DISEASES OF THE

INTESTINE
 DIAREEA
 Definition >3 feces/day, > 200 g/day

 Physiology:
– in gastrointestinal tract 9-10 l fluids (2l ingestion, the rest
secretions);
– Na - co-transport with Cl and glucose in small bowel and biliary
salts in terminal ileum; co-transport with H - HCO3; K absorbed with
H or Ca.
– In colon, Na absorbed through apical membrane canals
– parasimpatic is stimulating the peristalsis and electrolyte secretion;
simpatic nerves are doing the opposite.
– Enteric nervous system.
Figure 4.1 - Water fluxes through the intestine

©Copyright Science Press Internet Services

Functional design of small intestine
Acute Diarrhea
 Is just a little case of diarrhea…
 Second leading causes of all death worldwide
 Most common cause of morbidity and
mortality in children worldwide
 Accounts for 9% of hospitalizations in children
<5 years old in the United States
 You will likely suffer from diarrhea in the near
future!
 Definition
 Stool weight in excess of 200 gm/day
 3 or more loose or watery stools/day
 Alteration in normal bowel movement
characterized by decreased consistency and
increased frequency
 Less than 14 days in duration
 Epidemiology
 1.2-1.9 episodes per person annually in the
general population
 2.4 episodes per child <3 years old annually
 5 episodes per year for children <3 years
old and in daycare
 Seasonal peak in the winter
 Etiology
 Viral: 70-80% of infectious diarrhea in
developed countries
 Bacterial: 10-20% of infectious diarrhea but
responsible for most cases of severe
diarrhea
 Protozoars: less than 10%
 Viral Diarrhea
 Rotavirus
 Norovirus (Norwalk-like)
 Enteric Adenovirus
 Astrovirus
 Rotavirus
 Leading cause of hospitalization for diarrhea in
children
 Most prevalent during winter season
 Fecal-oral transmission: viral shedding can
persist for 21 days
 Acute onset of fever followed by watery
diarrhea (10-20 BM/day) and can persist for up
to a week
 Norovirus
 Most common cause of diarrheal
outbreaks/epidemics
 Multiple modes of fecal-oral transmission
 Acute onset of nausea and vomiting, watery
diarrhea with abdominal cramps and can
persist for 1-3 days
 Enteric Adenovirus
 Primarily affects children < 4 years old
 Fecal-oral transmission
 Clinical picture similar to rotavirus (fever
and watery diarrhea)
 Astrovirus
 Primarily affects children < 4 years old and
immunocompromised
 Seasonal peak in the winter
 Fecal-oral transmission: viral shedding can
occur for several weeks
 Fever, nausea and vomiting, abdominal pain,
and diarrhea lasting up to a week
 Summary of Viral Diarrhea
 Most likely cause of infectious diarrhea
 Rotavirus and Norovirus are most common
 Symptoms usually include low grade fever,
nausea and vomiting, abdominal cramps, and
watery diarrhea lasting up to 1 week
 Viral shedding can occur for weeks after
symptoms resolve
 Bacterial Diarrhea
 Campylobacter
 Salmonella
 Shigella
 Enterohemorrhagic Escherichia coli
 Campylobacter
 Most common bacterial pathogen
 Transmitted through ingestion of contaminated
food or by direct contact with fecal material
 Symptoms include diarrhea (+/- blood),
abdominal cramps (can be severe), malaise,
fever
 Usually self-limited and does not require
antibiotics
 Salmonella
 Most common in children <4 years old and a
peak in the first few months of life
 Transmitted via ingestion of contaminated food
and contact with infected animals
 Symptoms include fever, diarrhea, and
abdominal cramping
 Antimicrobial therapy can prolong fecal
shedding
 Shigella
 Fecal-oral transmission
 Symptoms include fever, abdominal
cramps, tenesmus, and mucoid stools with
or without blood
 Can lead to serious complications
 Antimicrobial treatment shortens duration
of illness and limits fecal shedding
 E. Coli O157:H7
 Transmission via contaminated food and water
 Symptoms include bloody diarrhea, severe
abdominal pain, and sometimes fever
 Can lead to serious complications
 Antibiotics have no proven benefit and may
increase the risk of complications
 Summary of Bacterial Diarrhea
 Can affect all age groups
 Fecal-oral transmission, often through
contaminated food
 Typical symptoms include bloody diarrhea,
severe cramping, and malaise
 Antibiotic treatment not always necessary
 History and Physical Exam
 3 main goals
– Estimate the level of dehydration
– Identify likely causes on the basis of history
and clinical findings
– Determine if additional studies and/or
medications are necessary
 History
 Onset, frequency, quantity, and character of
diarrhea
 Associated symptoms: nausea, vomiting,
fever, abdominal pain, tenesmus, malaise
 Recent oral intake
 Signs and symptoms of dehydration
 Physical Exam
 Vitals, vitals, vitals!
 Abdominal exam
 Presence of occult blood
 Signs of dehydration
 Laboratory Evaluation
 Unnecessary for patients who present within 1
day from onset of diarrhea
 Warning signs/symptoms: bloody diarrhea,
high fever, severe abd pain, dehydration, or
comorbid condition
 Fecal leukocytes followed by bacterial culture,
ova & parasites, viral antigens
 CBC, chemistries
Chronic Diarrhea
 Definition
 >3 weeks duration
 Average fecal daily weight in normal
person is 100-200grams/day
 Approach to Patient
 Patient should be questioned about the
onset, duration, pattern, aggrevants
(especially diet), relieving factors, and stool
characteristics
 Presence or absence of fecal incontinence,
fever, weight loss, pain, certain exposures-
travel, medications, contacts with diarrhea)
should be noted
 Approach to patient

