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Physiology and Pharmacology - Essay Example

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Physiology and Pharmacology. Smooth muscles are the muscles in the human body which are not under the conscious control of an individual that is they are involuntary. Smooth muscles are present in the most important operating systems of the human body…
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Physiology and Pharmacology
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? PHYSIOLOGY AND PHARMACOLOGY Physiology and Pharmacology Question of 4 (12 of 36 marks) Many drugs have been designed to relax smooth muscle, and can have different mode of actions and clinical applications. Discuss the possible mechanisms for smooth muscle relaxation, and, using examples of different drugs, explain how these mechanisms can be applied clinically to treat various medical conditions. Smooth muscles are the muscles in the human body which are not under the conscious control of an individual that is they are involuntary. Smooth muscles are present in the most important operating systems of the human body. They are present in the blood vessels, in the stomach as well as the small and large intestine, the urinary bladder, the air passages, uterine cavity as well as the cavernosal sinuses of the penis and clitoris. The contraction and relaxation of these muscles involves interplay of ions. The contraction in the smooth muscle is led to by the interaction of calcium and calmodulin to activate the myosin chains by phosphorylating it. Actin and myosin are involved in the contractile process. An alteration in the potential of the membrane results in the initiation of action potentials which in turn leads to contraction. For actin and myosin to bring about contraction, the myosin light chain kinase (MLC kinase) plays a very important role. This is because it is the function of the MLC kinase to phosphorylate the chain of myosin for contraction to occur. The relaxation of smooth muscle is brought about by the elimination of the stimuli that result in contraction or by the specific function of substances like atrial natriuretic factor which prevent contraction from occurring (Guyton & Hall 2006; Ganong 2005; Webb 2003). Relaxation of the smooth muscle needs a reduction in the amount of calcium within the cell and the working of the enzyme Myosin Light chain phosphatase. The reduction in the amount of calcium in the sarcoplasm results in the separation of the dephosphorylated heads of myosin from actin and thus relaxation occurs. Substances that attach to the receptors on the sarcolemma and lead to the activation of adenylate cyclase-cyclic AMP (cAMP) further result in the activation of protein kinases. These protein kinases lead to the phosphorylation of the myosin light chain kinase making it lose its activity by the reduction of its attraction for the Calcium- calmodulin complex. Furthermore, substances that lead to a rise in the cyclic GMP (cGMP) also promote the functioning of protein kinases. The work of these kinases is to enhance the functioning of the myosin light chain phosphatase and affect the functioning of the calcium ion pumps. They cause the reduction of the calcium ion inside the sarcoplasm and hence lead to relaxation of the smooth muscle. Also an increase in the polarity of the sarcolemma results in the closure of the voltage gated channels of calcium. This prevents the entry of calcium and hence leads to the relaxation of the smooth muscle (Seifter 2005; Webb 2003). Smooth muscle relaxing drugs are used for the treatment of various pathological conditions. Nitrite and nitrate drugs which include glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside are a class of drugs which function in a similar manner as nitric oxide. The function of these drugs is to increase the amount of cyclic GMP. This results in the activation of protein kinases and subsequent reduction of sarcoplasmic calcium ions. This provides for the relaxation of the smooth muscles. These drugs are used for the treatment of angina and acute hypertension. Calcium channels blockers are another class of drugs which are used to relax smooth muscles of all types. These drugs prevent the entry of calcium in the intracellular compartment and thus lead to relaxation of the smooth muscles. Their main function is for the purpose of vasodilation of the vessels and verapamil and diltiazem are examples of these classes of drugs. Drugs that lead to the opening of potassium channels also have a relaxation effect on the smooth muscle. This is because this leads to making the membrane stable and hyperpolarized. These drugs are either used as vasodilators for the cure of high blood pressure and cardiac failure or for the relaxation of the air passages. Nicorandil is an example of a potassium channel blocker which acts as a vasodilator and antihistaminic agents are used for the relaxation of smooth muscles in the air passage (Howland