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.Pathology 3 > GIT: Stomach > Flashcards

GIT: Stomach Flashcards

1
Q

glands in the ___ and ___ are mucus secreting

A

glands in the cardia and antrum are mucus secreting

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2
Q

glands in the ___ and ___ (____) have chief cells which secrete ___ and parietal cells which secrete ____ and ____

A

glands in the corpus and fundus (oxyntic) have chief cells which secrete pepsinogen and parietal cells which secrete acid and intrinsic factor

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3
Q

congenital hypertrophic pyloric stenosis is associated with ____, ____ and ____

A

congenital hypertrophic pyloric stenosis is associated with Turner syndrome, trisomy 18 and esophageal atresia

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4
Q

congenital hypertrophic pyloric stenosis is caused by concentric ____ of ____

A

congenital hypertrophic pyloric stenosis is caused by concentric hypertrophy of circular muscular coat

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5
Q

congenital hypertrophic pyloric stenosis is treated by ____

A

congenital hypertrophic pyloric stenosis is treated by surgery (myotomy)

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6
Q

acute gastritis affects the ____

full thickness mucosal injury = _____

A

acute gastritis affects the superficial mucosa (loss of surface epi.)

full thickness mucosal injury = ulcers

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7
Q

in acute gastritis, there is edema and congestion of the ____ and ____ are found in the surface epithelium and glands

A

in acute gastritis, there is edema and congestion of the lamina propria and neutrophils are found in the surface epithelium and glands

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8
Q

endoscopy of a patient with chronic gastritis would show ____

A

endoscopy of a patient with chronic gastritis would show normal to patchy/diffuse erythema +/- hemorrhage to boggy with thick mucosal folds

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9
Q

in chronic gastritis, ____ is found in the lamina propria

A

in chronic gastritis, inflammatory infiltrate (lymphocytes and plasma cells) is found in the lamina propria

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10
Q

in chronic gastritis, ____ is found in the surface epithelium and glandular lumen

A

in chronic gastritis, PMNs is found in the surface epithelium and glandular lumen

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11
Q

in chronic gastritis, ____ is found, mainly superficial, which is a maker of H. pylori infection

A

in chronic gastritis, reactive lymphoid aggregates is found, mainly superficial, which is a maker of H. pylori infection

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12
Q

describe what H. pylori infection can lead to

A
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13
Q

describe diagnosis of H. pylori (invasive vs. non-invasive)

A
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14
Q

in autoimmune gastritis, there are autoantibodies to ____

A

in autoimmune gastritis, there are autoantibodies to parietal cell antigens/intrinsic factor

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15
Q

in autoimmune gastritis, there is destruction of ___ glands which leads to ___ and ____

A

in autoimmune gastritis, there is destruction of oxyntic glands which leads to achlorhydria and increased gastrin levels

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16
Q

in autoimmune gastritis, there is an increased risk for ___ and ____

A

in autoimmune gastritis, there is an increased risk for gastric carcinoma and neuroendocrine tumors (carcinoids)

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17
Q

describe the effects of autoimmune gastritis

A
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18
Q

gastric ulcers are caused by a loss of mucosa that extends through ____ or deeper

A

gastric ulcers are caused by a loss of mucosa that extends through muscularis mucosae or deeper

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19
Q

describe acute gastric ulcers

A
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20
Q

the pathogenesis of acute gastric ulcers is related to ____ and ____

A

the pathogenesis of acute gastric ulcers is related to systemic acidosis and hypoxia (severe trauma and burns) and vagal stimulation (intracranial lesions)

21
Q

list the sites of peptic ulcer disease

A
22
Q

list clinical features of a peptic ulcer

A
  • clinical features:
    • burning epigastric pain 1-3 hours after meals
    • relieved by food and alkali
    • worse at night
    • associated weight loss
    • gastric outlet obstruction
23
Q

list complications of peptic ulcers

A
  • complications:
    • bleeding
    • perforation
    • gastric outlet obstruction
    • malignant transformation:
      • unknown in duodenal ulcer and exceedingly rare in gastric ulcer
24
Q

a risk factor for ___ gastritis is severe burns, which causes ____

A

a risk factor for acute gastritis is severe burns, which causes Curling ulcer

caused by hypovolemia → decreased blood flow to stomach → blood can’t “sweep away” the acid or bring nutrients → acute gastritis

