3.

3-B
ABDOMINAL SX IIB: DIARRHEA, CONSTIPATION and WEIGHT LOSS
DR. TENGCO

December 3, 2014
PLM CM

I.

Diarrhea & Constipation

A. Norm al Physiology
1. Neural Control
2. Intestinal Fluid Absorption and Secretion
3. Sm all Intestinal Motility
4. Ileocolonic Storage and Salvage
5. Colonic Motility and Tone
6. Colonic Motility after Meal Ingestion
7. Defecation
II. Diarrhea
A. Differentials
B. Acute Diarrhea
1. Acute Diarrhea from Infectious Agents
2. Acute Diarrhea from Other Causes
3. Approach to the Patient
C. Chronic Diarrhea
1. Causes
a. Secretory Causes
b. Osmotic Causes
c. Steatorrheal Causes
d. Inflammatory Causes
e. Dysm otility Causes
f.
Facitial Causes
g. Iatrogenic Causes
2. Approach to the Patient
III. Constipation
A. Approach to the Patient
B. Investigation of Severe Constipation
IV. Weight Loss
A. Physiology of Weight Regulation
B. Significance of Weight Loss
C. Causes of Weight Loss
D. Approach to the Patient
1. Physical Exam ination
2. Diagnostic Testing

DIARRHEA & CONSTIPATION

Among the most common patient complaints faced by
internists and primary care physicians
Account for nearly 50% of referrals to gastroenterologists.
Although diarrhea and constipation may present as mere
nuisance symptoms at one extreme, they can be severe or
life-threatening at the other.
Even mild symptoms may signal a serious underlyin g
gastrointestinal lesion, like:
o colorectal cancer
o systemic disorder (i.e. thyroid disease)
Given the heterogeneous causes and potential severity of
these common complaints, it is imperative to appreciate the:
o pathophysiology
o etiologic classification
o diagnostic strategies
o therapeutic principles
NORMAL PHYSIOLOGY
Functions of the human small intestine and colon:
o Digestion and assimilation of nutrients from food
o secretion and absorption of water and electrolytes
o storage and subsequent transport of intraluminal contents
aborally
o salvage of some nutrients after bacterial metabolism of
carbohydrate that are not absorbed in the small intestine
Normal Gastrointestinal Motility:
Functions at Different Anatomic Levels
Stomach and Synchronized MMCs (Migrating Motor
small bowel
Complexes)in fasting
Accommodation, trituration, mixing, transit
o Stomach ~3 h
o Small bowel ~3 h
Ileal reservoir empties boluses
Colon
irregular mixing, fermentation, absorption,
transit
Ascending, transverse: reservoirs
Descending: conduit
Sigmoid/rectum: volitional reservoir

CALDERON, GARCIA, HARDIN, MANABAT, SOLIS, VIOLAGO

It should be noted that the values above applies only to

individuals on typical "Western", low ruffage diets.
In developing nations, the average stool output of individuals
can vary considerab ly depending on the nature of dietary
intake, b ut is generally greater b ecause of higher fiber intake
Diseases

Diarrhea
Irritable Bowel Syndrome
Chronic Diarrhea
Chronic Constipation

Contributing Factors
Alterations on fluid and
electrolyte handling
Alterations in motor and
sensory functions of the colon

NEURAL CONTROL
1. Intrinsic innervation (enteric nervous system)
Comprised of several layers:
o Myenteric Plexus: regulates smooth-muscle function
o Submucosal Plexus: affects secretion, absorption, and
mucosal blood flow
o Mucosal Neuronal layer
Function of these layers are modulated by interneurons
through the actions of neurotransmitter amines or peptides :
o Acetylcholine
o Vasoactive Intestinal Peptide (VIP)
o Opioids
o Norepinephrine
o Serotonin
o Adenosine Triphosphate (ATP)
o Nitric Oxide (NO)
2.

Extrinsic innervation
part of the autonomic nervous system
modulate motor and secretory functions
Parasympathetic fibers convey visceral sensory and
excitatory pathways to the colon
o Small Intestine and Proximal Colon

Conveyed via the vagus nerve along the

branches of the superior mesenteric artery
o Distal Colon

Supplied by sacral parasympathetic nerves

(S2-4) via the pelvic plexus

Fibers course through the wall of the colon as

ascending intracolonic fibers
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Reaches the proximal colon in some instances

Sympathetic nerves
o modulates motor functions

excitatory to sphincters and inhibitory to

nonsphincteric muscle
o reaches the small intestine and colon alongside their
arterial vessels
chief excitatory neurotransmitters:
o Acetylcholine
o Tachykinins (substance P)
VISCERAL AFFERENTS
Convey sensation from the gut to the CNS
Course to the Spinal Cord:
Course along the sympathetic fibers (Initially)

Separate as they approach the spinal cord

Have cell bodies in the dorsal root ganglion

Enter the dorsal horn of the spinal cord

Course to the Brain:
Conveyed along the lateral spinothalamic tract and nociceptive
dorsal column pathway