et al 2006; Morton & Hall 1999). Question 2 of 4 (12 of 36 marks) Two drugs use to reduce cardiac output are calcium channel blockers and beta (receptor) blockers. Discuss their effects on the cardiovascular system and explain the possible mechanisms and clinical applications. Calcium is very important for the contractility of the muscles. In the case of reduction of blood supply to an organ, the intracellular movement of calcium increases owing to the depolarized state of the membrane which results due to the reduced oxygen supply. This further leads to the activation of enzymes that promote the breakdown of ATP and this result in the usage of stores of energy of the organ. This further deteriorates the ischemic condition of the organ. The calcium channel blockers are of utmost importance in these conditions as they provide for a guarding effect by the prevention of calcium entry into the cardiac cells as well as the cells of the smooth muscle of the cardiovascular system. The calcium channel blockers allow for the relaxation of the vasculature as well as the myocardium. Verapamil, Nifedipine and diltiazem are three important calcium channel blockers used for cardiac problems (Trevor et al 2008; Howland et al 2006). Nifedipine is a calcium channel blocker which leads to the dilatation in the arterioles. It has a greater effect on the peripheral vessels. It does not provide for any major effect on the conduction of the heart or the heart rate. Its property of providing for vasodilation makes it an effective drug for the treatment of variant angina which mainly results due coronary spasm. It is useful in the treatment of acute angina. Verapaeymil is a calcium channel blocker which reduces the atrioventricular conduction of the heart. It leads to a reduction in the heart rate as well as contraction and reduces the blood pressure and oxygen requirement as well. Diltiazem on the other hand also reduces the atrioventricular conduction and also reduces the heart rate. It can also assist in variant angina owing to its vasodilatory properties. Verapamil and diltiazem are used for the treatment of AV node arrhythmias (Trevor et al 2008; Howland et al 2006). Calcium channel blockers can thus be used for the treatment of angina, raised blood pressure and supraventricular tachycardia. The cardiac side effects of calcium channel blockers are atrioventricular blockade, depression of the sinus node and cardiac failure (Trevor et al 2008). Beta blockers act on both beta one and beta two receptors and are antagonists. The cardiac beta blockers are mainly beta one blockers. Beta blockers provide for an effective treatment in angina, arrhythmias, mycordial infarction as well as congestive heart failure. Propanolol is a beta blocker which acts on both beta 1 and beta 2 receptors. It has a direct cardiac effect and it also causes peripheral vasoconstriction. It decreases the output from the heart and also reduces the sinoatrial as well as the atrioventricular conduction of the heart. In the peripheries, owing to the reduced cardiac output, there is a fall in the blood pressure. This promotes a vasoconstriction peripherally and a low systolic as well as diastolic blood pressure is observed. These properties of propanolol make it an effective treatment form for high blood pressure, angina pectoris, hypertrophic cardiomyopathy, myocardial infarction as well as supraventricular tachycardia. Acebutolol, atenolol, metoprolol and esmolol are beta blockers which only act on the beta one receptors and they are used to prevent the side effects resulting from propranolol owing to its action on the beta beta two receptors. The function of these selective beta blockers is to reduce the blood pressure and to improve the tolerance to exercise in conditions like angina. Esmolol and acebutolol are effective for the treatment of supraventricular tachycardias owing to their action of reducing the atrioventricular conduction. The side effects of beta blockers are reduced heart rate as well as atrioventricular blockade. Heart failure may also result (Trevor et al 2008; Howland et al 2006). Question 3 of 4 (6 of 36 marks) A person drinks 1200 ml of distilled water. Use the data in the table to calculate the resulting increase in total body water (TBW), intracellular fluid (ICF), extracellular fluid (ECF), plasma and interstitial fluid (ISF). Repeat the calculations for ingestion of 1200 ml of isotonic NaCl. Discuss the clinical significance for the results in terms of expanding plasma volume in a patient who has just haemorrhaged. Compartment Volume of fluid (L) % of body fluid % of body weight Total body fluid 42 100 60 ICF 28 67 40 ECF 14 33 20 Plasma 2.8 6.6 (20% of ECF) 4 ISF 11.2 26.4 (80% of ECF) 16 Calculations for 1200 ml of distilled water Increase in total body water= 1.2 L Therefore, new Total Body Water= 42+1.2= 43.2 L Increase in intracellular fluid= 0.9 L Therefore, new ICF=28.9L Increase in extracellular fluid=0.3 L Therefore, new ECF=14.3L Increase in