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NP 730 Diagnostic Measures > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

Enzyme tests for liver INFLAMMATION

A
  • Tests for liver INFLAMMATION b/c elevation of these enzymes can be found in other tissues unrelated to liver
  • ALT
  • AST
  • ALP
  • GGT
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2
Q

Test for liver FUNCTION

A
  • Bilirubin
  • Albumin
  • Ammonia
  • Prothrombin
  • AFP - alpha fetoprotein (AFP)
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3
Q

Indications for liver function tests

A
  • Symptoms of liver disease
    • Jaundice
    • RUQ pain/swelling - protein and fluid imbalance
    • Itchy skin - pruritus (toxin buildup)
    • Dark (coca colored) urine - excreting bilirubin
    • Pale stool - excreting bilirubin
    • N/V
    • Easy bruising - problems w/clotting
    • Loss of appetite
    • Chronic fatigue
  • If patient has risk/concern for VIRAL hepatitis exposure or NAFLD/NASH
  • Medication monitoring: APA, lamisil, fibrates, statins, niacin
  • Disease monitoring
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4
Q

Which metabolic panel has LFTs included?

A

CMP - GGT, bilirubin and albumin left out

NOT BMP

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5
Q

Most specific liver enzyme test for hepatic injury

A

ALT

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6
Q

Causes for elevation of ALT

A
  • Found in hepatocytes; also comes from kidney, less from skeletal and cardiac mm
  • Hep A, B, C
  • Acute drug injury
  • EtOH and non-EtOH fatty liver
  • Genetic + autoimmune liver problems
  • Burns, skeletal trauma
  • LOOK AT HOW MUCH HIGHER ABOVE NORMAL RANGE (2x, 3x, 4x, etc)
  • Higher in infants than adults + children
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7
Q

AST present in which tissues?

A
  • Liver
  • Cardiac mm
  • Skeletal mm
  • Kidney
  • Brain
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8
Q

Causes for elevation in AST

A
  • Liver problems: hepatitis, cirrhosis, drug induced liver injury, metastasis, mononucleosis w/hepatitis
  • Skeletal mm problems: Trauma, non-cardiac surgery, severe burns, muscular dystrophy, heat stroke
  • Higher in infants + elderly vs adults
    • MM wasting cause in elderly
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9
Q

normal ALT + ⇡AST suggestive of?

A

Cardiac or mm disease

As opposed to liver issue

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10
Q

Causes of ALP elevation

A
  • Problem in hepatobiliary system
    • Biliary disease: think biliary tract disease (stones) or infiltrative disease
  • Pregnancy d/t placental synthesis
  • Bone diseases
    • Tumors, Paget’s, kids growing, hyperparathyroidism
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11
Q

⇡ALTs AND ⇡ ALP suggestive of?

A

Elevation of these suggest liver related issue

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12
Q

What to order next if elevation in ALP related to liver-biliary system?

A

GGT

BUT, no need to order if ALP and AST elevated

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13
Q

Causes of GGT elevation

A
  • Not specific
  • Liver problems: hepatitis, cirrhosis, liver tumors, hepatotoxic drugs
  • MI
  • EtOH ingestion
  • Pancreatitis or pancreatic cancer
  • EBV aka infectious mono
  • NOT PRESENT IN BONE
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14
Q

↑ ALP, ↑ GGT, (-) hCG = _______

A

BILIARY ISSUE

Get a pregnancy test as ALP is elevated in pregnancy

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15
Q

↑ ALP, ↓ GGT = ________

A

BONE ISSUE

Remember: no GGT in bone!

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16
Q

↑ ALT, ↑ AST, normal ALP = ___________

A

Hepatocellular issue (LIVER)

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17
Q

↑ ALP, normal AST/ALT = __________

A

Biliary but related to bone and other sources w/GGT

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18
Q

Degree of elevation categories

A
  • Borderline: < 2x ULN
  • Mild: 2-5x ULN
    • Start lab workup at this stage
  • Moderate: 5-15x ULN
  • Severe: > 15x ULN
  • Massive AST or ALT > 10,000 IU/L
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19
Q

Causes of Mild-moderately elevated ALT/AST

A
  • Common
    • NAFLD + EtOH (get hx)
  • Less common
    • Meds: OTC, vitamins, etc
    • Viral Hepatitis, B + C, A (acute s/s)
    • Hemochromatosis = elevated iron levels
  • Rare
    • Alpha I antitrypsin deficiency
    • Autoimmune disease (copper?)
    • Wilson disease (copper?)
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20
Q

AST : ALT > 2 indicative of?

