Pharma 5

Question 1

Skeletal muscle relaxants are classified into two categories:

Answer 1

1- Centrally acting
2- Peripherally acting

Question 2

What are the types of centrally acting skeletal muscle relaxants?

Answer 2

1) Benzodiazepine: Diazepam
2) GABA derivative: Baclofen
3) α2 receptor agonist: Tizanidine

Question 3

What are the different types of drugs acting at the neuromuscular junction (NMJ)?

Answer 3

1) Depolarizing neuromuscular blockers: Succinylcholine
2) Non-depolarizing neuromuscular blockers: Tubocurarine
3) Inhibitor of Ach release: Botulinum toxin

Question 4

What is the only direct acting skeletal muscle relaxant mentioned?

Answer 4

Dantrolene

Question 5

What mechanism do benzodiazepines like Diazepam utilize as skeletal muscle relaxants?

Answer 5

They bind to GABA-A receptors, potentiating GABAergic activity by increasing chloride conductance results in presynaptic inhibition in the spinal cord

Question 6

What is Baclofen’s mechanism of action as a muscle relaxant?

Answer 6

It is an analogue of GABA that binds to GABA-B receptors, reducing glutamate release and has analgesic effects.

Question 7

What effects does Tizanidine produce as a muscle relaxant?

Answer 7

It is an alpha 2 adrenoceptor agonist that inhibits the presynaptic release of neurotransmitters, reducing excitability of post-synaptic α-motor neurons.

Question 8

List some adverse effects of baclofen.

Answer 8

1) Sedation, drowsiness, confusion, depression, dizziness, ataxia, seizure.
2) Nausea, gastrointestinal disturbances.
3) Sudden withdrawal can precipitate hyperactivity and seizures.

Question 9

What are the adverse effects specifically associated with Tizanidine?

Answer 9

1) Drowsiness, fatigue, dizziness.
2) Dry mouth.
3) Hypotension.

Question 10

What are the uses of centrally acting skeletal muscle relaxants?

Answer 10

Used for spasticity associated with spinal cord injury, hemiplegia, amyotrophic lateral sclerosis, and multiple sclerosis.

Question 11

Are benzodiazepines commonly recommended as a first-line treatment for spasticity?

Answer 11

No, they are the only FDA approved for treatment but not often recommended as first-line.

Question 12

What is the anti-hypertensive activity of Tizanidine compared to clonidine?

Answer 12

Tizanidine has only 10% of the anti-hypertensive activity of the α2-adrenoceptor agonist (clonidine).

Question 13

What are some adverse effects of non depolarizing blocker

Answer 13

Histamine release leading to hypotension and bronchospasm, respiratory paralysis

Question 14

What is botulinum toxin and its source?

Answer 14

It is an inhibitor of acetylcholine release derived from the anaerobic bacillus Clostridium botulinum.

Question 15

How does botulinum toxin work at the neuromuscular junction?

Answer 15

It binds to a receptor on the presynaptic membrane of cholinergic nerve endings, inhibiting neurotransmitter release.

Question 16

What are the therapeutic uses of botulinum toxin?

Answer 16

1) To treat blepharospasm for local muscle paralysis.
2) To relieve focal spasticity and for cosmetic wrinkle removal.
3) To reduce hyperhidrosis (excessive sweating).
4) For prophylaxis of migraine.
5) Intra-vesical injections for severe overactive bladder syndrome.

Question 17

What is the mechanism of action of dantrolene?

Answer 17

Dantrolene is an antagonist at the ryanodine receptor (RyR1), regulating calcium release from the sarcoplasmic reticulum in skeletal muscle.

Question 18

List the uses of dantrolene.

Answer 18

1) Treatment of malignant hyperthermia and neuroleptic malignant syndrome.
2) Management of spasticity due to various disorders.

Question 19

What are the adverse effects associated with dantrolene?

Answer 19

1) Skeletal muscle weakness and dyspnea.
2) Dysphasia and somnolence.
3) Dose-dependent diarrhea and risk of hepatitis.

Question 20

What is malignant hyperthermia and its relation to anesthetics?

Answer 20

A rare but fatal complication associated with inhalation anesthetics and suxamethonium.

Question 21

What causes malignant hyperthermia at the cellular level?

Answer 21

It is genetically determined due to a defect in the ryanodine receptor (RyR1), affecting calcium release from the sarcoplasmic reticulum.

Question 22

What are the manifestations of malignant hyperthermia?

Answer 22

A sudden increase in intracellular calcium causes tachycardia, unstable blood pressure, hypercapnia, fever, hyperventilation, hyperkalemia, and metabolic acidosis.

Question 23

What is the treatment for malignant hyperthermia?

Answer 23

Dantrolene, a RyR1 receptor antagonist.

Question 24

What are the contraindications for using non depolarizing blockers?

Answer 24

Bronchial asthma, Myasthenia Gravis, concurrent use with aminoglycosides or quinidine

Question 25

What is Neostigmine and its function in relation to non depolarizing blockers?

Answer 25

It is a reversible cholinesterase inhibitor that prolongs the action of acetylcholine and reverses the block.

Question 26

What are neuromuscular blockers (NMB)?

Answer 26

Drugs that block cholinergic transmission between motor nerve endings and nicotinic receptors on skeletal muscle.

Question 27

How do neuromuscular blockers act at the neuromuscular junction (NMJ)?

Answer 27

They act as either antagonists (non-depolarizing type) or agonists (depolarizing type) at the receptors on the endplate.

Question 28

What are examples of non-depolarizing neuromuscular blockers?

Answer 28

D-Tubocurarine (prototype), Mivacurium, Atracurium, cisatracurium, Vecuronium, pancuronium.

Question 29

What is an example of a depolarizing neuromuscular blocker?

Answer 29

Suxamethonium (succinylcholine), which is an ester of acetylcholine.

Question 30

What is the absorption and distribution characteristic of neuromuscular blockers?

Answer 30

All members are not absorbed orally due to being polar compounds; they are administered parenterally and cannot cross the blood-brain barrier (BBB) or placental barrier.

Question 31

What are the two phases of depolarizing block at Nm receptors?

Answer 31

Phase 1: initial depolarization then paralysis due to maintained depolarization. Phase 2: muscle repolarizes but remains insensitive to acetylcholine leading to desensitization.

Question 32

What is Sugammadex and its role in neuromuscular blocking?

Answer 32

Sugammadex is a specific antagonist for rocuronium and vecuronium, acting by chelating them and reducing their plasma concentration but not pancuronium

Question 33

What are the therapeutic uses of neuromuscular blockers?

Answer 33

1) Endotracheal intubation, primarily using rocronium instead of suxamethonium. 2) Inducing skeletal muscle relaxation during surgical operations. 3) Controlling convulsions during electro-convulsive therapy (ECT).