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Pharm Sem 4 > Block 1 > Flashcards

Block 1 Flashcards

1
Q

acute regulation of blood pressure occurs through __ while long term regulation occurs through __

A

moment to moment- baroreceptor
long term- RAAS

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2
Q

what are the 6 classes of antihypertensive drugs

A

antiadrenergics (sympatholytics inhibit sympathetic activity)
ACE inhibitors
angiotensin receptor blockers
calcium channel blockers
direct vasodilators
diuretics

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3
Q

what are 2 compensatory responses to decreased blood pressure due to antihypertensive drugs

A

reflex tachycardia
increased renin activity (Na/H2O retention)

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4
Q

what suffix indicates an alpha-1 blocker

A

-zosin

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5
Q

what is the cause of orthostatic hypotension

A

venule dilation

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6
Q

what is the physiological effect of alpha-1 blocker usage

A

vasodilation (decreased arteriolar and venous resistance)
decreased BP

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7
Q

why are alpha-1 blockers used in combination with beta blockers for hypertension

A

the addition of beta blockers decrease the effect of reflex tachycardia

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8
Q

what drug class is used for hypertension with benign prostatic hyperplasia

A

alpha-1 blockers (alpha-1A)

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9
Q

alpha-1 blockers are coupled with what G protein class, what is the effect

A

Gq

there is a decrease in Ca2+ and myosin light chain kinase activity, leading to contraction

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10
Q

what are the 3 main adverse effects of alpha-1 blockers

A

reflex tachycardia
first dose syncope
orthostatic hypotension

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11
Q

what drug class can be used but is rarely used for hypertension due to adverse effects, development of tolerance, and advent of safer drugs

A

alpha-1 blockers

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12
Q

what is the main advantage of alpha-1 blockers

A

positive effect on lipid profile

(increases HDL and decreases LDL)

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13
Q

what is an example of a non-selective beta blocker

A

propanolol

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14
Q

what suffix indicates a beta blocker

A

-olol

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15
Q

what type of beta blocking activity does atenolol have

A

beta-1

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16
Q

what type of beta blocking activity does esmolol have

A

beta-1

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17
Q

what type of beta blocking activity does metoprolol have

A

beta-1

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18
Q

what type of blocking activity does labetalol have

A

alpha-1 and beta

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19
Q

what type of blocking activity does carvediol have

A

alpha-1 and beta

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20
Q

what are 2 physiological effect of beta blockers

A

decrease HR and SV (and as a result CO)- beta-1 activity
decreases renin release (decreases peripheral resistance)- beta-1 activity

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21
Q

decrease in release of angiotensin II allows for what physiological effect which aids in blood pressure

A

vasodilation

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22
Q

what are 3 effects of propranolol, a non-selective beta blocker, on the heart

A

decreased inotropy (contractility)
decreased chronotropy (rate of contraction/HR)
decreased dromotropy (AV conduction/prolonged PR interval)

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23
Q

does propranolol decrease systolic, diastolic, or both

A

both

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24
Q

what is an advantage of propranolol compared to other beta blockers

A

no postural hypotension due to no venodilation

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25
Q

what is the effect of propranolol on the kidneys

A

decreases renin release (beta-1)

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26
Q

what is the effect of propranolol, a non-selective beta blocker, on the respiratory tract

A

bronchoconstriction and precipitation of bronchial asthma (beta-2)

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27
Q

propranolol, a non-selective beta blocker, is contraindicated in patients with what conditions

A

asthma
COPD

*due to bronchoconstriction and propranolol being a nonselective beta blocker

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28
Q

what is the effect of propranolol, a non-selective beta blocker, on the eyes

A

decreased IOP

*due to decreased aqueous humor production

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29
Q

what is the effect of propranolol, a non-selective beta blocker on the CNS

A

sleep disturbances
sedation
depression

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30
Q

what is the effect of propranolol, a non-selective beta blocker, on skeletal muscle

A

antagonizes epinephrine induced tremors

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31
Q

what is the effect of propranolol, a non-selective beta blocker, on carbohydrate metabolism

A

blockage of epinephrine induced glycogenolysis which can cause fasting hypoglycemia

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32
Q

what is the effect of propranolol, a non-selective beta blocker, on insulin release