plasma= 0.06 L Therefore, new plasma volume= 2.86L Increase in ISF= 0.24L Therefore, new ISF=11.44L Calculations for 1200 mL isotonic NaCl Increase in total body water= 1.2 L Therefore, new Total Body Water= 42+1.2= 43.2 L Increase in intracellular fluid= 0 L Therefore, new ICF=28 L Increase in extracellular fluid=1.2 L Therefore, new ECF=15.2L Increase in plasma= 0.24 Therefore, new plasma volume= 3.04L Increase in ISF=0.96 Therefore, new ISF=12.16L In a patient who has just haemorrhaged, the main aim of treatment is to increase the plasma volume. If a solution from either distilled water or isotonic NaCl is to be chosen, isotonic NaCl is a better option. This is because isotionic NaCl remains in the plasma serves to increase the volume of plasma which is the main requirement following haemorrhagic blood loss. Distilled water is a hypotonic solution which gets evenly distributed in all the body compartments. In a haemorrhagic patient, the treatment of choice in the order of preference is whole blood, hemacecal, Ringer’s Lactate or isotonic NaCl (Guyton & Hall 2006; Bailey et al 2000). Question 4 of 4 (6 of 36 marks) Botulinum toxin is used locally for treating dystonia (involuntary skeletal muscle contraction) and in the beauty industry as an anti-wrinkle agent. Explain how it acts to reduce skeletal muscle contraction, and why it must be used with caution and cannot be given intravenously. Botulinum toxin is labelled to be one of the most dangerous poisons and an intake of a quantity as low as 0.0001 mg can prove to be fatal. With the assistance of research, this toxin has been started to be used as a cure for neuromuscular pathologies which are referred to as dystonias. Another significant use has been for the purpose of removing wrinkles on the face. Botulinum toxin is injected into the skeletal muscle where it basically functions by preventing the release of the neurotransmitter acetylcholine at the synaptic junction. Thus, the toxin prevents the exocytosis of the neurotransmitter at the synapse. The functioning at the synaptic junction is maintained by the formation of sprouts. The muscle is able to reach back to its normal functional capacity over a period of three months when the excocytotic capacity for the release of acetylcholine is achieved again and the sprouts revert making the muscle go back to its original state (Jankovic 2004; Sherwood 2010). Botulinum toxin mainly results in a “flaccid paralysis” of the muscle where it is injected. The toxin is given via the intramuscular route and it starts acting after the period of a few days up to 2 weeks. This is the time duration required for the action of the toxin on the nerve terminals of the muscle. Many people resort to using this toxin as a form of treatment for a long time and some may stop responding to the injections. This occurs because of the formation of antibodies against the toxin which prevent it from functioning. This is mainly seen to occur in people who use the toxin in high doses or it is also known to occur in those individuals who opt for the re-injection of the toxin before the completion of three months (Brody et al 2010). The toxin should be injected by an expert as many negative effects result. Inhalation of the toxin can result in ptosis, generalized weakness, blurring of the vision and dysphagia. In extreme cases, it can lead to a loss of respiratory function. The path of the administration of botulinum toxin is intramuscular and it should not be injected intravenously owing to the poisonous effects of the toxin which may result in death (Brody et al 2010). Bibliography BAILEY, H., LOVE, R. J. M. N., RUSSELL, R. C. G., WILLIAMS, N. S., & BULSTRODE, C. J. K. (2000). Bailey and Love's short practice of surgery. London: Arnold. BRODY, T. M., WECKER, L., & CRESPO, L. M. (2010). Brody's human pharmacology: molecular to clinical. Philadelphia, Mosby Elsevier. GANONG, W. F. (2005). Review of medical physiology. New York, McGraw-Hill Medical. GUYTON, A. C., & HALL, J. E. (2006). Textbook of medical physiology. Philadelphia, Elsevier Saunders. HOWLAND, R. D., MYCEK, M. J., HARVEY, R. A., CHAMPE, P. C., & MYCEK, M. J. (2006).Pharmacology. Philadelphia, Lippincott Williams & Wilkins. JANKOVIC J. (2004). Botulinum toxin in clinical practice. Journal of Neurology, Neurosurgery, and Psychiatry. 75, 951-7. MORTON, I., & HALL, J. (1999). Concise dictionary of pharmacological agents properties and synonyms. Boston, Kluwer Academic.  SEIFTER, J., SLOANE, D., & RATNER, A. (2005). Concepts in medical physiology. Philadelphia, PA, Lippincott Williams & Wilkins. SHERWOOD, L. (2010). Human physiology from cells to systems. [Pacific Grove (Calif.)], Brooks/Cole. TREVOR, A. J., KATZUNG, B. G., & MASTERS, S. B. (2008). Katzung & Trevor's pharmacology: examination & board review. New York, McGraw Hill Medical. WEBB, R. C. (2003). Smooth Muscle Contraction and Relaxation. Advance Physiology Education. 27. 201-206. Read More
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