Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
71 Cards in this Set
- Front
- Back
|
Which type of bilirubin is water-insoluble?
|
Unconjugated
|
|
|
Another name for unconjugated bilirubin is:
|
Indirect
|
|
|
Which type of bilirubin is produced directly from the breakdown of heme?
|
Unconjugated/Indirect bilirubin
|
|
|
The process that occurs in the liver to cause bilirubin to be water-soluble is called?
|
Glucuronidation
|
|
|
Which type of bilirubin is secreted in bile?
|
Conjugated/Direct
|
|
|
What effect does intestinal bacteria have on bilirubin?
|
Conversion to Urobilinogen
(which is yellow and gives stool/urine color) |
|
|
A patient with a cholangiocarcinoma causing complete biliary obstruction may demonstrate what characteristic stool finding?
|
White, acholic stools
(Siver stool of Thompson)--how lame to have your eponym be about poop |
|
|
Bilirubinuria is always associated with which type of hyperbilirubinemia?
|
If a patient has bilirubinuria, then the elevated bilirubin is CONJUGATED b/c indirect bili is not water soluble.
|
|
|
A patient presents with jaundice and bright yellow urine that is 3+ positive for bilirubin on dipstick. A likely clinical scenario that could accompany this is:
a) Gilbert syndrome b) Choledocholelithiasis c) Crigler Najjar syndrome d) loss of hepatocyte function due to drug effect |
b) A stone obstructing the bile duct is the only scenario listed that will cause conjugated bilirubinemia.
Crigler Najjar (failure of conjugation in hepatocyte), Gilbert (failure of hepatocyte to take up unconjug bili), and loss of hepatocyte function all cause indirect/unconjugated bilirubinemia |
|
|
Which of the bilirubin measurements is calculated, not measured?
|
Indirect (Unconjugated): remember-this is the early stuff.
|
|
|
The diazo-colorimetric method of hemoglobin measurement uses which of the following to calculate findings:
a) temperature b) light scatter c) Light transmisison at 540 nm d) Turbidity e) Color dye reaction |
Color dye reaction.
|
|
|
What is purpose of adding an accelerant to the diazo-colorimetric method?
|
Without accel, you measure mainly conjugated. With addition of accelerant, you maeasure conjug + unconjug (total). Subtract conjug from total and get (estimated) unconjugated.
|
|
|
One more time:
Conjugated is to _________ as Unconjugated is to _______ a) direct, total b) indirect, direct c) direct, indirect d) total, indirect |
Remeber: conjugated/unconjugated has to do with how the bili is in the body, while direct/indirect is the method of measurement. Indirect (Unconjugated) is the one you calculate *indirectly*
It's nice, because Indirect and Unconjugated both have prefixes, so you can remember they go together. |
|
|
Measuring absorbance by direct spectrophotmetry at 455nm can determine what?
|
Total bilirubin
|
|
|
What is the limitation of measuring bilirubin by direct spectrophotometry and how do we correct for this?
|
Interference by hemoglobin can occur so we simultaneously measure hemoglobin level at its other peak and subtract them to get real answer
|
|
|
What is delta hemoglobin?
|
With prolonged elevation, conjugated bilirubin can actually bind to albumin (delta-bili). This sticks around longer, as it cannot be excreted by liver/kidney. Makes it look like hyperbili is still present.
|
|
|
A patient with alcoholic cirrhosis and jaundice would be expected to have what changes in below parameters:
Type of hyperbili, AST/ALT, Alk Phos, Cholesterol, Pruritis |
Some unconjugated, but some conjugated; really high AST/ALT, not super-high Alk Phos, Normal cholesterol, no pruritis
|
|
|
A patient with a bile duct obstruction would be expected to have what changes in below parameters:
Type of hyperbili, AST/ALT, Alk Phos, Cholesterol, Pruritis |
Almost all conjugated, Not super-high AST/ALT, really high Alk Phos, Increased Cholesterol, Itching +
|
|
|
What is the half-life of Factor VII?
|
12 hours
|
|
|
A patient presents to an ER without CT or ultrasound equipment with jaundice and elevated PT. Before the workup can reveal whether he has cirrhosis or a bile duct obstruction, an simple medication can be given to help discern. What is it?
|
Parenteral Vitamin K.
