Pharmacology - gastric secretion Flashcards

moa of K+ pump inhibitors moa of histamine receptor antagonists what happens to ga secretion antacids? how buffering occurs misoprostol NSAID-induced gastric ulcers (16 cards)

1
Q

gastric secretions of the gastric pit

mucus cells secrete x
parietal cells secrete x
ECN-like cells secrete x
G cells secrete x
D cells secrete x
Chief cells secrete x

gastric pit + gastric gland

these all promote the secretion of HCl, gastric acid

A

mucus + bicarbonate
HCl
Histamine
Gastrin
Somatostatin
pepsinogen

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2
Q

the proton pump involves which 2 ions? moa? function?

responsible for secreting HCl into the stomach

A

H+/K+ ATPase

  • The H⁺/K⁺-ATPase (proton pump) actively pumps H⁺ out into the stomach lumen.
  • At the same time, K⁺ is pumped back into the parietal cell.
  • Cl⁻ Also Moves into the Stomach
  • Cl⁻ follows H⁺ into the stomach through Cl⁻ channels.This combines with H⁺ to form HCl (hydrochloric acid).
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3
Q

Regulation of the Proton Pump (What Stimulates It?)

3 main stimulators

A

✅ Gastrin → Released from G cells (acts on CCKB receptors).
✅ Histamine → Released from enterochromaffin-like (ECL) cells (acts on H₂ receptors).
✅ Acetylcholine (ACh) → From vagus nerve (acts on M3 receptors).

🔹 These three increase cAMP or Ca²⁺ inside parietal cells → Activates the proton pump → More acid secretion.

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4
Q

Proton Pump Inhibitors (PPIs) examples + INDICATIONS

A

Omeprazole, Pantoprazole

bind irreversibly to H⁺/K⁺-ATPase, preventing H⁺ secretion.

INDICATIONS:
- GERD
- pepti ulcers

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5
Q

Histamine in response to xx is secreted by the xxx cells, binds to xx receptors, activating xxx, increasing xxx, to increase the number of xx, increasing/decreasing gastric acid secretion from yy cells

A

ACh
enterochromaffin like cells
H2 receptors in the GI
adenylyl cyclase
cAMP
proton pumps
INCREASING
parietal cells

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6
Q

describe the action of ACh, and its impact on gastric acid secretion from parietal cells

A

ACh released from parasympathetic neurons
- binds to M3 ACh receptors
- activates PLC
- increases intra Ca2+
- increase number of proton pumps

INCREASES gastric acid secretion from parietal cells

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7
Q

describe the action of gastrin and its effect on gastric acid secretion

released by:
binding to:
activating:
increasing number of :
effect on gastric acid secretion from parietal cells? :

A

released by: G cells
binding to: CCK2 receptors
activating: PLC
increasing number of : proton pumps
effect on gastric acid secretion from parietal cells? : INCREASE

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8
Q

describe the action of SOMATOSTATIN and its effect on gastric acid secretion

A

released by: D cells
binding to: SST2R receptors
activating: DECREASING cAMP
increasing number of :
effect on gastric acid secretion from parietal cells? : DECREASING

**HOW DOES THIS WORK:
** - binding to SST2R receptors on enterochromaffin cells results in REDUCED HISTAMINE RELEASE + decreased acid secretion from the parietal cells —–> paracrine control

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9
Q

NSAIDs
- examples (reversible, irreversible, non-selective, selective)
- indications
-side effects

A

⚠️ Side Effects:

  1. Gastric ulcers, bleeding (due to COX-1 inhibition → less protective mucus in stomach).
  2. Renal injury (less prostaglandins → reduced kidney blood flow).
  3. Increased cardiovascular risk (except for aspirin, which reduces platelet aggregation).

2️⃣ Selective COX-2 Inhibitors (Lower GI Side Effects)
These selectively block COX-2, reducing inflammation without inhibiting stomach-protective COX-1.

1️⃣ Non-Selective COX Inhibitors (Block COX-1 & COX-2)
These inhibit both COX-1 (which protects the stomach & kidneys) and COX-2 (which causes inflammation & pain).

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10
Q

Class + Indication + MOA + side effects of
- paracetamol
- clopidogrel
- misoprostol
- cimetidine
- omeprazole
- gaviscon
- ibuprofen

A
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11
Q

effect of NSAIDs on gastric acid secretion + how is this mediated

A

promote HCl secretion

inhibit COX1, reducing prostaglandins

reduced prostaglandins LEADS TO –> histamine secretion from enterochromaffin cells

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12
Q

cox 2 relates to

A

Function: Produces prostaglandins that mediate inflammation, pain, and fever.

but increase cardiovascular risk (by reducing PGI2, which normally prevents clotting).

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13
Q

cox1 relates to

A

protect the stomach lining, regulate kidney function, and maintain platelet function.
🔹 Prostaglandins Produced:

PGE2, PGI2 (Prostacyclin) → Protects gastric mucosa.
Thromboxane A₂ (TXA2) → Promotes platelet aggregation (clotting).aglandins, protective function

– Inhibitory effects by eg NSAIDs, decrease prostaglandins, promoting HCl secretion, SIDE EFFECTS OF: gastric ulcers + blood in stool

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14
Q

PPI example + moa+ indications + side effects

A

Omeprazole
irreversibly inhibtis H+/K+ ATPase pump
reduces HCl secretion

INDICATION: benign gastric aicd ulceration ++ GERD

side effects: increased stomach pH reduces defences agaisnt infection via the GI tract

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15
Q

H2 receptor antagonist - example, moa, indications

A

Cimetidine
block H2 receptor –> reduces Hcl secretion
indication : gastric acid ulceration + NSAID associted gastric ulceration

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