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The Nervous System - Essay Example

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This paper 'The Nervous System' tells us that acetylcholine is synthesized in the neurons from choline and acetyl-CoA by the enzyme choline acetyltransferase. The destruction of acetylcholine into choline is catalyzed by the enzyme acetylcholinesterase. Opening calcium ion channels leads to the activation of exocytosis…
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The Nervous System
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QUESTION Describe the following events in the nervous system 1 The synthesis and destruction of acetylcholine. (5) Acetylcholine is synthesised in the neurons from choline and acetyl-CoA by the enzyme choline acetyltransferase. The destruction of acetylcholine into choline and acetate is catalysed by the enzyme acetylcholinesterase. 1.2 The role of calcium ions (Ca2+) in the mechanism of neurotransmitter release. (5) Opening calcium ion channels leads to the activation of exocytosis, i.e. release of neurotransmitters. 1.3 Give more information regarding the dorsal column-lemniscal sensory pathway e.g. describing the nerve fibres, velocity of impulse conduction, spatial orientation and type of impulses conducted. (5) The dorsal column-lemniscal pathway is an ascending somatic sensory pathway conveying tactile and proprioceptive information for the body and posterior third of the head. This pathway consists of A & A fibers characterised with high velocity (30 to 110 m/sec) of impulse conduction. The dorsal column-lemniscal pathway has also high degree of spatial orientation of the nerve fibres; particularly the medial fibers convey the information from the lower parts of the body while the lateral fibers related to higher segments. 1.4 The origin of spasticity in the muscles. (5) The spasticity in the muscles is related to the pyramidal insufficiency. This condition can occur if pyramidal pathways controlling voluntary movements are damaged by the mechanic or other agents. Intoxications, chronic neurodegenerative diseases, traumas, and metabolic disorders can play role in the origin of muscular spasticity. 1.5 The importance of the attenuation of sound by the structures in the outer- and middle ear. (5) The attenuation reflex is important protective mechanism providing the best sound perception. The contraction of the stapes muscle protects the inner ear from damaging. The role of outer ear structures is important also - they can reduce resonance in the middle ear. QUESTION 2 Explain synapse functioning regarding the following aspects: 2.1 Facilitation. (2) Facilitation is a progressive increase of neurotransmitter release at a synapse. This process leads to the occurrence of the reflexes after less intensity of additional stimulation. 2.2 Summation. (4) Summation is a process of gradual release of the transmitter and the transmission of the impulse from several presynaptic neurones to one postsynaptic neurone (spatial summation) or from only one presynaptic and one postsynaptic neurone (temporal summation). The summation leads to the release of sufficient the impulse is transmitted across the synaptic cleft. 2.3 One way conduction of impulses. (2) One way conduction of impulses is explained by the fact that the transmitter is only in the presynaptic membrane and the receptor molecules are only on the postsynaptic membrane. No exclusions 2.4 The effect of hypoxia. (2) Hypoxia can disrupt neuronal signal transmission at the synapse. Thus hypoxia suppresses the release of neurotransmitters at the presynaptic neurons. QUESTION 3 Pain is a protective mechanism for the body. Discuss the painconcept under the following headings: 3.1 Stimuli that excite pain receptors (nociceptors). (3) There are different stimuli related to mechanic, thermal or chemical damaging of the tissues. Correspondingly, there a different pain receptors: thermal, mechanical and polymodal. 3.2 What is the mechanism of the pain control (analgesic) system in the brain and spinal cord (6) The pain control system of CNS is represented by three major components: the periaqueductal grey and the nucleus raphe magnus (in the brain) and the pain inhibitory neurons of the dorsal horns in medulla spinalis. The opioid receptors of these structures are activated by endorphins or exogenous opiates and block the spreading of pain impulses. 3.3 Why is it difficult to localize slow, chronic pain (2) Chronic pain usually irradiate to other areas thus its localisation could be difficult. Furthermore, the efferent pain stimuli are conducted to CNS more slowly than acute pain. This peculiarity is related to the role of type C nervous fibers conducting impulses pf chronic pain with the velocity of 0.5-2.0 m/s. 3.4 Why can't a person sleep if he/she experiences pain (2) Insomnia occurs during pain episodes because of the release of neuromediators activating CNS and preventing falling asleep. 3.5 Name TWO causes of headache as a type of referred pain.