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Clin Med GI > GI Lab Medicine > Flashcards

GI Lab Medicine Flashcards

1
Q

What lab result is greatly increased in the early phase of acute pancreatitis?

A

Amylase
 Greatly increased (>3x ULN) in early phase of acute pancreatitis
 Within 3‐6 hours of onset of abdominal pain
 Tends to return to normal after 3‐5 days

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2
Q

What are two non-GI etiologies of increased amylase?

A

Current mumps infection, or salivary stones

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3
Q

What lab is more accurate than amylase for the diagnosis of acute pancreatitis?

A

Lipase
~98% specific if level is >3x ULN
~Also, remains elevated for up to 14 days, so useful for delay in seeking care

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4
Q

What are two non-GI etiologies of increased lipase?

A

DKA

HIV

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5
Q

Which is more specific and which is more sensitive, of amylase and lipase?

A

Amylase: more sensitive
Lipase: more specific

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6
Q

What is bilirubin?

A

 Breakdown product of RBCs, specifically “heme”

 Overproduction (hemolysis) or underexcretion (liver problem)

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7
Q

If you see a lot of indirect/unconjugated bilirubin, what does that tell you?

A

Increased bilirubin production -

hemolytic anemia, transfusion reaction

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8
Q

What is the most common cause of an “unimportant” increased indirect/unconjugated bilirubin?

A

Gilbert’s syndrome

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9
Q

If you see a lot of direct/conjugated bilirubin, what does that tell you?

A

Liver dysfunction:
~hepatitis cirrhosis
Biliary obstruction:
~gallstones, pancreatitis

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10
Q

Where does alkaline phosphatase originate?

A

bone, liver

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11
Q

How do you determine if an isolated elevated alkaline phosphatase is hepatic or bone origin?

A

GGT
~GGT elevated means alk phos elevation is from liver disease
~GGT normal means alk phos elevation is from bone

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12
Q

How can you help confirm an alcoholic liver etiology? (corresponding to acute alcohol use)

A

AST/ALT elevated in ratio of 2:1, elevated GGT

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13
Q

GI etiologies of elevated alkaline phosphatase

A

 Obstruction – gallstone,

hepatic/pancreatic cancer

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14
Q

Non-GI etiologies of elevated alkaline phosphatase

A

 Bone:

 Paget’s disease, metastatic bone tumor, osteomalacia, rickets

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15
Q

Where does lactic acid dehydrogenase originate?

A

Intracellular enzyme widely distributed in all tissues of the body

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16
Q

What is the GI clinical significance of elevated LDH?

A

 In GI setting, think:
 Ischemic bowel
 Liver disease (cirrhosis, alcoholism, acute viral hepatitis)
 May be significantly elevated in hemolysis / accompany an increase in unconjugated bilirubin

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17
Q

Total protein may be increased in:

A

 Marked dehydration

~hemoconcentration from vomiting, diarrhea

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18
Q

Total protein may be decreased in:

A 
~chronic liver disease
~nephrotic syndrome
~IBD
~severe dietary protein deficiency
~malabsorption
~alcoholism
~acute burns
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19
Q

What is the source of albumin?

A

 Synthesized by liver, so measurement can reflect the liver’s biosynthetic capacity

20
Q

How is albumin level useful?

A

 Consider chronic liver disease if below 3g/dL

 Level indicates severity in chronic liver disease

21
Q

In what liver conditions is albumin usually normal?

A

~acute viral hepatitis
~drug-related hepatotoxicity
~obstructive jaundice

22
Q

What is the source of gastrin?

A

 Hormone secreted by the antral G cells in stomach mucosa, stimulating gastric acid production
 Follows circadian rhythm, fluctuates in relation to meals

23
Q

Etiologies of increased gastrin levels

A

 Hypo/Achlorhydria (most common)

 Gastrinoma (Zollinger‐Ellison syndrome, levels >10x normal)

24
Q

H. pylori is bad because it invades the intestinal mucosa.

T/F

A

FALSE
 Generally does not invade gastroduodenal tissue
 Renders the underlying mucosa more vulnerable to acid peptic damage
 Host immune response to H. pylori incites an inflammatory reaction which further perpetuates tissue injury

25
Q

What are the gold standard and the preferred tests for H. pylori?

