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BMS150 Post-MT2 > Pathology - GI Cancers > Flashcards

Pathology - GI Cancers Flashcards

1
Q

Two main variants of esophageal carcinomas?

A
  • Adenocarcinoma
  • Squamous cell carcinoma
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2
Q

Risk factors for Adenocarcinoma? (3)

A
  • Long standing GERD
  • Barrett’s esophagus
  • Tobacco use
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3
Q

Protective factors against Adenocarcinoma?

A

Diets rich in fruits and vegetables

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4
Q

Risk factors for Squamous Carcinoma? (7)

A
  • Alcohol and tobacco use
  • Poverty
  • Caustic esophageal injury
  • Achalasia
  • Tylosis
  • Plummer-Vinson syndrome
  • Frequent consumption of very hot beverages
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5
Q

Are esophageal carcinomas common?

A

Yes relatively common - very deadly

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6
Q

Epithelial clones identified in nondysplastic Barrett metaplasia persist and __________ during progression to dysplasia and invasive carcinoma

A

Accumulate mutations

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7
Q

What mutations are present in esophageal carcinoma? (3)

A
  • Over expression of p53
  • Amplification of: c-ERB-B2, cyclin D1, cyclin E genes
  • Mutation of RB
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8
Q

Where does esophageal adenocarcinoma usually occur?

A

Distal 1/3 of the esophagus and may invade adjacent gastric cardia

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9
Q

In adenocarcinoma. tumors resemble what kind of cells? What do they produce?

A

Intestinal cells; mucin and form glands

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10
Q

Etiology of squamous cell carcinoma?

A

Loss of several tumor suppressor genes, including p53 and p16/INK4a

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11
Q

Half of squamous cell carcinomas occur where?

A

Middle 1/3 of the esophagus

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12
Q

How do early lesions of squamous cell carcinomas appear?

A

Small, grey-white, plaque-like thickenings

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13
Q

With progression, squamous cell tumor can ______ into and obstruct the lumen or _____ and infiltrate

A

protrude; ulcerate

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14
Q

What surrounding structures may squamous cell carcinoma invade?

A
  • respiratory tree, causing pneumonia
  • aorta, causing catastrophic exsanguination
  • mediastinum and pericardium
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15
Q

Clinical features of esophageal carcinomas? (5)

A
  • Dysphagia
  • Odynophagia
  • Obstruction
  • Weight loss
  • Hemorrage and sepsis (may occur)
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16
Q

Prognosis of esophageal carcinomas?

A

Poor – 5 year survival is 10% - 25% due to frequency of metastasis

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17
Q

75% of all gastric polyps are either ________ or ________

A

Inflammatory or hyperplastic

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18
Q

Gastric polyps usually develop in association with what?

A

Chronic gastritis

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19
Q

What increases the likelihood for presence of malignancy?

A

Larger polyps

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20
Q

Gastric adenomas make up ___% of gastric polyps

A

10%

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21
Q

Epidemiology of gastric adenoma?

A
  • Incidence increases with age
  • M > F
  • Age: 50-60 yo.
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22
Q

Gastric adenomas have a greater risk of cancer than ________

A

Colonic carcinomas

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23
Q

Etiology of gastric adenoma?

A
  • Gastric atrophy
  • Intestinal metaplasia
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24
Q

Where are gastric adenoma solitary lesions most commonly located?

A

Stomach antrum - higher malignant potential in the fundus

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25
Q

what is risk of progression to adenocarcinoma related to?

A

Size of lesion

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26
Q

Majority of adenomas composed of what?

A

Intestinal-type columnar epithelium

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27
Q

How are gastric adenocarcinomas classified? What are the classifications?

A

Classified based on location
- Diffuse = diffuse infiltrative growth patterns
- Intestinal = composed of glandular structures

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28
Q

Adenocarcinomas comprises what percent of gastric cancers?

A

90%

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29
Q

Why is it thought that incidence of gastric adenocarcinoma has decreased in North America?

A

Related to reduced rates of H. pylori infection and environmental factors

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30
Q

Gastric adenocarcinoma tends to develop in what setting?

A

Chronic inflammation

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31
Q

Genes of interest in gastric adenocarcinoma? (3)

A
  • p53 mutations common
  • lof of E-cadherin
  • Intestinal - mutations that increase signalling of ent pathway
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32
Q

Characteristic of advanced cancers?

A

Penetration below the submucosa into the muscular wall

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33
Q

Intestinal gastric adenocarconioma?

A

Composed of malignant cells forming neoplastic intestinal glands - resemble colonic adenocarcinoma

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34
Q

Diffuse gastric adenocarcinoma?