Projected beyond the thalamus and brainstem to the insula

and cerebral cortex to be perceived
Other afferent fibers synapse in the prevertebral ganglia and
reflexly modulate intestinal motility
INTESTINAL FLUID ABSORPTION AND SECRETION
Average day secretion:
Fluid that enter the GI tract:
9L
Residual fluid that reaches the colon:
~1 L
Stool excretion of fluid:
0.2 L/d
Fluid reabsorbed by the colon:
4X its usual volume
of 0.8 L/d
Colon
o Has a large capacitance and functional reserve
o Ma y recover up to 4 x its usual volume of 0.8 L/d, provided
the rate of flow permits reabsorption to occur
o Colon can partially compensate for excess fluid delivery to
the colon because of intestinal absorptive or secretory
disorders
o Sodium absorption in the colon:

Predominantly electrogenic

Uptake takes place at the apical membrane

Compensated for by the export functions of the

basolateral sodium pump
Neural and Non-neural mediators that regulate colonic fluid
and electrolyte balance
o Cholinergic
o Adrenergic
o Serotonergic
Angiotensin and aldosterone
o Also influence colonic absorption
o Reflects the common embryologic development of the
distal colonic epithelium and the renal tubules
SMALL INTESTINAL MOTILITY
Migrating Motor Complex (MMC)
o Intestinal Housekeeper
o serves to clear nondigestible residue from the small
intestine
o propagated series of contractions lasts on average 4 mins
o occurs every 6090 min
o usually involves the entire small intestine
After ingestion, small intestine produces irregular, ixing
contractions of relatively low amplitude
o Except in the distal ileum where more powerful
contractions occur intermittently and empty the ileum by
bolus transfers
ILEOCOLONIC STORAGE AND SALVAGE
Distal Ileum
o Acts as a reservoir, emptying intermittently by bolus
movements
o Allows time for salvage of fluids, electrolytes and nutrients
Segmentation by haustra compartmentalizes the colon
o Function:

Mi xing

Retention of residue

Formation of solid stools

o There is increased appreciation of the intimate interaction
between the colonic function and luminal ecology
The resident bacteria in the colon are necessary for the
digestion of unabsorbed carbohydrates vital source of
nutrients to the mucosa
CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

3.3-B

o also keeps pathogens at bay by a variety of mechanisms

Ascending and transverse colon function as reservoirs
(average transit, 15 h)
Descending colon acts as a conduit (ave transit, 3 h)
Colon
o Efficient at conserving sodium and water
o Important function in sodium -depleted patients in whom
the small intestine alone is unable to maintain sodium
balance
DISEASES
DIARRHEA

CONSTIPATION

CONTRIBUTING FACTORS
Alterations in the reservoir function of the
proximal colon or the propulsive function
of the left colon
Same as above
Disturbances of the rectal or sigmoid
reservoir
o Typically as a result of dysfunction
of the pelvic floor, anal sphincters,
or the coordination of defecation

COLONIC MOTILITY AND TONE

The small intestinal MMC only rarely continues into the colon.
Short duration or phasic contractions, the presominant
contractions in the colon, are irregular and non-propagated
mix colonic contents
High-amplitude propagated contractions (H APCs) (>75
mmHg) are sometimes associated with mass movements
through the colon and normally occur approximately five times
per day, usually on awakening in the morning and
postprandially
Colonic tone
o refers to the background contractility upon which phasic
contractile activity (typically contractions lasting <15 s) is
superimposed.
o an important cofactor in the colon's capacitance (volume
accommodation) and sensation
COLONIC MOTILITY AFTER MEAL INGESTION
The colonic phase and tonic contractility increase for a period
of ~2h
The initial phase (~10 min) is mediated by the vagus nerve in
response to mechanical distention of the stomach.
The subsequent response of the colon requires caloric
stimulation and is mediated at least in part by hormones, e.g.,
gastrin and serotonin.
DEFECATION
Puborectalis muscle
o Forms a sling around the rectoanal junction
o its tonic contraction is important to maintain continence
During defecation:
Sacral parasympathetic nerves relax this muscle

Facilitates the straightening of the rectoanal angle

Distention of the rectum results in transient relaxation of the

internal anal sphincter via intrinsic and reflex sympathetic
innervations

As sigmoid and rectal contractions increase the pressure within

the rectum, the rectosigmoid angle opens by >15

Voluntary relaxation of the e xternal anal sphincter (striated

muscle innervated by the pudendal nerve) in response to the
sensation produced by distention permits the evacuation of feces
o Valsalva maneuver : augments this evacuation process
by an increase in intraabdominal pressure
o Defecation can also be delayed voluntarily by contraction
of the external anal sphincter
DIARRHEA
Diarrhea is loosely defined as passage of abnormally liquid or
unformed stools at an increased frequency.
For adults on a typical Western diet, stool weight >200g/d can
generally be considered diarrheal
o Acute
o Persistent
o Chronic

if <2 weeks
if 2-4 weeks
if >4 weeks in duration

DIFFERENTIALS
Two common conditions, usually associated with the passage
of stool totaling>200 g/d
o Pseudodiarrhea
frequent passage of small volumes of stool