A

decreases and as a result can lead to postprandial hyperglycemia

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33
Q

propranolol, a non-selective beta blocker, should be used with caution in patients with what 3 conditions

A

diabetes (propranolol decreases the release of insulin)
asthma and COPD (due to bronchoconstriction )

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34
Q

all beta blockers block __

A

tachycardia, a warning sign of hypoglycemia

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35
Q

what is the effect of propranolol, a non-selective beta blocker, on lipid metabolism

A

inhibits stimulation of sympathetic leading to increased triglyceride levels

*chronic use leads to increased VLDL, decreased HDL, and no change in LDL. this results in an increased LDL:HDL ratio

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36
Q

propranolol, a non-selective beta blocker can be used for all forms of angina except ___

A

Prinzmental (vasospastic) angina

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37
Q

can propranolol be used for hypo or hyperthyroidism

A

hyperthyroidism

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38
Q

what consideration must be made to use propranolol, a non-selective beta blocker, for pheochromocytoma

A

it can only be used along with an alpha blocker

*if used without, there will be a significant increase in blood pressure

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39
Q

what are 2 examples of beta blockers with partial agonist activity (intrinsic sympathomimetic activity)

A

pindolol
acebutolol

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40
Q

what are 3 advantages to using pindolol or acebutolol, beta blockers with partial agonist activity (intrinsic sympathomimetic activity)

A

less bradycardia
less vasoconstriction
less bronchoconstriction

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41
Q

beta blockers with partial agonist activity (intrinsic sympathomimetic activity) such as pindolol and acebutolol are useful in patient with hypertension who also have

A

bradycardia
diabetes mellitus
peripheral vascular disease
abnormal lipid profile

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42
Q

what are 2 adverse effects of beta blockers on the CVS

A

bradycardia
AV block

*due to decreased cAMP

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43
Q

what is used as treatment for beta blockage poisoning

A

glucagon

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44
Q

what is an adverse effect of beta blockers on the respiratory system

A

bronchoconstriction

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45
Q

beta blockers are contraindicated in conditions including … (4)

A

bronchial asthma
diabetes mellitus
Raynaud’s disease
Prinzmental angina

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46
Q

what type of receptor blockage can be performed in those with peripheral vascular disease, COPD, or asthma

A

beta-1

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47
Q

what is an adverse effect of selective beta-1 blockage

A

bradycardia

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48
Q

what beta-1 blocker is used to treat supraventricular tachycardia, intra/postoperative hypertension, and hypertensive emergencies

A

esmolol

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49
Q

what type of blocking activity does Nebivolol have for hypertension

A

beta-1 with vasodilating properties

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50
Q

how can nebivolol, a selective beta-1 agonist, cause vasodilation

A

due to induction of endothelial NO synthase which causes release of NO, a vasodilator

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51
Q

what is the effect of nebivolol if there is an inhibitor of CYP2D6

A

loss of beta-1 selectivity

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52
Q

beta blockers are less preferred in what population group

A

elderly

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53
Q

beta blockers should be avoided with use of what other drugs (4)

A

digitalis and verapamil (causes further depression of SA and AV node)
insulin/other antidiabetics (masks effects of hypoglycemia)
indomethacin/other NSAIDS (decreases antihypertensive action of beta blockers)
cimetidine (inhibits propranolol metabolism)

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54
Q

what are the physiological effects of labetalol and carvediol, alpha and beta receptor blockers

A

vasodilation
no reflex tachycardia
no alteration in lipid or glucose levels

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55
Q

what drug is used in hypertension of pheochromocytoma

A

labetalol (alpha and beta blocker)

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56
Q

what drug is used in compensated (symptoms are stable or absent) heart failure

A

carvediol (alpha and beta blocker)

