Motility disorders

Dr.Prasanjanie Jayasinghe
Lesson Learning Out comes …
Students should be able to

1. Describe the mechanism of vomiting

2. Describe common GI motility disorders
3. Describe basis of diagnosis common motility disorders
4. Describe principles of management of common motility disorders
Outline
• Introduction
• Motor Disorders of the Oesophagus
• Paralytic Ileus
• Hirschsprung Disease
• Vomiting
Recap; GI Motility
GENERAL PATTERNS OF MOTILITY
• Peristalsis
• Segmentation & Mixing
• Basic electrical rhythm (BER) is initiated by the interstitial cells of Cajal
• Migrating motor complex (MMC)
Regulation
• Neuronal
• Hormonal
• Myogenic
• GI Reflexes
Common GI motility disorders
Upper GI motility Lower GI motility disorders
Achalasia:Loss of esophageal peristalsis, with failure of Paralytic Ileus
the lower esophageal sphincter (LES) to relax
Gastroesophageal reflux disease (GERD): Reflux of Irritable bowel syndrome
gastric contents from the stomach into the esophagus
Gastroparesis:Delayed gastric emptying without Hirschsprung disease: Also known as congenital
evidence of mechanical obstruction aganglionic megacolon, in which the distal section of
the colon that is missing ganglion cells fails to relax
Clinical Features
Upper intestinal motlity disorders Lower intestinal motility disorders
Abdominal distention Recurrent obstruction
Severe abdominal colicky pain Severe abdominal colicky pain
GERD Severe constipation
Intractable or recurrent nausea or vomiting Diarrhea
Stool incontinence
Motor Disorders of the Oesophagus
• Achalasia
• GORD
Achalasia

• Literally - failure to relax

• Food accumulates in the oesophagus -
massively dilated.
• The lower oesophageal pressure is
elevated in more than half of patients.
 Achalasia - Pathophysiology
Massively
dilatation of the
Esophagus

-Deficient Myenteric
plexus of esophagus/ Food accumulates Ulceration of the
Severe substernal pain or
at the LES and putridly esophageal
mucosa even rupture and death
-Defective release of infected
NO and VIP

Elevated lower
oesophageal
pressure
Clinical Features

• Long history of intermittent dysphagia, characteristically For both

liquids and solids from the onset.
• Spontaneous chest pain (oesophageal ‘spasm’)
• Severe substernal chest pain
• Regurgitation of food from the dilated oesophagus occurs, particularly
at night
• Aspiration pneumonia
Chest X-ray

• Dilated oesophagus
• Fluid level seen behind the heart.
• Absent fundal gas shadow
Barium swallow
• The oesophagus is dilated and
tapers inferiorly with a ‘bird-
beak’ appearance at the
gastro-oesophageal junction.
Esophageal Manometry
• Usually required for
confirmation of
diagnosis
• Elevated resting LES
pressure
• Incomplete LES
relaxation
• Absence of
peristalsis
Treatment

• Pneumatic/Balloon dilation of the sphincter or incision of the

esophageal muscle (myotomy).
• Injection of botulinum toxin into the LES( Inhibition of acetylcholine
release by )
• Surgical treatment
Gastroesophageal reflux disease ; Recap ;;
• LES incompetence, which permits
reflux of acid gastric contents into
the esophagus.
• A common condition
Small Intestine – paralytic (adynamic) ileus

• Commonly occurs after intraperitoneal surgery

• Symptoms - similar to bowel obstruction

(constipation, vomiting, abdominal discomfort and bloating.)
 Direct inhibition
Activation of opioid
Trauma to intestines
receptors
of smooth
Decrease
Muscle intestinal
Abdominal
peristaltic
surgeries Increased discharge Reflex inhibition activity
Peritoneum is of noradrenergic
irritated fibers in the
of smooth
splanchnic nerves Muscle
 Small Intestine
Contents are not
Diffuse decrease in irregularly distended
propelled into the
peristaltic activity by pockets of gas and
colon
fluid

• Marked • Intestinal peristalsis

distension returns in 6–8 h,
of bowel followed by gastric
loops with peristalsis, but colonic
air-fluid activity takes 2–3 days
levels to return
Treatment
• Management is conservative
• Nasogastric drainage -passing a tube through the nose down to the small
intestine and aspirating the fluid and gas for a few days until peristalsis returns.
• Antiemetics,intravenous fluids, and a slow and gradual introduction of oral
feeding

• Reduced by
• more widespread use of minimally invasive (eg, laparoscopic) surgery.
Postsurgical - early ambulation
Hirschsprung Disease(aganglionic megacolon)

• Genetically Determined Condition Of Abnormal Colonic Motility

• Characterized By Abdominal Distension, Anorexia, And Lassitude.
• The Disease Is Typically Diagnosed In Infancy, And Affects As Many As 1 In 5000
Live Births.
• Due to congenital absence of the ganglion cells in both the myenteric and
submucous plexuses of A segment of the distal colon, as a result of failure of the
normal cranial-to-caudal migration of neural crest cells during development.
• feces to pass the aganglionic region with difficulty, and children with the disease
may defecate as infrequently as once every 3 weeks.
Abdominal Xray -Dilatation of the small bowel with no gas
in the rectum.
Manometric studies - show failure
of relaxation of the internal sphincter, which is diagnostic
of
Hirschsprung’s disease
Rectal Biopsy – Stain for Ganglionic cells

Treatment
Resection of the aganglionic potion of the colon
Vomiting
• Vomiting is the forceful expulsion of contents of the stomach and often, the
proximal small intestine
• Starts with salivation and the sensation of nausea.
• Reverse peristalsis empties material from the upper part of the small intestine
into the stomach.
• The glottis closes (preventing aspiration ).
• The breath is held in mid inspiration.
• The muscles of the abdominal wall contract, increases intra-abdominal pressure.
• The LES and the esophagus relax, and the gastric contents are ejected.
The “vomiting center” - control the different
components of the vomiting act
 Irritation
Emotions Motion of
Pharynge
sickness Mucosa al
Irritation

vestibular Sympathetic
Diencephalon and
nuclei nerves and vagi 9th craniakl nerve
limbic system
Neucleua tractues
solitarius

Motor Impulses
Chemoreceptor trigger • Fifth, seventh, ninth, tenth, and
zone twelfth cranial nerves – UGI
Vomiting centre • Vagal and sympathetic nerves –
(area postrema on the
Multiple LGI
lateral walls of the
distributed nuclei • Spinal nerves- diaphragm and
fourth ventricle)
in the brain stem abdominal muscles.

Chemical
Changes
The chemoreceptor trigger zone

Chemical abnormalities in the body (e.g. emetic drugs, uremia, hypoxia

and diabetic ketoacidosis, Hormone changes ) are sensed by these
centers, which then send excitatory signs to the vomition centers.
Many of the antiemetic drugs act at the level of the chemoreceptor
trigger zone.
Consequences
• Dehydaration
• Electrolyte inbalances
• Acid-base derangments. – What is it??
• Malnutrition (Long term)
• Aspiration pneumonia
Summary
• Physiology of GI Motility
• Common Intestinal Motility Disorders
• Vomiting
Thank You