 On physical exam, check for thyroid mass,

wheezing on lung exam, heart murmurs,
edema, hepatomeg, abdominal mass, LAD,
perianal fistula, or anal sphincter laxity.
 Chronic Diarrhea

 If diagnosis is still unclear after initial

encounter, further testing is required
 Further work up should delineate secretory
vs. osmotic diarrhea vs. malabsorption vs
inflammatory
 Malabsorptive diarrhea
 Malabsorption suspected in patients with weight
loss, greasy stools, glossitis, anemia, and
hypoalbumenima
 If malabsorption suspected, a 72 hr stool specimen
should be sent for fecal fat determination, if +
suspect malabsorption
 Causes of malabsorption include pancreatic
insufficiency (confirmed by CT/pancreatic
function tests) and disease of small intestine--
Whipple’s disease, tropical sprue, intestinal
lymphoma (small bowel biopsies by EGD)
 Malabsorptive Diarrhea-Mucosal
Malabsorbtion
 Celiac sprue-hypersensitivity to gluten
 Tropical sprue-infectious disease of
unknown origin, seen in Indian
subcontinent, Asia, West Indies, North &
South America, central and southern Africa,
and Central America
-
 Mucosal Malabsorptive
 Tropical Sprue-tx with tetracycline and
folic acid
 Whipple’s->infection form Treponema-
whippelii.
 Diagnosed by + biopsy for PAS
macrophages
 Associated symptoms include
hypersomnolescence, arthralgias, fever,
hypotension, and LAD
 Intraluminal Malabsorbtion
 Other-Most commonly results from pancreatic
exocrine insufficiency when >90% of pancreatic
secretory function is lost
 Most commonly due to ethanol abuse
 Other causes include cystic fibrosis, pancreatic
duct obstruction
 Also SBO where bacteria deconjugate bile acids,
impairing fat digestion
 SBO one can see low B12, high folate, and
megaloblastic anemia
 Secretory vs Osmotic

 Secretory vs Osmotic –check stool osmotic

gap
 290-2x[NAstool + Kstool]
 If < 50, diarrhea falls under secretory
category
 Secretory Diarrhea

 Characterized by watery, large-volume

fecal outputs that are typically painless and
persist with fasting—one may do a 24 hr
stool quant.-should exceed one liter and not
decrease with fasting
 Usually stool pH is neutral, and fecal fat
test is negative
 Secretory diarrhea

 If secretory diarrhea confirmed, recommend

checking serum should be sent for:
 Gastrin (gastrinoma), VIP(VIPOMA),
glucagon (glucogonoma), serotonin (carcinoid),
calcitonin, histamine, and prostaglandins
 -if overproduction of one of these mediators is
documented,  abdominal CT scan is
recommended
 Secretory Diarrhea
 Carcinod present with watery diarrhea,
flushing, skin changes, bronchospasm, and
cardiac murmurs which are all symptoms
caused by secretion of serotonin, histamine,
catecholamines, kinins, and prostaglandins
by the tumor masses
 1/3 pts with carcinoid present with diarrhea
alone
 Secretory Diarrhea
 Medullary carcinomas of thryoid
(spontaneous or part of MENIIA) cause
secretory diarrhea because of the release of
calcitonin
 Sectretory Diarrhea

 Other conditions to consider include:

 Diseases like Crohn’s ileitis or resection of
<100cm of terminal ileum (dihydroxy bile
acids may escape absorption and stimulate
colonic secretion)
 TABLE 4 - 5. TYPICAL FEATURES OF
SECRETORY DIARRHEA

TABLE 4-5. TYPICAL FEATURES OF SECRETORY DIARRHEA

Voluminous, watery stools

Little or no fecal osmotic gap, stool pH near 7.0

Usually persists during fasting

Usually no pus, blood, or excess fat in stools

TABLE 4-6. MECHANISMS AND CAUSES OF SECRETORY DIARRHEA

Reduction in mucosal surface area

Postresection diarrhea

Short-bowel syndrom e

Extensive mucosal disease and Inflammation

Viral gas troenteritis

Celiac disease

Whipple`s dis ease

Crohn`s disease

Lymphoma

Absence of ion transport mechanism

Congenital chloridorrhea

Bacterial toxins

Cholera

Enterotoxigenic Escherichia coli

Shigella

Staphylococcus

Clostridium perfringens

Luminal secretagogues

Bile acids

Fatty acids, hydroxy-fatty acids

Phenolphthalein, ricinoleic acid, bisacodyl

Circulating secretagogues

Gastrin (Zollinger-Ellison s yndrome)

