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GIR Test 2 > B5-032 Gastric Ulcer > Flashcards

B5-032 Gastric Ulcer Flashcards

1
Q

main hormone produced by antral cells to stimulate parietal cells to produce acid

A

gastrin

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2
Q

main inhibitor of gastric acid secretion

A

somatostatin

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3
Q

main neurotransmitter secreted by vagus nerve to regulate acid secretion

A

ACh

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4
Q

promotes mucus secretion

A

prostaglandin

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5
Q

main risk factors for ulcers

2

A

H. pylori
NSAIDs

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6
Q

how does H. pylori cause ulcers in a majority of cases?

A

pangastritis of antral and fundic mucosa, causing reduced mucous production

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7
Q

how does H. pylori cause duodenal ulcers in a minority of patients?

A

causes antrum predominant gastritis which results in high gastric acid secretion

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8
Q

describe the characteristics of H. pylori bacterium

gram stain, shape, etc.

A

gram negative
helical rod shape
flagellae

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9
Q

major characteristics of peptic ulcer disease

A

periodic epigastric pain

(may be relieved with food or antacids)

pain occuring every 6-12 weeks, if on NSAIDs may have no pain

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10
Q

imaging modality of choice to diagnose peptic ulcer disease

A

EGD

CT if perforated

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11
Q

risk factors for peptic ulcer disease

4

A
  • Type A personality
  • steroids
  • NSAIDs
  • Zollinger Ellison
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12
Q

mucosal protective agents

3

A
  • sucralfate
  • pepto-bismol
  • misprostrol
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13
Q

identify the image

A

gastric ulcer

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14
Q

how might an ulcer present in an older person?

A

bleeding/perforation symptoms without preceding pain

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15
Q

what is the diagnostic modality of choice when perforated ulcer is suspected?

A

CT scan

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16
Q

what symptoms may lead you to suspect perforation?

A

severe abdominal pain
abdominal wall rigidity

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17
Q

what country has a highest incidence of H. pylori?

A

China

Hong Kong specifically, may be relevant to patient’s hx

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18
Q

how does H. pylori cause ulcers?

A
  • causes inflammation
  • activates T cells
  • chronic cellular damage
  • worsened by acid
  • H. pylori proteins channel into gastric epithelial cells
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19
Q

how do NSAIDs cause ulcers?

A
  • block COX-1 from synthesizing prostaglandings
  • decrease mucous barrier
  • worsened by acid
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20
Q

which form of gastritis is more likely to cause an ulcer in the stomach and not the duodenum?

A

pangastritis

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21
Q

what kinds of cells are in the gastric antrum?

4

A
  • G cells
  • D cells
  • mucous neck cells
  • surface mucous cells
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22
Q

why does antral gastritis cause duodenal ulcers?

A

decreased somatostatin causes increased gastric acid –> duodenal ulcer

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23
Q

H. pylori attaches to receptors called […] in the gastric mucosa

A

Lewis antigens

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24
Q

does H pylori invade gastric cells?

A

no

attaches to lewis antigen receptors

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25
Q

genes within this island form a special apparatus to transport bacterial product inside the host cell

A

cag pathogenicity island

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26
Q

treatment of H. pylori peptic ulcer disease

3 things

A
  • remove offending agent
  • acid suppression
  • mucosal protective agent
27
Q

why is ischemia of the stomach rarely seen?

A

heavily vascularized

28
Q

descibe the neural pathway of acid secretion

A

ACh from gastric enteric neurons -> M3 receptors -> intracellular Ca+ -> H+

29
Q

descibe the hormonal pathway of acid secretion

A

Gastrin from antral G cells -> CCK2 receptors -> intracellular Ca+ -> H+

30
Q

describe the paracrine pathway of acid secretion

A

histamine released from oxyntic ECL cells -> H2 receptors -> cAMP pathway

inhibited by somatostatin

31
Q

inhibits the paracrine pathway of gastric acid secretion

A

somatostatin

32
Q

how do PPIs block the proton pump?

A

sulfenamide binds to cysteine in HKATPase

33
Q

what is the duration of treatment for ulcers?

A

12 or more weeks

34
Q

how do you establish a refractory ulcer?

A
  • ensure patient has stopped NSAIDs
  • ensure H. pylori is cleared
  • ensure patient has been compliant with treatment
  • counsel about smoking
35
Q

how do gastrinomas cause ulcers?

A

increased gastrin -> increased gastric acid

36
Q

how does systemic mastocytosis cause ulcers?

A

excessive histamine –> increased gastric acid production

37
Q

oncologic gastric ulcers

3

A
  • MALT lymphoma
  • gastric adenocarcinoma
  • metastatic disease (breast cancer)
38
Q

symptoms of systemic mastocytosis

associated with gastric ulcers

A

pruritis, flushing, syncope, nausea, vomiting, diarrhea, fibromyalgia

39
Q

symptoms of Churg-Strauss

associated with gastric ulcers

A

eosinophilia, asthma, peripheral neuropathy, palpable purpura

40
Q

options of surgical treatment of gastric ulcers

rare but happens, 3

A
  • vagotomy
  • antrectomy
  • subtotal gastrectomy (both body and antrum)

or combination of above

41
Q

what is the main inhibitory method against acid secretion?

A

somatostatin

42
Q

H. pylori can lead to gastric ulcer in some, but duodenal ulcer in others. Why?

A

depends on if H. pylori infects the entire stomach or just the antrum

43
Q

how do NSAIDs cause gastric ulcers?

A

decreased mucous production by inhibiting COX-1 with reduced prostaglandin secretion

44
Q

what will happen when a tumor starts producing excess gastrin?

A
  • the basal and maximal acid output is increased because parietal cells secrete more acid
  • ulcers will develop in unusual locations
45
Q

primary gastric cells that secrete acid

A

parietal cells

46
Q

neurogenic control of acid secretion

A

vagus via ACh

47
Q

primary gastric cells that secrete gastrin

A

G cell in antrum

48
Q

primary cells that secrete somatostatin

A

D cells

49
Q

primary gastric cells that secrete pepsin

A

chief cells

50
Q

primary gastric cells to secrete histamine

A

ECLs

51
Q

final common pathway to secrete acid

A

H+K+ATPase

52
Q

indomethacin is an NSAID, which blocks

A

COX-1

53
Q

COX-1 inhibitors cause

A

decreased production of prostaglandins

54
Q

multiple, recurrent ulcers in unsual locations

A

gastrinoma

55
Q

a serum gastrin level can help rule in/out

2

A

gastrinoma
Zollinger Eillison

56
Q

what can be measure to determine if a patient is unknowingly taking NSAIDs?

A

serum salicylate

57
Q

older people who take NSAIDs can develop complications of ulcer disease without

A

prior symptoms

58
Q

side effect of Pepto Bismol

A

black stools

59
Q

enzymes responsible for production of prostaglandins in the stomach

A

COX 1 & 2

60
Q

constitutively expressed in the stomach and helps in the production of mucus and maintaining the integrity of the gastric mucosa

A

COX-1

61
Q

surgery that will remove gastrin producing antral G cells

A

distal gastrectomy

62
Q

surgery to decrease the parietal cell mass but with leaves the antrum intact

A

proximal gastrectomy

acid secretion will continue

63
Q

what two surgical options significantly decrease acid production?

A
  • vagotomy
  • distal gastrectomy

GIR Test 2 (18 decks)

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