism/thyroiditis
 Grave’s disease—autoimmune TSH receptor antibodies
 S/S
o Weight loss despite increased appetite, rapid heart rate, fine tremor, anxiety
o Increased nervousness, emotional instability



o Heat intolerance and excessive sweating
o Palpitations, frequent bowel movements
o Menorrhagia, brittle hair
o Sinus tach or AFIB
o Widened pulse pressure, warm, smooth moist skin
o Diffuse enlarged thyroid with thyroid bruits
o Lid lag, exophthalmos/proptosis
o Pretibial myxedema
 Diagnosis
o Positive thyroid stimulated Ab
o TFT
 Elevated T3/T4-more pronounced T3
 TSH extremely low or undetectable
 Treatment
o Radioactive iodine
 Will need hormone replacement
 Avoid in pregnancy
 Can worsen ophthalmopathy symptoms
o Methimazole or PTU
 MMI—serum sickness, jaundice, alopecia, hypoglycemia, nephrotic
 Agranulocytosis
 Need to monitor WBC and LFT
 PTU preferred in pregnancy—still crosses but less effects
 Arthritis, lupus aplastic anemia, thrombocytopenia, hepatic
necrosis
o Beta blockers—propranolol for symptomatic relief
o Thyroidectomy—compressive symptoms and not responsive to meds
o Ophtho symptoms—IV methylprednisolone
Toxic multinodular goiter
 Autonomous function nodules—elderly
 S/S
o Hyperthyroidism with diffusely enlarged thyroid
o No skin or eye changes
o Palpable nodule
 Diagnosis
o RAIU shows patchy areas of increased and decreased uptake
 Management
o Radioactive iodine and surgery if compressive
Toxic adenoma
 One autonomous functioning nodule
 S/S
o Clinical hyperthyroidism
o Can have compressive symptoms of dyspnea and dysphagia
o Stridor, hoarseness with laryngeal compression
 Diagnosis
o RADIU shows local uptake with hot nodule
 Management
o Radioactive iodine and surgery if compressive
Thyroid storm/thyrotoxicosis crisis




o
o
Frequently after a precipitating event or inadequately treated Grave’s
S/S
o Hypermetabolic state, palpitations, tachy, AFIB, higher fever, N/V
o Psychosis, tremors, seizures
o Can progress to coma and hypotension
Diagnosis
o Primary hyperthyroid TFT profile
o Elevated T3/T4 with low TSH
Management
o Anti-thyroid meds
 IV propylthiouracil (PTU)
 Methimazole
 Prevents conversion of T4 into T3
o Beta blockers for symptomatic therapy
o Supportive
 Steroids—inhibits peripheral conversion, impairs hormone production
 Antipyretics, but no aspirin
Hypocalcemia
 Etiology
 Can be pseudo due to reduced due to hypo-albumin but corrected is normal
 S/S
 Trousseau’s – carpal spasm with arm compression
 Chvostek’s – twitching of facial muscles when facial nerve is tapped
 Muscle spasms, cramps, tetant, laryngospasms, paresthesias (perioral and peripheral)
 Diagnosis
 Need to check calcium, phosphorous, and mag levels
 Treatment
 Need to lower severe elevations in phosphorous
 Need to treat low mag to correct calcium
 Calcium gluconate
Hyponatremia
 Hypertonic hyponatremia – low sodium with high serum osmolality
 Normally iatrogenic
 Mannitol, sorbitol, maltose, radiocontrast
 Unmeasured but osmotically active that the lab picks up
 Can also be severe hyperglycemia
 Isotonic hypernatremia – low sodium with normal osmolality
 High hyperlipidemia or hyperproteinemia
 Hypotonic hyponatremia – both sodium and osmolarity are low
 Hypovolemic hypotonic hyponatremia
o Excess salt loss via dehydration/GI loss or renal mechanisms
 Euvolemic hypotonic hyponatremia
o Inappropriate ADH mediation
o Medications, pain, post-op, stress, hormonal imbalance, tumor
o SIADH
 ADH produced in un-regulated way
 Inappropriate water reabsorption and retention
 Rise in total body water—serum concentration of sodium is decreased


o
o
Hypervolemic hypotonic hyponatremia
o Too much fluid accumulation due to dysfunction of other organs
o CKD, CHF, liver disease with cirrhosis
S/S

 Treatment
 Hypertonic saline when severe neuro decomp
 Risk of central pontine myelinolysis
o Flaccid paralysis, dysarthria, dysphagia
 Fluid restriction
 NS infusion
 1-2 mEg/L for 3-4 hours then tapered not to exceed 10-12 mEq/L in 24 hours
Hypoparathyroidism
 Etiology
 Parathyroidectomy or thyroidectomy
 Autoimmune, heavy metal toxicity (Wilson disease, hemochromatosis)
 Thyroiditis, hypomagnesemia (chronic alcoholism)
 DiGeorge (congenital) – parathyroid hypoplasia, thymic hypoplasia, outflow tract
defects of heart
 S/S
 Tetany, carpopedal spasms, muscle/abdominal cramps, paresthesias
 Tooth, nail, and hair defects
 Hyperreflexia
 Chvostek sign—contraction of eye, mouth, or nose muscles by tapping along the facial
nerve anterior to the ear
 Trousseau sign—spasm in hand and wrist with compression to the forearm
 Diagnostic studies
 Decreased PTH and serum calcium, increased phosphate levels
o Low serum mag—may worsen symptoms
 ECG—prolonged QT, T-wave abnormalities
 XR—chronic increased bone mineral density—lumbar and spine
 Management
 Correcting hypocalcemia—calcium and VD supplement
 Magnesium supplement
 Thiazide diuretics
 Avoid phenothiazines and furosemide
 Recombinant human PTH (teriparatide)—severe cases that do not respond to other
measures
Hypothyroidism
 Etiology
 Hashimoto’s—autoimmune with anti-thyroid antibodies
 Iatrogenic—radioactive treatment for Grave’s
 DeQuervain’s/Granulomatous painful subacute
o Post viral—coxsackievirus, EBV, mumps, measles
o Tender gland with fever, fatigue, dysphagia, otalgia
o Hyperthyroid state followed by hypothyroid state
o Elevated ESR
o Symptomatic treatment with NSAID and BB







 Aspirin
Medication induced
o Amiodarone, lithium, interferon-alpha
Acute suppurative—staph
o Painful, fluctuant thyroid, fever, overlying erythema, pharyngitis
o Elevated ESR, leukocytosis
o FNA with gram stain and culture
o ABX, drainage if abscess
Fibrous thyroiditis (Riedel)
o Dense fibrous tissue in the thyroid gland
o Female
o Asymmetric hard woody thyroid
o Need to r/o carcinoma
o Long term tamoxifen
o Can have extra-glandular involvement—sclerosing cholangitis, retroperitoneal
fibrosis, orbital pseudotumor
S/S
 Fatigue, lethargy, weight gain despite poor appetite
 Cold intolerance, hoarseness, constipation, weakness
 Oligomenorrhea, impaired fertility
 Dry skin and hair loss, eyebrow thinning on outer 1/3
 Bradycardia, diastolic HTN, mild hypothermia
 Lid lag, non-pitting edema of LE
 Carpal tunnel, delayed DRT in relaxation phase
Diagnosis
 Labs
o CMP
 Hyponatremia, anemia, hypercholesterolemia
o TFT
 TSH—high
 Free T4—low
o Antibodies
 Anti-thyroid peroxidase—Hashimoto’s
 Thyrotropin receptor blocking –Hashimoto’s
Treatment
 Levothyroxine therapy—calcium, iron, fiber decrease absorption
 Need to check for other autoimmune diseases
 Adjust dose every 4-6 weeks based on TSH value
 T4 needs increased in third trimester
Myxedema crisis
 Severe hypothyroidism
 S/S
o Obtunded, CO2 retention, coma
o AMS, hypothermia, hypoventilation, hyponatremia, hypotension, rhabdo,
hypoglycemia, AKI
 Can be precipitated by sepsis, cardiac disease, respiratory distress, CNS disease, noncompliance
 Treatment
o
o
o
o
IV thyroxine, passive warming, ABX if infection suspected
Do not give morphine—overly sensitive
Osteoporosis
 Etiology
 Loss of bone density over time  increased bone resorption and decreased bone
formation
 Primary—postmenopausal or senile
 Secondary – chronic disease of meds
o Prolonged high-dose steroids, low estrogen, heparin, anticonvulsants
 S/S
 Pathologic fracture
o Vertebral hip, distal radius, with/out trauma
o Postmenopausal – trabecular bone loss  vertebral compression and wrist
fracture
o Senile  trabecular and cortical bone loss  hip and pelvic fractures
 Spine compression
o MC in upper lumbar and thoracic
o Loss of vertebral height –shortening of statue, kyphosis
 Back pain – vertebral compression with/out fractures
 Diagnosis
 Labs—serum calcium, phosphate, PTH, ALP normal
o ALP may be elevated following fractures
 DEXA – demineralization
o Osteoporosis < 2.5
o Osteopenia 1.0 – 2.5
 XR- demineralization
 Management
 Lifestyle
o Vitamin D intake
o Exercise –weight-lifting, high impact
 Bisphosphonates
o Inhibits osteoclast bone resorption
o Can cause pull esophagitis
o ONJ
o PO—alendronate, risdronate, ibandronate
o IV—pamidronate, zoledronic acid
 PTH therapy—teriparatide
Paget disease of the bone
 Etiology RF
 Europe, NA, Australia
o Rare in Asia
 Femur > pelvis > tibia > skull > spine
 Increased osteoclastic bone resorption leading to disordered bone remodeling
o Increase in osteoclast bone resorption
o Increase in abnormal trabecular bone formation
o Larger, weaker, less compact bone
 Viral infection – RSV
 Environmental, genetic
 S/S




o
o
Asymptomatic
Bone pain
Increase warmth
Soft bone
o Bowed tibias, kyphosis, frequent fractures
 Skull involvement
o Deafness CNVIII
 Diagnosis
 ALP – elevated
 Calcium – normal
 Phosphate – normal
 XR – lytic phase (blade of grass/flame shaped lunacy) or sclerotic phase (coarsened
trabeculae)
Pheochromocytoma
 Etiology
 Catecholamine secreting adrenal tumor
 Secretes epi/norepi autonomously and intermittently
 90% benign
 May be associated with MEN2
 S/S
 Hypertension – temporary or sustained – can be up to 200/150
 Paroxysmal spells
 PHE  palpitations, headaches, excessive sweating
 Chest and abdominal pain, weakness, fatigue, weight loss
 Diagnosis
 Elevated 24H urinary catecholamines
o Metabolites  metanephrine and vanillylmandelic acid
 MRI or CT
 Labs – hyperglycemic or hypokalemia
 Management
 Adrenalectomy
 Preoperative
o Non-selective alpha-blockade
o Phenoxybenzamine or phentolamine for 7-14 days
o Begin beta blockers or CCB to control HTN
o Do not begin beta blockade without alpha first
Pituitary adenoma
 Etiology
 Benign microadenomas:
o Function as hypersecretion of hormones
o Non-functioning
 S/S
 Mass effect
o > 10mm
o HA due to stretching of dura and elevated ICP  papilledema
o Visual disturbance  bitemporal hemianopsia
o CSF rhinorrhea if erosion into cribiform plate
o CNIII palsy
o

o
o
Temporal lobe epilepsy
Types
 Prolactinomas MC
o Women – oligomenorrhea, amenorrhea, galactorrhea, infertility
o Men – impotence, decreased libido, hypogonadism, infertility
o Measure serum prolactin level
o Cabergoline or bromocriptine
 Somatotropinoma
o Secretes GH
o Acromegaly in adults and gigantism in children
o TSS + bromocriptine
o Octreotide
 Adrenocorticotropinomas
o Secretes ACTH
o Cushing’s Disease
 TSH secreting adenomas
o Secrete TSH
o Thyrotoxicosis, elevated T3T4, elevated TSH
 Diagnosis
 MRI
 Endocrine studies
 Management
 Transsphenoidal surgery – active or compressive tumors
o Except prolactinomas – observation if nonfunction, <10mm
Thyroid cancer
 Etiology and RF
 More common in women but prognosis is worse in men
 Types
 Papillary – MC
o Least aggressive
o Radiation exposure and young females
o Spreads via local extension
 Follicular
o Increased RF with iodine deficiency
o Slower growing
o Mets to lungs, bone, brain, and liver
 Due to vascular invasion
 Medullary
o Associated with MEN2 syndrome
o Parafollicular C cells—secrete calcitonin
o Cause symptoms related to secretion of calcitonin, prostaglandins, serotonin,
ACTH
o Measure calcitonin levels to monitor for residual disease
 Anaplastic
o Most aggressive
o RF—many years after radiation exposure; males > 65
o Dysphagia and vocal cord paralysis
thyroid nodule
 over 1cm to be palpated









