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GI > 4. Pathology of the Stomach Peptic Ulcer & Gastric Malignacies > Flashcards

4. Pathology of the Stomach Peptic Ulcer & Gastric Malignacies Flashcards

Part 2

1
Q

Gastric malignancy

A

stomach (gastric) cancer is the cancer that starts in the cells lining the stomach

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2
Q

the most common gastric cancer is

A

adenocarcinoma

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3
Q

gastric adenocarcinoma

A

cancer in cells that produce mucus

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4
Q

is the early stage of gastric adenocarcinoma asymptomatic

A

yes

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5
Q

what are symptoms associated in the late stage of gastric adenocarcinoma

A

indigestion
nausea or vomitting
dysphagia
GI bleeding
unintentional weight loss

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6
Q

How is gastric adenocarcinoma treated

A

surgery (resection)
chemotherapy
radiation

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7
Q

how is gastric adenocarcinoma divided

A

location
by micrograph

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8
Q

what are possible locations of gastric adenocarcinoma

A

Gastric cardia cancer begins in the top inch of the stomach, just below where it meets the esophagus

Non-cardia gastric cancer is cancer that begins in all other sections of the stomach.

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9
Q

what are possible classifications of gastric adenocarcinoma based on micrographs

A

Intestinal adenocarcinomas are well differentiated = the cancer cells look similar to normal cells under a microscope.

ØDiffuse adenocarcinomas are undifferentiated or poorly
differentiated = the cancer cells look different from
normal cells under a microscope

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10
Q

Most common benign tumors

A

adenoma

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11
Q

Most common malignant tumors:

A

Adenocarcinoma

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12
Q

Adenocarcinoma most commonly occur in what location of the stomach

A

antrum

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13
Q

what are the risk factors for Adenocarcinoma

A

H. pylori
Smoking
Nitrites
Smoked food
Menetrier’s disease
(E-cadherin)

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14
Q

What actions on the gastric epithelial do H. pylori and gastric cancer cause

A

oxidative stress + increased DNA damage =
inflammation of epithelial cells =
Impairment of DNA repair pathways = deactivation of tumor suppression gene and oncogenesis

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15
Q

What actions through the modulation of immune-inflammatory pathways do H. pylori and gastric cancer cause

A

Increase in:
Smad7
ROS, RNS
IL-17, IL-21
NF-kB activity

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16
Q

What response cells are involved with H. pylori and gastric cancer

A

dendritic cells
neutrophil
macrophage
t-cells

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17
Q

What is sodium nitrites commonly ingested with

A

preserved foods (meats)

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18
Q

What are nitrates commonly ingested with

A

nitrate consumed through the diet is converted to nitrite by bacteria

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19
Q

the combination of nitrite from processed meats and low pH of stomach acid creates

A

nitric oxide

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20
Q

How can smoking lead to gastric cancer

A

3 ways:

  1. (increase) inflammation
  2. (increase) NAchR - stimulation of growth factor = angiogenesis
  3. DNA damage can happen through the NachR - instability of genetics - angiogenesis = deactivation of suppression gene
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21
Q

Are nitrites by themselves safe?

A

yes

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22
Q

through what mechanism do nitrites become harmful

A

nitrites become harmful with they react with amines, found in the stomach. together they make nitroamines

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23
Q

Why are nitroamines harmful

A

nitroamines increase the risk of DNA damage

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24
Q

the combination of nitrite and low pH of stomach acid creates what

A

nitric oxide

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25
Q

DNA damage from n-alkylnitrosamine compounds can form

A

colon carcinoma

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26
Q

What two compunds are of concerned with smoked meats

A

PAH - Polycyclic aromatic hydrocarbon
HCA - heterocyclic amines

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27
Q

Why HCA and PAH involved in cancer development

A

the carcinogens at high temps can damage DNA which increases cancer development

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28
Q

what is menetrier disease

A

overexpression of tumor growth factor-a TGF-a, a ligand for tyrosine kinase epidermal growth factor receptor

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29
Q

What are characteristics of menetrier disease

A

giant mucosal folds in the proximal part of the stomach

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30
Q

what happens in menetrier disease

A

decreased acid
decreased digestion
decreased albumin (hypoalbumena)

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31
Q

How does e-cadherin affect gastric cancer

A

e-cadherin involves cell-to-cell junctions

with it we have abnormal growth of cells(dysplasia) leading to gastric cancer

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32
Q

how many ways can adenocarcinoma be diagnosed

A

depth of invasion
histology
growth pattern

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33
Q

what are the 2 stages of depth of invasion to diagnose adenocarcinoma?

A

Early and late

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34
Q

what are the 2 histology types to diagnose adenocarcinoma?

A

intestinal and diffused

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35
Q

What layers of the stomach are involved in the early depth of invasion of an adenocarcinoma diagnosis?

A

2 - mucosa + submucosa

36
Q

What layers of the stomach are involved in the late(advanced) depth of invasion of an adenocarcinoma diagnosis?

A

4 - mucosa + submucosa + serosa + muscularis propria

37
Q

what is the histological appearance of intestinal type adenocarcinoma?

