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AFN Pharm 1 > Pharm Exam 3: Anti-hypertensives 2/2 > Flashcards

Pharm Exam 3: Anti-hypertensives 2/2 Flashcards

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1
Q

What are your different vasodilator drug classes used in htn?

A
  1. CCB
  2. direct arterial vasodilators
  3. nitrates
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2
Q

how do the drug class vasodilators aid in the tx of HTN?

A

relax arteriole smooth muscle –> decreased SVR.

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3
Q

are vasodilators a good single tx method for htn?

A

no d/t compensatory reflexes –> increased HR, blood volume, sodium

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4
Q

if you are using a vasodilator to tx htn, adding a beta blocker will stop what 3 compensatory mechanisms from counteracting the VD?

A
  1. block increased renin release
  2. block increase in HR
  3. block increased cardiac contractility
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5
Q

if you are using a vasodilator to tx htn, adding a diuretic will stop what compensatory mechanisms from counteracting the VD?

A

inhibit decreased renal sodium excretion (i.e. will increase sodium excretion, thus decreasing blood volume)

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6
Q

which vasodilator drugs cause direct arterial vasodilation through the opening of potassium channels

A

minoxidil and hydralazine

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7
Q

MOA of minoxidil

A

opens potassium channels in arterioles –> smooth muscle relaxation and vasodilation

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8
Q

MOA of hydralazine

A
  1. promote K efflux from vascular smooth muscle –> hyperpolarization and muscle relaxation
  2. arterial dilation by smM relax and increase in cGMP
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9
Q

hydralazine dilates ________________ not ________ or _____________

A

arterioles; veins; epicardial arteries

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10
Q

s/e of hydralazine

A
  1. HA
  2. n/v
  3. flushing
  4. peripheral neuropathy
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11
Q

use of _______________ for tx of htn has a risk of tachyphylaxis

A

hydralazine

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12
Q

how much of hydralazine is bioavailable after first pass?

A

25%

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13
Q

why is hydralazine not a good choice of anti-htn, especially in the OR

A
  1. variable responses d/t acetylation
  2. 10-20 min onset
  3. reflex tachycardia, contractility, and activation of RAAS
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14
Q

what are the functions of NO

A
  1. relax vascular smM
  2. inhibit plt aggregation
  3. inhibit leukocyte-endothelial interactions
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15
Q

__________________ is a direct acting nitrodialator

A

sodium nitroprusside

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16
Q

what is the difference in a direct acting and indirect acting nitrodilator

A

direct - releases NO spontaneously; indirect must be nitrogenated (i.e. activated) before releases NO

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17
Q

in the smooth muscle, indirect acting nitrodilators are denitrogenated by ___________________

A

glutathion s-transferase

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18
Q

in the mitochondria, indirect nitrodilators are denitrogenated by ________________

A

aldehyde dehydrogenase

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19
Q

isosorbide dinitrate and mononitrate are the oral formulary for which medication?

A

nitroglycerine

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20
Q

what is an example of an indirect acting nitrodilator

A

nitroglycerine

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21
Q

nitroglycerine, at high concentrations _______________ responds, but at low concentrations ________________ responds

A

arteries; veins

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22
Q

what is the main clinical use of nitroglycerine

A

Angina

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23
Q

primary effects of nitroglycerine

A
  1. venous relaxation
  2. increased venous capacity
  3. decreased preload and pulmonary pressure
  4. Dilates epicardial coronary arteries
  5. Reduces myocardial O2 demand (by reducing PL)
  6. decreased heart size
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24
Q

what are the adverse effects of nitroglycerine

A
  1. orthostatic hypotension
  2. syncope
  3. throbbing headache
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25
what are some secondary effects of nitroglycerine
1. reflex tachycardia and contractility d/t baroreceptor response 2. decreased plt aggregation 3. Risk for tachyphylaxis
26
how does adenosine fx as a nitrodilator
1. activates purinergic receptors on endothelial cells to stimulate release of NO - VD on smM 2. blocks calcium entry at phase I of action potential - inhibiting contraction
27
effects of nitroprusside
1. dilates arteries and veins 2. increases cGMP --> relaxing of vascular smM
28
what are the byproducts of nitroprusside metabolism
cyanide + NO
29
Where is nitroprusside metabolized?
RBC
30
how do you treat cyanide toxicity from nitroprusside
1. stop NTP 2. give Sodium thiosulfate 3. 100% FiO2 4. can also give methylene blue for the methmyoglobin
31
T/F: adults are normally able to detoxify cyanide formed from sodium nitroprusside
True
32
when is cyanide toxicity with sodium nitroprusside risk increased?
1. large prolonged dosing 2. hepatic dz 3. renal dz
33
what are some signs of cyanide toxicity
1. hypertension 2. metabolic acidosis 3. lactate > 8 4. CV collapse Late signs: 1. hypotension 2. seizure/coma death 3. elevated SvO2
34
signs and sx of cyanide toxicity is often is preceded by ________________
tachyphylaxis
35
Calcium channel blockers as anti-htn cause __________________, through blockage of _______________ channels in smooth muscle of vessels
arterial dilation; L-type Ca channels
36
what are the 3 classes of calcium channel blockers?
1. dihydropyridines 2. phenylalkylamines 3. benzothiazepines
37
nifedipine, amlodipine, nicardipine, and felodipine are drugs in which calcium channel blocker drug class?
dihydropyridines
38
verapamil is what type of CCB?
phenylalkylamine
39
diltiazem is what type of CCB?
benzothiazepine
40
dihydropyridines have what function on blood pressure
cause arterial smM dilation, and small effect on veins
41
which CCB class acts mainly on the heart
phenylalkylamines (verapamil)
42
which CCB drug class has greater effects on vascular smooth muscle
benzothiazepines (diltiazem)
43
what are some common characteristics of CCB?
1. high 1st pass effect 2. highly protein bound 3. extensive metabolism
44
s/e of dihydropyridine CCBs
1. reflex tachycardia 2. flushing 3. edema
45
when should you caution use of dihydropyridine CCBs?
1. pts with pre-existing bradycardia 2. conduction defects 3. heart failure 4. avoid non-concomitant use with BB
46
what is the most effective prophylactic tx of variant angina
CCB
47
verapamil and diltiazem are effective in the tx of :
SVT and Afib/flutter with RVR
48
Verapamil should be used with caution in patients taking __________
digoxin --> dig toxicity
49
____________________ decreases contractile force, reduces myocardial O2 requirements, decreases arterial BP and ICP
CCB
50
in patients with moderate to severe htn, the most effective drug regimens will include which agent?
sympatholytic
51
what are your centrally acting sympatholytics?
clonidine and alpha-methyldopa
52
neurogenic alpha 1 blocker drugs
prazosin, doxazosin
53
neurogenic alpha 1 & 2 blocker
phentolamine
54
neurogenic Alpha 1 and beta 1 blockers
labatelol, carvedilol
55
neurogenic beta 2 agonists
isoproterenol
56
advantage of centrally acting sympatholytics
baroreflexes are retained --> decreased incidence of postural hypotension and sx'atic bradycardia
57
what is MOA of centrally acting sympatholytics as anti-htns
agonize alpha 2 receptors on the pre-synaptic terminal --> reduce sympathetic outflow from vasomotor centers in the brainstem
58
what is the effect of centrally acting sympatholytics
1. decreased CO 2. decreased HR 3. decreased contx 4. decreased SVR by dilation
59
why are alpha 2 agonists (centrally acting sympatholytics) not a primary anti-htn?
they cause sedation
60
___________________ is presynaptic alpha-2 agonist that reduces sympathetic outflow and increase vagal activity
clonidine
61
_____________ is a postsynaptic alpha 2 agonist that inhibits the reuptake of NE
dexmedetomidine
62
stimulation of the _______________ synaptic alpha-2 receptors --> sedative and analgesic effects
post-synaptic
63
stimulation of _____________ synaptic alpha 2 receptors --> decreased central sympathetic outflow
pre-synaptic
64
Alpha2 : Alpha 1 ratio of clonidine
220:1
65
alpha2 : alpha1 ratio of precedex
1620:1
66
which drug is more specific for alpha 2 receptors, clonidine or precedex?
precedex
67
what is the function/MOA of ganglionic blockers
competitively block nicotinic cholinoreceptors on post-ganglionic neurons of SNS and PNS
68
trimethaphan is what type of drug
ganglionic blocker
69
MOA of resperine
1. blocks the uptake and storage of biogenic amines 2. depletes NE, dopa, and serotonin
70
what are the adverse effects of reserpine
1. nightmares 2. depression 3. parkinsonism 4. increased peripheral cholinergic activity 5. antipsychotic effects
71
examples of selective alpha 1 antagonists
1. prazosin 2. terazosin 3. doxazosin 4. trimazosin
72
examples of drugs that are non-selective pre-synaptic and post-synaptic alpha blockers
1. phentolamine 2. phenoxybenzamine
73
alpha 1 adrenoreceptor antagonists are good in the treatment of htn when what other co-morbid condition is present?
BPH
74
Prazosin is a __________ selective antagonist
alpha 1
75
what s/e do you see with prazosin and doxazosin
postural hypotension, effects are pronounced with general anesthesia
76
minipress is aka __________________
prazosin
77
cardura is aka __________________
doxazosin
78
doxazosin is _________% less potent as prazosin
50
79
the most common side effects with alpha blockers
1. vertigo 2. dizziness 3. headache 4. orthostatic hypotension 5. reflex tachycardia 6. Na and fluid retention
80
__________________ should not be used in patients with heart failure or angina
Alpha blockers
81
what are your beta 1 selective antagonists
atenolol esmolol metoprolol
82
B1 selective antagonists effects:
1. cardio-selective 2. no vasodilating effects 3. decreases effects of myocardial remodeling
83
what is your non-selective B1/B2 antagonist?
propranolol
84
which beta blocker is a partial agonist
pindolol
85
pindolol has less _______________ with some vasodilation compared with other beta blockers
bradycardia
86
what are some adverse effects of non-selective beta antagonists
1. bronchospasm 2. block clinical signs of hypoglycemia 3. psychosis 4. depression 5. agitation 6. vivid dreams 7. profound bradycardia 8. hypotension 9. acute CHF
87
what are the uses for non-selective beta antagonists
1. migraine headaches 2. anxiety 3. IHSS 4. pheochromocytoma (AFTER, alpha blocker initiated)
88
A Beta 1 selective Blocker that also causes vasodilation mediated by increased endothelial release of NO
Nebivolol

AFN Pharm 1 (5 decks)

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