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Disease List

Cardiovascular

Stable Angina
Gen: d/t increased O2 demand. DM is the worst risk factor. HTN is most common RF.
Clinical: Substernal chest pain that is worse with exertion and better with rest or NG
Dx:
- 1st – Resting ECG: usully normal in stable angina
- 2nd – Stress: +  cardiac cath w angio (definitive test)
 Stress ECG: looking for ST depression.
 Stress Echo: wall motion tenderness.
 Pharm stress: uses IV adenoside or dypridamole or
dobutamine
- Other: Holter monitor
Tx:
- 1st – RFs reduction, ASA, B-blocker (atenolol, metoprolol), NG (PRN)
 NG adverse effects: HOTS (HA, ortho hypo, tolerance, syncope)
- 2nd – CCBs
- Other - ACEI/Diuretic if also have HF
- Surgical – PCI and CABG

Unstable Angina
Gen: O2 demand is unchanged. Supply is decreased secondary to reduced resting coronary flow. The
only difference b/w USA and NSTEMI is that NSTEMI also has elevation of cardiac enzymes
Clinical:
- Chronic angina with increasing frequency, duration, or intensity
- New onset that is severe and worsening
- Angina at rest
Dx:
-Same as stable angina. r/o MI in all pts and stabilize before attempting dx tests.
Tx:
- Hospital admission with cardiac monitoring, IV access, O2, pain control with nitrates and
morphine if nec.
- Aggressive acute medical management (no thrombolysis) ((MONA-BASH-C))
 ASA
 Clopidogrel
 Beta-blockers
 Enoxaparin
 Nitrates
 O2 if nec
 GP 2b/3a if nec (abciximab)
 Morphine (controversial cuz it can mask sx)
 Electrolyte replacement, especially K and Mg
o Cardiac cath/revascularization
 If medical therapy fails, ischemia changes persisting longer
than 48hrs
 OR coexisting hemodynamic instability, ventricular
arrhythmias, and new mitral regurg.
o After acute tx
 Continue ASA (or other antiplatelet) beta-blockers, and
nitrates
 Reduce RFs (statins, DM drugs, HTN, etc)

Variant (Prinzmetal) Angina
Gen: Transient coronary vasospasm.

Clinical: Episodes of angina at rest and a/w ventricular dysrhythmias. Classically at night
Dx: Hallmark is transient ST segment elevation during chest pain. Definitive test is coronary
angiography; spasms provoked with IV ergonovine or acetylcholine.
Tx: CCBs and nitrates. Rf lowering.

Myocardial Infarction
Clinical: Intense substernal pressure with radiation to neck, jaw, arms, or back. Commonly left side
- can also be epigastric discomfort or asx
- other sx: dyspnea, diaphoresis, weakness/fatigue, n/v, sense of impending doom, syncope
- sudden cardiac death – d/t Vfib
Dx:
- ECG:
 Anterior (LAD)
 ST elevation in V1-V4
 Q waves in V1-V4
 Posterior (Post. Descending artery from RCA)
 Large R wave in V1-V2
 ST segment depression in V1-V2
 Upright and prominent T waves in V1-V2
 Lateral (LCX)
 Q waves in I and AVL
 Inferior (RCA)****DO NOT GIVE NITRATES OR DIURETICS d/t
CV collapse
 Q waves in II, III, AVF
- Enzymes: dx gold standard for myocardial injury; drawn on admission and q8h 3x
 Troponins – most important initially
 CK-MB – reinfarction
Tx: in acute MI, aspirin, b-blocker, acei are the only agents shown to reduce mortality.
- MONA BASH C (see OME notes) for acute
- Maintenance: ASA, Beta-blocker, ACEI, statins
- Revascularization via thrombolysis (rural within 6hrs; ex is alteplase), PCI, or CABG. Best
within 90mins.
 Contraindications to thrombolytics therapy
 Trauma, previous stroke, recent surgery, dissecting
aortic aneurysn, active bleeding.
 Dual clopidogrel and ASA in stents
Complications: Many so look at individual sections for management of most
- Pump failure
- Arrhythmias
- Recurrent infarction
- Mechanical rupture
 Free wall
 IV septum
 Papillary muscle  produces MR
 Ventricular pseudoaneurysm (more likely to end up rupturing)
 Ventricular aneurysm (less likely)
- Acute pericarditis
- Dressler syndrome (aka post-MI syndrome)
 Immunologically based consisting of fever, malaise,
pericarditis, leukocytosis, and pleuritis, occurring weeks to
months after MI
 Tx: 1st – ASA. 2nd – Ibuprofen

Gen: Systolic failure common causes : ischemic heart dz, HTN resulting in cardiomyopathy, valvular
heart dz, myocarditis (post-viral). Diastolic common causes: HTN leading to hypertrophy (MCC),
valvular dz like AS, MS, and MR, and finally restrictive cardiomyopathy.
Clinical features:
- left sided s/s:
 dyspnea, orthopnea, PND, nocturnal cough, confusion,
diaphoresis and cool extremities
 displaced PMI (usually to the left) d/t cardiomegaly, pathologic
S3 gallop, S4 gallop, crackles/rales at lung base (pulm edema),
dullness to percussion and decreased tactile fremitus over
lower lung fields (pleural effusion), increased intensity of
pulmonic component of S2 (pulm HTN)
- right sided s/s:
 peripheral pitting edema, nocturia, JVD,
hepatomegaly/hepatojugular reflux, ascites, RV heave
Dx:
- CXR and ECG (not helpful for the actual dx but is uaully done anyway, cardiac enzymes, CBC,
echo (test of choice; EF <40% = systolic HF, EF >40% = diastolic EF), BNP >150
 BNP, echo (best), and cath are the better ones
- Other: Radionuclide ventriculography with tec-99, cardiac catheterization and angiography
to help find etiology.
Tx:
- Systolic dysfunction: standard tx is first ACEI and beta-blocker, then diuretic if sx. Also add
statins and ASA if CAD associated.
 RF modification: Na less than 2g/day, fluid restriction 1.5-
2.0L/day, weight loss, smoking, restrict ETOH, exercise,
monitor weight daily, annual flu and pneumococcal vaccine.
 Diuretics for sx: furosemide, thiazide
 Spironolactone for advanced stages: monitor K+ and renal
function (CI’d in renal failure)
 ACEI (1st line)– combo of diuretic and ACEI should be started in
most sx pts. ACEI reduces mortality in all stages of CHF. Should
be on even if asx. Monitor BP, K, BUN/Cr
 ARBs (-sartan) or hydralazine/isosorbide dinitrates in
blacks or if they can’t tolerate ACEI
 Beta-blockers: metoprolol, bisoprolol, and carvediol
 Also decreases mortality in post-MI HF
 Digoxin in severe pts after spironolactone hasn’t worked
 s/s of toxicity: N/V, anorexia, ectopic beats, AV block,
Afib, visual disturbances, disorientation
 Contraindicated in CHF
 Metformin – lethal lactic acidosis
 Thiazolidinediones (-zones) – fluid retention
 NSAIDs – may cause exacerbation
 Some antiarrhythmics that have negative inotropic
effects.
 ICD (defibrillator) or cardiac resynchronization therapy in
advanced cases
- Diastolic dysfunction: few options; mostly to treat sx only. No mortality benefit
 Beta blockers
 Diuretics
 Digoxin and spironolactone should NOT be used
- Acute decompensation: LMNOP (lasix, morphine, nitrates, O2, position)
 Do all tests listed first above.

heart disease: CAD. blood stasis. dizziness. COPD. surgery) . flushing.Atrial Fibrillation Gen: irregularly irregular. digoxin toxicity (PSVT with 2:1 block is MC association with dig). Dx: ECG . acute: vasovagal maneuvers. tx of choice). stress . irregularly irregular pulse. AV reciprocating tachy. excessive alcohol intake . Dx: ECG – narrow complex tachy. SOB. pericarditis and pericardial trauma (e. Chronic: same as acute without cardioversion. IV adenosine (1st line. angina. nausea . . exertional dyspnea. ventricular rate between 75-175 Causes: . aVF) Figure 1 Tx: same as Afib PSVT Gen: AV nodal reentrant tachycardia Causes: Ischemic HD. only a some make it through to ventricles Causes: Heart dz (HF is MC association). Atrial septal defect Dx: ECG – sawtooth at baseline with QRS every 2-3 p-wave. AV nodal reentry. MV dz . sick sinuc syndrome . pheochromcytomy Clinical features: fatigue. III. Prevention: Verapamil or beta-blockers. systemic illness .Narrow QRS complexes without P waves (or rare P waves) Figure 2 Tx: . rheumatic heart disease. acute  hemodynamically unstable – immediate electrical cardioversion  stable  beta blockers for rate control  cardioversion to sinus rhythm  anticoagulation with an INR 2-3 goal. excessive caffeeine or alcohol consumption. just beta blocker Atrial Flutter Gen: 250-350 atrial bpm. radiofrequency catheter ablation of AV node or accessory tract Wolff-Parkinson-White Syndrome Gen: Accession conduction through the bundle of kent that causes premature ventricular contraction d/t skipping AV node. including PE . IV verapamil or DC cardioversion  adenosine s/e: HA. Dx: ECG – irreg irreg. Med options include procainamide or quinidine . hyper/hypothyroidism . a short PR interval. Tx: . Best seen in the inferior leads (II. pulmonary dz. without P waves with a wavy baseline. Pts under 60 don’t even need anticoag. chest pressure. and a delta wave Tx: Radiofrequency ablation of accessory pathway.g. CAD. HTN. MI. Atrial flutter with rapid ventricular response. palpitations.

Immediate defibrillation and CPR  Intubation if indicated  Epinephrine and repeat defibrillation  IV amiodarone if refractory . VT or Vfib causes 75% of episodes of cardiac arrest. w/o a preceding PR interval prolongation. 1st degree  PR interval prolonged. Nonsustained and nml heart  none Ventricular Fibrillation Causes: Ischemic heart dz (MCC). prolonged QT syndrome. QRS follows each P wave. . absent heart sounds and pulse. Acute unstable  DC cardioversion followed by IV amiodarone . Afib + WPW Clinical: cant read BP. electrolytes. active ischemia with hypotension. impaired consciousness. unconscious Dx: ECG – no p waves or qrs can be identified Tx: . drug toxicity Torsades de pointes: . Nonsustained and underlying heart disease  ICD placement 1st. Acute stable  IV amiodarone . . Originates below bundle of His. No tx  type 2  P wave fails to conduct suddenly. lightheadness. Identify and treat causes . cardiomyopathies. Causes: CAD with prior MI (MCC). AV Block Figure 4 . antidepressants.Ventricular Tachycardia Gen – 3 or more PVCs in a row at a rate of 100-250. Pwaves unaffeceted. Sick sinus synrome is persistent spontaneous bradycardia that’s usually in the elderly. SCD. cannon A waves in the neck (both atria and ventricle contract at the same time and its like a brief JVD) Dx: ECG – wide and bizzare QRS complexes Figure 3 Tx: . Block is in AV node  Benign. amiodarone 2nd. Ecg shows twisting bow . Sinus Bradycardia  atropine and pacemaker if persistent . dyspnea. tx: IV magnesium Clinical: palpitations. antiarrhythmics) . drugs that causes torsades. 2nd degree  type 1 aka Wenchkebach  progressive prolongation of PR interval until a P wave fails to conduct (dropped QRS beat)  block is in AV node. therefore. no tx . a/w prolonged QT d/t genetics or drugs (TCA. rapid polymorphic form of VT that can lead to Vfib. Successful cardioversion: maintain IV amiodarone until implantable defibs. congenital defects. the QRS drops suddenly  Often brogresses to complete heart block  Site of block is within His-purkinje .

sustained handgrip  Increases with valsalva and standing  Rapidly increasing carotid pulse with two upstrokes (bisferious pulse) Dx: Echo established dx. vasodilators. Thyroid: hypo or hyper . no correspondence between P and QRS (AV dissociation  An ectopic ventricular pacemaker maintains a ventricular rate of 25-40 (so spread out QRS)  Tx is pacemaker. uncontrolled tachycardia . May also have dynamic outflow obstruction d/t hypertrophy of the interventricular septum Clinical: . and echo results consistent CHF Tx: Similar to CHF: Dig. viral. SLE. diuretics. Consider anticoagulation Hypertrophic Cardiomyopathy Gen: Most cases are autosomal dominant (mutation in sarcomeres).  Tx is pacemaker  Type 3 aka complete  Absense of conduction of atrial impulses to the ventricles. Signs  Sustained PMI  Loud S4  Systolic ejection murmur best heard at LLSB  Decreases with increased SVR and increased VR: squatting. cocaine . or arrhythmias. lyme dz. and transplant. adriamycin . which further increase with high HR and contractility or decrease ventricular filling. All should avoid strenuous exercise . Remove offending agent. Insult causes LV dysfunction Causes: . CXR. Infxn: Chaga’s sz. HIV . slceroderma . murmurs. uremia . Prolonged. Symptoms  Dyspnea on exertion  Angina  Syncope  Palpitations and arrhythmias  Cardiac failure and sudden death . Toxic: ETOH. Metabolic: thiamine or selenium def. doxorubicin. Associated extra sounds. Dilated Cardiomyopathy Gen – MC type of cardiomyopathy. hypophosphatemia. Cardiomegaly. straight leg raise. Clinical and fam hx are main components Tx: . Familial/genetic Clinical: S/S of L/R heart failure. idiopathic (50%) . Main problem is diastolic dysfunction d/t hypertrophy that elevate diastoic filling pressures. Pheochromocytoma. CAD with prior MI is common known cause . Sudden death Dx: ECG. Peripartum cardiomyopathy . lying.

positional that’s relieved by sitting up and leaning forward. Viral: Coxsackie. Acute Pericarditis Causes: Many but think about post-viral (esp coxsackie). chest pain (pleuritic. Less common Causes: . Afib . sarcoidosis . arrhythmia. chemo or rad induced .beta-blockers (improves diastolic filling and reduces myocardial contractility). PR depression . Lyme dz. parvovirus B19. treat underlying cause . post-MI (dressler). Complications: Pericardial effusion and cardiac tamponade Clinical: Cardinal manifestations: . ECG: low voltages or conduction abnormalities. HHV-6. increased RA/LA size with normal RV/LV size. arrhythmias. meds (sulfonamides). Echo: thickened myocardium. Other: SLE. pericardial friction rub . amyloidosis . Bacterial: GAS in rheumatic fever. Endocardial bx may be diagnostic Tx: . death Classic presentation is a young male Dx: Cardiac enzyme elevation and ESR Tx is supportive and of the underlying cause and complications. Echo for effusion (should be done in all pts to check). mycoplasma. Tx underlying disorder  Hemochromatosis – phlebotomy or deferoxamine  Sarcoidosis – glucocorticoids  Amyloidosis – none available  Give Digoxin if systolic dysfunction is present (except in amyloidosis d/t increased risk of toxicity. carcinoid syndrome . CHF. pericarditis. Look for recent illness . 2nd – CCBs. Tx: . etc . hemochromatosis . . Or present with fatigue. post-surgery (postpericardiotomy syndrome) for possible questions. Symptoms based off complications . Myocarditis Causes: .  In amyloidosis: myocardium appears brighter or may have a sparkled appearance . Surgery – Myomectomy of the septum in pts with severe dz Restrictive Cardiomyopathy Gen: infiltration causes impaired filling d/t less compliance. . most cases are self-limited in 2-6wks . fever. chest pain. idiopathic Clinical: elevated filling pressures cause dyspnea and exercise tolerance. idiopathic Clinical: may be asx. Pericardial effusion w or w/o tamponade Dx: ECG. Right-sided sx present for the same reason Dx: . etc .. ECG changes – diffuse ST elevation. Symptomatic pts: 1st . scleroderma .

Small and asx  repeat echo in 1-2 weeks Cardiac Tamponade Gen: accumulation of pericardial fluid. symptoms related to fluid overload and diminished cardiac output . iatrogenic – central-line placement. Pericardial Effusion Clinical – nonspecific but include muffled heart sounds. Anything that increase flow exacerbates the pulm HTN. -leads to pulm congestion. Echo: (best) increased pericardial thickness and sharp halt in filling . Pericardial fluid analysis to find cause Tx: Don’t do cenesis unless there’s tamponade. dullness at left lung base. post-MI with free wall rupture Clinical: . . Pulsus paradoxus  Exaggerated decrease in arterial pressure during inspiration (>10mmHg) Dx: . Diastolic dysfunction that has rapid filling early and then halted filling (vs. soft PMI. CT/MRI showing thickening and calcifications . and pericardium all equalize). pericarditis .. Treat underlying cause. CXR shows enlargement and may have “water-bottle” appearance. penetrating trauma . LA. pulm arter. RA. mainstay is NSAIDs (colchicine)  2nd but should be avoided if possible is glucocorticoids. ECG: low voltage. Cath for pressures in filling ventricles Tx: treat the underlying condition and symptoms. Narrowed pulse pressure . No pulmonary vascular congestion. rate is more important than amount. Effusion that mechanically impairs filling. Sometimes afib in advanced dz . Constrictive Pericarditis Gen: fibrous scarring of the pericardium leading to rigidity. tamponade where filling is impeded throughout diastole) Clinical: . pacemaker insertion. Immune-mediated damage d/t cross-reactivity between M protein of strep and valve tissue. Surgical pericadiectomy for advanced. muffled heart sounds . pericardiocentesis. Echo Tx: Pericardiocentesis if unstable. Beck triad: JVD. Surgery if d/t trauma (pericardial window) Mitral Stenosis Gen – almost all cases are d/t rheumatic heart dz. hypotension. Causes: . . LV. friction fub. Echo (best) . Equalization of intracardiac and intrapericardial pressures during diastole (RV. etc . Dx . signs  JVD  Kussmaul – JVD fails to decrease during inspiration  Pericardial knock – corresponds to abrupt cessation of filling  Ascites and depn edema  May lead to tamponade Dx: .

immobile aortic valve and dilated aortic root . “fish-mouth”-shaped orifice. The closer the opening snap is to S2. Dx: Echo – LA enlargement. palpitations. Chronic  Primary valvular: rheumatic fever. SLE. bicuspid aortic valve. Rheumatic fever Clinical: . thromboembolism (afib) . RHF in advanced dz. Aortic Regurgitation Causes: . no tx for asx)  Diuretics for pulm congestion and edema  Beta-blockers to decrease HR and CO . Signs  Murmur: harsh crescendo-decrescendo systolic murmur heard in second right intercostal space that radiates to carotid arteries  Soft S2. ECG: LVH. marfan syndrome. Causes: Calcification of tricuspid the elderly and bicuspid in the young. orthopnea. Surgical (for severe dz)  Percutaneous balloon valvuloplasty Aortic Stenosis Gen: Severe AS can lead to LV dilation with pulls the MV annulus apart. thick. ankylosing spondylitis. Cardiac catheterization  Definitive dx test but used only prior to surgery . and Afib. Med: (for mild sx. Sx  Angina  Syncope (exertional)  HF sx . Clinical . exertional dyspnea. PND . . LA abnormality . narrow. calcified MV. Other: CXR late findings – calcific aortic valve. chest pain . LVH. causing MR. enlarged LV/LA Tx: Aortic valve replacement is tx of choice and indicated in all sx pts. thickened. ECHO diagnostic in most cases. RHF. -Long standing MS can lead to pulm HTN. S2 may also be single since the aortic component may be delayed and merge into P2. heomptysis . Murmur: opening snap followed by a low-pitched diastolic rumble. Acute  Infective endocarditis  Trauma  Aortic dissection  Iatrogenic as during a failed replacement surgery . Ehlor-danlos. Tx: . Murmur followed by loud S1.  S4  Parvus et tardus – diminished and delated carotid upstrokes  Sustained PMI  Precordial thrill Dx: . the worse the stenosis (this is not a typo). RHF s/s .

cor pulmonale . Tx: Conservative if asx with vasodilators etc. Chronic  MVP  RF  Marfan  Cardiomyopathy Clinical: LVH sx. osteogenesis imperfecta. usually d/t RV dilation  LVF. Surgical correction IF pulmonary HTN is not present. angina. definitive is surgery and must perform replacement if its an Acute AR (e. MCC of MR in developed countries. . Behcet syndrome (causes blood vessel inflammation). Echo – performed serially in chronic. CXR will show LHF type findings. palpitations. Blowing holosystolic murmur at LLSB that intensifies with inspiration. Common in those with marfan.g. Clinical: usually asx unless the pt developt RHF/pulm HTN. Acute:  Endocarditis (MC staph aureus)  Papillary muscle rupture (from infarction) or dysfunction (from ischemia)  Chordae tendineae rupture . aortic dissection. Epstein anomaly – congenital malformation of tricuspid valve in which there is downward displacement of the valve into the RV. CXR/ECG – LVH and dilated aorta . Cardiac cath – to assess severity of AR and degree of LV dysfxn. Mitral Valve Prolapse Gen – presence of excessive or redundant mitral leaflet tissue d/t myxomatous degeneration of MV leaflets and/or chordae tendineae. osteo imperfecta. EDS. Surgical – replacement (must be performedbefore LV function is too compromised) Tricuspid Regurgitation Causes: . Sx: HF sx. Holosystolic murmur at the apex which radiates to the back or clavicular area. Reiter syndrome. Similar to MS murmur. Dx: Echo Tx: symptomatic. systemic HTN Clinical . RV Infarct. Dx: Echo will show dilation of the left heart. Tricuspid endocarditis in IVDU .  Aortic root disease: syphilitic aortitis. Dx: . Tx: Med – afterload. inferior wall MI. Complication of Lithium in preggers and WPW syndrome. post-MI) Mitral Regurgitation Causes: .. . shock . PE:  Widened pulse pressure  Diastolic decrescendo murmur best heard at LSB  Corrigan (water-hammer) pulse aka bounding  Austin flint murmur – low-pitched diastolic rumble d/t competing flow anterograde from the LA and retrograde from the aorta.

