GI Infections Flashcards

1
Q

host defences of the mouth

A

flow of liquids

saliva

lysozyme

normal bacterial flora

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2
Q

host defences of the oesophagus

A

Flow of liquids

Peristalsis

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3
Q

host defences of the stomach

A

acid pH

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4
Q

host defence of the small intestine

A
Flow of gut contents
Peristalsis
Mucus, bile
Secretory IgA
Lymphoid tissue (Peyer’s patches)
Shedding and replacement of epithelium 
Normal flora
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5
Q

host defence of the large intestine

A

Normal flora
Peristalsis
Shedding and replication
mucus

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6
Q

what is the role of the bacteria in the stomach and colon?

A

Selectively inhibit gastroenteritis from occurring on daily basis

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7
Q

is it worthwhile taking products with probiotics

A

no

Most bacteria from probiotics die in stomach before they reach colon – where they are meant to work

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8
Q

what are the majority of good bacteria like

A

99.9% anaerobes e.g. Bacteroides fragilis

E. coli

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9
Q

what is a purpose of good bacteria in the GIT

A

Good bacteria make supplementary vitamins (secondary metabolites)
- Vitamin K production

Needed to make cascade system required for absorbing nutrients

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10
Q

3 types of causative agents

A

bacteria

viruses

protozoa

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11
Q

helicobacter pylori is associated with which diseases

A

Assoc. with 90% of duodenal ulcers

Assoc. with 70-80% of gastric ulcers

Increased risk of gastric cancer (adenocarcinoma)
- Kills many

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12
Q

how does helicobacter pylori survive and be virulent

A

Ability to survive in acidic conditions

Catches to epithelial cell

Releases enterotoxins

Endothelial release neutrophils as lumen is agitated
- If sustained can lead to cancer

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13
Q

what area of the world is more effected by H pylori

A

50-90% of developing world infected
- crammed environments

In developed world there is low prevalence

Associated with socio-economic factors

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14
Q

mode of transfer of H pylori

A

Mode of transfer undefined

Transmission probably faecal-oral route

Oral-oral route also implicated

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15
Q

pathogenicity of H pylori

A

Acid tolerance

  • Turn acid into urea which causes ammonia production
  • Detoxifies the acid so bacteria can thrive

Ammonia is in breath test

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16
Q

3 methods of diagnosis for H pylori

A

endoscopy and biopsy (more invasive)

breath test

serology

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17
Q

3 methods of treatment for Gi infections

A

Proton pump inhibitor

Bismuth salts

Antibiotics (combination)

  • Amoxicillin
  • Clarithromycin
  • Metronidazole
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18
Q

what is gastroenteritis

A

non-specific term for various pathologic states of the gastrointestinal tract
- body takes in something which it subsequently tries to secrete/excrete

The primary manifestation is diarrhoea, but it may be accompanied by nausea, vomiting, and abdominal pain

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19
Q

definition of diarrhoea

A

universal definition does not exist

Definitions centre on:

  • Frequency, consistency, and water content
  • Disease of the small intestine and involving increased fluid and electrolyte loss
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20
Q

key symptoms of viral gastroenteritis (6)

A

abdominal cramps (1)

Vomiting

Profuse watery stools

Myalgias
- Sore head due to interferon

Fever

Headaches

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21
Q

key symptoms of bacterial dysentery (5)

A
Small volume stools
Fever 
Tenesumus
Bloody mucoid stools
suprapubic pain 

exotoxin stimulating enterocytes in number of different ways

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22
Q

what is the most common causative agent for gastroenteritis

A

viral (50-70%)

Norovirus, Caliciviruses, Rotavirus, Adenovirus, Parvovirus, Astrovirus

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23
Q

what is the second most common causative agent for gastroenteritis

A

bacterial (15-20%)

Salmonella, Shigella, and Campylobacter species

24
Q

what is the least most common causative agent for gastroenteritis

A

parasitic (10-15%)

Giardia lamblia, Entamoeba, Cryptosporidium

25
Q

invasive infection

A

The organism enters the mucosal cells, destroys them, causing diarrhoea usually with blood in the stool

26
Q

enterotoxic infection

A

The organisms do not invade the mucosa, but produce enterotoxins of which act as chemical mediators causing hypersecretion of the fluid. - - - Little damage to the tissue is done.

Produces proteins which cause a physiological response

27
Q

structure of norovirus

A

non-enveloped RNA virus (calciviridae)

28
Q

transmission of norovirus

A

aerosolised particles end up a distance away
- variety of different episodes

projectile vomiting

29
Q

how contagious is norovirus

A

very

10-100 particles needed for infection

30
Q

incubation period for norovirus

A

1-2 days approx

31
Q

clinical manifestation of norovirus

A

abrupt onset of vomiting & watery diarrhoea +/- fever and abdominal pain (similar to rotavirus).

32
Q

management of norovirus

A

self-limiting;

correct fluid / electrolyte balance.

33
Q

can norovirus have repeated infections

A

yes

strain specific immunity only lasts a few months.

