LFTs Flashcards
Elevations typical of inflammation/hepatocellar damage
ALT
AST
may see GGT
(bilirubin, bilirubin direct, bilirubin indirect- only see if inflammation is severe)
Elevations typical of cholestasis
Bilirubin
Bilirubin direct
Alkaline Phosphatase
may see GGT
If GGT and ALP are elevated..
Source is likely liver
Pattern indicative of reduced liver function
low albumin
low total protein
(may order separately:
PT- prolonged/high)
Which is worse?
Very high ALT & AST with nl albumin & PT/INR
OR
Normal ALT & AST w. slightly low albumin & minimally high PT/INR?
Normal ALT & AST w. slightly low albumin & minimally high PT/INR
This means that the liver is not functioning!
No direct relationship between severity of liver disease & transaminase levels
Liver inflammation/hepatocellular damage=
high ALT & AST
Cholestasis=
high All phos & high Direct Bilirubin
Reduced liver function=
High PT/INR, low albumin
Common cause of cholestasis?
Sx?
Choledocholithiasis
pain- biliary colic
jaundice
clay-colored stools (light colored)
cola colored urine
Isolated elevation in Indirect (unconjugated) bilirubin is often due to?
Gilbert syndrome
Alkaline phosphate is derived from..?
liver & bone
If only Alk phos is elevated, must get _____?
If elevated/not elevated, suggests..?
GGT
elevated= liver source
not elevated= bone source
Common cause of reduced liver function= ?
Cirrhosis
Explain why cirrhosis causes reduced liver function
Results from chronic liver disease ->
causes chronic inflammation/hepatocellular damage ->
scarring (fibrosis) - scarred liver does not function like healthy liver
Signs and sx of cirrhosis
fatigue portal HTN ascites jaundice easily bruising/bleeding
Can patients with nl ALT & AST levels have significant liver disease? Explain
Yes
Occurs in setting of chronic disease- like cirrhosis
Is ALT or AST more specific to the liver?
ALT
Risk factors for liver damage and disease
fam hx EtOH obesity DM hyperlipidemia meds/supplements autoimmune dz
Hepatitis risk factors -IVDU -high-risk sexual behavior foreign travel -hx of transfusions -tattoos
What is the easiest way to determine if a medication is causing elevation of ALT & AST?
Stop it and see if the lab value returns to nl
DDx for elevated transaminases (AST & ALT)
hepatitis alcoholic liver dz fatty liver disease meds hemochromatosis
(celiac, hypothyroidism = uncommon)
When to worry about elevated ALT & AST vs not
modest elevations are common- often asymptomatic
Worry if: other liver tests abnormal clinical signs and sx of disease >3-5 fold elevation of any level persistently abnormal for >6 months
DDx for mildly elevated AST & ALT
-Fatty liver (hepatic steatosis)- assoc. with obesity, type 2 DM, HLD
EtOH related
DDx for elevated AST
Alcoholic hepatitis
common bile duct obstruction
cholangitis
DDx for ALT/AST elevation with:
AST:ALT ratio of >1
EtOH liver disease (especially if GGT >2x normal)
DDx for ALT/AST elevation with:
AST:ALT ratio of < 1 (ALT higher)
acute or chronic viral hepatitis
NASH (nonalcoholic steatohepatitis)
DDx for ALT/AST elevation with:
associated increased Alk Phos
Cholestatic disease (choledocholithiasis)
NASH = ?
fatty infiltration + associated inflammation
Prevalence of NAFLD (non alcoholic fatty liver disease)/NASH in population
11% (accounting for 75% of chronic liver dz)
Risk factors for NAFLD/NASH
obesity
hypertriglyceridemia
insulin resistance & DM
Meds (estrogens, corticosteroids)
What labs would be elevated in pt with NAFLD/NASH?
ALT or ALT & AST
What is the usual initial imaging test you do to diagnose NAFLD/NASH?
why?
Ultrasound
increased echogenicity can detect steatosis
General approach to management of NAFLD/NASH
weight loss in obese pts
Hep A & B vaccinations
avoid alcohol
treatment of risk factors of cardiovascular dz
What is Hereditary Hemochromatosis?
