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Therapeutics > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

prototype drug for antimuscarinic agents

A

Atropine

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2
Q

Competitive antagonist mechanism

A

Anticholinergics that bind to the receptor and disrupts ACh binding.

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3
Q

Atropine effect on muscarinic receptors

A

They block them by being competitive antagonists at M1,2 and 3 at postganglionic

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4
Q

Atropine also has action on_____

A

Smooth muscle that lack innervation

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5
Q

Atropine effect on nicotinic receptor

A

Little effect on actions of ACh at nicotinic receptors

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6
Q

Atropine effect on CNS

A

Can produce partial block on M1 at high doses

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7
Q

Does acetylcholine bind pre or post synaptically

A

Post

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8
Q

effect of atropine on exocrine glands, what receptor does it act on?

A

decreased secretions
decreased sweating
M3 receptor

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9
Q

Therapeutic use of atropine on exocrine glands

A

Preanesthetic, peptic ulcers, OTC and cold remedies

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10
Q

Adverse effects of atropine on exocrine glands

A

Dry mouth
hyperthermia in children

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11
Q

effect of atropine on eye, what receptor does it block

A

Blocks M3 receptor.
Causes mydriasis

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12
Q

therapeutic use of atropine in eye

A

opthalmic examination or procedure

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13
Q

adverse effects of atropine on eye

A

exacerbation of glaucoma

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14
Q

effect of atropine on CVS, what receptor does it act on

A

Increase heart rate, M2 receptor

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15
Q

Therapeutic use of atropine in cardiovascular system

A

bradyarrythmia, heartblock

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16
Q

adverse/toxic effects of atropine on CVS

A

Tachycardia, increased risk of VF in acute MI

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17
Q

effect of atropine on respiratory tract, what receptors does it act on?

A

Block of vagal bronchoconstriction

M2 and M3

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18
Q

use of atropine therapeutically in respiratory tract

A

Treatment of COPD and asthma

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19
Q

effects of atropine on urinary bladder

A

decreased urinary frequency

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20
Q

toxic effects of atropine in urinary system

A

urine retention

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21
Q

effects of atropine in GI smooth muscle

A

decreased motility (might lead to constipation)

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22
Q

effects of atropine on GI smooth muscle

A

Constipation

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23
Q

effects of atropine on CNS

A

Blocks all muscarinic receptors

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24
Q

Therapeutic use of atropine on CNS

A

Anti motion sickness, anti parkinsosn

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25
Q

toxic effects of atropine on CNS

A

Coma, confusion, depression

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26
Q

Difference between tertiary amines like atropine and quaternary amines

A

Tertiary amines can be used in ocular and CNS application. Quaternary amines are mainly used in GI tractand peripheral applications

27
Q

Antagonist vs agonist size difference

A

Antagonist is much bigger

28
Q

Why do tertiary amines have CNS access

A

Nitrogen is not charged

29
Q

Structural difference between atropine and scopolamine? How does this change the effects?

A

Scopolamine has an extra oxygen. This makes it more lipophilic. Making it have better CNS access.

30
Q

How does clinical use in anti muscarinic drugs depend on drug duration

A

Less duration= less side effects

31
Q

Scopolamine use

A

Motion sickness treatment

32
Q

homatropine and tropicamide clinical uses

A

optical application

33
Q

benztropine clinical use

A

Parkinsons disease

34
Q

What two drugs are used in conjunction to treat parkinsons

A

Benztropine, L-Dopa

35
Q

Ipratropium clinical use

A

Same as atropine, but is charged. COPD

36
Q

How does ipratropium treat COPD

A

M3 Antagonist, dilates bronchi.

37
Q

What two drugs are used in conjunction to treat COPD

A

Albuterol and Ipratropium

38
Q

Longer acting analog of ipratropium

A

Tiotropium

39
Q

Glycopyrrolate used for

A

GI spasms and peptic ulcers

40
Q

Tolteridon clinical use

A

Acts selectively on M3 and used for Overactive bladder

41
Q

How do we treat antimuscarinic effects

A

Physostigmines

42
Q

How do physostigimines treat antimuscarinic effects

A

ACHe inhibitor

43
Q

Nm on which tissue? Nn on which tissue?

A

Skeletal muscle
post ganglionic

44
Q

what is a common feature between muscarinic and nicotinic receptors

45
Q

Features of neuromuscular blocking agents

A

They look like ACh

46
Q

Succinylcholine (SUX) structure

47
Q

2 main nicotinic blockers

A

Tubocurarine
SUX

48
Q

tubocurarine blocking mechanism

A

non-depolarizing nicotinic blockade

49
Q

SUX mechanism of blockade

A

Depolarizing blockade

50
Q

Mechanism of nicotinic receptros

A

ACh binds postsynaptically to nicotine and becomes inactive
Depolarizes membrane
sodium comes in
ACHe binds ACh and breaks it down
Goes back to active state

51
Q

Difference between tubocurarine and succinylcholine

A

Succinylchoine has permanent depolarization because ACh remains bound to receptor, Tubocurarine has non-depolarizing nicotinic blockade.

52
Q

Persistent depolarization definition

A

AChE does not break down ACh down and remains bound. Na+ channels stay in an inactive state and cannot reset to active state

53
Q

What is Succinylcholine (SUX) metabolized by? Rate of degradation compared to ACh and ACHe

A

Butyrylcholinesterase. Much slower than AChE.

54
Q

Butyrylcholinesterase breaks ACh down into

A

Choline. Increases BP

55
Q

Clinical use of Succinylcholine (SUX)

A

Skeletal muscle relaxation during anesthesia and electroconvulsant therapy.

56
Q

Indirect inhibitor of ACh RELEASE

A

Botulinum toxin

57
Q

Clinical use of botulinum toxin

A

Cerebral palsy, uncontrolled muscle spasms

58
Q

Hexamethonium action

A

blocks ALL of the sympathetic and Parasympathetic activity to treat HTN. Discontinued.

59
Q

effect of hexamethonium on blood vessel

A

Hypotension

60
Q

effects of hexamethonium on sweat glands

A

decrease sweat excretion

61
Q

effects of hexamethonium on Heart rate

A

increases HR

62
Q

effects of hexamethonium on eye

A

Pupillary dilation and blurred vision

63
Q

Effect of hexamethonium on gut

A

Deccreases gut motility

64
Q

effect of hexamethonium on bladder

A

Urinary retention

Therapeutics (46 decks)

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