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Pharm Sem 4 > Block 1 > Flashcards

Block 1 Flashcards

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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
what is the effect of propranolol on the kidneys
decreases renin release (beta-1)
26
what is the effect of propranolol, a non-selective beta blocker, on the respiratory tract
bronchoconstriction and precipitation of bronchial asthma (beta-2)
27
propranolol, a non-selective beta blocker, is contraindicated in patients with what conditions
asthma COPD *due to bronchoconstriction and propranolol being a nonselective beta blocker
28
what is the effect of propranolol, a non-selective beta blocker, on the eyes
decreased IOP *due to decreased aqueous humor production
29
what is the effect of propranolol, a non-selective beta blocker on the CNS
sleep disturbances sedation depression
30
what is the effect of propranolol, a non-selective beta blocker, on skeletal muscle
antagonizes epinephrine induced tremors
31
what is the effect of propranolol, a non-selective beta blocker, on carbohydrate metabolism
blockage of epinephrine induced glycogenolysis which can cause fasting hypoglycemia
32
what is the effect of propranolol, a non-selective beta blocker, on insulin release
decreases and as a result can lead to postprandial hyperglycemia
33
propranolol, a non-selective beta blocker, should be used with caution in patients with what 3 conditions
diabetes (propranolol decreases the release of insulin) asthma and COPD (due to bronchoconstriction )
34
all beta blockers block __
tachycardia, a warning sign of hypoglycemia
35
what is the effect of propranolol, a non-selective beta blocker, on lipid metabolism
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
36
propranolol, a non-selective beta blocker can be used for all forms of angina except ___
Prinzmental (vasospastic) angina
37
can propranolol be used for hypo or hyperthyroidism
hyperthyroidism
38
what consideration must be made to use propranolol, a non-selective beta blocker, for pheochromocytoma
it can only be used along with an alpha blocker *if used without, there will be a significant increase in blood pressure
39
what are 2 examples of beta blockers with partial agonist activity (intrinsic sympathomimetic activity)
pindolol acebutolol
40
what are 3 advantages to using pindolol or acebutolol, beta blockers with partial agonist activity (intrinsic sympathomimetic activity)
less bradycardia less vasoconstriction less bronchoconstriction
41
beta blockers with partial agonist activity (intrinsic sympathomimetic activity) such as pindolol and acebutolol are useful in patient with hypertension who also have
bradycardia diabetes mellitus peripheral vascular disease abnormal lipid profile
42
what are 2 adverse effects of beta blockers on the CVS
bradycardia AV block *due to decreased cAMP
43
what is used as treatment for beta blockage poisoning
glucagon
44
what is an adverse effect of beta blockers on the respiratory system
bronchoconstriction
45
beta blockers are contraindicated in conditions including ... (4)
bronchial asthma diabetes mellitus Raynaud's disease Prinzmental angina
46
what type of receptor blockage can be performed in those with peripheral vascular disease, COPD, or asthma
beta-1
47
what is an adverse effect of selective beta-1 blockage
bradycardia
48
what beta-1 blocker is used to treat supraventricular tachycardia, intra/postoperative hypertension, and hypertensive emergencies
esmolol
49
what type of blocking activity does Nebivolol have for hypertension
beta-1 with vasodilating properties
50
how can nebivolol, a selective beta-1 agonist, cause vasodilation
due to induction of endothelial NO synthase which causes release of NO, a vasodilator
51
what is the effect of nebivolol if there is an inhibitor of CYP2D6
loss of beta-1 selectivity
52
beta blockers are less preferred in what population group
elderly
53
beta blockers should be avoided with use of what other drugs (4)
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)
54
what are the physiological effects of labetalol and carvediol, alpha and beta receptor blockers
vasodilation no reflex tachycardia no alteration in lipid or glucose levels
55
what drug is used in hypertension of pheochromocytoma
labetalol (alpha and beta blocker)
56
what drug is used in compensated (symptoms are stable or absent) heart failure
carvediol (alpha and beta blocker)
57
what drug class does methyldopa belong to
centrally acting alpha2 agonist
58
what type of agonist is clonidine
alpha 2
59
what are the physiological effects of clonidine
decrease HR, CO, and total peripheral resistance
60
what are 4 side effects seen with clonidine use
dry mouth CNS depression (sedation) sodium and water retention (edema) also rebound hypertension if discontinued abruptly
61
methyldopa causes a decrease in heartrate instead of __
reflex tachycardia
62
