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DISEASES OF SMALL
INTESTINE
Coeliac disease (gluten-sensitive
enteropathy)
 Coeliac disease is a condition in which there is
an abnormal jejunal mucosa that improves
morphologically when the patient is treated
with a gluten-free diet and relapses when
gluten is reintroduced.
 Gluten is contained in wheat, rye and barley.
 Pure oats are not harmful.
 Aetiology
 The toxic portion of gluten is the peptide a -
gliadin.
 The exact mechanism by which gluten causes
damage to the intestinal mucosa is not known.
 Pathology
 There are absent or stunted small intestinal villi
with elongation of crypts (subtotal villous atrophy).
 There is a chronic inflammatory cell infiltrate in
the lamina propria, with an increase in
intraepithelial cell lymphocytes.
Clinical features
 Coeliac disease can present at any age but there
are two peaks in incidence: in infancy, after
weaning on to glutencontaining foods, and in
adults at 30-40 years. It often presents with non-
specific symptoms of tiredness and malaise, or
symptoms of small intestinal disease (steatorrhea,
diarrhea, malabsorption, features of malnutrition
and vitamin deficiencies)
 Physical signs are usually few and non-specific,
and related to anaemia and nutritional deficiency.
 There is an increased incidence of atopy and
autoimmune disease.
Investigations
 Distal duodenal biopsies are obtained endoscopically.
The mucosa shows the histological features described
above.
 Serum antibodies:
 Endomysial (EMA) antibodies
 tissue transglutaminase (tTG) antibodies
 Antigliadin and antireticulin antibodies (less commonly
used now)
 Blood count
 A mild anaemia is present in 50% of cases.
 There is almost always folate deficiency, commonly iron
 deficiency and, rarely, vitamin B12 deficiency.
 Radiology
 Small bowel barium follow-through may show a dilated
Management
 Treatment is with a gluten-free diet, which
should be continued lifelong, and nutritional
supplements if there are vitamin deficiencies.
Definitive diagnosis is confirmed when
symptoms resolve subsequently with a gluten-
free diet.
Complications
 There is an increased incidence of malignancy,
particularly intestinal lymphoma, small bowel
and oesophageal cancer.
 The incidence may be reduced by a gluten-
free diet.
Inflammatory bowel disease
 Two main forms are recognized:
 Crohn's disease, which affects any part of the
gastrointestinal tract
 Ulcerative colitis (UC), which affects the large
bowel only.
Aetiology
 It is probable that environmental factors operate in
a genetically predisposed individual.
 Environmental factors:
 Infective agents:
 Measles virus and Mycobacterium paratuberculosis have
been put forward as possible causes of Crohn's disease,
but a causal relationship has not been established.
 Smoking.
 Crohn's disease is more common in smokers and UC less
corrunon. In Crohn's disease smoking doubles the risk of
postoperative recurrence.
 Genetic:
 There is a familial tendency in both UC and Crohn's
disease; twin studies suggest a stronger genetic
influence in Crohn's disease than in Uc.
Crohn’s disease UC
Macroscopic Affects any part of GIT
from mouth to anus
Only the colon
Oral and perianal
disease
Starts in the rectum
and extends
proximally
Discontinuous
involvement (skip
lesions)
Continuous
Histology Transmural
inflammation
Mucosal inflammation
Granuloma present Granuloma absent
Clinical features
 Crohn's disease is a progressive chronic disease
with symptomatology depending on the region(s)
of involved bowel; the commonest site is
ileocaecal (in 40% of patients).
 The main feature in patients with small bowel
disease is abdominal pain, usually with weight
loss. Less commonly, terminal ileal disease
presents as an acute abdomen with right iliac
fossa pain mimicking appendicitis. Colonic
disease presents with diarrhoea, bleeding and
pain related to defecation. In p eri ana I disease
there are anal tags, fissures, fistulae and abscess
formation.
 UC presents with diarrhoea, often containing
blood and mucus. The clinical course may be
one of persistent diarrhoea, relapses and
remissions, or severe fulminant colitis
 Patients with IBD may have one or more
extraintestinal manifestations,
Non-gastrointestinal manifestations
of
inflammatory bowel disease
Eyes Uveitis, episcleritis, conjunctivitis
Joints Small joint arthritis', monoarticular arthritis
(knees and ankles), ankylosing spondylitis',
sacroileitis
Skin Erythema nodosum, pyoderma gangrenosum
(necrotizing ulceration of the skin, commonly on
the lower legs)
Liver Fatty change, primary sclerosing cholangitis,
chronic hepatitis, cirrhosis
Calculi Increased incidence of gall bladder and renal
calculi
Venous thrombosis
Vasculitis
Amyloidosis
Investigations
 The purpose of investigations is to define the nature of the
disease and the extent and severity of bowel involvement.
 Blood count:
 Anaemia is common and is usually the normochromic,
normocytic anaemia of chronic disease, although iron deficiency
anaemia may occur. The platelet count, ESR and C-reactive
protein are often raised in acute Crohn's disease, and the serum
albumin may be low in severe disease.
