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Cirrhosis of liver

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Cirrhosis of liver

  1. 1. CIRRHOSIS OF LIVER PORTAL HYPERTENSIONHEPATIC ENCHEPALOPATHY
  2. 2. Definition of cirrhosisCirrhosis is derived from Greek word kirros=orange or tawny and osis=condition-WHO definition :a diffuse process characterized by liver necrosis and fibrosis and conversion of normal liver architechture into structurally abnormal nodules that lack normal lobular organisation.
  3. 3. CAUSES OF LIVER CIRRHOSIS-Infections:post hepatitic cirrhosis(B,D,C).-Toxins:Alcohol.-Cholestatic liver disease:PBC,PSC…-Autoimmune diseases:autoimmune hepatitis.-Vascular disorders: cardiac cirrhosis,Budd-Chiari syndrome ,Veno occlusive disease-Metabolic and genetic :Wilson disease ,hemochromatosis,alpha 1- antitrypsin deficiency-Non alcoholic steato hepatitis(NASH). Cryptogenic.
  4. 4. Pathology of cirrhosis -nodularity(regenerating nodules).-fibrosis(deposition of dense fibrous septa)- fragmentation of sample.-abnormal liver architecture-hepatocyte abnormalities:pleomorphism,dysplasia,hyperp lasia-Gross pathology:irregular surface ,yellowish colour,small,firm
  5. 5. HISTOLOGICAL IMAGE OF A NORMAL AND A CIRRHOTIC LIVERNormal Cirrhosis Nodules surrounded by fibrous tissue
  6. 6. HISTOLOGICAL IMAGE OF CIRRHOSIS FibrosisRegenerative nodule
  7. 7. PATHOGENESIS OF LIVER FIBROSISNormal Hepatic SInusoid Retinoid droplets Fenestrae Hepatic stellate cell Space of Disse Sinusoidal endothelial cell Hepatocytes
  8. 8. PATHOGENESIS OF LIVER FIBROSISAlterations in Microvasculature in Cirrhosis • Activation of stellate cells • Collagen deposition in space of Disse • Constriction of sinusoids • Defenestration of sinusoids
  9. 9. NATURAL HISTORY OF CHRONIC LIVER DISEASE Natural History of Chronic Liver DiseaseChronicliver Compensated Decompensated cirrhosis cirrhosis Deathdisease Development of complications: • Variceal hemorrhage • Ascites • Encephalopathy • Jaundice
  10. 10. CLINICAL FEATURES• Hepatomegaly (although liver may also be small)• Jaundice• Ascites• Circulatory changes – Spider telangiectasia, palmar erythema, cyanosis• Endocrine changes – Loss of libido, hair loss – Men: gynaecomastia, testicular atrophy, impotence – Women: breast atrophy, irregular menses, amenorrhoea• Haemorrhagic tendency – Bruises, purpura, epistaxis, menorrhagia• Portal hypertension – Splenomegaly, collateral vessels, variceal bleeding, fetor hepaticus• Hepatic (portosystemic) encephalopathy• Other features – Pigmentation, digital clubbing
  11. 11. COMPLICATIONS OF CIRRHOSISComplications of Cirrhosis Result from PortalHypertension or Liver Insufficiency Variceal Portal hemorrhage hypertension Spontaneous bacterial Ascites peritonitisCirrhosis Hepatorenal syndrome Encephalopathy Liver insufficiency Jaundice
  12. 12. Diagnosis of cirrhosis• clinical+laboratory+radiologic+liver biopsy
  13. 13. DIAGNOSIS OF CIRRHOSIS – CLINICAL FINDINGSIn Whom Should We SuspectCirrhosis?• Any patient with chronic liver disease • Chronic abnormal aminotransferases and/or alkaline phosphatase• Physical exam findings • Stigmata of chronic liver disease (muscle wasting, vascular spiders, palmar erythema) • Palpable left lobe of the liver • Small liver span • Splenomegaly • Signs of decompensation (jaundice, ascites, asterixis)