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often associated with rectal urgency and accompanies

irritable bowel syndrome or anorectal disorders like
proctitis
o Fecal incontinence
involuntary discharge of rectal contents and is most
often caused by neuromuscular disorders or structural
anorectal problems
Although severe diarrhea and urgency my aggravate or
cause incontinence
o Overflow diarrhea
may occur in nursing home patients due to fecal
impaction that is readily detectable by rectal
examination
A careful history and physical examination generally allow
these conditions to be discriminated from true diarrhea.
ACUTE DIARRHEA
90% - infectious agents
10% - medications, toxic ingestions, ischemia, and other
conditions.
ACUTE DIARRHEA FROM INFECTIOUS AGENTS
often accompanied by vomiting, fever, and abdominal pain
fecal-oral transmission via direct personal contact or, more
commonly, via ingestion of food or water contaminated with
pathogens from human or animal feces
In the immunologically competent person, the resident fecal
microflora, is rarely the source of diarrhea and m ay actually
play a role in suppressing the growth of ingested pathogens.
Disturbance of the flora by antibiotics
o Lead to diarrhea by reducing the digestive function or by
allowing the overgrowth of pathogens, such as C. difficile
Acute infection or injury occurs when the ingested agent
overwhelms the host's mucosal immune and nonimmune
(gastric acid, digestive enzymes, mucus secretion, peristalsis,
and suppressive resident flora) defenses.
Established clinical associations with specific enteropathogens
may offer diagnostic clues.
HIGH RISK GROUPS
Travelers
Latin America, Africa, and
Enterotoxigenic or
Asia traveler'sdiarrhea
EnteroaggregativeE.coli
Campylobacter
Shigella
Aeromonas
Norovirus
Coronavirus
Salmonella
Russia (especially St.
Giardia-associated diarrhea
Petersburg)
Nepal
Campers, backpackers, and
swimmers in wilderness
areas
Cruise ships

Cyclospora
Giardia

Norwalk virus

3.3-B

Mycobacterium spp.
CMV
Herpes simplex
Cryptosporidium
Isospora belli
Microsporida
Blastocystis hominis
Agents transmitted venereally per rectum may contribute to
proctocolitis in patients with AIDS:
Neisseria gonorrhea
Treponema pallidum
Chlamydia
Patients with hemochromatosis are especially prone to
invasive, even fatal, enteric infections and should a void raw
fish:
Vibrio
Yersinia

Daycarepaticipants and their family members

Shigella
Giardia
Cryptosporidium
rotavirus

Institutionalized persons
Infectious diarrhea is one of the most frequent categories of
nosocomial infections in many hospitals and long-term care
facilities
most commonly C. difficile

The pathophysiology underlying acute diarrhea by infectious

agents produces specific clinical features that may also be
helpful in diagnosis
PATHOGENS
REMARKS
Preformed
Diarrhea
Bacterial Toxins
associated with:
o Marked vomiting
EnterotoxinAssociated with
o Minimal or no
producing
profuse watery
fever
Bacteria
diarrhea secondary
Occurs within few
to small-bowel
hours after
hypersecretion after ingestion
ingestion
Enteroadherent
Less vomiting
pathogens
Greater abdominal
cramping or
bloating
Higher fever
Cytotoxinproducing and
ALL causes high fever and abdominal pain
invasive
microorganisms
Invasive Bacteria
Often cause bloody diarrhea, referred to
and E. histolytica
as dysentery
Yersinia
Invades the terminal ileal and proximal
colon mucosa
Ma y cause especially severe abdominal
pain with tenderness mimicking acute
appendicitis

Consumers of certain foods

Consumption at a picnic,
Salmonella Campylobacter
banquet, or restaurant
or Shigella (chicken)
Undercooked hamburger
E. coli (O157:H7)
enterohemorrhagic
Fried rice
Mayonnaise or creams
Eggs
Uncooked foods or soft
cheeses
Seafood, especially if raw

Bacillus cereus
Staphylococcus aureus or
Salmonella
Salmonella
Listeria
Vibrio species, Salmonella,
or acute hepatitis A

Immunodeficient persons (person with AIDS)

Primary Immunodeficiency
IgA Deficiency
Common Variable Hypogammaglobulinemia
Chronic Granulomatous Disease
Secondary Immunodeficiency States (More Common)
AIDS
Senescence
Pharmacologic suppresion
Common enteric pathogens often cause a more severe and
protracted diarrheal illness, particularly in individuals with
AIDS:
CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

Infectious diarrhea may be associated with systemic

manifestations
PATHOGENS
RELATED SYSTEMIC DISEASE
Salmonella
Reactive arthritis (Reiters Syndrome)
Campylobacter
Arthritis
Shigella
Urethritis
Yersinia
Conjunctivitis
Yersinia
Autoimmune-type thyroiditis
Pericarditis
Glomerulonephritis
EHEC (O157:H7)
Hemolytic Uremic Syndrome
Shigella
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The syndrome of postinfectious IBS has now been

recognized as a complication of infectious diarrhea
Acute diarrhea can also be a major symptom of several
systemic infections including:
o Viral hepatitis
o Listeriosis
o Legionellosis
o Toxic Shock Syndrome
ACUTE DIARRHEA FROM OTHER CAUSES
CAUSES
REMARKS

Side Effects From

Medications

Occlusive or
Nonocclusive
Ischemic Colitis

Colonic
Diverticulitis

Ingestion of Toxins

Conditions Causing
Chronic Diarrhea

Probably
the
most
common
noninfectious causes of acute
diarrhea
Etiology may be suggested by a
temporal association between use
and symptom onset
Medications:
o Antibiotics
o Cardiac antidysrhythmics
o Antihypertensives
o NSAIDS
o Certain antidepressants
o Chemotherapeutic agents
o Bronchodilators
o Antacids
o Laxatives
Typically occurs in persons > 50
years
Often presents as acute lower
abdominal pain preceding watery,
then bloody diarrhea
Generally
results
in
acute
inflammatory changes in the sigmoid
or left colon while sparing the rectum
Ma y present with acute diarrhea

3.3-B

Vib rio spp.

Yersinia
If stool studies are unrevealing, flexible sigmoidoscopy with
biopsies and upper endoscopy with duodenal aspirates and
biopsies may be indicated.
Brainerd Diarrhea
o Abrupt-onset diarrhea that persists for at least 4 weeks,
but may last 13 years
o Thought to be of infectious origin
o Ma y be associated with subtle inflammation of the distal
small intestine or proximal colon
To exclude Inflammatory Bowel Disease (IBD), ischemic
colitis, diverticulitis, or partial bowel obstruction
o Structural examination by sigmoidoscopy
o Colonoscopy
o Abdominal CT scanning
o or other imaging approaches

Organophosphate insecticides
Amanita and other mushrooms
Arsenic
Preformed environmental toxins in
seafood
o Ciguatera
o Scombroid
Can also be confused with acute
diarrhea early in their course
Ma y occur in:
o Inflammatory Bowel Disease
o Other inflammatory chronic
diarrheas that may have an
abrupt rather than insidious
onset and exhibit features that
mimic infection

APPROACH TO THE PATIENT

The decision to evaluate acute diarrhea depends on its
severity and duration and on various host factors.
Most episodes of acute diarrhea are mild and self-limited, and
they do not justify the cost and potential morbidity of diagnostic
or pharmacologic interventions.
Indications for evaluation include:
o profuse diarrhea with dehydration
o grossly bloody stools
o fever 38.5 C
o duration >48 h without improvement
o new community outbreaks
o associated severe abdominal pain in patients older than 50
years of age, and elderly (>70 years)
o immunocompromised patients
In some cases of moderately severe febrile diarrhea
associated with fecal leukocytes (or increased fecal levels of
the leukocyte proteins) or with gross blood, a diagnostic
evaluation might be avoided in favor of an empirical antibiotic
trial.
The cornerstone of diagnosis in those suspected of severe
acute infectious diarrhea is microbiologic analysis of the stool.
Workup includes:
o Cultures for bacterial and viral pathogens
o Direct inspection for ova and parasites
o Immunoassays for:

Certain bacterial toxins (C. difficile)

Viral antigens (Rotavirus)

Protozoal antigens (Giardia, E. histolytica)

If a particular pathogen or set of possible pathogens is so
implicated:
o Whole panel of routine studies may not be necessary
o Special cultures may be appropriate (Rare)

Enterohemorrhagic and other types of E. Coli

CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

CHRONIC DIARRHEA
Diarrhea lasting more than 4 weeks warrants evaluation to
exclude serious underlying pathology.
Most of the causes of chronic diarrhea are noninfectious
Classification of chronic diarrhea is by pathophysiologic
mechanism
o Facilitates a rational approach to management

CAUSES
Secretory Causes
Secretory diarrheas are due to derangements in fluid and
electrolyte transport across the enterocolic mucosa.
They are characterized clinically b y watery, large-volume fecal
outputs that are typically painless and persist with fasting.
Medications
o Side effects from regular ingestion of drugs and toxins are
the most common secretory causes of chronic diarrhea.
o Surreptitious or habitual use of stimulant laxatives [e.g.,
senna, cascara, bisacodyl, ricinoleic acid (castor oil)]
o Chronic ethanol consumption d/t enterocyte injury with
impaired sodium and water absorption as well as rapid
transit other alterations
Environmental toxins (e.g., arsenic)
Bowel resection, mucosal disease, or enterocolic fistula
o inadequate surface for reabsorption of secreted fluids and
electrolytes
o worsen with eating
o resection of <100 cm of terminal ileum, dihydroxy bile
acids may escape absorption and stimulate colonic
secretion cholorrheicdiarrhea
o With disease (Crohns ileitis) or resection of <100 cm of
terminal ileum
Dihydroxy bile acids may escape absorption and
stimulate colonic secretion (Cholorrheic Diarrhea)
Ma y contribute to so-called idiopathic secretory
diarrhea in which bile acids are functionally
malabsorbed from a normal appearing terminal ileum
Certain Bacterial Infections
Partial bowel obstruction, ostom y stricture or fecal
impaction
o Paradoxically lead to increased fecal output due to fluid
hypersecretion

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Hormones
Ma y produce:
o Watery diarrhea (May exist alone)
Metastatic
o Carcinoid Syndrome
gastrointestinal
Episodic Flushing
carcinoid
Wheezing
tumors or,
Dyspnea
rarely, primary
Right Sided Valvular Disease
bronchial
Diarrhea is due to the release into the
carcinoids
circulation of potent intestinal
secretagogues including Serotonin,
histamine, prostaglandins, and various
kinins
Pellagra-like skin lesions m ay rarely
occur as the result of serotonin
overproduction with niacin depletion
Gastrinoma
Gastrin
One of the most common
neuroendocrine tumors
Most typically present with refractory
ulcers
Diarrhea most often results from fat
maldigestion owing to pancreatic enzyme
inactivation by low intraduodenal pH.
VIPoma
VIP pancreatic cholera (a.k.a Watery
Diarrhea Hypokalemia Achlorhydria
Syndrome)
Secretory diarrhea is often massive with
stool volumes >3L/d
Ma y be accompanied by:
o Life-threatening dehydration
o Neuromuscular dysfunction from
associated hypokalemia,
hypomagnesemia or
hypercalcemia
o Flushing
o Hyperglycemia
Medullary
Calcitonin
carcinoma of
Present with watery diarrhea caused by
the thyroid
calcitonin, other secretory peptides, or
prostaglandins
Systemic
Histamine
mastocytosis Ma y be associated with the skin lesion
urticarial pigmentosa
Ma y cause diarrhea:
o Mediated by histamine
o Due to intestinal infiltration by
mast cells
Colorectal
Prostaglandins
villous
Ma y rarely be associated with a
adenomas
secretory diarrhea that may cause
hypokalemia
Mediated by prostaglandins
Inhibited by NSAIDS
Congenital defects in ion absorption
o Congenital chlorridorrhea (Defective Cl /HCO3 e xchange):
results in alkalosis
o Congenital Sodium Diarrhea (Defective Na + /H+ exchange):
results in acidosis
o Addison's disease
Osmotic Causes
Osmotic diarrhea occurs when ingested; poorly absorbable,
osmotically active solutes draw enough fluid lumenward to
exceed the resorptive capacity of the colon.
Fecal water output increases in proportion to such a solute
load
Osmotic diarrhea characteristically ceases with fasting or
with discontinuation of the causative agent
Osmotic laxatives (Mg 2+, PO43, SO4 2)
o magnesium-containing antacids, health supplements, or
laxatives
o stool osmotic gap (>50 mosmol/L)
Serum osmolality (typically 290 mosmol/kg) - [2 x (Fecal
Sodium + Potassium Concentration)]
o Measurement of fecal osmolarity is no longer
recommended
Ma y be erroneous because carbohydrates are
metabolized by colonic bacteria, causing an increase in
osmolarity
Carbohydrate malabsorption
o Due to defects in brush-border disaccharidases and other
enzymes
o Leads to osmotic diarrhea with low pH
o lactase deficiency and other disaccharide deficiencies
o Lactase Deficiency
One of the most common cause of chronic diarrhea in
adults
CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

3.3-B

Diarrhea ensues because of malabsorbed lactose from

diet (milk and other dairy products)
Nonabsorbable carbohydrates
o Sorbitol
o Lactulose
o Polyethylene glycol
Steatorrheal Causes
Fat malabsorption may lead to greasy, foul-smelling, difficultto-flush diarrhea often associated with weight loss and
nutritional deficiencies due to concomitant malabsorption of
amino acids & vitamins.
Increased fecal output is caused by the osmotic effects of fatty
acids and by the neutral fat especially after bacterial
hydroxylation
STEATORRHEA - stool fat >7 g/d;
o Rapid-transit diarrhea may result in fecal fat up to 14 g/d
o daily fecal fat averages 15 to 25 g with small intestinal
diseases
o often exceeds 32 g with pancreatic exocrine insufficiency
Intraluminal maldigestion
o Bacterial overgrowth in the small intestine may
deconjugate bile acids and alter micelle formation,
impairing fat digestion and occurs in:
Stasis from blind-loop
Small-bowel diverticulum or dysmotility
Especially likely in elderly
o Most commonly results from pancreatic exocrine
insufficiency
Occurs when >90% of pancreatic secretory function is
lost
o Chronic pancreatitis
Usually a sequel of ethanol abuse
Most frequently causes pancreatic insufficiency
o Cirrhosis or biliary obstruction may lead to mild
steatorrhea due to deficient intraluminal bile acid
concentration
o Bariatic surgery
o Liver disease
o Other Causes:
Cystic fibrosis
Pancreatic duct obstruction
Somatostatinoma
Mucosal Malabsorption
o Celiac sprue/ Gluten-sensitive enteropathy
Most common, affects all ages
villous atrophy and crypt hyperplasia
(+) fatty diarrhea associated with multiple nutritional
deficiencies
Can mimic IBS
o Tropical sprue
Ma y produce a similar histologic and clinical syndrome
but occurs in residents of or travelers to tropical climates
Abrupt onset and response to antibiotics suggest an
infectious etiology
o Whipple's disease
due to the bacillus Tropheryma whipplei and histiocytic
infiltration of the small-bowel mucosa
less common cause of steatorrhea that most typically
occurs in young or middle-aged men
frequently
associated
with
arthralgias,
fever,
lymphadenopathy, and extreme fatigue
may affect the central nervous system and endocardium
o Mycobacterium avium-intracellulare infection in patients
with AIDS.
o Abetalipoproteinemia
Rare defect of chylomicron formation and fat
malabsorption in children
associated with acanthocytic erythrocytes, ataxia, and
retinitis pigmentosa
o Infections: Giardia
o Medications (e.g., colchicine, cholestyramine, neomycin)
o Amyloidosis
o Chronic ischemia
Postmucosal lymphatic obstruction
o Due to: congenital intestinal lymphangiectasia or acquired
lymphatic obstruction secondary to trauma, tumor, or
infection
o Ma y lead to:
Fat malabsorption
Enteric losses of protein (often causing edema)
Lymphocytopenia
o Carbohydrate and amino acid absorption are preserved
Inflammatory Causes
Inflammatory diarrheas are generally accompanied by pain,
fever, bleeding, or other manifestations of inflammation.
Mechanism of diarrhea:
o Exudation
o Fat malabsorption
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o Disrupted fluid/electrolyte absorption

