Unit 2 - Autonomics III Flashcards Preview

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Flashcards in Unit 2 - Autonomics III Deck (46):
1

what are sites of action of ganglionic blockers?

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

2

what are sites of action of neuromuscular blockers?

Nm (nicotinic receptor in NMJ)

3

what are sites of action of antimuscarinic drugs?

M1-5 (muscarinic receptors in parasympathetic endpoint)

4

what is the link between "atropine" and "belladonna"?

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

5

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

quaternary amines
-propantheline
-glycopyrrolate

6

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

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)

7

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

quaternary amines
-Ipratropium
-Tiotropium

8

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

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

9

is there selectivity between muscarinic receptors?

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

10

what does atropine do at the following doses?
-0.5 mg
-5 mg
->10 mg

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

11

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

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

12

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

cycloplegia, mydriasis
-block M3 receptors

13

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

bronchodilation, especially if constricted
-block of M3 receptors

14

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

relaxation, slowed peristalsis
-block of M1/3 receptors

15

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

relaxation of the bladder wall, urinary retention
-block of M3 receptors

16

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

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

17

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

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

18

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

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

19

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

none

20

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

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

21

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

tertiary amine that is well absorbed with central effects
-given by injection, mouth, or transdermal patch

22

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

atropine, homatropine, cyclopentolate, tropicamide
-produce mydriasis and cycloplegia

23

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

ipratropium and tiotropium
-cause bronchodilation in asthma and COPD

24

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

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)