cirrhosis best presentation about hepatitis

it is mainly focus about hepatitis or liver related problems

1. Cirrhosis By Dr. Afework Adam(MD,GP) 1 Dr.Afework A 10/8/2025

2. Outlines Introduction Pathophysiology of cirrhosis Evaluation of severity Complication of cirrhosis 2 10/8/2025 Dr.Afework A

3. cirrhosis Is development of fibrosis with architectural distortion and the formation of regenerative nodules Could be reversible 3 10/8/2025 Dr.Afework A

4. ….cont Liver fibrosis is a dynamic process that results from an imbalance between the production and dissolution of the extracellular matrix Result of the progressive accumulation and decreased remodeling of the ECM, which disrupts the normal architecture of the liver. Progression to cirrhosis or regression no approved anti-fibrotic drug 10/8/2025 Dr.Afework A 4

5. Cirrhosis Advanced fibrosis, scarring, and formation of regenerative nodules leading to architectural distortion. A number of etiologies with common pathologic features: degeneration and necrosis of hepatocytes , and replacement of liver parenchyma by fibrotic tissues and regenerative nodules , and loss of liver function. 5 10/8/2025 Dr.Afework A

6. Causes of cirrhosis 6 10/8/2025 Dr.Afework A

7. Risk factors for alcoholic liver disease Quantity Ingestion of 160 g/d is associated with 25–fold increased risk of developing alcoholic cirrhosis duration of alcohol intake --- 10yrs Sex- female >male Genetic Coinfection : HCV,HBV 7 10/8/2025 Dr.Afework A

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9. Alcoholic Cirrhosis alcoholic liver disease alcoholic fatty liver alcoholic hepatitis 3. alcoholic cirrhosis 1 & 2 are reversible 3 irreversible 9 10/8/2025 Dr.Afework A

10. 1.alcoholic fatty liver benign right upper quadrant discomfort tender hepatomegaly Nausea jaundice Reversible with cessation alcohol intake 10 10/8/2025 Dr.Afework A

11. 2.Alcoholic hepatitis Cytokine production is responsible for the systemic manifestations of alcoholic hepatitis Fever, spider nevi, jaundice, and abdominal pain Portal hypertension, ascites , or variceal bleeding can occur in the absence of cirrhosis Precursor for alcoholic cirrhosis Reversible with cessation of alcohol intake AST>ALT 11 10/8/2025 Dr.Afework A

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13. Post hepatitis : HBV,HCV 80% of acute HCV develop chronic hepatitis C 20–30% will develop cirrhosis over 20–30 years 5% of acute HBV develop chronic hepatitis B 20% -25%of those patients will go on to develop cirrhosis. 13 10/8/2025 Dr.Afework A

14. Cirrhosis from Autoimmune Hepatitis Post hepatitis antinuclear antibody (ANA) anti-smooth-muscle antibody (ASMA) 14 10/8/2025 Dr.Afework A

15. nonalcoholic steatohepatitis (NASH) Fatty liver:- DM, Dyslipidemia, obesity, drugs nonalcoholic steatohepatitis can progress to cirrhosis cryptogenic cirrhosis: nonalcoholic steatohepatitis As their cirrhosis progresses, they become catabolic and then lose signs of steatosis 15 10/8/2025 Dr.Afework A

16. Cardiac Cirrhosis long-standing right-sided congestive heart failure may develop chronic liver injury and cardiac cirrhosis-- Corpulmonale Back ward transmission of elevated venous pressure via the inferior vena cava and hepatic veins to the sinusoids of the liver Nutmeg liver Corpulmonale —hepatic congestion– compress vessel— heamorrhegic ischemia(Nutmeg liver) 16 10/8/2025 Dr.Afework A

17. s/s signs of congestive heart failure an enlarged firm liver ALP levels are characteristically elevated aminotransferases may be normal or slightly increased with AST usually higher than ALT AST>ALT- Alcoholic hepatitis - Cardiac cirrhosis Enlarged liver—cardiac cirrhosis --HIV 17 10/8/2025 Dr.Afework A

18. inherited metabolic liver diseases hemochromatosis -Iron Wilson's disease- Copper 1 antitrypsin ( 1 AT) deficiency cystic fibrosis. 18 10/8/2025 Dr.Afework A

19. Causes of cirrhosis summary 1.viral hepatitis 2.alcohol 3.drug 4.autoimmune 5.primary biliary , secondary biliary 6.cardiac 7.inherited metabolic liver disease 19 10/8/2025 Dr.Afework A

20. Diagnosis of cirrhosis Although cirrhosis is strictly speaking a histologic diagnosis, a combination of clinical, laboratory, and imaging features can help confirm a diagnosis of cirrhosis. Several physical findings suggestive of cirrhosis result in part from alterations in the metabolism of estrogen by the cirrhotic liver . An intense red coloration of the thenar and hypothenar eminences suggests palmar erythema . Terry’s nails are characterized by proximal nail bed pallor, which can also involve the entire nail plate, with predominant involvement of the thumb and index finger. Clubbing of the fingernails may result from the presence of arteriovenous shunts in the lung as a result of portal hypertension.

