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46 Cards in this Set
- Front
- Back
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definition of traveller's diarrhea
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*gastroenteritis
*affects travellers from developed nations who go to developing nations |
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most common pathogenic cause of traveller's diarrhea
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enterotoxigenic e. coli
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at risk populations
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*immunocompromised
*elderly *hospitalised |
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which foods commonly cause diarrheal illness, what pathogens are they associated with?
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*seafood: hep A and E, v. cholerae, salmonella
*chicken: salmonella, shigella, campylobacter *raw meat: E. coli *mayonnaise: salmonella, s.aureus |
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severe epidemic diarrheal illnesses occur in _________ and are caused by ___________
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*India, Bangladesh
*v. cholerae |
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countries most affected by diarrheal illness
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*SE Asia
*Africa *Latin America |
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what is osmotic diarrhoea?
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occurs when there is high concentration of solute in lumen, drawing water into lumen
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osmotic diarrhea - better or worse with fasting?
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stops when fasting
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example of osmotic diarrhoea
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malabsorption
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what is secretory diarrhoea
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involves active intestinal secretion of fluid and electrolytes + decreased absorption
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secretory diarrhoea - better or worse with fasting?
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persists during fasting - i.e. no better or worse
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example of secretory diarrhea
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enterotoxins (E.coli, cholerae)
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what is inflammatory diarrhea?
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occurs due to damage to intestinal mucosa; there is loss of fluids and blood + decreased absorption
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examples of inflammatory diarrhea
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Shigella dysentery
IBD |
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common causes of diarrhea
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*infective
- bacterial: salmonella, shigella, campylobacter, e. coli, s. aureus, clostridium - viral: norovirus, rotavirus, adenovirus, astrovirus - fungal: histoplasmosis - parasitic: giardia intestinalis, amoebic dysentery, schistosomiasis *non-infective - IBD, pseudomembranous colitis, diverticulitis, malignancy, drugs, malabsoprtion *endocrine - thyrotoxicosis, zollinger-ellison syndrome |
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v. cholerae - incubation period; duration
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incubation period - 2-3 days
duration - 7 days |
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pathophysiology of v. cholerae
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v. cholerae produces exotoxins --> bind to small intestine mucosa --> secretion of Cl and HCO3 ions into gut lumen --> water flows into lumen --> secretory diarrhoea (up to 13L/day)
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pathogenesis of salmonella typhi infection
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ingestion --> invades small intestinal mucosa --> enters Peyer's patches --> multiplies IN the macrophages --> transported to mesenteric LNs --> thoracic ducts --> blood stream:
*secondarily infect organs, esp those with reticulo-endothelial cells i.e. bone marrow, spleen, liver *can also infect brain, bone, heart and lung *gallbladder can be infected by haematogenous spread/direct extension from liver infection --> bacteria enters small intestine in larger no.'s than primary encounter --> strong inflammatory response in Peyer's patches --> ulceration and risk of perforation |
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how many people become carriers of salmonella typhi
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1-3%
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clinical stages of salmonella typhi infection
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1st week: fever, constipation (illeocecal valve blocked by swollen Peyer's patches)
2nd week: bacterial emboli to skin (<5 blanching "rose spots"); toxic, febrile, soft splenomegaly 3rd week: weight loss, toxic, febrile, psychosis/confusion/apathy, tachycardia, basal crepitations, marked abdo distention, liquid foul yellow green diarrhoea 4th week: recovery; relapses in 10% |
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pathophysiology of IBD
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*results from exaggerated and unregulated immune response to commensal microbes in the gut
*poorly understood important factors *genetic - positive FH is risk factors; - NOD2 gene, which encodes protein in gut epithelial cells *role of intestinal flora - defects in the intestinal wall allows luminal flora to access mucosal lymphoid tissue *abnormal T cell function --> excessive T cell activation |
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how does NOD2 gene contribute to IBD
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NOD2 gene encodes a protein in gut epithelial cells; when this protein binds to microbil components, NOD2 activates NF-kB , a transcription factor that induces cytokine production --> chronic inflammation
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list pharmacotherapies in the order that they should be used in patient with IBD
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*aminosalicylates
*corticosteroids *immunomodulators also consider non-pharmacological options (e.g. avoid aggravating foods) and surgical management |
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gives examples of aminosalicylates
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*sulfasalazine
*mesalazine |
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MoA of aminosalicylates
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unknown; probably anti-inflammatory effect through inhibition of PG and leukotriene synthesis
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give an example of corticosteroids used in IBD
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methylprednisolone
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MoA of corticosteroids in IBD
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*alters gene expression
*anti-inflammatory effect |
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give example of immunomodulator used in IBD
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infliximab
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MoA of immunomodulators in IBD
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*monoclonal antibody against TNF-alpha
*reduces inflammation |
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pathophysiology of pseudomembranous colitis
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*caused by C.difficile which is a commensal gut organism --> proliferates after exposure to broad spectrum antibiotics
*C. difficile --> cytotoxins --> inflammation in colon *pseudomembrane (consisting of inflammatory cells and debris) clings to colon membrane |
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what clinical features will make one suspect that someone has pseudomembranous colitis
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*fever, pain, bloody diarrhoea
*occurs following antibiotic use *nosocomial setting |
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when should diarrhoea be further investigated?
