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anti-hypertensives > anti-hypertensives > Flashcards

anti-hypertensives Flashcards

1
Q

primary / “essential” hypertension

A
  • 90-95% of all hypertensive cases
  • UNKNOWN CAUSE
  • affects 1/3 of US population
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2
Q

susceptive predisposing factors for primary hypertension

A
  • obesity
  • stress
  • high salt intake
  • poor Mg/K/Ca intake
  • lots of booze (except tequila)
  • smoking
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3
Q

non-susceptive predisposing factors for primary hypertension

A
  • family history
  • insulin resistance
  • age, gender
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4
Q

secondary hypertension

A

secondary to another disease:

  • sleep apnea
  • thyroid / parathyroid disease
  • primary aldosteronism
  • kidney disease / renovascular disease
  • adrenal d/o: cushings, pheochromocytoma
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5
Q

what population has highest prevalence/risk for hypertension?

A

(1) older black females
(2) white men
[ overall higher rates in men ]

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6
Q

Guidelines for hypertensive treatment come from?

A

The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

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7
Q

Pre-hypertension parameters

A

120 - 139 / 80 - 89

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8
Q

Stage I hypertension parameters

A

140 - 159 / 90 - 99

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9
Q

Stage II hypertension

A

> 160 / >100

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10
Q

Renin-Angiotensin System (RAS)

A

(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

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11
Q

Effects of Angiotensin II

A

(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)
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12
Q

Diuretics (class)

A
  • 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
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13
Q

Reserpine

A

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
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14
Q

Guanethedine

A

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
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15
Q

Guanadrel

A

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
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16
Q

Selective alpha-1 blockers (class)

A
  • 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
17
Q

alpha-methyldopa

clonidine

A

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 **
18
Q

direct-acting central alpha-2 agonists (class)

A
  • 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 **
19
Q

non-selective alpha/beta-adrinergic blockers (class)

A
  • 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
20
Q

specific contraindication for all drugs with intrinsic sympathomimetic activity (ISA):

A

Reynaud’s (exacerbates vasoconstriction in extremities)

  • CAN NOT GIVE:
    pindolol, penbutolol, cartelol, carteolol, labetalol, acebutolol
21
Q

non-selective beta-1/2 blockers (class)

A
  • 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)

22
Q

beta-1 selective blockers “cardioselective” (class)

A
  • 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

23
Q

Calcium entry blockers (class)

A 
verapamil
diltiazem
nifedipine
nicardipine
amlodipine
israpidine
felodopine

MOA: block calcium channels in smooth muscle, produces vasodilation, decresaed PVR

24
Q

Nifedipine

A

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 **

25
Q

Verapamil / Diltiazem

A

MOA: Blockade of Ca2+ channels in the vasculature, heart muscle and the AV node

Adverse effects: ankle edema, headache, dizziness, flushing, nausea

** NO REFLEX TACHYCARDIA **

Interactions: beta blockers & digitalis (caution for AV block)

26
Q

Sodium Nitroprusside

A

MOA: direct-acting ARTERIOLAR AND VENOUS vasodilator; nitrous oxide donor to cGMP (???)

Adverse effects:reflex tachycardia, possible cyanide poisoning

  • rapid onset, short acting, photosensitive
  • use IV in HTN EMERGENCY
27
Q

Hydralazine

A

MOA: direct-acting ARTERIOLAR (only) vasodilator

Adverse effects: reflex tachycardia, Na/fluid retention, hirsutism

  • for htn used with a diuretic and beta-blocker
  • used with pregnancy htn crisis/ pre-eclampsia
28
Q

Potassium channel openers (class)

A
  • minoxidil, diazoxide, pinacidil

MOA: vascular vasodilation: open K+ channels of smooth muscle of VASCULATURE (selective), K+ efflux, causes hyperpolarization (prevent contraction)

Adverse effects: reflex tachycardia, Na/fluid retention, hirsutism

  • minoxidil - s/e of hirsutism becomes therapeutic effect when used for baldness
  • diazoxide - use IV in htn crisis; also used to treat hypoglycemia due to reduced insulin secretion; adverse effects- hyperuricemia, hyperglycemia
29
Q

ACE inhibitors (class)

A

-pril: captopril, verapamil, lisinopril, ramipril

MOA: inhibit ACE / decr AT2, prevent breakdown bradykinin (active vasodilator)

Adverse effects: COUGH (due to high levels bradykinin), reduced aldosterone/HYPERKALEMIA

  • NOT EFFECTIVE in African-Americans
  • DRUG OF CHOICE in diabetics
  • also use with CHF
  • NO EFFECT on glucose or lipids
  • NO IMPOTENCE
  • CONTRAINDICATED IN PREGNANCY (fetal renal toxicity)
30
Q

Angiotensin II blockers

A

-artan: losartan, valsartan, irbesartan

MOA: selective blockade AT2 receptor; no effect on bradykinin

Adverse effects: sim ACE-I, reduced aldosterone/HYPERKALEMIA

    • NO COUGH **
  • CONTRAINDICATED IN PREGNANCY (fetal renal toxicity)
  • expensive
31
Q

Aliskiren

A

MOA: binds to and inhibits renin; prevents conversion angiotensinogen to AT1

Adverse effects: ANGIOEDEMA, hyperkalemia

32
Q 
New Bp goals:
In general-
Dm-
Cardiac failure-
Renal failure-
Renal failure with proteinuria-
A

General: < 120/80
Dm: < 130/80
Cardiac: <130/85
Renal with protein: 125/75

anti-hypertensives (1 decks)

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