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G.I & Nutrition > Physiology of Gastric Acid Secretion and Acid Peptic Disorder/Peptic Ulcer Disease > Flashcards

Physiology of Gastric Acid Secretion and Acid Peptic Disorder/Peptic Ulcer Disease Flashcards

1
Q

Does not being able to make acid in the stomach affect quality of life?

A

Not as much in developed world b/c food is free of most organisms

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2
Q

What product is produced by the cell? Parietal cells

A

acid and intrinsic factor

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3
Q

What product is produced by the cell? G-cells (antrum)

A

gastrin

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4
Q

What product is produced by the cell? D-cells

A

somatostatin

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5
Q

What product is produced by the cell? ECL cells (enterochromaffin-like cells)

A

histamine

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6
Q

What product is produced by the cell? Chief cells

A

pepsinogen

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7
Q

What product is produced by the cell? surface epithelial cells

A

mucus and bicarbonate

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8
Q

What product is produced by the cell? mucus neck cells

A

mucus and bicarbonate

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9
Q

On which surface of the parietal cell do signals result in second messenger activation?

A

basal surface

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10
Q

What is the final step in acid production at the level of the parietal cell?

A

proton pump on lumenal side of parietal cell

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11
Q

What inhibitory signals act on parietal cells?

A

somatostatin and prostaglandin E (Gi)

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12
Q

What excitatory signals act on parietal cells?

A
  1. vagus nerve acetylcholine works on ECL cells to produce histamine that acts on H2 receptors on the parietal cell (Gs)
  2. vagal acetylcholine acts directly on the parietal cell
  3. gastrin acts on ECL cells to produce histamine that acts on H2 receptors on the parietal cell (Gs)
  4. gastrin acts directly on the parietal cell
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13
Q

What two second messenger signaling pathways work within the parietal cell?

A

cAMP (histamine signal) and IP 3(gastrin and vagal signals)

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14
Q

Parietal cellular target for: atropine

A

vagal nerve stimulus

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15
Q

Parietal cellular target for: H2 receptor antagonists

A

H2 receptor

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16
Q

Parietal cellular target for: proglumide

A

gastrin recepptor

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17
Q

Parietal cellular target for: PPI

A

H+/K+ Atpase (proton pump)

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18
Q

What is the minor component of acid production stimulus?

A

neurocrine stimulus (seeing food/smelling food) –> 10-15% of acid production

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19
Q

Major pathway for acid production?

A

consumption of food –> distention of stomach –> inhibits somatostatin production –> allows gastrin dominance on acid secretion

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20
Q

How does acid production get shut off in stomach?

A

As stomach pH drops, D cells get switched on –> drives inhibition of gastrin and ECL production

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21
Q

How is the pH at the lining of the stomach maintained at 7?

A

bicarbonate secretion around mucus layer protects against back/auto-digestion of stomach

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22
Q

How does acid peptic disease occur if there is mucosal protection of stomach?

A

If the pH drops low enough, pepsinogen turns into pepsin which can autodigest the stomach

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23
Q

5 protective features that prevent autodigestion of the stomach

A
  1. thick mucus layer, 2. pH gradient, 3. bicarbonate secretion, 4. good mucosal blood flow to support epithelial growth, 5. prostaglandin production (COX 1 and 2)
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24
Q

What prostaglandin is constitutively expressed?

A

COX1

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25
Q

What prostaglandin is induced by inflammation?

A

COX2

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26
Q

Why do NSAIDs reduce mucosal cytoprotection and what is the consequence?

A

They block both COX1 and COX2 and can result in peptic ulcer disease

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27
Q

Aggressive factors in PUD (3)

A

acid, pepsin, bile salt

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28
Q

“no acid, no ulcer”

A

cannot have ulcers without acid –> may otherwise have atrophic gastritis

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29
Q

Effect of NSAIDs on the stomach

A

local caustic effect + COX inhibition

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30
Q

The major cause of gastric cancer

A

H pylori –> decreased mucosal protection and increased acid output

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31
Q

Two types of ulcers

A

duodenal and gastric ulcers

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32
Q

What kind of ulcer? pinpoint, epigastric burning pain

A

duodenal ulcer

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33
Q

What kind of ulcer? 1-3 hours after meals, empty stomach, relieved by foods or antacids

