troy apex1 > Unit 2 - ANS Pharm & Patho > Flashcards

Unit 2 - ANS Pharm & Patho Flashcards

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1
Q

how is phenylephrine metabolized

A

MAO

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2
Q

synthetic catecholamines

A

isoproterenol, dobutamine

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3
Q

2 neurotransmitters the ANS relies on

A

ACh & NE

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4
Q

NT of postganglionic PNS neurotransmission

A

cholinergic (ACh)

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5
Q

NT of postganglionic SNS neurotransmision

A

NE (adrenergic)

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6
Q

3 alpha selective drugs

A
  1. phenylephrine (α1)
  2. clonidine (α2)
  3. dexmedetomidine (α2)
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7
Q

infusion dose of phenylephrine

A

0.15-0.75 mcg/kg/min

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8
Q

HR effects of phenylephrine

A

significant reflex bradycardia may occur d/t baroreceptor activity

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9
Q

how does phenylephrine affect PAP

A

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

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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

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11
Q

how to treat phenylephrine overdose

A
  • alpha 2 blocker (phentolamine)
  • time (duration is brief)
  • do NOT use beta blocker
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12
Q

why are beta blockers contraindicated in phenylephrine overdose

A

induce pulmonary edema and catastrophic, irreversible CV collapse

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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)
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14
Q

location of α2 receptors in the nervous system

A
  • medulla
  • vagus nerve
  • locus coeruleus
  • dorsal horn of spinal cord
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15
Q

effect of α2 stimulation at medulla

A

decreased SNS tone

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16
Q

effect of α2 stimulation at vagus nerve

A

decreased PNS tone

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17
Q

effect of α2 stimulation at locus coeruleus

A

sedation, hypnosis

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18
Q

effect of α2 stimulation at dorsal horn of spinal cord

A

analgesia

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19
Q

effect of α2 stimulation in vasculature

A

vasoconstriction

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20
Q

effect of α2 stimulation in renal tubules

A

inhibits ADH (diuresis)

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21
Q

effect of α2 stimulation in pancreas

A

decreased insulin release

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22
Q

effect of α2 stimulation on platelets

A

increased platelet aggregation

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23
Q

effect of α2 stimulation in salivary glands

A

dry mouth (thick, viscous saliva)