 Endoscopy
 Other investigations
 Barium follow through
 CT scan
 MRI
 US
 Plain X-ray
Summary of treatments used in
inflammatory bowel disease
 5-ASA (aminosalicyclic
acid)
 Corticosteroids
 Liquid enteral nutrition
 Metronidazole
 Methotrexate
 Ciciosporin
 Infliximab (anti-TNF-a
antibody)
 5-ASA (in UC)
 Azathioprine/6-
mercaptopurine
 Methotrexate
 Infliximab
Remission induction Maintenance of remission

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Diseases of small intestine (1)بور .pptx

  • 2. Coeliac disease (gluten-sensitive enteropathy)  Coeliac disease is a condition in which there is an abnormal jejunal mucosa that improves morphologically when the patient is treated with a gluten-free diet and relapses when gluten is reintroduced.  Gluten is contained in wheat, rye and barley.  Pure oats are not harmful.
  • 3.  Aetiology  The toxic portion of gluten is the peptide a - gliadin.  The exact mechanism by which gluten causes damage to the intestinal mucosa is not known.  Pathology  There are absent or stunted small intestinal villi with elongation of crypts (subtotal villous atrophy).  There is a chronic inflammatory cell infiltrate in the lamina propria, with an increase in intraepithelial cell lymphocytes.
  • 4. Clinical features  Coeliac disease can present at any age but there are two peaks in incidence: in infancy, after weaning on to glutencontaining foods, and in adults at 30-40 years. It often presents with non- specific symptoms of tiredness and malaise, or symptoms of small intestinal disease (steatorrhea, diarrhea, malabsorption, features of malnutrition and vitamin deficiencies)  Physical signs are usually few and non-specific, and related to anaemia and nutritional deficiency.  There is an increased incidence of atopy and autoimmune disease.
  • 5. Investigations  Distal duodenal biopsies are obtained endoscopically. The mucosa shows the histological features described above.  Serum antibodies:  Endomysial (EMA) antibodies  tissue transglutaminase (tTG) antibodies  Antigliadin and antireticulin antibodies (less commonly used now)  Blood count  A mild anaemia is present in 50% of cases.  There is almost always folate deficiency, commonly iron  deficiency and, rarely, vitamin B12 deficiency.  Radiology  Small bowel barium follow-through may show a dilated
  • 6. Management  Treatment is with a gluten-free diet, which should be continued lifelong, and nutritional supplements if there are vitamin deficiencies. Definitive diagnosis is confirmed when symptoms resolve subsequently with a gluten- free diet.
  • 7. Complications  There is an increased incidence of malignancy, particularly intestinal lymphoma, small bowel and oesophageal cancer.  The incidence may be reduced by a gluten- free diet.
  • 8. Inflammatory bowel disease  Two main forms are recognized:  Crohn's disease, which affects any part of the gastrointestinal tract  Ulcerative colitis (UC), which affects the large bowel only.
  • 9. Aetiology  It is probable that environmental factors operate in a genetically predisposed individual.  Environmental factors:  Infective agents:  Measles virus and Mycobacterium paratuberculosis have been put forward as possible causes of Crohn's disease, but a causal relationship has not been established.  Smoking.  Crohn's disease is more common in smokers and UC less corrunon. In Crohn's disease smoking doubles the risk of postoperative recurrence.  Genetic:  There is a familial tendency in both UC and Crohn's disease; twin studies suggest a stronger genetic influence in Crohn's disease than in Uc.
  • 10. Crohn’s disease UC Macroscopic Affects any part of GIT from mouth to anus Only the colon Oral and perianal disease Starts in the rectum and extends proximally Discontinuous involvement (skip lesions) Continuous Histology Transmural inflammation Mucosal inflammation Granuloma present Granuloma absent
  • 11. Clinical features  Crohn's disease is a progressive chronic disease with symptomatology depending on the region(s) of involved bowel; the commonest site is ileocaecal (in 40% of patients).  The main feature in patients with small bowel disease is abdominal pain, usually with weight loss. Less commonly, terminal ileal disease presents as an acute abdomen with right iliac fossa pain mimicking appendicitis. Colonic disease presents with diarrhoea, bleeding and pain related to defecation. In p eri ana I disease there are anal tags, fissures, fistulae and abscess formation.
  • 12.  UC presents with diarrhoea, often containing blood and mucus. The clinical course may be one of persistent diarrhoea, relapses and remissions, or severe fulminant colitis  Patients with IBD may have one or more extraintestinal manifestations,
  • 13. Non-gastrointestinal manifestations of inflammatory bowel disease Eyes Uveitis, episcleritis, conjunctivitis Joints Small joint arthritis', monoarticular arthritis (knees and ankles), ankylosing spondylitis', sacroileitis Skin Erythema nodosum, pyoderma gangrenosum (necrotizing ulceration of the skin, commonly on the lower legs) Liver Fatty change, primary sclerosing cholangitis, chronic hepatitis, cirrhosis Calculi Increased incidence of gall bladder and renal calculi Venous thrombosis Vasculitis Amyloidosis
  • 14. Investigations  The purpose of investigations is to define the nature of the disease and the extent and severity of bowel involvement.  Blood count:  Anaemia is common and is usually the normochromic, normocytic anaemia of chronic disease, although iron deficiency anaemia may occur. The platelet count, ESR and C-reactive protein are often raised in acute Crohn's disease, and the serum albumin may be low in severe disease.  Endoscopy  Other investigations  Barium follow through  CT scan  MRI  US  Plain X-ray
  • 15. Summary of treatments used in inflammatory bowel disease  5-ASA (aminosalicyclic acid)  Corticosteroids  Liquid enteral nutrition  Metronidazole  Methotrexate  Ciciosporin  Infliximab (anti-TNF-a antibody)  5-ASA (in UC)  Azathioprine/6- mercaptopurine  Methotrexate  Infliximab Remission induction Maintenance of remission