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CVS II Pharmacology > Antihypertensive drugs > Flashcards

Antihypertensive drugs Flashcards

1
Q

treatment for HTN + angina pectoris

A

BB and/or CCB

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2
Q

HTN + BPH treatment

A

alpha blocker

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3
Q

HTN + DM treatment

A

ACEI or ARB

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4
Q

HTN + heart failure treatment

A

ACEI, ARB, BB, Diuretic

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5
Q

HTN + MI treatment

A

BB and ACEI

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6
Q

HTN + high cholesterol (dyslipidemia) treatment

A

Alpha blocker and CCB
Don’t give thiazide diuretics because they cause increased lipids

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7
Q

what drugs are recommended for stage I HTN

A

One of the following: diuretic, ACEI, ARB or CCB

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8
Q

what are the recommended drugs for stage II HTN

A

2 drug combo:
diuretic + ACEI, ARB, or CCB

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9
Q

In a study of a patient with refractory hypertension, which of the
following antihypertensive combinations will reduce the systolic
BP the most?
A. adding an alpha blocker to a beta blocker
B. adding an ARB to an ACEI
C. Adding K+ sparing diuretic to a thiazide diuretic
D. Adding a dihydropyridine CCB to a non-hydropyridine CCB

A

C. to balance out the ions

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10
Q

hich of the following activities can have the greatest
effect on blood pressure reading?
A. The consumption of three alcoholic drinks 12 h before the
measurement
B. The drinking of a cup of coffee 1h before the measurement
C. The smoking of a cigarette 15 minutes before the measurement
D. The use of a cuff that is one size too small for the patient.

A

C, smoking

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11
Q

what is the site of action or thiazide diuretics

A

DCT

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12
Q

what is the drug of choice for HTN during pregnancy (pre-eclampsia)

A

first choice is Labetalol (beta blocker) otherwise hydralazine, nifedipine, or nitroglycerin

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13
Q

what is the site of action of loop diuretics

A

loop of henle

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14
Q

what is the site of action of osmotic diuretics

A

everywhere but mostly on the proximal convoluted tubule

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15
Q

what is the site of action of carbonic anhydrase
Inhibitors

A

proximal convoluted tubule

These inhibitors work by blocking the enzyme carbonic anhydrase, which is crucial for the reabsorption of bicarbonate. This action leads to increased excretion of bicarbonate, sodium, water, and potassium, and it reduces the reabsorption of these substances in the proximal convoluted tubule.

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16
Q

what is the site of action of K+ sparing diuretics

A

collecting duct/dct

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17
Q

what is the drug(s) of choice for increased SV due to edema or increased renin angiotensin activity

A

Diuretics, ACEI, or ARB

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18
Q

What is the MOA of Thiazide diuretics

A

inhibit Na/Cl cotransport causing increased excretion of Na, K, Cl, Mg and HCO3 and decreasing Ca and uric acid

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19
Q

what is the only thiazide diuretic that does not increase plasma cholestero and TGs

A

indapamide

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20
Q

what type of diuretic is chlorothiazide

A

thiazide diuretic

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21
Q

what type of diuretic is hydrochlorothiazide

A

thiazide

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22
Q

what type of diuretic is indapamide

A

thiazide

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23
Q

what type of diuretic is chlorthalidone

A

thiazide

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24
Q

what type of diuretic is metolazone

A

thiazide

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25
Q

what is the MOA of loop diuretics

A

inhibit the Na+/K+ dichloride cotransport

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26
Q

what type of diuretic would not affect kidney stones

A

thiazide diuretics

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27
Q

what is the major adverse effect of loop diuretics

A

ototoxicity (when used in conjunction with aminoglycosides)

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28
Q

what type of diuretic is furosemide

A

loop diuretic

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29
Q

what type of diuretic is bumetanide

A

loop diuretic

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30
Q

what type of diuretic is torsemide

A

loop diuretic

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31
Q

what type of diuretic is ethacrynic acid

A

loop diuretic

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32
Q

what are the two osmotic diuretics

A

mannitol and glycerol

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33
Q

what is the MOA of osmotic diuretics

A

increase the osmotic pressure in the PT which leads to inhibition of reabsorption of water and electrolytes

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34
Q

what are the indications for mannitol and glycerol (osmotic diuretics)

