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

B5.028 - GI Cancers, Non Tubular Flashcards

1
Q
A

normal liver

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2
Q

liver cancer locations

A

hepatocyte - hepatocellular carcinoma, fibrolamellar carcinoma

bile ducts - cholangiocarcinoma

blood vessels

metastasis

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3
Q

features of hepatocellular carcinoma and risk factors

A

often arises in cirrhotic livers

risk factors:

viral hepatitis

alcohol

environmental (aflatoxin)

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4
Q

symptoms of hepatocellular carcinoma

A

often no symptoms

ill defined upper abdominal pain, fatigue, weight loss, hepatmegaly

jaundice if biliary obstruction

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5
Q

work up for hepatocellular carcinoma

A

may show elevated AFP ~50%

CT/MRI with vascular contrast often diagnostic

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6
Q

staging of HCC

A

T - size, number, vascular invasion

N - lymph nodes

M - metastasis

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7
Q

treatment of HCC

A

surgican resection

ablation, chemoembolization, chemo

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8
Q

prognosis of HCC

A

small tumors <2cm have good prognosis

large have poor prognosis and avg survival 2 yrs

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9
Q

molecular features of HCC

A

activation of beta catenin

inactivation of p53 - prominent in tumors with aflatoxin exposure

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10
Q

HCC precursor lesions

A

non cirrhotic

* small cell change

large cell change (not direct)

cirrhotic

* dysplastic nodules

* small cell change

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11
Q
A

cirrhosis with large nodule, precursor lesion

differential includes macrogenerative nodule, dyplastic nodule, HCC

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12
Q
A

top:

large cell change, large atypical nuclei are scattered among normal size hepatocytes

bottom:

small cell change, abnormal cells have high nuclear to cytoplasmic ration separated by thickened plates

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13
Q
A

cellular atypia

HCC

increased nuclear to cytoplasmic ration

distorted architecture

thickened cell plates

bile production (no mucin)

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14
Q
A

•Cellular atypia

–Increased nuclear to cytoplasmic ratio

–Distorted architecture

–Thickened cell plates (more than two cells thick)

–Bile production (no mucin)