A

duodenal ulcer

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34
Q

What kind of ulcer? nausea, vomiting, diffuse epigastric pain, weight loss

A

gastric ulcer

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35
Q

What kind of ulcer? onset immediately after meals, aggravated by food

A

gastric ulcer

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36
Q

What kind of ulcer? location at the duodenal bulb

A

duodenal ulcer

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37
Q

What kind of ulcer? location at the antrum

A

gastric ulcer

38
Q

What kind of ulcer? normal/high gastric acid production

A

duodenal ulcer

39
Q

What kind of ulcer? normal/low gastric acid production

A

gastric ulcer

40
Q

Uncomplicated ulcers are increasing/decreasing in incidence/prevalence

A

decreasing in us b/c of PPIs and histamin antagonist use, disappearance of H. pylori, judicious use of NSAIDs and introduction of coxibs/selectives, better management of ICU patients

41
Q

Bleeding ulcers are increasing/decreasing in incidence/prevalence

A

prevalence is unchanged resulting in increasing proportion overall

42
Q

Etiologies of PUD that reduce mucosal defense (2)

A

Aspirin/NSAIDs and H pylori gastritis

43
Q

Etiologies of PUD that increase acid/pepsin (2)

A

H pylori gastritis and hypersecretory states

44
Q

Zollinger Ellison Syndrome

A

non-beta islet cell tumor that hypersecretes gastric acid w/the loss of paracrine somatostatin secretion leading to fulminant PUD

45
Q

Pathophysiology of ZES

A

tumor produces gastrin –> blood stream –> drives ECL and stomach to make acid/histamine –> reduce pH –> switch on D cells locally but no paracrine function of somatostatin –> no feedback inhibition

46
Q

Can a local somatostatin analog turn off hypersecretion of acid?

A

No –> need a systemic one like octreotide

47
Q

Hallmark of ZES and diagnostic criteria

A

hypergastrinemia –> elevated acid output AND serum gastrin (these measurements have no value on their own; they have to exist together)

48
Q

What is appropriate hypergastrinemia?

A

There are no parietal cells –> pH increases –> somatostatin switches off –> gastrin goes sky high to try to make acid –> hypergastrinemia without hyperacidemia (e.g. atrophic gastritis)

49
Q

Diff Dx of appropriate hypergastrinemia

A

drugs (H2RA and PPI), atrophic gastritis, H. pylori pangastritis, chronic renal failure, vagotomy

50
Q

Diff Dx of inappropriate hypergastrinemia

A

ZES (sporadic or MEN1), retained antrum syndrome, antral predonominant H.pylori infection with G cell hyperplasia, massive intestinal resection (temporary), gastric outlet obstruction (reversible)

51
Q

Genetics of MEN1

A

two hit Rb hypothesis + autosomal dominant –> cloning of 11q13 resulting in increased Menin

52
Q

Clinical presentations of MEN1

A

parathryoid hyperplasia (early), pituitary adenomas, entero-pancreatic tumors +/- lipomas, adrenal hyperplasia, etc.

53
Q

BAO

A

how much basal acid do you make in an hour –> calculated by titration –> concentration is irrelevant, absolute amount is key

54
Q

MAO

A

maximal acid output or BAO after pentagastrin stimulation

55
Q

PAO

A

peak acid output –> alternate measure of stimulated acid secretion

56
Q

Control acid output

A

BAO in the presence of therapy (efficacy of Rx)

57
Q

Two processes in ZES

A

hormonal syndrome due to uncontrolled gastrin release + enteropancreatic neuroendocrine tumor with a potential for neoplastic growth

58
Q

Features of patient with ZES

A

duodenal ulcer (multiple or recurrent) w/ acid hypersecretion leading to diarrhea + not on NSAIDs + no H. pylori +/- MEN1

59
Q

Clinical presentation of ZES

A

abdominal pain, diarrhea, heartburn, initial perforation

60
Q

Idiopathic hypersecretion gastric analysis

A

BAO and MAO increased, increased parietal cell mass, increased meal-stimulated acid output, increased 24 hour secretory profile

61
Q

Acid response in duodenal ulcers

A

higher basal acid and higher meal-stimulated acid too

62
Q

4 possible causes for gastric hypersecretion in duodenal ulcers

A
  1. increased parietal cell sensitivity to gastrin secretagogues
  2. basal or meal-stimulated hypergastrinemia
  3. abnormality of inhibition (e.g. somatostatin deficiency)
  4. decreased bicarbonate secretion
    * usually always due to H. pylori
63
Q

