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Physiological Functions of the Colon

The physiological functions of the colon: include:-

 The recycling of nutrients--- depends upon: - further breakdown of ingested materials by microflora
metabolism.
 Mucosal absorption water and electrolytes.
 Secretion of electrolytes and mucous.

The absorptive and secretory capacities of the colonic mucosa are critical for regulating the
intraluminal fluid volume and contributing to serum fluids and electrolyte homeostasis.

 Storage and propulsion of faeces toward the rectum; which is important for act of normal
defecation.

Colonic Flora

The colon may contain as many as- 1011 -1012 CFU/ml faecal fluid. (More than 400 bacterial species);
bacterial population varies with dietary and environmental factors-and they contribute approximately
50-60% of faecal mass. Yeast and other fungi are normally present in very small numbers-while
Bacteria dominate the lumen of intestine.

Colonic Flora- feed on proteins sloughed from the intestinal epithelium; undigested proteins and non-
digestable; non-absorbed complex Polysaccharides.

 Most of these colonic species-are Anaerobes. Bacteroides species (especially B.fragilis)

predominate throughout the colon, comprising 65% of the total counts of the proximal colon and
almost 80% of the bacteria in the distal colon and rectum.

Other anaerobes include- Lactobacillus; Clostridia of various types.

 Aerobic bacteria –includes- Coliforms -Escherichia-mainly E.coli-—Klebsiella- Proteus and

enterococci-(mainly Streptococcus faecalis), are the predominant species.

 Functions of Colonic micro-flora:

It has become evident that a Symbiotic environment is present between the Gut Commensal Microflora
and the GIT-which, at least in part, is responsible for proper Homeostasis of the GIT.

 There are-several important Beneficial functions to the host, including:-

(1)- Metabolic-(Nutritive) - functions:-

 Colonic Flora-metabolise and ferment un-digested dietary complex carbohydrates (starch and non-
starch); producing Short-chain fatty acids (SCFAs); the principal source of nutrition for the
Colonocytes-and the gut-associated-lymphoid tissue.
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 Colonic Flora- metabolize Urea (the end product of Nitrogen metabolism); as they possess Urease
enzyme; producing Ammonia that absorbed via portal circulation into the liver where they are used
for AA.Synthesis and added to AA-pool.

 Colonic Flora Deconjugate Bile Salts by their enzymatic action; to produce free Bile Acids; which
then reabsorbed via portal V. into the liver where they are secreted again (colonic share of Entero-
hepatic circulation).

 Colonic Flora also produce certain vitamins, such as vitamin K and B12, which are absorbed by the
host.

(2)--Barrier functions: -

 Colonic bacteria suppress the growth of potentially pathogenic bacteria such as Clostridium difficile
a phenomenon termed “colonization resistance.”

 Colonic bacteria-maintain the anatomical and- immunogenic integrity of the Intestinal Mucosal
Barrier-through producing Short-chain fatty acids (SCFAs); the principal source of nutrition for the
Colonocytes-and the gut-associated-lymphoid tissue.

(3)- Trophic functions- includes control of epithelial cells regeneration; proliferation; differentiation
and angiogenesis.

 Hazardous Actions of the Enteric Resident Bacteria-

 Metabolism of un-digested Proteins by process of putrefaction results in formation of potentially

toxic metabolites, including phenols, indoles, and amines- which can lead to mucosal injury and
reactive hyperplasia, which have been hypothesized to promote carcinogenesis.
 Dysregulation of the enteric flora has been implicated in the pathogenesis of IBD and, to a lesser
extent, colorectal cancer.

Analysis of the micro- flora of patients with IBD; revealed markedly difference in flora compositions in
ulcerative colitis, Crohn’s disease, and healthy control patients.

 Normally-endotoxins produced by pathogenic bacteria; are prevented from absorption into the
blood due to presence of bile salts-however in O.J.-absence of bile salts in SB-will result in
endotoxinaemia may be responsible for the development of renal failure in these patients even-
after surgical intervention in jaundiced patients.
 Bacterial translocation- from the SB and colon in critically ill or traumatized patients is believed to
contribute to Sepsis and multiple organ system failure (MOF) -- in these patients.

Bacterial translocation-refers to- passage of viable bacteria and/or toxins from the GIT-Lumen to the
Mesenteric LNs- and beyond-this into the systemic blood-due to Damage of the anatomical and-
immunogenic integrity of the Intestinal Mucosal Barrier by different kinds of Systemic and local
injuries.

 Clinical conditions that may cause Bacterial translocation includes-

Immuno-deficiency- immunocompromised patients-,

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Protein/ Calorie- Malnutrition.

Major-Surgery- Trauma and Burn.

Major Sepsis as in- Peritonitis-especially- septic patients fed via TPN-

Intestinal Ischemia-and-Endotoxaemia.

 Bacterial translocation is thought to be- responsible for systemic inflammatory response Syndrome-
(SIR-S)-, (i.e. endotoxin-induced activation of the cytokine cascade, which in turn leads to Multi-
organ system failure - (MOF) and death. However in clinical trials-this hypothesis has, been
challenged because treatment with antibodies to the polysaccharide fraction of endotoxin has been
shown to be ineffective. So- other mechanisms-as- endothelial damage by activated Neutrophils,
may be responsible for MOF.
 In patients with major illness-as- Major Trauma- Burn -and Sepsis enteral feeding with complete
dietary elements - has beneficial effects over TPN-and- may protect the integrity of the gut barrier
and improve the immune function .-

The dietary components of enteral feeds which have been shown to enhance the ability of the intestinal
mucosa to resist bacterial translocation are: - are AAs-(Arginine, Glutamine) and Lipids (especially fish
oil).

Arginine and Lipids- have been shown to enhance immune functions and stimulate the secretion of
insulin, prolactin and growth hormone.

Glutamine is essential for all rapidly dividing cells including Enterocytes-and-has important role in
maintaining the integrity of the intestinal mucosa-and should be considered as essential AA-in critically
ill-and- Septic patients.

There is good evidence that in patients with major trauma-burn-and sepsis- glutamine-enriched-
intravenous or enteral nutrition may suppress the translocation of bacteria—through stimulation of the
secretory IgA levels-and decrease in the bacterial adherence to Enterocytes.

(I)--Recycling of Nutrients

During the digestive process, ingested nutrients are diluted within the intestinal lumen by Bilio-
pancreatic and SB- secretions. The SB- absorbs most of the ingested nutrients and some of the fluid
electrolytes and bile salts secreted into the lumen.

By the time the Chyme reaches the terminal ileum, most of the nutrients have been absorbed, leaving a
succus entericus composed of electrolyte-rich fluid, bile salts, and some undigested proteins; and
complex polysaccharides.

Normally- Nutrients such as Glucose, AAs, FAs and vitamins can be absorbed slowly through the colonic
mucosa, but only very small amounts of these substances actually reach the caecum under normal
circumstances.
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However, the ileal effluent is still rich in water, electrolytes, and nutrients that resist digestion-(some
undigested proteins; and starches-and non-starch complex polysaccharides).

