anti-hypertensives Flashcards
(32 cards)
primary / “essential” hypertension
- 90-95% of all hypertensive cases
- UNKNOWN CAUSE
- affects 1/3 of US population
susceptive predisposing factors for primary hypertension
- obesity
- stress
- high salt intake
- poor Mg/K/Ca intake
- lots of booze (except tequila)
- smoking
non-susceptive predisposing factors for primary hypertension
- family history
- insulin resistance
- age, gender
secondary hypertension
secondary to another disease:
- sleep apnea
- thyroid / parathyroid disease
- primary aldosteronism
- kidney disease / renovascular disease
- adrenal d/o: cushings, pheochromocytoma
what population has highest prevalence/risk for hypertension?
(1) older black females
(2) white men
[ overall higher rates in men ]
Guidelines for hypertensive treatment come from?
The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
Pre-hypertension parameters
120 - 139 / 80 - 89
Stage I hypertension parameters
140 - 159 / 90 - 99
Stage II hypertension
> 160 / >100
Renin-Angiotensin System (RAS)
(1) Decrease in perfusion sensed at juxtaglomerular apparatus in kidney activates RAS
(2) Kidneys release renin, meanwhile
(3) Angiotensinogen released from liver
(4) Renin converts angiotensinogen to angiotensin I
(5) Angiotensin Converting Enzyme (ACE) released from pulmonary and renal endothelium
(6) ACE converts AT1 to AT2
(7) AT2 is a potent arteriolar vasoconstrictor and has many stimulating effects throughout the body to increase BP
Effects of Angiotensin II
(1) Direct arteriolar vasoconstrictor
(2) Sympathetic activation / more NE release
(3) Renal tubules: stimulates Na, Cl reabsorption (associated water retention), and K excretion
(4) Adrenal cortex: stimulates release of aldosterone (which further directly stimulates Na/Cl reabsorption / K excretion at renal tubules)
(5) stimulates release ofADH from post. pituitary (which stimulates water retention at nephron collecting ducts)
- overall effect: water, salt retention, increases circulating volume to perfuse juxtaglomerular apparatus (feedback loop)
Diuretics (class)
- first line Rx for hypertension bc prevents cardiovascular complications of hypertension, more affordable
- thiazides (first line for htn), carbonic anyhydrase inhibitors, loop diuretics, K-sparing diuretics
Reserpine
MOA: prevents adrinergic transmission; depletes NE, DA, 5HT from strorage vesicles in presynaptic nerve endings CENTRAL and PERIPHERAL
Adverse effects: orthostatic htn (less catecholamines, less reflex increase in sympathetic tone secondary to position change, impotence, diarrhea, depression (central effect),
- slow onset, full effect takes weeks, seldom used
Guanethedine
MOA: prevents adrinergic transmission; depletes NE from vesicles in presynaptic nerve terminals PERIPHERALLY only
Adverse effects: orthostatic htn, impotence, diarrhea, NO DEPRESSION (no central action); sim to resperine
- poor GI absorption, full effect in weeks, NOT USED anymore bc of severe side effects
Guanadrel
MOA: prevents adrinergic transmission; depletes NE from vesicles in presynaptic nerve terminals PERIPHERALLY only;
Adverse effects: sim to guanethedine but less severe - orthostatic htn, diarrhea, impotence
- good GI absorption, rapid onset, shorter duration versus guanethedine
Selective alpha-1 blockers (class)
- prazosin, terazosin, doxazosin
MOA: Selective alpha-1 blocker (vasculature), decreases PVR
** favorable effect on lipid profile, does not interfere with glucose metabolism **
adverse effects: BIG first pass effect, fluid retention
- use in stage 1 or 2 htn with a diuretic and beta-blocker
alpha-methyldopa
clonidine
MOA: central-acting alpha-2 agonist; converted to alpha-methyl-NE (a false a2 agonist) suppresses central sympathetic outflow
Adverse effects: SEDATION/DROWSINESS, withdrawal syndrome (with rebound htn)
- limited use bc drowsiness, cannot stop taking abruptly bc withdrawal/rebound htn, ** htn in pregnancy **
direct-acting central alpha-2 agonists (class)
- clonidine, guanabenz, guanfacine
MOA: suppress central sympathetic outflow
Adverse effects: SEDATION/DROWSINESS, withdrawal syndrome (with rebound htn)
- limited use bc drowsiness, cannot stop taking abruptly bc withdrawal/rebound htn, ** NO htn in pregnancy **
non-selective alpha/beta-adrinergic blockers (class)
- 3rd generation beta blockers
MOA: decrease sympathetic output, block alpha-1 in vasculature (decr PVR), block cardiac beta-1 (decr HR, contractility), block renal beta-1 (decr renin, consequent decr-but not eliminate- AT2)
- labetalol: block ALPHA-1 & BETA-1/2 (beta-blockade more prominent); also HAS intrinsic sympathomimetic activity (ISA); can be given IV for HTN CRISIS
- carvedilol: block ALPHA-1 & BETA-1/2; NO ISA
- carteolol: NO alpha effect, only block beta-1/2, HAS ISA
specific contraindication for all drugs with intrinsic sympathomimetic activity (ISA):
Reynaud’s (exacerbates vasoconstriction in extremities)
- CAN NOT GIVE:
pindolol, penbutolol, cartelol, carteolol, labetalol, acebutolol
non-selective beta-1/2 blockers (class)
- 1st generation beta blockers
- NO ISA: propanolol, timolol
- HAS ISA: pindolol, penbutolol, cartelol
MOA: decrease sympathetic output, block cardiac beta-1 (decr HR, contractility), block renal beta-1 (decr renin, consequent decr-but not slim- AT2)
Adverse effects: bradycardia, interferes with lipid and glucose metabolism, bronchoconstriction (beta-2 blockade in airways)
**ALL ARE CONTRAINDICATED WITH ASTHMA, DIABETES
**PINDOLOL, PENBUTOLOL, CARTELOL CONTRAINDICATED WITH REYNAUD’S
Interactions: verapamil, diltiazem, digitalis (AV block)
beta-1 selective blockers “cardioselective” (class)
- metoprolol, atenolol, acebutolol, bisoprolol
- 2nd generation beta blockers
MOA: decrease sympathetic output, block cardiac beta-1 (decr HR, contractility), block renal beta-1 (decr renin, consequent decr-but not slim- AT2)
Adverse effects: bradycardia, interferes with lipid and glucose metabolism
- somewhat safer to give with asthma bc no beta-2 blockade, BUT selective for beta-1 blockade ONLY in low doses
ALL ARE CONTRAINDICATED WITH DIABETES
Calcium entry blockers (class)
verapamil diltiazem nifedipine nicardipine amlodipine israpidine felodopine
MOA: block calcium channels in smooth muscle, produces vasodilation, decresaed PVR
Nifedipine
MOA: blockade of Ca2+ channels SELECTIVE FOR VASCULATURE, NO DIRECT EFFECT ON HEART
Adverse effects: ankle edema, reflex tachycardia (only with short acting version), headache, dizziness, flushing, nausea
** MORE effective in African-Americans **
