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81 Cards in this Set
- Front
- Back
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Diarrhoea
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Frequent stools (> 3/day)
&/or Soft-liquid stools |
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Types of Diarrhoea
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Physiological
◦osmotic ◦secretory ◦motility Clinical ◦small bowel ◦large bowel ◦steatorrhoea |
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Osmotic
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goes on fasting
osmotic gap in stool eg, lactase deficiency, laxatives, malabsorption |
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Secretory
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continues while fasting
no osmotic gap eg, hormone-secreting tumours, ibd, infections |
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Abnormal motility
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irritable bowel syndrome
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Small bowel diarrhoea
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large volume
liquid brown or pale no blood or mucus may contain undigested food audible borborygmi Pain - periumbilical Examples – coeliac disease, Crohn’s disease, lactase deficiency, drug-induced |
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Large bowel diarrhoea
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small volume
may contain blood and mucus straining, tenesmus Pain - lower abdomen Examples - ulcerative colitis, ischaemic colitis |
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Steatorrhoea
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Bulky
Pale Oily or greasy Very offensive Floating Difficult to flush Examples – pancreatic insufficiency, advanced coeliac disease and other small bowel mucosal disorders |
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Symptoms of malabsorption
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COELIAC DISEASE
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an immunologically-mediated disorder of the small intestine caused by dietary exposure to triggering proteins in wheat, barley and rye
the hallmark is villous atrophy which resolves after removal of the offending proteins The manifestations are often non-gastrointestinal |
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Immunogenic proteins in coeliac disease
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Wheat
◦gliadins Barley ◦hordeins Rye ◦secalins ALL generally refferred to as glutens |
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Genetics of coeliac disease
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Coeliac disease in relatives
First degree 5-10% HLA-identical siblings 30% Identical twins >75% + HLA DQ2 or DQ8 necessary but not sufficient |
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HLAs
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Coeliac disease and Tissue Transglutaminase
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◦Found in gut mucosa as a repair enzyme (cross links extracellular matrix proteins)
◦Deamidates glutamine in gliadin to glutamate ◦Deamidation increases affinity of HLA DQ2/8 antigen-presenting cells for gliadin ◦The gliadin-transglutaminse complex is presented to T cells ◦Immune response leads to tissue i.e THE COMPLEX is the antigen |
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Pathogenesis of coeliac disease
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COELIAC DISEASE
PREVALENCE |
Clinical: 1:300 to 1:1000
Silent: 1:100 Occurs in Caucasians and non-Caucasians UNDERDIAGNOSED (1 in 8) |
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The Syndrome of coeliac disease
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Antibody Testing in Coeliac Disease
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Small Bowel Biopsy Coeliac
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Coeliac Disease
Dx |
Small bowel biopsy is essential
Repeat biopsy after gluten-free diet (6 months or longer) Gluten challenge and rebiopsy may be needed in children (to DDx viral gastro causes) |
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Coeliac Disease NON-Dx criteria
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Coeliac Tx
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• No wheat, barley, rye, (oats)
• Strict • Life-long Benefits of a gluten free diet Improved nutrition Reversal of metabolic deficiencies Improvement in bone density Reduction in malignancy risk |
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IBD
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Inflammatory bowel disease - epidemiology
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Prevalence up to 1:1000
Developed > developing countries ◦increased prevalence as countries “westernise” Any age but maximal 15-35 and 50-70 Males = females |
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Ulcerative colitis
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confined to colon
rectum always involved continuous inflammation for a variable distance •proctitis to pancolitis mucosa only affected |
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Crohn’s disease
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any part of GIT
•mostly ileum, colon or both transmural inflammation •mucosa + submucosa •deep ulcers, fissures discontinous inflammation •“skip” lesions strictures and fistulae granulomas typical (70%) |
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AETIOLOGY OF INFLAMMATORY BOWEL DISEASE
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Genetics and Crohn’s disease
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Complex and non-Mendelian
Increased risk in families – 3-20x increased risk in 1st degree relatives Concordance for site and clinical type in families Heterogeneity in HLA II studies Crohn’s disease – NOD2, IL-23R, ATG16L1 Multiple loci identified in Crohn’s disease and ulcerative colitis |