If the patient has cirrhosis, then Vit K should not help correct the factor levels much. If the patient has a stone, then the PT prolongation is likely due to a lack of absorption of Vit K (lack of bile salts) and should correct with IV Vit K. |
|
|
What pattern of gamma globulins do you expect to see in autoimmune hepatitis?
|
polyclonal IgG increase
|
|
|
What pattern of gamma globulins do you expect to see in primary biliary cirrhosis?
|
polyclonal IgM increase
|
|
|
What pattern of gamma globulins is common in all liver diseases?
|
Impaired hepatic synthesis of protein with increased immunoglobulin synthesis results in an albumin to globulin ration <1.
|
|
|
What leads to so-called physiologic jaundice of the newborn? What type of hyperbilirubinemia is it?
|
Unconjugated hyperbilirubinemia. The gut lacks the bacteria to convert Conjugated Bili to urobilinogen and it can't be excreted via stool. Conjug bili is thus converted back to Unconjug by beta-gluconaridase in gut. Fetal clearance of the Unconjug bili is via placenta. At birth, if the baby cannot pass enough bili through stool then becomes jaundiced. Also, hepatic enzymes aren't full-force yet.
|
|
|
Name the following characteristics of neonatal jaundice:
a) time of onset b) time of peak c) peak level and rate of increase |
a) onset at day 2-3 days
b) peaks at 4-5 days c) peak of 5-6 mg/dL (usually) and at a rate of <5mg/dL/day |
|
|
Two common causes of marked elevation in newborn bilirubin:
|
Hemolytic disease of newborn, sepsis
|
|
|
What is the CNS damage caused by hyperbilirubinemia termed? Why does this happen in infants?
|
Kernicterus
Underdeveloped blood-brain barrier |
|
|
A 7 day-old infant dies after severe hyperbilirubinemia. At autopsy, the cause is found to be due to biliary atresia. In addition, what CNS findings would you see?
|
Yellow-stained subthalamic nucleus, hippocampus, thalamus, globus pallidus, cerebellar nuclei, and cranial nerve nuclei.
|
|
|
Features in neonatal jaundice that raise the concern that it is not "physiologic:"
Timing of appearance and peak, length of jaudice, levels, type |
Appearance at <24 hours, rising bili past 1 week, persistance of jaundice past 10 days, level >12mg/dL, increase >5mg/dL/day, conjugated bili >2mg/dL. (Remember, Physiologic jaundice is more unconjugated--due to crappy liver enzymes).
|
|
|
A newborn with biliary atresia develops jaundice. What type of jaundice is most likely, and why will phototherapy not work?
|
The bilirubin is most likely conjugated (it's already been through the liver), and phototherapy works by converting unconjugated bili to conjug bili for water solubility and excretion.
|
|
|
When should phototherapy be considered in the treatment of neonatal jaundice?
|
As age increases, the threshold level increases. But it basically starts at 10mg/dL at 12 hours then increases 2mg/dL for each 12 hours of life.
|
|
|
When should exchange transfusion be considered in the treatment of neonatal jaundice?
|
>20mg/dL
|
|
|
Timing and type of hyperbilirubinemia related to:
Physiologic jaundice of Newborn |
>24 hours but less than 10 days; unconjugated
|
|
|
Timing and type of hyperbilirubinemia related to:
Breast milk Jaundice |
>7 days; unconjugated
|
|
|
Timing and type of hyperbilirubinemia related to:
Polycythemia, Hemolytic disease of newborn, erythroblastosis |
<24 hours, unconjugated
|
|
|
Timing and type of hyperbilirubinemia related to:
Hemoglobinopathies or RBC enzyme defects |
>7 days, unconjugated
|
|
|
Timing and type of hyperbilirubinemia related to:
Bowel obstructions like CF, Hirschsprung, ileal atresis |
>7 days, unconjugated
(*unconjugated* because the gut bacteria don't see the conjugated bili to help it get changed to urobilinogen and excreted, but the enzyme β-glucuronidase is present to "unconjugate" the bili to get it reabsorbed. |
|
|
Timing and type of hyperbilirubinemia related to:
Inherited disorders of bilirubin metabolism Extra: what are these disorders? (2) |
Unconjugated, >7days
Crigler-Najjar, Gilbert |
|
|
Timing and type of hyperbilirubinemia related to:
Biliary obstruction |
Conjugated, >7days
|
|
|
Timing and type of hyperbilirubinemia related to:
TORCH infections Extra: What are they? |
<24 hours, conjugated
Toxo, Rubella, CMV, Herpes, Others (Coxsackievirus, Syphilis, Varicella-Zoster Virus, HIV, and Parvovirus B19) |
|
|
Timing and type of hyperbilirubinemia related to:
Metabolic disorders such as storage diseases |
>7days, conjugated
|
|
|
Timing and type of hyperbilirubinemia related to:
Disorders of bilirubin transport Extra: What are they? (2) |
Conjug, >7 days
Rotor, Dubin-Johnson |
|
|
Timing and type of hyperbilirubinemia related to:
Allagille Syndrome |
Conjugated, >7days
|
|
|
What is the main use of transcutaneous bilirubin measurements?
