Hospital Acquired Infections And Adaptive Immune System Flashcards

1
Q

What is a hospital acquired infection?

A

Infections arising as a consequence of providing health care
The infection was not present or incubating on admission
Onset at least 48 hours after admission

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2
Q

What are the commonest types of hospital acquired infections?

A

UTIs
GI problems
Surgical wound infections

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3
Q

Name some viruses that were/are notorious for hospital spread and state which have available vaccines

A

HepB (vaccine)
Norovirus
Influenza (vaccine)
Chicken pox (vaccine)

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4
Q

Give examples of common bacteria causing HAQ infection

A
Staph aureus (inc MRSA)
Clostridium difficile 
E-coli
Klebsiella pneumoniae
Pseudomonas aureginosa
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5
Q

Name some features of clostridium difficile

A

Gram positive
Anaerobic
Produces spores - can survive for months in a clinical environment

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6
Q

Give some risk factors for HAQ infection

A
Extremes of age
Obesity/malnourished
Diabetes
Cancer
Immunosuppressed 
Smoker
Surgical patient 
Emergency admission
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7
Q

What are the 4 Ps of infection prevention and control?

A

Patient
Pathogen
Practice
Place

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8
Q

Name some interventions we do for the patient to reduce change of HAQ infection

A
Optimise pt conditions (good nutrition, controlled diabetes)
Antimicrobial prophylaxis 
Skin preparation 
Hand hygiene 
MRSA screens
Disinfectant body wash
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9
Q

Give 2 methods of ward deep cleaning and explain why they are impractical

A

Steam cleaning
Hydrogen peroxide vapour
Difficult because need whole wards clear of people for days at a time

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10
Q

Describe the I-Five pathway for dealing with HAQ infections

A
Identify (A-F)
Isolate
Investigate
Inform (infection control/other HCPs)
Initiate (appropriate treatment)
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11
Q

What does the A-F stand for when trying to identify HAQ infections?

A
A - abroad (travel Hx)
B - blood borne infections
C - colonised
D - diarrhoea/vomiting
E - expectorating (coughing up)
F - funny looking rash 
(Things to look for)
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12
Q

Describe the pathway for suspected C. Diff infection

A

Send stool sample (look for CDT)
Take blood samples for WCC, urea, creatinine and albumin
Isolate patient and inform infection control
Stop: antibiotics, PPIs, laxatives, immunosuppressants, opioids
Ensure regular assessment

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13
Q

What features would make a case of C. Diff infection severe?

A
Sepsis 
Temp >38.5
Evidence of severe colitis
Albumin <25
WBC > 15
Acute rising serum creatinine
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14
Q

What is the treatment for severe C. Diff infections?

A

Oral vancomycin for 10 days

Needs daily assessment and review

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15
Q

What is the treatment for non-severe C. Diff infection?

A

Metronidazole (oral) for 10 days

Regular assessment

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16
Q

When can patients who’ve had a C. Diff infection mix with other patients again?

A

No diarrhoea for at least 48 hours

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17
Q

How are T cells activated?

A

By antigen presenting cells

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18
Q

What is the difference between intracellular and extracellular microbes?

A

Replicate inside/outside the host cells

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19
Q

What are the 3 stages that an APC goes through after contact with a pathogen?

A

Capture
Processing
Presentation

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20
Q

Give some features of APCs

A

Located in strategic places (where B and T cells are)
Pathogen capture - can use phagocytosis or macropinocytosis
Diversity in pathogen sensors (PRRs)

21
Q

Where are dendritic cells found?

A

Lymph nodes
Mucous membranes
Blood

22
Q

Where are Langerhans’ cells present?

23
Q

Which type of APC presents to both T and B cells?

A

Dendritic cell

24
Q

Extracellular microbes trigger which immunity first?

A

Humoral immunity

Antibodies and complement

25
Intracellular microbes trigger which immunity?
Cell-dependent immunity | CD8 cells, macrophages and antibodies
26
Where do we find MHC class I molecules?
All nucleated cells
27
Where do we find MHC class II molecules?
Antigen presenting cells and B cells
28
Give the key features of MHC molecules
Codominant expression - both parental genes are expressed to increase the number of different MHC molecules Polymorphic genes - many different alleles of each gene therefore different individuals have different presentations of antigens Can accommodate many peptides - broad specificity
29
MHC class I presents peptides from ...
Intracellular microbes
30
MHC class II presents peptides form ...
Extracellular microbes
31
MHC class I mainly activates which type of cell?
CD8+ T cells
32
MHC class II mainly activates which type of cell?
CD4+ T cells (helper)
33
What is the function of the MHC molecules?
Bind peptide fragments derived from pathogens | Display these fragments on the cell surface for recognition by appropriate T cells
34
How can MHC molecules cause organ rejection?
MHC/HLA mismatch | Recognises as foreign so attacks it
35
How do T lymphocytes recognise antigens?
Have antigen receptors called T cell receptors (TCRs) | Recognise the MHC-peptide complex
36
How are T cells activated?
Not easily Must have TCR bound to MHC-peptide complex and co-stimulatory signals before the T cells will proliferate and differentiate
37
Extracellular microbes stimulate the production of which TH molecules?
TH2 and TH17
38
Intracellular microbes stimulate the production of which TH molecule?
TH1
39
What is the role of TH1?
Helps with T cell differentiation
40
What is the role of TH2?
Activation of eosinophils, B cells and mast cells
41
What is the role of TH17?
Chemotaxis to get neutrophils to site of infection for phagocytosis
42
Which type of immunoglobulin is most abundant in the primary response to an infection?
IgM
43
Which type of immunoglobulin is more abundant in the secondary response to an infection?
IgG
44
How can we tell whether something is a primary or secondary response to infection?
Measure the IgG and IgM levels
45
What is the role of IgG?
Opsonin Activates complement Neonatal immunity as transfers from maternal blood Toxin/virus neutralisation
46
What is the role of IgA?
Mucosal immunity - prevents the microbes from attaching
47
What is the role of IgE?
Immunity against helminths (worms) | Mast cell degranulation in allergies
48
What is the role of IgM?
Complement activation