Digestive Secretions: Saliva, Gastric, Pancreatic, Biliary
Key stimuli, composition and regulation of the major GI secretions.
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Questions Covered in This Set
11 cards to master
How much fluid enters the GI lumen daily, and how much is lost in stool?
~7 L of secretions (1.5 L saliva, 2 L gastric, 1.5 L pancreatic, 0.5 L bile, 1.5 L intestinal) plus ~2 L ingested; only ~100 mL is lost in stool.
Explain the two-stage model of saliva formation.
Acinar cells produce isotonic plasma-like fluid; duct cells reabsorb Na⁺ and Cl⁻ and secrete K⁺ and HCO₃⁻ but are water-impermeable, so final saliva is hypotonic, high in K⁺ and HCO₃⁻.
Why does saliva become more plasma-like at high flow rates?
There is less contact time for ductal modification, so less Na⁺/Cl⁻ reabsorption occurs — saliva is closer to isotonic (with still-high HCO₃⁻ from stimulated secretion).
How is salivary secretion regulated?
Almost purely neural with no important hormonal control, and BOTH autonomic limbs stimulate: parasympathetic (M3, IP₃/Ca²⁺, CN VII & IX) gives copious watery saliva; sympathetic (β-adrenergic, cAMP) gives scant thick protein-rich saliva.
Name the cell types of the oxyntic and antral gastric mucosa and their products.
Oxyntic: parietal (HCl + intrinsic factor), chief (pepsinogen), ECL (histamine), mucous neck cells. Antrum: G cells (gastrin), D cells (somatostatin).
Describe the parietal cell acid-secreting mechanism and the alkaline tide.
CO₂ + H₂O → (carbonic anhydrase) H⁺ + HCO₃⁻; H⁺/K⁺-ATPase pumps H⁺ into the canaliculus for K⁺; HCO₃⁻ exits basolaterally via Cl⁻/HCO₃⁻ exchange, alkalinising gastric venous blood and post-prandial urine.
What are the three stimuli of the parietal cell and their receptors/second messengers?
ACh (M3, Ca²⁺), gastrin (CCK-B, Ca²⁺), histamine (H2, Gs→cAMP). Histamine is the final common amplifier since ACh and gastrin also drive ECL cells.
Why are PPIs stronger than H2 blockers?
H2 blockers (ranitidine, famotidine) remove the histamine amplification of all stimuli, but PPIs (omeprazole) covalently inhibit the H⁺/K⁺-ATPase itself — the final effector.
How does somatostatin provide negative feedback on acid?
When antral pH falls below ~3, D cells release somatostatin, which inhibits gastrin and parietal cell acid secretion; secretin, GIP and prostaglandins also inhibit.
Contrast H. pylori and NSAID ulcer mechanisms.
H. pylori antral infection destroys D cells → less somatostatin → hypergastrinaemia → duodenal ulcer. NSAIDs block prostaglandin-driven mucus/bicarbonate defence → gastric ulcer.
List the three phases of gastric secretion with their contributions.
Cephalic ~30% (sight/smell/taste/chewing → vagus, abolished by vagotomy); gastric ~60% (distension, vagovagal & local reflexes, peptides/amino acids on G cells); intestinal ~10% (briefly stimulatory then inhibitory via secretin, CCK, enterogastrones).
