Title of the report

Inflammatory Bowel Disease

Prepared by

‫أحمد علي حسين‬

Sixth grade student

Supervised by

2020 1441
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 Acknowledgments
I would like to express my appreciation and gratitude to my supervisor
PROF. DR. Ali Abdul-Aziz Alshawi for his support and efforts that he
made for us.

Page Contents
3 Introduction
3 Ulcerative colitis
3 Etiology
4 Pathology
4 Clinical presentation
5 Investigations
8 Deferential diagnosis
8 Treatment
9 Complication
9 Prognosis
10 Crohn's Disease
10 Etiology
10 Pathology
11 Clinical presentation
12 Investigations
13 Deferential diagnosis
14 Treatment
14 Complication
14 Prognosis
15 Differences between ulcerative colitis and Crohn’s disease
16 References

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 Introduction
Inflammatory bowel disease (IBD) contain two major entities:
- Ulcerative colitis
- Crohn disease.
Crohn disease can affect any part of the gastrointestinal tract from the mouth down to the
perianal area, whereas ulcerative colitis affects the colon only. The pathologic
characteristics and clinical picture of these disorders are somewhat different, but with
substantial overlap.(1) Their pathogenesis remains poorly understood. Its inflammation is
chronic or recurring in nature. There is also an extraintestinal manifestations in patients with
IBD, like diseases of the liver and biliary tract that are common in IBD.(2) Although the
availability of population genetics and molecular biology has contributed to our
understanding of the pathogenesis of inflammatory bowel disease, the aetiology remains
unclear.(3)

Ulcerative colitis
Ulcerative colitis is a disease of the colon otherwise commonly involves the rectum and
extend in a proximal and continuous fashion to involve the rest of the colon with
extraintestinal manifestations. Its course has relapsing and remitting episodes of
inflammation in a chronic inflammation limited to the mucosal layer of the colon. The
prevalence of UC is stable (unlike Crohn’s disease, it is increasing). The Ashkenazi Jewish
population more commonly have ulcerative colitis and in early life, affects men and women
equally, but the disease in later life is more common in males. It is most commonly
diagnosed between the ages of 20 and 40. The disease has a marked geographical
distribution.(1,3,4)

Etiology:
Ulcerative colitis has range of etiologic factors include genetic factors, environmental
factors, NSAID drug use, psychological stress factors, immune system reactions, and low
levels of antioxidants. The cause of UC remains unknown. Genetic factors clearly have a
contribution as 10-20% has a first-degree relative with inflammatory bowel disease among
patients with UC. The mechanism of UC has been suggested to be related to a primary
abnormality of mucosal permeability, triggering an inflammatory response due to bacterial
antigens being able to cross the colonic mucosal barrier. Also, Multiple patients with UC
have alterations in intestinal microbiota in both the composition and function as lines of
evidence suggest that. Unlike crohn's disease, in UC smoking seems to have a protective
effect. Patients often comment that relapses are associated with periods of stress or drug
withdrawal. In other evidences, development of ulcerative colitis may be lowered after
appendectomy.(1,3,5,6)

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Pathology: (3,7)
In virtually all cases, the disease starts from the rectum and ascends proximally in continuity.
Only in those using topical rectal preparations the rectum doesn’t involved with the disease
(rectal sparing).
Normal or thin thickness of bowel wall, but the impression of a thickened bowel wall come
from edema, the accumulation of fat, and hypertrophy of the muscle layer. The mucosa is
largely involved by the disease and to a lesser extent, the submucosa. Very rarely muscular
layer and serosa involved by the disease; in patients with severe disease, such as toxic
dilatation, and it is not a primary ulcerative colitis pathogenesis, it is a secondary effect of
the severe disease.
It manifests as hemorrhagic inflammation with loss of the normal vascular pattern, petechial
hemorrhages, and bleeding in the early stage of the disease. Crypt abscesses which is formed
by undermining of the mucosa, are the hallmark of the disease.
Ulcerative colitis presented with infiltration of lamina propria with acute and chronic
inflammatory infiltrates, branching of the crypts, and villous atrophy. Inflammation of the
crypts of Lieberkühn and abscesses also represents a microscopic change. Accompanied by
a goblet cells discharge of mucus, which is reduced with the disease progresses. A
granulation tissue sooner covers the ulcerated areas.
Polypoidal mucosal excrescences are formed as a result of undermining of the mucosa and
an excess of granulation tissue, which known as inflammatory polyps or pseudopolyps.
(figure 1)
Pale, featureless, a haustral pattern to the colon means a chronic ‘burnt-out’ disease is the
cause.

