Antihypertensive Agents Flashcards

1
Q

Diuretics

1) How effective are they?
2) How do they work?

A

1) lower BP 10-15 mmHG

2) deplete body sodium stores

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2
Q

Chlorothiazide

1) Use
2) Mechanism of action
3) Major side effects

A

1) First line therapy for mild to moderate HTN with normal renal and cardiac function
2) Inhibits sodium-chloride transporter in the distal tubule and early collecting duct
3) Hypokalemia, hyperglycemia

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3
Q

Chlorthalidone

1) Use
2) Mechanism of action
3) Major side effects

A

1) First line therapy for mild to moderate HTN with normal renal and cardiac function
2) Inhibits sodium-chloride transporter in the distal tubule and early collecting duct
3) Hypokalemia, hyperglycemia

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4
Q

Hydrochlorothiazide

1) Use
2) Mechanism of action
3) Major side effects

A

1) First line therapy for mild to moderate HTN with normal renal and cardiac function
2) Inhibits sodium-chloride transporter in the distal tubule and early collecting duct
3) Hypokalemia, hyperglycemia

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5
Q

Furosemide

1) Use
2) Mechanism of action
3) Major side effects

A

1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity

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6
Q

Torsemide

1) Use
2) Mechanism of action
3) Major side effects

A

1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity

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7
Q

Ethacrynic acid

1) Use
2) Mechanism of action
3) Major side effects

A

1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity

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8
Q

Bumetanide

1) Use
2) Mechanism of action
3) Major side effects

A

1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity

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9
Q

Spironolactone

1) Use
2) Mechanism of action
3) Side effects

A

1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Bind to mineralocorticoid receptors and blunt aldosterone activity to act on the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis

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10
Q

Eplerenone

1) Use
2) Mechanism of action
3) Side effects

A

1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Bind to mineralocorticoid receptors and blunt aldosterone activity to act on the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis

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11
Q

Amiloride

1) Use
2) Mechanism of action
3) Side effects

A

1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Inhibit Na influx through luminal channels in the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis

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12
Q

Triamterene

1) Use
2) Mechanism of action
3) Side effects

A

1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Inhibit Na influx through luminal channels in the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis

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13
Q

Aliskiren

1) Use
2) Mechanism of action

A

1) Hypertension

2) Oran renin inhibitor

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14
Q

Catopril

1) Use
2) Mechanism of action

A

1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin

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15
Q

Enalapril

1) Use
2) Mechanism of action

A

1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin

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16
Q

Fosinopril

1) Use
2) Mechanism of action

A

1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin

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17
Q

Lisinopril

1) Use
2) Mechanism of action

A

1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin

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18
Q

What are three side effects of ACE inhibitors?

A

Dry cough from increased bradykinin levels
Hyperkalmeia
Angioedema
Hypotension in the presence of hypovolemia

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19
Q

What are the effects of ACE inhibitors on CO and HR

A

Remain unchanged

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20
Q

What are additional benefits of ACE inhibitors?

A

1) Improved renal hemodynamics in renal disease
2) decreased hypertrophy and remodeling in MI and HF
3) protects from diabetic nephropathy

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21
Q

Losartan

1) Use
2) Mechanism of action

A

1) Hypertension

2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion

22
Q

Valsartan

1) Use
2) Mechanism of action

A

1) Hypertension

2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion

23
Q

Candesartan

1) Use
2) Mechanism of action

A

1) Hypertension

2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion

24
Q

Irbesartan

1) Use
2) Mechanism of action

A

1) Hypertension

2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion

25
Q

What are the side effects of ARBs?

A

Same as ACEs, but reduced cough and angioedema

26
Q

Propranolol

1) Use
2) Mechanism
3) Effect on CO

A

1) Hypertension
2) Non-selective B1-B2 receptor antagonist
3) Decreases CO by decreasing HR and contractility

27
Q

Metoprolol

1) Use
2) Mechanism
3) Effect on CO

A

1) Hypertension
2) Selective B1 receptor antagonist
3) Decreases CO by decreasing HR and contractility

28
Q

Atenolol

1) Use
2) Mechanism
3) Effect on CO

A

1) Hypertension
2) Selective B1 receptor antagonist
3) Decreases CO by decreasing HR and contractility

29
Q

1) What are the side effects of beta blockers?

