lonic Equilibria and Resting Membrane Potentials Primary Hyperkalemic Periodic P
ID: 136549 • Letter: L
Question
lonic Equilibria and Resting Membrane Potentials Primary Hyperkalemic Periodic Paralysis A 10-year-old boy has sporadic attacks of muscle aralysis. The patient has four brothers, all of whom have suffered similar symptoms. The onset of these attacks is characterized by pain associated with contractures of the affected musc and contracture frequently occur without subsequent paralysis. An hyperkalemic. Plasma K+ levels are normal when the patient is not having an attack. Biopsies of the patient's muscle show a significantly diminished level of intracellular K+ (83 mmol/kg wet tissue) compared with control muscle (95 mmol/kg ATPase is normal. Paralytic attacks are accompanied by diuresis during an attack the excitability and conduction times of motor neurons are normal Microelectrode studies show that during an attack the magnitude of the resting membrane potential of skeletal muscle cells is diminished ompared with control muscle fibers. Electromyography shows that early in an attack the muscle contractures are associated with spontaneou action potentials in the affected muscle fibers. Later, during the paralytic phase of an attack, muscle cells become electrically inexcitable-the muscle cells do not respond electricall Later in the attack those muscles may become paralyzed and more flaccid. Episodes of pain is of blood samples taken duri ncreased K+ excretion. Electrophysiologic studies of the patient show that s the function of the neuromuscular junction timulation of the motor axons that innervate them. A paralytic attack can be relieved by treating the atient with an insulin injection. Long-term administration of the 32-agonist salbutamol dramatically diminishes the occurrence of episodes of potassium concentration in his skeletal muscle cells is diminished? What types of alterations of basic cellular processes might underlie this situation? 2. What explains the observation that the magnitude of the resting membrane potentials of the patient's skeletal muscle fibers is diminished during an attack? 3. Does the diminished resting membrane potential have anything to do with the spontaneous action potentials and contractures that occur early in an attack, before par paralytic phase of an attack, in which muscle cells are electrically inexcitable? 5. How might insulin terminate a paralytic attack? 6. How might long sets in? 4. How might the diminished resting membrane potential contribute to the rm administration of salbutamol diminish the occurrence of att of contractures and parExplanation / Answer
1.Periodic paralysis is a type of muscle disease which is heriditary in nature and is characterized by muscle weakness.its onset is hereditary.it is often known by the name as Hyperkalemic periodic paralysis.The increased influx of sodium through defective channels results in compensatory loss of muscle potassium,hence the hyperkalemia.The hyperkalemia associated with a decrease in the amount of potassium in skeletal cells shows that hyperkalemia is caused by efflux of potassium from the cells,but what cause this efflux is unknown.potassium efflux from muscle cells may occur because of less potassium accumulation by the Sodium,Potassium and ATPase or an increased rate of Potassium efflux or a combination of both.
2 Elevation of extracellular potassium and the resultant decrease in the intracellular potassium would misbalance the equilibrium of potassium potential and thereby decrease the intensity of the resting membrane potential.
3 The decreased magnitude of the resting membrane potential initially the muscle cells more closer to threshold for firing up the action potential.As a result any small fluctuations in the resting membrane potential may reach the threshold and thereby result in spontaneous action potentials and contractures of skeletal muscles.
4 Prolonged depolarization of the muscle cell plasma membrane will lead to voltage inactivation of Sodium channels in the membrane ,which result in the muscle cells being unable to fire an action potential.This is believed to be the cause of paralytic phase of an attack and is supported by the observation that during the paralytic phase,the patients skeletal muscle cells may be electrically inexcitable.
5 Shifting of potassium may be associated with insulin administration .hence insulin may terminate a paralytic attack.Insulin immediately promotes the uptake of potassium and exrusion of Sodium from cells and thus insulin restores cellular [otassium levels to normal.This cause the resting membrane potential for the affected skeletal muscle cells to come closer to the normal resting value.
6 Salbutamol Beta 2 agonist increases the activity of sodium,potassium and ATPase in skeletal muscles and leads to increased sequestration of potassium in muscle cells and thereby prevents potassium efflux.At the initial time of muscle weakness,episodes in many people may be prevented by inhalation of salbutamol,eating carbohydrates or intravenous calcium gluconate.Salbutamol terminates the attack
Related Questions
Navigate
Integrity-first tutoring: explanations and feedback only — we do not complete graded work. Learn more.