The Colon has the functional ability to recover these substances and avoid unnecessary losses of fluids,
electrolytes, nitrogen, and energy. To accomplish this, the colon depends highly on: - the colonic flora-
metabolism- and on its high absorptive capacity.

(A)--Urea Recycling:-

Urea is the end product of nitrogen metabolism in humans-(urease enzyme is not produced in humans).
However, colonic bacteria are rich in urease enzyme—so colonic flora metabolize Urea and produce
Ammonia-which is then absorbed via portal circulation into the liver and used for AA synthesis; added
to AA pool

 Ammonia production and absorption from the colon is decreased in:

 Broad-spectrum Antibiotics suppressing colonic flora.
 Oral administration of Lactulose lowering intraluminal PH and suppressing bacterial urease.
 In chronic Hepatic Disease-Ammonia produced by colonic flora can’t be reused by hepatocytes and
absorbed into the systemic blood crosses the blood-brain barrier and produces false
neurotransmitters, which result in hepatic coma.

(B)-Bacterial Fermentation-

Unlike most of the mucosal lining of the proximal GIT - colonic mucosa does not receive its primary
nutrition from the bloodstream. Instead, nutrient requirements are supplied from the metabolism-
(fermentation) - of colonic flora on the un-digested dietary products--this illustrates the essential
symbiotic interaction between the colon and its resident bacterial flora.

 The Rt. Colon-(caecum and ascending colon)-is the primary site for bacterial fermentation.
 The primary energy source for the Colonocytes and the gut-associated-lymphoid tissue is the
SCFAs-(especially-Butyrate)-
 Carbohydrates Fermentations:
 Dietary CHO-that pass un-digested; un-absorbed- into the colon are-

(1)-Resistant Starch-10% of dietary Starch.

(2)-Non-starch complex polysaccharides- (Dietary fibers).

Fermentable- Starches and -non-starch complex polysaccharides –-Although participate to add minimal
stool bulk -they are metabolized by the process of fermentation by colonic flora; to a varying degree-
producing Short-Chain FAs (Sch-FAs)- predominantly Acetate, Propionate, and Butyrate --- which are
the main source of nutrition and energy production for mucosa-(Colonocytes and Gut-associated
Lymphoid Tissue)..

(3)- Non-digestible; Non- fermentable Complex polysaccharides- –such as- lignin and psyllium-- and
Pectins-(present in pulpy fruits) and --Cellulose.
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Non-Fermentable polysaccharides called- (bulking agents) –are hygroscopic, thus leading to water
absorption into the colonic lumen and contribute to stool bulk-so they decrease intracolonic pressures
and enhance colonic motility –however they do not accelerate colonic transit in normal individuals.

However-in patients with idiopathic constipation- Supplementation with Diets rich in Non-Fermentable
polysaccharides shortens colonic transit time.

Dietary fibers- these are components of plant food; containing mixtures of fermentable and non-
Fermentable polysaccharides-which both are important for colonic health.

The main Dietary fibers sources in food includes-

Cereals--Wheat Bran-Oat--Beans—kidney Bean-Green Bean-Dates—Nuts-

Vegetables—

Fruits especially pulpy fruits; Kiwi--Raspberry; Blueberry; Grapes; Raisin-

 The end products of Carbohydrates-fermentation are-- Sch-FAs and Gas—(carbon dioxide, methane,
and hydrogen.)

Colonic Gases: highly variable due to dietary habits.

50% to 75% of flatus, gases produced by bacterial fermentation (mainly hydrogen and methane)

25-50% of flatus; swallowed air- (oxygen and nitrogen)

Short-Chain Fatty Acids: - Sch-FAs-Physiological Functions-

Sch-FAs- have important roles in colonic and also the overall human metabolism.

The three primary fatty acids produced are- Acetate, Propionate, and Butyrate in a ratio of 3: 1: 1-

 Sch-FAs are weak acids-and higher concentrations of SCFAs decrease the colonic luminal PH that
can alter the growth profiles of pH-sensitive pathogenic bacteria such as Escherichia coli and
Salmonella.-
 Absorption of SCh-FAs into the colonic mucosa- is efficient-(90-95% of Sch-FAs are absorbed); only
5% -10% are lost in the faeces-and constitute the main anions in the stool.
 They are metabolized in three main sites -

(a)--Colonocytes: - use Butyrate as their primary energy source. (Provide up to 70% of Colonocytes
energy needs)-this will reduce glucose oxidation, and spare other essential AAs for metabolism.

Human Colonocytes can use various energy sources- however Butyrate is metabolized in preference to
glutamine, glucose, or ketone bodies-, the Colonocytes relies on luminal bacteria to produce it through
the fermentation of dietary fiber-(as they do not produce it).

The lack of -Butyrate, such as that resulting from the inhibition of fermentation of dietary fibres- by
broad-spectrum antibiotics, will lead to loss of absorptive capacity of Colonocytes for Na and water
with resulting diarrhea.
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So; Diversion of the faecal stream by ileostomy or colostomy will result in atrophy of the distal colonic
mucosa-(Diversion Colitis)-due to lack of nutrition of colonic mucosa.

(b)--Hepatocytes: - metabolize all three SCh-FAs to various degrees for use in gluconeogenesis and
cholesterol synthesis- (Acetate).

(c) Muscle cells: - oxidize Acetate as energy source.

SCh-FAs also influence GI- Motility via the ileo-colonic brake mechanism, which is defined as the
suppression of gastric and distal ileal emptying- so prevents nutrients from reaching the ileo-
colonic junction.
Other physiologic effects of SCh-FAs on the colon- include stimulation of splanchnic blood flow,
mucosal cell regeneration and regulation of intraluminal pH for homeostasis of the bacterial flora.

Butyrate is the primary energy source for Colonocytes and may also play an important role in
maintaining cellular health by arresting the proliferation of neoplastic Colonocytes, while paradoxically
being trophic for normal Colonocytes. In addition, Butyrate serves to regulate and stabilize cell
adhesion molecules.

Acetate is primarily absorbed and transported to the liver, where it is the primary substrate for
cholesterol synthesis.

Propionate, which has a glycolytic role in the liver, may also lower serum lipid levels by inhibiting
cholesterol synthesis.

 Protein fermentation (putrefaction):-

 The un-digested proteins; and proteins from desquamated epithelial cells pass into the colon where
they are metabolized by colonic bacteria through process of putrefaction.
 Putrefaction of un-digested proteins- will results in: - formation of potentially toxic metabolites,
including phenols, indoles, and amines.
 The production of these toxins is inhibited -by presence of alternate Fermentable carbohydrates
sources (as energy source) and becomes accentuated more distally in the colon as carbohydrate
sources become scarcer. These toxic end products of bacterial metabolism can lead to mucosal
injury and reactive hyperplasia, which have been hypothesized to promote carcinogenesis.

