DIABETES MELLITUS

Characterized by metabolic disorders associated w absolute / relative deficiency of insulin production. People of ages around 40-60 are mostly affected.

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Clinically,it manifested by formation of trophic ulcers & slow healing of wounds.

AETIOLOGY & PATHOGENESIS Main factor of pathogenesis = organic/functional affection of -cells of pancreas islets. Lead to insufficient synthesis of insulin. Damage of -cells of pancreas can b due to (PRIMARY) : a. Infection b. Psychic trauma c. Removal of pancreas d. Tumor e. Sclerosis of pancreatic vessels f. Pancreatitis g. Regular overeating h. Insufficient intake of substances required 4 normal func. of insular apparatus i. Genetic predisposition SECONDARY insufficiency of -cells can b due to endocrine dysf(x) : a. Pituitary b. Adrenal hyperf(x) c. Thyroid Pathogenesis of DM also dpend on presence of excess insulin inhibitor : a. (nzyme insulinase) , wic produced in liver & is activated in ant. pituitary hyperf(x). b. Insulin antagonist c. a/b to insulin contained in blood of pt. hyperglycaemia is a symptom of disordered carb. metabolism. a. Increased blood sugar content is ass. W slowed glucose supply to muscles & fatty tissue & its slow phosphorylation. b. High blood sugar dpend also on intensified glucose supply from liver to blood & formation of glucose from glycogenic amino acid. c. Dis hyperglycaemia usually attended by glycosuria

Disorders of fat metabolism are delayed formation of higher fatty acids & neutral fats from carb. & enough supply of free FA to blood. a. Clinically this is manifested by wasting og pt b. Fat infiltration of liver = sign of upset fat metabolism. c. Severe disorder in fat metabolism is ketosis (accumulation in blood of acetone bodies & ketones intermediate products of oxidation of higher FA in liver. d. Diabetic coma can dev. in dis disorder of fat metabolism. Polyuria, loss of Na & partially K = symptoms of upset water-salt metabolism in DM a. Its pathogenesis is ass. w glycosuria wic elevates osmotic pressure in tubules to decrease reabsorption of water. b. Reabsorption of Na in kidney also decreased. A long-standing & incompletely compensated DM results in vascular changes (retinopathy,nephropathy) &atherosclerosis. a. Pronounced fluctuation in blood sugar increase pituitary xtvt,cause spastic atonia of vessels affect struc. of their walls,accelerates destruction of elastic fibres & promotes sclerosis & calcinosis Insulin deficit inhibits phosphorylation of vit. B6, wic often causes neuropathic complications of DM

CLINICAL PICTURE OF DM Excessive thirst (polydipsia); Increased appetite; Polyuria; Hyperglycemia; Glycosuria; Weakness; Decreased work capacity; Skin itching espc in perineal region;

Rubeosis (reddening of the face, the cheeks, supraciliary arches, the chin); Xanthosis (yellowish decolouration of the palms n soles assc. with upset conversion of vit. A in the liver n acc. of carotin in the skin); Patients skin is dry, rough, easily scaling, covered with traces of scratching; Furuncles, exematous n ulcerous lesions can be found; At points of insulin injection, there will be zones where fat is absent (insulin lipodystrophy); Muscles and Bones: o Muscular atrophy o Osteoporosis CVS: o Atherosclerosis of various arteries o Angina pectoris o Gangrene of the feet Respiratory system: o DM always concurs with bronchitis, pneumonia, TB GIT: o Oral mucosa n tongue are dry o Paradontosis o Pyorrhea o Appetite is very good, sometimes bulimia o Gastric juice studies show hypo- or achlorydia o Fat dystrophy of liver o Liver cirrhosis Kidney disease: o Arteriosclerosis of the kidneys n intracapillary glomerulosclerosis o Pyelonephritis may be also. Retinopathy: o Presence of exudates in the retina o Hemorrhages o Pigment abnormality in the yellow spot o Cataracts Changes in nervous system: o Polyneuritis

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Headache Deranged sleep Decrease work capacity

secretion of insulin(in healthy person) 2 dose does not increase sugar concent in blood

nd

Main laboratory methods used to diagnose DM n assess its gravity is based on: o Determination of sugar n ketone bodies in urine o Sugar level in blood on fasting stomach o Glucose tolerance tests o Sugar in urine maybe 5-8% n more o Morning urine of patients with latent DM maybe free from sugar, thus daily urine test should carried out o Urine taken after giving the patient a test meal or sugar can also be studied. Blood of healthy individual (fasting stomach) 4.46.6 mmol/L (80-120mg/100ml) of glucose Will increase to 28-44mmol/L (500-800mg/100ml) and more for diabetic pt But concent will be in normal if in mild dz so need to do 3-4 times per day lah! *if glycemia appears to exceed normal in repeated glucose tolerance tests, diagnosis of DM is +ve! After det bl sugar in fasting stomach- ask pt to drink 50g of glucose in 200ml of water- take bl specimen every 30mins for 3hrs Bl sugar level in healthy individual increase by nd about 50% during fez hr, 2 hr initial bl level is restored *the rise in bl level is higher in DM pt, increase in sugar concent is delayed while the initial level is not restored even in 3hrs ANOTHER TEST FOR GLUCOSE INTOLERANCE TESTanother portion of glucose given to pt in 1 hr following the fez dose.fez glucose intensify

Glucose oxidase & Samogyi-Nelson tests are used to det bl sugar o Glucose oxidase method is used to det true glucose of blood and is therefore most specific but normal glucose level is slightly underestimated compared with the Hagerdon and Jenson method o The sugar concent depend on how the blood is taken : glucose level is high in capillary than in the venous blood o Increase bl level xsemestinya DM but also maybe emotional excitation o GLYCOSURIA INDIRECTLY show hyperglycemia Present of sugar in urine also x semestinya show DM- since glycosuria may be due to decreased sugar permeability of kidneys Glucose Tolerance Testing Pt with clear sign of DM x require glucose tolerance testing Prednisolone or corticoglucose if person is predisposed to DM and normal result of glucose tolerance testing. Result of glucose tolerance testing dep on: o Fasting o Pathological processes in liver parenchyma o Injuries o Infections o Acute disorders of cerebral circulation o Strong emotions

Alkali Reserve Determination To predict approaching grave complication of DM e.g. diabetic coma. o sharply in moderate acidosis o Also in acidosis of other etiology like fasting or kidney dx.

COURSE (Onset can be acute or gradual) 1) Itching and furunculosis a. Characterize DM by its degree of severity and course and also the body response to therapy given into 3 levels: light, moderate, and grave. 2) Degree of hyperglycemia, glycosuria, presence of ketone bodies in urine and gravity of acidosis a. Characterize DM into: prediabetes, masked diabetes, and true diabetes mellitus. i. Prediabetes Cant be diagnosed acc given method e.g. in hereditary predisposition, obesity, newborns weigh over 4.5 kg. ii. Masked DM Detected by glucose tolerance test. iii. True DM diagnosed via cliniclaboratory findings. 3) DIABETIC COMA a. Grave maybe fatal complication of DM. b. Occur due to improper treatment of DM, or is complicated by acute infections, injuries, nervous stress. c. Pathogenesis: toxic accumulation in blood develop gradually that affect CNS precomatose condition (excessive thirst, epigastric pain, dyspepsia, headache, loss of appetite, pt breath smells acetone like rotten apples) first phase of coma (all precomatose condition symptoms intensify+ strong nervous excitement e.g. insomnia, restlessness, clonic convulsions, Kussmauls respiration second phase of coma wc shows marked inhibition (dizziness, no interest in surrounding, loses consciousness) deep coma(pt is motionless, face pallid or pink, muscle tone and tendon reflex, develop pathological reflex e.g. eyeball tone , eyeballs soft to touch, pupils narrow), d. Deep coma also shows: i. Kussmauls respiration heard at considerable distance, ii. Low and fast pulse, iii. Arterial pressure . iv. Hypothermia v. Oliguria and anuria develops

vi. Blood sugar markedly (22 55 mmol/l) vii. Alkali reserve of blood to 15-30% viii. No. ketone bodies with nonprotein residual nitrogen ix. Chloride content x. Leucocytosis as much as 50 x 10^9 per 1L of blood with neutrophilic shift to left. xi. Ketone bodies and sugar found in urine **they may develop without any distinct stage, thus develops sometimes abruptly without any precursors. xii. 4) Hypoglycaemic Coma a. Arise in the patient treated in insulin for DM b. Usually their diet lacks carbs, so insulin administration increase rate towards hypoglycaemic condition c. Early indication include: hungeeeerrrr, weakness, sweating, tremor, psychic and motor excitement,pupils dilated, blood sugar low, sugar and acetone is absent from urine. d. Patient will react quickly to treatment after IV infusion of hypertonic glucose 5) Treatment a. Diet therapy alone if patient is not disturbed by malnutrition,ketosis, contomittant disease b. If not, insulin is a must kalau antidiabetic preparations xeffective c. Insulins dose depends on the severity of patient condition d. To prevent the hypoglycaemic coma, kne administered glucose solution in hypertonic NaCl bfore insulin TAMMATUN KOIDOH!