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GI - anna > Gastroenteritis > Flashcards

Gastroenteritis Flashcards

1
Q

what are the risk factors of gastroenterititis

A 
Malnutrition (micronutrient) deficiency
Closed/ semi-closed communities
Exposure to contaminated food/water /travel
Winter congregating/ summer floods
Age <5 , not breastfeeding
Older age
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2
Q

pathogenesis of gastroenteritis

A

Osmotic/Malabsorptive (various mechanisms)
Secretory (toxin mediated)
Intestinal tight junction dysruption (leak-flux)
Inflammatory (mucosal invasion)
Intestinal motility (through the enteric nervous system)

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3
Q

how does diarrhoea happen

A

Adherence/attachment to the gastrointestinal mucosa
Cellular invasion
Production of exotoxins
Changes in epithelial cell physiology
Loss of brush border digestive enzymes, and/or cell death
Increased intestinal motility, net fluid secretion, influx of inflammatory cells, and/or intestinal hemorrhage

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4
Q 
≥3 unformed stolls/day more than 250g/day
no other cause (exclude laxatives)
hold shape of container
departure from normal bowel habit
use bristol stool chart
A

diarrhoea

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5
Q

inflammation of the intestine particularly the colon causing diarrhoea associated with blood and mucus
generally associatated with fever, abdominal pain, and rectal tenesmus

A

dysentry

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6
Q

volume of diarrhoea in large bowel and small?

A

Large volume tends to be small bowel, large bowel small volume

Yersinia enterocolitica may mimic appendicitis as it may invade mesenteric nodes

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7
Q

what should you ask in a history for gastroenteritis

A

associated symptoms
exposure history and predisposing factors
travel history
stool appearance

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8
Q

1 to 6 hours
gram positive
from starchy food (reheated Rice)
profuse vomiting

A

bacillus cereus

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9
Q 
1-6 hrs
gram positive coccus
preformed toxin in food, rapid absorption, acts on vomiting centres on brain
food left at room temp
milk, meat, fish
A

staphylococcus aureus

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10
Q

investigations for gastroenteritis

A

stool sample

Blood culture

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11
Q

gram negative rod, nonmotile, anaerobic, enterobacteriaceae

four species

A

shigella

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12
Q

what are the 4 species of shigella

A

s. dysenterae (serogroup A), S. flexneri (serogroup B), shigella boydii (C), s sonnei (D)

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13
Q

what species of shigella can cause the hemolytic-uremic syndrome (HUS) and what is it mediated by ?

A

s. dysenterae 1

and shiga toxin (Stx)

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14
Q

what are the symptoms of a shigella infection

A 
fever
abdominal pain
mucoid diarrhoea
watery/bloody diarrhoea
vomiting
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15
Q

what does shiga toxin do

A

binds to receptors found on renal cells, RBC and others
inhibit protein synthesis
cause cell death

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16
Q

ecoli classes

A

enteroToxigenic(ETEC)
enteroPathogenic (EPEC)
enteroInvasive (EIEC)
enteroAggregative (EAIC)

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17
Q

how does Ecoli produced toxin

A

Adhere to the intestinal epithelial cells, and elaborate Shiga toxin

Toxins bind to absorptive enterocytes on the luminal surface of the small and large intestines, enter the cell, and irreversibly inhibit protein synthesis, resulting in death of enterocytes.

