GIT: Stomach Flashcards
glands in the ___ and ___ are mucus secreting
glands in the cardia and antrum are mucus secreting
glands in the ___ and ___ (____) have chief cells which secrete ___ and parietal cells which secrete ____ and ____
glands in the corpus and fundus (oxyntic) have chief cells which secrete pepsinogen and parietal cells which secrete acid and intrinsic factor
congenital hypertrophic pyloric stenosis is associated with ____, ____ and ____
congenital hypertrophic pyloric stenosis is associated with Turner syndrome, trisomy 18 and esophageal atresia
congenital hypertrophic pyloric stenosis is caused by concentric ____ of ____
congenital hypertrophic pyloric stenosis is caused by concentric hypertrophy of circular muscular coat
congenital hypertrophic pyloric stenosis is treated by ____
congenital hypertrophic pyloric stenosis is treated by surgery (myotomy)
acute gastritis affects the ____
full thickness mucosal injury = _____
acute gastritis affects the superficial mucosa (loss of surface epi.)
full thickness mucosal injury = ulcers
in acute gastritis, there is edema and congestion of the ____ and ____ are found in the surface epithelium and glands
in acute gastritis, there is edema and congestion of the lamina propria and neutrophils are found in the surface epithelium and glands
endoscopy of a patient with chronic gastritis would show ____
endoscopy of a patient with chronic gastritis would show normal to patchy/diffuse erythema +/- hemorrhage to boggy with thick mucosal folds
in chronic gastritis, ____ is found in the lamina propria
in chronic gastritis, inflammatory infiltrate (lymphocytes and plasma cells) is found in the lamina propria
in chronic gastritis, ____ is found in the surface epithelium and glandular lumen
in chronic gastritis, PMNs is found in the surface epithelium and glandular lumen
in chronic gastritis, ____ is found, mainly superficial, which is a maker of H. pylori infection
in chronic gastritis, reactive lymphoid aggregates is found, mainly superficial, which is a maker of H. pylori infection
describe what H. pylori infection can lead to
describe diagnosis of H. pylori (invasive vs. non-invasive)
in autoimmune gastritis, there are autoantibodies to ____
in autoimmune gastritis, there are autoantibodies to parietal cell antigens/intrinsic factor
in autoimmune gastritis, there is destruction of ___ glands which leads to ___ and ____
in autoimmune gastritis, there is destruction of oxyntic glands which leads to achlorhydria and increased gastrin levels
in autoimmune gastritis, there is an increased risk for ___ and ____
in autoimmune gastritis, there is an increased risk for gastric carcinoma and neuroendocrine tumors (carcinoids)
describe the effects of autoimmune gastritis
gastric ulcers are caused by a loss of mucosa that extends through ____ or deeper
gastric ulcers are caused by a loss of mucosa that extends through muscularis mucosae or deeper
describe acute gastric ulcers
the pathogenesis of acute gastric ulcers is related to ____ and ____
the pathogenesis of acute gastric ulcers is related to systemic acidosis and hypoxia (severe trauma and burns) and vagal stimulation (intracranial lesions)
list the sites of peptic ulcer disease
list clinical features of a peptic ulcer
- clinical features:
- burning epigastric pain 1-3 hours after meals
- relieved by food and alkali
- worse at night
- associated weight loss
- gastric outlet obstruction
list complications of peptic ulcers
- complications:
- bleeding
- perforation
- gastric outlet obstruction
- malignant transformation:
- unknown in duodenal ulcer and exceedingly rare in gastric ulcer
a risk factor for ___ gastritis is severe burns, which causes ____
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
a risk factor for ___ gastritis is increased intracranial pressure which leads to ____
explain how this occurs
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
describe the mechanism of NSAID injury
- 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
intestinal gastric adenocarcinoma is associated with ____
intestinal gastric adenocarcinoma is associated with H. pylori
diffuse gastric adenocarcinoma is caused by a mutation in ____
diffuse gastric adenocarcinoma is caused by a mutation in E-cadherin
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)
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)
in diffuse gastric adenocarcinoma, there is a _____ appearance
in diffuse gastric adenocarcinoma, there is a linitis plastica appearance
describe what is seen in the image
intestinal gastric adenocarcinoma
describe what is seen in the image
diffuse gastric adenocarcinoma
describe what is seen in the image
signet ring cells (diffuse gastric adenocarcinoma)
early gastric carcinoma is confined to ___ and ___ regardless of ____
early gastric carcinoma is confined to mucosa and submucosa regardless of involvement of regional lymph nodes
list clinical features of gastric adencarcinoma
- 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
gastrointestinal stromal tumors are derived from ____
gastrointestinal stromal tumors are derived from cells of Cajal (the pacemaker cells)
describe the appearance of GIST
whorls and bundles of spindle-shaped or epithelioid cells
____ mutations are present in most GIST tumors
Kit mutations are present in most GIST tumors
___, a KIT inhibitor, is used for malignant GIST
imatinib (Gleevec), a KIT inhibitor, is used for malignant GIST
describe oral leukoplakia
- well-defined white patch or plaque caused by epidermal thickening or hyperkeratosis
oral leukoplakia is associated with…. (3 things)
oral leukoplakia is associated with:
- tobacco use
- chronic friction (ill-fitting dentures)
- HPV infection
oral leukoplakia are (removed or not removed?) with scraping
oral leukoplakia are not removed with scraping
oral leukoplakia range from ___ to ____
oral leukoplakia range from benign epithelial lesions to highly dysplastic lesions
oral hairy leukoplakia is seen in patients with ___ and is caused by ____
oral hairy leukoplakia is seen in patients with HIV and is caused by EBV
what words are used to describe oral hairy leukoplakia?
white, confluent, fluffy hyperkeratotic thickenings
there (is or is no) malignant potential in oral hairy leukoplakia
how does this differ from oral leukoplakia?
there IS NO malignant potential in oral hairy leukoplakia
oral leukoplakia has small chance of malignancy (there is dysplasia!)
describe erythroplakia aka erythroplasia
- red, velvety eroded area
- poorly circumscribed
- more atypical epithelial changes
- typically marked dysplasia
- malignant transformation in more than 50%
what words are used to describe erythroplakia?
red, velvety, eroded area
list the order of malignant potential seen in oral epithelial changes (oral leukoplakia, oral hairy leukoplakia, erythroplakia)
erythroplakia/erythroplasia >> oral leukoplakia
NO malignant potential in oral hairy leukoplakia