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24
Q

effect of α2 stimulation in GI tract

A

decreased GI motility

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25
protein binding of clonidine vs. dexmedetomidine
dex - 94% clonidine - 50%
26
MOA of clonidine
- acts as α2 agonist at central presynaptic receptors (medulla and locus coeruleus) - diminishes SNS outflow leading to sympatholysis (dec HR and BP)
27
how does clonidine affect vasculature
inhibits NE release, causing vasodilation
28
AEs of abrupt clonidine discontinuation
rebound HTN, tachycardia, arrhythmia
29
MOA of dexmedetomidine
stimulates presynaptic α2 receptors in the brain & spinal cord, leading to inhibition of neuronal firing decreased sympathetic drive = hypotension, bradycardia, sedation, analgesia
30
AEs of dexmedetomidine
HTN, tachycardia, dysrhythmias
31
what role does dexmedetomidine play in pain signals
inhibition of NE release plays a role in modifying propagation of pain signals
32
effects of dexmedetomidine's central sympatholytic effects
- anti-shivering - reduction in neuroendocrine stress response to surgery
33
AEs of rapid dexmedetomidine admin
can stimulate postsynaptic α2 receptors in arterial and venous circulations and cause vasoconstriction/HTN
34
which adrenergic agonist is not arrhythmogenic
phenylephrine
35
metabolism of epinephrine
- reuptake - MAO & COMT
36
receptor stimulation of epinephrine
β1 > β2, α1
37
receptors stimulated by norepinephrine
α1, β1 > β2
38
adrenergic agonists that decrease airway resistance
- epinephrine - isoproterenol
39
metabolism of NE
- reuptake - MAO & COMT
40
metabolism of dopamine
- reuptake - MAO & COMT
41
metabolism of isoproterenol
COMT
42
metabolism of dobutamine
COMT
43
metabolism of ephedrine
liver
44
receptors stimulated by dopamine
β1 > β2, α1
45
receptors stimulated by isoproterenol
β1 > β2
46
receptors stimulated by dobutamine
β1 > β2 > α1
47
catecholamines that increase RBF
- dopamine - dobutamine
48
net effect of epi in different tisuses/organs
- organs with higher incidence of β2 receptors (skeletal muscles) = vasodilation - higher incidence of α receptors (mesentery, kidneys) = vasoconstriction
49
effects of low vs. higher doses of epi
- lower: favor β effects (increased HR, CO, inotropy, pulse pressure, decreased SVR) - higher: favor α effects (increased SVR, decreas CO)ed
50
metabolic effects of epi
increased blood glucose hypokalemia d/t transcellular K+ shift
51
what is "epinephrine reversal"
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
52
effects of low vs. high doses of NE
low: favor beta-1 effects (increased HR, CO, inotropy, dromotropy) high: favor beta-1 and alpha effects (systemic vasoconstriction except coronaries, decreased HR)
53
NE effect on venous return
enhances by venous vasoconstriction
54
principal use of NE
increase total peripheral vascular resistance, increasing BP
55
HR changes with NE
may be clinically insignificant d/t vasoconstrictive stim. of baroreceptors to slow HR countered by beta-1 positive chronotropic effect
56
metabolic effects of NE
minimal- no BG increase
57
first line treatment of distributive shock states
NE
58
how does dopamine affect CO
increases by positive chronotropic, inotropic, and dromotropic activity via beta 1 receptors
59
dose, receptor & effects of low dose dopamine
- dose: < 3 mcg/kg/min - receptor: D1 - effects: vasodilation, increased renal and splanchnic blood flow
60
dose, receptor & effects of moderate dose dopamine
- dose: 3-8 mcg/kg/min - alpha 1 and beta 1 receptors in heart and periphery - increased contractility and BP
61
dose, receptor & effects of high dose dopamine
- dose: > 10 mcg/kg/min - pure alpha 1 agonist - increased BP
62
effects of postsynaptic D1 receptors
vasodilation of renal, GI, coronary, and cerebral vessels
63
effects of presynaptic D2 receptors
inhibit NE release, cause vasodilation
64
where are D2 receptors found
- pituitary gland - emetic center - kidney
65
how does dopamine affect vascular beds
highly variable effects depending on dose and receptor type/density
66
why does dopamine have to be given as an infusion
rapidly metabolized
67
useful and unique clinical effect of DA
increase contractility and BP while increasing RBF and UOP
68
complications assoc. with low-dose dopamine
CV, pulmonary, GI, immune, and endocrine compllications
69
metabolite of epi and NE
vanillylmandelic acid (VMA)
70
end-product of dopamine metabolism
homovanillic acid (HMA)
71
infusion dose of isoproterenol
0.015-0.15 mcg/kg/min
72
MOA of isoproterenol
potent sympathomimetic with beta-1 and beta-2 activity
73
uses of isoproterenol
- manage RV dysfunction - manage pulmonary congestion
