Digestion Phases: Cephalic and Gastric

Digestion Phases

Three Phases of Digestion

  • The digestion process is divided into three phases:

    • Cephalic

    • Gastric

    • Intestinal

Cephalic Phase

  • The cephalic phase begins when you:

    • Hear food

    • See food

    • Smell food

    • Think about food

  • "Cephalic" means brain, indicating the involvement of the brain in this phase.

  • Triggers saliva production in the mouth.

  • Two important enzymes are released in the mouth from salivary glands:

    • Salivary amylase: Begins the chemical digestion of carbohydrates.

    • Lingual lipase: Begins the chemical digestion of lipids.

  • These enzymes function optimally at a relatively moderate to slightly alkaline pH (pH above 5, around 5-7).

  • Acidic conditions inhibit their function.

  • Involves the parasympathetic nervous system, with neurons extending to the intestines.

  • Epithelium of the duodenum contains Brunner's glands, which produce mucus to protect against low pH.

  • Mucus production begins in the cephalic phase to prepare for the arrival of acidic food.

  • The sympathetic nervous system inhibits Brunner gland activity.

  • Increased sympathetic activity (fight or flight) shuts down mucus production, increasing the risk of duodenal ulcers.

Role of Acetylcholine (ACh)

  • The parasympathetic nervous system releases acetylcholine.

  • Acetylcholine stimulates:

    • G cells

    • Parietal cells

    • Chief cells

Submucosal Plexus

  • Nerve plexus located in the submucosa.

Sympathetic vs. Parasympathetic Nervous System

  • Sympathetic nervous system (fight or flight) inhibits Bruner gland activity.

  • Parasympathetic nervous system activates saliva and mucus production.

Stress and Digestion

  • Stress inhibits mucus production in the duodenum, increasing the risk of duodenal ulcers.

Gastric Glands and Pits

  • Cross-section of the stomach epithelium reveals gastric glands and gastric pits.

  • Gastric pits are lined with mucus-making cells.

  • Gastric glands branch out from the pits and contain different types of cells:

    • Parietal cells: Produce hydrochloric acid (HCl) and intrinsic factor (for B12 absorption).

    • Chief cells: Produce pepsinogen (inactive form of pepsin).

    • Enteroendocrine cells: Produce hormones.

Hormonal Control of Gastric Activity

  • Vagus nerve stimulates the submucosal plexus.

  • Submucosal plexus releases acetylcholine.

    • Acetylcholine lands on G cells, parietal cells, and chief cells.

G Cells and Gastrin

  • G cells produce gastrin in response to acetylcholine stimulation.

  • Gastrin goes into circulation and travels throughout the body.

  • Parietal cells have receptors for gastrin and makes hydrochloric acid.

  • Other stimuli for G cells include:

    • Caffeine

    • Alcohol

    • Amino acids

  • This explains why individuals with gastric ulcer issues are advised to limit alcohol and caffeine intake.

Parietal Cells

  • Parietal cells are stimulated by:

    • Gastrin

    • Acetylcholine (from vagus nerve via submucosal plexus)

    • Histamine (via H2 receptors) that came from cells known as ECL.

ECL Cells and Histamine

  • ECL cells (enterochromaffin-like cells) release histamine.

  • Histamine binds to H2 receptors on parietal cells, stimulating hydrochloric acid production.

  • ECL cells are stimulated by:

    • Gastrin

    • Acetylcholine

  • Stretch of stomach wall can also stimulate ECL cells.

  • More stomach stretch leads to increased histamine release, resulting in more hydrochloric acid production.

Chief Cells

  • Chief cells are stimulated by:

    • Gastrin

    • Acetylcholine from submucosal plexus.

  • Activated chief cells produce pepsinogen (an inactive enzyme).

  • Hydrochloric acid converts pepsinogen into pepsin (active enzyme).

  • Pepsin is used for the chemical digestion.

Function of Hydrochloric Acid

  • Begins chemical digestion of food (breaks covalent bonds).

  • Kills pathogens in the stomach.

  • Activates pepsinogen to pepsin.

Process of Activation

  • Pepsinogen is exposed to hydrochloric acid.

  • Lowers the pH to around 1.5 to 2, that's pretty acidic.

  • Activates pepsinogen to become pepsin.

D Cells and Somatostatin

  • D cells (Delta cells) release somatostatin in response to increased hydrochloric acid levels.

  • Somatostatin acts as a negative feedback mechanism.

  • Somatostatin inhibits:

    • G cells (reducing gastrin production)

    • Parietal cells (reducing hydrochloric acid production)

    • Chief cells (reducing pepsin production)

  • This helps regulate the pH in the stomach.