Vasoactive intestinal polypeptide (VIPom a, ganglioneuroma, neuroblastoma, pheochromocytoma)

Calcitonin, prostaglandins (medullary carcinoma of the thyroid)

Somatos tatin (som atos tatinom a)

Glucagon (glucagonoma)

Serotonin, kinins (carcinoid tumor)

Thyro xine (hyperthyroidism)

Histam ine (mastocytos is)

 Osmotic Diarrhea
 Most common cause is lactase deficiency
 Magnesium ingestion or factitious laxative
abuse
 Intraluminal maldigestion is also seen in
cirrhotics and bile duct obstruction-there is
impaired delivery of bile salts to small
intestine, leads to poor micelle formation
with ingested fats
 CRONIC DIARRHEA -Investigation-

 Blood: ESR; hemoleucograme ( anemia,

inflammation); proteinograme (hyposerinemia)

 Rectosigmoidoscopy, Colonoscopy with/without

biopsy/ UGI endoscopy ( celiac disease )

 Rx: small bowel/barium enema

 Chronic diarrhea: Abdominal X-Ray, US/ CT

TABLE 5-3. DIAGNOSTIC STUDIES FOR FECAL INCONTINENCE

Tests Information Obtained

Sigmoidoscopy Inflammation, strictures, tumors

Anorectal manometry Sphincter pressures

Rectal sensation, compliance

External sphincter responses

Pelvic floor neurophysiology External sphincter electromyography

Puborectalis electromyography

Pudendal nerve conduction

Proctography Rectal capacity

Anorectal angle

Perineal descent

Retention of contrast

Anal ultrasonography Anal sphincter integrity

 CONSTIPATION
1. Definition
2. Pathogenesis
3. Risk factors
4. Diagnosis and differential diagnosis
5. Treatment approaches
1. Definition

The patient’s view:

The following perceptions,
• Need for straining (52%)
•Hard pellet-like stools (44%)
•Inability to defecate when desired (34%)
•Infrequent defecation (33%)

The clinical view: ROME-CRITERIA (at least 2 in any 12week period);

•< 3 bowel movements (BM) per week
•Hard stools in > 25% of BM’s
•Sense of incomplete evacuation in >25% of BM’s
•Excessive straining in >25% of BM’s
•The necessity of digital manipulation
2. Causes
•Extrinsic
•Inadequate dietary fiber, fluid
•Ignoring urge to defecate
•Structural
•Colorectal: neoplasm,stricture,ischemia,volvulus,diverticular disease
•Anorectal: inflammation, prolapse, rectocele,fissure, stricture
•Systemic
•Hypokalemia
•Hypercalcemia
•Hyperparathyroidism
•Hypothyroidism
•Diabetes mellitus
•Addison’s disease
•Pregnancy
•Neurological
•CNS: Parkinson's disease, Multiple sclerosis, trauma, ischemia, tumor
•Sacral nerves: trauma, tumor
•Autonomic neuropathy
•Aganglionosis ( Hirschsprung’s disease )
•Drugs
•Analgesics
•Anticholinergics
•Anticonvulsants
•Antihistamines
•Antihypertensive
•Chemotherapeutic agents
•Diuretics
•Metal ions
•Uncertain Pathophysiology
Irritable bowel syndrome, Slow transit constipation (STC)
3. Risk factors

Risk situations, groups and factors:

•Infants and children

•People older than 55 yrs
•Recent abdominal or perianal/pelvic surgery
•Late pregnancy
•Limited mobility
•Inadequate diet (fluid or fiber)
•Medications especially in the elderly
•Laxative abuse
•Terminal care patients
•Travel
•History of chronic constipation
 4.

4. Diagnosis and differential diagnosis

•History taking
•Physical examination
•Diagnostic techniques
 •History taking
•Check for age of onset ( sudden or long term)
•Check for ROME- II criteria
•Check for neurological disorders
•Check for psychiatric conditions
•Check for family history of constipation?

•Physical examination
•Palpation of abdomen ( tumour )
•Percussion ( check for gases)
•Rectal palpation
•Consistency/impaction
•Presence of non-fecal masses or abnormalities (tumors, hemorrhoid,
fissures)
•Presence of blood
•Sphincter tone
 •Diagnostic techniques
•Stool analysis
•Weighing 3 days; < 100g avg means constipation

•Abdominal x-rays

•Radiological or endoscopic investigation

•Colon tumour, stenosis

•Abdominal echography
• Tumour mass
•Anorectal function tests
•Manometry
•Electromyography
•Rectal mucosal biopsy
•Colonic transit time (radiopaque marker)
Major alarm symptoms especially in patients >50yrs

•New onset constipation

•Anemia
•Weight loss
•Anal blood loss
•Positive occult blood test
•Sudden changes in defecation pattern and
appearance of stool
Barium proctography in a healthy subject (A)
Barium proctography in a healthy subject (B)
Barium proctography in a healthy subject (C)
Barium proctography in a healthy subject (D)
 DEFECOGRAFIA
-
Distal bowel in Hirschsprung`s disease