|
Screening otherwise healthy newborn infants for elevations of bilirubin to evaluate those at risk for jaundice.
|
|
|
In regards to drug-induced hepatitis, when do most events occur in relation to the drug dosage?
|
Within first 4 months of administration.
|
|
|
Which type of viral hepatitis is the most likely to become chronic?
|
HCV
|
|
|
What type of acute hepatic injury will raise the AST/ALT the most?
|
Ischemic or toxic injury
|
|
|
What level of AST will give you a 90% chance that the etiology of injury is toxic?
|
>3,000 U/L
|
|
|
A patient presents with AST of 600 U/L and an ALT of 600. Is the cause more likely alcohol or viral?
|
Viral. Viral infections often raise the AST to greater than 10x the upper limit of normal, while EtOH rarely does this.
|
|
|
A patient presents with AST of 300 and ALT of 145. Is the cause more likely alcohol or viral?
|
Alcohol. EtOH often raises the AST 2x's higher than the ALT. Viral patterns are usually closer to 1:1.
|
|
|
Which patients are more likely to have jaundice? Hep A, Hep b, Hep C, EtOH
|
Hep A, EtOH
|
|
|
Which levels correct first, bili or transaminases?
|
Transaminases
|
|
|
What is probably the best indicator of prognosis in acute hepatic injury?
|
PT >4.0s
|
|
|
What two isoenzymes make up serum amylase?
How do we differentiate? |
Salivary and pancreatic amylase
Electrophoresis, inhibition, or monoclonal antibodies |
|
|
If you put amylase on an electrophoresis gel how many bands do you see? Which are pancreatic and which are salivary?
|
6, first three are salivary, second 3 are pancreatic
|
|
|
How can we differentiate between salivary and pancreatic amylase using inhibition tests?
|
Salivary amylase is inhibited by wheat germ lectin.
|
|
|
When do serum amylase levels rise and normalize in acute pancreatitis?
|
Rise within 2-24 hours, fall to normal in 2-3 days.
|
|
|
Do high levels of amylase mean anything in the diagnosis of pancreatitis? What about prolonged elevation?
|
High levels don't reflect severity, but do increase liklihood that pancreatitis is the cause. Prolonged elevation suggests pseudocyst formation or complication
|
|
|
Why do most pancreatitis patients also have increased urine amylase?
|
The amylase is normally cleared by glomerulus. (Keep in mind--kidney failure patients might have increased plasma amylase...) Can calculate fractional excretion of amylase.
|
|
|
A 42 year-old gentleman presents with severe acute epigastric pain, nausea, and "stranding" (evidence of inflammation) of the pancreas on CT scan. Pancreatitis is the top of the differential, but serum amylase is barely elevated. What could be the cause?
|
If his pancreatitis is caused by hypertriglyceridemia, TGs may interfere with measure of amylase assay.
|
|
|
Name 10 non-pancreatic causes of hyper-amylasemia:
|
diabetic ketoacidosis, peptic ulcer disease, acute cholecystitis, ectopic pregnancy, salpingitis, bowel ischemia, intestinal obstruction, macromaylasemia, renal insufficiency, opioid administration (?)
|
|
|
What is macroamylasemia? What is the incidence?
What is the cause? |
1% incidence where apparently healthy individuals have elevated amylase and low urine amylase due to Ig-amylase complexes that are not cleared.
|
|
|
Is lipase specific for the pancreas?
|
Yes
|
|
|
When does lipase rise and fall in acute pancreatitis?
|
Rises like amylase in 2-24 hours of onset and remains elevated for 14 days.
|
|
|
How is lipase better than amylase for pancreatitis diagnosis?
|
Less renal clearance, so more predictable. Only pancreatic form exists.
|
|
|
What is Ranson criteria used for in treatment of pancreatitis?
|
Predict severity
Note: Lipase/Amylase levels do not predict severity. |
|
|
What two time frames are used to evaluate Ranson criteria?
|
Admission and 48 hours following
|
|
|
What criteria are used for Ranson criteria at admission?
|
Age, WBC, Glucose, AST, LDH
|
|
|
What criteria are used for Ranson criteria at 48 hours?
|
Urea, Calcium, PaO2, Base deficit, fluid sequestration, hematocrit
|
|
|
Most common causes of acute pancreatitis? (2)
|
Alcohol and Gallstones
|
|
|
What are some other causes of pancreatitis besides EtOH and gall stones?
|
Hypertriglyceridemia, Hypercalcemia, Viral, inherited, CF, scorpion bite
|
