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Cards HTN Tx


Firstline tx in HTN: MOA (eg, diuretics, BB) decrease vascular volume, decrease afterload and systolic BP
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.
Thiazide diuretics MOA = HCTZ & chlorthalidone: inhibit K+ & Na+ reabsorption in TAL.
Thiazide diuretics AEs = Volume depletion, low K+ & Na, hyperglycemia / insulin resistance; hyperuricemia/gout, photosensitivity, decreased placental flow. May increase serum cholesterol & digoxin
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
Cushing Syndrome: tx for HTN HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)
Beta blocker: MOA Blockade of parts of the sympathetic NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin
ACEI AEs Cough; Angioedema; Hyperkalemia & hyponatremia (2/2 low aldosterone); Rash. CI in pregnancy, and use cautiously in renal artery stenosis (RAS)
ARBs: MOA Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs
ARBs AEs Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS
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)
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)
DHP CCBs: AEs Ankle edema; Flushing; HA; Increased HR
Non-DHP CCBs (diltiazem, verapamil): AEs Bradycardia, constipation, hotn, edema, CHF, AV node block
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
Most single HTN meds lower BP: at most 20/10 mm Hg (so most pts on more than 1 drug)
Beta-1 stimulation causes (a), and beta-2 stimulation causes (b) (a) tachycardia; (b) bronchodilation
BBs (2) used for migraine, SVT, V-tach, tremors, EtOH W/D = Inderal (propranolol) and atenolol
BB used to reduce IOP in glaucoma = nadolol
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
CCBs are contraindicated in: CHF, LV dysfunction, AV block, sick sinus syndrome
First Line Tx for HTN *Thiazide*; beta; ACEI; ARB; other diuretics; CCB
ACEI MOA: Inhibit ACE inlung -> block formation of angiotensin II -> in vasodilatation and Na+ loss
ACEI work less well in AA popultion bc of: lower blood renin levels
Rx of choice for DM nephropathy ACEI (increase blood flow to kidneys -> promote renal repair); act synergistically with a diuretic
Presynaptic adrenergic release inhibitors: 2 types central and peripheral
Central presynaptic adrenergic release inhibitors (anti-adrenergic meds) MOA prevent adrenergic outflow from the brain, by stimulating inhibitory alpha-2 receptors (eg, clonidine)
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)
Sudden DC of anti-adrenergic meds can cause: rebound HTN
Firstline & 2ndline HTN tx in pregnant patient = 1st: methyldopa (Aldomet). 2nd: hydralazine
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
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)
Nitrates AEs hotn, rebound tachycardia, facial flushing, HA
JNC8: tx of uncomplicated HTN for most (non-AA) patients Firstline: ACEI, ARB, CCB, thiazide diuretics
JNC 8: essential HTN tx for AA patients CCBs and thiazide diuretics
For pts with DM regardless of race), HTN tx should include: ACEI or ARB
Hypertensive emergency tx nitroprusside (CI in PG) or labetolol; to 110 over several hours
HTN Compelling Indications: CHF 1st: ACE plus diuretic (HCTZ / Lasix); 2) Beta blocker (atenolol); 3) clonidine. Also ARB
HTN Compelling Indications: High Coronary Dz Risk Beta; ACEI; CCB; Diuretic
HTN Compelling Indications: Post-MI 1 Beta; 2 ACEI; CCB
HTN Compelling Indications: DM 1 ACEI; 2 Beta (for DM2); 3 Verapamil or clonidine
HTN Compelling Indications: Recurrent Stroke Prevention ACEI; Diuretic
JNC 8: in patients >60, start tx at: SBP >150 or DBP >90
JNC 8: in patients <60, start tx at: 140/90 (same used in pts >18 yo with either CKD or DM)
1stline (&2nd & 3rd) tx for uncomplicated isolated systolic HTN (elderly) 1) HCTZ; 2) Atenolol; 3) captopril or verapamil
HTN Compelling Indications: CKD 1 ACE; 2 BB (atenolol) or verapamil or HCTZ; 3 clonidine
Tx for BPH Prazosin +/- tamsulosin
Tx for migraine (w/HTN meds): 1 atenolol; 2 verapamil
Tx osteoporosis (w/HTN med): HCTZ
Tx for pre-op HTN Atenolol
1stline HTN tx in pregnancy 1 Methyldopa; 2 hydralazine
Created by: Adam Barnard Adam Barnard