A

Gastric-type mucous cells that don’t form glands but permeate the mucosa = form signet-ring cells

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35
Q

Clinical features of gastric adenocarcinoma? (initial and advanced)

A
  • Sx similar to PUD or chronic gastritis until advanced
  • Advanced: weight loss, anorexia, altered bowel habits, anemia
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36
Q

Prognosis of gastric adenocarcinoma?

A
  • If caught early, surgical resection results in 90% 5- year survival
  • If advanced, 5-year survival is 20%
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37
Q

Common metastasis of gastric adenocarcinoma? (2)

A
  • Supraclavicular sentinel lymph node
  • Ovaries
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38
Q

Most common site for lymphoma outside of lymph nodes?

A

Stomach (gastric lymphoma)

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39
Q

Where does gastric lymphoma arise?

A

Sites of chronic inflammation (most commonly from chronic H. pylori)

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40
Q

Where does gastric lymphoma originate?

A

Originate in GI tract at sites of pre-existing MALT

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41
Q

Gastric lymphoma tends to be _____ lymphoma

A

B-cell

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42
Q

Pathology of B-cell lymphomas? (3)

A
  • Dense lymphocytic infiltrate LP
  • Neoplastic lymphocytes infiltrate gastric glands
  • reactive-appearing B-cell follicles present
43
Q

Prognosis of gastric lymphoma?

A
  • 90% 5-year survival if caught at an early stage
  • 30-40% if discovered at more advanced stages
43
Q

Clinical features of gastric lymphomas? (7)

A
  • Underlying B-12 deficiency and anemia
  • Fatigue
  • Low-grade fever
  • Nausea
  • Constipation
  • Epigastric pain
  • Weight loss
44
Q

Why are clinical findings of gastric lymphomas those of underlying B12 deficiency?

A

Autoimmune deficiencies = lose intrinsic factor

45
Q

Most common neoplastic polyps?

A

Colonic adenomas

46
Q

Benign polyps are precursors to what?

A

Colorectal adenocarcinomas

47
Q

Risk factors for colonic adenomas?

A
  • 50% of adults in western world by age 50
  • If you have a relative with it, typically screened at 10 years before youngest age that relative was diagnosed
48
Q

Although adenomas exhibit _________, majority do not progress to adenocarcinomas?

A

Epithelial dysplasia

49
Q

Metaplasia?

A

Turns into a different kind of cell (eg. stomach cell becomes an esophageal cell)

50
Q

Dysplasia?

A

Transforms into an abnormal version of ITSELF

51
Q

What will you see with dysplasia?

A
  • Nuclear hyperchromasia, elongation
  • Epithelium fails to mature actively = REDUCTION IN GOBLET CELLS
52
Q

What is the most important characteristic that correlated with risk of malignancy of colorectal adenocarcinoma?

A

Size

53
Q

Most common malignancy of GI tract and major cause of morbidity and mortality worldwide?

A

Adenocarcinoma of the colon

54
Q

Peak incidence of adenocarcinoma of the colon?

A

60-70 yo.

55
Q

What is most closely associated with increased colorectal cancer rates?

A

Dietary factors - low intake of un-absorbable vegetable fiber and high intake of refined carbs and fats

56
Q

Reduced fiber content leads to what?

A

Decreased stool bulk and altered composition of intestinal microbiota

57
Q

What do deficiencies of vitamins A, C, and E do?

A

They are free radical scavengers - so more damage by oxidants

58
Q

High fat intake enhances what?

A

Hepatic synthesis of cholesterol and bile acids

59
Q

What may be protective against adenocarcinoma of the colon?

A

COX-2 inhibitors

60
Q

Two genetic pathways of adenocarcinoma?

A
  1. APC/beta-catenin pathways associated with WNT
  2. Microsatellite instability pathway
61
Q

What mutation is also common in adenocarcinoma of the colon? (proto-oncogene)

A

BRAF

62
Q

80% of sporadic colon tumors typically include mutation of ____ in the neoplastic process

A

APC

63
Q

What is APC a key negative regulator of?

A

Beta-catenin

64
Q

What happens with loss of APC function?

A

Beta-catenin accumulates and translocates to the nucleus

65
Q

What does beta-catenin activate?

A

MYC and cyclin D1 = promote proliferation

66
Q

Additional mutations following APC mutation?

A

KRAS and p53 lof

67
Q

What is micro-satellite instability?

A

Loss of mismatch repair genes, mutations accumulate in micro-satellite repeats

68
Q

Some microsatellite sequences are located in the coding or promoter region of genes involved in regulation of cell growth including: (2)

A
  • Type II TGF-beta receptor
  • Pro-apoptotic protein BAX
69
Q

Distribution of adenocarcinoma of the colon?