Other: . involvement of infected skin or MSK tissue . If negative culture. Px: Indication AND certain procedures . Vegetations occur and can embolize. valve dz – usually MS)  subcutaneous nodules  erythema marginatum  Sydenham’s chorea . CRP is used to monitor tx . Cardiobacterium. Eikenella. tx strep pharyngitis with penicillin or erythromycin to prevent RF . Nonbacterial Verrucous Endocarditis (aka Libman-Sacks)  Aortic valves (MC) in SLE pts  Formation of small. bx or incision of respiratory mucosa. Qualifying procedures  Dental. Can cause emboli  Treat underlying SLE and anticoagulate Atrial Septal Defect (L to R) Types: ostium secundum (MC). ostium primum. acute RF is tx with NSAIDs. tx valvular pathology of RHD Infective Endocarditis Gen: Don’t forget HACEK group: Haemophilus. warty vegetations on both sides of leaf-lets and may present with regurgitant murmurs. treat with a penicillin (or vanco) plus an AG. Nonbacterial Thrombotic Endocarditis (aka Marantic)  a/w debilitating illness like met cancer. Actinobacillus. Kingella. midsystolic rumbling murmur that increases with standing and the valsalva maneuver and decreases with squatting (so decreases with increased VR. only other one besides HOCM). Dx: TransEsophageal Echo is best (and classic clinical features) Tx: Parenteral abx based on culture for 4-6 wks. Qualifying cardiac indications  Prosthetic valves  Hx of IE  Congenital heart dz (unrepaired or repaired in last 6mos)  Cardiac transplant with valvulopathy . CHF. sinus venosus . .  Sterile deposits of fibrin and platelets form on valve.Clinical: Key signs – systolic clicks. Dx – Echo Tx – condition is usually benign Rheumatic Heart Disease Gen: RF may progress to RHD Dx: Requires two major criteria or one major and two minor . Minor  Fever  Elevated ESR  Polyarthralgias  Prior hx of RF  Prolonged PR interval  Evidence of preceding streptococcal infxn Tx: . Do not give abx for native MVP/MS or routine GI/GU procedures. Major (JONES)  migratory polyarthitis  cardiac involvement (pericarditis.

Pulmonary HTN . TEE is best for dx . Midsystolic murmur heard best over the back. also well-developed in upper and underdeveloped in lower. stroke from paradoxical emboli or afib Tx: Surgery if symptomatic Ventral Septal Defect (L to R) Gen: MC congenital defect Clinical: . . Murmur decreases with Valsalva and handgrip. CXR shows large pulm arteries and increased pulm markings . progressive aortic regurg . Severe HTN . . claudication with exercise and leg fatigue . heart failure . cold extremities. Delayed femoral pulses Dx . Perc balloon aortoplasty is also an option. CXR:  Rib notching  Aorta looks like a “3” d/t indentation of it Complications: . Dx: . ECG – biventricular hypertrophy when PVR is high . CXR – enlargemnt of the pulm artery and cardiac silhouette. eisenmenger Tx: same as ASD Coarctation of the Aorta Gen – if it’s a woman. Sx include HA. IE .Clinical: . Harsh. HTN in UE and hypotension in LE. atrial abnormalities Complications . RHF. Sternal lift (RV enlargement) . ECG – RBB and RAD. Possible Aortic regurg Dx: . Echo is best . RVF if advanced. blowing holosystolic murmur with thrill at 4 left intercostal space. fixed split S2 . ECG shows LVH . endocarditis . Increased P2 heart sound . mild systolic ejection murmur at pulmonary area secondary to increased flow. Aortic dissection Tx: Standard tx invloves surgical decompression. AFIB. Eisenmenger disease: irreversible pulm HTN causing reversal and LHF and cyanosis . usually asx until middle age and presents as exertional dyspnea . Rupture of cerebral aneurysms . Diastolic rumble . Complications . think Turner’s Clinical . the louder the murmur . . The smaller the defect.

Indomethacin indicated for closure. do NOT correct PDA. sx include insidious onset of HA. residual outflow obstruction. PGE1 can use to keep it open (in face of other abnormalities like Tetralogy) Tetralogy of Fallot (R to L) Gen: Tetrad – 1. seizures. . Tx HTN and sx - Aortic Dissection Gen: Type A (ascending)  surgical tx. Adults with PDA usually have nml pulmonary pressures Clinical: . HTN emergency may lead to posterior reversible encephalopathy syndrome (PRES) – a radiographic condition which is postulated to be caused by autoreguatory failure of cerebral vessels as well as endothelial dysfunction. Hypertensive Emergency/Urgency HTN emergency . AMS. high altitude. Murmur is typically crescendo-decrescendo best heard at LUSB Dx: . Tet spells: they will squat after exertion (exercise or crying) to increase SVR. .Patent Ductus Arteriosus (L to R) Gen: Associated with congenital rubella syndrome. Overriding aorta Clinical: . Beta-blockers may be needed if pt continues to be cyanotic . LE clubbings . HTN. Diaphoresis. MCCOD is SCD and HF  Complications after surgery include arrhythmias. RVH 4. . VSD 2. If severe pulmonary HTN or R-L shunt is present. and premature births. posterior cerebral white matter edema on MRI . either in the anterior (type A) or back/interscapular (type B) of chest. Wide pulse pressure and bounding peripheral pulses . tearing/ripping/stabbing pain. Loud P2 (pulm HTN)  RV hypertrophy  LVH . . HTN urgency is without end organ damage tx with PO meds or decrease BP over 24hrs. Echo is best. Pulse or BP asymmetry between limbs . Type B (descending)  medical tx. CXR shows same as other L to R shunts. Leading causes of death in adults are HF and IE. Pulmonary artery stenosis 3. EKG may show enlarged RA and RV . If pulmonary vascular disease is absent – surgical ligation . Morphine. Sx depns on degree of RV outflow obstruction . . and HF. Tx: . vision changes. Chest xray classically shows boot-shaped heart Tx: . Surgery is contraindicated. Additionally sometimes calcification of ductus arteriosus. which helps shunt blood from the RV to the lungs instead of the aorta. Cyanosis is the most common sx . Surgical preferably before 1st year of life. Echo is best for dx .>220 and/or >120 in addition to end-organ damage  immediate tx with IV meds. typically abrupt. O2. Continuous “machinery murmur” at left 2nd ICS both systolic and diastolic. Severe. pulmonary regurgitations. . . Complication = reversal of shunt Dx: . or hypotensive . Clinical: .

syncope/near-syncope. decreased hair. ischemic ulceration (usually on the toes) Dx: . Tx: . Diminished pulses.4 . TEE is best for unstable pt cuz its bedside. aortoiliac (sx in butt and hips instead of legs). usually asx. Rest pain is often prominent at nigiht . Ultrasound is test of choice . Immediate medical therapy for both types  IV beta blockers  IV sodium nitroprusside to lower systolic BP below 120mmHg . and decreased skin temp. Aortic angiography is the actual best test for determining extent of the dissection for surgery but its invasive. pain is throbbing . HLD. Smoking is most important RF. Conservative for intermittent  Stop smoking . TEE and CT are the preferred tests for acute dx. thick toenails. if present.3 is very severe cuz vessels are non compressible  claudication under . and palpable pulsatile mass requires emergent laparotomy. Open is gold standard but endovascular can be done too Peripheral Vascular Disease Gen: Sites – superficial femoral artery (MC). AAA Gen – most occur between the renal arteries and iliac bifurcation. . HTN. Unruptured: >5cm or sx  endovascular graft placement. Grey turner sign (ecchymoses on back and flanks) and Cullen sign (ecchymoses around umbilicus) are signs suggesting impending rupture.  Also CV collapse. muscular atrophy. More common in men but more likely to rupture in women. Clinical: . Neurologic – hemiplegia/hemianesthesia d/t obstruction of carotid. pulsatile mass on ab exam . Intermittent is very reproducible with same distance . .. Tx: . N/V Dx: . Clinical: . DM. popliteal. Type A – surgery . Rupture of AAA: Triad of abdominal pain. CXR shows widened mediastinum . hypotension. 1st test is ABI (DM pts have false readings)  >1. MRI is good but take awhile . . No further dx testing needed. CT abdomen only if stable and preop planning. incidental finding .7  rest pain under . CAD. Arteriography is gold standard Tx: . Aortic regurg (Esp type A) . Type B – medical  IV beta blockers  Pain control  Unrelenting sx require surgery. Ruptured: emergency repair. Dx: .

bypass if fogarty failure). Tx IV abx and surgically excise. if ulcer develop. Dx: Arteriogram is gold standard Tx: anticoagulation or emergent surgery (cutdown and fogarty balloon for embolectomy. tPa. DVT Gen: Virchow’s triad – endothelial injury. Luetic Heart -Complication of syphilitic aortitis with retrograde extension that causes aortic regurg. Surgical for rest pain. hypercoagulability (inherited examples – factor V leiden. Presents with small areas of iscemia. Dx: clinical Tx: leg elevation. swolen leg)  Occurs in extreme cases indicating major venous obstruction  Severe leg edema can compromise arterial supply leading to impaired sensory and motor  Venous thrombectomy is indicated. wet-to- dry dressings Superficial Thrombophlebitis Gen: In UE – usually at IV infusion sites. Mycotic Aneurysm -Aneurysm that results from damage to the aortic wall secondary to infxn. Clinical: Six Ps – pain. pulselessness. protein C and S deficiency.Tx is supportive. pigmentation. Compartment: assess for compartment syndrome Cholesterol Embolization Syndrome -d/t showers of cholesterol crystals from a proximal source triggered by interventions or thrombolysis. ischemic ulcerations. and severe refractory sx. Chronic Venous Insufficiency Clinical: aching of LE. paresthesisas. venous stasis. Do NOT anticoagulate. erythema along the course of a superficial vein Dx: clinical . paralysis. AT3 deficiency). calf pain Dx: Duplex US. PE . blue. edema. pallor. relieved by elevation of legs and worsened by recumbency. worse at end of day. . paralysis.see below. Acute Arterial Occlusion Gen: usually caused by embolization. ulcers. In LE – usually a/w varicose veins Clinical: local tenderness.  Graduated exercise  Asa and cilostazol and other RF decrease . IVC filter (only if absolute contraindication or failure of anticoagulation – prevents PE not DVT) Complications: . elastic stocking. MC site of occlusion is the common femoral artery. Happens in most pts. avoid long periods of standing. Tx with IV penicillin and surg repair. Unna boots. Options are angioplasty or bypass grafting. Phlegmasia cerulea dolens (painful. . Clincial: usually asx. MC source is heart (MC AFIb). polar. d-dimer Tx: anticoagulation (heparin to warfarin for 3-6mos). Postthrombotic syndrome: chronic venous insufficiency can result in ambulatory venous HTN -.

Tx: . CXR . FEV1/FVC ratio is <0. Sepsis = SIRS + infection source suspicion . RV is increased. Guidelines  Mild to moderate  Begin with anticholinergic and/or beta-agonist  ICS may be used at lowest dose  Theophylline may be considered after above  Severe  Above meds (triple inhaler therapy works combining ICS. TLC is increased . blood replacement isnt necessary just crystalloid solution with appropriate electrolyte replacement. indurated vein. renal fxn. Peak expiratory flow is low . For nonhemorrhagic hypovolemic shock. . oliguira. If all else to dx – pulmonary artery catheter and/or echo Other: . Remove and give systemic abx. pulse ox. NE or phenylephrine) . tachycardia. electrolytes. Cessation and O2 therapy are the only ones to lower mortality . AMS.beta. Cardiogenic: IVF is likely to be harmful if LV pressures are elevated. Dx: PFT values .000 or bands over 10% . Patients may need diuretics. Sx in all are hypotension. . VC is low. PT/PTT . Clinical monitoring includes serial FEV1 measurement. Septic Shock = hypotension persisting despite fluids . monitor for spread or cellulitis Suppurative thrombophlebitis – septic phlebitis d/t IV cannula. Hypo usually in young and old  Tachypnea over 20 or PaCO2 under 32  Tachycardia over 90  Increased WBC over 12. exercise tolerance. Urine output measuring is best for treatment monitoring. Shock Gen: PCWP is up in cardiogenic and down in all others. Multiple Organ Dysfunction Syndrome = altered organ function Pulmonary System Diseases COPD Gen – leads to chronic respiratory alkalosis with metabolic alkalosis as compensation. Continuous pulse ox . Fev1 is decreased . CVP is down in hypovolemic only.anti-M) . .70 . smoking cessation (most important): slows rate of decline but does not result in complete reversal. draw blood: CBC. SIRS is characterized by 2 or more  Fever or hypothermia (38 or 36). ECG. .000 or under 4. 2 large-bore caths . Different than cellulitis and lymphangitis because there’s less swelling and there is a palpable. fluid bolus .Tx: analgesics. Initial steps: . Vasopressors if fluid fails (dopamine (esp if cardiogenic).

Acute severe: inhaled beta2 agonist. May progress to PPV and intubation. methacholine or histamine decreases FEV1 by over 20% . Clinical: If the patient is having an attack. Mild persistent (sx 2 or more times per week. pneumococcal every 5 yrs for pts over 65 or under 65 with severe disease Complications: Acute exacerbations. frequent exacerbations): Daily ICS + LABA (alternative to ICS is LTA or theophylline) . IV steroids. possible IV magnesium (3 rd line). O2 to keep SaO2 between 90-93% (not higher because you lose respiratory drive and risks higher CO2 retention). it’s a bad sign and ventilation should be considered. chest PT. High-rest CT is best . Tx/Management: Avoid beta-blockers . Cromolyn sodium used for ppx only in kids .7  If bronchodilator results in increase in FEV1 or FVC by at least 12%. . vaccination (flu and pneumo). O2. Beta blockers are generally contraindicated . pulmonary HTN and cor pulmonale. doxy). foul-sputum. bronchoscopy Tx: . Primary Ciliary Dyskinesia. hemoptysis. Dyspnea. Asthma Dx: . levo. secondary polycythemia (>55% Hct in men or >47% in women). Acute hospitalized exacerbations  IV Steroids (plus taper) and Abx (azithro. chest physiotherapy. Bronchiectasis Causes: recurrent infxns. Vaccination: yearly flu. Pts should self monitor peak expiratory flow rate to self-adjust meds. recurrent/persistent PNA. Consider omalizumab and PO steroids. Clinical: Chronic cough with large amounts of mucopurulent. If CO2 increases. Cxr abnormalities. they should have hypocarbia cuz of the increased RR.  In asthma. Bronchial hygeine: hydration. fat-soluble vitamin replacement. PFTs reveal obstructive pattern. . . Moderate persistent (daily sx. CF (MCC).  O2 is hypoxemic  Pulm rehab . intubation if nec. Severe persistent (everyday with limited function): daily high dose ICS and LABA. Continuous O2 when PaO2 is at 55mmHg or O2 sat is less than 88% . consider abx depn on picture. Humoral immunodeficiency. Mild intermittent (sx 2 or less times per week): PRN albuterol . obstruction is considered reversible. inhaled recombinant human deoxribonuclease (breaks down DNA in respiratory mucus). inhaled bronchodilators Cystic Fibrosis -usually Peds but they can live till 30 now -tx is pancreatic enzyme replacement. abx. but not everyday): low dose ICS . PFTs are required for dx  Ratio under 0. Peak flow is also used in the emergent setting. AI dz. Abx for acute exacerbations . Dx: .

Lung Neoplasms
Random:
- pancoast tumor is a superior sulcus tumor. Usually squamous cell Ca. UE weakness d/t
brachial plexus invasion. a/w horner’s syndrome
- mets: MC sites are brain, bone, adrenal glands, and liver
- paraneoplastic
 SIADH – SCLC
 Ectopic ACTH – SCLC
 PTHrP – Squamous
 Hypertrophic pulmonary osteoarthropathy – adca and
squamous – severe long bone pain may be present
 Eaton-lambert syndrome – SCLC. Proximal muscle weakness
but IMPROVES on muscle use
 Digital clubbing
Staging/Dx: central lesions should be biopsied via bronchoscopy and peripheral lesions can use
transthoracic needle bx under fluorscopic or CT guidance.
- Pleural effusions should be tapped and sent to cytology.
- Pathology is required for cancer dx
- Always perform a bx for intrathoracic lymphadenopathy
Tx:
- NSCLC
 Surgery is best if theres not mets
 Radiation is an important adjunct
- SCLC
 For limited dz, combo oc chemo and radiation is used initially
 For extensive dz, chemo is used alone as initial tx. If pt
responds, then radiation is used as ppx for brain mets.
Figure 5

Mediastinal Masses – MCC is mets (usually from lung) in older pts
Common causes by location:
- Anterior mediastium (Ts)
 Thyroid
 Teratogenic tumors
 Thymoma
 Terrible lymphoma
- Middle: lung cancer, lymphoma, aneurysms, cysts, morgagni hernia
- Posterior: neurogenic tumors, esophageal masses, enteric cysts, aneurysms, bochdalek
hernia.
Clinical: usually asx. When they cause sx, its d/t to compression like cough, dysphagia, nerves etc
Dx: Chest CT is test of choice. If it looks benign and pt is asx then observation is tx.

Pleural Effusion
Gen: caused by – increased drainage of fluid into pleural space, increased production of fluid by cells
in the pleural space, or decreased drainage.
- Transudative: due to elevated hydrostatic pressure or decreased oncotic pressure
o CHF, cirrhosis, PE, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, atelectasis
- Exudative: caused by increased permeability of pleural surfaces or decreased lymphatic flow
because of damage to membranes or vasculature.
o Bacterial PNA, TB, malignancy, viral infxn, PE, collagen vascular disease.
o Meet at least one of Light’s criteria
 Pleural protein/serum protein > 0.5
 Pleural LDH/serum LDH >0.6
 LDH > 2/3rd the upper limit of nml serum LDH.

Pleural Fluid analysis
- elevated amylase: esophageal rupture, pancreatitis, malignancy
- Milk, opalescent: chylothorax (lymph in the pleural space)
- Frankly purulent: empyema (pus in space)
- Bloody: malignancy
- Exudative effusions that are primarily lymphocytic: TB
- pH < 7.2: parapneumonic effusion or epyema
Dx: CXR is initial, CT more reliable, thoracentesis is dx and tx for bigger effusions
Tx:
- Transudative
 Diuretics and sodium restriction
 Therapeutic thoracenesis if massive and causing dyspnea
- Exudative: treat underlying dz
o Parapneumonic (effusion in presence of PNA)
 Uncomplicated (effusion isnt infectious itself) – abx
 Complicated or empyema (the effusion is also infectious)
 Empyema – aggressive thoracentesis plus abx
 Chest tube drainage
 Intrapleural injection of thrombolytic agents
(streptokinase or urokinase)
 Surgical lysis of adhesions may be required.