Thus; providing adequate sources of various forms of dietary fibres-can serve positive roles in colonic
health and overall metabolism:-

 Dietary Fibers- Starches and non-starch Fermentable- complex polysaccharides -provide the
nutrition and energy source for colonic flora so; sparing protein fermentation and production of
toxic amines.-The end-metabolic products of CHO fermentation are SCh-FAs the main source of
nutrition and energy production for mucosa.
 Non-fermentable polysaccharides (lignin; psyllium which are plants components)-are not
metabolized ; but absorb water by hygroscopic action so; add bulk to stool and enhance colonic
motility - also, the presence of bulking agents decreases intra-colonic pressures and may serve to
prevent the formation of colonic diverticula.
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 Also- Non-absorbable, non-fermentable complex polysaccharides, such as-lignin and psyllium, may
decrease the production of Acetate and so- may have a beneficial effect on lowering serum
cholesterol levels.

(II)--Colonic Absorption-and- Secretion-

The total absorptive area of the colon is estimated to be approximately 900 cm2- the colon represents
the most efficient site of absorption in the GIT -per surface area.

The daily ileal effluent delivered into the caecum- is 1.0- 1.5 L of fluid/ day--while the total volume of
fluids in stool is only 100 - 150 mL/day.

The colon can increase its absorptive capacity to- as much as- 5-6 liters of water-and- 400-800 mEq of
sodium and chloride /day-when larger fluid loads entering the caecum, provided at a slow rate.

The colon absorptive capacity-depends upon the rate at which ileal fluids enter the caecum, and the Rt.
And Transverse Colon- have greater capacity to water- Na and CL- absorption than the Lt. Colon-- so
patients after Rt.Hemicolectomy there may have temporary diarrhea due to water and Na loss until the
rest of the colon adapts.

The single most important process occurring along the intestinal epithelial cells-which underlies its
absorptive and secretory functions is- the establishment and maintenance of an electrochemical
gradient of Sodium across the intestinal epithelial cells by a large number of Na+/K+ ATP-ases (sodium
pumps) embedded in the basolateral membrane-These pumps export 3- Sodium ions from the cell in
exchange for import two Potassium ions, thus establishing electrochemical gradient – (gradient of both
charge and sodium concentration) across the basolateral membrane of Colonocytes—The cell interior
has low Na concentration-and it is electronegative as the intestinal lumen.

 Water-Sodium- - Absorption:

Sodium Absorption-the Colonocytes have great capacity for Na- absorption-(The colon can absorb up to
90% of the 200 mEq of sodium found in the daily ileal effulent.)

Under normal physiological conditions- Na balance can be maintained by low dietary Na- (as low as
5mmol/day) - due to efficient colonic Na absorption.

Sodium Absorption: - occurs- by active transport (against electrochemical gradient) - - controlled by

Na-K- ATP-ase (at basolateral membrane) – via Na+/ K+-exchange, -and enhanced by aldosterone H.
and glucocorticoids H.

Also- Sodium Absorption occur through Na+- H+-exchanger-(electroneutral absorption).

Water is absorbed passively (depending on osmotic gradient) - created by active Na Absorption.

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 Factors stimulate active Na absorption include-

Aldosterone H. and Glucocorticoids H.

α-2- Adrenergic agonists’ as- Clonidine--while muscarinic cholinergic receptors Agonists-

(parasympathetic) - inhibits active Na-Cl absorption and stimulates active chloride secretion.

Somatostatin- stimulate Na-Cl-and water- absorption--also has potent anti-secretory effects on colonic
mucosa.

 In EC-Dehydration and Hypovolemia-there is enhanced Na-Cl-and water absorption as a part of

homeostatic mechanisms mediated via sympathetic stimulation acting on α-2- Adrenergic receptors
present in colonic mucosal cells-and-via- Aldosterone and Glucocorticoids Hs.
 Patients after Rt.Hemicolectomy there may have temporary diarrhea due to water and Na loss until
the rest of the colon adapts.
 After Total colectomy and ileostomy; there is much Na loss from ileal effulent-(ileal fluids contain
200 mEq Na/ L.) and the daily requirement of Na should increase to 80-100 mmol/day; however
this is compensated by the kidney by decrease renal excretion of Na.

 K+-Secretion-

The colon - secretes K+ by process of active secretion via- Na+/ K+-transporters, that depends on the
electrochemical gradient generated by Na+-K+-ATPase at the basolateral membrane that promotes K+
transport down an electrochemical gradient then by passive diffusion through apical potassium
channel-- and enhanced by aldosterone H. and glucocorticoids H.

The colon can secrete up to 45 mEq. Of K /day—also K secretion occurs as a part of mucous production
by colonic mucosa.

In patients with chronic renal failure- can remain normo-kalemic while ingesting a normal amount of
potassium before requiring dialysis due associated compensatory increase in colonic secretion and
faecal excretion of potassium enhanced by effect of Aldosterone H.

Many forms of Colitis such as (IBD), and infective colitis due to-(cholera, and shigellosis) - and Villous
neoplasm- are associated with increased potassium secretion due to excessive mucus production and
result in- Hypo-kalemia.

 Chloride-transport-

CL¯- -is absorbed mainly- by means of an energy-independent- passive mechanism; depending upon
the negative charge of the CL-(intestinal lumen is electronegative)-and the osmotic gradient created by
active Na Absorption.

CL¯- is also- absorbed in exchange of Hco3- secretion-(electroneutral absorption)—through exchanger

mechanism- Cl is absorbed- Hco3 is secreted.

Active Secretion of K-Cl- occurs at a basal rate-and depends upon Na+/K+/ CL¯-ATPase-(pump) - via-
Na+-K+-2-Cl¯−transporters at baso-lateral membrane that promotes K+ CL¯- transport down an
electrochemical gradient -then by passive diffusion through the apical Cl channels.
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Some forms of Colitis as (collagenous and microscopic colitis) - impair colonic absorption or produce
secretion of chloride.

 H+ and bicarbonate-Secretion-

H+ and HCO3¯- Secretion- is coupled to the absorption of Na+ and Cl¯− respectively-(electroneutral
absorption)-

 H+ is secreted in exchange of Na+ absorption— (Na+- H+-exchanger)

 Hco3¯- is secreted in exchange of CL- absorption--( CL¯ - Hco3¯-exchanger)

The supply of H+ and bicarbonate for these transportes-(exchangers) - is maintained by the hydration
of CO2- catalyzed by colonic carbonic anhydrase enzyme-and make the colon is involved to systemic
acid-base balance.

Changes in systemic pH induce changes in the activity of carbonic anhydrase, eliciting elimination of
H+-or HCO3¯- as needed to bring the systemic pH back to normal.

 Bile Acids-Absorption-

The colonic mucosa can absorb bile acids that escape absorption by the terminal ileum, thus making the
colon part of the Entero- Hepatic circulation. Bile acids are passively absorbed across the colonic
epithelium by nonionic diffusion.

When the colonic absorptive capacity for bile acids is exceeded, colonic bacteria de-conjugate bile
acids. De-conjugated bile acids can then interfere with sodium and water absorption, leading to
secretory- diarrhea.

Early after Rt. Hemicolectomy secretory- diarrhea occurs as a transient and temporary phenomenon-
due to—both water and Na loss and secretory effect of De-conjugated bile acids-

After extensive ileal resection -Diarrhea occurs permanently due to mal-absorption of bile acids.

