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Infection And Immunity > Hospital Acquired Infections And Adaptive Immune System > Flashcards

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?

A

Skin

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
Q

Intracellular microbes trigger which immunity?

A

Cell-dependent immunity

CD8 cells, macrophages and antibodies

26
Q

Where do we find MHC class I molecules?

A

All nucleated cells

27
Q

Where do we find MHC class II molecules?

A

Antigen presenting cells and B cells

28
Q

Give the key features of MHC molecules

A

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
Q

MHC class I presents peptides from …

A

Intracellular microbes

30
Q

MHC class II presents peptides form …

A

Extracellular microbes

31
Q

MHC class I mainly activates which type of cell?

A

CD8+ T cells

32
Q

MHC class II mainly activates which type of cell?

A

CD4+ T cells (helper)

33
Q

What is the function of the MHC molecules?

A

Bind peptide fragments derived from pathogens

Display these fragments on the cell surface for recognition by appropriate T cells

34
Q

How can MHC molecules cause organ rejection?

A

MHC/HLA mismatch

Recognises as foreign so attacks it

35
Q

How do T lymphocytes recognise antigens?

A

Have antigen receptors called T cell receptors (TCRs)

Recognise the MHC-peptide complex

36
Q

How are T cells activated?

A

Not easily
Must have TCR bound to MHC-peptide complex and co-stimulatory signals before the T cells will proliferate and differentiate

37
Q

Extracellular microbes stimulate the production of which TH molecules?

A

TH2 and TH17

38
Q

Intracellular microbes stimulate the production of which TH molecule?

A

TH1

39
Q

What is the role of TH1?

A

Helps with T cell differentiation

40
Q

What is the role of TH2?

A

Activation of eosinophils, B cells and mast cells

41
Q

What is the role of TH17?

A

Chemotaxis to get neutrophils to site of infection for phagocytosis

42
Q

Which type of immunoglobulin is most abundant in the primary response to an infection?

A

IgM

43
Q

Which type of immunoglobulin is more abundant in the secondary response to an infection?

A

IgG

44
Q

How can we tell whether something is a primary or secondary response to infection?

A

Measure the IgG and IgM levels

45
Q

What is the role of IgG?

A

Opsonin
Activates complement
Neonatal immunity as transfers from maternal blood
Toxin/virus neutralisation

46
Q

What is the role of IgA?

A

Mucosal immunity - prevents the microbes from attaching

47
Q

What is the role of IgE?

A

Immunity against helminths (worms)

Mast cell degranulation in allergies

48
Q

What is the role of IgM?

A

Complement activation

Infection And Immunity (9 decks)

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