Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

APEX > Unit 2 - ANS Pharm & Patho > Flashcards

Unit 2 - ANS Pharm & Patho Flashcards

1
Q

how is phenylephrine metabolized

A

MAO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

synthetic catecholamines

A

isoproterenol, dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

synthetic catecholamines

A

isoproterenol, dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 neurotransmitters the ANS relies on

A

ACh & NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

NT of postganglionic PNS neurotransmission

A

cholinergic (ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NT of postganglionic SNS neurotransmision

A

NE (adrenergic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 alpha selective drugs

A
  1. phenylephrine (α1)
  2. clonidine (α2)
  3. dexmedetomidine (α2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

infusion dose of phenylephrine

A

0.15-0.75 mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HR effects of phenylephrine

A

significant reflex bradycardia may occur d/t baroreceptor activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does phenylephrine affect PAP

A

increases d/t direct vasoconstrictive action in lung vasculature & increased venous return

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how can phenylephrine worsen ischemic event in a CAD patient?

A

CO decreased from strong baroreceptor reflex-induced bradycardia + abrupt increase in afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how to treat phenylephrine overdose

A
  • alpha 2 blocker (phentolamine)
  • time (duration is brief)
  • do NOT use beta blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why are beta blockers contraindicated in phenylephrine overdose

A

induce pulmonary edema and catastrophic, irreversible CV collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

3 locations of α2 receptors

A
  1. presynaptic (NE-releasing neurons in CNS & PNS)
  2. postsynaptic (smooth muscle, some organs)
  3. nonsynaptic (platelets)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

location of α2 receptors in the nervous system

A
  • medulla
  • vagus nerve
  • locus coeruleus
  • dorsal horn of spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

effect of α2 stimulation at medulla

A

decreased SNS tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

effect of α2 stimulation at vagus nerve

A

decreased PNS tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

effect of α2 stimulation at locus coeruleus

A

sedation, hypnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effect of α2 stimulation at dorsal horn of spinal cord

A

analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

effect of α2 stimulation in vasculature

A

vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

effect of α2 stimulation in renal tubules

A

inhibits ADH (diuresis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

effect of α2 stimulation in pancreas

A

decreased insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

effect of α2 stimulation on platelets

A

increased platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

effect of α2 stimulation in salivary glands

A

dry mouth (thick, viscous saliva)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

effect of α2 stimulation in GI tract

A

decreased GI motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

protein binding of clonidine vs. dexmedetomidine

A

dex - 94%
clonidine - 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA of clonidine

A
  • acts as α2 agonist at central presynaptic receptors (medulla and locus coeruleus)
  • diminishes SNS outflow leading to sympatholysis (dec HR and BP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does clonidine affect vasculature

A

inhibits NE release, causing vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

AEs of abrupt clonidine discontinuation

A

rebound HTN, tachycardia, arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA of dexmedetomidine

A

stimulates presynaptic α2 receptors in the brain & spinal cord, leading to inhibition of neuronal firing

decreased sympathetic drive = hypotension, bradycardia, sedation, analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

AEs of dexmedetomidine

A

HTN, tachycardia, dysrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what role does dexmedetomidine play in pain signals

A

inhibition of NE release plays a role in modifying propagation of pain signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

effects of dexmedetomidine’s central sympatholytic effects

A
  • anti-shivering
  • reduction in neuroendocrine stress response to surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

AEs of rapid dexmedetomidine admin

A

can stimulate postsynaptic α2 receptors in arterial and venous circulations and cause vasoconstriction/HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

which adrenergic agonist is not arrhythmogenic

A

phenylephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

metabolism of epinephrine

A
  • reuptake
  • MAO & COMT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

receptor stimulation of epinephrine

A

β1 > β2, α1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

receptors stimulated by norepinephrine

A

α1, β1 > β2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

adrenergic agonists that decrease airway resistance

A
  • epinephrine
  • isoproterenol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

metabolism of NE

A
  • reuptake
  • MAO & COMT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

metabolism of dopamine

A
  • reuptake
  • MAO & COMT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

metabolism of isoproterenol

A

COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

metabolism of dobutamine

A

COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

metabolism of ephedrine

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

receptors stimulated by dopamine

A

β1 > β2, α1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

receptors stimulated by isoproterenol

A

β1 > β2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

receptors stimulated by dobutamine

A

β1 > β2 > α1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

catecholamines that increase RBF

A
  • dopamine
  • dobutamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

net effect of epi in different tisuses/organs

A
  • organs with higher incidence of β2 receptors (skeletal muscles) = vasodilation
  • higher incidence of α receptors (mesentery, kidneys) = vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

effects of low vs. higher doses of epi

A
  • lower: favor β effects (increased HR, CO, inotropy, pulse pressure, decreased SVR)
  • higher: favor α effects (increased SVR, decreas CO)ed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

metabolic effects of epi

A

increased blood glucose

hypokalemia d/t transcellular K+ shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is “epinephrine reversal”

A

converting the pressor response (mediated by α receptors) to a depressor response (mediated by β2)

might see if giving epi to treat severe hypotension caused by alpha blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

effects of low vs. high doses of NE

A

low: favor beta-1 effects (increased HR, CO, inotropy, dromotropy)

high: favor beta-1 and alpha effects (systemic vasoconstriction except coronaries, decreased HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

NE effect on venous return

A

enhances by venous vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

principal use of NE

A

increase total peripheral vascular resistance, increasing BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

HR changes with NE

A

may be clinically insignificant d/t vasoconstrictive stim. of baroreceptors to slow HR countered by beta-1 positive chronotropic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

metabolic effects of NE

A

minimal- no BG increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

first line treatment of distributive shock states

A

NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how does dopamine affect CO

A

increases by positive chronotropic, inotropic, and dromotropic activity via beta 1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

dose, receptor & effects of low dose dopamine

A
  • dose: < 3 mcg/kg/min
  • receptor: D1
  • effects: vasodilation, increased renal and splanchnic blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

dose, receptor & effects of moderate dose dopamine

A
  • dose: 3-8 mcg/kg/min
  • alpha 1 and beta 1 receptors in heart and periphery
  • increased contractility and BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

dose, receptor & effects of high dose dopamine

A
  • dose: > 10 mcg/kg/min
  • pure alpha 1 agonist
  • increased BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

effects of postsynaptic D1 receptors

A

vasodilation of renal, GI, coronary, and cerebral vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

effects of presynaptic D2 receptors

A

inhibit NE release, cause vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

where are D2 receptors found

A
  • pituitary gland
  • emetic center
  • kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how does dopamine affect vascular beds

A

highly variable effects depending on dose and receptor type/density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

why does dopamine have to be given as an infusion

A

rapidly metabolized

67
Q

useful and unique clinical effect of DA

A

increase contractility and BP while increasing RBF and UOP

68
Q

complications assoc. with low-dose dopamine

A

CV, pulmonary, GI, immune, and endocrine compllications

69
Q

metabolite of epi and NE

A

vanillylmandelic acid (VMA)

70
Q

end-product of dopamine metabolism

A

homovanillic acid (HMA)

71
Q

infusion dose of isoproterenol

A

0.015-0.15 mcg/kg/min

72
Q

MOA of isoproterenol

A

potent sympathomimetic with beta-1 and beta-2 activity

73
Q

uses of isoproterenol

A
  • manage RV dysfunction
  • manage pulmonary congestion
74
Q

infusion dose of dobutamine

A

2-20 mcg/kg/min

75
Q

MOA of dobutamine

A
  • selective beta-1 agonism with mild beta-2 effects
  • increased contractility and HR
  • reduces vascular tone
76
Q

specific adverse events with dobutamine in CV surgery

A

extending a cardiac muscle infarction, increasing AV conduction

may trigger rapid ventricular rate in pts with A fib

77
Q

use of dobutamine in pulm HTN

A

decreases PAP and PVR via beta-2 stim

78
Q

MOA of ephedrine

A
  • directly stim. alpha and beta receptors
  • indirectly promotes NE release
79
Q

what causes indirect actions of ephedrine

A

endocytosis of ephedrine into adrenergic presynaptic terminals, displacing NE from secretory vesicles

NE activates target alpha-1 and beta-1 receptors

80
Q

why is tachyphylaxis seen with ephedrine

A

depletion of presynaptic NE causes ephedrine to be released from synaptic vesicles as a false NT

81
Q

T/F ephedrine crosses the BBB

A

true

82
Q

onset and duration of ephedrine

A

rapid onset
duration up to an hour (depending on dose)

83
Q

why should ephedrine be given to CAD pts cautiously

A

positive inotropic and chronotropic effects can increase O2 demand

84
Q

long-acting beta agonists

A
  • salmeterol
  • formoterol
85
Q

AEs of chronic beta2 agonist therapy

A
  • down-regulation of target receptors (tachyphylaxis)
  • airway hyperresponsiveness
86
Q

MOA of beta agonists

A

increase intracellular cAMP, decrease Ca2+

87
Q

how do beta agoinsts affect uterine smooth muscle

A

relaxation; tocolytic effect

88
Q

black box warning assoc. with beta agonists

A

long-acting beta agonists

risk of asthma-related death possibly d/t development of airway hyperresponsiveness