©Copyright Science Press Internet Services

 1

Main types of inflammatory bowel

disease (IBD)

 Ulcerative colitis
 Crohn’s disease
 2

Specific IBD syndromes

 Proctitis
 Proctosigmoiditis
 Left-sided ileitis
 Ileitis
 Ileocolitis
 24

Geographical distribution of IBD

(reproduced with permission, the AGA Teaching Project, 1992)

 25

Ethnic prevalence of IBD

50

40

30
Prevalence
(per 105)
20

10

0
White Black Hispanic Asian Other

(after Kurata et al, 1992) Ethnic Group

Incidence of IBD with respect to age
26

and sex

(reproduced with permission from Wells Medical Ltd, Binder 1993)

 27

Patterns of IBD incidence in previous

decades

(reproduced with permission from Wells Medical Ltd, Binder 1993)

 Def. chronic idiopathic inflammation of
colon starting from rectum
 Epidemiology:
– 2-10 / 100.000 loc (USA),
– maximum15-25 (secondary 55-65);
– Women more than males;
– Smoking more common;
– Ethnic Jews
 28

Aetiological theories of IBD

 Genetic
 Smoking
 Dietary
 Infection
 Immunological
 Psychological?
 Recent controversies in the
29

pathogenesis of IBD

 Genetics
 Mycobacterium paratuberculosis
 Measles virus
 30

Genetic factors
 It is estimated that between 10 and 20 genes
are involved
 Susceptibility loci have been located on
chromosomes 3, 7, 12 and 16
 The genetic contribution to the aetiology of
both Crohn’s disease and ulcerative colitis
is polygenic NOT Mendelian
 Pathological and anatomical features 23

distinguishing ulcerative colitis from Crohn’s

disease
 Clinical presentation of
12

ulcerative colitis
 Bloody diarrhoea
 Fever
 Cramping abdominal pain
 Weight loss
 Frequency and urgency of defecation
 Tenesmus
 General malaise
 Investigation
 Colonoscopy
 3

Endoscopic features of ulcerative

colitis

(reproduced with permission, Schiller et al, 1986)

Figure 4.1a - Endoscopic features of active
ulcerative colitis

©Copyright Science Press Internet Services

Figure 4.1b - Endoscopic features of active
ulcerative colitis

©Copyright Science Press Internet Services

Figure 4.2 - Ulcerative colitis in remission

©Copyright Science Press Internet Services

Figure 4.3 - Severe ulcerative colitis

©Copyright Science Press Internet Services

Figure 4.4 - Severe ulcerative colitis with
pseudopolyps

©Copyright Science Press Internet Services

 Investigation
 Barium enema
 Lab: ex stools – culture
 Lab: anemia, high sedimentation rate,
 Low Na, K,
 High creatinine, blood ureea, renal failure
 4

Radiological features of acute

ulcerative colitis

(from Wilson et al, 1991)

 5

Radiological features of chronic

ulcerative colitis

(from Wilson et al, 1991)

 6

Anatomical location of ulcerative colitis

 Intestinal complications of
7

ulcerative colitis
 Fibrosis
 Shortening of the colon
 Bleeding
 Stricture
 Bowel perforation
 Toxic megacolon
 Systemic complications of
8

ulcerative colitis
 Arthritis
 Iritis
 Erythema nodosum
 Pyoderma gangrenosum
 Sclerosing cholangitis
 Aphthous stomatitis
 Thromboembolic disorders
 9

Risk of cancer with ulcerative colitis

(reproduced with permission, the AGA Teaching Project, 1992)

 10

Risk of colectomy with pancolitis

Disease duration Risk of colectomy

Year of diagnosis 9%
Following 4 years 3% each year
Following years 1% per year
 Relapse of ulcerative colitis
11

during pregnancy
15

Relapse in
pregnant 10
women with
UC, who were
remission at
5
conception
(%)

0
1st 2nd 3rd Post-partum

(after Willoughby & Truelove, 1980)Trimester

 31

M. Paratuberculosis and Crohn’s

disease
Mycobacterium paratuberculosis has been
thought to have an aetiological role in
Crohn’s disease as:
 it causes a similar disease in the small
intestine in cattle (Johne’s disease)
 it can be found in milk
 it can be found in Crohn’s disease tissue,
although it is also found in other tissues
 32

Measles virus and IBD

Measles virus has been associated with Crohn’s
disease due to:
 good epidemiological links between
perinatal measles infection and subsequent
Crohn’s disease
 a possible increase in the incidence of
Crohn’s disease in children of mothers who
had measles during pregnancy
 tissue studies suggest a higher than expected
proportion of patients with Crohn’s disease

(Forbes, 1997)
Clinical presentation of Crohn’s
21

disease
 Diarrhoea
 Abdominal pain
 Bleeding
 Pyrexia
 Weight loss
 Fistulae
 Perianal disease
 General malaise
 Investigation
 Colonoscopy
 13

