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A 45 – year – old woman comes to the emergency department complaining of stomach upset and vomiting.

This suddenly occurred today, whereas over the past week she has been experiencing constipation, along with frequent urination. She also complains of muscles pains and weakness. Sometimes she feels as though her pain is originating from her bones. All this makes walking difficult for her. She has not noted any spasms in her muscles. She also states that she occasionally gets headaches and fatigue with the inability to conduct daily activities.

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Currently her vital signs are normal. Physical examination is insignificant except for hypotonia and hyporeflexia. Which ionic imbalance has resulted in these symptoms in this patient? Hypokalemia Hypocalcemia Hyperphosphatemia Hyperkalemia Hypercalcemia Explanation:Correct Answer (E): Hypercalcemia occurs when there is too much calcium in the extracellular fluid. This patient is displaying characteristic symptoms of high calcium which is lethargy, constipation, pain in the bones and weakness in the muscles.

Symptoms are displayed depending on how fast the calcium has increased. Mild prolonged hypercalcemia might produce mild symptoms. Most of the causes of hypercalcemia include hyperparathyroidism or malignancy. In malignancies an increase in calcium occurs either due to bony metastases or due to the release of parathyroid hormone related peptide (PTHrP).On presentation it is classic to notice a patient who has “kidney stones, bone pain, abdominal moans, and psychic groans.” The central nervous system symptoms include weakness, lethargy that may progress on to confusion and finally coma. Polyuria, dehydration, kidney stones are some of the renal manifestations. Gastrointestinal symptoms manifest as constipation, nausea, anorexia and sometimes gastric ulcers.

Syncope and arrhythmias are the rare cardiovascular effects.The normal calcium levels are between 8.5 – 10.2 mg / dl. In most cases of hypercalcemia the calcium levels are significantly increased. The increase is sudden in cases of malignancy and could be slower in other causes. Once malignancy is ruled out hyperparathyroidism is looked into.

An ECG is also recommended which characteristically shows a shortening of the QT interval.Incorrect Answer (A): Hypokalemia can result from increased loss of potassium, decreased intake or a shift of potassium into the intracellular space. Potassium levels below 3.5 mEq/ L are characterised under hypokalemia, with levels below 2.5 mEq/ L considered severe. Symptoms are more commonly related to the cardiac and muscular systems. Patients demonstrate muscular weakness through constipation, dyspnea, abdominal distention and exercise intolerance.

In hypokalemia there is the characteristic U wave present after the T wave on ECG.Incorrect Answer (B): Hypocalcemia is primarily caused by hypoalbuminemia. Other causes include; hypomagnesemia, hyperphosphatemia, medication or surgical effects, PTH deficiency or vitamin D deficiency. The main systems affected are the neuromuscular and cardiovascular systems. The Chvostek and Trousseau signs can be elicited in hypocalcemia. ECG shows prolongation of QT interval.Incorrect Answer (C): Increased phosphate intake, decreased excretion or increase in the extracellular phosphate levels can all lead to hyperphosphatemia.

Fatigue, nausea, vomiting and sleep disturbances are common symptoms. Sometimes patients note symptoms of hypocalcemia, namely muscle spasms, tetany, perioral tingling. Hypotension and a prolongation of the QT interval can be noticed on ECG.

Incorrect Answer (D): Hyperkalemia is classified for potassium levels greater than 5 – 5.5 mEq / L. Most commonly patients present with muscular and cardiac complaints. Muscle paralysis, palpitations, chest pain, nausea and paresthesias are common complaints. Increased intake with decreased excretion can be a cause, even an increase in extracellular potassium through metabolic acidosis, thermal or electrical burns or medications can all cause hyperkalemia.

Potassium levels and renal function tests should be checked. ECG is also vital which shows a widening of QRS complex, with a prolonged PR interval and amplified R wave.Educational Objective:Hypercalcemia is caused by an increase in extracellular calcium with a decrease in its excretion. It is most commonly caused by malignancy or hyperparathyroidism.