Figure 1 – Pseudopolyps of the bowel

Clinical presentation: (3,4,8)

An insidious onset of ulcerative colitis may present with minimal bloody stools, or an abrupt
onset can be with severe diarrhea and bleeding, abdominal pain, fever, and tenesmus.
It depends on the extent of diseases in large part. There are usually no systemic upset and
also extra-alimentary manifestations are rare if the disease confined to the rectum (proctitis),
the main symptoms will be rectal bleeding, mucous discharge, and tenesmus. Almost always
colitis associated with bloody diarrhea and urgency may be incapacitating in nature. Colicky
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abdominal pain, tenesmus, and incontinence are associated symptoms. Constipation
accompanied by frequent discharge of blood and mucus are signs of distal disease.
Extensive colitis associated with systemic illness also, characterized by fever, malaise, and
loss of appetite. Anemia, hypoproteinemia and electrolyte disturbance resulting from
diarrhea if it's profuse and bloody.
There is proximal spread of the disease to the splenic flexure occurs in 20%, and 30% of
patients have inflammation extending to the sigmoid colon. The more extensive the disease,
the more likely extraintestinal manifestations are to occur.

Classification of severity: (3,4,7)

• Mild: Four or fewer stools per day with or without blood, normal erythrocyte
sedimentation rate (ESR) with no signs of systemic toxicity. Also, mild crampy pain,
periods of constipation, and tenesmus are common. but severe abdominal pain, profuse
bleeding, fever, and weight loss are not part of the spectrum of mild disease.
• Moderate: Frequent loose, bloody stools (>4 per day), mild anemia not requiring blood
transfusions, and abdominal pain that is not severe. There are minimal signs of systemic
toxicity like low-grade fever.
• Severe: Frequent loose, bloody stools (≥6 per day), severe cramps and evidence of
systemic toxicity as presented by a fever, tachycardia, anemia, or an elevated ESR. And
also, there may be a rapid weight loss.
• Fulminant colitis: More than 10 stools per day, continuous bleeding, abdominal pain,
distension, associated with acute, severe toxic symptoms including fever and anorexia.
As the inflammatory process extends beyond the mucosa and involve the muscle layers
of the colon, there will be high risk of developing toxic megacolon.

Extraintestinal manifestations: (3,4,7)

• Musculoskeletal conditions: Ankylosing spondylitis, spondyloarthropathies.
• Cutaneous conditions: Erythema nodosum, pyoderma gangrenosum
• Ocular conditions: Scleritis, episcleritis uveitis
• Hepatobiliary conditions: Primary sclerosing cholangitis (PSC), fatty liver, and
autoimmune liver disease
• Hematopoietic/coagulation: Venous and arterial thromboembolism
• Pulmonary conditions: Airway inflammation, parenchymal lung disease, serositis, and
thromboembolic disease.

Investigations:

▪ Laboratory Studies (3,4,7,8)

o Complete blood cell count (CBC): Anemia, Thrombocytosis.
o Comprehensive metabolic panel:
- Hypoalbuminemia (ie, albumin < 3.5 g/dL)
- Hypokalemia (ie, potassium < 3.5 mEq/L)
- Hypomagnesemia (ie, magnesium < 1.5 mg/dL)
- Elevated ALP: More than 125 U/L suggests primary sclerosing
cholangitis.
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 o Inflammatory markers:
- Elevation of the erythrocyte sedimentation rate and C-reactive protein
level correlates with disease activity.
- Fecal calprotectin is a marker of activity of inflammation; it can also be
used to determine mucosal healing 3-6 months after treatment initiation.
- Fecal lactoferrin and alpha-1-antitrypsin studies are used to exclude
intestinal inflammation.

o Stool assays:
Stool studies are used to exclude other causes and to rule out infectious
enterocolitis. These tests include evaluation of fecal blood or leukocytes,
culture for bacterial pathogens, viral studies, Clostridium difficile titer,
and ova and parasite studies.

