Neural Control of GI Motility & Funtion Flashcards
2 reservoirs of the GI tract
*stomach (reservoir for ingested food)
*left colon/rectum (reservoir for feces)
function of sphincters in the GI tract
*control direction and rate of movement between functional zones
important sphincters (valves) in the GI tract
*lower esophageal sphincter
*pyloric valve
*ileocecal valve
*internal & external anal sphincters
voluntary vs. automatic elements of the GI tract
*entry to and exit from GI tract = voluntary control
*movement of contents through most of GI tract = automatic
layers of the GI tract
1) mucosa (enzymes, absorption, secretion)
-epithelium
-basement membrane
-lamina propria
-muscularis mucosa
2) submucosa (vascular, transport)
3) muscularis propria (motility, structural)
-circular smooth muscle layer
-longitudinal smooth muscle layer
-muscle fibers electrically connected
4) nerve plexes (secretion/motility control)
-submucosal (Meissner’s)
-myenteric (Auerbach’s) [b/w circular and longitudinal muscle layers]
5) serosa
enteric nervous system
*largest network of nerve cells outside CNS
*controls and regulates all GI functions (motility, secretion, absorption, blood flow)
*functions SEMI-AUTONOMOUSLY
*modulated by SYMP/PARASYMP balance
myenteric plexus
*aka Auerbach’s plexus
*controls MOTOR function: velocity and intensity of smooth muscle contraction
*sphincter tone (pylorus, IC valve)
*located between the circular and longitudinal muscle layers
submucosal plexus
*aka Meissner’s plexus
*controls EPITHELIAL function
*secretion and absorption
*mucosal blood flow
*located below the submucosal layer
sensory neurons of the enteric nervous system
*provides FEEDBACK to the CNS
*endings in epithelium, gut wall
*communicates with enteric plexi, spinal cord, and CNS via vagus
parasympathetic actions in the GI tract
*cholinergic; ACTIVATES GI tract (“rest and digest”):
1. increases gut motility
2. relaxes sphincters
3. increases secretion
4. gallbladder contraction
5. increases blood flow
sympathetic actions in the GI tract
*adrenergic; INHIBITS GI tract:
1. decreases gut motility
2. contracts sphincters
3. decreases secretions
4. gallbladder relaxation
5. decreases blood flow
patterns of gut motility
1) isolated contractions
2) segmentation
3) peristalsis
isolated contractions (pattern of gut motility)
*no net movement
*stimulated by radial stretching of gut wall by chyme (lumenal contents)
*mediated by myenteric plexus
segmentation (pattern of gut motility)
*no net movement
*chyme simultaneously pushed anterograde and retrograde
*facilitates MIXING of chyme & secretions, and absorption of nutrients and water (aids in digestion, not movement)
peristalsis (pattern of gut motility)
*propulsive movement
*propels chyme in oral to caudal direction (at a rate of 2-25 cm/sec)
*peristaltic wave begins on oral side of a gut segment and proceeds distally
gastrointestinal blood flow - overview
*arterial blood provided by: celiac artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA) [except upper 2/3 of esophagus & rectum]
regulation of GI blood flow
*splanchnic circulation is the most highly regulated blood flow in the body (5-10% of cardiac output when asleep; up to 25% after a meal)
*controlled by sympathetic nervous system and release of gut hormones (ex. somatostatin)
venous blood flow from GI tract
*venous blood flows from GI tract to the liver via portal venous system and subsequently into superior vena cava
*blood passes through hepatic sinusoids to hepatic veins to vena cava to right atrium
3 phases of swallowing
1) oral phase
2) pharyngeal phase
3) esophageal phase
oral phase of swallowing
*voluntary
*mediated by CNs V, VII, IX, and XII
*mastication physically breaks up food, leading to increased surface area accessible to enzymes
*enzyme secretion: amylase (salivary glands) and lingual lipase (tongue)
*tongue propels bolus from oral cavity to pharynx
pharyngeal phase of swallowing
*involuntary
*mediated by swallowing center, CN IX, and vagus
*soft palate elevation; closure of epiglottis
*food bolus passes pharynx into esophagus
esophageal phase of swallowing
*automatic
*mediated by myenteric plexus and vagus
*primary peristalsis: continuous movement from pharynx to stomach
*secondary peristalsis: initiated by local distension
*LES relaxation
lower esophageal sphincter (LES) - overview
*3cm band of circular muscle at the gastroesophageal junction
*tonically contracted
*resting pressure modulated by vagal tone and GI hormones
*function: prevents retrograde reflux of gastric contents into esophagus
*primary peristaltic waves trigger LES relaxation
gastroesophageal reflux disease (GERD) - simplified
*can be caused by reduced LES tone
