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;
44 Cards in this Set
- Front
- Back
What is hemosiderosis?
|
Deposit of iron (hemosiderin) - this causes hemochromatosis
|
|
The traid of sx. are?
|
micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation ("bronze" diabetes)
|
|
Possible complications include?
|
CHF, increased risk of hepatocellular carcinoma
|
|
What is primary form?
|
inherited, Autosomal recessive
|
|
What is secondary form due to?
|
chronic transfusion therapy
|
|
What are ferritin, iron, TIBC and transferrin saturation levels?
|
Ferritin increased, iron increased, TIBC decreased => transferrin saturation is increased
|
|
How much iron may the body contain?
|
As much as 50g, enough to set off airport metal detectors
|
|
How is this condition treated?
|
Phlebotomy, deferoxamine
|
|
bacteria convert conjugated bilirubin into what? what happens to some of this?
|
urobilinogen --> some which is reabsorbed, some which is excreted. (urobilinogen that's reabsorbed is converted to urobilin= yellow pigment in urine)
|
|
which is soluble in water/urine: conjugated or unconjugated bilirubin?
|
conjugted of course!
|
|
check out the 3 jaundice types: what are they? For each type: bilirubin type, urine bilirubin?, urine urobilinogen?
|
heptocellular (conjugated/uncongugated; urine bilirubin inc; urnine urobilinogen normal) obstructive (conjugated; urine bilirubin increased; urine urobilinogen decreased); hemolytic (unconjugated; urine bilirubin absent; urine urobilinogen increased)
|
|
What is the biochemical disorder in GILBERTS SYNDROME?
|
mild ↓ in UDP-glucuronyl transferase (this is key enzyme in conjugation of bilirubin)
|
|
what are the symptoms?
|
asymptomatic
|
|
what type of bilirubin is seen upon the lab findings in Gilbert's? Do you have do you have major hemolysis?
|
unconjugated bilirubin is elevated w/o overt hemolysis
|
|
What is the syndrome called when you have an ABSENCE of UDP-glc-ur-transferase?
|
Crigler-Najjar (CN) syndrome type 1 (type 2 is LESS severe)
|
|
when does it present in life? What is the prognosis?
|
presents early in life: pts die in a few years.
|
|
name 3 findings of Crigler Najjar syndrome?
|
jaundice, kernicterus, ↑ unconjugated bilirubin
|
|
type 2 is more sever or less severe? What do you treat it with?
|
less severe than type 1; treat type 2 with phenobarbital.
|
|
what do you treat type 1 with (name 2)?
|
plasmapheresis + phototherapy (breaks down unconj. Bilirubin)
|
|
What is Dubin Johnson syndrome?
|
↑↑ hyperbilirubin (conjugated) due to defective liver EXCRETION
|
|
what does the liver look on gross exam?
|
black liver grossly
|
|
what is the name of the less severe syndrome akin to Dubin Johnson?
|
Rotor's syndrome: also no black liver.
|
|
what is the pathophysiology of primary sclerosing cholangitis
|
segmental inflammation and fibrosis of bile ducts: unaffected parts are dilated.
|
|
what test do you do to see stricture/dilating/beading pattern in primary sclerosing cholangitis?
|
ERCP
|
|
what disease is primary sclerosing cholagitis associated with?
|
Ulcerative Colitis
|
|
What can prim. Scl. Cholangitis lead to?
|
2° biliary cirrhosis/sclerosis
|
|
what is the cause of Primary Biliary Sclerosis (PBS)? (compare the name/disease of PBS vs. PSC: primary sclerosing cholangitis)
|
autoimmune disorder with antimitochondrial antibodies
|
|
name 3 signs associated with PBS:
|
1) severe obstructive jaundice 2) itching 3) hypercholesterolemia (xanthoma)
|
|
What is the cause of SBS: secondary biliary sclerosis?
|
EXTRA-hepatic biliary obstruction → ↑ pressure in INTRA-hepatic ducts → ↑ injury/sclerosis
|
|
what is 2° biliary sclerosis associated with (name 3 things)?
|
ascending cholangitis (bacterial infection), bile stasis, and bile lakes
|
|
in liver cancers, is this common?
|
yes, #1 most common!
|
|
there is an ↑ incidence of hepatoma due to what diseases/exposures (name 7)
|
1) hep B, 2) hep C, 3) Wilson's disease, 4) hemochromatosis, 5) a-antitrypsin def 6) EtOH cirrhosis 6) carcinogens (e.g. aflatoxin B1)
|
|
How do hepatomas spread? How does this differ with renal cell ca. spread?
|
They BOTH commonly spread hematogenously!
|
|
What is major lab finding with hepatocelluar ca?
|
↑ AFP (alpha fetoprotein)
|
|
What is Reye's syndrome?
|
Hepato-encephalopathy: fatal: occurs in childhood
|
|
name 3 finding in Reye's:
|
1) fatty liver w/ microvesicular fatty change 2) hypoglycemia, 3) coma
|
|
is this associated with any outside factors/triggering factors?
|
yes: 1) viral infection (esp. VZV or influenza B) 2) salicylates!!!
|
|
if baby/child has fever what do you use in place of aspirin?
|
use acetaminophen (but with caution): i.e. acetaminophen OD hepato-toxicity
|
|
name 3 types of stones and tell me how they show up on CT scan:
|
1) cholesterol stone (radiolucent but 10-20% opaque due to calcification) 2) mixed stone = cholesterol + pigment (radiolucent) 3) pigment stone (radio-opaque)
|
|
Which is the most common type of gall stone?
|
mixed stone
|
|
name at least 5 out 9 risk factors for Cholesterol stones: is there a mnemonic?
|
1) obesity 2) Crohn's D 3) Cystic fibrosis 4) elderly 5) clofibrate 6) estrogens 7) multiparity 8) rapid weight loss 9) native American origin mnemonic = 4 F's fat, female….
|
|
name 4 risk factors for pigment stones:
|
1) pts with chronic RBC hemolysis 2) alcoholic cirrhosis 3) elderly 4) biliary infection
|
|
What is a good way to diagnosis stones?
|
ultrasound
|
|
What is CHARCOT'S TRIAD
|
1) epigastric/RUQ pain 2)fever 3) jaundice. present in 70% of those with bacterial cholangitis
|