How does H pylori affect the gut

A

secreates urease to neutralize local pH via production of ammonium –> attaches to host epithelium –> gastric acid secretion modified to permit maximal survival and induces inflammation to permit nutrition

  • non invasively evades host immune response
64
Q

Cohort effect

A

there is higher transmission of bugs like H pylori within an age cohort –> that group of people eventually age out of the population together –> leads to multimodal distribution of infection across the population

65
Q

H. pylori mode of transmission

A

person-to person

66
Q

Function of flagellae and spiral morphology of H pylori

A

penetration of mucus layer

67
Q

Does H pylori invade the mucosa

A

no

68
Q

3 ways H pylori affect acid secretion

A

antral predominant infection, asymptomatic chronic infection, pangastritis (with GU, cancer, lymphoma)

69
Q

The gastrin hypothesis

A

antral H pylori infection inhibits somatostatin production leading to unopposed gastrin release –> basal and meal hypergastrinemia lead to inappropriate hypersecretion of gastric acid –> consequent duodenal gastric metaplasia permits colonization in duodenal bulb –> local defenses are undermined + acid hypersecretion results in duodenal ulceration

70
Q

What is the spectrum of H. pylori infection?

A 
basically anything:
chronic gastritis
duodenal ulcers (90%)
gastric ulcers (70%)
gastric metaplasia/dysplasia/cancer
maltoma
non-ulcer dyspepsia
71
Q

T/F all H pylori sequelae begin with an acute infection

A

T –> acute infection followed by superficial gastritis is the starting point for any hyper or hypo secretory state

72
Q

H pylori pangastritis features

A

Hyposecretory state with chronic atrophic gastritis (leading to gastric ulcers or cancers) or lymphocytic predominance leading to maltomas

73
Q

H pylori antral predominance features

A

Hypersecretory state with propensity for duodenal ulcers

74
Q

Are distal or proximal stomach cancers associated with H. pylori?

A

both are but distal corpus/antral cancers are more associated than cardia/GEJ cancers

75
Q

Host factors in H. pylori that lead to increased pathogenicity

A

of lymphocytes, macrophages, PMNs, quantity of IL1, IL8, TNFalpha, genetic HLA loci, hypergastrinemia

76
Q

Bacterial factors in H. pylori that lead to increased pathogenicity

A

virulence factors: Vac A, Cag A, Ice A, etc.

77
Q

Environmental factors in H. pylori that lead to increased pathogenicity

A

nitroso compounds, salt, smoking, vitamin C

78
Q

CagA

A

gene that forms a pathogenicity island present in 50-60% of all Hpylori isolates –> marker of virulence –> CagA+ organisms are associated with increased cytokine release and increased inflammation and are closely related to gastric cancer

79
Q

IL polymorphism

A

IL1beta polymorphisms are proinflammatory run in families

80
Q

Are H pylori present once gastric atrophy turns to metaplasia –> dysplasia –> cancer?

A

no –> they are gone at this point

81
Q

Corpus gastritis

A

precursor to hypochlohydria and gastric atrophy (along the timeline to cancer) and results from Hpylori gastritis, proinflammatory phenotype, and CagA+ features

82
Q

What are the effects of NSAIDs on the GI system?

A

topical effects that are direct/indirect and cause GI erosions + systemic PG inhibition/antiplatelet effects

83
Q

What is the function of constitutive Cox1 on the GI system?

A

protection of gastric mucosa and hemostasis

84
Q

What is the function of inducible Cox2 on the GI system?

A

mediate inflammation/gastritis

85
Q

What Cox system does H pylori infection upregulate?

A

Cox2 inflammation

86
Q

What kind of Cox would the ideal NSAID inhibit?

A

Cox2

87
Q

In the absence of a Cox2 selective inhibitor, how can you prevent ulceration in NSAID-using patients?

A

use omeprazole or misoprostol (PPI or synthetic prostaglandins) to restore prostglandins that are missing due to Cox 1/2 dual inhibition

88
Q

Does H pylori affect Cox1?

A

not really

89
Q

T/F NSAIDS and H. pylori together increase the risk of ulcers

A

yes –> additive effect

90
Q

Curling’s ulcers are due to ___

A

burns

91
Q

Cushing’s ulcers are due to ____

A

head injury

92
Q

dyspepsia

A

ulcer like pain in the absence of ulcers: GERD, gallstones, pancreatitis, pneumonia, PE, MI, AAA

G.I & Nutrition (43 decks)

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