Digestive System Lecture: From Pharynx to Small Intestine

Context & Big Picture

• Continuation of the digestion unit (reproduction lecture is longer but digestion covers more ground).
• Material covered today: mouth ➜ pharynx ➜ esophagus ➜ stomach ➜ beginning of small intestine (duodenum/jejunum/ileum)
• Constant theme: structure dictates function (epithelial types, muscle layers, folds, sphincters).
• Practical/clinical threads woven throughout: choking/Heimlich, hiatal hernia, reflux (GERD), proton-pump inhibitors (PPIs), ulcers, alcohol absorption.
• Evolutionary aside: many animals separate food & air passages (e.g., fish Gill system) – humans share a single pharyngeal pathway, predisposing us to choking.

Pharynx ("common hallway")

• Shared conduit for BOTH digestion & respiration.
  • Transports food, liquids, air ➜ evolutionary cost = choking risk.
• Lined by stratified squamous epithelium (abrasion-resistant, rapidly sloughed/replaced).
• Pharyngeal skeletal muscles facilitate swallowing.
  • Swallowing starts voluntarily, transitions to involuntary (reflexive) control.
• Minimal chemical digestion here; mainly a passageway.

Esophagus

• Muscular tube posterior to cricoid cartilage; descends in mediastinum.
• Propulsive movement: peristalsis pushes bolus toward stomach.
• Passes through diaphragm at the esophageal hiatus (other two hiatuses = aortic & caval for aorta & IVC).
• Topography under diaphragm visualised as three apertures (aorta, IVC, esophagus).
• Swallowing sequence
  • Bolus ➜ oropharynx ➜ esophagus (UES relaxes).
  • Epiglottis folds over glottis to protect trachea.
  • Primary peristaltic wave begins.
• Lower esophageal “sphincter” (LES)
  • Physiologic, not anatomical; weak closure → reflux potential.

Esophageal Disorders

• Hiatal hernia
  • Portion of stomach protrudes through esophageal hiatus → constriction, pain.
• Dysphagia: difficulty swallowing (mechanical obstruction or neuro-motor deficit).
• GERD (gastro-esophageal reflux disease)
  • Acidic gastric contents splash into esophagus.
  • Burning = “heartburn.” LES insufficiency + recumbency after meals exacerbates.
  • Esophageal mucosa lacks thick mucus; HCl causes damage.

Stomach

General Functions

• Temporary storage for undigested food.
• Mechanical processing: strong muscular walls mash food.
• Chemical disruption: HCl breaks covalent bonds; enzymes initiate proteolysis.
• Secretes intrinsic factor (glycoprotein needed for vitamin B₁₂ absorption downstream).
• Produces chyme: 1.5–2 L of acidic "slurry".
• NOT a major absorption site.
  • Exceptions: alcohol, aspirin, lipid-soluble drugs, Helicobacter pylori (ulcer-causing) thrives here.

Gross Anatomy & Sphincters

• Curvatures: lesser (medial) & greater (lateral).
• Regions (superior ➜ inferior):
  1. Cardia – entry zone from esophagus.
  2. Fundus – dome (homology: uterine fundus).
  3. Body – bulk/mixing tank.
  4. Pylorus – funnels chyme to duodenum; guarded by pyloric sphincter (true, muscular).

Histology

• Simple columnar epithelium folded into rugae; surface peppered with gastric pits.
• Gastric pits open to gastric glands housing three key cells:
  1. Mucous cells – secrete protective mucus; lubricates chyme.
  2. Parietal cells – secrete H⁺ and Cl⁻ separately ➜ combine as HCl in lumen.
     • Also secrete intrinsic factor.
  3. Chief cells – release pepsinogen (inactive). In acid, converted to pepsin (protease).
• Collective secretions = gastric juice.

Mechanism of HCl Formation (Parietal Cell)

• Cellular CO₂ + H₂O ⟶ carbonic acid ⟶ \text{HCO}_3^- + \text{H}^+.
• \text{HCO}_3^- exchanged for Cl⁻ (basolateral antiporter) – "alkaline tide" into blood.
• Luminal H⁺/K⁺-ATPase (proton pump) exports H⁺, imports K⁺.
• Cl⁻ diffuses into lumen; H⁺ + Cl⁻ form HCl extracellularly.

Clinical & Ethical Angle – Proton-Pump Inhibitors (PPIs)

• Drugs: Prilosec, Prevacid = PPI; block the H⁺/K⁺-ATPase.
  • ↓ Acid → symptomatic relief of GERD but:
  • Interferes with normal digestion & B₁₂ absorption.
  • Higher gastric pH diminishes innate defense against pathogens.
  • Lifestyle fixes (meal timing, portion control) & antacids (e.g., Tums) can be preferable.

Stomach Digestion Summary

• Proteins & carbs begin chemical digestion here; fats minimal.
• Mucosal barrier is impermeable to water – limits absorption.
• Rapid turnover of epithelial cells protects against self-digestion.

Small Intestine: Structure & Segments

• Overall: ~20 ft long, ≈1 inch diameter; primary site of digestion completion & nutrient absorption.

1. Duodenum (~8 in.)
   • Receives acidic chyme + bile (liver/gallbladder) + pancreatic juice via common bile duct & pancreatic duct.
   • Major role = neutralize acid (lots of bicarbonate buffers), begin fat emulsification.
2. Jejunum (≈40–45 % of length)
   • Most plicae circulares & villi ➜ maximal absorption.
3. Ileum (remaining length)
   • Few/no plicae; contains MALT/Peyer’s patches (immune surveillance) to guard colon.
   • Terminates at ileocecal sphincter (entry to large intestine/cecum).

Surface-Area Adaptations

• Plicae circulares (plakae) – large circular folds in mucosa/submucosa.
• Villi – finger-like projections on plicae.
  • Each villus houses:
  • Capillary bed (absorbs sugars, amino acids, small peptides).
  • Lacteal (lymphatic) – absorbs chylomicrons/fats too large for capillaries.
• Microvilli on apical surface of enterocytes ("brush border" enzymes) – final enzymatic steps.
• Diffusive path: lumen ➜ enterocyte ➜ endothelial/lymphatic cell = 2 cell layers only.

Intestinal Secretions & Neutralisation

• Intestinal glands add mucus & water to keep chyme in solution.
• Bile = emulsifies lipids (↑ surface area for lipase).
• Pancreatic juice = digestive enzymes + bicarbonate (buffers HCl).

Motility Patterns

• Peristalsis – wave-like propulsion (left diagram in lecture).
• Segmentation – rhythmic churning/"kneading" to mix & expose chyme to mucosa (right diagram).
• Gastric stretch receptors trigger increased small-intestinal motility; parasympathetic input accelerates.
• When ileum fills, ileocecal sphincter relaxes; material passes into large intestine.

Integrative/Real-World Connections

• Heimlich maneuver importance stems from shared airway/foodway anatomy.
• Hiatal hernia & GERD link back to diaphragm anatomy & LES physiology.
• Ulcer development (\textit{H. pylori}) shows microbial survival in extreme pH; modern treatment combines antibiotics + acid modulation.
• Ethical consideration: Long-term PPI use vs. natural defense needs; diet-lifestyle modifications as first-line therapy.
• Segmentation/Peristalsis concepts extend to other tubular organs (ureters, vas deferens) discussed in prior reproductive lectures.

Key Numerical & Chemical References

• Stomach capacity: 1.5-2\text{ L} of chyme.
• Small intestine length: \approx 20\text{ ft}, diameter \approx 1\text{ in}.
• Duodenum length: \approx 8\text{ inches}.
• HCl pathway: \text{CO}2 + \text{H}2\text{O} \rightarrow \text{H}2\text{CO}3 \rightarrow \text{HCO}_3^- + \text{H}^+ ; luminal \text{H}^+ + \text{Cl}^- \Rightarrow \text{HCl}.
• Gastric pH normally \text{pH}\,1-2; PPIs raise it toward neutrality.

“Need-to-Know” Checklist for Exam Prep

• Identify pharynx/air–food double duty & associated risks.
• Trace the bolus: mouth ➜ pharynx ➜ esophagus ➜ stomach (regions) ➜ duodenum ➜ jejunum ➜ ileum.
• Explain how parietal cells make HCl & why PPIs work.
• Differentiate true vs. functional sphincters (LES vs. pyloric).
• Recognise cell types in gastric glands & their secretions.
• Correlate plicae/villi/microvilli structure with absorption efficiency.
• Compare peristalsis vs. segmentation (mechanics & purpose).
• Describe accessory organ contributions at duodenum (bile, pancreatic enzymes, bicarbonate).
• List clinical disorders (hiatal hernia, GERD, dysphagia, ulcers) and underlying anatomy/physiology.
• Recall approximate volumes/lengths (chyme capacity, small intestine dimensions).