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Block 4 Pharm > Anti-hypertensive Drugs > Flashcards

Anti-hypertensive Drugs Flashcards

1
Q

What is the average efficacy of diuretics’ ability to lower blood pressure when administered alone

A

about 10-15 mmHg

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2
Q

In what context of hypertension are diuretics used for

A

mild to moderate hypertension with normal cardiac/renal function

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3
Q

In what patients are the thiazides not particularly effective

A

patients with renal insufficiency

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4
Q

What are the 8 classes of drugs used to treat hypertension

A
  1. Diuretics
  2. Calcium channel blockers (CCBs)
  3. Centrally acting agents
  4. Alpha adrenergic blockers
  5. Beta adrenergic blockers
  6. Vasodilators
  7. Angiotensin converting enzyme inhibitor (ACE-I)
  8. Angiotensin receptor blockers (ARBs)
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5
Q

Of the 8 classes of drugs used to treat hypertension which 4 are considered to be the first line drugs of choice

A
  1. Diuretics
  2. CCBs
  3. ACE-Is
  4. ARBs
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6
Q

generally (not including the K+ sparing diuretics) what are the side effects of the diuretics

A

Hyponatremia, HYPERGLYCEMIA, Increased LDL/HDL ratio, HYPOKALEMIA, and metabolic alkalosis

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7
Q

What is the MOA of the thiazides

A

inhibits Na+/Cl co transporter

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8
Q

How do the thiazides decrease blood pressure

A
  1. Decreases fluid volume by preventing the reabsorption of Na+ in the DCT
  2. Stimulated PG production leading to vasodilation
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9
Q

What drugs can interfere with the ability of thiazides to treat hypertension

A

NSAIDs (interfere with the anti-hypertensive effect of PGs)

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10
Q

What drugs can be used with the thiazides to prevent hypokalemia

A

BB, ACEI, or ARBs (diminish K loss by blunting diuretic induced rise in renin and aldosterone levels)
or use with a K+ sparing diuretic

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11
Q

What class of drug will exacerbate the hyperlipidemic and hyperglycemic effects of the thiazides

A

Beta Blockers

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12
Q

Contraindication of the thiazides

A

existing hypokalemia

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13
Q

Relative contraindication of the thiazides

A

Pregnancy

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14
Q

What is the MOA of the loop diuretics

A

inhibits the Na+/K+/2Cl- co-transporter in TAL of hence

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15
Q

What is the prototype loop diuretic

A

furosemide

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16
Q

What are the differences in efficacy between the thiazide s and the loop diuretics

A

Furosemide has a short duration of action than thiazide, less effective in patients with normal renal function (due to rebound sodium retention)

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17
Q

What patient population are the loop diuretics usually reserved for

A

Patients refractory to thiazides, pts with moderate to severe renal insufficiency or CHF

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18
Q

What are the major side effects of the loop diuretics

A

Hyponatremia, HYPOKALEMIA, impaired diabetes control, increased LDL/HDL, REV. OTOTOXICITY

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19
Q

What drug can interfere with the ability of the loop diuretics to treat hypertension

A

NSAIDs (interfere with the anti-hypertensive effect of PGs)

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20
Q

What drug is to be avoided taken with the loop diuretics to avoid toxicities

A

Aminoglycosides (enhance ototoxicity and nephrotoxicity)

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21
Q

What are the 2 types (MOAs) of the K+ sparing diuretics

A

Aldosterone receptor antagonist (Spironolactone and eplerenone) and ENaC blocker (triamterene and amiloride)

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22
Q

In what context are the K+ sparing diuretics used to treat hypertension

A

NOT used alone for treatment, used in combo with other diuretics (usually to correct hypokalemia)

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23
Q

Generally adverse effect of the K+ sparing diuretics

A

HYPERKALEMIA

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24
Q

Adverse effect of spironolactone

A

gynecomastia

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25
Q

Contraindications of K+ sparing diuretics

A

any state that can lead to hyperkalemia, combination with drugs that inhibit the RAS (ACE-I, ARBs, BBs)

