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Pathology I > Hepatobiliary Pathology > Flashcards

Hepatobiliary Pathology Flashcards

1
Q

describe the liver structure

A
  • classic lobule
  • roughly hexagonal
  • consists of stacks of hepatocyte plates with intervening sinusoidal spaces
  • the center of the lobule is a central vein
  • portal triads at the angles of the hexagon
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2
Q

where do the sinusoids drain

A

in the central vein

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3
Q

what do the portal triads contain

A
  • contains connective tissue with terminal branches of the hepatic artery, portal vein and bile duct
  • contains lymphatic vessels and nerve
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4
Q

describe the dual blood supply liver blood flow

A
  • blood enters from the heaptic artery and the portal vein -> portal triads-> hepatic sinusoids ->central veins -> sublobular veins -> hepatic vein
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5
Q

what makes up the portal triad

A

-arteriole
- bile duct
- portal vein

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6
Q

what are the hepatocyte functions

A
  • protein synthesis
  • oxidation and conjugation of drugs, toxins
  • lipid metabolism
  • carbohydrate metabolism
  • produces bile- an exocrine secretion
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7
Q

what proteins are synthesized by the liver

A

albumin and other transport proteins, clotting factors, lipoprtoeins espcially VLDL

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8
Q

how does the liver oxidize and conjugate drugs and toxins

A

makes substances not easily excreted by the kidney more hydrophilic, to enhnace excretion: hydroxylation, carboxylation and conjugation

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9
Q

how does the liver do lipid metabolism

A

-stores or breaks down fatty acids from plasma
-synthesis and uptake of cholesterol

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10
Q

describe carbohydrate metabolsim of the liver

A

either converts glucose to glycogen for carbohydrate storage, or breaks down glycogen to glucose for energy usage

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11
Q

what do bile salts do

A

aid in emulsifying lipids in the GI tract

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12
Q

what are the reversible changes in hepatocyte injury

A
  • accumulation of fat (steatosis)
  • accumulation of bilirubin
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13
Q

what are the non reversible changes to hepatocyte injury

A

necrosis and/or apoptosis
- necrosis may follow hypoxia/ischemia and may be single cell death, zonal, regional
- necrosis or apoptosis may follow viral infection, toxin exposure, other inflammatory conditions

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14
Q

what are the 2 outcomes following hepatocyte injury and describe each

A
  • regeneration: by dividing hepatocytes near the site of injury or in more severe injuries by dividing stem cells
  • scar formation: most often a result of chronic injury . may progress to sirrhosis wherein the liver is made up of nodules of regerenating hepatocytes surrounded by dense bands of collagen
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15
Q

what are the causes of acute liver failure

A
  • acetominophen ingestion
    -autoimmune hepatitis
  • acute viral hepatitis
    -other drugs/toxins
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16
Q

what are the clinical features of acute liver failure

A
  • nausea, vomting, jaundice, fatigue, encephalopathy, coagulation defects and icterus
  • coagulopathy
  • hepatorenal syndrome
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17
Q

what is jaundice casued by

A

yellow coloration of the skin due to bilirubin retention and cholestasis

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18
Q

what is icterus

A

discoloration of the sclera

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19
Q

what is hepatic encephalopathy

A

symptoms ranging from behavioral abnormalities to confusion, stupor, coma and death

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20
Q

what is the cause of hepatic encephalopathy

A

elevated ammonia levels which impair neuronal function and causes cerebral edema

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21
Q

what is the histology for cholestasis

A

bile pigments within hepatocyte cytoplasm

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22
Q

what is coagulopathy

A

bruising and bleeding

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23
Q

what is hepatorenal syndrome

A

in patients without pre existing renal disease, acute liver failure can result in decreased renal perfusion leading to decreased urine output

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24
Q

what is chronic liver failure and describe it

A
  • cirrhosis
  • diffuse transformation of the liver into regenerative hepatocyte nodules surrounded by bands of dense fibrous connective tissue- scar
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25
Q

what are the most common causes of chronic liver failure

A

-chronic hepatitis B
- chronic hepatitis C
- nonalcoholic fatty liver disease
- alcohol relatde liver disease

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26
Q

describe cirrhosis

A
  • it does not indicate the presence of a specific disease, it is a common final pathway of a number of chronic liver diseases
  • not all chronic liver disease results in cirrhosis and not all cirrhosis results in end stage liver disease
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27
Q

what is portal hypertension

A

increased portal vascular resistance, portosystemic shunts may develop

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28
Q

what are ascites and what causes it

A
  • increased fluid in the peritoneal space
  • primarily due to portal hypertension
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29
Q

what is viral hepatitis caused by

A

hepatotrophic vrisues A, B, C, D, and E

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30
Q

describe hepatitis A, transmission, symptoms, and diagnosis

A
  • usually benign and self limited
  • ingestion of contaminated food/water from fecal- oral route of transmission
  • symtpoms: fever, fatigue, decreased appetite, jaundice at 2-12 weeks of infection
  • does not cause chronic hepatitis
  • diagnosis: detection of IgM antibodies
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31
Q

