Phases of Digestion – Key Vocabulary

Big-Picture Roadmap

  • Digestive activities occur in three sequential temporal windows:

    1. Cephalic Phase ("head‐related")

    2. Gastric Phase (food inside the stomach)

    3. Gastrointestinal / Intestinal Phase (chyme has reached the duodenum)

  • Each phase is defined by:

    • Primary stimulus (sight, stretch, pH, etc.)

    • Dominant effectors (nerves, local plexuses, hormones)

    • Ultimate goal (prime, intensify, or modulate stomach activity)

  • The body deliberately uses redundant control pathways—neural and hormonal—to ensure vital digestive shifts occur reliably.

Phase 1 – Cephalic (“Head”) Phase

  • Name origin: cephalic = “head” (Latin).

  • Triggers (all are pre-ingestion or oral events):

    • Thought, sight, smell, or taste of food.

    • Tactile sensation of food in the mouth.

  • Central integration:

    • Sensory input → cerebral cortex & hypothalamus → autonomic centers in the medulla oblongata.

    • Medulla ramps up parasympathetic (vagus) outflow to digestive organs.

  • Vagus-mediated stomach responses:

    • ↑ Secretion of gastric juice (HCl + pepsinogen + other enzymes).

    • Initiation of segmentation (mixing) contractions → “stomach rumbling” before food arrives.

  • Hormonal reinforcement:

    • Vagus stimulation ⟹ G-cells (endocrine) secrete gastrin → enters blood → feeds back to stomach.

    • Gastrin further ↑ HCl secretion & motility (positive feedback/“priming”).

  • Physiological theme: Prepare the battlefield before the army (food) arrives.

Phase 2 – Gastric Phase

  • Entry criterion: Food has been swallowed; stomach begins to fill.

  • Primary stimulus: Distension of the stomach wall.

    • Stretch receptors work analogously to arterial baroreceptors—membrane deformation encodes pressure/volume.

  • Neural loop:

    • Stretch receptor afferents travel via vagus nerve → medulla.

    • Medulla sends stronger vagal efferents back → enhanced gastric activity.

  • Resultant changes (intensifying Phase 1 actions):

    • Further ↑ gastric juice secretion.

    • Stronger segmentation contractions.

  • Progression to chyme handling:

    • Ongoing mixing + HCl ↓ pH & liquefies bolus → chyme.

    • Stomach begins peristaltic waves propelling chyme toward the pylorus & duodenum.

Phase 3 – Gastrointestinal (Intestinal) Phase

Strategic Goal
  • Protect the intestine by neutralizing gastric acid quickly.

  • Achieve this by allowing only small acidic batches of chyme into the duodenum at a time.

    • Cycle: “Push a bit → neutralize → push next bit… until stomach empty.”

Detection Mechanism in Duodenum
  • pH receptors (chemically identical concept to H⁺-sensitive chemoreceptors) monitor luminal acidity.

    • Normal duodenal pH ≈ \text{pH}\approx7 (neutral).

    • Arrival of gastric chyme drops it to acidic values (e.g., \text{pH}<3) → triggers response.

Three Parallel Communication Pathways (all inhibitory to stomach)
  1. Extrinsic Neural (long vagal reflex)

    • Acid detected → vagal afferents → medulla.

    • Medulla reduces parasympathetic vagal tone to stomach.

    • Less vagus activity = ↓ secretions & ↓ motility.

  2. Intrinsic / Local Neural Reflex

    • Enteric nerve plexuses of duodenum directly synapse with those of stomach.

    • Local inhibitory signals further ↓ gastric secretions & contractions (CNS not required).

  3. Hormonal Pathway

    • Duodenal endocrine cells release:

      • Secretin

      • Cholecystokinin (CCK)

    • Via bloodstream these hormones reach the stomach → inhibit HCl production & motility.

    • (They also act on pancreas, liver, gallbladder—covered in later material.)

Cyclic Feedback Logic
  • Acidic batch arrives → 3 pathways inhibit stomach → duodenum neutralizes acid (via pancreatic bicarbonate, etc.).

  • Once duodenal pH returns to ~neutral, pH receptors fall silent.

  • Medulla lifts inhibition → vagus re-activates stomach → next peristaltic pulse of chyme.

  • Cycle repeats until stomach is completely empty.

Key Definitions & Concepts (Quick-Reference)

  • Gastric juice: aqueous mix of \text{HCl}, pepsinogen/pepsin, intrinsic factor, mucus.

  • Segmentation: Non-propulsive mixing contractions that churn contents.

  • Peristalsis: Wave-like propulsion moving material distally.

  • Chyme: Semi-liquid stomach output (food + gastric secretions).

  • Secretin: Hormone that stimulates pancreatic bicarbonate, inhibits stomach.

  • CCK (Cholecystokinin): Hormone that stimulates gallbladder contraction, pancreatic enzyme secretion, inhibits stomach.

Integration & Redundancy Themes

  • The digestive system relies on both fast neural signals (vagus, enteric plexus) and slower hormonal signals (gastrin, secretin, CCK) for the same task → provides fail-safe control.

  • Similar strategy recurs across physiology (e.g., blood pressure control uses baro-reflex + renin-angiotensin system).

Everyday Manifestations & Clinical Relevance

  • “Mouth-watering” and stomach growling before eating = cephalic vagal activation.

  • Overeating can swamp the duodenum’s ability to neutralize acid, potentially irritating intestinal mucosa.

  • Drugs that block acid (e.g., PPIs) or block vagus (rarely used) can alter these phases.

Study Tips & Next Steps

  • Sketch a flow chart linking stimuli → pathway → stomach response for each phase.

  • Practice labeling where each hormone is produced and what organ it targets.

  • Complete the “Phases of Digestion” lab worksheet to solidify cyclic feedback understanding.