A

cerebral edema, acute glaucoma, acute renal failure

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35
Q

what are the adverse effects of osmotic diuretics

A

excessive plasma volume expansion which can lead to heart failure

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36
Q

what are the two carbonic anhydrase inhibitors

A

acetazolamide and Dorzolamide

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37
Q

what is the MOA of carbonic anhydrase inhibitors

A

Increase excretion of Na+, K+ and HCO3

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38
Q

what are the indications for carbonic anhydrase inhibitors

A

high altitude sickness, glaucoma, and overdose of acidic drugs (to alkalinize the urine)

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39
Q

what are the adverse effects of CA inhibitors

A

drowsiness and paresthesia

acetazolamide

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40
Q

what is the MOA of spironolactone

A

K+ sparing diuretic, aldosterone antagonist

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41
Q

what is the MOA of Eplerenone

A

K+ sparing diuretic (less gynecomastia risk)

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42
Q

what is the MOA of amiloride

A

K+ sparing diuretic, black Na+ reabsorption

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43
Q

what is the MOA of triamterene

A

K+ sparing diuretic, block Na+ reabsorption

44
Q

what are the clinical uses of K+ sparing diuretics (Spironolactone, eplerenone, amiloride, and triamterene)

A

spironolactone + ACEI increased survival in Heart failure and is also used to treat hirsutism due to antiandrogenic effect
amiloride is used for nephrogenic Diabetes insipidus caused by lithium

45
Q

what are the adverse effects of K+ sparing diuretics

A

hyperkalemia, nephrolithiasis, decreased libido and gynecomastia

46
Q

what is the treatment for hyperkalemia

A

patiromer

47
Q

what is the MOA of conivaptan

A

V1A and V2 receptor blocker

48
Q

What is the MOA of Tolvaptan

A

Selective V2 receptor blocker

49
Q

what are the clinical uses of conivaptan and Tolvaptan

A

Euvolemic and hypervolemic hyponatremia

50
Q

what are the adverse effects of conivaptan and Tolvaptan

A

Infusion site reaction and hypokalemia

51
Q

Which of the following diuretics causes hyperkalemia:
Acetazolamide, Spironolactone, HCTZ, or Furosemide?

A

spironolactone (also ace inhibitors)

52
Q

what is the suffix for ace inhibitors

A

“pril” (captopril, enalapril, etc.)

53
Q

what is the MOA of ACE inhibitors

A

prevent conversion of Angiotensin I to angiotensin II, decrease the release of aldosterone and prevent conversion of bradykinin to its inactive compound (this has a god vasodilatory effect)

54
Q

what is one of the side effects of ACE inhibitors as it relates to its effect on bradykinin

A

dry cough

55
Q

why are ACEI the drug of choice for patients with HTN + Diabetes

A

because it slows down renal damage (remember that diabetic patients tend to develop nephropathy)

56
Q

what are the clinical uses of ACEI

A

heart failure, LV systolic dysfunction (post MI), HTN + Diabetes, and stroke

57
Q

what are the adverse effects of ACEI drugs

A

hyperkalemia, angioedema, proteinuria, and elevated BUN and creatinine

58
Q

what are the contraindications of ACEI drugs

A
  1. Pregnancy may cause Fetopathy
    Oligohydramnios, IUGR, Hypocalvaria and renal failure
  2. Angioedema
  3. Bilateral renal artery stenosis
59
Q

what is the suffix for ARB (angiotensin II receptor blockers)

A

“Sartan” (losartan, valsartan, etc.)

60
Q

what is the MOA of ARB drugs

A

they block angiotensin II receptors with NO effect on bradykinin metabolism (unlike ACEI)

61
Q

what are the adverse effects of ARB drugs

A

hyperkalemia, angioedema

62
Q

what are the contraindications for ARB drugs

A

pregnancy

63
Q

what is the suffix for beta blockers

A

“OLOL”

64
Q

what are the three non-selective BB drugs

A

propranolol, nadolol, and timolol

65
Q

what are the four selective B1 blockers

A

metoprolol, atenolol, bisoprolol, and betaxolol

66
Q

what type of drug is acebutolol

A

beta-adrenergic partial agonist

67
Q

what type of drug is nebivolol

A

B-blocker and NO release

68
Q

what is the MOA of carvedilol and labetalol

A

non-selective beta and alpha blockers

69
Q

what are the clinical uses of beta blockers

A

CAD, tachyarrhythmias, migraine headaches, and anxiety

70
Q

what are the adverse effects of beta blockers

A

Bradycardia
Fatigue
Sexual disfunction
AV Block
Abrupt withdrawal can cause rebound hypertension due
To upregulation of # of receptors
Mask signs of Hypoglycemia