thyroid adenoma MC benign
 encapsulated
 follicular adenoma MC
 hurtle cell has eosinophilic staining—malignant potential
multinodular goiter—not encapsulated
bleeding into nodule causes pain and enlargement
hot nodule—low risk for malignancy
cold nodule—higher risk
high-res U/S is most sensitive test to detect thyroid lesions
 preferred over CT due to accuracy, lower cost, and lack of radiation
malignancy
 irregular or indistinct margins
 heterogenous echogenicity
 intramodular vascular markings
 microcalcifications
 complex cyst pattern
 size > 1cm
 rapid growth, fixed in place with no movement with swallowing
benign
 varied, smooth, firm, sharply outlined, discrete, painless
NEUROLOGY
o Bell palsy
 Etiology
 Idiopathic unilateral CNVII palsy
 Inflammation or compression
 Association with HSV reactivation
 More common on right side
 RF
 DM, pregnancy in 3T, post-URI, dental nerve block, HSV, zoster
 S/S
 Sudden onset ipsilateral hyperacusis (ear pain) 24-48h
 Unilateral facial paralysis
o Unable to life affected eyebrow, wrinkle forehead, smile
o Loss of nasolabial fold
o Drooping of corner of mouth
 Taste disturbance on anterior 2/3
 Biting inner cheek
 Eye irritation – decreasing lacrimation and inability to fully close eye
 Diagnosis
 Diagnosis of exclusion
 Management
 Prednisone if within 72 hours
 Artificial tears
 Acyclovir
o Cerebral aneurysm
 Berry – MC in Circle of Willis
 Diagnosed via angio
 Needs clipping
o
Cerebral vascular accident
 MC due to thrombotic, emboli, or CV occlusions
 Internal carotid
 MC is no symptom due to collateral flow
 Can cause hemispheric infarct
 Lacunar – history of HTN in 80%
 Small vessel disease – penetrating branches of cerebral arteries of pons, basal ganglia
 Pure motor MC – hemiparesis and hemiplegia
 Ataxic hemiparesis – clumsiness in leg > arm
 Dysarthria
 Pure sensory loss
 Diagnosis via CT – small punched out hypodense areas
 Treatment – aspirin with control of risk factors
 MCA – MC
 Contralateral sensory/motor loss and hemiparesis
o Greater in face and arm > leg and food
 Visual – contralateral homonymous hemianopsia
o Gaze preference toward side of lesion
 Dominant (usually L side)
o Aphasia
 Nondominant (usually R side)
o Spatial deficits, dysarthria, left-side neglect
 ACA
 Contralateral sensory/motor loss/ hemiparesis
o Greater in leg and food > upper extremities  abnormal gait
 Face spared – speech preservation, slow responses
 Primitive reflexes
 Gait apraxia
 Frontal lobe and mental status impairment
o Impaired judgement and confusion
o Personality changes – flat affect and apathy
 Urinary incontinence
 Gaze preference toward side of lesion
 PCA
 Visual hallucinations, contralateral homonymous hemianopsia – preserved macula
o Cortical blindness, lack of depth perception
 Crossed symptoms
o Ipsilateral cranial nerve deficits + contralateral muscle weakness
o Coma, drop attacks
 Memory deficits
 Basilar artery
 Cerebellar dysfunction, CN palsies, decreased vision, decreased bilateral sensory
 Eye movement abnormalities – nystagmus
 Coma
 Diagnosis
 Non-contrast CT to rule out hemorrhage
 May be normal in first 6-24 hours
 Treatment

o
o
Thrombolytics within first 3-4.5 hours
o tPA/alteplase given if no evidence of hemorrhage
o only effective on ischemic stroke
o CI if BP > 185/110, recent bleed/trauma, bleeding disorder
 Antiplatelet therapy
o Aspirin, clopidogrel
 Anticoag if cardioembolic
 Only lower BP if > 185/110 for thrombolytics or 220/120 in general
o If MAP > 130
Hemorrhagic stroke
 Spontaneous
 Etiology
o HTN related
o Basal ganglia
o Blind infarct bleeds due to pressure/necrosis
 S/S
o Worsening condition 1-2 days after stroke
o MC in embolic than thrombotic
o LOC, N/V, hemiplegia, hemiparalysis
o Symptoms gradually increasing in severity
 Diagnosis
o Non-contrast CT
o Do not perform LP if ICH is suspected – will herniate
 Treatment
o Supportive vs. hematoma evac
o If elevated ICP – head elevation + mannitol, hyperventilation
 SAH
 Etiology
o MC 2ndary to berry rupture or AVM
 S/S
o No focal neuro symptoms
o Sudden onset of worse HA
o Brief LOC, NV, meningeal irritation
o Nuchal rigidity, seizures
 Diagnosis
o CT
o If negative but high suspicion – LP – xanthochromia (RBCs) and high pressure
 Treatment
o Bed rest, no exertion or straining
o Anxiolytics, stool softeners
o Cautions of lowering BP—nicardipine
Intracranial hemorrhage
 Epidural hematoma
 Etiology
o Arterial bleed between skull and dura – middle meningeal artery
o Temporal bone fracture
 S/S
o Brief LOC  lucid period  coma
o HA, NV< focal neuro symptoms
o
o
o Rhinorrhea of CSF
 Diagnosis
o CT shows convex lens shaped bleed that does not cross sutures
 Management
o Herniation if not evacuated early
 Subdural
 Etiology
o Venous bleed between dura and arachnoid – cortical bridging veins
o Frequently no fractures
o Elderly and alcoholics
o Blunt trauma
 S/S
o Varies, focal symptoms
 Diagnosis
o CT shows concave crescent shaped bleed that crosses sutures
 Treatment
o Hematoma evac vs. supportive
 Intracerebral
 Etiology
o Intraparenchymal
o HTN, HVM, trauma, amyloid
 S/S
o HA, NV, LOC
o Hemiplegia, hemiparesis
o Not associated with lucid intervals
 Diagnosis
o CT shows intraparenchymal bleed
o Do not perform LP – herniation
Cluster headaches
 Etiology
 Predominately young middle-aged males
 S/S
 Severe unilateral periorbital/temporal pain – sharp lancinating
 Episodes last < 2 hours with spontaneous remission
 Several times a day over 6-8-week period
 Triggers – worse at night, EtOH, stress or ingestion of specific foods
 Ptosis, miosis, nasal congestion, rhinorrhea, lacrimation, conjunctival injection,
sweating, eyelid edema
 Can be mistaken for paroxysmal hemicrania – try indomethacin
 Management
 100% oxygen at 6-10L
 Anti-migraine meds
o SQ sumatriptan or ergotamine
 Frequently occur between early evening and early morning hours with peak time
between midnight and 3AM
 Prophylaxis
 Verapamil
Coma
o
o
 Unresponsive to environmental stimuli
Complex regional pain syndrome
 Etiology
 Occurs after nerve injury – surgical
 Multifactorial
 S/S
 Severe pain, swelling, changes in skin
 Allodynia – triggering of pain response from stimuli that doesn’t normally provoke pain
 Hyperalgesia – excessive pain from normally painful stimulus
 Swelling
 Dystrophic changes in skin and nails
 Alteration in skin temp and color
 Diagnosis
 Bone scans show early increased uptake of radiotracer
 Presence of continuing pain, allodynia, or hyperalgesia after nerve injury
 Edema, changes in skin blood flow
 Treatment
 Sympathetic blocks
 Anticonvulsants, antidepressants
 Early pain referral
 Early mobilization
Concussion
 Etiology
 Mild TBI – alteration in mental status with/out LOC
 Head trauma that causes temporary brain dysfunction of any sort
 S/S
 Confusion – blunted affect, blank expression
 Amnesia – retrograde or antegrade
 HA, dizziness, visual disturbances – blurred, diplopia, photophobia
 Delayed responses and emotional instability
 Signs of increase ICP – persistent vomiting, worsening HA, increasing disorientation,
changing LOC
 Vertigo and disquilibrium – incoordination N/V, loss of balance
 Seizure, confusion, disorientation
 Warning signs
o Worsening HA with focal neuro signs
o Diplopia
o Seizures
o Repeated vomiting
o Anisocoria
o Worsening LOC
o GCS < 14
 Diagnosis
 CT – evaluate acute head injuries
 MRI – prolonged symptoms > 7 – 14 days or worsening symptoms
 Management
 Cognitive and physical rest until all symptoms resolved
 Gradual return to activities and sports
o
o
Delirium
 Acute, abrupt transient confused state with identifiable cause – medication, infection
 Rapid onset
 Associated with fluctuating mental status changes
 Marked deficit in short-term memory
 Full recovery within 1 week
Dementia
 Progressive chronic intellectual deterioration of selective function
 Loss of memory, impulse control, motor, and cognitive functions
 Language dysfunction, disorientation, complex motor activities, inappropriate social interaction
 Alzheimer disease
 Etiology
o MC dementia after 60
 Downs syndrome gets it early
o Loss of brain cells, amyloid deposition (senile plaques), neurofibrillary tangles
(tau protein)
 S/S
o Short term memory loss 1st sign
 Recent recall (3 objects at 5 minutes) profoundly affected
o Reduced insight into deficits
 Anosognosia – don’t know what they don’t remember
o Inability to make new memories
o Progresses to long-term memory loss
o Disorientation, behavioral and personality changes
 Depression, irritability, apathy, social disengagement, agitation,
wandering
o Usually gradual in nature
o 5 As
 Amnesia
 Agnosia – don’t remember objects or people
 Apraxia – inability to perform a function or skill
 Aphasia – unable to express speech
 Anomia – unable to recall name of everyday objects
 Diagnosis
o CT – cerebral cortex atrophy
 Management
o AchE inhibitors
 Donepezil, Tacrine, Rivastigmine, Galantamine
 Reverses cholinergic deficiency and symptom relief
 Does not slow progression
o NMDA antagonist
 Memantine
 Reduce glutamate excitotoxicity
 May be used as adjunctive
o Treat depression
 SSRIs – no TCAs
o Minimize meds that interfere with cognition
 Benadryl
 Anti-psychotics

o
o
Vascular
 Etiology
o 2nd MC
o Chronic ischemia and multiple lacunar infarcts
o HTN most important controllable risk factor
o Often mixed with AD
 S/S
o Stepwise progression
o Cortical
 Forgetfulness, confusion, amnesia, executive difficulties, speech
abnormalities
o Subcortical
 Motor deficits, gait abnormalities, urinary difficulties, personality
changes
 Diagnosis
o CT/MRI abnormal
 Frontotemporal dementia/ Pick’s disease
 Etiology
o Rare
o Localized brain degeneration of frontotemporal lobes
o Progresses globally
 S/S
o Early alteration of personality, behavior, and executive functioning
o Marked personality changes with behavior symptoms – apathy, disinhibition
o Preserved visuospatial
o Aphasia
o No amnesia
o + Pick bodies
 Diagnosis
o Autopsy
o Not responsive to Parkinson drugs
 Diffuse Lewy body disease
 Diffuse in comparison to Parkinson disease
 S/S
o Visual hallucinations and delusions
o Episodic delirium
o Dysautonomia and sleep disorders
o Neuroleptic sensitivity
o Parkinsonism
o Dementia occurs later
 Treatment
o Do not give anti-psychotics or benzos
o Behavior
o Rivastigmine and donepezil
Serotonin syndrome
 AMS + autonomic instability + hyperthermia + tremor, clonus, hyperreflexia, mydriasis
 Cyproheptadine + benzo
Neuroleptic malignant syndrome
 Decreased dopamine
o
o
o
 AMS + autonomic instability + extreme muscle rigidity + hyperthermia + hyporeflexia
 Bromocriptine
 Dantrolene
Encephalitis
 Herpes
 Devastating symptoms
 Seizures and coma
 Temporal lobe predisposition with frequent hemorrhage
 Changes in EEG and MRI
 Treatment with acyclovir
 Rabies
 Fever and tingling at site of exposure
 Violent movements, uncontrolled excitement, fear of water, paralysis, confusion
 Diagnosis – brain biopsy shows Negri bodies
 Rabies prophylaxis after exposure and Ig plus vaccination
 West Nile
 Looks like polio
 Taking methotrexate, over 80, under 2  higher risk for symptoms and complications
 3 manifestations  encephalitis, aseptic meningitis, polio
Essential tremor
 Etiology
 Autosomal dominant
 Onset 60s
 Sustention tremor at 4-12Hz
 S/S
 Intentional tremor
o Postural, bilateral action tremor of hands, forearms, head, neck, or voice
o MC in upper extremities and head (titubation)
o Spares legs
 Tremor relieved with EtOH ingestion
 No abnormal exam findings other than tremor
 Diagnosis
 Alcohol challenge
 Ask about family history
 Look for stiffness, accentuation, gait
 Management
 Propranolol if severe or situational
 Primidone (barbiturate) if no relief or can be used in conjunction
 Alprazolam
 Look for meds that can cause tremor
o SSRIs, valproic acid, topiramate, albuterol, lithium, caffeine, amiodarone,
thyroxine, TCAs
Giant cell arteritis
 Etiology
 Over 50
 S/S
 New onset temporal HA
 Jaw pain
o
o
 Trouble with vision
 Diagnosis
 Elevated ESR
 Temporal artery biopsy
 Treatment
 High dose steroids
 Do not wait to start steroids until biopsy – steroids as soon as suspicion
Guillain-Barré syndrome
 Etiology
 Demyelinating polyradiculopathy of peripheral nerves
 Campylobacter jejuni (MC)
 Antecedent respiratory of GI infections – CMV, EBV, HIV, mycoplasma
 Immunizations, post-surg
 S/S
 Ascending symmetrical weakness and paresthesias
 Decreased DTR – LMN lesion
 May eventually involve muscles of respiration or bulbar – swallowing abnormalities
 CNVII palsy
 Autonomic dysfunction – tachycardia, hypo/hypertension, breathing difficulties
 Diagnosis
 CSF – high protein with normal WBC (albuminocytological dissociation)
 Electrophysiologic studies – decreased motor nerve conduction velocities and amplitude
 Management
 Plasmapheresis – best done early
o Removes harmful circulating auto-antibodies
o Equally as effective as IVIG
 IVIG – suppresses harmful inflammation/auto-antibodies and induces remyelination
o Recovery in a few months
 Mechanical ventilation for respiratory failure
 NO PREDNISONE
Huntington disease
 Etiology
 Autosomal dominant
 Mutation on chromosome 4 – unstable CAG repeat
o Onset depends on length of repeat
 S/S
 Onset 30-50yo
 Behavior  chorea  dementia
 Behavior
o Personality, cognitive, intellectual, irritability
 Chorea
o Rapid, involuntary, or arrhythmic movements of face, neck, trunk, limbs initially
o Worsened with voluntary movements and stress – disappear with sleep
 Dementia
o Develop before 50yo
o Primary executive dysfunction
 Gait abnormalities and ataxia – irregular and unsteady
 Incontinence and facial grimacing
o
 Restlessness and fragility
 Quick involuntary hand movements with brisk DTR
 Diagnosis
 CT – cerebral and caudate nucleus atrophy
o MRI shows similar findings
 Genetic testing
 PET – decreased glucose metabolism in caudate nucleus and putamen
 Management
 No cure – fatal within 15-20y onset
 Chorea management
o Antidopaminergics – typical/atypical antipsychotics
o Benzos for sleep
 Tetrabenazine
Intracranial tumors
 Astrocytoma
 Etiology
o Derived from astrocytes – glial cells that support endothelial cells of BBB
o Can appear in any part of the brain
o Infratentorial in children
o Supratentorial in adults
 Types
o Pilocytic/Grade 1 (Juvenile): localized
 Most benign
 MC in children and YA
 Can be cerebellar and desmoplastic infantile
o Diffuse/Grade II/low-grade
 Fibrillary, gemistocytic, protpplasmic
 Invade surrounding tissue but grow slowly
o Anaplastic/Grade III
 Rare but aggressive
o Grade IV (Glioblastoma “Multiforme”)
 MC primary CNS tumor in adults
o Subependymal giant cell
 Ventricular tumors associated with tuberous sclerosis
 S/S
o Focal deficits MC
 Location is key – MC in frontal and temporal
o HA worse in morning, may wake patient up at night, may be positional
o CN deficit, AMS, neuro deficits
o Ataxia, vision changes, weakness
o Increased ICP due to mass effect
 HA, N/V, papilledema, ataxia, stupor, drowsiness
 Diagnosis
o CT/MRI with contrast
o Brain biopsy
 Grade 1 – cystic, Rosenthal fibers
 Diffuse – microcysts and mucus like fluid
 Anaplastic – tentacle like projections
 Grade IV – cystic material, calcium deposits, blood vessels



Management
o Pilocytic – surgical excision + radiation
o Diffuse – surg if accessible + radiation
o Anaplastic – surg and radiation, maybe chemo
o Grade IV – surg, radiation, and chemo
Glioblastoma
 Etiology
o MC and most aggressive of all primary CNS tumors in adults
o Grade IV astrocytoma
 Primary
o Adults > 50
o Arises de novo
o MC and most aggressive
 Secondary
o MC < 45
o Malignant progression from low-grade astrocytoma (grade II/III)
 Risk factors
o Males >50, HHV-6, CMV, ionizing radiation
 Types
o Classic – 97%
 Extra copies of epidermal growth factor receptor gene
o Mesenchymal
 High rates of mutations and alterations
 S/S
o Focal deficits MC – frontal and temporal
 Frontal – dementia, personality changes, gait abnormalities, seizures,
expressive aphasia
 Temporal – partial complex/generalized seizures
 Parietal – receptive aphasia, contralateral sensory loss, hemianopsia,
spatial disorientation
 Occipital – contralateral homonymous hemianopia
 Thalamus – contralateral sensory loss
 Brainstem – papillary changes, nystagmus, hemiparesis
o HA worse in AM
o CN deficits – fixed and dilated pupil
o Increased ICP
o Cushing’s reflex – irregular respirations, HTN, bradycardia
 Diagnosis
o CT/MRI with contrast
 Non-homogenous mass with hypodense center
 May have hydrocephalus
o Brain biopsy
 Small areas of necrotizing tissue surrounded by anaplastic cells
 Hyperplastic blood vessels with areas of hemorrhage
 Management
o Surgical excision, radiation, chemo
o Poor prognosis
Meningiomas
 Etiology
o
o
o
o
o
o

S/S
o
o
o
Usually benign
Arise from meningothelial arachnoid cells of meninges
2nd MC CNS neoplasm
MC in women – estrogen receptors
Associated with NF -2
MC from dura or sites of dural reflection – venous sinuses or falx cerebri
Asymptomatic
Focal deficit
 Seizures, progressive spasticity, weakness
 Motor/sensory symptoms
 Rare to have symptoms due to ICP
 Diagnosis
o CT/MRI with contrast
 Intensely enhancing well-defined lesion attached to dura
 May see calcification on CT
o Brain biopsy
 Spindle cells arrange in whorled pattern
 Psammoma bodies
 Oligodendroglioma
 Oligodendrocyte – supportive glial tissue of brain
o Tumors found anywhere in cerebral hemis – frontal and temporal MC
 S/S
o Asymptomatic
o Focal deficits – seizures, HA< personality changes
 Diagnosis
o CT or MRI with contrast
o Biopsy
 Soft grayish pink calcified tumors with area of hemorrhage or cysts
 Chicken-wire capillary pattern with fried-egg shaped tumor
 Management
o Surgical resection
 Ependymoma
 Etiology
o Ependymal cells line ventricles
o MC in children
o MC in 4th ventricle  hydrocephalus
o Spinal cord  cauda equina
 S/S
o Infants – increased head size, irritability, sleeplessness, vomiting
o Adults – N/V, headache
 Diagnosis
o CT/MRI with contrast
 Hypointense T1, hyperintense T2, enhances with gadolinium
o Biopsy – perivascular pseudo-rosettes
 Management
o Surgical resection followed by radiation
Meningitis
 Etiology






o
Inflammation of dura
Newborn – E. coli
Childhood – strep pneumo
18-50 – strep pneumo; N. meningitidis – purpuric rash
Older or IC – Listeria monocytogenes, gram neg
S/S
 Fever, severe HA, stiff neck, N/V
 Photophobia, confusion, rash
 Nuchal rigidity, Kernig’s and Brudzinski signs
 Diagnosis
 LP with culture
 HSV PCR
 Blood cultures
 Treatment
 Vanc
 Ceftriaxone
 Ampicillin if concern for listeria
 Steroids for strep pneumo
 Viral/aseptic – supportive
 CSF analysis
 Fungal – high protein, low glucose, high OP
 Bacterial – high protein, low glucose, high WBC (polys mainly), high OP
 Viral – mild protein elevation, normal glucose, lymphs, normal to elevated OP
Migraine headaches
 Etiology
 MC in women
 Without aura more common
 Migraine with aura is classic, but less common
 MC of morning HA
 Vasodilation of vessels innervated by trigeminal nerve OR neurogenic inflammation
o Now though to be CGRP
 S/S
 Lateralized pulsatile throbbing HA
 Associated with N/V, photophobia, phonophobia
 4-72h duration
 Moderate to severe pain intensity
 Worse with activity, stress, lack/excessive sleep, EtOH, specific foods, OCP/menstruation
 Aura
o Visual changes MC
o Light flashes, scotomas, aphasia, weakness or numbness
o Last < 60m
o 5-30m before HA onset
 Management
 Abortives
o Triptans or ergotamine – serotonin 5HT-1 agonists – vasoconstriction
 SE – chest tightness from constriction, N/V, abdominal cramps
 CI – coronary artery or CVD, uncontrolled HTN, hepatic or renal disease,
pregnancy
o
o
Dopamine antagonists – IV phenothiazines – metoclopramide, promethazine,
prochlorperazine
 Antiemetics for N/V
 Given with diphenhydramine to prevent EPS, dystonic reactions
o IV fluids, dark quiet room
o Mild – NSAIDs, Tylenol
 Codeine or barbiturates may be used
 Caffeine
 Prophylactics – 2+ / week
o Anti – HTN – beta blockers, CCB
o TCAs
o Anti-consultants – valproate, topiramate
Multiple sclerosis
 Etiology
 Autoimmune inflammatory demyelinating disease
 Axon degeneration of white matter
 MC in women and young adults 20-50y
 CNS IgG production and T-cell reaction
 Types
 Single attack – never have another attack; technically don’t reach diagnostic criteria
 Relapse-remitting – MC, episodic exacerbations; increasing disability after each attack
 Relapsing progressive – slow constant decline along with relapses
 Secondary progressive – relapsing-remitting pattern that becomes aggressive
 Chronic progressive – just goes downhill, older patients
 S/S
 Sensory
o Pain, fatigue, numbness, paresthesias in limbs, muscle cramping
o Trigeminal neuralgia – suspect MS in young patients with TN
o Uhthoff’s phenomenon – worsening symptoms with heat
o Lhermitte’s sign – neck flexion causes nerve pain radiation from spine down legs
 Retrobulbar optic neuritis
o Unilateral eye pain worse with eye movements, diplopia, central scotomas,
vision loss
o + RAPD
 Motor – UMN
o Spasticity with positive (upward) Babinski
 Spinal cord symptoms
o Bladder, bowel, sexual dysfunction
 Charcot’s neurologic triad
o Nystagmus + staccato speech + intentional tremor
 Diagnosis
 Clinical + at least 2 discrete episodes of exacerbations
 MRI + gadolinium
o White matter plaques/hyper densities
o Proof of 2 white areas
 Lumbar puncture
o Elevated IgG in CSF
o Discrete bands in gamma globulin region on electrophoresis
 Management

o
Acute
o IV high dose steroids
o Immunomodulators – cyclophosphamide
o Plasmapheresis
 Relapse remitting
o Beta-interferon
o Glatiramer acetate
Myasthenia gravis
 Etiology
 Autoimmune peripheral nerve disorder
 MC in young women
 75% have thymic abnormality – hyperplasia or thymoma
 May be postpartum
 Patho
 Autoimmune antibodies against Ach nicotinic postsynaptic receptor at the NMJ
 Decreases Ach receptors
 S/S
 Ocular – first presenting symptom and more severe
o Extraocular involvement
o Diplopia, eyelid weakness
o Ptosis – more prominent with upward gaze
o Weakness worsened with repeated use
o Pupils spared
 Generalized progressive muscle weakness
o Less in the morning, worsens with repeated muscle use through the day
 Relieved with rest
o Normal sensation and DRT
o Bulbar (oropharyngeal weakness) with prolonged chewing and dysphagia
o Respiratory muscle weakness may lead to respiratory failure – myasthenic crisis
 Diagnosis
 + Ach receptor Ab
 + MuSK (muscle specific tyrosine kinase) Ab
 Edrophonium test – rapid response to short acting in limb MG
 CT/MRI chest for thymoma or thymus
 Ice pack test – on eye lid for 10 minutes – improvement of ocular symptoms
 Management
 AChE inhibitors
o Pyridostigmine or neostigmine
o Increase ACh by decreasing breakdown
o SE – abdominal cramps, diarrhea
o Cholinergic crisis – excess Ach
 Weakness, N/V/D, pallor, sweating, salivation, miosis, bradycardia,
respiratory failure
o if flaccid paralysis improves with edrophonium  myasthenic crisis
o if flaccid paralysis worsens with edrophonium  cholinergic crisis
 immunosuppression in myasthenic crisis for rapid response
o plasmapheresis or IVIG
o chronic – steroids, cyclosporine
 thymectomy if thymoma
o
 avoid FQ and aminoglycosides
Parkinson disease
 Etiology
 Loss of dopamine producing cells in substantia nigra
 Idiopathic dopamine depletion
 Onset 45-65yo
 Failure to inhibit Ach in basal ganglia  Ach is main excitatory, dopamine inhibitory
 S/S
 Tremor  first symptom
o Resting tremor MC at 3-6Hz
o “pill rolling”
o Worse at rest and with emotional stress
o Lessened with voluntary activity, intentional movement, and sleep
o Confined to one limb or side before generalized
o Handwriting abnormality – tiny writing
 Bradykinesia  slowness of voluntary movement and decreased in automatic
movements
o Lack swimming of arms while walking and shuffling gait – festinating gait
o Difficulty getting out of chairs
 Rigidity
o Increased resistance to passive movement, especially axial
o Festination  increased speed while walking
o Normal DTR
o Usually no muscle weakness
 Facial involvement – relatively immobile face
o “masked facies”
o Fixed facial expressions
o Myerson’s sign –tap the bridge of the nose repetitively causes sustained blink
o Decreased blinking
o Seborrhea of skin
o Soft voice
 Postural instability
o Late finding
 Management
 Levodopa/carbidopa  most effective treatment
o Levodopa converted to dopamine
o Carbidopa reduces the amount of levodopa needed – reduces SE
o SE – N/V, hypotension, somnolence, dyskinesia, wearing off bradykinesia with
long term use
 Dopamine agonists  bromocriptine, pramipexole, ropinirole
o Directly stimulates dopamine receptors
o Less SE than levodopa
o Used in young patients to delay levodopa use
o SE – orthostatic hypotension, nausea, HA, dizziness, sleep disturbances
 Anticholinergics  trihexyphenidyl, benztropine
o Block excitatory cholinergic effects
o < 70 with tremor predominance, does not improve bradykinesia
o SE – constipation, dry mouth, blurred vision, tachycardia, urinary retention
o CI – BPH, glaucoma