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Ulcerative colitis
Symptoms |
- bleeding
- diarrhoea - constipation if proctitis (rectal) - pain if severe A mucosal disease |
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Crohn’s disease - distribution
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Crohn’s disease
Symptoms |
- abdominal pain - diarrhoea if colonic involvement - constipation if ileal disease - bleeding ~ 50% - weight loss - systemic symptoms – fever, malaise, etc - impaired nutrition, esp. children - stenosis/obstruction - fistulas
A transmural disease |
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Crohn’s disease - fistula
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entero-enteric enterocutaneous enterovesical rectovaginal perianal
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IBD – systemic complications
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Ulcerative colitis –and cancer risk
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Ulcerative colitis – increased cancer risk
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Diagnosis of IBD
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History
◦duration and nature of symptoms, F/H, etc Stool examination and culture ◦exclude infection Colonoscopy +/- other endoscopic modalities Radiology ◦CT, MR, barium studies, AXR Histopathology ◦granulomas specific for Crohn’s disease but 70% only ◦acute and chronic changes |
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Management of ulcerative colitis
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Medications
◦5 –aminosalicylic acid – sulphasalazine, mesalazine, olsalazine, balsalazide ◦corticosteroids - prednisone, budesonide ◦immunosuppressives - azathioprine/6-MP,methotrexate, cyclosporin, etc ◦biologics - infliximab, adalimumab Surveillance for carcinoma Severe or resistant disease – surgery (ileoanal pouch or ileostomy) |
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Ulcerative colitis surgical options
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Management of Crohn’s disease
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Nutrition
Medications ◦5 –aminosalicylic acid – sulphasalazine, mesalazine, olsalazine, balsalazide ◦corticosteroids - prednisone, budesonide ◦immunosuppressives - azathioprine/6-MP,methotrexate, cyclosporin, etc ◦biologics - infliximab, adalimumab ◦antibiotics if infection/abscess NO SMOKING! Surgery ◦resection ◦stricturoplasty ◦perinal disease |
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Irritable bowel syndrome
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A functional disorder of the gastrointestinal tract manifested by:
◦abdominal pain &/or ◦disturbed defaecation &/or ◦bloating/distension |
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Irritable bowel syndrome
Epidemiology |
◦10-15% of the population affected
◦20-50% of referrals to gastroenterologist ◦Females > males 2:1 ◦Any age 50% onset < 35years 90% onset <50 years ◦Important condition time lost from work (2nd only to the common cold) medical costs anxiety |
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Irritable bowel syndrome
Clinical features |
◦Abdominal pain
◦Altered bowel habit diarrhoea &/or constipation ◦Distension/bloating ◦Flatulence ◦Mucus ◦Upper GI symptoms ◦Non-GI symptoms |
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Extraintestinal symptoms in IBS
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so maybe a gut-brain syndrome
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Irritable bowel syndrome
Features against a diagnosis of IBS |
◦rectal bleeding
◦anaemia ◦weight loss ◦nocturnal symptoms ◦fever ◦first symptom > 50 years of age ◦recent change in symptoms MAIN THING IS NOCTURNAL SX not present in IBS |
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Lactose intolerance/lactase deficiency
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Common
◦10% adults ◦Asians/Africans > caucasians Can be secondary ◦gastroenteritis; giardiasis; coeliac disease, etc Symptoms similar to IBS ◦diarrhoea, flatulence, bloating, rumbling Diagnosis ◦history, SB biopsy, lactose breath test, lactose-free diet Treatment – lactose-free diet; lactase supplements |
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Chronic Diarrhoea
Basic Pathophysiology |
• Imbalance between absorption and secretion
– Gut secretes ~9L of liquid /day – Stool volume usually about 200mL/day – Major function of the colon is to absorb liquid • So….. – Increased secretion – Decreased absorption – Increased transit will all lead to increased liquid excretion |
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WARNING SIGNS
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• Significant weight loss
• Bleeding • Systemic symptoms (eg: fever, arthralgias) • Evidence of inflammation |
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• 23 year old PhD student at Sydney University
• In Sydney (from Hong Kong) for 2 years • Previously well • Episodic diarrhoea for ~12 months • Seems to be worse during term – “my supervisor is a jerk” • Characteristics: – Mostly post-prandial – Resolved during a 48hr fast – Associated periumbilical cramping, rumbling – “Mushy” – No blood – Up to 3-4 times per day – Otherwise feels well, weight stable – Good exercise tolerance, etc – No significant family history • Physical Examination – Well – Normal physique – Afebrile – Abdomen soft, non-tender – Normal bowel sounds – Otherwise normal • Rigid sigmoidoscopy: – Normal appearing rectal mucosa • Investigations: – Full blood count – Erythrocyte sed. rate – C-Reactive protein – Thyroid function – Stool microscopy/culture/sensitivity -all normal • Upper endoscopy: – Normal upper gut appearance – A diagnostic test was performed…… • Small bowel biopsy for disaccharridases: – Lactase 3 (20-135 U/g prot.) – Sucrase 80 (35-280 U/g prot.) – Maltase 270 (60-930 U/g prot.) Feels well after abstaining from milk products |
