Costanzo | Physiology | Chapter 9 | Gastrointestinal Physiology | Study Guide

Chapter 8: Gastrointestinal Physiology Notes

I. Structure and Innervation

  • Wall Structure: From the lumen outward: epithelium, lamina propria, muscularis mucosae, submucosa, circular muscle, longitudinal muscle, and serosa.

  • Enteric Nervous System (Intrinsic): Consists of two plexuses:

    • Submucosal (Meissner’s) plexus: Controls secretion and blood flow.

    • Myenteric (Auerbach’s) plexus: Controls motility.

  • Extrinsic Innervation:

    • Parasympathetic: Primarily via the vagus nerve (upper tract) and pelvic nerve (lower tract). Usually excitatory (ACh).

    • Sympathetic: Fibers from celiac, superior/inferior mesenteric, and hypogastric ganglia. Usually inhibitory (Norepinephrine).

II. Regulatory Substances

  • Hormones: Released into circulation by endocrine cells.

    • Gastrin: Secreted by G cells; stimulates gastric H+ secretion and growth of gastric mucosa.

    • CCK: Secreted by I cells; stimulates pancreatic enzyme secretion and gallbladder contraction; inhibits gastric emptying.

    • Secretin: Secreted by S cells; stimulates pancreatic HCO3−​ secretion to neutralize H+.

    • GIP: Secreted by K cells; stimulates insulin secretion and inhibits gastric H+ secretion.

  • Paracrines: Act locally (e.g., Somatostatin inhibits all GI hormones; Histamine stimulates H+).

  • Neurocrines: Released by neurons (e.g., VIP relaxes smooth muscle; GRP stimulates gastrin).

III. Motility

  • Slow Waves: Spontaneous oscillations in membrane potential; frequency is highest in the duodenum (12/min) and lowest in the stomach (3/min). They originate in the interstitial cells of Cajal (pacemaker).

  • Gastric Motility:

    • Receptive Relaxation: Vagovagal reflex allowing the orad stomach to expand; mediated by VIP.

    • Mixing/Digestion: Occurs in the caudad stomach via retropulsion.

  • Small Intestine: Segmentation (mixing) and Peristalsis (propulsion).

IV. Secretions

  • Salivary: Hypotonic; contains α-amylase (starch) and lingual lipase (fats).

  • Gastric (HCl): Produced by parietal cells. Stimulation involves ACh, gastrin, and histamine (potentiation). Inhibited by low pH and somatostatin.

  • Pancreatic: Contains HCO3−​ (aqueous component) and digestive enzymes (enzymatic component).

  • Bile: Produced by the liver, stored in the gallbladder; essential for emulsifying dietary fats.

V. Digestion and Absorption

  • Carbohydrates: Must be broken down to monosaccharides (glucose, galactose, fructose). Glucose/galactose use SGLT1 (Na+-dependent); fructose uses GLUT5 (facilitated diffusion).

  • Proteins: Absorbed as amino acids, dipeptides, or tripeptides.

  • Lipids: Require micelles for solubilization. After absorption, they are re-esterified and packaged into chylomicrons for lymph transport.

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Chapter 8 Study Guide

I. Glossary of Key Terms

  • Chylomicron: A lipoprotein particle that transports lipids from the intestine to the rest of the body via lymph.

  • Enterokinase (Enteropeptidase): A brush-border enzyme that activates trypsinogen to trypsin.

  • Incretin: A GI hormone (like GIP) that stimulates insulin secretion.

  • Micelle: A small aggregate of bile salts and lipids that facilitates fat absorption in the aqueous environment of the intestine.

  • Potentiation: When the combined effect of two stimulants is greater than the sum of their individual effects.

  • Retropulsion: The back-and-forth movement of chyme in the stomach to increase mixing and reduce particle size.

  • Steatorrhea: The presence of undigested fat in the stool, often due to bile acid or pancreatic lipase deficiency.

  • Vagovagal Reflex: A reflex where both afferent and efferent limbs are carried in the vagus nerve.

