Swallowing, Gastric Emptying and Intestinal Motility Flashcards
Phases of swallowing
oral, pharyngeal, esophageal
Aspects of gastric motility
Receptive relaxation/Gastric accommodation, Mixing, Emptying, Migrating myoelectric complex
small intestine motility (3)
Segmentation, Peristalsis, Migrating myoelectric complex
large intestine motility (4)
Haustrations, Long-duration contractions, Mass movements
Defecation reflex
Swallowing: receptors, integration center, effectors
Deglutition
Initiated voluntarily
Reflex control of events moving food from mouth → stomach
Receptors: Touch receptors
-Primarily near opening of pharynx
Integration center: Swallowing center
-Medulla oblongata (lower pons)
Effectors: Pharyngeal and esophageal striated and smooth m.
-Cranial n.n.: pharynx and upper esophagus
-Vagus n.: lower esophagus
Swallowing: 3 Phases
Oral phase: Voluntary
-Bolus: tongue pharynx
- Pharyngeal phase: Involuntary
-Initiated by response to pressure
receptors in pharynx
-Directs bolus into esophagus via
relaxed upper esophageal sphincter (UES) - Esophageal phase: Involuntary
-Bolus from UES via peristalsis through
lower esophageal sphincter (LES) stomach
Pharynx propulsive function
food transfer to esophagus
Upper Esophageal Sphincter (UES) propulsive functions and protective effects
allows entry of food into esophagus
protects airway from swallowed material
Esophagus function and protective effects
transports bolus from pharynx to stomach
clears material refluxed from stomach
Lower Esophageal Sphincter (LES) function and protective effects
allows entry of food into stomach
protects esophagus from gastric reflux
Swallowing- oral phase
Tongue pushes bolus against hard palate
Touch receptors of the pharynx detect bolus
Swallowing reflex is initiated
Swallowing- pharyngeal phase
involuntary
Propels food from pharynx into esophagus
Respiration inhibited
1.Bolus is directed into pharynx
-Elevation of soft palate blocks entry
to nasopharynx
2.Epiglottis blocks entry to trachea
3.Pharyngeal m.m. push bolus into pharynx; UES relaxes
4.Peristaltic wave moves bolus
through UES
5. During pharyngeal stage of swallowing, respiration is
reflexely inhibited
Pressure peak travels during swallowing
pharynx -> upper sphincter of esophagus –> junction of smooth and striated muscle–> body of esophagus–> lower sphincter of esophagus
Swallowing: esophageal phase
After UES closes, LES begins to relax Primary peristaltic wave begins below UES -Reflex initiated by swallowing center Secondary peristalsis -Initiated by distention -Occurs only if primary wave is not sufficient
What kind of input modulates esophageal peristalsis?
Input from esophageal sensory fibers to the CNS
and ENS modulates both primary and secondary
esophageal peristalsis
Sphincters- general
Muscular barriers
High resting pressure in order to maintain separation
Regulate antegrade and retrograde movement
In general:
Proximal stimuli → relaxation
Distal stimuli → contraction
Facilitate unidirectional movement through G.I. tract
Coordination of:
-Other smooth muscle contractions
-Neural stimulation
-Humoral stimulation
Sphincters- general
Muscular barriers
High resting pressure in order to maintain separation
Regulate antegrade and retrograde movement
In general:
Proximal stimuli → relaxation
Distal stimuli → contraction
Facilitate unidirectional movement through G.I. tract
Coordination of:
-Other smooth muscle contractions
-Neural stimulation
-Humoral stimulation
Upper esophageal sphincter
Skeletal muscle
Regulated by swallowing center via cranial n.n.
Highest resting pressure of GI sphincters
Closed during inspiration
Limits air entry to esophagus
Lower esophageal sphincter
Smooth muscle
Primary function:
allows coordinated movement of food into stomach
prevents reflux of gastric contents into esophagus
LES resting tone:
-Intrinsic myogenic properties
-Cholinergic regulation
LES relaxation:
Intrinsic smooth muscle properties
Vagus n. (inhibition by VIP and NO)
LES relaxation occurs after UES returns to resting pressure
Swallowing or esophageal distention → decreases LES pressure
GERD
the most common symptom of
heartburn due to stomach acid reflux
into esophagus
is not a disease but a normal physiological process
stomach contents leak backwards from the stomach into the esophagus and irritates the lining of the esophagus
this occurs when the lower esophageal sphincter (LES) does not work properly
weak squamous lining of the lower esophageal section
decrease secretion of mucus and bicarbonate in saliva
Barrett’s esophagus
(pre-cancerous lesion):
it is most often diagnosed in people who have long-term GERD (chronic inflammation)
this condition is recognized as a complication of GERD
a condition in whichcolumnar cells replace squamous cell in themucosa of esophagus
the main cause of Barrett’s esophagus is thought to be an adaptation to chronic acid
exposure fromreflux esophagitis
its importance lies in its predisposition to evolve into esophagealcancer
it develops in about 10–20% of patients withchronic GERD.
