Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal 1 > Liver Function Tests > Flashcards

Liver Function Tests Flashcards

1
Q

What are the roles of the liver?

A
  • synthesis of protein, vitamins, and fats
  • storage of glycogen, triglycerides, iron, copper, and lipid soluble vitamins (A, D, E, and K).
  • glucose regulation (gluconeogenesis)
  • detoxification
  • excretory function (bile production/drainage).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the common Liver Function Tests (LFTs) or sometimes called Hepatic Function Panel or Complete Metabolic Panel (CMP)?

A

Markers that indicate hepatic function:

  • aspartate aminotransferase (AST)
  • alanine aminotransferase (ALT)
  • albumin
  • alkaline phosphatase
  • total protein
  • total bilirubin
  • direct bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are other labs that can be ordered for LFTs?

A

usually ordered in response to abnormal findings in your Hepatic Function Panel:

  • lactate dehydrogenase (LDH)
  • gamma glutamyl transpeptidase (GGT)
  • 5’ nucleotidase
  • coagulation factors (PT/PTT/INR)
  • acute hepatitis panel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What tests would you look at for hepatocellular injury (damage to the hepatocytes themselves)?

A
  • AST
  • ALT
  • LDH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What tests would you look at for cholestasis (flow of bile stops) or biliary excretory function?

A
  • Bilirubin
  • Alkaline phosphatase
  • GGT
  • 5’ nucleotidase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What tests would you look at for hepatic synthetic function (cirrhosis)?

A
  • albumin
  • PT
  • coagulation factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is most important when evaluating a patient and interpreting LFTs?

A

HISTORY AND PHYSICAL!!!

*Never cut corners because that’s how people die. Sometimes LFTs can be normal in a disease state.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are important question to ask in your history and physical (H&P)?

A
  • FMH (any issues with liver, bilirubin or anemia)
  • Social Hx (occupation, travel, alcohol or illicit drug use, sexual activity).
  • PMH/ PSH (home medications, surgeries)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some things you would see on a physical exam if someone presented with liver disease?

A
  • cachexia/temporal wasting
  • spider nevi/palmar erythema, gynecomastia, caput medusa.
  • ascites
  • hepatic encephalopathy
  • Virchow’s node/Sister Mary Joseph’s node
  • Pleural effusion
  • Neurologic issues
  • JVD
  • jaundice
  • parotid gland enlargement
  • asterixis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What would cause aminotransferases (AST/ALT) to be released into the blood?

A
  • toxins (EtOH, statins…)
  • viral hepatitis
  • ischemia/hypoperfusion
  • malignancy
  • Elevations in these enzymes indicate possible differentials.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is important about ASPARTATE aminotransferase (AST) and what is a normal value?

A
  • NORMAL= 8-45 U/L
  • formerly SGOT (serum glutamic-oxaloacetic transaminase).
  • found in mitochondria and in multiple organs (liver, heart, muscle).
  • In acute hepatitis, AST may elevate higher than ALT in the first 48 hours (half-life= 48 hours), then ALT will be higher after 48 hours.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is important about ALANINE aminotransferase (ALT) and what is a normal value?

A
  • NORMAL= 7-55 U/L
  • formerly SGPT (serum glutamic-pyruvic transaminase).
  • unlike AST, it is PRIMARILY PRODUCED by the LIVER hepatocytes. Thus it is more specific to liver disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Are AST elevations usually lower or higher than ALT elevations in the setting of hepatic injury?

A

lower (aka ALT is higher).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

If you see an AST:ALT ratio of 2:1, what should you think?

A

alcoholic liver disease

*higher levels indicate more damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the patterns of acute hepatic failure/fulminant (severe and sudden in onset) hepatic necrosis?

A
  1. LFTs usually 10x upper normal (in the 100s).
  2. hepatic encephalopathy= patient is lethargic, going in and out of consciousness, and/or can’t hold out their arms when asked to do so.
  3. prolonged PT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some causes that would cause LFTs to be 15x GREATER than normal?

A

Consistent with acute hepatitis from:

  • acute viral hepatitis
  • alcoholic hepatitis
  • toxins
  • acetaminophen
  • ischemia
  • Wilson’s disease
  • autoimmune
  • Budd-Chiari syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some causes that would cause LFTs to be LESS than 15x normal?

A 
- possible improving etiology of acute hepatitis. 
More chronic issue:
- chronic Hep C
- Chronic Hep B
- Wilson disease
- Viruses (EBV, HIV, CMV)
- primary biliary cirrhosis 
- hemochromatosis primary sclerosing cholangitis
- alpha-1 antitrypsin
- anorexia nervosa
- nonalcoholic fatty liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is important about alkaline phosphatase and what is a normal value?