▪ Radiological Assessment: (3,4,7,8)

o Abdominal imaging may be performed in patients who present with symptoms of
colitis. In patients with mild to moderate disease it is usually normal, but proximal
constipation, mucosal thickening or "thumbprinting" secondary to edema, and
colonic dilation in patients with severe or fulminant ulcerative colitis may be
identified.

o Double contrast barium enema in mild ulcerative colitis may be normal. A diffusely
reticulated pattern with superimposed punctate collections of barium in micro
ulcerations are the findings on barium enema.
Spiculated collar button ulcers, loss of haustrae, pseudo-polyps, shortening of the
colon, narrowing of the luminal caliber, and filiform polyps can be found in more
severe disease.
A foreshortened colon and lacks haustral markings (lead pipe colon) are findings in
long-standing ulcerative colitis. (figures 2,3,4)

Figure 1 Figure 2 Figure 3

Lead pipe appearance of colon in ulcerative colitis showed by double contrast barium enema

Barium enema should be avoided in patients who are severely ill since it may
precipitate ileus with toxic megacolon, because the inflammation in ulcerative colitis
is purely mucosal.

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 o Computed tomography (CT) and magnetic resonance imaging (MRI) are
nonspecific, and they have lower sensitivity for the detection of subtle early mucosal
disease than barium enema.
But they are equivalent in patients with established and severe disease.

o A thickened hypoechoic mucosal layer may be demonstrated by ultrasound with

doppler in patients with active ulcerative colitis.
Transmural bowel wall thickening may be associated with more severe cases.
However, these findings are not specific for ulcerative colitis.

▪ Endoscopy and biopsy (3,4,7,8)

Ulcerative colitis is almost always diagnosed by endoscopy (figure 5).
If the symptoms are mild flexible sigmoidoscopy may be performed, However, if
inflammation is found with flexible sigmoidoscopy, most physicians perform a full
colonoscopy.

Figure 5 – normal large intestine versus large bowel with ulcerative colitis

Loss of vascular markings due to engorgement of the mucosa, giving it an erythematous

appearance are the endoscopic findings in patients with UC. In addition, granularity of the
mucosa, touch friability, exudates, petechiae, edema, erosions, and spontaneous bleeding
may be present.
Macro ulcerations, profuse bleeding, and copious exudates are associated with more severe
cases. And due to prior inflammation, non-neoplastic pseudo-polyps may be present in areas
of disease involvement.

Both inflamed and normal-appearing mucosa should be biopsied. Crypt abscesses, crypt
branching, shortening and disarray, and crypt atrophy are features suggestive of UC. Mucin
depletion and Paneth cell metaplasia, may also be seen.
Increased lamina propria cellularity, basal lymphoid aggregates, basal plasmacytosis, and
lamina propria eosinophils are Inflammatory features of UC.
The diagnosis confirmed by findings on colonoscopy with biopsy. Also, this evaluation is
useful for surveillance for dysplasia or cancer, for documenting the extent of the disease,
and for monitoring disease activity.

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Differential Diagnoses: (4,7)
▪ Crohn disease
▪ Radiation colitis
▪ Infectious colitis
▪ Diversion colitis
▪ Medication associated colitis
▪ Graft versus host disease
▪ Solitary rectal ulcer syndrome
▪ Diverticular colitis

Treatment: (3,7)
Ulcerative colitis (UC) treatment is made on the basis of the disease:
o Stage: active, remission.
o Extent: proctitis, distal colitis, left-sided colitis, and pancolitis.
o Severity: mild, moderate, severe.

Medical treatment:
The 5-aminosalicylic acid (5-ASA) derivatives can be given per rectum (topically) or
systemically. They can be used for long term as a maintenance therapy. 5-ASA inhibit cyclo-
oxygenase (COX) enzyme system and protect the aspirin-related drug from degradation
before reaching the colon.

