INTESTINAL DISORDERS

Enjel A. Gabriel, M.D, FPCP, FPSG, FPSDE

COURSE SYLLABUS

Learning Objectives Instructional Design Learning Outcomes Assessment

1. To review the anatomy, Didactic lectures Knowledge of intestinal Long/short

histology, and physiology Case discussions diseases quizzes
of the SI and LI
Competence in Oral case
2. To known the common formulating presentation
intestinal disorders a diagnosis and differential
diagnosis
3. To know the clinical
manifestations of Competence in
intestinal disorders interpreting
laboratory and diagnostic
4. To know the different tests
diagnostic tests for
intestinal disorders Competence in decision-
making on appropriate
5. To know the differential diagnostic and
diagnosis of intestinal therapeutic
disorders management

6. To know the management

of intestinal disorders

Reference: Harrison”s Principles of Internal Medcine 20th ed

SHORT BOWEL SYNDROME
EPIDEMIOLOGY OF IBD
Ulcerative Colitis Crohn’s Disease

Incidence (North America) per person-

0–19.2 per 100,000 0–20.2 per 100,000
years

Second to fourth decades and seventh to Second to fourth decades and seventh to
Age of onset
ninth decades ninth decades

Ethnicity Jewish > non-Jewish white > African American > Hispanic > Asian

Female/male ratio 0.51–1.58 0.34–1.65

Smoking May prevent disease (odds ratio 0.58) May cause disease (odds ratio 1.76)

Oral contraceptives No increased risk Odds ratio 1.4

Appendectomy Protective (risk reduction of 13–26%) Not protective

Monozygotic twins 6–18% concordance 38–58% concordance

Dizygotic twins 0–2% concordance 4% concordance

Antibiotic use in the first year of life 2.9× the risk of developing childhood IBD
PRIMARY GENETIC DISORDERS ASSOCIATED WITH IBD

Name Genetic Association IBD Phenotype

Turner’s syndrome Loss of part or all of X chromosome Associated with UC and colonic CD

Granulomatous colitis, oculocutaneous

Hermansky-Pudlak Autosomal recessive chromosome 10q23 albinism, platelet dysfunction, pulmonary
fibrosis

X-linked recessive disorder, loss of WAS Colitis, immunodeficiency, severely

Wiskott-Aldrich syndrome (WAS)
protein function dysfunctional platelets, and thrombocytopenia

Granulomatous colitis, presents in infancy

Deficiency of the glucose-6-phosphate
Glycogen storage disease with hypoglycemia, growth failure,
transport protein type B1
hepatomegaly, and neutropenia

UC-like autoimmune enteropathy, with

Immune dysregulation polyendocrinopathy, Loss of FoxP3 transcription factor and T
endocrinopathy (neonatal type 1 diabetes or
enteropathy X-linked (IPEX) regulatory cell function
thyroiditis), dermatitis

Early-onset IBD Deficient IL-10 and IL-10 receptor function Severe, refractory IBD in early life
Different Clinical, Endoscopic, and Radiographic Features
Ulcerative Colitis Crohn’s Disease

Clinical
Gross blood in stool Yes Occasionally
Mucus Yes Occasionally
Systemic symptoms Occasionally Frequently
Pain Occasionally Frequently
Abdominal mass Rarely Yes
Significant perineal disease No Frequently
Fistulas No Yes
Small intestinal obstruction No Frequently
Colonic obstruction Rarely Frequently
Response to antibiotics No Yes
Recurrence after surgery No Yes
Endoscopic
Rectal sparing Rarely Frequently
Continuous disease Yes Occasionally
“Cobblestoning” No Yes
Granuloma on biopsy No Occasionally
Radiographic
Small bowel significantly abnormal No Yes
Abnormal terminal ileum No Yes
Segmental colitis No Yes
Asymmetric colitis No Yes
Stricture Occasionally Frequently
 Crohn’s Disease

