Digestive System 2
Lecture 12
Pathology and Clinical
Science 1 (BIOC211)
Department of BioscienceText Reference:
Grossman, S.C. & Porth, C.M. (2014). Porth’s Pathophysiology: concepts of
altered health states, (9th ed.). Philadelphia, U.S.A. Walters Kluwer Health -
Lippincott, Williams & Wilkins.
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Session Learning Outcomes
o Understand the causation, clinical features, treatment aims and prognosis for the following conditions:
o Disorders of Stomach.
• Gastritis
• Peptic Ulcer Disease
o Disorders of the Small intestine
• Malabsorption, Coeliac disease
• Small bowel bacterial overgrowth, Short bowel syndrome
• Infections of the small intestine,
− Travellers diarrhoea, Giardiasis
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GASTRITIS
http://4.bp.blogspot.com/_bw5UbZR_48Q/SvskUQKhXbI/AAAAAAAAA30/kpXTB8AKFQA/s320/gastritis.jpg
Inflammation of gastric mucosa, may be acute or chronic
o Aetiology
• Acute - aspirin or NSAID therapy
• Chronic –
– H Pylori 80%,
– viral - cyclomegalovirus & herpes simplex,
– autoimmune against
parietal cells
o Clinical Features
– dyspepsia, nausea, vomiting,
haematemesis, melaena
o Treatment
– treat underlying cause
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PEPTIC
ULCER
DISEASE
http://www.cytotec.in/wp-content/uploads/2010/10/stomach_ulcer2.jpg
Small round ulcers penetrating to
sub mucosa (muscularis) layer
occurring in the oesophagus,
stomach or duodenum
o May be acute or chronic
• Acute - no fibrosis
• Chronic - shows fibrous base
with presence of inflammatory
cells
• acid and pepsin act on tissues
(autodigestion) and ulcer may
extend further into the deeper
muscularis layer
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PEPTIC
ULCER
DISEASE
Duodenal Ulcerhttp://www.jaoa.org/content/108/1/25/F2.large.jpg
o Duodenal
• more common in younger age
group
• 5:1 to 2:1 male to female
o Gastric 90% seen on lesser
curve
• more common in older group
• 2:1 male to female
o 10% of patients have both
o Chronic ulcer show surface
debris, neutrophil activity,
granulation tissue
and fibrosis (collagen)
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PEPTIC
ULCER
DISEASE
http://www.sciencephoto.com/image/76496/530wm/C0012059-Helicobacter_pylori_bacteria,_SEM-SPL.jpg
Aetiology
• Helicobacter pylori found in
– 95% of duodenal ulcers
– 70% of gastric ulcers great
percentage of ulcers
• NSAIDS - reduce pro
inflammatory prostaglandins esp.
Cox 1 pathway
• hereditary - true genetic or familiar
H pylori clusters
• Smoking
• Imbalance in acid pepsin versus
mucosal resistance
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PEPTIC ULCER DISEASEo Clinical Features
o Epigastric pain or
heartburn
• 30 minutes to 2-3
hours after meals
• hunger pain at night
• relieved by food or
antacids
o nausea, vomiting
o weight loss
o anaemia
o occult blood in faeces
o Investigations
• gastroscopy
• barium X-rays
o Test for H Pylori
• breath test
• IgG antibodies
• stool test for
immunoassay
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PEPTIC
ULCER
DISEASE
o Treatment
• H Pylori eradication
– Drug Therapy - triple therapy
– 2 anti-microbials
– H2 antagonist or proton pump
inhibitors
– bismuth chelate may be added to
anti-microbials
• reduction of risk factors e.g.
smoking, alcohol
• surgery when complications arise
– partial gastrectomy
– vagotomy & pyloroplasty
o Complications
• Haemorrhage
• Perforation
• pyloric stenosis
• intestinal
obstruction
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STOMACH CANCER
Epidemiology
Fourth most common cancer globally (2008)
Half of the cases in Eastern Asia
Less than 30% of cases in developed countries
Aetiology
Genetic factors
Carcinogenic factors in the diet (e.g., N-nitoso
compounds and benzopyrene found in smoked and
preserved foods)
Autoimmune gastritis
Gastric adenomas or polyps
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STOMACH CANCER
Pathogenesis
Bacterial infection causes gastritis followed by atrophy,
intestinal metaplasia and carcinoma.
Clinical Features
Indigestion
Anorexia
Weight loss
Vague epigastric pain
Vomiting
Abdominal mass
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STOMACH CANCER
Treatment
Radical subtotal gastrectomy
Irradiation – for palliative care
Chemotherapy – for palliative care or metastatic spread
Diagnosis
Barrium x-ray studies
Endoscopy with biopsy
Cytologic studies
Routine screening for persons with atrophic gastritis or
gastric polyps
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STOMACH CANCER
http://medicalpicturesinfo.com/wp-content/uploads/2011/10/Stomach-cancer-51.jpg
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OVERVIEW SMALL INTESTINE
o Small bowel function
• Digestion and absorption of carbohydrates
(CHO), protein, lipids, calcium, B12, Iron (Fe)
o Small bowel disorder - clinical features
• diarrhoea,
• abdominal pain - site
• bloating
• weight loss
• nutritional deficiencies
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SMALL BOWEL INVESTIGATIONS
o Blood FBE, proteins, calcium, B12
o Autoantibodies, endomysium, tissue
transglutaminase, reticulin, gliadin
o Barium follow through
o Jejunal biopsy
o 3 day fat collection (100 gm fat intake)
o Lactose intolerance (intake of 50 gm
lactose)
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MALABSORPTION
Occurs as result of:
oDeficiency of digestive enzymes
oMucosal malabsorption from
damaged absorptive epithelium
oPost mucosal lymphatic obstruction
oSurgical removal due to disease
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COELIAC DISEASEMalabsorption syndrome - gluten sensitive, Enteropathy /
intolerance
• Gluten present in wheat, barley rye and oats
• Incidence 1:1000 UK, 1:300 Ireland
• Females greater occurrence, often begins in 40’s
• May be latent/ undiagnosed in genetically susceptibility persons
• Familial tendency - 10% have 1st degree relative with disorder
• HLA antigens A1, B8, DR3, DR7, DQ2, DQ8 seen in many patients
• Often associated with other auto-immune disorders egthyroid, diabetes, primary biliary cirrhosis, splenic atrophy, inflammatory bowel disease
• Proximal area most affected, less seen in ileum
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COELIAC DISEASE (GLUTEN SENSITIVITY ENTEROPATHY)
Angular stomatitis
http://images.paraorkut.com/img/health/images/a/angular_st
omatitis-337.jpg
Pathophysiology
Immune reaction to the Gliadin fraction -(gliadin) tissue transglutaminase, the autoantigens that produce anti endomysial antibodies
Immune response destroys the intestinal villi (partial or subtotal villous atrophy) seen as
• flat mucosal surface
• hyperplasia of crypts
• chronic inflammatory cells in lamina propria
Clinical Features
• Infants - steatorrhoea, weight loss
• Adults - bloating, abdominal pain, malaise, anaemia, weight loss, mouth ulcers, angular stomatitis
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COELIAC DISEASEo Investigations
• Tissue transglutaminase assay, anti endomysial antibodies,
Full Blood Evaluation (FBE), Fe studies, Calcium levels
• small bowel follow through
• duodenal jejunal biopsy
• bone density
o Treatment
• gluten free diet, replacement of nutrients
• pneumococcal vaccination (splenic atrophy)
o Complications
• high risk enteropathic T cell lymphoma, small bowel
cancers, head & neck squamous cell carcinoma
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COELIAC
DISEASE
Normal villi
Atrophied villi in Coeliac Disease
http://soulfoodheals.com/wp-content/uploads/2015/05/celiac_biopsy.jpg
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SMALL BOWEL BACTERIAL
OVERGROWTH
http://www.allergy-details.com/wp-
files/CeliacdiseasebacteriaovergrowthglutenfreedietE_coli_10000x_thumb.jpg
Bacterial over growth
Increase count and changes of the normal flora bacterial colonies in small
intestine
o Aetiology
• caused by low gastric acid
• Impaired intestinal motility
• Structural abnormalities allowing movement of bacteria from colon upward
• Jejunal diverticulosis
• Diabetic diarrhoea
• Scleroderma
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SMALL BOWEL BACTERIAL
OVERGROWTHo Clinical Features
• Diarrhoea watery
• Steatorrhoea
• B12 anaemia
o Investigations
• Tests to exclude coeliac
• B12 & Folate assays
• Endoscopy - aspirated specimen for culture
o Treatment
• Antimicrobials
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SHORT BOWEL SYNDROMEMalabsorption picture from chronic small bowel disease or
major small bowel resection.
E.g. Crohn's, radiation enteritis, mesenteric infarction
o Clinical Features
• Diarrhoea from non absorption of fluid
• Steatorrhoea
• Hypovolemia
• Weight loss
• Muscle loss
o Treatment
• Positive fluid balance
• Dietary assessment and management for micro and macro nutrients
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INFECTIONS OF THE SMALL
INTESTINE Infectious Diarrhoea
o Major cause of morbidity and mortality esp. in young or elderly
o Cause
o Faecal oral spread of organisms including campylobacter, shigella, salmonella, with short incubation period
o May cause secretory diarrhoea or mucosal inflammation and ulceration
Investigation
• Stool cultures
Treatment
• Fluid replacement
• Appropriate antidiarrhoeals and antibiotics
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INFECTIONS OF THE SMALL
INTESTINE Giardiasis - Protozoal infection with Giardia intestinalis or G
lamblia commonly found in contaminated water in tropical areas
http://www.sciencephoto.com/image/198864/530wm/F0022887-Giardiasis-SPL.jpg
Investigation
• 3 by stool cultures at 3 day intervals to identify the cysts
• Aspiration of fluid from endoscopic examination tested for cysts
Treatment
• Tinidazole / metronidazole
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Readings and ResourcesResources:
o Set Textbooks:
Colledge, N.R., Walker, B.R. & Ralston S.H. (2014). Davidson’s Principles and Practice of Medicine, (22nd ed.). Edinburgh.
Churchill Livingstone.
Grossman, S.C. & Porth, C.M. (2014). Porth’s Pathophysiology: concepts of altered health states, (9th ed.). Philadelphia,
U.S.A. Walters Kluwer Health - Lippincott, Williams & Wilkins.
o Additional textbooks:
Davies, A. & Moores, C. (2010). The respiratory system: basic science and clinical conditions, (2nd ed.). Edinburgh. Churchill,
Livingstone, Elsevier.
Field, M., Pollock, C., Harris, D. (2010). Systems of the Body: The Renal System; Basic Science and Clinical Conditions. (2nd
ed.). United Kingdom: Churchill Livingstone.
Jamison, J.R. (2006) Differential Diagnosis for Primary Care: a handbook for health care practitioners. (2nd ed.). Edinburgh.
Churchill Livingstone.
Lee, G. & Bishop, P. (2013). Microbiology and Infection Control for Health Professionals, (5th ed.). Frenchs Forest, NSW.
Pearson Education.
McCance, K.L. & Huether, S.E. (2014). Pathophysiology: the biological basis for disease in adults and children, (7th ed.). St.
Louis, MO. Elsevier.
Murphy, K. (2011). Janeway’s immunobiology, (8th ed.). New York. Garland Science.
Noble, A., Johnson, R. & Bass, P. (2010). The cardiovascular system: basic science and clinical conditions, (2nd ed.).
Edinburgh. Churchill, Livingstone, Elsevier.
Pagana, K.D. & Pagana, T.J. (2013). Mosby’s diagnostic and laboratory test reference, (11th ed.). St. Louis, MO. Elsevier.
Smith, M.E. & Morton, D.G. (2010). The digestive system: basic science and clinical conditions, (2nd ed.). Edinburgh.
Churchill, Livingstone, Elsevier.
VanMeter, K.C. & Hubert, R. (2014). Gould’s pathophysiology for health professions, (5th ed.). St. Louis, MO. Elsevier.
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