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Lack of insulin






↓ anabolism ↑ secrtion of glucagons cortisol ↑ catabolism

↓, growth harmone, catacholamine ↓

hyperglycemia à fatigue ↑ glcogenolysis

↓ ↑ gluconeogensisà wasting

glycosurea à vulvitis balantitis ↑ lipolysis à loss of wt.(type1)

↓ ↓

osmotic dyuresis à polyurea, polydepsia hypercatonemia à hypotension, ↓ body

temp

↓ ↓

salt & water depletion à tacycardia, hypotension acidosisà peripheral vasodilation

↓ hyperventilation, kussmaul

breathing

collapse à death Diab catoacidosis è death

Clini pic: - above together with pathogenesis.

Complica: - (A)Acute complic: - (a) Diabetic ketoacidosis(DKA)-it may b the initial sympt. complex that leads to diag. of type -1 DM. Pathophy: -DKA results form relative or absolute insuffi. With counter regulatory hormone excess(glucogon, CAs, cortisol & growth hormones) à ↑ gluconeogenesis n glycogenlysis & ketone bodies formation in liver as wellas substrate delivery from fat & mus.(free fatty acid, aminoacids to liver). Clinic pic: - nausea /vomiting, thirst/ polyuria, abd pain, tachypnoe(or kussmaul breathing/resp distress), tachycardia. Precipitating events à inadequate insulin administration, infec., infarction, drugs, preg. DKA may complicate into Diabetic coma. Rx of DKA: - Adminis’ of short –acting (soluble)*insulin-5U/hr, Fluid replacement therapy-i.v 0.9%*saline sol, 1litre in 30 min, K+ replacement therapy started cautiously. if infection –prescribe A/B. (b) Non-ketonic hyperosmolar DiabeticComa: - Chr by severe hyperglycemia(50mmol/l)without significant hyperketonaemia or acidosis. Rx: - differs from that of DKA in two respects(1st, these pts r relatively sensitive to insulin n approx half dose of insulin is recommended for Rx of DKA shud b emplpyed. 2nd, plasma osmolality shud b measured by using formulaà plasmaosmolality= 2(Na+)+2(K)+(glucose)+(urea). N value is 280-300 mmol/kg n conscious level is depressed when its high> 300mmol/kg.*Saline-0.45% shud b given until osmolality approache N, when 0.9% shud b substituted. To avoid thromboembolic complica. administer heparin .(c) Lactic Acidosis: - In coma due to LA the pt is likely to b taking biguanide for type 2 DM n is very ill n tachypnoe but not so profoundly dehydrated as it in DK coma.The pt’s breath doesn’t smell of acetone, ketonuria is mild or absent yet plasma bicarbonate n pH r markedly reduced. Diag: - high(usually> 5 mmol/l)concen of lactic acid in bld. Rx: - i.v *Sodium bicarbonate to achieve N pH (to above 7.2)along with insulin n glucose. (2)Chronic complic: -^Microvascular-Eye dis(retinopathy, macularedema)neuropathy-sensory n motor(mono- n polyneuropathy) autonomic nephropathy. ^Macrovascular-Coronary artery dis, Peripheral vascular dis, ^ others: - GIT (gastropathies, diarrhea), Genitourinary (urinopathy, sexual dysfunction), Infarctions, Catarracts, glaucoma. Rx of DM: - Type - 2 - ^ Adequate diet (wt ↓ diet for obesity n wt maintaining diet for non-obese) when diet is no longer effective, oral hypoglycemic drugs r prescribed(3 types)à *Sulfonylureas (inhibitor of enzyme reducing absorption of glucose)-Stimulates the insulin release from pancreatic β cells,.eg.1st gener -*Tolbutamide (500-3000mg), *Chloropropamide (100-500mg), 2nd gener-*Gilbenclamide, *Glucotrol. ^ Biguanides-*Metformin, *Gliformin500-3000mg. ^ α -glucoside inhibitors-Acarbose75-300mg, *Glibamide. Type-2 - ^ *insulin liporegular (shrt actng), *Actrapid, *Lente, *NPH humulin(intermediate acting), very rarely used long acting-*Ultralente.