89
Q

chemical precursor of epi

A

norepinephrine

90
Q

which adrenoreceptor is metabolized by the liver

A

ephedrine

91
Q

synthetic catecholamine derived from dopamine

A

isoproterenol

92
Q

catecolamine used in treatment of vasoplegia

A

Norepi

93
Q

precursor of norepi

A

dopamine

94
Q

common side effect of prazosin

A

orthostatic hypotension

95
Q

how do alpha antagonists lower BP

A

by preventing NE from acting on vascular smooth muscle alpha-1 receptors

96
Q

why do alpha antagonists cause orthostatic hypotension

A

can greatly impair compensatory vasoconstriction assoc.with baroreceptor response to sudden position changes

97
Q

MOA of phenoxybenzamine

A
  • noncompetitive, irreversible alpha antagonist
  • blocks α-mediated activity of NE and epi
  • results in decreased peripheral vascular resistance and BP
98
Q

how is clinical effect of phenoxybenzamine terminated

A

synthesis of new receptors

99
Q

what is phenoxybenzamine used for

A

preoperative management of pheo to normalize BP and prevent episodic HTN

100
Q

how to prevent significant acute-onset hypotension with phenoxybenzamine

A

low dose initiation increased over several days

101
Q

how should phenoxybenzamine-induced hypotension be treated

A

vasopressin and fluids
(irreversible alpha block makes NE and phenylephrine ineffective)

102
Q

MOA of phentolamine

A

competitive nonselective alpha receptor antagonist

103
Q

use of phentolamine

A
  • otherwise refractory HTN seen with abrupt clonidine discontinuation
  • local infiltration after IV extravasation of a vasoconstrictor like epi or NE
104
Q

why does phentolamine stimulate stomach acid secretion

A

affinity for 5HT3 receptors
also induces mast cell degranulation

105
Q

why should phentolamine be used cautiously in pts with CAD

A

causes baroreceptor-mediated reflex tachycardia

106
Q

MOA of prazosin

A
  • highly selective alpha 1 antagonist
  • α1:α2 1000:1
107
Q

effects of prazosin

A
  • decreased peripheral vascular resistance in arterioles and veins
  • increased venous capacitance
  • decreased preload and BP with little change in HR
108
Q

main use of terazosin

A

BPH

109
Q

why are terazosin, doxazosin, and tamulosin used in BPH treatment

A

large numbers of α1A receptors there

110
Q

MOA & use of yohimbine

A
  • selective α2 antagonist
  • widely marketed for ED, athletic performance, weight loss, HTN, diabetic neuropathy
111
Q

ANS effects of yohimbine

A
  • increased PNS activity (cholinergic)
  • decreased SNS activity (adrenergic)
112
Q

how might yohimbe affect antihypertensives

A

might diminish effect

113
Q

CV indications of beta blockers

A
  • HTN
  • SVT
  • A fib
  • CHF
  • IHD
  • reduces myocardial O2 consumption and improving perfusion
114
Q

AEs of abrupt discontinuation of long-term beta blockers

A

rebound tachycardia and HTN

115
Q

caution of beta blocker use in hypovolemia

A

may cause bradyarrhythmias and obtund CV response to hypovolemia, progressive heart block, heart failure

116
Q

beta blockers with membrane stabilizing activity

A

propranolol
acebutolol

117
Q

what is MSA?

A
  • membrane stabilizing activity
  • inhibition or abolition of AP propagation across the membrane
  • beta blockers with MSA act as antiarrhythmics
118
Q

beta-blockers with intrinsic sympathomimetic activity (ISA)

A

pindolol
labetolol
acebutolol

119
Q

prototypical nonselective beta blocker

A

propranolol

120
Q

MOA of propranolol

A
  • competitive β1 & β2 antagonism
  • prevents action of epi, NE, dopamine, dobutamine, and isoproterenol at these receptors
121
Q

AEs of β2 antagonism

A
  • bronchoconstriction
  • hypoglycemia
  • peripheral vascular constriction
  • aggravates Raynaud’s/PVD
122
Q

beta blocker with a very long half life

A

nadolol

123
Q

nonselective beta blocker with weak beta agonist effects

A

pindolol
assoc. with less HR slowing, less impact on BP

124
Q

CV effects of β receptor blockade

A
  • decreased HR
  • decreasd contractility
  • decreased AV conduction
  • moderates cardiac O2 cosumption
125
Q

cardioselective β blockers

A
  • metoprolol
  • atenolol
  • acebutolol
  • esmolol
  • bisoprolol
126
Q

cardioselective β blocker with weak beta agonist effects

A

acebutolol

127
Q

MOA of cardioselective β blockers

A
  • competitive cardioselective β1 antagonist
  • prevents action of epi and NE
128
Q

