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MOHDIII - Unit 2 > Hypertension Pharmacology > Flashcards

Hypertension Pharmacology Flashcards

1
Q

Targets of antihypertensive therapy

A
  • fluid balance (sodium & water)
  • renin angiotensin system (RAS)
  • central & peripheral control of SNS
  • tone of vascular smooth muscle
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2
Q

Classes of antihypertensive drugs

A
  • Diuretics
  • RAS blockers
  • Ca+ channel blockers
  • Sympatholytics
  • Vasodilators
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3
Q

Diuretics: initial & long term use

A
  • initial use: decrease extracellular fluid volume and CO
  • long term use: decrease vascular resistance; decreased response of VSM to vasoconstrictors, impaired release of NE/Epi
  • cellular mechanism: decrease in VSM Na+ & secondarily decrease in Ca2+
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4
Q

Diuretics: major use & adverse effects

A
  • use: alone of in combination, use in treatment of heart failure
  • adverse effects: most deplete K+ (except for K+ sparing diuretics)
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5
Q

Thiazide diuretics

A
  • chlorothiazide & hydrochlorothiazide
  • mechanism: block Na+Cl- symporter in distal convoluted tubule
  • effect: moderate diuresis, reduced by NSAIDs
  • adverse effects: hypkalemia, decreased uric acid & calcium excretion, thiazides & sulfonamides cross reactivity
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6
Q

High ceiling LOOP diuretics

A
  • furosemide, bumetanide, torsemide
  • mechanism: block Na, K+2Cl- co transporter in thick ascending limb of Loop of Henle
  • effect: use with edema, MOST EFFECT DIURETICS
  • adverse effects: hyokalemia, decreased uric acid excretion, deafness
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7
Q

Aldosterone receptor blockers

A
  • spironolactone & eplerenone
  • mechanism: collecting duct; block Na+ & water reabsorption, K+ sparing
  • use: resistant HTN, CHF HTN
  • adverse effects: HYPERKALEMIA*** not hypo
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8
Q

Potassium sparing diuretics

A
  • triameterene, amiloride
  • mechanism: late distal tubule & collecting duct Na+ channel blockers
  • diuretic effect in combo w/ thiazides: mild diuresis, weak HTN effect
  • adverse effects: HYPERKALEMIA
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9
Q

RAS inhibitors & HTN

A
  • blood levels of drugs & renin don’t correlate w/ effects
  • non renal RAS: vascular & brain
  • ACE/aldosterone escape: increased renin release, loss of negative feedback, RAAS and non RAAS mediated mechanism
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10
Q

Angiotensin II actions

A
  • vasocontriction–increasing blood pressure
  • stimulate thirst & secretion of aldosterone/ADH, increasing fluid/Na+
  • increase SNS: increasing cardiac activity and PVR
  • cardiac and vascular remodeling
  • feedback inhibition of renin release
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11
Q

ACE inhibitors

A
  • captopril, enalapril, lisinopril, fosinopril (PRILs)
  • mechanism: block conversion of angiotensin I to II, elevate bradykinin levels, decreased PVR, decreased aldosterone (increasing Na+/water excretion), reverse or reduce CV remodeling, increase plasma renin & renin activity
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12
Q

ACE inhibitors: use & adverse effects

A
  • use: mild/moderate HTN & heart failure

- adverse effects: DRY COUGH (20%), hyperkalemia, angioedema, hypotension, rash, pregnancy problems,

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13
Q

Angiotensin receptor antagonists (ARBs)

A
  • losartan, valsartan, candesartan, irbesartan
  • mehcanism: AT1 antagonist, vasodilation, increased Na+/water excretion, reduced plasma volume & cellular hypertrophy, increased plasma renin & renin activity
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14
Q

ARBs use and adverse effects

A
  • use: HTN & heart failure
  • adverse effects: hypotension, cough or angioedema but less than ACEIs (don’t start w/ this b/c don’t have as good long term effects, not used in combo w/ ACEIs), hyperkalemia, fetal renal toxicity
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15
Q

Renin inhibitor

A
  • aliskiren
  • mechanism: direct competitive inhibitor, increase plasma renin but NOT renin activity
  • use: HTN (not first line since long term CV outcome unclear)
  • adverse: diabetic/renal impairment, hypotension, dry cough, angioedema, hyperkalemia
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16
Q

Calcium channel blockers

A
  • cardioselective: verapamil, diltiazem
  • VSM selective: nifedipine, nicardipine, amplodipine (better for HTN)
  • mechanism: block voltage L-type Ca2+ channels, relax VSM & decrease PVR, decrease MAP (reflec increase SNS & HR–THEREFORE COMBINED WITH BETA BLOCKER), negative chronotropic-verapamil, diltiazem
17
Q

Calcium channel blockers (CCB) use & adverse effects

A
  • use: HTN (low renin), AFRICAN AMERICAN & OLDER PATIENTS W/ SYSTOLIC HTN: DIHYDROPYRIDINES MORE EFFECTIVE
  • adverse: contraindicated in heart failure (edema), depresses AV conduction/contractility, headache, gingival inflammation/hyperplasia
18
Q

Drugs acting on SNS

A
  • site of action: beta/alpha-adrenergic receptor antagonists, inhibitors of peripheral adrenergic transmission, central mediated anti hypertensives
19
Q