Muscle weakness is common along with bone pain, abdominal discomfort, polyuria, kidney stones, finally lethargy and weakness. ECG shows a shortening of QT interval. Treatment involves reducing the severity of symptoms and treating the underlying cause.References and further reading: Metabolism In: W. F Ganong, Review of Medical Physiology, 20th Edition, McGraw Hill, 2001, Pp 377 – 382.Question 02Topic: Excitable TissueSubtopic: Neuronal excitability in different casesConcepts to be tested: Demyelination: GBS, Loss of neurons ALSA 10 – year – old boy is brought to the emergency department by his parents because of his sudden inability to walk.

He had initially complained of difficulty holding his hands upright and also struggled with grasping objects. Slowly he felt that his legs were getting heavy and noticed that he was unable to walk steadily. There is no other complaints as of now. His parents state that two weeks ago he suffered from bloody diarrhea which received treatment. On physical examination it is noticed that he is taking shallow breaths.

His muscle strength is assessed to be 3/5  in the upper and lower limbs. He has absent patellar and ankle reflexes bilaterally. Biceps reflex is 1+.

Routine tests are unable to show any revealing signs. A lumbar puncture is then performed, and all values are normal except for an increase in protein is noted. What is the pathophysiologic process that is causing this boy’s symptoms? Neurodegenerative loss of motor neurons Autoimmune destruction of myelin Autoantibodies against the postsynaptic acetylcholine receptors Viral replication causes nerve cell chromatolysis Presence of neurotoxin inhibits the function of motor neurons Explanation:Correct Answer (B):According to the symptoms mentioned in the case above the child is suffering from Guillain – Barre Syndrome (GBS).

The physiological process involves a cross reaction against the body’s neural tissues of the peripheral nervous system. The classic form of the disease is a demyelinating neuropathy with ascending weakness.Typically a patient who has a history of a gastrointestinal or respiratory illness a few weeks prior, followed by proximal muscle weakness should be suspected of Guillain Barre Syndrome. It has been postulated that the infectious agents produce antibodies that cross react with gangliosides and glycolipids distributed on the myelin in the peripheral nervous system.  In severe form of GBS, severe inflammation results in axonal disruption and loss. Infections commonly associated are Campylobacter jejuni, Cytomegalovirus, Epstein – Barr virus, Mycoplasma pneumoniae and varicella zoster.The initial proximal muscle weakness can progress to involve the arms, truncal muscles, cranial nerves and respiratory muscles. The muscles of the lower limbs seem to affected first.

Patients find it difficult to walk despite the fact the muscle strength seems almost intact. In a vast majority of the cases cranial nerves may also be affected. These are manifested as diplopia, dysphagia, facial droop or ophthalmoplegia. Another characteristic feature of GBS are the diminished or loss of most the reflexes. Patients can also have autonomic responses such as tachycardia, bradycardia, anhidrosis or orthostatic hypotension.

Respiratory involvement can rarely lead to the requirement of respiratory support.Most lab tests are normal. Electromyography and nerve conduction studies might be useful. A lumbar puncture is indicative of GBS when there is an increase in protein with no increase in white blood cells. Patients with GBS are usually admitted. Treatment involves intravenous immunoglobulins or plasma exchange.Incorrect Answer (A): Degenerative process of the motor neuron system is characteristic of Amyotrophic Lateral Sclerosis (ALS). Most of their patients present with lower limb involvement with tripping, stumbling, and foot drop (“slapping gait”).

In the upper limb there is reduced finger dexterity, with wasting of the intrinsic hand muscles. Muscle cramps and persistent stiffness eventually become common. Some may face difficulty in swallowing and  also face emotional struggles.

Care involves a multidisciplinary approach. There is no cure for ALS currently.Incorrect Answer (C): Autoantibodies against the acetylcholine receptors is a feature of myasthenia gravis.