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57
Q

what drug class does methyldopa belong to

A

centrally acting alpha2 agonist

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58
Q

what type of agonist is clonidine

A

alpha 2

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59
Q

what are the physiological effects of clonidine

A

decrease HR, CO, and total peripheral resistance

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60
Q

what are 4 side effects seen with clonidine use

A

dry mouth
CNS depression (sedation)
sodium and water retention (edema)

also rebound hypertension if discontinued abruptly

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61
Q

methyldopa causes a decrease in heartrate instead of __

A

reflex tachycardia

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62
Q

what drug is mainly used in hypertension during pregnancy

A

methyldopa

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63
Q

what 2 drugs can be used in hypertensive patients with renal insufficiency

A

methyldopa
fenoldopam

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64
Q

what are 4 effects of methyldopa

A

sedation
increased prolactin secretion (due to decreased dopa inhibition)
hemolytic anemia
sodium and water retention (edema)

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65
Q

how does reserpine work as an antihypertensive drug

A

inhibits the transport of NE into vesicles by interfering with VMAT

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66
Q

what are the physiological effects of reserpine

A

decreased NE leads to decreased CO and total peripheral resistance, as well as decreased dopamine and serotonin

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67
Q

what are 2 main adverse side effects of reserpine

A

severe depression (can lead to suicidal ideations)
increased GI secretions

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68
Q

how does guanethidine work as an antihypertensive drug

A

blocks release of NE

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69
Q

what are 3 main adverse effects of guanethidine

A

diarrhea
edema
retrograde ejaculation

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70
Q

guanethidine should not be used with what drugs

A

TCA (antidepressants)- block NE reuptake
cocaine- block NE reuptake
amphetamines- stimulate release of NE

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71
Q

how does trimethaphan work as an antihypertensive drug

A

competitively blocks nicotinic receptors inhibiting ganglionic transmission

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72
Q

why is trimethaphan, a ganglionic blocker, not commonly used

A

it causes parasympathetic and sympathetic effects such as mydriasis, urinary retention, excessive orthostatic hypotension, and sexual dysfunctions

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73
Q

do vasodilators, which can be used for hypertension, mainly act on arteries or veins

A

arteries

74
Q

do dihydropyridine (-dipine) calcium channel blockers have a greater effect on cardiac or vascular calcium channels

A

-dipines have a greater effect on vascular calcium channels

75
Q

what calcium channel blocker produces the greatest decrease in AV conduction

A

verapamil

76
Q

what calcium channel blocker has the greatest frequency of adverse effects

A

nifedipine

77
Q

what type of calcium channel do calcium channel blockers block

A

L-type

78
Q

how does verapamil differ from other calcium channel blockers

A

it has an effect on both cardiac and vascular smooth muscle cells

79
Q

what 2 drugs can be used to treat supraventricular tachyarrhythmia

A

verapamil
diltiazem

80
Q

why may diltiazem be favored over verapamil for hypertention

A

diltiazem has less negative inotropic effect

81
Q

what drug class can be used to treat hypertensive patients with asthma, diabetes mellitus, angina, and peripheral vascular disease

A

dihydropyridines (-dipines)

82
Q

what are 3 side effects of calcium channel blockers

A

peripheral edema
cardiac depression
flushing/dizziness/HA/fatigue

83
Q

what is one of the main side effects of -dipines (calcium channel blockers)

A

gingival hyperplasia

84
Q

what calcium channel blocker should be avoided with use of beta blocker

A

verapamil

85
Q

__ increase the risk for MI in patients with hypertension, therefore slow release and long acting vasoselective calcium channel blockers are preferred

A

nifedipine

86
Q

verapamil and diltizam should be avoided in patients with __, __, and __

A

heart failure (HFrEF)
bradycardia
AV block

87
Q

what are 2 mechanisms in which drugs can act as vasodilators for relief of hypertension

A

NO release
opening in K+ channels

88
Q

what is the mechanism of action of hydralazine as an antihypertensive drug

A

causes release of NO–>activates guanylyl cyclase–>increased cGMP –>inactivation of myosin light chain kinase–>vasodilation

89
Q

vasodilatory drugs cause what response

A

reflex tachycardia

90
Q

orthostatic hypotension is due to __

A

venous dilation

91
Q

what 2 drugs can be used in pregnancy induced hypertension

A

methyldopa
hydralazine

92
Q

hydralazine is usually used in combination with what

A

beta blocker to counter reflex tachycardia and diuretic to decrease Na/H2O retention

