GI lab assessment

Question 1

RBCs - anemia causes?

Answer 1

• multifactorial: depends on etiology of liver disease
• liver disease due to alcoholism: GI blood loss, nutritional deficiency: B12 and folate (macrocytic anemia), alcohol is a direct toxin

Question 2

WBCs - neutropenia causes?

Answer 2

• sequestering of WBCs in spleen b/c of portal HTN because or cirrhosis

Question 3

Platelets - thrombocytopenia causes?

Answer 3

• sequesterin in spleen secondary to portal HTN

Question 4

Big cause of pancytopenia?

Answer 4

• alcohol

Question 5

Applications for LFTs?

Answer 5

• provide noninvasive method to screen for presence of liver disease
• used to measure efficacy of tx for liver disease
• used to monitor progression of liver disease
• can reflect severity of liver disease, particularly in pts who have cirrhosis

Question 6

What are the cons of LFTs?

Answer 6

• most don’t accurately reflect how well the liver is fining
• abnormal values can be caused by diseases unrelated to the liver
• tests may be normal in pts who ahve advanced liver disease
• need to also check PT, albumin

Question 7

What tests reflect injury to hepatocytes?

Answer 7

• enzymes are normally intracellular: released into bloodstream when hepatocytes are injured, damage or destruction of tissues or changes in cell membrane permeability permit leakage
• serum aminotransferases: ALT and AST (AST also in cardiac, skeletal muscle, kidneys, brain, pancreas and erythrocytes, so not a specific marker for liver)
• extent of liver necrosis correlates poorly with rise of aminotransferases
• ***highest elevations seen in viral hepatitis, ischemic hepatitis, toxicity
• rapid decline in aminotransferases usually sign of recovery but may reflect massive destruction of viable hepatocytes signaling acute liver failure

Question 8

Alkaline phosphatase - what are these enzymes, where are they found, What do levels reflect?

Answer 8

• refers to group of enzymes that catalyze hydrolysis of organic phosphate esters at an alkaline pH
• found in many areas of the body, it’s precise fxn isn’t known
• sources: liver, bone, sometimes intestinal tract
• in bone: enzyme is involved in calcification (see in growing kids)

Question 9

How do you differentiate source of AP?

Answer 9

• 5-nucleotidase:
  found in liver, intestine, brain, heart, blood vessels, endocrine pancreas
• in liver: subcellular locatio in hepatocytes
• increase in non-preg pt with increase in AP suggests that increase in AP from liver
• elevations in 5’ nucleotidase are seen in same types of hepatobiliary disease assoc with increase in AP
• however sometimes the 2 are discordant and can’t be totally reliable - have to think is something else going on?

Question 10

What can an increase in gamma-glutamyl transpeptidase (GGT) tell us?

Answer 10

• plays a role in amino acid transport
• elevated serum activity is found in diseases of the liver, biliary tract and pancreas corresponding to increases in AP
• major clinical value for conferring organ specificity to an elev AP
• also see early peaks in acute liver toxicity such as after alcohol binge (will also fall quickly)

Question 11

Bilirubin levels - elevation due to?

Answer 11

• bili is product of heme metabolism (80%)
• other 20% from other heme proteins

elevated bili due to:

• overproduction of bili (hemolysis)
• impaired uptake of bili
• impaired conjugation or excretion
• backward leaking from damaged hepatocytes or bile ducts (sclerosing cholangitis)

Question 12

elevations in conjugated and unconjugated bili?

Answer 12

• conjugated: relates only to hepatobiliaray disease, can’t diff from obstructive vs hepatocellular damage
• unconjugated: adheres tightly to albumin and doesn’t get filtered by kidneys
• increased levels of unconjugated are from increased production or decreased excretion usually not from hepatobiliary disease (could be from hemolytic anemia)
• UA - urobilinogen: positive when direct bilirubin is excreted via the kidneys

Question 13

unconjugated hyperbilirubinemia etiologies?

Answer 13

• overproduction: hemolysis, extravasation, shunt hyperbilirubinemia
• reduced uptake:
  portosystemic shunt, drugs, gilbert syndrome
• conjugation defect: acquired - neonatal, maternal milk, wilson’s disease, hyperthyroidism, chronic persistent hepatitis
  inherited: crigler-najjar I and II, gilbert’s syndrome

Question 14

Etiologies - if both conjugated and unconjugated hyperbilirubinemia?

Answer 14

• biliary obstruction
• intrahepatic cholestasis: primary biliary cirrhosis, primary sclerosing cholangitis, viral hepatitis, corticosteroids, intrahepatic cholestasis of pregnancy
• hepatocellular injury: acute or chronic
• hepatocellular defects of canalicular excretion or sinusoidal re-uptake: dubin-johnson or rotor syndrome

Question 15

Effects of high ammonia levels? Cycle of increased ammonia?

Answer 15

• hepatic encephalopathy: reversible impairment of neuropsych fxn assoc with impaired hepatic fxn
  increased ammonia concentrations play a role, one part of tx is to decrease ammonia levels
• cycle of increased ammonia: produced by catabolism of colonic bacteria in the GI tract, enters circulation via portal vein, intact liver clears ammonia from circulation BUT when there is advanced liver disease - liver can’t clear out ammonia

Question 16

How do you obtain an ammonia level?

Answer 16

• arterial ammonia level: most accurate method
• many factors can result in inaccurate results: fist clenching, use of tourniquet, whether sample was put on ice or not
• following ammonia level is necessary to know if tx aimed at helping liver is successful in lowering ammonia level

Question 17

Major site of albumin synthesis? What do serum levels reflect?

