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GI DRx > 04b: Liver Stuff > Flashcards

04b: Liver Stuff Flashcards

1
Q

Liver disease longer than (X) period of time is considered chronic

A

X = 6 months

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2
Q

Patients considered to be in fulminant hepatic failure presented with which symptoms only (X) weeks after onset of liver disease.

A

X = 6

Encephalopathy, hypoglycemia, hypoalbuminemia, low coag factors

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3
Q

The jaundice seen in liver disease is almost always associated with which other symptom?

A

Dark urine (due to high direct BR)

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4
Q

T/F: pruritis and maculopapular rash are important features of liver disease

A

False - rash-less pruritis is

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5
Q

T/F: liver disease symptoms include hypercoaguable states

A

True - decreased synthesis of antithrombin III, Protein C and S

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6
Q

List the key clinical signs that make liver disease in a patient obvious.

A
  1. Jaundice
  2. Muscle wasting
  3. Ascites
  4. Palmar erythema
  5. Spider angioma
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7
Q

Enlargement of the spleen in the setting of liver disease is usually due to:

A

portal hypertension

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8
Q

A cirrhotic liver feels (X) upon palpating

A

Firm and nodular

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9
Q

Liver function tests usually include (X) hepatocellular enzymes and (Y) canalicular enzymes.

A 
X = AST, ALT
Y = ALP, GGT
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10
Q

Most commonly used tests of hepatic synthetic function include:

A
  1. Albumin

2. PT (replaced by INR)

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11
Q

Most commonly used tests of hepatic excretory function include:

A

BR

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12
Q

(ALT/AST) is less specific to liver since it is also found in high concentrations in (X) cells.

A

AST

Pancreas, RBCs, muscle, kidney

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13
Q

An increase in (AST/ALT) that’s out of proportion to (AST/ALT) suggests alcoholic hepatitis/drug-induced injury.

A

AST&raquo_space; ALT

Likely due to extra-hepatic release as well

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14
Q

Increased levels of alkaline phosphatase is found as result of extra-hepatic reasons such as:

A
  1. bone disease (Paget’s)
  2. pregnancy
  3. intestinal injury (ischemia).
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15
Q

Increased levels of alkaline phosphatase (with normal AST/ALT) is found as result of hepatic diseases such as:

A
  1. Bile duct obstruction

2. Cholestatic liver diseases (primary biliary cirrhosis, sclerosing cholangitis, drug-induced cholestatic liver injury)

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16
Q

Hepatic cause for high ALP can be confirmed with (X) test.

A

X = GGT (should see parallel increase)

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17
Q

GGT is a (specific/sensitive) test for liver injury.

A

Sensitive (but not specific for any one disease since elevated in nearly all forms of liver disease)

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18
Q

T/F: liver disease can be ruled out with normal serum albumin levels.

A

False - long half-life of albumin means acute liver disease in patient may present with normal albumin

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19
Q

Based on the (short/long) half life of (X), which test is extremely useful for monitoring liver function in patients with acute liver injury?

A

Short;
X = clotting factors

PT/INR

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20
Q

List examples of diseases that present with hepatitic pattern of disease (high ALT/AST).

A
  1. Viral/autoimmune hepatitis

2. Acute drug toxicity (ex: acetaminophen)

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21
Q

List the most common diseases that would cause AST/ALT rise over 1000!

A
  1. Viral hepatitis
  2. Drug/toxin-mediated hepatitis
  3. Ischemic hepatitis
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22
Q

“Mixed” (cholestatic and hepatitic) pattern of liver disease is only really seen in which cases?

A

chronic diseases (cirrhosis, some cases of metastasis)

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23
Q

What are some causes for cholestatic pattern of liver disease (high ALP/GGT)?

A
  1. Bile duct obstruction
  2. Metastatic disease to liver
  3. Infiltrative disorders
  4. Granulomatous disease
  5. Autoimmune (preferentially affecting biliary ductules)
24
Q

BR is formed from breakdown of:

A

Heme:

  1. Myoglobin
  2. Hemoglobin
  3. Cytochromes
25
Q

T/F: Liver is major site of BR production.

A

False - spleen! 70-80% BR from hemoglobin from senescent RBCs

26
Q

In ecchymoses (bruises), (X) process is occurring in (Y) cells.

A 
X = Heme breakdown and BR formation
Y = macrophages
27
Q

BR formation: here is converted to (X) by (Y). What color is (X)?

A 
X = biliverdin
Y = heme oxygenase

Blue/green

28
Q

Biliverdin is converted to (X) via cytosolic (Y).

