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GI > Drug Induced Liver Disease, Hepatobiliary Neoplasia, GI/Liver Miscellaneous > Flashcards

Drug Induced Liver Disease, Hepatobiliary Neoplasia, GI/Liver Miscellaneous Flashcards

1
Q

DILD

A

Drug Induced Liver Disease

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2
Q

DILD Important?

A
  • 10% of acute hepatitis admissions
  • 6% of drug side effects
  • 15-20% of fulminant & subfulminant hepatitis
  • 20% of patients with jaundice & DILD will progress to fulminant failure
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3
Q

When does DILD happen?

A
  • within 5-90 days
  • after prolonged use
  • triad of rash, eosinophilia & fever rare
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4
Q

Clinical Setting of DILD?

A

-asymptomatic
-fatigue
-abnormal liver enzymes
-jaundice
-hepatic failure
(repeated exposure not required, even small doses)

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5
Q

Intrinsic Hepatotoxin

A
  • predictable injury
  • dose dependent
  • easily reproduced in animals
  • carbon tetrachloride
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6
Q

Idiosyncratic Hepatotoxin

A
  • unpredictable
  • not in animals
  • not dose dependent
  • most medications
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7
Q

Hepatocellular Injury

A 
acute hepatitis
fulminant hepatitis
chronic hepatitis
steatohepatitis
cirrhosis
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8
Q

Cholestatic Injury

A 
Cholestasis-impariment of bile flow
bland cholestasis
acute & chronic cholangitis
sclerosing cholangitis
vanishing bile duct syndrome
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9
Q

Oral Contraceptives

A

-Idiosyncratic
-bland cholestasis
-estrogen decreases membrane fluidity
-dec. Na+, K+ ATPase activity & bile salt transport
vascular complications
hepatic vein thrombosis (Budd-Chiari)
Peliosis hepatis
Focal nodular hyperplasia
Hepatic Adenomas
Hepatocellualr carcinoma: rare with current doses

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10
Q

Occupational Chemicals

A
  • obtain exposure history

- inhaled & contact

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11
Q

Angiosarcoma

A

25 patients per year
-hepatomegaly, inc. alkaline phosphatase
>70% pathogenesis is unknown
(polyvinyl chloride exposure?)

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12
Q

Acetaminophen in US

A
  • 85% of OTC poisonings
  • with ethanol, dec. glutathione, inc. P450 induction, inc. toxic metabolites, 2.5-4g may be hepatotoxic in alcoholics (unsafe at low doses with alcoholics)
  • well tolerated in patients with non-alcoholic liver disease
  • patients w/cirrhosis from other causes often have decreased P450 activity & normal glutathione level
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13
Q

Acetaminophen/Alcohol/Hospital

A
  • discontinue ethanol
  • hold acetaminophen
  • N-acetylcysteine give 140mg/kg then 70mg/kg q 4 hrs x 17 doses
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14
Q

N-Acetylcysteine

A
  • Therapeutic even with late presentation
  • Dosing within 10-36hrs lowers mortality from 58 to 37% (acetaminophen)
  • helpful in acute liver failure from non-acetaminophen etiologies `
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15
Q

Paracetamol

A
  • restricted to 16 500mg tablets per patient in stores (32 tablets in UK)
  • 72% drop in hospitalizations
  • 74% dec. in deaths/transplantation
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16
Q

Hepatocellular Carcinoma

A
  • most common primary cancer of liver (75%)
  • 5th most common neoplasm world wide
    • common in areas with viral hep B is endemic
    • 24,000/year in US due to inc. hep C
    • bad prognosis, 5 year survival is less than 5%
  • malignant epithelia neoplasm of liver composed of cells resembling hepatocytes
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17
Q

Hepatocellular Carcinoma Epidemology

A
  • 3x more common in males
  • 3x more common in Asian Americans & 1.5x more common in blacks
  • 50-60 years old
  • usually in patients with chronic liver disease (80% chronic viral hepatitis)
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18
Q

Common Sites for Liver Mets?

A

-colon, lung, breast, pancreas & stomach

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19
Q

Most common neoplasms in liver?

