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Pharmacology- Test 3 Material > 24- Antihypertensive Drugs > Flashcards

24- Antihypertensive Drugs Flashcards

1
Q

diltiazem

A

Calcium channel blocker

1: 1 cardiac:VSM
- block voltage sensitive L-type Ca channels
- relax VSM and decrease peripheral resistance
- decrease MAP– reflex increase sympathetic discharge and HR
- negative chronotropic
- used for HTN (especially low renin) blacks and older patients with systolic HTN
- side effects- headache, contraindicated in heart failure, depresses A-V conduction & contractility

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2
Q

verapamil

A

Calcium channel blocker

1: 1 cardiac:VSM
- block voltage sensitive L-type Ca channels
- relax VSM and decrease peripheral resistance
- decrease MAP– reflex increase sympathetic discharge and HR
- negative chronotropic
- used for HTN (especially low renin) blacks and older patients with systolic HTN
- side effects- headache, contraindicated in heart failure, depresses A-V conduction & contractility

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3
Q

amlodipine

A

Calcium channel blocker (dihydropyridine)
-10:1 VSM:cardiac
-block voltage sensitive L-type Ca channels
-relax VSM and decrease peripheral resistance
-decrease MAP– reflex increase sympathetic discharge and HR
-negative chronotropic
used for HTN (especially low renin) blacks and older patients with systolic HTN
side effects- headache, contraindicated in heart failure, depresses A-V conduction & contractility

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4
Q

nicardipine

A

Calcium channel blocker (dihydropyridine)

  • 10:1 VSM:cardiac
  • block voltage sensitive L-type Ca channels
  • relax VSM and decrease peripheral resistance
  • decrease MAP– reflex increase sympathetic discharge and HR
  • negative chronotropic
  • used for HTN (especially low renin) blacks and older patients with systolic HTN
  • side effects- headache, contraindicated in heart failure, depresses A-V conduction & contractility
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5
Q

nifedipine

A

Calcium channel blocker (dihydropyridine)

  • 10:1 VSM:cardiac
  • block voltage sensitive L-type Ca channels
  • relax VSM and decrease peripheral resistance
  • decrease MAP– reflex increase sympathetic discharge and HR
  • negative chronotropic
  • used for HTN (especially low renin) blacks and older patients with systolic HTN
  • side effects- headache, contraindicated in heart failure, depresses A-V conduction & contractility
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6
Q

chlorothiazide

A
  • inhibits Na/Cl transport in distal tubule and collecting duct
  • drug interaction- NSAIDs, sulfonamides
  • Side effects- hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, hyponatremia, muscle weakness
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7
Q

chlorthalidone

A
  • inhibits Na/Cl transport in distal tubule and collecting duct
  • drug interaction- NSAIDs, sulfonamides
  • Side effects- hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, hyponatremia, muscle weakness
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8
Q

hydrochlorothiazide

A
  • inhibits Na/Cl transport in distal tubule and collecting duct
  • drug interaction- NSAIDs, sulfonamides
  • Side effects- hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, hyponatremia, muscle weakness
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9
Q

bumetanide

A

Na/K/2Cl transport inhibition in thick loop of Henle
-used in severe HTN, renal insufficiency, cardiac failure
short duration of action
-drug interactions- allergic reaction (sulfonamide), can be inhibited by NSAIDs
-side effects- hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesmia

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10
Q

ethacrynic acid

A

Na/K/2Cl transport inhibition in thick loop of Henle

  • used in severe HTN, renal insufficiency, cardiac failure
  • short duration of action
  • drug interactions- can be inhibited by NSAIDs
  • side effects- hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesmia
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11
Q

furosemide

A

Na/K/2Cl transport inhibition in thick loop of Henle

  • used in severe HTN, renal insufficiency, cardiac failure
  • short duration of action
  • drug interactions- allergic reaction (sulfonamide), can be inhibited by NSAIDs
  • side effects- hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesmia
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12
Q

torsemide

A

Na/K/2Cl transport inhibition in thick loop of Henle

  • used in severe HTN, renal insufficiency, cardiac failure
  • short duration of action
  • drug interactions- allergic reaction (sulfonamide), can be inhibited by NSAIDs
  • side effects- hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesmia
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13
Q