(III)-Endocrine Function of the colon-

The colon contains Entero-endocrine (APUD-cells) that secrete numbers of GIT-Hormone peptides:

Somatostatin-stimulates- Na; Cl; and water absorption - also has potent anti-secretory effects on
colonic mucosa.

Enteroglucagon (Glucagon-like peptide- 2): Entero- trophic- - stimulate intestinal cellular proliferation
to the small intestinal mucosa, and the colon might participate in regulation of small intestinal mucosal
growth-- and may be responsible for the adaptive intestinal hypertrophy seen after massive small
bowel resection.

Peptide-YY --- (neuro-peptide-Y)—is released from the distal ileum and proximal colon in response to
luminal fat and is responsible for the so-called “ileal break,” which serves to slow gastric emptying and
SB-Transit.
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“Ileal Brake-Reflex.”—Presence of partially digested triglycerides in the ileum-(or infusion of partially

digested triglycerides into the ileum) -- has an inhibitory effect on jejunal motility and peristalsis and
increases small intestinal transit time- Peptide YY released from ileal endocrine cells has been
suggested as a possible mediator of this reflex which serves to allow more time for nutrient absorption
when the absorptive capacity of the more proximal small intestine is limited by accelerated transit or
mucosal disease.
Neurotensin: produced by the N cells primarily in the ileum-(also in the proximal small intestine and
colon)-in response to the presence of intraluminal fat.

 It inhibits gastric secretion and gastric emptying.

 It stimulates pancreatic bicarbonate and biliary secretion.

 It stimulates SB-and Colonic motility.

 Entero-trophic to SB- and colonic mucosa.

(IV)--Motility Function of the Colon

Colonic motility is a highly complex process, and is relatively slow compared with the proximal GI tract;
with marked regional variation between the right and left colon.

Motility Function of the Colon -is regulated through a combination of Myogenic, Neural, and Hormonal
factors—Myogenic Electrical activity of smooth muscle layer is especially important-and Neurological
and Hormonal factors act to modify the myogenic-initiated motor patterns.

Colon motility does not demonstrate cyclic motor activity characteristic of the migratory motor complex
(of the small intestine); however the colon displays intermittent contractions of either low or high
amplitude.

Regulation of colonic motility

(I)--Intrinsic Myo-Electrical Activity of the Smooth Muscle Layer -

The intrinsic Electrical Rhythm of the GI-Smooth Muscles-(Basic Electrical Rhythm) - depends upon the
pacemaker activity of the interstitial cells of Cajal - (ICC).

Interstitial cells of Cajal-(ICC) - are pleomorphic mesenchymal cells located within the muscularis
propria – (from smooth muscle part of Esophagus to internal anal sphincter) - interposed between
smooth muscle cells and nerve endings of the ENS- neurons.

The interstitial cells of Cajal - (ICC) - are the primary pacemaker cells governing the function of the
ENS and are important for GIT-Motility.

 There are 3- distinct populations of ICC—

 ICC-Myenteric-(MY)-form extensive networks in the myenteric plexus – (are distributed around the
ganglia and tertiary plexus- in the space between the circular and longitudinal muscle layers). –
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They have several long processes that branching out –contact- and electrically coupled to smooth
muscle cells in both circular and longitudinal muscle layers. -

 ICC-Intramuscular-(IM)--located in the intramuscular plane of both circular and longitudinal muscle

layers-in the septa that separate bundles of smooth muscle cells- and in close contact with varicose
processes of enteric motor neurons-(both excitatory and inhibitory).In the Colon-(and Stomach)-
ICC-IM- - are the subtype- involved in mediating enteric neurotransmission- -(respond to
neurotransmitters released by enteric motor neurons.)
 ICC-Submucosal-(SM) - form extensive networks in the inner border of the circular muscle layer- -
submucosal border-( deep submucosal plexus of Henle).-In the Colon- ICC-Submucosal-(SM)- serve
as the dominant pacemaker cells that generate the Pacemaker Potential - (Slow Waves)-at the
highest frequency.

 ICC-form extensive networks along the intestinal wall and are electrically coupled to one another,
to the smooth muscle cells, and synapse with -enteric motor neurons; so- mediate enteric
neurotransmission- between the enteric motor-neurons and smooth muscle cells.
 ICC- Generating Pacemaker Potential and; are electrically coupled to smooth muscle cells, via Gap
junctions which permit electrical coupling; so responses elicited in the ICC are Propagated and
transmitted to smooth muscle cells- and so—ICC - influence and regulate the smooth muscle
membrane potential and excitability.

 ICC-- governing the function of the ENS-as they synapse with the nerve endings of -motor neurons
of Auerbach Plexus; and express receptors, have second-messenger pathways, and ion channels
facilitating responses to enteric neurons neurotransmitters-

So-ICC-functions-

● Generating-and Propagate- Electrical Slow Waves-(Rhythmic Regular Rate of Electrical Discharges)-to

GIT-Smooth Muscles via Gap junctions - Slow Waves drive the Fundamental Rhythmicity of SB-
Contractions--(organize GIT- contractions into phasic contractions that are the basis for peristalsis and
segmentation.)-

● Form extensive networks along the intestinal muscularis propria and are electrically coupled to one
another, to the smooth muscle cells via Gap junctions, They also synapse to-enteric motor neurons of
Myenteric plexus; so- mediate enteric neurotransmission- between the EM- Neurons and smooth
muscle cells.

● Mediate neural input-(inhibitory and excitatory signals from the ENS)--serve as transducer of neural
signals-and mediate enteric neurotransmission- between the EM- Neurons and smooth muscle cells.

ICCs-are densely innervated by excitatory and inhibitory EM-Neurons; and express receptors for
different neurotransmitters.

Neurotransmitter released from enteric motor neurons binds primarily to receptors expressed by
interstitial cells of Cajal (ICCs). Activation (depolarisation or hyperpolarisation) of adjacent smooth
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muscle cells occurs by conduction of excitatory or inhibitory junction potentials via gap junctions
between ICCs and smooth muscle cells.

● Thus- the nerve endings of enteric motor neurons, interstitial cells of Cajal and smooth muscle cells
form functional units that release Neurotransmitters; and mediate and transduce neural signals into
mechanical responses.

● ICC-function as-mechano-sensitive cells-respond to stretch of intestinal wall.

Intrinsic Electrical Activity is based on:

Resting Membrane Potential of the intestinal smooth muscle (This normally is: --50 --65 mV and is
maintained by Na+-K+-ATPase activity.)-

There are 3-basic electrical activities-recorded from the colonic smooth muscle:-

(1)- Pacemaker Potential - -- (Slow Waves) – (Basic Electrical Rhythm) –

Spontaneous Regular Cycles of Depolarization/Repolarization- of the resting membrane potential

Generated in the interstitial cells of Cajal- ICC-Submucosal-(SM)- that are transmitted to colonic
smooth muscle cells-; so—ICC regulate the excitability of the colonic smooth muscle.

