GI - Diarrhoea & malabsorption Flashcards
Define diarrhoea
- volume
- frequency
Stool > 200 g/day and number of movements > 3/day
What are the mechanisms that cause diarrhoea?
osmotic, secretory, inflammatory & altered intestinal motility (can occur in combination)
What (2) are small volume stools typical of?
colonic diseases and IBS
What (2) are large volume (>750ml/d) stools typical of?
small bowel disease and secretory diarrhoea
What tests on faeces could help establish the mechanism or diagnosis for diarrhoea?
- MCS of stool
- Faecal electrolytes & osmolarity
- faecal fat
- faecal elastase
- C. difficile toxin
- faecal calprotectin
- faecal laxative screen
- faecal alpha-1 antitrypsin
What does Faecal elastase indicate?
Presence of faecal elastase = marker of exocrine pancreatic sufficiency
Hence lack of = insufficiency
What does Faecal calprotectin indicate?
marker of gastrointestinal inflammation
What does Faecal laxative screen indicate?
anthroquinones, bisacodyl, phenolphthalein
What does Faecal alpha-1 antitrypsin screen indicate?
marker of protein losing enteropathy
Describe osmotic diarrhoea
- cause
- stool volume
- stool osmotic gap
- effect of fasting
- stool leukocytes
- H2/methane breath test
- Presence of excess unabsorbed substrates in gut lumen
- Common cause: Fermentable carbohydrate malabsorption (FODMAPs)
- Stool volume typically 100)
- Stops with fasting
- Not present (normal faecal calprotectin)
- Increased breath hydrogen with malabsorption
Describe secretory diarrhoea
- cause
- stool volume
- stool osmotic gap
- effect of fasting
- stool leukocytes
- Due to active anion secretion from enterocytes
- Bacterial toxins (cholera, toxigenic E.coli), hormone secreting tumours (e.g. carcinoid, gastrinomas), laxative abuse, hyperthyroidism
- Stool volume > 1 litre/d, watery
- Normal osmolality (osmolar gap
Describe inflammatory diarrhoea
- cause
- stool volume
- stool leukocytes
- Altered membrane permeability →exudation of protein, blood, mucus
- Invasive bacteria (Shigella, Salmonella, Campylobacter, Clostridium difficile), Entamoeba histolytica, cytomegalovirus colitis, inflammatory bowel disease (IBD)
- Volume of faeces usually small
- Increased red blood cells and leukocytes (elevated faecal calprotectin). Stools may contain visible (‘frank’) blood and be associated with urgency, tenesmus and constitutional upset e.g. fever
Describe rapid transit as a cause of diarrhoea
- mechanism
- causes
Inadequate time for absorption of fluid (& nutrients)
Irritable bowel syndrome (IBS), thyrotoxicosis, diabetic neuropathy
Describe slow transit as a cause of diarrhoea
- mechanism
- causes
Bacterial overgrowth -> nutrient consumption -> bile salt inactivation (unable to solubilise micelles
Intestinal stasis due to anatomical defects (strictures, blind loops, surgical procedures)
List (4) classes of causes of luminal phase maldigestion
- Mechanical - Mixing disorders
- Post-gastrectomy - Reduced nutrient availability
- Co-factor deficiency e.g. pernicious anaemia
- Bacterial overgrowth (nutrient consumption) - Defective nutrient hydrolysis (digestion)
- Pancreatic insufficiency e.g. chronic pancreatitis - Reduced fat solubilisation (reduced bile salt concentration)
- Cholestasis, bacterial overgrowth
List (3) classes of causes of mucosal phase maldigestion & defective transport
- Inadequate absorptive surface
- Intestinal resection or bypass due to disease - Diffuse mucosal disease
- Coeliac disease, Crohn’s disease, Giardia infection
- Brush border enzyme deficiency e.g. lactase - Mucosal absorptive defects
- lymphoma, lymphatic obstruction, radiation damage
- vascular problems
42yo male
Three months of feeling unwell
Loose-stools, 6-8 times a day (normally once every 1-2 days)
Often bloody with mucous mixed in
Crampy abdominal pain prior to defecation
Urgency and tenesmus
Occasional nocturnal diarrhoea
Afebrile. Looks tired. Pale.
Abdominal examination: unremarkable
Constitutional symptoms: Feeling lethargic & sleeping poorly, occasionally “feverish”; weight loss 2-3 kg in past 3 months
Recent travel: 6 months ago holiday in Thailand. Was not unwell there.
Social History: Lawyer, lives with partner Paul
Mechanism of diarrhoea? DDx?
The clinical presentation is of bloody, mucousy diarrhoea with tenesmus This is usually due to an INFLAMMATORY mechanism
Common causes are:
- Infection (“dysentery”) e.g. Salmonella, Shigella, Yersinia, Entamoeba histolytica (amebiasis) and cytomegaloviral colitis
- Inflammatory bowel disease
- Ischaemic colitis
- Radiation colitis
How do you confirm the diagnosis of IBD?
colonoscopy and colonic biopsies
Describe what you’d see on colonoscopy & colonic biopsy of UC
- superficial ulceration with distortion of crypts
- acute and chronic diffuse inflammatory infiltrate
- goblet cell depletion
- crypt abscesses
- lymphoid aggregates but no granulomas
Rx of ulcerative colitis
–5-ASA compounds (sulphasalazine) and steroids.