describe hepatitis B

A
  • clinical vourse varies widely: acute hepatitis with clearance and recovery, nonprogressive chronic hepatitis, progressive chornic hepatitis leading to cirrhosis, fulminant hepatitis with massive liver necrosis , asymptomatic carrier state
  • HBV associated chronic hepatitis incurs an elevated risk for hepatocellular carcinoma
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32
Q

what is the prevalance of hepatitis B and what countries have it more

A

2 billion
- africa and asia

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33
Q

what is the transmission and testing for hep B

A
  • parenteral transmission- vaccine is 95% effective
  • detection of HBsAg, anti- HBcag, HBV DNA by PCR
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34
Q

what is the histology for hep B

A

ground glass

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35
Q

describe hepatitis C, transmission, diagnosis and treatment

A
  • affects ~170 million people worldwide
  • parenteral route of transmission
  • acute infection is generally asymptomatic (85% of time), but 80-90% of infected people develop persistent chronic infections leading to cirrhosis in about 20% over 2-3 decades
  • diagnosis: HCV RNA
  • treatable: antiviral combination therapy can cure 95% of infections
36
Q

where does inflammation usually occur in hep C infections

A

portal triad

37
Q

describe hepatitis D, diagnosis

A
  • dependent on HBV for its life cycle to progress
  • parenteral route of transmission
  • diagnosis by detecting HDV RNA
  • coinfection: clinically indistinguishable from HBV infection, usually self limited
  • superinfection: HBV carrier exposed to HDV, resulting in either severe acute hepatitis or exacerbation of chronic HBV
38
Q

describe Hepatitis E- transmission and diagnosis

A
  • enterically transmitted by fecal-oral
  • usually produces acute, self limited hepatitis
  • zoonotic, with animal reservoirs
  • diagnosis: IgM, HEV RNA
39
Q

descrbe bacterial infections of the liver

A
  • ascending infections involving the biliary tract
  • seeding via blood S. aureus and salmonella typhi
  • liver abscesses
40
Q

describe parasitic infectinos of liver

A
  • worms- schistosomiasis, liver flukes, echinococcus
  • enteamoeba histolytica
41
Q

what is autoimmune hepatitis

A
  • presence of autoantibodies
  • responds to immunosuppression
  • may be a genetic predisposition
  • may be associated with other autoimmune diseases
42
Q

what are examples of autoantibodies in autoimmune hepatitis

A

antinuclear antibodies (ANA), anti smooth muscle antibodies (ASMA)

43
Q

what is the remission percentage of patients with autoimmune hepatitis

A

90%

44
Q

what is the morphology of autoimmune hepatitis

A
  • necrosis and inflammation
  • may lead to cirrhosis
45
Q

what are the patterns of injury due to drugs and toxins

A
  • fatty change
  • fibrosis
  • cholestasis
  • necrosis
46
Q

what causes fatty change of liver

A

alcohol
- methotrexate
- tetracycline

47
Q

what causes fibrosis of the liver

A
  • alcohol
  • methotrexate
48
Q

what causes cholestasis

A

chlorpromazine

49
Q

what causes necrosis

A

acetominophen, carbon tetrachloride, mushroom toxins (amanita phalloides - death cap)

50
Q

what are the drug reaction types

A
  • predictable/ intrinsic
  • unpredictable/idiosyncratic
51
Q

what are the predictable drug reactions and another name for predictable drug reactions

A

acetaminophen
- intrinsic

52
Q

what are the unpredictable drug reactions and another name for unpredictable drug reactions

A

chlorpromazine
- idiosyncratic

53
Q

describe fatty liver disease - alcohol and non alcohol realted

A

-both feature varying degrees of steatosis, steatohepatitis, gradually increasing fibrosis which may eventually progress to cirrhosis

54
Q

what is steatohepatitis and what stain is used to see it

A

symptoms and lab abnormalities develop in the setting of an already fatty liver
- malaise, anorexia, upper abdominal discomfort
- masson trichrome stain

55
Q

what is NAFLD associated with

A

becoming increasingly common
-associated with type 2 DM, obesity, hyperlipidemia, and HTN

56
Q

what percentage of deaths from cirrhosis are from excessive alcohol consumption

A

40-50%

57
Q

what are the metabolic liver diseases

A
  • hemochromatosis
  • wilson disease
  • alpha 1 anti trypsin deficiency
58
Q

what is hemochromatosis and what stain is used to identify it

A
  • excessive absorption of iron, deposited in liver, pancreas, heart and other organs
  • may be acquired
  • usually hereditary with loss or impairment of regulatory control of intestinal iron absorption
  • mutation of HFE gene most common
  • prussian blue stain
59
Q

what does tissue deposition of hemosiderin lead to

A

gradually increasing fibrosis
- iron deposition in other organs can lead to fibrosis and atrophy of other organs in addition to changes in skin pigmentation

60
Q

describe wilson disease

A
  • autosomal recessive: loss of function mutation of ATP7B leading to imapired copper excretion in bile and failure to incorporate copper into ceruloplasmin
  • increased unbound copper in the circulation causes hemolysis
  • accumulation of toxic levels of copper in organs, pricipally liver brain and eye
61
Q

what is the morphology of wilson disease and what stain is used to identify it

A

liver: variable- fatty change, hepatitis (acute or chronic) ultimately cirrhosis
- eye: Kayser- Fleischer rings - deposits of copper in the limbus of the cornea
- copper stain