Etiology Clinical Manifestations Diagnosis Treatment

★ Sulfasalazine
★ Infectious Agents
★ Right lower quadrant pain ★ Barium contrast studies ★ Mesalamine
★ Diet ★ Endoscopy ★ Corticosteroids
★ Diarrhea
★ Genetics ★ Mucosal biopsy
★ Fever ★ Immunosuppressive agents
★ Immune System ★ Cross-sectional imaging
★ Weight loss Azathioprine
CT scan, MRI
★ Psychosocial factors
★ GI bleeding ★ Ultrasonography 6-Mercaptopurine

★ Perianal fissures/fistulas/ ★ Biochemical tests ★ Antibiotics

CRP, ESR, orosomucoid
abscesses
fecal A1-antitrypsin
chromium 51-labeled serum proteins
indium-111-labeled leukocytes
Crohn’s Disease
Extraintestinal Manifestations
Colitis-related SI pathology Miscellaneous
(malabsorption)
Skin amyloidosis
erythema nodosum Gallstones Thromboembolic
Cutaneous vasculitis Kidney stones (oxalate) complications
metastatic lesions Bacterial overgrowth Hepatobiliary disease
Oral Choleretic diarrhea primary sclerosing
apthuous stomatitis Steatorrhea cholangitis
Ocular Folate deficiency
Joints
Musculoskeletal
clubbing
osteomyelitis
osteomalacia
 Ulcerative Colitis
Epidemiology Etiology Clinical Diagnosis Treatment
Presentation Medical
★ Stool exam
★ Distribution: worldwide ★ Infection § Corticosteroids
★ Diarrhea ★ Sigmoidoscopy § Salicylates
high incidence - UK, ★ Food allergy
★ Colonoscopy § Immunosuppressive agents
US, Northern Europe, ★ Rectal bleeding
★ Environmental § Antibbiotics
Australia ★ Barium contrast
factors ★ Abdominal pain
★ Age and sex: examination Surgical
smoking - ★ Passage of mucus
young adults 20 – 40 ★ severe attacks failing to
★ Biopsy
yrs protective respond to medical therapy
women > men oral ★ complications of a severe
★ Ethnicity: attack
contraceptive e.g. perforation,
Jews (Ashkenazi >
agents acute dilatation
Sephardic)
(toxic megacolon)
★ Socioeconomic factors: ★ chronic continuous disease
slightly higher with impaired quality of life
incidence in ★ dysplasia or carcinoma
higher-salaried, better
educated population
Ulcerative Colitis
Extraintestinal Manifestations
Related to activity of colitis
Peripheral arthropathy
Erythema nodosum
Episcleritis
Apthuous ulceration of
the mouth
Fatty liver
Usually related to activity
of colitis
Pyoderma gangrenosum
Anterior uveitis
Unrelated to colitis
Sacroileitis
Ankylosing spondylitis
Primary sclerosing cholangitis
Rare
Pericarditis
Acute febrile neutrophilic
dermatosis (Sweet’s syndrome)
Amyloid
ORAL 5-ASA Preparations

Preparation Formulation Delivery Dosing Per Day

Azo-Bond

Sulfasalazine (500 mg)

Sulfapyridine-5-ASA Colon 3–6 g (acute)
(Azulfidine)

2–4 g (maintenance)

Olsalazine (250 mg)

5-ASA–5-ASA Colon 1–3 g
(Dipentum)

Balsalazide (750 mg) (Colazal) Aminobenzoyl-alanine–5-ASA Colon 6.75–9 g

Delayed-Release

Mesalamine (400, 800 mg)

Eudragit S (pH 7) Distal ileum-colon 2.4–4.8 g (acute)
(Delzicol, Asacol HD)

1.6–4.8 g (maintenance)

Mesalamine (1.2 g) (Lialda) MMX mesalamine (SPD476) Ileum-colon 2.4–4.8 g

Controlled-Release

Mesalamine (250, 500, 1000

Ethylcellulose microgranules Stomach-colon 2–4 g (acute)
mg) (Pentasa)

1.5–4 g (maintenance)

Delayed- and Extended-Release

Intellicor extended-release
Mesalamine (0.375 g) (Apriso) Ileum-colon 1.5 g (maintenance)
mechanism
IRRITABLE BOWEL SYNDROME

• Irritable bowel syndrome (IBS) is

a functional bowel disorder
characterized by abdominal pain
or discomfort and altered bowel
habits in the absence of
detectable structural
abnormalities.