A

Distributed equally over entire colon

70
Q

Tumors in proximal colon grow as what?

A

Polyploid, exophytic masses that extend along walls of the viscus

71
Q

Carcinomas in distal colon tend to be what kind of lesions? What do they produce?

A
  • Annular lesions
  • Napkin-ring constrictions and luminal narrowing
72
Q

Adenocarcinomas in the distal colon can be palpated in what exams? What do they feel like?

A
  • DRE
  • Firm palpable masses
73
Q

Clinical features of cecal and other right-sided colon cancers? (3)

A
  • Bleeding leading to iron deficiency anemia
  • Fatigue
  • Weakness
74
Q

Clinical features of left-sided colorectal carcinomas? (3)

A
  • Occult bleeding
  • Changes in bowel habits
  • Cramping in LLQ
75
Q

Most important prognostic factors for adenocarcinoma of the colon?

A
  • Depth of invasion
  • Presence or absence of lymph node metastases
76
Q

Most common site of metastatic lesions of adenocarcinoma of the colon? What is it a result of?

A

Liver - Result of portal drainage of colon

77
Q

Adenocarcinoma of the colon matastases?

A
  • Regional lymph nodes
  • Lungs
  • Bones
78
Q

When hepatic adenomas present as intra-hepatic masses, what may they be mistaken for?

A

Ominous hepatocellular carcinomas

79
Q

What type of adenomas have a tendency to rupture during pregnancy? What may this cause?

A

Subcapsular adenomas - may cause intraperitoneal hemorrage

80
Q

Epidemiology of hepatic adenomas?

A

Tend to occur in young women who have used oral contraceptives (but usually regress when terminated)

81
Q

Primary carcinomas of the liver?

A

Hepatocellular carcinoma (HCC)

82
Q

Where do hepatocellular carcinoma cases happen most?

A

Countries with high rates of chronic HBV infection

83
Q

Risk factors for hepatic carcinoma?

A
  • Long standing cirrhosis
  • Chronic viral infection
  • Chronic alcoholism
  • Food contaminants
84
Q

What is Aflatoxin?

A

Produced by fungus, which contaminates peanuts and grains and mutates p53

85
Q

Common driver mutations in hepatic carcinoma? (3)

A
  • Activating mutations in Beta-catenin genes
  • TERT mutations – upregulated telomerase
  • Inactivating mutations to p53
86
Q

Why is cirrhosis the major risk factor for HCC?

A

Repeated cycles of cell death and regeneration

87
Q

Tumor will often be well differentiated and can secrete what?

A

Bile

88
Q

What do hepatic carcinomas do early?

A

Invade vascular structures - migrate along portal vein or vena cava

89
Q

What are hepatic carcinomas less dependent on for metastasis?

A

Lymph node infiltration

90
Q

Clinical features of hepatic carcinoma? (4)

A
  • Ill defined upper abdominal pain
  • Malaise and fatigue
  • Weight loss
  • Abdominal fullness
91
Q

Prognosis of hepatic carcinoma?

A

Poor - majority of patients pass away within first 2 years

92
Q

Majority of pancreatic cysts are what type?

A

Non-neoplastic pseudocysts

93
Q

4th leading cause of cancer deaths?

A

Pancreatic cancer (ductal adeno-carcinoma)

94
Q

Risk factor for pancreatic cancer?

A
  • SMOKING
  • Chronic pancreatitis
  • Diabetes
95
Q

What do 90% of pancreatic cancers begin as?

A

Intraepithelial neoplasia

96
Q

Most frequently altered oncogene in pancreatic cancer?

A

KRAS

97
Q

Genetic alterations in pancreatic cancer?

A
  • KRAS
  • Inactivation of CDKN2A (encodes p16)
  • Inactivates p53
98
Q

Where do most pancreatic cancers arise?

A

In the head of the gland (60%)

99
Q

Ductal adenocarcinomas that form glandular structures secrete what?

A

Mucin

100
Q

Characteristic features of ductal adenocarcinoma?

A
  • Highly invasive
  • Elicits an intense non-neoplastic host reaction
101
Q

Clinical features of pancreatic cancer? (3)

A
  • Typically silent until tumor causes obstruction
  • Jaundice (post) from obstruction of common bile duct
  • Weight loss, anorexia, malaise
102
Q

Prognosis of pancreatic cancer?

A

Poor - 5-year survival rate less than 5%

103
Q

Higher mortality rate of any cancer?

A

Pancreatic cancer

BMS150 Post-MT2 (17 decks)

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