 Slow Waves- consisting of a rapid upstroke-(of partial Depolarization) - and a longer plateau phase
followed by Repolarization-(There are Fluctuation of Resting Membrane Potential by 5-15 mv) - the
period of high excitability corresponds to the plateau phase of the slow wave.
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The Frequency of Slow Waves; is important in determining the location of pacemaker dominance; as
this resides in cells that generate the highest frequency of pacemaker activity-(highest frequency of
Slow Waves).However in the Colon-Slow Waves have multiple frequencies without a dominant
rhythmicity-so the location of dominant Pacemaker is not well characterized

 Myoelectric activity of the colon-(Slow Waves) -is more complex than that of the SB-colonic slow
waves- are intermittent, and are of variable amplitude and frequency-(have multiple frequencies
without a dominant rhythmicity) – The predominant Slow waves and contractile rhythm recorded
from the human colon - corresponds to the slow wave frequency of 2 --4/minute.
 The Frequency of Slow Waves in the colon; determines the Maximum Frequency of Colonic
Contractions- (however-Not every Slow Wave is associated with a Muscle Contraction—only when
MPOs is superimposed on Slow Waves.)
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 Pacemaker potential (Slow Waves):

 Generated in ICC- and transmitted to smooth muscle cells; are characterised by Rhythmic and
Regular rate of electric discharges.—so- plays a Pacemaker Role in the setting the Fundamental
Rhythmicity of Colonic Contractions-( organize GIT- contractions into phasic contractions that are
the basis for peristalsis and segmentation.)-

 The Coordination of Slow Waves - and Spike Potentials- lead to - generation of Action Potential and-
the Initiation-and- determine Duration, and Frequency of Rhythmic Migratory small-intestinal
Contractions.

(2)-- Spike Potentials- Membrane Potential Oscillations-(MPOs)-

 Spike Potentials-(MPOs) - higher-amplitude rapid Oscillations of membrane potentials- originating

in the neurons of myenteric plexus of ENS.

 The membrane potential becomes- excitatory- "more depolarized-(more positive) - moves towards
the threshold for firing -/ or- inhibitory “hyperpolarized-(more negative).

 The frequency of the spike potentials, usually ranging between 1 -10 spikes per second.

 Upon-excitatory /inhibitory signals (Local and Systemic) - from neurons of the Myenteric plexus of
ENS-and various excitatory/ inhibitory hormones. MPOs – (excitatory or inhibitory junction
potentials )-originate and- –transmitted to ICC-via their synapse and -are propagated to smooth
muscle cells via Gap junctions -ICC transduce neural signals-and mediate enteric
neurotransmission- between the enteric motor- neurons and smooth muscle cells.

(3)--Action Potential-

 Upon excitatory stimulation- MPOs is superimposed upon- the plateau phase of Slow Waves –
membrane potential rises above threshold of activation of voltage-gated- L-type calcium channels,
the result is Ca2+ influx -and consequently, action potentials are generated in smooth muscle cells
superimposed on Slow Waves. – However- Upon inhibitory signals-and- Hyperpolarizing junctional
potentials do not reach the threshold potential required to generate an action potentials.
 Action Potential greatly augment Ca2+ entry and triggers smooth muscle contractions through
mechanisms of excitation-contraction coupling.-and so-
 Action Potential will regulates contractile strength and frequency.
 The Frequency of Action Potentials is affected by neuro-hormonal stimuli-with increased
frequencies associated with stronger contractions.

Note- ICC generate slow waves, and transmit MPOs from the- neurons of the Myenteric plexus to SMCs,
and the Action potentials generated in SMCs elicits muscular contractions.

In the Colon—

The Variable frequency and duration of action potentials—is thought to be the cause of irregular colonic
contractile activity. (In contrast to the Continuous-Regular Action Potentials- which is responsible for
the regular cyclical contractile activity-(of Stomach and SB).
 15

 Tonic colonic contractions-(Continuous partial contraction) - are generated by continuous action

potentials; as in ileo-caecal valve and IAS.

 The contractile behavior in most smooth muscle regions of the GIT-(including the Colon)- is phasic
in nature, consisting of a rhythmic contraction-relaxation cycle- timed by the occurrence of slow
waves. Phasic contractions are the basis for the major motility patterns of the GIT, such as
segmentation and peristalsis.

In Functional SB-Motility Disorders—as Chronic Intestinal Pseudo-obstruction-(CIPO) –and in acquired

slow-transit constipation without colonic dilatation to megacolon- ICC- abnormalities are recognized as
decreased ICC or an abnormal ICC-network—(Mesenchymo-Myopathy.)

(II)-Neural Regulation of colonic motility.-(Extrinsic and Intrinsic N.S)

(1)-- Enteric Nervous System- is specialized; Neural Plexus formed of N. Fibres and ganglionic cells;
that lies within the bowel wall. ENS- regulate colonic motility, as well as colonic blood flow, absorption,
and secretion. ENS-respond to Local and Systemic stimulation.

The ENS is an independently functioning system that can affect Motility, Secretion, Vascular Tone, and
Hormone Release in GIT; and can initiate physiologic motor activity in the absence of extrinsic
innervation.

ENS -Helps in the execution of sympathetic and parasympathetic signals.

 Myenteric (Auerbach) plexus, Plexus of nerve fibers and ganglion cells present interposed between
the outer longitudinal and inner circular smooth muscle layers of the muscularis propria-- and send
network of neural fibers into both layers, thus providing electrical continuity and conduction
through the whole muscle layer. The nerve endings of ENS- (Myenteric Plexus); are closely
associated with ICC—the Pacemaker cells of intestinal motility.
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Myenteric Plexus--Main function is to Control Motor Activity of the intestine--It Provide the basis for
Coordinated Electrical activity and Muscular Contractions of both circular and longitudinal smooth
muscles of the colon.

 Sub-mucosal (Meissner's) plexus; plexus of nerve fibers and ganglion cells present in intestinal
submucosal layer—with short N. Fibres from ganglion cells provide innervation to secretory cells,
Endocrine cells, and BVs.

Meissner Plexus— Main functions- Regulates colonic absorption and Secretion-- -- Vascular Tone- and
blood flow-

 Inter-connecting Neurons- provide intercellular communication signals between neurons along the
GIT.
 Sensory Neurons –receive sensory information from mechanoreceptors and chemoreceptors within
the bowel wall – sensory neurons-then provide Signals - to the motor neurons; that innervate target
organs-(Glands-Smooth muscles-BVs—and Endocrine Cells)—Also Afferent input from the Enteric
Neurons pass to the sympathetic neurons of the SM-and-IM Ganglia –then-pass through the visceral

afferent sympathetic fibers to Spinal Cord,  and then to Brain Stem—So- Autonomic nervous
system- Modulate the function of ENS-in response to Systemic stimuli.

(2) Autonomic nervous system:-.

Sympathetic and Parasympathetic systems- Modulate the function of ENS-in response to Systemic
stimuli.

(a)-Sympathetic innervation: -

Proximal Colon-Thoracic Splanchnic Ns-(T10 - T12).

