Never offer the devil (desire) a ride,He always want to be in the driving seat…!-- BK
CPC 4.2.3 – 2013 – ―yellow eyes‖• Fatigue / Anorexia..?• Nausea, Vomiting..?• Haematemesis… ?• Itching..?• Fever..?• Abdominal distension slow..?• Bleeding / Bruising..?• 10 stubbies/day /more..?• Many Tattoos..?• BMI – if low / High..?2Mr. T.D. 50 year old, presents to his GP. ‗My stomach appears bigand my wife has noticed a yellow tinge in my eyes‘.CASE STUDY 1Abd distension, fatigue, yellow discoloration of eyes for 1 weekPresenting Symptoms:• Liver failure…• Liver failure…• Portal Hypertension• Obstructive jaundice.• Hepatitis.• Cirrhosis.• Vit-K deficiency.• Alcoholic hepatitis.• Viral Hepatitis (B/C)• Anorexia / Obesity –steatosis.• Differential Diagnosis:• Hepatitis: Alcoholic/Infective/Malignant/Drug/Toxins• Acute / Chronic? Primary/Secondary?• ―HBV / HCV, CMV, Lepto, Dengue, Melioidosis.
Case2: Mr.GG, 48y, fatigue & yellow…• Abdominal distension, fatigue, yellowsclera – 6 weeks.• Hardware business, Alcohol 40units / wk.• Travel: Thailand, had tattoo / surgery /transfusion.. *• PE: abdomen nil sig. mild RUQtenderness. No organomegaly.• Differential: Acute hepatitis.– CMV, Lepto, Hep A,B,C..– Hepatitis - Alcohol– Chronic hepatitis.– Drugs, toxins,3AST = 1320 U/lALT = 1780 U/lAlk. Phos. = 133 U/lGGT = 192 U/lHep B SerologyHep B sAg +iveHep B sAb <10Hep B cAb IgM +iveHep B e Ag +iveHep B eAb –ive
4CPC 4.2.2 - 2010• George, 62 year old farmer from Tully, presentsto his GP with fatigue. His wife has asked him toconsult you as his eyes look a bit yellow.• Fatigue: Progressing 2wk. Unable to get out.• nausea : no• vomiting/haematemesis : no• Anorexia, wt loss: yes thinks lost a bit of weight.• bowel habit : constipated, stool pale, no blood.• 2 x episodes fatigue last 2 years preceded by 2weeks of fever. Lab: ―liver not working so well.then felt better and has not been to see GP since.• Banana farmer from Greece - 26 years ago.
5Laboratory Investigations:• FBC: Hb 13.8 g/dl, PCV 45%; WBC 7000/mm3, 70%N, 25% L; Platelets 200,000/mm3• Blood film: Normocytic, normochromic cells• Bilirubin: Total serum Bilirubin = 98 μmol/l, (Direct 67)• Liver enzymes:• Aspartate amino transferase (AST) = 182 U/l• Alanine amino transferase (ALT) = 55 U/l• Alkaline Phosphatase = 190 U/I• Serum Protein: Total protein = 59 g/l, Albumin = 20 g/l,• Hepatitis B Surface Antigen (HbsAg): PositiveHep B sAg +iveHep B sAb <10Hep B cAb IgM +iveHep B e Ag +iveHep B eAb –ive
6Differential Diagnosis:• Viral fever -?– Yellow fever, Relapsing fever, Dengue, Ebola,– Leptospirosis (common in Tully) - ?• Hepatitis – Acute / Chronic - ?• Chronic Hepatitis B – why chronic?• History & presentation in Hep. A & C ?• Other causes of Jaundice?• Alcoholic liver disease ?• Toxins, chemical, Reyes syndrome?• Hemolytic / Anemia - ?• Malignancy - ?
"When you speak, speak the truth;perform when you promise;discharge your trust... Withhold yourhands from striking, and from takingthat which is unlawful and bad..."-- From Wings of Fire, book by Dr. APJ Abdul Kalam, Foremer President of India.
9Pathology ofCommon Liver DisordersDr. Venkatesh M. Shashidhar.Assoc.Prof & Head of Pathology
18Jaundice Clinical Types:Stool Urine Ser. chem. DiagnosisDark Normal Un.Conj / ID Hemolysis.Pale Dark Conj./D + ALP CholestasisPale Dark ID+D ALT/AST Hepatitis.Variable Variable Variable Cong. Syndr.
A wise man watches his faults moreclosely than his virtues; othersreverse the order.--Napoleon Hill
20Pathology of Viral HepatitisDr. Venkatesh M. Shashidhar.Assoc.Prof & Head of Pathology
21Viral Hepatitis: Introduction• Viral Hepatitis:– Specific – Heptitis B, C, D (serum), A, E– Non-Specific - Many viruses CMV, EBV, etc.– Acute, Chronic (CPH, CAH), Fulminant.• Specific viral hepatitis important cause ofmorbidity & mortality.• Horizontal transmission – Blood.. Sex.• Vertical transmission – Mother to fetus.• Hepatitis Cirrhosis Hepatic Ca. (not in A/E)
22Hepatitis A• faecal-oral spread, Travel / exposure.• Relatively short incubation period (2-6wk)• Epidemics common, may be sporadic.• Direct cytopathic virus (immune in B & C)• No carrier state – prolonged immunity.• Usually mild illness, full recovery usual.• Rarely – severe or fulminant.• IgM Ab is diagnostic. (no IgG tests).
24History Hep B Virus:• In 1965 - Dr. Blumberg who wasstudying haemophilia, found anantibody in two patients which reactedagainst an antigen from an AustralianAborigine. Later the antigen was foundin patients with serum type hepatitis andwas initially designated "AustraliaAntigen". Later proved to be hepatitis Bvirus surface antigen (HBsAg). Dr.Blumberg was awarded the Nobel Prizein 1976.
25Hepatitis B• Spread by blood, Sex & birth (serum hepatitis..)• Relatively long incubation period (4-26wk)• liver damage by antiviral immune reaction• Carrier & Chronic state exist.• Relatively serious infection – chronic• Complications: cirrhosis, carcinoma.• Diagnosis: Viral serology (HBs, HBc & HBe)IgM anti-HAVantibodyAcute Hepatitis AHBsAg Hepatitis B orcarrier – exp./inf.HBeAg Active hepatitis BinfectionAnti-HCV antibody Hepatitis C virusexposureHCV RNA Active hepatitis Cinfection
26Viral Hepatitis B: SerologySequence of serologic markers for hepatitis B viral hepatitis demonstrating (A)acute infection with resolution and (B) progression to chronic infection.
36Fulminant Hepatitis:• Hepatic failure with in 2-3 weeks.• Reactivation of chronic or acute hepatitis• Massive necrosis, shrinkage, wrinkled• Collapsed reticulin network• Only portal tracts visible• Little or massive inflammation – time• More than a week – regenerative activity• Complete recovery – or - cirrhosis.
43Learn from the mistakesof others. You cant livelong enough to makethem all yourself…!61% of 5th year students exceeded ‘sensible’ limitsDrugs and alcohol were taken mainly for pleasure and wereperceived as a normal part of life for many students…Capability of advising patients…?http://www.lycaeum.org/research/researchpdfs/1996_webb_1.pdf
"The past, the present and thefuture are really one: they aretoday!"-Harriet Beecher StoweThe past has gone and future you cannot see. The present, when you can do something, that is the Gift(Present) with which you can make your future & past memorable.- Sai Baba
Drug Induced Zonal Hepatitis:46• Autopsy specimen in a case ofacetaminophen (paracetamol /NSAID) overdose.• Prominent hemorrhagic necrosisof the centrilobular zones of allliver lobules.• greater activity of drug-metabolizing enzymes in thecentral zones.• Other agents that produce suchinjury are carbon tetrachloride,toxins of the mushroom Amanitaphalloides.• Patients either die in acutehepatic failure or recover withoutsequelae.
Reye Syndrome:48• Acute disease of children• Following a febrileillness, commonlyinfluenza or varicellainfection with use ofaspirin.• Microvesicularsteatosis, hepaticfailure, andencephalopathy.• Cerebral edema and fataccumulation in the brain.• Pathogenesis remainsunknown (Aspirin..)Fat stain (oil-red o)
Toxemia of Pregnancy:49• Abnormal LFT in 3-5% of preg.• Acute Fatty Liver of Pregnancy• Intrahepatic Cholestasis of Preg.• Hypertension, proteinuria, edemaand coagulation abnormalities(pre-eclampsia) with convulsions& coma (eclampsia).• HELLP syndrome(hemolysis, elevated liver enz. &low plt).• Patchy hemorrhages overcapsule, DIC• Fibrin thrombi in portal vessels.• Hepatocellular necrosis.
71Learn from the mistakesof others. You cant livelong enough to makethem all yourself…!61% of 5th year students exceeded ‘sensible’ limitsDrugs and alcohol were taken mainly for pleasure and wereperceived as a normal part of life for many students…Capability of advising patients…?http://www.lycaeum.org/research/researchpdfs/1996_webb_1.pdf
Alcoholic Hepatitis:83• Centrilobular necrosis. Ballooned degenerating hepatocytes (BC) Mallory bodies(MB) Many Neutrophils, few lymphocytes & Macrophages.• The central vein(or terminal hepatic venule (THV), is encased in connectivetissue (C) (central sclerosis). Fat-laden hepatocytes (F) are evident in the lobule.The portal tract displays moderate chronic inflammation.
110Diagnosis pathway:• Jaundice?– Mild increase, Mixed (combined)• Synthesis?– Total protein, albumin – Low & PT abnormal.• Obstruction & Bilirubin Clearance ?– Alk Phos is up a bit – but not high – some obstruction.• Hepatocyte Direct Injury:– ALT & AST are up a bit, but not dramatically.• Discussion:– Chronic Mild compromise - chronic Activehepatitis. (In CPH LFT will be normal)ALT: 52AST: 58Alk Phos: 150Bilirubin 3.9 (direct 1.8)
111• 28y Male, 3 weeks after visiting eastTimor, presents with malaise, fatigue, lossof appetite. Mild icterus. AST & ALT mildelevation. Total bil 3.9mg/dl (Direct 2.8).Which of the following would be positive?
113Chronic Hepatitis:• Passive CPH• Limited Periportalinflammation.• Mild Periportal fibrosis• No hepatocyteNecrosis.• LFT normal or mildchange.• Late cirrhosis• Active CAH• ExtensiveInflammation• More fibrosis.• Necrosis ofhepatocytes.• LFT abnormal.• Early cirrhosis & othercomplication.
“Nearly all men can stand adversity,but if you want to test a manscharacter, give him power!”— Abraham Lincoln