Clinical Lab in GI Disease Flashcards
What are the diagnostic criteria for acute pancreatitis?
Need two of three:
Abdominal pain characteristic of disease
amylase and/or lipase at least 3x the ULN
characteristic imaging findings
Which is better for pancreatitis and why: amylase or lipase?
lipase because it is more sensitive and more specific
also remains elevated longer than amylase
IN FACT: CURRENT REC IS FOR LIPASE ALONE
What are some other causes for elevated pancreatic enzymes?
macroamylasemia/macrolipasemia renal failure acute appendicitis cholecystitis intestinal ischemia/obstruction peptic ulcer disease gynecological disease diabetes (esp lipase) parotid/salivary gland (amylase only)
What are the two most common causes of acute pancreatitis?
gallstones and alcohol
What are some other less common causes of acute pancreatitis?
post-ERCP, trauma/injury
Genetic - like CF mutations
Drugs (azathioprine, sulfonamides, NSAIDs, steroids, tetracycline)
Viral infections (mumps, rubella, EBV, CMV, hepatitis)
Hypertrigliceridemia
Hypercalcemia
What are the first tier LFT labs?
transaminases bilirubin alk phos GGT albumin prothrombin time/INR
What is the general pattern of liver labs in hepatocellular injury/necrosis?
ALT and AST significantly elevated, moreso than alk phos
What is the general pattern of liver labs in cholestatic disease?
alk phos elevated higher than ALT/AST
What is the general pattern of liver labs in infiltrative liver disease?
elevated AP with either normal or just slightly elevated AST/ALT
Which transaminase is more specific for liver disease?
ALT
AST is also found in muscle and red cells, so with extensive muscle breakdown, both ALT and AST will rise
Which transaminase has a longer half-life?
ALT
So Liver and Longer
Where on the cell is alk phos located?
on the hepatocyte membrane bordering the bile canaliculi, which is why it elevated in obstructive disease
Where in the body are other alk phos isoemzymes located?
bone and placenta
also elevated in other GI and kidney diseases
What can you use to confirm a liver course of an elevated alk phos?
GGT - there are few reasons to order a GGT other than this!
What are the main causes of acute rises in transaminases?
Viral hepatitis Drug-induced hepatitis alcoholic hepatitis Ishcemic "shock liver" acute ductal obstruction autoimmune hepatitis Wilson's disease
ALT is often in the thousands with acute hepatitis. If it’s over 5,000 U/L, though, what should you consider?
Acetaminophen
hepatic ischemia
unusual viruses like HSV
What are the four main causes of chronic hepatitis?
Hep C
Hep B
NASH
Alcoholic liver disease
What is the time cutoff for hepatitis to be called chronic?
over 3 months
What are some common causes of cholestasis?
Stones Primary biliary cholangitis primary sclerosing cholangitis drug-induced stasis infiltrative/malignancy severe inflammation
Which suggests liver disease: elevated unconjugated bilir (indirect) or elevated conjugated bili (direct)?
conjugated (direct)
elevations in unconjugated (indirect) suggest hemolysis
Jaundice will become visible at what bili level?
> 2.5 mg/dL
Can bilirubin help you determine whether liver disease is hepatocellular, cholestatic or infiltrative?
not really
What are some causes for unconjugated hyperbilirubinemia besides hemolysis?
resorption of large hematoma
ineffective erythropoiesis (like B12 def)
neonatal physiologic hyperbilirubinemia
Gilbert syndrome
What is the typical pattern of LFTs in alcoholic hepatitis?
AST > 2 x ALT
but AST less than 400 UL
What are the two main autoantibodies seen in autoimmune hepatitis?
type 1 with anti-smooth muscle and antinuclear
type 2 with liver-kidney microsome type 1
Who gets PBC and how do they present?
middle aged women
presenting with fatigue and pruritus
What will labs look like in PBC?
increased alk phos increased IgM Fal soluble bitamin deficiencyes high HDL later increased Bili
If you did a biopsy of a liver with PBC, what would you see?
granulomatous infiltration of the septal bile ducts
What is the main antibody seen in PBC?
anti-mitochondrial antibodies
What symptoms occur in stage I of acetaminophen toxicity?
anorexia
nausea
vomiting
What symptoms occur in stage II?
RUQ pain
AST and ALT elevation (and sometimes bili, PT and/INR)
What symptoms occur in stage III?
vomiting and jaundice
LFTs peak
sometimes renal failure and pancreatitis
What happens in stage IV?
resolution or progression to multiple organ failure and sometimes death
What are two major causes of iron overload liver damage?
hereditary hemochromatosis or multiple blood transfusions
What will iron labs look like in iron overload? How do you confirm?
Transferrin saturation will be high
Ferritin also high (?)
liver biopsy
What gene is defective in Wilson disease?
ATP7B
How will wilson disease present?
Kayser-Fleischer ring hepatitis splenomegaly hypersplenism Coomb's neg hemolytic anemia portal hypertension neuro-psychiatric disease
How do you test for Wilson disease?
urinary copper (high)
ceruloplasmin (low)
hepatic Cu (high)
genetic testing
What causes Crigler Najjar type 1? Who gets it?
Absent UDPGT activity (so unconjugated hyperbilirubinemia)
newborns and it’s fatal due to kernicterus unless they get a liver transplant.
What causes Crigler Najjar type 2?
milder deficiency of UDPGT, so milder form than Type 1 and fortunately more common
can survive to adulthood
What are the two other genetic bilirubin metabolism disorders that cause conjugated hyperbilirubinemia and asymptomatic jaundice?
Dubin-Johnson
Rotor syndrome
What percentage of newborns will have jaundce?
60%
What are the typical causes for neonatal jaundice?
usually immaturity of conjugating enzymes
hemolytic disease
bruising (cephalohematoma)
sepsis
What’s the major concern with jaundice in newborns?
acute encephalopathy and kernicterus