93
Q

what are 3 adverse effects of hydralazine

A

precipitation of angina
precipitation of arrhythmias
Lupus-like syndrome

94
Q

any drug which is metabolized in which way can cause lupus

A

acetylation

95
Q

what is the mechanism of sodium nitroprusside

A

causes release of NO–>activates guanylyl cyclase–>increased cGMP –>inactivation of myosin light chain kinase–>vasodilation

96
Q

how does the vasodilatory effect of sodium nitroprusside differ

A

it causes vasodilation of both arterioles and venules

*since it causes vasodilation of venules, it can produce orthostatic hypotension

97
Q

what 3 antihypertension drug can be given in hypertensive emergencies

A

sodium nitroprusside (causes NO release)
minoxidil/diazoxide (K+ channel openers)
labetolol (alpha and beta blocker)

98
Q

what is the main adverse effect of sodium nitroprusside

A

cyanide toxicity/poisoning

99
Q

what is the treatment for cyanide poisoning caused by sodium nitroprusside

A

sodium/amyl nitrate+sodium thiosulfate/hydroxocobalamin

*produces a less toxic form of cyanide which can be excreted in the urine

100
Q

does opening of K+ channels cause arteriolar dilation, venule dilation, or both

A

arteriolar

101
Q

what hypertension drug can also be used for baldness

A

minoxidil (opens K+ channels)

102
Q

what is the main adverse effect of diazoxide

A

decreased insulin release–> hyperglycemia

*hyperpolarization (due to K+ channel opening) decreases insulin release

103
Q

what is the mechanism of action of fenoldopam

A

D1 agonist which causes arteriolar dilation through increasing cAMP

104
Q

what are the 2 main adverse effects of fenoldopam

A

reflex tachycardia
increased IOP (avoid in those with glaucoma)

105
Q

what 2 diuretic classes can cause hypokalcemia

A

loop
thiazide

106
Q

how do thiazides work to decrease blood pressure

A

they decrease Na/H2O in the distal convoluted tubules leading to decreased blood volume and cardiac output

thiazides also decrease peripheral resisitance

107
Q

what diuretics are particularly useful in treatment of hypertension in African Americans and the elderly

A

thiazides

108
Q

what are the 6 main adverse effects of thiazide diuretics

A

hyponatremia
hypokalemia
hypercalcemia
hyperuricemia
hyperglycemia (inhibition of insulin release)
increased Digoxin toxicity

109
Q

what states always increases risk of Digoxin toxicity

A

hypokalemia

110
Q

how do loop diuretics cause vasodilation

A

enhancing prostaglandins

111
Q

what are the 5 main side effects of loop diuretics

A

acute hypovolemia
hypokalemia
ototoxicity
hypocalcemia
hypomagnesemia

112
Q

what are the 2 possible mechanisms of potassium sparing diuretics

A

antagonism of mineralocorticoid receptors
inhibition of Na+ influx through blocking Na+ channels

113
Q

K+ sparing diuretics can cause __

A

hyperkalemia

114
Q

ACE inhibitors have the suffix __

A

-pril

115
Q

what is the mechanism of action of ACE inhibitors

A

prevent the conversion of angiotensin I–> angiotensin II,, therefore decreasing vasoconstriction effect

116
Q

why may the use of ACE inhibitors lead to a cough and/or angioedema

A

there is an increase in bradykinin

117
Q

what are the physiological effects of ACE inhibitors

A

increase bradykinin level
decrease angiotensin II–> decreased aldosterone
decreased aldosterone–>increased renin–> increased angiotensin I
decrease Na+/H2O retention
increased K+

118
Q

what antihypertensive drug class can be used for patients with diabetes mellitus

A

ACE inhibitors

119
Q

what antihypertensive drug class can be used for patients with diabetic neuropathy

A

ACE inhibitors

120
Q

what antihypertensive drug classes can be used for heart failure

A

ACE inhibitors
beta blockers
angiotensin receptor blockers (ARBs)

121
Q

what antihypertensive class can be used post MI

A

ACE inhibitors

122
Q

what antihypertensive drug class can be used for autosomal dominant polycystic kidney disease

A

ACE inhibitors

PKD stimulates the release of renin, leading to increased BP

123
Q

what are some side effects of ACE inhibitors

A

dry cough (bradykinin effect)
hypotension
angioedema
acute renal failure (due to azotemia with rise in creatinine)
teratogenicity

124
Q

ACE inhibitors are contraindicated with

A

pregnancy
bilateral kidney stenosis
NSAIDs (decrease action of ACR inhibitors)
hyperkalemia (when given with K+ sparing drug)

125
Q

why are ACE inhibitors contraindicated with renal artery stenosis

A

loss of angiotensin II leads to decreased efferent resistance. this causes glomerular capillary pressure to drop and GFR to decrease

126
Q

why are NSAIDs contraindicated in use with ACE inhibitors

A

NSAIDs cause inhibition of prostaglandin production, causing kidney afferent arteriole vasoconstriction and reduced GFR

127
Q

ACE inhibitors are contraindicated in hereditary angioedema, why

A

in hereditary angioedema, there is a deficiency of C1 esterase inhibitor which causes an increase in bradykinin, which can further worsen angioedema

128
Q

why are ACE inhibitors useful in diabetic nephropathy

A

there is a decrease in vasoconstriction of efferent arterioles and less protein crosses the glomerular filter into the tubule of the nephron

129
Q

what suffix indicates an angiotensin receptor blocker (ARB)

A

-sartan

130
Q

angiotensin receptor blocker (ARB) and ACE inhibitors have similar effects. what makes them different in terms of their adverse effects

A

ARBs do not interfere with bradykinin degradation, so there is no dry cough or angioedema

131
Q

why is there an increase in bradykinin in hereditary angioedema

A

deficiency of C1 esterase inhibitor

132
Q

what are the physiological effects of angiotensin receptor blockers

A

increased renin, ang I, and ang II
decreased aldosterone, Na/H2O retention, increased K+

133
Q

Aliskiren belongs to what drug class

A

Aliskiren

134
Q

Aliskiren is a renin inhibitor not often used due to what reasons

A

acute renal failure
intolerable diarrhea

135
Q

what is the preferred antihypertensive drug in patients with angina

A

beta blockers
calcium channel blockers

136
Q

what is the preferred antihypertensive drug in patients with diabetes

A

ACE inhibitor
angiotensin receptor blocker

137
Q

what is the preferred antihypertensive drug in patients with heart failure

A

ACE inhibitors
angiotensin receptor blocker
beta blocker

138
Q

what is the preferred antihypertensive drug in patients post-MI

A

beta blocker
ACE inhibitor

139
Q

what is the preferred antihypertensive drug in patients with BPH

A

alpha blocker

140
Q

what is the preferred antihypertensive drug in patients with dyslipidemia

A

alpha blocker
calcium channel blocker
ACE inhibitor
angiotensin receptor blocker

141
Q

what is the preferred antihypertensive drug in patients with chronic kidney disease

A

ACE inhibitor
angiotensin receptor blcoker

142
Q

what is the mechanism of action of Bosentan as a treatment for pulmonary hypertension

A

endothelin-A receptor blocker

*endothelin is a vasoonstrictor

143
Q

what is the mechanism of action of Epoprosteol as a treatment for pulmonary hypertension

A

acts as a prostacyclin (vasodilator)

144
Q

what are the adverse effects of Epoprostenol

A

flushing, jaw pain, diarrhea

145
Q

what is the mechanism of action of Sildnafil and Tadalafil

A

inhibit phosphodiesterase type 5 which will decrease cGMP breakdown, allowing cGMP to act as a vasodilator

146
Q

calcium channel blockers should be limited to patients without ___

A

evidence of R sided heart failure

147
Q

what is the mechanism of Riociguat as a treatment for pulmonary hypertension

A

increases cGMP

148
Q

what is the mechanism of action of Selexipag

A

it’s a prodrug hydrolyzed to act as a prostaglandin I receptor agonist

149
Q

what 4 drugs can be used for hypertension in pregnancy

A

methyldopa
labetalol
nifedipine
hydralazine

150
Q

what is the mechanism of statin drugs

A

inhibit HMG CoA reductase, preventing the synthesis of cholesterol

151
Q

what is the impact on LDL levels with the use of statins

A

HMG CoA reductase is inhibited
a decrease in cholesterol leads to an upregulation of LDL receptors, increasing the uptake of LDL from the blood to the liver and decreasing serum LDL