  14. 14. DIAGNOSIS OF CIRRHOSIS – LABORATORY STUDIESIn Whom Should We SuspectCirrhosis?Laboratory • Liver insufficiency • Low albumin (< 3.8 g/dL) • Prolonged prothrombin time (INR > 1.3) • High bilirubin (> 1.5 mg/dL) • Portal hypertension • Low platelet count (< 175 x1000/µl) • AST / ALT ratio > 1
  15. 15. DIAGNOSIS OF CIRRHOSIS – CAT SCAN CT Scan in CirrhosisLiver with an irregular surface Collaterals Splenomegaly
  16. 16. DIAGNOSTIC ALGORITHMDiagnostic Algorithm Patient with chronic liver disease and any of the following: • Variceal hemorrhage • Ascites • Hepatic encephalopathy Physical findings: Laboratory findings: Yes No Enlarged left hepatic lobe Thrombocytopenia Splenomegaly Impaired hepatic synthetic Stigmata of chronic liver function disease Radiological findings: Yes No • Small nodular liver • Intra-abdominal collaterals • Ascites • Splenomegaly • Colloid shift to spleen and/or bone marrow Yes No Liver biopsy not necessary for the Liver biopsy diagnosis of cirrhosis
  17. 17. Management of cirrhosis-Specific treatment in some pre cirrhotic lesions:wilson disease— Dpenicillamine,,hemochromatosis--- phlebotomy,,antiviral drugs for chronic viral hepatitis-in established cirrhosis---treatment of complications-screening for hepatocellular carcinoma-liver transplantation-maintenance of nutrition
  18. 18. CHILD-PUGH CLASSIFICATION OF PROGNOSIS IN CIRRHOSISScore 1 2 3Encephalopathy None Mild MarkedBilirubin (mg/dl) < 2.0 2.0-3.0 > 3.0Albumin (g/dl) > 3.5 3.0-3.5 < 3.0Prothrombin time <4 4-6 >6(seconds prolonged)Ascites None Mild MarkedAdd the individual < 7 = Childs Ascores: 7-9 = Childs B > 9 = Childs C
  19. 19. MELD SCORE• MELD = 3.8(SERUM BILIRUBIN –MG/DL)+11.2 IN INR + 9.6 IN SERUM CREATININE – MG/DL+ 6.4
  20. 20. PORTAL HYPERTENSIONDefinition:it is an increase in portal venous pressure.-normal portal pressure:5-10mmHg.-portal hypertension;>12mmHg-normal portal blood flow:1-1.5L/minute-- increased resistance to portal blood flow +hyperdynamic circulation-----formation of porto systemic collaterals that diver blood to systemic circulation bypassing the liver
  21. 21. MECHANISMS OF PORTAL HYPERTENSIONMechanisms of Portal Hypertension • Pressure (P) results from the interaction of resistance (R) and flow (F): P=RxF • Portal hypertension can result from: • increase in resistance to portal flow and/or • increase in portal venous inflow
  22. 22. THE NORMAL LIVER OFFERS ALMOST NO RESISTANCE TO FLOW Normal Liver Hepatic veinSinusoid Liver Coronary Portal vein vein Splenic vein
  23. 23. ARCHITECTURAL LIVER DISRUPTION IS THE MAIN MECHANISM THAT LEADS TO AN INCREASED INTRAHEPATIC RESISTANCE Cirrhotic Liver Portal systemic collaterals Distorted sinusoidalarchitecture leads to increased resistance Portal vein Splenomegaly
  24. 24. AN INCREASE IN PORTAL VENOUS INFLOW SUSTAINS PORTAL HYPERTENSION An Increase in Portal Venous Inflow Sustains Portal Hypertension 20 Distorted sinusoidalarchitechure Portal vein ↑ Flow Mesenteric veins Splanchnic vasodilatation