A

metastatic tumors

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20
Q

Presentation of Hepatocellular Carcinoma

A
  • decompensation of chronic liver disease
  • jaundice, encephalopathy, ascites, bleeding
  • others: mild-moderate upper abdominal pain, weight loss, diarrhea, bone pain, dyspnea
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21
Q

Classifications of Hepatocellular Carcinoma

A
  • based on microscopic/macroscopic appearance (doesn’t predict behavior)
  • Predictors: size, differentiation, invasion & metastasis, presence or absence of cirrhosis
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22
Q

Gross Pathology of Hepatocellular Carcinoma

A

highly variable

  • yellow (from bile production), invasive
  • multiple nodules (tumor originating in multiple sites), cholestasis (tumor obstruct ducts)
  • 20% arise without cirrhosis
  • highly vascularized (biopsy cause hemorrhage)
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23
Q

Hepatocellular Carcinoma: Histologic patterns

A
  • Micro-Trabecular
  • MacroTrabecular
  • Acinar
  • Solid
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24
Q

Hepatocellular Carcinoma Pain

A

from stretching of capsule

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25
Q

Hepatocellular Carcinoma Microscopy: 1

A

-well differentiated with trabeculae of cells resembling normal hepatocytes

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26
Q

Hepatocellular Carcinoma Microscopy: 2

A

-moderately differentiated hepatocellular carcinoma with bigger cells less resembling normal hepatocytes and very abnormal architecture

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27
Q

Hepatocellular Carcinoma Microscopy: 3

A

-moderately differentiated (still) but very large neoplastic cells and even more disturbed architecture

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28
Q

Hepatocellular Carcinoma Microscopy: 4

A

-poorly differentiated hepatocellular carcinoma with pleomorphic dyscohesive neoplastic cells invading non-neoplastic liver from below

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29
Q

Hepatocellular Carcinoma Microscopy: 5

A

-anaplastic hepatocellular carcinoma with markedly pleomorphic cells with huge nuclei, some multinucleated, some bizarre

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30
Q

Alpha-Fetoprotein

A

-major fetal serum globulin
>20mcg/L in 60% of patients with hepatocellular carcinoma (also elevated with acute/chronic liver injury, gonadal tumors, pregnancy, gastric cancers)
-specificity 91%
>200mcg/L specificity 99% (sen. 22%)

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31
Q

Treatment of Hepatocellular Carcinoma

A
  • surgical resection
  • majority of patients not eligible due to tumor extent or underlying liver dysfunction
  • various other treatments including injecting poison into the tumor (ethanol)
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32
Q

Hepatic Adenomas (Hepatomas)

A
  • more common in patients who have taken or are taking anabolic steroids, androgenic steroids of estrogenic steroids
  • commonly compress surrounding normal liver, which may cause some necrosis of it, with repair response forming a capsule
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33
Q

Hemangioma

A
  • most common benign tumor in liver
  • usually <2cm, commonly sucapsular
  • composed of blood-filled vascular spaces
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34
Q

Hepatoblastoma

A
  • rare malignant epithelial neoplasms in children

- malignant tumors in children have more primitive appearance, similar to embyronal appearance of site (blastoma)

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35
Q

Cholangiocarcinoma

A
  • malignant epithelial neoplasm with biliary differentiation, arising from cholangiocytes
  • uncommon (7,000/year in US) (3,000 extrahepatic)
  • males, 50-70
  • associated with primary sclerosing cholangitis (PSC)
  • extrahepatic 2/3 at bifurcation of common hepatic bile duct (Klatskin tumors)
  • KRAS mutation in 50% of intra and 15% of extrahepatic, p53 mutation in 33%
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36
Q

Cholangiocarcinoma Appearance/Spread

A
  • tan-white & firm b/c they have a desmoplastic reaction and they don’t make bile
  • more tendency to spread via lymphatics
  • less tendency to spread via blood vessels than hepatocellular carcinoma
  • embedded in dense fibrous matrix, abnormal tubular structures
37
Q

Symptoms of Extrahepatic Cholangiocarcinoma

A

-pruritus (66%), RUQ abdominal pain (constant dull ache 50%), weight loss 50%, fever 20%, clay-colored stools and dark urine

38
Q

Signs of Extrahepatic Cholangiocarcinoma

A

-jaundice (90%), hepatomegaly (40%), RUQ mass (10%

39
Q

Labs of Extrahepatic Cholangiocarcinoma

A

high bilirubin (>10)
high alkaline phosphatase (2-10x normal)
initially normal ALT & AST

40
Q

Symptoms of Intrahepatic Cholangiocarcinoma

A

dull RUQ pain & weightloss

41
Q

Signs of Intrahepatic Cholangiocarcinoma

A

only those of underlying liver disease

42
Q

Labs of Intrahepatic Cholangiocarcinoma

A

normal or slightly elevated bilirubin

elevated alkaline phosphatase

43
Q

Cholangiocarcinoma Diagnosis

A

biopsy (cytology)