Preganglionic sympathetic nerves-arise from-T11 and T12 spinal segments-pass through paravertebral
thoracic sympathetic chain ganglia without synapse and exit as thoracic Splanchnic Ns, and then pass
through Aortic plexus to synapse with neurons of SM- ganglia- Post-ganglionic sympathetic fibers then
course along SMA-Branches- -(peri-vascular plexus in the Meso-colon) -to reach the bowel wall and
supply proximal colon-

Distal Colon- lumbar splanchnic (L1 – L2).

The preganglionic sympathetic nerves arise from L1 – L2 spinal segments- pass through paravertebral
lumbar sympathetic chain ganglia without synapse and exit as lumbar Splanchnic Ns.-; and then pass
through Aortic plexus to synapse with neurons of IM- ganglia. Post-ganglionic sympathetic fibers
follow the branches of the IMA and superior rectal artery; (peri-vascular IM- Plexus in the Meso-colon);
to reach the bowel wall and supply distal colon and upper rectum.

Post-ganglionic sympathetic fibers- pass both to – Inhibitory neurons of the ENS--and Directly into
Smooth Muscle-- Secretory cells—BVs—

Sensory Afferent input from sensory neurons of ENS- pass to the sympathetic neurons of the SM-and-
IM-Ganglia-(sympathetic visceral afferent pathway)-
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 Sympathetic stimulation- is Inhibitory Adrenergic-( via stimulation of α2-adrenergic receptors

Noradrenaline is the neurotransmitter)-- through both direct inhibition of the smooth muscle; and
also acts indirectly by stimulating inhibitory neuron of ENS-( which hyperpolarize cholinergic

neurons in the myenteric plexus) Resulting in  suppress colonic motility and secretion-and
causing VC to mesenteric BVs and decrease Blood Flow.

Clonidine-(α2-agonist) - decreases colonic motility and secretion-and enhances mucosal absorption of

fluid and salt.

(b)--Parasympathetic innervation: -

Proximal Colon-Vagal N.-(Coeliac branch of posterior Vagus N.)

Preganglionic Parasympathetic-(vagal) fibers run through Coeliac and SM- Plexus without synapse;
then follow branches of the SMA-(mixed with sympathetic fibres in the peri-vascular plexus);
Preganglionic Vagal Nerve fibres synapse into neurons of ENS.

The Preganglionic Vagal fibres synapse with 2-types of post-ganglionic motor neurons of ENS:-

 Excitatory; Cholinergic neurons. Acetyl Choline is the neuro-transmitter.

 Inhibitory; non-cholinergic, non-adrenergic- (Peptidergic neurons). VIP is the neuro-Transmitter.)

Postganglionic Parasympathetic fibers are very short; (arising from their postganglionic neurons of
ENS)--passing very short course to innervate the target tissue-(Glands and Smooth Muscles) —
however-the Parasympathetic Motor input to smooth muscles: is more complex, with projections of
Preganglionic fibres to both Inhibitory and Excitatory ENS-Motor neurons.

 So; Vagal stimulation -- can elicit several motor responses; and have two Functionally Different

effects-one is Excitatory--(cholinergic-mediated via Acetyl Choline)  increased motility-- the other

is Inhibitory--(Peptidergic- mediated via VIP)  decrease motility. So--the effects of vagal
stimulation on Intestinal Motility are more difficult to predict; and there is delicate interplay
between net stimulatory and inhibitory effects in response to vagal activity.

Distal Colon-(S2 - S4) - Pelvic Splanchnic Nerves-(Nervi erigentes)

Preganglionic Parasympathetic fibres join the Pelvic plexus; then Parasympathetic fibres to distal colon
ascend into; Superior hypogastria plexus without synapse; then leave it by a separate trunk which then
follow arterial branches of IMA-And SRA-( inferior mesenteric and superior rectal plexus); by which
they are distributed to the distal colon-(and upper rectum).

The Preganglionic Parasympathetic fibres enter the colonic wall; and synapse with neurons of the
myenteric and submucosal Ganglia of ENS; from which short Post-ganglionic Parasympathetic fibers
pass to supply colonic smooth muscles; BVs; and glands.

Parasympathetic stimulation- is Sretetory-Motor to the colon.

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Patterns of Colonic Motility-

It is well known that patterns of intestinal motility illustrate considerable variability from one segment
of bowel to another.

 The contractile behavior in most smooth muscle regions of the GIT--(including the Colon)- is phasic
in nature, consisting of a rhythmic contraction-relaxation cycle- driven-and-timed by the occurrence
of slow waves. Phasic contractions are the basis for the major motility patterns of the GIT, such as
segmentation and peristalsis.

There are two patterns of colonic motility:-

(1)--Segmental contractions:

These are- intermittent; (low amplitude; short duration); annular contractions of the circular muscle
layer; occur in both ante-/ and retro-grade directions- dividing the colonic lumen into segments-and-
result in the segmented appearance of the colon-(haustration).- Haustration form from the concomitant
constricted and relaxed segments of the colon.

 Annular contractions form, relax and re-form in different locations in a random fashion; at a
frequency of 3-8 times/minute.
 Segmental contractions: move the colonic contents over short distances in both antegrade and
retrograde direction; resulting in--slow forward progression of faecal matter; so-delaying colonic
transit; allowing thorough mixing; microflora metabolism-and increase the time available for
absorption of water and exchange of electrolytes.
 Retro-grade Segmental contractions dominates in the right and transverse colon; so tends to
confine the liquid faecal matter to the caecum and ascending colon - (storage Function)

(2)--Propagated contractions: These are coordinated; strong- propulsive contractions- either high-
amplitude (>100 mm Hg) propagated contractions (HAPCs) –or- low-amplitude (<60 mm Hg)
propagated contractions (LAPCs).

Peristalsis Reflex-is the basis of propagated colonic contractions-

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 The LAPCs- move luminal contents forward at a rate of 0.5 - 1.0 cm/s and typically last for 20 to 30
seconds.
 The HAPCs- (Mass contractions)-occur 2-3 times per day, (primarily after meals; awakening, and
after exercise.)--involving a longer segment of colon. Mass contractions: propel larger volumes of
faecal matter to the distal colon and emptying of the transverse and descending colon into the
sigmoid colon and rectum; (an important role in initiation of defecation-feeling the desire to
defecate.)
 Increased Myoelectrical activity and propulsive contractions are initiated at the transverse colon;
propagated distally towards descending and sigmoid colon.
 The HAPCs- (Mass contractions) - can be induced by luminal distention, by the parenteral
administration of the cholinesterase inhibitor –neostigmine- or by intraluminal stimuli, that is,
glycerol, Bisacodyl, and oleic acid.

Normal-Colonic Motor Function-(compared to Motor Functions of the SB-and Stomach)-

 Colonic Motility-in contrast to SB-and-Stomach is lacking the Migrating Myoelectric Complex-(MMC)

 Normal-Colonic contractile activity is irregular-(not Cyclic) due to Variable frequency and duration
of action potentials and constitutes a major proportion of colonic motor activity -. (In contrast to
the Continuous-Regular Action Potentials- which is responsible for the regular cyclical contractile
activity-(of Stomach and SB).

 Colonic motor activity may vary from- no activity - (quiescence) - isolated contractions- bursts of
contractions-or propagated contractions.