Which lab elevation makes it even more suggestive of this issue?

A

ALCOHOLIC LIVER DISEASE (still get hx)

GGT > 2x ULN

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21
Q

Common causes of ALT/AST elevation in ASYMPTOMATIC patients

A
  • Autoimmune
  • (B) Hep
  • (C) Hep
  • Drugs, toxins
  • EtOH
  • Fatty liver
  • Growths (TUMOR)
  • Hemodynamic disorder (CHF)
  • Iron (hemochromatosis), Copper (Wilson’s), alpha-1 antitrypsin deficiency
  • Muscle injury
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22
Q

Work-up of mildly elevated transaminases

A

First confirm by either repeating labs or performing clarifying test (GGT)

Only go through algorithm if acutely ill. Repeat in 3-4 weeks to see trend

Fatty liver disease RFs: high cholesterol, abd obesity, HTN, etc

Viral Hep RFs: IV drug use, high risk sexual activity (no protection), etc

Check iron panel - ferritin level - hemochromatosis

Albumin, Hep B, C; Abd U/S

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23
Q

Why is having excess fat in liver a problem?

A

Makes it more difficult for liver to function

Fat → inflammation

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24
Q

NAFLD

A
  • Non-alcoholic fatty liver disease
  • Has little to no inflammation
  • Signs + Symptoms
    • Metabolic syndrome (HTN, lipids, high TG level + low HDL, elevated BG) → need to be well-controlled to manage liver inflammation
  • NAFLD fibrosis score = HIGH → GI referral → biopsy
    • Inflammation → scarring → fibrosis
  • Can progress to fibrosis and cirrhosis
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25
Q

NASH

A
  • Non-alcoholic steatohepatitis
  • Inflammation present
  • See LFTs elevation → see CHRONIC damage
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26
Q

Liver disease progression

A

Hepatitis → Fibrosis → Cirrhosis → Cacner

Inflammation → scarring → severe scarring leaving irreversible damage → cancer

27
Q

Fibrosis

Cirrhosis

ESLD

Liver failure

A

Fibrosis: Inflammation starts to scar. Scar tissue replaces the normal, healthy tissue. It is difficult for blood to flow through a scared, stiff liver. Healthy liver has to compensate for the inflamed, scared liver.

Cirrhosis is scared liver. Scared tissue replacing healthy tissue, can’t function well, eventually will not function (fail).

  • Complications of cirrhosis: bleeding, edema, jaundice, itchy, diabetes, sensitivity to medications (ie liver not processing), toxin build up in brain, varices
  • Chronic liver failure, cause death if no transplant to replace
  • Not all end w/end stage liver disease, but put pt at risk more for cancer and disease

End stage liver disease: DECOMPENSATION, ex: hepatic encephalopathy, variceal bleed, ascites, kidney failure, lung transplant

Cancer: transplant.

Liver failure: loss of function, confusion, disorientation, coma

28
Q

Bilirubin transport (picture)

A
  • Bilirubin byproduct of RBCs breakdown
  • SPLEEN → breakdown of heme → unconjugated bilirubin needs attachment to albumin → LIVER → unconjugated biliubin > conjugated bilirubin (via GBT) → INTESTINES → urobilinogen > stercobilin
    • Stercobilin gives stool brown color
    • Pool pale = bilirubin not able to get into intestines!
  • Unconjugated NOT excreted in urine, only conjugated bilirubin
29
Q

Conjugated bilirubin in liver suggests a problem in…

A

Something wrong POST-HEPATIC

30
Q

High levels of unconjugated bilirubin suggests a problem in…

A

INTRAHEPATIC

31
Q

Direct bilirubin

A

Looks for water soluble (conjugated) bilirubin

32
Q

Indirect bilirubin

A

Total bilirubin - direct bilirubin

33
Q

Total bilirubin =

What does this tell you?

