Gastrointestinal malabsorption Flashcards
What are the UK’s common causes of malabsorption? (x3)
Coeliac disease, chronic pancreatitis and Crohn’s disease.
What is the aetiology of gastrointestinal malabsorption? (x6)
- LOW BILE: cholangitis, ileac resection, biliary obstruction, cholestyramine (drug that binds to bile to prevent its reabsorption)
- PANCREATIC INSUFFICIENCY: cancer, cystic fibrosis
- ENZYME INSUFFICIENCY: lactase deficiency (lactose intolerance)
- INFLAMMATORY CONDITIONS: IBD
- MUCOSAL ABNORMALITY: Coeliac disease
- STRUCTURAL ABNORMALITIES: resection, short bowel syndrome (usually from surgery)
- INFECTION: Whipple’s disease (systemic infection), HIV
- BACTERIAL OVERGROWTH
- INTESTINAL HURRY: post-gastrectomy dumping, post-vagotomy, gastrojejunostomy
Why does ileac resection lead to low bile?
Ileum is responsible for bile salt absorption. When this does not occur (e.g. ileac resection), less bile can be synthesised.
What are the main roles of the ileum?
Bile salt and vitamin B12 absorption.
What are the signs of gastrointestinal malabsorption? (x5)
Deficiency signs such as anaemia (low Fe, B12, folate), bleeding disorders (low Vitamin K), oedema (from low protein; low osmotic pressure), metabolic bone disease (low Vitamin D), neurological features (neuropathy).
What is coeliac disease?
Systemic autoimmune disease triggered by dietary gluten peptides found in wheat, rye, barley and related grains, and leading to GI symptoms, malabsorption and a diverse range of systemic manifestations.
What is the aetiology of Coeliac disease? (x1 and x3)
- Almost all carry HLA-DQ2 or HLA-DQ8 that present gluten peptides (such as gliadin) in a manner that activates an antigen-specific T cell response. DQ2/DQ8 is a major factor in the genetic predisposition, though most that are DQ2-/DQ8-positive never develop coeliac disease.
- Other environmental and genetic factors are unknown, though it is believed that the time of initial gluten exposure, GI infection leading to gluten antigen mimicry, or damage to the intestinal-epithelial barrier leading to abnormal exposure of the mucosa to gluten peptides also contribute.
What are the risk factors of Coeliac disease? (x4)
Increased gluten exposure in early life increases risk, T1DM, autoimmune thyroid disease, family history.
! What is the pathophysiology of Coeliac disease?
Both innate and adaptive immune activation in the duodenum and proximal jejunum leading to villous atrophy, hypertrophy of intestinal crypts, and increased numbers of lymphocytes in the epithelium and lamina propria (i.e., damage and loss of villi). The secretion of duodenal hormones such as CCK and secretin may also be reduced. Locally, these changes lead to GI symptoms and malabsorption.
What is the epidemiology of Coeliac disease: Prevalence? Where? Gender?
1/2000 in the UK. More common in the West; rare in Asia. More common in women.
What are the symptoms of Coeliac disease? (x9)
- May be asymptomatic.
- Abdominal discomfort and distension.
- Steatorrhea (pale, bulky with offensive smell and difficult to flush away)
- Diarrhoea
- Tiredness, malaise, weight loss
- Failure to ‘thrive’ in children
- Amenorrhoea in young adults
- Apthous ulcers
- Angular stomatitis
- N&V
What are the signs of Coeliac disease? (x4)
- Signs of anaemia
- Signs of malnutrition: short stature, abdominal distension and wasted buttocks in children. Triceps skinfold thickness give an indication of fat stores.
- Signs of vitamin or mineral deficiencies e.g. osteomalacia, easy bruising (Vitamin K)
- Dermatitis herpetiformis: intense, itchy blisters on elbows, knees or buttocks
What investigations are there for Coeliac disease? (x6)
- BLOOD: low Hb, iron and folate, albumin, calcium and phosphate
- SEROLOGY: IgG anti-gliadin (AGA), Ig-TTG (IgA antibody), and IgG anti-endomysial transglutaminase antibodies. As IgA deficiency is common (1 in 50 with Coeliac disease), Ig levels should be measured to avoid false negatives
- STOOL: culture to exclude infection, faecal fat tests for steatorrhea
- D-XYLOSE TEST: reduced urinary excretion after an oral xylose load indicate small bowel malabsorption
- ENDOSCOPY: biopsy of duodenal mucosa
- SKIN BIOPSY: for patients with skin lesions suggestive of dermatitis herpetiformis.
What would you observe in endoscopy of Coeliac disease patient?
Villous atrophy in the small intestine (esp. jejunum and ileum) giving the mucosa a flat smooth appearance.
What would you observe in biopsy of Coeliac disease patient? (x4)
Duodenal villous atrophy, crypt hyperplasia in duodenum. The epithelium adopts a cuboidal appearance, and there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria.
How is Coeliac disease non-medically managed?
Withdraw from gluten (wheat, rye, barley).
How is Coeliac disease medically managed? (x2)
Vitamin and mineral supplements. Oral corticosteroids may be used if the disease does not subside with gluten withdrawal.
What are the complications of Coeliac disease? (x8)
Iron, folate and Vitamin B12 deficiency, autoimmune conditons (such as DERMATITIS HERPETIFORMIS), osteomalacia, ulcerative jejunoileitis (chronic ulcerative condition of small intestine), hyposplenism (so offer flu and pneumococcal vaccine), gastrointestinal lymphoma (particularly T cell), bacterial overgrowth, and cerebellar ataxia.
What is the prognosis of Coeliac disease?
Strict adherence to gluten-free diet leads to intestinal recovery and resolution of symptoms within weeks. Histological changes may take longer to resolve. Though there is no cure and a gluten-free diet needs to be followed for life.
What does IBS stand for?
Irritable bowel syndrome.
