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Pharma > Hypertension > Flashcards

Hypertension Flashcards

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

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

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

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

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

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

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

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
Q

hydralazine

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

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
Q

minoxidil

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

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
Q

nitroglycerin

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

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
Q

nitroprusside

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

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
Q

riociguat

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

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
Q

dilitazem

A

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
Q

verapamil

A

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
Q

Amlodipine

A

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
Q

Nicardipine

A

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
Q

Nifedipine

A

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
Q

Chlorothiazide

A

Thiazide diuretic

Block Na/Cl symproter in distal tubule

Moderate Diuresis

Reduced by NSAIDs

Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity

36
Q

chorthalidone

A

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
Q

hydrochlorothiazide

A

Thiazide diuretic

Block Na/Cl symproter in distal tubule

Moderate Diuresis

Reduced by NSAIDs

Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity

38
Q

Bumetanide

A 
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
Q

ethacrynic acid

A 
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
Q

furosemide

A 
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
Q

torsemide

A 
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
Q

Amiloride

A

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
Q

triamterene

A

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
Q

eplerenone

A

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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