A

glandular

38
Q

what is the predilection of intestinal type adenocarcinoma?

A

mean age men

39
Q

what are the risk factors of intestinal-type adenocarcinoma?

A

diet high in smoked and salted foods

pickled vegetables

lack of citrus fruits

green leafy vegetables

cigarette smoking

40
Q

intestinal-type adenocarcinoma is associated with

A

chronic gastritis
H pylori
autoimmune gasritis
partial gastrectomy
gastric adenomas

41
Q

what is the histology of intestinal-type adenocarcinoma?

A

bulky tumors that are either tubular or papillary

42
Q

what is the predilection of diffuse type adenocarcinoma?

A

mean age 48 for men and women but more common in young

43
Q

what is the clincial appearance of diffuse type adenocarcinoma?

A

poorly differentiated discohesive malignant cells

44
Q

what is another name for diffuse type adenocarcinoma?

A

linitis plastica or signet ring cell adenocarcinoma

45
Q

Why is diffuse type adenocarcinoma refered to as linitis plastica?

A

because of its thickened and rubbery hard gastric wall due to an extensive infiltration with signet ring cells

46
Q

what happens with diffuse adenocarcinoma enters systemic circulation

A

it travels and effects other parts of the body which will be known as krukenburg tumor

47
Q

whats an example of a krukenburg tumor

A

ovarian
has signet rings
cellular stroma background (fibroblasts)

48
Q

what is the Borrmann classification

A

classifies gastric cancer

49
Q

the Borrmann classification has how many types

A

4

50
Q

the Borrmann classification least aggressive

A

type 1

51
Q

the Borrmann classification most aggressive

A

type 4

52
Q

the Borrmann classification type 1

A

polypoid (minimal invasion)

53
Q

the Borrmann classification type 2

A

fungating carcinoma (raised margin, shallow ulceration)

54
Q

the Borrmann classification type 3

A

ulcerated carcinoma (infiltration of malignant cells)

55
Q

the Borrmann classification type 4

A

infiltrating carcinomas (more diffused malignant cells that affect the stomach rapidly and has a leather appearance)

56
Q

What is GIST

A

a soft tissue carcinoma cancer in the nerve cells that are found in the walls of the stomach

57
Q

Where does GIST arise from

A

interstitial cell of Cajal that is located in the muscularis propria

58
Q

ICC or interstitial cells of Cajal are sometimes referred to as

A

pacemakers of the GI tract

59
Q

what is the predilection of GIST

A

elder males

60
Q

increased GIST is associate with

A

Neurofribromatosis type I and carneys triad

61
Q

signs of Neurofribromatosis type I

A

cafe au lait spots
soft bumps

62
Q

carneys triad

A

3 types of endocrine tumors happening at once - lungs, stomach, adrenal

63
Q

what is the pathogenesis of GIST

A

tyrosine kinase gene c-KIT (70%)

platelet derived growth factor receptor alpha (10%)

64
Q

activation of tyrosine kinase gene c-KIT does what

A

promote tumor proliferation

inhibit tumor suppressor genes

65
Q

what are the 3 forms of GIST

A

spindle cell
epithelioid cells
mixed

66
Q

foregut carcinoid tumor

A

stomach duodenum

67
Q

midgut carcinoid tumor

A

jejunum and ileum (aggressive)

68
Q

Hindgut carcinoid tumor

A

appendix and colorectum (large intestines)

69
Q

Most commonly associated lymphomas

A

2; MALT and diffuse large B-cell gastric lymphoma

70
Q

where does MALT originate

A

H. pylori chronic gastritis

71
Q

MALT untreated becomes what

A

diffused B

72
Q

MALT lymphoma can mimic what

A

(6)
erythematous gastritis
ulcer scar
polyp
ulcer
mass
thickened fold

73
Q

How do you treat MALT

A

antibiotics
surgery
radiation
therapy
chemotherapy
targeted therapy

74
Q

What are the two types surgical procedures for gastrectomy

A

total
partial

75
Q

what is a partial gastrectomy

A

plyorus preservation by removal of part of the stomach

76
Q

what type of surgery is gastric bypass surgery

A

temporary; puts less pressure on the stomach

77
Q

what are surgical procedures for gastrectomy complications

A

anatomic leak
bile reflux
dumping syndrome
malnutrition
internal hernia
narrowing at the attachment site
post surgery gastroparesis

78
Q

anatomic leak

A

leak at the attachment site

79
Q

bile reflux

A

bile flows backwards into stomach

80
Q

dumping syndrome

A

food travels to your small intestine before it is broken down enough

81
Q

internal hernia

A

part of your small intestine bulge through the membrane that attaches your intestine to your abdominal wall

82
Q

narrowing at the attachment site

A

the site that connects your partial stomach or esophogus and small intestine narrows

83
Q

post surgery gastroparesis

A

the stomach doesnt process food as quickly as it should

84
Q

what is the recovery time for gastrectomy

A

2 months

85
Q

regaining energy levels and getting used to new habits after a gastrectomy takes

A

3 to 6 months or even longer

GI (5 decks)

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