Gastroenteritis and infective colitis Flashcards

1
Q

What is gastroenteritis?

A

Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.

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2
Q

What is the aetiology of gastroenteritis? (x4)

A
  • Viruses: rotavirus, adenovirus, calicivirus, Norwalk virus, small round structured virus
  • Bacterial: Campylobacter jejuni, E. coli, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica
  • Protozoal: Entamoeba histolytica, Cryptosporidium parvum, Giardia lamblia
  • Toxins contained in contaminated foods or water
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3
Q

What are the toxins that cause gastroenteritis? (x7 +3)

A

Toxins that come FROM Staph. Aureus (improperly cooked meat, old rice), Clos. Botulinum (canned food), Clos. Perfringens (improperly cooked meat), Bacillus cereus (old rice), Salmonella (eggs and poultry), Listeria and Campylobacter (milk and cheeses), mushrooms, heavy metals, seafood

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4
Q

What is the pathophysiology of gastroenteritis? (x2) Which pathogen or toxin (produced by a pathogen) can cause worse disease?

A
  • NON-INFLAMMATORY MECHANISMS: e.g., V. cholerae and enterotoxigenic E. coli produce ENTEROTOXINS that cause enterocytes to secrete water and electrolytes
  • INFLAMMATORY MECHANISMS: e.g., Shigella and enteroinvasive E. coli release CYTOKINES and INVADE and damage the epithelium, with greater invasion and bacteriaemia in the cause of Salmonella typhi.
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5
Q

What are the risk factors of gastroenteritis? (x5) (How should this inform your history?)

A

Recent travel, recent antibiotic use, recent intake of at-risk food (enquire about how cooked, source and whether anyone else is ill), poor hygiene, contact history (faecal-oral transmission)

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6
Q

What is the epidemiology of gastroenteritis: Where?

A

Higher prevalence in the developing world – especially Africa.

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7
Q

What are the symptoms of gastroenteritis? (x5)

A
  • Sudden onset nausea and vomiting
  • Anorexia
  • Diarrhoea (bloody or watery)
  • Abdominal pain/discomfort
  • Fever
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8
Q

How does onset of symptoms differ depending on aetiology of gastroenteritis?

A

If aetiology is from a TOXIN, onset is early (1-24 hours). If aetiology is bacterial/viral/protazoal, onset is 12 hours or later.

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9
Q

How may the toxin involved in gastroenteritis affect a patient’s history? (x2 examples)

A

Botulinum causes paralysis; mushrooms can cause fits, renal or liver failure.

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10
Q

What are the signs of gastroenteritis? (x4)

A
  • Diffuse abdominal tenderness
  • Abdominal distension
  • Bowel sounds increased
  • Pyrexia, dehydration, hypotension if severe
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11
Q

What are the investigations for gastroenteritis? (x4 (x3 and x6))

A
  • Diagnosis typically done clinically based on signs and symptoms.
  • BLOOD: FBC (raised WBC; sometimes low Hb/platelets is haemolytic uraemic syndrome manifests as complication of E. coli), blood culture (helps identification if bacteraemia present), U&Es (dehydration sign)
  • STOOL: faecal microscopy for polymorphs (WBCs), parasites, oocysts, culture, electron microscopy (for viral infections), analysis for toxins (especially Clostridium difficile as a differential – infectious colitis)
  • AXR: to exclude differentials for abdominal pain
  • USS: to exclude differentials for abdominal pain
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12
Q

How is gastroenteritis generally managed? (x3)

A
  • Fluid and electrolyte replacement with oral rehydration solution containing glucose and salt. IV rehydration may be necessary if symptoms severe
  • Antibiotics ONLY if severe or the infective agent has been identified
  • Public Health: often a notifiable disease
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13
Q

How is botulism gastroenteritis managed?

