Digestion: Cephalic & Gastric Phases

Digestion Phases

Cephalic Phase

  • Triggered by:
    • Hearing food
    • Seeing food
    • Smelling food
    • Thinking about food
  • Cephalic = Brain
  • Triggers saliva production.
  • Two important enzymes released from salivary glands:
    • Salivary amylase: begins carbohydrate digestion (chemical digestion)
    • Lingual lipase: begins lipid digestion (chemical digestion)
    • Enzymes function best at a moderate to slightly alkaline pH (above 5, around 5-7).
  • Involves parasympathetic nervous system:
    • Neurons extend to the intestines.
    • Stimulates Brunner's glands in the duodenum epithelium.
    • Brunner's glands produce mucus to protect epithelium cells from low pH.
    • Mucus production begins in the cephalic phase to prepare for acidity later.
  • Parasympathetic nervous system releases acetylcholine.
    • Acetylcholine stimulates G cells, parietal cells, and chief cells.
Submucosal Plexus
  • Activated with food; see food, smell food, think about food.
Sympathetic Nervous System
  • Inhibits Brunner gland activity (fight or flight response).
  • When inhibited, mucus is not produced, leading to potential duodenal ulcers.
  • Stress inhibits mucus production because the sympathetic nervous system prioritizes immediate survival (fight or flight) over digestion.

Gastric Phase

  • Processes occurring in the stomach.
Stomach Epithelium
  • Cross section reveals gastric glands and gastric pits.
  • Food molecules can enter the gastric pit, lined with mucus-making cells.
  • Gastric pit branches into a 3D structure forming the gastric gland.
  • Gastric gland contains:
    • Parietal cells
    • Chief cells
    • Enteroendocrine cells
  • Enteroendocrine cells: produce hormones.
  • Chief cells: produce pepsinogen.
  • Parietal cells:
    • Responsible for hydrochloric acid (HCl) production in the stomach (but don't directly secrete HCl).
    • Produce intrinsic factor (important for B12B_{12} absorption).
Hormonal Control of Gastric Activity

Important cells in the gastric gland:
* G cells
* Parietal cells
* Chief cells

Process
  • Vagus nerve stimulates the submucosal plexus.
  • Submucosal plexus releases acetylcholine (ACh).
  • ACh binds to receptors on G cells.
  • G cells produce gastrin (hormone).
  • Gastrin enters circulation and travels throughout the body, but only parietal cells have receptors for it.
  • Gastrin binds to parietal cells, stimulating them to produce hydrochloric acid (HCl).
Other Stimuli for G Cells
  • Caffeine
  • Alcohol
  • Amino acids (in food)
  • These stimulate G cells to produce gastrin, leading to more acid production.
Parietal Cell Stimulation

Besides gastrin, parietal cells are also stimulated by:
* ACh (from vagus nerve and submucosal plexus)
* Histamine (via H2 receptors)

  • ECL cells: release histamine, which binds to H2 receptors on parietal cells.
  • ECL cells are stimulated by:
    • Gastrin
    • ACh
Chief Cell Stimulation
  • Chief cells are stimulated by:
    • Gastrin
    • ACh
  • Chief cells produce pepsinogen (inactive enzyme).
Functions of Hydrochloric Acid (HCl)
  • Begins chemical digestion of food by breaking covalent bonds.
  • Kills pathogens in the stomach.
  • Activates pepsinogen to pepsin.
  • Pepsinogen is exposed to hydrochloric acid (pH 1.5-2) to activate, turning it into pepsin.
Key Points
  • Parietal cells do not directly secrete hydrochloric acid.
  • Chief cells do not secrete pepsin; they secrete pepsinogen.
Feedback Mechanism
  • As hydrochloric acid levels increase, pH decreases.
  • Low pH stimulates D cells.
  • D cells release somatostatin (hormone).
  • Somatostatin acts as a negative feedback:
    • Inhibits G cells, reducing gastrin production.
    • Directly inhibits parietal cells, reducing hydrochloric acid production.
    • Inhibits Chief cells, reducing pepsin production.
Stomach Stretch
  • Stretching of the stomach wall leads to:
    • More stimulation of ECL cells.
    • More histamine release.
    • Increased hydrochloric acid production (if you have a lot of food).
Producing Hydrochloric Acid and Gastric Ulcers
Parietal Cells
  • Parietal cells don't directly secrete hydrochloric acid because it would destroy them.
  • HCl production related to gastric ulcers - where too much gets released.
Stomach Anatomy Reminder:
  • Rugae: folds in stomach that increase surface area.
  • Mucus layer: protects stomach lining from acid.
Ulcer Cause
  • H. pylori (Helicobacter pylori):
    • Bacteria that live in the mucus layer.
    • Irritate the epithelium of the stomach.
    • Reduces mucus production in that area.
    • Protons (acid) can then damage epithelial cells causing bleeding and gastric ulcers.
Ulcer Treatments
  • Antibiotics:
    • To kill H. pylori (bacterial cause).
    • They're not specific and can harm bacteria needed for mental health.
  • Proton Pump Inhibitors (PPIs):
    • Prevents potassium from attaching to the hydrogen-potassium antiporter (proton pump).
    • If the potassium can't attach, the pump can't work.
    • Protons can't get into the lumen of the stomach.
  • H2 Blockers:
    • Histamine can't attach to the H2 Receptor.
    • Less stimulation of parietal cells.
    • Reduced proton production.
Alkaline Tide

As bicarbonate ions are shuttled out of the parietal cell and into the bloodstream:
* pH of the blood INCREASES, becomes more alkaline
* Creates "Alkaline Tide"

Medication Examples
  • PPIs (Proton Pump Inhibitors):
    • Prilosec (OTC)
    • Nexium (OTC)
  • H2 Blockers:
    • Zantac
    • Tagamet
    • Pepcid AC