A

gold standard: tissue biopsy

preferred: Urea Breath Testing (UBT)

26
Q

What medications interfere with the results of a gastrin level test?

A

Must be off H2 blockers for 24 hours; off PPIs for 6 days

27
Q

What is the procedure for a Urea Breath Test and how does it work?

A

 Hydrolysis of urea into CO2 and ammonia by H. pylori
 Patient drinks a labeled urea solution & blows into a tube
 If H.pylori is present, the urea is hydrolyzed and labeled CO2 is detected in breath samples

28
Q

What medications must be stopped before doing a Urea Breath Test?

A

Off antibiotics/bismuth for 4 weeks; antacids for 2 weeks

29
Q

What is the gold standard for diagnosis of celiac disease?

A

small bowel biopsy

30
Q

You do celiac antibody testing when the patient has not eaten gluten for 14 days.
T/F

A

FALSE
 Test while patient is on gluten‐rich diet
 If already gluten‐free, resume consumption of
gluten for 2‐12 weeks before testing
 After gluten‐free diet is initiated, Ab levels remain elevated for 1‐12 months
 Can test if recently went gluten‐free

31
Q

What antibody is pathognomonic for celiac?

A

 Presence of IgA EMA is pathognomonic for celiac

32
Q

When would you order a stool culture?

A

 When suspect bacterial etiology

 Salmonella, Campylobacter, Shigella

33
Q

When would you order a fecal lactoferrin?

A

 Used most widely in assessing patients with IBD

34
Q

What is the significance of fecal leukocytes?

A

 Usually present in patients with stools containing blood and mucus / infection with invasive organisms
 If positive, patients may merit more extensive diagnostic evaluation / possibly empiric antibiotic therapy

35
Q

When would you order ova & parasite testing?

A

 Suspect parasitic etiology

 Giardia, Entamoeba histolytica, Cryptosporidium

36
Q

What is the most common test for C.diff and how effective is it?

A

 Most common test is assay for antigen in stool
 High specificity (typically >95%)
 Low sensitivity (60‐95%)
 If negative result: repeat 1‐2 times

37
Q

What is the gold standard test for C.diff? (not most common test, just gold standard test)

A

 Gold standard is cell cytotoxicity assay
 Detects toxin by its cytotoxic effect in cell cultures
 Sensitivity = 94‐100%
 Specificity = 99%
 Lab dependent, high cost, delay 1‐3 days

38
Q

With acute diarrhea, what criteria would lead you to do further testing rather than simply recommending supportive therapy?

A
  1. Severe illness: T>38.5C, abd pain, bloody, >6 stools/24h, dehydration
  2. Immunocompromised: AIDS, post-transplant
  3. Patient > 70 yrs of age
39
Q

If you determine that further testing is necessary for acute diarrhea, what do you do?

A
  1. Fecal leukocytes
  2. Routine stool culture
  3. C.diff assay if recent hosp or abx
  4. O & P if:
    ~diarrhea > 10 days
    ~travel to endemic region
    ~community water-borne outbreak
    ~HIV infection or MSM
40
Q

What are two etiologies of fecal fat?

A

celiac disease

pancreatic insufficiency

41
Q

Dietary fat should be restricted before performing a fecal fat test.
T/F

A

FALSE.
 Dietary fat should be at least 50–150 g/d for 2 days before collection
 All stools should be collected for 72 hours and refrigerated

42
Q

What are two etiologies of fecal occult blood?

A

~GI bleed (upper or lower)

~colon cancer

43
Q

What can cause a false negative fecal occult blood test?

A

vitamin C

44
Q

What is the purpose of SAAG testing?

A

To determine whether ascites is caused by portal hypertension.
A high SAAG (> 1.1 g/dL) indicates patient’s ascites is due to portal hypertension with 97% accuracy.
A low SAAG (< 1.1 g/dL ) indicates ascites not associated with increased portal pressure, e.g. TB, pancreatitis, nephrotic syndrome.

45
Q

What is the test used to screen for immunity to Hepatitis B?

A

~look for a positive anti-HBsAg blood serum level

~this antibody appears in most individuals after clearance of HBsAg and after successful vaccinations

46
Q

If a patient has both elevated GGT and MCV, what is most likely?

A

serious drinking problem

Clin Med GI (13 decks)

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