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

Pharm Exam 3: Anti-hypertensives 2/2 Flashcards

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
Q

what are some secondary effects of nitroglycerine

A
  1. reflex tachycardia and contractility d/t baroreceptor response
  2. decreased plt aggregation
  3. Risk for tachyphylaxis
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26
Q

how does adenosine fx as a nitrodilator

A
  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
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27
Q

effects of nitroprusside

A
  1. dilates arteries and veins
  2. increases cGMP –> relaxing of vascular smM
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28
Q

what are the byproducts of nitroprusside metabolism

A

cyanide + NO

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29
Q

Where is nitroprusside metabolized?

A

RBC

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30
Q

how do you treat cyanide toxicity from nitroprusside

A
  1. stop NTP
  2. give Sodium thiosulfate
  3. 100% FiO2
  4. can also give methylene blue for the methmyoglobin
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31
Q

T/F: adults are normally able to detoxify cyanide formed from sodium nitroprusside

A

True

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32
Q

when is cyanide toxicity with sodium nitroprusside risk increased?

A
  1. large prolonged dosing
  2. hepatic dz
  3. renal dz
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33
Q

what are some signs of cyanide toxicity

A
  1. hypertension
  2. metabolic acidosis
  3. lactate > 8
  4. CV collapse
    Late signs:
  5. hypotension
  6. seizure/coma death
  7. elevated SvO2
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34
Q

signs and sx of cyanide toxicity is often is preceded by ________________

A

tachyphylaxis

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35
Q

Calcium channel blockers as anti-htn cause __________________, through blockage of _______________ channels in smooth muscle of vessels

A

arterial dilation; L-type Ca channels

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36
Q

what are the 3 classes of calcium channel blockers?

A
  1. dihydropyridines
  2. phenylalkylamines
  3. benzothiazepines
37
Q

nifedipine, amlodipine, nicardipine, and felodipine are drugs in which calcium channel blocker drug class?

A

dihydropyridines

38
Q

verapamil is what type of CCB?

A

phenylalkylamine

39
Q

diltiazem is what type of CCB?

A

benzothiazepine

40
Q

dihydropyridines have what function on blood pressure

A

cause arterial smM dilation, and small effect on veins

41
Q

which CCB class acts mainly on the heart

A

phenylalkylamines (verapamil)

42
Q

which CCB drug class has greater effects on vascular smooth muscle

A

benzothiazepines (diltiazem)

43
Q

what are some common characteristics of CCB?

A
  1. high 1st pass effect
  2. highly protein bound
  3. extensive metabolism
44
Q

s/e of dihydropyridine CCBs

A
  1. reflex tachycardia
  2. flushing
  3. edema
45
Q

when should you caution use of dihydropyridine CCBs?

A
  1. pts with pre-existing bradycardia
  2. conduction defects
  3. heart failure
  4. avoid non-concomitant use with BB
46
Q

what is the most effective prophylactic tx of variant angina

A

CCB

47
Q

verapamil and diltiazem are effective in the tx of :

A

SVT and Afib/flutter with RVR

48
Q

Verapamil should be used with caution in patients taking __________

A

digoxin –> dig toxicity

49
Q

____________________ decreases contractile force, reduces myocardial O2 requirements, decreases arterial BP and ICP

A

CCB

50
Q

in patients with moderate to severe htn, the most effective drug regimens will include which agent?

A

sympatholytic

51
Q

what are your centrally acting sympatholytics?

