Flashcards in GI assessment Deck (59):
from GI disease could be?
1. Multifactorial—depends on etiology of liver disease
2. Liver disease due to alcoholism:
Liver disease due to alcoholism?
1. GI blood loss
2. Nutritional deficiency—B12 and folate (macrocystic anemia)
3. Alcohol as a direct toxin
1. Why does this happen?
1. Sequestering of WBCs in the spleen because of portal hypertension
2. Results in the patient being ?
(Etiology of portal HTN: ?
cirrhosis of the liver)
why does this happen?
Sequestering in the spleen secondary to portal hypertension
Liver Function Tests
3. Alkaline Phosphatase
Applications of LFTs?
1. Provide a noninvasive method to screen for the presence of liver disease
2. Used to measure the efficacy of treatments for liver disease
3. Used to monitor progression of liver disease
4. Can reflect the severity of liver disease, particularly in patients who have cirrhosis
Assess liver function not destruction or failure? 2
Albumin and PT
Cons of LFTs
1. Most do not accurately reflect how well the liver is functioning
2. Abnormal values CAN be caused by diseases unrelated to the liver
3. The tests may be normal in patient’s who have advanced liver disease
Tests that reflect injury to hepatocytes?
1. Alanine aminotransferase (ALT)*
2. Aspartate aminotransferase (AST)
1. ALT and AST is normally located where?
2. When are they released intot he blood stream?
1. Enzymes are normally intracellular:
2. Released into the blood stream when hepatocytes are injured
---Damage or destruction of tissues or changes in cell membrane permeability permit leakage
AST is also produced in what type of cells?
1. cardiac muscle,
2. skeletal muslce,
4. the brain
6. lungs and
Extent of ____________ correlates poorly w/ the rise of aminotransferases?
Highest elevations seen in what diseases? 3
1. viral hepatitis,
2. ischemic hepatitis,
Rapid decline in aminotransferases usually a sign of ________ but may reflect what?
2. massive destruction of viable hepatocytes signaling acute liver failure
1. What does alkaline phosphatase refer to?
2. Found where?
3. Sources? 3
4. In bone it is involved in what?
5. MAJOR value of elevated serum alkaline phosphatase in diagnosis of liver disease is recognition of what?
1. Refers to a group of enzymes that catalyze the hydrolysis of organic phosphate esters at an alkaline pH
2. Found in many areas of the body it’s precise function is not known
-sometimes the intestinal tract
4. In bone the enzyme is involved in calcification
5. MAJOR value of elevated serum alkaline phosphatase in diagnosis of liver disease is recognition of cholestatic disease!
1. Found where? 6
2. In the liver where is it located?
3. An increase in a non-pregnant patient with an increase in AP suggests the increase in AP is from where?
4. Elevations in 5’-nucleotidase are seen in the same types of ________________ associated w/ an increase in AP
HOWEVER sometimes the two are discordant and cannot be totally reliable
1. Found in the
-blood vessels, &
2. In the liver subcellular location in hepatocytes
4. hepatobiliary disease
Gamma-glutamyl Transpeptidase (GGT):
1. PLays an important role in what?
2. Elevated serum activity is found in diseases of the what? 3
3. Major clinical value is for what?
4. In what else do we see this in?
1. Plays a role in amino acid transport
2. Elevated serum activity is found in diseases of the
-pancreas corresponding to increases in AP
3. Major clinical value is for conferring organ specificity to an elevated AP level
4. Also see early peaks in acute liver toxicity such as after an alcohol binge
1. Bilirubin the 80% the product of what?
2. Other 20% of the time?
1. Bilirubin is the product of heme metabolism (80%)
2. The other 20% is from other heme proteins
Elevated bilirubin is due to:
1. Overproduction of bilirubin
2. Impaired uptake of bilirubin
3. Impaired conjugation or excretion of bilirubin
4. Backward leaking from damaged hepatocytes or bile ducts
1. Relates only to what kind of disease?
2. What can it not differentiate though?
1. relates to only hepatobiliary disease
2. It does not differentiate it from obstructive vs. hepatocellular damage
Why does unconjugated bilirubin not get filtered by the kidneys?
adheres tightly to albumin
Increased levels of unconjugated bilirubin levels are caused by what 2? (not caused by?)
1. from increased production
2. or decreased excretion
usually not from hepatobiliary disease
UA—urobilinogen: is positive when direct bilirubin is what?
excreted via the kidneys
See slide 15
see slide 15
See slide 16
See slide 16
1. What is Hepatic encephalopathy?
2. Increased concentrations of what play a role in this?
3. What is one part of treatment because of this?
1. Reversible impairment of neuropsychiatric function associated w/ impaired hepatic function
2. Increased ammonia concentrations play a role
3. One part of treatment is to decrease the ammonia levels
Cycle of increased ammonia:
3 steps of normal ammonia clearance?
4 What happens when there is advanced liver failure?
1. Produced by the catabolism of colonic bacteria in the GI tract
2. Enters the circulation via the portal vein
3. The intact liver clears the ammonia from the circulation
4. When there is advanced liver disease the liver cannot clear the ammonia
Obtaining an ammonia level:
1. Whats the most accurate way?
2. Many factors can result in inaccurate results? 3
3. Following the ammonia level is necessary why?
1. Drawing an arterial ammonia level is the most accurate method to determine a level
2. Many factors can result in inaccurate results:
-Use of a tourniquet
-Whether the sample was put on ice or not
3. to know if treatment aimed at helping the liver is successful in lowering the ammonia level
what two tests?
