Hepatology: Abominal Radioraphy, Hepatitis, Encephalopathy, Sbp

Front 1

Abdominal Radiography: Abdominal Series
• SBO:
• Gallstone ileus:
• Hernia:
• String of pearls:
• Gasless abdomen:
• Colitis:
• Obstruction versus ileus:

Back 1

• SBO: see multiple air-fluid levels
• Gallstone ileus: see air in the biliary tree
• Hernia: see bowel extending beyond inguinal line
• String of pearls: bowels filled with fluid; high degree of obstruction; very little air
• Gasless abdomen: either esophageal obstruction and nothing going through or marked obstruction
because the loops are filled with fluid.
• Colitis: often do not see haustra. In long-standing UC, see a "lead pipe" (no haustra) image of the
sigmoid/descending colon.
• Obstruction versus ileus: clues suggestive of obstruction include asymmetric dilation of bowel, no air in
the cecum/rectum, a definite point of transition, alternating levels of air-fluid.
U/S: Hepatobillary. CT: Masses

Front 2

Ascities: Work up

Back 2

On physical exam will palpate through fluid wave transmission. If you suspect ascities and not on physical exam than look on U/S. If new on set ascities have to perform paracentesis. If patient is cirrhotic with fever, leukocytosis, and altered mental status have to rule out infection. Send ascities fluid for cell count, albumin, protein, bacterial culture. Others LDH, glucose amylase, cytology, AFB.

Front 3

Ascities: SAAG

Back 3

SAAG = Serum albumin - Ascities albumin
High gradient >1.1g/dl (cirrhosis, alcoholic hepatitis, cardiac ascities, fulminant hepatic failure, budd chiari syndrome, massive hepatic metastases, veno occlusive disease, portal vein thrombosis, myxedema, fatty liver)
Low gradient <1.1 - (Nephrotic syndrome, peritoneal carcinomatosis, pancreatic ascities, TB peritonitis, billiary ascities, collagen vascular disease

Front 4

Ascities: Treatment

Back 4

Dietary salt restriction. Spironolactone 100mg daily and furosemide 40mg daily. Fluid restriction only if hyonatremic.

Front 5

Paracentesis: Indications

Back 5

• Indications for Diagnostic Paracentesis
• New onset ascites
• Patients with ascites and fever, leukocytosis or other signs/symptoms of infection
• Patients with cirrhosis who have ascites at the time of hospitalization
• Patients with cirrhosis and ascites who have worsening of their clinical condition or deterioration in
laboratory parameters (i.e. acidosis, azotemia)
• Indications for Therapeutic Paracentesis
• Tense ascites
• Respiratory distress

Front 6

Spontaneous Bacterial Peritonitis: Definition

Back 6

>250 PMN or WBC >500cells/mm3 with positive fluid culture.
Culture negative neutrocytic ascities: PMN count >250cells/mm3 with neative fluid culture subtract 1PMN for ever RBC.

Front 7

SBP: Common Pathogens and Risk Factors

Back 7

E. coli. K. pneumoniae. Enterobacteriaceae, strep pneumoniae. Enterococcus.

Sever liver disease. GI hemorrhage. Prior SBP. Ascitic fluid protein <1g/dL

Front 8

SBP: Clinical Signs, Diagnosis, Treatment

Back 8

Fever, ascities, altered mental status, vomiting, diarrhea, and abdominal pain.

Diagnosis with abdominal paracentisis

Treat with antibiotic, cephalosprin (ceftriaxone or cefotaxime) high dose 2gm/day.
Prophylaxisis Cipro 750mg PO weekly

Front 9

Hepatic Encephalopathy: Diagnosis and Percipating Factors, Treatment

Back 9

Any patient with abnormal liver function and altered mental status. Patient will have asterixis on physical exam and elevated serum ammonia levels. Precipating factors include GI bleeding, infection, increased dietary intake, azotemia, constipation, volume depletion, hypoglycemia.

Front 10

Hepatic Encephalopathy: Treatment

Back 10

Correct precipitating cause. Lactulose 30cc TID titrate up to 3-4 soft bowel movements a day.

Front 11

• Liver Tests
• Aminotransferases (AST, ALT):
• ALT (SGPT)
• AST (SGOT)
• High levels of AST and ALT (about 10× normal)
• In alcoholic liver disease,
• Alkaline phosphatase:
• Albumin and prothrombin time:
• Bilirubin:

Back 11

• Liver Tests
• Aminotransferases (AST, ALT):
• ALT (SGPT) is more specific for the liver
• AST (SGOT) can be derived from the liver, heart or skeletal muscle
• High levels of AST and ALT (about 10× normal) usually indicate acute hepatocellular injury
• In alcoholic liver disease, AST and ALT are generally modestly elevated (about 5-6× normal) and the
AST/ALT ratio is around 2
• Alkaline phosphatase: derived from liver, intestine, bone, kidney, and placenta.
• GGPT, 5’-nucleotidase are more “liver specific” enzymes
• Alkaline phosphatase is increased in biliary obstruction, cholestasis, and space occupying lesions
• Albumin and prothrombin time: markers of synthetic function
• Bilirubin: marker of clearance

Front 12

Patterns of LIver INjury
• Hepatocellular:
• Cholestasis:
• Biliary obstruction
• Isolated Hyperbilirubinemia:
• Conjugated:
• Unconjugated:
• Infiltrative:

Back 12

• Hepatocellular: ↑↑ aminotransferases + ↑ alkaline phosphatase ± ↑ bilirubin
• Viral, autoimmune, or drug-induced hepatitis, ischemic, toxic, hereditary, nonalcoholic steatohepatitis
(NASH)
• Cholestasis: ↑↑alkaline phosphatase + ↑ bilirubin ± ↑ aminotransferases
• Hepatocellular dysfunction:
• Biliary epithelial damage from hepatitis, cirrhosis
• Intrahepatic cholestasis from medications, sepsis, primary biliary cirrhosis, CHF
• Biliary obstruction
• Isolated Hyperbilirubinemia:
• Conjugated: impaired excretion (hepatocellular injury, Dubin-Johnson)
• Unconjugated: overproduction (hemolysis) or impaired conjugation (Gilbert’s, Crigler-Najjar)
• Infiltrative: ↑ alkaline phosphatase ± ↑

Front 13

Abnormal LFT Pneumonic

Back 13

• Autoimmune hepatitis/Hepatitis A
• Hepatitis B
• Hepatitis C
• Drugs/Medications: acetaminophen, NSAIDs, antibiotics, statins, anti-epileptics, anti-TB.
• EtOH
• Fatty Liver/Nonalcoholic steatohepatitis
• Granulomatous
• Hemochromatosis/Wilson’s/α1-antitrypsin deficiency

Front 14

Back 14