Defecation
Reflex
Defecation
• Reflex phenomenon with voluntary control.
• It is a neurophysiological process that leads to expulsion of
faeces.
• Has both reflexive & voluntary components.
• Center for defecation is present in sacral portion of the spinal
cord.
• Efferent pathway- cholinergic parasympathetic fibers in pelvic
nerves.
• Coordinates enteric, autonomic and somatic nervous systems.
Defecation Reflexes
1. Intrinsic Reflex (enteric)
• Mediated by the myenteric plexus.
• Rectal stretch activates peristaltic contractions.
• Internal anal sphincter relaxes.
2. Parasympathetic Reflex (spinal)
• Strong reflex is mediated via pelvic splanchnic nerves (S2-S4).
• Regulated by Autonomic nervous system.
• Afferent: rectal stretch to spinal cord.
• Efferent: parasympathetic signals; intense peristalsis
• Anal sphincter relaxes.
3. Voluntary Control (somatic)
• Acted upon the external anal sphincter via the pudendal nerve.
• Allows suppression or initiation of defecation.
• There’s conscious control from cortical centers.
Position of External and Internal Anal Sphincters.
Pathway
1. Receptors for defecation reflex are stretch receptors located in the
wall of rectal rectum.
2. Afferent information from the wall of rectum is conveyed to sacral
segment (S3) of spinal cord via pelvic nerve.
3. Efferent input from spinal cord to rectum and internal anal sphincter
comes via pelvic nerve and to external anal sphincter via somatic nerve.
4. Higher center, especially cortex influences spinal cord center via
corticospinal pathway.
5. Relaxation of internal anal sphincter is due to inhibitory signals that
originate in myenteric plexus in response to peristaltic wave approaching
anus. This allows the fecal matter to press onto the anal canal.
Rectal distension
Spinal cord
Relaxes internal anal sphincter
Powerful contractions of abdominal
muscles, rectum and colon
Relaxation of external anal sphincter
Mechanism
• The individual sits on toilet and strains. This increases intra-abdominal
pressure, which forcefully expels the rectal contents through the anal
canal. This is assisted by relaxation of external anal sphincter, decreased
anorec- tal angle and relaxation of puborectalis muscle.
• 1. Evacuation of bladder is preceded by a deep breathing that pushes the
diaphragm downward.
• 2. Contraction of respiratory muscles increases intratho- racic and intra-
abdominal pressures.
• 3. Contraction of abdominal wall muscle further increases abdominal
pressure.
• 4. When all these mechanisms elevate the intra-abdom- inal pressure to
about 200 cm of H2O, the feces is forced out through the external anal
sphincter.
Applied Aspect
1. Hirchsprung’s Disease
2. Diarrhea
3. Constipation
4. Irritable Bowel Syndrome
5. Inflammatory Bowel Disease (Crohn’s Disease & Ulcerative Colitis)
Hirchsprung’s Disease
Cause
1. Entire neuronal plexuses in the wall of colon
are congenitally absent.
2. The enteric neurons are usually markedly
absent in the anus and distal part of the
rectum.
3. Failure of migration of neural crest from
cranial to caudal region results in absence of
ganglion in both myen- teric and submucosal
plexuses in distal part of colon and rectum.
4. This prevents relaxation of rectal outlet and
inter- nal anal sphincter in response to rectal
filling. Thus, obstruction occurs to the outflow
of feces and feces accumulate behind the
obstruction.
5. Consequently, distention of the colon ensues.
Features
• Manifests as abdominal distention, anorexia and lassitude.
• In severe cases, symptoms appear in new- borns as early as third
day after birth.
Treatment
• Surgical dilation.
Diarrhea
• Physiologically it may be due to either
increased secretion as occurs in cholera
or increased GI motility.
• In any case, acute diarrhea results in
dehydration and hypovolemia.
• Oral rehydration therapy is the
immediate treatment to prevent volume
and electrolyte loss. Oral rehydration
solution (ORS) contains salt, electrolytes,
and glucose. ORS contains both Na+ and
glucose so that Na+ is absorbed via SGLT
1 (Na+-glucose co-transporter). Glucose
facilitates Na+ transport.
Constipation
• Physiological basis: decreased
intestinal motility.
• It causes stasis of chyme in large
intestine, which facilitates water
absorption and dehydration of
intestinal contents.
• Chyme hardens, feces become more
solid.
• Treatment- distending rectum by inert
material.
Irritable Bowel Syndrome
• Also known as- mucous colitis, spastic colon,
irritable colon, and colonic neurosis.
• Commonly misdiagnosed as chronic amebiasis.
• It is a functional disorder characterized by
alteration of bowel habits & abdominal pain.
• No morphologic, histologic, microbiologic or
biochemical abnormalities in IBS. Changes in gut
motility is observed.
• Constipated variety: frequency of high altitude
peristaltic contraction is less, non propulsive
segmentation contractions are more.
• Food induced hypermotility of colon.
• Emotional stress is seen to aggravate motility
disorder.
Clinical features
• Female to male ratio- 1:3
• Painless functional diarrhea.
• Painless simple constipation.
• Alternating diarrhea and constipation.
• Bloating of abdomen.
• Pain due to spasm of colon and small intestine.
Inflammatory Bowel
Disease
Crohn’s Disease and Ulcerative Colitis
• Crohn’s disease or regional enteritis is an
idiopathic chronic ulcerative IBD, characterized
by transmural, non-caseating granulomatous
inflammation, affecting most commonly the
segment of terminal ileum and/or colon, though
any part of the gastrointestinal tract may be
involved.
• Ulcerative colitis is an idiopathic form of acute
and chronic ulcero-inflammatory colitis
affecting chiefly the mucosa and submucosa of
the rectum and descending colon, though
sometimes it may involve the entire length of
the large bowel.
Features
• Polyarthritis, uveitis, ankylosing spondylitis, skin lesions and hepatic
involvement is seen.
• More frequent in 2nd and 3rd decades of life.
• Females are affected more then males.
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