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Hypertension Flashcards

(44 cards)

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1
Q

Atenolol

A

B1 receptor antagonist

B1 and B2: propranolol, B1: metoprolol, atenolol
• Mechanism of action:
– Non-selective B1- B2 or selective

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2
Q

Metoprolol

A

B receptor antagonist

B1 and B2: propranolol, B1: metoprolol, atenolol
• Mechanism of action:
– Non-selective B1- B2 or selective

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3
Q

Propranolol

A

B receptor antagonist

B1 and B2: propranolol, B1: metoprolol, atenolol
• Mechanism of action:
– Non-selective B1- B2 or selective

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4
Q

Doxazosin

A

alpha1 receptor antagonist

Mechanism of action:
– Blockade of

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5
Q

Prazosin

A

alpha receptor antagonist

Mechanism of action:
– Blockade of a1-receptors on VSM
– Dilation of arterioles and capacitance veins
• Use: alone or in combination for hypertension
– Pheochromocytoma
• Side/adverse effects:
– Reflex tachycardia, orthostatic hypotension, fluid
retention
– GI upset, palpitation, tinnitus, headache, dizziness,
urinary incontinence
– Water retention-use with diuretic or a-antagonist

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6
Q

Terazosin

A

alpha receptor antagonist

Mechanism of action:
– Blockade of a1-receptors on VSM
– Dilation of arterioles and capacitance veins
• Use: alone or in combination for hypertension
– Pheochromocytoma
• Side/adverse effects:
– Reflex tachycardia, orthostatic hypotension, fluid
retention
– GI upset, palpitation, tinnitus, headache, dizziness,
urinary incontinence
– Water retention-use with diuretic or a-antagonist

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7
Q

carvedilol

A

Mixed a/b antagonist

non-selective B and a1 receptor
antagonist
– Antioxidant and antiproliferative
• Use: hypertension and heart failure

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8
Q

Labetalol

A

Mixed a/b antagonist

non-selective B and a1 receptor
antagonist, mix of four stereoisomers
• Use: chronic hypertension and hypertensive
emergencies

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9
Q

reserpine

A

Inhibitor of peripheral transmission

Mechanism of action:
– Deplete NE from adrenergic nerve endings
– Inhibits reuptake of NE into storage terminal
– Decrease peripheral resistance and CO
• Use: mild to moderate hypertension
resurgence in use low dose in combination with
thiazide diuretic
• Adverse effects:
– Postural hypotension
– Sedation, dry mouth, nightmares
– Sodium and water retention-add diuretic

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10
Q

alpha-methyldopa

A

Central mediated agent
Brainstem a2 receptor

Mechanism of action:
– Stimulate brainstem a2 adrenergic receptors
• decrease sympathetic outflow
– Vagal activity to heart increased
– Decreased peripheral vascular resistance and CO
• Use: resistant hypertension-clonidine
– Pregnancy-induced hypertension-methyldopa
• Side/adverse effects:
– Withdrawal syndrome-rebound hypertension
– Sedation, dry mouth, depression, drowsiness
– Sodium and water retention-add diuretic
– Postural hypotension-elderly

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11
Q

clonidine

A

CNS mediated agent

Mechanism of action:
– Stimulate brainstem a2 adrenergic receptors
• decrease sympathetic outflow
– Vagal activity to heart increased
– Decreased peripheral vascular resistance and CO
• Use: resistant hypertension-clonidine
– Pregnancy-induced hypertension-methyldopa
• Side/adverse effects:
– Withdrawal syndrome-rebound hypertension
– Sedation, dry mouth, depression, drowsiness
– Sodium and water retention-add diuretic
– Postural hypotension-elderly

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12
Q

Guanabenz

A

CNS mediated agent

Mechanism of action:
– Stimulate brainstem a2 adrenergic receptors
• decrease sympathetic outflow
– Vagal activity to heart increased
– Decreased peripheral vascular resistance and CO
• Use: resistant hypertension-clonidine
– Pregnancy-induced hypertension-methyldopa
• Side/adverse effects:
– Withdrawal syndrome-rebound hypertension
– Sedation, dry mouth, depression, drowsiness
– Sodium and water retention-add diuretic
– Postural hypotension-elderly