A
  • NORMAL= 45-115 U/L

- derived from liver and bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do you determine if an elevated alkaline phosphatase is coming from the liver or bones?

A

Order GGT:

  • if 4x ELEVATED then this is consistent with cholestasis; aka the biliary tree).
  • if not elevated, then think bone fracture, abnormal bone formation (Paget’s disease), 3rd trimester of pregnancy, or just youth.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is important about gamma glutamyl transpeptidase (GGT) and what is a normal value?

A
  • NORMAL= 9-48 U/L
  • mainly located in hepatocytes and biliary epithelial cells.
  • Again, elevation with elevated ALT leads to a cholestasis picture.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is 5’ nucleotidase?

A
  • found in multiple organs (liver, brain, and intestines), but is released into serum from ONLY HEPATOBILIARY tissue.
  • found near the bile canalicular membrane of hepatocytes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Is 5’ nucleotidase ever elevated in conditions other than liver disease?

A

Rarely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is important about lactate dehydrogenase (LDH) and what is a normal value?

A
  • NORMAL= 122-222 U/L

- found in multiple areas of the body and used mostly for MI, or hemolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is important to know about ammonia?

A
  • it is produced in the body during normal protein metabolism and by intestinal bacteria (primarily those in the colon).
  • if the liver is functioning properly, it will clear the ammonia (by converting it to urea for the kidneys to excrete). If it is not, then you will see a rise in ammonia levels leading to HEPATIC ENCEPHALOPATHY (disconnect in motor functions due to effects on nervous tissue in the brain).
  • poor correlation of blood serum ammonia and hepatic function however, because everyone reacts to ammonia levels differently.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is important to know about PT (Prothrombin Time)/INR (International Normalized Ratio)?

A
  • PT assesses EXtrinsic pathway of clotting. This will INCREASE in liver disease due to decreased synthesis of both vitamin K-dependent and -independent clotting factors; mostly factor 7.
  • In severe and/or chronic liver disease (both the PT and aPTT may be prolonged).
  • INR will be elevated due to vitamin K dependent coagulation factors 2, 7, 9 and 10.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the MELD score?

A

score calculated from 3 components: total bilirubin, creatinine, and INR to prioritize patients for liver transplant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Again what labs would point you to a Hepatocellular pattern?

A
  • AST/ALT greater than alkaline phosphatase
  • possible elevation of serum bilirubin
  • possible abnormal tests of synthetic function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Again what labs would point you to a Cholestasis pattern?

A

We are now lower in that biliary tree so think:

  • elevation of ALKALINE PHOSPHATASE out of proportion to AST/ALT.
  • serum bilirubin may be abnormal
  • GGT abnormality (elevated).
  • synthetic function tests can be abnormal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is important about albumin and what is a normal value?

A
  • NORMAL= 3.5-5 g/dL
  • low levels point to chronic disorder of the liver.
  • not accurate if malnourished in last 24-48 hours.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is important about PT/INR and what are normal values?

A
  • NORMAL PT= 9.5-13.8 seconds
  • NORMAL INR= 0.9-1.1
  • prolongation suggests vitamin K deficiency that may be related to malabsorption or hepatocellular dysfunction.
31
Q

What is bilirubin?

A

end product of heme degradation

32
Q

What is important about hyperbilirubinema and what is a normal value of total serum bilirubin?

A
  • NORMAL= 0.2-1.2 mg/dL
  • fractionate to direct (conjugated) and indirect (unconjugated) to help with Dx.
  • level >2.5 mg/dL is required to produce jaundice.
  • if elevated with normal alkaline phosphatase, then likely genetic disorder or hemolysis.
33
Q

What is important about DIRECT (conjugated) bilirubin and what is a normal value?

A
  • NORMAL= 0-0.3 mg/dL
  • job of the liver is to make non-water soluble (unconjugated) bilirubin, water soluble by conjugating it (direct bilirubin), so that it can be excreted in bile.
  • values >1.0 mg/dL always abnormal in infants (so do something).
  • if elevated, means decreased excretion from bile ductules.
34
Q

What are 3 possible problems that you should consider if DIRECT bilirubin in elevated (past 0.3 mg/dL)?

A
  1. extrahepatic/biliary obstruction
  2. intrahepatic cholestasis
  3. hepatocellular injury
35
Q

How does the liver conjugate bilirubin from the blood?

