Algorithm A

Treatment of paroxysmal atrial fibrillation

No comprise of circulation Compromise of circulation

See algorithm A Cardioversion 400 J

Cardioversion 800 J

Amiodarone 300 mg

Algorithm A

Onset of Paroxysmal atrial fibrillation

< 30 min before 3 hrs 3 hrs – 7 days 7 days – mths > 6 mths

1, 2, 3, 4, 5 2, 3, 4, 5 3, 4, 5 4, 5 5

RX: - *Sublingual Propafenone 450-600mg, Ibutilid. *Sublingualual β blockers – Propanolol, Atenolol, Meteprolol. *IV procainamide 1- 2mg, Propafenone 140mg, Ibutilid 10-15mg, Nibetam 1-4mg. *Quinidine 200mg, (first day give 1000mg ↑ 200mg 2t/d, max 2g), Amiodarone 1200 – 1600mg 1d max dose10g (5-7days). *Electrical defibrillation (cardioversion) - Pharmaco therapy is not effective due to remodelaltion of myocardium. *Prevention therapy pf paroxysmal A Fib: - Class I: Chinidine, Eathacizine, etc. Effect by 60%, Class II: β blockers, effect before 50 – 60%, Class III: Sotalol, amiodarone. Effect by 80 – 90%, Class IV: Verapamil, diltiazem, effect by 40 – 50%.

22. Shock: - Def: - is Acute circulatory failure with inadequate or inappropriate distributed tissue perfusion resulting in generalized cellular hypoxia. Patho: - (i) sympatho adrenal system-HyptoTà stimulation of barorecptors n chemorecptors à ↑ symp nervous activityà release of CAs à vasocontriction with ↑ myocardila contractility, ↑ heart rate. In renal cortex ↓ blood perfusion-à renin- angiotensin -aldosterone system actvationà Na n water retention.-à restore the circul vol. (ii) Neuroendocrine-à release of pituitary hormones(ACTH, vasopressin n endogenous opioid peptides), release of cortisol(fliud retention n antagonizes insulin), release of glucagons. (iii) release of pro& antinflam. mediators. Classifi: - ^Traumatic shock - (i) pain shock-uncontrolled painà disorder in NS-à stop of tonus supply of vessels-à vasodilation.--à ↓ BP.Clinicalà In 90-95mmHg, compensatory mech. r working. At the level of 80mmHg can diagnose shock. BP, 80mmHG-serious ↓ functionn of organs. Can access by checking kidney function(urine production-1ml/1min).BP70-65mmHg-stop production of urine tells about stopped macrocirculation.After 70-65Hg 1st stage à 2nd stage begins(morpho. disorders in peripheral system). Rx: - If BP-80mmHg-stop pain by narcotics(morphine n phentanyl). If BP < 80mmHg p give sympathomimetics to induce vasoconstriction. (ii) traumatic shock associated with Hypovolemia (bleeding, dehydration)-à Hypovolemia (↓ vol of bld return to heart)à ↑ heart rate to provide normal heart output & ↑ periph resistance bcoz of symp system(noradrenaline). Rx: - (cant give nor adrenaline bcoz already vasoconstriction which may lead to microcirculation is order) Fluid, electrolytes infusion. If severe continous bleeding infuse cogulantfactors of bld or fresh bld containing coagulation factors. Absolute indicat. for conserved bld transfusion r hb< 50mg/L, untreatable anemia, chr.myeloleucosis, aplastic anemia. ^Cardiogenic shock -< 90(in nonHT), < 100(HT), thready pulse, pale skin, anuria/oliguria, marble skin covers on dorsal side of palm on expressed pale skin r visible blue veins > 4-5 its branches. Degrees of shock -1st 90-60, 2nd 60-40, 3rd < 40. Types of Card shock: -reflectory, arrhythmic, real, a reactive. Mechanism of C.shock: - appearance of strong anginal pain & /or ↓ stroke n minute vol of bld-à sympathetic adrenal activity thru barorecptors à vasoconstriction à ↓ BP n ↓ regional bld supply. Reason of ↓ minute volà syst dysfunction due to big sized foci of affected n also diastolic or both. Clinic: - tacy-or bradysystolia. Rx: - (i) vasopressor is not good bcos of already vasoconstriction..Drugs which can ↑ heart contractility or ↑ art bld supply to the tissue. *1st step-inotropic stimulation (β 1-adrenostimulators e.g.Dobutamine. β 1-adrenoreceptors r localized in the myopcardium n in coronary artà ↑ heart contractility & little dilation of coronary art. (ii) if tachysystolia -cardioversion, if bradysystolia - cardiostimulation. (iii) in Real C.shock-Myocardial disorders, ischemic part of myocardium cant participate in heart contraction n no effect of Dobutamine on that ischemic myocardial part. So give *phosphodiesterse inhibitor e.g.Amrirone. Direct indication of thrombolytics when shock starts from cardiac ischemia. Aorta-coronary shunting is best to ↑ blood supply in the intact part of myocardium à ↑ heart output. Control ballon tubation.-In aorta, ballon is connected with compressor synchronises with ECG, aortic valves close à ballon dilates n occludes the way à bld moves to up & to coronary art. ^Toxico-infecshock: - oxins in the bld, intra bacterial & intracellular factors-à dilation of vesselsà DIC synd. Toxico-infectious shock developed ^ in the beginning with hyperergic reaction. ^ crisis in pt with pneumonia without A/B therapy so immunologic answers reaching at critical level n ↑ bact no.it has 2 outcomes-recovery n death from crisis. Clinic: - pyrexia, rigorsor hypothermia, nausea, vomit, vasodilation, warmperiph, ↑ puls, cutaneous vasoconstriction. Sign: - jaundice, bleeding due to coagulopathy, rash n minigism. Rx: - * Dobutamine for good heart contractility, *cortcosteroids for inflammatory reaction. *Heparin or other anticoagulant with direct fast effect. ^Anaphylacticshock: - profound vasodilatation(warm peripheries, low BP), erythema, urticaria, angio-edema, pallor, cyanosis, bronchospasm, rhinitis, edema of face, pharynx, larynx, pulm edema, hypovolemia due to capillary leak, nausea vomit, abd cramps, diarrhea.

