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Quizzes > Health & Medicine > Diseases & Conditions

Take the Myasthenia Gravis Quiz: Test Your Neurotransmitter Knowledge

Think you can spot the neurotransmitter deficiency in myasthenia gravis? Start now!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
paper art neuromuscular junction with missing acetylcholine, question marks for myasthenia gravis quiz on coral background

Ready to flex your neurology know-how? In this Myasthenia Gravis Quiz: Neurotransmitter Deficiency Test, you'll uncover which of the following neurotransmitters are deficient in myasthenia gravis, refine your grasp of symptoms of myasthenia gravis, and explore myasthenia gravis neurotransmitter deficiency. Ideal for students and anyone interested in autoimmune neuromuscular disorders quiz challenges, it's a fun, free way to test and expand your expertise. Dive in, tackle each question, then deepen your learning with our quiz on neurotransmitters or power up with a synaptic transmission quiz . Start now and see your score!

Which neurotransmitter is primarily deficient in myasthenia gravis at the neuromuscular junction?
Acetylcholine
Dopamine
GABA
Serotonin
Myasthenia gravis results from autoantibodies against acetylcholine receptors, reducing postsynaptic response to acetylcholine. This leads to decreased effective neurotransmission at the neuromuscular junction. The net result is a functional deficit of acetylcholine signaling. NCBI: Myasthenia Gravis
Autoantibodies in myasthenia gravis are directed against which structure?
Nicotinic acetylcholine receptor
Muscarinic acetylcholine receptor
Voltage-gated calcium channel
GABA receptor
In myasthenia gravis, pathogenic IgG autoantibodies bind to the nicotinic acetylcholine receptor on the postsynaptic membrane at the neuromuscular junction. This blocks receptor function and promotes receptor internalization and complement-mediated damage. Other receptor types are not the primary autoantigen in MG. NCBI: Myasthenia Gravis
Which characteristic best describes the muscle weakness in myasthenia gravis?
Fatigable muscle weakness
Spastic paralysis
Flaccid paralysis without fatigue
Constant muscle stiffness
The hallmark of myasthenia gravis is fatigable muscle weakness that worsens with activity and improves with rest. This pattern reflects the progressive loss of neuromuscular transmission during sustained muscle use. Spasticity and constant stiffness are features of other neuromuscular disorders. Mayo Clinic: Myasthenia Gravis
Which ocular symptom is most commonly seen in myasthenia gravis?
Ptosis
Nystagmus
Photophobia
Diplopia without eyelid droop
Ptosis, or drooping of the eyelid, is often the earliest and most common ocular manifestation of myasthenia gravis. It occurs due to weakness of the levator palpebrae superioris muscle. Patients may also develop diplopia, but ptosis is more specific. NCBI: Myasthenia Gravis
The edrophonium test is diagnostic for myasthenia gravis because edrophonium is:
A short-acting acetylcholinesterase inhibitor
A presynaptic calcium channel blocker
A central GABA agonist
A long-acting nicotinic receptor agonist
Edrophonium is a rapid-onset, short-acting acetylcholinesterase inhibitor that temporarily increases acetylcholine levels at the neuromuscular junction. In patients with myasthenia gravis, this leads to a transient improvement in muscle strength. The test helps confirm the diagnosis clinically. Mayo Clinic: Edrophonium Test
Pyridostigmine is used in myasthenia gravis primarily to:
Inhibit acetylcholinesterase
Block nicotinic receptors
Increase GABA release
Mimic dopamine
Pyridostigmine is an acetylcholinesterase inhibitor that prolongs the action of acetylcholine in the synaptic cleft at the neuromuscular junction, improving neuromuscular transmission. It does not block nicotinic receptors nor influence GABA or dopamine. This is a cornerstone symptomatic treatment for myasthenia gravis. NCBI: Pyridostigmine
Myasthenia gravis is classified as which type of hypersensitivity reaction?
Type II (antibody-mediated)
Type I (immediate)
Type III (immune complex)
Type IV (cell-mediated)
Myasthenia gravis involves IgG autoantibodies directed against postsynaptic acetylcholine receptors, leading to receptor destruction and impaired transmission. This mechanism is characteristic of type II hypersensitivity. Type I through IV refer to other immune mechanisms not directly relevant here. NCBI: Myasthenia Gravis
Which thymic abnormality is commonly associated with myasthenia gravis?