  25. 25. CAUSESCAUSES OF PORTAL HYPERTENSION ACCORDING TO SITE OF ABNORMALITYExtrahepatic post-sinusoidal Budd-Chiari syndromeIntrahepatic post-sinusoidal Veno-occlusive diseaseSinusoidal Cirrhosis• Cystic liver disease• Partial nodular transformation of the liver• Metastatic malignant diseaseIntrahepatic pre-sinusoidal Schistosomiasis• Sarcoidosis• Congenital hepatic fibrosis• Vinyl chloride• DrugsExtrahepatic pre-sinusoidal Portal vein thrombosis due to sepsis* (umbilical, portal pyaemia) or procoagulopathy (thrombotic diseases, oral contraceptives, pregnancy), or secondary to cirrhosis• Abdominal trauma, including surgery• Malignant disease of pancreas or liver• Pancreatitis• Congenital
  26. 26. Clinical complications of PHTVARICES:esophageal,gastric,anorectal,retroperit oneal.-portal hypertensive gastropathy and colopathy.-caput medusae-ascites-congestive splenomegaly-hepatic encephalopathy
  27. 27. VARICES INCREASE IN DIAMETER PROGRESSIVELYVarices Increase in DiameterProgressively No varices Small varices Large varices 7-8%/year 7-8%/yearMerli et al. J Hepatol 2003;38:266
  28. 28. PROGNOSTIC INDICATORS OF FIRST VARICEAL HEMORRHAGE Variceal hemorrhage Varix with red signs Predictors of hemorrhage: • Variceal size • Red signs • Child B/CNIEC. N Engl J Med 1988; 319:983
  29. 29. Treatment of portal hypertension-treatment of complications:variceal bleeding,,,ascites…-endoscopic procedures:sclerotherapy +band ligation+prophylactic propranolol
  30. 30. TREATMENT OF ACUTE VARICEAL HEMORRHAGETreatment of Acute Variceal Hemorrhage General Management: • Iv acess and fluid resuscitation • Do not overtransfuse (hemoglobin ~ 8 g/dL) • Antibiotic prophylaxis Specific therapy: • Pharmacological therapy: terlipressin, somatostatin and analogues, vasopressin + nitroglycerin • Endoscopic therapy: ligation, sclerotherapy • Shunt therapy: TIPS, surgical shunt
  31. 31. ENDOSCOPIC VARICEAL BAND LIGATIONEndoscopic Variceal BandLigation• Bleeding controlled in 90%• Rebleeding rate 30%• Compared with sclerotherapy: • Less rebleeding • Lower mortality • Fewer complications • Fewer treatment sessions
  32. 32. THE TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNTTransjugular Intrahepatic PortosystemicShunt Hepatic vein TIPS Splenic Portal vein vein Superior mesenteric vein
  33. 33. MANAGEMENT OF UNCOMPLICATED ASCITESManagement of UncomplicatedAscites Definition: Ascites responsive to diuretics in the absence of infection and renal dysfunction Sodium restriction • Effective in 10-20% of cases • Predictors of response: mild or moderate ascites, Urine Na excretion > 50 mEq/day Diuretics • Should be spironolactone-based • A progressive schedule (spironolactone  furosemide) requires fewer dose adjustments than a combined therapy (spironolactone + furosemide)
  34. 34. MANAGEMENT OF UNCOMPLICATED ASCITES: DIURETIC THERAPYManagement of Uncomplicated Ascites Diuretic Therapy Dosage • Spironolactone 100-400 mg/day • Furosemide (40-160 mg/d) for inadequate weight loss or if hyperkalemia develops • Increase diuretics if weight loss <1 kg in the first week and < 2 kg/week thereafter • Decrease diuretics if weight loss >0.5 kg/day in patients without edema and >1 kg/day in those with edema • Side effects • Renal dysfunction, hyponatremia, hyperkalemia, encephalopathy, gynecomastia
  35. 35. EARLY DIAGNOSIS OF SPONTANEOUS BACTERIAL PERITONITIS (SBP) Early Diagnosis of SBP • Diagnostic paracentesis: • If symptoms / signs of SBP occur • Unexplained encephalopathy and / or renal dysfunction • At any hospital admission • Diagnosis based on ascitic fluid PMN count >250/mm3Rimola et al., J Hepatol 2000; 32:142
