The Case of the Off-Rhythm Bongo Player - Essay Example

and number] in format: 12 May 2002] Case Study: The Case of the Off-Rhythm Bongo Player The most likely cause of Bado's hypocalcemia comes from documentation written on the Health A to Z site in which the explanation for the onset of hypocalcemia is a result of the removal of his thyroid gland wherein "hypocalcemia can be caused by hyperparathyroidism, by failure to produce 1, 25-dihydroxyvitamin D, by low levels of plasma magnesium, or by failure to get adequate amounts of calcium or vitamin D in the diet. Hyperparathyroidism involves the failure of the parathyroid gland to make parathyroid hormone. Parathyroid hormone controls and maintains plasma calcium levels." (Health A to Z: Hypocalcemia). As a result of the removal of his thyroid, it actually caused his low levels of blood plasma Calcium level to be at the level it was tested at. As explained by Jason Bardi reports from the Scripps Institute, "calcium is a second messenger and regulates many different intracellular processes, including gene expression within cells." (Bardi, 2004) and "the transfer or spread of this excitability to a neuronal network, manifested as electro-graphic and clinical seizures, occurs via synaptic transmission." (Wellmer J, Su H, Beck H, Yaari Y and Eur J Neurosci, 2002) The effect on ion channels and effect on threshold are distinctive in the sense that "native calcium channels have been classified by both their electrophysiological and pharmacological properties and are generally divided into low-threshold (T-types) and high threshold (L-, N-, P/Q- and R-types). The L-, N-, P/Q- and R-type channels typically activate at membrane potentials near -30 mV and display diverse kinetic, voltage-dependent and pharmacological properties.1 The availability of specific pharmacological agents targeting the high threshold channels has permitted elucidation of many of their physiological functions. The T-type calcium channels describe a class of molecules that transiently activate at relatively negative potentials (-60 mV) and for which a general lack of high-affinity selective blockers has made their exact physiological contributions lag behind those of the high-voltage activated isoforms" (Snutch, 2005) The effect on Bado's muscles including the aching, twitching and tingling fingers is based on how the calcium mediates constriction and relaxation of blood vessels. This includes those excitable cells which controls the nerve impulses like those occurring in his twitching fingers. More definitively explained by Jane Higdon of the Linus Pauling Institute at Oregon University, calcium plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones, such as insulin. Excitable cells, such as skeletal muscle and nerve cells, contain voltage-dependent calcium channels in their cell membranes that allow for rapid changes in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions into the muscle cell. These calcium ions bind to activator proteins within the cell that release a flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein, troponin-c, initiates a series of steps that lead to muscle contraction. The binding of calcium to the protein, calmodulin, activates enzymes that breakdown muscle glycogen to provide energy for muscle contraction. (Higdon, 2003) As explained in the following afflictions, cell excitability and effects on the skeletal muscle are discussed: a) Hyperkalemia: "In acute hyperkalemia, the ratio of intracellular to extracellular K+ is decreased. The gap between the resting membrane potential to the excitability threshold is decreased and the nerve conduction is initiated more easily. If this continues it progresses to weakness of muscles. Gradual hyperkalemia, as in chronic renal failure, will cause an increase in both the intracellular and extracellular concentration with little change in the ratio. Hence, the signs and symptoms related to hyperkalemia are less intense. The converse occurs in acute hypokalemia. Hyperpolarisation of the resting membrane leads to decreased nerve cell excitability. This results in generalised weakness, and ultimately paralysis (Paralytic ileus, respiratory insufficiency). In chronic hypokalemia, there will be minimal or no change in the K+ gradient and no change in the resting membrane potential." (Reddy, 1998) "Potassium, a positively charged ion, helps to regulate water balance, nerve conduction, and muscle contraction. Hyperkalemia may lead to various signs and symptoms, such as diarrhea, nausea, abdominal cramps, weakness, and, with increasing severity, abnormal heart rhythms and muscle paralysis." (We Move Glossary of Terms) b) Hypokalemia: This is defined as another potassium condition wherein "Hypokalemia is defined as a potassium level less than 3.5 mEq/L. Moderate hypokalemia is a serum level of 2.5-3 mEq/L. Severe hypokalemia is defined as a level less than 2.5 mEq/L. " (Garth, 2005) "Common symptoms include the following: Palpitations Skeletal muscle weakness or cramping Paralysis, paresthesias Constipation Nausea or