Thymoma
Thymic atrophy
Thymic cyst
Thymic lipoma
Thymoma or thymic hyperplasia is found in a majority of patients with myasthenia gravis and may contribute to the production of pathogenic autoantibodies. Thymic atrophy or cysts are not typically linked to MG pathogenesis. Thymectomy can improve symptoms in many cases. NCBI: Myasthenia Gravis
Which of the following distinguishes Lambert-Eaton myasthenic syndrome from myasthenia gravis?
Presynaptic voltage-gated calcium channel antibodies
Antibodies against acetylcholinesterase
Postural tremor
IgA-mediated receptor blockade
Lambert-Eaton syndrome involves autoantibodies against presynaptic P/Q-type voltage-gated calcium channels, reducing acetylcholine release. Myasthenia gravis targets postsynaptic acetylcholine receptors. The presynaptic versus postsynaptic distinction is critical for diagnosis and management. NCBI: Lambert-Eaton Syndrome
Which sign is most indicative of a cholinergic crisis rather than worsening myasthenia gravis?
Miosis and bradycardia
Increased muscle weakness without muscarinic signs
Hyperreflexia
Elevated creatine kinase
Cholinergic crisis from excess acetylcholinesterase inhibitor leads to muscarinic overstimulation: miosis, bradycardia, salivation, and gastrointestinal hyperactivity. In contrast, myasthenic crisis shows pure neuromuscular weakness without these parasympathetic signs. Mayo Clinic: Cholinergic Crisis
Single-fiber electromyography in myasthenia gravis typically shows which finding?
Increased jitter and blocking
Decreased amplitude of motor unit potentials
Continuous muscle fiber activity
Low-frequency repetitive discharges
Single-fiber EMG in MG reveals increased neuromuscular jitter (variability in action potential timing) and blocking (failure of transmission). These findings reflect compromised safety factor at the neuromuscular junction. Other EMG patterns are characteristic of different disorders. NCBI: EMG in Myasthenia Gravis
Which autoantibody is found in a subset of seronegative myasthenia gravis patients?
Anti-MuSK antibody
Anti-GAD antibody
Anti-myelin basic protein antibody
Anti-acetylcholinesterase antibody
Anti-MuSK (muscle-specific kinase) antibodies are present in about MuSK-positive patients who lack AChR antibodies. These patients often present with different clinical features and require tailored therapy. Other listed antibodies are not associated with MG pathogenesis. NCBI: MuSK Antibodies
The ice pack test improves ptosis in myasthenia gravis by:
Reducing acetylcholinesterase activity
Increasing membrane depolarization
Enhancing sodium channel opening
Stimulating sympathetic outflow
Cooling reduces the activity of acetylcholinesterase at the neuromuscular junction, thereby increasing the availability of acetylcholine. This temporary effect improves muscle strength and ptosis in MG patients. Other mechanisms do not explain the specific improvement with ice. Mayo Clinic: Ice Pack Test
Repetitive nerve stimulation in myasthenia gravis typically shows:
A decremental response in compound muscle action potential amplitude
An incremental response in amplitude
No change in amplitude
A single prolonged potential
Low-frequency repetitive nerve stimulation in MG produces a characteristic decremental (decreasing) response in CMAP amplitude due to impaired synaptic transmission. An incremental response is seen in Lambert-Eaton syndrome. Normal amplitude suggests no NMJ disorder. NCBI: Electrophysiology in MG
How do corticosteroids like prednisone help treat myasthenia gravis?
Suppress autoimmune antibody production
Block acetylcholine receptors
Enhance acetylcholine release
Stimulate thymic growth
Prednisone and other corticosteroids suppress the immune system, reducing the production of pathogenic autoantibodies against acetylcholine receptors. This leads to improved neuromuscular transmission over weeks to months. They do not directly affect receptor function or release of acetylcholine. NCBI: Immunosuppression in MG
Plasmapheresis is beneficial in myasthenia gravis because it:
Removes circulating autoantibodies
Inhibits neuromuscular transmission
Blocks presynaptic calcium channels
Increases acetylcholinesterase activity
Plasmapheresis mechanically filters the blood to remove circulating pathogenic autoantibodies, producing rapid symptomatic improvement in MG. It does not directly alter enzyme activity or receptor function. The effect is temporary, so repeat treatments may be needed. Mayo Clinic: Plasmapheresis