A 
X = BR
Y = Biliverdin reductase
29
Q

T/F: both biliverdin and BR are water insoluble.

A

False - biliverdin water soluble

30
Q

Which structural feature of BR accounts for its poor water solubility?

A

Intramolecular H bonds

31
Q

T/F: unconjugated BR is transported to liver bound to albumin

A

True

32
Q

T/F: Hepatic uptake of BR is rate-limiting in its metabolism.

A

False - very rapid carrier mediated uptake

33
Q

Once BR enters hepatocyte, (X) regulate its cytosolic diffusion and prevent efflux back into plasma.

A

X = ligandins and FA binding proteins (bind to BR)

34
Q

BR conjugating enzyme:

A

UGT (BR Uridine diphosphate glucoronosyltransferase)

35
Q

BRDG transported across (X) and into biliary tree via which transporter?

A

X = canalicular membrane

MRP2 transporter

36
Q

In the gut, bacteria have which effect on BRDG?

A
  1. Deconjugation (back to BR)

2. Reduction (to urobilinogen)

37
Q

T/F: Urobilinogen is yellow.

A

False - colorless

38
Q

T/F: Urobilinogen is mainly excreted by the kidneys.

A

False - only 2%

39
Q

Urine urobilinogen (increases/decreases) when there’s total bile duct obstruction.

A

Decreases/disappears

40
Q

Urine urobilinogen is increased in which general disease states?

A

BR overproduction (ex: hemolysis)

41
Q

Jaundice with no bilirubinuria usually means that the serum bilirubin is (conjugated/unconjugated). Why?

A

Unconjugated (can’t be excreted in urine); conjugated BR would be excreted by kidney if significant amounts were circulating in serum

42
Q

DDx for conjugated hyperbiliruminemia.

A

Mnemonic: BICH

  1. Bile duct obstruction
  2. Inherited (Dubin-Johnson, Rotor’s)
  3. Cholestatic disease
  4. Hepatitis
43
Q

Dubin-Johnson follows (X) inheritance pattern and involves point mutation in gene for (Y). Highest incidence in which ethnic group?

A 
X = AR
Y = MRP2 protein (nonfunctional)

Iranian Jews

44
Q

24 y.o. M presents with upper resp tract infection and jaundice. He reports this has happened before when he had the flu. Serum BR is 4 mg/dL and mostly conjugated. Likely diagnosis is (X).

A

X = Dubin-Johnson Syndrome

45
Q

In (X) inherited etiology of hyperbilirubinemia, liver tissue is darkly pigmented, often black.

A

X = Dubin-Johnson Syndrome

46
Q

DDx for unconjugated hyperbiliruminemia.

A
  1. Hemolysis
  2. Ineffective erythropoeisis
  3. Neonatal/breast milk jaundice
  4. Drug-induced
  5. Inherited (Crigler-Najjar, Gilbert’s)
47
Q

T/F: Over 90% of newborns have high BR levels with over 50% becoming jaundiced.

A

True

48
Q

T/F: Hemolysis usually causes severe elevation of BR (over 10 mg/dL).

A

False - usually mild between 1-4 mg/dL

49
Q

Why might ineffective erythropoeisis be a cause for (conjugated/unconjugated) hyperbilirubinemia?

A

RBC destruction in bone marrow leads to large BR load

50
Q

Crigler-Najjar Syndrome is inherited in (X) pattern involving (Y) protein.

A 
X = AR
Y = UGT (conjugates BR)
51
Q

Crigler-Najjar Type I: (X) protein is (defective/absent) and therapy involves (Y).

A

X = UGT
Absent (severe, death by 18 mo)
Y = liver transplant

52
Q

Crigler-Najjar Type II: (X) protein is (defective/absent) and therapy involves (Y).

A

X = UGT
Defective (mild form, survival to adulthood)
Y = Phenobarbital therapy (increases expression of UGT)

53
Q

Patient with Crigler-Najjar Type II presents with jaundice. You would expect urine BRDG to be (low/normal/high).

A

Normal (high circulating BR is unconjugated)

54
Q

Gilbert’s Syndrome is condition characterized by (constant/intermittent) (conjugated/unconjugated) hyperbilirubinemia. Which protein involved?

A

Intermittent (bouts);
unconjugated

UGT (levels either reduced or protein defective with reduced activity)

55
Q

T/F: Gilbert’s Syndrome patients typically don’t require Rx.

A

True

GI DRx (11 decks)

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