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GI block > Pathology- hepatobiliary neoplasia > Flashcards

Pathology- hepatobiliary neoplasia Flashcards

1
Q

Most common neoplasm in liver?

A

metastatic tumors

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2
Q

most common primary sites of liver mets are?

A

Cancer Sometimes Penetrates Benign Liver

  • colon, stomach, pancreas, breast, lung
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3
Q

what type of patients get hepatocellular carcinoma?

A
  • males >60yo
  • pts w/ chronic liver disease manifest to HCC esp after cirrhosis.
  • metabolic diseases like heriditary hemochromatosis and alpha1 antitrypsin deficiency, and metabolic syndrome increase risk of HCC
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4
Q

4 hepatocarcinogens to know

A

1) alcohol (itself is a risk factor for HCC but also synergizes with HBV and HCV and possibly smoking)
2) HCV
3) HBV
4) aflatoxin (in africa and asia)- also synergizes with hbv and hcv to increase hepatocarcinogenesis.

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5
Q

what are two of the most common EARLY mutations found in HCC? what toxins associated with these mutations?

A
  • activation of beta catenin (demonstrate genetic instability and more likley to be unrelated to HBV)

&

  • inactivation of p53 ( esp associated with aflatoxin)
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6
Q

how does the IL-6/JAK/STAT pathway play into the pathogenesis of Hepatocellular carcinoma?

A
  • IL-6 is an inflammatory cytoking which is overproduced in many chronic hepatitides –> IL-6 then suppress hepatocyte differentiation & promote hepatocyte proliferation by regulatign the function of transcription factor HNF4-alpha
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7
Q

Gross pathologic appearance of hepatocellular carcinoma?

A

highly variable. Can be yellwo from bile production, can be green, can be white etc.

  • can have yellow nodules in multiple sites with a background of green liver w/ severe cholestasis suggesting that tumor has obstructed bile ducts (even the common bile duct)
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8
Q

how would intrahepatic mets present?

A
  • usually small satellite tumor nodules around larger, primary mass and are more common once tumors reach 3cm in size
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9
Q

What is the most common route for extrahepatic mets?

A

hepatic venous system

  • extra hepatic spread via lymphatic channels is less common
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10
Q

in HCC, hematogenous mets to portal vein and IVC would cause what problems?

A
  • hematogenous mets esp to LUNG occur late in disease
  • usually invade portal vein –> cause portal HTN
  • or invade inferior vena cava which can extend into right side of heart
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11
Q

what causes nutmeg liver?

A
  • nutmeg liver = vascular congestion of liver
  • many HCC are highly vascularized which can cause peritoneal hemorrhage and passive congestion of the liver.
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12
Q

Who gets fibrolamelllar hepatocellular carcinoma?

A
  • no gender prediliction or identifiable predisposing conditions but most occur < 35yo
  • it’s a distinctive variant of HCC
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13
Q

gross pathologic presentation of fibrolamella hepatocellular carcinoma?

A
  • single large, hard scirrhous tumor w/ fibrous bands coursing through it
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14
Q

microscopic presentation of fibrolamellar hepatocellular carcinoma?

A
  • well differentiated cells rich in mitochondria (oncocytes) growing in nests and cords separataed by parallel lamellae or dense collagen bundles.
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15
Q

what is this?

A

well differentiated hepatocellular carcinoma w/ trabeculae of cells resembling normal hepatocytes

  • nonneoplastic liver on the left side.
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16
Q

What is this?

A

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

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17
Q

what is this?

A
  • moderately differentiated still but very large neoplastic cells (compare to size of scattered inflammatory cells) and even more disturbed architecture
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18
Q

what is this?

A
  • poorly differentiated hepatocellular carcinoma w/ pleomorphic dyscohesive neoplastic cells invading non-neoplastic liver from below
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19
Q

what is this?