And what population is it mostly seen in?
Hereditary disorder of iron metabolism
-autosomal recessive
Caucasians
Classic triad in Hereditary Hemochromatosis
cirrhosis
DM
bronze skin pigmentation
What are the steps to diagnosing Hereditary Hemochromatosis?
- Elevated ALT & AST, or 1st degree relative
- check serum transferrin saturation
- If TS <45= normal, no further eval
- If TS > 45 - check genotype
If not identified, hereditary hemochromatosis can lead to?
cirrhosis leading to a hepatocellular carcinoma
What is the most common pt to be diagnosed with autoimmune hepatitis?
Age/gender
40s-50s
female
What is Wilsons disease?
very rare hereditary disorder of cellular copper transport
-autosomal recessive
What is a notable physical feature of patients with Wilsons disease?
Kayser-Fleischer rings (in about 1/2 pts with dz)
Other than elevated ALT/AST, what other lab abnormality would you see in a pt with Wilson disease?
Low ceruloplasim (the major copper-carrying protein)
Approach to an asymptomatic pt with mildly elevated ALT/AST
Step 1
Check for risk factors for hepatitis, liver damage, & conditions assoc. with NAFLD/NASH
Step 2
Consider other causes of elevated ALT/AST (celiac, hypothyroidism, adrenal insufficiency)
Step 3
Consider screening for rare liver conditions (autoimmune hepatitis, Wison disease)
Step 4
Ultimately may need specialty consult- GI or Hepatologist
Describe Hep A infection
what kind of hep, chronic/not, route
- causes “infectious/ endemic hepatitis”
- does not lead to chronic disease
- spread fecal-oral route
What are the main sx of Hep A?
fever and jaundice (looks like hepatitis)
Management of Hep A
supportive care
post-exposure prophylaxis (vaccine)
Prevention of Hep A
- Hygiene- hand washing
- vaccinate children between 12-23 months
- vaccinate those who are at risk of complications from HAV (traveling, MSM, drug users, w/ chronic liver disease, contacts of people w/ HAV)
What will labs show in pt with Hep A?
Elevated ALT & AST
Can also see elevated bilirubin
When testing for Hep A, what is an good marker of acute or recent infection?
IgM anti-HAV antibodies
Describe Hep B
transmission, chronic/not?
Transmitted by blood, sexual contact, parenteral contact
Leading cause of cirrhosis and hepatocellular carcinoma worldwide
Hep B- Acute vs chronic sx
Acute: varies
Chronic: usually asymptomatic until late disease
Prevention of Hep B
- Avoid high risk behaviors
- Vaccination (infants, children, MSM, IVDU, people with HIV)
What labs would you see n acute vs chronic Hep B?
Acute: Elevated ALT/AST (in the hundreds or thousands)
Chronic: Elevated ALT/AST (mildly elevated)
What is Hep B surface antigen (ABsAg) and when is it highest?
Protein on surface of the virus
During incubation-beginning of acute phase (Infective phase)
What is Hep B surface antibody (anti-HBs) appear and what does it indicate?
- appears during recovery
- usually indicates recent infection or immunity
- also in vaccinated person
When does Total Hep B core antibody appear and what does it indicate?
At onset of sx in acute phase and persists for life
Indicates previous or ongoing infection of HBV in undefined time frame
What does IgM antibody to Hep B core antigen (IgM anti-HBc) indicate?
acute or recent infection with HBV (less than 6 months)
If someone has anti-HBs + does not have anti-HBc, what does that indicate?
Immunity from vaccination
What is Hep C the leading cause of?
leading cause of liver transplants in the U.S.
How is Hep C transmitted?
- IVDU (most common)
- received donated blood
- needle-stick injuries
- birth (HVC-infected mother)
Can also be spread infrequently through:
sex
sharing personal items (toothbrush/razors)
Explain the process of testing for HCV
- HCV antibody
- If +, check for HCV RNA
- If HCV RNA is +, pt has HCV. If HVC RNA not preset- infection might have cleared or HCV antibody was false +
(Because Hep C does not provide immunity to re-infection!)
