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gastrointestinal > Lecture 17- GI infections > Flashcards

Lecture 17- GI infections Flashcards

1
Q

the gut is a tube- great way to get toxins into the body. name some potential toxins

A
  • Chemical
  • Bacterial
  • Viruses
  • Protozoa
  • Nematodes (roundworms)
  • Cestodes (tapeworms)
  • Trematodes (flukes)
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2
Q

Main defence against toxins:

A

commensal bacteria

  • When we have an imbalance in commensal bacteria , ingesting other toxins are more likely to make us ill
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3
Q

role of bacteria in the colon

A

produce short chain fatty acids (SCFA)

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4
Q

name 3 SCFA

A

butyrate

acetate

propionate

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5
Q

butyrate

A

energy source for colonocytes, helps regulate gut environment

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6
Q
  • Acetate-
A

involved in cholesterol metabolism

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7
Q
  • Propionate-
A

helps regulate satiety

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8
Q

what icnreases composition of gut microbiotia

A

high fibre diet

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9
Q
  • …………..disrupt diversity of gut microbiota (bad)
A

Sweeteners

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10
Q
  • Gluten free diet people without gluten sensitivity or coelicac disease-
A

have a lower numbers of key species

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11
Q

drug which causes increased GI infections

A
  • proton pump inhibitors
  • antibiotics (meat) linked to obesity
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12
Q
  • Probiotics
A

– live bacteria and yeasts put in foodà probs die in stomach

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13
Q
  • Prebiotics-
A

essentially food for the microbiota (accessible carbs and fibreà seen as more useful

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14
Q

GI defences

A
  • Sight , smell, memory
  • Saliva (bacteriostatic secretions)
  • Gastric acid (acidic environment)
  • Small intestinalsecretions (bile)
  • Colonic mucus
  • Anaerobic environment (small bowel, colon)
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15
Q

proximal gut microbiome

*

A
  • Proximal gut is relatively sterile
    • Stomach is microaerophilic environment e.g. H.pylori (not anaerobic yet)
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16
Q

how much bacteria in the colon

A
  • 10^11 bacteria in the colon (anaerobic environment)
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17
Q
  • More than ………of faecal matter is bacteria
A

20%

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18
Q
  • Benefits of gut microbiome
A
  • Harmful bacterial cannot compete for nutrients
  • Microbiome produces antimicrobial substances
  • Helps to develop newborns immune system
  • Produces certain nutrients (VitK)
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19
Q
  • Microbiome started when we
A

come out the birth canal

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20
Q

obesity and fut microbiota

A

seems to be less diverse pop of bacteria

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21
Q
  • Inflammatory bowel disease-
A

less diversity

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22
Q
  • Microbiome composition affects response
A

to chemotherapy

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23
Q
  • Microbiome competition affects
A

insulin response to food

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24
Q

Faecal microbiota transplant (FMT)

A

Stool is a biologically active complex mixture of living organisms with therapeutic potential

  • Route of admin
    • NG/duodenal tube (unappealing)
    • Upper GI endoscopy
    • Colonoscopy
    • Transplant can be in caecum (allowed to move throughout colon)
      • Distributed throughout length of the colon
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25
Q

which disease has FMT been used to treat

A
  • E.g. pseudomembranous colitis has been treated by faecal enemas since 1985
  • C.diff
  • IBD
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26
Q

Where do you get faeces from

A
  • 10-25 year olds
  • Donors do not use (in past 3 months)
    • Antibiotics
    • Laxative
    • Diet pills
  • Do not have GI disease
  • Completely screen for diseases e.g. HIV, hepatitis
  • Transplant takes place within one hour
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27
Q

bacteria infections in the gut

A
  • Gram negative rods
    • Salmonella
    • Campylobacter
    • Shigella
    • Enterotoxigenic E.coli
  • Gram positive
    • Clostridium difficile
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28
Q

Salmonella- gastroenteritis

  • Symptoms
A
  • Nausea
  • Vomiting
  • Diarrheal (mostly non-blood)
  • Abdominal cramping
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29
Q

salmonella transmission

A
  • -ingesting food and water contaminated by salmonella bacteria (symptoms develop 48 hours later)
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30
Q

