Pharm 13 Drugs Which Stimulate Cholinergic Junctions

Front 1

Bethanecol
1) Drug class
2) Actions
3) Advantages over its analog?

Back 1

1) Choline ester
2) Stimulant of GI tract and bladder, good post surgery
3) More specific (has almost no CV effects) and less labile than Ach, resistant to almost all AchE

Front 2

Pilocarpine
1) Based on which drug/drug class
2) Acts predominantly where?
3) Therapeutic uses

Back 2

1) Muscarine/muscarinic agonist
2) At parasympathetic synapses
3) Xerostomia (dry mouth) and glaucoma (causes outflow of fluid from anterior chamber)

Front 3

Muscarine
1) Drug class
2) Actions
2) Toxicity

Back 3

1) Muscarinic agonist
2) Parasympathomimetic
3) Toxic mushrooms

Front 4

Nicotine
1) Drug class
2) Actions

Back 4

1) Nicotinic agonist
2) Actions difficult due to biphasic effect. Act at all autonomic ganglia, adrenal medulla, and also directly stimulate carotid and aortic bodies to increase RR and HR (think when smoking RR and HR increase)

Front 5

Mechanism of action of AchE

Back 5

1) Carbonyl carbon of Ach binds active center on AchE
2) Choline is split of
3) Acetylated AchE is then hydrolyzed to release more free enzyme

Front 6

Edrophonium
1) Drug class

Back 6

1) Truly reversible anti AchE, meaning does not covalently bind AchE and is hydrolyzed quicly

Front 7

Physostigmine
1) Drug class
2) Action
3) Therapeutic uses

Back 7

1) Carbamate, poorly reversible anti AchE
2) Has tertiary N that binds AchE as Ach does. Carbamates enzyme is not quickly hydrolyzed.
3) Glaucoma

Front 8

Neostigmine
1) Drug class
2) Action
3) Therapeutic uses

Back 8

1) Carbamate, poorly reversible anti AchE
2) Has quaternary N that binds AchE as Ach does. Carbamates enzyme is not quickly hydrolyzed.
3) Atony of GI and bladder, myasthenia gravic (in which there is autoimmune destruction of nicotinic R)

Front 9

DFP (Diisopropyl phophoroflouridate)
1) Drug class and general structure
2) Mechanism of action
3) Sites of action
4) Reactivator of Ach

Back 9

1) Irreversible Anti AchE

2) P molecule binds covalently to AchE active center
3) Lipid soluble so has effects in CNS
4) Pralidoxime, displases P

Front 10

Treatment for antiAchE poisoning do to either:
1) Reversible antiAchE
2) Irreversible antiAchE

Back 10

1) Atropine, muscarinic antagonist
2) Pralidoxime, reactivator for skeletal muscle paralysis

Front 11

Pralidoxime
1) Drug class
2) Mechanism of action
3) Therapeutic use

Back 11

1) Reactivator
2) Nucleophilic O pulls P of of AchE
3) antiAchE poisoning if administered quickly

Front 12

Botulinum toxin
1) Drug class, site of action
2) Therapeutic uses

Back 12

1) Blocks release of Ach at NMJ, leading to paralysis
2) Blepharospasm, strabismus, hemifacial spasm, facial wrinkles (Botox)

Front 13

Atropine
1) Class of drug derived from what?
2) Structure consists of what?
3) Actions

Back 13

1) Muscarinic antagonist derived from belladona
2) Has both an organic base and organic acid moiety
3) Parasympatholytic, binds receptor competitively

Front 14

Scopolamine
1) Class of drug
2) Site of actions

Back 14

1) Muscarinic antagonist
2) Has CNS effects at therapeutic doses, unlike atropine. Causes drowsiness, amnesia. At larger doses excitement, restlessness, amnesia.

Front 15

Place in order from lowest dose to highest dose the effects of muscarinic antagonists:
UT and GI inhibition, pupil dilation and increased HR, inhibition of gastric secretion, decreased salivation or sweating

Back 15

Lowest
Decreased salivation/sweating
Increased HR, pupil dilation
Decreased UT and GI activity
Decreased gastric secretions
Highest

Front 16

Match the following Muscarinic receptors with appropriate site of action: M1, M2, M3, M4
a) salivation, bladder, GI, blood vessels
b) heart, Ach feedback inhibition
c) forebrain, movement control
d) autonomic ganglia, brain

Back 16

M1, d
M2, b
M2, a
M4, c

Front 17

Benztropine
1) Drug class

Back 17

1) Muscarinic blocker

Front 18

d-tubocurarine
1) Drug class
2) Mechanism of action
3) Onset, duration
4) Side effects
5) Therapeutic uses

Back 18

1) Nicotinic blocker
2) Binds competitively with Ach to R via two N groups widely separated
3) 4-6 min., 80-120
4) Releases histamine, CV problems with HR increase
5) Muscle relaxant

Front 19

Metocurine
1) Drug class

Back 19

1) More potent derivative of d-tubocurarine with quartinary N

Front 20

Pancuronium
1) Drug class
2) Structure
3) Onset/duration
4) Side effects

Back 20

1) Competitive nicotinic blocker
2) Steroid derivative with Ns at either end
3) Onset 4-6 min, lasts 120-180 min
4) Inhibits vagus paraympathetic activity at heart, inhibits NET, blocks M2 receptor

Front 21

Atracuronium
1) Drug class
2) Advantages over previous drugs

Back 21

1) Competitive nicotinic blocker derived from d-tubocurarine
2) slower duration of activity, less cumulative tendency, ie less histamine, and less CV effects, no HR increase

Front 22

Vecuronium
1) Drug class
2) Advantages over previous drugs

Back 22

1) Competitive nicotinic blocker derived from pancuronium
2) no vagal effect, shorter duration, less cumulative effects

Front 23

Hexamethonium
1) Drug class
2) Structure
3) Site of action

Back 23

1) Competitive nicotinic blocker
2) Two choline moieties at either end with six carbons in between
3) Acts selectively at autonomic ganglia

Front 24

Succinylcholine
1) Drug class
2) Sites of action
3) Therapeutic uses
4) Onset/duration

Back 24

1) Depolarizing nicotinic blocker
2) Mostly active at NMJ but some action at autonomic ganglia
3) Tracheal intubation, used as muscle relaxant
4) 1-2 min, 5-8 min

Front 25

Decamethonium
1) Drug class
2) Site of action

Back 25

1) Depolarizing nicotinic blocker
2) Selectively at NMJ

Front 26

Depolarizing blockers
1) Describe biphasic effect and physical outcomes

Back 26

Initial NMJ stimulation because they are nicotinic agonists leads to faciculation. After repeated depolarization, Na channels enter inactive state and paralysis ensues.