Mainstay of treatment for any ‘flare up’ is corticosteroids, either topically or systemically
with a widespread anti-inflammatory action.

Azathioprine and cyclosporin (immunosuppressive drugs) can be used to maintain remission

and also, can be used as steroid-sparing agents.

Monoclonal antibodies have entered clinical practice more recently; infliximab and
adalimumab both act against tumor necrosis factor alpha TNF-a, which has a central role in
inflammatory cascades.

Indications of surgery:
The most common indication for surgery is failure of medical management.

Indications for urgent surgery in patients with UC are:

1. Toxic megacolon refractory to medical management.
2. Fulminant attack refractory to medical management.
3. Uncontrolled colonic bleeding.

Indications for elective surgery in UC are:

1. Long-term steroid dependence.
2. Dysplasia or adenocarcinoma found on screening biopsy.
3. The presence of disease for 7-10 years.
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Surgical options are:
1. Total colectomy (panproctocolectomy) and ileostomy.
2. Total colectomy.
3. Ileoanal pouch reconstruction or ileorectal anastomosis.
4. Subtotal colectomy with end-ileostomy is recommended in an emergency situation.

Maintenance Therapy:
Maintenance therapy is recommended for all patients with ulcerative colitis (UC), once
remission has been achieved, to prevent relapse.
For disease that responded to acetylsalicylic acid (ASA) or steroids oral amino-salicylates
are indicated.
With proven effectiveness for maintenance of remission, alternatives are Azathioprine and
6-mercaptopurine, particularly for those who are unable to maintain remission with 5-ASA
preparations or steroid dependent patients.
Maintenance therapy should continue with infliximab or azathioprine for patients who were
induced with infliximab.
For the induction of remission in steroid-refractory or steroid-dependent moderate to severe
ulcerative colitis, Anti-tumor necrosis factor (anti-TNF) agents are effective.

Complications: (3,4,7)
Acute
- Toxic dilatation.
- Perforation.
- Hemorrhage.

Chronic
- Dysplasia or Colo-rectal Cancer.
- Strictures.
- Extra-alimentary manifestations: skin lesions, eye problems, and liver disease.

Prognosis: (4,7)
Disease-related mortality may be associated with UC. However, overall mortality is not
increased or slightly higher as compared to the general population. May be observed among
elderly patients with the disease. Patients who develop complications (shock, malnutrition,
anemia) also have increased mortality. Also, patients with UC who undergo any form of
medical or surgical intervention, have increased mortality as the evidences suggested.
Toxic megacolon is the most common cause of death of patients with UC.
3-5% of patients with UC develop colonic adenocarcinoma, and as the duration of disease
increases, the risk increases. Increased risk of colorectal cancer significantly among patients
with extensive ulcerative colitis over a long period.

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 Crohn's disease
It is an idiopathic, chronic transmural inflammatory disease with a course going to affect
any part of the alimentary tract, including most commonly involvement of terminal ileum.
Crohn’s disease varies in incidence among ethnic groups in the same geographic region. For
example, Ashkenazi Jewish population members of Eastern European are at 2-4 folds higher
risk of having Crohn’s disease than other populations members living within the same area.
Interestingly, CD prevalence of the Jewish population in Europe or the United States is
higher than that in Israel, suggesting that also, environmental factors are important.
Incidence appears to have been increased over the last four decades, thought to be a
consequence of improved diagnostic modalities, environmental factors, or both.
Crohn’s disease is slightly more common in females than in males as many evidences
suggest that. Most commonly CD diagnosed between 25-40 years of age, with a second peak
of incidence around the 70 years of age. (3,8)

