B5.032 Prework 1 Gastric Ulcers Flashcards

1
Q

definition of gastric ulcer

A

5 mm or greater break in the lining of the stomach that extends into the submucosa on biopsies or has an appreciable depth during upper endoscopy

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2
Q

how does pepsin play a role in causing gastric ulcers

A

enzyme active at acidic pH

pepsin can digest proteins within ulcer base and grow ulcer

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3
Q

epidemiology of gastric ulcers

A

0.14-0.19% annual incidence in US
17-22% in China (H.pylori more prevalent)
incidence inclines with improvements in sanitation

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4
Q

major complications of ulcers

A

GI bleeding (0.02-0.006% incidence)
perforation (0.004-0.014% incidence)
overall:
bleeding in 10% of ulcer, perforation in 1%

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5
Q

why is acid a necessary component of the digestive system?

A

acid helps with protein digestion by converting pepsinogen to pepsin
promotes absorption of nonheme iron, vitamin B12, and meds such as ketoconazole and thyroxine
prevent bacterial overgrowth

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6
Q

parietal cell

A

main cell that makes acid

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7
Q

gastrin

A

main hormone produced by antral G cells to stimulate parietal cells to secrete acid

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8
Q

somatostatin

A

main inhibitor of acid secretion

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9
Q

vagus nerve/ Ach

A

main neurotransmitter that regulates acid secretion by modulating the secretion of gastrin, somatostatin and histamine

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10
Q

H+K+ATPase

A

final common pathway from acid secretion from all stimuli

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11
Q

how is H+ secreted

A

occurs in exchange for uptake of K+ ions to maintain neutral electric charge inside the cell
K+ in gastric juice exceeds plasma K+ 2-4 fold

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12
Q

main defenses against gastric ulcer

A

mucus secretion
bicarb secretion
pH gradient across epithelial surface into lumen

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13
Q

mucus secretion as a defense against acid

A

firm adherent viscous layer that covers the gastric surface
composed of 95% water and 5% cross linked mucin glycoproteins that are produced by MUC genes
prostaglandin secretion promotes mucus secretion

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14
Q

major causes of ulcers

A

H. pylori
NSAIDs
idiopathic
Zollinger Ellison

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15
Q

discuss H.pylori infections

A

majority of people have pangastritis involving both antral and fundic mucosa that lowers stomach defenses by reducing mucous protection
minority of patients have an antrum predominant gastritis which results in high gastric acid secretion (major mechanism of duodenal ulcer formation)

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16
Q

clinical presentation of ulcers

A

epigastric pain
periodicity (every 6-12 weeks)
some older patients may not develop ab pain and present with bleeding or perforation

17
Q

diagnosis of ulcers

A

EGD is procedure of choice for uncomplicated

CT scan is the diagnostic modality of choice for perforated ulcers

18
Q

special considerations about ulcer causes

A

type A personality is a risk factor
combo of steroids + NSAID increases risk 8 fold
HP proportion declining, but idiopathic is growing (20-30% in US are idiopathic)

19
Q

treatment of gastric ulcers

A

mainstay is medical management

20
Q

types of medical management for gastric ulcers

A

treat HP or remove offending NSAID agent
antacids only 67% effective
anti secretory agents to reduce acid production
mucosal protective agents

21
Q

types of anti secretory agents

A

H2 blockers

proton pump inhibitors

22
Q

types of mucosal protective agents

A

sucralfate
pepto bismol
misoprostol

23
Q

H2 blockers

A

competitive inhibitors of histamine stimulated acid secretion and markedly suppress acid secretion

24
Q

PPIs

A

inhibit H+K+ATPase
final common pathway
“big guns” for acid suppression
pro-drugs and must be activated by acid

25
Q

sucralfate

A

ulcer exposes positively charged proteins which can bind to the sulfate anions in sucralfate
covers the surface of the ulcer and prevents further damage

26
Q

pepto bismol

A

can form complexes with mucus to coat ulcers
also has activity against HP infection
turns stools black
colonic bacteria convert bismuth salts to bismuth sulfide that turns stool black

27
Q

misoprostol

A

PGE analog which can enhance mucosal defense mechanisms and also inhibit gastric secretion through inhibition of histamine stimulated cyclic AMP pathway

28
Q

refractory gastric ulcers

A

most heal within 8 weeks