Endoscopic appearance of Crohn’s

disease

(reproduced with permission, Schiller et al, 1986)

Figure 4.15 - Severe Crohn`s colitis

©Copyright Science Press Internet Services

Figure 4.19 - Cutaneous opening of a perirectal
fistula

©Copyright Science Press Internet Services

Figure 4.20 - Typical perianal changes of Crohn`s
disease

©Copyright Science Press Internet Services

CROHN’S DISEASE
-Radiology-
 14

Radiological features of Crohn’s

disease

(reproduced with permission (courtesy of Dr Sten Norby

from McGraw-Hill) Rasmussen, Denmark)
 15

Anatomical location of Crohn’s disease

Intestinal complications of
16

Crohn’s disease

 Fistulae
 Abscesses
 Adhesions
 Strictures
 Obstruction
 17

Perianal complications of Crohn’s

disease
 18

Risk of cancer with Crohn’s disease

and ulcerative colitis

(adapted from Hamilton, 1985, with permission)

Systemic complications of
19

Crohn’s disease

 Arthritis
 Gallstones
 Malabsorption
– Lactase deficiency
– Vitamin B12 deficiency
 Renal stone formation
 22

Differences in clinical presentation between

ulcerative colitis and Crohn’s disease
Ulcerative colitis Crohn’s disease
Symptoms
Pain * ***
General malaise *** **
Fever * *
Diarrhoea *** *
Stools
Blood *** *
Mucus * **
Pus * **
The number of * symbols indicates the frequency with which each
symptom is present
 Pathological and anatomical features 23

distinguishing ulcerative colitis from Crohn’s

disease
Ulcerative colitis Crohn’s disease
Localisation Distal Segmental, proximal
Rectum affected Always 50% of cases
Intestinal wall Normal thickness Thickened
Adhesions Rare Common
Inflammation Superficial layers All layers
Ulcerations Superficial Deep
Mucous membrane Denuded Cobblestones
Granulomas 0–4% 50–70%
Lymphocytic infiltration Rare Always
Fistulae Rare Common
Intestinal Semiology

“As you could kill time

without injuring eternity”
Henry David Thoreau
 Colorectal cancer
 Def: Acquired genetic disease, due to prolonged
exposure to carcinogens
 Epidemiology
– The 4th malignant localization after lungs, stomach, sin.
– 10% of total deaths by cancer in developed countries
– Increase cases of morbidity and mortality, affecting
1:20 persons with a growth of economic standards.
– sex: more frequent in men than women
– race: white > black, asian
– Geographical variability: increase > 30/100.000 in
North America, West Europe, Australia, New Zeeland;
decrease in less developed countries. In Romania - 15-
20/100.000
– Age: exponential rise over 50 years of age
– Increased risk factors: high caloric report, sedentarism,
beer consumption,(smoking = adenomes)
 Colorectal cancer-Etiopathogenesis
 Genetic Factors
– Hereditary genetic anomalies (hereditary CCR - 25% of total
CCR); sporadic CCR, non-hereditary (75%).
– Hereditary genetic anomalies confirm an increased susceptibility
for cancer.
– Sporadic form: multi-stage process of carcinogenization with
accumulation of genetic anomalies under the action of
environemental factors,hereditary playing a minor role.
– 2 major forms of hereditary CCR: a) polyposis cancer ,syndroms
of familial adenomatosis polyposis- 1% cancer; b) HNPCC:
hereditary non-polyposis colorectal cancer - 5% din CCR
Molecular genetic events in evolution of colon cancer
Genetic alterations in progression to colorectal cancer
Genes altered in colon cancer

TABLE 3 - 10. GENES ALTERED IN COLON CANCER

Sporadic tumors with
Gene Chromosome Class Function
alterations, %
K - ras 12 50 Protooncogene Signal transduction
APC 5 60 Tumor supressor ?Cell adhesion
DCC 18 70 Tumor supressor ?Cell adhesion
p53 17 75 Tumor supressor Cell cycle control (G1/S arrest)
DNA Mismatch Maintains fidelity of DN A
hMSH2 2 repair replication
DNA Mismatch Maintains fidelity of DN A
hMLH1 3
repair replication
 Colorectal Cancer - symptomatology-
 age >50 years, more frequent in men than in females.
 Personal history: RCUH (post-colecystectomy)
 Family history- familial polyposis syndrome and Lynch

 ASYMPTOMATIC-(the rate of doubling of the tumors of 2 years)

 Abdominal coilcative pain -subocclusive/occlusive syndrom
 Change in bowel habits: constipation/false diarrhea
 Inferior digestive tract hemorrhage (rectorhagia)
 SG: weight loss/ important asthenia (anemia), loss of appetite
 S. given by distant causes: hepatic metastasis- jaundice; increase in
abdominal volumn – carcinomatous ascites
 Colorectal Cancer – objective
examination-
 normal
 palpation: Tumoral formation (more often if of suboclusive
phenomenon)
 SG: cashexia/ iron deficiency anemia picture: palor/ asthenie
headache/tachycardia, anginal pain/ platonychia
 Hepatomegaly MTS hepatic/ increase in abdominal volume because of
carcinomatous ascites
 RECTAL TOUCH IS A PART OF GENERAL CLINICAL
EXAMINATION.
Mucocutaneous pigmentation in Peutz-Jeghers syndrome

