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
Q

what is the median age of autoimmune gastritis diagnosis?

A

60

26
Q

what are the clinical features of autoimmune gastritis?

A

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
Q

what are 3 uncommon forms of gastritis?

A

eosinophilic (allergies, immune disorders, parasites); lymphocytic (varioliform gastritis)- women, celiac disease; granulomatous- crohn disease most common

28
Q

PUD results from what?

A

imbalances between defense mechanisms and damaging factors that cause chronic gastritis

29
Q

nearly all peptic ulcers are associated with what?

A

H. pylori infections, NSAIDs, or cigarette smoking

30
Q

what are the complications associated with PUD?

A

bleeding (iron deficiency anemia or hematemesis), perforation, obstruction (acquired pyloric stenosis) mucosal atrophy and intestinal metaplasia, dysplasia, gastritis cystica

31
Q

how are peptic ulcers described morphologically?

A

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
Q

heaped up margins of peptic ulcers are characteristic of what?

A

cancers

33
Q

hypertrophic gastropathies are characterized how?

A

by giant cerebriform enlargement of the rugal folds due to hyperplasia without inflammation

34
Q

What are two examples of hypertrophic gastropathies?

A

menetrier disease and zollinger-ellison syndrome

35
Q

what are the symptoms associated with menetrier disease?

A

hypoproteinemia, weight loss, and diarrhea

36
Q

what are the symptoms associated with zollinger-ellison syndrome?

A

peptic ulcers

37
Q

what are the risk factors for menetrier disease?

A

none

38
Q

what are the risk factors for zollinger-ellison syndrome?

A

Multiple endocrine neoplasia

39
Q

which hypertrophic gastropathy is associated with adenocarcinoma?

A

menetrier disease