Internal Medicine EOR Review (UPDATED TABLE GUIDE).

Internal Medicine EOR Review (UPDATED TABLE GUIDE). Internal Medicine EOR Review Cardiology (20%) Angina Pectoris Stable Unstable Prinzmetal Predictable pattern* Aggravated c exertion; alleviated c rest or NTG; Caused by FIXED* plaque EKG: STd ONLY* Outpatient Setting Unpredictable pattern* New onset while RESTING*; NOT alleviated c rest EKG: STd or TWi* MUST ADMIT* Unpredictable/EPISODIC pattern* Triggered by COCAINE*, alcohol or triptans* EKG: STe +/- reciprocal changes MUST ADMIT* S/Sx & PE SUBSTERNAL CP usually brought on by EXERTION (due to low supply & high demand) WITHOUT necrosis*. Described as “pressure/burning/tightness”, usually NOT SHARP or altered by breathing or positioning. POORLY* localized; radiation to ARM*, LOWER JAW*, back, epigastrium, shoulders. By definition lasts < 30 minutes but usually only lasts 1-5 minutes; (+) Levine’s Sign (clenched fist on chest) Associated sx: SOB/DOE, DIAPHORESIS*, cool/clammy skin; ATYPICAL* presenters: Female, Diabetics, Elderly Dx F/L: EKG* - STd classic* (especially horizontal/downsloping STds) ● Resting EKG is normal in half of pts (therefore not definitive) ● May also have TWi, nonspecific ST changes, poor RWP & pseudonormalization of T waves* ● WILL NOT HAVE PATHOLOGIC Qs or STe* S/L: Stress Testing - Most useful NONinvasive SCREENING tool* ● Stress EKG ○ (+) if STd, hypo/hypertension, arrhythmias or cardiac sx develop ● Myocardial Perfusion Imaging Stress c Thallium-201 or 99m-technetium sestamibi ○ Used when baseline EKG has abnormalities* ○ Exercise if able to tolerate exercise (C/I in asthmatics) ○ Pharmacologic: Dobutamine, Adenosine or Dipyridamole if unable to exercise (C/I in asthmatics) ● Stress Echocardiogram or cardiac MRI can also be used for further evaluation (esp. Valvular etiologies) Gold Standard: Coronary Angiography* Cardiac Enzymes (CEs): ALL NEGATIVE* Pharmacologic Definitive (Revascularization) > NTG (Vasodilator) ● Decreases preload & afterload; SL route most effective* ● Used in acute setting; max dose 0.4mg x3 SL (Total of 1.2mg) ● S/E: HA (MC*), flushing, hypotension (keep out of light) ● C/I: SBP < 90mmHg; RVMI; use of PDE-5 inhibitors (Sildenafil aka Viagra, Cialis, etc.) > Beta blockers ● Increase diastolic timing by prolonging coronary filling times* & reduces demand; reduces mortality* ● F/L drug for CHRONIC MANAGEMENT* > CCBs (NON-DIHYDROPYRIDINES: Cardizem & Verapamil) ● Prolongs diastolic filling times; DoC for Prinzmetal angina* ● Also used for pts unable to take BBs (bronchospasms; ↓HR) > ASA ● F/L if ACS is suspected. Can be used as 2ry prophylaxis ONLY* (1) Percutaneous Transluminal Coronary ANGIOGRAPHY* (PTCA) > 1/2 vessel dz* NOT involving LCA with NORMAL EF* > 50-55% --------------------------------------------------------- (2) Coronary Artery Bypass Graft (CABG) > 3 vessel dz*, LCA (left main coronary artery) involvement or LVEF < 40% --------------------------------------------------------- Outpatient Regimen: DAILY ASA, SL NTG PRN, DAILY BB & STATIN* Don’t forget lifestyle modifications if preventing angina in primary care setting! (Control of DM, HTN, cholesterol, diet, etc.) Cardiac Arrhythmias / Conduction Disorders Typos: AFib - IRREGULARLY irregular*; Junctional has INVERTED/ABSENT P waves c NARROW QRS (NOT idioventricular) Idioventricular has ABSENT P waves c WIDE QRS complexes* Tx: ACLS Protocols (Stable: Meds; Unstable [SBP < 90mmHg/AMS]: Electrical Therapy) Cardiomyopathy CM Dilated (MC*) SAGGY LV* Restrictive STIFF MYOcardium* Hypertrophic STIFF LV* > Viral: MCC: Enteroviruses (Coxsackie B*; echovirus) > Toxic: Alcohol*, cocaine, anthracyclines (Doxorubicin), radiation therapy > Other: Pregnancy*, infiltrative, autoimmune, metabolic (thyroidism), > Takotsubo CM (Apical LV ballooning) aka “Broken Heart Synd.” > Infiltrative Dz: Amyloidosis MCC*, sarcoidosis, myocardial fibrosis, hemochromatosis*, metastatic dz, scleroderma*, chemotherapy, radiation therapy; Loffler syndrome > Inherited genetic disorder (autosomal dominant*) of inappropriate LV/RV hypertrophy* (esp. septal*) > Obstructive in 70% of pts SYSTOLIC* dysfunction c LOW EF* Poor systolic contraction* Fatigue, sx of CHF, laterally displaced PMI, CP/DOE, arrhythmias; S3*** DIASTOLIC* dysfunction Tends to have more R sided sx: JVD, edema, Giant A wave, etc. (+)Kussmaul SIGN* (JVP ↑ c insp.) DIASTOLIC* dysfunction (LOW LV volume*) Syncope/DOE; SUDDEN death* ↑ c valsalva & standing ↓ c hand grip & squatting > Echo: VENTRICULAR* (esp LV) dilation & REDUCED EF*; LV hypokinesis* > CXR: Cardiomeg., edema, effusion > EKG: S Tach, wide QRS/BBBs*, +/- arrhythmias > CXR: ENLARGED atria*; edema > EKG: Low voltage*, LAA/RAA > Echo: ATRIAL* dilation c NORMAL ventricles; DIASTOLIC* dysfunction. > Definitive Dx for Etiology: Endomyocardial Bx* EKG: LVH; ventricular arrhy. Echo: LVH & SAM* (systolic anterior motion) of MITRAL valve c MR* Standard Regimen: ACEIs, diuretics, BBs (only if STABLE), Digoxin, Na+ restriction; AICD if EF < 35% Definitive: Heart Transplant Tx underlying condition. Hemochromatosis: Chelation Sarcoidosis: Steroids BBs Gold Standard* S/L: CCBs (Verapamil*) if BB C/I Avoid exertion & athletic sports Septal Myectomy: Recurrent syncopal episodes or worsening ICD: Hx of syncope or event seen on Holter monitor* Congestive (Decompensated) Heart Failure S/Sx & PE Baseline worsening* Pulmonary congestion, DOE, rales, pink FROTHY* sputum; S3/S4; PMI enlarged Dx CXR: Vascular congestion/cephalization, Kerley B lines, cardiomegaly*, Batwing/Butterfly edema pattern EKG: RVH, RBBB, RAD, low voltage if effusion present, S.Tach; Poor RWP Labs: ANP & *BNP*, troponin (flat trending*; r/o MI), BMP (Na+, BUN, K+) Tx Acute exacerbation: LMNOP (Lasix, morphine, NTG, O2 & Positioning) c CPAP/BiPAP ventilation Chronic Management: Tx of underlying HF etiology (CM, structural abnormality, infiltrative dz) Coronary Vascular Dz (CAD) Patho INADEQUATE TISSUE PERFUSION; ischemia* due to coronary blood supply & demand imbalance. ● Fatty streak formation* (FORMATION OF FATTY STREAKS) ○ Lipid deposition in WBCs lead to smooth muscle proliferation. Can form as early as adolescence. FATTY STREAKS are the first step in atherosclerotic plaque*. ● Formation of early plaque* (FORMATION OF FOAM CELLS) ○ LDL enters endothelium in fatty streak leading to LDL oxidation*, attracting macrophages/smooth muscle cells to ingest harmful LDL* (now called “FOAM CELLS”). ○ Foam cells attract more macrophages, fibroblasts* & inflammatory cells. ● Formation of fibrous (mature) plaque* (FORMATION OF FIBROUS CAP) ○ Proliferating smooth muscle cells & connective tissue incorporates into mature plaque forming “FIBROUS CAP” resulting in narrowing of coronary arterial lumen* & calcification. ● Myocardial Ischemia ○ The narrowing results in ischemia due to lower blood flow when demands increase. ○ Pts usually become symptomatic with 70% lumen occlusion. ○ Progressive compromise leads to collateral circulation (this is why elderly do better c MIs) S/Sx, Dx & Tx Revolves around PREVENTATIVE medicine & risk factor management* (Lifestyle modifications) Pearls MCC of CAD is ATHEROSCLEROSIS* Other causes: coronary artery vasospasm, AS/AR, pulmonary HTN, severe systemic HTN, HOCM RFs: DM (worst factor); smoking (most important MODIFIABLE* RF); hyperlipidemia, HTN, males, age (> 45y for males; > 55y in women); FHx of CAD; obesity, hyperhomocysteinemia, elevated CRP. Endocarditis MC Etiologies ● ACUTE Bacterial Endocarditis: Staphylococcus aureus ● SUBacute Bacterial Endocarditis: Streptococcus viridans (usually due to dental procedure) ● Endocarditis in IVDA: MCC: Staphylococcus aureus (esp. MRSA); also Candida & Pseudomonas. ● Prosthetic Valve Endocarditis: Staphylococcus epidermidis ● Non-Infectious Endocarditis: Libman-Sacks (SLE); Marantic (Metastatic CA) ● Colon CA Setting: Streptococcus bovis ● Recent GI/GU Procedure: Enterococci ● HACEK Organisms: Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella S/Sx & PE Often presents c PERSISTENT FEVERS OF UNKNOWN ORIGIN*; SOB, weakness, malaise, anorexia PE: New murmur (usually LSB); Roth spots (retinal hemorrhages c pale centers*), petechiae* on conjunctiva, Janeway lesions (NONtender erythematous macules on palms/soles); Osler nodes (TENDER nodules on pads of digits); splinter hemorrhages of proximal nail bed, hepatomegaly, clubbing, glomerulonephritis. Duke Criteria: 2 Major OR 1 Major + 3 Minor OR 5 Minor Major Criteria Minor Criteria > SUSTAINED BACTEREMIA (3 sets @ least 1 hour apart*) ● 2 (+) BCxs by organism known* to cause infxn > ENDOCARDIAL INVOLVEMENT (Do TTE first*; TEE after) ● (+) Echocardiogram (vegetations, abscess, valve perforation, prosthetic dehiscence) ● NEW* valvular regurgitation (AR/MR) > PREDISPOSING CONDITION (Valvulopathy, IVDA, catheters) > FEVER (> 38°C/ 100.4°F) > VASCULAR/EMBOLIC PHENOMENA (Janeway lesions, ICH) > IMMUNOLOGIC PHENOMENA (↑ESR/RF/glomerulonephritis) > (+) BCXS NOT MEETING MAJOR CRITERIA (Unknown organism) > ECHO NOT MEETING MAJOR CRITERIA (Old murmur worsened) Tx (MedBullets) > Empiric tx for NON prosthetic valve pts ● Vancomycin + Ceftriaxone or Vancomycin + Gentamicin x4-6 weeks ● Another option from PEARLS: Nafcillin + Gentamicin x4-6 weeks > Empiric tx in PROSTHETIC VALVE pt: Vancomycin + Gentamicin + Rifampin* x 4-6 weeks > Fungal: Amphotericin B x6-8 weeks but often need surgical intervention > Surgical Valve Replacement: CHF, Pts refractory to therapy, abscesses, recurrent systemic emboli, fungal infxn > Pending BCxs: If acute: Start empiric tx right away; If subacute: Can opt to wait for BCxs > Prophylaxis: Amoxicillin (2g, 30-60 min prior to procedure); Clindamycin if PCN allergy (+) ● Administer in dental procedures, I&Ds, rigid bronchoscopy, respiratory surgery or if h/o valve dz/endocard. Heart Murmurs / Valvular Heart Dz > MCC of valvulopathy in the U.S: Mechanical degeneration; in the world: Rheumatic fever* *Waiting on Harvey to finish* Hyperlipidemia Etiologies Familial hypercholesterolemia, physical inactivity, metabolic syndrome, DM, CKD, HYPOTHYROIDISM* Drugs: Steroids, protease inhibitors (antivirals used to tx HIV* & HCV*: saquinavir, ritonavir) S/Sx & PE Pts are usually asx. Remember your OSCE: Severe hypertriglyceridemia can cause pancreatitis* Xanthelasma (lipid plaques on eyelids); Xanthoma (lipid nodules commonly found in Achilles tendon), HTN, corneal arcus (white opaque ring at the border of the cornea) Dx Lipid panel: Total cholesterol: > 200 mg/dL; LDL: > 130 mg/dL ● Familial hypercholesterolemia: Heterozygotes: > 300 mg/DL; homozygotes have levels > 700. 