Gastric Acid Secretion – Regulation & Output

Gastric Acid Secretion – Regulation & Output


GASTRIC ACID SECRETION – REGULATION & OUTPUT

  • Gastric acid – Secreted by gastric glands in gastric mucosa.

GASTRIC GLANDS IN STOMACH:

1. In pyloric & cardiac regions:

  • Gastric glands are “Mucous” type.
  • Secrete only mucous & HCO3.
  • In pylorus referred “Mucus-secreting pylorus gland”.
  • Contains less parietal & chief cells.

2. In body & fundus regions:

  • Glands contain secretory cells.

Cell types:

2a. Parietal/Oxyntic cells –

  • Secrete hydrochloric acid (HCl) & Intrinsic factor of castle.

2b. Chief/Zymogen/Peptic cells –

  • Secrete pepsinogen.

2c. G cells –

  • Secretes Gastrin.

2d. Delta (D) cells –

  • Secretes Somatostatin.

2e. Entero-chromaffin like (ECL) cells –

  • Secretes Histamine.

COMPOSITION OF GASTRIC ACID:

  • In human – 2.5 L (105ml/hr) gastric juice secreted daily.
  • Gastric acid pH is less than 3 (usually 1-2).

Important constituents:

  • HCl (H+ & Cl).
  • Anions (HPO4-2 & SO4+2).
  • Cations (Na2+, K+, & Mg2+).
  • Pepsinogen & Pepsin.
  • Mucus.
  • Lipase.
  • Intrinsic factor of castle.

REGULATION OF ACID SECRETION:

  • Gastric acid secreted by parietal cell activation in gastric mucosa.

1. ACTIVATORS FOR ACID SECRETION: 

  • Mainly Histamine – H2 receptors.
  • Acetylcholine (M3 receptor).
  • Gastrin.

Mechanism:

Ach & gastrin acts indirectly.

  • By releasing histamine.
  • Also by stimulating H+-K+-ATPase (proton pump).

Vagal (Parasympathetic) stimulation –

  • Increases acid secretion.
  • Through acetylcholine.

Clinical application:

Proton Pump/H+ inhibitors:

  • By blocking H+ receptors/inhibiting proton pump –> Blocking acid secretion.

Anti-muscarinic drugs:

  • Blocks muscarinic receptors.
  • Ex: Pirenzepine.

2. INHIBITORS OF ACID SECRETION:

  • Somatostatin –.
  • By directly inhibiting parietal cells & gastrin secretion
  • Secretin
  • Cholecystokinin (CCK).
  • GIP & VIP –  
  • Inhibit gastric secretion by stimulating somatostatin release.

PGE2 –

  • By inhibiting parietal cells & gastrin release.
  • Best established inhibitor – Low pH (Acid itself).
  • Stomach & duodenal acidification inhibits acid secretion.
  • By inhibiting gastrin release from G cells.

CONDITIONS:

1. Increased gastric acid secretion:

  • In duodenal ulcer.
  • Gastric ulcer.
  • ZES.

2. Reduced gastric acid secretion:

  • After vagotomy.
  • In Pernicious anemia.

GASTRIC ACID OUTPUT:

  • Measurement of gastric acid output – Clinical importance.
  • Two important parameters – 

1. Basal Acid Output (BAO) –

  • Rate of acid secretion in absence of any stimulations.
  • Normal BAO – < 10 (2 – 5) mmol/hr.

2. Maximal Acid Output (MAO)/Total Acid Output –

  • Rate of acid secretion produced by stimulants like histamine/ pentagastrin.
  • Normal MAO – < 50 mmol/hr.
  • Values reflects total parietal cell population in stomach.
  • Hence, referred Parietal cell mass”.
Exam Question
 

GASTRIC ACID SECRETION – REGULATION & OUTPUT

  • Parietal/Oxyntic cells secrete Hydrochloric acid (HCl) & Intrinsic factor of castle.
  • Chief/Zymogen/Peptic cells secretes pepsinogen.
  • Delta (D) cells secrete Somatostatin.
  • Pylorus contains “mucus-secreting pylorus gland”.
  • In human – 2.5 L (105ml/hr) gastric juice secreted daily.
  • Important cationic constituents in acid – Na2+, K+, & Mg2+.
  • Main activators of acid secretion are mainly Histamine (H2 receptors), Acetylcholine (M3 receptor) & Gastrin.
  • Vagal (Parasympathetic) stimulation increases acid secretion through acetylcholine.
  • Proton Pump/H+ inhibitors act by blocking H+ receptors.
  • Inhibitors of acid secretion are Somatostatin, Secretin, Cholecystokinin (CCK), GIP & VIP.
  • Best established inhibitor of acid secretion is “Low pH” (Acid itself).
  • Normal BAO – < 10 (2 – 5) mmol/hr.
  • Maximal Acid Output (MAO)/Total Acid Output values reflect total parietal cell population in the stomach, hence referred “Parietal cell mass”
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