21. Gynecomastia is the enlargement of the male breast with palpable tissue. Spider telangiectasias (or angiomata ) are dilated arterioles characterized by a prominent central arteriole with radiating vessels. Compression of the central arteriole with a pinhead results in blanching followed by reformation of the “spider” after release of pressure on the arteriole. In general, more than 2 to 3 spider telangiectasias are considered abnormal.

22. Dilated abdominal veins ( caput medusae ) with flow away from the umbilicus, toward the inferior vena cava in the infraumbilical area and toward the superior vena cava in the supraumbilical area, suggest intrahepatic portal hypertension On the other hand, dilatation of veins in the flank with blood draining toward the superior vena cava suggests inferior vena caval obstruction. Parotid enlargement is also a feature of cirrhosis, especially alcoholic cirrhosis. Usually secondary to fatty infiltration , fibrosis, and edema rather than a hyperfunctioning gland

23. Dupuytren's contracture- Nodular fibrosing lesions with bands radiating distally The ulnar side of the hand is affected, with the fourth and fifth fingers usually involved first.

24. Evaluation of severity of cirrhosis 28 10/8/2025 Dr.Afework A

25. Complication of cirrhosis 29 10/8/2025 Dr.Afework A

26. Portal Hypertension Portal circulation -a high compliance, low-resistance system that is able to accommodate a large blood volume -dual blood supply *75% portal v *25% hepatic a 30 10/8/2025 Dr.Afework A

27. Portal Hypertension Portal pressure gradient >5 mm Hg. Normal HVPG is 3-5 mmHg. a measure of sinusoidal pressure Initial and main consequence of cirrhosis. Responsible for the majority of its complications. May occur before a formal anatomical diagnosis of cirrhosis is established. 31 10/8/2025 Dr.Afework A

28. Pathophysiology of PH in cirrhosis Increased intrahepatic resistance due to cirrhosis and regenerative nodules and active intrahepatic vasoconstriction Structural in 70%, functional in 1/3 rd Increased splanchnic blood flow secondary to vasodilatation within the splanchnic vascular bed. Increases in portal resistance or portal flow can contribute to increased pressure. OHM’ ҆ S LAW: Δ P = F × R PHN almost always results from increases in both portal resistance and portal flow 32 10/8/2025 Dr.Afework A

29. Measurement of PH Direct Portal Vein Pressure Indirect HVPG only sinusoidal and postsinusoidal TE/MRE US 33 10/8/2025 Dr.Afework A

30. Non-invasive History and physical examination IX: Lab evidence of hepatic dysfunction Low platelet count Ultrasound, Fibroscan, MRE.. Esophagogastroduodenoscopy(EGD) 34 10/8/2025 Dr.Afework A

31. ….PH Imaging- Ultrasound, CT, MRI Recanalized paraumbilical vein, spontaneous splenorenal circulation, and dilated left and short gastric veins. Portal vein diameter >13 mm, reduction of portal vein velocity. A reversal of flow within the portal system is 100% specific and sufficient to diagnose CSPH. Splenomegaly: sensitive but not specific. 35 10/8/2025 Dr.Afework A

32. ….PH -pre-hepatic -intra-hepatic -post-hepatic 36 10/8/2025 Dr.Afework A

33. Ascites The most common complication of cirrhosis Cirrhosis is the most common cause of ascites i [~ 85 %]. 5 – 10% of patients with compensated cirrhosis per yr Poor prognosis (5-year survival~30%) Uncomplicated not infected, refractory or associated with impairment of renal function. 37 10/8/2025 Dr.Afework A

34. Evaluation 38 10/8/2025 Dr.Afework A

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36. ….ascites Diagnostic paracentesis is indicated in : All patients with new-onset grade 2 or 3 ascites P atients hospitalized for worsening ascites or any complication of cirrhosis Recommendation Neutrophil count and culture of ascitic fluid culture † should be performed to exclude bacterial peritonitis Neutrophil count >250 cells/µl denotes SBP II-2 1 Ascitic total protein concentration should be performed to identify patients at higher risk of developing SBP ‡ II-2 1 The SAAG should be calculated when the cause of ascites is not immediately evident, and/or when conditions other than cirrhosis are suspected § II-2 1 Cytology should be performed to differentiate malignancy-related from non-malignant ascites II-2 1