Dysphagia
common problem in elderly people with difficulty
in swallowing, food getting caught in esophagus
risk of aspiration, choking and malnutrition
difficulty in swallowing due to abnormalities in:
structural - anatomical structures
- abnormal tongue, cannot propel bolus backward
- diverticula (outpouchings of pharyngeal or
esophageal wall) in which food is trapped.
functional - abnormal swallowing reflex
- neurological defect and control of oropharyngeal
swallowing, peristalsis, and esophageal sphincter
relaxation, or to defects in muscle layers.
disease state:
- neurological disorders
- stroke
- Parkinson’s disease
- myasthenia gravis
- xerostomia
Achalasia
(failure to relax):
special form of dysphagia
complete lack of peristalsis within esophagus
LES does not relax and increased LES pressure
food is retained at the level of LES
caused by:
- nerve degeneration (enteric nervous system)
- lack of NO synthase, VIP, etc
- Chagas disease (infection protozoa: Trypanosoma cruzi)
What does the radiography look like in achalasia?
bird’s beak
Incompetent LES
The LES acts like a guard that prevents anything that gets into the stomach from refluxing into the esophagus, it acts as a pressure barrier at the gastro-esophageal junction
Incompetent LES or transient relaxation of LES are the most common symptoms
of reflux. Physiologically, a well functioning LES will remain closed except in:
- primary peristalsis-within 2 sec after a swallow, leads to LES relaxation for
5-10 sec (release of NO & VIP) and then contracts
- secondary peristalsis-LES relaxation occurs as a reflex after distention of
proximal striated or more distal esophageal smooth muscle
- transient LES relaxation are not associated with pharyngeal contraction or
esophageal peristalsis and persists for more than 10 sec.
control of LES function are not completely understood
various drugs, hormones, and neuro-humoral agents produce stimulatory or inhibitory effects on the LES by binding with specific receptors
cessation of excitatory cholinergic activity and release of NO and VIP leads to LES relaxation
GERD is secondary to an incompetent lower esophageal sphincter
as the real cause to incompetent LES is not known it is sometimes referred to as idiopathic LES Incompetence
Diffuse esophageal spasms
diffuse esophageal spasms (DES) are irregular, uncoordinated, and sometimes powerful contractions of the esophagus
it is characterized by contractions that are of normal amplitude but are uncoordinated, simultaneous, or rapidly propagated
these spasms can prevent food from reaching the stomach, leaving it stuck in the esophagus
it can cause dysphagia, regurgitation and chest pain
the cause of esophageal spasm is unknown
may caused by disruption of the nerve activity that coordinates the swallowing action of the esophagus
in some people, very hot or very cold foods may trigger an episode
What does radiography look like in DES?
corkscrew appearance
Hiatal hernia
a hiatus hernia or hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm
in hiatal hernia, it is easier for stomach acids to come up into the esophagus
this causes a burning feeling in the throat and chest
symptoms similar to GERD
Functional divisions of the stomach: roles in motility
LES and Cardia: prevention of reflux, entry of food, regulation of belching
Fundus and body: reservoir, tonic force during emptying
Antrum and pylorus: mixing, grinding, sieving, regulation of emptying
Receptive relaxation
Initiated by swallowing (esophageal peristalsis)
LES and stomach (fundus & body) relax
Vagovagal reflex
Vasoactive Intestinal Peptide (VIP)
Pressure in stomach does not increase despite increased volume
Disruption of vagus n. → rapid pressure increase
Vagotomy
Gastric accomodation
Relaxation in response to
gastric filling
-Activate dilation of fundus
Early changes in volume do not result in increased gastric pressure
-Allows for storage
After threshold: rapid increase in pressure for increased volume
Vagus n.
