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GIR Test 2 > B5.028 GI Cancers- Non Tubular > Flashcards

B5.028 GI Cancers- Non Tubular Flashcards

1
Q

HCC risk factors

A

often arises in cirrhotic livers, only 10% non cirrhotic
-HBV present in many non-cirrhotic patients
risk factors:
-hep B and C
-alcohol
-environmental

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2
Q

HCC symptoms/presentation

A
  • often no symptoms
  • ill-defined upper abdominal pain, fatigue, weight loss, abdominal mass/hepatomegaly
  • jaundice if biliary obstruction present
  • often older age
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3
Q

work up for HCC

A

labs: may show elevated serum AFP ( in 50%)
imaging: CT/MRI with vascular contrast often diagnostic

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4
Q

staging of HCC

A

T(tumor): size, number, vascular invasion, invasion of adjacent structures
N (lymph nodes)
M (metastasis)

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5
Q

treatment of HCC

A 
surgical resection (if possible, not usually possible in cirrhotic liver)
ablation, chemoembolization, chemotherapy
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6
Q

prognosis of HCC

A 
small tumors (<2 cm) have a good prognosis with possibility for cure
large tumors have a poor prognosis and average survival of 2 years
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7
Q

molecular features of HCC

A
  • activation of beta-catenin (40%)

- inactivation of p53 (60%), prominent in tumors associated with aflatoxin exposure

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8
Q

HCC precursor lesions

A 
non-cirrhotic livers:
-small cell change
-large cell change
cirrhotic livers:
-dysplastic nodules
-small cell change
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9
Q

what do you do if you find an HCC precursor lesion?

A

surveillance cancer screening

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10
Q

differential of cirrhosis with large nodule

A

macroregenerative nodule
dysplastic nodule
HCC

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11
Q

features of large cell change

A

large hepatocytes with large, often atypical nuclei scattered among normal size hepatocytes with round, typical nuclei

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12
Q

features of small cell change

A

abnormal cells have a high nuclear-to-cytoplasmic ratio and are separated by thickened plates

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13
Q

cellular atypia

A

increased nuclear to cytoplasmic ratio
distorted architecture
thickened call plates
bile production (no mucin)

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14
Q

fibrolamellar carcinoma HCC variant description

A 
clinical and labs:
-young patients, 5-35
-non-cirrhotic liver
-almost always negative for AFP
gross appearance:
-firm with fibrous band running through tumor
-central scar
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15
Q

microscopic appearance of fibrolamellar carcinoma

A

hepatocytes with lots of mitochondria, giving a pink “oncocytic” appearance

  • growth is nested or cord like pattern
  • dense collagen fibers is the hallmark
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16
Q

what is cholangiocarcinoma

A

cancer arising from biliary tree/bile duct

-can arise in any area: intrahepatic or extrahepatic

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17
Q

risk factors for cholangiocarcinoma

A

chronic inflammation, cholestasis

  • liver flukes
  • chronic inflammatory conditions
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18
Q

clinical presentation of cholangiocarcinoma

A

asymptomatic

symptoms of biliary obstruction of liver mass

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19
Q

location of cholangiocarcinomas

A

intrahepatic- 10%
perihilar- 50-60%
distal- 20-30%

20
Q

gross appearance

A

tan-white solid nodule, may be multiple

non-cirrhotic liver

21
Q

microscopic appearance of cholangiocarcinoma

A

adenocarcinoma (forms glands, produces mucin)

cells with enlarged nuclear to cytoplasmic ratio, glands are angulated instead of round

22
Q

precursor lesions of cholangiocarcinoma

A

dysplasia of normal bile ducts
BilIN (biliary intraepithelial neoplasia), grade 1-3
some cystic neoplasms

23
Q

cholangiocarcinoma staging

A

depends on location of tumor (intrahepatic, perihilar, distal)
size, vascular invasion, invasion of adjacent structures

