DISTURBANCES OF BOWEL MOTILITY

Lecturer: Dina C. Gonzales MD MHPEd FPCP FPSG

FPSDE

DIARRHEA

Loosely defined as passage of

abnormally
liquid or unformed
stools at an increased frequency
May also refer to change in the
usual frequency, stool volume and
consistency
from
formed
to
semiformed to semi liquid
Passage of unusually loose or
watery stools
Increased frequency of at least
3x/day
Frequent passing of formed
stools is NOT diarrhea

Water is absorbed and secreted in the

different parts of the intestine.
Approximately 2 liters of water are
coming from exogenous sources (food
and fluid intake) while about 7 liters
are secreted by the digestive glands
and organs.

Water and fluids absorbed through the

intestines come from two main sources
exogenous and endogenous sources.
Food and fluid intake are examples of
exogenous sources. Whereas saliva, gastric
juices, intestinal secretions, pancreatic
juices, and biliary secretions account for the
endogenous sources.
In children, the passage of stools with
less than 5ml/kg of water is still considered
normal.

- About 5.5 liters are absorbed back in

the duodenum and jejunum, 2 liters in
the ileum, and 1.3 liters in the colon
and rectum. In normal conditions, this
exchange of fluids results in a stool
output with less than 200 ml of water
in adults.In children, the normal water
content of the stool is less than 5
ml/kg of body weight.

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-Enkephalins

Water is absorbed into the enterocyte

together with glucose and electrolytes (Na+,
K+, Cl-).

In the Intestines, water is absorbed in the villi,

while secretion occurs in the crypts.
REGULATIONS OF INTESTINAL SECRETION

Enkephalin
Opioid neurotransmitter that binds to delta
receptors to reduce cAMP levels.f
Enkephalinase
Enzyme that degrades enkephalins
VIP (Vasoactive intestinal Peptide
Increase cAMP levels.
Cyclic AMP
Induces secretion of water and electrolytes.

In
normal
conditions,
enkephalin
is
produced so it can bind to delta receptors in the
enterocyte. This binding inhibits the formation of
cAMP, thus preventing the hypersecretion of
water.
Enkephalinase is the enzyme that degrades
enkephalin.
The enkephalin-enkephalinase interaction
results in adequate levels of enkephalin binding
to delta receptors which inhibits the formation of
cAMP from ATP. On the other hand, VIP and
prostaglandins stimulate the conversion of ATP
to cAMP.

OPIODS AND THEIR RECEPTORS

Opioids

Opioid Receptors
(mu)
d (delta)
has
decreases
inhibitory
cAMP
effects
on formation
intestinal
smooth
muscles

Exogenous
-Morphine
-Loperamide
Endogenou
s

+++

+++

- The balance between the actions of

enkephalins, and VIP and prostaglandins
regulates the amount of cAMP being
produced. This maintains physiologic

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levels of cAMP which then results in the

normal rate of water and electrolyte
secretion.
DIARRHEA
- Imbalance
absorption.

between

secretion

and

Condition
Hypersecreti
on
Malabsorptio
n
Hypersecreti
on
with
Malabsorptio
n

Secretio
n

Absorptio
n
Normal

Normal

CONSTIPATION
Usually implies failure to produce a stool
over 24 hours.
May be characterized by straining, or
infrequent passage of small, hard stools.
Ranges from 3 bowel movements per day to
3 bowel movements per week.
Fewer than 3 bowel movements per week.
Questions to ask: Diarrhea and
Constipation
Duration
Frequency
Number of episodes
Interval between bowel movements
(constipation)
Character of the stool
Consistency, Presence of blood, mucus
Amount per episode
Stool caliber
Accompanying manifestations
Abdominal pain
Fever
Vomiting, Nausea
Abdominal distention
Flatulence
Anal pain
Intake of medications that can precipitate
and/or alleviate the symptoms.
Offending Agents
Food source/ preparation
Water source
Associated illnesses/conditions
Diabetes
Thyroid disorders
Stroke
Pancreatic disease
Previous abdominal surgery

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CONSTIPATION AS DEFINED BY WGO (2007)

DIARRHEA

ACUTE : < 2 weeks

PERSISTENT: 2- 4 weeks
CHRONIC: > 4 weeks
Acute Diarrhea
>90% Infectious causes
Symptomatology: Vomiting, Abdominal Pain,
Fever
10% Medications, toxic ingestion, ischemia,
other conditions.