what drug is mainly used in hypertension during pregnancy
methyldopa
63
what 2 drugs can be used in hypertensive patients with renal insufficiency
methyldopa fenoldopam
64
what are 4 effects of methyldopa
sedation increased prolactin secretion (due to decreased dopa inhibition) hemolytic anemia sodium and water retention (edema)
65
how does reserpine work as an antihypertensive drug
inhibits the transport of NE into vesicles by interfering with VMAT
66
what are the physiological effects of reserpine
decreased NE leads to decreased CO and total peripheral resistance, as well as decreased dopamine and serotonin
67
what are 2 main adverse side effects of reserpine
severe depression (can lead to suicidal ideations) increased GI secretions
68
how does guanethidine work as an antihypertensive drug
blocks release of NE
69
what are 3 main adverse effects of guanethidine
diarrhea edema retrograde ejaculation
70
guanethidine should not be used with what drugs
TCA (antidepressants)- block NE reuptake cocaine- block NE reuptake amphetamines- stimulate release of NE
71
how does trimethaphan work as an antihypertensive drug
competitively blocks nicotinic receptors inhibiting ganglionic transmission
72
why is trimethaphan, a ganglionic blocker, not commonly used
it causes parasympathetic and sympathetic effects such as mydriasis, urinary retention, excessive orthostatic hypotension, and sexual dysfunctions
73
do vasodilators, which can be used for hypertension, mainly act on arteries or veins
arteries
74
do dihydropyridine (-dipine) calcium channel blockers have a greater effect on cardiac or vascular calcium channels
-dipines have a greater effect on vascular calcium channels
75
what calcium channel blocker produces the greatest decrease in AV conduction
verapamil
76
what calcium channel blocker has the greatest frequency of adverse effects
nifedipine
77
what type of calcium channel do calcium channel blockers block
L-type
78
how does verapamil differ from other calcium channel blockers
it has an effect on both cardiac and vascular smooth muscle cells
79
what 2 drugs can be used to treat supraventricular tachyarrhythmia
verapamil diltiazem
80
why may diltiazem be favored over verapamil for hypertention
diltiazem has less negative inotropic effect
81
what drug class can be used to treat hypertensive patients with asthma, diabetes mellitus, angina, and peripheral vascular disease
dihydropyridines (-dipines)
82
what are 3 side effects of calcium channel blockers
peripheral edema cardiac depression flushing/dizziness/HA/fatigue
83
what is one of the main side effects of -dipines (calcium channel blockers)
gingival hyperplasia
84
what calcium channel blocker should be avoided with use of beta blocker
verapamil
85
__ increase the risk for MI in patients with hypertension, therefore slow release and long acting vasoselective calcium channel blockers are preferred
nifedipine
86
verapamil and diltizam should be avoided in patients with __, __, and __
heart failure (HFrEF) bradycardia AV block
87
what are 2 mechanisms in which drugs can act as vasodilators for relief of hypertension
NO release opening in K+ channels
88
what is the mechanism of action of hydralazine as an antihypertensive drug
causes release of NO-->activates guanylyl cyclase-->increased cGMP -->inactivation of myosin light chain kinase-->vasodilation
89
vasodilatory drugs cause what response
reflex tachycardia
90
orthostatic hypotension is due to __
venous dilation
91
what 2 drugs can be used in pregnancy induced hypertension
methyldopa hydralazine
92
hydralazine is usually used in combination with what
beta blocker to counter reflex tachycardia and diuretic to decrease Na/H2O retention
93
what are 3 adverse effects of hydralazine
precipitation of angina precipitation of arrhythmias Lupus-like syndrome
94
any drug which is metabolized in which way can cause lupus
acetylation
95
what is the mechanism of sodium nitroprusside
causes release of NO-->activates guanylyl cyclase-->increased cGMP -->inactivation of myosin light chain kinase-->vasodilation
96
how does the vasodilatory effect of sodium nitroprusside differ
it causes vasodilation of both arterioles and venules *since it causes vasodilation of venules, it can produce orthostatic hypotension
97
what 3 antihypertension drug can be given in hypertensive emergencies
sodium nitroprusside (causes NO release) minoxidil/diazoxide (K+ channel openers) labetolol (alpha and beta blocker)
98
what is the main adverse effect of sodium nitroprusside
cyanide toxicity/poisoning
99
what is the treatment for cyanide poisoning caused by sodium nitroprusside
sodium/amyl nitrate+sodium thiosulfate/hydroxocobalamin *produces a less toxic form of cyanide which can be excreted in the urine
100
does opening of K+ channels cause arteriolar dilation, venule dilation, or both
arteriolar
101
what hypertension drug can also be used for baldness
minoxidil (opens K+ channels)
102