1. Liver is the major site where what is synthesized?
2. What is the most important serum plasma protein?
3. This serum level reflects what? 3
4. Hypoalbuminemia can reflect other disorders such as?
1. Liver is the major site where serum proteins are synthesized
2. Albumin is the most important serum plasma protein
3. The serum level reflects the:
-Rate of synthesis
-Rate of degradation
-Volume of distribution
4. Hypoalbuminemia can reflect other disorders:
-When present with chronic liver disease it reflects the severity of the liver disease
When albumin goes down how does this affect PT?
1. The liver is the site of synthesis for the what?
2. How does severe liver disease affect this?
3. Instead of measuring the individual clotting factors the what is measured?
4. What else is also measured?
1. 11 blood coagulation proteins
2. clotting factor deficiency occurs
Amylase & Lipase
1. Both secreted by what?
2. How are they affected by acute pancreatitis? 2
3. The level of elevation DOES NOT correlate with the level of what?
It is important to correlate elevations of these enzymes with the history and clinical exam of the patient as well as with other studies
-Both can rise in acute pancreatitis—lipase remains elevated longer so is thought to be more accurate
-Both may be in the normal range in acute pancreatitis
3. damage to the pancreas
1. Main source in humans is what? 2
2. It is also secreted by what? 2
3. It rises early in what disease and is the first to drop?
1. Main source in humans is
2. It is also secreted by the
-kidneys and the
3. It rises early in pancreatitis and is the first to drop
4. Function of amylase is to cleave starch into smaller polysaccharides
1. Activity of all lipases is inhibited by what?
2. Activity of the lipase in the pancreas depends on what?
3. It remains elevated longer in ____________ so sometimes it alone is tested for?
1. bile acids
2. co-lipase and prevents the bile salts from degrading it
4. Function of lipase is to hydrolyze triglycerides into glycerol and free fatty acids
Can't give what kind of vanco to clear C. Diff?
Stool examination includes:
1. Microscopic exam:
2. Stool culture
3. Ova and Parasites (O & P) X 3
4. Clostridium difficile toxin
5. Testing for occult blood in the stool
What are the componenets of the microscopic stool analysis?
2. Epithelial cells
4. Fat globules
Microscopic General? 3
+ epithelial cells—
1. What would RBCs in the stool suggest? 3
2. What would epithelial cells in the stool suggest?
3. WBCs? 2
2. irritated GI tract
1. Fecal fat is detected by what?
2. Increased amounts can indicate what?
1. detected with Sudan stain
2. increased amounts can indicate malabsorption or pancreatitis
Normal analysis microscopic:
2. Epithelial cells?
3. Neutral fat globules?
2. Epithelial cells---------------present
3. Neutral fat globules---------0-2+
What are Charcot-Leyden crystals----sometimes found in ?
parasitic infections (especially amebiasis)
1. What is the normal color?
2. If its clay color?
2. Clay color-------------biliary obstruction
3. Tarry----------------- > 100 mL blood upper GI tract
4. Red--------blood in large intestine, or undigested beets or tomatoes
What is infectious diarrhea defined as?
Acute diarrhea due to viruses & bacteria is self-limited & when evaluation fails to ID a pathogen noninfectious etiologies need to be considered
For infectious diarrhea what would we see?
FECAL ANALYSIS--+for occult blood and WBCs support bacterial etiology
Infectious diarrhea etiologies?
1. Viruses most common cause
2. Bacteria usually show signs of fever
3. Parasites when persistent diarrhea or travel to endemic area or exposure
When would we obtian stool cultures for infectious diarrhea?
1. Immunocompromised patients
2. Patients w/ comorbidities—increased risk for complications
3. Patients w/ inflammatory bowel disease
4. Patients w/ severe inflammatory diarrhea (including bloody diarrhea)
5. Routine stool cultures test for: Shigella, Salmonella, Campylobacter**
C difficile Colitis often develops with what kind of pts?
1. Develops in patients treated w/ antibiotics or hospitalized patients
2. Now also becoming more common in peds and geriatric pts.
C Diff: Can test stool directly for what?
Can test stool directly for toxins A & B using ELISA which is found in 95% of patients w/ infected stool
Sensitivity of test is 72-84%
C diff aka?
1. Metronidazole (Flagyl)
2. Oral vancomycin
When to send a stool samples for O & P:
1. Persistent diarrhea (associated w/ Giardia, cryptosporidium and Entamoeba hystolytica)
2. Persistent diarrhea following travel to countries w/ endemic parasites such as Russia, Nepal, or mountainous regions (even our Rocky mountains!)
3. Persistent diarrhea w/ exposure to infants in daycare centers (associated w/ giardia & cryptosporidium)
4. Bloody diarrhea w/ few or no fecal leukocytes
Ova and Parasites.
Specimens sent on consecutive days: How should we manage that? 2
1. Separated by at least 24 hrs for O & P examinations
2. Parasite excretion is intermittent in contrast to bacterial pathogens
H pylori Tests
1. Endoscopic Biopsy:
2. Serologic tests for IgG AB**
3. Antigen in stool detects active infection & if negative confirms eradication**
4. Urease breath tests:
Endoscopic Biopsy: H. Pylori
What two things are we testing during this?
1. Kit for rapid urease test—urease converts urea in kit to ammonia changing pH changes color
2. Culture—can be used to determine antibiotic resistance
Urease breath tests: H pylori
1. What is this test based on?
3. What can the test determine?
1. Based upon the hydrolysis of urea by H. pylori to CO2 & ammonia
2. A labelled carbon isotope is given by mouth—H. pylori liberates CO2 can then be detected in breath samples
3. Test can determine if infection is active or if Rx has been successful
Carcinoembryonic Antigen (CEA)
1. Is a marker for what?
2. Who else is this elevated in? 4
1. Marker for colon cancer
2. Also elevated in >30% of patients w/