o
o
Amantadine
o Increases presynaptic dopamine release
o Improves long-term levodopa induced dyskinesias
o Early mild symptoms
 MAO-B inhibitors – selegiline, rasagiline
o Increases dopamine in striatum
 COMT inhibitors – entacapone, tolcapone
o Adjunctive treatment
o Prevents dopamine breakdown
o SE – GI, brown discoloration of urine
 Deep brain stimulation
Peripheral neuropathies
Seizure disorders
 Partial/focal – confined to small area of brain
 Common cause is hippocampal sclerosis
 Simple partial
o Consciousness fully maintained
o EEG – focal discharge at onset of seizures
o Focal sensory, autonomic, motor symptoms
 Sensory – paresthesias, numbness, pain, heat, cold, sensation of
movement, olfactory, flashing lights
 Motor – jerky, rhythmic, movements on area or spread to other parts of
affected limb
 Autonomic – abdominal (N/V, pain, hunger); CV (sinus tach)
o May be followed by transient neuro deficits lasting up to 24h
 Complex partial – temporal lobe
o Consciousness impaired
o Starts focally
o EEG – interictal spikes with slow waves in temporal area
o Aura – seconds – minutes  impair consciousness
 Sensory/autonomic/motor symptoms of which patient is aware of
 May precede accompany or follow
o Automatisms
 Lip smacking, manual picking, patting, coordinated motor movement
 Management
o Lamotrigine, carbamazepine – less expensive
o Levetiracetam, valproate – more expensive
 Generalized seizures – diffuse brain movement in both hemispheres
 Absence – nonconvulsive
o Brief lapse in consciousness – patient unaware of attacks
o Brief staring episodes, eyelid twitching, no pot-ictal phase
o MC in childhood – ceases around 20
o Can be brought on by hyperventilation
o EEG –bilateral symmetric 3Hz spike and wave
o Management – ethosuximide, valproate
 Tonic-clonic
o Tonic phase – LOC  rigidity, sudden arrest of respirations  clonic phase
o Clonic phase  repetitive, rhythmic jerking  postictal phase
o Postictal phase  flaccid coma/sleep with variable duration


o May have incontinence, tongue biting, or aspiration with confusion
o Auras are pre-warnings
o EEG – generalized high-amplitude rapid spiking
o Management – valproate, phenytoin, carbamazepine, lamotrigine
 Juvenile myoclonus
o Sudden brief, sporadic involuntary twitching with no LOC
o May be 1 muscle or groups of muscles
o Begin age 10-16
o Clumsy in AM
o Patients will also have absence seizures
o Will progress to generalized tonic-clonic during puberty
 Worsens in puberty unlike absence
o Management – valproate, lamotrigine, levetiracetam, topiramate, zonisamide
 Avoid sleep deprivation and alcohol
 Atonic
o Drop attacks with sudden loss of postural tone
 Status epilepticus
o Repeated generalized seizures without recovery > 30m
o Major cause is non-compliance
o Management
 ABCs
 Lorazepam or diazepam  phenytoin  phenobarbital
 Thiamine + D50
 Place in lateral decubitus
 Febrile
o Simple
 < 15 minutes
 Associated with high fevers  when fever is rising
 Generalized tonic/clonic activity
 Generally, LP not needed
 Risk of epilepsy low
 Antipyretics nor anticonvulsants are effective nor recommended
o Complex
 > 15 minutes
 Multiple seizures in 24h
 Focal features
 Good prognosis but need more extensive evaluation – EEG and MRI
 Still do not need antipyretics and anticonvulsants
o Factors affect recurrence
 Family history
 Short time before onset of fever and seizure
 Abnormal neuro signs
 40% risk for second seizure in 2 years
o Management – phenobarbital
Psychogenic non-epileptic seizures
 Even patients with epilepsy can have them
 Psych consult is normally requested
o Treat overwhelming anxiety, somatization, conversion disorder
Alcohol withdrawal
o
 Generalized tonic-clonic seizures up to 48 hours after EtOH withdrawal
 Treat with benzos + other EtOH withdrawal symptoms
 Seizure drugs
 Ethosuximide – absence seizures
o Monitor CBC, UA, LFTs
 Valproic acid
o Increase GABA effects
o Absence, complex partial, tonic clonic
o Acute mania in bipolar
o Pancreatitis, hepatotoxicity, thrombocytopenia
o Monitor LFT, CBC
 Lamotrigine
o Absence, grand mal, partial complex
o Rash, SJS< HA, diplopia
 Phenytoin
o Tonic-clonic, complex partial
o Status epilepticus after benzo
o Seizure prophylaxis
o Monitor drug levels, CBC, UA
o Significant drug interactions
o Rash (EM/SJS), gingival hyperplasia, nystagmus, slurred speech
o Hirsutism, teratogenic, arrhythmias
 Carbamazepine
o Seizure, bipolar, trigeminal neuralgia, central DI
o Hyponatremia (causes SIADH), SJS, increases LFT
 Topiramate
o Grand mal, partial
o Weight loss, hyperthermia, nephrolithiasis
 Benzos
o Generalized, absence, anxiety, sedation, status epilepticus
o Sedation, ataxia, paradoxical
o Flumazenil reverses – can give seizures – then can’t give benzos
 Phenobarbital
o Status epilepticus after phenytoin
o Febrile seizures in children
o Permanent neuro deficit if injected into or near peripheral nerve
Syncope
 Vasovagal – MC
 Migraine
 Standing long periods with locked knees
 Cardiac causes
 3rd degree block
 Tachyarrhythmias
 Aortic dissection
 Pulmonary embolus
 Valve abnormalities
 Autonomic dysfunction
 Multisystem atrophy
o
o
 Aggressive treatment for HTN
 Micturition – older men
 Cough, vomiting, carotid sinus pressure
 Valsalva
 Work-up
 H/P
 EKG
 Orthostatic BP
 Evaluate for seizure if cardiac eval is negative
Tension headaches
 Etiology
 MC overall headache
 Mental stress
 S/S
 Bilateral band/vise-like constant daily HA
 Mild to moderate intensity
 May have peri-cranial tenderness
 Worsened with stress, fatigue, noise, or glare
 Not worsened with activity
 Not pulsatile
 No N/V or neuro symptoms
 Management
 NSAIDs, aspirin, Tylenol, anti-migraine meds
 TCAs in severe or recurrent
Transient ischemic attacks
 Etiology
 Focal brain, spinal cord, retinal ischemia without acute infarction
 Lasting < 24 hours
 MC due to embolus
 50% have CVA within 1st 24-48h especially if DM, HTN
 S/S
 ICA
o Amaurosis fugax – monocular vision loss
o Weakness in contralateral hand
o ICA/MCA/ACA – cerebral hemi-dysfunction
 Sudden HA, speech changes, confusion
o PCA – somatosensory deficits
 Vertebrobasilar – brainstem/cerebellar symptoms
o Gait and proprioception, dizziness, vertigo
 Diagnosis
 CT to rule out ICH
 Carotid doppler – if stenosis > 70% need endarterectomy
 CT angio
 Echo to look for embolic sources
 ECG to look for fib
 ABCD2 score
o Age, BP, clinical, duration, diabetes
o Score > 3 reasonable to admit


Management
 Aspirin + dipyridamole or clopidogrel
 Thrombolytics CI
 Supine to increase cerebral perfusion
 Avoid lowering BP unless > 220/120
 Reduce modifiable risk factors – DM, HTN, fib
UROLOGY/RENAL
o Acid base disturbances
 AG-metabolic acidosis
 Etiology
o Methanol
o Uremia
o DKA, alcoholic KA
o Propylene glycol
o Isoniazid, infection
o Lactic acidosis
o Ethylene glycol
o Rhabdo, renal failure
o Salicylates
 Too much acid or too little bicarbonate
 Low bicarb!
 NAG-metabolic acidosis
 Hyperchloremic
 Diarrhea
 Metabolic alkalosis
 Etiology
o Elevated serum bicarb
o Vomiting
o Exogenous alkali or contraction alkalosis
o Post-hypercapnia
 High bicarb level
 Respiratory acidosis
 Etiology
o Anything that decreases respiration
o CNS – opioids, sedatives, trauma, pneumonia, CP arrest
o Chronic – COPD, obesity, NM disorders
 High CO2
 Respiratory alkalosis
 Etiology
o Hyperventilation
o Anxiety, mech ventilators, salicylates
 Low CO2
o Acute kidney injury
 1. Increased serum creatinine > 50%
 2. Elevated BUN
 3 levels of AKI
 Risk, injury, failure
 Phases




Oliguric maintenance phase
o Decrease urine output, azotemia, hyperkalemia, metabolic acidosis
 Diuretic phase
o Increased urine output, hypertension, hypokalemia
 Recovery
Prerenal – reduced renal perfusion
 Etiology
o Hypovolemia
o Dehydration/volume depletion – GI disease (V/D), diuretics
o Hypotension
o Edematous states – heart failure and cirrhosis
o Hemorrhage
o Anemia?
o Nephrons are structurally intact
o MC type
 S/S
o Can lead to intrinsic if not corrected
 Diagnosis
o BUN/Cr ratio > 20:1
o High specific gravity due to concentrating
o Low FeNa
o Normal UA
 Management
o Volume repletion to restore volume and perfusion
Postrenal – obstruction
 Etiology
o Severe prostatic hypertrophy
o Malignancy along GU tract
o Hydronephrosis from renal calculi
 Management
o Removal of obstruction – cystoscopy, TURP, ureteral stenting, etc.
o Need to watch for post-obstructive diuresis/polyuria
 High FeNa – like ATN, but not ATN
Intrarenal – direct damage to kidney
 Etiology
o Nephrotoxic, cytotoxic, prolonged ischemia
o Structural, functional nephron damage result in cellular cast formation
 Acute tubular necrosis
o Ischemic – prolonged prerenal, hypotension, hypovolemia
o Nephrotoxic
 Exogenous – aminoglycosides, contrast dye, cyclosporine
 Ampho B
 Endogenous – crystal precipitation (gout), myoglobinuria, lymphoma,
Bence-Jones proteins
o MC type of intrinsic
o Diagnosis
 UA
 Renal tubular epithelial cell casts and muddy brown casts
 Low specific gravity due to inability to concentrate
o
 FeNa > 2
 Hyperkalemia, phosphatemia
 Elevated BUN: Cr
o Management
 Remove offending agents, IV fluids
 Furosemide
 Acute tubulointerstitial nephritis
o Inflammatory or allergic response in interstitium
o Drug hypersensitivity – PCN, NSAIDs, sulda
o Infection – strep, legionella, CMV, EBV
o Autoimmune – SLE, sarcoid
o S/S
 Fever, eosinophilia, maculopapular rash, arthralgias
 UA
 WBC casts
 Elevated serum IgE
o Management
 Remove offending agent
 Glomerular/ acute glomerulonephritis
o Hematuria – RBC casts only
o HTN, azotemia, proteinuria
o Management – high dose steroids, cytotoxic agents
 Vascular
o Microvascular – TTP, HELLP syndrome, DIC
o Macrovascular – AAA, renal artery dissection, malignant hypertension
Chronic kidney disease
 Etiology
 DM MC cause of ESRD due to diabetic nephropathy
 Hypertension
 Glomerulonephritis
 PKD
 Staging
 Based on creatinine clearance / eGFR
 Stage 1 – normal or elevated eGFR
o Kidney damage with normal GFR – proteinuria, abnormal UA
 Stage 2 – 90 – 60
 Stage 3 – 60 – 30
 Stage 4 – 30 – 15
 Stave 5 -- < 15
 Symptoms
 Slowly progressive
 Weakness, decreased exercise tolerance, anorexia, chronic sour taste
 Pruritis, uremic frost, hypertension, edema and progressive dyspnea
 Diagnosis
 Proteinuria – best predictor of disease progression
o Spot UAlbumin/UCreatinine ratio – especially in AM
 Urinalysis
o Abnormal sediment – broad waxy casts




o
o
eGFR
elevated BUN/Cr
renal US shows small kidneys
labs
o progressive anemia, decreased EPO
o hypocalcemia, hyperphosphatemia, hyperkalemia, slowly progressive AGmetabolic acidosis
 management
 fluid restriction
 diuretics
 dietary phosphate restriction and phosphate binders
 secondary prevention of other co-morbidities – CVD is high – frequently die of cardiac
not renal
Acute interstitial nephritis
 Etiology
 Drugs
o NSADs, PCN, cephalosporins, sulfonamides
 Infection
o Legionella, CMV, strep, TB, EBV
 S/S
 N/V malaise
 Oliguria, mild proteinuria
 Fever, rash, hypertension, hematuria
 Diagnosis
 Elevated creatinine
 Eosinophilia and eosinophiluria
 Urine sediment of white cells, white casts
 FENa > 1
 Management
 Discontinuation of offending agent
 Steroids
 Dialysis
Benign prostatic hyperplasia
 Etiology
 Natural progressive prostate enlargement as you age
 S/S
 Obstructive
o Hesitancy, decreased stream force, sensation of incomplete emptying, double
voiding, straining, dribbling
 Irritative
o Urgency, frequency, dysuria, nocturia
 Diagnosis
 Rule out neurologic disease of bladder innervation
 UA to rule out infection
 PSA
 DRE – uniformly enlarged, firm, rubbery prostate
 Management
 Observation


o
o
5-A-reductase inhibitors – finasteride, dutasteride
o Androgen inhibitor to suppress prostate growth
o Takes time to work – up to 6 months
o Has positive effect on clinical course
o SE – sexual or ejaculatory dysfunction, decreased libido
Alpha blockers – tamsulosin
o Provides rapid symptom relief but no effect on clinical course
o SE – dizziness, orthostatic hypotension, retrograde ejaculation
Surgical – TURP

