Слайд 2CIRRHOSIS
• End stage liver disease (irreversible)
• Result from many causes of chronic
![CIRRHOSIS • End stage liver disease (irreversible) • Result from many causes](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-1.jpg)
liver disease:
• Viral Hepatitis (especially B and C)
• Alcoholic liver disease
• Non-alcoholic fatty liver disease
Слайд 3CIRRHOSIS
• Liver tissue replaced by fibrosis and nodules
• Smooth liver surface replaced
![CIRRHOSIS • Liver tissue replaced by fibrosis and nodules • Smooth liver](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-2.jpg)
by nodules
• In advanced cirrhosis, liver becomes shrunken
Слайд 4CLINICAL FEATURES
• Hyperammonemia
• Asterixis, confusion, coma
![CLINICAL FEATURES • Hyperammonemia • Asterixis, confusion, coma](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-3.jpg)
Слайд 5HYPERAMMONEMIA
TREATMENT
• Low protein diet
• Lactulose
• Synthetic disaccharide (laxative)
![HYPERAMMONEMIA TREATMENT • Low protein diet • Lactulose • Synthetic disaccharide (laxative)](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-4.jpg)
• Colon breakdown by bacteria to fatty acids
• Lowers colonic pH; favors formation of NH4+ over NH3
• NH4 + not absorbed → trapped in colon
• Result: ↓plasma ammonia concentrations
Слайд 6CIRRHOSIS
CLINICAL FEATURES
• Jaundice
• Loss of bilirubin metabolism
• Hypoglycemia
• Loss
![CIRRHOSIS CLINICAL FEATURES • Jaundice • Loss of bilirubin metabolism • Hypoglycemia](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-5.jpg)
of gluconeogenesis
• Coagulopathy
• Loss of clotting factors
• Elevated PT/PTT
• Hypoalbuminemia
• May cause low oncotic pressure
• Contributes to ascites, edema
Слайд 7• Elevated estrogen
• Normally removed by liver
• Gynecomastia in
![• Elevated estrogen • Normally removed by liver • Gynecomastia in men](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-6.jpg)
men
Testicular atrophy
• Spider angiomata
• Palmar erythema
Слайд 8CAPILLARY FLUID SHIFTS
• Capillary hydrostatic pressure (Pc)
• Drives fluid out of
![CAPILLARY FLUID SHIFTS • Capillary hydrostatic pressure (Pc) • Drives fluid out](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-7.jpg)
capillaries into tissues
• Capillary oncotic pressure (∏c )
• Proteins (albumin) pull water into capillaries
• Resists movement of fluid out of capillaries
Слайд 9PORTAL HYPERTENSION
• Blood flows portal vein → liver → hepatic vein
• Cirrhosis
![PORTAL HYPERTENSION • Blood flows portal vein → liver → hepatic vein](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-8.jpg)
→ obstructed flow through liver
• High pressure in portal vein (“hypertension”)
Слайд 12VENOUS COLLATERALS
VENOUS ANASTAMOSES
• High portal pressure opens “venous collaterals”
• Connection between
![VENOUS COLLATERALS VENOUS ANASTAMOSES • High portal pressure opens “venous collaterals” •](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-11.jpg)
portal-systemic veins
• Normally small, collapsed vessels
• Engorge in portal hypertension
• Key collaterals:
• Umbilicus – physical exam finding: “caput medusa”
• Esophagus – upper gastrointestinal bleeding
• Stomach – upper gastrointestinal bleeding
• Rectum – hemorrhoids which may also bleed
Слайд 18PORTAL VEIN THROMBOSIS
• Rare cause of portal hypertension
• Acute onset abdominal
![PORTAL VEIN THROMBOSIS • Rare cause of portal hypertension • Acute onset](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-17.jpg)
pain
• Splenomegaly (palpable spleen one exam)
• May result in gastric varices with bleeding
• Liver biopsy will be normal
Слайд 19ASCITES
• Accumulation of fluid in peritoneal cavity
• In liver disease, from
![ASCITES • Accumulation of fluid in peritoneal cavity • In liver disease,](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-18.jpg)
