Liver - Angelfire
Liver
Dr. Oliver followed his notes very closely so I am just going to include the additional information. He also stated that he will finish the remaining liver slides on the 31st following the breast lectures.
Pediatric Liver Disease:
The most famous one is Reye's syndrome.
• This is only seen in kids 90% of patients with PBC
• Chronic, progressive cholestatic disease seen in middle aged women (remember that most autoimmune diseases are seen more in women)
• Pathology- cholestasis, destruction of bile ducts by non-necrotizing granulomatous inflammation called florid duct lesion, hepatocyte necrosis from portal inflammation called piecemeal necrosis, scarring and eventually ending up with micronodular cirrhosis
• Slide- portal triad, granuloma (similar to Robbins 19-29)
• Slide-piecemeal necrosis
• Slide- liver with cirrhosis, greenish color from cholestasis (Robbins 19-28)
3. Primary Sclerosing Cholangitis
• Seen in middle aged patients (important distinction is M:F is 2:1)
• Famous person that died from this- Walter Payton
• Etiology- thought to be some kind of autoimmune disease
• 70% of those with PSC have ulcerative colitis but only 4% of those with ulcerative colitis develop PSC
• Pathology- bile duct degeneration, “onion skin” concentric periductal fibrosis obliteration and scarring of ducts caused by cholestasis and biliary cirrhosis
• Slide- ulcerative colitis without PSC (Curran 5.42, p. 97)
• Slide- onion skin fibrosis with bile duct in the middle (Robbins 19-30)
• Slide- Xray of dye injected into biliary tract
Anomalies of the Biliary Tract
1. Von Meyenburg Complexes:
• Most common, clusters of dilated portal bile ducts in the fibrous stroma under the capsule
2. Polycystic Liver Disease
• Multiple cysts in the liver lined by biliary epithelium
3. Congenital hepatic fibrosis (Curran 5.1)
• More fibrosis: fibrotic portal tracts and fibrous septa
4. Caroli’s Disease
• Multiple ducts communicating with the biliary tree
Circulatory Disorders or Vascular Liver Diseases
1. Liver Infarcts (Robbins 19-33)
• Dual blood supply so infarcts are rare and localized unless main hepatic artery thrombosis
• Infarcts of Zahn, occlusion of branches of portal vein, secondary atrophy with portal HTN
2. Portal Vein Obstruction/Thrombosis
• Extrahepatic (infectious pylephlebitis or inflammation of vein)
• Intrahepatic (cirrhosis, tumors, ab pain, ascites, esophageal varices)
• Banti’s syndrome- subclinical occlusion of portal vein causing idiopathic portal hypertension + splenomegaly
• Slide- infarct of liver, pale wedge shaped infarct
3. Passive congestion
• Rt. Sided heart failure causes backflow of blood down inferior vena cava, and liver is the first thing it goes to so you get congestion of liver
• Nutmeg liver, centrolobular area is where it backs up
4. Centrilobular Necrosis (Robbins 19-34)
• Lt. Sided heart failure, shock, vascular insuffiency
• Centrolobular area is the furthest from the blood supply so it is the most susceptible to infarct
5. Cardiac Sclerosis (Cirrhosis)
• Centrolobular liver fibrosis due to chronic CHF
• Just scarring not true fibrosis
6. Peliosis Hepatitis
• Irregular blood filled cystic spaces, usually with no endothelial lining
• Just pooled blood
• Associated with ananbolic steroids, oral contraceptives, cat scratch fever
7. Hepatic Vein Thrombosis (Budd-Chiari Syndrome) Robbins 19-35
• Acute or chronic
• Tremendous congestion of the liver, can involve the entire liver
• Due to: Pregnancy (can cause stasis), postpartum, oral contraceptives (thrombotic), PNH (paroxysmal nocturnal hemoglobinuria), HCC(hepatocellular carcinoma), webs in hepatic veins
• 30% idiopathic
Pregnancy and Hepatic Disease
1. Preeclampsia/ Eclampsia (Robbins 19-37)
• Hemorrhagic disease, hemorrhage under capsule
• HEELP (hemorrhage, elevated liver enzymes and low platelets)
2. Acute fatty liver of pregnancy
• Usually 3rd trimester, mild to severe hepatic failure
• Looks like Reye’s syndrome-microvesicular steatosis
• If severe enough, termination of pregnancy might be needed to save the woman
3. Intrahepatic Cholestasis of Pregnancy
• Benign condition due to estrogen related derangement of bile acid metabolism
• Mild cholestasis and increased risk of gallstones
Liver and Transplantation
1. Drug Toxicity
• Soon after transplant administered
• Nonspecific cholestasis/ necrosis
2. Graft vs. Host disease
• Not from liver transplant but from bone marrow transplant
• Acute GVH 10-50 days after BM transplant, signs of acute hepatitis
• Chronic GVH >100 days and limited to portal tracts
3. Rejection of implanted livers
• Opposite of GVH- patient’s immune system rejects the graft and fights it
• Acute-portal inflammation, hepatocyte injury
• Chronic- vascular problem
4. Veno-occlusive disease nodular regenerative hyperplasia
• Follows BM transplant (more common in allografts)
• Subendothelial deposition of collagen in central vein
5. Nonimmunologic damage to liver allograft
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