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46 Cards in this Set

  • Front
  • Back
definition of traveller's diarrhea
*gastroenteritis
*affects travellers from developed nations who go to developing nations
most common pathogenic cause of traveller's diarrhea
enterotoxigenic e. coli
at risk populations
*immunocompromised
*elderly
*hospitalised
which foods commonly cause diarrheal illness, what pathogens are they associated with?
*seafood: hep A and E, v. cholerae, salmonella
*chicken: salmonella, shigella, campylobacter
*raw meat: E. coli
*mayonnaise: salmonella, s.aureus
severe epidemic diarrheal illnesses occur in _________ and are caused by ___________
*India, Bangladesh
*v. cholerae
countries most affected by diarrheal illness
*SE Asia
*Africa
*Latin America
what is osmotic diarrhoea?
occurs when there is high concentration of solute in lumen, drawing water into lumen
osmotic diarrhea - better or worse with fasting?
stops when fasting
example of osmotic diarrhoea
malabsorption
what is secretory diarrhoea
involves active intestinal secretion of fluid and electrolytes + decreased absorption
secretory diarrhoea - better or worse with fasting?
persists during fasting - i.e. no better or worse
example of secretory diarrhea
enterotoxins (E.coli, cholerae)
what is inflammatory diarrhea?
occurs due to damage to intestinal mucosa; there is loss of fluids and blood + decreased absorption
examples of inflammatory diarrhea
Shigella dysentery
IBD
common causes of diarrhea
*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
v. cholerae - incubation period; duration
incubation period - 2-3 days
duration - 7 days
pathophysiology of v. cholerae
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)
pathogenesis of salmonella typhi infection
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
how many people become carriers of salmonella typhi
1-3%
clinical stages of salmonella typhi infection
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%
pathophysiology of IBD
*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
how does NOD2 gene contribute to IBD
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
list pharmacotherapies in the order that they should be used in patient with IBD
*aminosalicylates
*corticosteroids
*immunomodulators

also consider non-pharmacological options (e.g. avoid aggravating foods) and surgical management
gives examples of aminosalicylates
*sulfasalazine
*mesalazine
MoA of aminosalicylates
unknown; probably anti-inflammatory effect through inhibition of PG and leukotriene synthesis
give an example of corticosteroids used in IBD
methylprednisolone
MoA of corticosteroids in IBD
*alters gene expression
*anti-inflammatory effect
give example of immunomodulator used in IBD
infliximab
MoA of immunomodulators in IBD
*monoclonal antibody against TNF-alpha
*reduces inflammation
pathophysiology of pseudomembranous colitis
*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
what clinical features will make one suspect that someone has pseudomembranous colitis
*fever, pain, bloody diarrhoea
*occurs following antibiotic use
*nosocomial setting
when should diarrhoea be further investigated?
*prolonged illness (>1 week)
*immunocompromised/elderly
*travel history
*outbreak of infection
*dysenteric (pain, fever, severe diarrhoea with blood and mucus)
what key investigation do you perform in someone with severe diarrhoea
*stool microscopy/culture looking for ova, cysts, parasites; test for C. difficile toxins
metabolic consequences of severe, prolonged diarrhoea
*loss of water --> hypovolaemia --> shock or ATN
*loss of electrolytes
- decreased bicarb --> metabolic acidosis
- decreased K --> arrythmias
*loss of blood --> Fe deficiency anaemia
definition of IBS
*chronic/recurrent abdo pain
*bloating
*altered bowel habits

all of these unexplained by biochemical/structural abnormalities
possible pathogenic factors contributing to IBS
*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
epidemiology of CD vs UC
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
areas affected CD vs UC
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
macroscopic features: CD vs UC
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
microscopic features: CD or UC
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
clinical features: CD vs UC
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
Investigations for UC
*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
MoA of sulfasalazine
*sulfa drug of unknown mechanism
*poorly absorbed anti-inflammatory agent with greatest action in intestines
mechanical obstruction more likely in UC or CD
CD
how can UC cause toxic megacolon?
severe UC --> damage to muscularis propria and neural plexus --> shutdown of neuromuscular function --> massive dilatation of bowel --> leakage of faecal matter/perforation --> peritonitis
Main complications of UC
*toxic megacolon --> perforation
*peri-anal diseases (fissure, fistula)
*bleeding
*colorectal adenocarcinoma