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GI II Exam 1. > Robbin's Tables > Flashcards

Robbin's Tables Flashcards

1
Q

Normal values of bilirubin: conjugated and unconjugated

A

conjugated - .1 - .3

unconjugated - .2 - 9

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2
Q

Dasabuvir

A

NS5B
CYP3A4
N, pruritus, insomnia

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3
Q

Preeclampsia

A

maternal HTN
proteinuria
peripheral edema
coag abnormalities

+ hyperreflexia and convulsions = eclampsia

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4
Q

HNF1-alpha hepatocellular adenoma

A

inactivating HNF1alpha mutation
fatty and devoid of cellular architectural atypic
LFABP is NOT expressed (typically always is)

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5
Q

What levels are elevated in:
a. Steatosis
b. Steatohepatitis
c, Steatofibrosis/cirrhosis

A

a. alk phos, ggt
b. AST, ALT, alk phos, bilirubin
c. coag probs hypoprotein

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6
Q

Elbasvir

A

fatigue, HA, N when combined with Grazoprevir

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7
Q

When is infarct of hepatic artery a problem?

A

in liver transplantation –> leads to infarction of major ducts of biliary tree

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8
Q

Simeprevir

A

NS 3/4 protease inhibitor

must be taken with food

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9
Q

Ledipasvir

A

fatigue, HA, asthenia when combined with sofobuvir

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10
Q

Pattern of Injury: Cholestatic Hepatitis

A

antibiotics

statins

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11
Q

Glasgow alcoholic hepatits score

A

predicts mortality based on

  1. age
  2. serum bilirubin
  3. BUN
  4. PT time
  5. peripheral WBC count

greater than/equal to 9 –> better survival is received glucocorticoids

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12
Q

What is cholestasis?

A

impaired bile formation and bile flow that leads to bile pigmentation in the haptic parenchyma

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13
Q

Grazoprevir

A

NS 3/4 protease inhibitor

fatigue, HA, N

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14
Q

Classic Tetrad of Hemochromatosis

A
  1. Cirrhosis with hepatoemegaly
  2. Abnormal skin pigmentation
  3. DM
  4. Cardiac dysfunction
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15
Q

Mallor Denk bodies

A

accumulations of intermediate filaments found within hepatocytes

  1. Alc Liver disease (main one)
  2. NAFLD
  3. Wilson Disease
  4. Chronic biliary obstruction
  5. PBC
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16
Q

Pattern of Injury: Hepatocellualr necrosis

A

acetaminophen

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17
Q

PBC Morphology Highlights

A
  1. patchy distribution
  2. bile accumulation is periportal
  3. feathery degeneration and ballooned, bile-stained hepatocytes
  4. Mallory Denk Bodies
  5. Marked hepatomegaly

End stage livers have a green pigmentation!!

some pts develop portal HTN rather than severe cholestasis

18
Q

Pattern of Injury: Fatty liver disease

A

ethanol
aspirin (reye)
corticosteroids

19
Q

Dagnosis for

  1. HNF1-alpha hepatocellular adenoma
  2. Beta catenin hepatocellular adenoma
  3. Inflammatory hepatocellular adenoma
A
  1. stain for LFABP –> will be absent
  2. beta catenin nuclear translocation; glutamine synthetase is positive
  3. inc CRP and serum amyloid in serum; areas of fibrotic storm, mononuclear inflammation, ductular reactions, dilated sinusoids, telangiectatic vessels
20
Q

Pattern of Injury: Neoplasms

A

vinyl chloride
alcohol
oral contraceptives
thorotrast

21
Q

Velpatasvir

A

with sofosbuvir = first once daily single tablet regime

HA, fatigue

22
Q

Pattern of Injury: Fibrosis and cirrhosis

A

alcohol

vitamin A

23
Q

Pattern of Injury: Granulomas

A

amiodarone

allopurinol

24
Q

Sofosbuvir

A

NS5B

prodrug, nucleotide analog

25
Q

What cytokines activate stellate cells?

A

proliferation - PDGF, TNF
contraction - ET-1
chemotaxis - MCP-1, PDGF

422,

26
Q

Ombitasvir

A

nausea, purities, insomnia

CYP3A4

27
Q

Why are women more susceptible to alc liver disease?

A

estrogen increases gut permeability to endotoxins –>
increases expression of LPS receptor CD14 in Kupffer cells –> increased production of pro inflammatory cytokines and chemokine

28
Q

What can a PPI due in hemochromatosis?

A

reduces intestinal iron absorption and decreases maintenance phlebotomy blood volume requirement

29
Q

Paritaprevir

A

NS 3/4 protease inhibitor
CYP3A4
N, pruritus, insomnia

30
Q

What levels are raised in hepatic steatosis? alcoholic hepatitis?

A

a. serum bilirubin, alk phos

b. AST > ALT, hyperbilirubinemia, alk phos

31
Q

Mxns of liver injury due to iron

A
  1. lipid per oxidation via iron catalyzed free radicals
  2. stimulations of collagen formation by activation of hepatic stellate cells
  3. Interaction of reactive oxygen species and iron with DNA leading to cell death and possibly HCC
32
Q

Three ways Cu is toxic to liver

A
  1. promotes formation of free radicals
  2. binds to sulfhydryl groups of cellular proteins
  3. displaces other metals from hepatic metal-enzymes
33
Q

What is unique about aflatoxin in HCC?

A

leaves molecular signature - mutation in codon 249 of p53 gene

34
Q

Criteria for Metabolic Syndrome

A
  1. DM or insulin resistance or impaired glucose tolerance or impaired fasting glucose
  2. BP (140/90), microalbuminuria, central obesity, dyslipidemia
35
Q

Stupid high liver enzyme levels

A

ischemic hepatitis
acetaminophen OD
acute viral hep

36
Q

Pattern of Injury: Cholestatic

A

contraceptives

anabolic steroids

37
Q

What are the three types of hepatic adenomas?

A
  1. HNF1-alpha: no risk of malignant transformation
  2. Beta catenin Activated: very high risk (cut out even if asx); associated with OCs and anabolic steroids
  3. Inflammatory: small, but definite risk (cut out even if asx)
38
Q

Pattern of Injury: Vascular lesions

A

oral contraceptives
high dose chemo
anabolic steroids

39
Q

Maddrey Discriminant Function

A

if at or above 32, have high risk of mortality and may benefit from glucocorticoids

*alcoholic hepatitis

40
Q

Associated Conditions with Wilson Disease

A 
renal calculi 
infertility 
hemolytic anemia
subQ lipomas 
RTA
41
Q

What is the histo hallmark of ascending cholangitis?

A

influx of periductular neutrophils directly into bile duct epithelium and lumen

GI II Exam 1. (25 decks)

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