what is the main adverse effect of diazoxide
decreased insulin release--> hyperglycemia *hyperpolarization (due to K+ channel opening) decreases insulin release
103
what is the mechanism of action of fenoldopam
D1 agonist which causes arteriolar dilation through increasing cAMP
104
what are the 2 main adverse effects of fenoldopam
reflex tachycardia increased IOP (avoid in those with glaucoma)
105
what 2 diuretic classes can cause hypokalcemia
loop thiazide
106
how do thiazides work to decrease blood pressure
they decrease Na/H2O in the distal convoluted tubules leading to decreased blood volume and cardiac output thiazides also decrease peripheral resisitance
107
what diuretics are particularly useful in treatment of hypertension in African Americans and the elderly
thiazides
108
what are the 6 main adverse effects of thiazide diuretics
hyponatremia hypokalemia hypercalcemia hyperuricemia hyperglycemia (inhibition of insulin release) increased Digoxin toxicity
109
what states always increases risk of Digoxin toxicity
hypokalemia
110
how do loop diuretics cause vasodilation
enhancing prostaglandins
111
what are the 5 main side effects of loop diuretics
acute hypovolemia hypokalemia ototoxicity hypocalcemia hypomagnesemia
112
what are the 2 possible mechanisms of potassium sparing diuretics
antagonism of mineralocorticoid receptors inhibition of Na+ influx through blocking Na+ channels
113
K+ sparing diuretics can cause __
hyperkalemia
114
ACE inhibitors have the suffix __
-pril
115
what is the mechanism of action of ACE inhibitors
prevent the conversion of angiotensin I--> angiotensin II,, therefore decreasing vasoconstriction effect
116
why may the use of ACE inhibitors lead to a cough and/or angioedema
there is an increase in bradykinin
117
what are the physiological effects of ACE inhibitors
increase bradykinin level decrease angiotensin II--> decreased aldosterone decreased aldosterone-->increased renin--> increased angiotensin I decrease Na+/H2O retention increased K+
118
what antihypertensive drug class can be used for patients with diabetes mellitus
ACE inhibitors
119
what antihypertensive drug class can be used for patients with diabetic neuropathy
ACE inhibitors
120
what antihypertensive drug classes can be used for heart failure
ACE inhibitors beta blockers angiotensin receptor blockers (ARBs)
121
what antihypertensive class can be used post MI
ACE inhibitors
122
what antihypertensive drug class can be used for autosomal dominant polycystic kidney disease
ACE inhibitors PKD stimulates the release of renin, leading to increased BP
123
what are some side effects of ACE inhibitors
dry cough (bradykinin effect) hypotension angioedema acute renal failure (due to azotemia with rise in creatinine) teratogenicity
124
ACE inhibitors are contraindicated with
pregnancy bilateral kidney stenosis NSAIDs (decrease action of ACR inhibitors) hyperkalemia (when given with K+ sparing drug)
125
why are ACE inhibitors contraindicated with renal artery stenosis
loss of angiotensin II leads to decreased efferent resistance. this causes glomerular capillary pressure to drop and GFR to decrease
126
why are NSAIDs contraindicated in use with ACE inhibitors
NSAIDs cause inhibition of prostaglandin production, causing kidney afferent arteriole vasoconstriction and reduced GFR
127
ACE inhibitors are contraindicated in hereditary angioedema, why
in hereditary angioedema, there is a deficiency of C1 esterase inhibitor which causes an increase in bradykinin, which can further worsen angioedema
128
why are ACE inhibitors useful in diabetic nephropathy
there is a decrease in vasoconstriction of efferent arterioles and less protein crosses the glomerular filter into the tubule of the nephron
129
what suffix indicates an angiotensin receptor blocker (ARB)
-sartan
130
angiotensin receptor blocker (ARB) and ACE inhibitors have similar effects. what makes them different in terms of their adverse effects
ARBs do not interfere with bradykinin degradation, so there is no dry cough or angioedema
131
why is there an increase in bradykinin in hereditary angioedema
deficiency of C1 esterase inhibitor
132
what are the physiological effects of angiotensin receptor blockers
increased renin, ang I, and ang II decreased aldosterone, Na/H2O retention, increased K+
133
Aliskiren belongs to what drug class
Aliskiren
134
Aliskiren is a renin inhibitor not often used due to what reasons
acute renal failure intolerable diarrhea
135
what is the preferred antihypertensive drug in patients with angina
beta blockers calcium channel blockers
136
what is the preferred antihypertensive drug in patients with diabetes
ACE inhibitor angiotensin receptor blocker
137
what is the preferred antihypertensive drug in patients with heart failure
ACE inhibitors angiotensin receptor blocker beta blocker
138
what is the preferred antihypertensive drug in patients post-MI
beta blocker ACE inhibitor
139