 

 

40. Hypothyroidism: - Def: -Hypothyroidism is a cl synd resulting from a defici. of throid hormones leading to a generalized hypometabolism with deposition of glycosaminoglycans in intracellular places esp in skin n mus. (bcoz of ↓ destruction of glucseaminoglycans). Etio: - primary- ^ Hashimoto’s thyroiditis à (i)with goiter, (ii)idiopathic thyroid atrophy presumably end-sage autoimmune thyroid dis, following either Hashimoto’s thyroiditis or Grave’s dis, (iii)neonatal hypothyroidism due to placental transmission of TSH-recpetors blocking Ab. ^ Radioactive iodine therapy for Grave’s dis, ^ Subtotal thyroidectomy for Grave’s dis or nodular goiter. ^ Excessive iodine intake, ^ subacute thyroiditis, ^ Rare causes-Iodine insufficiency, other goitrogens eg lithium, antithyroid drug therapy, inborn errors of thyroid hormones synthesis as a rule due to enzyme defects protease. Secondary- Hypopituitarism due to pituitary adenoma, pituitary ablative therapy or pitiuitary destruction. Tertiary- hypothalamic dysfunction(rare)periph resistance to action of thyroid hormone. Clini pic: -^General-tiredness, somnolence, wt gain, cold, intolerance, hoarseness, goiter(primary), ^Cardiorespiratory-bradycardia, HT, xanthelasma, pericardial n pleural effusion, ^Neuromuscular-mental retardation in children, cerebellar ataxia, depression, psychosis, delayed relaxation of tendon reflexes, muscle pains n stiffness. ^GIT-constipation, ascites, ^Reproductive-menorrhagia, infertility, glactorrhea, impotence, marked slowing of growth n development in children, ^dermatological-dry, rough skin n hair, puffyface n alopecia n myxedema. ^Hematological-macrocytosis, anemia(fe deficit, normochromic, folate defic, pernicious anemia (b12 –def). Clini pic. infants n children: - in infants- resp difficulty, cyanosis, jaundice, poor feeding, hoarse cry, umbilical hernia, marked retardation.In severe cases so called Cretinism may take place(mental retardation, short stature, characteristic puffy appearance of face n hands, neuro- signs of pyramidal n extrapyramidal tract abnormalities). Lab & diag: -↓ serum T-4, ↑ TSH, Nonspecific abnormalities include-elevation of enzymes eg LDH, Creatininekinase, ↑ cholesterol, triglyceride↑, ↓ serum Na. In severe prolong hypothyroidism in ECG classicly demonstrates sinus bradycardia with low voltage complexes n ST n T-wave abnormalities. Rx: - ^ In all forms of Hypothyroidism replacement therapy with thyroid hormones r usedà (a) L-thyroxine (levothyroxine) à in young pts with mild HypoTH, initial dose is 0, 05 mg daily.in pts with severly hypoTh n cardiovascular problems, the initial dose is 0.0125-0.025mg daily may then b↑ slowly (under ECG-control). (b) Thyrecomb(levothyroxine+liothyroxine+potassium iodide) Thyreotom (levothyroxine +liothyroxine) à used in pts with inhibition of conversion of T4 to T3. Rx secondary hypothyriosis: - compensation of other endocrine glands insuff. (hypocorticism, hypogonadism) Dose of L-T4 must ↑ about 25%during preg n lactation. Older pts metabolise T4 more slowly n the dose of L-T4 will gradually ↓ with age.

 

 