It affects the neuromuscular junction in the skeletal muscles. The hallmark is weakness of muscles that increases on activity and decreases on rest. Some patients also present with ocular weakness towards the end of the day.

Weakness in respiratory muscles has to be identified immediately for treatment. Pyridostigmine is given for symptomatic treatment. Incorrect Answer (D): Viral replication leading to the destruction of nerve cells is more commonly seen in polio infection. The anterior horn motor neurons are the most affected.

Flaccid paralysis along with muscle atrophy are characteristic of polio infection. In non paralytic polio fever, headache and gastroenteritis can be symptoms exhibited. Rehabilitation following paralysis is a mode of therapy. Vaccination has been proven to be the single best method of protection against polio.Incorrect Answer (E): Neurotoxin that inhibits motor neuron function is found in botulinum spores. This neurotoxin either prevents the release of acetylcholine or binds itself to the acetylcholine.

This eventually leads to hypotonia and flaccid paralysis. Initially patients present with nausea, vomiting, diplopia, dilated/ fixed pupils, a dry mouth and respiratory muscle weakness. The toxin has to identified to pinpoint the disease. Supportive care is the prime method of treatment.

Educational Objective:Guillain Barre Syndrome is caused by antibodies produced against the body’s own myelin tissue. A respiratory or gastrointestinal infection precedes the symptoms of GBS. Proximal muscle weakness is noticed before other muscles weakness.

The lower limbs show weakness in gait and strength. Cranial nerves and autonomic system can also be affected. Reflexes are almost all absent in GBS. Treatment involves plasmapheresis or intravenous immunoglobulin therapy.References and further reading: 03Topic: Excitable TissueSubtopic: Neuronal excitability in different casesConcepts to be tested: Toxins: Tetrodotoxin and saxitoxin A student is graphing out the effects of a possible toxin on the muscle action potential. Below is a regular action potential graph and besides it is the effects of a possible toxin that has been ingested.

It has been suggested that this toxin causes motor dysfunction and weakness in few hours of ingestion, with rapid ascending paralysis. Death can occur 4 – 6 hours later after ingestion due to respiratory muscle failure. What toxin is the student most likely researching about? Tetrodotoxin Botulinum Toxin Ciguatoxin Tetanus Toxin BatrachotoxinExplanation:Correct Answer (A): Image Source: https://en. student is studying the effects of Tetrodotoxin. This is a neurotoxin can be ingested through various forms of puffer fish, gastropod mollusc, eggs of horseshoe crabs, newts and various other types of exotic fish.

Tetrodotoxin blocks the diffusion of sodium through the sodium channel.  This prevents depolarization and formation of action potentials in the nerve cells. This toxin affects the central and peripheral nervous systems. Nausea, vomiting and diarrhea occur early on. Lip and tongue paraesthesias along with facial and extremity numbness is also reported within hours.

Hypoventilation and speech difficulties develop, along with ascending paralysis in the next 24 hours. Cardiac dysfunction, seizures and eventual coma may develop. Supportive therapy is vital in this case. Endotracheal intubation and working on cardiac dysfunction is vital in this case. Attempts are made to remove the toxin from the gastrointestinal tract.

Incorrect Answer (B): Botulinum toxin works on the neuromuscular junction. It’s acts by interfering with neural transmission by blocking the release of acetylcholine. This leads to muscle overactivity and eventual flaccid paralysis. The patient can also have droopy eyes, dysarthria, descending paralysis and respiratory weakness. Supportive care is necessary for patient treatment. Incorrect Answer (C) and (E): Ciguatoxin and batrachotoxin are toxins that block the inactivation of fast acting Na+ channels. Ciguatoxin accumulates among the reef fish and batrachotoxin are found on certain species of frogs.

