intestinal peristalsis physiology and motility disorders
TRANSCRIPT
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Dr. Subhasish Deb
Burdwan Medical College
Dept of General Medicine
Dr Subhasish Deb, BMCH
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Smooth muscles
of GIT made of
many muscle
bundles
Outer=
LONGITUDINAL
Inner= CIRCULAR
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Smooth muscles of a bundle
connected with GAP JUNCTIONS
Adjacent bundles also connected
with GAP Junctions
Stimulation of 1 bundle stiml the
other bundle thus acts as an
electrical syncitium
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Interstitial cells of CAJAL Present between long and circular
layer
Can produce pacemaker activity (like heart)
Electrical
activity
spreads via
gap
junctons
Interstitial cell of cajalDr Subhasish Deb, BMCH
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The RMP is fluctuating between -65 to -45mV
This Basic Electrical Rhythm(BER) is initiated
by interstitial
cells of Cajal
BER aka
Slow Waves
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Ca channels present allow Ca2+ to enter
continuously
This raises the RMP from -65 to -45
when K+ channels open
Efflux of K and the RMP comes back to
-65mV
These are NOT ACTION POTENTIALS
They do NOT CAUSE CONTRACTIONS
RATE OF SLOW WAVES:
I. Stomatch : 3/min
II. Duodenum : 12/min
III. Jejunum, ileum : 9/min
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So excitibility of GIT soomth muscles increases progressively and decr progressively
IF peak of this wave touches the threshholdpotential -40mV, voltage sensitive Ca channles open –- Ca influx –- Contraction
When repolarisation occurs, it still finds the slow wave above the threshhold so another spike is produced
These Aps at the top are called SPIKE POTENTIALS
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Key Points:
1. Action potentials = Spike potential
2. How many spikes(Aps) produced
depends on how long the slow
wave remains above TP
3. If slow wave does not reach TP
then no APs
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Muscle excitability can ne changed by change in RMP.
RMP to -50mV = more excitability (slow waves will be frequently over TP, more spikes)
RMP to -70mV = less excitability
Factors inc RMP:1. Muscle Stretch : more Ca influx through
channels
2. Acetylcholine : vagus
3. Parasympathetic stimulation
4. Some hormones
Factors decr RMP:1. Nor epinephrine
2. Sympathetic stimulation
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ENTERIC NERVOUS SYSTEM
Can work independent of higher
impulses (thus also called mini brain)
Considered as 3rd part of ANS
Consists of 2 neuronal layers
1. Myentric plexus (Aurbach’s plexus) in
muscular layer
2. Missner’s plexus in submucosa
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Missner’s plexus
Submucosal
Mainly regulates secretion from mucosal &
submucosal glands
Blood flow in these layers determine
absorption
Aurbach’s plexus
In Muscular layer
Mainly concerned with motility
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Stimulus for peristalsis:
1. Stretch by food bolus – stimulates sensory
neurons which then stimulate myenteric
plexus
2. Chemical signals or irritation of mucosa
Peristalsis: for it to occur, the oral side
of the GIT to the food bolus should
contract and the anal side should relax
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The myenteric plexus has 2 sets of neurons:
1. Ascending (signal moves towards oral side)
2. Descending (signal moves towards anal side)
When sensory system (stretch) stimuates
ascending fibres, they release Ach & Sub P
which are positive neuro transmitters – go
on stimulating fibres towards oral side
Contraction of muscles behind the food
bolus
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At the same time sensory neurons also
stimulate the descending neurons. They
release NO and Vaso Inhibitory Peptide(VIP)
This causes relaxation of smooth muscle
distal to the food bolus
Food particle moves forward, causes local
stretch in the new area ad the whole thing
repeats.