23. Iron def anaemia: - Anaemia charct ↓ RBC & or Hb in 1vol of blood, anaemia is a synd not disease. Etio: - ^ Inadequate stores provided at birth, ^ diminished intake of fe, ^ ↑ demand of fe during pubertal period pregnancy lactation, ^ ↓ absorption of fe g pathology of GIT, ^ Apparent or occult bleeding eg ulcers, ^ disorder of fe transport eg hereditary atranferinemia, ^ not enough used of fe from its depo eg infection, ^ disorder of deposition of fe eg hepatitis. Patho: - In normal fe in the body, ^ heme feà Hb 70%, myoglobin 5-10%, fe containing enzymes1%, ^ non hem fe feritin+hemosederin30%, transferin and other enzymes. Fe stores in liver, B.marrow & spleenà.due to ↓ fe in the body char’c by ↓ or complete exhaustion of fe reserve(disappearance of hemosederins in liver & spleen ↓ sideroblast & siderocyte in bone marrow)in the bld ↓ fe serum level and ↓ saturation of transferine with feà not enough entrance of fe into mitochondria of erthrokarocytesà ↓ synthesis of hem & globin & ↓ activity of fe dependent enzyme eg catalyseà ↑ sensitivity of RBC to hemolytic oxydatives.so ↓ feà non effective ↑ haemopoesis & ↓ life of RBC. Clinic manife: - ^ anaemic syndrome(dyspnoea on excertion, dizziness, headache, palpitation, disturbances of mood, fatigue). ^ Sederopeniaà dirorder of skin, glossitis, dryness of the skin, trophic disorder of nails, hair, mucous of mouth and tongue, disorder of digestive system(esophageal varices, dysphagia enteritis and colitis). Diag: - ^ bld analy-(hypochromic, microcytic, ↓ CI, ↓ MCV, normogenerative anaemia, ↑ ESR in severe & moderate grades, anisocytic poikilocytic, Rt ↑). ^ Bioche anal: - ↓ serum fe level < 30µg/dl, ↑ total fe binding capacity, ↓ saturation of transferine with fe < 20%, ↓ serum feritin. ^ B.marrow specimen in case of necessity-erythroid hyperplasia, normoblast have scanty fergmented cytoplasm with poor hemoglobolisation, absence of hemoserderin. Rx: - (i) excluding etiological factor, (ii) dietary management, (iii) fe medication eg *sorbifer 100g 1tab twice a day, *actiferin, best drug is maltofer minimal course 3-6months decreased dose 1 and half for 1-2yrs. D.D: - blood analysis

24. Aplastic anaemia & partial aplasia: - Def: - The hypoproliferative A associated with B marrow damage charct by marked reduction or absence of erythroid granulocytic & megakaryocytic cells in B marrow with resultant pancytopenia. Aplastic A is: - (i)Accquired A: - 2 forms- ^myelotoxic (radiation cytostatics, insecticides, organic solvents & DDT), ^ immune (damage of B marrow heamopoeisis by drugs (eg levimycitin, sulphanilamines, uroseptics & gold salts). Patho: - ↓ polypotent stem cells in B marrow (under influence of above mention factors) à incomplete haemopoesis à pancytopenia. Clinic: - ac. onset & fast progressive, severe anaemic synd, bleeding from nose, gums, vagina, GIT, early menstrual flow, thrombocytopenia, rectal haemorrhage, severe neutropenia. Physical ex: - cutaneous & conjuntival pallor & haemorrhages (petechia, ecchymosis, gum bleeding). Lab diag: - ↓ RBC, normochromic, normocytic, ↓ Rt, thrombocytopenia & leucopenia. same B marrow diag. signs. (ii) congenitial: - fanconi, dyskeratosis, shwachma synd. (fanconi à it is autosomal recessive type disorder in DNA synthesis, Clinic pic: - develops early in pts life, anaemia, different degrees of haemorrahagic diathesis due to thrombocytopenia, 2^nd dary infect. bc of granulocytopenia, different skeletal defects à microcephalia, absence of ulnar bone, short height, changes in all sysyem (eg hrt & kidney failure, hypogonadism, DM, aplastic Lab diag: - hyporegenerative↓ Rt, thrombocytopenia, granulocytopenia, ↑ lymphoctes, B marrow aspiration fatty tissue > 50%(in N< 50%) & few haematopoetic cells, marked ↓ in erythroid, megakarocytes, granulocytes. Diag: - is based on

presence of somatic disorders with pancytopenia. Rx: - transfusion of RBC, thrombocytes & prophylactic infusion of desferal, in 2^nd dary immunization GCC & cyclosporins on the back ground of haemo transfusion & in some cases spleenoectomy. Radical Rx transplantation of B marrow.

D.D: - with vit b12 & folic acid def, mylodysplastic synd, acute leukemia (in B marrow they r rich in cellular elements) & metastasis of cancer in B marrow(we can find cancer cells). Rx: - ^exclude etiological factors, ^replacement therapy(transfusion of RBC and thrombo concentrate). ^prophylaxis & Rx of infect. & fungal complication (A/B, & antifungal (eg diflucan, nystatin), ^Rx for idiopathic aplastic Aà antilymphocytic globulin, GCC, cyclosporins & haemopoetic growth factors (eg erythropoietin, transplantation of B marrow).

25. Megaloblastic anaemia: - Def: - MA is disorder cause by impaired synthesis of DNA of myeloid cells(erythroid granulocytic megakarcytic) RBC r effected most severely. large cells of embronial haemopoesis, megablast r found in B marrow they r larger & different in structure of nuclei then of RBC. Etio: - MA due to vit b12 & or folic acid à ^ elementary (veg diet). ^ abn in vit b12 utilisation at level gastric casal factor produce by parietal cells. casal factor+ vit b12 complex can be absorb in upper part of intestine and in the bld vit b12+transport protein(transcobalin)can be send to different tissue (a) gastric pathology (operation, inflamm., absence of casal factor). (b) upper intestinal pathology(malabsorption synd, inflamm.) (c) def of transport protein due to liver patho. ^ ↑ demand of B12 (lactation, preg, growing age). ^ parasites in intestine (eg tapeworm which consumpts all b12 for its proliferation). ^ tumour of any localization needs B12 for their proliferation. Patho: - B12 forms 2 co-enzymes, ^methycobalamine à function is to transform uridine monophosphate in RNA into thiamin MP. In def of B12è ↓ activity of MCà DNA ia abn in cells named as megaloblast à megalocytes. ^Dezoxyadenozyl cobalamine à it participates in lipid metabolism(DC transferes methylmalonic acid into succinic acid). In def of DCà ↓ concentration of succinic acid but methymalonic acid is toxic for peripheral nervesà it inhibits myeline formationà cant transmit iipulseà myolosis(↓ sensitivity function of peripheral nerves). Clini pic: - ^anaemic synd, ^funicular mylosis (it’s a neuro. disorder will be parasthesia). ^changes in GIT(gastritis autoimmune, changes in tongue ie hunter glossitis violet colour shinny pattern atrophy of papilla). ^hepatosplenomegaly à pallor or jaundice bc of hemolytic components. Diag: - ^ bld: - microcytic, hyperchromic, megalocytes, isocytosis, macrocytosis, piokilocytosis, jolly bodies, cabot rings in megaloblast & cytes. Rt↓ may be thrombocytopenia & leucopenia, hemolytic jaundice (leucopenia+↓ phagocytosis leads to 2ndary infection). ^ In B marrowà megaloblastic type of haemopoesis. ^ serum cobolamine, follate levels r low. ^ methylmalonic aciduria & ↑ serum methylmalonic acid. Rx: - para - enteral *cyancobalamine 1000µg/daily for 2 wks minimumà then weekly until haemotocrit becomes Nà then montly 500µg. D.D: - Anaemia with impaired synthesis of DNA(aplasticA & myelodysplastic synd. in B marrow high level cellular elements & megaloblastic haemoposis in megaloblastic A & +ve effect of vit b12 & or folic acid Rx.

26. Chronic leukemia’s: - |A| Chr. myeloid leukemia: - Def: - ia a malignant myeloproliferative disorders of primitive hemopoetic stem cell with specific chrosomal aberration(Ph chromosome). Etiopatho: - Ionizing radiation ↑ incidence of CML. Patho: - (cytogenetic & molecular background) all leukemia cells in pt with CML contain a specific cytogenetic marker (PH chromosome) it represents a balanced translocation bw long arm of chromosomes 9 & 22.T(9: 22).Thus PH chromosomes appears somewhat shorter than couterpart & 9q+somewhat longer than N9.this translocation resulting in breakpoint cluster region/abelson proto-oncogene chimeric gene that expresses an abn fusiob protein altered tyrosin kinase activity. The PH chromosome is represent in erythroid, neutrophilic, basophilic, monocytic, megakaryocytic & suggesting the cell of origin may be a pleuripotential stem cell. Charcterised: - by excessive ↑ of quantity of myeloid precussors cells(with envolvment of myeloid, erthroid, megakaryocytic lines)myeloid hyperplasia of spleen, liver, lymphnodes & other organs. Clinic feat + diag: - ^ synd. of intoxication à weakness, anorexia, weight loss, subfebrile temp. ^ enlargement of liver, spleen & lym.nodes. ^ pain in bones due to hyperplasia of myeloid tissue. ^ Anaemic synd. ^ heamorrhagical synd. 3 phases: - ^chronic - (weakness, fatigue, moderate weight loss, sweating. anaemia, fever, haemorrhage, sensation of masss in left upper abd quadrant, lymphadenopathy.Lab testà ↑ WBC, ↑ esonophil & basophil, ↓ ery Hb, thrombocytopenia the platelet counts is N or ↑, neutrophil alkaline phospatase activity is low or zero, B marrow is hypercellular(70-90%)with a myeloid to erythroid ratio10: 1 to 30: 1 megakarcytes may be ↑ in no less than 5%blast & promyelocytes in bone marrow or bld, PH chromosome is present in abt 90-95%of pts). ^Accelerated/progressive- (signs of progression of dis WBC count > 25× 10/l with myelocytes, promyelocytes & blast 5-30% in bone marrow, blast in blood > 15%, thrombocytopenia< 100× 10/l with bleeding, severe anaemia, ↑ spleenomegaly, ↑ fever, infect.). ^Blastic phase(blast crisis)- polyclonic stage may be blastic crisis whn> 30% blast in bone marrow, 20%blast in bld or > 20%, myeloid crisis in 25% lymphoid crisis in 25%. Rx: - 2 object. ^ control haematological manifestation of the dis. ^ prevention the progression of dis to blastic stage & prolong survivalè *Interferon α (roferon, reafiron enteron)r used in intial stageè *chemotherapy hydroxyurea2-3g/d best drug for CML is *busulfan(myeleran, myelosen)r standard Rx used to stabilized ptsè low doses of *cytarabine combined with interferonα è symptomatic Rx. ^Rx options for acclerated phase à *bone marrow transplantation, α interferon high dose of *cytarabine, hydroxyurea, busulfan, supporitive transfusion therapy, symptomatic Rx. Rx options for blastic phaseà combined *chemotherapy-5azacitidine & mitoxantron, antracyclin & cytosineà vincristin & predinisolon, allogenic bone marrow transplantation, hydroxyurea, high doses of cytarabine. Rx for meningeal CML or neural leukemia: - (cranial irradiation, intratecal cytarabine) symptomatic Rx.

|B| Chr. lymphocytic leukemia- Def: - Is a malignant clonal lympho proleferative disorder of younger cell precussor of lymphopoiesis with primary defeat of b.marrow. Etio & patho: - 90%pts r over 50yrs ♂ & ♀ ratio is 2: 1, pts dis is of B-cell lineakage & have T-cell linkeage in 2%. Etio fact: -^ hereditary factors, ^ genetic abn, ^ viral theory viruses HTLV-1, HTLV-2, ^ radiation, ^ chemically mutagenic factors(after mutations of one cell precussors of lymphopoisis, monoclinic growth of tumor begin in bone marrow with differentiated & maturation of young malignant cell to mature lymphocyte, this dis id charct by lymphoid proliferation in bone marrow, bl, & lymphoid tissue and suprresion of N naemopoiesis the cause of cytopenia may be auto immune. Classifi: - RAI staging system. ^ stage 0à absolute lymphocytosis w/o adenopathy hepatosplenomegaly, anaemia, thrombocytopenia. ^ stage1à absolute lymphocytosis with lymphoadenopathy w/o heaptosplenopathy, anaemia & thrombocytopenia. ^ stage2à absolute lymphocytosis with either with hepato or splenomegaly with or w/o lymphoadenopathy. ^ stage3à absolute lymphocytosis & anaemia (Hb< 11g/dl)with or w/o lymphoadenopathy hepatosplenomegaly. ^ stage4à absolute lymphocytosis & heapatoaplenomegaly, anaemia. Clinic feat: - ^ intoxicative synd (weakness, sweating, fatigue, sub-febrile t, Weight loss). ^ lymphoadenopathy can occur nodes r painless don’t fused with skin, elastic mobile w/o

Hepatosplenomegaly in intial stage. ^ recurrent infection. ^ anaemia due to auto-immune process. ^ bleeding due to thrombocytopenia. ^ hepatosplenomegaly. ^ may be cancer. Lab sign: - ^ intial stage in heamogram(moderate monoclonal leucocytosis, lymphocytosis, specific botkin gumbercht shadows). ^ Progressive stageè ↑ of lymphocytic leucocytosis(50*10/l-800-900*10/l). ^ in blacric crisisè blast > 20-30%. Rx acc. to stage: - * stage 0 no Rx indicated. *stage 1 observation chemotherapy with oral alkylating agent 9 chlorambucil with or w/o GCC. *stage 2è oral alkylating agent with or w/oGCC +vincristrin+ prenisolone. ^ stage 3è alkylating agent +prenisolone+ fuldarabin combine chemotherapy & CVP or bone marrow transplantation or splenoectomy & irradiation of spleen. ^ stage4 à alkylating agent+ prenisolone+ fudarabin combine with chemotherapy & CVP, CHOP & bone marrow transplantation.

27. Hemorrhage diathesis: - Def: - is dis charact by tendency to bleeding & repeated haemorrhages. this is combine grp of bleeding dis according to their main sympt. Etiopatho: - ^ disorder of bld coagulation & anti coagulation system. ^ abn of platelet count(werlhoff dis, thrombocytopenic purpura or thrombocytopathy). ^ vascular dis (eg haemorrhagic vasculitis). ^ combine of list factors hereditary or acquired diathesis. Types of bleeding: - ^ haemotomic (haemotomas of skin & various organs, haemoarthorosis bleeding from GIT lungs uterus) due to coagulopathy with ↑ time of coagulation (N 3-5 min). ^ spoty petechial (bruisis petechia, bleeding)due to path of thrombocyte with N time of coagulation & ↑ time of bleeding (thrombocytopathy, thrombocytopenia, thromboastheina). ^ vasculitic purpura due to vascular disorder. ^ angiomatosic. Classif: - (i) HD cause by disorder of bl coagulation(time of coagulation is ↑). (a) disorder of synthesis of thromboplastin (eg haemophilia A, B, C). (b) disorder of synthesis of thrombine (eg defic. of factor X). (c) disoreder of synthesis of fibrine (eg defect of factor XIII). (ii) HD cause by disorder of gigantic cells & thrombocytic system (a) autoimmune thrombocytic purpura, (b) thromboasthenia (eg disturbance of count or function). (iii) HD caused by vacular disorder associated with bleeding (eg H vasculitis, osler webber rendu dis, scurvy dis, H fever). (iv) Hd caused by combine disorder (eg von-willebrand dis (angiohaemophilia). Clini manife: - for all haemophilia. (i) bleeding tendency from 1^st month of life & more difficulty begin when child becomes physically active. (ii) bleeding episode can develop spontenously w/o trauma or provoking causes. (iii) repeated haemoarthrosis of knee elbows & other joints is common & can result in progressive destruction of joints. (iv) haemotomas often occurs in mus. & spft tissues. (v) several bleeding in retro peritoneum, bowel wall peptic ulcers & mesenteric bleeding can be dangerous for life. Diag: - ^werlhoff dis: - myelogram in b-marrow ↑ megakaryocytes, thrombocytopenia, ↑ bleeding time 15-20min & more but time of coagulation is N, antithrombocytic Ab in bl & spleen↑. ^Haemophelia: - ^cl manifestation. ^quantitative determination of factor VIII concentration. ^correction test, plasma, which has not one of anti-hemophilic factors VIII.IX, or XI is added into testing bl. if there is no correction in one of test tube so there is no corresponding factor in testing bl. Medical tacti: - ^ factor VIII is changeable, ^ medication containing factorVIII eg cryprecipitat, ^ direction bl transfusion 3t/24hrs(1/2 period of factorVIII is 6-8hrs), ^ symptomatic therapy & Rx: - consequences of haemorrhages. Rx werlhoff’s dis: - *GCC eg predinisolone 1-1.5mg/kg in tabs of body masss, * to stop bleeding eg anthraxzon, dizizon, *spleenectomy, *cystostatic drugs eg cyclophosphan, imuran, *symptomactic therapy of bleeding & post haemorrhagic anaemia.

28. Ac & chr GN: - Acute GN: - Def: - is an ac. diffused damage of K developing on the immune based & primary localized in glomeruli, most arises after different infect. (eg streptococcal infect. AGN are primary & 2^nd dary. Etio: - ac. Infect. (eg acute tonsilitsà nephretogenic strain of streptoc, viral infect. eg hep B, Idiopathic). Risk factors: - cooling, humidity, ↓ immunity, vaccination. Patho: - Immune path - streptococcal infect. or other infect.à anti strep Ab productionà immune complex formation(strepAg+Ab+compliment)à immune complex fixation on theGBM à immune inflamm. à cl manif.. Clini pict: - ^ Urinary synd - proteinurea, leucocytiurea, cylinder(hyaline it indicates inflam. of tubules, wax it indicates abt more deep inflamm. more specific for chr. Process. ^ Hypertensive synd. - Na & water retension. 3 mecha. (activation renin angiotension aldosterone system, sympathetic adrenal system, ↓ drepressor f of K. ^ edema synd.- ↓ GFR, ↑ Na reabsorption à water retension ↑ total bili circulating volà activation of 2^nd dary hyperaldosteronismà ↑ sensitivity of distal parts of nephronà again water retensionà ↑ vessel preameability à edema. Diag: - ^ urine analy - proteinurea, hematurea (93%micro & 7%macro), (100%cases) rarely leucocytiurea & cylinderurea. ^ nechiprorenko testà in1ml urine RBC 1000, WBC 2000-4000, cast20 above figures r N. ^ Biochem: - ac. phase indicators of inflame., ↑ fibrinogen, α 2globulin, c-reative protein, ↑ ESR, moderate anaemia (due to hypervolemia)no changes in creatinine level in urine. ^ Immunological testà immune reaction(presence of circulat. immune complex, ↑ anti streptolysin O, ↓ Y-lymphocytes & ↑ B lymphocytes. ^ reberg testà in intial phase GFR ↓ due to ↑ tubular reabsorption. ^ X-ray- ac. HT ↑ hrt borders(N in recovery). ^ ECGà LV hypertrophy(N in recovery)T-ve in metabolicdisorders. ^ biopsy. Diag: - ac. onset, proteinurea not< 2g/24hrs, micro & very seldom macro hematurea, transient HT, edema, absence chr systemic dis & previous renal pathology. Complic: - ^ hrt failure3%. ^ encephalopathy, eclampsia, epilepsy with loss of consiousnes. ^ sometimes ac. vision loss due to edema of optic disc. ^ ac. RF chart by anurea & azotemia. Rx: - ^strong bed regimen 2-4wks, hospital pt 4-8wks till main sympt. Disappears. ^dietà limitation of fluid & saltà first 2d hungry period & water according to diauresisà 2-3d diet rich in K+, diuresis+300-500ml of water from previous 24hrsà 4-5days protein 60-g/24hrsdiet regimen till Bp N. ^à A/B(if etioà previous infect. penicillin & semi penicillin)à Diuretics for HT & edema more preferable central acting diuretics eg *clophylinium, dopigidium, hemiton, à Immunesuppresive(in nephritic variant *prednisone 60-120mg/d gradually ↓ dose & is given for 4-8wksà if edema with marked ↓ diuresis we give heparin

20000-30000 units/day for 4-6wks heparin improves micro-circulation anti inflammatory effect & moderate immuno suppressive effect. if only proteinurea for long time give NSAIDs eg *indometacin.

Chronic GN- Def: - is chr diffuse K dis develops on immune based there is primary effection of glomerulià envolment of other structure of K. duration of chr GN is progressive, nephrosclerosis & RF. chr GN primary or 2^nd dary(also knw as nephropathy). Patho: - formation of anti strep Ab fixes on GBMà react with strepAgà damage of GBMà new formation of Ab to affected GBMà fixation immune complex (autoAb+autoAg+compliment) à inflamm. & further damage of GBM(deep damage)then clini manifest.. Etio: - untreated GN, chr Gn as complication of ac. dis (eg bacterial endocarditis, sys vasculitis, primary chr GN without preliminary factors). Clinic: - ^urinary, ^HT, ^edema synd.. clini vari: - ^ latent GN in 44% may be isolated urinary synd.(moderate proteinurea, slight leucocytourea and hematurea). HT latent form progress very slowly exacerbation after 15yrs prognosis is 10yrs. ^ hematuremic 6% morp var diffuse proliferation of mesangium (GBM not changed) constant sign hematurea in glomeruli IgA deposits(berger’s dis)chr. RF develops very late. ^ hypertonic 20%predominantly HT synd. urine changes not marked proteinurea not more than 1g/24hrs, slight hematurea, changes in CVS depends upon stage & duration of HT, morp var mesangio proliferative & seldom membrano proliferative duration quite like in latent form. In hypertonic form always chr. RF. ^ nephritic 22% severe edema with massive proteinurea > than 3, 5g/24hrs, hypoalbumiemia, hyperα 2globulinemia, hypercholestrolemia, hypertriglyceridemia.morp var membranous GN or mesangio proliferative. Diag: - ^ macrohematurea more constant cylindurea in exacerbation ↑ ESR, hyperα 2globulinemia, ↑ fibronigen, C-reactive protein. ^ Biochem anal: - hypercholesterolemia, ↑ triglycerides, ↓ total proteins, ↑ creatinine, ↑ urea, ↑ nitrites, GFR depends upon stage 1^st stage of RF & next stage ↓. ^ X-ray - LV hyper. & signs of arthresclerosis, CT, ECG, optic fundus exam. can be edema of optic nerve diff changes in vessels, biopsy of K(biopsy as diag. & control method esp whn we used Gcc). Morp classify: - ^ mesangioà immunue complex deposit on mesangium 3 types mesangio capillary, mesangio membranous & mesangial proliferative. ^ membrano proliferativeà difuse proliferation of mesangial cells & infiltration of glomeruli by macrophages ↑ mesangial matrix thickening & reduplication of GBM. ^ minimal changesà insignificant expansion of mesangium may be focal thickening of GBM capillaries. ^ membranous GNà diffuse thickening of capillaries due to changes in GBM. ^ fibroblasticà sclerosis of capillaries of glomerular loops, thicking & sclerosis of capsule. ^ membranous nephropathy(non proliferative)diffuse thicking of GBM with sub epithelial projections or spikes around immune deposits. ^ rapidly progressive GNà majority of glumeruli contains areas of fibronoid necrosis & crescent in bowman’s space composed of proliferating periteal epithelial cells infiltrating macrophages & fibrin. ^ diffuse proliferative GN/ac. GNà diffuse ↑ incellularity of tufts of most glomeruli due to infiltration by neutrophils & monocytes & proliferation of glomerular endothelial & mesangial cells.

29. Chronic pyelonephritis: - Def: - Its infective-inflammatory affection of mucous membrane of UT calyces, pelvis & interstitial tissue of kidney(K). Etio: - infect. (bact or viral) eg.E.coli(50-60%), proteus vulgaris, cocci (streptococcus-hematogenic, nephretogenic, staphylococcus) etc. Patho: - Enterance of infection into mucosa of urinary tract(UT)system or interstitium thru hematogenous, lymphogenous or spreading from adjacent organs involved in inflammatory process, ascending pathway, when there is urodynamic disorder. Vesico-ureteral refluxà 1^st ly infection starts from mucosa of calyces-pelvic systemà infect. into interstitium & tubules. Favour. conditi: - for producing inflame. or causing secondary PN - ^congenital anomalies (eg nephroptosis, dystopia), ^urodynamic disorder (eg vesico-ureter reflux), ^reinfection, ^Kidney stones, ^↓ immunity. Chr. PN: - it occurs due to inadequate Rx of ac. Process. clnic.pic: - is not so expressed. Difficut to diagnose esp in latent phase. Morpholo: - K affection is irregular (ie.why morph changes r focal.Focus of inflame.à WBC, lymphocytes, monocytes infiltration.-à scar conn tissue formationà Progressive scarring involving tubulesà dystrophy of distal tubules located in medullaà then atrophic changes.-à wrinking of K. Classifi: - ^ primary n seconadary, ^ acc to cl picture. Clini pic: - ^ intoxication synd- ↑ temp, chills, headache, weakness. ^ specialrenalsynd- dysuria (pain in beginning of urination-urethritis, pain during whole urination-inflam. of whole urinary tract., dull pain-affection of pelvis), lumbar pain. (i)latent: - (20% pts)minimal sympt., pt doesn’t know abt his dis, moderate urine analysis changes after flu or during prophylactic investigation. Dis gradually progresses, dull inflammatory process with gradual development of sclerosis. During provocation (flu, preg etc)à activisation of process. (ii)Recidive: - more bright cl sympt.- periodic intoxication sympt. i.e.periodic ↑ in {temp, chills, dysuria(frequent& painful urination)n nicturia}, chararectristic lumbar pain(uni- or bilateral).pain is due to distension of capsule due to edema., stasis of urine. (iii)Progressive: - continousprogressive inflame. process. Constant ↑ temp, chills, severe sweating, temp-hectic character, always dysuria n nicturia, lumbar pain constant.Macrohematuria5-10% bcos of involvement of fronical parts of calcyces into inflammatory processà affection of nearby veins. Irrespect of cl. picture, chr. PNà sclerotic changes in Ki.e.why HT. In beginning à slight ↑ BP(15-25%), later high level of BP(70%). Diag: - ^ urine analy -proteinuria not> 1g/day, leucocyturia, hematuria(specific-due to injury by stones in pelvis, nonspecific-necrosis of papilla), ^ Microb. urine analy. - to reveal microbe, bacteriuria> 100000 microbes/ml daily. ^ nichoparenky test-WBC, RBC in uine. ^ Zimnitsky test-↓ specific gravity 1012-1014(due to involvement of medullar part of K where occurs concentration of urine). ^ USI-to reveal localistation of K stones, adenoma of prostate gland if present. ^ cystography-to reveal vesico-ureter reflux. ^ X-ray & excretory urography - asymmetry of excretion of contrast by K(1^st min) (bcos of retention of contrast in dilated calyces), ureter dilated. ^ Radionuclear renography-isotope iv administration à check K filtration rate. In progression of disà ↓ size of K, irregular contours, irregular calyces, irregular calyx-pelvic complex, asymmetry of kidneys. D.D: - (i) Urinary tract infect. - PN can b with affection of lower parts of UT. *Cystitis-common in ♀.freq. urination, pain during urination, impairative poses & pain in suprapubic area. *Ac. anterior urethritis-common in males. burning pain in beginning of urination. & also discharges from urinary tract.in chr urethritis -sympt. r minimal. *ac. prostitis n total urethritis-↑ painful n difficult urination. In chr. Prostitis -freq. urination, nicturia, impairative poses, sex funct disorder. (ii) GN-its always bilateral diffuse, on 1^st place –massive proteiburia (nephrotic synd)in PN-leucocyturia on 1^st place. (iii) Synd. of art HT -young age, in anamnesis cystitis, K stones. X-ray-deformation of calyx-pelvic complex. (iv) Isolated leucocyturia-excluding TB of K. (v) Lumbar pain-osteochondrosis. (vi) Focal affection of K-abscess, cyst, tumour of K. Diag: - ^ Recidives of infect dis of urinary tract, ^ metabolic disorders, ^ presence of other risk factors of PN. Rx: - ^ restoration of urodynamics ^ Uroseptics/antibact, ^ immuno modulation in case of long term dis. In primary PN- *uroseptics /antibact -better 2drugs together for 7 -*Levomycetin, Sulphanylamides-long acting drugs (against Gram+ve & -ve)1-2gm/d for 7-10d.*Nitrofuran eg.Furadonin, Furagin, solafur-0.4g/d for 6-8d.*Nalidic acid eg.Negran, Nevigramon 0.5-1gm for 3t. Chinolones. *Pipemidic acid (urotractin / palin)-1cap 2t/d for 7d. *5NOC -nitrofuran+oxychinolones-0.4g. * Physiol solution with diurtics(Lasix-20-40mg) to drain kidney from bacterias.Diet-normal diet. Art.HT -diuetics, β -blockers etc.*Herbal uroseptics-eg Cranberry.

30. Chr. renal failure(CRF). Def: - is a functional diagnosis charct by a progressive and generally irreversible decline in GFR. Etio: - ^dis with primary affection of glomeruls (eg GN), ^with primary affection of tubules & interstitium (eg chr PN, interstial nephritis), ^dis of urinary system (eg urine stone dis, hydronephrosis, neoplasm of urinary system), ^defects of renal vesels (eg stenosis of renal artery, HT), ^diffuse conn tissue dis, ^metabolic dis (eg DM, amyliodosis, gout, disorder of ca metabolism), ^congenitial renal dis (eg polycystosis, hypoblasia of K, pseudo gout). Patho: - (i) by products, nitrogen slag(urea, creatinine, uric acid)delay in an organism & they cant be eliminated by other way, delaying of C is indicator of CRF degree. (ii) disorder of water electrolyte balance è on early stage con f of K is changing, residual nephrons must eliminate much more soluble substances/1 min. for that they need to ↑ urination volà developing of polyurea & isosthenureia à hypokalemia. (iii) disorder of acid base balanceà acidosis due to losing of bicarbonates & ↑ of tubular secretion of hydrogen ions & organic acids. (iv) changing of phosphor ca metabolism hypocalemia, hyperphosphademia. (v) production erythropoetine is defectedà anaemia. (vi) renin last to be producingà HT & retension of sodium. Classifi: - 3 stages based on GFR & ↑ of bl creatinine rate (i) latent stageà ↑ bl creatinine by 0, 2-0, 25mmol/l GFR declines 20-50 %. (ii) azotemic stageà ↑ bl creatinine 0, 7mmol/l GFR declines by 5-20%. (iii) terminal stageà ↑ bl creatinine rate more than 0, 7mmol/l GFR declines less 5% from norm. Clini manife: - ^electrolyte disorderà hyperkalemia, sodium retension, hypocalemia, hyperphosphatemia, ^CVS abnà accelerated atherosclerosis, HT, pericarditis, myocardial dysfunct. ^hematological abnà anaemia erytropoetin def & fe def, leucocyte dysfun., infect, haemorrhagic diathesis deftive in platelet function, ^GIT disorderà anorexia, nausea, vomiting, GI bleeding & disorder of taste, ^Renal osteodystrophyà osteomalacia, ostetis fibrosa, osteosclerosis, osteoporosis. ^neurological abnà insomnia, fatigue, peripheral neuropathy. ^myopathy esp of proximal muscles. ^ endrocrine and metabolic disordersà glucose intolerance, insulin resistance, insulin degradation, hypoglycemia (xi)hyperuricemia(x)pruritus soft tissue calcification, uremic frost. Treatmentè the therapeutic approaches to slow the progression of renal disease(i)treatment of HT(ii)prevention of hyperparathyroidism(iii)dietary(iv)treatment of hyperlipidaemia, (v)avoidance of toxic agents (vi)control of bl coagulation and electrolyte balance and glycemic control in diabetic pts. Rx for H Tà ACE inhibitors eg enalapril 5-10mg/day (ii)prevention of hyperparathyroidism à renal failure is usually associated with low serum ca level and high serum phosphate level(phosphate retension)and 2^nd dary hyperthyroidism. (iii)dietary à restriction of intake of protein and phosphate, protein intake upto 40g/day and milk intake shud be reduced. (iv)if hypocalcemia persist and the serum concentration is N vit D may be used this requires careful monitoring bc of risk of hypercalacaemia eg alphacalcidol 0, 25-0, 50µg/day (v)for electrolyte and fluid balance recommended intake of fluid in 2-3l/day sodium intake shud be restricted to 3-5g/day if necessary loop diuretics may be given (vi)acidosis shud be corrected if serum bicarbonate concentration is lower than 18mmol/l or below 15mmol/l egca carbonate 2-6g/day or sodium bicarbonate 1-6g/day (vii)hyperlipidaemia may speed progression of renal failure mech is unknw statins or gemfibrozil may be used but more experience used of antilipid drugs in uraemic pts(viii)for anaemia by ↓ production of erythropoietin in K and corrected by exogenous erythropoietin for pt receiving dialysis treatment administrating subcutaneously 50IU/kg weight 1-3 times a week and fe drugs orally or IV.

31. Chronic gastritis: - Def: - chr gastritis is a cl anatomical dis characterized by chr inflamm. of gastric mucosa, disorder of physiological regenerationà progressive atrophy of specialized glandular epithelium with motoric disorders & secretory & incretory f disorder. Etio: - ^Exogenic fac - diet, professional factors(acidic & alkaline stem etc), alcohol abuse, smoking, drugseg NSAID, K+ drugs, A/B, infection of gastric mucosa(h.pylori). ^Endogenic fac – metabolic & endrocrine disorders, tissue hypoxia(hrt insuff, portal HT, fe def, food allergy). Classifi: - ^acc to etiologyà endogenic & exogenic, ^acc to pathogenisisà type A(autoimmune) typeB(h.pylori) typeC(chemical), ^acc to morphologyà superficial, atrophic, gastric atrophy, gastric reconstruction (instestinal metaplasia, pylorisation of glands & atrophic hypertrophic gastritis), ^acc to localizati. à diffused or pangastritis, limited(entral, pyloroduodenal) fundal, ^acc to functional symptà with N or moderate ↑ secretory f, with secretory insuff(accholoridia), ^acc to clini course à phase (exacerbation, remission) stages (compensative, subcompensative & deompensative), ^acc to formsà rigid antrum gastritis, gigantic hypertrophic (menentri dis)polpous gastritis, erosive heamorrhagic. Clinic manif: - Symtoms r less specific dull pain in epigastrium, gastric dyspepsia in pangastritis pain or discomfort after food without irradiation to epigastrium in antral chr gastritis b late pain(2-3hrs after meal) intensive periodic rhythmic spastic pain. typical acidism (constant hrt burning & acidic eructation)in exacerbation Wt ↓, diffuse pain in epigastrium, white coated tongue surface. Lab diag & Instru: - ^endoscopic biopsy from diff parts, ^check gastric secretory f(it’s a 2 phasic method investigation with thin tube to check basal acidic production in 1^st hr & stimulated acidic production 2^nd by histamine or pantgastron in normal SAP 3 times ↑ after adequate irritation but in atrophic gastritis it is ↓), ^PH metry, ^for erosive gastritisà reaction gregorson method. Rx: - ^diet regimenà avoid spicy fatty food, alcohol, smoking, ^A/B(max10-14days Rx) in case of h.pylori eg *amoxicillin 1000mg/2 d, is bacteriocidic, * claritomycin 500mg/2d, is bacteriostatic or *metronidazole 400mg/2d, *omeprazole20mg /2d, *lanzoprazole 60mg/2d, *ranitidine 20mg/d & bismuth is for mucousal defence 0.5g 3-4times b4 meal. D.D: - organic cause of dyspepsia à gastic ulcer dis, gasro esophageal dis, hepato biliary system dis eg hep, GB dis with stones & f dis of biliary tract, alcohol ceasatio, endrocrinological dis eg DM, thyroid dis, electrolyte abn, drugs eg ca antagonist, hypolipidemic drugs, narcotic anaelgics, NSAID, fe drugs, potassium, glycoside, antidepression, A/B. Diag: - clini bld analysisà anaemia shud be checked, Biochemical analysis to check enzymes, proteins. Stool analysis to check bl, mucous, pus. Abd US, esophagogastroscopy, CT. Functional dyspepsia diagnostic criteria à (i)dyspeptic synd. with duration 12weeks in 1yr.(ii)we must exclude organic causes by fibro gastroscopy.

32. Pep. ulcer dis of stomach & duodeneum: - Def: - peptic ulcer dis is a chr heterogenic dis of gastro duodenal zone with diff variants of course charct by formation of local ulceral defects of gastric & or duodenal mucousal coverings(in period of active stage). Etio fac: - h pylori infect., genetic predispose., emotional stress, irregular nutrition, smoking, drugs, risk 1^st grp of bld, genetic def of α antitrypsin- *Primary ulcerative dis(h.pylori). *2^nd dary or symptomatic stress ulcers(burn, MI, sepsis, operation)drug induced ulcer, endrocrine ulcer, zollinger Alison syndrome, dyscirculative hypoxemic ulcer, toxic, ulcer in dis of liver, pancrease & bladd. Patho: - UD develops due to disturbance in bw factors of defence of gastric mucosal covering and prevalence agrresive factors. Defence factors include suff mucous formation, regeneration of epithelial cells, secretion of prostraglandins bicarbonates, suff micro-circulation, cytoprotection & immune defence. Factors of aggressionà acid, pepsin, h.pylori, duodenal reflux, disturbances of motor evacuative function, smoking. H pylori produces protein inhibitor of hcl, Forms ammonia by ureaseà ammonia ↑ gastrin secretionà ↑ acid produc., h pylori distructs muccin of gastric mucosa by mucunase protease phospholipase & penetrates into epithelial cells & distructs mucosal wall. this phenomenon is attaching effacing lesion causing production of IL 1 & ILH, Tumor necrosis factor, lysosomal enzymes which stimulate inflamm. process. h pylori produces 2 toxins vacculia & caga, toxin vac A ia vacculisic toxin(main ulcerogenic toxin) caga a stimulates production of IL hinducing degeneration of epithelial cells & inflammatory infiltration. h.pylori delays degeneration and process of epithelisation. Clinic pic: - ^ depending upon the location of peptic ulcer è 2 main synd. *painà epigastric pain connected with meals. Ulcer in cardial or fundal partà pain arises after 30-60min after meal(early pain)à pylori & antrum ulcer pain arises in 1, 5-2hrs after meals(late pain)à night & hungry pain in duodenal ulcer. pain reduces or disappears after vomiting or after taking antacids or spasmolytic *dyspeptic synd.à esophageal intestinal duodenal dyspepsia, hrt burn, eructation, nausea, vomiting & constipation. appetite is N or high. Diag: - ^ fibroesogastroduodonoscopy we define 4 stages of ulcer defectà ac.Stage fresh ulcer, 2^nd stage ↓ periulceral edema, 3^rd plain borders of ulcer, 4^th stage scar and then white. ^ X-ray: - of Stomach for discover of scar deformation, evacuating motor disturbances, degree of pyloro duodenal stenosis, for DD with infiltrative form/cancer. ^ intragastric PHmetry 24hrs. ^ diag. of H pylori infec.à non invasive method urease resp. test, PCR, serological test, immunological test. invasive methodà biopsy of mucosal wall(PCR, bacteriological method Culture of biopsy material. ^ Bld analysisà Hb level. ^ greigerson reaction in stool. Early late compli: - *penetration, * perforation, *bleeding, *stenosis, *malignancy. Rx: - medical regimen, diet & pharamacological therapyà ^drugs for↓ intra gastric PH eg *antacids, antisecretory drugs ^H2 blockers eg *ranitidine, roxatidine, ^PPI eg *omeprazole, lanzoprazole, pariet.^cytoprotective drugsà *de-nol, venter, bismuth. ^eradication therapy if H pylori infection.1^st line PPI *omeprazole20mg/2d, *clarithromycin 500mg/2d, *amoxicillin 1000mg 2d. 2^nd line therapy if absence of +ve effect *bismuth subsalicylate 120mg/4d.* tetracyclin 500mg/4d *Metronidazole 500mg/3d all above medication for 7d.

33. Chronic hepatitis: - Def: - is a chr. Diffuseor focal inflamm. A spectrum of disease between ac. Hepatitis & cirrhosis. Etio: - Infectious, paracytogenic, toxicoallergic, metabolic, α 1 antitripcine def, idiopathic autoimmue hepatitis. Patho: - liver injury largely caused by an immune mediator hoste reaction to the infection, depends on the etiology of the disease.- ^ toxic hepatoicytes are progressively affected (necrobisis), ^ Virus nature- presence of virus in the liver cells & cytopathic effect of virus kill the hepatocytes & inflmmates the conn. Tissue, ^ cholistatic hepatitis- obstruction & bile conjestion & poisoning. Classi: - ^ according to etio & pathogenesis- *chr.HBV / HCV / HDV/ HVF. *autoimmune hepatitis, * drug induced hepatitis, *cryptogenic hepatitis (unknown etio), * α 1 antitripcine def., * Willson & conovalouse disease, * primary sclerosing cholangitis, * Primary bilary cirrhosis. ^ Activity of necro inflamm. Process (minimum, slight marked, mod. Marked, severe marked). ^ According to stage- 0 stage fibrosis absent, 1^st slight marked periportal fibrosis, 2^nd moderate marked fibrosis with porta portal septs. 3^rd severe marked fibrosis with porta portal septs. 4^th liver cirrhosis- initial, sub compensated & decompenstaed. Clinic: - Dyspeptic sympt, jaundice, hepato + speenomegaly, dysfunction of liver, malaise, anorexia, ↓ appetite, bitter taste in mouth, nausea, fatigue, eructation, upp abd discomfort, heaviness or dull pain in right hypocondrium, signs of chr. Liver disease – spider navy, fluid retention. Lab: - ^ bio chem.bld Anal (*syndrome of injured cells-cytolasis-> ↑ ALT ↑ AST, * inflammatory synd - ↑ γ globulins ↑ ESR ↑ c-reac protein, * sund of cholicystatsis ↑ Dir.billirubin, ↑ alakaline phosphatase, ↑ cholestrol, ↑ bile acids, * syndrome of hepatocyte insuff↑ indirect BR, ↓ albumin, ↓ prothrombin, ↑ ammonia, ↑ phenol)(ii)viral markers. ^Bld anal- anemia, leucopenia, thrombocytopenia, ESR. ^ Fuctional test- hyperbilirubinemia, hyperproteinemia, hyper γ globulinemia + protein sedemenation test (activity of transaminases, aldolase, alkaline phosphatase, ↓ colinestorase, ↓ prothrombim index). Diag: - biopsy of liver, cholestatic synd (jaundice- sub hepatic), severe skin itching, hyperbilirubinemia, ↑ alkaline phosphatase, cholesterol, ESR, sub febrile Temp. D.D: - alcoholic liver disease, recrudescent acute viral hepatitis, primary bilary cirrhosis. Progn: - drug etiology (drug is eliminated), viral etiology (slow and resistant), autoimmune (good). Rx: - removal of cause of hepatitis, during excerbations liver should be spared & regeneration of liver cells, bed rest, diet, parentral use of vitamins, glucose. *autoimmune- corticosteroids (to suppress the inflamm reaction, it alters the immune response, long time survival. *Hep B virus- interferone α 5-10million IU, 3/wk 4-6months. *Hep C virus- interferone α 3million IU 3/wk for 12months. *corticosteroids are contraindiacatedà viral replication is enhanced. Complicat: - liver cirrhosis.

34. D.D of hepatomegaly & hepatosplenomegaly: - Causes hepatomegaly- (HG)à *CHF, *hepatitits, * steatosis of hepar, * echinococcus, *abscess, *cancer of hepar, *cyst in hepar. Causes hepatosplenomegaly - *cirrohsis, *bld dis(ac. & chr leukemia), *genetic dis, *hemachromatosis, *amyloidosis, *lymphogranulomatosis, *nonhodgkin’slymphoma.

Causes splenomegaly- *infarction of spleen, * abscess, *cyst, *sarcoidosis, *Gossheydis, *felter synd. (i)CHF à before ↑ hepar must b dyspnea n tachycardia after exerc. test, edema of legs if standing for long hrsà ↑ hepar. Cause of ↑ hepar in CHF is ↓ function of LV. Causes of CHF(3 groups)-à *CVS dis-MI, IHD, *extracardiac à anemia, chr bronchitis.cor pulmonale, *intoxication divided into 2 gps i.e.pharma (A/B)n non pharma(alcohol n smoking).Aus + invest: - systolic mumrmur in th apex n pathologic sympt. in ECG n echoCG. (ii)hepatitisà necrosis of hepatocytes, inflamm. & products of necrosis passes to bld. Clinical: - absent. D Dis is determined by biochemical n enzyme activity of bld n biopsy of hepar. (iii)Steatosis of heparà Clinic: - absent. All investigations r normal, only in USI ↑ hepar. cause of steatosis-pt who use200ml alcohol in a week(alcohol passes into hepatocytes with lipids n cholesterol. alcohol comes out from hepatocytes but lipids r left into them. final stage of steatosis is necrosis n cirrhosis. Diag: - biopsy of hepar. (iv)Echinococcus à (1to 2 pts in 100000 popln)Its asymptomatic. Diag: - CT, USI, MRI. but biopsy of liver is choice of method. Punction of liquor from cyst determines c.agent. (v)Abscess à Cl.signs: - intoxication signs-temp ↑ in morning n evening n ↓ temp durin day time, reveal pain in hepar & ↑ pain at palpation, inflamm. of other organs eg Gallbladder, pancreas. Bld anal: - signs of inflamm. -↑ WBC. Diag: - USI n X-ray. If deformation of borderline b/w abscess n hepatocytes, we will diagnostic laproscopy n dissection of this part(if big size is affected –lobectomy. (vi)Cancer of liver) -à cl.signs- ↑ hepar > 5cm from N size, intoxication sign, cachexia, all signs of portal HT(↑ liver, ↑ Bp in vena porta, ascites but spleen is N.this D.D b/w cirrhosis n cancer of hepar). Diag: - CT scan. biopsy is not done bcoz metastsis can happen.Rx: - radiotherapy, pharma therapy, resection of hepar, liver tranpantation from pig. Only hepatosplenomegalyà (i)liver cirrhosisà hepatosplenomegaly without ascites is dis of bld, hepatosplenomegaly with ascittesis liver cirrohsis. Diag: - of L.cirrohsis by USI, Ct scan, determine pressure v.porta to determinme portal HT(fibroesophagoscopy, rectomanoscopy) n biops of liver. (ii)leukemia à bld anal: -anemia, difference b/w acute n chronic leukemia(in ac.-blastocytes a lot, leucocytosis.in chr-lympholeucocytosis, WBC> 90%).Rx of leukemia- bonemarrow transplantation.n hematransfusion of WBC n platelets. (iii)Genetic dis (wilson’s dis caused by enzymedefect, ↑ Copper in bldà passes to brain, hepar, kidneys n eyes) we determine Cu in bld. (iv)hemachromatosisà itsgenetic dis defect of enzyme.this Fe must pass from bld to bone marrow in normal.if ↓ activity of this enzymeà ↑ Fe in the bld & ↓ Fe in bone mwrrowà Fe goes into all organs i.e.skin, hepar, kidneys, brain. Fe color same as color of skin. Diag: - Fe> 30mmol/l(in normal 12 -20mmol/l).Rx: -pharm drugs of gold, adsorbents of Fe. but Rx is not effective. Duratioin of life -5to 8 yrs. (v) Amyloidosis à its divided into primary n secondary. Clinic: - periodic high temp, nodules in skin, dysfunction of all organs n system eg.heart, kidneys, brain. Diag: - biopsy of nodules.Cause of death is renal failure. Causes of secondary.Amyloidosisà myeloma, plasmacytoma, osteomyelitis, TB, chr. dis of lung seg chr bronchitis n bronchoectasis. Senile Amyloidosis in pts > 60yrs.In secondary A, amyloid passes into 2 organs hepar, kidney -à deformation of hepar ↑ pressure in v.porta à ↑ liver.cause of death is chr renal failure.Diag: - Biopsy of liver. Classifi: - of A-AL(amyloid light), genetic primary A are AF(amyloid family) n AA(primary amyloidosis), AS(amyloid senile), AH(Amyloid hemodialysis).For prevention of quick death—give crizanol. (V) Lymphogranulomatosis à ↑ l.nodes.Stenberg cells r revealed.Diag: - biopsy of l.nodes. (vi) Nonhodgkin’s disà eg lymphosarcoma.if in bone marrow passes blastcells its called lymphoblast.Clinic of LG: - ↑ temp, anemia-white color of skin, ↑ Hepar n ↑ spleen, ↑ nodules.1^st ↑ one lymp nome. in 2^nd stage ↑ lymp group.3^rd ↑ all l.nodes from one part of diaphragm.in 4^th stage ↑ from both sides of diaphrafm. Rx: - radiotherapy, pharm.therapy.Duration of life-5yrs bcoz not specific therapy.

35. D.D of jaundice: - Def: - Jaundice(J) may b caused by ↑ conjugated & ↑ unconjugated bilirubin. Causes of Unconjuga. hyperbilirubinemia(UBemia) – ^ ↑ production of B(hemolysis). ^ ↓ uptake of B. ^ failure of conjugation by liver. Causes of Conjugated hyperbilirubinemia(CBemia)-^ hepatocellular damage. ^ obstruction of bile ducts either within liver (intrahepatic colestasis) or of major bile duct(extra hepatic obstructive J). J is also classified: - prehepatic (hemolytic)J, hepatic J, posthepatic /obstructive/mechanicalJ. Etio: - Hemolytic J(family history, racial origin, drug history, sympt. of anemia), Hepatic J(flu sympt., rashes, joint pains, contact with J, bld transfusions, infect., drug history, alcoholic intake, previous J), Obstructive J(abd pain pale stools, dark urine, itching). Phy. Signs: - *For hemolytic J(splenomegaly, reduced stature).*For hepatic J(alcohol-dupuytren’s contractures, parotid enlargement; endocrine-spider naevi, gynaecomastia, testicular atrophy, loss of hair, red hands; hypoprotienemia-white nails, ascites, edema; prothrombin time prolonged-bruising; portal HT-splenomegaly, veins around umbilicus).*For obstructive J(scratch marks, mass in abd, Gall bladder-obst J+GB is palpable & without pain i.e.Courvoisier’s law). Liver func.tests: - In UBemia/hemolytic (↑ DB, AST, ALT, ALK-P r normal), in hepatocellular