25
Q

a risk factor for ___ gastritis is increased intracranial pressure which leads to ____

explain how this occurs

A

a cause of acute gastritis is increased intracranial pressure which leads to Cushing ulcer

increased intracranial pressure → increased vagal stimulation → increased ACh → binds to parietal cell and increases acid production

26
Q

describe the mechanism of NSAID injury

A
  • inhibition of enzyme COX
    • rate limiting step in converting arachidonic acid to PGs
    • PGs protect gastric mucosa
      • maintain blood flow, increase mucus and bicarb. secretion and augment epithelial defenses
  • direct irritant
    • denudation of surface epi., increased mucosal permeability to ions
27
Q

intestinal gastric adenocarcinoma is associated with ____

A

intestinal gastric adenocarcinoma is associated with H. pylori

28
Q

diffuse gastric adenocarcinoma is caused by a mutation in ____

A

diffuse gastric adenocarcinoma is caused by a mutation in E-cadherin

29
Q

in diffuse gastric adenocarcinoma, ____ cells can be seen when the single cells proliferate (since they are detached from one another because of the mutation in E-cadherin)

A

in diffuse gastric adenocarcinoma, signet ring cells can be seen when the single cells proliferate (since they are detached from one another because of the mutation in E-cadherin)

30
Q

in diffuse gastric adenocarcinoma, there is a _____ appearance

A

in diffuse gastric adenocarcinoma, there is a linitis plastica appearance

31
Q

describe what is seen in the image

A

intestinal gastric adenocarcinoma

32
Q

describe what is seen in the image

A

diffuse gastric adenocarcinoma

33
Q

describe what is seen in the image

A

signet ring cells (diffuse gastric adenocarcinoma)

34
Q

early gastric carcinoma is confined to ___ and ___ regardless of ____

A

early gastric carcinoma is confined to mucosa and submucosa regardless of involvement of regional lymph nodes

35
Q

list clinical features of gastric adencarcinoma

A
  • mostly asymptomatic in early stages
  • non-specific weight loss, anorexia, abdominal pain
  • pyloric outlet obstruction
  • prognosis depends upon depth of invasion and nodal status
  • Krukenberg tumor: bilateral ovarian spread
  • Virchow node: left supraclavicular lymph node
36
Q

gastrointestinal stromal tumors are derived from ____

A

gastrointestinal stromal tumors are derived from cells of Cajal (the pacemaker cells)

37
Q

describe the appearance of GIST

A

whorls and bundles of spindle-shaped or epithelioid cells

38
Q

____ mutations are present in most GIST tumors

A

Kit mutations are present in most GIST tumors

39
Q

___, a KIT inhibitor, is used for malignant GIST

A

imatinib (Gleevec), a KIT inhibitor, is used for malignant GIST

40
Q

describe oral leukoplakia

A
  • well-defined white patch or plaque caused by epidermal thickening or hyperkeratosis
41
Q

oral leukoplakia is associated with…. (3 things)

A

oral leukoplakia is associated with:

  • tobacco use
  • chronic friction (ill-fitting dentures)
  • HPV infection
42
Q

oral leukoplakia are (removed or not removed?) with scraping

A

oral leukoplakia are not removed with scraping

43
Q

oral leukoplakia range from ___ to ____

A

oral leukoplakia range from benign epithelial lesions to highly dysplastic lesions

44
Q

oral hairy leukoplakia is seen in patients with ___ and is caused by ____

A

oral hairy leukoplakia is seen in patients with HIV and is caused by EBV

45
Q

what words are used to describe oral hairy leukoplakia?

A

white, confluent, fluffy hyperkeratotic thickenings

46
Q

there (is or is no) malignant potential in oral hairy leukoplakia

how does this differ from oral leukoplakia?

A

there IS NO malignant potential in oral hairy leukoplakia

oral leukoplakia has small chance of malignancy (there is dysplasia!)

47
Q

describe erythroplakia aka erythroplasia

A
  • red, velvety eroded area
  • poorly circumscribed
  • more atypical epithelial changes
    • typically marked dysplasia
  • malignant transformation in more than 50%
48
Q

what words are used to describe erythroplakia?

A

red, velvety, eroded area

49
Q

list the order of malignant potential seen in oral epithelial changes (oral leukoplakia, oral hairy leukoplakia, erythroplakia)

A

erythroplakia/erythroplasia >> oral leukoplakia

NO malignant potential in oral hairy leukoplakia

.Pathology 3 (8 decks)

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