2ry causes: TSH, FBGL, HgbA1C, Alkaline phosphatase, UA Tx Best meds to lower LDL: Statins* Best meds to lower TGLs: Fibrates* Best meds to increase HDL: Niacin* (except diabetics; Niacin ↑ BGL; use Fibrates & Statins) Target Levels: LDL: < 100 ( < 70 in diabetics*) HDL: > 40 (MedBullets) - 60 (PEARLS) TGLs: < 150 Total: < 200 Screening: (High Risk if > 1 RF: HTN, smoking, FHx) > For males @ 20-25 & females @ 30-35y w ↑ risk > For males @ 35 & females @ 45y for ↓ risk > Anyone c CAD RFs > 20y; (+) FHx for familial hyperchol. Initiation of Statin Therapy - Diabetics between 40-75 y/o - Anyone > 21y c LDL > 190 - Anyone c CAD or stroke - ≥ 7.5% (Pearls); ≥ 10% (MedBullets) Framingham Risk Pharm > Niacin (Nicotinic acid; Vitamin B3) ● S/E: Flushing* (taking ASA prior prevents this); HA; pruritus, warm sensation; HYPERurecemia/glycemia* ● C/I: PUD, hyperglycemia, hepatotoxicity, paresthesias, N/V/D; dry skin > Statins ● S/E: Myositis/Rhabdo* (esp. when used c fibrates/niacin); liver toxicity/hepatitis*, more S/E when used c tetracycline & abx. ● Strongest statins: Atorvastatin & Rosuvastatin*; less S/E c Pravastatin & Rosuvastatin; give @ bedtime* > Fibrates (Gemfibrozil; Fenofibrate) ● S/E: Bile lithogenicity (gallstones*); myositis/myalgias/rhabdo (esp when used c statins) ● C/I: Hepatobiliary dz or severe renal dz > Bile Acid Sequestrants (Cholestyramine; Colestipol; Colesevelam) ● Safe in pregnancy* (excreted through feces); usually always used in conjunction c another lipid lowering agent; used for pruritus associated c biliary obstruction* ● S/E: N/V, abd pain, bloating, increased LFTs; increases TGLs!*; impairs Digoxin, warfarin & fat-soluble vitamin absorption (either take these 1 hour prior to BAS or 4 hours post BAS ingestion) > Ezetimibe: Adjuvant therapy to statins in pts c ACS; S/E: Increases LFTs > PCSK9 Inhibitors (Alirocumab; Evolocumab): Indicated in hyperlipidemia despite max dose statin* Pearls Hypercholesterolemia: Caused by Hypothyroidism, pregnancy & kidney failure Hypertriglyceridemia: Caused by DM, ETOH, obesity, steroids, estrogen HTN *ASK GALEAS IF EOR HAS UPDATED HTN GUIDELINES OR IF IT’S STILL GOING BY OLD ONE* Etiologies > MCC of HTN in GENERAL: Idiopathic* 2ry Causes by Demographic: > MCC of 2ry HTN: Renal Artery Stenosis > MCC of 2ry HTN in young males: ETOH > MCC of 2ry HTN in young female: OCPs 2ry Causes by Systems: > Cardiovascular (AR; Coarctation of the Aorta) > Renal (Glomerular Dz, RAS, Polycystic kidney Dz) > Endocrine (Cushing's, Conn’s, Pheochromocytoma, ↑thyroid) > Drug-Induced (OCPs, glucocorticoids, NSAIDs, phenylephrine) S/Sx & PE Asx “Silent Killer” until complications arise (SOB, CP, HA, vision changes due to retinopathy, S4 gallop) Dx Elevated BP on ≥ 2 readings on ≥ 2 different visits* Tx Pharmacology F/L: Lifestyle modifications (Low salt diet, wt loss, exercise, smoking cessation) for 6 months - 1 year Pharmacologic Tx by Demographic & Comorbidities (PEARLS & MedBullets Cross Referenced) ● Uncomplicated HTN in Caucasians without comorbidities: Thiazides, ACEIs/ARBs & BB ● Uncomplicated HTN in African American without comorbidities: Thiazide with CCB ● HTN in Diabetics/CKD: ACEIs/ARBs ● HTN in Hyperthyroidism: BBs ● HTN in CHF: ACEIs/ARBs with BBs & Diuretics ● HTN in Migraines: BBs ● HTN in Osteoporosis, Hypocalcemia: Thiazides ● HTN in Pregnancy: Alpha-Methyldopa or Labetalol > HCTZ (Cardioprotective) ● Prevents Na+/water reabsorption @ the DISTAL diluting tubule, lowering Ca+ urinary excretion ● S/E: ↓Natremia, ↓Kalemia, ↑Calcemia, ↑Uricemia, ↑BGL ● Use with caution in Diabetics* & pts with Gout* > Loop Diuretics ● Inhibits water transport across Loop of Henle, increasing excretion; strongest class of diuretics ● S/E: ↓Natremia, ↓Kalemia, ↓Calcemia, ↑Uricemia, ↑BGL, ↓chloremic metabolic ALKALOSIS; ototoxicity* ● C/I: Sulfa allergy* > Potassium Sparing Diuretics ● Inhibits aldosterone-mediated Na+/H2O absorption, sparing K+; weak diuretic .