o Hypersecretion or hypermotility from release of cytokines
and other inflammatory mediators
The unifying feature on stool analysis is the presence of
leukocytes or leukocyte-derived proteins such as calprotectin
o Can lead to anasarca if exudative protein loss is severe
Idiopathic inflammatory bowel disease
o Crohn's disease and chronic ulcerative colitis
most common organic causes of chronic diarrhea in
adults
Range in severity from mild to fulminant and lifethreatening
Ma y be associated with:
Uveitis
Polyarthralgias
Cholestatic liver disease (Primary Sclerosing
Cholangitis)
Skin Lesions (Erythema nodosum, Pyoderma
gangrenosum)
Microscopic colitis
o includes both lymphocytic and collagenous colitis
o an increasingly recognized cause of chronic watery
diarrhea, especially in middle-aged women and those on
NSAIDS
o Biopsy of a normal-appearing colon is required for
histologic diagnosis
o Ma y coe xist with symptoms suggesting IBS or with celiac
sprue
o responds well to anti-inflammatory drugs (e.g., bismuth), to
the opioid agonist loperamide, or to budesonide
Immune-related mucosal disease
o Primary or secondary forms of immunodeficiency
o Lead to prolonged infectious diarrhea
o With selective IgA deficiency or
common variable
hypogammaglobulinemia, diarrhea is particularly prevalent
and often the result of giardiasis, bacterial overgrowth or
sprue
o Eosinophilic Gastroenteritis
Eosinophilic infiltration of the mucosa, muscularis or
serosa at any level of the GI tract
may cause diarrhea, pain, vomiting, or ascites
(+) atopic history, Charcot-Leyden crystals (d/t extruded
eosinophilic contents) and peripheral eosinophilia (5075% of patients)
While hypersensitivity to certain foods occurs in adults,
true food allergy causing chronic diarrhea is rare
Infections
o Invasive bacteria, viruses, parasites
o Brainerd diarrhea
Other Causes:
o Radiation enterocolitis
o Chronic Graft-vs-host disease
o GI malignancies
o Behet's syndrome
o Cronkite-Canada syndrome

Dysmotility Causes
Primary dysmotility is an unusual etiology of true diarrhea
o Dysmotility induced diarrhea is usually as secondary to
other conditions
Hypermotility with resultant diarrhea:
o Hyperthyroidism
o Carcinoid syndrome
o Certain drugs (e.g., prostaglandins, prokinetic agents)
Stasis with secondary bacterial overgrowth causing diarrhea:
o Primary visceral neuromyopathies
o Idiopathic acquired intestinal pseudo-obstruction
Intestinal dysmotility:
o Diabetic diarrhea, often accompanied by peripheral and
generalized autonomic neuropathies
Disturbed intestinal and colonic motor and sensory responses:
o Irritable bowel syndrome symptoms of stool frequency
Typically cease at night
Alternate with periods of constipation
Accompanied by abdominal pain relieved with
defecation
Rarely result in weight loss
Postvagotom y
Facitial Causes
accounts for up to 15% of unexplained diarrheas
Either as a form of Munchausen syndrome (deception or
self-injury for secondary gain) or eating disorders
Some patients covertly:
o Self-administer laxatives
o Surreptitiously add water or urine to stool sent for analysis
(para kunwari may sakit sila para maka gain ng attention or
para pumayat due to diarrhea)

CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

3.3-B

Patients are:
o Typically women
o Often with histories of psychiatric illness
o Disproportionately from careers in health care
Hypotension and hypokalemia are common co-presenting
features
The evaluation of such patients may be difficult:
o Contamination of the stool with water or urine is suggested
by very low or high stool osmolarity,respectively
o Such patients often deny this possibility when confronted
but they do benefit from psychiatric counseling when they
acknowledge their behaviour.

Iatrogenic Causes
Cholecystectomy
Ileal resection
Bariatic surgery
Vagotomy, fundoplication

APPROACH TO THE PATIENT

The laboratory tools available to evaluate the very common
problem of chronic diarrhea are extensive, and many are
costly and invasive.
As such, the diagnostic evaluation must be rationally directed
by a careful history and physical examination, and simple
triage tests are often warranted before complex investigations
are launched.
The history, physical examination, and routine blood stud ies
should attempt to:
o characterize the mechanism of diarrhea
o identify diagnostically helpful associations
o assess the patient's fluid/electrolyte and nutritional status
Patients should be questioned about the:
o Onset
o Duration
o Pattern
o Aggravating factors (especially diet)
o Relieving factors
o stool characteristics of their diarrhea
o Family history of IBD or sprue
Look for:
o presence or absence of fecal incontinence
o fever
o weight loss
o pain
o certain exposures (travel, medications, contacts with
diarrhea)
o common extraintestinal manifestations (skin changes ,
arthralgias, oral aphthous ulcers)
Blood chemistries may demonstrate electrolyte, hepatic, or
other metabolic disturbances.
Physical findings may offer clues such as :
o thyroid mass
o wheezing
o heart murmurs
o edema
o hepatomegaly
o abdominal masses
o lymphadenopathy
o mucocutaneous abnormalities
o perianal fistulae
o anal sphincter laxity
Therapeutic trial is often appropriate, definitive, and highly cost
effective when a specific diagnosis is suggested on the initial
physician encounter
Persistent symptoms require additional investigation.
Certain diagnoses may be suggested on the initial encounter
However, additional focused evaluations may be necessary to
confirm the diagnosis and characterize the severity or e xtent of
disease so that treatment can be best guided
Cause of chronic diarrhea remains unclear after initial
encounter in 2/3 of cases and further testing is required
o Quantitative stool collection and analyses
Can yield important objective data that may
establish a diagnosis or characterize the type of
diarrhea as a triage for focused additional studies

l analyses
should be performed:
Electrolyte concentration
pH
Occult blood testing
Leukocyte inspection (or leukocyte protein
assay)
Fat quantitation
Laxative screens

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MEDICINE 1 // ABDOMINAL SYMPTOMS II: DIARRHEA, CONSTIPATION & WEIGHT LOSS

Initial Management Based on Accompanying Symptoms or

Features

b. Evaluation Based on Findings From a Limited Age

Appropriate Screen for Organic Disease

CONSTIPATION
persistent, difficult, infrequent, or seemingly incomplete
defecation
Because of the wide range of normal bowel habits,
constipation is difficult to define precisely.
Stool frequency alone is not a sufficient criterion for the
diagnosis of constipation because many constipated patients
describe a normal frequency of defecation but complains of:
o excessive straining
o hard stools
o lower abdominal fullness
o sense of incomplete evacuation
Stool form and consistency are well correlated with the time
elapsed from the preceding defecation.
Hard, pellety stools = SLOW transit
Loose, watery stools = R APID transit
Hard, pellety stools and very large stools are more difficult
to expel.
Psychosocial factors may also be important.
Chronic constipation generally results from inadequate fiber
or fluid intake or from disordered colonic transit or anorectal
function
Idiopathic constipation
o Patients exhibit delayed emptying of the ascending and
transverse colon with prolongation of transit (often in the
proximal colon) and a reduced frequency of highamplitude propagated contractions (HAPCs)
Outlet obstruction to defecation or evacuation disorders delayed colonic transit
o Usually corrected by biofeedback retraining of the
disordered defecation
Constipation of any causes may be exacerbated by
hospitalization or chronic illnesses that lead to physical or
mental impairment and may result in inactivity or physical
immobility.

APPROACH TO THE PATIENT

A careful history should explore the patient's symptoms and
confirm whether he or she is indeed constipated based on:
o frequency (e.g., <3 bowel movements per week)
o consistency (lumpy/hard)
o excessive straining
o prolonged defecation time
o need to support the perineum or digitate the anorectum
There is no underlying cause in majority (~90%) of cases
o Responds to ample hydration, exercise, and
supplementation of dietary fiber (15-25 g/d)
Rectal examination should exclude fecal impaction and most of
the important diseases that present with constipation and
possibly indicate features suggesting and evacuation disorder
(e.g., high anal sphincter tone)
(+) weight loss, rectal bleeding, or anemia with constipation in
patients >40 years flexible sigmoidoscopy plus barium
enema or colonoscopy alone to exclude structural diseases,
e.g., cancer or stricture
Patients with more troublesome constipation may be helped by
bowel-training regimen
o Osmotic laxative
o Evacuating with enema or glycerine suppository as
needed
o 15-20 min distraction- and straining-free bowel
movement after breakfast

Excessive straining hemorrhoids

Weakness of pelvic flor or injury to pudendal nerve

obstructed defecation from descending perineum
syndrome
A good diet and medication history and attention to
psychosocial issues are keys.
INVESTIGATION OF SEVERE CONSTIPATION
Patients who do not respond to simple measures (~5%) are
assumed to have severe or intractable constipation
Measurement of colonic transit
o
taken after 5 days should indicate passage of 80% of
the markers out of the colon
o Radioscintigraphy is used to characterize colonic
function over 24-48 hours with low radiation exposure
and to assess gastric, small bowel and colonic transit
Pelvic floor dysfunction
o Inability to evacuate the rectum, a feeling of persistent
rectal fullness, rectal pain, the need to extract stool from
the rectum digitally, application of pressure on the
posterior wall of the vagina, support of the perineum
during straining, and excessive straining
Simple clinical test to document a nonrelaxing puborectalis
muscle
o Have the patient strain to expel the index finger during
digital rectal exam
o Motion of the puborectalis posteriorly during straining
indicates proper coordination of pelvic floor muscles
Measurement of perineal descent
o Patient in left decubitus
o Inadequate descent (<1.5 cm) - pelvic floor dysfunction
o Perineal ballooning during straining relative to bony
landmarks (>4 cm) - excessive perineal descent
Anorectal manometry detects excessively high resting (80
mmHg) or squeeze anal sphincter tone, and identifies rare
syndromes, e.g., Hirschsprungs disease
Defecography reveals soft abnormalities, e.g., changes in
rectoanal angle and anatomic defects of the rectum

CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

3.3-B

WEIGHT LOSS
SIGNIFICANT UNINTENTIONAL weight loss in a previously
healthy individual is often a harbinger of underlying systemic
disease
Inquiry should always be made about changes in weight
>LOSS OF 5 % OF BODY W EIGHT OVER 6 TO 12 MONTHS
should prompt further evaluation.
PHYSIOLOGY OF WEIGHT REGULATION
Appetite and metabolism are regulated by an intricate network
of neural and hormonal factors.
Weight loss occurs when energy expenditure exceeds
calories available for energy utilization.
Mechanisms of weight loss include:
o decreased food intake
o malabsorption
o loss of calories
o increased energy requirements
Food intake may be influenced by a wide variety of factors:
o visual, olfactory, and gustatory stimuli
o genetics
o psychological factors
o social factors
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MEDICINE 1 // ABDOMINAL SYMPTOMS II: DIARRHEA, CONSTIPATION & WEIGHT LOSS

SIGNIFICANCE OF W EIGHT LOSS

Unintentional weight loss, especially in the elderly, is not
uncommon and is associated with increased morbidity and
mortality rates
Cancer patients with weight loss have decreased:
o performance status
o response to chemotherapy
o median survival
Marked degrees of weight loss also predispose to infection.
Patients undergoing elective surgery, who have lost more
than 10 lb (4.5 kg) in 6 months, have higher surgical mortality
rates.
CAUSES OF W EIGHT LOSS

ELDERLY

YOUNGER
INDIVIDUALS

CAUSES OF W EIGHT LOSS

Depression
Cancer
Benign gastrointestinal disease
Diabetes mellitus
Hyperthyroidism
Psychiatric disturbances (including eating
disorders)
Infection (especially with HIV)

3.3-B

New onset DM is often accompanied by weight loss,

reflecting glucosuria and loss of the anabolic actions of
insulin.
Adrenal insufficienc y may be suggested by increased
pigmentation, hyponatremia, and hyperkalemia.
APPROACH TO PATIENT
Confirm that weight loss has occurred.
Almost half of patients who claim significant weight loss have
no actual change in wt. when it is measured objectively.
If (+) weight loss:
o determine the time interval over which it has occurred
o In the absence of documentation, changes in belt notch
size or the fit of clothing may help confirm loss of weight.
Routine documentation of weight during office visits is
therefore important.
ROS:
o focus on s/s that are associated with disorders that
commonly cause weight loss
o These include:
Fever
Pain
SOB or cough
Palpitations
Changes in pattern of urination
Evidence of neurologic disease
GI disturbances, including difficulty eating, dysphagia,
anorexia, nausea, and change in bowel habits.
Use of cigarettes, alcohol, and all medications should be
reviewed
Ask about previous illness or surgery as well as diseases in
family members.
Signs of depression, evidence of dementia, and social factors,
including financial issues that might affect food intake.
PHYSICAL EXAMINATION
Weight determination and documentation of VS.
Skin
o Pallor
o Jaundice
o Turgor
o Scars from prior surgery
o Stigmata of systemic disease
Search for:
o oral thrush or dental disease
o TG enlargement
o Adenopathy
o Respiratory or cardiac abnormalities
o Detailed examination of the abdomen often lead to clues
for further evaluation
Rectal exam, including prostate exam and testing of stool for
occult blood, should be performed in men
All women should have a pelvic examination, even if they
have had a hysterectomy.
Neurologic examination should include mental status
assessment and screening for depression.
DIAGNOSTIC TESTING
Laboratory testing should confirm or exclude possible
diagnoses elicited from the Hx & PE
If GI s/s are present, upper and/or lower endoscopy and
abdominal imaging with either CT or MRI have a relatively
high yield.
Flexible sigmoidoscopy plus barium enema or colonoscopy
particulary for patients >40y/o to exclude structural diseases
(cancer or strictures)
o Colonoscopy - most cost-effective
o Barium enema - Advantageous to patients with isolated
constipation
Melanosis Coli indicates usage of anthraquinone laxatives
Megacolon or cathartic colon may be detected b y colonic
radiography
Measurement of serum Ca, K, and TSH -> identify p x w/
metabolic d/o

Lung and gastrointestinal cancer are the MOST COMMON

MALIGN ANCIES in patients presenting with weight loss.
In YOUNGER individuals, patients with medical causes of
weight loss usually have S/S that suggest involvement of a
particular organ system.
Gastrointestinal tumors, including those of the pancreas
and liver, may affect food intake early in the course of illness,
causing weight loss before other symptoms are apparent.
Lung cancer, depression and isolation, Chronic
pulmonary disease and CHF can produce anorexia and may
also increase resting energy expenditure.
Presenting sign of infectious diseases such as HIV infection,
tuberculosis, endocarditis, a nd fungal and parasitic
infections.
Hyperthyroidism or pheochromocytoma

CALDERON, GARCIA, HARDIN, MANABAT, SOLIS

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