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Download Practical of Clinical Chamistary
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Exp.1 Determination of Blood Glucose Concenteration Clucose is the transport form of carbohydrate in the body.Ingested starch and sugar are converted in to glucose by digestive enzymes and by the liver. When dietary source of glucose are not available the liver synthesizes glucose from glycogen by (glycogenolysis pathway) or from protein by (gluconeogenesis pathway), all cells use glucose as an important energy source, especially, the brain and spinal cord. Insulin is produced by specialized cells in the pancreas, it reduce blood glucose by facilitating its entry into the body cells. In deficiency of insulin, as in diabetes mellitus type1 , there will be increase of blood glucose by reducing the tissue utilization, while in diabetes mellitus type2, there will be antibodies developed against insulin which reduce its effectiveness, this lead to increase blood glucose level. Hyperglycemia Type1 insulin dependent diabetes mellitus(IDDM) Type2 non insulin dependent diabetes mellitus(NIDDM) Gestatinal diabetes Hypoglycemia Occure when blood glucose is below 2.2 mmol/L (40mg/100ml). Neonatal hypoglycemia : transient hypoglycemia in neonate of diabetic mother. GTT is used in investigating abnormalities of carbohydrate metabolism, and cases in which glucoseuria has been found. Glucoseuria Normal urine contains 1- 15mg/dL of glucose Glucosuria occurs if the concenteration of glucose exceed this level, its occurred when glucose in the filtrate exceed the tubular reabsorption capacity in the followings: 1- If plasma glucose is more than 11 mmol/L 2- If there is renal impairment of reabsorption as in pregnancy. Cholesterol is found in all cells of the body. The adernal gland contains 6% cholesterol. It is a precursor if the adernal and sex hormones Cholesterol may be synthesized from tow- carbon units (acetyl- Co A) in many body tissues, particularly liver, intestine and skin. Most cholesterol is excreted from the body via the bile. Liver cells oxidize the molecule by adding hydroxyl and carbonyl groups to form colic acid. There are excerted in the bile where they are instrumental in the absorption of fats, includind cholesterol itself. Hypercholesterolemia Primary hypercholesterolemia is due to rised LDL levels, because of LDL receptor deficiency. Secondary hypercholesterolemia is due to nephrotic syndrome, obstructive jaundice and diabetes mellitus. Hypocholestrolemia Cholesterol in the plasma tend to fall during starvation and as the result of prolonged debilitating illness. Hyperthyrodism also reduces serum cholesterol. Very low values occurs in abetalipoprotenemia and to a extent in familial hypobetalipoprotenemia The diferent types of lipproteins, which are called high-density lipoprotein (HDL), lowdensity lipoprotein (LDL), very low- density lipoprotein (VLDL), and chylomicrons have a relatively low density compared with other plasma proteins. Lipoprteins also differ in their electric charge and can be separated by Electrophoresis. Uric acid is a waste product of purine metabolism in man. Purines can be synthesized in the body or can be ingested foodstuffs, which contain abnormal amount of nuclear proteins such as liver and pancreas,contain large quantities of purines. Hyperuricaemia 1- Primary hyperuricaemia due to genetic disorders in uric acid metabolism. 2- Reduced rate of excretion. a- Renal glomerulr dysfunction. b- Treatment with thiazide diuretics. c- Acidosis. Hyperuricamia is, in many causes, due to an accelerate production of uric acid. Secondary to degradation of unusually large quantities of purines. If the plasma level of uric acid becomes unusually high (hyperuricaemia), it may precipitate in the tissue in the form of sodium urate crystals. Upon ingesting the crystals, microphages an inflammatory response leading to the syndrome known as gout. Urea is the detoxification product of the amino acids. Urea production is increased when excess protein in ingested or when body protein is catabolized. The concenteration of urea in the body water depends upone the rate of production by the liver and the rate of removel by the kidneys. Normal renal function depends on a normal filtration rate, normal tubular function and normal blood supply. Causes lead to increase serum urea concenteration a- increase prodction b- decreases GFR. c- post renal uremia. d- Kidney disease. Causes lead to decreases serum urea concenteration: 1- Malnutrition 2- Homodilution 3- Very sever liver disease 4- In born error of urea cycle 5- In appropirate ADH secretion.