34
Q

can norovirus survive in the environment

A

Very resilient in the environment

Have to be diligent in cleaning procedures – can self perpetuate

35
Q

3 types of salmonella

A
  1. Gastroenteritis is most common form of Salmonellosis
  2. Enteric Fever- Typhoid Fever
  3. Bacteremia
36
Q

how can a pt contract salmonella

A

Eating foods produced from infected animals; meat, milk, poultry, eggs, and drinking contaminated water; and from fecal-oral trans.

37
Q

incubation period for salmonella

A

8-48 hrs

38
Q

signs/symptoms of salmonella

A

can be asymptomatic

or after 2 days of eating infected food 
- Cramps
- Watery or bloody diarrhoea
-  Fever 
-  sometimes vomiting 
Lasts 1-4 days
39
Q

how to diagnose salmonella

A

stool, Presence of fecal WBC’s variable

40
Q

how to treat salmonella

A

supportive (IV hydration)

Antibiotics usually not necessary for Salmonella gastroenteritis (Bactrim, Amp, or Cipro indicated in pt’s c increased risk of mortality, Typhoid fever, or Bacteremia)

41
Q

when and where was the first recognised UK hospital C.diff outbreak

A

Stoke Mandeville Hospital, Aylesbury 2003
- Over 3 month period

150 cases
12 deaths

42
Q

how can a pt get C.diff

A

common cause of nosocomial antibiotic-associated diarrhea (AAD)
- over prescribing
- Only contract when over exposed to antibiotics
- Broad spectrum antibiotics get rid of competitive inhibition
Lying but start to thrive

Most common infectious cause of acute diarrheal illness in LTCFs

  • Unnecessary disease
  • Poor standards of health care lead to C.diff outbreak
43
Q

unique features of c.diff

A

anaerobic and forms spores

survive> 5 months and hard to destroy

44
Q

what is the infective dose of C.diff

A

less than 10 spores

45
Q

risk factors for CDI

A

Exposure to antimicrobials (prior 2-3 months)

Exposure to healthcare (prior 2-3 months)

Infection with toxogenic strains of C. difficile

Old age > 64 years

Underlying illness

Immunosuppression & HIV

Chemotherapy (immunosuppression & antibiotic-like activities)

Tube feeds and GI surgery

Exposure to gastric acid suppression meds ??

46
Q

microbiology features of C.diff

A

Gram positive spore forming bacillus (rods)

Obligate anaerobe

Part of the GI Flora in

  • 1-3% of healthy adult
  • 70% of children < 12 months

Some strains produce toxins A & B
- Both damaging to enterocytes in colon

Toxins-producing strains cause C. diff Infection (CDI)

CDI ranges from mild, moderate, to severe and even fatal illness (35% mortality)
- Hard wearing, chestnut spores

47
Q

transmission of C Diff

A

Faecal – oral route
- Contaminated hands of healthcare workers
- Contaminated environmental surfaces.
High level of disinfection needed

Person to person in hospitals and LTCFs

48
Q

2 reservoirs of C diff

A

Human: colonized or infected persons

Contaminated environment

49
Q

3 clinical manifestations of C diff

A

Illness caused by toxin-producing strains of C. difficile ranges from

  • Asymptomatic carriers = Colonized
  • Mild or moderate diarrhoea
  • Pseudo membranous colitis that can be fatal
50
Q

3 time scales of which pt can contract C diff

A

Acquire in hospital

Or arrive with

Or leave asymptomatic and return
- Spores in colon already and then become susceptible

51
Q

median time between exposure to onset of CDI symptoms

A

2–3 days

52
Q

5 symptoms of CDI

A

Watery diarrhoea ( > 3 unformed stools in 24 or fewer consecutive hours)

Loss of appetite

  • Become malnourished
  • -May fail to communicate this

Fever

Nausea

Abdominal pain and cramping

53
Q

CDI pathogenesis

A

Changes in intestinal microbiota
- Organisms flourish

Produces A and B toxin

54
Q

pseudomembranous colitis

A

Consequence of immune response

Plaque are inflammatory infiltrate

  • Cannot absorb nutrients
  • Sections need resected

Irreversible
- Not resume to normal pathology

55
Q

4 treatments of CDI

A

Oral rehydration

Antibiotics

  • Metronidazole, vancomycin Probiotics
  • despite being caused by antibiotics

Colectomy

Faecal transplants

  • Works but unpleasant
  • Revert microbiome to that of close family member
56
Q

case definition of CDI

A

Clinical: presence of diarrhoea AND

Laboratory: A stool test result positive for toxigenic C. diff or its toxins OR colonoscopic / histopathologic findings demonstrating evidence of pseudomembranes

57
Q

4 ways to try and prevent GI infections

A

Use of statutory powers
- Norovirus outbreak – in pt or staff – practicing dentist needs to self exclude

Safe food handling & handwashing

Infection control – enteric precautions for diarrhoea & vomiting

  • SICPs
  • Barrier nursing/patient isolation

Missuse of antibiotics

  • Esp in elderly pt groups
  • Surveillance