Neuromuscular Pharmacology

Question 1

What is the mnemonic for s/s of potentially lethal poison exposures (organophosphates) on nicotinic receptors?

Answer 1

MATCH

M- muscle weakness, fasiculations

A- adrenal medulla activity increased

T- tachycardia

C- cramping of skeletal muscles

H- hypertension

Question 2

What is Pralidoxime?

Answer 2

an antidote for organophosphate poisoning (but NOT against carbamate-type inhibitors like neostigmine)

Question 3

What is pancuronium?

Answer 3

a NMJ blocker- paralyzes respiratory muscles

Question 4

What is the mnemonic for s/s of potentially lethal poison exposures (organophosphates) on muscarinic receptors?

Answer 4

DUMBBELLS

D- defecation

U- urination

M- miosis

B- bradycardia

B- bronchospasm, bronchorrhea

E- emesis

L- lacrimation

S- salivation

Question 5

____ and _____ are used to overcome poisoning by nondepolarizing agents but they would worsen NMJ blockade by succinylcholine.

Answer 5

Edrophonium and neostigmine

Question 6

Name an agonist to the Nm receptor.

Answer 6

succinylcholine

Question 7

Name an AChE inhibitor.

Answer 7

• neostigmine
• nerve gas

Question 8

This blocks the release of GABA, causing failure of motor reflex inhibition–> excessive contractions occur .

Answer 8

tetanus toxin

Question 9

What can block voltage-gated sodium channels?

Answer 9

lidocaine

Question 10

Black widow spider venom forms pores allowing _____.

Answer 10

excessive Ca++ influx, clumping of vesicles, and explosive ACh release

Question 11

What do these s/s indicate?

MATCH

M- muscle weakness, fasiculations

A- adrenal medulla activity increased

T- tachycardia

C- cramping of skeletal muscles

H- hypertension

Answer 11

potentially lethal poison exposures (organophosphates) on nicotinic receptors

Question 12

Name 2 cholinesterase inhibitors.

Answer 12

1. AChE
2. BuChE

Question 13

Name something that increases vesicular ACh release.

Answer 13

increased Ca++

Question 14

_____ is lysed by tetanus toxin after the toxin has been transported in retrograde fashion to the spinal cord.

Answer 14

Synaptobrevin

Question 15

Synaptobrevin is lysed by ______ at the NMJ to prevent vesicle fusion and ACh release, producing flaccid paralysis.

Answer 15

botulinum toxin

Question 16

This is an Nm receptor agonist that opens the channel and allows depolarization but not repolarization –> produces flaccid paralysis.

Answer 16

succinylcholine

Question 17

How does succinylcholine work?

Answer 17

it’s an Nm receptor agonist that opens the channel and allows depolarization but not repolarization –> produces flaccid paralysis

Question 18

Edrophonium and neostigmine are used to overcome poisoning by nondepolarizing agents but they would worsen _______.

Answer 18

NMJ blockade by succinylcholine

Question 19

This is a NMJ blocker that paralyzes respiratory muscles.

Answer 19

pancuronium

Question 20

AP depolarization opens ______, allowing ____ influx.

Answer 20

voltage-gated Ca++ channels; Ca++

Question 21

Name 2 inhibitors of vesicular ACh release.

Answer 21

1. hemicholinum
2. botulinum toxin

Question 22

What is lidocaine used for?

Answer 22

blocking voltage-gated Na+ channels

Question 23

Synaptobrevin is lysed by botulinum toxin at the NMJ to prevent vesicle fusion and ACh release, producing ______.

Answer 23

flaccid paralysis

Question 24

Synaptobrevin is lysed by _____ after the toxin has been transported in retrograde fashion to the spinal cord.

Answer 24

tetanus toxin

Question 25

The AP depolarization is mediated via Na+ ion inward current through \_\_\_\_.

Answer 25

voltage-gated sodium channels

Question 26

What is the effect of Botox?

Answer 26

decreased ACh release

Question 27

\_\_\_\_\_ forms pores allowing excessive Ca++ influx, clumping of vesicles, and explosive ACh release.

Answer 27

Black widow spider venom

Question 28

This is an Nm receptor antagonist that blocks channel opening and depolarization to produce flaccid paralysis.

Answer 28

curare

Question 29

What do these s/s indicate? DUMBBELLS D- defecation U- urination M- miosis B- bradycardia B- bronchospasm, bronchorrhea E- emesis L- lacrimation S- salivation

Answer 29

potentially lethal poison exposures (organophosphates) on muscarinic receptors

Question 30

Edrophonium and neostigmine are used to overcome ______ but they would worsen NMJ blockade by succinylcholine.

Answer 30

poisoning by nondepolarizing agents

Question 31

Name 3 antidotes for organophosphate poisoning.

Answer 31

1. Pralidoxime (but NOT against carbamate-type inhibitors like neostigmine) 2. atropine 3. diazepam

Question 32

Name a competitive antagonist to the Nm receptor.

Answer 32

curare

Question 33

Synaptobrevin is lysed by botulinum toxiin at the NMJ to prevent \_\_\_\_\_\_\_, producing flaccid paralysis.

Answer 33

vesicle fusion and ACh release

Question 34

Name 2 inhibitors of depolarization.

Answer 34

1. curare 2. snake alpha-toxins

Question 35

How does curare work?

Answer 35

it's an Nm receptor antagonist that blocks channel opening and depolarization to produce flaccid paralysis

Question 36

What is the initial sign of organophosphate poinsoning?

Answer 36

muscarinic excess with double vision

Question 37

Name a inhibitor of muscle contraction.

Answer 37

dantrolene

Question 38

How does tetanus toxin work?

Answer 38

it blocks the release of GABA, causing failure of motor reflex inhibition and excessive contractions occur