©Copyright Science Press Internet Services

Colorectal Cancer –Paraclinical exploration
 Digestive endoscopy: anuloscopy, flexibil
rectosigmoidoscopy , colonoscopy
– Essential exam for diagnosis of intestinal
disease, completed with a histological exam
and therapy.
Flexible sigmoidoscopic view of the distal rectum

©Copyright Science Press Internet Services

 Colorectal Cancer –paraclinical
exploration
 Radiological examination of the colon is realized with
BaSo4 through barium enema done with simple or double
contrast method.
 Some Rx on empty bowel may show obstacle.
 Colorectal Cancer –paraclinical
exploration
 Barium enema
Colonic Polyposis
Barium enema with double contrast
Computerized Tomographic examination (ECHO) for
evaluation of local extension and MTS
Computerized Tomographic examination(ECHO) For
evaluation of local extension and MTS
 Colorectal Cancer
EPIDEMIOLOGY
Incidence in the world

– Fourth malignant
localization after lungs,
stomach and breasts.
– 1023 000 new annual
cases and 529.000
deaths
– 10% of total deaths due
to cancer in developing
countries.
 Europe in 2000
highest increased
incidents 300.000
new cases
 Czech Republic,
Hungary, Slovakia,
Germany have
incidents much
higher ( 2x than
USA in general)
 Net increase in the tendency of colorectal cancer (all statistic
reports).
 Increase in colorectal cancer incidents with proximal localization

1000000

500000

0
1975 1990 1996 2003
 with 4016 deaths in 2002 (OMS report) Romania registered a
mortality rate of 11,3/100 000.
 For both localizations levels of mortality presented an intentional
increase of constancy and continuity, with a higher increased rate for
colon cancer.
 In the last 40 years mortality doubled, an important increase in
comparison with other European countries.

12

10

6
Mortalitate
4

0
1969 1975 1996 2002
 Territorial distribution of mortality levels (standardized indicators) for
colon and rectal cancer.

 Incidents higher in western part of the cities and in Bucharest.

 The study which took place between 1994-1996 using data acquired
from city hospitals from Moldova revealed a higher level of mortality
for colon cancer for cities Neamţ ,Galaţi, Botoşani.
IRITABLE BOWEL SYNDROME
Functional
gastrointestinal
disorders - a
frequent cause for
referral to
gastroenterologist
 Epidemiology

-Prevalence: 10%-20% (5 and 65%);

-more frequent in women; (2:1);
-all age affected.
-20 - 30% presented to doctor
-1%-3% - GP consultation
SYMPTOMS BASED DEFINITION -which
definition?-
DEFINITION -which definition?-
 DEFINITION -LIMITS-
 Symptoms based definition due to the
absence of a specific biologic “marker”.
 Overlap between the definition of irritable
bowel syndrome and other functional
disorders.
 The present definition are not able to
differentiate between the subgroups of
IBS patients.
 The present definition criteria seem to
have a different gender sensibility.
 ROME II DEFINTION
 At least 12 weeks or more, which need not to be consecutive, in
the proceeding 12 months of abdominal discomfort or pain that
has two out of three features:
– 1. Relieved with defecation; and/or
– 2. Onset associated with a change in frequency of stool; and/or
– 3. Onset associated with a change in form (appearance) of stool.

 Symptoms that cumulatively Support the Diagnosis of Irritable

Bowel Syndrome:
– Abnormal stool frequency (> 3 bowel movements/day and less than 3
bowel movements per week);
– Abnormal stool form (lumpy/hard or loose/watery stool);
– Abnormal stool passage (straining, urgency, or feeling of incomplete
evacuation);
– Passage of mucus;
– Bloating or feeling of abdominal distension
 DEFINITION

Functional intestinal disorder in which

abdominal discomfort or pain is
associated with defecation or a change
in bowel habit and with features of
disordered defecation.
 PATHOPHYSIOLOGY
-MECANISMS-

 Digestive motility disorders;

 Visceral hypersensibility;
 Involvement of intestinal infection;
 Alimentary intolerance and allergy;
 Alteration of perception due to
psychiatric disorders.
PATHOGENIC MECANISMS
- Intestinal hypersensibility -
 COMORBIDITY

 About 50% of IBS patients from primary care and gastroenterology

clinics have at least one comorbid somatic symptom.
 Comorbidity substantially alters the quality of life of IBS patients and
adds an additional cost for its treatment.
 The presence of commorbidity was suggested to be a new diagnostic
criterion.
 Specific comorbide somatic condition are Fibromyalgia, Chronic
fatigue syndrome, Chronic pelvic pain, Temporo-mandibular joint
disorder.
 Overlap with other functional gastrointestinal disorders: functional
dyspepsia, non-cardiac chest pain, functional anorectal pain, fecal
incontinence.
 COMORBIDITY
 Overlap with psychiatric disorders such as: depressive syndromes,
anxiety disorder, somatisation.
 Figure 5.33 - Visceral sensations