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Ach
Sub P
NO
VIPAurbach’s plexus
Stomach
Missner’s plexus
Intestine
Vagus
Sensory nerve
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Parasympathetic control:
(directly innervaye neurons of both the plexus thus the
myenteric & missner’s plx can be considered as post
ganglionic fibres of para sys)
Inc motility
Inc digestion
Inc absorbtion
Sympathetic control: via postganglionic fibre
Dec motility
Dec digestion
Dec absorbtion
(directly affect splanchnic vessels- vasoconstriction-
diverts blood to other areas)
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1. Intra gut reflex: Local reflex
Local irritaton/dilatation – inc secretion, contraction
2. Ganglionic reflex: Gastrocolic
Enterogastric
Coloileal
3. Cns reflex: Vago vagal reflex (senry input from stomach to
medulla via vagus and back to stomach via vagus)
Defecation reflex
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Esophagus: Achalasia, GERD
Stomach: Gastroparesis
Small intestine: Ileus
Colon: Hirschsprung disease
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Achalasia is a primary esophageal motility disorder
characterized by the absence of esophageal peristalsis
and impaired relaxation of the lower esophageal
sphincter (LES) in response to swallowing.
Signs and Symptoms:
• Dysphagia (m/c)
• Regurgitation
• Chest pain
• Weight loss
Physical exam and lab studies are non contributary
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Pathophysiology:
LES pressure and relaxation are regulated by
excitatory (eg, acetylcholine, substance P) and
inhibitory (eg, nitric oxide, vasoactive
intestinal peptide) neurotransmitters.
Here there is lack of inhibitory
neurotransmission.
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Barium Swallow shows Bird’s Beak
appearance
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Other investigations:
1. Esophageal manometry:
incomplete LES relaxation on swallowing
High LES resting pressure
Absent esophageal peristalsis
2. Prolonged esophageal pH moitoring :
To rule out GERD
3. Esophageogastroduodenoscopy
To rule out CA of GEJ and fundus
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Treatment:
1. Pharmacological:
Ca channel blockers, nitrates – for elderly pts
who cannot undergo pnuemaic dilatation or
surgery
Endoscopic intrasphincteric injection of
botulinum toxin to block acetylcholine
release at the level of the LES
2. Surgical: Laparoscopic Heller myotomy, preferably with
anterior (Dor; more common) or posterior
(Toupet) partial fundoplication
Peroral endoscopic myotomy (POEM)
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Gastroesophageal reflux disease occurs when
the amount of gastric juice that refluxes into
the esophagus exceeds the normal limit,
causing symptoms with or without associated
esophageal mucosal injury (ie, esophagitis)
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Signs and Symptoms:
(typical esophageal)
Heart burn
Regurgitation
Dysphagia
(Atypical extraesophageal symptoms)
Coughing and/or wheezing
Hoarseness, sore throat
Otitis media
Noncardiac chest pain
Enamel erosion or other dental manifestations
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Investigations: Upper GI endoscopy
Esophageal manometry
Ambulatory 24-hour pH monitoring: Criterion standard in establishing a diagnosis of gastroesophageal reflux disease
Management principles:1. Control symptoms
2. Heal esophagitis
3. Prevent recurrent esophagitis and complications
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Management:
Life style modification- Losing weight (if overweight)
Avoiding alcohol, chocolate, citrus juice and tomato-based products
Avoiding peppermint, coffee and possibly the onion family
Eating small, frequent meals rather than large meals
Waiting 3 hours after a meal to lie down
Refraining from ingesting food (except liquids) within 3 hours of bedtime
Elevating the head of the bed 8 inches
Avoiding bending or stooping positions
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Pharmacotherapy:
H2 receptor antagonists (eg, ranitidine,
cimetidine, famotidine, nizatidine)
Proton pump inhibitors (eg, omeprazole,
lansoprazole, rabeprazole, esomeprazole,
pantoprazole)
Prokinetic agents (eg, aluminum hydroxide)
Antacids (eg, aluminum hydroxide, magnesium
hydroxide)
Surgical options:
Transthoracic and transabdominal
fundoplications are performed for
gastroesophageal reflux disease, including partial
(anterior or posterior) and circumferential wraps