-Modulates
-Vagotomy results in decreased accommodation
Enteric nervous system
Overview: gastric mixing and emptying- Excitatory portion
Excitatory: Gastric Mixing (Antrum)
Increased gastric contractility
Stomach contents:
(+) stimuli for increasing contractility
-Volume of chyme (distension)
- Fluidity of chyme
ENS: Acetylcholine and Substance P
Gastrin
Gastric mixing and emptying: inhibitory portion
Inhibitory: Gastric Emptying
Duodenum contents:
(-) stimuli for gastric emptying
-Duodenum has to be ready to receive food
-Stimuli in duodenum inhibit gastric emptying:
Fatty acids & monoglycerides; Acidic pH; Volume/distension,
Hypertonicity, Amino acids & peptides
Neural responses: Intrinsic & extrinsic
Hormonal response:
Cholecystokinin (CCK), Secretin, Gastric Inhibitory Peptide (GIP)
Effects on gastric motility and emptying: volume of chyme
increased volume stimulates motility and emptying
Effects on gastric motility and emptying: degree of fluidity
increased fluidity allows more rapid emptying
Effects on gastric motility and emptying: presence of fat, acid, hypertonicity or distension (in duodenum)
these factors in the duodenum inhibit further gastric motility and emptying until the duodenum has coped with factors already present
Effects on gastric motility and emptying: emotion
stimulates or inhibits motility and emptying
Gastric contractions: Slow waves, APs, pacemaker
Pacemaker zone: sets rate of gastric peristalsis
-Body of stomach
~ 3 – 5 slow waves/min.
Contraction force:
-Degree of depolarization
-Duration of membrane depolarization
Acetylcholine & Gastrin
-Increase amplitude and duration
-Increase contractility
Norepinephrine
-Decreases contractilityGastric contractions: Slow waves, APs, pacemaker
Pacemaker zone: sets rate of gastric peristalsis
-Body of stomach
~ 3 – 5 slow waves/min.
Contraction force:
-Degree of depolarization
-Duration of membrane depolarization
Acetylcholine & Gastrin
-Increase amplitude and duration
-Increase contractility
Norepinephrine
-Decreases contractilityGastric Mixing
Propulsion
Grinding
Retropulsion
Trituration:
-reduction of solid particle size
-> 2 mm do not leave the stomach
during the gastric phase (right after
a meal)
-Emptying is delayed until solids are
mechanically broken down
Gastric Emptying rates
Liquid > Carbohydrate > Protein > Fat
Isotonic > hypertonic or hypotonic
Duodenal contents affecting gastric emptying
Receptors in duodenum:
- pH, osmolarity, fatty acids/monoglycerides, amino acids/peptides
Gastric emptying slowed by:
- Byproducts of fat and protein digestion
- Hypertonic chyme
-
Duodenal contents delaying gastric emptying: coordinated events
Coordinated Events (Neural and Hormonal):
Relaxation of the fundus
Inhibition of antral contractions
Stimulation pyloric sphincter contractions (phasic)
Pyloric Sphincter (hormonal and neural regulation)
Hormonal Regulation:
Increased constriction:
-CCK, GIP, Secretin, Gastrin
Neural Regulation:
Sympathetic → constriction
Parasympathetic: Vagus n.
- Constriction: Acetylcholine - Relaxation: VIP
Migrating Myoelectic complex: Stomach
Fasting State -occurs every 75 – 90 (120) min -starts about 2 hrs after meal Stomach → ileum -“Cleans” tract -Removes remaining ingested contents (solids > 2mm) Burst of antral electrical activity (~ 5-10 min) Very strong antral contractions Relaxation of pylorus
Vomiting
Complex reflex reaction (Emesis)
-Integration includes medullary “vomiting center”
Stimuli include:
- Gastric & duodenal distention, irritants
- Dizziness, inner ear dysfunction, motion sickness
- Drugs
- Genitourinary injury
- Emetics: chemicals that can cause vomiting
Chemoreceptor trigger zone (brain 4th ventricle)
Gastric/Duodenal receptors (ex: ipecac)
Reflex response of vomiting
Reverse peristalsis (small intestine → pylorus) Pyloric sphincter relaxes, stomach relaxes Abdominal m.m. contraction Pylorus and antrum contract LES relaxes Gastric contents → esophagus UES relaxes -Retching: UES remains closed
3 Primary Types of Small Intestinal Motility
Segmentation:
-Mixing
Peristalsis
-Propulsion
Migrating myoelectric complex
-Sweeping of undigested contents during fasting state
Small intestine: 1. Segmentation
Postprandial period: - Alternating contractions of circular smooth m.
