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Pathology > Liver 2 > Flashcards

Liver 2 Flashcards

1
Q

Most common cause of incidental elevation of serum transaminase

A

NAFLD

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2
Q

Reverses NALFD histologic changes in biopsy proven steatohepatitis

A

Pioglitazone

stimulator of tf PPAR-y modulating expression of insulin sensitive genes

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3
Q

In children, NAFLD histologic injury is characterized by inflammation and scarring at the rather than neutrophilic infiltrates

A

portal tract and periportal region

mononuclear infiltrate

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4
Q

Affects children younger 4 years with viral illness
Pernicious vomiting, irritability, lethargy and hepatomegaly
Normal serum trans
Aspirin admin during viral illness
Mitochondrial injury leading to diffuse hepatocellular microvesicular steatosis (mitoch enlargement, electron lucency, disruption of cristae, loss of dense bodies)
Cerebral edema
Skeletal, kidney and heart present with microvascular fatty change

A

Reye syndrome

Others: tetracycline, valproate, ackee fruit HAART

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5
Q

Prolonged conjugated hyperbilirubinemia lasting beyond first 14d of life

May be extrahepatic or neonatal hepatitis

Jaundice, dark urine, acholic stool

A

Neonatal cholestasis

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6
Q

Most common alteration in cholestasis of sepsis from microbial product (endotoxemia) is

A

Canalicular cholestasis

prominent bile plugs in dilated canaliculi in centrilobular region

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7
Q

Cardinal feature of PBC is

A

non suppurative destruction of small and medium sized intrahepatic bile duct

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8
Q

Autoantibodies directed against several mitochondrial acid dehydrogenase
Immune resp against enzymes targetting intrahepatic ducts

A

Primary biliary cirrhosis

Destruction of duct, inflammation and scarring with cirrhosis and liver failure

Inc ALP

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9
Q

Tx of PBC with this dramatically improves course greatly slowing progression
Inhibit apoptosis of biliary epicand inhibit immune response

A

ursodeoxycholic acid

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10
Q

Most revealing in precirrhotic stage with destruction of interlobular bile duct by lympho and plasma cell with or without granuloma termed as

Portal-portal septal fibrosis
Nodular regenerative hyperplasia
Periportal periseptal chronic cholestasis with feathery degeneration

A

florid duct lesion

PBC

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11
Q

Progressive fibrosis, destruction of extra and intrahepatic bile duct of all sizes
Patchy changes with beading alternating normal and dilated duct
Assoc with IBD:
HLA-DR, ANCA, immunologically mediated

A

Primary sclerosing cholangitis

Ulcerative colitis

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12
Q

Circumferential fibrosis aka onion skinning
Tombstone scar - button scar tissue

Dx: MRI pf ducts
Biliary intraepithelial neoplasia may be harbinger of cholangiocarcinoma

Inc ALP

A

Primary sclerosing cholangitis

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13
Q

Full developed cases of hemochromatosis present with

A

1 cirrhosis all
2 DM 75-80
3 skin pigmentation 75-80

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14
Q

Defect in regulation of iron intestinal absorption leading to accum of 0.5-1 y due to mutations of the gene

Manifests after 20g of iron has accumulated

A

Hereditary hemochromatosis

HFE on ch6 Interacts with hepcidin by liver to form a web of iron control networks

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15
Q

Downregulates iron absorption in itestine and mac into plasma

A

Hepcidin

dec in all genetic forms of hemochromatosis

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16
Q

Lipid peroxidation by free rad
Stimulation of collagen
Interaction with DNA

A

Iron toxicity to cell

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17
Q

Hemosiderin deposits in organs

Golden yellow granules in cytoplasm staining blue with Prussian blue

Absent inflamm but very dark liver

Skin discoloration due to melanin not iron (slate gray)

Pseudogout from calcium dep

Atrophic testes

A

Liver, pancreas, myocardium, pituitary

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18
Q

Triad of hemochromatosis

Risk for HCC: 200x

A

Hepatomegaly
Skin pigmentation
DM

loss of libido
impotence

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19
Q

Accumulation of copper in liver, brain, eyes due to mutation of

A

Wilson disease

ATP7B

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20
Q

Copper is bound to the alpha2 globulin to form ceruloplasmin

But mutation of ATP7B leads to inability to excrete it in bile

A

apoceruloplasmin

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21
Q

Free radicals
Binding to sulfhydryl groups of cellular proteins
Displacing other metals in hepatic metalloenzyme