Spontaneous Pneumothorax
Tx
- primary spontaneous
o if small and pt is asx – observation (should resolve in 10 days). Small chest tube may benefit
some
o if larger or sx – supplemental O2, needle aspiration/chest tube
- secondary spontaneous (d/t underlying lung dz) – chest tube
Tension Pneumo
Causes: mechanical ventilation w/ barotrauma, CPR, trauma
Clinical features: Hypotension, JVD/neck veins, shift of trachea away, decreased BS, hyperresonance
Tx: medical emergency
- immediate chest decompression with a large-bore need (in 2nd or 3rd ICS of midclavicular
line) followed by chest tube

Interstitial Lung Disesase – general
-PFTs: FEV1/FVC ratio is increased. All lung volumes are low. Low DLco.
-CT can usually be enough for dx. Bx to confirm.
-CXR: reticular, reticulonodular, ground-glass, honeycombing. Depn on severity
ILD – a/w granulomas
Sarcoidosis
- systemic noncaseating granulomatous diseases almost always involving lungs. Usually black
women
- Clinical features
o Consitutional
o Lungs – dry cough, dyspnea
o Skin
o Erythema nodosum, plaques, nodules
o Eyes – anterior uveitis MC
o Heart – arrhythmias, etc (uncommon but MCCOD)
o Msk – arthralgias and arthitis and bone lesions
o Neuro – bell’s palsy, optic nerve dysfunction, papilledema, peripheral neuropathy.
- Dx
o CXR – bilateral hilar adenopathy

o Elevated ACE in serum
o Hypercalciuria and hypercalcemia
o Definitive dx is noncaseating granulomas on transbronchial bx plus clinical.
o PFTs a/w ILD
- Tx: Systemic corticosteroids. Mtx if unresponsive
Histiocytosis X
- 90% of pts are smokers
- variants include eosinophilic granuloma (localized to bone or lung), and 2 systemic forms –
Letterer-Siwe dz and Hand-Schuller-Christian syndrome
- dyspnea and nonproductive cough
- steroids sometimes helpful. May need transplant
Wegener granulomatosis (WeCkner’s)
- necrotizing granulomatous vasculitis
- affects vessels of lungs, kidneys, upper airway, and sometimes other organs
- manifestations: upper and lower respiratory infxns, glomerulonephritis, and pulm nodules.
- Dx: C-ANCA increases likelihood. Gold standard is bx.
- Tx: immunosuppression (cyclophosphamide for ex) and glucocorticoids.
Churg-Strauss syndrome
- granulomatous vasculitis in pts with asthma
- presents with pulm infiltrates, rash and eosinophilia
- a/w P-ANCA
- Tx: systemic glucocorticoids

ILD – Environmental/Pneumoconiosis
Coal Worker’s pneumoconiosis – inhaltion of coal which contains carbon and silica
Asbestosis
- develops 15-20 years later
- increased risk of bronchogenic carcinoma (smoking is synergistic) more commonly, and
malignant mesothelioma.
- CXR shows hazy infiltrates with bilateral linear opacities and may show pleural plaques
- No specific tx.
Silicosis
- Localized and nodular peribronchial fibrosis (upper lobes are more common)
- Can be acute or chronic; CXR findings of egg shell calcifications
- a/w increased risk of TB
- sources include mining, stone cutting, and glass manufacturing
- tx is removal from exposure.
Berylliosis
- aerospace or nuclear industry workers
- acute disease  diffuse pneumonitis. Chronic dz  looks like sarcoidosis
- beryllium lymphocyte proliferation test is useful
- glucocorticoid tx for acute and chronic

ILD a/w Hypersensitivity
Hypersensitivity Pneumonitis
- chronic exposure can lead to ILD
- causes
o farmer’s lung – moldly hay aka spores of thermophilic actinomycetes
o bird-breeder’s lung – bird shit
o air-conditioner lungs - spores of thermophilic actinomycetes
o bagassosis – moldy sugar cane aka spores of thermophilic actinomycetes
o mushroom worker – compost aka spores of thermophilic actinomycetes
o dx by serum IgG and IgA to antigen
o acute form is flu-like. Chronic is more insidious
o tx is removal

Pulmonary Alveolar Proteinosis .. Definitive dx is bx. hyperthermia) . more common in men . Hypoventilation – leads to hypercapnia with secondary hypoxemia . CXR has a ground glass appearance with bilateral alveolar infiltrates that resemble a bat shape. DKA. bilateral infiltrates on chest imaging. Increased CO2 production (e. Do NOT give steroids cuz they are at increased for infxn. CT scan is best and shows diffuse infiltrates. Hemorrhagic pneumonitis and glomerulonephritis. acute onset ( <1wk) .. Figure 6 .A-a gradient is nml if hypoventilation or low inspired PO2 is the only mechanism . CXR follow clinical severity . A-a gradient. congenital heart dz  Not responsive to O2 . dry cough. AI dz caused by IgG abs against the glomerular and alveolar basement membranes (Type 2 HSR against Type IV collagen) .g. dx: Cxr has ground glass or honeycombed.g. . treatment not really effective: O2.Alveolar Filling Disease Goodpasture syndrome . ILD – Miscellaneous Idiopathic Pulmonary Fibrosis . hypercapnia (PCO2 >50) -To determine cause of hypoxemia. Hemoptysis and dyspnea.. (abx are not helpful) Radiation Pneumonitis – interstitial inflammation leading to fibrosis. Tx: steroids Acute Respiratory Failure -General criteria for resp failure: hypoxia (PaO2 <60).g. sepsis. Similar clinical and radiographic features to infectious PNA . steroids. lung transplant Cryptogenic organizing pneumonitis (COP) . and rales . Lung bx required for definitive .. Shunting  Little or not ventilation in perfused areas (d/t collapsed or fluid-filled alveoli)  Causes: atelectasis or fluid buildup (PNA or pulm edema). PE)  Typically leads to hypoxia without hypercapnia  MC mechanism of hypoxemia and responsive to supplemental O2 . pulmonary edema) or perfusion (e. cyclophosphamide. then both PaCO2 and A-a gradient are elevated. Tx: steroids. V/Q Mismatch  Caused by defect in either alveolar ventilation (e. response to O2 differentiates between to mechanisms. and corticosteroids.g. Exclude all other causes . you need: PaCO2 level. Diffusion impairment (e. hypoxia.Eosinophilic PNA – fever and peripheral eosinophilia that may be acute or ILD .If V/Q mismatch or shunting is present. response to supplemental O2 . Tx: lung lavage and GCSF. caused by accumulation of surfactant-like protein and phospholipids in the alveoli . dyspnea. ILD) causes hypoxia without hypercapnia ARDS Definition . Treat with plasmapheresis. may be normal.

pulmonary edema not explained by fluid level or CHF (e. OSA) . permanent lung injury causing scarring and honeycomb . barotrauma secondary to high pressure ventilation (pneumothorax)  tracheomalacia (softening) can be caused by prolonged ET intubation over 2 weeks so a tracheostomy is placed at 2 weeks to prevent . oral CCBs. mechanical ventilation – High PEEP and low tidal volumes Complications: . stress ulcers . acute pancreatitis.. asthma. endothelin receptor antagonists (e. Sepsis is most common RF (so any infection) . abnormal movement of IV septum . ILD. prostacyclins.. toxic inhalation . fractures. ileus. Intracranial HTN . secondary to pulmonary disease Causes: usually COPD. The lower. Echo – dilated pulm artery. pulmonary vascular obliteration (collagen vasc dz) . obstruction (PE. massive transfusions. CXR – enlarged pulmonary arteries . abnormal PaO2/FiO2 ratio (<300. ECG – RVH/RAD .. bosentan) . PAH – use vasoactive agents like sildenafil. decrease in exercise tolerance . Severe trauma.g. near-drowning . Drug OD. Transplant. OSA.g. renal failure . chronic hypoxemia. O2 and other supportive care . passive d/t resistance in the heart (e. dilatation/hypertrophy of RA and RV. Causes: . caused by massive intrapulmonary shunting that is not improved by 100% supplemental O2 (requires high PEEP) Causes . recurrent PE. hyperkinetic (left to right shunts like ASD or PDA) .. nosocomial PNA . idiopathic primary – young women Signs: Loud P2 and subtle lift of sternum (RV dilatation). pneumoconioses Clinical: . RHF signs Dx: . CHF) .. critical illness myopathy Pulmonary Hypertension Def: mean pulmonary arterial pressure greater than 25mmHg at rest. multiple organ failure . line-associated infxns . COPD. Right heart catheterization – reveals increased PA pressure Tx: . Cariopulmonary bypass Tx: . the worse) . pulm artery stenosis) . usually underlying dz . pulmonary vasoconstriction (eg. CF. no clinical evidence of CHF or PCWP <18mmHg) . Aspiration of gastric contenst .g. Cor Pulmonale Gen: RVH with eventual RVF resulting from pulmonary HTN.

 100% cancer rate by 3rd or 4th decade. air embolism – trauma to thorax. fat embolism – long bone fractures (AMS. septic embolism – IVDU . then CT of chest. dental abnormalities. signs of RVF . . petechiae) . Continue for 3-6mos depn on RFs. Both UC and Crohn’s increases risk. Resulting in hypoxemia and hypercapnia leading to tachypnea. IVC filter if anticoagulation is CI’d GI Diseases -note EGD may appear as upper endoscopy Colorectal Cancer Dx: Colonoscope best. CXR: enlargement of RA. desmoid tumors. protein C/S def. benign soft tissue tumors. and PA . LMW heparin with goal of INR 2-3 bridged with warfarin or novel oral anticoagulant for long-term. A-a gradient is elevated. pelvis + PE to determine staging. ab.  Turcot . Leading to low PaO2 and low PaCO2 creating respiratory alkalosis. Random: . pregnancy/estrogen use Pathophysiology: Blood flow decreases in some areas of the lung and creates dead space. cyanosis and clubbing . sebaceous cysts. Also present elsewhere. indwelling venous/arterial lines . Liver MC site. RVH . Supplemental O2 . ECG: RAD. UC is just more so (surveillance after 8years). tPA  Consider when pt is hemodynamically unstable or evidence of RHF . If found.  CRC 100% by about 40.. schistosomiasis Random RFs – factor V Leiden. o This prevents new clots not existing one o LWMH has less complications than regular IV heparin. . Dx: note – V/Q scan is used if pt has significant renal insufficiency and thus CTA is CI’d Figure 7 Tx: . Thrombolytic (treats current clot)  Streptokinase. dyspnea. Sydromes:  FAP  AD mutations in the APC tumor suppressor gene. P pulmonale (peaked P waves)..  Hundreds of polyps in colon and commonly the duodenum. nephrotic syndrome. PPX colectomy  Gardner  FAP (so AD)plus oseomas. AT3 def. Echo: RV dilatation but nml LV size and function Tx: underlying dz and supportive care Pulmonary Embolism Sources: . RV. amniotic fluid embolism – during or after delivery . parasternal lift Dx: .

juvenile (under 10 yo) are highly vascular and common . genitals. childhood numerous colon polyps. rectal mass and feeling of incomplete evacuation.g. female genital tract. leukocytosis  Dx – CT ab/pelvis with contrast is test of choice  Barium and colonoscopy are contraindicated  Tx for uncomplicated  Outpatient: PO abx (cipro and metro for ex  Inpatient: IVF. IV Abx (cephalosporin plus metro for ex) . Single or multiple hamartomas (low malignant potential) that may be scattered through entire GI tract (small bowel and colon MC)  Pigmented spots around lips.  AD or AR polyps plus cerebellar medulloblastoma or glioblastoma multiforme  Peutz-Jeghers  AD. tubular is MC and has smallest risk of malignancy . brain. pancreas. stomach. oral mucosa. Diverticulosis Dx: for diverticulosis alone – barium enema is the test of choice Tx: high-fiber and psyllium Complications . LLQ. Only SMALL risk of CRC  Hereditarry nonpolyposis CRC – early onset CRC withOUT polyps  Lynch 1 – just CRC  Lynch 2 – family cancer syndrome. Painless rectal bleeding – usually no tx is needed unless its severe and you need surgery . NPO. breast. biliary tract). Diverticulitis  Complications  Abscess formation that can be drained percutaneously under CT guidance or surgery  Colovesical fistula  Obstruction  Perforation – surgery immediately  Clinical – fever. tenesmus. Lynch 1 plus increased number and early occurrence of other cancers (e. tubulovillous is intermediate . Rectal cancer: hematochezia. and palmar surfaces  Intussusception or GI bleeding may occur  Familial juvenile polyposis coli  Rare. o L side obstructs and R side bleeds (melena not hematochezia). shape: sessile is more likely to be malignant vs pedunculated. face. villous is greatest risk .. hyperplastic MC . inflammatory (pseudopolyps) are a/w UC Adenomatous polyps . skin. Higher recurrence rate Polyps Nonneoplastic . Think ECO  CRC is the mCC of large bowel obstruction in adults.

-Tx: stop offending agents and supportive measures (IVF. Arterial thrombosis  Atherosclerosis  Sx more gradual and less severe . perf. also: anorexia. cephalosporins -profuse watery diarrhea with crampy abdominal pain -complications: toxic megacolon. Typically stops on its own. Tx: . Angiodysplasia/AV malformation/Vascular ectasia – common cause of lower GI bleeding in adults over 60. Tx if necessary can be done by colonoscopic coagulation of the lesion or right hemicolectomy if really bad. Surgical decompression is last resory Pseudomembranous Colitis – C diff -MCC are clindamycin. . Heparin for venous thrombosis . Arterial Embolism  From heart  Sx are more sudden and painful than others . Intestinal infarction: shock and lactic acidosis. -tx: Surgical revascularization Ogilvie Syndrome -sx and radio evidence of LBO but there is no mechanical obstruction usually after trauma or surgery or serious illness or 2/2 to drugs. Acute Mesenteric Ischemia Types: . Plain ab film first to exclude other stuff.  Direct intra-arterial thrombolytics if necessary for embolus. Dx via colonoscope. Surgery resection if peritonitis develops Chronic Mesenteric Ischemia -caused by atherosclerosis -postprandial abdominal angina -significant weight loss can occur -dx: mesenteric arteriography. vomiting. support: IVF and broad-spec abx .  Tx for complicated is typically surgery. ampicillin. Venous thrombosis  Sx may be present for several days or weeks with gradual worsening  Hypercoagulability Clinical: Classic – severe abdominal pain that is disproportionate to PE . Check lactic acid when AMI suspected Dx: Mesenteric angiography is test of choice. mild GI bleeding. or advanced peritoneal signs . anasarca (widespread edema). arterial causes: direct intra-arterial infusion of papaverine (vasodilator) during arteriography. electrolyte repletion) -decompression is next step if above fails. electrolyte disturbances -dx: c diff toxins in stool -ab xray to r/o megacolon or perforation -leukocytosis Tx: . Nonocclusive ischemia  Splanchnic vasconstriction 2/2 to low CO  Usually critically ill pts .

Hepatic Encephalopathy -Precipitants: alkalosis. IV vasopressin (alternative to octreotide) other: TIPS and liver transplant B. Clinical: . asterixis. avoid toxic agents 3. Caput medusa D. hyperreflexia. oral vanco if resistant or can’t tolerate Chronic Volvulus Gen: MC site is the sigmoid colon. acute onset of colicky ab pain . Adding Vaccinations for hep A and B -Complications and associated clinical features 1. treat complications 4. Emergent surgery for cecal. Esophageal varices . pain films:  sigmoid – omega loop sign (bent inner-tube shape)  cecal – coffee bean sign (distension of cecum and small bowel) . N/V Dx: . hypokalemia. d/c offending med . treat underlying cause 2. Hepatorenal syndrome . TIPS 2. shifting dullness. obstipation. Paracentesis. liver transplant 5. infxn. Varices/Portal HTN A. rigidity. methotrexate) NASH Congestion secondary to RHF AI hepatitis PBC Inherited metabolic diseases (Wilson. hypovolemia -Clinical: AMS. fluid wave.massive hematemesis or melena ppx: nonselective beta-blocker acute: ligation. Rectal hemorrhoids C. IV octreotide (splanchnic vasoconstriction). Followed by cecum. rifaximin (decreases production) 3. barium enema shows bird’s beak Tx: sigmoidoscope decompression for sigmoid. Paracentesis for dx and Tx Tx: Low sodium and diuretics. Ascites – d/t portal HTN and hypoalbuminemia Dx: Distension. sedatives. metronidazole is drug of choice  don’t use in infants or pregnant . Cirrhosis Gen: Fibrotic replacement of damaged hepatocytes -Causes: Alcohol (MCC) Chronic Hep B and Hep C Drugs (acetaminophen. endoscopic sclerotherapy. hereditary hemochromatosis) Alpha 1 antitrypsin def Hepatic venoocclusive disease (after BM transplant) -Management 1. musty odor of breath -Tx: Lactulose (promotes excretion).. sigmoidoscopy: preferred dx and tx for sigmoid volvulus . GI bleeding. anorexia. US. distension .

liver transplant 5. gynecomastia. testicular atrophy 6. also psych disturbances). d-penicillamine . liver (primarily) .hypothyroid. Accumulates as ferritin and hemosiderin that lead to hydroxyl free radicals to affect: . joints – MC sites are 2nd and 3rd MCPs. rebound tenderness. Dx: . Hyperestrinism -spider angiomas.. liver bx . thyroid . nephrocalcinosis). HCC Management 1. treat complications 4. skin . pancreas . renal involvement (aminoaciduria. liver transplant . eye.cirrhosis .decreased TIBC/elevated transferrin saturation . elevated LFTs. heart – cardiomyopathy leading to CHF and arrhythmias .DM .markedly elevated serum iron and ferritin . zinc  prevents uptake of dietary copper  given alone in presymptomatic pts and pregnant pts or given in conjunction with d-penicillamine . strep pneumo -ab pain. 1st degree relatives must be screened Tx: . SBP -E coli. fever. etc. hips.hyperpigmentation .Vit K ineffective -Tx with FFP 7.low ceruloplasmin. Coagulopathy . monitor copper levels and liver and other signs of dz Hemochromatosis Gen: AR dz of iron absorption – screen siblings. palmar erythema. hyponatremia. hypotension. vomiting. Adding Vaccinations for hep A and B Wilson Disease Gen: AR mutation in the ATP7B gene Clinical features: deposition in liver.liver bx is required to for dx . gonads – hypogonadism in both sexes. low UOP -only tx is transplant 4. may lead to sepsis -Dx by increased WBC/PMNs from paracentesis -Tx: broad-spec abx (cefotaxime) until sensitivities 5. hypothalamus Dx: . secondary to renal hypoperfusion resulting from vasoconstriction of renal vessels.azotemia. Functional renal failure .-happens in advanced liver disease. CNS (EPS like parkinsonian. oliguria. avoid toxic agents 3.prolonged INR first then PTT . chorea.if diagnosed. klebsiella. knees . treat underlying cause 2.

asymptomatic or could have RUQ pain/fullness. and cirrhosis). infxn Clinical: UGI bleed. tumors. . . . Source can be anywhere along biliary tract Causes: Trauma (MCC). systemic. Fibrolamellar (not a/w hep and cirrhosis).Orgs: E Coli. -Dx: US or CT with IV contrast. papillary thyroid carcinoma. Liver transplant in advanced Hepatocellular Adenoma -benign liver tumor usually seen in young females. Complication: Anaphylactic shock --.paraneoplastic syndromes: erythrocytosis.MCC is biliary tract obstruction. LFTs. jaundice. Especially if a/w hep b or c -chemical carcinogens (aflatoxin. Tx: resuscitation. hypercalcemia. Klebsiella.Hep B/C serology. coagulation tests. No tx necessary usually Hepatocellular Carcinoma (HCC) Gen: 2 pathologic types: nonfibrolammelar (a/w HBV. Hydatid Liver Cysts Cause: infection from the tapeworm Echinococcus. Ligation or embolization may be necessary.hemochromatosis. Usually small and asx. Resectable and better. hypertrophic pulmonary osteodystrophy. Dx: . imaging. and anaerobes. Bx contraindicated d/t risk of rupture -Tx: resect if too large or about to rupture. proteus. Adols and YAs. RFs: -cirrhosis.liver bx – required . Usually unresectable and poor prognosis. Focal Nodular Hyperplasia – benign liver tumor without malignant potential in women with reproductive age. OCPs or pregnancy can increase size and cause complications like obstruction and rupture. OCP use.more likely to rupture than turn malignant. There is NO a/w OCPs. With RUQ pain and jaundice. and RUQ pain Dx: Arteriogram is diagnostic. Hemobilia Gen: bleeding into the duodenum from the CBD.HCV. Cavernous Hemangiomas -MC type of benign liver tumor. carcinoid syndrome. AFP is useful as a screening. wilson’s -hepatic adenoma (10% risk) -smoking -glycogen storage dz type 1 Clinical: -ab pain. . high cholesterol.Dx: CT or US -Tx: D/C OCPs and surgiccally resect if they don’t regress and they are large.AAT def . Liver Abscess – MC in R lobe Pyogenic: . .Clinical: Sick as shit. Cysts MC occur in the right lobe of the liver Tx: Surgical resection followed by Mebendazole. anabolic steroid use . thorotrast) . liver dz . surgery. hypoglycemia.either from rupture or spilling contents during surgery.genetic testing Tx: repeated phlebotomies and treat any complications. thrombocytosis. Other causes are spread of infxn or trauma . enterococcus. vinyl chloride.