Etiology:
It is incompletely understood but is thought to involve a complex of environmental and
genetic factors, both appear to influence the risk for developing the disease.
14 to 15 times the relative risk is higher among first-degree relatives of patients with Crohn’s
disease than that of the general population, with a family history reporting in about 20% of
patients.
As in UC, an increased permeability of the mucous membrane also found in CD, leading to
increased luminal antigens passage, which then induce a cell-mediated inflammatory
response.
There is an increased risk of CD in high socioeconomic status patients. Breastfeeding is
suggested to be protective against the development of Crohn’s disease. High prevalence of
CD with smoking, and is associated with the increased risk for both the need for surgery and
the risk of relapse after surgery for Crohn’s disease. Some studies have suggested that after
appendicectomy the risk of Crohn disease is increased. Also, there is role for mucosal
immune response and epithelial damage in the disease. (1,3,5,6,8,9)

Pathology: (3,8)
Focal, transmural inflammation of the intestine, is the pathological hallmark of Crohn’s
disease. The disease can be present with a spectrum of pathological lesions. The earliest one
is the aphthous ulcer, up to 3 mm in diameter, surrounded by a halo of erythema.
Aphthous ulcers typically arise over lymphoid aggregates in the small intestine. The highly
characteristic lesions of Crohn’s disease are granulomas which are present in up to 70% of
intestinal specimens obtained during surgical resection, they are noncaseating, found in both
areas of active disease and normal intestine, in any layer of the bowel wall, and also in
mesenteric lymph nodes.
Aphthae coalesce, as disease progresses, into larger, stellate shaped ulcers. When multiple
ulcers fuse in a direction parallel to the longitudinal axis of the intestine, linear or
serpiginous ulcers may form. Cobblestoned appearance of the mucosa may arise with
transverse coalescence of ulcers.

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Inflammation can be transmural with advanced disease resulting in fibrosis with stricture
formation, intra-abdominal abscesses, fistulas, and, rarely, free perforation. Adhesion of the
inflamed bowel to other loops of bowel or other adjacent organs due to serosal involvement.
There are skip lesions that are separated by intervening normal-appearing intestine, so the
CD is characteristically discontinuous.

Macroscopically, resection specimens show a narrow lumen, fibrotic thickening of the

intestinal wall and fat wrapping. The bowel just proximal to the stricture is usually dilated
and there are deep mucosal ulcerations in the strictured area with linear or snake-like
patterns. Cobblestone appearance formed by edema in the mucosa between the ulcers.
(figure 6)
Microscopically, involvement of all layers of the intestinal wall by focal areas of chronic
inflammation associated with lymphoid aggregates, and non-caseating giant cell
granulomas.
Thickened muscularis propria with multifocal arterial occlusions in it, also there will be
deep, fissuring ulceration within affected areas. Characteristically, there may be completely
normal areas immediately next to areas of severe inflammation, unlike in UC.

Figure 6 – Cobblestone appearance of the small intestine with crohn's disease

Clinical presentation:
Crohn’s disease most commonly present with fever, abdominal pain (often RIF), tender
mass may be palpable, diarrhea, secondary anemia of chronic disease and weight loss.
Failure to thrive in children and adolescents or have retarded growth.
However, the clinical features depend on which segment of the gastrointestinal tract is
predominantly involved, the intensity of inflammation, and the presence or absence of
specific complications like intestinal fistulation (ileo-colic, ileo-ileal, ileo-cutaneous) or
obstructive symptoms caused by narrowing and fibrosis of the intestine. Rarely free
perforation with features of peritonitis and only in Crohn’s colitis there may be rectal
bleeding. (10–12)

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Extraintestinal manifestations: (4)
- Arthritis or arthropathy: Sacroiliitis, ankylosing spondylitis.
- Eye involvement: Uveitis, iritis, and episcleritis.
- Skin involvement: Erythema nodosum, pyoderma gangrenosum.
- Hepatobiliary involvement: Primary sclerosing cholangitis, gallstones, pyogenic
liver abscess
- Secondary amyloidosis
- Renal stones: Calcium oxalate, uric acid kidney stones.
- Bone loss
- Pulmonary involvement: Bronchiectasis, chronic bronchitis, interstitial lung
disease, bronchiolitis obliterans with organizing pneumonia, sarcoidosis, necrobiotic
lung nodules, and pulmonary infiltrates with eosinophilia syndrome.