A

Botulinum antitoxin IM and manage in ITU

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14
Q

What are the complications of gastroenteritis? (x5)

A
  • Dehydration, electrolyte imbalance, prerenal failure
  • Secondary lactose intolerance (particularly in infants)
  • Sepsis (particularly Shigella and Salmonella)
  • Haemolytic uraemic syndrome in E. coli
  • Guilian-Barre syndrome (rapid-onset weakness from autoimmune peripheral nerve damage) weeks following Campylobacter gastroenteritis
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15
Q

What is the prognosis of gastroenteritis?

A

Good as the majority of cases are only self-limiting.

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16
Q

What is the difference between gastroenteritis and infectious colitis?

A

Gastroenteritis refers to inflammation of the gastrointestinal tract, usually the stomach and intestines. Colitis refers to inflammation of the colon. They also differ in their aetiology – as I will discover shortly.

17
Q

What is infectious colitis?

A

AKA PSEUDOMEMBRANOUS COLITIS. Large bowel inflammation with mucosal destruction and inflammatory exudates forming pseudomembranes on the bowel wall associated with toxin-releasing Clostridium difficile bacilli.

18
Q

What is the aetiology of infectious colitis? (x2 points)

A

Colonic overgrowth of C. difficile Gram-positive bacteria leading to disturbance of gut microflora, nearly always brought about by antibiotic use. Transmission is also a risk through faecal-oral route, fomites or direct exposure to contaminated environment.

19
Q

What antibiotics are more suggestive of infectious colitis? (x3)

A

Clindamycin, ampicillin, and broad-spectrum cephalosporins

20
Q

What is the pathophysiology of infectious colitis?

A

C. difficile releases two potent toxins: toxin A (enterotoxin) and toxin B (cytotoxin). Toxin A inactivates Rho-GTPase (epithelial cytoplasmic protein) causing intestinal hypersecretion, disaggregation of epithelial actin microfilaments and cell death. Both toxins also disrupt intracellular tight junctions and cause an inflammatory response leading to pseudomembrane formation and inflammatory exudates (increased vascular permeability).

21
Q

What are pseudomembranes?

A

Composed of an exudate made of WBCs, fibrin and mucus and are thin yellowish membrane with intact underlying epithelium.

22
Q

What is the epidemiology of infectious colitis: Population? Hospitals?

A

C. difficile carried asymptomatically in 2% of the population. Pseudomembranous colitis common in hospitals where there is both increase carriage of C. difficile and antibiotic use.

23
Q

What are the symptoms of infectious colitis? (x2)

A

Remember it is a large intestine issue, so no upper GI symptoms like vomiting: Watery diarrhoea which may become bloody, and crampy abdominal pain.

24
Q

What are the signs of infectious colitis? (x3)

A

Pyrexia, abdominal tenderness. In severe cases, toxic megacolon or perforation.

25
Q

What are the investigations for infectious colitis? (x3)

A
  • BLOOD: FBC (increased WCC), high CRP, lactate, blood culture (excludes other organisms)
  • STOOLS: demonstration of C. difficile toxin by ELISA. Stool culture only used to exclude differentials
  • SIGMOIDOSCOPY: visualises colitis and pseudomembranes
26
Q

How is infectious colitis medically managed? (x2)

A
  • Oral metronidazole or vancomycin. IV in critically ill. Empiric therapy is appropriate (antibiotics before diagnosis)
  • Supportive treatment: rehydration and electrolyte imbalance from diarrhoea
27
Q

How is infectious colitis managed after relapse?

A

Repeat treatment. In second relapse, taper vancomycin over 6 weeks plus probiotics started during final week of vancomycin and continued for two additional weeks.

28
Q

How is infectious colitis surgically managed? Indication?

A

Subtotal colectomy with ileostomy for patients over 65 with WCC over 20x10^9/L or plasma lactate between 2.2 and 5 mEq/L.

29
Q

What are the complications of infectious colitis? (x3)

A

Toxic megacolon, perforation, septic shock.

30
Q

What is the prognosis of infectious colitis?

A

Recovery is prompt with treatment. 25% relapse on stopping treatment.