 “Colonic Motor response to Eating” –

 20

 Eating is accompanied by a brisk increase in tone and phasic contractile activity throughout the
colon-the previous term-(“Gastro-Colonic reflex.”-Is not accurate as this response is preserved even

after a gastrectomy-
 Colonic Motor response to Eating-may begin within a few seconds after eating and last, to a varying
degree, for up to 2 ½ hours.
 Meal composition and caloric content both influence the response:-

▪ Mixed meal containing more than 500 kcal predictably elicits a response.

▪ Lipids are the most potent and longer duration stimuli, whereas; carbohydrate meals is less potent
and fairly short-lived; peptides and AAs- appear to inhibit the response.
▪ Gastric distention and chemical stimulation by nutrients elicit a response.

 The precise mechanisms mediating the Colonic Motor response to Eating –are unknown-however
neuro-hormonal mechanisms have been implicated-

It was found that-Cholinergic, Opiate, and Serotoninergic 5-HT3- receptors- may be involved in
mediating the response-as-Atropine, Naloxone, and the 5-hydroxytryptamine type 3 receptor (5-HT3)
antagonist-( Ondansetron)- inhibit the Colonic Motor response.

The early, particularly the immediate-phase after eating- is likely to be neurally mediated.

The later phase- timely coincides with arrival of Chyme into the ileum and may be mediated by humoral
factors such as Peptide YY, Neuropeptide-Y, and Neurotensin released from the ileal mucosa.

Factors enhance colonic motility:-

 There seems to be a circadian rhythm of colonic motility, with maximum peaks of activity
immediately after waking and after meals ;( Sleep is associated with a decrease in colonic motility.)

 Food ingestion: results in an increase of overall colonic motility for approximately 2 hours post-
prandial.

 High-caloric meal-(more than 500 kcal)-especially fatty meal.

 Dietary Fiber content:-non-digestible; non-fermented complex Polysaccharides- (present in grains;

vegetables and pulpy fruits); increase faecal bulk by water absorption and so; enhance colonic
motility.

In normal subjects, supplementation with- non-starch polysaccharides-(NSPs) - does not shorten

colonic transit time, although it does increase faecal bulk (by water absorption)—

However- In patients with-chronic idiopathic constipation, NSPs, in the form of psyllium seeds, shorten
colonic transit time and increase stool bulk.

 Physical Activity: - Walking and Exercise; enhance colonic motility.

 Emotional State:-Emotions have a variable effect on colonic motility; they either increase or
decrease motility via vagal or sympathetic stimulation respectively.

 Drugs- α2-adrenergic agonist-(clonidine) - morphine, and-cholinergic antagonist (atropine)

decrease the tone and relax colonic smooth muscles.
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Functional Classification

The Colon is a heterogeneous organ with regional- biomechanical, pharmacologic, and thus functional
differences.

 Caecum and Ascending Colon (Right Colon)-

The Ileo-caecal valve- regulates the intermittent aboard flow of ileal contents into the colon, mainly
after meals, and prevents reflux of bacteria into the ileum. If the ileum becomes distended,  the valve
will relax and allow the passage of contents from the small intestine into the colon.

Colonic Transit is influenced by-the rate of delivery of faecal fluids into the proximal colon. However- In
humans the ileo-colonic sphincter plays only a minor role in regulating ileo-colonic transit.

Ileal fluids entering the colon at the ileo-caecal junction remains in the caecum and right colon for an
extended period. Here, the resting propulsion rate is only 1 cm/hour; also; there are frequent retro-
pulsive contraction waves extending from the transverse colon back toward the caecum.

This allow -storage and mixing of ileal effluent; permit aerobic and anaerobic metabolism of residual
carbohydrate and protein by the colonic flora, thereby producing multiple by-products, most of which
are then absorbed through the remaining colon.

The ascending colon (along with the transverse colon) - is involved in sodium and water absorption –
so; regulating intraluminal fluid volume and consistency.

There is evidence for adaptation in these regional functions. Within 6 months after Rt. Hemicolectomy,
Scintigraphic Techniques; showed isotope movement from SB-to-Colon normalizes in response to the
augmented storage capacity in the residual transverse and descending colon.

 Transverse Colon-

The Myoelectrical activity of T. Colon-is characterized by- basic electrical rhythm-(Slow Waves) - and
muscle-generated pressure waves; more frequent than that identified in the right colon-(so-more rapid
propulsive function); so; T. Colon is generally believed to function as a rapid conduit between the Rt.
And Lt. Colon.

The transverse colon (along with the ascending colon) - is involved in sodium and water absorption –
so; regulating intraluminal fluid volume.

 Descending and Sigmoid Colon-(Left Colon)-

There is diminished rate of fluid and electrolyte transfer seen in the descending and sigmoid colon; so
Lt. Colon is the site for final modulation of intraluminal faecal contents; as regard to volume and
consistency before evacuation.

Propagated Mass contractions: These are coordinated; strong-(high amplitude); propulsive contractions
that involve a long segment of colon, due to increased Myoelectrical activity; that are initiated at the
transverse colon; and propagated distally towards descending and sigmoid colon. This will propel larger
 22

volumes of faecal matter to the Lt. Colon and emptying of the transverse and descending colon into the
sigmoid colon and rectum; (an important role in initiation of defecation.)

 Formation of Stool:

Distal Colon- (descending and sigmoid colon) - - is the site for final modulation of intraluminal faecal
contents; as regard to volume and consistency before evacuation.

 Stool consistency depends mainly upon-

 Fluids and dietary fibres intake-

 The rate at which colonic faecal contents moves through the colon is important in determining
whether the stool is liquid, semi-formed, soft or hard.

 The Faecal Mass is formed of:

 Water- 70%-
 Solids components--30%-

50% - Enteric Bacterial Flora-

50%- undigested-un-absorbed food particles; desquamated intestinal epithelial cells.

Normal Colonic Emptying—Colonic Transit-

Colonic-Transit is the result of complex GI- contractions that promote the aboral movement of
intestinal Chyme.

 Generally-GIT-Transit is variable between individuals and affected by-

 Diet- Caloric Fat- and-Dietary Fiber content-
 Physical Activity and- Emotional State-

Colonic Transit-is a highly complex process, is relatively slow compared with the proximal GI tract; and
extremely variable-(The faecal stream does not move along a regular laminar flow-and there is marked
regional variation in transit between the proximal and distal colon.

 The propagation of SB-Chyme slows distally- particularly in the terminal ileum before passing the
ileo-caecal valve into the colon- so-there is a buildup of intestinal contents distally-and the terminal
ileum may function as a temporary reservoir for Chyme before it passes into the colon.

Studies have confirmed that- the flow of intestinal Chyme from the SB- into the colon is regulated
across the ileo-caecal valve-and that- pulsatile filling of the caecum is associated with propagating
distal ileal contractions.

