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MSII Pharmacology > Unit 2 - Autonomics III > Flashcards

Unit 2 - Autonomics III Flashcards

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?

A

none

20
Q

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

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?

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?

A

atropine, homatropine, cyclopentolate, tropicamide

-produce mydriasis and cycloplegia

23
Q

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

A

ipratropium and tiotropium

-cause bronchodilation in asthma and COPD

24
Q

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

A

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

25
Q

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

A

glycopyrrolate, dicyclomine, methscopolamine

-reduce transient hypermotility

26
Q

what is glycopyrrolate often given together with?

A

opioid anti-diarrheal drugs

27
Q

what antimuscarinic drugs act on the genitourinary tract? what is their application?

A

oxybutynin, glycopyrrolate, tolterodine

-treat transient cystitis, postoperative bladder spasms, or incontinence

28
Q

what is tolterodine specific for?

A

relatively specific for urinary bladder, and now commonly used (Detrol)

29
Q

how is tropicamide in terms of metabolism and acting?

A

rapidly metabolized, short acting

30
Q

what is the mnemonic for overdose of atropine and other muscarinic antagonists? why do these occur?

A

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
Q

what is “atropine fever”?

A

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
Q

what are effects of ganglion-blocking drugs on CNS?

A

antinicotinic actions

  • reduction of nicotine craving
  • amelioration of Tourette’s (mecamylamine only)
33
Q

what are effects of ganglion-blocking drugs on eye?

A

moderate mydriasis and cyclopegia

34
Q

what are effects of ganglion-blocking drugs on bronchi?

A

little effect

-asthmatics may note some bronchodilation

35
Q

what are effects of ganglion-blocking drugs on GIT?

A

markedly reduced motility

-constipation may be severe

36
Q

what are effects of ganglion-blocking drugs on genitourinary tract?

A

reduced contractility of bladder

-impairment of erection and ejaculation

37
Q

what are effects of ganglion-blocking drugs on heart?

A

slight tachycardia in young adults

-reduction in force of contraction and cardiac output

38
Q

what are effects of ganglion-blocking drugs on blood vessels?

A
  • reduction in arteriolar tone, with marked reduction in venous tone
  • blood pressure decrease and orthostatic hypotention may be severe
39
Q

what are effects of ganglion-blocking drugs on glands?

A

reduction in salivation, lacrimation, sweating, and gastric secretion

40
Q

what are effects of ganglion-blocking drugs on skeletal muscle?

A

no significant effect

41
Q

what is the mechanism of ganglionic blockers?

A

competitively inhibit Nn receptors at both sympathetic and parasympathetic ganglia
-lack of selectivity causes broad range of undesirable effects, thus largely abandoned

42
Q

what is special about mecamylamine?

A

it can cross the BBB and is the only ganglion-blocking drug available today, to treat Tourette’s

43
Q

explain the pharmacology of NMJ blockers?

A

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
Q

what is the mechanism of nondepolarizing blockers? what is the prototypical one?

A

prevent opening of the end plate channel

-tubocuraine act competitively with ACh at Nm (can be overcome by AChE and increased ACh)

45
Q

what is the mechanism of depolarizing blockers? what is the prototypical one?

A

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
Q

explain what Botox is

A

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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