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13
Q

Captopril

A

ACE inhibitor

Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity

Adverse/toxic effects:
– Dry cough (20%) and altered taste
– Hyperkalemia-due to inhibition of aldosterone
secretion
– Angioedema
– Hypotension
– Rash
– Pregnancy problems (fetal renal damage
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14
Q

Enalapril

A

ACE inhibitor

Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity

Adverse/toxic effects:
– Dry cough (20%) and altered taste
– Hyperkalemia-due to inhibition of aldosterone
secretion
– Angioedema
– Hypotension
– Rash
– Pregnancy problems (fetal renal damage
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15
Q

Fosinopril

A

ACE inhibitor

Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity

Adverse/toxic effects:
– Dry cough (20%) and altered taste
– Hyperkalemia-due to inhibition of aldosterone
secretion
– Angioedema
– Hypotension
– Rash
– Pregnancy problems (fetal renal damage
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16
Q

Lisinopril

A

ACE inhibitor

Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity

Adverse/toxic effects:
– Dry cough (20%) and altered taste
– Hyperkalemia-due to inhibition of aldosterone
secretion
– Angioedema
– Hypotension
– Rash
– Pregnancy problems (fetal renal damage
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17
Q

Candesartan

A

ARB

Mechanism of action:
– AT1 receptor antagonists
– Vasodilation
– Increase Na+ and H2O excretion
– Reduce plasma volume
– Decrease cellular hypertrophy
– Increase plasma renin and renin activity
Adverse/toxic effects:
– Hypotension
– NO cough or angioedema
– Hyperkalemia
– Fetal renal toxicity
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18
Q

irbesartan

Study These Flashcards
A

ARB

Mechanism of action:
– AT1 receptor antagonists
– Vasodilation
– Increase Na+ and H2O excretion
– Reduce plasma volume
– Decrease cellular hypertrophy
– Increase plasma renin and renin activity
Adverse/toxic effects:
– Hypotension
– NO cough or angioedema
– Hyperkalemia
– Fetal renal toxicity
19
Q

Losartan

Study These Flashcards
A

ARB

Mechanism of action:
– AT1 receptor antagonists
– Vasodilation
– Increase Na+ and H2O excretion
– Reduce plasma volume
– Decrease cellular hypertrophy
– Increase plasma renin and renin activity
Adverse/toxic effects:
– Hypotension
– NO cough or angioedema
– Hyperkalemia
– Fetal renal toxicity
20
Q

Valsartan

Study These Flashcards
A

ARB

Mechanism of action:
– AT1 receptor antagonists
– Vasodilation
– Increase Na+ and H2O excretion
– Reduce plasma volume
– Decrease cellular hypertrophy
– Increase plasma renin and renin activity
Adverse/toxic effects:
– Hypotension
– NO cough or angioedema
– Hyperkalemia
– Fetal renal toxicity
21
Q

Aliskiren

Study These Flashcards
A

Renin Inhibitor

Mechanism of action:
– Direct, competitive inhibitor of renin
– Increase plasma renin but not renin activity
• Use: hypertension
– Not first line since long term CV outcomes unclear
• Side/adverse effects:
– Diabetic or renal impairment: hyperkalemia in combo with
ACEIs and ARBs
– Hypotension
– Dry cough but much less than with ACE inhibitors
– Rare: angioedema
– Hyperkalemia due to inhibition of aldosterone

22
Q

Ambrisentan

Study These Flashcards
A

Vasodilator

Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists

ETa receptor blocker:

Use: primary pulmonary hypertension
• Side/adverse effects:
– Edema
– Headache
– Spermatogenesis inhibition
– Respiratory tract infection
– Decreased hematocrit
– Hepatic effects
23
Q

