intestinal peristalsis physiology and motility disorders

Dr. Subhasish Deb

Burdwan Medical College

Dept of General Medicine

Dr Subhasish Deb, BMCH

Smooth muscles

of GIT made of

many muscle

bundles

Outer=

LONGITUDINAL

Inner= CIRCULAR


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


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

The RMP is fluctuating between -65 to -45mV

This Basic Electrical Rhythm(BER) is initiated

by interstitial

cells of Cajal

BER aka

Slow Waves


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


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


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


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


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


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


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


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


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.


Ach

Sub P

NO

VIPAurbach’s plexus

Stomach

Missner’s plexus

Intestine

Vagus

Sensory nerve


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)


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


Esophagus: Achalasia, GERD

Stomach: Gastroparesis

Small intestine: Ileus

Colon: Hirschsprung disease


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


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.


Barium Swallow shows Bird’s Beak

appearance


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


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)


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)


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


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


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


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


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


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


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)


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


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.


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


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


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)


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


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.


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.


Swenson, Soave, Duhamel, and Boley

procedures

The pull-through procedure repairs the colon by

connecting the functioning portion of the bowel

to the anus.


THANK YOUDr Subhasish Deb, BMCH

intestinal peristalsis physiology and motility disorders

Health & Medicine