  36. 36. TREATMENT OF SPONTANEOUS BACTERIAL PERITONITIS (SBP)Treatment of Spontaneous BacterialPeritonitis • Recommended antibiotics for initial empiric therapy • i.v. cefotaxime, amoxicillin-clavulanic acid • oral nofloxacin (uncomplicated SBP) • avoid aminoglycosides • Minimum duration: 5 days • Re-evaluation if ascitic fluid PMN count has not decreased by at least 25% after 2 days of treatment Rimola et al., J Hepatol 2000; 32:142
  37. 37. HEPATIC ENCEPHALOPATHYHepatic Encephalopathy 60
  38. 38. TYPE C HEPATIC ENCEPHALOPATHY IS THE ENCEPHALOPATHY OF CIRRHOSISType C Hepatic Encephalopathyis the Encephalopathy ofCirrhosis• Neuropsychiatric complication of cirrhosis• Results from spontaneous or surgical / radiological portal-systemic shunt + chronic liver failure• Failure to metabolize neurotoxic substances• Alterations of astrocyte morphology and function (Alzheimer type II astrocytosis)
  39. 39. STAGES OF HEPATIC ENCEPHALOPATHY Stages of Hepatic EncephalopathyStage Mental state Neurologic signs 1 Mild confusion: limited attention Incoordination, tremor, span, irritability, inverted sleep impaired handwriting pattern 2 Drowsiness, personality changes, Asterixis, ataxia, dysarthria intermittent disorientation 3 Somnolent, gross disorientation, Hyperreflexia, muscle marked confusion, slurred speech rigidity, Babinski sign 4 Coma No response topain,
  40. 40. STAGES OF HEPATIC ENCEPHALOPATHYStages of Hepatic Encephalopathy Confusion Drowsiness Somnolence Coma 1 2 3 4 Stage
  41. 41. HEPATIC ENCEPHALOPATHY IS A CLINICAL DIAGNOSISHepatic Encephalopathy Is AClinical Diagnosis• Clinical findings and history important• Ammonia levels are unreliable• Ammonia has poor correlation with diagnosis• Measurement of ammonia not necessary• Number connection test• Slow dominant rhythm on EEG
  42. 42. HEPATIC ENCEPHALOPATHY PRECIPITANTS Hepatic Encephalopathy Precipitants Sedatives / hypnoticsExcess protein GI bleedingTIPS Diuretics Serum K+ Plasma volume Temp Azotemia Infections
  43. 43. PATHOPHYSIOLOGY OF HEPATIC ENCEPHALOPATHYHepatic EncephalopathyPathogenesis Toxins NH3 Shunting Failure to GABA-BD metabolize receptors NH3 Bacterial action Protein load
  44. 44. ASTERIXIS IS THE HALLMARK IN THE DIAGNOSIS OF HEPATIC ENCEPHALOPATHYAsterixis
  45. 45. NUMBER CONNECTION TESTNumber Connection Test Draw a star 70(NCT)Time tocomplete____________________ End 6 10 25 4 7 9 23 1 11 5 Begin 14 8 243 2 Sample handwriting 13 12 1715 16 22 18 2119 20
  46. 46. TREATMENT OF HEPATIC ENCEPHALOPATHYTreatment of Hepatic Encephalopathy • Identify and treat precipitating factor • Infection • GI hemorrhage • Prerenal azotemia • Sedatives • Constipation • Lactulose (adjust to 2-3 bowel movements/day) • Protein restriction, short-term (if at all)
  47. 47. ACTIONS OF LACTULOSE Actions of Lactulose NH3 Decreased pH NH4+ Lactic acid NH3 LactuloseUrease-producing Increasebacteria cathartic effect
  48. 48. HEPATIC ENCEPHALOPATHY – TREATMENT SUMMARY Hepatic Encephalopathy Treatment: SummaryIncrease ammoniafixation in liver:• Ornithine aspartate• Benzoate Flumazeni l Shunt occlusion or reduction Decrease ammonia production in gut: • Lactulose • Antibiotics • Adjustment in dietary protein

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