Title: Mouth and Stomach
Course: Anatomy and Physiology
Date: Spring 2025, Wednesday, February 26
Ingestion: Taking in food.
Digestion: Breakdown of food into smaller components.
Mechanical Digestion: Involves teeth, stomach, and intestines.
Chemical Digestion: Breakdown by digestive enzymes.
Absorption: Uptake of nutrient molecules into the bloodstream.
Compaction: Consolidation of feces.
Defecation: Elimination of waste.
Definition: Mechanical processing of ingested food.
Purpose: Facilitate swallowing and increase surface area for digestion.
Characteristics:
Partially voluntary and reflexive process.
Structures involved:
Lips & Cheeks: Retain food inside the mouth.
Teeth: Cut and grind food.
Tongue: Manipulates food, forming a bolus.
Muscles of Mastication:
Masseter & Temporalis: Elevate the jaw.
Pterygoids: Lateral movement of the jaw.
Regulation by salivary nuclei in the brainstem.
Stimuli: Mechanoreceptors and chemoreceptors in the oral cavity.
Anticipation of food can trigger salivation.
Autonomic Nervous System controls:
Parasympathetic: Stimulates salivation.
Sympathetic: Inhibits salivation.
Muscle activity coordinated by the swallowing center in the medulla oblongata.
Oral Phase: Voluntary control.
Tongue forms bolus and pushes it posteriorly for swallowing.
Involuntary reflex begins here.
Mechanisms to prevent backflow:
Soft palate and root of tongue raise to block nasal passage.
Bolus tips the epiglottis, closing the trachea.
Pharyngeal constrictor muscles drive the bolus downward.
Respiratory Protections:
Breathing is automatically suspended.
Larynx is elevated by extrinsic muscles.
Vestibular folds close to prevent air entry.
Esophageal Phase: Involuntary movement of food.
Peristalsis transports the bolus.
Lower Esophageal Sphincter: Relaxes to allow food into the stomach.
Hormonal influences from gastric and intestinal enteroendocrine cells.
Role of Central Nervous System (CNS):
Enteric Nervous System: Main control source for digestive functions.
Composed of over 100 million neurons, can function independently of CNS.
Submucosal Plexus: Regulates gland activity.
Myenteric Plexus: Regulates smooth muscle contractions in digestive tract.
Short (Myenteric) Reflexes: Intrinsic control via local stimuli in digestive tract.
Long (Vagovagal) Reflexes: Extrinsic control involving CNS autonomics. Can be triggered by both internal and external stimuli.
Sensory stimuli from pharyngeal mechanoreceptors relay to swallowing center.
Receptive Relaxation: Parasympathetic stimulation via vagus nerves prepares stomach for food.
Antral Pump: Strong contractions help prepare food for duodenum, controlling pyloric sphincter.
Approximately 3mL of chyme enters the duodenum at a time.
Relaxation of the stomach allows sphincter to open for gradual chyme release.
Duodenum Overfilling: Inhibits gastric motility.
Typical stomach emptying: Around 4 hours.
Controlled by the emetic center in the medulla oblongata.
Triggering factors include:
Overstretching of stomach/duodenum.
Chemical irritants.
Viscera trauma or intense pain.
Psychological or sensory stimuli.
Process involves relaxation of lower esophageal sphincter and intense abdominal contractions.
Mechanical and chemical digestion occurs through:
Churning from peristaltic contractions.
Action of gastric enzymes and HCl.
Absorption: Very minimal nutrients absorbed in the stomach.
Activities increase after food intake; decrease as stomach empties.
Phases based on site of control:
Cephalic Phase: Brain response to food anticipation.
Gastric Phase: Local response in stomach.
Intestinal Phase: Response in small intestine.
Overlapping phases that can occur simultaneously.
Stimulatory Events:
Anticipation related to the sight and thought of food,
Taste and smell stimulation.
Increased secretion of HCl via vagus nerve stimulation.
Inhibitory Events:
Emotional states reducing parasympathetic activity.
Sympathetic stimulation can override parasympathetic effects.
Stimulatory Factors:
Activation from swallowed food and stomach distension increases pH.
Stimulates secretion of HCl and intrinsic factor via long and short reflexes.
Inhibitory Factors:
Excessive acidity decreases gastric secretions.
Primarily inhibitory phase:
Pyloric sphincter restricts chyme entry into the duodenum.
Intestinal hormones decrease gastric activity via enterogastric reflex triggered by chyme acidity and fats.
Signals inhibit gastric activity both locally and from CNS.
Hormones stimulate bile release from the liver and insulin from the pancreas.
Cephalic Phase Events:
1a: Sight and thought of food activate brain centers.
1b: Taste and smell receptor stimulation.
2a: Stomach distension activates long and short reflexes.
2b: Food chemicals increase gastric activity.
Intestinal Phase Events:
3a: Presence of food in the duodenum stimulates further digestive secretions.
Inhibitory Signals:
Loss of appetite, depression affects appetite stimulation.
Excessive acidity inhibits gastric activity.