24
Q

cholangiocarcinoma treatment

A

surgical resection

25
Q

cholangiocarcinoma prognosis

A

poor, 15% survival at 2 years

26
Q

liver metastasis

A

most common cause of liver tumor
usually multiple nodules, can be very large before symptoms occur
colon, lung, breast, pancreas most common primary sites for spread to liver (most are adenocarcinomas)

27
Q

pancreatic acinar cells

A

exocrine function

secrete enzymes for digestion

28
Q

islets of Langerhans

A

endocrine function

insulin, glucagon, somatostatin secretion

29
Q

characteristics of pancreatic ductal adenocarcinoma

A

most common pancreatic cancer
4th leading cause of cancer deaths
one of the highest mortality rates of any cancer

30
Q

pancreatic ductal adenocarcinoma risk factors

A

cigarette smoking
chronic pancreatitis
diabetes
familial BRCA2 and CDKN2A mutations

31
Q

pancreatic ductal adenocarcinoma clinical presentation

A 
older individuals (60-80)
usually asymptomatic
may have features of biliary obstruction
32
Q

pancreatic ductal adenocarcinoma locations

A

head - 60%
body - 15%
tail- 5%
entire gland - 20%

33
Q

pancreatic ductal adenocarcinoma pathogenesis

A 
multiple molecular alterations occurs
early alterations
-telomere shortening (almost all tumors)
-KRAS mutations (90%)
later alterations
-mutation and inactivation of many genes
34
Q

pancreatic ductal adenocarcinoma gross appearance

A

tan-white, firm mass

usually singular

35
Q

microscopic appearance of pancreatic ductal adenocarcinoma

A

adenocarcinoma = proliferation of atypical glands with mucin production
densely fibrotic stroma
inflammatory cells

36
Q

precursor lesions of pancreatic ductal adenocarcinoma

A

dysplasia of the pancreatic ducts
-PanIN (pancreatic intraepithelial neoplasia) 1-3
molecular alterations occur in the precursor lesions

37
Q

treatment for pancreatic ductal adenocarcinoma

A

resection if possible and without metastasis

38
Q

staging of pancreatic ductal adenocarcinoma

A

based on size, invasion of large arteries (celiac axis, superior mesenteric artery, common hepatic artery)

39
Q

describe pancreatic neuroendocrine tumors

A

less common than ductal adenocarcinomas (only 2% of pancreas tumors)
may occur anywhere in the pancreas
can be benign or malignant

40
Q

types of pancreatic neuroendocrine tumors

A

may be functional or non-functional

  • in pancreas, neuroendocrine cells secrete hormones
  • insulin, gastrin, somatostatin, glucagon, VIP
  • 90% of insulinomas are benign
  • 60-90% of non-insulinomas are malignant
41
Q

features of insulinoma

A 
secrete insulin
symptoms of hypoglycemic episodes
labs: high insulin, low glucose
treatment: resection
benign in 90%
42
Q

features of gastrinoma

A

secrete gastrin (Zollinger-Ellison syndrome)
-stimulated parietal cells in the stomach to produce acid
symptoms of hypersecretion of gastric acid and severe peptic ulceration
treatment: resection

43
Q

nonfunctional neuroendocrine tumors

A

no hormone secretion
usually asymptomatic, unless blocking bile ducts
treatment: resection

44
Q

gross appearance of pancreatic neuroendocrine tumors

A

similar for functional and non-functional

solid, tan-red nodule

45
Q

pancreatic neuroendocrine tumor histology

A

similar for functional and non-functional
architectural patterns: nested, cords, solid
cells: uniform cells, moderate amount of cytoplasm, nuclei with granular chromatin (salt and pepper)
positive for chromogranin stain

46
Q

pancreatic neuroendocrine tumor treatment and staging

A

treatment: resection
staging: based on size, invasion to adjacent structures

GIR Test 2 (20 decks)

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