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26
Q

Selected drug interaction of the K+ sparing diuretics

A

NSAIDs (PG synthesis), ACE-I, ARBs, BBs

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27
Q

What is the common MOA of the Calcium channel blockers

A
  1. inhibit Ca2+ influx into vascular smooth muscle thru L-type Ca channels
  2. relax peripheral arterial vascular smooth muscle and decrease TPR (due inhibition of MLCK activity due to decrease in Ca-calmodulin)
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28
Q

What are the 2 main types of Ca Channel blockers

A

dihydropyridines and non-dihydropyridines

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29
Q

What differentiates dihydropridines and non-dihydropyridines

A

Non-dihydropyridines also reduce Ca current in CARDIAC pacemaker cells and reduce conduction in AV node –> lower HR and contractility (due to decrease Ca-induced Ca release from myocyte SR) –> reduce cardiac output

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30
Q

MOA of Nifedipine (prototype)

A

Dihydropyridine –> selective vasodilator of vascular smooth muscle

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31
Q

How is Nifedipine metabolized? How does that impact who is administered it?

A

P450 system - avoid in patients with liver disease and consider drug interactions that interfere with P450 system

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32
Q

Side effects of Nifedipine

A

acute tachycardia (reflex sympathoexcitation), peripheral edema (arteriolar dilation > ventilation)

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33
Q

MOA of Diltiazem

A

non-dihydropyridine –> inhibits sinus node as well as L-type Ca channels of myocytes and vascular smooth muscle –> reduces both cardiac output and peripheral resistance

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34
Q

Side effects of Diltiazem

A

bradycardia (slowed rate and conduction)

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35
Q

MOA of verapamil

A

non-dihydropyridine –> potent effect of the heart with more pronounced reduction of currents –> reduces both cardiac output and resistance

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36
Q

Side effects of verapamil

A

constipation and bradycardia

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37
Q

Relative contraindication for CCBs

A

pts with liver failure (drugs are metabolized by liver) and patients with SA or AV node conduction disturbances should NOT be given verapamil nor diltiazem (caution in pts on BBs for this reason)

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38
Q

MOA of the sympatholytic drugs to treat hypertension

A

reduce sympathetic drive to the heart and/or blood vessels –> decreased venous return, cardiac output, TPR, and renin release

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39
Q

MOA of the centrally acting agents for treating hypertension

A

reduce sympathetic output from the vasopressor centers in the brainstem

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40
Q

MOA of Clonidine (prototype)

A

alpha2 agonist at medullary cardiovascular regulatory centers –> decreases symp. outflow from CNS to vascular smooth muscle

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41
Q

Side effects of Clonidine

A

sedation, dry mouth, contact dermatitis (due to transdermal patch)

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42
Q

Why is Guanfacine a better choice over clonidine

A

has a longer half-life, less chance of rebound (hypertensive crisis)

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43
Q

What are the significant dangers when a patient misses a dose of Clonidine or abruptly stops taking it

A

rebound hypertension

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44
Q

MOA of methyldopa

A

crosses BBB and in converted to methyl-NE and acts as alpha2 agonist as well as competes with L-DOPA for DOPA decraboxylase preventing the production of dopamine and NE or EPI in peripheral nerves

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45
Q

What medication with methyldopa interfere with

A

L-DOPA for parkinsons

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46
Q

What are the side effects of methyldopa

A

Sedation

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47
Q

Contraindication for methyldopa

A

liver disease

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48
Q

In what specific condition is methyldopa used most extensively in

A

Hypertension during pregnancy

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49
Q

What is the MOA of reserpine

A

blocks VMAT vesicular transporter, prevents storage of NE centrally and peripherally

50
Q

How is reserpine generally administered to treat hypertension

A

Given in combination with diuretics (side effects are significant in doses used for monotherapy)- low dose combo is highly efficacious with minimal side effects

51
Q

Side effects of reserpine

A

DEPRESSION, nasal congestion

52
Q

Selected drug interactions of reserpine

A

potentiates effects of CNS depressants and MOAI (counteract the effects of reserpine)

