Enteric Nervous System & Motility d/o Flashcards
What is the nervous system comprised of?
- CNS: brain, spinal cord
- PNS: somatic and autonomic (sympathetic, parasympathetic, enteric/ENS)
T/F The enteric nervous system can function independently of the CNS.
True.
the ENS receives input from the CNS and ANS, but it can function independently (reason why any part of the GI tract can be transplant from one person to another, but note that the transplant lack endogenous connections with the patient’s native vagus nerve and sympathetic nervous system)
Where are the neurons and glial cells of the enteric nervous system derived from?
How do theese cells populate the gut in the developing embryo?
neural crest cells
populate the gut in a linear fashion
(foregut->midgut->hindgut)
What are the 2 major ganglionated plexuses of the ENS?
Where are they normally found in the GI trat?
What do they innervate?
Where are IPAN cells found?
sub-mucosal plexus (Meissener’s)
• lies between the inner circular muscle layer and the mucosa
• primarily found in the small and large intestines but NOT in the esophagus/stomach
• innervate secretory cells, endocrine cells, and blood vessels in the mucosa and submucosa
myenteric plexus (Auerbach’s plexus)
• lies between inner circular and outer longitudinal layer
• extends from the upper esophagus to the internal anal sphincter
• provides motor innervation to the 2 muscle layers and secretomotor innervation to the mucosa
• ganglia connected to each other via internodal strands; branches from the intermodal strands
What are IPANs?
Where are they found? *be careful!*
What do they sense?
Where do they project to?
IPANs (intrinsic primary afferent neurons)
-primary receptors are located within the submucosal layer (but their cell body can be either in the submucosal or myenteric plexus)
respond to a variety of stimuli (chemical, stretch, distension)
project from the submucosal layer to the
• Myenteric plexus
• Brainstem via vagus n.
• Spinal cord via DRG
What are the major excitatory and inhibitory NTs of the GI?
excitatory : ACh, Substance P, Tachykinin
inhibitory: NO, VIP
serotonin: motor, sensory, and secretory functions; contained largely in interneurons
What are the 3 types of neurons found in the GI?
Where are they normally found?
What happens if you ablate each subset of neurons?
motor neurons
• act on smooth muscle, blood vessels, mucosal glands and mucosal cells; can be inhibitory or excitatory
• ablation -> flaccid bowel -> dysphagia, gastroparesis, bloating, constipation (or diarrhea)
interneurons
• interposed between sensory and motor neurons; role in amplifying and distributing signals throughout the gut
• ablation -> dysphagia, constipation, or diarrhea
sensory neurons
• found in plexuses (submucosal, myenteric)
• IPANS respond to a variety of stimuli (chemical, stretch, distension)
• ablation -> aperistalsis (no trigger!)
GI motility disorders can be caused by:
myopathic processes – usually a CT d/o (scleroderma, polymyositis, dermatomyositis, SLE) or congenital d/o (hollow visceral myopathy)
neuropathic processes – occurs due to injury to ENS, ANS, or CNS
both
Esophagus
layers?
muscle layers? what do they form?
innervation?
4 layers: mucosa, submucosa, muscularis propria, and adventitia (no serosa unlike the rest of the GI tract!)
2 muscle layers – inner circular + outer longitudinal; forms the
- UES: skeletal muscle; contracted at rest to prevent inspired air from being swallowed; innervated by pharyngeal branch of vagus n.
- LES: smooth muscle; contracted at rest to prevent reflux of gastric contents into the esophagus
innervation
- intrinsic: ENS
- extrinsic: parasympathetic (vagus) + sympathetic
LES tone is determined by: (3)
inner-circular muscle layer
fibers of R diaphragmatic crus
phrenoesophageal ligament
What is the pathophysiology of esophageal dysmotility? (5)
What are the features of these 5 esophageal d/o?
Achalasia – loss of NO neurons in LES, resulting in LES contraction and subsequent aperistalsis of the esophageal body
Hypertensive LES – loss of NO neurons or excess ACh that results in elevated resting pressure in LES, but esophageal peristalsis is normal (ie LES relaxation during swallowing is normal)
Diffuse esophageal spasm – uncoordinated peristalsis where the smooth muscle contracts or spasms all at once
Nutcracker esophagus – increased amplitude of contractions of the esophagus, but esophageal peristalsis is normal
GERD – due to TLESRs , where the LES relaxes via a vaso-vagal reflex in response to stomach distension (food/gas)
Stomach
function?
layers?
muscle layers?
innervation?
accommodation, trituration, emptying
4 layers: mucosa, submucosa, muscularis propria, and serosa
4 muscle layers
innervation
- intrinsic: ENS
- extrinsic: parasympathetic (vagus) + sympathetic (thoracic)
What are ICCs?
What do they do in the stomach? small intestines?