B-adrenergic receptor antagonists

A
  • B1 & B2: propranolol; B1: meoprolol, atenolol
  • mechanism: decreased CO, renin secretion
  • use: alone or in combo for HTN
  • adverse: nausea, vomiting, confusion, dizziness, fatigue, SLEEP DISORDERS-lipophilic propranolol
20
Q

When to avoid using B-blockers

A
  • asthmatics or peripheral vascular disease
  • diabetic: inability to elevate glucose
  • promote development of type 2 diabetes
  • *withdrawal: rebound HTN**
21
Q

A-adrenergic receptor antagonists

A
  • prazosin, doxazosin
  • mechanism: block a1 receptors on VSM, dilation of arterioles
  • use: alone or in combo for HTN (PHEOCHROMOCYTOMA)
  • adverse: reflect tachycardia, orthostatic hypotension, fluid retention, GI upset, palpitation, tinnitus, headache, dizziness, urinary incontinence
  • *water retention-use with diuretic or B-antagonist**
22
Q

Alpha & Beta adrenergic antagonists

A
  • labetalol: mix of four stereoisomers, use: chronic HTN & HTN emergencies
  • carvedilol: antioxidant & antiproliferative, use: HTN & heart failure
23
Q

Inhibitors of adrenergic transmission

A
  • mechanism: deplete NE from adrenergic nerve endings, inhibits reuptake of NE, decrease PVR and CO
  • use: HTN, resurgence in use, combine w/ thiazide diuretic
  • adverse: postural hypotension, sedation, dry mouth, nightmares, Na+/water retention–this is why you add diuretic
24
Q

Central mediated anti hypertensives

A
  • clonidine, alpha-methyldopa (prodrug)
  • mechanism: stimulate brainstem a2 receptors (decreased SNS outflow), vagal activity to heart increased, decreased, PVR & CO
  • use: resistant HTN–conidine, pregnancy induced HTN–methyldopa
  • adverse: rebound HTN, sedation, dry mouth, depression, drowsiness, Na+/water retention–add diuretic, postural hypotension in elderly
25
Q

Vasodilators

A
  • hydralazine, minoxidil, nitroprusside, riociguat, nitroglycerin, epoprostenol, bosentan, ambrisentan
  • mehcanism: direct dilators of VSM, decrease PVR, BARORECEPTOR ACTIVATION (THERFORE USE WITH DIURETICS & B-ANTAGONISTS)
26
Q

Hydralazine

A
  • vasodilator: reduced intracellular calcium, ARTERIOLES, decreased PVR/MAP, reflex increase in HR, contractility, CO**
  • use: HTN in combo w/ diuretic & B-blocker
  • adverse: headache, anorexia, nausea, dizziness, sweating, angina or ischemic arrhythmias w/ ischemic heart disease due to reflex tachycardia, increased renin/fluid retention, IMMUNE RESPONSE: LUPUS
27
Q

Minoxidil

A
  • vasodilator: ARTERIOLES, decreased PVR, activated K+ channels (VSM relaxation), reflex increase in HR, contractility, CO
  • use: resistant HTN in combo with diuretic & B-blocker
  • adverse: fluid retention: contraindicated in HF, pericardial effusion and cardiac tamponade, reflex tachycardia, ABNORMAL HAIR GROWTH (topical use for alopecia)**
28
Q

Nitroprusside

A
  • vasodilator: direct vasodilator, generates NO, effects VEINS & ARTERIES to reduce preload/afterload
  • use: produce HYPOtension in surgery & HYPERTENSIVE emergency
  • adverse: rapid decrease in MAP, cyanide accumulation (infusions>48hrs and/or impaired renal function)
29
Q

Nitroglycerin

A
  • vasodilator: VEINS, generates NO
  • use: HYPOtension in surgery, HTN emergencies
  • pharmacokinetics: short duration of action, tolerance
  • adverse: headaches indicates that drug is working
30
Q

Epoprosterol

A
  • vasodilator: prostacyclin (PGI2)
  • mechanism: direct vasodilator via cAMP, counteracts TXA2
  • use: potent antihypertensive must be administered CONTINUOUSLY
  • USED FOR PRIMARY PULMONARY HYPERTENSION*
31
Q

Endothelin receptor blockers

A
  • nonselective: bosentan, ETa receptor blocker: ambrisentan
  • use: PULMONARY HTN
  • adverse: edema, headache, spermatogenesis inhibition, respiratory tract infection, decreased hematocrit, hepatic effects
  • *VASODILATORS**
32
Q

Riociguat

A
  • vasodilator: directly stimulates guanylyl cyclase, increases cGMP
  • use: pulmonary HTN, thromboembolic pulmonary HTN, combine w/ ET receptor blockers
  • adverse: headache, dizziness, nausea, diarrhea, hypotension, BIRTH DEFECTS
33
Q

Stage 1 HTN treatment

A
  • monotherapy: ACE inhibitor, ARB, CCB, thiazide diuretic or two dug combo
34
Q

Stage 2 HTN treatment

A
  • TWO DRUG COMBO

- ACE inhibitor or ARB w/ thiazide diuretic or ARB w/ CCB

35
Q

Pharmacological approach

A
  • monotherapy vs. combination therapy
  • advantages of combined therapy: different classes w/ complementary actions, lower dose, fewer side effects, improved compliance

MOHDIII - Unit 2 (23 decks)

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