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*prolonged illness (>1 week)
*immunocompromised/elderly *travel history *outbreak of infection *dysenteric (pain, fever, severe diarrhoea with blood and mucus) |
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what key investigation do you perform in someone with severe diarrhoea
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*stool microscopy/culture looking for ova, cysts, parasites; test for C. difficile toxins
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metabolic consequences of severe, prolonged diarrhoea
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*loss of water --> hypovolaemia --> shock or ATN
*loss of electrolytes - decreased bicarb --> metabolic acidosis - decreased K --> arrythmias *loss of blood --> Fe deficiency anaemia |
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definition of IBS
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*chronic/recurrent abdo pain
*bloating *altered bowel habits all of these unexplained by biochemical/structural abnormalities |
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possible pathogenic factors contributing to IBS
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*abnormal gut motility
- delayed transit in constipation predominant IBS; accelerated transit in diarrhea predominant IBS - may benefit from anticholinergics *psychiatric disorders - higher prevalence of anxiety, depression and personality disorders in patients than controls; - stress episodes can exacerbate IBS; - SSRIs may relieve IBS *food intolerance - fructose, lactose, sorbitol can exacerbate IBS in some patients *neural hypersensitivity - hyperexcitable dorsal horn neurons in response to gut irritation; genetic susceptibility |
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epidemiology of CD vs UC
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CD
*3/100,000 *peak - 20s-30s *more common in white and Jews *smoking is RF UC *more common - 4-12/100,000 *peak: 20-25 *more common in whites and females *NOT smoking is a RF |
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areas affected CD vs UC
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CD:
*all parts but most commonly - small intestine ALONE (40%) - small intestine + colon (30%) - colon ALONE (30%) UC: - colon (only mucosa and submucosa) - disease begins in rectum and ascends |
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macroscopic features: CD vs UC
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CD:
*skip lesions *transmural - thick rubbery intestinal wall due to inflammation, fibrosis, oedema + hypertrophy of MP *strictures, fistulas, sinus formation (esp. perinanal) UC: *affected areas are continuous (no skip lesion) *affects only mucosa and submusoca *pseudopolyps (areas od attempted regeneration) *no strictures, sinuses or fistulas |
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microscopic features: CD or UC
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CD:
*mucosal inflammation (with neutrophils and lymphocytes) *crypt abcesses *chronic mucosal damage --> loss of villi *fissuring, stricture (fibrosis of mucosa, submucosa, MP) *transmural inflammation *non-caseating granulomas (50%) UC: *mucosal inflammation *crypt abcesses *mucosa ulceration with ulcers filled with granulation tissue *flattening of villi *no granulomas *increased risk of dysplasia --> carcinoma |
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clinical features: CD vs UC
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CD:
*intermittent attacks of fever, diarrhoea, abdo pain (separated by months) *may have occult blood loss --> anaemia *flare-ups may be induced by emotional stress *complications from stricture, sinus, fistula formation (e.g. B12 deficiency from terminal ileal involvement) *Extra-intestinal manifestations: - bones/joints - osteoporis, polyarthritis - skin: erythema nodosum - nails - clubbing - eyes - iritis, scleritis - kidneys - nephroliathiasis *5x increase in GIT cancer risk UC: - intermittent bloody, mucoid diarrhoea with crampy lower abdo pain - 30% of patients needs colectomy in 1st three years - extra-intestinal manifestations *bones/joints, eyes, skin, nails, kidneys as with CD - 20-30x increase in CRC risk |
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Investigations for UC
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*FBC, ESR, CRP, EUC, Fe studies, coag studies
*Stool - MCS, O + parasites, WBC, C. difficile *3 views of abdo (erect, supine, & chest) --> obstruction and perforation *CT colonography *Colonoscopy/sigmoidoscopy + biopsy |
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MoA of sulfasalazine
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*sulfa drug of unknown mechanism
*poorly absorbed anti-inflammatory agent with greatest action in intestines |
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mechanical obstruction more likely in UC or CD
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CD
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how can UC cause toxic megacolon?
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severe UC --> damage to muscularis propria and neural plexus --> shutdown of neuromuscular function --> massive dilatation of bowel --> leakage of faecal matter/perforation --> peritonitis
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Main complications of UC
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*toxic megacolon --> perforation
*peri-anal diseases (fissure, fistula) *bleeding *colorectal adenocarcinoma |