Bladder cancer
 Etiology
 Transitional cell carcinoma – urinary bladder, urethra, ureter, renal pelvis
 Papillary – growing into bladder
 Sessile – growing down into muscular
 RF
 Males, Caucasian, age, family history
 Cigarette, industrial factors, chemo, radiation, chronic bladder infections
 S/S
 Hematuria (MC microscopic), urgency, frequency, dysuria, abdominal pain
 Advanced – gross hematuria, weight loss, fatigue from anemia
 Diagnosis
 H/P
 UA with cytology
 CT abdomen and pelvis with/out contrast
 Cystoscopy
 Bladder biopsies
 Histo
 Papillary
o 70%
o Wart-like, cauliflower, attached to stalk
 Nonpapillary/sessile
o Flat
o 30%
o More likely to be invasive, worse outcome
 Management
 TURBT with mitomycin or chemo
 Radical cystectomy
Epididymitis
 Etiology
 STI – younger men, urethritis
 Non-STI
o Older men, GNR bacteria from recurrent UTIs
 S/S
 Fever, positive urine analysis and culture
 Swollen painful epididymis
 Gradual onset scrotal pain, erythema, swelling
 Fever, chills
 Diagnosis
o
o
 Positive Prehn’s sign – relief of pain with elevation
 Normal cremasteric reflex
 Scrotal US
 UA – pyuria, culture
 CBC – leukocytosis
 Management
 Symptomatic treatment
o Bed rest, scrotal elevation
 STI – doxy 100mg BID x 10d + Ceftriaxone
 Enteric – FQ
Erectile dysfunction
 Etiology
 Near-consistent or consistent inability to attain or maintain a rigid erection
 Organic
o PVD/PAD/CVD
o Psychological
 SSRIs, TCAs, beta-blockers, HCTZ, CCB
 Diagnosis
 H/P
 Testosterone level
 Duplex US to evaluate penile blood flow
 Management
 PDE5-I – sildenafil, tadalafil, vardenafil
o Increase nitric oxide levels
o SE – HA, flushing, hearing loss, change in color vision
o CI in use with nitrates or CV disease
 Intracavernosal injection – prostaglandin E2
 Vacuum pumps
Glomerulonephritis
 Primary
 Focal segmental glomerulosclerosis
 Membranoproliferative
 IgA nephropathy
o MC in children
o Henoch-Schonlein Purpura – systemic IgA vasculitis
 Anti – GBM
o Pulmonary involvement – Goodpasture’s
 Pulmonary hemorrhage
 Secondary
 DM nephropathy, HIV- associated nephropathy, hypertensive urgency, TTP, HUS
 S/S
 Hypertension, edema, oliguria
 Diagnosis
 AKI, rapid rise in creatinine, anemia, hyperkalemia, severe hyperlipidemia,
hypoalbuminemia, severe proteinuria
 Renal biopsy
 Management
 Plasmapheresis, dialysis, aggressive immunosuppression


o
o
o
o
High dose IV steroids
IV cyclophosphamide
Hydrocele
 Etiology
 Peritoneal fluid between parietal and visceral layers of tunica vaginalis
 Imbalance of secretion and reabsorption of fluid
 S/S
 Small, soft collections to massive tensive collections of fluid
 Pain and disability correlate with size
 Diagnosis
 Transillumination – differentiation for hematocele, hernia, solid mass
 Scrotal US
 Management
 Excision of hydrocele sac
 Aspiration is unsuccessful due to reaccumulating fluid
Hydronephrosis
 Etiology
 Stones, transitional cell carcinoma, clots, fibrosis, enlarged lymph nodes
 S/S
 Pain, change in UO
 Hypertension, hematuria
 Increased serum creatinine
 Bladder distention
 Diagnosis
 US
 CT
o Dilation of collecting system
Hypervolemia
 Etiology
 Hypertonic saline
 Mineralocorticoid excess
 CHF, nephrotic syndrome, cirrhosis
 S/S
 Peripheral and presacral edema
 Pulmonary edema
 JVD
 Hypertension
 Decreased hematocrit
 Decreased serum protein
 Decreased BUN: creatinine
Hypovolemia
 Etiology
 Extra renal losses
 Sweating, respiratory loss
 GI N/V/D
 Dehydration
 Severe hyperglycemia
 Diuretics

o
S/S
 Poor skin turgor
 Dry mucous membranes
 Flat neck veins
 Hypotension
 Increased hematocrit
 Increased serum protein
 Increased BUN: creatinine ratio > 20:1
 UNa < 20 mEq/L
Nephrotic syndrome
 Etiology
 Membranous nephropathy – adults
o Basement membrane thickening with little or no cellular proliferation or
infiltration
o Idiopathic, SLE, viral hepatitis, malaria, drugs
o Caucasian males > 40
o Immune complex deposition
 Minimal change disease – MC in children
o No evidence of immune complex deposition but podocyte damage
o Viral infections, allergies, SLE, Hodgkin
 Lupus
 Focal segmental glomerulosclerosis – adults
o Thickened glomerular basement membrane
o Idiopathic, HTN (AA), heroin, HIV
 Membranoproliferative glomerulonephritis
 Amyloidosis
 S/S
 Edema – peripheral, periorbital (children), worsen in AM
o Pitting LE, scrotal edema
o Due to hypoalbuminemia and low oncotic pressure
 Anemia, DVT – hypercoagulability
o Increased fibrinogen and clotting factors as liver tries to make more proteins to
raise oncotic pressure
 Frothy urine, pulmonary edema, pleural effusions
 Diagnosis
 24-hour urine protein collection
o > 3.5g/day
 UA – proteinuria
o Oval fat bodies – Maltese cross shaped
 Hypoalbuminemia, hyperlipidemia
 Renal biopsy to differentiate
 Management
 Corticosteroids in MCD and FSGS
o Steroid responsiveness most important determinant of prognosis
o Cyclophosphamide and cyclosporine if not responsive
 Edema reduction – diuretics
o Increased protein diet, fluid restriction
 Proteinuria reduction – ACEI/ARB

o
o
Hyperlipidemia reduction – diet modification and statins
Nephritis
 Etiology
 IgA nephropathy/ Berger’s disease
o MC AGN in adults
o Young males shortly after URI or GI due to IgA immune complexes
 Post infectious
o MC after GABHS
o 10-14d after skin (impetigo) or pharyngeal infection
 Membranoproliferative/mesangiocapillary
o SLE, viral hep (HCV, HBV)
o Mixed nephritic/nephrotic picture
 Rapidly progressive glomerulonephritis
o Poor prognosis with rapid progression to ESRD
 Goodpasture’s – only presents with RPGN
o Kidney failure and hemoptysis due to anti-GBM antibodies
o Most URI
 Vasculitis – only presents with RPGN
o Lack of immune deposits, + ANCA antibodies
o Microscopic polyangiitis – small renal vessels – P-ANCA
o Granulomatosis with polyangiitis – necrotizing vasculitis – C-ANCA
 S/S
 Hematuria – cola-colored urine, dark urine
 Edema – peripheral periorbital
 Hypertension due to sodium and water retention
 Fever, abdominal pain, flank pain
 AKI – oliguria, low urine output
 Diagnosis
 UA
o Hematuria with RBC casts, dysmorphic RBC, proteinuria, elevated SG
 Elevated BUN, Cr
 Renal biopsy GS
 IgA – IgA mesangial deposits on immunostaining
 Post-infectious – increased anti-streptolysin (ASO) titers, low serum complement
 RPGN – crescent formation on biopsy
 Goodpasture’s – linear IgG deposits
 Management
 IgA – ACEI + steroids
 Post- infectious – supportive +/- abx
 Membranoproliferative/lupus nephritis – steroids or cyclophosphamide
 RPGN – steroids + cyclophosphamide
 Goodpasture’s – high dose steroids + cyclophosphamide + plasmapheresis
Polycystic kidney disease
 Etiology
 PKD1
 PKD2 – progresses later and slower
 Ciliopathy – abnormal renal cyst development and growth
 Autosomal dominant

o
S/S
 As cysts grow, eGFR falls
 Weakness, decreased exercise tolerance, anorexia
 Cysts produce extra amounts of EPO – no anemia unlike CKD
 Recurrent gross hematuria
 Flank pain
 Cyst infection
 Diagnosis
 Renal US
 CT/MRI more sensitive
 Management
 Low sodium diet with low protein
 Aggressive BP control
 Associated with aneurysms, especially in CNS and Circle of Willis
 Screen in symptomatic
 Associated with pancreatic and splenic cysts
 PKD2 – liver cysts
 MVP
Prostate cancer
 Etiology
 MC non-cutaneous cancer in men
 Adenocarcinoma
 Bi-modal age distribution
o 40-60 – rarer but more aggressive
o 70+ -- indolent
 Peripheral zone
 RF
 Cigarette smoking
 Family
 Chemical and radiation exposure
 Recurrent or chronic UTI
 AA
 High dietary fat
 S/S
 Increased urinary retention and difficulty voiding
 Difficulty urination, frequency, nocturia
 Bone pain, weight loss, rectal mass
 Mets to bladder wall
 Diagnosis
 CBC, CMP, UA
 PSA
 Prostate biopsy
 Assigned Gleason score
o Primary pattern seen + second most common
o Score of 6 - 10
 Management
 Watchful waiting
 Radical prostatectomy


o
o
o
XRT
Orchiectomy or chemical orchiectomy if hormone dependent
Prostatitis
 Etiology
 Acute
o > 35 – E. coli
o < 35 – Chlamydia and Gonorrhea
o Viral in children – mumps
 Chronic
o E. coli, enterococci
 S/S
 Fever/chills in acute, malaise, arthralgias
 Irritative symptoms – frequency, urgency, dysuria
 Obstructive symptoms – hesitancy, poor stream, straining, incomplete emptying
 Lower back and abdominal pain
 Perineal pain in acute
 Chronic – recurrent UTI/intermittent dysfunction
 Diagnosis
 Acute – exquisitely tender hot boggy prostate
 Chronic – nontender boggy prostate
 UA
o Chronic
 UA can be normal however expressed prostatic fluid can have high
white count
 Avoid prostatic massage in acute – can lead to bacteremia
 Management
 Acute
o > 35 – FP or TMP-SMX 4-6 weeks
o < 35 – treatment for STI – Ceftriaxone + doxy or azithromycin
 Chronic
o FQ, TMP-SMX 6-12 weeks
Pyelonephritis
 S/S
 Fever, chills, flank/abdominal/back pain
 Tachycardia, dysuria, gross hematuria
 CVA tenderness, N/V
 Diagnosis
 UA
o Pyuria, leukocyte esterase, WBC casts
o Urine culture definitive
 Management
 FQ
Renal calculi
 Types of stones
 Calcium oxalate – MC
o Thiazide
 Calcium phosphate
o Thiazide




o
Struvite – infectious/staghorn/triple phosphate calculi
o Chronic low dose suppressive PO abx
Cysteine stones – genetic, start forming when young; liver is source
Uric acid – radiolucent on KUB/plain film
o Oral bicarb for urinary alkalization
S/S
 Severe acute flank pain
 Migratory as stone moves
 Gross hematuria, N/V
 Diagnosis
 Non-contrast CT
 Hang-up locations
 Uretero-pelvic junction
 Uretero-vesicular junction
 Management
 Stones < 5 mm
o 80% chance of spontaneous passage
o Fluids, analgesic, anti-emetics
o Tamsulosin
 Stones > 7mm
o Extracorporeal lithotripsy to break up larger stones
o Uretoscopy + stenting
o Percutaneous nephrolithotomy
 Most invasive
 Large stones > 10mm, struvite
Renal cell carcinoma
 Etiology
 MC kidney CA in adults
 Originates in epithelial lining of PCT
 Men > women
 AA > White
 Risk factors
 50% tobacco exposure, obesity, HTN
 Family history – tuberous sclerosis
 HD, chemical exposures
 S/S
 Classic triad
o Hematuria, flank pain, abdominal mass
 more commonly found incidentally due to US and CT
 weight loss, fatigue, fever – advanced
 blood work
o anemia from blood loss
o polycythemia from excess EPO
o Hypercalcemia from PTH-like protein
 Stauffer syndrome
o Hepatic dysfunction with elevated LFTs in absence of mets
 Scrotal varicocele – new onset or right sided
 HTN from excess renin production

o
o
Diagnosis
 US, CT, MRI
 Histo
 Mixed adenocarcinoma containing clear cells and granular
 Treatment
 Surgery curative if tumor limited to kidney
Renal vascular disease
 Etiology
 Narrowing renal arteries – can be unilateral or bilateral
 MC of secondary HTN
 Progressive atherosclerotic disease leading to occlusion
o Advancing age, male sex, tobacco, hypertension, CAD
 Fibromuscular dysplasia
o Young women
o Develop relatively sudden otherwise unexplained new onset hypertension, AKI,
hyperkalemia
 S/S
 Unexplained hypertension complications
 Sudden severe new-onset hypertension
 Sudden worsening of long-standing but well controlled HTN
 Stable HTN now with sudden unexplained onset AKI and hyperkalemia
 Stable HTN with new recurrent flash pulmonary edema due to renin/aldo surges
 RAS
 Sudden progressive or worsening HTN so new drug is started
o BP no better but now AKI and hyperkalemia
 Suspect if AKI after the initiation of ACEI
 Use of ACEI/ARB is absolute CI if bilateral due to risk of AKI and hyperkalemia
 Diagnosis
 Abdominal bruit
 Renal US not good enough
 Renal artery duplex
 CT angio or MRA
 Catheter guided angio is GS
 Management
 Atherosclerotic
o Angioplasty with stenting or renal artery bypass
 Fibromuscular
o Repetitive beaded pattern on angio
o Balloon angio only without need tor stenting or bypass effective
Testicular cancer
 General
 MC age 15-35
 RF
o Abnormal testicle development
o History of cryptorchidism
o Klinefelter
o MC in white
 S/S
o
o
 Discomfort or pain in testicle
 Heavy feeling in scrotum
 Pain in back or lower abdomen
 Enlargement, lump, or swelling in testicle
 Nodule unable to separate from testicle
 Diagnosis
 Firm lump that does not transilluminate
 Can trigger epididymitis symptoms
 Blood tumor markers
o AFP, beta-HCG
o LDH
 US scrotum
 Path exam after removal
 Treatment
 Radical orchiectomy
 Seminoma – exclusively with radiation
 All others with radical retroperitoneal lymph node dissection
 Histo
 Seminoma – men in 30s/40s; lacks tumor markers
 Non-seminoma – more common and grow more quickly
 Stromal tumor – rare but cannot differentiate between cancerous
Testicular torsion
 Etiology
 Neonates and post-pubertal boys MC but can be any age
 May have inciting event or spontaneously
 S/S
 Irreversible damage after 12 hours of ischemia
 Moderate to severe testicular pain with profound diffuse tenderness and swelling
 Negative cremasteric reflex
 N/V
 Asymmetric high-riding testis
 Diagnosis
 US
 Management
 Detorsion and fixation surgically
Urinary tract infection
 Etiology
 Coliform bacteria
 Sexually active young women
 Men – underlying disease – obstruction, stones, tumor
 S/S
 Irritative – frequency, dysuria, urgency
 Suprapubic discomfort
 Gross hematuria
 Diagnosis
 UA + C/S
 Treatment
 3-7 days antibiotics – nitrofurantoin, TMP-SMX, cephalosporin