A

via UDP-glucuronyltransferase (UGT1A1 gene is most important). Conjugation is necessary for excretion of bilirubin across the bile canalicular membrane into bile.

36
Q

What is normal for INDIRECT (unconjugated) bilirubin?

A
  • NORMAL= 96% of total bilirubin is in unconjugated form.
37
Q

What are some possible problems that you should consider if INDIRECT (unconjugated) bilirubin in elevated?

A
  • Bilirubin overproduction from hemolysis, hematoma, or ineffective erythropoiesis.
  • Reduced uptake from cirrhosis or Gilbert’s syndrome.
  • Impaired conjugation from impaired UDP-glucuronosyltransferase, Crigler-Najjar syndrome, or Gilbert’s syndrome.
38
Q

What is Gilbert’s syndrome?

A
  • most common inherited impairment of conjugated bilirubin excretion.
  • you will have a transient elevation of UNCONJUGATED bilirubin due to UGT1A1 reduction in activity, preventing the unconjugated bilirubin from entering the hepatocytes.
  • serum bilirubin is usually
39
Q

When is Gilbert’s syndrome most often diagnosed?

A

at or shortly after puberty or in adult life during routine examination.

40
Q

Is Gilbert’s syndrome often symptomatic?

A

NO, but may become intermittently jaundiced with acute illness/stress.
*Remember 2.5 mg/dL is the minimum you need to become jaundiced.

41
Q

What is Crigler-Najjar Syndrome?

A
  • RARE inherited (autosomal recessive) disorder of UDP-glucuronosyltransferase causing COMPLETE failure of bilirubin-glucuronide conjugation.
  • causes jaundice/kernicterus (bilirubin encephalopathy).
  • Types 1 and 2
42
Q

What is Type 1 Crigler-Najjar syndrome?

A
  • more severe of the 2 causing elevated unconjugated (indirect) bilirubin (20-45 mg/dL) with no detectable constitutive expression of UGT1A1 activity in hepatic tissue.
  • usually LFTs are normal otherwise.
  • Dx in infancy
43
Q

What is Type 2 Crigler-Najjar syndrome?

A
  • lower average unconjugated bilirubin, normal LFTs, less kernicterus, some UGT1A1 activity (aka less severe).
  • may not be Dx until later in life.
44
Q

What is Dubin-Johnson syndrome?

A
  • RARE inherited metabolic disorder causing an inability to transport bilirubin-glucuronide through hepatocytes into canaliculi.
  • causes elevated CONJUGATED (direct) bilirubin with normal LFTs.
  • usually asymptomatic benign process.
  • may see jaundice/icterus with an illness.
45
Q

What is the cardinal feature of Dubin-Johnson syndrome?

A
  • grossly dark/black liver.
46
Q

What is Rotor syndrome?

A
  • RARE benign, autosomal recessive disorder causing impaired excretion of conjugated bilirubin.
  • only abnormality seen on lab tests is an elevation of total serum bilirubin, mainly due to predominant rise in CONJUGATED (direct) bilirubin.
  • liver is NOT pigmented like it is in Dubin-Johnson’s
47
Q

What is Hereditary Hemochromatosis?

A
  • autosomal recessive mutation of HFE gene (classic or Type 1) causing impaired iron homeostasis and thus increased intestinal iron, leading to fibrosis and cirrhosis of liver.
48
Q

What is the “bronze diabetic” or classic triad of hereditary hemochromatosis?

A

cirrhosis, DM, and skin pigmentation

*most pts will be asymptomatic.

49
Q

What la elevations will you see with hereditary hemochromatosis?

A
  • elevated iron studies
  • elevated AST/ALT or serum ferritin (>1000 ug/L)= do liver biopsy, which will show iron deposition in a periportal distribution.
50
Q

How do you treat hereditary hemochromatosis?

A

phlebotomy to reduce iron stores and then once stabilized, do maintenance phlebotomy every 2-3 months.
*check family members also

51
Q

What is alpha-1 antitrypsin (AAT) deficiency?

A
  • autosomal recessive most common cause of liver disease in children, due to lack of alpha-1 antitrypsin, which is produced by the hepatocytes to inhibit proteolytic elastase in the lungs and other organ systems.
  • affects lungs, liver, and skin
52
Q

What are the 2 alleles that we need to know for alpha-1 antitrypsin (AAT) deficiency?

A
  1. Z allele= most common resulting in emphysema and eventual cirrhosis or hepatocellular carcinoma.
  2. null allele= rare, worst= no AAT, so no liver issues but really bad lung issues.
53
Q

How does AAT deficiency present?