amiloride

A

inhibit Na influx through luminal channels

  • act on the collecting duct
  • used to avoid excessive K depletion and enhance the natriuretic effects of other diuretics
  • drug interaction- can be inhibited by NSAIDs
  • side effects- hyperkalemia (increased risk by renal disease, renin inhibitors, angiotensin II blockers), hyerchloremic acidosis
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14
Q

triamterene

A

inhibit Na influx through luminal channels

  • act on the collecting duct
  • used to avoid excessive K depletion and enhance the natriuretic effects of other diuretics
  • drug interaction- can be inhibited by NSAIDs, acute renal failure when used in combination with indomethacin
  • side effects- hyperkalemia (increased risk by renal disease, renin inhibitors, angiotensin II blockers), hyerchloremic acidosis
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15
Q

eplerenone

A

Aldosterone Receptor Antagonist

  • bind to mineralocorticoid receptors and blunt aldosterone activity
  • act on the collecting duct
  • used to avoid excessive K depletion and enhance the natriuretic effects of other diuretics
  • drug interaction- can be inhibited by NSAIDs
  • side effects- hyperkalemia (increased risk by renal disease, renin inhibitors, angiotensin II blockers), hyerchloremic acidosis
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16
Q

spironolactone

A

Aldosterone Receptor Antagonist

  • bind to mineralocorticoid receptors and blunt aldosterone activity
  • act on the collecting duct
  • used to avoid excessive K depletion and enhance the natriuretic effects of other diuretics
  • drug interaction- can be inhibited by NSAIDs
  • side effects- hyperkalemia (increased risk by renal disease, renin inhibitors, angiotensin II blockers), hyerchloremic acidosis
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17
Q

captopril

A

ACE inhibitor

  • inhibits production of angiotensin II from angiotensin I thus reducing aldosterone secretion
  • inhibits breakdown of bradykinin
  • leads to inc. Na+ and H2O excretion
  • decreases peripheral vascular resistance (CO and HR unchanged)
  • improved intra-renal hemodynamics in CKD
  • dec. cardiac hypertrophy and remodeling
  • Diabetes
  • Adverse effects: dry cough, alt. taste, hyperkalemia (dec. aldosterone), angioedema, rash, pregnancy problems, hypotension in presence of hypovolemia
  • NSAIDs may inhibit effects
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18
Q

enalapril

A

ACE inhibitor

  • inhibits production of angiotensin II from angiotensin I thus reducing aldosterone secretion
  • inhibits breakdown of bradykinin
  • leads to inc. Na+ and H2O excretion
  • decreases peripheral vascular resistance (CO and HR unchanged)
  • improved intra-renal hemodynamics in CKD
  • dec. cardiac hypertrophy and remodeling
  • Diabetes
  • Adverse effects: dry cough, alt. taste, hyperkalemia (dec. aldosterone), angioedema, rash, pregnancy problems, hypotension in presence of hypovolemia
  • NSAIDs may inhibit effects
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19
Q

fosinopril

A

ACE inhibitor

  • inhibits production of angiotensin II from angiotensin I thus reducing aldosterone secretion
  • inhibits breakdown of bradykinin
  • leads to inc. Na+ and H2O excretion
  • decreases peripheral vascular resistance (CO and HR unchanged)
  • improved intra-renal hemodynamics in CKD
  • dec. cardiac hypertrophy and remodeling
  • Diabetes
  • Adverse effects: dry cough, alt. taste, hyperkalemia (dec. aldosterone), angioedema, rash, pregnancy problems, hypotension in presence of hypovolemia
  • NSAIDs may inhibit effects
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20
Q

lisinopril

A

ACE inhibitor

  • inhibits production of angiotensin II from angiotensin I thus reducing aldosterone secretion
  • inhibits breakdown of bradykinin
  • leads to inc. Na+ and H2O excretion
  • decreases peripheral vascular resistance (CO and HR unchanged)
  • improved intra-renal hemodynamics in CKD
  • dec. cardiac hypertrophy and remodeling
  • Diabetes
  • Adverse effects: dry cough, alt. taste, hyperkalemia (dec. aldosterone), angioedema, rash, pregnancy problems, hypotension in presence of hypovolemia
  • NSAIDs may inhibit effects
21
Q

candesartan

A

AT1 Receptor Blockers (ARB)

  • vasodilation, inc. Na+ and H2O excretion, reduce plasma volume, dec. cellular hypertrophy, inc. plasma renin and renin activity
  • similar s/fx to ACEIs but dec. cough and/or angioedema
  • can lead to hyperkalemia if given with ACEIs or K+ sparing diuretics
22
Q

irbesartan

A

AT1 Receptor Blockers (ARB)

