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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
toxic effects of atropine on CNS
Coma, confusion, depression
26
Difference between tertiary amines like atropine and quaternary amines
Tertiary amines can be used in ocular and CNS application. Quaternary amines are mainly used in GI tractand peripheral applications
27
Antagonist vs agonist size difference
Antagonist is much bigger
28
Why do tertiary amines have CNS access
Nitrogen is not charged
29
Structural difference between atropine and scopolamine? How does this change the effects?
Scopolamine has an extra oxygen. This makes it more lipophilic. Making it have better CNS access.
30
How does clinical use in anti muscarinic drugs depend on drug duration
Less duration= less side effects
31
Scopolamine use
Motion sickness treatment
32
homatropine and tropicamide clinical uses
optical application
33
benztropine clinical use
Parkinsons disease
34
What two drugs are used in conjunction to treat parkinsons
Benztropine, L-Dopa
35
Ipratropium clinical use
Same as atropine, but is charged. COPD
36
How does ipratropium treat COPD
M3 Antagonist, dilates bronchi.
37
What two drugs are used in conjunction to treat COPD
Albuterol and Ipratropium
38
Longer acting analog of ipratropium
Tiotropium
39
Glycopyrrolate used for
GI spasms and peptic ulcers
40
Tolteridon clinical use
Acts selectively on M3 and used for Overactive bladder
41
How do we treat antimuscarinic effects
Physostigmines
42
How do physostigimines treat antimuscarinic effects
ACHe inhibitor
43
Nm on which tissue? Nn on which tissue?
Skeletal muscle post ganglionic
44
what is a common feature between muscarinic and nicotinic receptors
ACHe
45
Features of neuromuscular blocking agents
They look like ACh
46
Succinylcholine (SUX) structure
ACh dimer
47
2 main nicotinic blockers
Tubocurarine SUX
48
tubocurarine blocking mechanism
non-depolarizing nicotinic blockade
49
SUX mechanism of blockade
Depolarizing blockade
50
Mechanism of nicotinic receptros
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
Difference between tubocurarine and succinylcholine
Succinylchoine has permanent depolarization because ACh remains bound to receptor, Tubocurarine has non-depolarizing nicotinic blockade.
52
Persistent depolarization definition
AChE does not break down ACh down and remains bound. Na+ channels stay in an inactive state and cannot reset to active state
53
What is Succinylcholine (SUX) metabolized by? Rate of degradation compared to ACh and ACHe
Butyrylcholinesterase. Much slower than AChE.
54
Butyrylcholinesterase breaks ACh down into
Choline. Increases BP
55
Clinical use of Succinylcholine (SUX)
Skeletal muscle relaxation during anesthesia and electroconvulsant therapy.
56
Indirect inhibitor of ACh RELEASE
Botulinum toxin
57
Clinical use of botulinum toxin
Cerebral palsy, uncontrolled muscle spasms
58
Hexamethonium action
blocks ALL of the sympathetic and Parasympathetic activity to treat HTN. Discontinued.
59
effect of hexamethonium on blood vessel
Hypotension
60
effects of hexamethonium on sweat glands
decrease sweat excretion
61
effects of hexamethonium on Heart rate
increases HR
62
effects of hexamethonium on eye
Pupillary dilation and blurred vision
63
Effect of hexamethonium on gut
Deccreases gut motility
64
effect of hexamethonium on bladder
Urinary retention

Therapeutics (46 decks)

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