Can they generate contractions?
intercalated cells of cajal (aka pacemaker cells of the GI) - sets the frequency, velocity, and direction of the peristaltic waves
stomach: generates the intrinsic slow wave (3cpm) that migrates circumferentially and distally towards the pylorus
intestines: generate spontaneous slow waves (11-13 cpm)
Slow waves do not lead to contractions unless they coincide with an action potential
What is the MMC?
What is their role?
How does their role change with fasting or fed states?
Migrating Motor Complex (MMC) “housekeeper of the GI tract”
serves to clean out debris in the GI tract during fasting periods (antrum contracts more slowly, but more intensely than the small bowels)
fasting state: ACTIVE MMC
fed state: MMC stops
What can you use to measure stomach motility?
EEG – measures the slow waves and the increases in amplitude after a meal
What is the physiology in transferring food from the stomach to the duodenum?
Fundus relaxes via vagal-mediated reflex to accommodate food
• note: the fundus has high tone, little phasic activity
irregular contractions (chaotic) develop in the lower body and antrum breaks up food into smaller particles (<1mm)
• note: the antrum has low tone, high phasic/peristaltic activity (contracts in response to electrical slow waves
**food empties into proximal duodenum via pyloric sphincter **
What are 4 pathophysiological causes of stomach dysmotility? (4)
Gastroparesis – delayed gastric emptying in the absence of mechanical obstructions (ie cancer, ulcers, stones)
Functional dyspepsia – sensory d/o - postprandial fullness, early satiety, epigastric discomfort in the absence of structural disease
Dumping Syndrome
Rumination Syndrome
What is gastroparesis?
causes?
Symptoms?
how is it diagnosed?
Treatments?
Complications?
delayed gastric emptying in the absence of mechanical obstructions (ie cancer, ulcers, stones)
causes:
- severe hypothyroidism
- chronic intestinal pseudo-obstruction
- ischemia
- CT d/o
- abdominal sugery
- Rx: anti-cholinergics, opioids, TCAs
- diabetes (diabetic gastroparesis)***
Sx: nausea, vomiting, early satiety, epigastric/RUQ pain, weight loss, reflux
Dx:
- EGD (to look for obstructions) - NONE
- GES (quantifies emptying) = delayed
Trmts:
- metoclopramide and domperidone (dopamine antagonists/prokinetics)
- erythromycin
- Tegaserod (5HT agonist) to accelerate gastric emptying
- Botox
Complications:
- Mallory-Weiss tear
- bezoar formation
- reflux esophagitis
- malnutrition
- electrolyte d/o
What is functional dyspepsia?
Symptoms?
Treatments?
Complications?
sensory d/o with the absence of structural disease
Sx: postprandial fullness, early satiety, epigastric discomfort
- NO weight loss (comp. to gastroparesis)
Trmt: prokinetics do not help
What is the law of the intestines?
“Local stimulation of the gut produces excitation above and inhibition below the excited spot. These effects are dependent on the activity of the local nervous mechanism.”
Small Intestines
function?
layers?
muscle layers?
innervation?
absorption of nutrients
4 layers: mucosa, submucosa, muscularis propria, and serosa
2 muscle layers: inner circular + outer longitudinal
innervation:
- intrinsic: ENS
- extrinsic: parasympathetic (vagus) + sympathetic (thoracic)
What is the SITZ test? What is it used for?
assesses colonic transit time
used to distinguish between normal transit time, slow transit time, and functional outlet obstruction
uses a capsule containing 24 markers, patient swallows it and after a certain period, an Xray is taken to assess location and number of the markers
If >5 markers present, this indicates an abnormality with colonic motility
What is Hirschsprung’s disease?
What is the pathophysiology behind it?
What are the symptoms?
How is it diagnosed?
How is it treated?
cause: aganglionosis due to failure of the neural crest cells to migrate into the distal colon (rectum, sigmoid colon)
pathophysiology: IAS fails to relax properly as a result of aganglionosis,resulting in accumulation of colonic contents and subsequent dilation of the distal colon
Sx: failure to thrive, distention, bloating, constipation, vomiting; severe cases noted at birth
- *dx**:
- anorectal manometry and/or full thickness rectal biopsy
- digital rectal exam will cause ass explosion because putting in the finger in relieves the IAS obstruction…be careful!
Trmt: myotomy to remove aperistaltic area
Vomiting center in the medulla receives information from these 3 areas.
What stimulates these areas?
1) Vagal and sympathetic afferents (from the GI tract, the heart, the vestibular system) - stimulated by irritants (toxins, infections, inflammation, stretching)
2) chemoreceptor trigger zone (CTZ) afferents – located on the area postrema on the floor of the 4th ventricle (outside of the BBB, and is therefore very sensitive to chemical stimuli, toxins, NTs, and Rx).
3) afferent stimuli from higher-order CNS (cortex, thalamus, and hypothalamus) – transmits unpleasant tastes, offensive odors, or somatic pain