• No clear diagnostic markers exist

for IBS; thus the diagnosis of the
disorder is based on clinical
presentation.
Differential Diagnosis
Diarrhea-predominant symptoms
• Crohn’s disease
• Ulcerative colitis
• Microscopic colitis
• Infectious
• Clostridium difficile infection
• Small bowel bacterial
overgrowth
• Celiac disease
• Lactose intolerance
• Hyperthyroidism
• Neuroendocrine tumor
Constipation-predominant symptoms
• Strictures (cancer, inflammatory bowel,
diverticulitis, ischemia)
• Colonic inertia
• Pelvic floor dysfunction
• Neurologic disease
• Medication
• Hypothyroidism
Pain-predominant symptoms
• Aerophagia, bloating
• Intermittent small bowel obstruction
• Acute intermittent porphyria
• Ischemia
• Chronic pancreatitis
• Lymphoma of GI tract
• Endometriosis
Diagnostic tests

Ø Laboratory tests
q CBC, complete metabolic panel, C-reactive protein
q Thyroid profile if suspicion for thyroid disease is high
q Test for celiac disease in non-constipated patients with IBS

Ø Stool sample evaluation

q Check for occult blood
q Exclude C. difficile infection in IBS-D + recent antibiotics

q Check for ova and parasites based on travel history

q Fecal calprotectin measurement to identify inflammation

Ø Colonoscopy, Radiologic/Imaging tests

q case-by-case basis
Probiotics Prebiotics

live microorganisms that when nondigestible food ingredients

administered in adequate that stimulate growth and/or

amounts confer a health benefit activity of bacteria in the GI tract.

on the host

Antibiotic treatment
A low FODMAP diet reduces
benefits a subset of IBS
IBS symptoms.
patients
• Neomycin 500 mg BID
for 10 days
• Rifaximin,nonabsorbed
oral antibiotic

Because altered colonic flora (gut dysbiosis) may contribute to the pathogenesis of IBS,
this has led to great interest in using antibiotics, prebiotics, and probiotics to treat IBS.
• A diet rich in FODMAP (fermentable oligo-
saccharides, disaccharides,
monosaccharides, and polyols) often triggers
symptoms in IBS patients.

• FODMAPs are poorly absorbed by the small

intestine and fermented by bacteria in the
colon to produce gas and osmotically active
carbohydrates .

• At the same time, on entering the colon,

FODMAPs may serve as nutrient for the
colonic bacteria and promote the growth of
gram negative commensal bacteria which
may induce epithelial damage and subclinical
mucosa inflammation.

• Fructose and fructans induce IBS symptoms

in a dose-dependent manner. In contrast, a
low FODMAP diet reduces IBS symptoms.

• Low FOMAP diets appeared to be superior to

national guidelines for IBS management
COLONIC DIVERTICULOSES
Incidence and Epidemiology
• In the United States, diverticulosis affects 60% of
the population aged >60 and up to 30% of individuals
with diverticular disease will experience recurrent
symptoms.
• Diverticular disease has become the fifth most costly
gastrointestinal disorder in the United States and is
the leading indication for elective colon resection.
• The incidence of diverticular dis- ease is on the rise.
Fortunately, only 20% of patients with diverticulosis
develop diverticular disease and 4% require
hospitalization.

Two types of diverticula occur in the intestine

a. true and false (or pseudo diverticula).
a True diverticiula
saclike herniation of the entire bowel wall
b.Pseudo diverticulum
involves only a protrusion of the mucosa and
submucosa through the muscularis propria of the
colon

The type of diverticulum most commonly affecting the

colon is the pseudo diverticulum.

Diverticula commonly affect the left and sigmoid colon;

the rectum is always spared.

Iin Asian populations, 70% of diverticula are seen in the

right colon and cecum as well.
RECTAL PROLAPSE

Anatomy and Pathophysiology

• Rectal prolapse (procidentia) is a circumferential,
full-thickness protrusion of the rectal wall through
the anal orifice.
• It is often associated with a redundant sigmoid
colon, pelvic laxity, and a deep rectovaginal septum
(pouch of Douglas).