74
infusion dose of dobutamine
2-20 mcg/kg/min
75
MOA of dobutamine
- selective beta-1 agonism with mild beta-2 effects - increased contractility and HR - reduces vascular tone
76
specific adverse events with dobutamine in CV surgery
extending a cardiac muscle infarction, increasing AV conduction may trigger rapid ventricular rate in pts with A fib
77
use of dobutamine in pulm HTN
decreases PAP and PVR via beta-2 stim
78
MOA of ephedrine
- directly stim. alpha and beta receptors - indirectly promotes NE release
79
what causes indirect actions of ephedrine
endocytosis of ephedrine into adrenergic presynaptic terminals, displacing NE from secretory vesicles NE activates target alpha-1 and beta-1 receptors
80
why is tachyphylaxis seen with ephedrine
depletion of presynaptic NE causes ephedrine to be released from synaptic vesicles as a false NT
81
T/F ephedrine crosses the BBB
true
82
onset and duration of ephedrine
rapid onset duration up to an hour (depending on dose)
83
why should ephedrine be given to CAD pts cautiously
positive inotropic and chronotropic effects can increase O2 demand
84
long-acting beta agonists
- salmeterol - formoterol
85
AEs of chronic beta2 agonist therapy
- down-regulation of target receptors (tachyphylaxis) - airway hyperresponsiveness
86
MOA of beta agonists
increase intracellular cAMP, decrease Ca2+
87
how do beta agoinsts affect uterine smooth muscle
relaxation; tocolytic effect
88
black box warning assoc. with beta agonists
long-acting beta agonists risk of asthma-related death possibly d/t development of airway hyperresponsiveness
89
chemical precursor of epi
norepinephrine
90
which adrenoreceptor is metabolized by the liver
ephedrine
91
synthetic catecholamine derived from dopamine
isoproterenol
92
catecolamine used in treatment of vasoplegia
Norepi
93
precursor of norepi
dopamine
94
common side effect of prazosin
orthostatic hypotension
95
how do alpha antagonists lower BP
by preventing NE from acting on vascular smooth muscle alpha-1 receptors
96
why do alpha antagonists cause orthostatic hypotension
can greatly impair compensatory vasoconstriction assoc.with baroreceptor response to sudden position changes
97
MOA of phenoxybenzamine
- noncompetitive, irreversible alpha antagonist - blocks α-mediated activity of NE and epi - results in decreased peripheral vascular resistance and BP
98
how is clinical effect of phenoxybenzamine terminated
synthesis of new receptors
99
what is phenoxybenzamine used for
preoperative management of pheo to normalize BP and prevent episodic HTN
100
how to prevent significant acute-onset hypotension with phenoxybenzamine
low dose initiation increased over several days
101
how should phenoxybenzamine-induced hypotension be treated
vasopressin and fluids (irreversible alpha block makes NE and phenylephrine ineffective)
102
MOA of phentolamine
competitive nonselective alpha receptor antagonist
103
use of phentolamine
- otherwise refractory HTN seen with abrupt clonidine discontinuation - local infiltration after IV extravasation of a vasoconstrictor like epi or NE
104
why does phentolamine stimulate stomach acid secretion
affinity for 5HT3 receptors also induces mast cell degranulation
105
why should phentolamine be used cautiously in pts with CAD
causes baroreceptor-mediated reflex tachycardia
106
MOA of prazosin
- highly selective alpha 1 antagonist - α1:α2 1000:1
107
effects of prazosin
- decreased peripheral vascular resistance in arterioles and veins - increased venous capacitance - decreased preload and BP with little change in HR
108
main use of terazosin
BPH
109
why are terazosin, doxazosin, and tamulosin used in BPH treatment
large numbers of α1A receptors there
110
MOA & use of yohimbine
- selective α2 antagonist - widely marketed for ED, athletic performance, weight loss, HTN, diabetic neuropathy
111
ANS effects of yohimbine
- increased PNS activity (cholinergic) - decreased SNS activity (adrenergic)
112
how might yohimbe affect antihypertensives
might diminish effect
113
CV indications of beta blockers
- HTN - SVT - A fib - CHF - IHD - reduces myocardial O2 consumption and improving perfusion
114
AEs of abrupt discontinuation of long-term beta blockers
rebound tachycardia and HTN
115
caution of beta blocker use in hypovolemia
may cause bradyarrhythmias and obtund CV response to hypovolemia, progressive heart block, heart failure
116
beta blockers with membrane stabilizing activity
propranolol acebutolol
117
what is MSA?
- membrane stabilizing activity - inhibition or abolition of AP propagation across the membrane - beta blockers with MSA act as antiarrhythmics
118
beta-blockers with intrinsic sympathomimetic activity (ISA)
pindolol labetolol acebutolol
119
prototypical nonselective beta blocker
propranolol
120
MOA of propranolol
- competitive β1 & β2 antagonism - prevents action of epi, NE, dopamine, dobutamine, and isoproterenol at these receptors
121
AEs of β2 antagonism
- bronchoconstriction - hypoglycemia - peripheral vascular constriction - aggravates Raynaud's/PVD
122
beta blocker with a very long half life
nadolol
123
nonselective beta blocker with weak beta agonist effects
pindolol assoc. with less HR slowing, less impact on BP
124
CV effects of β receptor blockade
- decreased HR - decreasd contractility - decreased AV conduction - moderates cardiac O2 cosumption
125
cardioselective β blockers
- metoprolol - atenolol - acebutolol - esmolol - bisoprolol
126
cardioselective β blocker with weak beta agonist effects
acebutolol
127
MOA of cardioselective β blockers
- competitive cardioselective β1 antagonist - prevents action of epi and NE
128
why is metoprolol useful in IHD
exerts moderating effect on HR, limiting its increase during exercise and stress
129
use of metoprolol
- angina - heart failure - MI - A fib - HTN
130
dose of metoprolol
2.5-5 mg increments to max of 15mg
131
first-line drug for rapid periop control of HR and BP
esmolol
132
metabolism of esmolol
nonspecific esterases found in RBC
133
use of atenolol
- decrease cardiac work, reduce myocardial O2 demand - HTN - chronic angina - MI survivors - some cases of A fib
134
atenolol dosing
PO 25-200 mg once or twice a day IV 5-10 mg
135
MOA of labetolol
alpha 1 and nonselective beta blockade (ratio of beta to alpha block is 7:1)
136
primary indication of labetolol
acute HTN
137
effects of alpha 1 antagonism with labetolol
vasodilation decreased vascular resistance
138
considerations for labetolol in pts with asthma or COPD
may produce bronchospasm
139
how does labetolol affect HR
due to mixed activity, produces vasodilation without triggering baroreceptor-increased HR
140
half-life and metabolism of labetolol
- about 6 hours - metabolized in liver - eliminated by kidneys
141
MOA & effects of carvedilol
- antagonist at alpha-1, beta-1, and beta-2 receptors - impaired arterial vasodilation - modest HR reduction
142
beta blocker with antioxidant and anti-inflammatory properties
carvedilol
143
use of carvedilol
success in managing pts with heart failure, LV dysfunction, HTN, acute MI
144
propranolol's use as an antidysrhythmic is best related to its:
membrane stabilizing ability
145
which beta blocker has intrinsic sympathetic activity
labetolol
146
which beta blocker undergoes renal metabolism
atenolol
147
what receptors does nicotine activate
acts as ACh analog at postganglionic neurons (Nn subtype) in SNS and PNS
148
CV effects of nicotine
unopposed sympathomimetic activity = increased vascular tone heart may receive conflicting signals from SNS & PNS, affecting rhythm
149
use of methacholine
provocative agent to identify RAD in patients without clinically apparent asthma
150
MOA of methcholine
activates M3 receptors to evoke bronchoconstriction, increase airway secretions, and impair peak expiratory flow rates
151
MAO and use of bethanechol
relatively M3 selective in GI and urinary tract; used for nonobstructive urinary retention in periop period
152
antimuscarinic with greatest affect on HR
atropine
153
antimuscarinic with greatest degree of sedation
scopolamine
154
antimuscarinic with greatest antisialagogue effects
scopolamine
155
structure of antimuscarinics
atropine, scopolamine - tertiary amines glyco - quarternary amine
156
antimuscarinics that cross the BBB
atropine & scopolamine
157
why can low dose (< 0.1) mg atropine worsen bradycardia
by blocking presynaptic M1 receptors on preganglionic PNS fibers
158
s/s atropine toxicity assoc. with 0.5-1 mg
- increased HR - dry mouth - lack of sweating - feeling thirsty - mild pupil dilation
159
s/s atropine toxicity assoc. with 2-5 mg dose
- tachycardia - palpitations - mydriasis - cycloplegia - restlessness - confusion
160
s/s atropine toxicity assoc. with > 5 mg dose
- tachycardia - mydriasis - cycloplegia - hot flushed skin - fever - hallucinations - coma
161
CNS s/s muscarinic toxicity
- excitation, restlessness - sedation, confusion, stupor - hallucinations, delirium - seizures - coma, death
162
treatment for muscarinic toxicity
- oxygenation - ventilation - physostigmine 1-2 mg IV
163
primary inhibitory neurotransmitter in CNS
GABA
164
agents that enhance GABA
- isoflurane - sevoflurane - desflurane - propofol - benzos - barbiturates - etomidate
165
synthetic catecholamines
isoproterenol, dobutamine
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