–Topical therapy (suppositories/enemas) used for distal disease.
–Immunosupressants used in severe or recurrent disease
–Surgery for severe or refractory cases (this is curative)
Rx of Crohn’s disease
Steroids, 5-ASA compounds, immunosupressants (e.g. azathioprine, methotrexate), biologicals (monoclonal Ab), surgery
26yo female
~ 10 year history of intermittent diarrhoea with bloating & flatulence
Up to 2-5 bowel motions per day (erratic), no blood
No weight loss
Stress, dairy products and some fruits make her symptoms worse
She tried a gluten free diet on advice of a friend and felt better.
SHx: Office manager, lives with partner
FHx: Sister is “gluten intolerant”
PHx: Depression
Meds: Nil. Non-smoker.
DDx?
- Irritable bowel syndrome
- Coeliac disease
- Infection such as Giardia
- Inflammatory bowel disease
How do you diagnose irritable bowel syndrome?
1. Typical clinical Hx “Rome III” criteria •Symptoms for at least 3 months •Recurrent abdominal discomfort or pain associated with (2 or more of): –Improvement of symptoms with defecation –Change in stool appearance (form) –Change in stool frequency
- Exclude other Dx
Presence of “red-flag” symptoms or signs such as weight loss, rectal (PR) bleeding, nocturnal symptoms, and age >45 should prompt further investigation before a diagnosis of IBS is made
How do you diagnose coeliac disease? (c.f. screen)
- demonstration of small bowel damage (villous atrophy, crypt hyperplasia and raised intra-epithelial lymphocytosis) whilst a person is consuming gluten, and
- improvement in histology, serology and clinical picture following a gluten free diet
How do you screen for coeliac disease?
–blood test measuring antibodies to transglutaminase (tTG-IgA) and gliadin (“deamidated gliadin peptides”, DGP-IgA and DGP-IgG).
–The DGP assay replaces the older and less accurate anti-gliadin antibodies (AGA-IgA, AGA-IgG) test.
If antibodies are abnormally elevated (positive), a small bowel biopsy showing villous atrophy is required to confirm the diagnosis
What (3) might cause false negative serology results in Coeliac disease screening?
–Gluten free diet (especially if > 6 weeks)
–IgA deficiency (seen in 3% of coeliac disease – that is why the total IgA level is measured or the IgG isotype of DGP assessed
–Immunosuppression e.g. prednisolone
How can you test for coeliac disease if a person is already following a gluten free diet?
HLA-DQ2/8 gene test. This is seen in most (99.6%) patients with coeliac disease. If negative, it can be used to exclude coeliac disease.
6 week gluten challenge (~4 serves gluten/day) followed by small bowel biopsy
How can you exclude infection and inflammatory bowel disease?
- Faecal assessment
- Inflammatory markers
- Gastroscopy and colonoscopy with biopsies may be required in some instances
(4) pathogenesis of irritable bowel syndrome
Serotonin (5-HT) a key mediator in IBS
- disordered intestinal motility
- altered perception of nociceptive stimuli (visceral hypersensitivity)
- psychogenic factors
- post-infectious component in some people
“Stress” and small bowel bacterial overgrowth can be a trigger
Role of genetics is unclear
Rx of IBS
•Dietary modification
- Avoiding common food triggers – FODMAPs
- Avoiding caffeine, alcohol, smoking
•Pharmacological therapies
- Probiotics
- Antispasmodics, antidiarrhoeals, laxatives
- Antibiotics (Rifaximin) to treat bacterial overgrowth
- ? Increase fibre ? Decrease fibre
•Psychological therapies
-Relaxation, cognitive behaviour therapy, hypnotherapy
62yo male
6 month history of pale, smelly, greasy stools, difficult to flush
Frequently feels bloated and nauseated after meals. More lethargic and has lost 15 kg weight in past 6 months. Denies drinking alcohol for the past 2 years
PHx:
- Hypertension
- Ex-smoker.
- Heavy drinker in the past
- Alcoholic pancreatitis 10 years ago, subsequent two recurrent episodes
O/E: Bruises on arm. Evidence of subcutaneous fat loss. Several spider naevi on chest. Abdominal exam normal. No hepatic flap or fetor
DDx?
- Defective nutrient hydrolysis (digestion): Pancreatic insufficiency due to chronic pancreatitis or pancreatic cancer
- Reduced nutrient availability: Poor oral intake (especially if still an alcoholic); bacterial overgrowth
- Reduced fat solubilisation (reduced bile salt concentration): Cholestasis (failure of bile flow) due to underlying liver disease; bacterial overgrowth will inactivate bile salts
- Diffuse mucosal disease: e.g. coeliac disease, Giardia infection, brush border enzyme deficiency
- Mucosal absorptive defects: e.g. lymphoma, lymphatic obstruction
What features suggest malabsorption might be present and how can we confirm it?
- History of steatorrhoea, lethargy, weight loss
- Examination findings of bruising, muscle wasting, weight loss
Confirm it by:
•Nutrient levels (Iron studies, B₁₂, folate, vitamins)
•Faecal assessment: Increased faecal fat
Differing clinical picture associated with peritonitis
- red
- grey
- white
–Red: vasodilated, warm peripheries, flushed (bacterial peritonitis)
–Grey: shutdown, clammy, sweaty (chemical peritonitis/severe pancreatitis/MI/PE)
–White – pale, shut down, cold peripheries (haemorrhagic shock)