  • vasodilation, inc. Na+ and H2O excretion, reduce plasma volume, dec. cellular hypertrophy, inc. plasma renin and renin activity
  • similar s/fx to ACEIs but dec. cough and/or angioedema
  • can lead to hyperkalemia if given with ACEIs or K+ sparing diuretics
23
Q

losartan

A

AT1 Receptor Blockers (ARB)

  • vasodilation, inc. Na+ and H2O excretion, reduce plasma volume, dec. cellular hypertrophy, inc. plasma renin and renin activity
  • similar s/fx to ACEIs but dec. cough and/or angioedema
  • can lead to hyperkalemia if given with ACEIs or K+ sparing diuretics
24
Q

valsartan

A

AT1 Receptor Blockers (ARB)

  • vasodilation, inc. Na+ and H2O excretion, reduce plasma volume, dec. cellular hypertrophy, inc. plasma renin and renin activity
  • similar s/fx to ACEIs but dec. cough and/or angioedema
  • can lead to hyperkalemia if given with ACEIs or K+ sparing diuretics
25
Q

aliskiren

A

Renin Inhibitor

  • direct competitive renin inhibitor
  • orally active, new drug
  • dose dependent decrease in renin
26
Q

ambrisentan

A

Selective Endothelin Receptor Blocker

  • specifically ETa receptor blocker
  • used in PHTN
  • S/Fx: edema, HA, spermatogenesis inhibition, respiratory tract infection, dec. hematocrit, hepatic effects
27
Q

bosentan

A

Non-selective Endothelin Receptor Blocker

  • used in PHTN
  • S/Fx: edema, HA, spermatogenesis inhibition, respiratory tract infection, dec. hematocrit, hepatic effects
28
Q

epoprostenol

A

Vasodilator

  • exerts effects through prostacyclin (PGI2)
  • direct vasodilator via cAMP and counteracts effects of thromboxane A2
  • Use: potent antihypertensive but must be administered continuously (primary PHTN)
29
Q

hydralazine

A

Vasodilator

  • mechanism unknown
  • requires presence of NO to have effect
  • preferential effect on arterioles
  • dec. peripheral vascular resistance and MAP
  • reflex inc. in HR, contractility, CO (pronounced)
  • Use: mild to mod. hypertension in combo with diuretic and BB
  • S/fx: HA, anorexia, nausea, dizziness, sweating, angina or ischemic arrhythmias d/t reflex tachy, inc. renin and fluid retention, lupus
30
Q

minoxidil

A

Vasodilator

  • preferential effect on arterioles
  • dec. peripheral vascular resistance
  • reflex inc. in HR, contractility, CO, renin secretion, and fluid retention
  • Use: resistant HTN in combo with diuretic and BB
  • S/fx: fluid retention (contraindicated in HF), pericardial effusion and tamponade, reflex tachy, abnormal hair growth
31
Q

nitroglycerin

A

Vasodilator

  • preferential effect on veins
  • generates NO which activates guanylyl cyclase, inc. in cGMP
  • Use: to produce hypotension in surgery and hypertensive emergencies
  • Short DOA and tolerance can develop
  • S/fx: headache (HA)
32
Q

nitroprusside

A

Direct Vasodilator

  • generates NO which activates guanylyl cyclase, inc. in cGMP
  • effects on veins and arteries to reduce preload and afterload
  • use: to produce hypotension in surgery and hypertensive emergencies
  • S/Fx: rapid dec. in MAP, cyanide accumulation (infusions > 48hrs or renal impairment)
33
Q

riociguat

A

Vasodilator

  • inc. NO and cGMP activity
  • used in PHTN
34
Q

atenolol

A

Cardiac selective beta-blocker (Beta 1)

  • decrease HR, contractility, renin secretion, and sympathetic outflow.
  • avoid in asthmatics, PVD, bradycardia, AV block, insulin dependent diabetics.
  • Can decrease BG
  • S/E: NV, confusion, dizziness, fatigue, and withdraw rebound HTN.
35
Q

metoprolol

A

Cardiac selective beta-blocker (Beta 1)

  • decrease HR, contractility, renin secretion, and sympathetic outflow.
  • avoid in asthmatics, PVD, bradycardia, AV block, insulin dependent diabetics.
  • Can decrease BG
  • S/E: NV, confusion, dizziness, fatigue, and withdraw rebound HTN.
36
Q

propranolol

A

Non-selective Beta-blocker (block Beta1 and beta2)