Hydrochloric Acid Production

  • Parietal cells do not directly secrete hydrochloric acid; instead, they produce the components.

Mechanism of Hydrochloric Acid Production

  • CO2 from the blood diffuses into the parietal cell.

  • Water can also split, creating protons.

  • CO2 reacts with water to form carbonic acid (H<em>2CO</em>3H<em>2CO</em>3), which dissociates into hydrogen ions (H+H^+) and bicarbonate ions (HCO3−HCO_3^-).

    • Bicarbonate is shuttled out of the parietal cell into the bloodstream via a bicarbonate-chloride shift.

    • Chloride ions (Cl−Cl^-) are transported from the blood into the parietal cell.

Gastric Pit Environment

  • The chloride ions diffuse through a leaky channel goes into the gastric pit/gland.

  • Hydrogen ions are pumped out of the parietal cell into the gastric pit via a proton pump (H+/K+ ATPase).

  • Proton pump requires ATP.

Helicobacter Pylori (H. Pylori)

  • H. Pylori bacteria can live in the mucus layer of the stomach.

  • They move toward the surface for protons (energy) and retreat deeper into the mucus to avoid high proton concentrations.

  • H. Pylori irritates and inflames the epithelium of the stomach, reducing mucus production.

  • This exposes epithelial cells to acid, causing damage and potentially gastric ulcers.

Gastric Ulcers

  • Gastric ulcers can result from H. Pylori infection or other factors that reduce mucus production.

  • One treatment involves antibiotics to reduce H. Pylori populations.

  • However, antibiotics can affect gut bacteria, which are important for serotonin production.

  • Alternative approaches to acid control

    • Proton pump inhibitors (PPIs):

      • Inhibit the potassium from attaching to the hydrogen-potassium antiporter.

      • Prilosec and Nexium are examples.

    • H2 blockers:

      • Block histamine from binding to H2 receptors and stimulating acid production.

      • Zantac, Tagamet and Pepcid AC are examples.

Alkaline Tide

  • Bicarbonate ions ($$HCO_3^-$) transported into the blood cause an alkaline tide.

  • This raises the pH of the blood in the capillaries near the parietal cells.

Gastric Phase

  • Key aspects:

    • Increase in gastrin.

    • Gastric motility (activity of the stomach).

  • Stomach functions primarily as a storage bag for chemical digestion with limited nutrient absorption.

  • Motility: increases the level of gastrin.

Factors affecting Gastrin Level

  • Increases gastrin:

    • Caffeine

    • Alcohol

    • Amino acids

    • Increased pH: Higher pHs lead to an increase in gastrin through reduces the negative feedback from said D cell in the form of somatostatin.

  • Distension of the gastric wall: leads to ECLs producing histamine. Plus is there an activation of the motor neurons to release ACH.

Stomach Capacity

  • Stomach's storage capacity varies; typically holds 1 to 2 pints normally.

  • Competitive eaters demonstrate extreme capacity; the current Nathan's Hot Dog Eating Champion is 72 hot dogs and buns in ten minutes. That is an ungodly amount of fats, sodium, calories.

Factors that affects Gastrin Levels and Motility

  • The amount of stimuli affects the level of gastrin and motility.

    • Maybe it's the level of pH.

    • Maybe it's the amount of distension.

    • Maybe it's the amount of caffeine.

    • Maybe it's the amount of alcohol.

Sponging Effect

  • The level of stimulus of an increase in the amount of gastrin can be absorbed by food.

  • But, eventually, the food and the liquids will eventually saturate, stopping its absorbtion.

Liquid effect.

  • If you want to actually be able to eat a really big dinner later on, like a nice sized lunch and you want to get ready for a really good dinner coming up, Drink few liquids with your meal because the more liquids you drink the more you dilute the hydrochloric acid and the more you dilute the acid the longer it takes to chemically break down the food and to leave your stomach.

Environment Changes

  • As pH decreases, salivary amylase and lingual lipase activity are inhibited, but pepsin activity increases.

  • These enzyme changes, allow certain enzymes to be active where others aren't as active.

Chyme

  • The mixture of foods, liquids, and secretions in the stomach is called chyme.

  • The stomach mixes the food until it's liquidy enough to pass through the pyloric sphincter.

  • The pyloric sphincter has the job of preventing the fluid from leaving unless it's really liquidy enough.

  • More solid chyme stays near the upper part of the stomach while more liquidy chyme is near the pyloric region.

Vomit Factor.

  • Think about being sick and how watery the chucks can appear at times. The time frame of when you got sick allows all the chunks and food you consumed to become liquified.