1 g/dL Tx: Medical usually fails. After resolution do ERCP to decompress (sphincterotomy). low grade fever and leukocytosis -Dx: US that may show: thickened GB wall. emphysematous chole. -Dx: First test is imaging US/CT to find absecess and then Serologic (IgG immunoassay) establishes diagnosis. -Followed with early cholecystectomy.Charcot’s triad . -Note: Hepatic Abscess is the most dreaded complication and has a high mortality rate. jaundice. Transplant if progressed to cirrhosis. infxn. Jaundice Figure 8 Cholelithiasis and related diseases Stones: Black stones are usually d/t hemolysis and alcoholic cirrhosis Cholithiasis: biliary colic. Amebic: -MC in men. Perc drainage may be necessary if large (high risk of rupture) or refractory to treatment. Budd-Chiari Gen: Caused by occlusion of hepatic venous outflow leading to microbascular ischemia and congestion resembling cirrhosis clinically. Elective surgery if symptomatic Acute Cholecystitis: obstruction and inflammation (not infection) . diarrhea. NPO.RUQ pain that is constant. -Tx: IV metronidazole. analgesics. -Dx: 1st – US 2ND – ERCP (Gold standard) -Tx: ERCP Cholangitis . mostly idiopathic. pregnancy. perforation. serum ascites albumin gradient >1. trauma. Murphy’s sign. Dx: Hepatic venography. electrolytes. May require surgical drainage.ERCP/PTC after acute phase -Tx: IVF and IV abx. other RFs include cholecystoenteric fistula and porcelain gallbladder . Carcinoma of the Gallbladder -most are adenocarcinomas and in the elderly with a dismal prognosis -a/w gallstones in most cases. particularly. myeloproliferative DOs. Treatment is still removal or drainage.Dx: US/CT. pericholecystic fluid. Choledocholithiasis -Sx: RUQ/epigastric pain and jaundice.RUQ pain. -Note: acalculous cholecystitis is usually found in severe ICU pts. cholecystoenteric fistula with gallstone ileus. homosexual men. cancer. chronic inflamm. elevated LFTs .Tx: IV abx and percutaneous drainage. LFTs also elevated. . Surgery to place a stent in IVC or portacava. N/V hepatomegaly. Pentad – add AMS and septic shock (hypotension) -Dx: 1st – US (shows dilatation so usually good enough) . distended GB and stones -CT if identifying complications: gangrenous chole. Causes: Hypercoagulable states. IV ABX. Transmitted through fecal-oral route -Entamoeba histolytica -Clinical: fever. RUQ pain. and fever. Or do it emergently if no response to abx. empyema of GB -HIDA scan when US is inconclusive -If no GB is visualzied then cholecystitis is confirmed -Tx: Initially – IVF.

CT. estrogens. bronchus. N/V and anorexia. and heart valve dysfunction (tricuspid insufficiency and pulmonary stenosis) Acute Pancreatitis Gen: Inflammation resulting from prematurely activated pancreatic digestive enzymes that involve pancreatic autodigestion.most common site is appendix (can also be found in small bowel. -Hemorrhage -Grey turner sign: flank ecchymoses -Cullen: periumbilical ecchymoses -Fox sign: ecchymosis of inguinal ligament Dx: Labs are supportive CT is confirmatory -Lipase. Worse when supine and after meals. pancreas). – excess serotonin can lead to carcinoid syndrome: cutaneous flushing. ERCP -dx: HIDA scan with CCK. and others -Postop complications . MC location). HIV meds. peritoneal signs.Scorpion bites . infect.S.PSC is the major risk factor in the U. Coxsackie B) -Drugs: sulfonamides. Untreated can lead to rupture. wheezing abd pain. rectum. Low EF = dyskinesia -Tx: lap chole or endoscopic sphincterotomy. Lacks true epithelial lining. then debridement and abx are indicated . thiazide diuretics. .Pseudocyst -Encapsulated fluid that appears 2-3 weeks after acute attack. Appendicitis -Clinical diagnosis -signs of perforation: high fever. Clonorchis sinensis infestation (Hong Konx) Clinical: Obstructive jaundice and weight loss Dx: Cholangiography (aka ERCP or PTC) with stenting to help with obstruction Biliary Dyskinesia -motor dysfunctin of the sphincter of Oddi causing biliary colic without any evidence of stones on US. marked leukocytosis. etc.ETOH and gallstones are equally common . LFTs. kidney.Primary Biliary Cirrhosis vs.Post-ERCP .Proximal 1/3rd of CBD (aka Klatskin tumor.Necrosis -Sterile vs infected? Do a CT-guided percutaneous aspiration for gram stain -If infected. distal extrahepatic (best chance at resection). Primary Sclerosing Cholangitis Figure 9 Cholangiocarcinoma Gen/types: Most are adenocarcinomas . GALAW Complications: . intrahepatic (least common) .. tachycardia. furosemide.Viral infections (mumps. obsturction. other RFs – UC. diarrhea. hypercalcemia -Uremia -Blunt abdominal trauma (MCC in kids) Clinical: Ab pain radiating to the back. Can be severe (necrotizing) Causes: . sweating. choldochal cysts. toxic appearance) -carcinoid tumors originate from neuroendocrine cells and secrete serotonin .Pancreatic cancer -Hypertriglyceridemia.

ERCP is the gold standard but not routinely done. Early enteral nutrition in the first 72 hrs through NJ tube. NPO. If over 5cm – drain percutaneously or surgically. Chronic Pancreatitis Gen: Persistent inflammation with fibrotic tissue replacement and alteration of pancreatic ducts (stricture and/or dilation).CT with calcifications plus clinical presentation is diagnostic . recent glucose intolerance. -Dx: CT -Tx: If under 5cm –observation.Narcotic addiction (MC) . wt loss.DM . CT for staging -Tumor markers: CA-19. low-fat meals -Surgical: goal is to relieve pain -pancreaticojejunostomy – decreases dilated ducts – MC procedure -pancreatic resection Pancreatic Cancer (painless jaundice is NOT common in pancreatic cancer) Clinical: Ab pain (90% of pts). Clinical: same as acute but can also have steatorrhea and diabetes leading to malabsorption and weight loss. Dx: . eventually leads to irreversible damage and impairs endocrine/exocrine functions. migratory thrombophlebitis. If more than 30% of pancreas is necrosed. Tx: -Mild: supportive. -Amylase and lipase are NOT elevated Complications: . IVF -Severe: ICU (3 or more Ransom criteria). MCC is chronic alcoholism.Malabsorption/steatorrhea (late manifestation) -pseudocyst -pancreatic ductal dilation -CBD obstruction -Vitamin B12 malabsorption -Effusions -Higher risk of panc carcinoma Tx: -Medical tx: -Narcotics for pain -NPO -Panc enzymes and H2 blockers given together (enzymes decrease endogenous secretions after meals and H2 blockers prevent enzymes from getting degraded) -Insulin -Alcohol abstinence -Frequent. CEA Tx: -Whipple procedure . and Courvosiier sign (palpable GB) Dx: -ERCP is best for the actual panc cancer -Then. small-volume. ppx abx with Imipenam should be considered. Pain control. . jaundice.Hemorrhage (as shown by signs listed above): CT with IV contrast is study of choice -ARDS -Pancreatic ascites/pleural effusion -Ascending cholangitis -Abscess: 4-6 weeks later and less threatening then necrosis.

Worldwide = Chagas .=idiopathic (MCC) and AdCa of proximal stomach. Colonoscopy is the initial test. If bile without blood = LGI. then do colonoscopy -Occult blood – Colonsocopy first. -Melena – first EGD.weight loss. spinach.S. -neoplasm LGI Causes -Diverticulosis (painless) -angiodysplasia -IBD -CRC -polyps -ischemic colitis -hemorrhoids. Side note – if BUN/Cr is elevated.odynophagia – late in course -hematemesis. GI Bleeding UGI Causes (if melena. -ERCP/PTC with stent for palliation if biliary obstruction is present and the tumor is unresectable. charcoal. If nothing then EGD -Radionuclotide testing can detect blood at slower flow rates but doesn’t localize -Arteriography definitively locates (can also tx with vasoconstrictor) -Ex lap is last resort – not responding to resuscitation Dysphagia DDX Chart Figure 10 Esophageal Cancer Gen – SCC d/t smoking and drinking usually. If nothing found. If blood = UGI (usually) -Hematemesis – EGD is initial test -Hematochezia – first r/o anorectal cause (hemorrhoids for ex). fistula -aspiration PNA d/t involvement tracheobronchial tree Dx: UGD with bx and mets workup if positive Tx: Palliative is usual tx. gastric erosions. and licorice). Esophagectomy if low staged or chemo + radiation Achalasia Gen – incomplete relaxation of the LES and aperistalsis of esophagus. Adca – GERD/Barrett’s Clinical . iron. note that dark stools can also result from bismuth. CP.dysphagia (solids then liquids) . Increased risk of SCC Causes – U. duodenitis -mallory-weiss tear -hemobilia -Dieulafoy’s vascular malformation – submucosal dilated arterial lesions that can cause massive GI bleeding -Aortoenteric fistulas – after aortic surgery/grafting – can lead to fatal hemorrhage – perform endoscopy or surgery immediately. anorexia . anal fissures -small intestine (dx after r/o UGI and colon) Tests: NG tube is often performed before anything. hoarseness. its more likely UGI -PUD -Reflux esophagitis -Esophageal varices -Gastric varices.

boerhaave syndrome . Tx: see Gen Mallory-Weiss Syndrome/Boerhaave Syndrome -forceful vomiting causing a tear in the mucosa at the GE junction  Mallory -forceful vomiting causing transmural tear  Boerhaave -hematemesis is always present and EGD is diagnostic -most mallory tears stop bleeding without treatment -otherwise surgery is required to oversew the tear or angiographic embolization. Tx: nothing really effective. CP. acids. correct nutritional deficiency Schatzki Ring (Distal esophageal webs) -a circumferential ring in the lower esophagus that is ALWAYS accompanied by a sliding hiatal hernia -usually d/t ingestion of alkali. arms.circular muscle layer of LES is incised Diffuse Esophageal Spasm Gen: Nonperistaltic spontaneous contraction of several segments of esophagus.sublingual NG. recurrent pulm complications secondary to aspiration Dx – Barium swallow  UGI endoscopy to r/o secondary causes  manometry to confirm Tx: . Sliding = GERD. Plummer-Vinson Syndrome (upper esophageal webs) Key features: upper esophageal web causing dysphagia.force dilatation: pneumatic balloon is most effective . Dysphagia. iron def anemia. bleach or detergents in suicide attempts -alkali causes full-thickness necrosis and perforation  esophagectomy -complications: stricture formation and risk of eso cancer -bougienage for stricture Esophageal Diverticula Upper 1/3rd – Zenker – underlying motility disorder – failure of the cricopharyngeal muscle to relax during swallowing leads to increased pressure and outpouching pharyngeal constrictors – dx with barium swallow – tx is cricopharhyngeal myotomy Mid 1/3rd – Traction – d/t traction from contiguous mediastinal inflammation and adenopathy (like pulmonary TB) – usually no treatment Lower 1/3rd – Epiphrenic – underlying motility disorder – a/w DES or achalasia – dx with barium swallow – tx esophagomyotomy Esophageal Perforation Causes: blunt trauma. (regurg is uncommon) Dx: Initial – Barium swallow showing “corkscrew esophagus”. and back. koilonychia (spoon-shaped fingernails) and atrophic oral mucosa -precursor for SCC -Tx: esophageal dilatation.botulinum toxin during endoscopy . nitrates.antimuscarinic agent (dicyclomine) (usually unsuccessful) . regurgitation.Clinical – Equal difficulty swallowing solids and liquids (vs. Manometry is diagnostic. Dysphagia. Paraesophageal = possible strangulation and needs surgery. weight loss. Sphincter function is normal Clinical: Non cardiac chest pain that mimics angina and may radiate to the jaw.surgical: “Heller myotomy” . CCBs may help in early stages . cancer). Can try nitrates and CCBs and TCAs for symptoms Esophageal Hiatal Hernias Gen: Think of sliding and paraesophageal. Acid suppression helps healing. Dx: barium upper GI series and EGD.

bismuth subsalicylate. May add chemo Gastric Lymphoma -Non-hodgkin’s lymphoma in the stomach that presents similar to gastric cancer -complications include bleeding. NG suction. replace electrolyte/volume deficits.Irish node – left axillary adenopathy Dx: EGD with biopsy followed by ab CT for staging Tx: surgical resection with extended LN dissection.Sister Mary Joseph – periumbilical LN . signs of peritonitis. UGD is dx and tx -resusitation and endoscopy. hemodynamic instability -upright CXR (free air under diaphragm). Ulcerative. and tetracycline fro 1 week. Bx is gold standard for H pylori though -triple therapy: PPI + amoxicillin + clarithromycin for 2 weeks.Virchow node – supraclavicular fossa nodes . supplement nutrition. Dx: -Contrast esophagram is definitive -CXR usually shows air in the mediastinum Tx: -small  IVF. H2 Blockers -large/unstable  surgery within 24hrs. IV ABX.Clinical: pain (severe retrosternal/chest/shoulder). epigastric fullness/early satiety. SIRS sx. -peptic ulcer disease is the MCC UGI bleed Acute/Chronic Gastritis . effusion. NPO. surgery usually necessary -most common with duodenal ulcers and prepyloric (type 3) gastric ulcers -GI bleeding -may be slow leading to anemia or rapid leading to shock -stool guaic. obstruction. Quadruple therapy: PPI.acute is very similar to PUD. surgery if nec. metronidazole. -Complications -perforation -acute severe ab pain. pneumothorax. polypoid. superficial spreading. saline load test -initially. relationship between eating and pain is not consistent. weight loss -barium swallow and upper endoscopy. and perf . Peptic Ulcer Disease -urea breath test can be initial test. linits plastica Metastases: -Krukenburg – ovary -Blumer’s shelf – rectum (pelvic cul-de-sac) – can palpate on DRE . Hamman sign (mediastinal crunch produced by the heart beating against air-filled tissues). CT is most sensitive -emergency surgery to close perf and vagotomy or vagotomy/pylroplasty -can progress to sepsis and death if untreated -gastric outlet obstruction -N/V.same dx and tx as gastric cancer Small Bowel Obstruction Gen: . -H pylori is the most common cause for acute or chronic -Autoimmune gastritis leads to chronic atrophic gastritis with serum antiparietal and anti-intrinsic factor antibodies (and possible development of pernicious anemia) Gastric Cancer Gen: The majority are AdCa.

cholelithiasis. minimal gas in colon Tx: -IVF and potassium -NG decompression -abx -surgery (lysis of adhesion and resect any necrotic bowel) if complete obstruction. severe pain. SBO.closed loop obstruction. NG suction. intussusception.Steroids for acute exacerbations and if no response to metro -steroids plus other immunosuppressants . skip lesions. mesenteric fat creeping Extraintestinal manifestations: uveitis. 2. anorectal disease. minimal distension. etc -causes hypochloremic. . metabolic alkalosis Sx: proximal – frequent vomiting.Distal – less vomiting and significant ab distension.Partial vs complete: partial can pass gas . correct electrolyte. pseudopolyps. ankylosing spondylitis. malignancy (less common than UC). more obvious on xray. pyoderma gangrenosum. shock. malabsorption of B12 and bile acids (so therefore DEAK vitamins def and cholelithiasis) Tx: . where the lumen is occluded at 2 points. erythema nodosum. Paralytic Ileus CXR: ileus vs SBO  ileus will have gas all throughout the intestines. joint pain and arthritis -dx: PAS positive macrophages in the lamina propria containing non-acid-fast gram-positive bacilli -tx: abx for up to 1-2 years Tropical Sprue -celiac sprue but lives in tropical region -same clinical and endoscopy findings -tx is abx and folic acid for 6 months or so Crohn’s disease Dx: endoscopy with bx – aphthous ulcers. the blood supply can be compromised (strangulation  perf. -hypokalemia is significant cause -failure to pass contrast medium beyond a fixed point is diagnostic -tx: IVF. aphthous oral ulcers. tube placement if necessary (no surgery) Celiac Sprue -best antibody test is anti-TTG -a/w vitamin deficiencies -osteoporosis (vit d) -easy bleeding (vit K) -megaloblastic anemia (poor folate and B12 absorption) -a/w dermatitis herpetiformis (papulovesicular lesion seen on the extensor surfaces) -Dx: biopsy of duodenum shows flattening of villi -tx: avoid gluten Whipple disease -inflammation secondary to infection and villi damages -weight loss.. and SMA syndrome Dx: Ab plain films – dilated loops. carcinomatosis. air-fluid levels proximal to obstruction. nephrolithiasis Complications: fistulae. diarrhea. arthritis.Sulfasalazine (better for UC but still works as anti-inflammatory) -metronidazole if no response to 5-ASA . strictures. chrons. strangulation.incarcerated hernias. noncaseating granulomas. 3 – malignancy. Causes: 1 – adhesions. Other pathology: transmural inflammation. cobblestone. NPO. hypokalemic. persistent partial.

palpitations muscle weakness -elderly: weight loss. -bile acid sequestrants (cholestyramine. Labs: Factors that increase TBG (and therefore total T4) include pregnancy. pretibial myxedema. ankylosing spondylitis. irritability. diffusely enlarged glang (with a viral illness) -Plummer disease and Hashimoto – bumpy. TBG is decreased by anabolic steroids. sclerosing cholangitis -dx: initial  stool cultures to r/o infectious causes. . toxic megacolon. Confirm with colonoscopy -complications: IDA. monitor leukocyte count for agranuloctosis -Immediate control of adrenergic sx: Propranolol -Non-pregnant with Graves disease -start methimazole + propranolol. cholangiocarcinoma. strictures. Used for refractory and complicated disease. Endocrine and Metabolic Disease Hyperthyroidism -causes . pyoderma gangrenosum. A radioiodide scan shows diffuse uptake -Plummer disease (multinodular toxic goiter) -hyperfunctioning areas that produce high T4 and T3 levels and decreases TSH levelsresulting in thyroid atrophy -Scan will have patchy appears on the scan -Toxic thyroid adenoma -Hashimoto thyroiditis and subacute granulomatous thyroiditis: both can cause transient hyperthyroid. Taper propranolol and continue methimazole -Pregnany with graves -PTU is preferred -Radioactive iodine ablation -leads to hypothyroidism in most pts. liver disease. iodine-induced. excessive levothyroxine -Clinical features -classic: nervousness. heat intolerance. diffuse enlargement -Subacute thyroiditis: exquisitely tender. -screening colo after 8 years with disease -Tx: -steroids for acute exacerbatioins -Topical Sulfasalazine is the mainstay (5-ASA is the active metabolite) -immuosuppresive to prevent relapses if refractive -surgery is often curative (unlike Crohns) and involves total colectomy. hemorrhage. -Young women usually.Graves (diffuse toxic goiter): MCC . IgG antibody binds to the TSH receptors and triggers excess synthesis.AI disorder. -other (rare): postpartum thyroiditis. -Tx: note . Afib -Graves: exophthalmos. thyroid bruit.for all pts on antithyroid medication. E+ disturbance. sweating. and aspirin. fecal leukocytes. OCPs. colon cancer. insomnia. tremor. weakness. colestipol) -surgical for complications -nutritional support Ulcerative Colitis -only involves mucosa and submucosa and is continuous -PMNs accumulate in the crypts of the colon (crypt abscesses -clinical: usually abdominal pain and hematochezia -extraintestinal: same as crohn’s with emphasis on arthritis. weight loss. hyperactivity. sclerosing cholangitis. diarrhea. irregular -Toxic adenoma – single nodule amongst atrophic gland.

mild normocytic anemia. PTU. -consider in the elderly with Graves. Least aggressive. dexamethasone (impairs peripheral conversion to T3 and supports adrenals) Hypothyroidism Random: Myxedema Coma – rare condition that presents with a depressed state of consciousness. meds (lithium) -Secondary/Tertiary: pituitary and hypothalamic disease respectively. iodine. anti- microsomal -goiter is MC feature -iatrogenic: surgery. a/w HLA-B35 -prodrometransient hyperthyroidismeuthyroidhypothyroid states -painful thyroid gland -Dx: radioiodine uptake is low. Labs: Other labs besides high TSH – elevated LDL and decreased HDL. Causes: -Primary: -Hashimoto’s (chronic thyroiditis) MCC and a/w other AI diseases (e. Supportive. Biggest RF is radiation. lupus. pernicious anemia) . Lymph spread to cervical nodes commonly -Tx: lobectomy with isthmusectomy or total Follicular: . antithyroglobulin abs. pts with solitary toxic nodule. Low TSH to begin with. corticosteroids for severe. betablockers. radioiodine therapy. Both have low TSH and T4. or stress (surgery. and respiratory depression. or those that are refractory to meds. IV thyroxine and hydrocortisone. Thyoid Storm -rare. Subacute lymphocytic thyroiditis – transient. Thought to present after years of untreated hypothyroidism that’s precipitated by a stress factor. childbirth for ex) . DKA. Papillary: -MCC..Supportive therapy. and high ESR -Tx: NSAIDs for mild. Most cancer are solid RFs: -Head and neck radiation (during childhood) -Gardner and Cowden syndrome for papillary cancer -MEN 2 for medullatry. Clinical (other than the typical) -menorrhagia -hoarseness -nonpitting edema (glycosaminoglycan in intersitial tissues) -non tender goiter Subclinical hypothyroidism: elevated TSH and normal T4. treat if thyroxine if symptomatic. nonspecific hypothyroidism signs. life-threatening complication of thyrotoxicosis look for AMS -usually a precipitating factor: infection. -US  cystic and solid.g. Cold suggests malignancy. Tx: medical emergency.Type IV HSR: antiperoxidase abs (90%). Similar to viral but painless Hashimotos (see above) Thyroid Cancer Nodule – FNA is the initial test of choice and is reliable in all but follicular (encapsulated) -Radioactive scans can be used when answer is indeterminate. Thyroiditis Subacute (viral) thyroiditis (subacute granulomatous thyroiditis) -usually follows viral illness. profound hypothermia.