  • decrease HR, contractility, renin secretion, and sympathetic outflow.
  • blockade of beta2 leads to vasoconstriction and bronchoconstriction.
  • avoid in asthmatics, PVD, bradycardia, AV block, insulin dependent diabetics.
  • Can decrease BG
  • S/E: NV, confusion, dizziness, fatigue, and withdraw rebound HTN.
37
Q

doxazosin

A

Competitive alpha1 antagonist

  • dilates arteries and veins.
  • Use: HTN and pheochromocytoma.
  • S/E: orthohypotension, relef tachycardia, fluid retention, GI Sx.
38
Q

prazosin

A

Competitive alpha1 antagonist

  • dilates arteries and veins.
  • Use: HTN and pheochromocytoma.
  • S/E: orthohypotension, relef tachycardia, fluid retention, GI Sx.
39
Q

terazosin

A

Competitive alpha1 antagonist

  • dilates arteries and veins.
  • Use: HTN and pheochromocytoma.
  • S/E: orthohypotension, relef tachycardia, fluid retention, GI Sx.
40
Q

carvedilol

A

Non-selective Beta-blocker (Beta 1 and 2) and Alpha1 blocker

  • beta:alpha block= 1:1
  • decrease HR, contractility, renin secretion, and sympathetic outflow.
  • blockade of beta2 leads to vasoconstriction and bronchoconstriction.
  • avoid in asthmatics, PVD, bradycardia, AV block, insulin dependent diabetics.
  • Can decrease BG
  • S/E: NV, confusion, dizziness, fatigue, and withdraw rebound HTN.
41
Q

labetalol

A

Non-selective Beta-blocker (beta 1 and 2) and alpha 1 blocker

  • beta:alpha block= 3:1
  • decrease HR, contractility, renin secretion, and sympathetic outflow.
  • blockade of beta2 leads to vasoconstriction and bronchoconstriction.
  • avoid in asthmatics, PVD, bradycardia, AV block, insulin dependent diabetics.
  • Can decrease BG
  • S/E: NV, confusion, dizziness, fatigue, and withdraw rebound HTN.
42
Q

methyldopa

A

Centrally acting sympatholytic

  • stimulates alpha2 receptors in the brain stem (alpha2 agonist)
  • Decrease sympathetic outflow, increased vagal tone on the heart.
  • Decrease SVR and CO.
  • Use: pregnancy-induced HTN
  • S/E: sedation, dry mouth, Na/H20 retention, rebound HTN, and orthohypotension (esp elderly)
43
Q

clonidine

A

Centrally acting sympatholytic

  • stimulates alpha2 receptors in the brain stem (alpha2 agonist)
  • Decrease sympathetic outflow, increased vagal tone on the heart.
  • Decrease SVR and CO.
  • Use: resistant HTN
  • S/E: sedation, dry mouth, Na/H20 retention, rebound HTN, and orthohypotension (esp elderly)
44
Q

endothelin

A

Endothelial Derived Constrictor

  • amino acid peptide released from damaged or traumatized endothelial cells
  • powerful vasoconstrictor that helps prevent excessive bleeding from torn arteries
  • produced by endothelin converting enzyme
  • ETa- vasoconstriction, ETb- Vasodilation
  • endothelin blocking drugs used to treat PHTN
  • inc. release believed to contribute to cycle of vasoconstriction when endothelium damaged by HTN
45
Q

nitric oxide

A

Endothelia Derived Relaxant

  • created by endothelial-derived nitric oxide synthase from arginine and oxygen
  • lipid soluble gas that diffuses out of cell and acts upon smooth muscle to convert cGTP to cGMP which causes relaxation of blood vessel (vasodilation)
  • chronic HTN can damage endothelial lining and impair synthesis of NO
46
Q

nitric oxide synthase

A

-synthesizes NO from arginine and oxygen in endothelial cells lining vasculature

47
Q

prostacyclin

A

Endothelial Derived Relaxant

  • synthesized from arachidonic acid by COX-1
  • increases cAMP in vascular smooth muscle and mediates relaxation
  • also inhibits platelet aggregation
48
Q

thromboxane

A

-produced from arachidonic acid and mediates platelet aggregation and vasoconstriction

Pharmacology- Test 3 Material (10 decks)

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