Shiga toxins can then enter the bloodstream via damaged intestinal epithelium and cause the death of vascular endothelial cells by the same mechanism

Endothelial cell lysis is accompanied by platelet activation and aggregation, cytokine secretion, vascular constriction contributing to fibrin deposition, and clot formation within the capillary lumen

Microangiopathy propagates distally as the toxins are carried to the kidneys, causing the clinical syndrome of hematuria and renal failure (HUS). The development of HUS is associated primarily with serotypes that produce Shiga toxin 2

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18
Q 
bloody diarrhoea
very low infectious dose
food - beef (raw milk, water)
person to person direct/indirect
children and elderly at risk of complications
outbreak potential
A

E Coli 0157

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19
Q

effect of verotoxin (VTEC)

A

mild to severe (Death)
bloody diarrhoea
haemorrhagic collitis

20
Q

Haemolytic Ureamic Syndrome (HUS) presentation

A 
abdomen pain
fever
pallor
petechiae
oliguria
blood diarrhoea
under 16 years old
21
Q

Haemolytic Ureamic Syndrome (HUS) signs

A 
High white cells
Low platelets
Low HB
Red cell fragments
LDH>1.5 x normal
May develop after diarrhoea stopped
22
Q

Haemolytic Ureamic Syndrome (HUS) investigations and what treatments should be avoided

A

Send stool culture samples: all patients with bloody faeces

Send U&E, FBC, film, LFT, clotting, urine, (dipstick/micro), lactate dehydrogenase

Close monitoring
Admission usually needed
Look for: acute renal failure, thrombocytopaenia, haemolytic anaemia

NO antibiotics: may precipitate HUS
NO anti-motility agents
NO NSAIDS

23
Q

produces heat liable and heat stable toxin
Heat stable toxin similar to cholera and Yersinia toxins
Travel related

A

enteroTOXIgenic (ETEC)

24
Q

Attaching and effacing lesions. No toxin, not invasive
Synthesises, secretes and inserts its own receptor into cell membranes
Non breastfed children
Can be asymptomatic

A

enteroPATHOgenic (EPEC)

25
Q

Watery diarrhoea, rare dysentery
Demonstrates invasion
Sereny test

A

enteroINVASIVE (EIEC)

26
Q

Travellers diarrhoea
New kid on the block
Cytogenic, secretogenic, proinflammatory

A

enteroAGGREGATIVE (EAIC)

27
Q 
Gram negative, Enterobacteriales family
16- 48 hrs incubation
Sporadic – rarely outbreaks
Low inoculum
Invasive
Pain, blood (30%), fever
May be admitted
food hygiene (raw poultry especially)
Sel limiting 
macrolide (maybe if co-morbid factors: but increasing resistance)
less likely to spread person to person 
Most common
A

Campylobacter

28
Q

corkscrew appearance

A

campylobacter

29
Q

campylobacter post infectious consequences

A 
Guillain Barré (1-2 weeks after infection)
Reactive arthritis ( associated with HLA B-27)
Miller-Fischer variant
30
Q

Motile gram negative bacilli. Enterobacteriales family
8-72 hours hrs incubation
Fecal oral route
Food: poultry, meat, raw egg
animal gut, multiplies in food
Toxin and invasion
D&V, blood, fever (severity depends on inoculum)
Achloridia, IBD and sickle cell disease associated with more severe

A

salmonella

31
Q

Non spore forming Gram positive rod. It has 1 to 5 flagella
Infection acquired from contaminated food -unpasteurised milk products, deli counter
It can grow at low temperature

Extract of cell membrane causes monocytosis ……. in rabbits
Rarely causes monocytosis in humans !!!
Despite the name 67% csf has neutrophils
Effect of iron overload
Food borne transmission, mother to child
A

Listeria monocytogenes

32
Q

what can invasive listeria monocytogenes causes

A

meningitis/bacteriaemia

brain abscess, rhomboencephalitis

33
Q

what are examples of viruses causing viral gastroenteritis

A

Rotavirus

Norovirus

34
Q 
Commonest cause in kids <3 yrs 
~ all kids get it before 5
person-person 
Faecal oral
Direct & indirect
Usually in the winter
Subclinical or mild in adults
Immunocompromised? can be severe
Range of clinical effects
Mild watery to profuse and shock
May have moderate fever first, vomiting then diarrhoea
Not bloody
Self limiting
Lasts a week Children may have post infection malabsorption 
which leads to more diarrhoea
Repeat infections: milder each time
Can cause outbreaks 
PCR diagnosis on faeces
Hydration is the key to management
Oral where possible in mild to moderate
A