Bosentan

Study These Flashcards
A

Vasodilator

Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists

Non-selective ET receptor blocker

Use: primary pulmonary hypertension
• Side/adverse effects:
– Edema
– Headache
– Spermatogenesis inhibition
– Respiratory tract infection
– Decreased hematocrit
– Hepatic effects
24
Q

epoprostenol

Study These Flashcards
A

Vasodilator

Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists

Prostacyclin (PGI2
)
• Mechanism of action:
– Direct vasodilator via cAMP
– Counteracts thromboxane A2
• Use: potent antihypertensive but must be
administered continuously
– Primary pulmonary hypertension
25
hydralazine
vasodilator Mechanism of action: – Direct dilators of VSM-different mechanisms – Decrease peripheral vascular resistance – Baroreceptor activation of compensatory mechanisms • Use: – Hypertension-hydralazine and minoxidil – Hypertensive crises-nitroprusside – Pulmonary hypertension-epoprostenol, bosentan, ambrisentan, riociguat – Used in combination-diuretics and B-antagonists Mechanism of action: unclear – Reduced intracellular calcium – Preferential effect on arterioles vs arteries and veins – Decreased peripheral vascular resistance, MAP – Reflex increase in HR, contractility, CO (pronounced) • Use: mild to moderate hypertension in combination with diuretic and B-blocker • Side/adverse effects: commonly occurring – Headache, anorexia, nausea, dizziness, sweating – Angina or ischemic arrhythmias with ischemic heart disease due to reflex tachycardia – Increase renin and fluid retention – Immune response: Lupus
26
minoxidil
Vasodilator Mechanism of action: – Direct dilators of VSM-different mechanisms – Decrease peripheral vascular resistance – Baroreceptor activation of compensatory mechanisms • Use: – Hypertension-hydralazine and minoxidil – Hypertensive crises-nitroprusside – Pulmonary hypertension-epoprostenol, bosentan, ambrisentan, riociguat – Used in combination-diuretics and B-antagonists Mechanism of action: – Preferential effect on arterioles vs veins – Decreased peripheral vascular resistance – Activates K+ channels, VSM relaxation – Reflex increase in HR, contractility, CO, renin secretion and fluid retention • Use: resistant hypertension in combination with diuretic and B-blocker • Side/adverse effects: – Fluid retention: contraindicated in heart failure – Pericardial effusion and cardiac tamponade – Reflex tachycardia – Abnormal hair growth (topical use for alopecia)
27
nitroglycerin
vasodilator Mechanism of action: – Direct dilators of VSM-different mechanisms – Decrease peripheral vascular resistance – Baroreceptor activation of compensatory mechanisms • Use: – Hypertension-hydralazine and minoxidil – Hypertensive crises-nitroprusside – Pulmonary hypertension-epoprostenol, bosentan, ambrisentan, riociguat – Used in combination-diuretics and B-antagonists ``` Mechanism of action: – Preferential effect on veins – Generates nitric oxide which activates guanylyl cyclase, increase in cGMP • Use: to produce hypotension in surgery and hypertensive emergencies • Pharmacokinetics: – Short duration of action – Tolerance • Side effects: – Headache ```
28
nitroprusside
vasodilator Mechanism of action: – Direct dilators of VSM-different mechanisms – Decrease peripheral vascular resistance – Baroreceptor activation of compensatory mechanisms • Use: – Hypertension-hydralazine and minoxidil – Hypertensive crises-nitroprusside – Pulmonary hypertension-epoprostenol, bosentan, ambrisentan, riociguat – Used in combination-diuretics and B-antagonists ``` Mechanism of action: – Direct vasodilator – Generates nitric oxide which activates guanylyl cyclase, increase in cGMP – Effect on veins and arteries to reduce preload and afterload • Use: to produce hypotension in surgery and hypertensive emergencies • Adverse/toxic effects: – Rapid decrease in MAP – Cyanide accumulation (infusions>48 hours and/or impaired renal function) ```
29
riociguat
vasodilator Mechanism of action: – Direct dilators of VSM-different mechanisms – Decrease peripheral vascular resistance – Baroreceptor activation of compensatory mechanisms • Use: – Hypertension-hydralazine and minoxidil – Hypertensive crises-nitroprusside – Pulmonary hypertension-epoprostenol, bosentan, ambrisentan, riociguat – Used in combination-diuretics and B-antagonists ``` Mechanism of action: – Directly stimulates guanylyl cyclase – Increases cGMP • Use: – Primary pulmonary hypertension – Thromboembolic pulmonary hypertension – Combined with ET receptor blockers • Side/adverse effects: – Headache, dizziness, nausea, diarrhea – Hypotension – Birth defects ```