Causes: -Prolactinoma -Meds (e. TSH Hypopituitarism: GH deficiency and hypogonadotropic hypogonadism are the MC problems Clinical: Mass effect . -may be a/w iodine def -needs tissue biopsy to look for vascular or capsule invasion -tx: total thyroidectomy with postop iodine ablation -variant: Hurthle cell carcinoma – cells contain abundant cytoplasm. and oval nuclei with prominent nucleoli (orphan annie). HTN. Medullary: parafollicular C cells – produces calcitonin. diabetes insipidus. Pituitary Adenomas Hormonal hypersecretion effects in order: Prolactin. H2 blockers. -hematogenous route so therefore distant mets can happen. or panhypopituitarism -Dx by MRI (calcification of suprasellar region). Bromocriptine or cabergoline (less s/e) 3. MEN2a + b -total thyroidectomy with radical neck dissection when LN involvement (which is most of the time) Anaplastic: tx – chemoradiation and palliative surgery. Surgery Acromegaly -GH-secreting pituitary adenoma after epiphyseal closure (gigantism if before) -Cardiomyopathy (hypertropic) is the MCC of death -Non growth clinical features: DM and hyperhidrosis.. and GH are usually lost first Causes: . estrogen) -pregnancy -renal failure -suprasellar mass lesions (compressions) -hypothyroidism -idiopathic Tx: 1. Oral glucose suppression test fails to suppress GH confirms if the IGF-1 level is equivocal -MRI of pituitary -don’t just do a random GH level Tx: transphenoid resection -radiation therapy if IGF levels remain elevated -octreotide or other somatostatin analog to suppress GH secretion Craniopharyngioma -rathke’s pouch remnant -suprasellar sx. for which medical management should be tried first) Hyperprolactinoma Gen: High levels of prolactin inhibit secretion of GnRH which leads to decreased FSH/LH and leads to decreased production of estrogen/testosterone  hence the hypogonadotropic hypogonadism being the MC problem. verapmis.hypothalamic or pit tumor MCC . tightly packed mitochondria. psychiatric meds. GH. treat is surgical w or w/o radiation Hypopituitarism Gen: loss of hormones are unpredictable but LH. parasellar manifestations. ACTH. Radioiodine resistant. OSA -30% also have hyperprolactinemia Dx: IGF-1 (somatomedin C) is significantly elevated. FSH.HA and bitemporal hemianopsia Dx: MRI is the study of choice. Treat underlying cause 2. May cause hyperprolactinemia.g. Also get hormone levels Tx: Transphenoidal surgery in most pts (except prolactinomas. metoclopramide.

cirrhosis for ex) -SIADH – volume expanded without edema Causes: many random ass ones like neoplasms. Chlorpropamide also increases ADH and enhances effect Nephrogenic – sodium restriction and thiazide diuretics. trauma. mild hypernatremia Dx: -Urine: low specific gravity and low osmolality indicate DI -Serum Osmolality -nml: 250-290 mOsm/kg -primary polydipsia: 255-280 -DI: 290-310 -***water deprivation test is required -Normal patients and polydipsia patients will have an increase in urine osmolality after dehydration without further response to ADH -Central DI pts will not have an increase in urine osmolality after dehydration but will have a response to ADH -Nephrogenic DI will not respond to dehydration or ADH Tx: Central – DDAVP. things affecting hypothalamus Nephrogenic DI -MCC is chronic lithium use. edema is not seen because of natriuresis occurs despite hyponatremia (so volume expansion correction wins out) -volume expansion increases atrial natriuretic peptide -volume expansion leads to decrease proximal tubule Na absorption -RAA system is inhibited Hyponatremia pearls -hypovolemic hyponatremia – volume contracted -hypervolemic hypernatremia – volume expaned with edema (CHF. hemochromatosis). etc Clinical features: acute hyponatremia . Congenital mutation in ADH receptor gene or the aquaporin-2 gene. cavernous sinus thrombosis. infiltrative (sarcoidosis. pulm disorders. CNS disorders. loss of libido -ADH (hypothalamic lesion): DI -MSH: decreased skin and hair pigmentation Dx: low levels of target hormones and normal/low trophic hormones. polydipsia. . head trauma. Sheehan syndrome. Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) Pathophysiology: Excess ADH from the posterior pituitary or an ectopic source  leading to water retention and excretion of concentrated urine leading to hyponatremia and volume expansion  despite the volume expansion. -depletion of sodium leads to increased reabsorption in the proximal tubules which means that less water reaches the distal tubules. loss of secondary sex. surgery Clinical: -GH: growth failure (decreased muscle mass in adults). MRI may help Tx: replace Diabetes Insipidus Types: Central DI is most common – low ADH secretion by posterior pituitary -mostly idiopathic. Clinical: Colorless polyuria (5-15 L a day). increased LDL -Prl: failure to lactate -ACTH: adrenal insufficiency -TSH: hypothyroidism -Gonadotropins: infertility. amenorrhea. leading to decreased urine volume.radiation.

urine cAMP. myopathy. volume expansion without edema. PUD. panc. (and diuretics if severe hypercalcemia) Cushing Syndrome Gen: Syndrome – any cause of excess glucocorticosteroids. NM irritability d/t hypocalcemia (hyperreflexive. HTN. and virilizing. cataracts Dx: low serum calcium.e. mucosal neuromas. coma. ab striae. leads to brain swelling and neuro disorders like seizures. buffalo hump. gout. osteoporosis. normal thyroid and adrenal function. pituitary tumors 2a – medullary thyroid.Pts with pituitary tumor causing cushings will also have the hyperpigmentation (elevated ACTH to MSH) but pts with other types of cushings will NOT have hyperpigmentation Dx Figure 11 Tx: taper steroids or surgery Pheochromocytoma MEN Syndrome: AD with incomplete penetrance 1 – Parathyroid. ab striae. moon facies. normal Cr. natiuresis. Tx: -underlying cause -asymptomatic ---water restriction -symptomatic -restrict water and NS -hypertonic saline in severe cases but be careful cuz of CPM!!!!! -Na replacement should not exceed 0. death. osteitis fibrosa cystic -groans: muscle pain and weakness. DM -more specific: easy bruising. oral calcium in less severe -vitamin D supplementation Primary Hyperparathyroidism If PTH is normal with high calcium. sleep disturbances. shortened QT interval. lanugo hair. pheo . lethargy -other: polydipsia. hyperPTH 2b – medullary thyroid. acne. grand mal seizures). fatigue. Appearance (central obesity. weight loss Dx: Primary: PTH levels (note that in presence of hypercalcemia. anxiety. serum PTH inappropriately low. constipation -Psych overtones: depression. prolonged QT interval. chloride/phosphorus is >33 is diagnostic. marafanoid. Secondary: high PTH and a low or low-nml serum calcium. not exogenous steroids) -asceptic necrosis of femoral head with exogenous steroids -infections more likely due to impaired immunity . pheo. rickets/osteomalacia. high serum phosphate. hirsutism. a nml PTH is abnormal). hypercalciuria. d/t renal failure or vit d def Tx: surgery. low phosphate. its still primary hyperparathyroidism Clinical: -Stones: nephrolithiasis. easy bruising) -androgen excess manifesting as masculinization in females is only seen in ACTH-depn forms (i. Dx: Dx of exclusion – hyponatremia. low urine cAMP Tx: IV calcium gluconate in severe cases. HTN. anorexia. hypouricemia and low BUN. polyuria. facial nerve tap. panreatitis. Disease – pituitary adenoma Clinical: -nonspecific: obesity. nephrocalcinosis -bones: bone aches and pains.5mEq/L per hour Hypopituitarism Clinical: cardiac arrhythmias. Chronic can be asymptomatic or just have N/V because the brain adjusts via chronic loss of Na and K to decrease edema. BP cuff inflation.

can be carcinoma or hyperplasia -peripheral edema will be absent **-adenoma is cured by adrenalectomy but hyperplasia (bilateral) is NOT cured by surgery. But first do alpha blocker (phenoxybenzamine) followed by beta blocker Primary Hyperaldosterone -always suspect in a hypertensive pt with hypokalemia (and metabolic alkalosis) who is NOT on a diuretic. Positive if aldo:renin ratio is over 30:1 -to find cause: adrenal venous sampling for aldosterone levels – one side = unilateral.arise from chromaffin cells in the adrenal medulla or sympathetic cells extra-adrenal Lab: associated findings: hyperglycemia.Gen – most common extra-adrenal site is the organ of Zuckerkandl (aortic bifurcation) . Diabetes Mellitus (random) -Type 2 has a high concordance in twins so has a much stronger genetic component -type 1 is a/w HLA-DQ/DR . Most likely an adrenal adenoma. blood pressure will be low and thus RAA will be inactivated.imaging Tx: adenoma = surgery. Usually 21-hydroxylase deficiency -decreased cortisol and aldosterone leads to increased ACTH causing bilateral adrenal hyperplasia -virilization in females: female infants are born with ambiguous external genitalia but normal female ovaries and uterus. Dx: plasma ACTH level  high? primary low? Secondary.primary: Addison’s disease (idiopathic) is MCC in industrialized world and infectious disease (TB is MCC). Usually after abrupt steroid cessation or increased need after infection or surgery. Dx: -initial test: plasma alodosterone/renin. Bilateral hyperplasia = spironolactone Adrenal Insufficiency Gen: -secondary to chronic steroid use is the MCC worldwide. HLD. -MC clinical findings -weight loss -weakness/anorexia -pigmentation -nausea -postural hypotension -abdominal pain -hypoglycemia -hyperpigmentation in and hyperkalemia/hyponatremia fr low aldo occus in primary only -aldosterone is reliant on the RAA system. So since no mineralocorticoids are produced. Shows up as emesis and shock early in life Dx for 21 def: high levels of 17-hydroxyprogesterone Tx: Medically – cortisol and mineralocorticoid to shut off excess ACTH via negative feedback Surgically correct genital abnormalities early in life. not ACTH. HMA followed by CT Tx: surgical resection with early ligation of venous drainage. two sides = bilateral . Tx: Primary  daily po glucocorticoid and daily fludrocortisone (mineralocorticoid) Secondary gluco but no fludro Congential Adrenal Hyperplasia 1_ = HTN _1 = virilization -AR disease. (men have no abnormalities at birth) -21 def can be severe and salt wasting causing hypotension (with hyponatremia and hyperkalemia also from lack of aldo). hypokalemia Dx: urine VMA. Tx with steroids .

Laser photocoagulation is the tx -CN III involvement: remember that the pupils are spared -increased susceptibility of infection is d/t impaired WBC function. low glu. leads to an osmotic diuresis resulting in hyperglycemia. use insulin instead. C-peptide. low glu. proinsulin Insulinoma: high insulin. -metformin is contraindicated in patient with renal failure (creatine over 1. IVF. gabapentin. abdominal pain -kussmaul respiration (rapid.20 -critical to intervene before micro turns to proteinuria to prevent ESRD -hold metformin for 48hrs after radiocontrast to prevent renal damage -key characteristics of prolferative retinopaty are new vessel formation and scarring that can lead to vitreal hemorrhage and retinal detachment leading to blindness. hyperosmalarity >320. serum pH >7.3 (no acidosis) -tx: aggressive IVF. convulsions. Gastroparesis – metoclopramide DKA Gen: can occur in both types but is more common in type 1. (vs alcoholic KA which can be euglycemic) -HAGMA (required) -ketonemia (required) -potassium: initially high because of acidosis but as insulin is given a rapid hypokalemia can occur. high proinsulin Exogenous insulin: high insulin.02 to 0. Severe hyperglycemia. reduced blood supply and neuropathy -Neuropathy tx: NSAIDs. low glucose. normal proinsulin .5 -2 hour post-prandial over 200mg -screen all aduls over 45 q 3yrs with fasting glucose test -BP goal in type 2 is less than 130/80 and LDL is under 100 -most oral hypoglycemic agents are contraindicated in pregnancy. K ppx *ensure pt is NOT hypokalemic before insulin administration Complications – cerebral edema if glucose drops too quickly (add some glucose in IVF when its at about 250). Tx: Insulin. polyphagia. deep breathing) -fruity (acetone) breath -volume depletion is always present -polydipsia. polyuria. low-dose insulin (add some glucose in IVF when its at about 250) Hypoglycemia Clinical: sx occur at a blood glucose level of 40-50mg. low C-peptide Sulfonylurea: high insulin. 1. elevated epinephrine levels causing adrenergic sx. weakness -AMS (drowsy to coma) Dx: -serum glocose usually 450-850mg. often preciptiated by stress. plasma insulin. hyperchloremic nongap metabolic acidosis d/t large IVF Hyperosmolar hyperglycemic nonketotic syndrome -typically elderly type 2 diabetics. CNS findings are common (seizures for ex) -severe dehydration and osmotic diuresis -Labs: glucose >900mg.5 in men. TCAs. ketoemia. and there’ll be neuroglycopenic sxs (lethargy. and volume depletion Clinical features -N/V. high C-peptide. metabolic acidosis. high C-peptide. etc) Labs: measure glucose.4 in women) -sliding scale regular insulin is used for control for in-patient people -definitin of microalbuminuria: 30 to 300mg/day albumin-creatinine ratio of 0.-Dx of diabetes include one of the following -2 fasting glucose greater than 125mg -single glucose level over 200mg with symptoms -increased glucose level on oral glucose tolerance test -HGBA1C > 6.

hyperglycemia -tx: resect Somatostatinoma – classic triad: gallstones. hypoK. acidosis). -TIAs can involve either the carotid or the vertebrobasilar system -Lacunar stroke – small vessel thrombotic disease is d/t thickening of vessel walls not by thrombosis (Subclavian Steal Syndrome: -caused by stenosis of subclavian artery proximal to origin of vertebral artery – exercise of left arm causes the ipsilateral vertebral to supply the subclavian instead. dysarthria. . steatorrhea VIPoma – watery diarrhea (leading to dehydration. UE claudication -tx: surgical bypass) Clinical: -ACA – contralateral LE and face -MCA – aphasia. Dx: 1st – CT without contrast. hyperglycemia. diabetes. clumsy hand -thalamus: pure sensory deficit. junction of second and third portions of the duodenum inferiorly. diplopia. or obstructure. achlorhydria (VIP inhibits gastric acid secretion). -complications: GI hemorrhage. plasma and urine sulfonylurea levels Tx: glucose obviously. If pt is an alcoholic. and vertigo contralateral: homonymous hemianopsia with basilar –PCA lesions -Lacunar -internal capsule: pure motor hemiparesis -pons: dysarthria. give thiamine first! Insulinoma: Dx: 72-hour fast and do above labs Tx: resection 80-90% cure rate Zollinger-Ellison Syndrome (Gastrinoma) -90% are in the gastrinoma triangle: formed by cystic duct superiorly. Supportive – ECG. and neck of the pancreas medially. -leads to decreased cerebral blood flow and symptoms of vertebrobasilar arterial insufficiency -BP is left arm is less than in right arm. 2nd – MRI. stomatitis. Carotid duplex but MRA is the definitive for stenosis of the head and neck. but in ZES the gastrin increases substantially) -Tx: high dose PPI and attempt resection Glucagonoma -clinical: necrotizing migratory erythema (usually below the waist). perforation. Other: anti-insulin abs. Tx: -acute: -ABCs -tPA if within 3 hours and no obvious bleed risk. and hypercalcemia). decrease in pulse in left arm. dysphagia. glossitis. (normal response is for gastrin to be inhibits. Tx is resection CNS and PNS Diseases Ischemic Stroke Gen: -the most important risk factors are age and HTN. contralateral hemiparesis -Vertebral/basilar – ipsilateral: ataxia. Mets to the liver -Secretin injuection test is diagnostic test of choice. Po preferred if possible.

limb rigidity. vomiting. sudden transient LOC. retinal hemorrhages. Early and adjuvent -Amantadine: mild benefir. death. haloperidol. IVF. hydrocephalus (communicating). AMS. rebleeding. lower BP gradually. SIADH Tx: Gradual BP reduction (do not cause hypotension and reduce cerebal blood flow) -if BP is >160/105 Subarachnoid Hemorrhage Common sites: -junction of anterior communicating artery with anterior cerebral artery -junction of posterior communicating artery with the internal carotid -bifucation of the MCA Clinical: Thunderclap HA. PSP causes progressive bradykinesia. AV malformation -usually located in the basal ganglia Clinical: Abrupt onset of a FND that worsens steadily over 30mins-90mins. do NOT perform LP cuz may cause a herniation -Once diagnosed. hydrocephalus. order a cerebral angiogram to detect site of bleeding for surgical clipping. vasospasm. signs of increase ICP -pinpoint pupils: pons -poorly reactive pupils: thalamus -dilated pupils: putamen Dx: Noncontrast CT Complications: increased ICP. seizures. Complications: seizures. (or give clopidogrel or ticlopidine) -Don’t give anticoagulants after stroke in the acute setting -no hypertensives unless very high and/or controlling post-TPA -goal is to prevent future strokes: CEA if symptomatic and >70% occlusion Intracerebral hemorrhage Gen: -HTN (particularly a sudden increase in BP) is the MCC -other: amyloid angiopathy. SIADH Tx: Surgical consult for clipping -stool softeners. reserpine) Shy-Drager syndrome = parkinsonian sxs + autonomic insufficiency Progressive Supranuclear Palsy -like PD. LP (diagnostic) if negative – blood in the CSF and xanthochromia (fr RBC lysis) -If papilledema is present. analgesia. CCB (nifedipine) for vasospasm Parkinson Disease Gen: loss of dopamine-containing neurons in substantia nigra AND locus ceruleus Tx: -Carbidopa-Levodopa is drug of choice -S/E: dyskinesias (chorea) after 5-7 years -shows an “on and off” effect later in the disease -Dopamine-receptor agonists (bromocriptine. HA/vomiting. Don’t use in older pts or demented -Amitriptyline -DBS if not response or severe disease before 40 Meds that cause PD: Neuroleptic drugs (chlorpromazine. vasospasm. brain tumors. eary disease -Anticholinergics (trihexyphenidyl and benztropine) -particularly helpful tremor. meningeal irritation. Dx: Noncontrast CT. -don’t give aspirin for the first 24 hrs -aspirin if over 3 hrs and after 24hrs post-tpa. perphenazine. cognitive decline but does NOT cause tremor and DOES cause ophthalmoplegia . Good for early on -Selegiline: MAOB inhibitor which increases dopamine activity. pramipexole). rebleeding. drugs (cocaine and anticoags).

