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Block 7 - GI > Stomach Path > Flashcards

Stomach Path Flashcards

1
Q

What cells is the body of the stomach composed of?

A

foveolar cells that secrete protective mucus

glands w/ parietal cells (secrete HCl) and chief cells (secrete pepsin)

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2
Q

What cells is the antrum of the stomach composed of?

A

G cells producing gastrin - promotes secretion of HCl and pepsin

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3
Q

What are internal and external injurious agents to the stomach?

A

internal - pepsin, HCl, bile

external - drugs, alcohol, bacteria

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4
Q

What are the defensive forces of the stomach?

A

mucus, bicarb, cell regeneration, blood flow, prostaglandins

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5
Q

What does the tern “gastritis” refer to?

A

any inflammation, ulceration/erosion, irritation

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6
Q

What are the symptoms of gastritis?

A

nausea, abdominal bloating, heartburn, hiccups, epigastric pain, bleeding with possible hematemesis and melena, coffee ground emesis

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7
Q

What are the histologic features of chronic gastritis?

A

lymphocytes and plasma cells in lamina propria
with or without ACTIVITY (inflammation - PMNs)
can destroy parietal cells and glands –> metaplasia

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8
Q

What features are present with chronic gastritis due to H. Pylori?

A

both active and chronic gastritis

T and B lymphocytes, then infiltration of lamina propria and epithelium by neutrophils

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9
Q

What feature is H. pylori gastritis known for producing?

A

lymphoid follicles and germinal centers

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10
Q

What is different about the features of autoimmune gastritis as opposed to that caused by H. pylori?

A

NO active inflammatory component with neutrophils

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11
Q

How does H. pylori colonize the stomach?

A

uses flagella to burrow into mucus and reach niche close to epithelial layer
senses acidic pH of lumen by chemotaxis and swims away
adhesins help it adhere to epithelial cells

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12
Q

How does H. pylori damage the stomach?

A

produce urease that breaks down urea to carbon dioxide and ammonia –> ammonium that neutralizes gastric acid, allowing survival
ammonia and other products are toxic to epithelial cells

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13
Q

How can H. pylori be detected?

A

CLO test - if it turns red indicates pH change - means H. pylori

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14
Q

What antibodies are present in autoimmune chronic gastritis?

A

anti-intrinsic factor

anti parietal cell

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15
Q

What are the two patterns of H. pylori associated chronic gastritis?

A

diffuse antral - chronic inflammation w activity - in individuals w peptic ulcers
multifocal atrophic - gastric atrophy and partial replacement by intestinal epithelium - individuals who dev gastric carcinoma and ulcers

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16
Q

What is the treatment for H. pylori?

A

antibiotics plus acid suppressants

PPIs

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17
Q

What are possible complications of H. pylori?

A

gastric or duodenal ulcers

increased risk of gastric adenocarcinoma and lymphoma (MALT)

18
Q

What are the consequences of AIG (autoimmune gastritis)?

A

destruction of parietal cells and eventual replacement of normal gastric mucosa by intestinal metaplasia and fibrosis
decreased intrinsic factor –> dec B12 –> pernicious anemia
hyperplasia of G cells –> hypergastrinemia - trophic effect on ECL cells that can transform into carcinoid tumors
inc risk of adenocarcinoma

19
Q

What is seen microscopically in acute gastritis?

A

superficial neutrophilic infiltrates (above BM), mucosal edema, reactive and regenerative changes of surface epithelium, maybe erosions

20
Q

What is acute erosive gastritis?

A

acute gastritis with necrosis of epithelial cells

21
Q

What is the pathogenesis of acute gastritis due to?

A

compromise of mucosal defenses

increased acid production/decreased bicarb production

22
Q

What agents are associated frequently with acute gastritis?

A

heavy NSAID use, excessive alcohol, smoking, severe physical stress, chemo/radiation, bile reflux from duodenum, iron pills

23
Q

What are the clinical features of acute gastritis?

A

mild epigastric discomfort to hematemesis, melena and potentially fatal blood loss

24
Q

What is an ulcer?

A

breach of gastric mucosa that extends through muscularis mucosa into submucosa or beyond

25
Q

What are the most common causes of gastric or duodenal ulcers?

A

increased acid/pepsin secretion
H. pylori
NSAIDs

26
Q

Where in the stomach and duodenum do ulcers typically occur?

A

stomach - lesser curvature and antrum

duodenum - first part

27
Q

What are peptic ulcers?

A

can be gastric or duodenal
single sharply punched out defects with clean base due to peptic digestion of necro-inflammatory debris
flat rim (unlike rolls in cancer)
usually chronic gastritis in adjacent mucosa

28
Q

What are the four zones of a chronic active ulcer?

A

necrotic fibrinoid debris
mixed acute and chronic inflammation
granulation tissue
fibrosis/scar

29
Q

What two conditions are key for the dev of most peptic ulcers?

A

H. pylori inf

mucosal exposure to gastric acid and pepsin

30
Q

What is the difference between duodenal and gastric ulcers?

A

duodenal have increased gastrin and acid levels

gastric have normal or reduced gastric acid production

31
Q

What is the major cause of PUD in people who are heliobacter negative?

A

NSAIDs - inhibit COX1 that produces a prostaglandin that protects stomach lining

32
Q

What are risk factors for NSAID-related gastroduodenal toxicity?

A

older age
higher doses
prolonged use

33
Q

What is the relationship between ulcers and cancer?

A

cancers often ulcerate but ulcers rarely become malignant (never with duodenal and rarely with gastric)

34
Q

What are complications of PUD?

A

GI bleeding
Perforation - can penetrate into adjacent organ
Gastric outlet obstruction - inflammation or scar formation in outlet area

35
Q

Where do duodenal ulcerates vs. gastric ulcers penetrate?

A

duodenal - posteriorly into pancreas

gastric - into left hepatic lobe

36
Q

What are signs and symptoms of gastric outlet obstruction?

A

early satiety, nausea, vomiting, postprandial abdominal pain, weight loss

37
Q

What are stress ulcers?

A

usually multiple and shallower than peptic ulcers - don’t penetrate muscularis propria
heal w no fibrosis or scarring
in stomach mostly

38
Q

What conditions are stress ulcers seen in?

A

severe trauma
use of gastric irritant drugs (NSAIDs, corticosteroids)
extensive burns (Curling ulcers)
CNS trauma (Cushing ulcers)

39
Q

What are the main causes of peptic ulcers?

A

H. pylori
NSAIDs, corticosteroids
Zollinger Ellison syndrome

40
Q

What are the types of gastric tumors?

A

adenocarcinoma
MALT lymphoma
Carcinoid

41
Q

What are the symptoms of gastric malignancies?

A

nausea, vomiting, early satiety, GI blood loss

iron deficiency anemia

Block 7 - GI (28 decks)

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