30
dilitazem
Ca channel blocker (cardioselective) Mechanism of action: – Block voltage sensitive L-type Ca2+ channels – Relax VSM and decrease peripheral resistance – Decrease MAP-reflex increase sympathetic discharge and HR – Negative chronotropic -verapamil and diltiazem Use: – Hypertension (esp. low renin) – African Americans and older patients with systolic hypertension: dihydropyridines more effective • Adverse effects: – Contraindicated in heart failure (edema) – Depresses A-V conduction and contractility – Headache
31
verapamil
Ca channel blocker (cardioselective) Mechanism of action: – Block voltage sensitive L-type Ca2+ channels – Relax VSM and decrease peripheral resistance – Decrease MAP-reflex increase sympathetic discharge and HR – Negative chronotropic -verapamil and diltiazem Use: – Hypertension (esp. low renin) – African Americans and older patients with systolic hypertension: dihydropyridines more effective • Adverse effects: – Contraindicated in heart failure (edema) – Depresses A-V conduction and contractility – Headache
32
Amlodipine
Ca channel blocker (vasoselective) Mechanism of action: – Block voltage sensitive L-type Ca2+ channels – Relax VSM and decrease peripheral resistance – Decrease MAP-reflex increase sympathetic discharge and HR – Negative chronotropic -verapamil and diltiazem Use: – Hypertension (esp. low renin) – African Americans and older patients with systolic hypertension: dihydropyridines more effective • Adverse effects: – Contraindicated in heart failure (edema) – Depresses A-V conduction and contractility – Headache
33
Nicardipine
Ca channel blocker (vasoselective) Mechanism of action: – Block voltage sensitive L-type Ca2+ channels – Relax VSM and decrease peripheral resistance – Decrease MAP-reflex increase sympathetic discharge and HR – Negative chronotropic -verapamil and diltiazem Use: – Hypertension (esp. low renin) – African Americans and older patients with systolic hypertension: dihydropyridines more effective • Adverse effects: – Contraindicated in heart failure (edema) – Depresses A-V conduction and contractility – Headache
34
Nifedipine
Ca channel blocker (vasoselective) Mechanism of action: – Block voltage sensitive L-type Ca2+ channels – Relax VSM and decrease peripheral resistance – Decrease MAP-reflex increase sympathetic discharge and HR – Negative chronotropic -verapamil and diltiazem Use: – Hypertension (esp. low renin) – African Americans and older patients with systolic hypertension: dihydropyridines more effective • Adverse effects: – Contraindicated in heart failure (edema) – Depresses A-V conduction and contractility – Headache
35
Chlorothiazide
Thiazide diuretic Block Na/Cl symproter in distal tubule Moderate Diuresis Reduced by NSAIDs Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity
36
chorthalidone
Thiazide like diuretic Block Na/Cl symproter in distal tubule Moderate Diuresis Reduced by NSAIDs Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity
37
hydrochlorothiazide
Thiazide diuretic Block Na/Cl symproter in distal tubule Moderate Diuresis Reduced by NSAIDs Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity
38
Bumetanide
``` Loop diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid ```
39
ethacrynic acid
``` loops diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid ```
40
furosemide
``` loop diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid ```
41
torsemide
``` loop diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid ```
42
Amiloride
K sparing diuretic ``` Mechanism of action: late distal tubule and collecting duct – Na+ channel blockers • Diuretic effect in combination with thiazides – Mild diuresis – Weak antihypertensive effect • Adverse effects: – Hyperkalemia ```
43
triamterene
K sparing diuretic ``` Mechanism of action: late distal tubule and collecting duct – Na+ channel blockers • Diuretic effect in combination with thiazides – Mild diuresis – Weak antihypertensive effect • Adverse effects: – Hyperkalemia ```
44
eplerenone
Aldosterone receptor antagonist ``` Mechanism of action: collecting duct – Block sodium and water reabsorption – Also potassium sparing • Diuretic effect: – Mild diuresis • Use: – Resistant hypertension – CHF with hypertension • Adverse effects: – Hyperkalemia ```

Pharma (39 decks)

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