53
Q

MOA of alpha adrenergic antagonists

A

act at post synaptic receptors to block arterial and venous constriction

54
Q

MOA of phenoxybenzamine

A

non-selective alpha adrenergic antagonist

55
Q

Indications for phenoxybenzamine

A

used exclusively for htn due to pheochromocytoma

56
Q

Side effects of phenoxybenzamine

A

tachycardia (baroreflex)

57
Q

MOA of prazosin (prototype)

A

selective a1 adrenergic antagonist

58
Q

what are the advantages of terazosin and doxazosin over prazosin

A

longer half life, terazosin and doxazosin can be dosed once/day

59
Q

Side effects of Prazosin

A

Hypotension (1st dose), fluid retention (best results obtained when taken with a diuretic)

60
Q

Benefits of Prazosin/other selective a1 antagonists

A

do not impair exercise tolerance, less tachycardia than direct vasodilators or non-specific a-antagonists, DECREASES LDL/HDL

61
Q

MOA od BBs

A

B-adrenergic antagonist: decrease myocardial contraction and CO, decrease renin secretion (and ATII), reduce sympathetic action thru CNS effects (lipophilic ones)

62
Q

MOA of propanolol (1st gen)

A

Non-selective BB, lipophilic, short half life

63
Q

Indications for propanolol

A

mild to moderate hypertension, used as an adjust to prevent reflexive tachycardia from direct vasodilators, MI or arrhythmia

64
Q

Indication for Prazosin/Terazosin/Doxazosin

A

Second line for chronic hypertension

65
Q

MOA of nadolol

A

non-selective BB

66
Q

Advantage of nadolol over propanolo

A

longer half life, allows single daily dosing, hydrophilic

67
Q

MOA of pindolol

A

non selective B-antagonist with partial B-agonist activity

68
Q

Advantages of pindolol over other BBs

A

produces less bradycardia than other BBs (potentially eliminated some of the side effects of BBs)

69
Q

Indication for pindolol

A

chronic hypertension, pts with symptomatic bradycardia or postural hypotension

70
Q

MOA of metoprolol

A

B1 selective antagonist (fewer respiratory effects), lipophilic (so may have central sympatholytic effect)

71
Q

Indication for metoprolol

A

Hypertension, long term angina rx

72
Q

MOA for atenolol

A

B1 selective antagonist, hydrophilic

73
Q

Indications for atenolol

A

Chronic hypertension, MI, angina, HF

74
Q

MOA for labetolol

A

mixed alpha/beta adrenergic receptor antagonist

75
Q

Side effect of labetolol

A

lipophilic, higher incidence of orthostatic hypertension

76
Q

MOA of Carvedilol

A

non-selective alpha receptor and beta blocker and NO generator (vasodilatory), lipophilic

77
Q

General side effects of beta blockers

A

ALL: bradycardia, increased serum TGs, decreased HDL levels, hyperglycemia (less so with cardioselective), low exercise tolerance
Non-selective: increased airway resistance
Lipophilic: insomnia, mild chronic fatigue, depression

78
Q

Drug interactions with the BBs

A

CCB’s increase the risk of conduction disturbances (reduces contractility and conduction)

79
Q

What are the contraindications for the BBs

A

cardiogenic shock, sinus bradycardia, ASTHMA, severe congestive heart failure (protective in compensated heart failure)

80
Q

Why should you taper a patient off a BB

A

rebound tachycardia

81
Q

What should you worry about with a diabetic patient on a BB

A

BB can mask and prolong insulin induced hypoglycemia

82
Q

What patient populations are BB mono therapy less efficacious in

A

African Americans and the elderly

83
Q

MOA of Hydralazine

A

vasodilator of small vessels (primarily arterioles)

84
Q

Indications for hydralazine

A

Drug resistant hypertension and emergencies

85
Q

Side effects of hydralazine

A

tachycardia, angina aggravation (reduced venous return can compromise coronary blood flow), fluid retention, lupus-like syndrome

86
Q

What drug will interfere with hydralazine efficacy

A

NSAIDs (probably due to PGs synthesis)

