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GI Motility Part 1
L-8
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Learning objectives
Role of enteric nervous system (ENS) ingastrointestinal motility
Types of motility & their functions
Mastication
Deglutition
Motor functions of the stomach (Gastricperistalsis, gastric emptying,)
The mechanism of vomiting- causes,consequences of protracted vomiting
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Learning outcomes
8.1 Briefly describe the function of ENS inGI motility
8.2 Briefly describe the mechanism ofdeglutition
8.3 Outline the basic physiologic
mechanism preventing or minimizinggastro esophageal reflux
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Learning outcomes contd
8.4 State the basic physiologic defect inAchalasia
8.5 Briefly describe the motor functions of
the stomach
8.6 Briefly describe how gastric emptyingis regulated ?
8.7 Briefly describe the basic physiologicmechanism of vomiting
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MASTCATION or Chewing
First mechanical process to which food is
subjected in the mouth. Its an voluntaryact.
Muscles of mastication are:
Masseter, internal and external pterygoids,temporal muscles and buccinator.
Movements of upper & lower jaw by thesemuscles bring about the apposition of two
rows of teeth, which grinds or breaks thefood. Tongue helps in rolling over thefood.
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Purpose served by mastication
-solid, large food particles are broken &reduced to a size convenient forswallowing.
- helps to break the indigestible cellulosecovering in fruits & vegetables.
- chewing results in reflex salivation
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- serves to mix food with saliva, so as tomoisten & lubricate & thereby facilitate act
of swallowing. - Helps to mix with digestive components
of saliva.
Physical act of chewing thus helps intaste, smell and appreciation of othersensory qualities of the food.
By mastication finally the bolus is formed.
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DEGLUTITION
It is the act of swallowing. The passage of
bolus from the oesophagus to stomach. Process is complicated since pharynx
forms a common passage for both
respiration & food passage. Divided into 3 stages:
1. Oral Phase (voluntary)
2. Pharyngeal phase (involuntary)
3. Oesophageal phase (involuntary)
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Deglutiion (act of swallowing)
Is a sequentially programmed reflex
Initiated voluntarily
Multiple responses triggered in a specifictimed sequence
Involves highly coordinated contraction of
several musclesSwallowing center located in the medulla
Receptors in the pharyngeal wall
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Oral phase
When the bolus is ready for swallowing, it
is voluntarily squeezed or rolled posteriorlyinto the pharynx by pressure of thetongue upwards & backwards against the
hard palate.
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Pharyngeal phase
As bolus enters posterior aspect of oral cavity,
around pharynx, receptors get stimulated &send impulses to medullary deglutition center,which initiates series of coordinated automaticpharyngeal muscle contractions.
Now the bolus can enter into nasal cavities,trachea or oesophagus. So first two entries hasto be blocked.
1. soft palate is pulled upwards to close theposterior nares, which prevents reflux of foodinto nasal cavities.
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2. Vocal cords of the larynx are strongly
approximated, and larynx is pulledupwards & anterior by the neck muscles.
These actions cause the epiglottis to swingbackwards over the opening of larynx,which prevents entry of food into trachea.
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3. Palatopharyngeal folds pulled medially
to approximate each other. These foldsform a saggital slit through which foodpasses, this selectively allows onlyproperly masticated food.
What is deglutition apnoea ?
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4. Upward movement of larynx also pullsup & enlarges the opening of the
esophagus. At the same timepharyngoesophageal sphincter relaxes,thus allowing bolus to move freely into
oesophagus from pharynx.
5. Peristalsis starts in superior part of the
pharynx then spreads over downward.
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Pharyngeal phase Tongue pressed
against hard palate Uvula elevated,
touches posteriorpharyngeal wall
Elevation of larynx Epiglottis swings
backwards
Closure of vocal
folds
Food prevented
from re-enteringmouth
Seals off nasalpassage
Food prevented
from re-enteringrespiratory passage
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1 2
5
3
4
Tongue
Uvula
Bolus
Epiglottis
Laryngeal opening
Esophagus
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Deglutition reflex Receptors: Pressure receptors on the
pharyngeal wall, especially onthe tonsillar pillars
Afferents: V, IX, X nerves
Center: Medulla oblongata (deglutition
centre)
Efferents: V, IX, X , XII nerves
Effectors: Muscles of tongue, pharynx,
larynx
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Define Pristalisis
constriction behind the bolus andrelaxation appears in front of the boluswhich results in forward movement ofbolus (oral to aboral direction).
