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
What are the gold standard and the preferred tests for H. pylori?
gold standard: tissue biopsy | preferred: Urea Breath Testing (UBT)
26
What medications interfere with the results of a gastrin level test?
Must be off H2 blockers for 24 hours; off PPIs for 6 days
27
What is the procedure for a Urea Breath Test and how does it work?
 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
What medications must be stopped before doing a Urea Breath Test?
Off antibiotics/bismuth for 4 weeks; antacids for 2 weeks
29
What is the gold standard for diagnosis of celiac disease?
small bowel biopsy
30
You do celiac antibody testing when the patient has not eaten gluten for 14 days. T/F
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
What antibody is pathognomonic for celiac?
 Presence of IgA EMA is pathognomonic for celiac
32
When would you order a stool culture?
 When suspect bacterial etiology |  Salmonella, Campylobacter, Shigella
33
When would you order a fecal lactoferrin?
 Used most widely in assessing patients with IBD
34
What is the significance of fecal leukocytes?
 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
When would you order ova & parasite testing?
 Suspect parasitic etiology |  Giardia, Entamoeba histolytica, Cryptosporidium
36
What is the most common test for C.diff and how effective is it?
 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
What is the gold standard test for C.diff? (not most common test, just gold standard test)
 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
With acute diarrhea, what criteria would lead you to do further testing rather than simply recommending supportive therapy?
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
If you determine that further testing is necessary for acute diarrhea, what do you do?
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
What are two etiologies of fecal fat?
celiac disease | pancreatic insufficiency
41
Dietary fat should be restricted before performing a fecal fat test. T/F
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
What are two etiologies of fecal occult blood?
~GI bleed (upper or lower) | ~colon cancer
43
What can cause a false negative fecal occult blood test?
vitamin C
44
What is the purpose of SAAG testing?
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
What is the test used to screen for immunity to Hepatitis B?
~look for a positive anti-HBsAg blood serum level | ~this antibody appears in most individuals after clearance of HBsAg and after successful vaccinations
46
If a patient has both elevated GGT and MCV, what is most likely?
serious drinking problem