and glatiramer acetate can be helpful if started early in the course Symptomatic: baclofen or dantrolene for muscle spasticity. decreased pupillary reaction -Internuclear ophthalmoplegia -lesion in the MLF results in ipsilateral medial rectus palsy on attempted lateral gaze and horizontal nystagmus of abducting eye (contralateral to lesion) -cerebellar involvement -loss of bladder control -autonomic -cerebral involvement -neuropathic pain (commonly hyperesthesia and trigeminal neuralgia) Dx: -clinical: 2 episodes -MRI -CSF with oligoclonal bands of IgG -abnormal evoked potentials Tx: Acute -High-dose IV corticosteroids Dmards: recombinant beta-1a and beta-1b. Very sensitive to neuroleptic agents’ side effects aka anti-psych aka anti-dopamine. pimozide. cerebral edema) Multiple Sclerosis Gen: -classic location of plaques is at the angles of the lateral ventricles -demyelination of white matter -must have 2 episodes of symptoms for diagnosis Clinical: -transient sensory deficit (MC initial presentation) -fatigue -motor symptoms (pyramidal tract involvement) -visual disturbances -Optic neuritis: monocular vision loss and painful movement. hep. neuroleptics are used for hallucinations and psychotic features. delerious patient unless there are contraindications (e.a/w with OCD -onset before 21yo -tx: clonidine. haloperidol Dementia vs. Clincal: -abrupt ascending weakness/paralysis of all 4 extremities. -Pick’s disease (frontotemporal dementia) has severe personality changes.Tourette Syndrome . HIV). you must avoid anticholinergics! -Dementia with lewy bodies initially have visual hallucinations then EPS features and fluctuating mental status. -Perform an LP in any febrile.g. Can lead to respiratory arrest. central scotoma. CMV. carbamezapine or gabapentin for neuropathic pain Guillain-Barre Syndrome (AIDP) Gen: -primarily affects motor nerves (but not only motor) -usually preceded by a viral or mycoplasmal infxn of URI or GI (esp: campy. Deliruim Figure 12 -Since pts with alzheimer’s already have low acetylcholine. However. .

neck trauma Vertigo Peripheral vs Central: Peripheral is more sudden. and cysts in multiple organs. severe. tensilon test. pancoast. with or without ataxia and/or weakness. a/w N/V. ipsilateral hemiparesis. and ipsilateral position/vibration Transverse Myelitis -usually thoracic horizontal aspect -cause is usually unknown. Younger women and older men. MS. Cavernous hemangiomas of the brain. low threshold for intubation (FVC of 15) Meds that exacerbate sx: aminoglycosides and tetracyclines. azathioprine or cyclorsporine. beta-blockers. renal angiomas. vertebrobasilar insufficiency. No inflammation. Also decreased motor NCS Tx: supportive  IVIG/PLEX. quinidine and procainamide and lidocaine. EMG (decremental response). CVA. -areflexia -autonomic features (arrhytmias. progression is rapid -LE weakness or plegia. Improved with rest. urinary retention (or other sphincter issues) -Dx with MRI -Tx: high-dose steroid Horner’s Syndrome – Causes – idiopathic. Pseudohypertrophy of calves Dx: CPK  DNA testing (no longer bx) Tx: Prednisone Becker MD is the exact same but some dystrophin is present VHL – AD. can be after viral infxns. no associated FNDs. but normal cell count. a/w RCC and pheos. Never give steroids. Central: tumor. areflexia. thymoma on CT. tachy. Duchenne Muscular Dystrophy Gen: XLR. Myasthenia Gravis Gen: Autoantibodies against nicotinic acetylcholine receptors at the NMJ. Lambert-Eaton which is abs against presynaptic calcium channels and sxs improve with repeated stimulation) Dx: AchR abs. plex/ivig. Muscles stimulated freq go weak. (vs. brainstem stroke. back pain. Tx: AchE. sensory deficits below the level of the lesion. hypotension) are dangerous complications Dx: CSF – elevated protein. Fischer-variant: ophthalmoplegia. migraine-associated vertigo Peripheral: . Syringomyelia -MC a/w arnold-chiari malformation -sx may include bilateral loss of pain and temp over the shoulder (cape-like) but preservation of touch -dx via MRI -tx depns on size (surgery) Brown-Sequard Syndrome -spinal hemisection usually at cervical region -usually caused by trauma/crush injury of spinal cord -contralateral loss of pain and temp. thymectomy. Clinical: Proximal fatigue as muscles are used more. intense nystagmus (vertical only). internal carotid dissection.

tinnitus. No atrophy Myopathy – acquried (vs dystrophy). normal sensation. EXCEPT IF LYME IS SUSPECTED -bilateral bell’s is found in GBS Trigeminal Neuralgia Dx: Clinical. sodium. Normal reflex. no anti-sm or dsdna -similar to SLE but does NOT affect CNS or kidneys and skin is usually not seen . Dx with dix-hallpike -Meniere: vertigo. cognition. Always do preg test before prescribing Figure 13 ALS Hallmark: upper and lower motor neuron signs Unaffected: bowel/bladder. Tx with sodium restriction and duretics -Acute Labrynthitis: viral. Seizures -if pt is unknown. brachial and lumbosacral Roots (radiculopathy) – pain is the key finding Peripheral nerve – weakness is worse distally. Several days -Ototoxic drugs: aminoglycosides. Tx is mainly supportive. extraocular muscles. no fasciculation. and hearing loss. sensation. sexual fxn. atazia Brainstem – specific CN findings. Atrophy and diminished reflexes late in course. MRI to r/o CPA tumor Tx: carbamezapine Localizing the lesion Cerebral cortex – contralateral motor and sensory Subcortical – hemiparesis is usually complete Cerebellar – incoordination. gait unsteadiness. some loop diuretics -acoutic neuroma (schwannoma) of 8th CN: ataxia. glucose. Often a/w a right hemiparesis Bell’s Palsy -unilateral. usually asymmetric NMJ – fatigability. and BUN -status epilepticus: treat with IV diazepam -anticonvulsants are teratogenic. Connective Tissue and Joint Diseases SLE Types: -Spontaneous SLE -Discoid lupus (skin lesions without systemic disease) -drug-induced -antihistone abs. Dx is helped with clinical or electrical evidence of 2+ regional involvement. -BPV: Tx with meclizine or epley maneuver. Symmetric if proximal. immediate check calcium. -steroids is the treatment. tinnitus. intention tremor. Riluzole is a glutamate-blocking agent that may prolong life. crossed hemiplegia (ipsi face and contra body) Spinal – level of lesion corresponds to the sensory level Plexus – motor and sensory involve more than one nerve. Normal sensation. hearing loss. nystagmus. Aphasia Conduction – disturbance in repetitition Global – all areas. both upper and lower parts of the face.

5g/day. telangiectases (over fingers and under nails) Dx: almost all have ANA -Limited = anticentromere ab -Diffuse = antitopoisomerase ab Tx: symptomatic Sjogren Syndrome Gen: -in patients with SS. cellular casts -CNS – seizures. ANA negative -risk of neonatal lupus in infants of affect women -Neonatal lupus -skin lesions. Lupus anticoagulant positive (yes I said anticoagulant) and/or anticardiolipin. -treat with long term anticoagulant (despite prolonged labs) Dx: 4 or more present at any time -mucocutaneous signs (each count as one) -butteryfly rash -photosensitivity -oral or nasopharyngeal ulcers -discoid rash -arthritis -pericarditis. valvular and septal defects) -Lupus anticoagulant: clotting.Raynaud Phenomenon -usually initial sx in both types -sclerodactyly -GI findings like dysphagia in both -pulmonary is MCCOD -pulm fibrosis is more common in diffuse -heart and renal -CREST is found in limited Calcinosis of digits. secondary is with another connective tissue disease . methyldopa. and quinidine -ANA-negative lupus -arthritis. psychosis -immunologic: positive LE prep. search for occult non-hodgkins lymphoma (LAD or HSM) -primary is SS alone. false-positive test result for syphillis (RPR). subacute cutaneous lupus -serology: Ro (anti-SSA) positive. raynaud. Prolonged PTT or PT that is NOT corrected by adding normal plasma. isoniazid. raynauds. recurrent miscarriages. chlopromazine. anti-SM Ab (either is diagnostic) -ANA Tx: -avoid sun exposure -NSAIDs for less severe sx -steroids for acute exacerbations -long term: Hydroxychloroquine (annual eye exam needed because of retinal toxicity) -glomerulonephritis: cyclophosphamide Scleroderma (diffuse and limited) Clinical: . transposition of great vessels). procainamide. -agents: hydralazine. sclerodactyly. anti-dsDNA. pleuritis -hematologic: basically pancytopenia -renal disease: proteinuria >0. esophageal dysmotility. cardiac (AV block.

RA. They take about 6 weeks so bridge with NSAIDs and then remove NSAIDs. subluxation and instability. -all RA pts should have cervical spine xrays before any surgery -Labs: RF (titers correlate with disease severity). -start DMARDs immediately. positive serum ACPA or RF. DMARDs for long term. -best is MTX -S/E: gi upset. infliximab) figure 14 Gout Pathogenesis: PMNs phagocytize monosodium urate crystals and release inflammatory mediators and proteolytic enzymes causing inflammation. sulfinpyrazone) if 24-hr urine uric acid is under 800mg because this indicated undersecretion. corticosteroids for exacerbation = pain relief. elevated CRP and ESR. increase ACH) -otherwise symptomatic tx Mixed Connective Disease -overlap syndrome with clinical features similar to SLE. fatigue. arthritis. bone marrow suppression (coadminister folinic acid) -others: leflunomide. Increased production -HGPRT deficiencies – Lesch-Nyhan syndrome -PRPP overactivity -increase cell turnover states Decreased excretion (most cases) -renal disease -NSAIDs. Use if excretion is more than 800mg. Watch for SJS . Contraindicated if hx of renal stones or renal dysfunction -allopurinol (xanthine oxidase inhibitor) decreases uric acid synthesis. sx lasting at least 6 weeks. diuretics.Clinical: dry eyes. systemic sclerosis. anticitrullinated peptide/protein antibodies -Dx: arthritis of 3 or more joints. arthralgias. sulfasalazine. interstitial nephritis and vasculitis Dx: ANA and RF can be present -Anti Ro/La aka SSA/SSB -risk of neonatal lupus with anti ssa -Schirmer test: filter paper inserted in eye to measure lacrimal output -salivary gland is most accurate but no necessary Tx: Pilocarpine or Cevmeline for ocular secretions (anti-cholinesterase inhibitors. anti-TNF (etanercept. dry mouth and tooth decay. hydroxychloroquine. Tx: -acute -NSAIDs (indomethacin is usually picked) -avoid aspirin and acetaminophen -Colchicine if they can’t take NSAIDs -Prednisone is 3rd line -PPx -wait till patient has had >2 attacks -uricosuric drugs (probenecid. radiographic changes consistent with RA (erosions and periarticular decalcification) -Tx: NSAIDs. and polymyositis -anti-U1-RNP antibodies Rheumatoid Arthritis -can involve any joint except DIP -cervical spine is common at C1-2. acidosis -Avoid thiazide and loop diuretics Dx: Joint aspiration and synovial fluid analysis – needle-shaped and negatively birefringent urate crystals. never use in acute gout.

-Dx: ESR elevated. No real chronic treatment Inclusion Body Myositis -Insidious onset with progressive proximal AND distal weakness. Clinical dx -Tx: Corticosteroids. -1st – NSAIDs. campylobacter. spondylodiscitis -tx: NSAIDs. chlamydia. decreased/absent peripher pulses. joint swelling. -acute tx is same as gout. temporal arteritis Med – PAN. vision (ophth artery involvement). -aspirate: weakly positively birefringent. osteoporosis. Asymmetrical -also lose deep tendon reflexes -no real labs or antibodies Polymyalgia Rheumatica -elderly patients. AV heart block. microscopic polyangiiitis Small – HSP. Kawasaki. -complications: restrictive lung dz. 2nd – MTX or anti-tnf Vasculities Large vessel – Takayasu arteritis. jaw -dx: ESR. yersinia -asx polyarthritis -no specific test.Pseudogout (Calcium Pyrophosphate Deposition Disease) -increase risk with age and OA of the joints. Churg-Strauss. hypersensitivity vasculitis. a/w hemochromatosis and hyperparathyroidism. BP discrepancies. Fibromyalgia -1st line tx is amitriptyline Ankylosing Spondylitis -stong a/w HLA-B27. anti-TNF Reactive Arthritis/Reiter Syndrome -don’t have to have the classic triad -common orgs: salmonella. constitutional. Behcet syndrome Temporal/Giant Cell Arteritis -granulomatous -a/w polymyalgia rheumatica and aortic aneurysm and dissection -HA. cauda equina. arterial bruits -granulomatous vasculitis of aortic arch and its major branches -Dx: arteriogram . nail pitting. prone to spinal fractures -other manifestations: anterior uveitis. r/o other shit with synovial analysis -Tx: 1st line – NSAIDs. shigella. ethesitis. Smaller joints more common. Negative RF -bilateral sacroiliitis is a prereq for dx -LBP and stiffness improve with activity. Bx confirms -Tx: start prednisone immediately. spinal fx. 2nd – Sulfasalazine. azathioprine Psoriatic Arthritis -asx and polyarticular. aortic insufficiency are the important ones. Wegner. rod-shaped and rhomboid crystals. Monitor ESR for improvement Takayasu Arteritis -young asian woman. sausage digits. a/w temporal arteritis -hip and shoulder muscle pain.

protein and blood -AIN: RBCs. Tx is steroids Buerger Disease (Thomboangiitis Obliterans) -young male smokers -segmental inflammation that may lead to digit gangrene and autoamputation -tx: smoking cessation Hypersensitivty Vasculitis -response to a drug. and bicarb (for hyperkalemia) -postrenal failure: both kidneys must be obstructive for Cr to rise. it is defined by lab and clinical findings of uremia. -UA: -prerenal = hyaline casts -muddy brown = ATN -acute glomerulonephritis = RBC casts. seizures etc). elevated ESR. Severe  add cyclophosphamide Behcet Syndrome -painful oral and genital ulcers. and platelet dysfunction -pts may show restless legs – pain only relieved by moving legs (neuropathic) . P-anca may be present -Tx: initial  steroids. HIV. (rituximab may work also) Polyarteritis Nodosa -nervous system and GI. >2-3% ATN) -rhabdo tx: IVF. anemia. GI (N/V. mannitol. vesicles on LE) -dx is bx. Churg-Strauss Syndrome -asthma. pericarditis (absolute indication for dialysis). and drug reactions. neuropathy. or other -skin lesions (palpable purpura. surgery may be required to recannulate stenosed vessels. treat HTN. eye involvement.-Tx: steroids first. pulm. C-anca. eosinophils CKD – random -defined as >3 months -ESRD is not defined by BUN/Cr. ESR elevated. arthritis. Tx is withdrawal of offender and steroids. -PMN invasion of all layers and fibrinoid necrosis leading reduced luminal area causing ischemia -necrosis is segmented leading to rosary sign as a result of aneurysms -Dx: bx or mesenteric angiography. Lung bx confirms -tx: cyclophosphamide and sterodis. WBCs with casts. renal (glomerulonephritis) -Dx: CXR. NO pulm -a/w hepatitis B. hematuria. skin lesions. CNS -often in middle easteners -dx is bx. Renal and GU diseases AKI – random -whenever a pt has elevated creatinine levels. eosinophilia -a/w p-ANCA -tx: steroids We(C)gner’s Granulomatosis -sinusitis. anorexia). -Uremia: Neuro dysfunction (AMS. the first step is to determine the baseline Cr -oliguria is ALWAYS found in prerenal failure -FENa is most useful in oliguria ( <1% = prerenal. infection.

proteinuria. HTN. HTN. Gross hematuria after URI or exercise is common -mesangial IgA and C3 on EM and IF Hereditary Nephritis (Alport syndrome) -XL or AD with variable penetrance -hematuria. hypoalbuminemia and edema. edema. Hematuria and HTN often present -resistent to steroids alone MemBRANous glomerulonephritis -MCC in adults -spike and dome on EM -can be due to Hep B and others IgA Nephropathy -asx recurrent hematuria/mild proteinuria. high-frequency hearing loss without deafness. progressive renal failure Secondary Glomerular DOs Diabetic nephropathy – MCC of ESRD HTN nephropathy Lupus Membranoproliferative GN -Usually due to hep c -common a/w cryoglobulinemia PSGN (PIGN) -MCC of nephritic syndrome -GAS infection of URT or impetigo -coca-cola urine. think glomerular dz -initial test: urine dipstick and UA -Nephritic syndrome: hematuria. hyperlipidemia. MCC of glomerular hematuria. azotemia Primary Glomerular Diseases Minimal Change Dz -nephrotic syndrome -MC in kids – lymphoma has been a/w it -fusion of foot processes on EM -tx: steroids Focal segmental glomerulosclerosis -nephrotic -more common in minorities. ethylene glycol.-correct hyperphosphatemia with calcium citrate (a phosphate binder) -intoxications that can be dialyzed: methanol. pyuria.5g/day). magnesium-containing laxatives Proteinuria Nephrotic syndrome -key features: urine protein ( >3. aspirin. hypercoagulable state -dx: dipstick  UA (fatty casts)  24 urine collection or albumin/Cr ratio Hematuria -defined as >3 erythrocytes/HPF on UA -gross painless hematuria = bladder or renal cancer until proven otherwise -if microscopic. proteinuria . lithium.

pulm hemorrhage. sulfas. UTI. cephalos. rifampin. and psych disturbance .treat underlying cause or remove agent Renal Tubular Acidosis – leads to NAGMA (hypochloremic) 1 (distal) -inability to secrete H+ -urine pH >6 -hypokalemia -nephrolithiasis and nephrocalcinosis DO occur -tx: sodium bicarb for acidosis and phosphate salts 2(proximal) -inability to reabsorb HCO3 -caused by fanconi’s in kids. sickle cell. tx is supportive Goodpasture Syndrome -triad: proliferative crescentric GN. anticoagulants. ataxia. causing nicotinamide def -leads to similar features as pellagra (niacin def): dermatitis. treat infection etc Renal Papillary Necrosis -most commonly a/w analgesic nephropathy (NSAIDS). PPIs -infection (esp kids): streptococcus and legionella -collagen vascular diseases and AI diseases Clinical: AKI with fever rash and eosinophilia. and IgG antiglomerular BM antibody. diuretics. diarrhea. and HAART Wegner’s PAN Acute Interstitial Nephritis Causes: -acute allergic rxn to meds is MCC: pens. UT obstruction. ACEI. diabetes. phenytoin. edema. MM in adults -so increase HCO3 excretion -nephrolithiasis and nephrocalcinosis DO NOT occur -tx: underlying disease (do NOT give bicarb cuz you can reabsorb) 4 (hyperaldosteronism) – still NAGMA surprisingly -decreased Na absorption and H and K secretion in distal tubule -results in hyperkalemia and acidic urine (so alkalosis) . pyuria and hematuria may be present Dx: UA – looks for eosinophils Tx: remove agent. light/heavy chain dz Sickle Cell Nephropathy HIV Nephropathy -proteinuria.ephrolithiasis and nephrocalcinosis rare Hartnup Syndrome -AR inheritence of defective neutral amino acid transporter -tryptophan for example. Cyclophosphamide and steroids can decrease formation of new abs Dysproteinemias – amyloidosis. alcoholism. and hematuria -Histo often resembles a collapsing form of FSGS -tx: prednisone. -lung disease usually precedes renal -linear IF pattern -treat with plasmapheresis to remove antibodies. allopurinol. and renal transplant rejection -Dx: excretory urogram – note change in papilla or medulla . -self limited.

acetazolamide. HTN. hyperPTH.seen in the AR disease. -diseases that precipitate: gout. antacids. HCO3 – leading to rickets in kids. Surgery if unsucessful (bypass) Sickle Cell Nephropathy -sickling in the microvasculature leading to infarction. -ACEI may be helpful Nephrolithiasis Gen: -ureterovesicular junction is the MC site of impaction. Abdominal bruit in fibromuscular. hexagon-shaped crystals (UA) . and high frequencies UTIs. UTIs. serratia. MVP. cystinuria. US. AA. Occurs mostly in the renal papilla and can lead to renal papillary necrosis. infection. If survive treat with respiratory management and renal replacement therapy Medullary Sponge Kidney -characterized by cystic dilation of the collecting ducts -may present with hematuria. or asx -may be a/w hyperparathyroidism (adenoma) -Dx: IVP -Tx: treat stones and infections Renal Artery Stenosis (Renovascular HTN) Gen: MCC of secondary HTN. type 1 RTA -Meds: loop diuretics. K. PO4. often severe HTN that is refractory to medical management. hematuria. Stenosis can be d/t atherosclerosis (MCC) or fibromuscular dysplasia in young females Clinical: Sudden. other cysts -Dx: US is confirmatory -Tx: drain if symptomatic and treat complications -ARPKD: infants usually -hepatic fibrosis is always present -pulmonary hypoplasia or full-on hydramnios and Potter sequence -dx is US. UA. RTA 2 -treat with supplementation and hydration ADPKD -AD or AR will correlate with severity and age of onset -ADPKD: pain. or nephrolithiasis. RF. stones. berry aneurysm.-give supplemental nicotinamide Fanconi Syndrome -acquired proximal tubule dysfunction that leads to defective transport of glucose. IVP -urine pH under 5. chemo (Uric acid stones) Types: -calcium oxalate: radiodense -uric acid: radiolucent and cannot be seen on ab radiograph – require CT. Na. Dx: Renal arteriogram is diagnostic but do not use if renal railure -RF  MRA Tx: Initial – revascularization with percutaneous transluminal renal angioplasty (PRTA) – best for fibromuscular dysplasia. Stenosis causes activation of RAA.5 promotes -gout or chemo -struvite (staghorn): radiodense rectangular prisms -recurrent UTIs with urease-producers (Proteus. klebsiells. crohn’s. enterobacter) -facilitated by alkaline urine – creates ammonium magnesium phosphate stones -cysteine: radiolucent .

phenacetin analgesics. Local excision is the most common route of spread. urine cytology. brain. Likely to recur after removal. or gonadotropins – feminization or masculinization. Cystoscopy and bx (definitive). Tx: radical nephrectomy (+adrenal gland is radical) for all Bladder Cancer Gen: 90% are transitional cell. nodular. -paraneoplastic: EPO secreting – PV. bone Rfs: smoking. exposure to heavy metals (mercury. flank/ab mass.Clinical: Sunden colicky flank pain that radiates to the groin and UA with hematuria. or if PSA has risen >0. industrial carcinogens (aniline dye.g. HTN Clinical: triad – hematuria.75 per year (PSA velocity) -carcinoma is hard. transrectal ultrasound (TRUS) with biopsy is indicated regardless of if the other test is normal. renin – HTN. LN dissection. liver. cadmium). removal of prostate/uterus/ovaries/ anterior vag wall. RFs: smoking. PTHrP – hypercalcemia. and irregular on DRE Tx: -disease in a pt that has less than 10 years  observation -localized disease  radical prostatectomy -complication: ED and urinary incontinence -locally invasive: give radiation therapy + androgen deprivation (see below) -Mets: reduce testosterone with -orchiectomy if pt is non-compliant with meds -anti-androgens (flutamide) -leuprolide (LH releasing hormone against -GnRH antagonists (Degarelix) Renal Cell Carcinoma Gen: Tumor thrombus invades renal vein or IVC and spread hematogenously to lung. flank/ab pain. Dx: CT without contrast aka spiral CT is gold standard for all types of stones -renal US in preggers Tx: -most stones: analgesia and vigorous fluids -Extracorporeal shock wave lithotripsy if pain isn’t controlled -best for stones 5mm-2cm -Percutaneous nephrolithotomy if lithotripsy fails -best for >2cm -prevention -hydration and avoiding purines (red meat) -thiazide diuretics reduce urinary calcium. DX: Renal US. Then stage Tx: -CIS: intravesical chemo A (lamina propria): transurethral resection B (muscle invasion): radical cystectomy. ADPKD. long-term tx with cyclophosphamide Clinical: painless hematuria Dx: UA and culture to r/o infection. ileal conduit) C (perivesicular fat): same as B D (mets): cystectomy and chemo Testicular Cancer . Constitutional sx.. and urinary diversion (e. cortisol – cushings. Cannot sit still. azo dyes). Then CT for staging. esp in pts with hypercalcemia -allopurinol in pts with UA stones Prostate Cancer Dx: If PSA is over 10 OR DRE is abnormal. Then. chronic diaylsis (multicystic dz develops).

50ml/kg for next 10. Do the CT and tumor markers after removal to compare. remove to confirm dx. tumor markers. Nongermcells are usually benign. Also signs of dehydration. coma. if renal failure  dialysis .Gen: more common 20-35. consider epididymitis (E coli infection in young and old. FNDs  confusion. Sx are worse when sodium increase was rapid. don’t correct >8 in the first 24 hrs. Tx: like hyponatremia. klinefelter Dx: PE. staging Tx: -if suspected based off PE and US. infarction may occur and you have to remove it. electrolytes and Acid-Base Disorders Maintenance fluids calculation -100 ml/kg for first 10 kg. G+C in adults) Fluids. PO oral fluids or D5W -hypervolemic hypernatremia – give diuretics and D5W. restlessness. seizures. to avoid cerebral edema -hypovolemic hypernatremia: give isotonic fluids to restore hemodynamics then replace free water deficit (Water deficit = TBW (1-actual Na / desired Na) -isovolemic hypernatremia: central DI – give vasopressin. RFs: cryptorchidism (surgical correction reduces but doesn’t eliminate risk). -if ruled out. 20ml/kg for every 1 kg over 20 so all adults just do 1500ml + (20xkg over 20) eg: 70 kg man: 1500 + (20x50) = 2500ml/kg/day divided by 24 = 104ml/hr Hyponatremia Causes/Classification: Figure 15 -urine Na concentration less than 40mmol/L is consistent with SIADH -note: hypothyroidism causes reduced GFR and thus hyponatremia (unknown how) Tx: -hypovolemic hyponatremia is obviously IVF replacement -isotonic and hypertonic hyponatremia: tx underlying disorder -hypotonic hyponatremia -mild (120-130): withhold free water -moderate (110-120): loop diuretics (given with saline to prevent renal concentration of urine d/t high ADH) -severe (<110): hypertonic saline to improve by 1-2 per hr -do not increase sodium more than 8mmol/L during the first 24 hrs in order to prevent CPM Hypernatremia Figure 16 Clinical: neuro sx predominate: AMS. -seminoma  add radiation -nonseminomatous  add retroperitoneal LND with or w/o chemo Penile Cancer -a/w HSV and HPV18 -presents as exophytic mass and treatment is local excision Testicular Torsion -will be in a higher position comparatively plus acute pain -surgical emergency  detorsion and orchipexia bilaterally -if delayed beyond 6hrs. Germ cells is most common (seminatous and non-seminomatous). weakness. US (initial).

malignancy) – bisphosphonates (pamidronate) and calcitonin -glucocorticoids if vitamin D-related (intox. coma and paralysis late -ECG: similar to hyperkalemia -tx: IV calcium gluconate for emergent sx. and renal impairment d/t excessive intake of calcium and certain absorbable antacids (calcium carbonate. So high PTH but low calcium. IV for severe Hypermagnesemia -Renal failure is the MCC -loss of DTRs is classic first sign. -hemodialysis if renal failure Potassium – need to correct magnesium in order to correct K (whether high or low) -serum K is affected by pH: Alkalosis leads to hypokalemia. a/w mental retardation and short metacarpal bones -cardiac manifestations: arrhythmias. total calcium is normal but free calcium lower because more is bound to albumin.g. alkalosis. AMS) -coexisting hypocalcemia is common because of decreased release of PTH and bone resistance to PTH when Mg is low -coexisting hypokalemia: in muscle and myocardium one affects the other -ECG: loss of t wave (like hypoK) prolonged QT  Torsades -PO mg for mild. acidosis can lead to hyperkalemia -if HTN and hypokalemia  think excessive aldosterone -Hypokalemia -causes: usually GI losses (urine K less than 20) or renal losses (urine K over 20)or insulin administration -random: Bartter syndrome -abx: bactrim and Amp B -epinephrine -hypokalemia predisposes to digoxin toxicity Hypomagnesemia -ETOH is a common cause -NM and CNS hyperirritability (twitching. Acid-Base Disorder equations 1. Use PCO2 to determine acidosis/alkalosis . Long term – calcium carbonate and vit D -Hypercalcemia -milk-alkali syndrome: hypercalcemia. granulomatous disorders) or MM are the cause. seizures. This is why you get symptoms (perioral numbness for ex) when hyperventilating -Hypocalcemia -pseudohypoparathyroidism: end organ resistance to PTH. especially acute alkalotic states: in respiratory alkalosis. hyperreflexia. milk) -cardiac manifestation: short QT -Tx: -1st step: IVF (1st) and diuretics -inhibit bone resorption in patients with osteoclastic disease (e. AR disorder. Saline and furosemide. but low in vit D def -normal vitamin D levels increase both calcium and phosphate -normal PTH levels increase calcium but decreases phosphate -tx: if symptomatic. prolonged QT -serum PO4 will be high in renal failure and hypoparathyroidism. Dialysis Hyperphosphatemia – tx is phosphate-binding antacids: aluminum hdroxide or carbonate. Dialysis if necessary.Calcium -changes in pH alter calcium binding. IV calcium gluconate.

2. pregnant women -microcytic. -alpha-thal -HbH disease: mutation/deletion of three alpha-loci -similar sxs and tx as beta-thal-major. calculated osmolar gap = 2Na + glu/18 + BUN/2. but Vomiting causes met alkalosis -first step in met alkalosis is to determine ECF volume (contraction vs expansion) -saline-sensitive: contraction usually with co-existing hypkalemia. May cause iron overload so typically given with defuroxamine. HEME/ONC Diseases Microcytic Anemias -retic count will typically be less than 2% cuz it’s a production problem -IDA -menstruation or GI typically.6 calc – serum osmolarity = osmolar gap. SO doesn’t work for ethanol cuz its in the calculation -diarrhea causes NAGMA. Delta gap = actual – normal if delta gap plus given HCO3 is more than 24 +/.2 if actual is more than expected then you have co-existing respiratory acidosis classic example of met acid and resp acid is an asthmatic child who has a PaCO2 that goes from abnormal to normal. adolescent women. -urine chloride will be low (less than 10) -saline-insensitive: expansion usually with HTN (d/t excess mineralocorticoids from adrenal pathology) -urine chloride will be high (>20) -tx with saline or aldosterone (until adrenal path fixed) -respiratory acidosis: -increased PaCO2  increased cerebral blood flow  increased CSF pressure. ringed sideroblasts in bone m arrow . RDW is typically high unlike the other micro anemias -nutritionial deficiency: kids 6mos-3years because of only human milk. and myelodysplastic dz -labs: increased iron and ferritin and TIBC saturation is normal/elevated (distinguishes it from IDA). typically mediterranean people. If over 10 then you have something else there  methanol or ethylene glycol or isopropyl alcohol. then you have a co-existing met acidosis 5. resulting in CNS depression. collagen vascular dz. severe anemia.2.2. hypochromic RBCs on blood smear -only consider IV iron if the cause is poor absorption or can’t tolerate oral iron -Thalassemias -Beta-thal -major -homozygous mutation. Winter’s formula: expected pCO2 = (1. Means impending resp failure required intubation if actual is less than expected then you have co-existing respiratory alkalosis 4.8 + Ethanol/4. massive HSM. expansion of marrow space (xray = crew-cut of skull) -dx: hemoglobin electrophoresis – HbF and HbA2 elevated -blood smear may have target cells -tx: transfusion dependent.5 x HCO3 + 8) +/. Electrophoresis will show high HbH -4 loci deletion cause hydrops fetalis -Sideroblastic anemia -caused by abnormality in RBC iron metabolism -hereditary or acquired – acquired causes include drugs (chloramphenicol. INH. lead exposure. Anion Gap = Na – (HCO3 +Cl) 3. then you have a co-existing met alkalosis if delta gap plus given HCO3 is less than 24 +/. alcohol).

dementia. High methylmalonic acid and homocyteine (vs Folate def) -antibodies to IF can dx pernicious anemia -schilling test: adding IF will result in more absorbed B12 and less in urine = pernicious anemia -Tx parenteral once a month – cyanocobalamin -Folate def -similar to B12 but no neuro and methylmalonic acid wont be high Normocytic Anemias – Production problem -decreased retic response <2% -Aplastic Anemia -BM failure leading to pancytopenia -causes: idiopathic. HIV). gold. membrane defects (e. sickle cells. sulfonamides. mechanical valves). demyelination of posterior columns.g. -Dx: peripheral blood smear showing macrocytic RBCs and hypersegmented neutrophls. carbamezapine). transfusion if nec.. folate supplements (folate is depleted in hemolysis) Sickle Cell Anemia -AR disorder.g. infections (e. radiation. They will have a constant osmolality on UA. incontinence. toxins (snake bite or brown recluse spider) -high (>2. transfusion rxns. chemicals (benzene.g.. -Clinical (other than obvious) -high-output heart failure: many die from CHF -aplastic crises: generally precipitated by parvo B19. EBV. hemoglobinopathies (e. Glutamic acid replaces valine at the 6 position of the beta-chain -Sickle cell trait is a/w isosthenuria – the inability to concentrate or dilute urine. insecticides) -expected signs of pancyto. ileal resection. clostridial sepsis). hypersplenism. Can transform to acute leukemia -Dx: BM bx for definitive – reveals hypocellular marrow and the absence of progenitors of all 3 hematopoietic cell lines -Tx: BMT. meds (chloramphenicol. decreased haptoglobin and Hgb/Hct -Clinical: jaundice. infections (e. Consider pyridoxine -Anemia of chronic disease -can be micro or normo (usually normo apparently) Macrocytic Anemias -B12 deficiency: -causes: Pernicious anemia (MCC). competitors (Diphyllobothrium latum and blind loop syndrome (bacterial overgrowth)) -clinical: anemia. CMV. Bartonella. not bilirubin  indicates intravascular) -spherocytes or helmet cells suggest extravascular -Tx-general: underlying cause.5%) reticulocyte count because BM is responding appropriately until it can’t keep up with hemolysis -labs: elevated retic.. LDH. underlying causes -Anemia of chronic disease (disscussed earlier) Normocytic Anemias – Hemolytic Anemia (HA) Intravascular hemolysis – microangiopathic HA (e. Hereditary spherocytosis). viral (HPV. -tx: remove offending agents. DIC. IVIG infusion. dark urine (from hemoglobinuria. transfusion if nec. crohn’s.g. impotence. HBV. thalassemia). alcoholism. poor diet (strict vegetatians (no fish or meat)). paroxysmal nocturnal hemoglobinuria (PNH). IV RhoD Ig infusion Extravascular hemolysis – Intrinsic RBC enzyme deficiency (e.g. gastrectomy. HCV. sore tongue. G6PD). warm or cold-agglutinin autoimmune hemolyitic anemia (most cases). Treat with transfusion -Dx: confirmed with hemoglobin electrophoresis -Tx: . malaria).g.

which anchors CD55 and CD59. or myelodysplasia -Dx: -Ham test: cells are incubated in acidified serum. WBC. aka other AI diseases). Measurement of G6PD levels is diagnostic -Tx: avoid and support Autoimmune Hemolytic Anemia (AIHA) -Warm: more common. -idiopathic (elderly) or d/t infection (mycoplasma pneumoniae or infectious mononucleosis) -Dx: Direct Coombs -if coated with IgG then its warm AIHA. hemolysis ensues -Best: flow cytometry for CD55 59 -TX: .e. RBC transfusions/chemo agents. collagen vascular disease (SLE. -vaccines for encapsulated bacteria -ppx with penicillin between 4mos-6years -folic acid supplements d/t chronic hemolysis -supportive management (hydration and pain control) for pain crises -hydroxyurea: enhances Hb F -transfusion based on clinical picture -BMT Hereditary Spherocytosis -AD defect in spectrin -Spherocytosis causes: HS. drugs like alpha-methydopa -Cold: IgM autoantibody that binds optimally at 0-5deg -causes complement activation and intravascular hemolysis. Leads to accumulation of H2O2 which denatures Hgb and it precipitates into a heinz body -Precipitants: SNP D and fava beans. hyperthermia. dimercaprol/dapsone and fava beans and infection -Dx: blood smear – heinz bodies and bite cells. IgG autoantibody that binds to RBC membranes best at 37 deg and results in extravascular hemolysis. Cold agglutination also -Tx: only if severe -Warm: glucocorticoids. -Cod: avoiding cold. that normally inhibit complement. ABO incompatibility. hepatic veins  budd-chiari) -ab. G6PD def. May have spherocytosis -if coated with complement then cold AIHA. msk pain -may evolve into aplastic. bactrim). AIHA -Dx: Osmotic fagility to hypotonic saline (spherocytes cant tolerate swelling and they rupture) -negative direct coombs test -Tx: splenectomy Glucose-G-Phosphate dehydrogenase deficiency -XLR (so mostly men). Sequestrated in the liver. Nitrofurantoin. Sulfonamides (i. triggering the alternative complement pathway leading to lysis of PNH cells -Sugar water test: serum mixed is sucrose.g. immunosuppression/splenectomy/RBC transfusions/folate suppl. steroids do NOT work Paroxysmal Nocturnal Hemoglobinuria (PNH) -acquired disorder resulting in deficient glycosylphosphatidylinositol. back.. and platelets -Clinical -chronic intravascular hemolysis reesulting in chronic PNH and elevated LDH -pancytopenia -thrombosis of venous systems can occur (e. Can be secondary to lymphoma/leukemia. primaquine. -splenomegaly is a common feature (sequestration) -usually idiopathic. Leads to lysis of RBC.

which are then removed by splenic macs -2 forms -acute: kids after viral infection. no splenomegaly -Dx: Plt <20. Thrombotic Thrombocytopenic Purpura -lack functional ADAMTS13 and this leads to ultra large vWF multimers -microthrombi (mostly platelet thrombi) occlude small vessels leading to microangiopathic HA (schistocytes). 2nd is intracranial bleed. Platelets aggregate leading to venous thrombosis (DVT/PE) -decrease in plt clount by 50% suggests HIT -Dx: antiplatelet factor IV ab or serotonin release assay -Tx: stop heparin. start thrombin inhibitor (lepirudin. -tx: adrenal corticosteroids. splenectomy in increasing order for severity. Emergency. Rest is normal. -PT and PTT normal -TTP=HUS + fever + AMS HUS = microangiopathic HA + thrombocytopenia + renal failure -Tx: immediate large volume plasmapheresis -platelet transfusions are contraindicated Heparin-Induced Thrombocytopenia -antibodies against heparin-platelet factor 4 complex -few days after heparin.000. Common – hemarthroses causing joint destruction -Dx: only PTT prolonged -Tx: analgesia and immobilization for hemarthroses. IVIG. Suspect if unsuspected hemorrhage occurs in a male pt with positive family hx -AIDS d/t past transfusion is the MCCOD. It also is the typical carrier for factor VIII -mucosal/cutaneous bleeding and menorrhagia -Dx: -prolonged bleeding time but nml plt count – PTT may be prolonged (cuz the FVIII degradation) so increased PTT and increased bleeding time -decreased titers or activity of FVIII -reduced ristocetin-induced plt aggregation -Tx: Desmopressin (DDAVP) 1st. Its synthesized by megakaryocytes and endothelial cells Hemophilia A -XLR disorder. doesn’t spontaneously resolve -clinical: petechiae and ecchymoses. -Hemo B: XLR def in FIX . Spontaneously resolve -chronic: 20-40 yo women. -Iron/folate supp -Eculizumab (mab that inhibits complement activation) Immune (Idiopathic) Thrombocytopenia -autoimmune IgG coat and damage platelets. FVIII concentrate mainstay when necessary for bleeding episodes. pre-surgery or dental work. If needed. dabigatran) Bernard-Soulier Syndrome -AR disorder of platelet adhesion (to subendothelium) d/t def in platelet glycoprotein GPIb-IX Glanzmann Thrombasthenia -AR disorder in platelet aggregation d/t def in glycoprotein GPIIb-IIIa von Willebrand Disease -AD disorder (MCC inherited bleeding DO) resulting in def vWF and thus disrupts plt aggregation and adhesion. FVIII concentrate 2nd -Only clotting factor not made in the liver. argatroban. bleeding of mucous membranes.