what is the preferred antihypertensive drug in patients with BPH
alpha blocker
140
what is the preferred antihypertensive drug in patients with dyslipidemia
alpha blocker calcium channel blocker ACE inhibitor angiotensin receptor blocker
141
what is the preferred antihypertensive drug in patients with chronic kidney disease
ACE inhibitor angiotensin receptor blcoker
142
what is the mechanism of action of Bosentan as a treatment for pulmonary hypertension
endothelin-A receptor blocker *endothelin is a vasoonstrictor
143
what is the mechanism of action of Epoprosteol as a treatment for pulmonary hypertension
acts as a prostacyclin (vasodilator)
144
what are the adverse effects of Epoprostenol
flushing, jaw pain, diarrhea
145
what is the mechanism of action of Sildnafil and Tadalafil
inhibit phosphodiesterase type 5 which will decrease cGMP breakdown, allowing cGMP to act as a vasodilator
146
calcium channel blockers should be limited to patients without ___
evidence of R sided heart failure
147
what is the mechanism of Riociguat as a treatment for pulmonary hypertension
increases cGMP
148
what is the mechanism of action of Selexipag
it's a prodrug hydrolyzed to act as a prostaglandin I receptor agonist
149
what 4 drugs can be used for hypertension in pregnancy
methyldopa labetalol nifedipine hydralazine
150
what is the mechanism of statin drugs
inhibit HMG CoA reductase, preventing the synthesis of cholesterol
151
what is the impact on LDL levels with the use of statins
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
statin use is good for both __ and __ use
hyperlipidemia hypertriglyceridemia
153
what are 3 adverse effects of statin use
hepatotoxicity (increased serum transaminase) myalgia and myopathy (increase in serum creatine kinase) rhabdomyolysis (destruction of skeletal muscles)
154
what are precautions which must be taken with statin use
liver functioning test monitoring of creatine kinase
155
there is an increased risk of myopathy if statins are taking with use of what other drugs
fibrates amiodarone verapamil (also microenzyme inducers and inhibitors)
156
why should statins be taken in the evening
cholesterol synthesis occurs predominantly at night
157
what is the mechanism of nicacin
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
what are the effects of niacin use in hyperlipidemia
decreases plasma VLDL decreases plasma TG decreases plasma LDL increases plasma HDL
159
what are 4 adverse effects of niacin use
cutaneous flushing hyperuricemia/gout acanthosis nigricans hepatotoxicity
160
-fibro- indicates what drug class
fibrates
161
what is the mechanism of fibrates as a hyperlipidemia drug
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
the main effect of fibrates is
decreases triglycerides
163
what are w adverse drug reactions of fibrates
cholesterol stone formation myopathy (when given with statins)
164
fibrates can lead to toxicity of __ and __by displacing then from albumin binding sites
warfarin sulfonylureas
165
fibrates are contraindicated with use in those with __ or __ disease
renal liver
166
cholestyramine, colestipol, and colesevelam are what class of drug
bile acid sequestrants (resins)
167
what is the mechanism of cholestyramine, colestipol, and colesevelam (bile acid sequestrants)
they bind with bile acid to form a non-absorbable resin-bile acid complex which can then be excreted in stool
168
what is the main effect of cholestyramine, colestipol, and colesevelam, all of which are bile acid sequestrants
decreased LDL
169
what are the adverse effects of bile acid sequestrants (resins)
increases VLDL and triglycerides GI disturbances malabsorption of lipid soluble vitamins (decreases vit K causes hypoprothrombinemia)
170
bile acid sequestrants are contraindicated in what condition
hypertriglyceridemia
171
what is the mechanism of action of the cholesterol absorption inhibitor ezetimibe
prevents intestinal (dietary and biliary) absorption of cholesterol by inhibiting NPC1L1
172
the main use of Ezetimibe, a cholesterol absorption inhibitor, is in combination with what other drug
statins
173
what is the mechanism of action of omega-3 fatty acids
reduction of hepatic triglyceride synthesis and increased triglyceride clearance
174
what drug class can be used with hypertriglyceridemia in patients with cardiovascular disease or diabetes
omega 3 FA
175
what is the main adverse effect of omega 3 FA
prolonged bleeding time
176
what is the mechanism of action of Alirocumab and Evolocumab, both PCSK9 inhibitors
inhibition of PCSK9 improves the clearance of LDL
177
what drug can be used for familial hypercholesterolemia not responding to oral therapy
PCSK9 inhibitors
178
what type of drug is Lomitapide which is used to treat hypercholesterolemia
MTP inhibitor (MTP is needed for the formation of VLDLs)
179
what type of drug is bempedoic acid
ATP citrate lyase inhibitor
180

Pharm Sem 4 (2 decks)

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