71
Q

what is the most common cause of hypoglycemia

A

insulin

72
Q

do you need to be cautious when using beta blockers with patients with asthma

A

yes

73
Q

what is the suffix for calcium channel blockers for vascular tissues (dihydropyridines)

A

“DIPINE” (amlodipine, nifedipine, felodipine, isradipine, nicardipine, and clevidipine

74
Q

what are the heart (non-hydropyridine) CCB drugs

A

diltiazem and verapamil (they work directly on the heart)

75
Q

what are the clinical uses of non-hydropyridines

A

arrhythmias with tachycardia

76
Q

what is the MOA of dihydropyridines

A

block L-type Ca++ channels causing vasodilation and decrease peripheral resistance

77
Q

what are the adverse effects of dihydropyridines

A

reflex tachycardia (due to vasodilating of peripheral vessels), ankle edema, and gingival hyperplasia

78
Q

what is the MOA of non-dihydropyridines

A

decrease heart rate and conduction velocity

79
Q

what are the adverse effects of non-dihydropyridines

A

AV conduction block and constipation

80
Q

what is the MOA of Clonidine

A

activates presynaptic alpha 2 receptors (vasodilation)

81
Q

what are the clinical uses of clonidine

A

mild to moderate HTN

82
Q

what are the adverse effects of clonidine

A

edema, rebound HTN after withdrawal

83
Q

what alpha 2 agonist is safe for pregnancy

A

alpha Methyl Dopa

84
Q

What is the MOA of Guanethidine

A

binds to storage vesicles and inhibits release of NE

85
Q

what neuronal blocking agent is contraindicated in people taking tricyclic antidepressants

A

guanethidine

86
Q

what is the MOA of reserpine

A

binds to storage vesicles and destroys them causing depletion of NE, DA, and serotonin (NO LONGER USED due to severe side effects of suicidal thoughts)

87
Q

what is the MOA prazosin, doxazosin and terazosin

A

Selective antagonists of peripheral alpha 1 receptors

88
Q

what are the clinical uses of selective alpha 1 blockers

A

HTN, and BPH

89
Q

what are the adverse effects of selective peripheral alpha 1 blockers

A

first dose syncope (orthostatic hypotension), incontinence in women, retrograde ejaculation

90
Q

what type of necrosis do you see in malignant HTN

A

fibrinoid

91
Q

what type of necrosis do you see in TB

A

caseous

92
Q

what are the four direct acting vasodiator drugs

A

hydralazine, sodium nitroprusside, minoxidil, and fenoldopam

93
Q

what is the MOA of hydralazine

A

prodrug of NO

94
Q

what is the associated syndrome of hydralazine seen in slow acetylators

A

SLE like syndrome

95
Q

what is the MOA of sodium nitroprusside

A

cGMP vasodialtion

96
Q

what is the clinical use of sodium nitroprusside

A

given for IV HTN crisis (note that is can cause cyanide poisoning if administered too quickl/high dose so you have to start with sodium nitrite then Na thiosulfate of Vit B12

97
Q

what is the common name for the direct acting vasodilator, Minoxidil

A

rogaine

98
Q

what is the MOA of the direct vasodilator fenoldopam

A

stimulates D1 and alpha 2 receptor

99
Q

what is the direct renin inhibior drug

A

aliskiren

100
Q

what is the MOA of the renin inhibitor aliskiren

A

it blocks conversion of angiotensinogen to AGI

101
Q

what are the adverse effects of aliskiren

A

hyperkalemia, angioedema also NOT SAFE IN PREGNANCY

102
Q

why are ACEI or ARB the to drugs that are indicated for the combo of HTN and DM

A

bc ACEI and ARB protect pt. from getting nephropathy which is common in DM

103
Q

what are the antiHTN drugs that can cause rebound HTN

A

BB and alpha-2 agonists

104
Q

what antiHTN drugs cause hyperkalemia

A

ACEI, ARB, K+ sparing diuretics, and renin inhibitors

105
Q

what antiHTN drugs are contraindicated in pregnancy

A

ACEI, ARB, and renin inhibitors

106
Q

what AntiHTN drugs cause reflex tachycardia

A

CCB’s (esp. dihydropyridines) and direct acting vasodilators

CVS II Pharmacology (9 decks)

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