Patients View
Straining (52%)
Hard pellet-like stools (44%)
Inability to defecate when desired (34%)
Infrequent defecation (33%)
Clinical View: Rome Criteria III
< 3 bowel movements per week
Hard stool in > 25% of BM
- Incomplete evacuation in >25% of BMs
- Need for digital manipulation to facilitate
evacuation
- For patients not taking laxatives: (2) of the
above in any 12 week period during previous
12 months.

See Figures on Diarrhea (Last Page)

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Systemic
Amyloidosis
Scleroderma
Polymyositis
Pregnancy

Pathogenesis of Constipation
Motility Disorders
- Insufficient nutrition:
Inadequate fiber intake,
Low fluid intake
- Impaired Colon Motility:
Colinic Hernia
Slow transit constipation
Irritable bowel syndrome
Intestinal myopathy
Ogilvie syndrome
Drugs
Secondary Causes of Constipation
A. Gastrointestinal
- Colorectal Neoplasm
- Ischemia
- Volvulus
- Megacolon
- Diverticular Disease
- Anorectal Prolapse
- Rectocele, Stenosis
- Megarectum
B. Surgical
- Abdominal/ Pelvic Surgery
- Colonic/ Anorectal Surgery

C. Psychological
- Depression
- Eating Disorders
D. Drugs
- Opiates
- Antidepressants
- Anticholinergics
- Antipsychotics
- Antacids (Al, Ca)
- Ca channel blockers
- Iron Supplements

Neurological
Parkinsons
Multiple Sclerosis
Autonomic Neuropathy
Aganglionosis
Spinal Lesiosn
Cerebrovascular Disease
CLASSIFICATIONS OF PATHOPHYSIOLOGICAL
SUBGROUPS:
A.

Functional constipation (slow-transit

constipation) Two or more of the following in
at least 25% of defecations:

Straining
Lump or hard stools
Sensation of incomplete defecation
Sensation of anorectal obstruction
Manual maneuvers to facilitate defecations
Fewer than three defecations per week

Irritable Bowel Syndrome

At least 3 months with onset at least 6 months
previously of recurrent abdominal pain or
discomfort associated with 2 or more of the ff:
Improvement with defecation
Onset associated with a change in
frequency of stool
Onset associated with a change in form
(appearance of stool)
Outlet Obstruction
STOOL FORMS

E. Endocrine/ Metabolic
- Hypercalcemia
- Hyperparathyroidism
- Diabetes Mellitus
- Hypothyroidism
- Hypokalemia
- Uremia
- Addisons
- Porphyria
F. Lifestyle
- Inadequate fiber/fluid
- Inactivity
Normal Stool Form: Types 3,4,5

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Hard or lumpy stools can indicate that a

patients intestinal transit time is too slow for
them.
Studies have shown that stool form
correlates to transit time: therefore, sophisticated
testing of transit time is rarely required.

The Etiology of IBS remains an enigma.

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FIGURES AND TABLES FROM THE LECTURE:

Association Between Pathobiology of Causative Agents and Clinical

Features in Acute Infectious Diarrhea
Agents
TOXIN
PRODUCERS
A. Preformed
Toxin
B. cereus
S. aureus
C. perfringens
B. Enterotoxin
V. cholera
ETEC
Klebsiella sp.
Aeromonas
C.
Enteroadhere
nt
EPEC
Enteroadhere
nt E coli
Giardia
Helminths
Cryptosporidi
osis
D. Cytotoxin

Incubation

Vomiting

Abdominal
Pain

Fever

Diarrhea

1-8h

3-4+

1-2+

0-1+

3-4+,
watery

8-72h

2-4+

1-2+

0-1+

3-4, watery

1-8 days

0-1+

1-3+

0-2+

1-2+,
Watery,
Mushy

8-24h

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producers
C. difficile

1-3 days

0-1+

3-4+

1-2+

Hgic E.coli

12-72h

0-1+

3-4+

1-2+

1-3+,
usually
watery,
occ, bloody
1-3+
usually
watery,
quick
bloody

Agents

Incubation

Vomiting

Abdominal
Pain

Fever

Diarrhea

1-3 days

1-3+

2-3+

3-4+

1-3+,
watery

12h-11
days

0-3+

2-4+

3-4+

1-4+,
Watery or
bloody

12h-8 days

0-1+

3-4+

3-4+

1-2+,
bloody

INVASIVE
ORGANISMS
A. Minimal
Inflammation
Rotavirus
Norwalk agent
B. Variable
Inflammation
Salmonella
Campylobacte
r
Aeromonas
V.
parahaemolyti
cus
Yersinia
C. Severe
Shigella
EIEC
E. histolytica

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