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BDS2 BAMS > GI Infections > Flashcards

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
invasive infection
The organism enters the mucosal cells, destroys them, causing diarrhoea usually with blood in the stool
26
enterotoxic infection
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
structure of norovirus
non-enveloped RNA virus (calciviridae)
28
transmission of norovirus
aerosolised particles end up a distance away - variety of different episodes projectile vomiting
29
how contagious is norovirus
very 10-100 particles needed for infection
30
incubation period for norovirus
1-2 days approx
31
clinical manifestation of norovirus
abrupt onset of vomiting & watery diarrhoea +/- fever and abdominal pain (similar to rotavirus).
32
management of norovirus
self-limiting; | correct fluid / electrolyte balance.
33
can norovirus have repeated infections
yes strain specific immunity only lasts a few months.
34
can norovirus survive in the environment
Very resilient in the environment Have to be diligent in cleaning procedures – can self perpetuate
35
3 types of salmonella
1. Gastroenteritis is most common form of Salmonellosis 2. Enteric Fever- Typhoid Fever 3. Bacteremia
36
how can a pt contract salmonella
Eating foods produced from infected animals; meat, milk, poultry, eggs, and drinking contaminated water; and from fecal-oral trans.
37
incubation period for salmonella
8-48 hrs
38
signs/symptoms of salmonella
can be asymptomatic ``` or after 2 days of eating infected food - Cramps - Watery or bloody diarrhoea - Fever - sometimes vomiting Lasts 1-4 days ```
39
how to diagnose salmonella
stool, Presence of fecal WBC’s variable
40
how to treat salmonella
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
when and where was the first recognised UK hospital C.diff outbreak
Stoke Mandeville Hospital, Aylesbury 2003 - Over 3 month period 150 cases 12 deaths
42
how can a pt get C.diff
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
unique features of c.diff
anaerobic and forms spores | survive> 5 months and hard to destroy
44
what is the infective dose of C.diff
less than 10 spores
45
risk factors for CDI
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
microbiology features of C.diff
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
transmission of C Diff
Faecal – oral route - Contaminated hands of healthcare workers - Contaminated environmental surfaces. High level of disinfection needed Person to person in hospitals and LTCFs
48
2 reservoirs of C diff
Human: colonized or infected persons Contaminated environment
49
3 clinical manifestations of C diff
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
3 time scales of which pt can contract C diff
Acquire in hospital Or arrive with Or leave asymptomatic and return - Spores in colon already and then become susceptible
51
median time between exposure to onset of CDI symptoms
2–3 days
52
5 symptoms of CDI
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
CDI pathogenesis
Changes in intestinal microbiota - Organisms flourish Produces A and B toxin
54
pseudomembranous colitis
Consequence of immune response Plaque are inflammatory infiltrate - Cannot absorb nutrients - Sections need resected Irreversible - Not resume to normal pathology
55
4 treatments of CDI
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
case definition of CDI
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
4 ways to try and prevent GI infections
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

BDS2 BAMS (54 decks)

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