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II. 50 Question-and-Answer Quiz

  1. Which layer of the GI wall contains the myenteric plexus? Between circular and longitudinal muscle.

  2. Which division of the ANS is generally inhibitory to the GI tract? Sympathetic.

  3. What is the neurotransmitter for receptive relaxation? VIP.

  4. Which cells secrete gastrin? G cells.

  5. Where are I cells located? Duodenum and jejunum.

  6. What is the primary stimulus for secretin release? H+ in the duodenum.

  7. Which hormone stimulates insulin before blood glucose rises? GIP.

  8. What paracrine inhibits all GI hormone secretion? Somatostatin.

  9. Which enzyme begins starch digestion in the mouth? Salivary α-amylase.

  10. Where are the interstitial cells of Cajal located? Myenteric plexus.

  11. What is the slow wave frequency in the stomach? 3 waves/minute.

  12. What is the slow wave frequency in the duodenum? 12 waves/minute.

  13. Which reflex causes the urge to defecate? Rectosphincteric reflex.

  14. What is the "pacemaker" of the GI tract? Interstitial cells of Cajal.

  15. Which hormone causes gallbladder contraction? CCK.

  16. Which GI hormone family does GIP belong to? Secretin-glucagon family.

  17. What is the effect of secretin on gastric H+ secretion? Inhibitory.

  18. Which vitamin requires intrinsic factor for absorption? Vitamin B12​.

  19. Where is Vitamin B12​ absorbed? Ileum.

  20. Which cells produce HCl? Parietal cells.

  21. What are the three stimulants of HCl secretion? ACh, gastrin, and histamine.

  22. Which drug inhibits the H+-K+ ATPase? Omeprazole.

  23. What is the pH optimum for pancreatic lipase? 6.0.

  24. Which enzyme activates all other pancreatic proteases? Trypsin.

  25. What is the only essential component of gastric juice? Intrinsic factor.

  26. Which amino acids are the most potent stimuli for gastrin? Phenylalanine and tryptophan.

  27. What is the second messenger for histamine in parietal cells? cAMP.

  28. Which phase of HCl secretion is triggered by the smell of food? Cephalic phase.

  29. What percentage of HCl secretion occurs in the gastric phase? 60%.

  30. What is the primary bile acid precursor? Cholesterol.

  31. What converts primary bile acids to secondary bile acids? Intestinal bacteria.

  32. What is the major form of carbohydrate absorption? Monosaccharides.

  33. Which transporter moves glucose into cells via Na+ cotransport? SGLT1.

  34. How is fructose absorbed? Facilitated diffusion (GLUT5).

  35. What activates pepsinogen? Low gastric pH (H+).

  36. Which condition involves a gastrin-secreting tumor? Zollinger-Ellison syndrome.

  37. What is the byproduct of hemoglobin breakdown in the liver? Bilirubin.

  38. Which organ is the primary site for iron absorption? Small intestine.

  39. Where is the satiety center? Ventromedial nucleus of the hypothalamus.

  40. Which hormone increases appetite? Ghrelin.

  41. Which hormone decreases appetite and is made by fat cells? Leptin.

  42. What is the role of the Kupffer cells? Phagocytosis of bacteria in the liver.

  43. What happens to the pK of bile acids when they are conjugated? It decreases.

  44. What is the composition of saliva relative to plasma? Hypotonic.

  45. What is the major stimulus for the intestinal phase of pancreatic secretion? CCK.

  46. What does PYY do? Inhibits ghrelin and appetite.

  47. Which reflex causes relaxation of the orad stomach? Receptive relaxation.

  48. Which part of the esophagus is striated muscle? Upper one-third.

  49. What is the effect of vomiting on blood pH? Metabolic alkalosis.

  50. What causes the "clay-colored" stool in jaundice? Decreased fecal stercobilin.

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III. Short Answer Questions

  1. Explain the importance of the enterohepatic circulation of bile salts.

    • Answer: It allows 95% of bile salts to be reused by the liver, decreasing the need for new synthesis from cholesterol and ensuring high concentrations are available throughout the small intestine for fat digestion.

  2. Describe the mechanism of "potentiation" in gastric H+ secretion.

    • Answer: Potentiation occurs because ACh, gastrin, and histamine use different receptors and second messengers. Histamine potentiates the effects of ACh and gastrin, meaning blockers like cimetidine are more effective than expected because they also block the potentiated responses.

  3. Why does an oral glucose load stimulate more insulin than an intravenous one?

    • Answer: Oral glucose triggers the release of the GI hormone GIP (an incretin), which stimulates the pancreas to release insulin in addition to the direct effect of the glucose itself.

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IV. Essay Questions

  1. Discuss the integrated response of the GI tract to the arrival of a fatty meal in the duodenum.

    • Focus: Discuss I cells releasing CCK, which causes: (1) Gallbladder contraction/Sphincter of Oddi relaxation for bile; (2) Pancreatic enzyme secretion; (3) Inhibition of gastric emptying to allow time for digestion; and (4) The role of micelles in lipid absorption.

  2. Compare and contrast the digestion and absorption of carbohydrates and proteins.

    • Focus: Discuss that carbohydrates must be monosaccharides for absorption, whereas proteins can be amino acids, dipeptides, or tripeptides. Mention specific transporters like SGLT1 for glucose/galactose and H+-dependent cotransport for small peptides.

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