AIM Step 10
3rd Year MBBS
MSK Pharmacology
3rd Year MBBS
MSK Pharmacology
Student Memory Support
Skeletal-Muscle Relaxants and Neuromuscular Blockade
High-yield flashcards, mnemonics, comparisons and clinical hooks for rapid KMU revision.
Generated according to the supplied Step 10 framework. :contentReference[oaicite:0]{index=0}
1. High-Yield Flashcards
Tap each question to reveal the answer.
How are skeletal-muscle relaxants classified according to their main site of action?
Neuromuscular blockers, centrally acting spasmolytics and directly acting dantrolene.
What is the receptor target of non-depolarizing neuromuscular blockers?
Nicotinic Nm receptors at the motor end plate.
How do non-depolarizing neuromuscular blockers produce paralysis?
They competitively block Nm receptors, preventing adequate end-plate depolarization.
Why can neostigmine reverse a non-depolarizing block?
It inhibits acetylcholinesterase and raises acetylcholine, which competes with the blocker.
Which neuromuscular blockers are directly encapsulated by sugammadex?
Rocuronium and vecuronium.
What is the mechanism of Phase I succinylcholine blockade?
Persistent motor-end-plate depolarization keeps sodium channels inactivated.
Which finding distinguishes Phase I succinylcholine blockade from non-depolarizing blockade on train-of-four testing?
Phase I block produces uniform reduction without marked fade.
What causes succinylcholine apnea in a susceptible patient?
Deficient or atypical plasma butyrylcholinesterase causes delayed drug metabolism.
What is the immediate management of prolonged succinylcholine apnea?
Maintain sedation, oxygenation and controlled ventilation until recovery.
Why is succinylcholine dangerous after major burns or denervation?
Increased extrajunctional receptors cause excessive potassium release and severe hyperkalemia.
What receptor mediates the antispastic action of baclofen?
The GABAB receptor in spinal motor pathways.
Which receptor is activated by tizanidine?
Central α2-adrenergic receptors.
Which drugs are the major triggers of malignant hyperthermia?
Succinylcholine and volatile inhalational anesthetics.
What is the primary cellular abnormality in malignant hyperthermia?
Uncontrolled calcium release from the skeletal-muscle sarcoplasmic reticulum.
Why is dantrolene effective in malignant hyperthermia?
It reduces sarcoplasmic-reticulum calcium release, decreasing contraction and hypermetabolism.
2. Mnemonics
Mnemonic Title
Sites of Action
N-C-D
Meaning: Neuromuscular junction, Central nervous system, Direct skeletal-muscle action.
Mnemonic Title
Succinylcholine Serious Effects
H-A-M
Meaning: Hyperkalemia, Apnea and Malignant hyperthermia.
Mnemonic Title
Central Spasmolytics
B-T-D-C
Meaning: Baclofen, Tizanidine, Diazepam and Cyclobenzaprine.
Mnemonic Title
Malignant Hyperthermia Early Clues
C-R-T
Meaning: Rising Carbon dioxide, Rigidity and Tachycardia may precede marked fever.
3. Memory Tables
Depolarizing versus Non-Depolarizing Neuromuscular Blockade
| Feature | Non-depolarizing block | Succinylcholine Phase I |
|---|---|---|
| Receptor action | Competitive antagonist | Depolarizing agonist |
| Initial fasciculations | Absent | Present |
| Train-of-four | Fade present | Uniform reduction |
| Neostigmine | Can reverse | May prolong block |
| Major risk | Residual paralysis | Hyperkalemia and apnea |
Important Centrally Acting Spasmolytics
| Drug | Target | Main use | Key caution |
|---|---|---|---|
| Baclofen | GABAB agonist | Spasticity | Abrupt withdrawal |
| Tizanidine | Central α2 agonist | Spasticity | Hypotension and sedation |
| Diazepam | GABAA enhancement | Spasm or spasticity | Sedation and dependence |
| Cyclobenzaprine | Central motor suppression | Acute painful spasm | Antimuscarinic effects |
4. Rapid Revision Points — Last-Minute Revision
- Neuromuscular blockers cause paralysis but do not provide unconsciousness or analgesia.
- Rocuronium, vecuronium, atracurium and pancuronium are non-depolarizing blockers.
- Non-depolarizing blockade produces train-of-four fade.
- Sugammadex reverses rocuronium and vecuronium by direct binding.
- Atracurium may release histamine; cisatracurium causes less histamine release.
- Succinylcholine causes fasciculations before Phase I paralysis.
- Succinylcholine should be avoided when severe hyperkalemia is likely.
- Baclofen withdrawal may produce rebound spasticity, agitation or seizures.
- Rising carbon dioxide and rigidity may appear before severe fever in malignant hyperthermia.
- Dantrolene treats the calcium-release abnormality, while cooling treats hyperthermia.
KMU Exam Trap
Neostigmine reverses competitive non-depolarizing blockade but may prolong an initial Phase I succinylcholine block.
Neostigmine reverses competitive non-depolarizing blockade but may prolong an initial Phase I succinylcholine block.
5. Clinical Memory Hooks
Burn patient requiring intubation
→
Increased extrajunctional receptors
→
succinylcholine may cause severe hyperkalemia.
→
Increased extrajunctional receptors
→
succinylcholine may cause severe hyperkalemia.
Apnea lasting hours after succinylcholine
→
consider butyrylcholinesterase deficiency
→
ventilate until recovery.
→
consider butyrylcholinesterase deficiency
→
ventilate until recovery.
Multiple sclerosis with spasticity
→
baclofen activates GABAB receptors
→
reduced spinal excitation.
→
baclofen activates GABAB receptors
→
reduced spinal excitation.
Rigidity with rising carbon dioxide during anesthesia
→
malignant hyperthermia
→
stop triggers and give dantrolene.
→
malignant hyperthermia
→
stop triggers and give dantrolene.
Weak breathing with train-of-four fade after surgery
→
residual non-depolarizing block
→
delay extubation and reverse appropriately.
→
residual non-depolarizing block
→
delay extubation and reverse appropriately.
6. Starred High-Yield Exam Points
“`
- ⭐ Non-depolarizing blockers are competitive antagonists at nicotinic Nm receptors.
- ⭐ Succinylcholine Phase I block is persistent depolarization and is not reversed by neostigmine.
- ⭐ Prolonged succinylcholine apnea is managed with ventilation, oxygen and continued sedation.
- ⭐ Severe burns, denervation and neuromuscular disease increase succinylcholine-related hyperkalemia risk.
- ⭐ Succinylcholine and volatile anesthetics are the major malignant-hyperthermia triggers.
- ⭐ Dantrolene reduces calcium release from the skeletal-muscle sarcoplasmic reticulum.
- ⭐ Residual neuromuscular weakness can impair ventilation and airway protection despite visible limb movement.
“`