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Session 9 Flashcards

1
Q

GI defences

A

-Sight, smell, memory
-Saliva- bacteriostatic secretions
-Gastric acid
-SI secretions (bile)
- Colonic mucus
- Anaerobic environment (small bowel, colon)
- Commensal gut bacteria

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2
Q

Proximal gut is what type of environment

A

Sterile

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3
Q

What kind of environment is stomach

A

Microaerophilic environment

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4
Q

What kind of envionrment is colon

A

Anaerobic

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5
Q

Benefits of gut micro biome

A

Harmful bacteria cannot compete for nutrients
Micro biome produces anti microbial substances
Helps to develop newborns immune system
Produces certain nutrients Vit K

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6
Q

Bacteria in colon produce

A

SCFAs- short chain fatty acids

Acetate, propionate, butyrate

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7
Q

What is Butyrate

A

Energy source for colonocytes, helps regulate gut environment

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8
Q

What is Acetate

A

Involved in cholesterol metabolism

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9
Q

What is Propionate

A

Helps regulate satiety

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10
Q

Gut microbiota and health

A

Obesity = less diversity
IBD = less diversity

Affects response to chemotherapy and insulin response to food

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11
Q

Microbiota and diet and medications

A

Good = high fibre diet, probiotics, prebiotics

Bad = sweeteners, gluten free diet, PPIs, antibiotics in meat = obesity

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12
Q

FMT used for

A

Faecal microbiota transplant (FMT)

Pseudomembranous collitis
Crohn’s
C. difficile

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13
Q

Route of administration for FMT

A

NG/duodenal tubes
Upper GI endoscopy
Colonoscopy
Transplant can be put in Caecum

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14
Q

Where do you get faeces from

A

10-25 year olds

Donors do not use antibiotics, laxatives or diet pills in last 3 months, do not have GI disease, screened for inflammatory markers, Hep and HIV

Fresh stool to transplantation or storage within 1 hour- stool is centrifuged, filtered and diluted

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15
Q

Bacterial infections of the gut organisms

A

Gram negative rods-
Salmonella, Campylobacter, Shigella, Enterotoxigenic E-coli

Gram positive- Clostridium difficile (gram positive)

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16
Q

Symptoms and spread of salmonella

A

Nausea, vomiting and diarrhoea (mostly non-bloody), fever, abdo cramps

Self-limiting (2-3 days)

Spread by ingesting contaminated food and water

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17
Q

What happens inside gut in salmonella infection

A
  • Gain access to enterocytes (endocytosis)
  • Move to submucosa where encounter macrophages
  • Macrophages transfer salmonella to reticuloendothelial system where they multiply inside cells
  • Causing lymphoid hyperplasia
  • Re enter gut from the liver
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18
Q

Symptoms and spread of Campylobacter

A

fever, abdo cramping, diarrhoea (can be bloody)

Days to weeks (generally self-limiting)

Needs to multiply within host before symptoms appear (food infection not poisoning)

Faeco-oral route

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19
Q

Features of campylobacter

A

-Spiral/S shaped organism
-Microaerophillic mainly (do not ferment carbs)
- Releases cytotoxin (similar to cholera)

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20
Q

Treatment of campylobacter

A

Fluid/electrolyte replacement
Consider antibiotics if bloody diarrhoea

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21
Q

Symptoms and spread of Shigella

A

bloody diarrhoea with mucus and abdominal cramping

Usually resolves in a week

Spread from infected stools, person to person, sometimes flies, only small dose needed

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22
Q

Pathogenesis of Shigella

A

Causes shigellosis which is a dysentery commonly affecting young children

Invades large intestine colonocytes, multiplies in cells and invades neighbouring cells

Kills colonocytes and forms abscesses in the mucosa

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23
Q

Symptoms and spread of Enterotoxigenic E. coli ETEC

A

Travellers diarrhoea

Spread by faecal oral route by contaminated water

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24
Q

Pathogenesis of ETEC

A

Commensal of colon but also can be a pathogen

Adheres to enterocytes (produces enterotoxins), causes hypersecretion of chloride ions, water leaves cells into gut lumen

25
Summary of gram negative rods different types of diarrhoea
Diarrhoea Can be bloody- Shigella!! (Campylobacter) Watery- ETEC, salmonella
26
Which gram negative rods have potential for HUS
Shigella, campylobacter
27
Duration of gram negative rods longest to shortest
Campylobacter, shigella = weeks Salmonella and ETEC = days
28
What is HUS
Haemolytic uraemic syndrome Triad = anaemia, thrombocytopenia, AKI
29
Symptoms of Clostridium difficile
Asymptomatic (most people) Varying degrees of diarrhoea Abdominal cramping In a few cases: pseudomembranous colitis, toxic megacolon, surgery needed
30
Pathology of C. difficile
Gram positive, anaerobic, spore forming bacillus Minor component of GI tract Following antibiotic therapy, can colonise gut and release toxins (toxins A and B)
31
Spread of C. difficile
Can be transferred via faecal oral route Spores are very difficult to get rid of from an environment (Like hospital)
32
What are toxins A and B of clostridium difficile
A- enterotoxin that results in excessive secretion and inflammation B- cytotoxin
33
What can precipitate C. difficile proliferation
Antibiotics- especially broad spectrum
34
What is psuedomembranous colitis
Inflammatory condition Elevated yellow plaques join to form a pseudo membrane
35
Treatment of C. difficile infection
Remove offending antibiotic Fluid resuscitation Metronidazole/Vancomycin Probiotics
36
Viral and parasitic causes of gastroenteritis
37
Features and spread of gastroenteritis caused by Rotavirus
very common cause in under 5s, adults rarely affected Double stranded RNA Spread by faecal-oral route (small dose required)
38
Symptoms and treatment of viral gastroenteritis rotavirus
Vomiting with a fever are first symptoms Diarrhoea follows- lasting up to a week Treatment- manage dehydration
39
Pathology of diarrhoea in rotavirus
Chloride secretion- creates gradient for the movement of Na into lumen, water moves by osmosis SGLT1 disruption- reduced movement of Na/glucose into enterocytes, higher osmotic load in gut, water moves by osmosis Brush border dysfunction- general malabsorption
40
Features and spread of norovirus
Most common cause of non bacterial gastroenteritis in the world Any age as many strains, only needs small dose Resistant to cleansing
41
Symptoms and treatment of norovirus
Incubation is 1-2 days and symptoms lasts 1-3 days Infects the SI and damages microvilli (brush border enzymes disruption) Vomiting, water diarrhoea, fever Oral rehydration therapy
42
Pathology of symptoms in norovirus
Watery diarrhoea= anion secretion, so movement of water into gut lumen Vomiting= vomiting due to delayed gastric emptying
43
Pathology of symptoms of norovirus
Vomiting = delayed gastric emptying Watery diarrhoea = anion secretion, so movement of water into gut lumen
44
Types of parasitic gastroenteritis
Protozoa that infect intestinal tract Cryptosporidium: sporozoan (non motile) Giardia Lamblia: flagellate (motile) Entamoeba: amoeba (move by extending cytoplasmic projections)
45
Transmission of Cryptosporidium
Faecal-oral route, survive and spread via bodies of water
46
Disease pathology of Cryptosporidium
Ingestion of Oocyst- reproduces inside epithelial cells of distal SI, excreted in faeces to continue cycle
47
Symptoms and treatment of cryptosporidium
Water diarrhoea that is normally self limiting Malabsorption (brush border enzymes affected), chloride secretion Supportive- fluids, anti-parasitic treatment in at risk groups e.g. AIDS
48
Spread of Giardia
Faecal-oral route, water supplies often affected in developing countries
49
Symptoms of Giardia
Most asymptomatic but symptoms more common in children 10+ day incubation period Diarrhoea, abdominal cramping, can last up to 6 weeks- common cause of persistent diarrhoea
50
Treatment of Giardia
Antibiotics and fluid rehydration therapy Post Giardia infection, lactase deficiency is common (lactose intolerance)
51
Pathology of Giardia
2 stage life cycle 1- Cyst ingested, stomach acid/pancreatic enzymes release parasite from cyst, multiplies in SI Damages proximal SI causing symptoms, villous atrophy 2- Parasite goes back into cysts stage in colon- excreted to repeat cycle
52
Entamoeba spread
Higher prevalence in developing countries Faecal-oral route (poor sanitary conditions, MSM)
53
Entamoeba symptoms and treatment
80% asymptomatic Diarrhoea (bloody?) or liver abscess (rare) Anti-protozoals/metronidazole Severe colitis/toxic megacolon may need surgery
54
Pathology of Entameeba
Infection follows ingestion of cysts Excystation occurs in colon where trophozoites invade mucosa (bloody diarrhoea and inflammatory changes occurs) Infection can spread to liver (abscesses form) Cysts then pass out with faeces- infect others
55
What is travellers diarrhoea
ETEC is most common cause Passing 3 or more loose/water stools (+/- fever and abdo pain) Greater than 14 days of symptoms makes it less likely to be bacterial
56
Treatment of travellers diarrhoea
Antibiotics only for vulnerable/immunosuppressed Halves duration of symptoms 1.5 days on average
57
Risk of getting diarrhoea
Places you visit (south and east Asia, Central America, west and North Africa) Dietary exposure Less than 6, PPIs, Blood group O
58
Prevention of travels diarrhoea
Good hand hygiene, food and water precautions
59
Mild vs moderate travellers diarrhoea treatment
Mild/moderate = less than 6 stools in 24 hours: Hydration and anti diarrhoea agents Severe = more than 6 stools in 24 hours: IV fluids and antibiotics

GI (22 decks)

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