152
Q

statin use is good for both __ and __ use

A

hyperlipidemia
hypertriglyceridemia

153
Q

what are 3 adverse effects of statin use

A

hepatotoxicity (increased serum transaminase)
myalgia and myopathy (increase in serum creatine kinase)
rhabdomyolysis (destruction of skeletal muscles)

154
Q

what are precautions which must be taken with statin use

A

liver functioning test
monitoring of creatine kinase

155
Q

there is an increased risk of myopathy if statins are taking with use of what other drugs

A

fibrates
amiodarone
verapamil
(also microenzyme inducers and inhibitors)

156
Q

why should statins be taken in the evening

A

cholesterol synthesis occurs predominantly at night

157
Q

what is the mechanism of nicacin

A

decreases HSL in adipose tissue and inhibits FA breakdown
inhibits synthesis of VLDL (and LDL) in the liver
decreases secretion of VLDL (and LDL) in the plasma

158
Q

what are the effects of niacin use in hyperlipidemia

A

decreases plasma VLDL
decreases plasma TG
decreases plasma LDL
increases plasma HDL

159
Q

what are 4 adverse effects of niacin use

A

cutaneous flushing
hyperuricemia/gout
acanthosis nigricans
hepatotoxicity

160
Q

-fibro- indicates what drug class

A

fibrates

161
Q

what is the mechanism of fibrates as a hyperlipidemia drug

A

activation of PPARalpha and increased expression of LPL
increased LPL increases lipolysis of triglycerides, cellular FA uptake, and beta oxidation in FA in liver and skeletal muscle

decreased secretion of VLDL from liver decreases triglyceride levels

decrease Apo-CIII (further increases LPL)

increase ApoAI and ApoAII–> increases HDL

162
Q

the main effect of fibrates is

A

decreases triglycerides

163
Q

what are w adverse drug reactions of fibrates

A

cholesterol stone formation
myopathy (when given with statins)

164
Q

fibrates can lead to toxicity of __ and __by displacing then from albumin binding sites

A

warfarin
sulfonylureas

165
Q

fibrates are contraindicated with use in those with __ or __ disease

A

renal
liver

166
Q

cholestyramine, colestipol, and colesevelam are what class of drug

A

bile acid sequestrants (resins)

167
Q

what is the mechanism of cholestyramine, colestipol, and colesevelam (bile acid sequestrants)

A

they bind with bile acid to form a non-absorbable resin-bile acid complex which can then be excreted in stool

168
Q

what is the main effect of cholestyramine, colestipol, and colesevelam, all of which are bile acid sequestrants

A

decreased LDL

169
Q

what are the adverse effects of bile acid sequestrants (resins)

A

increases VLDL and triglycerides
GI disturbances
malabsorption of lipid soluble vitamins (decreases vit K causes hypoprothrombinemia)

170
Q

bile acid sequestrants are contraindicated in what condition

A

hypertriglyceridemia

171
Q

what is the mechanism of action of the cholesterol absorption inhibitor ezetimibe

A

prevents intestinal (dietary and biliary) absorption of cholesterol by inhibiting NPC1L1

172
Q

the main use of Ezetimibe, a cholesterol absorption inhibitor, is in combination with what other drug

A

statins

173
Q

what is the mechanism of action of omega-3 fatty acids

A

reduction of hepatic triglyceride synthesis and increased triglyceride clearance

174
Q

what drug class can be used with hypertriglyceridemia in patients with cardiovascular disease or diabetes

A

omega 3 FA

175
Q

what is the main adverse effect of omega 3 FA

A

prolonged bleeding time

176
Q

what is the mechanism of action of Alirocumab and Evolocumab, both PCSK9 inhibitors

A

inhibition of PCSK9 improves the clearance of LDL

177
Q

what drug can be used for familial hypercholesterolemia not responding to oral therapy

A

PCSK9 inhibitors

178
Q

what type of drug is Lomitapide which is used to treat hypercholesterolemia

A

MTP inhibitor (MTP is needed for the formation of VLDLs)

179
Q

what type of drug is bempedoic acid

A

ATP citrate lyase inhibitor

180
Q
A

Pharm Sem 4 (2 decks)

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