vomiting Abdominal cramping Polyuria, nocturia, or polydipsia Psychosis, delirium, or hallucinations Depression Physical: Findings may include the following: Signs of ileus Hypotension Ventricular arrhythmias Cardiac arrest Bradycardia or tachycardia Premature atrial or ventricular beats Hypoventilation, respiratory distress Respiratory failure Lethargy or other mental status changes Decreased muscle strength, fasciculations, or tetany Decreased tendon reflexes Cushingoid appearance (eg, edema)" (Garth, 2005) c) Hypercalcemia: Other than what has been outlined in the discussions above, the following can be added to the definition and symptoms of hypercalcemia: Symptoms of hypercalcemia depend on the underlying cause of the disease, the time over which it develops, and the overall physical health of the patient. Mild elevations in calcium levels usually have few or no symptoms. Increased calcium levels may cause the following: Nausea Vomiting Alterations of mental status Abdominal or flank pain (The workup of patients with a new kidney stone occasionally reveals an elevated calcium level.) Constipation Lethargy Depression Weakness and vague muscle/joint aches Polyuria Headache Severe elevations in calcium levels may cause coma. Elderly patients are more likely to be symptomatic from moderate elevations of calcium levels. Hypercalcemia of malignancy may lack many of the features commonly associated with hypercalcemia caused by hyperparathyroidism. Hypercalcemia associated with renal calculi, joint complaints, and ulcer disease is more likely to be caused by hyperparathyroidism. (Hemphell, 2005) d) Hypocalcemia: Hypocalcemia is a more serious disease of the two (hypocalcemia and hypercalcemia) and occurs when "a low bood calcium level, occurs when the concentration of free calcium ions in the blood falls below 4.0 mg/dL (dL=one tenth of a liter). The normal concentration of free calcium ions in the blood serum is 4.0-6.0 mg/dL." (Brody, 2002) The "symptoms of severe hypocalcemia include numbness or tingling around the mouth or in the feet and hands, as well as in muscle spasms in the face, feet, and hands. Hypocalcemia can also result in depression, memory loss, or hallucinations. Severe hypocalcemia occurs when serum free calcium is under 3 mg/dL. Chronic and moderate hypocalcemia can result in cataracts (damage to the eyes). In this case, the term "chronic" means lasting one year or longer." (Brody, 2002) To treat a patient with hyperkalemia intravenous calcium can be given to the patient in order to counteract the muscular and cardiac effects of hyperkalemia including those patients with a cardiac arrhythmia, but, this can only be used for a period of an hour, then alternate treatments should then begin. Methods such as intravenous insulin and glucose will move the required potassium to the intramuscular cells. Curate may help Bado in the short term to deal with the muscular problems that he is having in order to stop the twitching of the fingers but a more plausible methodology would be to treat the thyroid problem. Amphetamines would not likely help Bado with respect to relieving his symptoms as "Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. The net effect is an increase of neurotransmitter release into the synapse" (Handly, 2006) and add to the muscle degradation that Bado is experiencing now. Reflecting on the problem experienced by Bado and the information provided through the case study, it would be apparent that information that had been lacking is in obtaining further physical symptoms that Bado was experiencing. There was a brief discussion of his thyroid being removed but was not expanded on. It would be important to know why his thyroid was removed and the symptoms he was experiencing from that. The process used in approaching this problem was in just answering the problems as they were pronounced; but, the better method of analyzing this case would have been to get further background information on his childhood ailments or symptoms that could have explained why this was now becoming such a problem. There may have been hidden signals in his past that could have helped in preventing his situation that now exists. It's better to treat the symptoms and not the problems. Works Cited Bardi, Jason. "Inflammation and the Brain". 2004. Scripps Research Institute. 24 Feb 2006, Brody, Tom. "Hypocalcemai" Health A to Z. 24 Feb 2006, Garth, David. "Hypokalemia". 2005. eMedicine. 24 Feb 2006, Handy, Neal. "Toxicity, Amphetamines". 2006. eMedicine. 24 Feb 2006, Hemphill, Robin. "Hypercalcemia". 2005. eMedicine. 24 Feb 2006, Higdon, Jane. "Calcium". 2003. Linus Pauling Institute. 24 Feb 2006, "Hyperkalemia". We Move Glossary. 24 Feb 2006, Wellmer J, Su H, Beck H, Yaari Y and Eur J Neurosci. "Intrinsic Bursting Alone Does Not Beget Seizures". 2002. 16:259-266. 24 Feb 2006, Reddy, V.J. "Potassium and Anaesthesia". 1998. Singapore Medical Journal, 24 Feb 2006 Snutch, Terrance. "Targeting Chronic and Neuropathic Pain: The N-type Calcium Channel Comes of Age". NeuroRx 2:662-670, 2005. 24 Feb 2006, Read More