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Peristalsis
constriction relaxation
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Peristalsis
Stimulus: Stretch of the gut wall
Speed: variable 2-25cm /min
Regulation: enteric NS (myentric plexus) ismust, modulated by extrinsic nerves i.e
sympathetic inhibits & parasympatheticstimulates. Can be blocked by atropine.
Function: propulsion of chyme from oral to
aboral direction.
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Oesophageal stage
Exhibits primary peristalsis, mostly continuationfrom pharynx , which passes all the way to
stomach. If it fails reaching stomach, sec peristalisis starts
from distended portion of oesophagus wherefood is retained.
Receptive relaxation of lower oesophagealsphincter(normally under tonic contraction withintramural pressure of 30 mm Hg) occurs aheadof the peristalitic wave, allows food to enter
stomach. Receptive relaxation of stomach also occurs.
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Applied aspects
Gastro esophageal reflux disease (GERD)
Frequent reflux of gastric contents into esophagus,due to incompetence of LES (sphincter nothaving tone). Symptom is heart burn, & this isthe commonest cause of unexplained chest pain.
AchalasiaLES fails in receptive relaxation, so bolus gets heldup in esophagus.
Dysphagia
Difficulty in swallowing. Esophageal musclescontract in a uncoordinated manner, may be dueto neural disorders.
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MOTILITY IN STOMACH
For purpose of describing movements
stomach is visualized to be consisting of 2parts- Orad (fundus & body), Caudad(lower part)
1. Receptive relaxation 2. Mixing & churning
3. Gastric emptying
All these observed when stomach is full.
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Receptive relaxation
To receive bolus orad part of stomach
relaxes. Due to vagally mediated reflexwhen the bolus reaches LES.
Advantages of relaxation:
As digestive processes are slow , stomachcan act as reservoir, gets sufficient timefor digestive juices to act.
Intragastric pressure doesnt rise much ( if
increases gastroesophageal reflux willoccur).
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2. Mixing & churning
These movements achieved by gastricperistalisis ( at a rate of 3/min) + closureof the pyloric sphincter.
Effects of these movements are-
Breaking down of coarse food chunks
Thorough mixing of gastric juice with food
Squirting of gastric chyme into duodenum(ejecting of small volume of chyme in thinspurt)
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Enterogastric reflex: inhibitory reflex arisingfrom duodenum which prevents gastric
emptying 1. Degree of distension of duodenum
2. Degree of irritation of duodenum
3. Degree of acidity of duodenum(pH
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Gastric motility disorders:delayed gastric emptying(gastroparesis), rapid gastric emptying (dumpingsyndrome.
Reasons of abnormally delayed gastric emptying:
1) Pylorus and duodenum may be obstructed by an ulceror tumor, or by something large and indigestible that
was swallowed. (2) The pyloric sphincter at the exit of the stomach may
not open enough or at the right times to allow food topass through. These reflexes depend on nerves thatsometimes become damaged.
(3) The normally rhythmic, 3/min contractions of thelower part of the stomach can become disorganized sothat the contents of the stomach are not pushed towardsthe pyloric sphincter
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Rate of emptying stomach intoduodenum based on the type of food
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Gastric peristalisis in empty stomach(Migrating myoelectric complex MMC)
Empty stomach remains quiescent for 75-90mins, after this a MMC develops.
MMC is a wave of depolarization which is
immediately followed by an wave of muscularcontraction (hunger contractions).
MMC sweeps the whole stomach, then travelsduodenum, rest part of intestine, terminates at
terminal part of ileum taking about 10 mins.Again stomach rests for 75-90 mins then the
MMC repeats.
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Vomiting (emesis)
Oral expulsion of upper GI contentsresulting from contractions of the gut andmuscles of the thorax and abdomen.
Retrograde or reverse peristalsis
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Causes of vomiting & mechanism
Poison ingestion (by irritation)
Increased intracranial tension (symptomof a disease)
Uremia ( effects on chemoreceptor triggerzone in medulla)
Impairment of gastric motility( increaseintragastric pressure).
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Mechanism of vomiting in intestinalobstruction:
Aff input to vomiting center in medulla, reflexlysends efferent impulses to abdominal muscles &diaphragm
Retrograde peristalsis in stomach
Intragastric pressure increases
LES relaxes & vomitus ejected via esophagus(closure of glottis prevents aspiration of
vomitus)
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Consequences of Protractedvomiting:
Dehydration due to loss of GI secretions
Loss of hydrogen ions leads metabolic
alkalosis Prolonged vomiting leads to malnutrition
Loss of chloride ions ( hypochloremia)