Lecture 4 - Liver 1 Flashcards
LFTs commonly include?
hepatic panel = LFT
Bilirubin Albumin ALT AST ALP Total Protein
Less commonly included in LFTs?
GGT
LDH
PTT/INR
Platelets
Review: ALT is found primarily in the liver whereas AST is found in skeletal muscles and erythrocytes. So?
ALT elevations are generally more specific for hepatic injury
Transaminitis?
Elevation of transaminases (ALT/AST), often discovered on routine labs in otherwise asymptomatic pt
DDx is vast (so requires a thorough history, PE, repeat labs, hepatitis panel, hepatitis US, GI referral)
2:1 elevation in AST:ALT often indicates what? (particularly in light of elevated GGT)
alcohol-related liver disease
AST/ALT catalyze transfer of a-amino groups from aspartate/alanine to a-keto group of ketoglutaric acid to generate oxalacetic/pyruvic acids.
Both enzymes require what?
pyridoxal-5’-phosphate (Vit B6) (a deficiency which has a greater effect on ALT, hence the 2:1 ratio)
(alcoholic liver disease = pyridoxal-5’-phosphate deficiency)
GGT is an enzyme that is present in hepatocytes, biliary epithelial cells, renal tubules, pancreas, intestine (mechanisms of alteration are similar to ALP).
Note that GGT levels can also be observed in a variety of non-hepatic diseases as well
Many diseases of the liver, regardless of cause, may be responsible for altered GGT serum levels.
Because of lack of specificity, but HIGH SENSITIVITY, GGT can be useful for IDing causes of altered ALP levels
GGT elevated, with AST/ALT ratio > 2, may support the diagnosis of alcoholic liver disease
Disproportionate elevation in alkaline phosphatase (ALP) compared to ALT/AST…
LFT w/ cholestatic pattern
Most common causes of pathological elevation of ALP?
Liver/bone disease
Hepatic ALP is present on the surface of bile duct epithelium. Cholestasis enhances the synthesis and release of ALP, and accumulating bile salts increase its release from the cell surface
Pathologic increase in portal pressure indicated by?
pressure gradient b/w portal vein and IVC > 10 mm HG
Most common etiology of portal HTN?
Cirrhosis
Jaundice is result of accumulation of bilirubin in body tissue but isn’t clinically apparent until what level?
greater than 2 mg/dL
Unconjugated bilirubin (+albumin) is found where?
Found in the blood… then… arrives at the liver where it becomes conjugated and moved through the biliary system to the small intestine for excretion
Prehepatic jaundice is shown by elevated levels of unconjugated (indirect) bilirubin, most commonly due to?
- overproduction of bilirubin
- impaired bilirubin uptake by the liver
- abnormalities of bilirubin conjugation
Unconjugated hyperbilirubinemia causes?
Increased bili production: Hemolytic anemias, hemolytics rxns, hematomas, pulm infarct
Impaired bili uptake/storage: posthepatitis hyperbilirubinemia, Gilbert syndrome, Crigler-Najjar syndrome, drug rxns (TMP-SMX)
Plasma elevation of BOTH unconjugated and conjugated bilirubin can be to?
(this is often referred to as conjugated hyperbilirubinemia, even though both fractions of bilirubin are elevated)
Hepatocellular disease
Impaired canalicular disease
Biliary obstruction
Conjugated hyperbilirubinemia from hepatocellular dysfunction could be caused by?
hepatitis
cirrhosis
Examples of conditions of biliary obstructions causing hyperbilirubinemia are?
choledocholithiasis
biliary atresia
carcinoma
Clinical findings of unconjugated hyperbilirubinemia (prehepatic jaundice)?
Mild jaundice (maybe only scleral icterus)
Normal stool/urine color
Splenomegaly if etiology is hemolytic disorder (note that sickle cell anemia will likely NOT present w/ splenomegaly)
Clinical findings of hepatic/conjugated jaundice (hepatocellular disease)?
So, cirrhosis and hepatitis
Malaise, anorexia
Low grade fever
RUQ pn
Dark urine
amenorrhea
enlarged/tender liver
spider teleangiectasias
palmar erythema
ascites
gynecomastia
Clinical findings of conjugated jaundice from cholestatic syndromes?
Jaundice
Pruritus
light colored stool
Clinical findings of conjugated-biliary obstruction jaundice?
(post hepatic)
RUQ pn
wt loss (suggestive of carcinoma)
pruritus
dark urine
light-colored (acholic)
- Lab studies for jaundice?
- Radiographs for jaundice?
- What else can you do, for bile ducts maybe?
- Hepatic labs, CBC, CMP, UA
- Hepatic US
- ERCP, if biliary obstruction is suspected
Endoscopic technique in which a specialized side-viewing upper endoscope is guided into duodenum, allowing for instruments to be passed into the bile and pancreatic ducts…
Indicated for?
ERCP
indicated in jaundiced patient suspected of having biliary obstruction
Tx approach for jaundice?
Aimed at underlying etiology
SHould be referred (GI) for underlying etiology
Parameters for acute liver failure?
Severe acute liver injury w:
encephalopathy
AND
impaired synthetic fx (INR>1.5)
(w/in 8 weeks of onset of dz, in a pt w/o preexisting liver dz)
Most common cause of acute liver failure?
Acetaminophen (45%)
risk increased in pts w/ DM
By definition, pts w/ acute liver failure have severe acute liver injury (hepatic encelopathy, INR>1.5)
Other ssx?
Fatigue/malaise/lethargy anorexia N/V RUQ pn pruritus jaundice abd distension (from ascites)
Lab finding for acute liver failure?
- INR>1.5
- markedly elevated aminotransferase levels
- Elevated bilirubin and ALK PHOS
- Low platelet count (<150,000)
elevated ammonia
elevated amylase/lipase
elevated BUN/Cr
Acute liver failure admission/in patient mgmt parameters?
IV fluid/electrolyte replacement
Dietary monitoring
Gastroprotective measures (IV PPI, H2 to prevent stress gastropathy)
(and of course other tx as indicaated by etiology)
Most common causes of viral hepatitis in US?
Hep A
Hep B
Hep C