A

anaplastic hepatocellular carcinoma w/ markedly pleomorphic cells w/ huge nuceli, some multinucleated, some bizarre

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20
Q

what symptoms do pts with hepatocellular carcinoma present with?

A
  • decompensation of liver like jaundice, encephalopathy, ascites, bleeding
  • other symptoms: mild- mod upper abd pain, weight loss, diarrhea, bone pain, dyspnea

** usually in pts w/ chronic liver disease (80% chronic viral hepatitis)

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21
Q

symptoms, signs, diagnosis of HCC?

A
  • symptoms: most pts have ill defined upper abd pain, malaise, fatigue and weight loss
  • signs: some pts have jaundice, fever, and GI or esophageal variceal bleeding

**Clinical manifestations of HCC often masked by underlying cirrhosis or chronic hep

  • Dx- lab studies may help but are rarely conclusive
22
Q

alpha-fetoprotein measurement

A
  • major fetal serum globulin

>20 mcg/L in 60% of HCC pts but it is also elevated w/ acute or chronic liver injury, gonadal tumors, pregnancy, and some gastric cancer

* 91% specific

>200 mcg/L specificity of 99 but sensitivity only 22%

23
Q

how to early diagnose HCC?

A

** imaging studies most valuable for detection of small tumors

  • US to identify distinctive nodules of all kinds
  • CT and MRI w/ vascular contrast studeis
  • increasing arteralization in process of conversion from high grade dysplastic nodule to early HCC and then to fully developed HCC
24
Q

tx of HCC?

A
  • HCCs < 2cm in diameter can be removed surgically or ablated
  • larger tumors- radiofrequency ablation for local control. chemoembolization can also be used.
25
Q

prognosis of HCC? how does HCC progress?

A
  • HCC progressive enlargement of primary mass until it disturbs liver function or mets to the lungs or other sites
  • 5 year survival of large tumors is bad. pts die within first 2 yrs
26
Q

cause of death of HCC?

A

1) tumor burden
2) GI or esophageal variceal bleeding
3) liver failure w/ hepatic coma
4) rupture of tumor with fatal hemorrhage –> rare

27
Q

precursor lesions of HCC?

A
  • hepatocellular adenoma esp those w/ beta catenin activating mutations
  • cellular dysplasias in chronic liver disease, found at any stage of chronic sliver disease, means that pt needs more aggressive cancer surveillance.

* small cell change is thought to be directly premalignant

* large cell change - marker of increased risk of HCC in liver as a whole but in hep b may also be directly premalignant.

28
Q

what is this?

A
  • hepatocellular dysplasia
  • larce cell change shows scattered hepatocytes esp neat portal tracts and septa that are larger than normal hepatocytes and have large and often multiple, often moderately pleomorphic nuclei, but the nuclear to cytoplasmic ratio is normal.
29
Q

what is this?

A

hepatocellular dysplasia

  • small cell change has hepatocytes with high nuclear to cytoplasmic ratio and mild nuclear hyperchromasia and or pleomorphism.
  • hepatocytes w/ small cell change often form tiny expansile nodules wihin single lobule

** small cell change is most of the slide except RLQ.

30
Q

hepatocellular dysplastic nodules - low grade vs high grade

A
  • low grade nodules lack cytologic or architectural atypia. Portal tracts present within them often in near normal distribution –> blood supply remains mix of portal venous and hepatic arterial blood
  • high grade nodules have cytologic and architectural changes but arent sufficient for diagnosis. Sometimes you see subnodule in larger nodule. portal tracts are fewer and arteries feeding the growing lesion come to predominate over the portal venous flow.
31
Q

what drugs can cause hepatocellular adenomas?

A

OCPs and anabolic steroids

32
Q

how are hepatocellular adenomas detected and what are they?

A
  • they’re benign neoplastic or semi-neoplastic hepatocyte proliferations
  • detected incidentally w/ abd imaging or when causing abd pain from rapid growth (cause pressure on liver capsule) or hemorrhagic necrosis (lesion outstrips blood supply)

** rupture of hepatocellular adenoma may lead to intraabdominal bleeding –> surgical emergency.

33
Q

what is this?

A

hepatocellular adenoma: benign, usually expansile, rounded, soft, tan tumor mass, +/- capsule

34
Q

what is this?

A
  • hepatic adenoma on the left and non neoplastic liver on the right (dark reddish area)
35
Q
A
36
Q

what is this?

A

hepatic adenoma on the left- composed of near normal looking hepatocytes in a mass lacking normal lobular architecture

37
Q

what gene is affected in a subtype of hepatocellular adenoma affecting mostly women?

A
  • HNF1-alpha inactivation (encodes a tf)
  • almost no risk of malignant transformation
  • fatty and devoid cellular architectural atypia
  • liver fatty acid binding rptein is absent (LFABP is a downstream regulated protein of HNF1) d/t inactivating mutation of HNF1-alpha.

**LFABP immunostaining shows its absence in tumor is diagnostic of mutation.

38
Q

what mutation is a subtype of hepatocellular adenoma associated with OCPs and anabolic steroids?

A
  • beta catenin activation
  • found in womena nd men
  • very high risk of malignant transformation and should be resected even when asymptomatic
  • associated with neoplasia and malignancy in many organs including liver
  • high degree of cytologic or architectural dysplasia.
  • immunostaining for beta catenin shows nuclear translocation (activated state) which is diagnostic.
39
Q

what mutation is associated with inflammatory subtype of hepatocellular adenoma?

A
  • activating mutation in gp130, a coreceptor for il-6 –> constitutive JAK-STAT signaling and overexpression of acute phase reactants
  • found in mena nd women
  • increasing incidence associated w/ NAFLD
  • have areas of fibrotic stroma, mononuclear inflammation, ductular reactions, dilated sinusoids, telangiectatic vessles
  • small risk of malignant transformation and should be resected even when asymptomatic
  • immunostain for CRP
40
Q

what’s the most common benign tumor in liver?

A

hemangioma

41
Q

what is this?

A

hemangioma- usually <3cm and commonly subcapsular

-composed of blood-filled vascular spaces

42
Q

what is a rare malignant epithelial neoplasm of liver in children?

A

hepatoblastoma-

** malignant tumors in children tend to have a more primitive appearance similar to the embryonal appearance of the site (hence the suffix -blastoma)

43
Q

what is this?

A

cholangiocarcinoma

  • malignant epithelial neoplasm with biliary differntiation arising from cholangiocytes
  • uncommon
  • more in males

50-70 age group

  • strong association w/ primary sclerosing cholangitis (PSC)
44
Q

what mutations are associated with cholangiocarcinoma?

A
  • KRAS in 50% of intraheptatic and 15% of extrahepatic

p53 mutation in 33%

-tend to be tan-white and firm bc they have desmoplastic reaction and dont make bile

45
Q
A
46
Q

how do cholangiocarcinomas usually spread?

A

via lymphatics

  • less via blood vessels unlike HCC
47
Q

symptoms of intrahepatic cholangiocarcinoma?

A
  • dull RUQ pain and weight loss
48
Q

signs of intrahepatic cholangiocarcinoma?

A
  • only those of underlying liver disease
49
Q

labs of intrahepatic cholangiocarcinoma?

A

normal or slightly elevated bilirubin, elevated alk phosphate

50
Q

Diagnosis, tx, prognosis of cholangiocarcinoma?

A

diagnosis- biopsy or cytology

tx- surgical resection with variable but poor resutls

prognosis- bad. 5 year survival 5-10%

51
Q

what is this?

A

liver mets- generally multiple, commonly rounded and sometimes hemorrhagic and partially necrotic

** liver mets can increase size of liver and obstruct bile ducts turning liver green.

It can obstruct portal vein causing ascites and splenomegaly

It allows normal liver function d/t reseve capacity of the liver.

GI block (12 decks)

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