A

Conjugated + unconjugated

If it’s hyperbilirubinemia

34
Q

Prehepatic: dysfunction of and condition

A
  • Unconjugated bilirubinemia issue
  • Typically second to hemolysis
  • Something is going wrong in breakdown of RBCs
  • Hemolytic anemia
35
Q

Intrahepatic conditions

A
  • Unconjugated bilirubinemia
    • Disorders of enzyme metabolism impending conjugation (Gilbert syndrome)
  • Conjugated bilirubinemia
    • Intrahepatic choleestasis or hepatocellular damage from inflammation
      • Flow of bile impaired from liver cells where it is produced to small intestine
36
Q

Posthepatic condition

A
  • Conjugated bilirubinemia
    • Blockage in biliary system keeps bilirubin from being transported (stones, tumor)
    • Will often see pale stools and dark urine → d/t inability to excrete through biliary, goes into urine instead
37
Q

Indications for Hepatic panel

A
  • Acute jaundice
  • Elevated bilirubin in asymptomatic patient
  • Direct/Indirect bilirubin included: ALT, albumin, ALP, AST, +/- GGT
38
Q

Urobilinogen indication for decreased levels

A
  • Biliary disease - POSTHEPATIC
    • Prevention of moving from biliary system into bowels
    • Obstruction of conjugated bilirubin to bowel → less urobilinogen → PALE STOOLS
39
Q

Urobilinogen indication for increased levels

A
  • Increased in hemolytic process, hepatic disease
    • Some goes back to liver, can’t be re-processed by liver and sent to gut… so “extra” goes to kidney
40
Q

Bilirubinuria

A
  • Conjugated bilirubin in urine (coca-colar urine)
  • Unconjugated bilirubin is albumin bound (NOT WATER SOLUBLE = NOT IN URINE)
    • Not in hyperbliirubinemia
41
Q

Urine testing chart

Hemolytic disease, hepatic disease, and biliary obstruction

A
42
Q

Albumin

What, function, decreased levels indication

A
  • Protein made in liver
  • Helps keep fluid in blood stream and not leak out of blood stream into tissues → edema, ascites
  • Helps carry nutrients and hormones throughout body
  • Bound to unconjugated bilirubin
  • Low levels = severe liver disease (late finding)
    • Edema, ascites, trouble with drug metabolism/excretion
43
Q

Ammonia

High levels indicate…

A
  • Waste product of intestinal bacteria
    • Broken down in liver → urea + glutamine
  • If liver damaged → ammonia buildup → hepatic encephalopathy
    • Lethargy, agitation, disorientation → coma if untreated
    • Give lactulose to bind to ammonia and excrete in stool
44
Q

Prothrombin time (PT)

Longer PT indication

A
  • Measures time required for prothrombin to be converted to thrombin
    • Dependent on Vitamin K which is stored in liver
    • Non-functioning liver cannot carry out this process leading to prolonged PT and bleeding risk and clotting irregularities
45
Q

Alpha fetoprotein (AFP)

A
  • Tumor marker in adults…should only exist in small amounts
  • Made in fetus liver and yolk sac (decreases after age 1)
  • Increased in hepatocellular carcincoma
  • Get serial levels to follow cirrhosis patients
    • Increase should raise suspicion for HCC - cancer!!
    • Not a screening tool for hepatocellular carcinoma but should get aFP if have cirrhosis
46
Q

Ultrasound liver

Indications

A
  • First line - low cost
  • Can differentiate fatty changes vs cystic lesion vs solid lesion
    • Fatty liver
    • Screen for lesion
    • BEST FOR GALLSTONES
    • Gallbladder polyps
  • Not invasive
  • Can do in pts w/o s/s
  • Abnormal → MRI
47
Q

Fibro scan (Elastography)

Indication

A
  • U/S of liver that detects fibrosis
  • Used as surveillance in those with known fibrosis (degree of)
48
Q

Liver MRI

Indications

A
  • Gold standard imaging for the liver
  • Indications
    • Fatty liver
    • Cyst, lesion
    • Biliary duct dilation
    • Choledocholithiasis
    • Angioma, tumor
49
Q

Liver CT

Indications

A
  • Best if need image of entire abdomen
  • Generalized abd pain
  • Pelvic CT - appendicitis, gyn abnormality
  • Indications
    • Fatty liver
    • Cyst, lesion
    • Biliary duct dilation
    • Choledocholithiasis
    • Angioma, tumor
50
Q

Gallbladder function and process

A
  • Stores bile made from liver → releases bile to cystic duct → common bile duct → small intestine to aid in digestion
51
Q