 The flow of Chyme across the ileo-colonic junction-(is estimated at 1–2 L/ day) - with increased
flow seen post-prandial especially the first hour.
 In-Proximal Colon-(RT and T.Colon) –
 The Ileal fluids entering the colon at the ileo-caecal junction remains in the caecum and right colon
for an extended period. Here, the progression rate is Slow- only 1 cm/hour; also; there are frequent
 23

retro-pulsive contraction waves extending from the transverse colon back toward the caecum- (for
storage and mixing of colonic contents).
 Proximal Colon is involved in sodium and water absorption –-so; regulating intraluminal fluid
volume and consistency.
 In T-Colon-there are more rapid propulsive contractions-; so; T. Colon is generally believed to
function as a rapid conduit between the Rt. And Lt. Colon.
 In Distal Colon- (descending and sigmoid colon)-

 There is diminished rate of fluid and electrolyte transfer – so- is the site for final modulation of
intraluminal faecal contents; as regard to volume and consistency before evacuation.
 Propagated Mass contractions: These are coordinated; strong-(high amplitude); propulsive
contractions that involve a long segment of colon, due to increased Myoelectrical activity; that are
initiated at the transverse colon; and propagated distally towards descending and sigmoid colon.
This will propel larger volumes of faecal matter to the Lt. Colon and emptying of the transverse and
descending colon into the sigmoid colon and rectum; (an important role in initiation of defecation.)
 Generally; in most persons with normal bowel function, terminal ileal content from a meal reaches
the caecum after 3-4 hours and the recto-sigmoid by 24 hours.
 Some of the faecal stream entering the caecum flows through the colon past faeces remaining from
earlier periods; as portions of the stream may be retained in the periphery of haustrae, where it
may fail to progress to rectum for 24 hours-period or more.

Mixing of the faecal matter in the colon results in; about 25% of single meal residue may passed in the
stool after 3–4 days.

Colonic Transit Studies-

In many cases- symptoms of SB-and colonic Dysmotility overlap-(usually include nausea; ± vomiting;
abdominal pain, Bloating; diarrhea, or constipation)-

However-before final diagnosis of primary SB- Dysmotility; organic lesions as- tumor, stricture should
be excluded by endoscopy/ contrast studies.

Radiopaque Marker - can provide all of the necessary information regarding the overall colonic transit. -
While - Scintigraphy is a useful-as a research tool that allows more thorough assessment of regional
colonic transit.

Recent advances in the Wireless capsule technology and the development of video capabilities-enables
the assessment of the whole GIT-transit time as well as regional transit times.

The standard radiopaque markers, have been shown to correlate well with both Scintigraphic
measurement and the Wireless capsule technology in assessment of colon transit.

(1)--Radiopaque Marker Methods-(single capsule-/-single radiograph Method)

Patient ingest a single capsule containing 24 commercially available radio-opaque rings at day-0.

A single Abdominal radiograph-(from diaphragm-to-pubis) obtained 5 days after ingestion of the

capsule will reveal all the required information: - There are three basic results:-
 24

 If < - 20% of the markers-(5 or fewer markers) - are retained, this should be considered a
“normal” study.

 If-- ≥ 20% of the markers-(6 or more markers) - are retained in the recto-sigmoid, a functional-
pelvic outlet obstruction is thought to exist.

 If-≥ 20% of the markers--(6 or more markers) - are retained and diffusely scattered throughout

the colon, this is suggestive of slow-transit and colonic inertia.

Normally- the mean total colonic transit time is 30- hours in males and 38-hours in females.

(2)-Colonic Scintigraphy

Delayed-release capsule –-99mTc –labelled polystyrene pellets- and incorporated into a gelatin capsule
coated with a pH-sensitive polymer, (methacrylate polymer)-

Following ingestion, this capsule will remain intact through the acid pH of the stomach and duodenum
but will dissolve in the distal ileum where the pH is typically between 7.2 - 7.4--releasing the
radioisotope within the Caecum.

Multiple images-using a gamma camera are obtained-at-4, 24, and 48 hours after administration of the
capsule.

The colonic distribution of the radioisotope is highly sensitive and specific for identifying the overall-
rapid or slow colonic transit.

There are 3 major patterns of slow colon transit-

 Generalized slow colon transit with- diffuse retention of the radiotracer throughout the length of
the colon.
 Colon inertia with marked right-sided retention of the radiotracer proximal to the splenic flexure.
 Functional Outlet Obstruction- Retention of the radiotracer in the recto-sigmoid.

Recent Reports-stated that-

Whole-Gut Scintigraphy is recommended in patients with a suspected diffuse GIT- Motility Disorder/
or—when symptoms cannot be classified as either upper or lower GI-in origin to measure both total and
regional transit times”; including SB-and Colon transit as well as gastric emptying.

In patients with severe idiopathic constipation- abnormal gastric emptying and small-bowel transit may
exist-So- It is important to exclude significant upper GI Dysmotility-(before deciding surgery- (subtotal
colectomy) – as surgery may not correct their symptoms and surgery should be offered only to patients
if transit abnormality is limited to the colon.

(3)-- Motility Capsule-(Wireless-pH-Pressure)-

This involve-ingestion of Wireless capsule that measures pH, pressure, and temperature as it traverses
the GIT.

The use of Smart-Pill (Smart-Pill Corp., Buffalo, NY)-that incorporates mini-camera and video recording
capabilities-enables the physicians to study whole GIT-transit time as well as regional transit times.
 25

Once the capsule is activated and ingested, data regarding temperature- pH, and video images are
transmitted to a receiver.

The results are interpreted as- The colon transit time is the time from- entry of the capsule into the
caecum, determined by a sudden drop in pH- to the time the capsule passes out of the colon,
determined by a sudden drop in temperature accompanied by loss of pressure recording.

It has the advantage of-it is performed in the ambulatory setting with the avoidance of any ionizing
radiation-Also- this technique can be used for- measuring gastric emptying time, small-bowel transit
time, and colon transit time-

This technology is promising in the evaluation of GI transit but is not currently used as a standard
investigation-In Recent Studies -the wireless capsule was recently compared to the more standard
radiopaque marker method of evaluating colonic motility and found to be comparable.

Bowel Habits:-

The frequency of defecation is variable between individuals (as it is influenced by social and dietary
factors) - Bowel habits vary between 1-3 motions/day- to- 3 motions/week.

The frequency of defecation: - is just as variable among individual as is their perception of abnormal
stool frequency. An individual who passes more than three loose stools daily is considered as having
diarrhea, whereas passage of fewer than three stools weekly - is considered as having constipation.

Any frequency within that range is considered normal, although many individuals will still seek medical
advice for what they perceive as diarrhea or constipation.

 Diarrhea: - is defined as passage of- too loose or too frequent motion-(is usually said to be present
if stools contain more than 300 mL of faecal fluid daily.) and/or-more than 3-motions/day.

In inflammatory and infective diseases of the colon (and small bowel): produce Diarrhea by: excessive
fluid secretion by the inflamed mucosa-(most important); and impairment mucosal absorption&
decrease in transit time(less important).

Hydroxy fatty acids; Bile Salts; Castor oil: produce diarrhea by stimulation of fluid secretion by colonic
mucosa

 Constipation is defined as: infrequent stools (fewer than -3 motions per week) –or-hard consistence
of the stools-or- excessive straining,-or incomplete evacuation.