GI lab assessment Flashcards
1
Q
RBCs - anemia causes?
A
- 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
2
Q
WBCs - neutropenia causes?
A
- sequestering of WBCs in spleen b/c of portal HTN because or cirrhosis
3
Q
Platelets - thrombocytopenia causes?
A
- sequesterin in spleen secondary to portal HTN
4
Q
Big cause of pancytopenia?
A
- alcohol
5
Q
Applications for LFTs?
A
- 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
6
Q
What are the cons of LFTs?
A
- 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
7
Q
What tests reflect injury to hepatocytes?
A
- 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
8
Q
Alkaline phosphatase - what are these enzymes, where are they found, What do levels reflect?
A
- 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)
9
Q
How do you differentiate source of AP?
A
- 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?
10
Q
What can an increase in gamma-glutamyl transpeptidase (GGT) tell us?
A
- 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)
11
Q
Bilirubin levels - elevation due to?
A
- 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)
12
Q
elevations in conjugated and unconjugated bili?
A
- 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
13
Q
unconjugated hyperbilirubinemia etiologies?
A
- 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
14
Q
Etiologies - if both conjugated and unconjugated hyperbilirubinemia?
A
- 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
15
Q
Effects of high ammonia levels? Cycle of increased ammonia?
A
- 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
16
Q
How do you obtain an ammonia level?
A
- 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
17
Q
Major site of albumin synthesis? What do serum levels reflect?
A
- 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
18
Q
Why do we look at PT if we are concerned abot liver fxn?
A
- 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
19
Q
Significance of amylase and lipase?
A
- 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
20
Q
Source of amylase? When are levels elevated? Fxn?
A
- 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
21
Q
Activity of lipase is dependent on? When is it elevated? Fxn?
A
- 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
22
Q
Components of stool examination?
A
- 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
23
Q
Normal and not so normal stool analysis?
A
- 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
24
Q
How can you dx infectious diarrhea? Etiologies? When should you obtain stool cultures?
A
- 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
25
C diff is common in what pops? How can you test stool? Tx?
- 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)
26
When should you send stool samples for O & P?
- 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
27
How can you test for H pylori?
- 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
28
H pylori tests - sensitivity and specificity?
- 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
29
What is CEA a marker for? Use?
- 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