A

clonidine and alpha-methyldopa

52
Q

neurogenic alpha 1 blocker drugs

A

prazosin, doxazosin

53
Q

neurogenic alpha 1 & 2 blocker

A

phentolamine

54
Q

neurogenic Alpha 1 and beta 1 blockers

A

labatelol, carvedilol

55
Q

neurogenic beta 2 agonists

A

isoproterenol

56
Q

advantage of centrally acting sympatholytics

A

baroreflexes are retained –> decreased incidence of postural hypotension and sx’atic bradycardia

57
Q

what is MOA of centrally acting sympatholytics as anti-htns

A

agonize alpha 2 receptors on the pre-synaptic terminal –> reduce sympathetic outflow from vasomotor centers in the brainstem

58
Q

what is the effect of centrally acting sympatholytics

A
  1. decreased CO
  2. decreased HR
  3. decreased contx
  4. decreased SVR by dilation
59
Q

why are alpha 2 agonists (centrally acting sympatholytics) not a primary anti-htn?

A

they cause sedation

60
Q

___________________ is presynaptic alpha-2 agonist that reduces sympathetic outflow and increase vagal activity

A

clonidine

61
Q

_____________ is a postsynaptic alpha 2 agonist that inhibits the reuptake of NE

A

dexmedetomidine

62
Q

stimulation of the _______________ synaptic alpha-2 receptors –> sedative and analgesic effects

A

post-synaptic

63
Q

stimulation of _____________ synaptic alpha 2 receptors –> decreased central sympathetic outflow

A

pre-synaptic

64
Q

Alpha2 : Alpha 1 ratio of clonidine

A

220:1

65
Q

alpha2 : alpha1 ratio of precedex

A

1620:1

66
Q

which drug is more specific for alpha 2 receptors, clonidine or precedex?

A

precedex

67
Q

what is the function/MOA of ganglionic blockers

A

competitively block nicotinic cholinoreceptors on post-ganglionic neurons of SNS and PNS

68
Q

trimethaphan is what type of drug

A

ganglionic blocker

69
Q

MOA of resperine

A
  1. blocks the uptake and storage of biogenic amines
  2. depletes NE, dopa, and serotonin
70
Q

what are the adverse effects of reserpine

A
  1. nightmares
  2. depression
  3. parkinsonism
  4. increased peripheral cholinergic activity
  5. antipsychotic effects
71
Q

examples of selective alpha 1 antagonists

A
  1. prazosin
  2. terazosin
  3. doxazosin
  4. trimazosin
72
Q

examples of drugs that are non-selective pre-synaptic and post-synaptic alpha blockers

A
  1. phentolamine
  2. phenoxybenzamine
73
Q

alpha 1 adrenoreceptor antagonists are good in the treatment of htn when what other co-morbid condition is present?

A

BPH

74
Q

Prazosin is a __________ selective antagonist

A

alpha 1

75
Q

what s/e do you see with prazosin and doxazosin

A

postural hypotension, effects are pronounced with general anesthesia

76
Q

minipress is aka __________________

A

prazosin

77
Q

cardura is aka __________________

A

doxazosin

78
Q

doxazosin is _________% less potent as prazosin

A

50

79
Q

the most common side effects with alpha blockers

A
  1. vertigo
  2. dizziness
  3. headache
  4. orthostatic hypotension
  5. reflex tachycardia
  6. Na and fluid retention
80
Q

__________________ should not be used in patients with heart failure or angina

A

Alpha blockers

81
Q

what are your beta 1 selective antagonists

A

atenolol
esmolol
metoprolol

82
Q

B1 selective antagonists effects:

A
  1. cardio-selective
  2. no vasodilating effects
  3. decreases effects of myocardial remodeling
83
Q

what is your non-selective B1/B2 antagonist?

A

propranolol

84
Q

which beta blocker is a partial agonist

A

pindolol

85
Q

pindolol has less _______________ with some vasodilation compared with other beta blockers

A

bradycardia

86
Q

what are some adverse effects of non-selective beta antagonists

A
  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
Q

what are the uses for non-selective beta antagonists

A
  1. migraine headaches
  2. anxiety
  3. IHSS
  4. pheochromocytoma (AFTER, alpha blocker initiated)
88
Q

A Beta 1 selective Blocker that also causes vasodilation mediated by increased endothelial release of NO

A

Nebivolol

AFN Pharm 1 (5 decks)

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