Cholinesterase inhibitors in myasthenia gravis lead to what change in end-plate potential?
Increased amplitude of the end-plate potential
Decreased frequency of miniature potentials
Shortened time to threshold
Reduction in quantal content
By inhibiting acetylcholinesterase, these drugs increase acetylcholine concentrations in the synaptic cleft and thus raise the amplitude of the end-plate potential. Frequency of miniature potentials is unchanged, and quantal content relates to vesicle release rather than breakdown of acetylcholine. NCBI: Physiology of NMJ
Which cytokine is implicated in thymic hyperplasia associated with myasthenia gravis?
Interleukin-6 (IL-6)
Interferon-gamma
Tumor necrosis factor-beta
Interleukin-10
IL-6 has been found elevated in thymic tissue of MG patients and contributes to B-cell proliferation and autoantibody production. Other cytokines play roles in general immune responses but are not as directly linked to thymic pathology in MG. NCBI PMC: IL-6 in MG
Neonatal transient myasthenia gravis occurs because:
Maternal IgG crosses the placenta
Fetal thymus overproduces acetylcholine receptors
Neonatal acetylcholinesterase deficiency
Developmental immaturity of motor end plates
Autoantibodies from an affected mother cross the placenta and transiently impair neonatal neuromuscular transmission. These antibodies are cleared over weeks, resolving symptoms. The condition is self-limited and distinct from congenital myasthenic syndromes. NCBI: Maternal Antibodies
The relationship between end-plate current (I) and channel conductance (g) is given by:
I = g × (Vm – Erev)
I = g + (Vm – Erev)
I = g/(Vm – Erev)
I = (Vm – Erev)/g
Ohm’s law for ionic currents at the end-plate is I = g × (Vm – Erev), where Vm is membrane potential and Erev is reversal potential. This defines how conductance and driving force influence current. Other formulas misrepresent the relationship. NCBI: Electrophysiology
Complement activation in myasthenia gravis contributes to pathology by:
Mediating postsynaptic membrane damage
Enhancing acetylcholine release
Inhibiting antibody production
Blocking vesicle docking
Binding of autoantibodies to acetylcholine receptors activates complement, leading to membrane attack complex formation and destruction of the postsynaptic membrane. This reduces receptor density and impairs transmission. Complement does not affect presynaptic release directly. NCBI: Complement in MG
Which HLA haplotypes are most commonly associated with early-onset myasthenia gravis?
HLA-B8 and DR3
HLA-A2 and DQ6
HLA-B27 and DR4
HLA-Cw6 and DP2
Early-onset myasthenia gravis shows a strong genetic association with HLA-B8 and DR3, reflecting an autoimmune predisposition. Other HLA types are implicated in different autoimmune diseases but not predominantly in MG. NCBI: Genetics of MG
How does anti-MuSK antibody–mediated myasthenia gravis differ pathologically from anti-AChR MG?
IgG4 subclass that does not fix complement
Complement-dependent receptor destruction
Presynaptic acetylcholine depletion
Formation of immune complexes
Anti-MuSK antibodies are predominantly IgG4 subclass, which typically does not activate complement, leading to receptor disorganization rather than complement-mediated lysis. Anti-AChR antibodies are mainly IgG1/3 and fix complement. This distinction affects clinical features and therapy. NCBI PMC: MuSK MG
The safety factor for neuromuscular transmission is reduced in myasthenia gravis due to:
Decreased postsynaptic receptor density
Increased vesicle docking sites
Enhanced quantal release
Shortened end-plate potential
Autoantibody-mediated loss of acetylcholine receptors reduces the postsynaptic response to each quantum of acetylcholine, lowering the safety factor. This makes it harder to reach threshold for muscle fiber action potential. Vesicle docking and quantal release are presynaptic events unaffected directly. NCBI: Safety Factor
Which parameter defines quantal size at the neuromuscular junction affected in myasthenia gravis?
Amplitude of miniature end-plate potentials
Number of release sites
Frequency of nerve firing
Duration of receptor channel opening
Quantal size refers to the response produced by a single vesicle of acetylcholine, which is measured as the amplitude of miniature end-plate potentials (MEPPs). Myasthenia gravis affects quantal content more than quantal size by reducing receptor numbers. Number of release sites influences quantal content, not size. NCBI: Quantal Transmission
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Study Outcomes

