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PHARM 4 ANS > Endogenous/Drug effects on receptor > Flashcards

Endogenous/Drug effects on receptor Flashcards

1
Q

Norepinephrine has a low affinity/efficacy at what two receptors?

A

B2 & B3

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2
Q

EPI binds to what receptor causing bronchodilation?

A

B2

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3
Q

At low concentrations, epinephrine binds to what receptor?

What is the effect?

A

B2

vasodilation

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4
Q

At high concentrations, epinephrine binds to what receptor?

What is the effect?

A

A1

vasoconstriction

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5
Q

List 3 bronchodilators?

A

Epi
isoproterenol
albuterol

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6
Q

What can block NET? What is the result?

A

Cocaine and TCA(amitriptyline)

increased available Norepi

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7
Q

Methylxanthines (caffeine)

A

bronchodilation

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8
Q

Phenylephrine cause increase myocardial contractility by 2-3x WHY?

A

post junctional A1 receptors on heart

more prominent in failure or ischemia due to receptor upregulation

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9
Q

Sympathomimetic drugs such as ephedrine do what?

A

act using endogenous NT

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10
Q

Sympathomimetic drugs act primarily on what receptors

A

A1 and B1

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11
Q

Epi (agonist) primarily stimulates what receptors?

A

B1,2,3

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12
Q

Norepi stimulates_____, but minimal______ receptor activity?

A

B1

B2

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13
Q

Dopamine is a ____receptor agonist?

A

Beta

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14
Q

Stimulation of SNS causes 80% release of____from adrenal medulla.

A

Epi

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15
Q

Catecholamines are?

A

sympathetic amines with hydroxy substitutions 3 and 4 of benzene ring

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16
Q

Cocaine does what?

A

blocks reuptake of NE

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17
Q

Tyramine is

A

from fermented food, contraindicated with mao inhibitor

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18
Q

Tyramine, amphetamine, ephedrine cause what?

A

increase available nor epi, reuptake inhibition

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19
Q

Epinephrine in large doses may cause

A

PVC, tachycardia, fibrillation

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20
Q

The negative SE of EPI may exacerbated in

A

MI and anesthetic agents

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21
Q

In the presence of a beta blocker EPI will act as

A

vasoconstriction

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22
Q

EPI causes increased coronary blood flow via

A

metabolic adenosine

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23
Q

EPI via A1 causes high vasoconstriction where?

A

skin vasculature

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24
Q

Epinephrine indirectly increase blood pressure why?

A

Positive inotropic and chronotropic

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25
Q

Place in order affinity for A1&A2
Isoprotenrol
epi
norepi

A

epi
norepi
isoproterenol
epi>=NE»i

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26
Q

Place in order affinity for B1
Isoprotenrol
epi
norepi

A 
B1
Isoprotenrol 
epi 
norepi 
i>epi=NE
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27
Q

Place in order affinity for B2&B3
Isoprotenrol
epi
norepi

A

Isoprotenrol
epi
norepi
i>=epi»NE

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28
Q

Dobutamine would be a good choice for what patient?

A

Short term cardiac decompensation states(post CT surg, acute MI, CHF

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29
Q

In severe CHF dobutamine would be a shit choice. Why?

A

down regulation of b adrenergic receptors would decrease its effectiveness.

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30
Q

Dobutamine facilitates AV conduction and may cause

A

ventricular ectopy.

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31
Q

Dobutamine predominantly simulates which receptor

A

B1

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32
Q

Dobutamine is more prominent inotrope or chronotrope?

A

inotrope

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33
Q

Pheonochromocytoma will cause an increase of ______release by the _____of _______%?

A

norepi
adrenal medulla
97%

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34
Q

A low dose of epi 2-10mcg will cause

A

B3 lipolysis

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35
Q

Epi can cause an increase in this electrolyte______. Why?

A

Potassium

Increased Na-K pump action

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36
Q

Ephedrine may cause this adverse action______ if taken with ________.

A

HTN crisis

moa inhibitors

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37
Q

Isoproterenol and epinephrine are

equally effective in stimulating

A

release of free fatty acids and in

energy production

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38
Q

The duration of action of isoproterenol is somewhat longer than

A

epi

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39
Q

Inotropic

A

force of contraction

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40
Q

Chronotropic

A

rate

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41
Q

Dromotropic

A

conduction speed

42
Q

Metaproterenol is a?

