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MSII Pharmacology > Unit 2 - Autonomics III > Flashcards

Unit 2 - Autonomics III Flashcards

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1
Q

what are sites of action of ganglionic blockers?

A

Nn (autonomic nicotinic receptors; postganglionic adrenal, sympathetic, and parasympathetic)

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2
Q

what are sites of action of neuromuscular blockers?

A

Nm (nicotinic receptor in NMJ)

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3
Q

what are sites of action of antimuscarinic drugs?

A

M1-5 (muscarinic receptors in parasympathetic endpoint)

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4
Q

what is the link between “atropine” and “belladonna”?

A

atropine (in nightshade and jimsonweed) and scopolamine (in hebane) cause mydriasis (pupil dilation) due to their antimuscarinic activity
-dilated pupils were considered beautiful in Renaissance italy

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5
Q

what is the structure for antimuscarinic drugs that work on GIT? examples?

A

quaternary amines

  • propantheline
  • glycopyrrolate
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6
Q

what is the structure for antimuscarinic drugs that work on periphery? examples?

A

tertiary amines (better absorbed and penetrate CNS better to have more central effects)

  • pirenzepine (peptic disease)
  • dicyclomine (peptic disease, hypermotility)
  • tropicamide (mydriatric, cycloplegic)
  • tolterodine (urinary incontinence)
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7
Q

what is the structure for antimuscarinic drugs that work on asthma? examples?

A

quaternary amines

  • Ipratropium
  • Tiotropium
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8
Q

what is the structure for antimuscarinic drugs that work on Alzheimer’s? examples?

A 
tertiary amines (better absorbed and penetrate CNS better to have more central effects)
-benztropine
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9
Q

is there selectivity between muscarinic receptors?

A

no; antagonists are essentially non-selective in that they do not discriminate well between the subtypes

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10
Q

what does atropine do at the following doses?

  • 0.5 mg
  • 5 mg
  • > 10 mg
A

0.5 mg: slight cardiac slowing (paradoxical), some xerostomia, inhibition of sweating

5 mg: tachycardia, palpitation, markedly high xerostomia, some blurring of near vision

> 10 mg: hallucinations and delirum, coma

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11
Q

what do muscarinic blocking drugs do to the CNS? the mechanism?

A

sedation, anti-motion sickness, anti-Parkinson, amnesia, delirium
-block of muscarinic receptors, unknown sub-types

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12
Q

what do muscarinic blocking drugs do to the eye? the mechanism?

A

cycloplegia, mydriasis

-block M3 receptors

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13
Q

what do muscarinic blocking drugs do to the bronchi? the mechanism?

A

bronchodilation, especially if constricted

-block of M3 receptors

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14
Q

what do muscarinic blocking drugs do to the GIT? the mechanism?

A

relaxation, slowed peristalsis

-block of M1/3 receptors

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15
Q

what do muscarinic blocking drugs do to the GUT? the mechanism?

A

relaxation of the bladder wall, urinary retention

-block of M3 receptors

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16
Q

what do muscarinic blocking drugs do to the heart? the mechanism?

A

initial slight bradycardia, especially at low doses (0.5 mg), then tachycardia at higher (5 mg)

  • bradycardia from blocking inhibitory presynaptic receptors
  • tachycardia from block of M2 receptors in SA node
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17
Q

what do muscarinic blocking drugs do to the blood vessels? the mechanism?

A

block of muscarinic vasodilation; doesn’t manifest unless a muscarinic agonist is present
-blockage of M3 receptors on endothelium of vessels

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18
Q

what do muscarinic blocking drugs do to the glands? the mechanism?

A

marked reduction of salivation, moderate reduction of lacrimation/sweating, less reduction of gastric secretion
-block of M1/3 receptors

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19
Q

what do muscarinic blocking drugs do to the skeletal muscle? the mechanism?

20
Q

what antimuscarinic drugs act on the CNS? what is their application?

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A
  1. benzotropine, trihexyphenidyl, biperiden
    - to treat the manifestations of Parkinson’s disease
  2. scopolamine
    - prevent/reduce motion sickness
21
Q

what is the structure of scopolamine, and how is it given?

Study These Flashcards
A

tertiary amine that is well absorbed with central effects

-given by injection, mouth, or transdermal patch

22
Q

what antimuscarinic drugs act on the eye? what is their application?