(2) The intensive headache could be related to tugging on the venous sinuses, damaging the tentorium, or stretching of dura mater. Frequently the stimulation of nociceptors of supratentorial brain structures leads to the referred facial pains referred through n. trigeminus while the stimulation of subtentorial nociceptors can lead to the occipital pain referred through the second servical nerve. Question 4 Explain each of the following: 4.1 Function(s) of the microcirculation. (2) Microcirculation is the blood circulation throughout the microvascular network represented by the capillaries, metarterioles, and arteriovenous anastomoses between arterioles and venules. Microcirculation is crucial for oxygen and nutrients provision and the washout of metabolic by-products in the tissues. In the disease microcirculation could be worsened thus dystrophic processes can take place in the tissues. 4.2 Edema. (2) Oedema is swelling of tissues related to the extravasation of liquid part of blood or lymph. This process can occur during exudative phase of inflammation, due to vasodiltation caused by the pharmacological or toxic agents, due to hypoproteinaemia, and poor blood circulation. 4.3 Ejection fraction. (3) Ejection fraction is the proportion of blood ejected from the left ventricle with each heart beat. Normally it's equal to 50% or more. 4.4 Afterload on the heart. (3) Afterload is the resistance of vessels that the heart muscle should overpass for blood ejection. Increased aortic pressure and systemic vascular resistance rise afterload as well as ventricular dilatation or aortic valve stenosis. Question 5 Discuss the role of the Frank-Starling mechanism in control of the cardiac output of the heart. (10) The Frank-Starling mechanism is the capability of increasing of heart muscle contraction and stroke volume in response to increased venous return. Increased venous return increases end-diastolic volume and heart preload. Increased heart preload is related to the stretching of the cardiomyocytes. Myocyte stretching increases the length of sarcomeres and the force of ejection. This process caused length-dependent activation. Question 6 Give a brief description of the mechanisms involved in the control of the blood pressure. (20) There are following mechanisms involved in the control of the blood pressure: 1. Adrenergic responses of autonomic nervous system 2. Capillary shift mechanism providing the need volume of circulating blood 3. Hormonal responses (e.g. catecholamines, renin and angiotensin, vasopressin etc) 4. Kidney and fluid balance mechanisms (i.e. fluid and sodium retention helps to restore blood pressure) Question 7 Give a brief discussion of the following: 7.1 The hormonal control of tubular reabsorption. (12) Tubular reabsorption is controlled mainly by the mineralocorticoids (aldosteron) stimulating active reabsorption of sodium and passive reabsorption of water and vasopressin (antidiuretic hormone). 7.2 The osmoreceptor-ADH feedback system. (14) Hypovolaemia and hypotension stimulates the osmoreceptors in the hypothalamus thus the release of antidiuretic hormone is increased. Contrarily hypervolaemia and arterial hypertension inhibit the release of vasopressin. These mechanisms are an example of negative feedback system. 7.3 The role of urea in the mechanism for excretion of a concentrated urine. (12) Urea is osmoactive agent and one of the main constituents of urine. Thus urine specific gravity depends on the content of urea. Question 8 Define the following: 8.1 Filtration fraction. (2) The filtration fraction is the fraction of plasma water removed by the process of ultrafiltration. 8.2 Juxtaglomerular cells. (2) The juxtaglomerular cells (JG cells) are smooth muscle cells in the walls of the afferent arteriole that release renin. 8.3 Macula densa. (2) Macula densa is the part of the juxtaglomerular apparatus. It's located in the proximal distal tubule of the nephron and sensitive to the sodium concentration. 8.4 Pressure diuresis (2) Pressure diuresis is associated with increased mean arterial pressure i.e. increased mean arterial pressure results in increased diuresis. This phenomenon plays an important role in the regulation of blood pressure. 8.5 Plasma clearance. (2) Plasma clearence is the inverse of the time constant that describes the rate of spesific substance removal from the body divided by its volume of distribution. In other words, there is the ratio of the rate of a substance removal to its concentration in the blood. 8.6 A buffer. (2) A buffer is a substance having pH of dissociation which is close to the pH of its environment. A buffer helps to provide the minimal change of blood pH. Question 9 Activation of the complement system uses multiple means of destroying invaders. Discuss the most important effects of the complement activation. (15) There are following effects of complement activation: Opsonisation (i.e. increase of susceptibility to phagicytosis) Inflammation (by the activation of cellular mechanisms of inflammatory response) Lysis (by the influence of hydrophobic domains of lipid cellular membranes) Immune complex clearance (by the binding the immune complexes to erythrocytaric receptors and their further destruction in the spleen and liver. Question 10 Discuss the functions of the different types of T-cells. (10) Dependently on the clusters of differentiation there are classified following types of T-lymphocytes: CD8 -cytotoxic T-cells or T-killers. These cells release specific proteins destroying infected cells. CD4 - T-helpers. These cells regulate both T- and B-lymphocytes functions through cytokine release. Suppressor (CD4,CD25) T cells suppress activation of the immune system and maintain immune system homeostasis. They are important for the prevention of autoimmune disorders. Question 11 Discuss the following events in blood coagulation: 1. formation of prothrombin activator (4) There are intrinsic and extrinsic pathways of the formation of prothrombin activator. Both involve protease proenzymes of blood serume and form a prothrombin activator, which is a complex of factor Xa and its two cofactors, factor Va and procoagulant phospholipid on the surface of activated platelets or tissue cells. formation of thrombin (3) The prothrombin activator cuts prothrombin molecule into two fragments one of which is the enzyme thrombin. 