rotavirus

35
Q

describe the rotavirus vaccine

A

Oral
Live attenuated
Excreted in faeces
From sept 2013
1200 babies/yr need hospital treatment
2 doses
2 and 3 months
120 cases per 100,000 children < 1 yo per year
2 in 100,000 with vaccine
Risk of intususseption increases as babies get older
So 1st dose is not given to babies over 15 weeks
No dose given to babies over 24 weeks
Capable of coughing spitting & sneezing oral vaccine: careful technique!

36
Q

‘Winter Vomiting Disease’- lately all year round!
Affect all ages: HIGHLY infectious
5 billion viruses per gram of faeces
Faecal-oral/droplet routes of spread
Person to person (or on contaminated food/water)
Environmental survival on fomites for days- weeks
Low infectious dose
Community circulation is the reservoir
Asymptomatic shedding (48 hrs post cessation of symptoms)
Abrupt & unpredictable onset
D&V explosive & sudden!
Vomiting can lead to widespread environmental contamination & onward transmission

All lead to potential for numerous and large outbreaks especially in hospitals, schools etc

A

norovirus

37
Q

norovirus symptoms

A

Also some general systemic symptoms
Short incubation (<24 hours): lasts 2-4 days
Diagnosis: PCR on stool
PCR on vomit using red Copan viral swabs
Usually self limiting : very unpleasant
Hydration is the key
Can contribute to death in frail elderly patients
Early ward closure/isolation/cohorting required

38
Q

inflammation of lining of stomach, small and large intestine

A

gastroenteritis

39
Q

what is the pathophysiology of gastroenteritits

A

enteric pathogens cause diarrhoea via several mechanisms:
stimulation of net fluid and electrolyte secretion
increased propulsive muscle contractions
mucosal destruction and increased permeability
nutrient malabsorption

40
Q

what investigations would you do for gastroenterititis

A 
stool microscopy (HX of giardia, amoeba)
stool culture (eg salmonella, campyl, shigella)
stool toxin for C diff (enter- and cyto-toxin)
blood cultures (Salmonella)
PCR (norovirus)
FBC (assess WCC)
U&Es (renal function)
AXR
41
Q

what is the treatment for gastroenteritis

A 
usually supporting (oral rehydration + IV fluids)
specific C.diff managments
42
Q

what are the two short incubation (1-6hrs) pathogens

A 
staph aureus (gram positive coccus, very fast preformed toxin, acts on vomiting centre on brain, milk/meat/fish)
bacillus cereus (gram positive bacillus rod, profuse vomiting, REHEATED RICE)
43
Q

What are the two medium incubation pathogens

A

salmonella (12-48hrs)
[outbreaks can also cause bacteriaemia
pultry/meat/rawegg
blood diarrhoea, vomiting, fever]

listeria monocytogenes (9-48hrs) [fever, muscle aches, diarrhoea, pregnant women may have mild sympoms, unpasteurised milk products, deli counter, gram positive rod]

44
Q

what are the two longer incubation pathgogens

A

campylobacter (16-48hrs)
[most common, usually self limiting, associated with food hygiene, guillan barre syndrome complication]
e.coli 0157 (1-14 days) [rare but mobidity and outbreaks, produces verotoxin and shiga-like toxins, verotoxins, blood diarrhoea, notify health protection unit, avoid ABs -> can progress to haemolytic uraemic syndrome)

45
Q

management of c.diff

A

non severe = metrondiazole PO 400 m tds (10 days)

severe = vancomycin 125mg qds PO/NG +/- metrondiazole (10 days) isolate patient

46
Q

4Cs causing C diff

A

cephalosporins
clindamycin
ciprofloxacin
co-amoxiclav

GI - anna (14 decks)

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