2) Who should avoid beta blockers?

A

1) Nausea/vomiting, dizziness, sleep disorders with propranolol
2) Asthmatics, PVD, cardiac conduction delay

30
Q

Prazosin

1) Use
2) Mechanism

A

1) HTN and pheochromocytoma

2) blockade of a1 receptors –> dilation of arterioles and capacitance veins

31
Q

Terazosin

1) Use
2) Mechanism

A

1) HTN and pheochromocytoma

2) blockade of a1 receptors –> dilation of arterioles and capacitance veins

32
Q

Doxazosin

1) Use
2) Mechanism

A

1) HTN and pheochromocytoma

2) blockade of a1 receptors –> dilation of arterioles and capacitance veins

33
Q

What are the side effects of a1 antagonists?

A

Reflex tachycardia, fluid retention, orthostatic hypotension

34
Q

Labetalol

1) Use
2) Mechanism

A

1) Hypertensive emergencies IV, HTN orally

2) B blocking and vasodilating effects of combined a and B antagonism (B>a)

35
Q

Carvedilol

1) Use
2) Mechanism

A

1) Reducing mortality in HF, HTN

2) B blocking and vasodilating effects of combined a and B antagonism (1:1 ratio B:a)

36
Q

Clonidine

1) Use
2) Mechanism

A

1) resistant hypertension

2) stimulate presynaptic a2 receptors decreases sympathetic outflow and baroreceptor response

37
Q

Methyldopa

1) Use
2) Mechanism

A

1) pregnancy induced hypertension

2) stimulate presynaptic a2 receptors decreases sympathetic outflow and baroreceptor response

38
Q

Nifedipine

1) Use
2) Mechanism

A

1) HTN esp. w low renin, AA with systolic hypertension

2) Block voltage sensitive L-type Ca++ channels in the vascular smooth muscle

39
Q

Nimodipine

1) Use
2) Mechanism

A

1) HTN esp. w low renin, AA with systolic hypertension

2) Block voltage sensitive L-type Ca++ channels in the vascular smooth muscle

40
Q

Amlodipine

1) Use
2) Mechanism

A

1) HTN esp. w low renin, AA with systolic hypertension

2) Block voltage sensitive L-type Ca++ channels in the vascular smooth muscle

41
Q

Verapamil

1) Use
2) Mechanism

A

1) HTN esp. with low renin

2) Block voltage sensitive L-type Ca++ channels in the heart (cardiac and AV node selective)

42
Q

Benzothiazepine

1) Use
2) Mechanism

A

1) HTN esp. with low renin

2) Block voltage sensitive L-type Ca++ channels in the heart (cardiac and AV node selective)

43
Q
What are the effects on:
1) PVR
2) Baroreceptor Reflex
3) HR
when using calcium channel blockers?
A

1) decrease PVR
2) decreased baroreceptor reflex increases in HR
3) decreased HR

44
Q

Hydralazine

1) Use
2) Mechanism

A

1) mild to moderate HTN in combination with diuretic and B-blocker
2) acts through the release of NO (NO required)

45
Q

Minoxidil

1) Use
2) Mechanism

A

1) resistant HTN in combination with diuretic and B-blocker

2) opens K channels and hyperpolarizes the cell, closing Ca++ voltage gated channels

46
Q

Nitroprusside

1) Use
2) Mechanism

A

1) Produce hypotension in surgery and HTN emergencies

2) direct vasodilation by generating NO, increasing cGMP

47
Q

Nitroglycerin

1) Use
2) Mechanism

A

1) Cardiac surgery and HTN emergencies

2) generates NO increasing cGMP –> vasodilation with preferential effect on veins over arteries**

48
Q

Epoprostenol

1) Use
2) Mechanism

A

1) Primary pulmonary HTN

2) synthetic analog of prostacyclin (PGI2) –> direct vasodilation and counteracts thromboxane A2

49
Q

Bosentan

1) Use
2) Mechanism

A

1) Primary pulmonary HTN

2) Non-selective Endothelin receptor blocker

50
Q

Ambrisentan

1) Use
2) Mechanism

A

1) Primary pulmonary HTN

2) Selective endothelia receptor blocker of ETa receptor