MOA of salmonella

A
  • Salmonella gain access to enterocyte via endocytosis
  • Move to submucosa where encounters macrophages
  • Macrophages transfer salmonella to RES where they multiply inside cells
  • Lymphoid hyperplasia
  • Re-enter gut from the liver
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31
Q

prognosis of salmonella

A
  • Prognosis – self limiting (may need oral resus)
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32
Q

Campylobacter

A
  • Bacteria is spiral shaped
    • Microaerophilic (do not ferment carbs)
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33
Q

Campylobacter- gastroenteritis symptoms

A
  • Fever
  • Abdominal cramping
  • Diarrhoea (can be bloody)
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34
Q

Campylobacter- gastroenteritis transmission

A
  • Eating poultry
  • Foaeco-oral route
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35
Q

Campylobacter- gastroenteritis MOA

A
  • Needs to multiply within host before symptoms appear (food infection- not poisoning)
    • Longer incubation period e.g. 1-7 days)
  • Releases a cytotoxin (similar to cholera)
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36
Q

camplobacter prognosis

A
  • Can last days to week- generally self limiting
  • Fluid/electrolyte resus
  • Consider Abx if bloody
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37
Q

Shigella- gastroenteritis causes

A
  • shigellosis- dysentery commonly affecting young children
38
Q

transmission of shigella

A
  • Spread from infected stool
  • Person to person (sometimes flies)
  • Only need small dose to cause infection
39
Q

MOA of shigella

A
  • Invades large intestine colonocytes, multiplies and invades neighbouring cells
  • Kills colonocytes and forms abscesses in the mucosa
40
Q

symptoms of shigella

A
  • Blood diarrhoea with mucus and abdominal cramping
41
Q

prognosis of shigella

A
42
Q

Enterotoxigenic E.coli

A
  • Commensal of the colon but can also be a pathogen
    • Flagella helps transport
43
Q

Enterotoxigenic E.coli -gastroenteritis transmission

A
  • Faecal oral route by contaminated water
  • Common cause of travellers diarrhoea
44
Q

Enterotoxigenic E.coli -gastroenteritis MAO

A
  • Adheres enterocytes in small intestine
  • Produces enterotoxins
  • These cause hypersecretion of chloride
  • Water leaves cells in the gut lumen
45
Q

different strains of e.coli cause different

A

symptoms and need different treatment

46
Q

gram negative bacteria which cause bloody diarrhoea

A

shigell, campylobacter

(colon involvement)

47
Q

Hemolytic-uremic syndrome (HUS) potential

A

shigell and campylobacter

  • anaemia
  • thrombocytopenia
  • AKI
48
Q

duration of gram engative infections shrotest to longest

A

ETEC, salmonella (days), shigella (week), campylobacter (weeks)

49
Q

which is the main gram positive bacteria which causes gastroenteritis

A

clostridium difficile

50
Q

clostridium difficile

A
  • Gram positive
  • anaerobic
  • spore forming bacillus
  • minor component of GI tract but can be transferred via faecal oral route
51
Q

why is C.diff common in hospitals

A

spore very difficult to get rid of from environment e.g. hospital

up to 20% of hospitalised pts become colonised with C.difficile

52
Q

MOA of C.diff

A
  • Following antibiotic therapy C difficile can colonise gut (imbalance in microbiota and release toxins A and B
    • A- enterotoxin results in excessive secretion and inflammation
    • B- cytotoxin
53
Q

cause of C.diff

A

Most antibiotics can precipitate C.difficile proliferation- esp broad spectrum.

54
Q

symptoms of c.diff

A
  • Asymptomatic – most people
  • Varying degrees of diarrhoea (mild to terrible, rarely bloody)
  • Abdominal cramping
55
Q

rare complications of C,diff

A
  • Pseudomembranous colitis
  • Toxic megacolon (worst case scenario)- surgery
56
Q
  • Pseudomembranous colitis
A
  • Inflammatory condition
  • Elevated yellow plaques which join to form a pseudomembrane
57
Q

megacolon

A

needs surgery

58
Q

treatment of C.diff

A

Treatment

  • Remove offending antibiotic
  • Fluid resus
  • Metronidazole/vancomycin
  • Probiotics
59
Q

viruses which can cause gastroenteritis

A

rotavirus

noravirus

60
Q

Parasites which cause gastroenteritis

A
  • Cryptosporidium
  • Giardia
  • Entamoeba
61
Q

Viral gastroenteritis- Rotavirus characteristics

A
  • Common in under 5s
  • The virus
    • dsRNA
62
Q
  • transmission of rotavirus
A
  • faecal oral route (only small dose required)
  • adults rarely affected (immunity lasts into adulthood)
63
Q

symptoms of rotavirus

A
  • fever and vomiting first
  • diarrhoea follows
64
Q

diarrhea in rotavirus

A
  • chloride secretion
    • creates gradient for movement of Na into lumen
      • water moves by osmosis
      • diarrhoea
  • SGLT 1 disruption
    • Reduced movement of Na/glucose into enterocyte
    • Higher osmotic load in gut
    • Water moves by osmosis
  • Reduce brush border enzyme function- malabsorption
65
Q
  • Treatment of rotavirus
A

Managing dehydration

66
Q

Viral gastroenteritis- Norovirus can affect

A
  • Can affect any age – huge number of strains- don’t develop immunity
67
Q
A
68
Q

norovrius

A
  • RNA virus
  • Only requires small dose-highly contagious
69
Q
  • norovirus Transmission
A
  • Person to person
  • Resistant to cleaning
70
Q
  • MOA norovirus
A
  • Incubation 1-2 days
  • Symptoms last 1-3 days
  • Affecting small intestine and damages microvilli (brish border enzyme disruption)
71
Q
  • Symptoms norovirus
A
  • Vomiting
    • Delayed gastric emptying
  • Watery diarrhoea
    • Anion secretion- movement of water into gut
  • Fever
72
Q
  • Treatment of norovirus
A
  • Oral rehydration therapy
73
Q
  • Protozoal infects the intestinal tract
A
  • Cryptosporidium- sporozoan
    • Non motile
  • Giardia lamblia- flagellate
    • Motile - flagella
  • Entamoeba- amoeba
    • Motile- move by extending cytoplasmic projections
74
Q

Cryptosporidium is a

A

sporozoan- protozoa

75
Q

transmission of cryptosporidium

A
  • Faecal oral route but can also survive and spread via bodies of water
76
Q

who does Cryptosporidium effect

A
77
Q

MOA of cryptosporidium

A

MOA

  • Disease is caused by ingestion of oocysts (cyst containing parasitic)
    • Reproduces inside the epithelial cells of the distal small intestine
    • Oocysts are excreted in faces and continue cycle
78
Q

Symptoms of cryptosporidium

*

A
  • Watery diarrhoea (S.intestine)
    • Malabsorption (brush border enzymes affected)
    • Chloride secretion
79
Q

Treatment of cryptosporidium

A
  • Fluids
  • Occasionally need an anti-parasitic treatment if pt immunocompromised e.g. HIV
80
Q

giardia is a

A

flagellate

81
Q

symptoms of giardia

A
  • Most infections asymptomatic (symptoms in children)
  • If symptomatic (appear after 10+ days incubation period)
    • Diarrhoea
    • Abdominal cramping
    • Can last 6 weeks
  • Common cause of persistent diarrhoea
82
Q

transmission of giardia

A
  • Faecal oral route with water supplies often affected
83
Q
  • MOA of giardia
A

Life cycle in 2 stages

84
Q
  • Treatment of giardia
A

Antibiotics and fluid rehydration therapy (lactase deficiency common after infection- lactose intolerance)

85
Q

entamoeba has a higher prevalence in

A

developing coutnries

86
Q

entamoeba symptom

A
  • Most cases are asymptomatic (80%)
    • Diarrhoea
    • Liver abscesses (rare)
87
Q

transmission of entamoeba

A
  • Transmission
    • Faecal oral route
88
Q

MOA of entemoeba

A
  • MOA
    • Infection following ingestion of cysts
    • Excystation occurs in colon where trophozoites invade mucosa
      • Bloody diarrhoea and inflammatory changes occur (similar to IBD)
      • Infection can spread to liver- abscesses
    • Cysts then pass out with faeces- infect others
89
Q

treatment of entamoeba

A
  • Treatment
    • Anti-protozoal= metronidazole
    • Severe colitis/toxic megacolon= surgery
90
Q

travellers diarhhoea

A

gastrointestinal (35 decks)

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