37. treatment Salt restriction (2 g/day) Diuretics Large volume paracentesis TIPS(trans jugular intrahepatic portosystemic shunt) Liver trasplant

38. Spontaneous bacterial peritonitis bacterial infection of ascitic fluid without any intra-abdominal surgically treatable source of infection. The source of infection is mostly hematogenous Etiologies; E.coli S.viridans S.aures

39. …..SBP Clinical features: Signs/symptoms of peritonitis : abdominal pain, tenderness, vomiting or diarrhoea, ileus Signs of systemic inflammation : hyper- or hypothermia, chills, altered mental status Worsening liver function,altered WBC count, HE, shock, renal impairment, GI bleeding. Asymptomatic!

40. ….SBP Diagnosis Ascitic fluid PMNs >250/mm3 PMNs >250 highest sens and >500 has highest specif Manual counting, Automated counting, Reagent strips Culture positive in ~40%; GNB-E. coli and Gram-positive cocci mainly streptococcus sp and enterococci Community-GNB; Nosocomial-GPC Culture-negative SBP : ascitic PMNs >250 but culture negative Bacterascites : culture positive, PMNs <250

41. ….SBP Treatment SBP resolves with antibiotic therapy in ~90% of patients Cefotaxime 4g iv/day for 5 days High ascitic fluid conc, 77-98% efficacy Cefotaxime or amoxicillin/clavulanic acid effective in patients who develop SBP while on norfloxacin Px Repeat ascitic fluid analysis after 48hr of antibiotic treatment At least 25% decrement in PMNs

42. 10/8/2025 Dr.Afework A 46 Secondary prophylaxis prior hx of SBP

43. Esophageal varices and variceal bleeding Varices develop in order to decompress the hypertensive portal vein and return blood to systemic circulation Clinical feature: signs and symptoms of CLD Painless but massive hypotension with/without shock Investigation; emergency endoscopy BG CBC,OFT,PT and PTT

44. factors predicting the risk of bleeding the severity of cirrhosis (Child's class) height of wedged-hepatic vein pressure the size of the varix the location of the varix endoscopic stigmata: red wale signs, hematocystic spots, diffuse erythema , bluish color, cherry-red spots, or white-nipple spots tense ascites

45. Hepatorenal syndrome[HRS] Renal failure in a patient with advanced liver disease in the absence of an identifiable cause of renal failure ~30% of patients who develop SBP has HRS 49 10/8/2025 Dr.Afework A

46. ….HRS T1-HRS: rapid and progressive impairment in renal function(increase in serum creatinine of >=100% compared to baseline to a level >=2.5 mg/dl in >2 weeks). 60-70% have identified ppt factors Survival ~1 month T2-HRS: stable or less progressive impairment in renal function. No ppt factors identifiable Survival ~3 months 50 10/8/2025 Dr.Afework A

47. Clin J Am Soc Nephrol1: 1066 –1079, 2006. doi : 10.2215/CJN.01340406 51 10/8/2025 Dr.Afework A

48. Clin J Am Soc Nephrol1: 1066 –1079, 2006. doi : 10.2215/CJN.01340406 52 10/8/2025 Dr.Afework A

49. Hepatic Encephalopathy is a brain dysfunction caused by liver insufficiency and/or PSS It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma 53 10/8/2025 Dr.Afework A

50. Pathophysiology Multiple factors Production of neurotoxins Altered permeability of the BBB, and Abnormal neurotransmission 54 10/8/2025 Dr.Afework A

51. Neurotoxins Ammonia Produced primarily in the colon Bacteria – proteins Ammonia Enterocytes – glutamine Ammonia In cirrhosis blood ammonia level is increased Reduced hepatocyte function Portosystemic shunting Have a direct effect on brain edema, astrocyte swelling, and the transport of neurally active compounds such as myoinositol  HE 55 10/8/2025 Dr.Afework A

52. Pathophysiology of Hepatic encephalopathy 56 10/8/2025 Dr.Afework A

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55. Reading assignment Hepatopulmonary syndrome Portopulmonary Hypertension COAGULATION DISORDERS 59 10/8/2025 Dr.Afework A

56. Thankyou!!! 10/8/2025 Dr.Afework A 60