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Indications of Fundoplication:
Patients with symptoms that are not completely
controlled by proton pump inhibitors
Patients with well-controlled reflux disease who
desire definitive, one-time treatment
The presence of Barrett esophagus
The presence of extraesophageal manifestations
Young patients
Poor patient compliance with regard to
medications
Postmenopausal women with osteoporosis
Patients with cardiac conduction defects
Cost of medical therapy
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Aka delayed gastric emptying
paresis (partial paralysis) of the stomach,
resulting in food remaining in the stomach
for an abnormally long time
May occur due to:
1. Damage of vagus nerve
2. Improper functioning of muscle of stomach
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Signs and symptoms:
Chronic nausea (93%)
Vomiting (especially of undigested food) (68-84%)
Abdominal pain (46-90%)
A feeling of fullness after eating just a few bites (60-86%)
Causes:1. DM- autonomic neuropathy
2. CTDs- scleroderma, Ehler Danlos
3. Parkinson’s disease
4. Abdominal surgery- injury to vagus
5. Idiopathic- autoimmune response triggered by viral inection
Diagnosis: gastric emptying scan (radio nucleotide)
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Treatment:
Dietary changes
Low fiber diet
Avoid fat
Smaller meals spaced 2-3 hrs apart
Prokinetic medications
Domperidone, cisapride, erythromycin,
metochopramide
Adjustment of insulin dose for DM
Jejunostomy tube, parenteral nutrition
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hypomotility of the gastrointestinal tract in
the absence of mechanical bowel obstruction
Although certain older terms such as
gallstone ileus and meconium ileus persist in
usage, they are now misnomers.
Pathophysiology:
The exact pathogenesis of ileus remains unclear.
Postoperative ileus may be mediated via
activation of inhibitory spinal reflex arcs.
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Although ileus has numerous causes, the
postoperative state is the most common
setting for the development of ileus.
Physiologic ileus spontaneously resolves
within 2-3 days, after sigmoid motility
returns to normal. Ileus that persists for
more than 3 days following surgery is termed
postoperative adynamic ileus or paralytic
ileus
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Risk Factors:
gastrointestinal surgery or other GI procedures
electrolyte imbalance diabetic ketoacidosis
(DKA) and other causes of metabolic acidosis
hypothyroidism
medications (e.g. opiates or antimuscarinics)
severe illness (Inflammation with peritonitis)
spinal cord injury, those with injury above
thoracic vertebrae 5 (T5) will have
hypomotility problems within the bowel
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Treatment:
NPM + nasogastic suction + parenteral nutrition
(to avoid perforation)
Bowel movements may be stimulated by
lactulose, erythromycin.
a systematic review of randomized controlled
trials show that chewing gum, as a form of 'sham
feeding', may stimulate gastrointestinal motility
Correction of underlying cause (electrolytes,
thyroid)
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Hirschsprung disease is a developmental
disorder characterized by absence of ganglia
in the distal colon, resulting in a functional
obstruction
should be considered in any newborn that
fails to pass meconium within 24-48 hours of
birth
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Pathophysiology:
Normal motility is primarily under the control of
intrinsic neurons. In the absence of extrinsic
signals, bowel function remains adequate, owing
to the complex reflexive architecture of the
enteric nervous system (ENS)
Enteric ganglion cells are derived from the neural
crest during embryonic development.
One possible etiology of Hirschsprung disease is
the arrest of aboral neuroblast migration.
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Diagnosis:
Definitive diagnosis is made by suction biopsy of
the distally narrowed segment. A histologic
examination of the tissue would show a lack of
ganglionic nerve cells.
Treatment:
surgical removal (resection) of the abnormal
section of the colon, followed by reanastomosis.
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Swenson, Soave, Duhamel, and Boley
procedures
The pull-through procedure repairs the colon by
connecting the functioning portion of the bowel
to the anus.
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THANK YOUDr Subhasish Deb, BMCH