Incidence and Epidemiology

• Rectal prolapse is six times more common in
women than in men.
• The incidence of rectal prolapse peaks in
women >60 years.
• Women with rectal prolapse have a higher
incidence of associated pelvic floor disorders
including urinary inconti- nence, rectocele,
cystocele, and enterocele.
• About 20% of children with rectal prolapse will
have cystic fibrosis.
• All children presenting with prolapse should
undergo a sweat chloride test.
• Less common associa- tions include Ehlers-
Danlos syndrome, solitary rectal ulcer
syndrome, congenital hypothyroidism,
Hirschsprung’s disease, dementia, mental
retardation, and schizophrenia.
RECTAL PROLAPSE

Management:

Medical
• Stool bulking agents
• Fiber supplements

Surgical
• Mainstay of management
• Two approaches:
Transabdominal
approach
• have been
associated
with lower
recurrence
rates

Transperineal approach
• for patients with
significant
• comorbidities
FECAL INCONTINENCE
• Fecal incontinence is the involuntary
passage of fecal material for at least 1 month
in an individual with a developmental age of
at least 4 years.
• Prevalence (US): 0.5–11%.
• Epidemiology:
• majority of patients are women >65.
• higher incidence of incontinence among
parous women
• ½ of patients also suffer from urinary
incontinence.
• Etiology:
• majority of incontinence is a result of
obstetric injury to the pelvic floor, either while
carrying a fetus or during the delivery.
• An anatomic sphincter defect may occur in
up to 32% of women following childbirth
regardless of visible damage to the
perineum.
• Risk factors at the time of delivery :
• prolonged labor, the use of forceps, and the
need for an episiotomy.
• Symptoms: can present after two or more
decades following obstetric injury.
Diagnosis:
Management:
History and physical examination + DRE
Medical management
Neurogenic dysfunction
• strategies to bulk up the stool, which help in increasing
• Weak sphincter tone on DRE and
fecal sensation.
• loss of the “anal wink” reflex (S1-level
• fiber supplementation, loperamide, diphenoxylate, and
control)
bileacid binders.
Perianal scars may represent surgical injury.
• these agents harden the stool and delay frequency
of bowel movements and are helpful in patients with
Other studies
minimal to mild symptoms.
• anal manometry,
Biofeedback
• pudendal nerve terminal motor latency
a form of physical therapy
(PNTML)
• helps strengthen the external sphincter muscle while
• endoanal ultrasound.
training the patient to relax with defecation to avoid
unnecessary straining and further injury to the
sphincter muscles
Surgical Management
Overlapping sphincteroplasty
• Historically, the “gold standard” for the treatment of
fecal incon- tinence with an isolated sphincter defect
• Poor long term results with a 50% failure rate over 5
years.
Alternative therapies:
• Sacral Nerve Stimulation (SNS)
• Collagen-enhancing injectables
• Magnetic “Fenix” ring
ANORECTAL DISEASES
Anatomy and Pathophysiology

• Hemorrhoidal cushions are a normal part of the

anal canal.
• Three main hemorrhoidal complexes traverse the
anal canal— the left lateral, the right anterior, and
the right posterior.
• Engorgement and straining lead to prolapse of
this tissue into the anal canal.
• Over time, the anatomic support system of the
hemorrhoidal complex weakens, exposing this
tissue to the outside of the anal canal where it is
susceptible to injury.

Classification
• External hemorrhoids:
• originate below the dentate line
• covered with squamous epithelium
• associated with an internal component
• painful when thrombosed
• Internal hemorrhoids
• originate above the dentate line
• covered with mucosa and transitional
zone epithelium
• represent the majority of hemorrhoids.
ANORECTAL ABSCESSES

Anatomy and Pathophysiology

an abnormal fluid-containing cavity in the anorectal region.

results from an infection involving the glands surrounding the anal
canal.
Anorectal abscesses ;
perianal in 40–50% of patients, ischiorectal in 20–25%,
intersphincteric in 2–5%, supralevator in 2.5%

Presentation and Evaluation

Hx: Perianal pain and fever are the hallmarks of an abscess.