  1. Identify Deficient Neurotransmitters -

    Pinpoint which of the following neurotransmitters are deficient in myasthenia gravis by recalling the primary chemical messenger affected at the neuromuscular junction.

  2. Explain Neuromuscular Mechanisms -

    Describe how antibody-mediated damage disrupts acetylcholine receptor function and leads to the characteristic symptoms of myasthenia gravis.

  3. Analyze Symptom Patterns -

    Assess common clinical presentations of myasthenia gravis to connect neurotransmitter deficiency with muscle weakness and fatigability.

  4. Differentiate Disorder Types -

    Contrast myasthenia gravis with other autoimmune neuromuscular disorders based on their distinct neurotransmitter profiles and pathophysiology.

  5. Apply Quiz Insights -

    Use feedback from the scored quiz to reinforce your grasp of myasthenia gravis neurotransmitter deficiency and correct misconceptions.

  6. Evaluate Knowledge Gain -

    Interpret your quiz results to measure growth in understanding symptoms of myasthenia gravis and related neurotransmitter function.

Cheat Sheet

  1. Acetylcholine Receptor Autoimmunity -

    In myasthenia gravis, autoantibodies target nicotinic acetylcholine (ACh) receptors at the neuromuscular junction, reducing receptor density and causing functional ACh deficiency (Harrison's Principles of Internal Medicine; NEJM). This core mechanism defines which of the following neurotransmitters are deficient in myasthenia gravis and underpins all subsequent symptoms.

  2. Symptoms & Fatigue Pattern -

    Patients typically present with fluctuating muscle weakness that worsens with activity, often starting with ocular muscles (ptosis, diplopia) and progressing to bulbar or limb involvement (Mayo Clinic; Johns Hopkins Medicine). Recognize the hallmark fatigability as a direct consequence of impaired synaptic ACh transmission.

  3. Neurophysiologic Diagnostics -

    Repetitive nerve stimulation shows a decremental response, while single-fiber EMG reveals increased jitter and blocking, confirming impaired ACh-mediated transmission (AAEM guidelines). The edrophonium (Tensilon) test transiently boosts ACh levels, improving strength - key facts for any myasthenia gravis quiz.

  4. Acetylcholine Restoration Therapy -

    Pyridostigmine, an acetylcholinesterase inhibitor, prolongs ACh availability in the synaptic cleft and enhances muscle contraction (NIH MedlinePlus). Immunosuppressive agents like prednisone and azathioprine further reduce autoantibody production, addressing the myasthenia gravis neurotransmitter deficiency at its source.

  5. Thymus Involvement & Remission Strategies -

    Thymic hyperplasia or thymoma occurs in many patients, and thymectomy can induce long-term remission by modulating autoimmunity (American Academy of Neurology). Regular respiratory monitoring and individualized immunotherapy plans are essential in managing this autoimmune neuromuscular disorder quiz content.

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