Answer 17

• liver is major site where serum proteins are synthesized
• albumin is most impt serum plasma protein
• serum level reflects the:
  rate of synthesis, rate of degradation, and volume of distribution
• hypoablbuminemia can reflect other disorders:
  systemic inflammation
  malnutrition
  when present with chronic liver disease it reflects the severity of liver disease

Question 18

Why do we look at PT if we are concerned abot liver fxn?

Answer 18

• liver is site of synthesis for 11 blood coag. proteins
• when there is severe liver disease clotting factor deficiency occurs so instead of measuring individual clotting factors the PT is measured
• as liver disease progresses the PT should increase b/c albumin is decreased and clotting factors aren’t beign produced
• INR is measured as well

Question 19

Significance of amylase and lipase?

Answer 19

• both secreted by pancreas as well as other tissues
• both can rise in acute pancreatitis - lipase remains elevated longer so it is thought to be more accurate
• both may be in normal range in acute pancreatitis
• the level of elevation doesn’t correlate with the level of damage to the pancreas
• it is impt to correlate elevations of these enzymes with the hx and clinical exam of pt as well as other studies

Question 20

Source of amylase? When are levels elevated? Fxn?

Answer 20

• main source is pancreas and salivary glands
• it is also secreted by kidneys and reticuloendothelial system
• it rises early in pancreatitis and is first to drop
• fxn: to cleave starch into smaller polysaccharides

Question 21

Activity of lipase is dependent on? When is it elevated? Fxn?

Answer 21

• several sources of lipase in the body
• activity of all lipases is inhibited by bile acids
• activity of lipase in pancreas depends on co-lipase and prevents bile salts from degrading it
• it remains elevated longer in pancreatitis so sometimes it alone is tested for
• fxn of lipase: hydrolyze triglycerides into glycerol and free fatty acids

Question 22

Components of stool examination?

Answer 22

• in general: looking at bulk, color, pH, and osmolality
• microscopic exam:
  RBCs (cancer, infection, IBS), epithelial cells (irritated GI tract), WBCs (infection, IBS), fat globules
• stool culture
• ova and parasites x 3
• C diff toxin
• testing for occult blood in the stool
• fecal fat: detected with sudan stain, increased amts can indicate malabsorption or pancreatitis

Question 23

Normal and not so normal stool analysis?

Answer 23

- micro:
RBCS - none
epi cells - present 
charcot-leyden crystals - sometime found in parasitic infections (esp amebiasis)
neutral fat globules: 0-2+

color:

• normal - brown
• clay color - biliary obstruction
• tarry - 100 mL blood upper GI tract
• red - blood in large intestines, or undigested beets or tomatoes
• black - blood

Question 24

How can you dx infectious diarrhea? Etiologies? When should you obtain stool cultures?

Answer 24

• acute diarrhea due to viruses and bacteria is self-limited and when eval fails to ID a pathogen noninfectious etiolgies should be considered
• fecal analysis: for occult blood and WBCs support bacterial etiology
• etiologies:
  viruses = most common
  bacteria = show signs of fever
  parasites = when persistent diarrhea or travel to endemic area or exposure

obtain stool cultures when:

• immunocompromised pts
• pts with comborbidities - increased risk for complications, - pts with IBD
• pts with severe inflammatory diarrhea (bloody)
• routine stool culture test for: shigella, salmonella, and campylobacter

Question 25

C diff is common in what pops? How can you test stool? Tx?

Answer 25

• develops in pts tx with abx or hosp pts
• now also more common in peds and geri pop
• can test stool directly for toxins A & B using ELISA which is found in 95% of pts with infected stool
• sensitivity of test: 72-84%
• also called pseudomembranous colitis
• tx:
  metronidazole (flagyl)
  oral vanco (has to be oral - IV won’t work)

Question 26

When should you send stool samples for O & P?

Answer 26

• peristent diarrhea (assoc with giardia, cryptosporidium and entamoeba hystolytica)
• peristent diarrhea following travel to countries w/ endemic parasites such as Russia, Nepal or mount. regions (even the Rockies)
• persistent diarrhea with exposure to infants in daycare (assoc with giardia and cryptosporidium)
• bloody diarrhea with few or no fecal leukocytes (not bacterial)

specimens sent on consecutive days:

• sep by at least 24 hrs for O&P exams
• parasite excretion is intermittent in contrast to bacterial pathogens

Question 27

How can you test for H pylori?

Answer 27

• endoscopic bx:
  kit for rapid urease test: urease converts urea in kit to ammonia changing pH and color
  culture can be used to determine abx resistance

noninvasive:
- serologic tests for IgG AB (will stay + for months to years, not all that helpful)
- ag in stool detects active infetion and if negative confirms eradication (do this after tx)
- urease breath tests:
based upon hydrolysis of urea by H pylori to CO2 and ammonia
- a labelled carbon isotope is given by mouth - H pylori liberates CO2, this is detected in breath samples
- test can determine if infection is active or if Rx has been successful

Question 28

H pylori tests - sensitivity and specificity?

Answer 28

• serum ELISA: not that sensitive (85%) or specific (80%)
• urea breath test and stool ag test both very sensitive (91-100) and specific (94-99)
• invasive - endoscopy culture is 100 specific but 70-80 sensitive

Question 29

What is CEA a marker for? Use?

Answer 29

• for colon cancer
• also elevated in more than 30% of pts with breast, lung, liver and pancreas adenocarcinomas
• use:
  monitoring for persistent, metastatic or recurrent adenocarcinoma of colon after surgery
  determination of prognosis for pts with colon cancer
  NOT useful for local recurrence or screening b/c of low sensitivity and specificity