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A

atropine, homatropine, cyclopentolate, tropicamide

-produce mydriasis and cycloplegia

23
Q

what antimuscarinic drugs act on the bronchi? what is their application?

Study These Flashcards
A

ipratropium and tiotropium

-cause bronchodilation in asthma and COPD

24
Q

how is ipratropium given? how does it compare to tiotropium?

Study These Flashcards
A

ipra: given via aerosol to maximize bronchial effects and minimize central effects
tiot: longer acting (1-2 days duration)

25
what antimuscarinic drugs act on the GIT? what is their application?
glycopyrrolate, dicyclomine, methscopolamine | -reduce transient hypermotility
26
what is glycopyrrolate often given together with?
opioid anti-diarrheal drugs
27
what antimuscarinic drugs act on the genitourinary tract? what is their application?
oxybutynin, glycopyrrolate, tolterodine | -treat transient cystitis, postoperative bladder spasms, or incontinence
28
what is tolterodine specific for?
relatively specific for urinary bladder, and now commonly used (Detrol)
29
how is tropicamide in terms of metabolism and acting?
rapidly metabolized, short acting
30
what is the mnemonic for overdose of atropine and other muscarinic antagonists? why do these occur?
dry as a bone, blind as a bat, red as a beet, mad as a hatter - dry: reduced sweating, lacrimation, salivation - blind: blocked accommodation and excessive dilation - red: inhibited sweat glands increases body temp, and antagonism of alpha1 receptors block vasoconstriction - mad: inhibition of CNS muscarinic receptors causes complex consequences
31
what is "atropine fever"?
blockade of thermoregulatory sweating causes hyperthermia - sweat glands are symapthetic, but use cholinergic post-ganglionic fibers - very dangerous and potentially lethal in infants and small children
32
what are effects of ganglion-blocking drugs on CNS?
antinicotinic actions - reduction of nicotine craving - amelioration of Tourette's (mecamylamine only)
33
what are effects of ganglion-blocking drugs on eye?
moderate mydriasis and cyclopegia
34
what are effects of ganglion-blocking drugs on bronchi?
little effect | -asthmatics may note some bronchodilation
35
what are effects of ganglion-blocking drugs on GIT?
markedly reduced motility | -constipation may be severe
36
what are effects of ganglion-blocking drugs on genitourinary tract?
reduced contractility of bladder | -impairment of erection and ejaculation
37
what are effects of ganglion-blocking drugs on heart?
slight tachycardia in young adults | -reduction in force of contraction and cardiac output
38
what are effects of ganglion-blocking drugs on blood vessels?
- reduction in arteriolar tone, with marked reduction in venous tone - blood pressure decrease and orthostatic hypotention may be severe
39
what are effects of ganglion-blocking drugs on glands?
reduction in salivation, lacrimation, sweating, and gastric secretion
40
what are effects of ganglion-blocking drugs on skeletal muscle?
no significant effect
41
what is the mechanism of ganglionic blockers?
competitively inhibit Nn receptors at both sympathetic and parasympathetic ganglia -lack of selectivity causes broad range of undesirable effects, thus largely abandoned
42
what is special about mecamylamine?
it can cross the BBB and is the only ganglion-blocking drug available today, to treat Tourette's
43
explain the pharmacology of NMJ blockers?
interfere with transmission at axon terminals, and are very useful as skeletal muscle relaxants - inhibit Nm to facilitate surgery or artificial ventilation - can be nondepolarizing or polarizing
44
what is the mechanism of nondepolarizing blockers? what is the prototypical one?
prevent opening of the end plate channel | -tubocuraine act competitively with ACh at Nm (can be overcome by AChE and increased ACh)
45
what is the mechanism of depolarizing blockers? what is the prototypical one?
persistently occupies receptor to keep it open - "desensitizes" end plate to cause persistent depolarization - succinylcholine causes initial depolarization and contractions, but tension can't be maintained without periodic relaxation and depolarization at end plate, so continuous depolarization results in muscle relaxation and flaccid paralysis
46
explain what Botox is
C. botulinum toxin type A that degrades SNAP-25 that mediates fusion of synaptic vesicles with presynaptic terminal membrane - highly toxic at high concentrations - low concentration injection used to treat increased muscle tone (blocks ACh release)

MSII Pharmacology (43 decks)

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