Investigations: (4,11,12)
▪ Laboratory studies
o Complete blood cell count (CBC): Anemia, leukocytosis.
o Comprehensive metabolic panel:
- Hypoalbuminemia
- Iron and micronutrients deficiencies.
- Elevated liver enzymes.
o Inflammatory markers:
- ESR and CRP may correlate with disease activity, however, a normal ESR
or CRP levels don’t exclude the disease.
- A noninvasive surrogate marker of intestinal inflammation in IBD called
fecal calprotectin.
- Fecal lactoferrin is significantly correlated with histologic inflammation.

o Stool studies:
Check for the presence of white blood cells, occult blood, routine
pathogens, parasites, Clostridium difficile toxin, ova, rule out infectious
etiologies.

▪ Radiological studies:
o Plain Abdominal Radiography: It is a nonspecific test; however, if there is concern
about obstruction or perforation it can be useful. There will be mural thickening and
dilatation, small bowel and colonic mucosal abnormalities, and abnormal fecal
distribution with areas of colonic involvement without fecal material.

o Barium Contrast Studies: It's useful noninvasive method for evaluating features
such as fistulation, pseudodiverticula, and the severity and length of colonic strictures.

o Small bowel follow-through (SBFT): In patients with suspected Crohn disease an

upper GI SBFT and spot films of the terminal ileum can be used. Entero-enteric and
entero-colonic fistulation can also be detected by SBFT.

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 Edema and ulceration of the mucosa may appear as thickening and distortion of
valvulae conniventes in the small bowel. Separation of the barium-filled bowel loops
suggest there is edema of the deep layers of the bowel wall. Cobblestone appearance
result from tracking of deep ulcerations, both transversely and longitudinally.

o Enteroclysis: It is similar to SBFT with better visualization of CD in the small

intestine. Overall, it is reserved for complicated cases.

o Computed Tomography (CT) Scanning: It is helpful for extramural complications

as well as renal and hepatobiliary complications. Ct scan can show bowel wall
thickening, mesenteric edema, bowel obstruction, fistulae, and abscesses.

o Magnetic Resonance Imaging (MRI): It has higher sensitivity and specificity than
ileo-colonoscopy. It is especially useful for pelvic and perianal disease evaluation
when investigating for perianal fistulae and abscesses.

o Ultrasonography: It is a quick, inexpensive, and noninvasive method for screening,

used for the diagnosis of IBD or for repeated evaluation for complications.

▪ Endoscopy:
o Ileo-colonoscopy: For the evaluation of suspected ileocolonic CD, the findings will
be, cobblestone appearance, defined by focal ulcerations adjacent to areas of normal
appearing mucosa along with nodular mucosal changes. Also, there are skip lesions,
pseudo-polyps. Normal appearing rectal mucosa (ie, rectal sparing) is common in CD.
Biopsies are obtained to assess for histologic evidence of inflammation, these biopsies
are confirmatory for the disease rather than diagnostic.

o Upper endoscopy: It is performed in patients with suspected CD associated with

upper gastrointestinal symptoms (eg, dyspepsia, early satiety, vomiting). The findings
visualized as esophageal ulceration, gastric inflammation, and duodenal ulceration
and/or inflammation.

o Video capsule endoscopy: It is an alternative method for visualizing the small bowel
mucosa without radiation exposure. This method can detect lesions like ulcerations
of the small bowel not visible by other studies.

Differential diagnosis: (4,11)

- Diverticular colitis
- Ulcerative colitis
- Irritable bowel syndrome
- Infectious colitis
- Appendicitis
- Celiac disease
- Lactose intolerance
- Other: appendicitis, diverticulitis, ischemic colitis, and a perforating or obstructing
bowel cancer.

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Treatment: (3,8,11,12)

Medical treatment:
- Steroids: are CD mainstay of treatment, induce remission in 70–80% of cases with
moderate to severe disease.
- Aminosalicylates
- Antibiotics: Especially in perianal disease, drugs like metronidazole and
ciprofloxacin may be used.
- Immunomodulatory agents: Azathioprine is now standard maintenance therapy.
- Monoclonal antibody: Patients with severe, active disease, Infliximab and
Adalimumab are used.
- Nutritional support

Surgical treatment:
Because of the high rate of disease recurrence after segmental bowel resection, surgical
resection will not cure CD. So the guiding principle of surgical management is preservation
of intestinal length and function.