difficulty voiding and have blood in the stool.
PE:a large fluctuant area is usually readily visible.
Routineaboratory evaluation
elevated white blood cell count.
Diagnostic procedures
CT scan or MRI has an accuracy of 80% in determining
incomplete
drainage
Rigid or flexible sigmoidoscopic examination may be done
at the time of
drainage to evaluate for inflammation within the
rectosigmoid region Colonoscopy
Small-bowel series

Management:
1. Incision and drainage
2. Antibiotics
ANAL FISTULAS
 ANAL FISSURES
Incidence and Epidemiology
• occur at all ages but are more common in the third through the fifth decades
• most common cause of rectal bleeding in infancy.
• prevalence is equal in males and females.
• associated with constipation, diarrhea,
• infectious etiologies, perianal trauma, and Crohn’s disease.

Anatomy and Pathophysiology

• Trauma to the anal canal occurs following defecation;this injury occurs in the
anterior or, more commonly, the posterior anal canal.
• Irritation caused by the trauma to the anal canal results in an increased
resting pressure of the internal sphincter. ‘
• The blood supply to the sphincter and anal mucosa enters laterally.
Therefore, increased anal sphincter tone results in a relative ischemia in the
region of the fissure and leads to poor healing of the anal injury.
• A fissure that is not in the posterior or anterior position should raise
Management
suspicion for other causes, including tuberculosis, syphilis, Crohn’s disease,
and malignancy.
Medical Management
a. Acute fissure : 60-90% healing
Presentation and Evaluation
• Stool softeners ,increased dietary fiber,
Hx: pain associated with defecation., bright red
• topical anes- thetics, glucocorticoids,
PE: most fissures are located in either the posterior or anterior position.
sitz baths
A lateral fissure is worrisome because it may have a less benign nature,
b. Chronic fissures are those present for >6 weeks.
and systemic disorders should be ruled out.
aimed at decreasing the anal canal resting
A chronic fissure is indicated by the presence of a hypertrophied anal
pressure
papilla at the proximal end of the fissure and a sentinel pile or skin tag at
• nifedipine ointment
the distal end
• botulinum toxin type A
Anal manometry : elevation in anal resting pressure
Surgical management
• anal dilatation
• lateral internal sphincterotomy.
ACUTE APPENDICITIS
typical location in the right lower quadrant, to the pelvis, right flank, right upper
quadrant (as may be observed during pregnancy), or even the left side of the
abdomen for patients with malrotation or who have severely redundant colons.
 Maneuvers
Symptoms
•Obturator sign
•Anorexia Ø Palpating in the left lower quadrant
•Constipation causes pain in the right lower
•Diarrhea quadrant
•Fever
•Migration of pain to •Iliopsoas sign
right lower quadrant Ø Internal rotation of the hip causes
•Nausea pain, suggesting the possibility of
•Vomiting an inflamed appendix located in the
pelvis
Signs
•Rovsing’s sign
•Abdominal tenderness Ø Extending the right hip causes pain
along pos- terolateral back and hip,
•Cervical motion
suggesting retrocecal appendicitis
tenderness
•Psoas sign
•Obturator sign
•Rovsing’s sign
•Palpable mass
Diagnosis
• Hx and PE
• Laboratory tests
Ø CBC, UA, pregnancy test, cervical cultures
• Abdominal Xray
• Imaging Tests
Ø US, CT scan

Management:

• Medical
Ø Antibiotics, drainage of abscess
Ø Fluids and electrolytes
Ø Bowel rest

• Surgical
Ø Open vs Laparoscopic
Acute Peritonitis
Types:
q Primary/ Spontaneous Bacterial
Peritonitis
q Secondary Bacterial Peritonitis

SSx: abdominal pain, tenderness, fever

Dx: Laboratory tests

Abdominal Xray
Imaging studies/ CT

Mgt: Medical
Surgical
In Summary:

1. We reviewed the anatomy, histology, and physiology of the SI and LI

2. We leaned the common intestinal disorders

3. We learned the clinical manifestations of intestinal disorders

4. We learned the different diagnostic tests for intestinal disorders

5. We learned the differential diagnosis of intestinal disorders

6. We learned the management of intestinal disorders