• -That all took weeks and cost thousands
• Nothing wrong with a clinical approach – Avoid lactose for two weeks – Then challenge Diagnosis = lactose intolerance • The main clue is that the diarrhoea resolved after a 48 hour fast – osmotic diarrhoea • Confirmed by – Normal endoscopy with selective intestinal lactase deficiency – Response to lactose reduced diet |
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Lactase Deficiency
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• Congenital
• Acquired (primary Adult) • Secondary |
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Acquired Lactase Deficiency
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• Usually develops before age 6
• 50% will develop symptoms with 200 ml milk • Bloating, discomfort, flatulence, diarrhoea |
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Lactase Deficiency World-Wide
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• Northern European: 2 to 15%
• Latino patients: 50 to 80% • Ashkenazi Jews: 60 to 80% • African Americans: 60 to 80% • American Indians: 80 to 100% • Asians: 95 to 100% |
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Diagnosis of Lactase Deficiency
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Clinical
• Association of typical symptoms with lactose intake, relief by 1 week lactose free diet and +ve re-challenge Special tests (usually not necessary) • Hydrogen breath test • Specific lactase assay of small bowel biopsy |
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Lactase Def. Mx
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• Intolerance (due to enzyme def.) is not
allergy • Reduce diary products – Small amounts of milk are OK – Lactase tablet or liquid – Lactose free milk – Soy milk • Maintain calcium intake – Tinned fish with bones (are you kidding???) – Calcium supplements |
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Chronic Diarrhoea
4 basic mechanisms |
• Exudation (bowel disease)
• Osmotic • Secretory • Motility |
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Osmotic Diarrhoea
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• Poorly absorbed osmotically active agent
within lumen • Faecal H2O rises in parallel • Diagnosis: – Stops when solute removed (or total fast) – Increased Osmotic gap |
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Osmotic gap
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• Osmotic gap = 290 - 2 x (Na+K)
• Stool cannot sustain osmotic gap with plasma so rather than osmolality rising, Na/K concentrations fall in presence of osmotic load |
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Causes of osmotic diarrhoea
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• Carbohydrate malabsorption
– Excessive ingestion of poorly absorbed CHO (lactulose, sorbitol, mannitol, fructose, fibre) – Malabsorption (lactase or other enzyme deficiency) • Other solutes – Bowel prep (PEG, citrate, sulfate, phosphate) |
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Case 2
• 56 year old with 2-3 loose BMs per day • Slowly progressive over 2 years • Feels lethargic but ~well • Good appetite • Lost 10kg over past year |
• Past history:
– 6 hospitalisations with abdominal pain in 1990s • Diagnosis of recurrent acute pancreatitis • No episodes of pain for >1year – Recent diagnosis of diabetes mellitus • On oral Rx – Practising Barrister – Smokes 50 cigs/day – Drank ~100g alcohol/day until mid 90’s • ~10 standard drinks • Characteristics of diarrhoea: – Minimal hypogastric cramping – 3-4 times/day – Large volume with oil droplets – Wife makes him use outside loo: • “Smells like someone cut a dog in half” – Difficult to flush – No blood – Confirmation of the “type” of diarrhoea – Confirmation of the underlying process • Confimation of the “type” of diarrhoea – 72 hour faecal fat determination (yuk): • 90 g fat (Normal <5g/day) • Confirmation of the underlying process: – Options: • Pancreatic exocrine function testing • Pancreatic imaging • Progress – Started on pancreatic enzyme replacement with each meal – Resolution of diarrhoea – Gaining weight |
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Rumbing noise
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means inc peristalisis
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Hypogastric cramping
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means clonic sounding
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Mechanism of diarrhoea in
chronic pancreatitis |
• Maldigestion - failure to digest fat when
<10% function remains. Protein/cho maldigestion is lesser problem • Presentation – abdominal pain (pancreatic), – weight loss, – Diarrhoea, vitamin deficiencies, and – Diabetes often co-exists |
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Maldigestion v Malabsorption
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• Maldigestion
– Digestion takes place within the lumen – Requires enzymes, bile salts, correct pH, appropriate motility/contact time – eg pancreatic failure • Malabsorption – Absorption is a mucosal function – Requires intact mucosa, brush border enzymes (transport, disaccharidases), blood & lymph – eg coeliac disease |
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Management of chronic alcoholic
pancreatitis |
• Abstinence from alcohol
• Enzyme supplementation • Acid suppression • Analgesia – Significant risk of opioid dependence • Endoscopic therapy? • Surgery? |
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When someone says they are a barister
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think alcholic
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Case 3
• 25yr old with long history of intermittent “nagging” symptoms: – Bloating – Loose stools – Lethargy – Preesented when rejected from donating blood due to anaemia • Hb:110; microcytic |
