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Pharmacology > GI Disorders 2: Gastric Acid Secretion > Flashcards

GI Disorders 2: Gastric Acid Secretion Flashcards

1
Q

Gastric Secretion

what is in gastric juice?

What are peptic ulcers?
What is GERD?

A
  • gastric juice includes proenzymes (prorennin, pepsinogen), HCl, intrinsic factor
  • disturbances in secretions - peptic ulcer, GERD

Peptic ulcers: open sores on inside lining of stomach and upper portion of SI
GERD: stomach acid frequently flows back into esophagus

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2
Q

Parietal cells

What do they do?
what do they express?

A
  • secrete isotonic solution of HCl

- expresses K+ proton ATPase which pumps protons (H+/K+ ATPase) into the stomach lumen for gastric juice

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3
Q

Stimulators of parietal cell acid output (3)

A
  • histamine
  • gastrin
  • acetylcholine
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4
Q

Inhibitors of parietal cell acid output (2)

A
  • prostaglandin E2/I2 (majority of cells in GI)
  • somatostatin (peptide secreted by D cells)
  • somatostatin not selective so it is not controlled
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5
Q

G cells

secrete?

A
  • in gastric antrum, secrete gastrin
  • gastrin releases CCK
  • stimulate parietal cells (and ECL cells)
  • this axis is dominant controlling mechanism of acid
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6
Q

Neuroendocrine cells (enterochromaffin like cells)

secrete?

A
  • secrete histamine which acts on parietal cells through H2 receptors to increase cAMP
  • stimulate acid output
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7
Q

Mucus-secreting cells

secrete? (2)
pH?

A
  • mucus-secreting cells are abundant in the gastric mucosa
  • create a gel-like protective barrier
  • secrete HCO3-
  • secrete mucin
  • maintains mucosal surface pH at 6-7
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8
Q

H. pylori

A
  • peptic ulcers
  • G- bacillus
  • chronic gastritis
  • inflamm induces G cells to secrete gastrin
  • increase risk of stomach cancer
  • therapy w/ antibiotics and reduce ulcer symptoms
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9
Q

Agents for treating peptic ulcers or GERD (3 general)

A
  • antisecretory agents
  • buffers
  • cytoprotectants (act on mucus layer)
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10
Q

Histamine H2 Receptor Antagonists

Name (ending)
efficacy compared to PPIs?

A
  • cimetidine, ranitidine, nizatidine, famotidine
  • can be IM/IV except famotidine
  • less efficacious than PPIs
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11
Q

Histamine H2 Receptor Antagonists

MOA?
decrease?
promote?

A
  • competitively ant. histamine actions
  • reduce parietal cell cAMP levels
  • used to inhibit acid secretion, reduce histamine and gastrin induced acid secretion
  • decrease basal and food stimulated acid secretion
  • promote healing of gastric duodenal ulcers
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12
Q

Histamine H2 Receptor Antagonists

AE (2 main)

A
  • rare AE
  • *gynecomastia, galactorrhea, decrease in sexual function in men (cimetidine only)
  • *thrombocytopenia (low platelet count) due to suppression of bone marrow
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13
Q

Proton Pump Inhibitors

Name (ending)

A
  • omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole
  • most potent for treating acid, directly act on pump
  • oral, can be injected
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14
Q

Proton Pump Inhibitors

MOA?
how long does this last?

A
  • weak base
  • accumulates in acid environment of canaliculi of parietal cell
  • binds to proton pump irreversible
  • reduce the amount of H+ pumped into stomach lumen
  • effect stays until new proton pumps are made
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15
Q

Proton Pump Inhibitors

AE (1)

A
  • well tolerated generally
  • *hypergastrinemia
  • not enough acid so G cells secrete more gastrin which can be cancerous
  • may mask symptoms of gastric cancer
  • not for pregnant/breastfeeding women, liver disease
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16
Q

Misoprostol

MOA (3)
receptor?

A
  • oral stable analogue of prostaglandin E1
  • acts directly on prostaglandin EP2/3 receptors on ECL cells to inhibit basal and food-induced gastric acid secretion
  • may contribute to maintenance of mucosal barrier
  • stimulates mucin (EP4 receptor) and bicarbonate (EP1/2 receptor)
  • promotes healing of ulcers
  • prevent gastric damage with chronic NSAID use
17
Q

Misoprostol

AE (1)

A
  • diarrhea - strong GI contractions
  • abdominal cramps
  • *uterine contractions - avoid in pregnancy
18
Q

Antacids

Types (2)

A
  • salts of magnesium or aluminum
  • MgOH2 - insoluble powder that forms MgCl2 in stomach
  • Al(OH)3 forms Al(Cl)3
19
Q

Antacids

MOA (2)

A
  • neutralize acid and inhibit activity of peptic enzymes

- healing of duodenal ulcers if given for a long enough time (less effective for gastric ulcers)

20
Q

Antacids

AE
difference b/w the 2?

A
  • mag salts are fast acting and cause diarrhea
  • al salts are slow acting and cause constipation
  • mixture of 2 preserve normal bowel function
  • poorly absorbed drugs and can chelate certain drugs
  • prescribed with simeticone (anti-foaming agent to relieve bloating)
21
Q

Drugs the protect mucosa

Name (2)

A 
Bismuth chelate (Pepto bismol)
- OTC for mild GI symptoms

Sucralfate

22
Q

Bismuth chelate

MOA (3)

A
  • toxic on bacillus, prevent H. pylori adherence to mucosa
  • forms protective barrier over ulcer and enhances prostaglandins, mucus, bicarbonate secretion
  • inhibit proteolytic enzymes
23
Q

Bismuth chelate

AE (3)

A
  • nausea, vomiting
    • blackening of tongue and feces as bismuth reacts with H2S to make bismuth sulfide
    • tinnitus
    • encephalopathy (Reye’s Syndrome) if renal excretion impaired (not for kids) - brain damage due to chelation
24
Q

Sucralfate

MOA

A
  • complex of al hydroxide and sulfated sucrose that forms a viscous paste in acidic media (releases aluminum)
  • binds positively charge proteins in ulcer forming a barrier for 6 hours to protect lining
  • reduces degradation of mucus via pepsin
  • stimulate secretion of mucus, bicarbonate, prostaglandins (unknown mech)
25
Q

Sucralfate

AE

A
  • minimal systemic

- rare constipation due to Al, toxicity

26
Q

Treatment of H. pylori infection

what kind of therapy?

A
  • rapid, long-term healing of ulcers
  • triple therapy with antibiotics to eradicate infection and a PPI to reduce symptoms
  • amoxicillin, metronidazole, clarithromycin, tetracycline
27
Q

What is the dominant mechanisms controlling acid secretion?

A

gastrin-ECL-parietal cell axis

G cells release gastrin which acts on CCK receptor of ECL cell and causes histamine release which binds to H2R on parietal cell causing H+ release

28
Q

What releases ACh?

Effect?

A

postganglionic cholinergic neruons release ACh

act on M3R of parietal cell to cause H+ release

29
Q

Somatostatin

where in the axis does it act?
effect?
secreted by?

A
  • act on SST2R receptors of G cells, ECL cells, parietal cells
  • inhibits H+ release
  • stomach D cells secrete somatostatin
30
Q

Why is there a risk of ulcer with NSAID use?

A
  • NSAID blocks AA in being formed to PGE2 which would normally act on EP2/3 receptor on ECL cells and downstream inhibit acid release of parietal cells.
  • overproduction of acid that can damage stomach

Pharmacology (12 decks)

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