Indications for surgical intervention:

- Failure of medical therapy.
- Acute onset of severe disease.
- Persistent symptoms despite long-term steroid use.
- Crohn’s colitis +/− toxic megacolon (rare).
- Recurrence of symptoms when high-dose steroids are tapered.
- Drug-induced complications (Cushing’s disease, hypertension).
- Malignancy risk.
- Development of disease complications:
- Obstruction
- Perforation
- Complicated fistulas
- Hemorrhage

Complications: (3,8,11)
- Recurrent intestinal obstruction.
- Perianal disease.
- Bleeding.
- Malignant change.
- Intestinal fistula.
- Perforation.
- Fulminant colitis.

Prognosis: (4,8)
Complications such as strictures, fistula, or abscess caused by chronic bowel inflammation.
There is no surgical cure in Crohn’s disease, usually there is development of recurrence.
And 70% recur within 1 year of a bowel resection and 85% by 3 years, if recurrence is
defined endoscopically.
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Differences between ulcerative colitis and Crohn’s disease: (3,7,11)

Ulcerative colitis Crohn's Disease

Affect the colon only Affect any part of the gastrointestinal tract,
but particularly the small and large bowel
Mucosal disease Affects the full thickness of the bowel wall
Confluent disease in the colon and rectum Characterized by skip lesions and
cobblestone appearance

Doesn’t causing fistulation and stricturing More commonly causes stricturing and
fistulation
There is no granuloma There are non-caseating granulomas
Doesn’t associated with perianal disease Associated with perianal disease
Doesn’t affect the terminal ileum Affecting the terminal ileum may produce
symptoms mimicking appendicitis
Resection of the colon and rectum cures the Recurrence is common after resection
patient
Bleeding is common Bleeding is uncommon

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 References
1. Peppercorn MA, Cheifetz AS, Rutgeerts P, Robson KM. Definitions, epidemiology,
and risk factors for inflammatory bowel disease in adults. UpToDate Inc. 2020.
2. Friedman G, Bitton A, Rutgeerts P, Robson KM. Overview of hepatobiliary
disorders in patients with inflammatory bowel disease. UpToDate Inc. 2020.
3. Bailey HH, Love RJM, Williams NS, O’Connell PR, McCaskie AW. Bailey &
Love’s Short Practice of Surgery. 27th ed. 2018. 1240–1271 p.
4. Peppercorn MA, Kane S V, Rutgeerts P, Robson KM. Clinical manifestations,
diagnosis, and prognosis of ulcerative colitis in adults. UpToDate Inc. 2020.
5. Snapper SB, McGovern DPB, Rutgeerts P, Robson KM. Genetic factors in
inflammatory bowel disease. UpToDate Inc. 2020.
6. Snapper SB, Abraham C, Rutgeerts P, Robson KM. Immune and microbial
mechanisms in the pathogenesis of inflammatory bowel disease. UpToDate Inc.
2020.
7. Basson MD, Anand B. Ulcerative colitis. Medscape. 2019.
8. Brunicardi FC, Hunter JG, Kao LS, Matthews JB, Pollock RE. Schwartz’s Principles
of Surgery. 11th ed. McGraw-Hill Education; 2019. 1246–1286 p.
9. Rendi M, Swanson PE, Upton MP. Crohn Disease Pathology. Medscape. 2017.
10. Thompson CW, McLatchie G, Borley N, Chikwe J. Oxford handbook of clinical
surgery. 4th ed. Oxford University Press; 2013. 392–395 p.
11. Ghazi LJ, Praveen K Roy. Crohn disease. Medscape. 2019.
12. DeMeester SR, McFadden DW, Matthews JB, Fleshman JW. Shackelford’s
SURGERY of the ALIMENTARY TRACT. 8th ed. Elsevier; 2019. 976–996 p.

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