Gallstone conditions

A
  • Result of too much cholesterol or too few bile salts
  • Cholelithiasis - presence of too much gallstones
  • Cholecystitis - inflammation of gallbladder
  • Biliary colic - intermittent symptoms fo cholecystitis
52
Q

Gallbladder workup + tx

A
  • RUQ pain? Associated with fatty food?
  • RUQ U/S
  • LFTs
  • Lipase
  • CBC
  • Surgery? gallbladder removal as there were too many stones
  • Infection? more urgent!!!
53
Q

Gallbladder workup + tx

A
  • RUQ pain? Associated with food? What types of food? (fatty)
  • RUQ U/S
  • LFTs
  • Lipase
  • CBC
  • Surgery? gallbladder removal as there were too many stones
  • Infection? more urgent!!!
54
Q

No gallbladder?

A

Difficulty digesting fats. Bile released into small intestine → bile salt diarrhea

55
Q

Pancreatitis causes and acute symptoms

A
  • Gallstones, choledocholithiasis (stones in common bile duct)
  • Heavy EtOH use (acute or chronic)
  • High TGs
  • Acute?
    • Acute LUQ, epigastric or periumbilical pain, starts intermittent → constant → N/V + worse after eating and w/lying down
56
Q

Pancreatitis lab workup

A
  • Labs: CBC, CMP, UA, lipase, LDH, TGs
    • Lipase: pancreatic enzyme, more sensitive and specific than amylase
57
Q

Pancreatitis imaging

A

U/S 1st line → Abd CT

58
Q

Hepatitis A testing

HAV IgM, HAV IgG, Total

A
  • Test for anti-HAV immunoglobulin
    • HAV IgM (+) = acute infection - should only be ordered if symptoms acute
      • Presents 3-4 weeks after exposure, normalize within 8 weeks
    • HAV IgG (+) = past infection or immunity (develop 2 weeks post infection after IgM increases and last 10 years post infection)
    • Total HAV antibody - does not distinguish between IgG and IgM
59
Q

Hepatitis A pathology

A

Transmitted via fecal-oral route or through contaminated food or water - contagious

Symptoms: fatigue, N/V, upper abd pain jaundice, dark urine, itching

Not chronic - only acute

Vaccine - after 2006 - get one if traveling to underdeveloped country

60
Q

Hepatitis B pathology

Vaccine

A

Transmitted through blood and bodily fluids, needles, sexual contact

More asymptomatic, contributing to silent spread

  • Can be mild and resolve or become chronic
    • If not cleared after ∼6 months = chronic
  • Vaccine
    • Given to all infants at birth
    • At risk pops: healthcare workers, ESRD, DM, Hep C, HIV…
    • 3 dose series
    • Antibody titers confirm immunity/response to vaccine
61
Q

Hepatitis B markers

what do each indicate?

A
  • Hep B surface antigen
    • Presence implies acute or chronic infection
    • Person is infectious → able to spread virus as it’s in system
  • Hep B surface antibody
    • Indicates recovery and immunity from Hep B infection
    • Develops after vaccination
    • Does not develop in chronic carries - ACUTE
  • Hep B core antibody
    • Appear 4 weeks after infection and persist for life
    • Only present if prior infection, will not develop post vaccination
    • Implies prior or chronic infection
  • Hep B IgM antibody (IgM andti-HBc)
    • Occurs with acute infection
    • Lasts for 6 months
      • Positive implies infection within last 6 months
62
Q

Hepatitis B scenarios (slide 5)

A
63
Q

Hepatitis C pathology

Screening

A
  • Transmitted through blood/bodily fluids
  • No vaccine available
  • 1x lifetime screen for all adults aged ≥ 18 years
    • Screening for all pregnant women during each delivery
64
Q

Hepatitis C markers

HCV antibody test + HCV RNA + Viral genotyping

A
  • HCV antibody test
    • Reactive or non-reactive
    • Can take 4-10 weeks to become positive - be sure to retest
    • Remains positive for life - can develop it again
      • Will be positive in person who had it already in past
    • If someone has no hx of Hep C infection - use this test to confirm
  • HCV RNA
    • Ordered to confirm (+) HCV antibody test
    • Once infection tx/resolved → negative
  • Viral genotyping ordered for + HCV RNA
    • Determine type and length of tx

NP 730 Diagnostic Measures (11 decks)

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