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 Anorectal manometry
 Anorectal manometry catheter
 Distal balloon 320 ml
 Diagnosis
 Alarm symptoms
– onset in elderly;
– increasing intensity;
– waking up the patient;
– fever;
– Weight loss;
– rectoragia;

 Exclusion of other disease

 INVESTIGATIONS

– Sedimentation rate, hemoleucogram

– Proctoscopy <45 ani)
– Abdominal Ultrasound

 Additional investigations
– Colonoscopy or double contrast barium enema (>45 ani)
– coproculture
– Occult blood loss
 Colon spastic

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N-benzoyl-L-tyrosyl-para-aminobenzoic acid

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MALABSORPTION
 Points to be discussed.
– Introduction
– Clinical
– Differentials
– Workup
– Treatment
Introduction:
Clinical term that encompasses defects occurring during the
digestion and absorption of food nutrients by the gastrointestinal
tract.

• The digestion or absorption of a single nutrient component

may be impaired, as in lactose intolerance in lactase
deficiency.

• When a diffuse disorder such as celiac disease affects the

intestine, the absorption of almost all elements is impaired.
Pathophysiology:
3 major phases of digestion and absorption of food
materials.
 Luminal phase: dietary fats, proteins, and carbohydrates
are hydrolyzed and solubilized by secreted digestive
enzymes and bile.

 Mucosal phase: relies on the integrity of the brush-border

membrane of intestinal epithelial cells to transport digested
products from the lumen into the cells.

 Post absorptive phase: reassembled lipids and other key

nutrients are transported via lymphatic and portal
circulation from epithelial cells to other parts of the body.
Pathophysiology of bacterial overgrowth

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Pathophysiology of lactase deficiency

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Clinical: symptomatology

 Diarrhea
– Diarrhea is the most common symptomatic complaint.
– Diarrhea frequently is watery, reflecting the osmotic load received
by the intestine.
– Bacterial action producing hydroxy fatty acids from undigested fat
also can increase net fluid secretion from the intestine, further
worsening the diarrhea.
 Steatorrhea
– Steatorrhea is the result of fat malabsorption.
– The hallmark of steatorrhea is the passage of pale, bulky, and
malodorous stools.
– Such stools often float on top of the toilet water and are difficult to
flush. Also, patients find floating oil droplets in the toilet
following defecation.
 Weight loss and fatigue
– Weight loss is common and may be pronounced; however, patients
may compensate by increasing their caloric consumption, masking
weight loss from malabsorption.
– The chance of weight loss increases in diffuse diseases involving
the intestine, such as celiac disease and Whipple disease.
 Flatulence and abdominal distension
– Bacterial fermentation of unabsorbed food substances releases
gaseous products, such as hydrogen and methane, causing
flatulence.
– Flatulence often causes uncomfortable abdominal distention and
cramps.
 Edema
– Hypoalbuminemia from chronic protein malabsorption or from
loss of protein into the intestinal lumen causes peripheral edema.
– Extensive obstruction of the lymphatic system, as seen in intestinal
lymphangiectasia, can cause protein loss.
– With severe protein depletion, ascites may develop.
 Anemia
– Depending on the cause, anemia resulting from malabsorption can
be either microcytic (iron deficiency) or macrocytic (vitamin B-12
deficiency).
– Iron deficiency anemia often is a manifestation of celiac disease.
– Ileal involvement in Crohn disease or ileal resection can cause
megaloblastic anemia due to vitamin B-12 deficiency.
 Bleeding disorders
– Bleeding usually is a consequence of vitamin K malabsorption and
subsequent hypoprothrombinemia.
– Ecchymosis usually is the manifesting symptom, although
occasionally, melena and hematuria occur.
 Metabolic defects of bones
– Vitamin D deficiency can cause bone disorders such as osteopenia
or osteomalacia.
– Bone pain and pathological fractures may be observed.
– Malabsorption of calcium can lead to secondary
hyperparathyroidism.
 Neurological manifestations
– Electrolyte disturbances such as hypocalcemia and
hypomagnesemia can lead to tetany, manifesting as the Trousseau
sign and the Chvostek sign.
– Vitamin malabsorption can cause generalized motor weakness
(pantothenic acid, vitamin D) or peripheral neuropathy (thiamine),
a sense of loss for vibration and position (cobalamin), night
blindness (vitamin A), and seizures (biotin).
 Physical findings:
 General
– Patients may have orthostatic hypotension.
– Fatigue
– Signs of weight loss, muscle wasting, or both may be present.
– Patients may have signs of loss of subcutaneous fat.
 Abdominal examination
– The abdomen may be distended, and bowel sounds may be
hyperactive.
– Ascites may be present in severe hypoproteinemia.
 Dermatological manifestations
– Pale skin may reveal anemia.
– Ecchymosis due to vitamin K deficiency may be
present.
– Dermatitis herpetiformis, erythema nodosum, and
pyoderma gangrenosum may be present.
– Pellagra, alopecia, or seborrheic dermatitis
 Neurological examination
– Motor weakness, peripheral neuropathy, or ataxia may
be present.
– The Chvostek or Trousseau sign may be evident due to
hypocalcemia or hypomagnesemia.
 Cheilosis, glossitis, or aphthous ulcers of the
mouth
 Peripheral edema
TABLE 5-33. SELECTED SYMPTOMS AND SIGNS OF NUTRIENT DEFICIENCIES
Symptoms or sign
Weakness, weight loss, muscle
wasting
Pallor
Follicular hyperkeratosis
Perifollicular petechiae
Dermatitis
Bruising, purpura
Easily plucked, alopecia
Corkscrew hairs, coiled hair
Possible nutrient deficiency
Protein, calorie
Folate, iron, vitamin B12
Vitamin A, vitamin C
Vitamin C
Protein, calorie, niacin, riboflavin, zinc,
vitamin A, essential fatty acids
Vitamin C, vitamin K
Protein, zinc, biotin