Symptoms increase over the subsequent 6 – 12 hours after exposure to the toxin. Abdominal pain, nausea and painful defecation are some of the first symptoms. Neurological symptoms include lingual and circumoral paraesthesias, dental pain, myalgias, respiratory paralysis and coma.

If the patients presents in a few hours gastric decontamination can be attempted with activated charcoal. Other symptoms are managed with supportive care.Incorrect Answer (D): The tetanus toxin cleaves the synaptobrevin which is necessary for binding the neurotransmitter containing vesicles. Therefore GABA and glycine containing vesicles are not released which leads to a loss of inhibitory action. This leads to the uncontrolled muscle contractions characteristic of tetanus. Generalised tetanus presents with lockjaw, neck stiffness, reflex spasms, and eventually rigidity on the extensor muscles of the limbs. Treatment includes cleaning the wound, supportive care and giving tetanus immunoglobulin. Educational Objective:Tetrodotoxin is a neurotoxin that can be ingested from puffer fish.

It blocks the fast action sodium channels thereby preventing depolarisation and the formation of action potentials. Nausea, vomiting, lip paraesthesias, hypoventilation and ascending paralysis result from this toxin ingestion. Supportive therapy is the main course of treatment in this case.References and further reading:https://emedicine.medscape.

com/article/818763-overviewQuestion 04Topic: Excitable TissueSubtopic: Neuronal excitability in different casesConcepts to be tested: NMJ Blockers, BotulinumA 45 – year – old women has come to her plastic surgeon’s office to get some injections for her forehead. She states that she is unhappy with the line that have increased on her forehead. She also complains that her eyebrows seem droopy. She states that there are “crow’s feet” that are emerging on the side of her eyes. She claims she is very unhappy with these as they are making her look older than she is. One of her friends recently got the BOTOX injection and she looked marvellous after that. She now wants to go in for the same to fix all the problems she stated. Through what mechanism does the toxin in this injection work? Blocking of the fast action Na+ channels Cleaves synaptobrevin preventing the release of GABA Block the inactivation of  fast action Na+ channels Blocks the release of acetylcholine from the presynaptic motor neurons Blocks small conductance chloride channelsExplanation:Correct Answer (D):BOTOX, which is botulinum toxin, works in the neuromuscular junction by inhibiting the release of acetylcholine from the presynaptic motor neurons.

The botulinum is produced by Clostridium Botulinum, which is a gram positive bacteria. Clinically a person can get infected through ingesting the spores or having the spores infest a wound. Once in the system the toxin binds to the cholinergic nerve terminals and decreases the release of acetylcholine, causing a neuromuscular blocking effect. In some cases the toxin binds to the acetylcholine itself preventing its action.When infected with the toxin patients initially a patient presents with nausea, vomiting, diplopia, dysphagia, dilated pupils and a dry mouth. After this flaccid paralysis can be noticed in a descending manner. Respiratory weakness might be mild but can rapidly progress to respiratory failure. Gastric dilation, paralytic ileus, orthostatic hypotension and bladder distention can also be noted.

Antitoxin is administered along supportive treatment depending on the symptoms manifested.Botulinum toxin also has plenty of therapeutic uses these days. Small doses of the toxin has been cultured to use clinically for various purposes. Some of them include; use in focal dystonias like cervical dystonia or blepharospasm, hemifacial spasm, tremors, tics, spasticity of stroke or traumatic brain injury, cosmetic purposes like hyperkinetic facial lines and hypertrophic platysma muscle bands. Incorrect Answer (A): Tetrodotoxin and saxitoxin block the fast acting Na+ channels, thus preventing an action potential.

It acts on the central and peripheral nervous system. Lip, tongue and facial paresthesias are the first to appear. Salivation, vomiting, diarrhea and abdominal pain also appear early. Rapid ascending paralysis with speech difficulties and hypoventilation is also noticed. Patients should be treated immediately with supportive care.Incorrect Answer (B): The inhibition in the release of GABA and glycine vesicles is noticed in tetanus toxin infection.