41. Hyperthyroidism: - Def: -It’s a cl synd results from high levels of circulating thyroid hormones due to different causes.More common ♀.The synd consists of one or more following pictures, *thyriotoxicosis, *Goitre(diffuse thyroid enlargement in Grave’s dis), *ophthalmopathy, *Dermopathy so called pretibial myxedema. Etio: - ^common- Grave’s dis, Toxic multinodular goiter, Solitary toxic nodule or adenoma. ^Uncommon - Acute thyroiditis (viral eg, d-quervains, autoimmune, post-irradiation, post-partum), Gestational thyriotoxicosis, Exogenous iodine, Drugs eg amiodaron, thyriotoxicosis, factitia(secrets T4 consumption. ^Rare: - TSH-secretory pituitarty tumors, metastatic differentiated thyroid carcinoma, hCG producing tumors, hyperfunction ovarian teratoma. Patho. of Grave’s dis: - Its an autoimmune dis of unknown cause such as DM. The Hyperthyroidism results from production of IgE antibodies which iteract with TSH-receptors on the thyroid follicular cells n stimulate thyroid hormones, production n goiter formation. these antibodies r known as thyroid stimulating Ig or TSH-receptors Ab. this production of Ab cause is not clear but genetic predisposition n environmental factors r the key factors. The trigger factors for HyperTH is genetically predisposed, may b infection(viral or bacterial, preg, or iodine excess). Clini pic: - ^ goiter, ^Cardiorespiratory (palpitation, sinus tachycardia, AFib, ↑ pulse pressure, ankle edema in absence of cardiac failure, cardiomyopathy n cardiac failure dyspnea on exertion). ^Neuromuscular (nervousness, irritability, emotional lability, psychosis, tremor, hyper-reflexia, mus. weakness, proximal, periodic paralysis). ^GIT-(wt ↓, despite normal/↑ appetite, hyperdefecation, diarrhea n steatorrhea), ^Dermatological(↑ sweating’pruritis, palmar erythema, pretibial myxedema, pigmentation, vitilago), ^Ocular(40% pts), (lid retraction, lid lag, grittiness, excessive lacrimation, chemosis, exophthalmoses, corneal ulceration, ophthamiplegia, diplopia, papilloedema, loss of visul acuity), ^Others (heat intolerance, fatigue, apathy, gynecomastia, lymphadenopathy, thirst /due to ↑ sweating).Thyreotoxicosis for long time à DM(type depends upon genetic predisposition).HyperTh may lead to defici. of GCà adrenal crisis. Lab diag: -^ hormonal status à ↑ FT3, ↑ FT4’suppression of TSH, ^thyroid Ab may b present.TSH-R stimulating Ab r specific for Grave’s dis. ^ Iodine-123 or technetium scan is useful to evaluate the size of gland or the presence of hot or cold nodules.(normal uptake-6th hr is 5-15%, 24hr is 30-50%)in Grave’s dis its elevated. ^Thyroid USI-can measure the size of gland or individual nodules n for evaluating the results of therapy. Rx: - 3 methods- ^ antithyroid drug therapy-*Propylthiouracil 100-150mg every 6hrs initially n ↓ dose in 4-8 wks to 50-200mg 1 or 2 daily. *Methimazole-40mg 2ti/day. ^ Surgi treat: - subtotal thyroidectomy. ^ radioactive iodine therapy. Rx ophthalmopathy - ^sort couse coricosteroids-prednisone 100mg for 7-14days, then gradual ↓ dose for 6-12 wks.^if corticosteroidtherapy is not effective, external X-ray therapy to retro bulbar are may b helpful. ^ orbital compression may b used. Subacute thyroiditis -its an acute inflamm. disorder of thyroid gland due to viral infection. Patho examn: - moderate thyroid enlargement n mild inflammatory reaction involving capsule of thyroid gland. Histological features include destruction of thyroid parenchyma (i.e.follicular) n presence of many multinuclear cells n granulomas n this may lead to ↑ of thyrpoid hormones à short time thyrotoxicosis. Clini: - thyriotoxicosis symptom+inflamm symptoms(sever pain in ant surface of neck, swallowing n cough n is reffred to head, ears n neck)(body temp ↑ to 39-40C, chill, headache, weakness, ringing in ears appears, tearfulness, irritation, ↑ sweating, tachycardia. Rx subacute thyroiditi: -in most cases-NSAID. if severe pain, fever, malaise, short course of *GC -prednisone 20mg 3 times for 7-10 days. *levothyroxine is indicated during the hypothyroid phase of the illness.