87
Q

MOA of Minoxidil

A

vasodilator of arterioles via K+ channel opener

88
Q

Indications for Minoxidil

A

drug resistant hypertension

89
Q

Side effects of Minoxidil

A

tachycardia, angina aggravation (reduced venous return can compromise coronary blood flow), fluid retention, hypertrichosis

90
Q

MOA of Nitroprusside

A

vasodilation of small vessels (primarily arterioles and veins), does not stimulate increase cardiac work

91
Q

Indications for Nitroprusside

A

Emergencies: immediate onset brief duration

92
Q

Side effects of Nitroprusside

A

cyanide poisoning

93
Q

Contraindication for hydralazine

A

coronary artery disease (vasodilation in unobstructed coronary vessels “steal” blood from obstructed regions)

94
Q

MOA of the ACE-Is

A

blocks production of angiotensin II and Ang-II mediated vasoconstriction: decreases TPR, increases bradykinin –> vasodilation, and reduces aldosterone secretion

95
Q

MOA of captopril (Prototype)

A

ACE-I

96
Q

MOA of Enalapril

A

ACE-I

97
Q

MOA of Lisinopril

A

ACE-I

98
Q

Why would you prescribe Lisinopril over captopril and enalapril

A

Captopril - has a shorter half life
Enalapril - longer half life BUT has to be converted to an active metabolite
Lisinopril - water soluble and excrete unchanged by the kidney, longer half life

99
Q

Side effects of Lisinopril

A

DRY COUGH, hyperkalemia, angioedema (more common in african americans)

100
Q

Drug interactions with Lisinopril

A

K+ sparing diuretics: can exacerbate hyperkalemia

101
Q

Contraindications of Lisinopril

A

Pregnancy (Ang II in important in fetal renal development) and bilateral stenosis

102
Q

Therapeutic benefits of lisinopril

A

prolongs survival in pts with HF or LV disfunction after an MI, preserves renal function in pts with diabetes

103
Q

MOA of the ARBs

A

Bind to the angiotensin II receptors and inhibit there mediation of receptor vasoconstriction and sodium retention, but do not inhibit bradykinin metabolism (do not produce dry cough)

104
Q

MOA of Losartan

A

ARB: selective AT1 receptor antagonist, short half life

105
Q

Side effect of Losartan

A

Hyperkalemia

106
Q

Contraindication for losartan

A

Pregnancy

107
Q

Drug interactions for losartan

A

K+ sparing drugs (worsen hyperkalemia)

108
Q

What patient population is losartan less effective in

A

Salt sensitive hypertensive pts (African americans)

109
Q

What pt population should you reduce the dose of losartan

A

Liver disease (met by the liver) and hypovolemia

110
Q

What drug(s) would be a good combination with the thiazides

A

K+ sparing diuretics and BBs

111
Q

What drugs are a good combo with the CCBs

A

ACE-I

112
Q

What are the bad combos of drugs

A

ACE-I/ARB and K+ sparing diuretics

ACE-I and ARBs

113
Q

What ant-hypertensive would be recommended for a diabetic patient

A

ACE-I or ARBs, AAs, CCBs (few effects on carb met)

114
Q

What ant-hypertensive would be recommended for a pt with heart failure

A

ACE-I and diuretics

115
Q

What ant-hypertensive would be recommended for a pt with MI

A

BBs, and ACE-I (prevent LV remodeling)

116
Q

What ant-hypertensive would be recommended for a pregnant pt with hypertension

A

methyldopa

117
Q

What ant-hypertensive would be recommended for an african american pt with uncomplicated hypertension

A

CCBs or diuretics as first line, or BBs, ACE-I, ARBs in combo with a diuretic

118
Q

What ant-hypertensive would be recommended for a hyperlipidemic pt

A

Alpha blockers (decrease LDL/HDL ratio), CCBs, ACE-I, ARBs have little effect on lipid profile

119
Q

What drug should be avoid in obstructive airway disease

A

BBs

120
Q

At what blood pressure should you treat a pt under 60 without diabetes with anti-hypertensives

A

140/90

121
Q

At what blood pressure should you treat a pt over 60 without diabetes with anti-hypertensives

A

150/90

Block 4 Pharm (9 decks)

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