Night blindness, keratomalacia,

Vitamin C, vitamin A
photophobia
Conjunctival inflammation Vitamin A
Glossitis Vitamin A, riboflavin
Bleeding or receding gums, mouth Riboflavin, niacin, folate, vitamin B12,
ulcers protein
Decreased taste Vitamin A, vitamin C, vitamin K, folate
Burning or sore mouth and tongue Zinc, vitamin A
Vitamin B12, vitamin C, niacin, folate,
Angular stomatitis or cheilosis
iron
Tetany Riboflavin, niacin, pyridoxine, iron
Paresthesias Calcium, magnesium
Loss of reflexes, wrist drop, foot drop,
Thiamine, pyridoxine
loss of vibratory and position sense
Vitamin B12, vitamin E
Dementia, disorientation Niacin, vitamin B12
Ophthalmoplegia Vitamin E, thiamine
Depression Biotin, folate, vitamin B12
TABLE 5-1. CLASSIFICATION OF DISEASES THAT CAUSE
INTESTINAL MALABSORPTION
Premucosal Mucosal Postmucosal
Pancreatic Congenital
Celiac sprue
insufficiency lymphangiectasia
Hepatobiliary Secondary
Tropical sprue
disease lymphangiectasia
Bacterial
Whipple`s disease
overgrowth
Rapid intestinal
Eosinophilic enteritis
transit
Brush border enzyme
Gastrectomy
deficiency
Lymphoma
Short-bowel syndrome
Prolonged malnutrition
Radiation enteritis
Parasitic infection
Mesenteric ischemia
Massive small-bowel resection can cause
significant malabsorption
TABLE 5-16. PREDI CT ED NUT RITIO NAL OUT COM E IN P ATIENTS W HO HAV E HAD MASSIV E
INTESTI NAL RES ECTIO N

Remaining Jejunal length, cm Colon Nutritional outcome

0-50 - TPN

+ TPN

51-100 - IVFM/TPN

+ Modified oral diet

101-150 - Regular or modified oral diet

+ Regular diet

151-200 - Modified oral diet

+ Regular diet

>200 - or + Regular diet

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Differentials:
 Zollinger-Ellison Syndrome

Other Problems to be Considered:

– Amino acid deficiencies (cystinuria)
– Cystic fibrosis
– Hartnup disease
– Tropical jejunitis
– Whipple disease
 Workup :
TABLE 5-32. INITIAL EVALUATION OF PATIENT WITH POSSIBLE
MALABSORPTION
History and Physical Examination
Initial blood tests
Complete blood count
Prothrombin time
Standard electrolytes
Calcium
Magnesium
Blood urea nitrogen
Creatinine
Alkaline phosphatase
Cholesterol
Total protein and albumin
Follow-up laboratory tests
Serum iron
Serum folate
Serum vitamin B12
Serum vitamin A
Plasma 25-hydroxy vitamin D
Urinary oxalate excretion
Stool for Sudan stain
Stool for ova and parasites
 Imaging studies:
– Small bowel barium studies.
– CT-scan of the abdomen.
– Endoscopic retrograde cholangiopancreatogram
– Plain abdominal x-ray film.
 Other studies:
– Tests of fat malabsorption.
– D-xylose test.
– Test of carbohydrate absorption.
– Test of bile salt absorption.
– Schilling test.
 Procedures:
– Upper endoscopy with small bowel mucosal biopsy
» Establishing a definitive diagnosis of malabsorption of the
mucosal phase often can be achieved by histological
examination of biopsied mucosal specimens obtained during
routine upper endoscopy.
» Examples of conditions that can be diagnosed this way include
celiac sprue, giardiasis, Crohn disease, Whipple disease,
amyloidosis, abetalipoproteinemia, and lymphoma.

 Histologic Findings: Depending on the cause, the

histologic features of malabsorption vary.
– A frequently encountered histologic finding is villous
atrophy, which is seen in celiac disease, tropical
sprue, viral gastroenteritis, bacterial overgrowth,
inflammatory bowel disease, immunodeficiency
syndromes, lymphoma, and radiation enteritis.