A

Copper toxicity

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22
Q 
Mimics fatty liver, moderate steatosis, steatohepatitis
Acute hepatitis and chronic hepatitis 
Cirrhosis 
Rhodamine stain demonstrates copper 
Orcein stain for copper assoc protein

Copper 250 ug/g dry weight is diagnostic

A

Wilson disease

Tx D penicillamine
Zinc salt

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23
Q

Copper affects the of the brain

Copper deposits in eyes as

A

Basal ganglia putamen atrophy cavitation

Kayser Fleischer ring (green brown deposit in descemet of limbus)

Also hepatolenticular degeneration

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24
Q

Round to oval cytoplasmic globules in hepatocytes
PAS (+)
Diastase-resistant

retaining AAT
Cholestasis with hepatocyte necrosis
Childhood cirrhosis
HCC in 2-3a% of adult

Deficiency in persons with PiZZ genotype causing pulmonary emphysema by accumulated misfolded AAT

A

A1 antitrypsin deficiency

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25
Q

Low serum levels of protein inhibitor AAT bec of a mutation in the allele

A

PiZZ on ch14 of AAT gene

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26
Q

Portal vein obstruction
Intra or extrahepatic thrombosis

Esophageal varices
Splenomegaly
Intestinal congestion

A

Impaired blood inflow

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27
Q

Cirrhosis
Sinusoid occlusion
Systemic circulatory compromise

Ascites
Esophageal varices
Hepatomegaly
Elevated trans

A

Impaired hepatic blood flow

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28
Q

Hepatic vein thrombosis
(Budd-Chiari)
Sinusoidal obstructive syndrome

Ascites
Hepatomegaly
Abd pain
Elevated transaminase
Jaundice
A

Hepatic vein outflow obstruction

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29
Q

Fibrotic partially recanalized vascular channel
Splenomegaly, esophageal v
Subclinical thrombosis of portal vein from neonatal omphalitis or umbilical vein cath

A

Banti syndrome

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30
Q

Thrombosis of portal vein radicle resulting in sharply demarcated area of red blue discoloration

A

Infarct of Zahn

No necrosis
Hepatocellular atrophy
Congestion of sinusoid

Hepatoportal sclerosis

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31
Q

Sickle cell disease causes this type of hepatic necrosis

A

Panlobular parenchymal

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32
Q

DIC causea occlusion of hepatic

A

sinusoid

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33
Q

Variegated mottled appearance hemorrhage necrosis in centrilobular region alternating with pale midzonal area called

Sharp demarcation of vaible periportal and necrotic pericentral hepatocytes

A

Nutmeg liver in cirrhosis

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34
Q

Thrombosis of one or more major hepatic vein

Hepatomegaly
Ascites
Abdominal pain

A

Budd-Chiari syndrome

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35
Q

Budd Chiari rf

A 
Polycythemia vera
Pregnancy 
Postpartum state
OCP use
PNHG
HCC
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36
Q

Swollen red purple
Liver with tense capsule
Severe centrilobular necrosis and congestion
If slow, centrilobular fibrosis

A

Budd Chiari

Tx: portosystemic shunt

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37
Q

Sinusoidal obstruction syndrome is an outflow problem formerly known as venoocclusive disease from toxic injury to sinusoidal endo

Rf

A

Bush tea (bec of pyrrolizidine alkaloid)

20-30d post BMT
Cyclophosphamide
Actinomycin D
Mithramycin 
Total body radiation
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38
Q

Most common hepatic neoplasm are

A

Metastatic carcinoma from colon, lung, breast

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39
Q

Angiosarcoma of liver is due to exposure to

A

vinyl chloride

arsenic

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40
Q

Most common benign lesion of the liver

Well circ endothelial cell lined vascular channel and intervening stroma
Red blue soft nodules less than 2cm beneath capsule