44
Q

Cholangiocarcinoma Treatment

A

surgical resection (poor results)

45
Q

Cholangiocarcinoma Prognosis

A

bad, 5 year survival 5-10%

46
Q

Gallbladder Carcinoma

A 
-7,000per year in US
females, hispanics & Native Americans
exophytic or infiltrating patterns of growth
microscopic (usually glandular)
-70 year old
47
Q

Symptoms of Gallbladder Carcinoma

A

-abdominal pain, jaundice anorexia, nausea, vomiting, malaise, weight loss
SIGN: RUQ mass

48
Q

Diagnosis/Treatment of Gallbladder Carcinoma

A

-biopsy (cytology)
-surgery (rarely feasible)
prognosis bad (5% 5 year survival)

49
Q

Jaundice (hyperbilirubinemia)

A

Conjugated (direct): obstruction, hepatitis, Dubin-Johnson

Unconjugated (indirect): hemolysis, hepatitis, Gilbert

50
Q

Jaundice in Neonates

A
  • common, “physiologic” due to liver immaturity (hepatic machinery for conjugating & excreting bilirubin not fully operational until 2 weeks old)
  • severe can injure brian, treated with UV light
51
Q

Biliary Atresia

A
  • progressive inflammatory & fibrosing disease of extrahepatic bile ducts, of unknown etiology, with gradually complete obstruction of bile flow caused by destruction of extrahepatic bile ducts
  • 1:10,000 live births
  • causes 1/2 of neonatal cholestasis
  • most common cause of death from liver disease in early childhood
52
Q

Biliary Atresia Microscope

A

-Fibrosis obliterating on extrahepatic bile duct

53
Q

Biliary Atresia Progression

A
  • typically become jaundiced at 3-6 weeks of age
  • have conjugated hyperbilirubinemia
  • disproportionately high GGT
  • mild-moderately high ALT & AST
  • poor prognosis improved by early surgery (hepatoportoenterostomy) but many still need liver transplant
54
Q

Alagille Syndrome

A
  • syndrome paucity of intrahepatic bile ducts
  • neonatal jaundice, pruritis and cholestasis
  • “arteriohepatic dysplasia”
  • autosomal dominant
  • 70% sporadic new mutations
  • dut to mutation in JAGGED 1 gene for ligand for NOTCH 1 receptor
55
Q

Alagille Syndrome: Microscopy

56
Q

Alagille Syndrome: Prognosis

A

-good unless misdiagnosed and surgerized

57
Q

Dubin-Johnson Syndrome

A
  • hereditary conjugated hyperbilirubinemia

- defective excretion of bilirubin conjugates and other organic anions across hepatocyte canalicular membrane

58
Q

Dubin-Johnson Syndrome: Microscope

A

-brown-black pigment in the liver: lysosomes containing polymers of epinephrine metabolites

59
Q

Dubin-Johnson Syndrome: Symptoms

A

-usually asymptomatic, with normal life expectancy, but may have recurring or fluctuating chronic jaundice

60
Q

Gilbert Syndrome

A
  • autosomal recessive deficiency of uridine diphosphate-glucuronyltransferase (UGT) enzyme conjugates bilirubin
  • 9% of population homozygous
  • males
  • usually diagnosed in young adults with mild, primarily unconjugated hyperbilirubinemia (febrile illness, physical exertion, fasting or hemolysis) and no other manifestations of this disease
61
Q

Gilbert Syndrome: Prognosis

A

-benign, maybe better than average because have slightly higher bilirubin than average & incidence of colon cancer, cancer mortality in general and atherosclerotic heart disease are inversely proportional to bilirubin level

62
Q

Primary Biliary Cirrhosis

A
  • auto-immune, slowly progressive cholestatic disease
  • typically in late middle-aged women
    male: female 1:6
  • usually present with pruritis, fatigue, hepatomegaly, elevated alkaline phosphatase eventually get jaundice, xanthomas, steatorrhea
63
Q

Primary Biliary Cirrhosis: Pathology

A
  • dense lymphocytic inflitrate in and around interlobular bile ducts with granulomas and bile duct destruction and loss, and progressive portal fibrosis
  • associated with anti-mitochondrial antibodies (90%)
64
Q