Coeliac Disease (Sprue)
• Hypersensitivity to gluten (protein) – Wheat – Barley – Rye • Corn and rice (but not oats) are OK • Broad Spectrum of Disease – Australian Study (Busselton, WA): – 1:250 – 50% asymptomatic |
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Pathogenesis of Coeliac
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• DQ2: 90% of coeliacs
20% of general population • 10% have a first degree relative with CD • Autoantigen: Transglutaminase (tGT) – Catalyses glutamine to glutamate – Deamidates glutamine at posn 65 of A-gliadin – The tGT-gliadin complex stimulates an immune response in coeliac disease |
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Common Features of Coeliac
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• Steatorrhoea (most do NOT have this)
• Osteomalacia / osteoporosis • Anaemia (Fe def. / Folate def.) • Miscarriages • Splenic atrophy • Angular stomatitis • Weight loss • Abdominal pain, bloating • Depression • Lethargy |
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Case 4
• 22 year old medical student • 3 month history of diarrhoea • Associated generally unwell – Lethargic – Lost ~2kg • Characteristics: – Up to x10 per day – Small amounts – Assoc. hypogastric cramping – Mushy, “slimey” – Noticed small amount of blood ~50% of time – Feeling on incomplete evacuation • No recent travel or antibiotics • Investigations: – Full blood count Mild normocytic anaemia Mild leucocytosis – Eryth. sed. Rate 50mm/Hr (N: <10mm/Hr) – C-Reactive protein 60 U/L (N: <5U/L) – Stool Examination: • No parasites • Profuse RBCs and WBCs • Normal culture • A diagnostic test was performed……. |
• DDX
– Ulcerative colitis – Crohn’s colitis – Infective colitis • Biopsies consistent with ulcerative colitis • Rx: – rectal steroid foam – Oral sulphasalazine |
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Sigmoidoscopy in IBD
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Diarrhoea in IBD
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• Exudative
• Associated with inflammation • Stool contains mucus, exudate and blood • Continues despite fasting • Poor rectal compliance = frequent, small stools |
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Approaches to diarrhoea
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1. Are we sure this is diarrhoea?
eg: incomplete evacuation = ???? Rectal mass 1. Does it fit a common disorder? 3. Pathophysiological approach |
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Commonest causes of “diarrhoea”
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• Irritable Bowel Syndrome
• CHO malabsorption (lactose intolerance) • Recent antibiotics (C. difficile or overgrowth) • Drugs (and alcohol) |
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Irritable Bowel Syndrome
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• Clinical hallmark:
– abdominal pain associated with altered bowel habit, pain relieved by defaecation • Absence of other pathology • Pathophysiology: – altered motility of unknown cause (minimal inflammation, altered CCK, serotonin and neurokinins) with abnormal sensitivity to distension • Beware of patients with water bottles |
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Alcohol and diarrhoea
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• Altered motility
• Altered permeability • Small intestinal mucosal injury separation of the tip of the villus epithelium forming blebs (malabsorption of various nutrients) • Pancreatic disease (malabsorption) |
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Pseudo-diarrhoea
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• Faecal impaction may also present
with diarrhoea • Some people with normal stool volume complain of diarrhoea |
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Faecal Incontinence
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• May accompany diarrhoea
– Severe &/or – Elderly • Many report “diarrhoea” rather than incontinence due to embarrassment – Careful history taking – Assess rectal tone, neurological examination |
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Pathophysiological Approach to
Diarrhoea |
• Altered bowel integrity
• Osmotic • Secretory • Motility |
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Altered bowel integrity
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• Bowel diseases, eg inflammation, neoplasia,
infection (eg HIV) • Fistula (eg: s. bowel to colon) • Short bowel – BUT diarrhoea is not usually a prominent feature of small bowel Crohn’s disease • Localise to site (eg large vol-small bowel) • Endoscopy/biopsy/ barium studies |
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Osmotic diarrhoea
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• Commonest example is lactose intolerance
• Sorbitol • NB: Lactulose • Non-absorbable solutes attract water into lumen • Surreptitious laxative abuse |
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Secretory diarrhoea
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• Hallmark is continuing diarrhoea despite
complete fast • May need to admit and keep nil by mouth with IV fluids • Absence of blood or inflammation • Usually acute diarrhoea, not chronic |
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Commoner secretory diarrhoeas
(none are common) |
• Luminal secretogogue
– Bile salt diarrhoea • Loss of <100cm terminal ileum – Bacterial toxins • Cholera toxin • Circulating secretogogue – Tumours (VIPoma, MTC, Carcinoid, Z-E syndrome) |
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Motility
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• Too fast
– Thyrotoxicosis – Post-abdominal surgery – IBS/ just before a viva exam • Too slow (produce bacterial overgrowth) – Primary intestinal hypomotility (elderly) – Scleroderma, diabetic autonomic neuropathy • Abnormal – Irritable bowel syndrome |