A

cavernous hemangioma

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41
Q

Congenital bile duct hamartoma
Bile duct like structure separated by bland collagenized stroma
No malignant potential but if multiple may indicate fibropolycystic disease of liver

A

Von Meyenburg complex

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42
Q

Localized well demarcated poorly encap lesion
Hyperplastic hepatocyte nodules with central stellate fibrous scar
Abnormal vascular flow through congenital or acquired anomaly alternating areas of regeneration and atrophy
Incidental finding in women of reproductive age in resp to estrogen
No risk for malig

A

Focal nodular hyperplasia

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43
Q

Benign neoplasm of women using OCP, regresses on discontinuation
Well demarcated uncapsulated pale yellow tan sheets of cords of cells resembling normal hepatocyte
Absent portal tract but significant neovasc

Significant bec
Mistaken for HCC
Risk of rupture if subcap esp at pregnancy
If B catenin mutated, harbors risk of HCC

A

Hepatic adenoma

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44
Q

3 types of hepatocellular adenomai

A

1 mutation of HNF1A or CYP1B1 in women using OCP (little risk for malignancy)
2 activating mutations of B catenin related to anabolic or steroid use in men (ihigh risk of malig transformation)
3 Inflammatory 50% (inc exp of acute phase reactant serum amyloid A and CRP) in obese women with FL express serum amyloid protein

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45
Q

Type of hepatocellular dysplasia characterized by scattered large hepatocyte with pleomorphic multiple nuclei
Markers of molecular change

A

Large cell change

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46
Q

Smaller than normal hepatocyte with normal but hyperchromatic oval or angulated nuclei, thickened cell plate and high nuclear cytoplasmic ratio
Directly premalignant

A

Small cell change

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47
Q

Major pathway for HCC
Large size encompassing adjacent hepatic lobules without displacing all of portal tracts
High risk for malignant transformation

A

Dysplastic nodule

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48
Q

HCC etiologies

A

HBV infection
HCV infection
Alcoholic cirrhosis
Aflatoxin fr Aspergillus flavus

Others alpha 1 antitrypsin, hemochromatosis, tyrosinemia (most likely)

216 risk if combined

49
Q

Develops from small cell high grade dysplastic nodule in cirrhotic liver

Arise from both mature hepatocyte and progenitor cell or ductal or oval cells

Nodule vasc by imaging clear indication

Structural and numeric chromosomal abn indicative of genomic instability

Inflamm and regeneration leading to mutation in B catenin and TP53

A

HCC

HBV and HCV not oncogenic HBV-X is.

contributes to inflammation and inc cell turnover

50
Q

Unifocal
Multifocal with variable size
Diffusely infiltrative

Yellow white punctuated with strong propensity for vascular invasion

Better diff variant of globules of bile found within cytoplasm of cells and pseudocanaliculi

A

HCC

51
Q

Clinical variant of hcc in young male and female adults
No association with cirrhosis or risk factors
Single tumor with fibrous band coursing through it resembling focal nodular hyperplasia
Better prog

A

Fibrolamellar carcinoma

52
Q

Rapid inc in liver size
Sudden worsening of ascites
Bloody ascites, fever, pain

Marker:

A

HCC

Alpha fetoprotein

False positive in yolk sac and cirrhosis hepatitis pregnancy and massive necrosis

Radio screening at 6 mo interval look for early dysplastic nodules or small HCC

53
Q

Broad spec tyrosine kinase inhibitor giving benefit to those with advanced disease

A

Sorafenib

54
Q

Right-sided cardiac decompensation leads to passive congestion of the liver

Left-sided cardiac failure or shock may lead to hepatic hypoperfusion and hypoxia causing centrilobular necrosis

A

Chronic Passive Congestion

55
Q

Distinctive centrilobular fibrosis

A

Cardiac sclerosis

Cardiac cirrhosis

56
Q

Loss of inhibution of proteases released from neutrophils lead to panacinar emphysema

A

Alpha-1 Antitrypsin Deficiency

57
Q

Accumulation of abnormal alpha-1 leads to

A

Liver disease

58
Q

Panlobular giant cell transformation of hepatocytes

Lobular disarray with focal apoptosis and necrosis

Prolonged conjugated hyperbilirubinemia in neonates

2 major etiologies:
cholangiopathies like biliary atresia
neonatal hepatitis

A

Neonatal cholestasis

59
Q

Fine foamy appearance due to droplets of bile pigment that accumulates within hepatocytes