Tetanus toxin cleaves the synaptobrevin which is necessary for binding the neurotransmitter containing vesicles. Which results in the loss of inhibitory action. Uncontrolled contractions is commonly noted in this in the form of lockjaw, reflex spasms and rigidity of the extensor muscles.

Treatment is through wound care, tetanus immunoglobulin and supportive therapy.Incorrect Answer (C): Ciguatoxin and batrachotoxin prevent the inactivation of the fast acting Na+ channels. Ciguatoxin accumulates among the reef fish and batrachotoxin are found on certain species of frogs. Nausea, abdominal pain and painful defecation are some of the first symptoms to present themselves once a person is infected. Neurological symptoms can lead to respiratory paralysis and coma.

Treatment includes gastric decontamination and supportive therapy.Incorrect Answer (E): Chlorotoxin is found in a deathstalker scorpion, and it is known to block small conductance chloride channels. In humans this has been used to therapeutically detect cancerous cells namely glioma, melanoma, small cell lung carcinoma, neuroblastoma and medulloblastoma. This also helps in guiding therapy. References and further reading:Synaptic and Junctional Transmission In: Barrett K, Brooks H, Boitano S, Barman S, Ganong’s Review of Medical Physiology, 23rd Edition, McGraw Hill Medical, 2010.

Pp 119 05Topic: Excitable TissueSubtopic: Electrical Activity in the HeartConcepts to be tested: Action Potential in the Nodal Tissue: different phasesA student is tracing out the action potential of the Sinoatrial node of the heart. She is trying to learn all the different channels that play a role in the function of the heart. She noted that three channels play a particular role in the function of the SA node. Below is a tracing she has made of the different phases of the action potential of the SA node. What channel plays a vital role in the arrow marked portion of the graph? Outflux of K+ ions Influx of Ca2+ ions Influx of Na +  ions Outflux of Ca2+ ions Influx of K+ ionsExplanation:Source: https://commons.wikimedia.

org/wiki/File:2020_SA_Node_Tracing.jpgLicence:  Creative Commons Attribution 3.0 UnportedCorrect Answer (C):The slow influx of Na+ ions (phase 4) causes the depolarisation to reach threshold level. At the end of repolarization  the membrane potential is highly negative at – 60 mV. This causes the ion channels to conduct the slow, inward, depolarizing Na+ current. Because of it unusual activation it has been dubbed the funny or “f” channel. This depolarising currents eventually cause the SA node to spontaneously depolarize. Incorrect Answer (A): Outflux of K+ ions occur during repolarization (phase 3).

The K+ channels open which causes the hyperpolarizing K+ currents to move outward. At this time the Ca2+ channels also close decreasing depolarisation. Incorrect Answer (B): The rapid influx of Ca2+ occur at threshold level of depolarization (Phase 0). At about – 50 mV the transient T – type calcium channel opens first. This enables the Ca2+ to first enter the cell and further depolarise the cell.

When it reaches – 40 mV the long lasting L – type calcium channel opens for a rapid influx of the Ca2+ reaching action potential.Incorrect Answer (D) and (E): Outflux of Ca2+ and influx of K+ doesn’t occur during the nodal action potential. Educational Objective: A nodal action potential goes three phases.

The initial phase 4, is initiated by the slow influx of Na+ ions which enables depolarisation to reach threshold level. Then at phase 0, there is a rapid influx of Ca2+ ions favouring action potential to reach its threshold. Finally in phase 3, K+ ions move out of the cell to favour repolarisation. This continuous flow of ions favours the SA and AV node to conduct electrical impulses through the heart.

References and further reading:Electrical Activity of the Heart In: Barrett K, Brooks H, Boitano S, Barman S, Ganong’s Review of Medical Physiology, 23rd Edition, McGraw Hill Medical, 2010. Pp 491 – 492

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