Pathology of the GI Tract- SI and Colon (3) Flashcards

1
Q

what is the role of G cells in the antral glands?

A

they release gastrin to stimulate luminal acid secretion by parietal cells within the gastric fundus and body

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2
Q

when is gastrin released?

A

in response to vagal and gastrin-releasing peptide (GRP) stimulation secondary to ingestion of peptides, amino acids, gastric distention, and an elevated stomach pH

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3
Q

when is gastrin release decreased?

A

in response to paracrine inhibition by somatostatin and decreased stomach pH

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4
Q

most gastric adenocarcinomas involve what?

A

the gastric antrum; the lesser curvature is involved more often than the greater curvature

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5
Q

what nerve mediates acid stimulatory effects in the stomach?

A

vagus nerve

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6
Q

what are 2 congenital abnormalities of the stomach that we discussed?

A

pyloric stenosis and ectopia

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7
Q

what happens when ectopic pancreatic tissue is present in the pylorus?

A

inflammation and scarring may lead to obstruction (they can mimic invasive cancer)

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8
Q

what is acute gastritis?

A

a mucosal inflammatory process; when neutrophils are present, the lesion is referred to as acute gastritis; when inflammatory cells are rare or absent, the term gastropathy is used

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9
Q

where are prostaglandins found in high numbers?

A

in the gastric mucosa and gastric juice

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10
Q

when are stress ulcers most common?

A

in individuals with shock, sepsis, or severe trauma

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11
Q

what are curling ulcers?

A

ulcers occurring in the proximal duodenum and associated with severe burns or trauma

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12
Q

what are cushing ulcers?

A

gastric, duodenal, and esophageal ulcers arising in persons with intracranial disease; they carry a high incidence of perforation

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13
Q

what are 2 etiologies for chronic gastritis?

A

infection with h. pylori; autoimmune gastritis

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14
Q

what is the most common cause of chronic gastritis?

A

infection with the bacillus helicobacter pylori

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15
Q

what can long-standing chronic gastritis that involves the body and fundus lead to?

A

it may ultimately lead to mucosal atrophy and/or intestinal metaplasia–> both are risk factors for adenocarcinoma

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16
Q

what does chronic gastritis expose the epithelium to?

A

inflammation-related free radical damage and proliferative stimuli leading to gastric dysplasia–> over time this can result in carcinoma

17
Q

how does h. pylori present? (like how does the stomach look)

A

most often presents as predominantly antral gastritis with normal or increased acid production

18
Q

what is H. pylori infection associated with in the US?

A

poverty, household crowding, limited education, african american or mexican american ethnicity, residence in rural areas, and birth outside of the US

19
Q

what is the carrier of h. pylori?

A

humans are the primary carriers, suggesting that transmission is primarily by the fecal-oral route

20
Q

what are three examples of the diagnostic tests used for H. pylori infections?

A

serologic test, fecal bacterial antigen detection, urea breath test

21
Q

what are the effective treatments for H. pylori?

A

combinations of antibiotics and proton pump inhibitors

22
Q

what is autoimmune gastritis characterized by? histologically

A

diffuse mucosal damage of the oxyntic (acid-producing) mucosa within the body and fundus

23
Q

what is autoimmune gastritis characterized by in general?

A

antibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions; reduced serum pepsinogen I concentration; endocrine cell hyperplasia; vitamin B12 deficiency; defective gastric acid secretion (achlorhydria)

24
Q

what is progression of autoimmune gastritis like?

A

progression to gastric atrophy probably occurs over 2-3 decades, and anemia is seen in only a few patients; because of the slow onset and variable progression, patients are generally diagnosed only after being affected for many years

25
what is the median age of autoimmune gastritis diagnosis?
60
26
what are the clinical features of autoimmune gastritis?
they are related to deficiency in cobalamin--> atrophic glossitis, megaloblastosis of RBCs and epithelial cells; peripheral neuropathies and subacute combined degeneration of spinal cord; malabsorptive diarrhea
27
what are 3 uncommon forms of gastritis?
eosinophilic (allergies, immune disorders, parasites); lymphocytic (varioliform gastritis)- women, celiac disease; granulomatous- crohn disease most common
28
PUD results from what?
imbalances between defense mechanisms and damaging factors that cause chronic gastritis
29
nearly all peptic ulcers are associated with what?
H. pylori infections, NSAIDs, or cigarette smoking
30
what are the complications associated with PUD?
bleeding (iron deficiency anemia or hematemesis), perforation, obstruction (acquired pyloric stenosis) mucosal atrophy and intestinal metaplasia, dysplasia, gastritis cystica
31
how are peptic ulcers described morphologically?
round to oval, sharply punched out defect- the mucosal margin may overhang the base slightly, particularly on the upstream side, but it is usually level with the surrounding mucosa
32
heaped up margins of peptic ulcers are characteristic of what?
cancers
33
hypertrophic gastropathies are characterized how?
by giant cerebriform enlargement of the rugal folds due to hyperplasia without inflammation
34
What are two examples of hypertrophic gastropathies?
menetrier disease and zollinger-ellison syndrome
35
what are the symptoms associated with menetrier disease?
hypoproteinemia, weight loss, and diarrhea
36
what are the symptoms associated with zollinger-ellison syndrome?
peptic ulcers
37
what are the risk factors for menetrier disease?
none
38
what are the risk factors for zollinger-ellison syndrome?
Multiple endocrine neoplasia
39
which hypertrophic gastropathy is associated with adenocarcinoma?
menetrier disease