A

bronchodilator
selective B2 agonist
resistant to methylation by COMT

43
Q

Terbutaline is a

A 
Terbutaline is a
bronchodilator
selective B2 agonist 
can be give subq 0.25mg can repeat Q15 
rapid onset
44
Q

Albuterol is

A

bronchodilator
selective B2 agonist
works in 15 min

45
Q

Levalbuterol is

A

bronchodilator
selective B2 agonist
R-enantiomer= less SE

46
Q

Ritodrine is

A

Tocolytic

selective B2 agonist

47
Q

Phenylephrine is epinephrine minus

A

hydroxyl group at pos 4

48
Q

Phenylephrine is an A1 selective agonist but acts on ________at high doses.

A

B1

49
Q

Baroceptor response often stay intact if using

A

clonidine or dexmedetomidine

50
Q

Fenoldopam is

A

D1 receptor agonist

vasodilator for acute treatment of severe HTN

51
Q

Amphetamine and dextroamphetamine

A

Acts indirectly by releasing biogenic amines
from storage sites in nerve terminals
– Activates RAS
– Can cause psychosis (5-HT mediated)
– Anorectic, locomotor stimulant (DA mediated

52
Q 
Phenoxybenzamine
6 things
what is it?
where does it bind? 
causes?
enhanced by what?
Useful in two things?
A

-Phenoxybenzamine-vasodilator
-Blocks A1 & A2 irreversibly/Antagonists
-Causes decrease in SVR and increase in CO
(reflex)
– Hypotension enhanced with b2 agonists
– Useful in pheochromocytoma and in
-autonomic hyperreflexia, SC injury

53
Q 
Phentolamine
5
what is it
use
duration
S/E
contra in who
A 
Phentolamine
Blocks A1 &A2 receptors COMPETITIVELY
– Mainly used in preoperative management of
pheochromocytoma
• Same as phenoxybenzamine, but short-lived (~15
min following IV bolus)
– Causes release of histamine
• Contraindicated in CAD
54
Q

Prazosin

A

Prazosin/CHF
Potent A1 receptor antagonist/no A2 blockade (no increase in NE release)
• Blocks A1 receptors in arterioles
• Decreases SVR & venous return to heart
– Does not usually cause increase in HR or SV
• half-life 2-3 hours
• Terazosin (Hytrin®) is structural analog of
prazosin
– Also has high specificity for A1 receptors

55
Q

A1-Adrenergic Antagonists
Therapeutic uses
2

A

A1-Adrenergic Antagonists
Therapeutic uses
-CHF/A1 receptor blockade dilates arteries
• Decrease afterload and preload
-BPH
• A1 receptor antagonists reduce resistance in some
patients
• A1 receptors in bladder trigone and urethra contribute to
blockage
• Essential hypertension & prostatic hypertrophy
(prazosin, doxazosin, terazosin)

56
Q

Yohimbine

inhibits what

A 
Erectile dysfunction (Yohimbine)
• Blockade with selective antagonists
(yohimbine) can increase sympathetic
outflow
A2 receptor antagonist
• Increase SNS activity
• Inhibits the function of monoamine
oxidase enzymes
57
Q

Therapeutic Uses of A Blockers
(Antagonists)
5

A
  • Hypertension
  • Pheochromocytoma
  • Benign prostatic hyperplasia
  • Peripheral vascular disease
  • Erectile dysfunction (Yohimbine)
58
Q 
Beta Antagonists (B-Blockers) used to treat
4 cardiac issues
A

Used to Tx: CAD, HTN, HF, tachydysrhythmias

59
Q

Cardiac selective (β1 receptor) drugs

A

Atenolol, metoprolol, esmolol
-Relative selectivity; much less vascular, bronchial smooth
muscle, and metabolic effects

60
Q

Beta blockers Intrinsic sympathomimetic activity (ISA) (partial
agonist activity) drugs

A

Pindolol, acebutolol
Less slowing of HR at rest; exercise induced ↑ HR still blunted
like non-ISA β-blockers

61
Q

Beta blocker Membrane stabilizing activity (MSA)

A

Acebutolol, labetalol, metoprolol, pindolol, and

propranolol

62
Q

Beta blocker that vasodilates

A

Nebivolol vasodilates via endothelial dependent

NO pathway

63
Q

B antagonists block

A

renin release caused by
SNS stimulation
Reduction in plasma renin activity causes anti-HTN

64
Q

Beta blockers cause these negative effects on the heart

A

decreased sinus rate, spontaneous &

depolarization of ectopic foci

65
Q

Propranolol is life threating to what patient population? Why

A

COPD & asthma

blocks B2 receptor

66
Q

Beta blockers cause hypoglycemia. Why ?

4

A

Beta blockers cause hypoglycemia. Why ?
Metabolic effects
– Catecholamines promote glycogenolysis and mobilize glucose in response to hypoglycemia
-B adrenergic antagonists may block this response
-B2 receptor blockade may inhibit hepatic
response to insulin-induced hypoglycemia
-B3 adrenergic antagonists attenuate the
release of free fatty acids from adipose tissue

67
Q

Propranolol

A

non selective beta
Interacts with B1& B2 receptors with equal
affinity
Highly lipophilic with large VD
• Crosses BBB
– Lacks intrinsic sympathomimetic activity
– Extensively metabolized
– Propranolol may be administered IV for
management of life-threatening dysrhythmias
or to patients under anesthesia
• 1-3 mg administered slowly
• If bradycardia is profound - atropine may be used

68
Q

Metoprolol

A 
Metoprolol
– β1/β2-receptor affinity (30:1); membrane
stabilizing activity (MSA); no ISA
– Primarily liver metabolism
– ½ as potent as propranolol
– Short elimination half-life 3.5 hrs
69
Q

Atenolol

A

β1/β2-receptor affinity (30:1); no MSA or ISA
activity
– Primarily excreted via kidneys; no first-pass
metabolism
– Elimination half-life 6.5 hrs, so once daily dosing

70
Q

Pindolol

A

Nonselective β–blocker that has MSA and

ISA

71
Q

Acebutolol

A

β1-selective with ISA

72
Q

Esmolol

A

β1-selective; IV rapid onset and offset
(<10 min.)
– Rapid hydrolysis by non-specific esterases

73
Q

Esmolol

A

Esmolol
• B1 selective adrenergic antagonist with very
short duration of action t1/2B 8-9 minutes
• Esmolol has an ester linkage (nonspecific
esterases – red blood cells)
• Rapidly hydrolyzed
• Onset (2 minutes) and cessation of B
adrenergic blockade are rapid
• Peak hemodynamic effect in 10 minutes
• Esmolol has little, if any, ISA
• Anesthesia uses:
– Rapid, brief control of ↑ HR (i.e.: to prevent tachycardia
from intubation stimulation)
– Infusions can be quickly terminated if needed

74
Q

POISE

A

Dont hold beta blockers, control rate <80

beta blocker time out

75
Q

Labetalol

A 
Competitive antagonists
at A1 and B receptors
– Selective a and nonselective b blocker
– Racemic mixture with 4 stereoisomers
a1 blockade leads to arteriolar dilation
b1 blockade leads to decrease in BP by blocking
reflex sympathetic stimulation
• 5x-10x more potent b blocker than a  blocker (7:1)
• Extensively metabolized in liver
• Elimination half life of 5 hrs
• Onset 2-5 minutes, peak 5-15 minutes, and DOA 2-4
hrs
• 5-10 mg TTE every 10 minutes
76
Q

Adverse Effects of Beta Blockers

8

A 
• Bronchoconstriction
• Bradycardia, A-V block, cardiac
arrest
• Decreased cardiac output
• Sudden withdrawal problems
• Hypoglycemia problems
• Diminished exercise performance
• Possible changes in blood lipids
• Potential CNS effects
77
Q

use__________for bronchial asthma

drug

A

albuterol

78
Q

use__________for cardiogenic shock

drug

A

dopamine/dobutamine

79
Q

use__________for rhinitis

drug

A

phenylephrine

80
Q

use__________for HTN

drug

A

prazosin

81
Q

use__________for angina pectoris

drug

A

propranolol

82
Q

use__________for supraventricular arrhythmias

drug

A

atenolol

83
Q

use__________for BPH

drug

A

terazosin or prazosin

84
Q

Therapeutic Uses of Beta
Blockers
8

A
  • Hypertension
  • Ischemic heart disease
  • Cardiac arrhythmias
  • Obstructive cardiomyopathy
  • Congestive heart failure
  • Open-angle glaucoma B1
  • Migraine headache
  • Muscle tremor, performance anxiety propranolol
85
Q

Indirect acting irreversible muscarinic?

A

echothiopate

86
Q

indirect acting reversible muscarinic?

3

A

edrophonium, neostigmine, physostigmine

87
Q

Bethanechol

A

M3 muscarinic agonist
Used post-op to treat urinary retention and
abdominal distention
– Treat neurogenic G.I. atony and megacolon
(increase intestinal motility)

88
Q

Pilocarpine

A

m3 muscarinic
Pilocarpine - topical miotic, glaucoma (decrease
intraocular pressure

89
Q

Muscarinic Agonists

Clinical Uses

A 
Reduces IOP by causing contraction of
ciliary body
• facilitates aqueous humor outflow
• can be treated with cholinergic agonists or
cholinesterase inhibitors
90
Q

Atropine

A

CNS effects occur with high doses of
atropine
– effects from restlessness to somnolence
– toxic doses cause more prominent symptoms
• disorientation, hallucinations, and delirium
– larger (toxic) doses cause depression,
circulatory collapse

91
Q

scopolamine

A 
less likely to change heart 
depresses RAS
– may cause delayed awakening from anesthesia
– used for motion-sickness
• blocks medullary impulses arising from vestibular
overstimulation
• transdermal (postauricular) provides sustained blood
levels
Scopolamine in therapeutic doses may be
used for sedation
– can be combined with an opioid
– drowsiness, amnesia, and fatigue
– Intravenous dosing (0.3-0.6 mg
92
Q

Glycopyrrolate
chem structure
doesn’t do what
why

A

Glycopyrrolate is a quaternary amine
– devoid of sedative effects
– does not cross BBB

93
Q

Muscarinic relatively contraindicated

A

in narrowangle
glaucoma
• causes flow obstruction
• interferes with flow of aqueous humor

94
Q

Scopolamine produces sedation

A 
Scopolamine produces sedation by
decreasing activity of the RAS (100x
more than atropine)
– Also effects other areas of brain resulting
in amnesia
• May have delayed awakening
• Physostigmine is effective in reversing
restlessness or somnolence from CNS
effects of tertiary amine
antimuscarinics
95
Q

Scopolamine produces sedation by

A 
Scopolamine produces sedation by
decreasing activity of the RAS (100x
more than atropine)
– Also effects other areas of brain resulting
in amnesia
• May have delayed awakening
• Physostigmine is effective in reversing
restlessness or somnolence from CNS
effects of tertiary amine
antimuscarinics
96
Q

Tiotropium - DOA

A

> 24 hrs

97
Q

Most potent antisialagogue in order order of potency

A

scopolamine
glycopyrrolate
atropine

98
Q

Horner Syndrome

A 
Stellate ganglion
– Superior, middle, and cervicothoracic ganglia
– Spinal segments T1-4/5 synapse here
– Provide SNS innervation of ↑ ext., head, neck
– So?
– Horner syndrome
• Ptosis
• Miosis
• Anhidrosis
• Enophthalmos
• Redness of face and conjunctiva
99
Q

Dopamine

A

Precursor of NE
• Effects are mediated through D1 receptors
• Low doses primarily activate D1 receptors
– Vascular postjunctional D1 receptors in renal
and mesenteric blood vessels
– 0.5-3.0 mcg/kg/min
• Moderate DA dosages act on B1 receptors
– 3.0 - 10 mcg/kg/min
Higher dosages 10 - 20 mcg/kg/min primarily act
at a1 receptors
– Leads to vascular vasoconstriction
– Low dose increased renal blood flow and GFR
– Moderate dose increases myocardial contractility and
increase in CO
– High dosages vasoconstriction
• Benefit to renal perfusion may be lost
– Dopamine is an important central neurotransmitter
• Peripherally administered dopamine has no central side
effects
• Substrate for MAO & COMT
– Half-life of about a minute

100
Q

Ipatropium/tiotropium

A

quaternary compounds used to treat reactive
airway disease
– used as an inhalant
– does not impair mucociliary elevator
– toxicity not usually a problem since this
compound is poorly absorbed from lungs into
circulation

101
Q

Echothipoate

A

irreversible indirect

glaucoma

102
Q

Carvedilol is similar to ___________and good for

A

labetalol, chf

PHARM 4 ANS (6 decks)

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