A

feathery degeneration

Neonatal cholestasis

60
Q

Cholestatic hepatocytes
Dilated canalicular spaces
Apoptotic cells
Kupffer cells with regurgitated bile pigments

A

Intrahepatic cholestasis

61
Q

Bile duct proliferation
Edema, bile pigment retention
Swollen and degenerating hepatocytes

A

Extrahepatic cholestasis

62
Q

Viral hepatitis transmitted via oral fecal routes

A

Hep A
Hep E

Vowels hit the bowels

63
Q

Most common blood transfusion hepatitis

A

Hep C

64
Q

Placental barrier, blood and sexually transmitted

A

Hep B

65
Q

Only DNA hepadna
Infectious particle:
Sand nuclei

A

Hep B

Dane

66
Q

Empty cytoplasm with scattered remnants of cytoplasmic organelles

A

Ballooning degeneration

67
Q

Eosinophilic globules

A

Councilman bodies

68
Q

Connecting portal-to-portal, central-to-central, or portal-to-central regions of adjacent lobules

A

Bridging necrosis

69
Q

Hepatocyte apoptosis
Continued interface hepatitis
Bridging necrosis

A

Chronic hepatitis

70
Q

Hallmark of chronic hepatitis

A

deposition of fibrous tissue

bridging fibrosis

71
Q

Hepatocytes with finely granular cytoplasm

Chronic Hep B infection

A

Ground glass hepatocytes

72
Q

Lymphoid aggregates

Macrovesicular steatosis

A

Chronic hepatitis C infection

73
Q

Hepatic insufficiency that:
progresses from onset of symptom to hepatic encephalopathy within 2 to 3 weeks
occurs in individuals who do not have chronic liver disease

A

Fulminant hepatitis

74
Q

Massive loss of liver mass
Liver is transformed into a limp, red organ covered by a large wrinkled capsule
Muddy red, mushy appearance

A

Fulminant hepatitis

Hepatitis B

75
Q

Pipestem fibrosis

A

Schistosomiasis

Bilharziasis

76
Q

Result of sudden and massive hepatic destruction (fulminant hepatic failure)
End stage of progressive chronic damage to liver
Transplantation offers the best hope for survival

A

Hepatic failures

77
Q

Acute liver illness that is associated with encephalopathy within 6 months after the initial diagnosis

A

Acute liver failure

78
Q

Within 2 weeks of onset of jaundice

A

Fulminent liver failure

79
Q

Within 3 months of onset of jaundice

A

Sub-fulminant liver failure

80
Q

Caused by massive hepatic necrosis, most often induced by drugs or toxins

A

Acute liver failure

81
Q

Drug accounting for almost 50% of cases

A

Acetaminophen

82
Q

Jaundice
Hypoalbuminemia
Hyperammonemia (encephalopathy)
Fetor hepaticus

A

Hepatic failure

83
Q

Musty or sweet and sour body odor

Formation of mercaptans by the action of intestinal bacteria on methionine

A

Fetor hepaticus

84
Q

Protosystemic shunting

A

Caput medusae
Esophageal varcies
Hemorrhoids

85
Q

Impaired estrogen metabolism
Palmar erythema
Spider angioma
Hypogonadism and gynecomastia

A

Hepatic failure

86
Q

Associated with elevated ammonia levels

Promote generalized brain edema

A

Hepatic encephalopathy

87
Q

Drug for hepatic encephalopathy

A

Lactulose

88
Q

Delta waves slowing on EEG

A

hepatic and uremic encephalopathy

89
Q

Fluctuating neurologic signs include rigidity, hyperreflexia, and asterixis

Nonrhythmic, rapid extension-flexion movements of head and extremities

A

Hepatic encephalopathy

90
Q

Appearance of renal failure in individuals with severe chronic liver disease
Drop in urine output, associated with rising blood urea nitrogen and creatine

Treatment of choice: liver transplantation

A

Hepatorenal syndrome

91
Q

Chronic liver disease
Hypoxemia
Intra-pulmonary vascular dilations

Only curative treatment is liver transplantation

A

Hepatopulmonary syndrome

92
Q

Key mediator in hepatopulmonary syndrome

A

Nitric oxide

93
Q

Etiology of liver abscess usually caused by bacteria

A

Pyogenic liver abscess

94
Q

Neutrophilic infiltrate

Liquefactive necrosis

A

Pyogenic liver abscess

95
Q

Usually caused by echinococcal and amebic infections

A

Nonpyogenic liver abscess

96
Q

Eosinophilic infiltrate
Laminated cystic wall with hooklet in echinococcosis
Anchovy paste-like material

A

Nonpyogenic liver abscess

97
Q

Water lily sign

Camalote sign

A

Hydatid infection

Detachment of endocyst membrane which results in floating membranes within pericyst that mimic appearance of water lily

98
Q

Chronic and progressive hepatitis of unknown etiology

Pathogenesis: T cell-mediated autoimmunity
(+) for anti-smooth muscle antibodies

A

Autoimmune hepatitis

99
Q

Progressive alcohol consumption is the leading cause of liver disease

Three distinctive forms:
Hepatic steatosis (fatty liver disease)
alcoholic hepatitis
cirrhosis

A

Alcoholic liver disease

100
Q

Mallory bodies

A

Alcoholic liver disease

101
Q

Small lipid droplets accumulate in hepatocyte steatosis

A

microvascular steatosis

102
Q

Large, clear lipid globules displace the nucleus to periphery
Completely reversible

A

Hepatic steatosis

103
Q

Eosinophilic cytoplasmic clumps in hepatocytes

A

Mallory bodies

104
Q

Prominent activation of sinusoidal stellate cells and portal tract fibroblasts

A

Sinusoidal prevenular fibrosis

Alcoholic hepatitis

105
Q

Scattered larger nodules create a hobnail appearance on the surgsce of the liver

A

Macronodular cirrhosis

Alcoholic cirrhosis

106
Q

Brown, shrunken, nonfatty liver

A

Alcoholic cirrhosis

107
Q

Broad expanses of tough, pale scar tissue created by ischemic necrosis and fibrous obliteration of nodules

A

Laennec cirrhosis

Alcoholic cirrhosis

108
Q

Uniform micronodules created by regenerative activity of entrapped parenchymal hepatocytes

A

Micronodular cirrhosis

Alcoholic cirrhosis

109
Q

Hepatic steatosis in individuals who:
do not consume alcohol
do so in very small quantities (<20 g/week)

Most common cause of CLD in the United States

A

Nonalcoholic fatty liver disease (NAFLD)

110
Q

Simple hepatic steatosis

Non-alcoholic steatohepatitis (NASH)

A

NAFLD

111
Q

Steatosis
Mallory bodies
Hepatocyte death (ballooning degeneration and apoptosis)
Sinusoidal fibrosis

A

Steatohepatitis (NASH)

112
Q

Benign neoplasms developing from hepatocytes

Most frequently occurs in young women who have used oral contraceptives

A

Hepatic adenoma

113
Q

Chronic viral infection (HBV, HCV)
Chronic alcoholism
Non-alcoholic steatohepatitis (NASH)
Food contaminants (primarily aflotoxins)

A

Hepatocellular carcinoma

114
Q

Pallor
Green hue
Strong propensity for invasion of vascular structures

A

Hepatocellular carcinoma

115
Q

Large, hard “scirrhous” tumor with fibrous bands
Separated by parallel lamellae of dense collagen bundles
Better prognosis

A

Fibrolamellar carcinoma

116
Q

Malignancy of the biliary tree, arising from bile ducts within and outside of the liver

A

Cholangiocarcinoma

117
Q

Primary sclerosing cholangitis
HCV infection
Previous exposure to Thorotrast
Clonorchis/Opistorchis infection

Classified into intrahepatic and extrahepatic forms

A

Cholangiocarcinoma

118
Q

Perihilar extrahepatic form of cholangiocarcinoma is called

A

Klatskin’s tumor

Pathology (24 decks)

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