Cardiology
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| Firstline tx in HTN: MOA (eg, diuretics, BB) | decrease vascular volume, decrease afterload and systolic BP
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| Most potent type of diuretics & MOA = | loop (furosemide): inhibit Cl reabsorption in TAL -> Na follows Cl and H2) follows Na&Cl. Results in high K+ losses.
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| Thiazide diuretics MOA = | HCTZ & chlorthalidone: inhibit K+ & Na+ reabsorption in TAL. Decrease plasma volume, increase Na excretion
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| Thiazide diuretics AEs = | Volume depletion, low K+ & Na, hyperglycemia / insulin resistance; hyperuricemia/gout, photosensitivity, decreased placental flow. May increase serum cholesterol & digoxin
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| Hypertensive Emergency: tx | Controlled, gradual lowering of BP; 10% decrease in first hour, then 15% over next 3–12 hrs to BP of no less than 160/110; rapid correction of BP to normal levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
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| Cushing Syndrome: tx for HTN | HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)
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| Beta blocker: MOA | Blockade of parts of the sympathetic NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin
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| ACEI AEs | Cough; Angioedema; Hyperkalemia & hyponatremia (2/2 low aldosterone); Rash. CI in pregnancy, and use cautiously in renal artery stenosis (RAS)
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| ARBs: MOA | Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs
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| ARBs AEs | Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS
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| CCBs: MOA | Inhibit Ca+ influx -> block vascular smooth mx contractility -> vasodilatation & afterload reduction (aoso preload). Also coronary vasodilatation: CCBs are used in coronary artery spasm (Prinzmetal, Raynaud)
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| CCBs: Dihydropyridines (DHPs) vs nonDHPs | DHPs more vascular selective (fewer cardiac conduction fx): tx HTN/angina. NonDHPs more cardio-selective with more inhibitory fx on SA/AV node (CAUTION in CHF)
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| DHP CCBs (amlodipine, nifedipine): AEs | Ankle edema; Flushing; HA; Increased HR
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| Non-DHP CCBs (diltiazem, verapamil): AEs | Bradycardia, constipation, hotn, edema, CHF, AV node block
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| HTN lifestyle mods | Wt reduction (BMI 18.5 - 25) (biggest fx on bp); ETOH; aerobic activity 30 min; Na+ to 2.4 mg/day; K+; DASH diet
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| Most single HTN meds lower BP: | at most 20/10 mm Hg (so most pts on more than 1 drug)
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| Beta-1 stimulation causes (a), and beta-2 stimulation causes (b) | (a) tachycardia; (b) bronchodilation
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| BBs (2) used for migraine, SVT, V-tach, tremors, EtOH W/D = | Inderal (propranolol) and atenolol
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| BB used to reduce IOP in glaucoma = | nadolol
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| BBs are contraindicated in: | any resp dz (asthma, COPD, DF); type 1 DM. Also pt may have W/D and increase in CP (2/2 CAD) bc of increased HR & thus increasing O2 demand
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| CCBs are contraindicated in: | CHF, LV dysfunction, AV block, sick sinus syndrome
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| First Line Tx for HTN | *Thiazide*; beta; ACEI; ARB; other diuretics; CCB
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| ACEI MOA: | Inhibit ACE in lung -> block formation of angiotensin II -> increased vasodilatation and Na+ loss
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| ACEI work less well in AA popultion bc of: | lower blood renin levels
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| Rx of choice for DM nephropathy | ACEI (increase blood flow to kidneys -> promote renal repair); act synergistically with a diuretic
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| Presynaptic adrenergic release inhibitors: 2 types | central and peripheral
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| Central presynaptic adrenergic release inhibitors (anti-adrenergic meds) MOA | prevent adrenergic outflow from the brain, by stimulating inhibitory alpha-2 receptors (eg, clonidine)
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| Peripheral presynaptic adrenergic release inhibitors (anti-adrenergic meds) MOA | prevent norepinephrine release from peripheral nerve terminals (eg, in heart) -> block alpha-1 receptors (eg, prazosin)
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| Sudden DC of anti-adrenergic meds can cause: | rebound HTN
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| Firstline & 2ndline HTN tx in pregnant patient = | 1st: methyldopa (Aldomet). 2nd: hydralazine
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| Secondary indications of anti-adrenergic meds | Central: nicotine/heroin W/D; Ppx for migraine, glaucoma, DM-assoc diarrhea. Peripheral: BPH; asthma (relax smooth mx); meds lower LDL & inc HDL
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| Nitrates MOA | 1) dilate large myocardial arteries -> increase blood flow to heart; 2) reduce venous tone -> blood pooling in periphery -> reduces preload -> reduces cardiac work (so: increase O2 supply & decrease O2 demand)
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| Nitrates AEs | hotn, rebound tachycardia, facial flushing, HA
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| JNC8: tx of uncomplicated HTN for most (non-AA) patients | Firstline: ACEI, ARB, CCB, thiazide diuretics
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| JNC 8: essential HTN tx for AA patients | CCBs and thiazide diuretics
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| For pts with DM regardless of race), HTN tx should include: | ACEI or ARB
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| Hypertensive emergency tx | nitroprusside (CI in PG) or labetolol; to 110 over several hours
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| HTN Compelling Indications: CHF | 1st: ACE plus diuretic (HCTZ / Lasix); 2) Beta blocker (atenolol); 3) clonidine. Also ARB
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| HTN Compelling Indications: High Coronary Dz Risk | Beta; ACEI; CCB; Diuretic
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| HTN Compelling Indications: Post-MI | 1 Beta; 2 ACEI; CCB
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| HTN Compelling Indications: DM | 1 ACEI; 2 Beta (for DM2); 3 Verapamil or clonidine
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| HTN Compelling Indications: Recurrent Stroke Prevention | ACEI; Diuretic
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| JNC 8: in patients >60, start tx at: | SBP >150 or DBP >90
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| JNC 8: in patients <60, start tx at: | 140/90 (same used in pts >18 yo with either CKD or DM)
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| 1stline (&2nd & 3rd) tx for uncomplicated isolated systolic HTN (elderly) | 1) HCTZ; 2) Atenolol; 3) captopril or verapamil
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| HTN Compelling Indications: CKD | 1 ACE; 2 BB (atenolol) or verapamil or HCTZ; 3 clonidine
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| Tx for BPH | Prazosin +/- tamsulosin
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| Tx for migraine (w/HTN meds): | 1 atenolol; 2 verapamil
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| Tx osteoporosis (w/HTN med): | HCTZ
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| Tx for pre-op HTN | Atenolol
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| 1stline HTN tx in pregnancy | 1 Methyldopa; 2 hydralazine
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| Pt just started on ACEI develops weakness. What test (lab, UA, CT, US) is most specific to dx pt? | Renal US
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| HTN Tx in CVD | BB
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| HTN Tx in DM | ARB
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| Alternate to ACEI if CHF or other intolerance | ARB
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| HTN tx if BP >20/10 over goal: | 2 meds
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