A 25 year-old preschool teacher, Sandy Thompson, has not been feeling like herse

Question

A 25 year-old preschool teacher, Sandy Thompson, has not been feeling like herself lately. She has been feeling quite tired and her co-workers have commented on her droopy eyelids. Additionally, she is experiencing weakness in her arms and legs, has difficulty talking clearly and even her students’ parents have been concerned that Sandy hasn’t been looking very happy at work. One day at lunch, Sandy started to choke on her food, causing one of her coworkers to perform the Heimlich maneuver on her. While the scare didn’t cause any permanent damage, Sandy is convinced that it is time to go see a doctor. When she finally arrives at her appointment with Dr. Wayne, she explains to Dr. Wayne what has been going on, and the doctor decides to run a few blood tests. Sandy’s blood work results are presented below. Test Result Normal Range Blood pressure 115/73 90-120/60-80 Hematocrit (%) 36.5 36-38 Glucose (mg/dl) 94 70-110 Sodium (mmol/L) 144 135-145 Potassium (mmol/L) 4.3 3.5-5.0 AChE Activity Test (%) 100 100 Antibodies for ACh receptors Present Not Present Questions 1. What symptoms is she experiencing? 2. What levels from her blood work are abnormal? 3. How would antibodies against ACh receptors affect the neuromuscular junction? 4. How would antibodies against the ACh receptors affect the influx of Na+ into the cell? 5. How would antibodies against the ACh receptors affect the levels of Ca2+ inside the sarcoplasmic reticulum? What effect does this have on the actin and myosin filaments? 6. Sandy is diagnosed with myasthenia gravis. How is this treated/managed

Explanation / Answer

1. The symptoms that are experienced by Sandy are:

a) Ptosis or drooping eyelids.

b) Double vision (Diplopia), wherein there is difficulty in seeing clearly.

c) Difficulty in swallowing leading to choking.

d) Weakness in arms and legs

e) Not feeling happy or a little depressed.

2) Sandy has antibodies to ACh Receptors, which is abnormal. In normal individuals, no antibodies should be present against ACh receptors. This is because ACh receptors are self antigens and should not be recognized as non self by immune system.

Further, levels of sodium are increased to near the higher limit, which may indicate development of Hypernatraemia.

3. The impulse generated by axon of motor neuron reaches the neuromuscular junction or synapse formed with the muscle fiber. Acetylcholine is released at the synapse in response to an action potential generated by a nerve impulse. Acetylcholine binds to the acetylcholine receptors (nicotinic receptors) present on motor end plate. Motor end plate is a specialized area present in post-synaptic membrane of muscle fiber. This causes sodium channels to open and entry of sodium ions into the cell. As a result, the membrane potential becomes more positive, causing dephosphorylation of the membrane. An action potential is generated, which reaches the sarcolemma membrane. Calcium is released from the sarcolemma reticulum stores. It binds to troponin, causing acting binding sites on myosin to be exposed. This causes actin to bind troponin and induce muscle contraction.

Antibodies to ACh receptors will not allow the receptors to bind acetylcholine. The postsynaptic membrane will not be able to generate an action potential. As a result, muscle contraction will be inhibited.

4. The antibodies prevent the binding of acetylcholine to its nicotinic receptors. Hence, sodium channels are not open. This will prevent the flow of sodium ions inside the cell.

6. The inability of sodium ions to enter the cell will prevent generation of action potential. Hence, calcium ions are not released from its stores in sarcolemma. Hence, it cannot bind to troponin. Troponin will remain bound to myosin in trophomyosin. Hence, actin-binding sites are blocked, preventing myosin binding to actin and preventing sliding of actin and myosin fibers. This will prevent muscle contraction.

7. Myasthenia gravis is treated with inhibitors to acetylcholine esterase (AChE). AChE is the enzyme that cleaves acetylcholine at neuromuscular junction. As this enzyme is inhibited, more acetylcholine is present to bind at NMJ. This will alleviate symptoms of the disease.

Corticosteroids and immunosuppressants can be administered to suppress immune system and prevent antibody production.

Plasmapheresis is conducted which is a type of dialysis that removes the antibodies produced against ACh receptors. Monoclonal antibodies can be administered against specific white blood cells involved in antibody production. Normal immune responses can be improved by administration of intravenous immunoglobulins. Surgery of thymus gland may decrease the immune response.

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