Gastrointestinal Physiology Flashcards
Secretin
Source: S cells lining duodenum
Stimulated by acid entering duodenum
Inhibits stomach motility and gastric acid secretion
Stimulates aqueous (bicarb) secretion from pancreas
Stim. gastric chief cells to release pepsinogen
CCK
Source: I cells in dueodenum and jejunum
Stimulated by fat and amino acids entering duodenum
Inhibits emptying of stomach
Stimulates enzyme secretion by pancreas (acinar cells) and potentiates aqueous secretion
Causes contraction of gall blabber and relaxation of sphincter of Oddi
Gastrin
Sources:
- G cells of stomach
- Stimulated by stomach distention
- Acts to increase acid secretion (parietal cells)
- Stimulates growth of gastric mucosa
GIP (glucose insulinotropic peptide)
Source: duodenum
Stimulated by fat, CHO, amino acid
Inhibits stomach acid motility and secretion
In gallbladder: increases insulin, decreases glucagon
Events during swallowing
- Pharyngeal phase: Food in pharynx –> sensory from CN IX and X to medulla, efferent impulses sent back
- Relaxation of UES (skeletal muscle)
- Primary peristaltic wave
- Relaxation of LES (smooth mucles) via VIP acting as an inhibitory NT
- Fails in achalasia (abnormal enteric nerves)
- Tone not maintained in GERD, stomach acid refluxes back into esophagus - Relaxation of proximal stomach (receptive relaxation)
Stimulation of gastric motility
- Increased parasym via ACh and gastrin
**- **Local distention
- Atropine (ACh receptor antagonist) alone cannot slow stomach b.c GRP/Gastrin bypass ACh
Inhibition of gastric motility
- Low pH of stomach contents inhibits release of gastrin
- Feedback from duodenal overload (neural and hormonal)
Stomach emptying
Liquids > carbs > proteins > fat
Pyloris is a sphincter that controls rate of empyting
CCK, GIP, secretin slow stomach emptying by increasing contraction of pyloric sphincter
Migrating Myoelectric Complex (MMC)
- Propulsion during fasting, begins in stomach and moves undigested material from stomach –> small intestine –> colon
- Repeats every 90-120 min during fasting
- Correlated with high motilin levels (hormone of small intestine)
- Prevents backflow of bacteria from colon into illeum
Defacation
- Reflex of the CNS
- Filled rectum –> relaxation of internal anal sphincter and contraction of external anal sphincter –> voluntary relaxation of EAS with propulsive contraction of distal colon = poop!
- Lack of functional innervation of EAS = involuntary pooping when rectum fills
Salivary secretions
- Parotid gland secretions (25%) - entirely serous, rich in a-amylase
- Submandibular (70%) and sublingual (5%) gland secretions - mixed (mucus and serous), rich in mucin glycoproteins
- Under control of parasym - promotes secretion
Fxns: lubrication, protection, digestion
Sjogren syndrome (autoimmune, destroys salivary and lacrimal glands)
Xerostomia (dry mouth)
Myenteric Plexus (Auerbach’s)
- Between longitudinal and circular muscle laters
- From proximal esophagus to rectum
- Enhances peristalsis (increases tone, intesity, and velocity of contractions)
Submucosal plexus (Meissner’s)
- Between the circular muscle nad submucosa
- Small and large intestine
- Controls local intestinal secretions, absorption, and contraction of submucosal muscle
Types of receptors in the enteric nervous system
- Mechanoreceptors: sense SM stretch, signals through myenteric plexus to stimulate contractions
- Chemoreceptors: sense chemical composition of chyme, control luminal pH during influx of acidic chyme
- Osmoreceptors: sense osmolarity of chyme, control amount of chyme entering small intestine and secretions to buffer chyme (don’t want to chyme to exert an osmotic force)
PNS Activation of the Enteric Nervous System
Parasym preganglionics (vagus and pelvis nerves) terminate on postganglionic cholinergic/peptidergic neurons in plexuses
- PNS activation = increased gut motility, relaxation of sphincters, enhanced secretions
Vagovagal reflexes: both afferent and efferent impulses are carried by vagus
PNS Innervation of ENS
- Vagus innervates proximal 2/3 (pharynx –> beginning of distal colon)
- Pelvic nerves innervate distal 1/3 of colon
- ACh major NT (some postgang fibers release peptides)
- Activation promotes digestion and absorption
SNS innervation of ENS
- Postganglionic fibers from celiac plexus, hypogastric, superior & inferior mesenteric ganglia
- NE major NT. Many inhibit excitatory ACh neurons
- Inhibits/reduces digestion and absorption
Interstitial Cells of Cajal
- Pacemakes in the GI tract - generate slow waves
- In myenteric plexus
- Contraction of GI muscle wall occurs when AP is generated at the peaks of slow waves (above -40mV) –> stimulated of PNS
Order of secretory unit in exocrine pancreas
Acinus –> intercalated duct –> intralobular duct –> interlobular duct –> main pancreatic duct
Na+ and HCO3- secretion (aqueous secretion) by pancreatic duct cells
- Diffusion of CO2 from blood
- CO2 dissociates to carbonic acid –> H+ and HCO3-
- H+ pumped out through Na+/K+ exchanger or proton pump (removed)
- HCO3- also enters via Na+/HCO3- exchanger
- HCO3- accumulates, enters lumen through Cl-/HCO3- exchanger (depends on available Cl- in lumen, which depends on opening of apical Cl- channel)
Note: Cl- channel (CFTR) is activated by secretin –> increases cAMP –> opens channel –> bicarb can be secreted. Absent in CF patients, can’t secrete bicard
- Negative charge of lumen (from Cl-) pulls Na+ in across tight jxns
*ACh and secretin stimulate bicarb secretion
What is the “exchange hypothesis” in pancreatic aqueous secretions?
- Electrolye composition of aqueous secretion is a fxn of the rate of secretion
- Fast secretion = more bicarb (less time for exchange)
- Slow secretion = less bicarb, more like plasma
What causes cystic fibrosis?
- Defective CTFR channel
- Cl- isn’t replensihed in lumen, bicarb can’t be secreted by the exchanger
- Ducts become clogged with thick mucous without the aqueous secretions –> causes dyspnea