Primary Biliary Cirrhosis: Microscopy

A

-dense lymphocytic infiltrate in and around interlobular bile ducts, with granulomas and bile duct destruction and loss

65
Q

Primary Sclerosing Cholangitis

A
  • probably auto-immune fibrosing cholangitis of intra & extra hepatic bile ducts
  • associated with inflammatory bowel disease (70%)
  • early middle-aged men, male:female 2:1
66
Q

Primary Sclerosing Cholangitis: Pathology

A

-onion-skinning fibrosis of bile ducts

67
Q

Primary Sclerosing Cholangitis: Presentation

A
  • ususally fatigue, pruitis, jaundice
  • commonly have endoscopic retrograde cholangio-pancreatography showing characteristic “beading” of bile ducts due to strictures & dilatations
68
Q

Budd-Chiari Syndrome

A
  • portal hypertension due to thrombosis of hepatic veins
  • manifestations: hepatomegaly, ascites, abdominal pain
  • due to polycythemia vera, other myeloproliferative disease, pregnancy, postpartum state, oral contraception, paroxysmal nocturnal hemoglobinuria, abdominal cancer
69
Q

Budd-Chiari Syndrome Cause

A
  • 30% idiopathic
  • associated with hypertrophy of caudate lobe
  • commonly fatal in develops acutely
  • 50% 5 year survival if develops chronically
70
Q

Acute Cholecystitis

A

common (middle aged females)

90% have gallstones obstructing neck of gallbladder or cystic duct

71
Q

Acute Cholecystitis: symptoms

A

-steady severe abdominal pain (RUQ), fever, anorexia, nausea

72
Q

Acute Cholecystitis: signs

A
  • patients lie still b/c pain is aggravated by movement

- voluntary/involuntary guarding

73
Q

Murphy’s Sign

A

acute cholecystitis

  • while palpating the area of the gallbladder, patient asked to inspire deeply causing increased pain
    (sen. 97%, spec. 48%)
74
Q

Acute Cholecystitis: Labs

A

leukocytosis

inc. alkaline phosphatase

75
Q

Acute Cholecystitis: Complications

A

gangrene 20%

rupture 2%

76
Q

Acute Cholecystitis: Treatment

A

cholecystectomy

77
Q

Acute Acalculous Cholecystitis

A

10% of gallbladders removed for Acute Cholecystitis contain no gallstones

  • usually seriously ill patients with
    1. postoperative state after major surgery
    2. severe trauma
    3. severe burns
    4. sepsis
  • stasis & sludging of bile in gallbladder probably = major etiological factors
78
Q

Chronic Cholecystitis

A

-associated with gallstones (almost always) infection with E. coli or enterococci (1/3)

79
Q

Chronic Cholecystitis: Symptoms

A

biliary cholic or indolent RUQ pain, epigastric distress, nausea, intolerance for fatty foods

80
Q

Chronic Cholecystitis: Diagnosis

A

ultrasound: gallstones & thickened gallbladder wall

81
Q

Chronic Cholecystitis: Treatment

A

cholecystectomy

82
Q

Choledocholithiasis

A

gallstones in bile ducts (obstruction)

83
Q

Choledocholithiasis: Complications

A

biliary obstruction, acute/chronic pancreatitis, acute/chronic cholangitis, acute/chronic cholecystitis (if cystic duct), liver abscess, chronic liver disease, secondary biliary cirrhosis

84
Q

White Bile

A

-biliary secretion w/high mucus content being aspirated from the gallbladder intraoperatively in a case of biliary obstruction

85
Q

Cholangitis

A

inflammation of the biliary tree (often with infection)

  • almost always caused by choledocholithiasis complicated by bacterial infection of the normally sterial biliary lumen
  • uncommon: tumors, stents, acute pancreatitis, benign strictures
86
Q

Ascending Cholangitis

A

-infection of intrahepatic biliary ducts
Acute: usually due to bacteria (E. coli, Klebsiella, Clostridium, Bacteroides, Enterobacter, Enterococcus)
Chronic: usually due to parasites (Cryptosporidium, Fasciola hepatica, Schistosoma or Clonorchis sinensis)

87
Q

Symptoms of Ascending Bacterial Cholangitis

A

-fever, chills, abdominal pain, jaundice

88
Q

Pathology of Ascending Bacterial Cholangitis

A

-purulent bile fills and distends bile ducts, can get liver abscess formation

89
Q

Treatment of Ascending Bacterial Cholangitis

A

-relief of obstruction and antibiotics

GI (19 decks)

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