PTT.BM bx is essential for diagnosis and reveals at least 10% abnml plasma cells.Disseminated Intravascular Coagulation -Causes: infection (MCC). Anemia. *pts who’ve had 2 or more events should be permanently anticoagulated with warfarin Multiple Myeloma -proliferation of a monoclonal immunoglobulin. Renal failure. OB (placenta and uterus have tissue factor) – amniotic fluid emboli. -Recurrent infections 2/2 deprivation of normal plasma cells. LAD. Bone lesions (lytic) -Renal failure d/t -myeloma nephrosis – Ig precipitation in the tubules leads to casts of Bence jones protein -hypercalcemia also plays a role in renal impairment. D-dimer. splenomegaly and hyperviscosity -hyperviscosity syndrome can lead to retinal vessel dilation and hemorrhage  blindness -Dx: IgM >5mg. neuro. Fibrin split products. Pts with disorder DO NOT respond to heparin -Antiphospholipid antibody syndrome -can present with thrombosis. Decreased inhibition of factors V and VIII -Protein S def -cofactor of protein C. rattlesnake venom -labs are all abnormal: -Increased: PT. usually IgG or IgA -plasma cells take over normal cells in the BM -Signs: CRAB – calcium (hyperCa). recurrent preg loss. major tissue injury. shock. >50 . malignancy. Bence-jones. absence of bone lesions -Tx for hyperviscosity – chemo and plasmapheresis Hodgkin Lymphoma Gen -bimodal age: 15-30. abruptio placentae. ATIII is normally an inhibitor of thrombin. so def leads to increased thrombosis.other: peripheral smear shows RBCs in rouleaux formation from hyperglobulinemia -Tx: autologous stem cell transplant if younger and early in dz. Waldenstrom Macroglobulinemia -proliferation of plasmacytoid lymphocytes that produce IgM paraprotein. retained dead fetus. so same thing -Factor V Leiden -MC hereditary hypercoagulability disorder among whites -Protein C unable to inactivate FV -Prothrombin gene mutation -Hyperhomocysteinemia. bleeding time -decreased: fibrinogen (if it was nml/elevated then that r/o DIC). or thrombocytopenia (yes I said that right – also has false PTT prolongation) -see notes from earlier -Protein C def -AD. plt count -schisotcytes -tx: supportive. which causes hyperviscosity -sx: constitutional. TT. MCCOD -osteolytic lesions are d/t release of osteoclast-activating factor by the plasma cells -Dx: -Serum and urine protein electrophoresis (M protein) . and maybe cryoprecipitate (clotting factors and fibrinogen) or FFP (clotting factors) Inherited Hypercoagulable States -ATIII deficiency -AD inheritance. .

17) that often presents with pancytopenia. frequent infections -Dx: CBC: WBC = 50. night sweats. CML usually discovered on routine blood work (marked leukocytosis with left shift). CML follows indolent course and transforms to acute leukemia in a blast crisis -a/w t(9. leukomoid reaction which has increased leukocyte alk phos) What’s my age again? ALL = less than 15. Oncovin (vinchristine). weight loss) Dx: LN bx – RS cells are required Tx: Chemo + Radiation Non-hodgkins Lymphomas (NHL) -Epidemiology: burkitt = africa. hydroxydaunomycin (doxorubicin). splenomegaly.Low-grade. -histo: lymphocyte predominance (few Reed-sternberg (RS) cells). not attributed to infected. exposure to radiation or chemo. Can also have HSM and LAD.22) resulting in activated tyrosine kinase.e. also HSM and LAD -Dx: BM bx is required[ -watch for tumor lysis syndrome: medical emergency Chronic Lymphocytic Leukemia -MCC leukemia and typically over 60 yos -morphologically mature lymphocytes but functionally defective (i. Can be treated with all-trans retinoic acid and chemo -may have skin nodules -ALL (lymphoblasts) -MCC malignancy in kids under 15 -most responsive to therapy -may have testicular involvement or anterior mediastinal mass (T-ALL) -clinical features result from decrease in non-WBCs.B sx (fever.000-200. While intermediate and high-grade tumors are more responsive to chemo and have better chance of cure if they are treated figure 17 Acute Leukemias – affect more immature cells -2 types -AML (myeloblasts) -Adults. don’t differentiate into antibody-producing plasma cells) -nontender LAD. nodular sclerosis (bands of collagen surrounding pools of RS cells). Adult T-cell lymphoma = Japan and the Caribbean -Rituximab is often used in combo with CHOP (cyclophosphamide. mixed cellularity (large number of RS cells). -Dx: -WBC: leukocytosis with left shift and eosinophilia -blood smear: immature granulocytes and decreased leukocyte alk phos activity (vs. lymphocyte depletion (worse prognosis) Clinical: painless LAD that spreads by continuity from one LN to the next +/. should be biopsied . down’s -variant: APL t(15. Prednisone----CDVP) chemo -Any node over 1cm present for more than 4 weeks. Hence the treatment: TKIs (imatinib or other inibs) -constitutional sx are usually the initial sx. indolent tumors are unlikely to be cured but have better 5-year prognosis. AML/CML =40-60. smudge cells Chronic Myeloid Leukemia -middle aged. CLL = greater than 65 .000 and the rest is low -blood smear is often diagnostic: absolute lymphocytosis (mostly mature).

abnml shaped platelets -BM bx shows increased megakaryocytes -Jak2 mutation in ½ the pts -tx is antiplatelet agents such anagrelide and low-dose ASA. peptrostreptoccus. bacteroides other: s aureus. upper cavitation = TB -Culprits oral anaerobes: Prevotella. H/H (>50) -decreased EPO -BM bx confirms Tx: Repeated phlebotomy to lower Hct Essential Thrombocytosis -platelets over 600.= fluoroquinolone or cetazidime . Sometimes hydroxyurea Infectious Diseases Pneumonia -CAP -uncomplicated without significant comorbidities: azithromycin or clarithromycin -uncomplicated with comorbidities: flouroquinolone (levo or moxi) -hospitalized (not acquired) pt: fluroquinolone alone or ceftriaxone plus azithromycin -Hospital-acquired PNA: tailor towards gram-neg rods -ceftazidime or cefepime -imipenem -pipercillin/tazobactam -Ventilator-associated PNA: Combo of 3 drugs 1.Polycythemia Vera Gen: -increase in RBC mass independent of EPO -mutations in JAK2 tyrosine kinase in most cases Clinical -hyperviscosity: HA. Reactive must be r/o -smear shows hypogranular. people with renal failure or chronic lung disease. Aminoglycoside OR fluoroquinolone 3. s pneumo. aerobic gram-neg bacilli -foul-smelling sputum is consistent with anaerobic infxn and clues into the dx. Presents with GI sx and hyponatremia Lung Abscess -Dependent zones for aspiration leading to abscess: posterior segments of the upper lobes and superior segments of the lower lobes (more likely R side) -lower cavitation = aspiration.000. dyspnea classic: pt who complains of severe pruritis after a hot bath/shower -thrombotic phenomena (DVT. -Tx: until cavity is gone or CXR is improved -gram + = ampicillin or amoxicillin/clavulanic acid. MI. or vanco for aureus -anaerobes = clindamycin or MTZ -gram . visual impairment. Vancomycin OR linezolid -Legionella PNA is common in organ transplant recipients. and smokers. CVA) -bleeding -HSM and HTN Dx: -1st: R/O secondary polycythema -CBC: elevated RBC count. dizziniess. Ceftazidime or cefepime OR pip/tazo OR imipenam 2. fusobacterium. amp/sulbactam. weakness pruritis.

and choroidal tubercles in the eye -HIV pts: normal dx clues go out the window – PPD negative. VZV. reticulonodular infiltrates on CXR. and no granulomas Dx/Tx: -If PPD positive. Even if the pt had a BCG vaccine -PPD positivity -normal pt. west nile -Entero: polio for ex -less common: measles.cefotaxime or ceftriaxone + ampicillin + vancomycin -IC’d: Listeria. -If there’s no active disease. FND -Dx: -CSF will have lymphocytosis with nml glucose similar to viral meningitis (asceptic) -CSF PCR is a better test -MRI is imaging modality of chocie. T-cell lymphoma -Clinical -prodrome: HA. H flu -ceftiaxone or cefotaxime + vancomycin -Adults 18-50: S pneumo. H flu . next step is CXR to r/o active disease. N mening. malaise. and myalgias -acutely ill with signs of meningitis. no risk factors: >15mm is positive -Risk factors: >10mm is positive -Immunocompromised or abnormal CXR: >5mm -If symptomatic or has abnml CXR.ceftiaxone or cefotaxime + vancomycin -Elderly >50: S pneumo. gram-neg bacilli. and behavioral abnormalities. S pneumo. nuchal rigidity. Encephalitis -Organisms (usually viruses) -HSV -Arbovirus: EEE. AMS -MC orgs and empiric treatment -Neonates: GBS. S pneumo -ceftazidime (for psuedo) + amp + vanc -Aseptic: enterovirus and HSV usually. Supportive tx -CT is rec’d before LP to look for elevated ICP or lesions. delirium. mumps. or fungi -self-limiting. rabies.Tuberculosis -Xray findings in healed primary TB (so not active infxn): -Ghon complex: calcified primary focus with an associated LN -Ranke complex: Ghon complex undergoes fibrosis and calcification -Miliary TB: may present with organomegaly. Listeria -Empiric tx: cefotaxime + ampicillin + vancomycin (AG if <4weeks) -Kids >3mos: Neisseria meningitidis. parasites. Listeria . give isoniazid (plus B6 aka pyridoxine) for 9mos to decrease risk of active infection. cerebral aspergillosis -noninfectious: metabolic. -Tx: only have treatment for HSV (acyclovir) and CMV (ganciclovir or foscarnet) Viral Hepatitis . EBV. atypical CXR findings. next step is sputum acid-fast test -active TB = RIPE(S) tx and isolation until sputum is negative for acid-fast bacilli -only discontinue tx if LFTs rise to 3-5x the upper limit Meningitis -acute triad: fever. can also be certain bacteria. N meningitidis. prion disease -nonviral infectious causes: Toxoplasmosis. CMV. sputum more likely to be negative. E coli.

Lower UTI -no fever -presence of epithelial cells or bacteria without WBCs on UA indicates contamination -thus WBCs aka pyuria (greater than 10 leukocytes) is best indicator -don’t need a urine Cx unless elderly. Or give low-dose TMP-SMX for 6mos. uncomplicated UTI (any of these options) -Oral TMP/SMX for 3 days -Nitrofurantoin for 5-7 days – do not give if early pyelo is suspected -Fosfomycin 1 dose – don’t give if early pyelo is suspected -Cipro for 3 days -Phenazopyridine can be given for dysuria -Pregnant women -amp. If from wound. pregnant. IVF. bacteriuria. -wound contamination is another source -symmetric. HCV is a/w with cryoglobulinemia -HCV does not cause significant acute illness -HAV serology: anti-HAV persists for life. and leukocyte casts -obtain urine Cx in ALL pts with suspected pyelo -imaging if complicated or fails tx (renal US. -Tx -Acute. Then switch to PO for 2 weeks . Can be killed by cooking at high temps. or oral cephalosporins for 7-10d -Do NOT give Fluoroquinolones (can cause fetal arthropathy) -Men: same as women but for 7 days -Recurrent: PPX – single dose of TMP/SMX after intercourse or at 1st sx. -RNA is more useful for HCV -Chronic HBV tx: IFN-alpha -HCV treatment -IFN-alpha and ribavirin -newer cures: all end in –vir Botulism -results from preformed toxins (usually improperly stored food). IV amp plus gent until afebrile. recurrent UTIs. amox. stool. or use of a diaphragm. CT. then add cleaning and penicillin. elderly. Pyelonephritis -add less common organisms to the differential: Enterococcus faecalis and S aureus -complications -sepsis -emphysematous pyelonephritis: gas-producing bacteria in diabetics -chronic pyelo and scarring . descending flaccid paralysis (starts from face). or gastric contents -Tx: antitoxin (toxoid) and supportive respiratory care. -Dx: identifying toxin from serum. diabetes. or uroseptic -hospitalize.rare unless there’s underlying renal dz -UA: look for pyuria. IVP or retrograde urogram) -Tx: based on gram-stain -uncomplicated pyelo -TMP-SMX or fluoroquinolone for 10-14days for most gram negs -amoxicillin for gram-pos -a single dose of ceftriaxone or gentamicin if often given before PO tx -repeat cx after 48hrs.-HBV is a/w polyarteritis nodosa (PAN). unable to tolerate PO. sx lasting over a week. so IgM is acute and IgM is previous infection. if fails to respond  imaging -if patient is very ill. Usually a/w GI issues.

vibrio vulnificus -acute sinusitis = H influenzae -usually treat with a staphyloccal penicillin or a cephalosporin IV until signs of infection improve -Erysipelas is a cellulitis that is usually confined to the dermis and lymphatics -usually caused by GAS -*spectrum: cellulitis  erysipelas  necrotizing fasciitis -tx: PCN or erythromyciin -Necrotizing Fasciitis (deep soft tissue infection that goes to the fascial planes) -strep pyogenes (GAS) and C perfringens -pain out of proportion. IV if serious. -dx: clinical only and r/o other causes of ulcer -tx: azithromycin or ceftriaxone -Lymphogranuloma Venereum (caused by C. Tx: permethrin of all hairy areas. breaks in skin = GAS -wounds/abscesses = S aureus -immersion in water = Pseudomonas. and multiorgan failure -rapid surgical exploration and excision of devitalized tissues is absolutely necessary followed by broad-spec abx. aeromonas hydrophilia. -Tetanus -exotoxin in contaminated wounds that blocks inhibitory transmitters in the NMJ -Tx . give doxy or tetracycline -chancroid: painful genital ulcer(s) that can be deep with ragged borders and with a purulent base. crepitus. Tx partners -Cellulitis -local trauma. clothes. Acute is MC in younger men.Prostatitis -acute is less common than chronic. or towels -severe pruritis of pubes. trachomatis) -painless ulcer followed by tender inguinal LAD (unilateral usually) a few weeks later and constitutional symptoms -complication: proctocolitis may develop with perianal fissures and rectal strictures. necrosis. exquisitely tender prostate in acute disease) -UA and Urine Cx shows numerous sheets of WBCs and positive cx in acute -Chronic: presence of WBCs in expressed prostatic secretions -Tx: -acute: TMP/SMX or a fluoroquinolone and doxycycline. Other hairy areas can be involved too -Dx: visual inspection. gram-negs predominate and is more serious and requires tx -recurrent exacerbations and UTIs are common in chronic prostatitis -Dx: -avoid DRE because it my cause bacteremia (but its described as a boggy. can lead to cutaneous anesthesia -complications: sepsis. No constitutional findings. PO for 4-6weeks if mild -Chronic: fluoroquinolone for a long time (difficult to tx) Figure 18 Random infectious stuff -HSV-1 is a/w Bell’s palsy -Culture of HSV is the gold standard -syphillis: if allergic to PCN. Unilateral tender inguinal LAD (buboes) that appears 1-2 weeks after ulcer. toxic shock syndrome. Transmitted via sex. May even get lymphatic obstruction and elephantiasis -tx is doxycycline -Pediculosis Pubis (pubic lice aka crabs) -org: Phthirus pubis.

-complications (both gono and staph): destruction of surrounding structures.Rash start peripherally and spreads centrally. linezolid. -ICU and respiratory support (if nec) and give diazepam for tetany -passive immunization with single IM dose of tetanus IG followed by active with Td -Common bugs and osteomyelitis (OM) -catheter septicemia = S aureus -prothetic joint = coag-neg staph (s epidermis) -diabetic foot ulcer = polymicrobial -nosocomial = Pseudomonas -IVDU.systemic abx (tetracyclines. fluoroquinolones.000 -tx: staph drugs (MSSA or MRSA) for immunocompetent. Extend to gram-neg coverage if immunocompromised. daptomycin. fungal -sickle cell = salmonella -OM dx and tx -ESR/CRP are very useful in monitoring response to tx -needle aspiration or bone bx is the most direct and accurate way for dx -MRI is the most effective imaging study -Tx: IV abx (high bone penetration – cephalosporins. vanc. Rosacea -Tx: topical MTZ for acute. bactrim). Do not give in pregnancy (must have 2 negative preg tests before treatement and use 2 forms of birth control starting 1 month before till 1 month after treatment. and often progresses within days in a migratory or additive pattern -tenosynovitis in hands and feet -disseminated: fever. sepsis -Lyme disease -serologic studies are the most important to confirm dx. -tx is doxy. macrolides. 2nd topical retinoids. If CNS manifestations or pregnant. Systemic abx are used for maintenance -isoretinoin if refractory . rash -tx: ceftriaxone -Acute infectious arthritis (other than Gonococcal) -S aureus is MCC -Dx: joint aspiration for any infectious arthritis (including Gono) look for WBC over 50. chills. Beings 4-5 days after fever. avascular necrosis. and clindamycin) for 4-6wks and surgical debridement -Gonococcal Arthritis -acute monoarthritis (knee MC) or oligoarthritis. 3rd topical erythromycin or clindamycin -Moderate/severe nodular pustular acne: after trying above…1st . give chloarmphenicol Figure 19 Figure 20 Figure 21 Skin and Hypersensitivity Disorders Acne Vulgaris -Mild/moderate: 1st – topical benzoyl peroxide. 2nd – oral retinoids (isoretinoin) as last resort. neutropenia = pseudo. Tx is doxy -amoxicillin is given to kids under 8 or pregnant women -Rocky mountain spotted fever .

oral mucosa. sarcoidosis. fungal infxns. Otherwise tx is supportive Erythema multiforme -erythematous macules/papules that resemble target lesions that can become bullous. pregnancy. Usuallly affects the trunk. red. typically located over the anterior aspect of the tibia -usually in young women and resolves in a few weeks -causes: GAS. idiopathic -look for and treat underlying condition.Tinea versicolor -well demarcated hypo and hyperpigmented lesions that are well-demarcated. meds (OCPs. behcet dz. Only tx is antihistamines supportively Erythema Nodosum -painful. But think HSV -acyclovir -Spectrum for drug reactions: EM  SJS  TEN -aggressive IVF and supportive care Lichen Planus -4 Ps: Pruritic. abx). Polygonal. flat-topped Papules -MC seen on wrists. Tb. sulfa. subQ nodules. -KOH prep: spaghetti and meatballs -tx: oral or topical* antifungals Seborrheic dermatitis -dandruff may progress to yellowish flakes with surrounding scaly erythematous patches if severe -Tx: -sunlight -dandruff shampoo -topical ketoconazole or corticosteroids if severe Contact Dermatitis -irritant -not immune-mediated and doesn’t need sensitization -rash appears right after exposure -allergic -type IV HSR – takes hours to days Pityriasis Rosea -hearld patches and christmas tree pattern -NOT contagious -spontaneously remits. and genitalia -tx with glucocorticoids Bullous Pemphigoid -B for basement on IF (hemidesmosome) -systemic or topical steroids Pemphigus Vulgaris -Pimp Dez (desmosomes (IgG ab against desmoglien)) -fish net on IF -starts in oral mucosa (cuz dez is doing oral) -systemic steroids or other immunosuppressant . Purple. syphilis. amiodarone. May be painful or pruritic -may be caused by meds (sulfa or PCN or other). IBD. shins.

Dermatophytes -topical antifungals except for tina capitis (will have associated hair loss and maybe itching) or oncyhmycosis (oral griseofulvin) Psoriasis -1st line tx is topical corticosteroids. New and effective treatment are the vitamin D derivatives calcipotriene and calcitriol Other Figure 22 .