2. formation of fibrin (3) Thrombin cleaves fibrinopeptide A and B chains of fibrinogen. This process results in the release of fibrin monomer which is polymerized to insoluble polymer molecules of fibrin. 3. clot retraction (5) Clot retraction results from the contraction of platelet pseudopodas attached to fibrin strands. This process is dependent on the contractile protein thrombosthenin presented in the platelets. Question 12 1. define thrombi and emboli (5) Thrombus is the blood clot in the vessel while embolus is the matter transported from a distant site by the blood stream and blocking the blood circulation by the vessel bstrlusion. There are many different reasons of embolism: air, amniotic fluid, fat, migrating thrombi etc. 2. discuss the cause of thromboembolic conditions (5) Thromboembolism is the obstruction of the blood vessel by a blood clot that has been transported from a distant site by the blood stream. Question 13 13. Discuss proteins under the following headings: 13.1 The influence of plasma amino acid concentrations on protein intake. (3) Low concentration of aminoacids influences on the alimentary behaviour - the persons faced to the challenge of protein food craving. The intake of meat, fish, poultry, dairy products, nuts, leguminous plants, etc is increased and the level of aminoacids is normalised. 13.2 The role of vitamin B6 and zinc in protein metabolism. (5) Vitamin B6 (piridoxin) is the precursor of pyridoxal phosphate which is a coenzyme for synthesis of aminoacids and some neurotransmitters (serotonin, norepinephrine). The processes of transamination requires the presence of pyridoxal phosphate. Zinc is essential trace element which is contained in some hormones (insulin) and enzymes. Both zinc deficiency and surplus can lead to the disorders of protein metabolism. 13.3 The influence of the presence of peptides in the duodenum on stomach emptying.(5) Normal motility and stomach emptying depends on the presence of peptides in the duodenum. If regulatory peptides (e.g. secretin) are presented in high concentratons than gastric motility is decreased. 13.4 The function of exocrine and endocrine stomach secretions in protein digestion. (8) There are several mechanisms providing protein digestion in the stomach. The secretion of hydrochloric acid is important for the activation of pepsinogen to pepsin (the proteolytic enzyme). Endocrinic secretion of APUD and enteroendecrinic cells of the stomach leads to the release of histamine, gastrin and other biologically active substances participating in the regulation of protein digestion. 13.5 The function of exocrine secretions of the small intestine and pancreas in protein digestion. (8) Pancrease produces trypsinogen and chemotrypsinogen and small intestine cells release enterokinase converting inactive trypsinogen into active trypsin. The conversion of chemotrypsinogen into active chemotrypsin is occur under the action of trypsin or active chemotrypsin. 13.6 The role of the liver in protein metabolism. (8) Liver is the chemical laboratory of the body where many processes of protein metabolism are occurred, e.g. deamination and transamination of aminoacids, synthesis of non-essential aminoacids, synthesis plasma proteins including albumin, coagulation factors, etc. 13.7 Explain how gastrointestinal obstruction will influence the plasma protein concentration (8) Gastrointestinal obstruction decreases the concentration of plasma protein. This phenomenon occurs due to the intensive fluid secretion in the gastrontestinal tract and albumin losses. Question 14 Discuss the function of the lower esophageal sphincter (LES) as well as the consequence of insufficient dilatation of this sphincter during the swallowing process. (10) The lower esophageal sphincter works as a one way valve, it prevents chyme returning up the oesophagus. Nevertheless, if this sphincter is not dilated properly so called achalasia can occur. This health disorder is characterised by dysphagia i.e. swallowing disorder and regurgitation of undigested food. Question 15 Give a summary of the neural control of the gastrointestinal function. (15) Gastrointestinal function is regulated by the sympathic and parasympathic autonomous nervous system. The parasympathetic innervation of the gastrointestinal tract is provided by the vagal nerve (upper part of abdominal viscera) and the pelvic nerve (lower segments of colon and rectum). The sympathetic innervation is supplied by the branches of the paravertebral chain, prevertebral coeliacomesenteric and caudal mesenteric ganglia. Parasympathetic stimuli activate the peristalsis and secretion whereas the sympathetic stimuli produce opposite effect. References: Guyton, A.C. & Hall, J.E. 2000. Textbook of Medical Physiology. 11th edition. Philadelphia: W.B. Saunders. Read More
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