Slow process of propulsion & retropulsion - Time for digestion & absorption - Mixes chyme with digestive secretions - Maximizes contact with mucosal layer
Small intestine: 3. Migrating Myoelectric Complex
Propulsive movement initiated during fasting
Moves undigested material:
Stomach & small intestine → colon
New wave starts in stomach once previous wave passes distal ileum
Pylorus and ileocecal sphincter are relaxed
3 phases: Quiescence, small disorganized contractions, strong propagating contractions (~ 5-10 min)
Repeats every ~ 75-120 min during fasting
Correlated with high levels of circulating motilin (small intestinal hormone)
Prevents backflow of bacteria from colon into ileum
Small intestine: 3. Migrating Myoelectric Complex
Propulsive movement initiated during fasting
Moves undigested material:
Stomach & small intestine → colon
New wave starts in stomach once previous wave passes distal ileum
Pylorus and ileocecal sphincter are relaxed
3 phases: Quiescence, small disorganized contractions, strong propagating contractions (~ 5-10 min)
Repeats every ~ 75-120 min during fasting
Correlated with high levels of circulating motilin (small intestinal hormone)
Prevents backflow of bacteria from colon into ileum
Basic electrical rhythm of intestinal contractions
slow waves
- Duodenum (highest rate: ~ 11-13/min)
- Jejunum (~10-11/min)
- Ileum (~8-9/min)
What to bursts of APs on top of slow waves do?
increase strength of contractions for
intestinal motility
- Hormones
- Enteric nerve plexuses
- Parasympathetic and Sympathetic via ENSLaw of intestine:
contraction behind & relaxation in front of bolus
- Intrinsic reflex (ENS)
intestinointestinal reflex
: distention in one segment, relaxation in the rest
of the small intestine
- Long range coordination: Extrinsic and intrinsic
~ 2-4 hrs. for chyme to move through small intestine
Ileocecal sphincter
Normally contracted Tone coordinated primarily by: - Enteric neural reflexes - Long-range extrinsic neural reflexes - Hormones Distention in ileum → relaxation Distention in ascending colon → constriction Gastroileal reflex - Increased gastric activity → increased ileal motility and relaxation of sphincter
Goal: control rate of chyme entering colon so that colon can effectively absorb water and salts
3 types of colonic motility
haustrations
long-duration contractions
mass movements
Haustrations
Short-duration contractions (~ 8 sec stationary pressure waves)
Circular m. mixing contractions (not propulsive)
Long-duration contractions (~ 20-60 sec)
Taeniae coli
Mixing contractions, may propagate short distances in either direction
Antipropulsive movements in proximal colon: retain chyme
Goal: slow movement through colon for absorption
Mass movements
High-amplitude propagating contractions (high intensity)
Sweep length of colon (cecum to rectum)
1-3/day (1-10/day)
High variability in colonic motility rates among individuals (vs. small intestinal motility)
Regulation of colonic motility
Primarily neural regulation (ENS, PNS, SNS)
Intrinsic control; Extrinsic modulation
Local reflexes: Colonic distention Contraction behind (ACH and Substance P) and relaxation (VIP and NO) in front of bolus
Long-range reflex: Gastric distention
Gastrocolic reflex
Stomach distention results in generalized increase in colonic motility
ANS regulation of colonic motility
Parasympathetic: increased motility
Vagus n. via ENS:
Increased mixing contractions in proximal colon
Pelvic n.n. via ENS:
Increased contractions and propulsive movements in distal colon
Sympathetic: Inhibits motility
Postganglionics via abdominal sympathetic ganglia
Internal anal sphincter
Internal anal sphincter (IAS):
Smooth muscle
Involuntary control
Majority of tone
extrenal anal sphincter
Striated muscle
Voluntary & involuntary control
Defecation reflex
Expulsion of undigestible residues
Requires extrinsic neural input
– Higher CNS & spinal cord coordination via
pelvic n.n.
Distention of rectum →
Reflex relaxation of IAS
Rectosphincteric reflex: VIP & NO
Reflex constriction of EAS
Postponed defecation:
Accommodation of rectum
IAS: contract
EAS: relaxDefecation definition
Coordinated series of voluntary and involuntary events including:
Voluntary relaxation of EAS
Contraction of abdominal m.m.
Relaxation of pelvic muscles
Hirschsprung’s Disease
disease (congenital megacolon)
Congenital failure of enteric neural plexus development
Impair motility function
Aganglionic segment, remains contracted
-Commonly just above the IAS becomes dilated
Rectosphincteric reflex impaired
-Dilation of colon proximal to site of obstruction
Treatment: Symptoms alleviated by surgical excision of the diseased segment
Irritable Bowel Syndrome
Irritable Bowel Syndrome or Disease (IBS/IBD) is a group of inflammatory
conditions of the colon and small intestine.
Due to visceral hypersensitivity due to sensitization of afferent neural pathways
-respond abnormally to stimuli
-idiopathic, distension, inflammation, GI infections, etc
-Partially dysmotility
The major types of IBD are Crohn’s disease and ulcerative colitis
Although very different diseases, may present any of the following symptoms:
Abdominal pain, vomiting, diarrhea, rectal bleeding, severe internal cramps
Diagnosis by assessment of inflammatory markers is stool followed by colonoscopy with biopsy of pathological lesions.