portal hypertension +/- low albumin
Слайд 20SAAG
SERUM ASCITES ALBUMIN GRADIENT
• Test of ascitic fluid
• Two reasons
![SAAG SERUM ASCITES ALBUMIN GRADIENT • Test of ascitic fluid • Two](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-19.jpg)
for new/worsening ascites
• Portal hypertension
• Malignancy (leaky vasculature)
• Sample of ascitic fluid via paracentesis
• Serum albumin – ascites albumin = SAAG
Слайд 21SAAG
SERUM ASCITES ALBUMIN GRADIENT
• SAAG >1.1 g/dL
• Large difference
![SAAG SERUM ASCITES ALBUMIN GRADIENT • SAAG >1.1 g/dL • Large difference](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-20.jpg)
between serum and ascites albumin
• High pressure driving fluid (not albumin) into peritoneum
• Seen in portal hypertension
SAAG <1.1 g/Dl
Albumin levels similar between serum and ascites
• Leaky vasculature leading to fluid/albumin into peritoneum
Seen in malignant ascites (malignant cells in peritoneal cavity)
Слайд 22ASCITES TREATMENT
• Sodium restriction
• Spironolactone (drug of choice)
• Potassium-sparing diuretic
![ASCITES TREATMENT • Sodium restriction • Spironolactone (drug of choice) • Potassium-sparing](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-21.jpg)
• Blocks aldosterone distal tubule
• Most effective drug for ascites
• Loop diuretics (2nd line)
• Large volume paracentesis
• TIPS
Слайд 23TIPS
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
Transjugular Intrahepatic Portosystemic Shunt
• Treatment of portal
![TIPS TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT Transjugular Intrahepatic Portosystemic Shunt • Treatment of](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-22.jpg)
hypertension
• Creation of channel in liver
• Connects portal vein to hepatic vein
Слайд 24SBP
SPONTANEOUS BACTERIAL PERITONITIS
• Ascitic fluid infection
• Bacteria in gut gain
![SBP SPONTANEOUS BACTERIAL PERITONITIS • Ascitic fluid infection • Bacteria in gut](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-23.jpg)
entry into ascitic fluid
• Usually E. coli and Klebsiella; rarely strep/staph
• Fever, abdominal pain/tenderness
• ↑ ascitic absolute PMNs (≥250 cells/mm3)
• Common treatment:
• 3rd generation cephalosporin (cefotaxime)
• Gram positive and gram negative coverage
• Achieves good levels in ascitic fluid
Слайд 25MELD SCORE
MODEL FOR END-STAGE LIVER DISEASE
• Scoring system for chronic liver
![MELD SCORE MODEL FOR END-STAGE LIVER DISEASE • Scoring system for chronic](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-24.jpg)
disease or cirrhosis
• Estimates 3-month mortality from liver disease
• Point system using:
• Bilirubin level
• Creatinine level
• INR
• >40 = 71% mortality
<9 = 2% mortality
Слайд 26CHILD-PUGH CLASSIFICATION
• Five variables to predict risk/survival
• Points for encephalopathy,
![CHILD-PUGH CLASSIFICATION • Five variables to predict risk/survival • Points for encephalopathy,](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-25.jpg)
ascites, bilirubin, albumin, PT
• Score ranges from 5 to 15
• 5 or 6: Child-Pugh class A cirrhosis
• 7 to 9: Child-Pugh class B cirrhosis
• 10 to 15: Child-Pugh class C cirrhosis (worst)
Слайд 27CIRRHOSIS
DIAGNOSIS
Gold standard is liver biopsy
• Not required if diagnosis is
![CIRRHOSIS DIAGNOSIS Gold standard is liver biopsy • Not required if diagnosis](/_ipx/f_webp&q_80&fit_contain&s_1440x1080/imagesDir/jpg/1175796/slide-26.jpg)
clear from history
• Done only when biopsy will change management
• Imaging (ultrasound, CT, MRI)
• May show small, nodular liver
• Not sensitive or specific for diagnosis
• More helpful for detection of hepatocellular carcinoma
• Clinical diagnosis (common)
• Presence of ascites
• Low platelet count
• Spider angiomata