62
Q

what are the clinical features of wilson disease

A
  • acute/chronic liver disease or neurophsychiatric signs may be presenting factors
  • diagnoses by decreased serum ceruloplasmin, increased hepatic copper content, increased urine copper
  • treamtnet: copper chelation therapy; zinc based therapy nhibits copper uptake in the gut
63
Q

describe alpha 1 anti trypsin deficiency

A
  • autosomal recessive, mutations resulting in misfolding and loss of function of alpha-1 AT which normally inhibits proteases
  • alpha-1AT synthesized mainly by hepatocytes- the abnormal form accumulates in hepatocytes -> apoptosis
  • before they die hepatocytes accumulate cytoplsamic globular inclusions
  • may progress to hepatitis and eventually cirrhosis
64
Q

describe the clinical presentation of alpha 1 AT and the stain used to identify it

A
  • only effective tx for severe liver disease is transplant
  • the lung is also often involved resulting in emphysema
  • periodic acid-Schiff stain
65
Q

what are the benign hepatic tumors

A
  • focal nodular hyperplasia
  • cavernous hemangioma
  • hepatocellular adenoma
66
Q

what are the maligant hepatic tumors

A
  • hepatocellular carcinoma (HCC)
  • tumors metastatic to the liver - more common
67
Q

describe focal nodular hyperplasaia

A
  • may be single or multiplt
  • develop in non cirrhotic liver
  • result from focal chronic hypoperufsion of an area of the liver reuslting in scarring and compensatory hyperperfusion -> focal hepatocyte hyperplasia
  • most common in younger women ages 20-50
68
Q

describe hepatocellular ademona

A
  • usually arises in a non cirrhotic liver
  • most common in reproductive age women stimulated by estrogen
  • sheets of sheets of hepatocytes normal to atypical
  • rare cases progress to malignancy
69
Q

describe cavernous hemangioma

A
  • most common benign liver tumor
  • tumor of benign blood vessles, variably dilated
70
Q

describe hepatocellular carcinoma

A

-incidence varies widely throughout the world- highest in eastern asia and sub saharan african
- expossure to HBV and aflatoxin - aspergillus flavus- markedly increases risk of HCC
- incidence of HCC in western countries is rising mainly due to increased HCV
- chronic liver diseases are the most common setting for HCC development
- main risk factors include: HBV, HCV, aflatoxin exposure and increasinly NAFLD

71
Q

what is the histology of hepatocellular carcinoma

A

the neoplastic liver cells grow with distorted architecture, forming thickened cords and pseudoglandular spaces

72
Q

where is the gallbladder located

A

inferior and adherent to the liver

73
Q

what is the function of the gallbladder

A
  • concentrate, store and excrete bile
  • receives dilute bile from the common hepatic duct
  • in response to hormones from enteroendocrine cells or to parasympathetic stimulation the gallbladder contracts and delivers bile to the duodenum via the cystic duct and the common bile duct
74
Q

what are the layers of the gallbladder wall

A
  • mucosa
  • muscularis externa
  • connective tissue/adventitia
  • serosa
75
Q

describe the gallbladder mucosa

A
  • contains epithelium and lamina propria
  • occasional mucous glands near the neck
  • surface epithelium is simple columnar
76
Q

describe the surface epithelium of the gallbladder mucosa

A
  • resembles intestinal absorptive cells
  • apicolateral junctional complexes
  • short microvilli
  • complex lateral plications surrounding intercellular spaces
77
Q

describe gallstones

A
  • affects 10-20% of adults in the US
  • two types of stones: cholesterol stones and pigment bile salt sontesw
78
Q

what are the cholesterol stone risk factors

A
  • dyslipidemia
  • female
  • insulin resistance
  • gallbladder stasis
79
Q

what are the pigment stone factors

A
  • chronic hemolysis- malaria, sickle cell
  • biliary infection
  • various GI disorders, chron disease
80
Q

describe gallbladder carcinoma

A
  • occurs at older age with slight female predominance
  • usually not resectable at the time of diagnosis
  • mean 5 year survivial approximately 5-12%
  • though to arise primarily in a background of chronic gallbladder inflammation
81
Q

how does cholestasis appear on histology

A

bile pigments within hepatocyte cytoplasm

82
Q

what is the typical histology for a hepatitis C infection

A

chronic inflammation of a portal tract

83
Q

what is the typical resemblance physically and histologically of a focal nodular hyperplasia

A

central stellate scar on the tumor
- histologically: can resemble cirrhosis but is a focal lesion

84
Q

what is the histological appearance of hepatocellular adenoma

A

cords of hepatocytes are seen surrounding an artery without portal tracts

85
Q

what is the histological presentation of a hepatocellular carcinoma

A
  • neoplastic liver cells grow with distroted architecture
  • form thickened cords and pseduoglandular spaces

Pathology I (24 decks)

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