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15
Q

fibrolamellar carcinoma

A

different clinical presentation, histology and molecular changes

young patients, 5-35

non cirrhotic liver

almost always negative for serum AFP

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16
Q

fibrolamellar carcinoma gross appearance

A

firm with fibrous bands running through tumor

central scar

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17
Q
A

fibrolamellar carcinoma

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18
Q
A

fibrolamellar carcinoma

microscopic

* hepatocytes with lots of mitochondira, giving a pink oncocytic appearance

* growth is in nested or cord like pattern

* dense collagen fibers is the hallmark

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19
Q
A

fibrolamellar carcinoma

•Microscopic

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

–Growth is in nested or cord-like pattern

–Dense collagen fibers is the hallmark

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20
Q

features of cholangiocarcinoma

A

cancer arising from biliary tree/bile duct

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21
Q

risk factors for cholangiocarcinoma and clinical presentation

A

chronic inflammation, cholestasis

liver flukes, chronic inflammation

asymptomatic, sympotoms of biliary obstruction or liver mass

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22
Q
A

cholangiocarcinoma

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23
Q

gross appearance of cholangiocarcinoma

A

tan white solid nodule; may be multiple

non cirrhotic liver

24
Q
A

cholangiocarcinoma

•Microscopic

–Adenocarcinoma

•Forms glands, produces mucin

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

25
Q
A

cholangiocarcinoma

•Microscopic

–Adenocarcinoma

•Forms glands, produces mucin

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

26
Q

precursor of cholangiocarcinoma

A

precursor lesion is dysplasia of normal bile ducts

BilIN - grade 1,2,3

some cystic neoplasms

27
Q

staging of cholangiocarcinoma

A

depends on location of tumor, size, invasion

28
Q

treatment of cholangiocarcinoma

A

surgical resection

29
Q

prognosis of cholangiocarcinoma

A

poor, 15% at 2 years

30
Q

liver tumors usually caused by

A

metastasis

usually multiple nodules

cna be very large before symptoms occur

colon, lung, breast, pancrease most common primart sites

31
Q

most liver metastasis are

A

adenocarcinomas (glandular microscopic shape, mucin production

32
Q

acinar cells

A

exocrine function

secrete enzymes for digestion

33
Q

islet of langerhans

A

endocrine function

insulin, glucagon, somatostatin secretion

34
Q

tumor types of the pancreas

A

ducta cells - pancreatic adenocarcinoma

islets of langerhans - neuroendocrine tumors

35
Q

features of pancreatic ductal adenocarcinoma

A

most common cancer of the pancreas

4th leading cause of cancer deaths

36
Q

risk factors for pancreatic ductal adenocarcinoma

A

cigarettes

chronic pancreatitis

diabetes

familial BRCA2, CDKN2A

37
Q

location of pancreatic ductal adenocarcarcinoma

A

head of pancreas - 60%

body - 15%

tail - 5%

entire gland - 20%

38
Q

molecular pathogenesis of pancreatic ductal adenocarcinoma

A

multiple molecular alterations occur

early alterations - telomere shortening, KRAS mutations

later - mutation and inactivation of many genes

39
Q

gross and microscopic appearance of pancreatic ductal adenocarcinoma

A

gross - tan-white, firm mass, usually singular

micro - proliferation of atypical glands with mucin production

40
Q
A

carcinoma of the pancreas

41
Q
A

Carcinoma of the pancreas. Poorly formed glands are present in densely fibrotic stroma within the pancreatic substance; some inflammatory cells are also present. The cells would be positive for mucin (adenocarcinoma)

42
Q

precursors of pancreatic duct adenocarcinoma

A

dysplasia of pancreatic ducts - PanIN

43
Q
A

pancreatic intraepithelial neoplasia grade 3 involving small pancreatic duct

44
Q

treatment of pancreatic ductal adenocarcinoma

A

resection

45
Q

staging of pancreatic duct adenocarcinoma

A

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

46
Q

describe pancreatic neuroendocrine tumors

A
  • Pancreatic neuroendocrine tumors (PanNETs) are less common than pancreatic ductal adenocarcinoma (2% of pancreas tumors)
  • May occur anywhere in the pancreas

–Single or multiple tumors possible

•Can be benign or malignant

47
Q

what type of PanNET are most common

A

insulinomas, most are benign (90%)

60-90% non insulinomas are malignant

48
Q

features of insulinomas, treatment, labs, symptoms

A

•Insulinoma

–Secrete insulin

–Symptoms of hypoglycemic episodes (blood glucose <50mg/dL)

  • Confusion, stupor, loss of consciousness
  • Treat by giving food, parenteral glucose

–Labs: high insulin, low glucose

–Treatment: resection

–Benign in 90%

49
Q

describe gastrinomas (treatment, symptoms, features)

A

•Gastrinoma

–Secrete gastrin (Zollinger-Ellison syndrome)

•Stimulates parietal cells in the stomach to produce acid

–Symptoms of hypersecretion of gastric acid and severe peptic ulceration

•Typical medical management does not work

–Treatment: Resection

50
Q

non functional neuroendocrine tumors

A

no hormone secretion

usually asymptomatic, unless blocking bile ducts

treatment: resection

51
Q

gross and histo of pancreatic endocrine tumors

A

gross - similar for functional and non functional, solid tan-red nodule

histo - 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”

* posiitve for chromogranin stain

52
Q
A

a well circumscribed solid mass in pancreas is typical fro low grade neuroendocrine tumors

53
Q
A

neuroendocrine tumor: nested and corded growth pattern, Nuclei have stippled chromatin “salt and pepper”

54
Q
A

pancreatic neuroendocrine tumor: solid growth, salt and pepper chromatin

55
Q
A

diffuse positive staining for chromogranin is shown. neuroendocrine

56
Q

treatment/staging of pancreatic neuroendocrine tumors

A

resection

staging based on size, invasion of adjacent structures

GIR Test 2 (17 decks)

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