why is metoprolol useful in IHD

A

exerts moderating effect on HR, limiting its increase during exercise and stress

129
Q

use of metoprolol

A
  • angina
  • heart failure
  • MI
  • A fib
  • HTN
130
Q

dose of metoprolol

A

2.5-5 mg increments to max of 15mg

131
Q

first-line drug for rapid periop control of HR and BP

A

esmolol

132
Q

metabolism of esmolol

A

nonspecific esterases found in RBC

133
Q

use of atenolol

A
  • decrease cardiac work, reduce myocardial O2 demand
  • HTN
  • chronic angina
  • MI survivors
  • some cases of A fib
134
Q

atenolol dosing

A

PO 25-200 mg once or twice a day
IV 5-10 mg

135
Q

MOA of labetolol

A

alpha 1 and nonselective beta blockade
(ratio of beta to alpha block is 7:1)

136
Q

primary indication of labetolol

A

acute HTN

137
Q

effects of alpha 1 antagonism with labetolol

A

vasodilation
decreased vascular resistance

138
Q

considerations for labetolol in pts with asthma or COPD

A

may produce bronchospasm

139
Q

how does labetolol affect HR

A

due to mixed activity, produces vasodilation without triggering baroreceptor-increased HR

140
Q

half-life and metabolism of labetolol

A
  • about 6 hours
  • metabolized in liver
  • eliminated by kidneys
141
Q

MOA & effects of carvedilol

A
  • antagonist at alpha-1, beta-1, and beta-2 receptors
  • impaired arterial vasodilation
  • modest HR reduction
142
Q

beta blocker with antioxidant and anti-inflammatory properties

A

carvedilol

143
Q

use of carvedilol

A

success in managing pts with heart failure, LV dysfunction, HTN, acute MI

144
Q

propranolol’s use as an antidysrhythmic is best related to its:

A

membrane stabilizing ability

145
Q

which beta blocker has intrinsic sympathetic activity

A

labetolol

146
Q

which beta blocker undergoes renal metabolism

A

atenolol

147
Q

what receptors does nicotine activate

A

acts as ACh analog at postganglionic neurons (Nn subtype) in SNS and PNS

148
Q

CV effects of nicotine

A

unopposed sympathomimetic activity = increased vascular tone
heart may receive conflicting signals from SNS & PNS, affecting rhythm

149
Q

use of methacholine

A

provocative agent to identify RAD in patients without clinically apparent asthma

150
Q

MOA of methcholine

A

activates M3 receptors to evoke bronchoconstriction, increase airway secretions, and impair peak expiratory flow rates

151
Q

MAO and use of bethanechol

A

relatively M3 selective in GI and urinary tract; used for nonobstructive urinary retention in periop period

152
Q

antimuscarinic with greatest affect on HR

A

atropine

153
Q

antimuscarinic with greatest degree of sedation

A

scopolamine

154
Q

antimuscarinic with greatest antisialagogue effects

A

scopolamine

155
Q

structure of antimuscarinics

A

atropine, scopolamine - tertiary amines

glyco - quarternary amine

156
Q

antimuscarinics that cross the BBB

A

atropine & scopolamine

157
Q

why can low dose (< 0.1) mg atropine worsen bradycardia

A

by blocking presynaptic M1 receptors on preganglionic PNS fibers

158
Q

s/s atropine toxicity assoc. with 0.5-1 mg

A
  • increased HR
  • dry mouth
  • lack of sweating
  • feeling thirsty
  • mild pupil dilation
159
Q

s/s atropine toxicity assoc. with 2-5 mg dose

A
  • tachycardia
  • palpitations
  • mydriasis
  • cycloplegia
  • restlessness
  • confusion
160
Q

s/s atropine toxicity assoc. with > 5 mg dose

A
  • tachycardia
  • mydriasis
  • cycloplegia
  • hot flushed skin
  • fever
  • hallucinations
  • coma
161
Q

CNS s/s muscarinic toxicity

A
  • excitation, restlessness
  • sedation, confusion, stupor
  • hallucinations, delirium
  • seizures
  • coma, death
162
Q

treatment for muscarinic toxicity

A
  • oxygenation
  • ventilation
  • physostigmine 1-2 mg IV
163
Q

primary inhibitory neurotransmitter in CNS

A

GABA

164
Q

agents that enhance GABA

A
  • isoflurane
  • sevoflurane
  • desflurane
  • propofol
  • benzos
  • barbiturates
  • etomidate

APEX (54 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions