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Physiology: Esophageal and Gastric - Coggle Diagram
Physiology: Esophageal and Gastric
Process of Normal gastric Contractility and Emptying
Functions:
Motor: Reservoir, mixing adn grinding, controlled emptying
Secretory: HCl secretion, Mucosal barrier, pepsinogen secretion, Intrinsic Factor
Function of Motility: Accomodate meal, grind down solids, regulated emptying of stomach contents
Neuromuscular activity: Receptive relaxation of fundus, peristaltic waves of corpus and antrum, antral peristaltic waves
Modulated via: CNS, PNS, Sympathetic, Enteric Nervous System
Electrophysiology
Pacemaker along greater curve at proximal or mid corpus
Gastric slow waves from ICC
Propagate in longitudinal and circumferential direction
Migrate toward pyloruis, and cooridnated propulsive peristaltic activity
Fasting Stomach
Migratory Motor Complex: 3 Sequences of activity
Phase 1: Quiescence phase
Phase 2: random and irregular contraction phase
Phase 3: Burst of uninterrupted phasic contractions
Meal Reponse
Solid
emptying occurs in 2 phases (intial lag, linear emptying)
Solid is help in proximal solid, and as liquid empties, solid move to antrum for trituratio
Antrum and pylorus grinds large -> Small particles, empties in linear fashion
Motor
On initiation of swallowing, gastric fundus relaxes to accommodate incoming food
Tone and phasic contractions are inhibited as meal enters proximal stomach
Accommodation results in 2-3 fold increase in gastric volume
Retention of food in stomach until distributed to the antrum
Liquid
Trituration of meal is accomplsihed with propulsive force generated by tonic contractions (proximal sotmach adn ressitance of the antrum)
Liquids rapidly disperse through stomach
Rate depends on volume, nutrient content and osmolarity
Antropyloric Motility
Trituration is functin of coordinated contractions
Waves originating in proximal antrum -> Pylorus
Midantrum point, pylorus ios open to allow liquids and liquified solid
At distal antrum, terminal antrum contraction closes pylorus
Solid particles continue to move in and out of antrum until broken down
Gastric Emptying
Neuronal control
Intrinsic myenteric plexus, Extrinsic postganglionic sympathetic fibers
Preganglionic parasympathetic fibers of vagus nerve
Hormonal Control
CCK: Relax fundic tone, decreases antral contraction, and increase pyloric tone
Other hormones can control gastric emptying
Mucosal Protective Mechanisms
Mucous Layer, HCO3-, Epithelial tight junctions, Mucosal blood flow (modulated by prostaglandins)
Esophageal Protective functions
Esophageal peristalsis propagates acoid bolus down the esophagus
Basic saliva neutralises acid
Esophageal submucosal Glands secrete bicarb in response to acid reflux
In response to acid, blood flow increased to esophagus to clear H+
Stomach
Gastric Secretion
Cells
Gastric Epithelial Cells (Mucus, HCO3)
Cells of Gastric glands
Cells of lamina propria (mast cells: Histamine, Plasma cells: Immunoglobulins)
Neurocrine Secretion (Ach, VIP, Somatostatin)
Gland Type
Cardiac
Mucous: Mucus, Pepsinogen II
Endocrine (D cells; Somatostatin)
Oxyntic
Mucous (Mucus, Pepsinogen I and II)
Patiental (HCl, intrinsic factor)
Function of Gastric Acid
Facilitate peptic hydrolysis of dietary proteins
Inactivate ingested microorganisms
Facilitate intestinal absorption of calcium, B12, iron
Activation
Neurocrine (ACh from vagal efferences)
Endocrine (Gastrin from antral G cells)
Paracrine (histamine from mast cells, ECL Cells)
Chief (Pepsinogen and Leptin)
Enterochromaffin-line Cells (histamine)
D Cells (Somatostatin)
Enterochromaffin (ANP, Serotonin, Adrenomedullin)
Pyloric
Mucous (Mucus, pepsinogens II)
G Cells (Gastrin)
Enterochromaffin (ANP, Serotonin)
D Cells (Somatostatin)
Pathways of H+ Scretion
Mucosal Nerves (ACh stimulates parietal cells, gastrin release, inhibit somatostatin release)
Gastrin (stimulated by increase gastric pH, amino acids, gastric distension, ACh) and stimulates histamine release + pareital cell
Luminal H+ (Gastrin release is inhibited once gastric pH <2.5-3)
Somatostatin (Secretion is stimulated by gastric acid, gastrin, and VIP, Inhibits histamine and gastrin release, inhibits histamine-mediated activation of parietal cell
Prostaglandins (autocrine secretion from macrophages and endothelial cells of man lamina propria, inhibit histamine related parietal cell activation, inhibit gastrin related histamine release)
TGF-alpha
VIP
Phases
Cephalic: Vagally mediated stimulation of parietal cell triggered by thought of food, sight, smell, taste and mastication
Gastric: Distension, high pH, peptides, caffeine trigger vaso-vagal and local reflexes, Gastric, Gast cells, ECL cell which release histamine and activate pareital cells
Intestinal: Distension, Hypertonicity, Carbohydrates, fat, Low pH triggers Vago-vagal and local refelxes, somatostatin,CCK, Secrettin -> Pancrease -> HCO3-
Regulation