Which of the following neurotransmitters is deficient in Myasthenia gravis?

SCTIMST Staff Nurse - 2015 (Set-A)

Medical & Surgical Nursing

Medium

Appeared in: SCTIMST Staff Nurse - 2015 (Set-A)

Explanation

Myasthenia Gravis (MG) is a chronic autoimmune disorder affecting the neuromuscular junction.
In MG, the immune system produces antibodies that block, alter, or destroy the nicotinic acetylcholine receptors on the muscle cell surface.
This destruction of receptors prevents acetylcholine from binding and stimulating muscle contraction, leading to a state of functional deficiency and resulting in muscle weakness and fatigability.
Although acetylcholine is still produced and released, its effect is significantly diminished due to the lack of available and functioning receptors.

Option B: Dopamine deficiency is the hallmark of Parkinson's disease, not Myasthenia Gravis. It primarily affects the basal ganglia, leading to symptoms like tremors, rigidity, and bradykinesia.
Option C: Serotonin is primarily associated with mood, sleep, and appetite regulation. Imbalances are linked to depression and anxiety, not the primary muscle weakness seen in Myasthenia Gravis.
Option D: Nor-epinephrine (norepinephrine) is a key neurotransmitter in the sympathetic nervous system, involved in the 'fight-or-flight' response, alertness, and blood pressure control. It does not play a primary role in the neuromuscular junction pathology of MG.

Clinical Relevance

Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Pathophysiology of Myasthenia Gravis and neurotransmitter function as background academic context rather than a clinical decision trigger.
A key nursing priority for patients with MG is monitoring for myasthenic crisis, a life-threatening condition characterized by severe muscle weakening, leading to respiratory failure. Nurses must be vigilant about respiratory status, including rate, depth, and oxygen saturation.
Patient education is crucial. Nurses should teach patients to conserve energy, schedule activities after medication administration when muscle strength is greatest, and recognize signs of crisis.
What if the patient presents with similar weakness but also has symptoms of diarrhea, abdominal cramping, and excessive salivation after a dose of their MG medication? This could indicate a cholinergic crisis (overmedication), not a myasthenic crisis (undermedication). The key intervention is to hold the anticholinesterase medication and prepare to administer the antidote, atropine, if ordered.

How to Approach the Question

First, identify the key concepts in the question: 'Myasthenia gravis' and 'deficient neurotransmitter'.
Recall the basic pathophysiology of Myasthenia Gravis. The name itself gives a clue: 'my-' (muscle) and '-asthenia' (weakness). It's a disease of muscle weakness.
Access your knowledge about the neuromuscular junction, the site where nerves communicate with muscles. Remember that acetylcholine is the primary neurotransmitter at this junction.
Evaluate the options based on this knowledge. Acetylcholine is directly involved in muscle contraction.
Eliminate the other options by recalling their primary functions: Dopamine (Parkinson's, movement control), Serotonin (mood), and Nor-epinephrine (sympathetic response). This confirms Acetylcholine is the most logical answer.

Concept Tested & Keywords

Concept Tested: Pathophysiology of Myasthenia Gravis and neurotransmitter function.
Stem keywords: neurotransmitter, deficient, Myasthenia gravis
Lead-in keywords: Which
Negative lead-in flag: false

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