 Fluids
 Follow up UA if hematuria
 Needs further work-up in men
o Interstitial cystitis
 Etiology
 Women, 40+
 S/S
 Pain, difficulty voiding with full bladder
 Urinary urgency, frequency, dyspareunia
 Frequent urination in small amounts throughout the day and night
 Pain or discomfort with full bladder, relief after urinating
 Diagnosis
 Exclusion
 UA with C/S, cytology, to R/O bladder CA
 Cystoscopy with bladder biopsies
 Cracking of bladder wall and bleeding with distention
o Hunner’s ulcers/patches/lesions
o Glomerulations
 Management
 Supportive and symptom drive
 Hydrodistension can alleviate symptoms for a while
 Amitriptyline
 TENS
 Acupuncture
 Avoid caffeine, nicotine, citrus and acids
 Bladder training
o Varicocele
 Etiology
 Dilation of pampiniform plexus of spermatic veins
 Generally left-sided
 S/S
 Bag of worms
 May be dull, aching, left sided scrotal pain with standing
 Diagnosis
 Clinical
 US
 Management
 If right sided – underlying pathology caused IVC obstruction – need eval
 Surgical ligation or embolization
CRITICAL CARE
o Acute abdomen
 Older adults more likely to have severe disease and atypical symptoms
 Pregnancy!
 Appendicitis and cholecystitis
 Visceral, parietal/somatic, referred
 Fever not always tell-tale for infection – older adults more likely to present with hypothermia
 Bowel sounds
 Absence suggests peritonitis
o
o
 Hyperactive suggests blood or inflammation
 Tinkling or complete absence bowel obstruction
 Bruit – AAA
 CT study of choice
Acute gastrointestinal bleed
 Upper
 Etiology
o Gastric/duodenal ulcers
o Gastritis
o Esophagitis
o Varices
o Portal hypertensive gastropathy
o Angiodysplasia
o Mallory-Weiss tear
 S/S
o Vomiting blood or coffee-ground material
o Melena – black tarry stools
 Diagnosis
o Endoscopy
o Hematemesis – proximal to ligament of Treitz
 Management
o IV access with fluid resuscitation and transfusion if necessary
o Acid suppression
 Lower
 Etiology
o Anatomic – diverticulosis
o Vascular – angiodysplasia, ischemic, radiation-induced
o Inflammatory – IBD, infectious
o Neoplastic
o Hemorrhoids MC rectal bleeding
 S/S
o Hematochezia – maroon or bright red blood or clots
o Left colon – bright red
o Right colon – dark or maroon
 Diagnosis
o Colonoscopy
 Management
o General supportive measure with fluid resuscitation and transfusion if necessary
Acute glaucoma
 Elevated intraocular pressure resulting in optic nerve damage and decreased visual acuity
 Decreased drainage via trabecular meshwork
 Precipitating factors
 Mydriasis – pupil dilation closes the angle
o Dim lights, anti-cholinergics, sympathomimetics
 S/S
 Severe sudden onset unilateral ocular pain
 N/V, headache
 Vision changes, intermittent blurring with halos around lights
 Peripheral vision loss


o
 Conjunctival injection, steamy cornea, mid-dilated, fixed, nonreactive pupil
 Eye feels hard
Diagnosis
 Elevated IOP
 Cupping of optic disc
Management
 Acetazolamide – decrease IOP by decreased humor production
 Topical beta blocker (timolol) – decrease pressure by decreasing humor production
 Miotic/cholinergics (pilocarpine, carbachol) – papillary constriction
 Peripheral iridotomy definitive treatment
Shock
 Inadequate organ perfusion and tissue oxygenation
 Determined by:
 Low cardiac out put
 Low systemic vascular resistance
 Hypovolemic – loss of blood or fluid volume due to hemorrhage or fluid loss
 Etiology
o Hemorrhagic – GI bleed, AAA rupture, trauma, ectopic pregnancy, PP
hemorrhage
o Non-blood fluid loss – vomiting, bowel obstruction, pancreatitis, severe burns,
DKA
 S/S
o Rapid peripheral vasoconstriction and increased cardiac activity
o Sustained arterial vasoconstriction with sodium and water retention
o Tachycardia, hypotension, oliguria/anuria, elevated SVR
o Pale cool dry skin/extremities
o Slow cap refill, low skin turgor, dry membranes, AMS
 Blood loss
o 15-30% to get tachycardia
o 30-40% for decreased systolic pressure
o >40% for lethargy and no urine output
 Diagnosis
o Vasoconstriction, hypotension, decreased CO, decreased PCWP
o CBC – elevated Hgb/Hct hemoconcentration
 Decreased is a late sign
o Decreased CVP
 Management
o ABCDEs, 2 large bore IVs or central line
o Volume resuscitation with crystalloids
o Control hemorrhage
o Prevent hypothermia
 Cardiogenic – cardiac and myocardial dysfunction
 Etiology
o Poor tissue perfusion results in low cardiac output
o Often systolic
o Often produces respiratory distress
o CARDIAC DISEASE – MI, myocarditis, valves
 Management
o Oxygen, isotonic fluids – avoid aggressive IV fluid treatment
o


Inotropic support – increase myocardial contraction and output
 Dobutamine, epi
o Treat underlying cause
Obstructive – obstruction of blood flow to physical obstruction of heart or great vessels
 Etiology
o Pulmonary embolism
 Cyanosis, tachycardia, hypotension, VQ mismatch
 S1Q3T3
o Pericardial tamponade
 Blood in pericardial space prevents venous return to heart
 Muffled heart sounds, hypotension, elevated JVP
o Tension pneumothorax
 Positive air pressure causes external pressure on heart
 Hyperresonance to percussion and decreased breath sounds on affected
side
 Mediastinal and tracheal shift to contralateral side
o Aortic dissection
 Proximal dissections
 Amy also cause hypovolemic shock
 Management
o Oxygen, fluids, inotropic support
o Treat underlying cause
 Heparin, thrombolytics
 Pericardiocentesis
 Needle decompression
 Surgical intervention
Distributive – excess vasodilation and altered distribution of blood flow
 Low CO, SVR, PCWP
 Etiology
o Septic shock
 Overactive host response to infective organism
 Peripheral vasodilation from cytokines, low SVR
 S/S
 Hypotension with wide pulse pressure, bounding arterial
peripheral pulse
o ONLY SHOCK ASSOCIATED WITH ELEVATED CO
 Warm flushed extremities with fast cap refill time
 Classification
 SIRS
o Temperature > 38C/100.4F or < 36C/96.8F
o Pulse > 90
o Respiration >20 or PaCO2 < 32mmHg
o WBC > 12,000 or < 4,000
 Sepsis – SIRS plus source of infection
 Severe sepsis – SIRS + evidence of organ dysfunction
 Septic shock – Sepsis + refractory hypotension
 Management
 IV ABX
 IV fluids
o
o
o

 Vasopressors
Anaphylactic shock
 Etiology
 IgE-mediated severe systemic hypersensitivity reaction
 Within minutes of exposure
 S/S
 Pruritus, hives, angioedema  respiratory distress, stridor,
hoarseness
 Management
 Epinephrine 0.3mg IM of 1:1000
 Antihistamines
o Diphenhydramine 25-50mg IV for H1
o Ranitidine IV for H2
 Steroids
 Observe for 4-6 hours due to biphasic reaction
Neurogenic
 Etiology
 Acute spinal cord injury
 Unopposed vagal tone
 S/S
 Bradycardia and hypotension due to loss of sympathetic tone
 Warm dry skin with normal o low heart rate
 Wide pulse pressure
 Management – fluids, pressors, steroids
Endocrine
 Adrenal insufficiency
 Managed with hydrocortisone 100mg IV
HEMATOLOGY
o Acute/chronic leukemia
 ALL
 Etiology
o MC childhood malignancy
o Downs syndrome
 S/S
o Pancytopenia, fever, fatigue, lethargy, bone pain
o CNS symptoms – HA, stiff neck, visual changes, vomiting
o Pallor, fatigue, HSM, lymphadenopathy
 Diagnosis
o BMB with hypercellular with > 20% blasts
 Management
o Hydroxyurea or intrathecal methotrexate
 CML
 Etiology
o Starts indolent – can turn acute
o Philadelphia chromosome
o Median age 55-65
o Elevated neutrophil count
 S/S
o
o
o
o



AML






Etiology
o MC acute leukemia in adults
o Average age is 65 – more common in men
o Chemicals, radiation, tobacco, chemo
o Fanconi anemia, trisomy 21
S/S
o Complications of pancytopenia – anemia, neutropenia, thrombocytopenia
o Weakness, fatigue, infections
o Hemorrhagic findings – gingival bleeding, ecchymosis, epistaxis, menorrhagia
Diagnosis
o Auer rods
Sick upon presentation
Tumor lysis syndrome
o Hyperuricemia, hyperkalemia, hypocalcemia
o Manage with allopurinol, IV fluids
CLL

o
Fatigue, anorexia, weight loss, low-grade fever, excessive sweating
Abdominal fullness
Blurred vision, respiratory distress, priapism
Chronic stable
 Months – years
 Asymptomatic
o Accelerated phase
 Transient, lasting 4-6 months
 Fever, bone pain, splenomegaly
 Anemia, thrombocytopenia, renal failure, RUQ pain, sternal pain,
elevated uric acid
o Blast crisis
 Within 5 years untreated
 > 30% blast cells in blood or BM
Diagnosis
o Median WBC of 150K
o Philadelphia chromosome
Treatment
o Gleevec
Etiology
o MC leukemia in adults overall
 S/S
o Asymptomatic
o Fatigue, DOE< infections
 Diagnosis
o Smudge cells on peripheral smear – also called basket cells
o CBC
 Lymphocytosis – > 100,000
 Management
o Observation if indolent
o Chemo if symptoms
Anemia of chronic disease

o
Etiology
 Hepcidin-induced alterations in iron metabolism – reduced absorption of iron from GI
 Decreased EPO production
 S/S
 Known underlying chronic condition with inflammatory component
 Labs
 Mild anemia – 10-11
o Normocytic and normochromic
 Iron studies
o Low serum iron
o Low/normal TIBC/transferrin
 Increased in IDA
o Normal/increased serum ferritin
 Decreased in IDA
 Management
 Mange the chronic disease
Clotting factor disorders
 Hemophilia A – factor VIII
 Etiology
o X-linked
 Hemophilia B/Christmas disease – factor IX
 Etiology
o X-linked
o More common in males
 S/S
o Spontaneous bleeding, bruising, hematomas
o Mucocutaneous bleeding
o Hematuria
o Changes in neuro function, HA, hemarthroses, jaundice, splenomegaly
 Diagnosis
o CBC, UA
o Prolonged aPTT with normal or prolonged PT
 Corrects with mixing studies unless inhibitor is present
o Thrombocytopenia and platelet dysfunction
 Management
o Plasma derived factor IX or recombinant FIX
o Coagulation factor concentrates
o Antifibrinolytics – aminocaproic acid, tranexamic acid
o Analgesics for pain
 Hemophilia C – Factor XI
 Etiology
o Autosomal recessive
 Von Willebrand disease
 Etiology
o MC inherited bleeding disorder
o Autosomal dominant commonly
 S/S
o Bleeding is mild and do not experience a significant bleeding challenge
o Ingestion of aspirin or other NSADs can precipitate bleeding
o
o
o Epistaxis longer than 10 minutes
o Easy brusing
o Excessive bleeding following dental extractions
o Heavy menstrual bleeding
 Diagnosis
o Normal CBC and PT and aPTT
o VWF antigen, activity and factor VIII activity
 Management
o Desmopressin – promotes release of VWF from endothelial cell storage sites
o VWF replacement therapy
G6PD deficiency anemia
 Etiology
 MC enzymatic disorder of EBC
 X-linked
o Males – all RBC affected, more severe case
o Females – do not have severe anemia since half RBC express normal allele
 S/S
 Asymptomatic without hemolysis in steady state
 Acute hemolysis
o Oxidant injury from medications, illness, foods
 Fava beans, red wine
 Legumes, blueberries, soy, tonic water
 Chlorpropamide, dapsone, methylene blue, nitrofurantoin
 Pyridium, primaquine
o Jaundice, pallor, dark urine
o Abdominal pain/back pain
o Bite cells/blister cells; Heinz bodies
 Management
 Aggressive hydration for acute hemolysis
 Transfusion for severe anemia
 Avoidance of unsafe drugs
 Dietary restrictions
Hypercoagulable state
 Factor V Leiden
 Etiology
o Mutation in factor V
o MC inherited thrombophilia in Caucasian individuals
 S/S
o Higher risk of developing DVT
o Increased risk of miscarriage
 Pregnancy loss during 2nd or 3rd trimester due to placental abruption
 Protein C
 Etiology
o Congenital or acquired
o Vitamin K dependent
 S/S
o Elevated risk of DVT
 Diagnosis
o Protein S antigen assay
o

o
Protein S
 Etiology
o Vitamin K dependent
o Autosomal dominant
 S/S
o Increased risk of blood clots
o Arterial thrombosis
 Diagnosis
o Cannot test if on blood thinners
o Protein S antigen assay
 Antiphospholipid
 Etiology
o Primary condition or in underlying disease usually SLE
 S/S
o Thrombotic events
 Diagnosis
o Antiphospholipid antibodies
Idiopathic/Immune thrombocytopenic purpura
 Etiology
 Reduced platelet lifespan due to anti-body mediated destruction
 Inciting events
o Infections – viral
o Immune alteration – autoimmune conditions (antiphospholipid syndrome, SLE,
CLL)
 S/S
 Often asymptomatic
 If symptoms – related to thrombocytopenia and bleeding
 Bleeding – skin and mucus membranes
o Platelet-type bleeding
o Petechiae – do not blanch under pressure; occur in dependent areas of the body
o Purpura – coalescence of petechiae
o Epistaxis
 Thrombocytopenia – platelet count < 100,000
 Fatigue
 Lack of other abnormal hematologic findings – WBC, RBC, or other coagulation
parameters
 Diagnosis
 Inquire about recent infections, medications, underlying conditions, bleeding symptoms
 Labs
o Peripheral smear
 Rule/out not due to platelet clumping, no morpholic abnormalities
o HIV/HCV testing
 Diagnosis of exclusion
o Isolated thrombocytopenia (count < 100K) without anemia or leukopenia and
without another apparent cause
 Primary ITP – H/P and labs do not reveal potential etiologies
 Secondary ITP – underling condition (HIV, HCV, SLE, CLL)
 Management





o
o
Based on bleeding symptoms and platelet count
Risk greatest if < 10,000
Platelet count > 30,000, no bleeding – observe, no treatment
Platelet count < 30,000 or bleeding symptoms – steroids, IVIG
Platelet count < 20,000 or bleeding symptoms – splenectomy, rituximab, TPO receptor
agonist
Iron deficiency anemia
 Etiology
 GI/GU bleed
 Menses, pregnancy
 Repeat blood donation, gastric surgery, poor diet
 S/S
 Pica, fatigue, pallor, HA, irritability
 Pagophagia – pica for ice
 Restless leg syndrome
 Hematologic effects
 Microcytosis – low MCV
 Low reticulocyte count
 Hypochromic – low MCHC
 Reactive thrombocytosis – elevated platelets
 Elevated RDW
 Iron panel
 Total iron decreased
 TIBC increased
 Transferrin decreased
 Ferritin decreased
 Treatment
 PO iron first
o Continue for 3-6 months after restoration of normal values
o Enhanced absorption in acidic environment
 Take with vitamin C
 Empty stomach
 IV iron
o Chronic, uncorrectable bleeding
o Intestinal malabsorption
o Non-adherence
o 2 doses IV = 6 months oral
Lymphoma
 Hodgkin
 Etiology
o From germinal center
o Associated with EBV
o Bimodal age distribution – 20s and 60s
 Younger MC
 S/S
o Painless lymphadenopathy – firm, nontender, freely mobile
 Supraclavicular, cervical, mediastinal
 Alcohol may induce LN pain
o
o Systemic B symptoms
 Treatment
o Local disease – I, II, IIIA – radiation
 Non-Hodgkin
 Aggressive, present acutely with rapidly growing mass, systemic B symptoms
o Burkitt, adult T cell, diffuse large B cell
 Indolent are insidious – slow growing lymphadenopathy, HSM
o Follicular lymphoma, CLL
o Elevated white count, small rubbery LN in neck
 Peripheral LN typically
 Labs
o Elevated LDH
o Hypercalcemia, hyperuricemia
 Management
o Place on allopurinol
Multiple myeloma
 Etiology
 Genetic, environmental
 Overproduction of monoclonal IgG, IgA light chains
 Men > women; African American; older age
 S/S
 Bone pain in spine and ribs, pathologic fractures
 Infection – pneumococcal
 Renal failure due to protein deposition
 Spinal cord compression
 Hypercalcemia
 Anemia
 Diagnosis
 Lucent lesions/moth eaten lesions on skeletal survey
 Serum protein electrophoresis (SPEP)
o Elevated M protein and IgG
o Decreased levels of uninvolved immunoglobulins
 24-hour urine electrophoresis (UPEP)
o Bence Jones proteins – lambda light chains – monoclonal proteins
 CMP
o Hypercalcemia
o Elevated creatinine
o Low albumin
 Elevated ESR
 CBC – anemia, thrombocytopenia, or leukopenia
o Rouleaux formation – RBCs stick together due to increased plasma proteins
 Management
 Chemo
 Bisphosphonates
 Most treatments cause neuropathy
 Thalidomide derivatives – ASA or VTE prophylaxis
 Proteasome inhibitors – neuropathy and prophylactic acyclovir for zoster risk
 Stages

o
o
Monoclonal gammopathy
o Small M protein spike, no bone lesions
o Follow-up SPEP in 6 months
 Asymptomatic myeloma (smoldering)
o Elevated M protein but no bone lesions or end organ damage
 Clinical myeloma
o Elevated M protein with bone lesions
Sickle cell anemia
 Etiology
 Presence of HgS – sickle mutation in the beta globin
 Vaso-occlusive phenomena and hemolytic anemia
 S/S
 Pain, chronic anemia, pigment gallstones
 Episodes of acute worsening
 Low serum EPO due to renal disease – or increased plasma viscosity
 Folate/iron deficiency
 Acute drops in Hg – aplastic crisis, spleic sequestration, hyperhemolytic crisis
 Lab findings
 Low Hg – 8-10
 Sickled cells
 Howell jolly bodies
 Mildly increased WBC
 Management
 Prophylactic PNC started in newborn period until 5yo
 Immunizations
 Blood transfusions for those at risk
 Prevention of pain episodes – hydroxyurea – increase production of fetal hemoglobin
 Lifelong cure – hematopoietic cell transplant
 Cardiac complications – major cause of death
o Pulmonary HTN, HTN, MI
 Osteo due to salmonella
Thalassemia
 Alpha
 Etiology
o More common
o Tropical and subtropical Asia and India
 Minima
o ¼ altered
o Asymptomatic, no anemia, RBC’s not microcytic
 Minor
o 2/4 altered
o Resembles mild beta
o Mild anemia, hypochromic, microcytic
o Target cells
 Deletional form of hemoglobin H disease/ intermedia
o ¾ altered
o More severe
o Needs direct sequencing of DNA to diagnoses



o
Beta

o Have all symptoms of chronic hemolytic anemia
Bart’s hydrops fetalis
o 4/4 altered
o Incompatible with life
Management
o No iron
o Symptomatic management
Etiology
o Mediterranean
o Looks like IDA until proven otherwise
 Major
o Both chains impaired – excess alpha chains
o Onset 6 months of life
o S/S
 Growth retardation, abdominal swelling with HSM
 Jaundice
 Organ damage due to transfusion iron
 Severe and chronic anemia
o Early changes
 Skeletal, liver and GB, spleen, kidneys
o Late
 Cardiac, pulmonary, chronic pain, endocrine – growth failure, thyroid
o Hypochromic, microcytic, elevated iron, increased indirect bili and LDK
o Electrophoresis shows elevated F
 Minor
o One normal beta globin
o Majority is asymptomatic
o Increased splenic volume
o Similar picture of IDA
o Increased Hct and low MCV
o Normal RDW
o Elevated A2 and F
Thrombotic thrombocytopenic purpura
 Etiology
 Reduced activity of VWF cleaving protease ADAMTS13
 Can be acquired or hereditary
 Small-vessel platelet rich thrombi
 S/S
 Severe mircoangiopathic hemolytic anemia and thrombocytopenia in previously healthy
individual
 Fatigue, dyspnea, petechiae, or other bleeding
 Organ involvement
o CNS – confusion, HA, transient focal neuro, numbness, weakness, seizures,
coma
o GI – N/V/D
o Renal insufficiency
 Median platelet counts 10,000
 “pentad” thrombocytopenia, fever, ARF, and severe neuro findings – more obsolete


Diagnosis
 Peripheral smear
o Prominent schistocytes, helmet cells due to mechanical shearing of RBCs as they
pass through microthrombi
 Elevated indirect bili, low haptoglobin, increased retic, elevated LDH
 Management
 Plasma exchange (PEX)
 Steroids
 Rituximab
 Caplacizumab
o Vitamin B12 and folic acid deficiency anemia
 B12D
 Etiology
o Inadequate intake – vegans
o Defective production of intrinsic factor – pernicious anemia MC
o Defective absorption
 ZE, IBD, resection, pancreatic insufficiency
 General
o Absorbed in terminal ileum
o MMA – increased levels
o Homocysteine – elevated in B12D and folate
 S/S
o Demyelination
o Smooth tongue, painful beefy red tongue
o Weight loss, decreased appetite
o Paresthesia
o Weakness, unsteady gait, decreased vibratory sense
o Dementia/psychosis
 Treatment
o Cyanocobalamin
 FAD
 Etiology
o Decreased nutrition intake – alcoholics, pregnancy
o Defective absorption – small bowel disease
o Medications – EtOH, Bactrim, MTX, OCP, phenobarbital, phenytoin, nitric oxide
 S/S
o Same as B12, but no neuro symptoms
 Treatment
o Folic acid supplementation
INFECTIOUS DISEASE
o Botulism
 Etiology
 Food-borne – symptoms develop within 12-36h
 Wound (IVDU/heroin) – 10 days
 S/S
 N/V, diplopia, bilateral ptosis, progressive descending motor loss with flaccid paralysis
 Speech and swallowing affected
 Diagnosis
o
o
 Blood – taken prior to anti-toxin
 Stool, vomit, and food
 Need to alert staff
 Treatment
 Anti-toxin
 Food borne – any unabsorbed needs to be removed
o Abx not recommended
 Wound
o Benzylpenicillin and flagyl
o Surgical debridement
Candidiasis
 Esophageal
 Need HIV test
 Presentation
o Odynophagia, dysphagia, GERD
 Diagnosis
o EGD with biopsy and brushing
 Treatment
o Fluconazole x 21 days
 Candidemia – nosocomial
 Risk factors
o Abdominal surgery, neutropenia, ABX use, central lines with TPN, transplant
o PICC line users who mess with them
 Presentation
o FUO with sepsis
 Diagnosis
o Blood cultures
 Treatment
o PO fluconazole x 14 days
 Vaginal
 Etiology
o Preceding ABX exposure
 S/S
o Vulvar itching, erythema, thick discharge
 Diagnosis
o Wet prep with KOH stain
 Treatment
o Topical -azole cream
o Fluconazole 100-200mg PO
Chlamydia
 Chlamydia trachomatis
 Gram-negative obligate intracellular
 MC reportable STI
 S/S
 Men – asymptomatic
o Urethritis, urethral pruritus, dysuria
 Women – commonly asymptomatic
o Screen all women under 25 and anyone with high risk behavor annually


o
o
o
o Urethritis, cervicitis, dysuria, and/or PID
 Both can present with reactive arthritis
Diagnosis
 NAAT of discharge or urine
Treatment
 1g azithromycin PO once
 100mg doxycycline PO BID x 7 days
Cholera
 Non-inflammatory diarrhea
 Rice water stool leading to massive electrolyte and water loss
 Diagnosed with stool culture
 Treatment
 Oral rehydration
 Azithromycin or cipro in severe cases
Cryptococcus
 Etiology
 AIDS and immunocompromised patients
 S/S
 Pulmonary – cough and pleuritic chest pain
 Fever, cough, duspnea, HA< weight loss
 AMS with vomiting
 Cutaneous lesions if disseminated infection
 Treatment
 Ampho B in combo with flucytosine followed by fluconazole
 Meningitis
 MC cause of fungal meningitis
 Diagnosis
o High opening pressure on LP
o CSF culture and antigen
 Treatment
o Ampho B + flucytosine
o Fluconazole for 1 year
Cytomegalovirus
 Immunocompetent
 Asymptomatic/mild and self-limiting
 Nonspecific complaints of fever, lymphadenopathy, sore throat, fatigue
 Immunocompromised
 Major organ dysfunction
 Disseminated disease or death
 Congenital
 Brain liver, lung, or growth problems
 Most commonly – hearing loss
 Reactivation
 AIDS with CD4 < 50 or transplant
o Retinitis MC
o Need eye exam biannually
o #1 cause of AIDS associated blindness
 Pneumonitis with diffuse infiltrates
o
o
 Esophagitis, hepatitis, pancreatitis, colitis
 Polyradiculopathy, encephalitis
 Diagnosis
 CMV serologies with IgM and IgG
 CMV PCR
 Biopsy to look for viral inclusion bodies
 Treatment
 Immunocompetent do not require treatment
 Ganciclovir 14-21 days then valganciclovir until immune recovery
 CMV retinitis
o Intraocular ganciclovir implant + PO ganciclovir
Diphtheria
 Corynebacterium diptheriae
 S/S
 Acutely ill patient with fever
 Sore throat, malaise, cervical lymphadenopathy, low-grade fever
 Membranous pharyngitis that bleeds
 Exotoxin produces widespread organ damage
o Myocarditis/AV block, nephritis, hepatitis
o Neuritis with bulbar and peripheral paralysis
 Diagnosis
 Clinical
 Micro cultures from respiratory secretions – gram positive rods in a “Chinese character”
distribution
 Positive toxin assay
 Treatment
 Erythromycin 500mg 4x daily x 14d
 PCN x 14d
 Horse serum antitoxin
 Respiratory isolation and admission
Epstein-Barr infection
 Age of diagnosis is key
 Kids – asymptomatic
 Adults –clinical manifestations
 Elderly – rare due to seroconversion
 Infectious mono – primary infection transmitted via respiratory secretions
 S/S
 Fever, sore throat, lymphadenopathy
o Posterior cervical, axillary, inguinal
 Rash after aminopenicillins
 Exudative pharyngitis, palatal petechiae, HSM, atypical lymphocytes
 Diagnosis
 Monospot – heterophile agglutination test
 Recovery
 Fever resolves within 2 weeks
 Persistent fatigue
 Treatment
 Rest


o
o
o
Education on avoiding contact sports
Steroids – respiratory distress, CNS complications, splenic rupture, autoimmune
hemolytic anemia
 Chronic active
 Illness lasting > 6 months with fever and organ involvement
 Bone marrow hypoplasia, HSM, hepatitis, pneumonitis
Gonococcal infections
 Neisseria gonorrhea – gram negative diplococci
 Can infect any mucocutaneous surface
 S/S
 Yellow, creamy, profuse discharge
 PID, asymptomatic, septic arthritis, ocular, disseminated
 Diagnosis
 NAAT – urine or discharge
o If urine – no voiding 2 hours prior
 Treatment
 Ceftriaxone 250mg IM + 1g PO Azithromycin
o Can use 100mg Doxycycline PO BID x 7 days instead of azithromycin
Herpes simplex infection
 Etiology
o Subclinical shedding more common with HSV2
o Recurrences more common in HSV2
 Presentation
o Prodrome of local tingling, shooting pains
o Fever, malaise, HA
o Inguinal lymphadenopathy if genital
o Recurrent attacks tend to be less severe and shorter
o Herpes labialis – cold sores and fever blisters
o Herpetic gingivostomatitis – primary infection that is worse than the cold sore
 Meningoencephalitis – Mollaret’s meningitis
o High protein and elevated lymph on LP
 Need to check HSV PCR
o Confused patient with trouble word finding
o MRI with temporal lobe involvement
 Diagnosis
o Ulcerations
o Tzanck smear – multi-nucleated giant cells
o Viral culture
o PCR – preferred, more sensitive and test of choice for CSF
o Serum HSV Ab—need to specify type 1 or 2
 Treatment
o Acute – acyclovir 400mg TID x 5 days
o < 6 episodes per year – treat per episodes
o > 6 episodes – acyclovir 400mg PO BID
Histoplasmosis
 Etiology
 Bird and bat droppings in Ohio and Mississippi River Valley
 S/S
 Asymptomatic
o
 Pulmonary – patchy infiltrates with hilar nodes
 Disseminated in AIDS and immunocompromised – rash
 Diagnosis
 Antigen test – urine most specific
 May have elevated LDH
 CXR – hilar lymphadenopathy, diffuse nodular infiltrates
 CT – cerebral histo or adrenal involvement
 Treatment
 Ampho B + itraconazole
Human immunodeficiency virus infection
 Etiology and RF
 Sexual contact – receptor > penetrative
 Transmission risk decreases with circumcision
 Screening
 Ages 13-64 at least once
 High risk behaviors 1/year
 Those treated for STI
 Pregnant women
 Before starting TB treatment
 Testing
 4th gen HIV
 Ab and p24 Ag test – positive as early as 3 weeks
 Follow up with Western blot to confirm
 S/S
 Acute – mono-like
o Highly infectious, rapid initiation of therapy
o Fever, swollen nodes, rash, sore throat
 Asymptomatic
o Most common
o Median duration 10 years
 Symptomatic
o Clinical symptoms of immune dysfunction
o Opportunistic infections
o Non-infectious illnesses – cancers, CV events
 CD4+ count
 > 500 – normal, can see swollen nodes
 200-500 – risk for recurrent infections thrush, HSV, TB, LH lymphoma
 < 200 – AIDS diagnosis, PJP, KS
 50-100 – CMV, toxoplasmosis, cryptococcus
 <50 – M. avium
 Viral load – if < 20, no virus able to transmit, overall goal of HARRT
 Treatment
 Triple drug therapy
 2NRTIs + integrase inhibitor
 Pregnancy
 C-section if VL > 1000
 Intrapartum IV AZT
 Baby takes AVRs for 6 weeks

o
o
 No breastfeeding
Infections
 PJP
o S/S
 Insidious fever, dyspnea, non-productive cough
 Hypoxia at rest or with exertion
 Tachypnea, tachycardia, crackles pneumothoraxes
o Imaging –CT
 Diffuse bilateral interstitial ground glass infiltrates
o Treatment
 TMP-SMX
 Clindamycin + primaquine
 Steroids
 Toxoplasmosis
o Etiology – ingesting infected oocytes from soil, cat litter, or meat
o S/S
 Asymptomatic
 AIDS < 100 – reactivation
 CNS presentation
 HA, AMS, new onset seizures
 Dissemination – uveitis, pneumonitis
o Diagnosis
 Serologies, PCR of tissue
 Imaging – ring enhancing mass lesions
 Definitive – biopsy
o Treatment
 Pyrimethamine + sulfadiazine + leucovorin
Influenza
 Strains
 A – pandemic
 B – later in flu season
 Airborne transmission – droplet?
 Presentation
 Respiratory illness
 1-2 incubation
 Fever, chills, malaise and fatigue
 Diffuse myalgias, dry cough, SOB, HA
 Symptoms 1-2 weeks
 Diagnosis
 Rapid antigen test for A or B
 Viral PCR
 Treatment
 Need to begin within 48 hours of symptom onset – Tamiflu (oxeltamivir)
 Can cause secondary pneumonia – staph or strep
 Prevention!
Lyme disease
 Borrelia burgdorferi

o
Early
 Erythema migrans
 Conjunctivitis and diffuse urticaria
 Malaise, fatigue, HA, fever, chills, aches
 Early disseminated
 Neurologic and/or cardiac
 Neural
o Meningitis
o Cranial neuropathy
o Motor or sensory radiculoneuropathy
 Cardiac
o AV block
o Myopericarditis
o Cardiomyopathy
 Late disseminated
 Arthritis
o Migrated MSK pain with joint swelling in large joints
o Can lead to cartilage and bone erosion
 Neuro
o Encephalopathy
o Encephalomyelitis
 Diagnosis
 Need to meet criteria
o Recent history of residing or traveling to endemic area
o Risk factor for tick exposure
o Symptoms consistent with early or late lyme disease
 Do not test
o Asymptomatic patients
o Non-specific symptoms – high risk of false positives
 Serology
o ELISE IgG and IgM
 Positive – perform western blot
 Negative – nothing further
o Western blot IgM and IgG
 Positive and clinical history – treat
 Negative – supersedes ELISE
 Treatment
 Doxy or ceftriaxone
Parasitic infections
 Giardiasis
 Etiology
o Hiking and camping
 S/S
o Watery diarrhea alternating with steatorrhea
o Abdominal cramping and bloating
 Diagnosis
o Stool antigen test
o Stool O and P
o Wet mount shows trophozoites

o
o
Treatment
o Metronidazole
 Amebiasis
 Etiology
o Developing countries, crowded, unsanitary
 S/S
o Asymptomatic
 Diagnosis
o Stool O/P
o Stool antigen
 Treatment
o Metronidazole
Pertussis
 S/S
 Catarrhal stage
o Similar symptoms as URI with mild cough
o Most contagious stage
o Adolescents and adults
 Lacrimation and conjunctival injection
 Paroxysmal stage
o Coughing spells increase in severity
o Long series of coughing with little or no inspiratory effort
o May gag, develop cyanosis
o More bothersome at night
o Complications arise during this stage
 Apnea
 Pneumonia
 Weight loss
 Seizures and encephalopathy
o Posttussive vomiting
o Triggers
 Inhalation of steam, mist, respiratory irritants
 Convalescent stage
o Cough subsides
 Diagnosis
 Clinical
 Can do PCR of nasopharyngeal swabs
 Management
 Macrolide – erythromycin (14d), azithromycin (5d), clarithromycin (7d)
 Allergy – TMP-SMX (14d)
Pneumocystis
 Etiology
 HIV/AIDS CD4 < 200
 Severe malnutrition
 Transplant
 High dose steroids
 S/S
 Insidious onset of fever, dyspnea, non-productive cough, reduced exercise tolerance
 Hypoxia at rest/exertion, tachypnea, tachycardia, crackles, pneumothoraxes


o
o
o
Diagnosis
 Diffuse bilateral interstitial ground glass infiltrates, lobar or nodular changes
Treatment
 Empirically
 TMP-SMX
 Trimethoprim TID + dapsone
 Clindamycin + primaquine
 Steroids
 Hold off on ARV to prevent immune reconstitution inflammation syndrome
Rabies
 Rhabdovirus – lyssavirus
 Hosts
 US – bats, raccoons, skunks, foxes
 Globally – dogs
 Presentation
 1-3 months after exposure
 Pain at bite progressing to paresthesia
 Nonspecific HA, fever
 Late symptoms – extreme behavior, uncontrolled excitement, confusion, hydrophobia,
seizure
 Diagnosis
 During incubation – nothing useful
 Symptomatic – direct fluorescent Ab staining of skin biopsy taken from nape of neck
with PCR
 Treatment
 Clean wound immediately
 Post exposure prior to symptom onset
o Human rabies Ig –given around wound; rest given at distal anatomic site
 Rabies vaccine
o 4 shots – days 0, 3, 7, 14
 Once symptomatic, no treatment
Rocky Mountain spotted fever
 Rickettsia rickettsii
 Presentation
 Fever, HA< N/V, muscle pain
 Maculopapular rash on hands and feet spread to trunk
 AMS
 Diagnosis
 History
 Indirect immunofluorescence
 IgM and IgG
 Decreased platelets and WBC elevation
 Treatment
 Doxy 100mg PO BID x 10-14 days
Salmonellosis
 Presentation
 High fever, malaise, HA, abdominal pain, bloody diarrhea, mucus
 Typhoid fever – HSM, macular rash on trunk, intractable fever, bradycardia

o
o
o
Diagnosis
 Blood and stool culture
 Treatment
 Ceftriaxone, FQ
Shigellosis
 S/S
 Abrupt onset watery bloody diarrhea
 Tenesmus
 Diagnosis – stool culture
 Elevated WBC
 Treatment
 Self-limiting
 Cipro if severe, TMP-SMX
Syphilis
 Primary – chancre –painless ulcer
 Secondary
 Generalized maculopapular rash with palmar and plantar involvement
 Skin rash, mucosal ulceration, lymphadenopathy
 Condyloma lata
o Most infectious presentation
o Darkfield biopsy
o Need to check for HIV
 Tertiary
 Neurosyphilis – new onset psychosis/AMS
 Staging
 Early latent – acquired within 12 months
 Late latent – more than 12 months
 Diagnosis
 Primary – dark field microscopy
o RPR can be negative
 Secondary and tertiary
o RPR – titer correlates to disease activity
 Needs to decrease 4-fold post treatment
o FTA-ABS – confirmatory test
o Non-reactive RPR but positive FTA-ABS – history of successfully treated syphilis
o Reactive RPR and negative FTA-ABS – false positive
 Treatment
 Primary – PCN G 1g
 Secondary – PCN G once per week x 3 weeks
 Tertiary or NS – PCN IV via continuous infusion x 14 days
 Allergy – doxycycline
 Need to repeat titer 6 months after treatment
Tetanus
 S/S
 Localized tetanus with muscle rigidity, painful spasms
 Rigidity, opisthotonos (muscle spasms of head, neck, and spine)
 Autonomic dysfunction
 Trismus – lockjaw

o
o
Diagnosis
 Clinically
 Wound culture, serum toxin
 Treatment
 ICU for organ support
 Tetanus Ig
 Abx – flagyl or PCN
 Vaccine
 TDaP
 Booster ever 10 years
 Give booster after high risk exposure if > 5 years since last vaccine
Toxoplasmosis
 Etiology
 Parasitic infection
 Transmitted by ingesting infected soil, cat litter, contaminated meat
 Pregnant women who change the litter box
 S/S
 Asymptomatic at primary infection
 Mono-like symptoms
 AIDS patients –CNS
o HA, AMS, focal neurologic symptoms
o New onset seizures
 Diagnosis
 Toxoplasma serologies IgG IgM and PCR of CSF and tissue
 Imaging – MRI shows ring enhancing mass lesions
 Definitive diagnosis is biopsy
 Treatment
 Pyrimethamine + sulfadiazine + leucovorin
Tuberculosis
 Latent
 Exposed but not active
 Still requires treatment
 Diagnosis
o TST vs. interferon-gamma release assay
 Treatment
o INH x 6-9 months
o INH + RIF x 3 months
o INH + Rifapentine weekly X 3 months
 Higher toxicity but shorter duration
o all INH needs pyridoxine supplements to prevent neuropathy
 active
 upper lobe infiltrates, cavitation
 needs airborne isolation
 diagnosis
o acid-fast stain and culture
 obtained in AM
 need 3 consecutive negative AFB smears to remove isolation
precautions

o
 culture takes 6 weeks
o MTB PCR
 Quick answer
 Also send interferon – gamma release assay
Treatment
o INH x 9 months
 Hepatitis, peripheral neuritis – monitor LFTs
 Need pyridoxine supplementation
o RIF x 9 months
 Reddish – orange discoloration of bodily fluids (urine, feces, tears)
 Need to avoid ethanol – strong CYP450 inducer
o ETH x 1st 2 months
 Retrobulbar neuritis – optic neuritis
 Red-green colorblindness
 Need vision testing and color discrimination testing done prior to
starting
o PYR x `1st 2 months
 Hepatotoxicity with hepatic injury
 Hyperuricemia – acute gouty arthritis
In the bone – Potts disease

Varicella zoster
 Transmission – respiratory secretions – highly contagious as CPX
 Zoster – contact precautions
o Multiple dermatomes – airborne isolation
 Shingles
 S/S
o Burning, tingling prdrome
o Vesicular eruption in dermatomal pattern
o Disseminated – immunocompromised
 Post-herpetic neuralgia
o Pain control during outbreak
o Increased risk of CVA within 6 months
 Diagnosis
o Clinical
o Can obtain serology or viral culture
 Treatment
o Antivirals within 3 days of rash
o Mild to moderate – PO valacyclovir
o Severe or disseminated – IV acyclovir
 Prevention
o Zostavax – live virus
o Shingrix – not live, 2 dose series
o After shingles, wait until lesions are healed before vaccine