*drugs that reduce LES tone worsen GERD (anticholinergics, xanthines, etc)
achalasia
*failure of the LES to relax with swallowing
*can be primary or acquired
*presents with dysphagia
*can be treated with LES botox injections, interventional endoscopy, or surgery
physiologic functions of the stomach
*food reservoir (2-4 L)
*grinding and mixing
-pacemaker drive 3 cycle/min contraction (body to antrum, mixing food and gastric juice)
-pylorus remains tonically contracted
*regulated emptying
-at end of each contraction wave, the pylorus opens to allow 10 ml of chyme into duodenum
-gastric emptying half-life about 1-2 hours
factors that modulate the emptying rate of the stomach
*increase: food volume, increased vagal tone, and gastrin
*decrease: duodenal distension, high chyme osmolality, duodenal pH < 3.5, protein & fats
dumping syndrome
*when the pylorus is bypassed/removed during surgery, it can lead to rapid, unregulated entry of chyme into small bowel, leading to acute osmotic load
*sx: bloating, nausea, vomiting, abdominal pain, diarrhea, hypotension, hypoglycemia
*rx: diet modification (multiple small meals)
gastroparesis
*reduced or absent gastric motility caused by diabetes, vagal disruption, or idiopathic
*sx: early satiety, nausea, vomiting, weight loss, abdominal pain, malnutrition
*dx: gastric emptying scan
*rx: improve DM control; diet modification; metoclopramide (D2 receptor antagonist)
regulation of peristalsis in small intestine
1) cephalic phase of digestion (sight, smell, taste of food leads to increased vagal tone and increased peristalsis)
2) gastroenteric phase (food distension of the stomach and duodenum lead to increased peristalsis)
3) GI hormones (stimulation or inhibition)
migrating motor (myoelectric) complex (MMC)
*purpose = clean out gut bacteria in preparation for next meal
*appears between meals and during the night
*single waves start in stomach, sweep along small bowel to distal ileum every 90 min
*clears residual lumen contents
ileus
*absent or impaired small bowel peristalsis caused by surgery, drugs (opioids), or critical illness
*compromises nutrition
*can prolong hospital stays
intestinal pseudo-obstruction
*clinical picture of small bowel obstruction in absence of any physical or anatomical blockage
*absent peristalsis caused by neuromuscular disorders (scleroderma) or vasculitis
functions of ileocecal valve
*one-way valve: prevents backflow of colonic contents into small intestine lumen
-IC valve is tonically constricted
-helps reduce SB bacterial colonization
ileocecal valve reflexes
*mediated by cecal myenteric plexus and ANS
1. gastroileal: gastric distension relaxes the ICV and stimulates ileal peristalsis, promoting movement of chyme into cecum
2. cecal stretch: cecal back-pressure contracts the ICV and inhibits ileal peristalsis, stopping movement of chyme into cecum
resection of ileocecal valve
*commonly resected in cancer, Crohn’s disease, etc
*uncontrolled diarrhea (loss of ileal brake)
*small intestine bacterial overgrowth
colon has 2 functional organs
*right colon = electrolytes and H2O absorption
*left colon = storage of fecal matter
colonic motility patterns
1. haustrations (non-propulsive: local circular contractions facilitate electrolytes and water absorption)
2. mass movements (propulsive: longitudinal contractions transport feces from right to left colon)
*gastrocolic reflex (distension of stomach and duodenum initiates colonic mass movements via ANS)
constipation
*impaired motility leads to excess water absorption and hard feces
diarrhea
*increased motility or unabsorbable osmoles leads to reduced water absorption and liquid stools
internal anal sphincter
*circular smooth muscle
*autonomic control
external anal sphincter
*striated skeletal muscle
*voluntary control
recto-anal inhibitory reflex (RAIR)
*rectal distension leads to RELAXATION of internal anal sphincter
*mediated by enteric nervous system
defecation reflex
*rectal distension leads to increased sigmoid peristalsis
*mediated by enteric nervous system and parasympathetic spinal circuit
voluntary defecation
*mediated by skeletal motor nerves
*external anal sphincter relaxation
*increased abdominal wall pressure
Hirshsprung’s Disease
*absent myenteric plexus in distal colon leads to failure of internal anal sphincter relaxation, leading to severe constipation and colonic dilation
*diagnosed by absence of recto-anal inhibitory reflex on anorectal manometry
*treated by surgical resection of the aganglionic section of distal colon
impact of spinal cord injury or neuropathy on defecation
*disrupted pelvic motor and/or sensory nerve function, leading to loss of voluntary bowel control
*colonic myenteric reflexes are usually intact and can be used to re-train bowel function