 

42. D.D of edema syndrome: -the differences bw the 3 major causes of edema: -

Cardiac: -^History - Dyspnoea with excertion often asso with orthopnea or paroxymsal noctural dyspnoea. ^ Phy.Exam- ↑ JVP, peripheral cyanosis, cool extremities. ^ Lab- ↑ urea nitrogen to creatinine, ↑ uric acid, liver enzymes. Hepatic: -^History- Dyspnoea is rare except if asso with severe degree of ascities, most often ethanol abuse. ^ Phy.Exam- Ascities, BP low than in renal or cardiac dis, one or more signs of chr liver dis eg encephalopathy. ^ Lab- In severe case ↑ albumin. cholesterol, transferring, fibrinogen & liver enzymes, depending on the cause & acuity of liver injury. tendency towards hypokalemia and resp alkalosis. Renal: -^History - Usually chrn may be asso with uremic signs and symptoms ↓ appetitie, metallic or fishy taste. ^ Phy.Exam- BP↑, hypertensive or diabetic retinopathy in selected cases, periorbital edema may be prominent, pericardial friction rub in advanced cases with uremia. Lab- Albuminuria, hypoalbuminemia, sometimes ↑ creatinine & urea nitrogen, hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia & anaemia usually normocytic. The disturbution of edema is an important guide to the cause, edema limited to one leg or to one or both arms is usually the result of venous or lymphatic obstruction. edema resulting from hypoproteinemia. Characteristically is generalized, but it is esp evident in the very soft tissue of the eyelids abd face and tends to be more pronounce in the morning bc of the recumbent posture assumed during the night. Edema associated with hrt failure tends to be more extensive in the legs and accentuated in the evening. the colour, thickness and sensitivity of the skin r significant. local tenderness and warmth suggest inflamm, local cyanosis may signify venous obstruction.in individuals who have had repeated episodes of prolonged edema the skin over the envolved area may be thickened, indurated & often red.elevation in isolated part of body usually reflects venous obstruction, generalized localization indicates CHF. In pts with obstruction of sup vena cava edema is confined to face, neck and upper extremities.

 

 

43. Multiple myeloma: - Def: - multiple myeloma malignant proliferation of plasma cells dis results from uncontrolled plasma cells. Etio: -cause is unknown, myeloma occurs with ↑ frequency in those exposed to radiation & nuclear. the neoplastic event in myeloma may involve cells earlier in B cell differentiation than the plasma cells. interleukin 6 may play a role in driving myeloma cell proliferation. Classifi: - ^ solitary bone plasma cytoma, ^ extramedullary cytoma. Patho & clinic: - ^ bone pain is the most common esp on the back and ribs which usually worsen at night and is precipated by movement, ^ renal syndrome renal failure manifest contribute to hypercalemia proteinurea and benjons protein50mg/l. ^ anaemia normochromic, normocytic, ^ bacterial infection is most common as pneumonia, pyleonephritis, ^ neurologic syndrome-lethargy, weakness, confusion, hyperviscosity, headache.(vi)bleeding.criterea of diagnose. criterea of diagnose- stage1-benjons proteins< 4gm/l, HB↓, serum, ca, osteolysis id absent.Stage 2-bencejons proteins > 4 but < 12g/l, HB↓ 80-100, serum ca 2-5mmol/l osteolysis of bone.Stage 3-bencejons protein↑ 12gm/l, HB ↓ < 80gm/l, serum ca> 2.58mmol/l, osteodestruction. Rx: -standard of treatment-*mephalan 8gm/m2 body surface, *cyclophosphide 200mg/m20, *chlorambucil 8mg/m2, *predinisolone 25-60/m2..if its cancer we used chemotherapy and radiotherapy or transplantation of bone marrow.