A
  • in childhood= jaundice, ascites, poor nutrition

- adolescence or adulthood= anorexia, ascites, peripheral edema.

54
Q

How do you Dx AAT deficiency?

A
  • serum alpha-1 antitrypsin level with a PCR based of of that for the Z (severe), S (mild), or null (worst) alleles.
55
Q

What is the treatment for AAT deficiency?

A
  • no cure

- just symptomatic relief: diuretics for edema, vitamin support, and phenobarb for jaundice.

56
Q

What is primary biliary cirrhosis?

A
  • T cell mediated autoimmune intra-lobular bile duct damage, leading to cholestatic pattern of LFTs (AST/ALT elevations and alkaline phos elevation).
  • 95% cases are female.
57
Q

What are the primary symptoms of primary biliary cirrhosis?

A
  • pruritus
  • fatigue
  • hyperpigmented skin (jaundice)
  • hepatosplenomegaly
  • weight loss
  • RUQ discomfort
  • xanthomas
58
Q

** What is the classic test for primary biliary cirrhosis? (BOARD QUESTION)

A
  • ANTIMITOCHONDRIAL ANTIBODIES (AMA)
59
Q

What other labs will you see with primary biliary cirrhosis?

A
  • elevated ESR
  • elevated serum lipids
  • elevated ceruloplasmin
  • elevated alkaline phos
60
Q

*** What is primary sclerosing cholangitis? (BOARD QUESTION)

A
  • fibrosis of biliary ducts (both intra and extrahepatic) and associated with ULCERATIVE COLITIS.
61
Q

What labs will you see with primary sclerosing cholangitis?

A
  • cholestatic pattern of LFTs (AST/ALT elevations and alkaline phos elevation).
62
Q

What is nonalcoholic fatty liver disease?

A
  • hepatic steatosis without secondary cause (alcohol).
  • etiology unclear but most likely due to insulin resistance.
  • LFTs usually mildly elevated, bilirubin and albumin usually normal.
63
Q

What are the 2 types of nonalcoholic fatty liver disease?

A
  1. Nonalcoholic fatty liver (NAFL)= no inflammation

2. Nonalcoholic steatohepatitis (NASH)= infllammation

64
Q

What is Wilson’s disease?

A
  • autosomal recessive that causes abnormal copper excretion leading to cirrhosis and neurological deficits (dysarthria, ataxia, dystonia).
65
Q

What will you classically see with Wilson’s disease?

A
  • Kayser-Fleischer rings (corneal deposits).

- ceruloplasmin levels=

66
Q

How is the liver related to thyroid function?

A

it produces thyroxine-binding globulin, which is required for conversion of T4 to T3.

67
Q

What is the first and easiest imaging modality we should consider?

A
  • ultrasound= will show cirrhosis, what common bile duct looks like (dilation…), Hep C, helps distinguish between solid and cystic masses, and helps direct percutaneous biopsies for interventional radiology.
68
Q

What is the second imaging modality we should consider?

A

CT scan for visualizing hepatomegaly, intrahepatic tumors, portal hypertension, or biliary tree dilatation.
*more expensive

69
Q

What is the third imaging modality we should consider?

A

MRI= most accurate technique for identification of liver LESIONS (hemangiomas, fatty infiltrates, or tumors).
*high cost and any implantable metal devices CANNOT get an MRI (BIG MAGNET=BADNESS).

70
Q

For what is positron emmission tomography (PET) scan used?

A

smaller lesions or metastatic disease

*shows bright colors

71
Q

What is cholescintigraphy (HIDA scan)?

A

nuclear medicine exam useful in cholecystitis or evaluation of cystic duct/common bile duct/ampulla.
*takes a couple hours (long time).

72
Q

What is magnetic resonance cholangiography (MRCP)?

A

noninvasive test used to look at intrahepatic and extrahepatic bile ducts, stones, structures, or dilation.

73
Q

What is endoscopic retrograde cholangiopancreatography (ERCP)?

A

INVASIVE procedure, but more reliable than MRCP to evaluate malignant vs benign stricture, can extract stones, or insert stents.
*risk of pancreatitis post-exam.

74
Q

What is percutaneous transhepatic cholangiography (PTC)?

*What I saw at the Cleveland Clinic

A

INVASIVE procedure that helps evaluate anatomy of biliary tree. Can find site of obstruction and clarifies inconclusive scans.
*risk of fever, bacteremia, peritonitis, intraperitoneal hemorrhage

Gastrointestinal 1 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions