Clinical approach to diarrhoea Flashcards
What is diarrhoea?
excessively frequent and loose bowel movements
>300g/24 hours
What is malabsorption?
imperfect absorption of food material by the small intestine
What are the main types of diarrhoea?
Osmotic
Exudative
Secretory
Motility
What is osmotic diarrhoea?
non-absorbable solute
- deficiency in digestive enzymes
- lactulose
- magnesium salts
- sorbitol
What is exudative diarrhoea?
intestinal mucosal damage
- infections
- IBD
- Coeliac
- irradiation
- ischaemia
- colon cancer
What is secretory diarrhoea?
impaired electrolyte transport
- bacterial endotoxins
- bile salts
- laxatives
- hormone producing tumours
What is motility diarrhoea?
increased transit through GI tract
- IBS
- thyrotoxicosis
- autonomic neuropathy (DM)
- drugs
What are the 3 phases of malabsorption?
- luminal phase
- mucosal phase
- transport phase
What are the main processes underlying the luminal phase of malabsorption?
- reduced nutrient availability
- impaired fat solubilisation
- defective nutrient hydrolysis
What are the main processes underlying the mucosal phase of malabsorption?
- mucosal loss and damage
- enterocyte deficit
What are the main processes underlying the transport phase of malabsorption?
- vascular inflammation/disease
- lymphatic damage/disease
What clues in the history are important to consider for malabsorption?
- time course and severity
- impact of fasting on Sx
- volume and consistency of stools
- floating stools (steatorrhoea)
- malaena (bloody stools)
- nocturnal Sx
- constitutional Sx (anorexia/weight loss, fever, vomiting)
What are causes of diarrhoea that may present in the history?
PMHx:
childhood illness
IBS
previous GI surgery
Drugs
SHx/FHx: foreign travel dietary factors (intolerances) ethnicity contacts with similar Sx
What are some clinical features of malabsorption?
angular stomatitis, glossitis (iron/vitamin B12 deficiency)
osteomalacia (vitamin D and Ca deficiency)
Leukonichia (protein deficiency)
Tetany (Ca deficiency)
Bruising (Vitamin K deficiency)
Oedema (protein deficiency)
What are the main investigations ordered for diarrhoea?
Bloods
(FBC, ESR, U&E, TFTs, LFTs, CRP, iron studies, coeliac serology, vitamin B12 and folate)
Imaging
(barium/meal swallow study, CT/MRI)
Stool tests
(calprotectin, elastase, M C and S)
Functional studies
(hydrogen breath test - H. pylori, Schilling test)
Endoscopy
(OGD with D2 biopsies, colonoscopy, capsule endoscopy)
Gut hormone profile (Gastrin, glucagon, VIP, PP)
Urinary catecholamines
What is the Schilling test used to investigate?
Ordered to identify vitamin B12/cobalamin deficiency
Looks at how well vitamin B12 is absorbed from the GI tract in the patient (examination of stool)
Why are urinary catecholamines (CATU) ordered in diarrhoea?
some diseases increase catecholamine production, urinary screening is often coupled with a catecholamine blood test
In adults, urinary catecholamines are used to screen for PHAEOCHROMOCYTOMA
In children, CATU screening is performed to identify NEUROBLASTOMAS
What is irritable bowel syndrome (IBS)?
functional GI disorder a disorder of gut-brain axis interaction Sx are usually combos of the following: - motility disturbance - visceral hypersensitivity - altered mucosal and immune function - altered gut microbiota - altered CNS processing
What is the demographic for IBS in the western world?
~20% of adolescent/adult Westerns have symptoms consistent with IBS
What are the Rome IV criteria for IBS Dx?
recurrent abdo pain
for at least 1 day/week for last 3 months (on average)
associated with 2 or more of the following:
- related to defecation
- change in frequency of stool
- change in form/appearance of stool
Criteria fulfilled for preceding 3 months with Sx for the preceding 6 months for Dx
What are the main methods of management for IBS?
Ix/reassurance Diet Lifestyle advice Medications (symptom relief) - Anti-spasmodic (mebeverine, peppermint oil) - Altering intestinal transit (Opiates: loperamide, laxatives) - probiotics - Antidepressants
What is Coeliac disease?
inflammatory condition of small intestinal mucosa
mot marked proximally
improves morphologically when gluten is removed from diet
What is gluten?
breakdown product of wheat protein
Gluten: gliadins (alpha, omega, gamma) and glutenins subcomponents
The specific aa sequence found in gliadin is also found in rye and barley
What is the pathogenesis of Coeliac disease?
inherited auto-immune condition
HLA-DQ2 genotype (95% association, but not causal as genetic risk is polygenic)
HLA-DQ2 genotype present in 20% of population
likelihood of 1st degree relative having CD is 10-15%
Auto-antibodies:
- anti-gliadin
- anti-reticulin
- anti-endomysial
What is the prevalence of Coeliac in the UK?
iceberg effect in that only symptomatic CD (with +ve histology) is seen
There are also many other people with asymptomatic CD (positive histology) and latent CD (-ve histology)
What are the Sx of Coeliac that present during childhood?
failure to thrive/short stature
diarrhoea/steatorrhoea
vomiting (50% of patients)
abdo pain/distension
What are the Sx of Coeliac that present in adulthood?
fatigue (80-90%) anaemia (85%) diarrhoea/steatorrhoea (75-80%) weight loss mouth ulcers infertility
What are the criteria for Sx of Coeliac in adults?
4 intestinal biopsies
i) abnormal mucosa on gluten consumption (histological change may be minimal)
ii) improvement on gluten-free diet (over 3-6 months)
How long can it take for mucosal healing to occur after initiation of a gluten-free diet in Coeliac?
may take up to 2 year, or could remain incomplete
Sx should improve in 3-6 months of complete restriction of gluten
What are the histological markers of Coeliac disease?
flattening of cilia on enterocytes
erythema of duodenal mucosa
elongation of intestinal crypts
What is the sensitivity and specificity of the IgA anti-endomyosial test?
Sensitivity: 85-98%
Specificity: 97-100%
What is the sensitivity and specificity of the IgA anti-tTG?
Sensitivity: 95-98%
Specificity: 94-95%
What is tTG? What is its function?
tissue transglutaminase
deamidates the glutamine residues on gliadin
this makes it more immunogenic and increases the binding affinity to MHC class II molecules on T cells
-> stronger adaptive immune response generated
What is the sensitivity and specificity of the IgA anti-gliadin?
Sensitivity: 75-90%
Specificity: 82-95%
What is the sensitivity and specificity of the IgG anti-gliadin?
Sensitivity: 69-85%
Specificity: 73-90%
What other conditions are associated with coeliac disease?
(other autoimmune conditions) T1DM thyrotoxicosis IgA deficiency Sjogren's disease osteoporosis primary biliary cirrhosis
What is Sjogren’s disease?
F > M
affects body parts where fluid is produced e.g. tears and saliva
causes dryness in these areas
No cure for disease, treatments are for symptomatic relief
What is dermatitis herpetformis?
complication present in 2-5% of patients with CD
pr: 1:20,000 in UK
M>F
improved by gluten free diet
Dx: granular IgA at dermo-epidermal junction of unaffected skin
What are the treatment options of Coeliac disease?
gluten free diet
dietary supplements (Fe, folate, Ca, vitamin B12)
screening for bone abnormalities and hyposplenism
(prophylactic antibiotics may be given for the latter)
What are the benefits to a Coeliac sufferer adhering to a gluten-free diet?
improvement of Sx reduced risk of complications: - osteoporosis - malignancies - autoimmune diseases
What is the follow-up protocol for Coeliac patients?
6 monthly outpatients repeat small intestinal biopsy after 1st 6 months blood tests Sx assessment nutritional assessment dietary compliance
Close monitoring during pregnancy
What factors are important to check when there is a poor response/relapse of Coeliac?
- dietary compliance
- correct Dx
- co-incident disease
(ulcerative jejuna-ileitis, microscopic colitis, malignancy)
What types of malignancy are associated complications of Coeliac disease?
- lymphoma
- small bowel (adeno)carcinoma
- oesophageal/colonic carcinoma