 

 

44. Haemoblastosis: is the cancer of bld due to mutation of haemopoetic cells.

Leukaemia: this is result of genetic mutation in one or a few bone marrow cells, which begins in bone marrow: - ^ Ac. leukaemia (mutated cells without maturation or with partial diefferentiation). ^ Chr. leukaemia (mutated cells differentiated to mature forms), disease- Chr. myelogenous leukaemia, Chr lymphocytic leukaemia, Chr cubleukaemic myelosis, Erythremia, Paraproteinemic haemoblastosis (multiple myeloma, Waldenstroms’ disease) Acute leukaemia: - is a disease from group of haemoblastosis, malignant cancer of the haemopoetic tissue due to genetic mutation in one or a few bone marrow cells, pathomorphological substrate of this growth are leukaemic abnormal haemopoetic progenitor blastic cells with their subsequent distributed differentiation in certain parts of haemopoesis. Classifi: - *M0: Ac. Myeloblastic leukaemia without maturation, *M1: Ac. Myeloblastic leukaemia with Azurophilic granules and chromosome aberration, del (5), (7), (8). *M2: Ac. Myeloblastic leukaemia with partial differentiation, translocation (8, 21), (6, 9). *M3: Ac. Promyelocytic leukaemia; translocation (15, 17).*M4: Ac.Myelomonocytic leukaemia; translocation (4, 11); some signs of mono and myelo leukaemia. *M5: Ac. Monoblastic leukaemia. *M5a: Ac. Monoblastic leukaemia without maturation; translocation (9, 11). *M5b: Ac. Monoblastic leukaemia with maturation; translocation (10, 11). *M6: Ac. Erythroblastic leukaemia (erythromyelosis). *M7: Ac. Megakaryoblastic leukaemia (Megakaryocytes; precursor of thrombocytes. Etiology: -Due to genetic mutation in one or few bone marrow cells. factors which ↑ risk of leukaemia. ^ risk factors maybe inherited. Some genetic disorders, such as Down’s synd. are associated with ↑ risk. ^ Radiation. ^ Some drugs (Levomycin, Butadion, Cytostatics). ^ Chemical (Varnish, paints, Benzenes). ^ Virus, (virus HTLV– 1). Retrovirus from pt with T-cell, S- leukaemia. Cytopatho: -According to growth of monoclonalà one malignant haemopoetic cell after mutation is an ancestor of tumoral clone in bone marrowà Leukaemial cells don’t have normal functions, discrepancy between a process of proliferation & differentiation with a blockade of differentiationà During 3 months one such cell form 1 kg of the new cells (blastic transformation of bone marrow)à clinic sympt. begin. Malignant cells suppress a growth of normal cells and then anaemia and thrombocytopenic develop. During the development of acute leukaemia malignant cells go into blood, skin, nervous system, liver, spleen, lymph nodes, kidney, etc. Clinical signs: ^ Hyperplastic syndrome: enlargement of lymph nodses (mod. lymphadenopathy) in 50-75% of pts, ↑ spleen, ↑ liver 50-60%, leukaemic skin infiltrations, pain in bones, meningeal leukaemia. Failure of production of normal bld cells by replacement of marrow by leukaemic cells. ^ Anaemic synd; most common. ^ Haemorrhagical synd; due to thrombocytopenia. Intra & subcutaneous elements, bruises, profuse bleeding (50-60%) - < 20000 thrombocytes. ^ Intoxication, weakness, subfebrile temperature. ^ Secondary infect. (80%); ↑ temp, stomatitis, necrotic tonsillitis, pneumonia due to neutropoenia. Lab: - leucocytes may be ↑, ↓ or Nor (50 %), granulocytopoenia is very common (< 1000 cells in 50 %), anaemia of different degrees (severe degree is common), thrombocytopenia is frequently observed & platelet counts < 20000 / UL are common. Circulating blast cells are absent from peripheral bld in approximately 15% of pts initially sometimes blast cells level ↑ ↑ to 80 – 90 % initially. ^ definite diag – exam. of bone marrow aspirate more than 30% blastic forms (main criteria of diagnosis). All blastic cells are similar morphologically but special cytochemical reaction can be used to differentiate between them. Prevalence of their certain forms is determined by the haematological variant of leukaemia (ac. ymphoblastic, ac. myeloblastic, ac. monoblastic). Only the youngest and most mature cells can be revealed in blood of most patients with ac. leukaemia, while intermediate forms are absent (Hiatus Leukaemicus) Rx: -*Cytotoxic chemotherapy - profound suppression of leukaemic cells is necessary in order to permit recovery of normal haemopoesis. *1st - Remission induction therapy: 1 – 2 courses of intensive therapy. Prophylactic Rx of meningeal leukaemia; -(Cytostatics, Radiation to head with high doses – x-ray). *2nd - Post – remission therapy; consolidation therapy; 1 – 2 courses of intensive short course (reduce subclinical body burden of tumour). *3rd - Maintenance therapy; months to years of less intensive therapy to further recurrence orautologous bone marrow transplantation / allogenic (I.V transfusion of stem cells from healthy donor; siblings) bone marrow transplantation. Rx Ac. Myeloblastic Leukaemia: - *Cytosine Arabinoside (ARA – C). *Anthracycline; eg: Rubamycin is combined with ARA – C (7d ARA – C & 3d Rubamycin or 5d ARA – C & 2d Rubamycin) & 6 – Thioguanine in some regimens in severe cases. *Mitoxanthrone has also been used in combination with ARA – C. Rx Ac. Lymphoblastic Leukaemia: - *Vincristin, *Anthracyclin combined with vincristin (Oncovin), *Prednisolone combined with vincristin, *Adriablastin combined with vincristin. Progno: - better in children as they usually have acute lymphosis. 92 – 95% children have remission after 1st line therapy. Rx of complication: -*Antimicrobial therapy, *Infusion of platelet, treatment of bleeding, *Rx of neuroleukaemia (cytostatics, radiation of head with high doses “x-ray therapy”), metastasis in CNS causing encephalitis, meningitis, *Rx of severe anaemia (erythrotransfusion), *Detoxification therapy, *Immunotherapy.

 

 

45. Lymphogranulamatosis & lymphomas: - Def: - is malignant affection of lymphoid tissue with specific morphological picture formation of granulomas & presence of Sternberg reed cells with ability to spread via the lymphatic system with occasional involvement of internal organs. Hodgkins disease is a malignant disease of lymphatic tissue. the source of the growth are T-cells or macrophages disease of lymphatic tissue. Morpho: - ^ lymphohistiocytic, ^ nodular fibrosis, ^ mixed cell variety, ^ lymphocyte depleted variety. Classifi: -^ local-charc by involvement of 1 or 2 adjacent LN, ^ Regional-charct by invotvment of 2 or more non adjacent LN region, same side of diaphragm. ^ Generalized-charct by involvement of any grp of LN on both sides of diaghragm. ^ Disseminated or diffuse-involvement of internal organs, soft tissue & skin. Clinic: -3 major syndrome. ^ growth of tumour proper spreads by lymphatic system n into extralymphatic sites that envolves internal organs. ^ tumor induced toxaemia. ^ immunological abnormalities. Diag: - ^ grp of general symptoms (t 38c, night sweat, weight & itching. ^ ↑ LN. ^ involvement of internal organs as tumor metastasis to lungs, liver, bones and GIT with symptoms cough with sputum, pain in right hypochondrium, bone pain, diarrhea, abdominal pain, upset sensitivity. ^ the syndrome of immunologic abnormalities is manifested by ↑ susceptibility to infectious disease, immune disorders can cause autoimmune hemolytic anaemia which is manifested jaundice & fever. enlargement of peripheral LN. Lab-Diag: - ↑ ESR, neutrophils, leucocytes with Left shift, leucopenia, anaemai-this cause of anemia is autoimmune hemolysis which id due to formation of AB to RBC. by coombs & aggregate haemagglutination.hypoalbuminaemia, ↑ α globulins, fibrinogen. Rx: -method depends on stage of disease. ^ radiotherapy, ^ polychemotherapy ^ surgical removal of the spleen & LN nonspecific therapy is also used & another four programme *cyclophosphan, *vincrisrtine, *prednisone, the prevention-measure to prevent the onset of disease of the disease is unknown, 2nd dary prophylaxis r only possible they r Rx in time, maintainance care, correction of immunity, Rx of intercurrent infec & abstention from excessive insolation. Prognosis: - disease is timely & Rx is started during its early stage 80% of pts with stage I and II can be cured. prognosis with disease of III and IV stages long remission r possible.

 

 

46.Non specific ulcer disease: -

ULCERATIVE COLITIS: - is an idiopathic inflammatory condition that involves the mucosal surface of colon resulting in diffuse friability and erosions with bleeding. Etio: - unkonown, ^ genetic factor, ^Path. Immune reaction provoke by (allergic reaction, infect, virus, diatery factor, microtrauma). Location: - Rectosegment 50-70%; Lt side colon 30%; whole colon 20%. Patho: - ^ degeneration mucose epithel, ^ occlusion sub epith. Capillaries, ^ inflamm. of lamina propria, plasma cells, mast cells, ^ crypt abcess, necrosis, ulcer. Clinic: - Diarrhoea, pian before & after defication, pain in left side, mucouse + bld stool. Non specific Signs: - 3-5 min before & 10min after defication, Mucouse + bld in stool. Clinic Classif: -1st º (< 4 time stool, intermitant bld), 2nd º (stool + blood, severe diahorrea, fever, anemia, hypoalbuminemia), 3rd º (severe diarrhea 20-40, bleeding severe, hypovolumia, impaired nutrition, anemia, hypoalbuminemia). Diag: - Bld- anemia, leucocytosis, ↑ ESR, Rectomanoscopy (15-20cm), Fibrocolonoscopy – whole intestine, Xray- barium anema, Biopsy, Serology test. Complic: - bleeding, stenosis, penitartion, perforation, malignancy. D.D: - ^colitis cause by inf.agents (eg.salmonella, shigella).^crohns dis of colon.^ischemic colitis. ^Radiation colitis. ^ Colitis induced by drugs. ^malignancy of colon. Rx: - ^ mild attack(*mesalazine1, 5-2g/day orally or * sulfasalazine 3-4g/day. ^ mod. Attack(*oral prednisolone 60mg/day weekly reduction of daily dose for 10mg later on for 5mg according to l.improvement. *Mesalazine or sulfasaline orally if necessary topical steroids and or enema mesalazine or sulfasalazine). ^ severe attack (IV nutri or enteral utrition with elemental diet correction of fluid & electrolyte disturbances bld transfusion, *albumins *prednisolone 100mg.I.V *mesalazine or sulfasalazine orally in septic toxic situations with special regard to anerobes. ^ Therapy during remission (*mesalazine 1gm or sulfasalazine 2g, fiber rich diet, agents to control diarrhea). Surgery: - ^ resection of intestine, ^ transplanation, artificial anastomosis, artificial prosthesis.

CHRONS DISE: - Non specific inflammatory disease that affect distal ileum & colon, but can occur in any part of GIT. Etio: - unkown, Genetic predisposition, dietary + infection. Patho: - ^cryptits + crypto abcess, ^ granuloma formation, ^ transmural spread of inflamm, ^ bowel wall thick, ^ extensive fibrosis. Clininc: - ^terminal ileum + ascending colon 50%. ^ terminal ileum30%. ^ colon done 25%. Diag: - ^Diatal part- rectomonoscopy, Proximal part- fibrocolonoscopy + biopsy, Duodenum- laparascopy. Morpho: - Chronsà inflamm involves all layers of colon wall (ulcer in all layers). Non specific ulcerà only on epithelium, ulcer localized. Endoscopy: - Hyperemia+ ulcer, hyperemia + ulcer + sclerosis, deformation with polyps. Xray- irigoscopy deformation of ileum and polyp. Symptoms: - pain (constant) but ↑ before and after defication, diarrhea + bld, mucus. D.D: -^ Non specific ulcerative colitis, ^carcinoma of ileum, ischemic causes. Rx: - * Prednisolone 1wk/ 60m, * Melsalazin 2wk/40mg (3-4t | 0.5g/d| 3wk 30mg- 4th wk 25mg), * Sulfasalazin 5wk 20mg, 6th wk 15mg, 7wk 10 mg à if not effective give Azithroprin 2-3mg/d/kg not more tha 3months, * Metronidazole 500-1000mg/d not > 4wk. Remission: -Same dose of melasazin & sulfasalazin. Surgery: - ^ resection of intestine, ^ transplanation, artificial anastomosis.

Prophy: - effective Rx in 10%, in 90% not effective, 15-25% of pt die within a year. Surgery effective in 40-50% of pt.

 


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