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PPE > I&I > Flashcards

I&I Flashcards

1
Q

What is microbioata?

A

-Normal commensal bacteria carried on skin and mucous membranes which are harmless or even beneficial.

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2
Q

What are the 4 ps of prevention? Describe how each category works

A
  • Patient -> anything that the patient can do to minimise infection eg MRSA screen, disinfectant bodywash, stop smoking, keep nutrition good
  • Pathogen -> factors which try to overcome prevention -> virulence factors eg toxin production, abx resistance
  • Place -> what can be done to the built environment to minimise infection -> easy clean furnishings, single use medical devices, good food hygiene and kitchen facilities
  • Practice -> goverment policies and training on infection prevention. hand hygiene, ppe etc
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3
Q

What is the gram status/shape of staphylococcus/streptococcus? How do you differentiate between the two?

A
  • Positive cocci
  • Staphylococcus are often in clusters (grapes)
  • Strep pneumonia -> diplococci
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4
Q

What is the gram status/shape of neisseria?

A

-gram negative diplococci

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5
Q

What is the gramstatus/shape of E.coli, Klebsiella, salmonella and haemophilus?

A

-Gram negative bacilli

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6
Q

What is the gram status/shape of clostridium?

A

-Gram positive rods

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7
Q

What are the ideal features of an antibiotic?

A
  • Highly selective
  • Minimal DDIs
  • Short time course
  • Minimal off target effects
  • Easy formulary ie oral with long half life
  • Reach site of infection
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8
Q

Which categories of Abx affect cell-wall synthesis? How do they work? Give examples

A
  • B lactams -> penecillin (amoxicillin, cephalosporins (ceftriaxone) Carbapenems (meropenem)
  • Glycopeptides (vancomycin)
  • bind to penecillin binding protein or cell wall cross linking enzyme to prevent cross linking of peptidoglycan
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9
Q

Which catagories of Abx affect protein synthesis? give examples

A
  • Tetracyclines -> doxycycline
  • Aminoglycosides -> gentamicin
  • Macrolides -> erythromycin
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10
Q

Which catagories of Abx affect nucleic synthesis? How do they work? give examples

A
  • Quinolones -> ciprofloxacin
  • Trimetheprim
  • Rifampicin
  • Bind to enzymes involved in DNA replication to prevent nucleic acid synthesis/assembly
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11
Q

What are the 3 main mechanisms of resistance in bacteria?

A
  • Drug inactivating enzymes eg b-lactamases
  • Altered drug targets so abx has lower affinity eg methicillin resistance
  • Altered uptake eg increased efflux or decreased permeability
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12
Q

How do bacteria acquire resistance? Describe each method

A
  • Chromosomal gene mutation -> one bacteria has altered chromosomes -> Abx kills rest of bacteria -> the resistant one multiples
  • Horizontal gene transfer -> conjugation between two bacteria passes transposon, transduction by a bacteriophage, transformation by uptake of plasmid
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13
Q

Give two penicillin containing abx which may be misgiven in hospital in a penicillin alergic

A
  • Co-amoxiclav (amoxicillin + clavulanic acid)

- Tazocin (piperacillin + tazobactam)

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14
Q

Which organisms do penicillins target?

A

-Mainly strep and staph

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15
Q

Which organisms do cephalosporins treat? What special considerations are given to ceftriaxone?

A
  • Broad gram negative spectrum

- Ceftriaxone has good activity in CSF. Also concern over associated infection with c.diff

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16
Q

What target organisms do carbapenems treat? When can this be used in penicillin allergy?

A
  • V broad spectrum of gram negative bacteria inclusing anaerobes
  • Generally safe in penicillin allergy other than anaphylaxis
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17
Q

What are the target organisms of vancomycin? When is it given orally?

A
  • Gram positive

- C.diff

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18
Q

When are tetracyclines used? When should it not be used and why?

A
  • For gram positives with penicillin allergy
  • Atypical pneumonia
  • Chlamydia
  • Children under 12 due to deposition causing yellow staining of bones and teeth
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19
Q

What are the target organisms of gentamicin? When is it used?

A
  • Gram negatives

- Gram neg sepsis

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20
Q

When is eythromycin used?

A

-Alternative to mild gram pos infection in penicillin allergic

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21
Q

When is trimethoprim used and what is an alternative? How does it work?

A
  • UTI
  • Nitrofurytoin
  • Inhibits bacterial DHFR preventing folic acid synthesis necessary for dna synthesis
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22
Q

Describe the treatments of candida

A
  • Fluconazole/clotrimazole

- Nystatin for oral

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23
Q

What is aciclovir and when is it used?

A
  • Antiviral which inhibits DNA polymerase

- Herpes simplex, varicella zoster

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24
Q

What is oseltamivir? How does it work?

A
  • Tamiflu

- Inhibits viral neuroamidase

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25
Q

What is metronidazole and when is it used?

A
  • Antibacterial and antiprotozoal

- Anaerobic bacteria, amoebae, giardia and trichomonas

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26
Q

How is neisseria meningitidis spread? State 3 virulence factors. What are the life threatening complications of meningitis? What is the treatment for meningitis?

A
  • Resp secretions
  • LPS endotoxin, pili and polysaccharide capsule
  • Sepsis
  • Raised ICP
  • AKI
  • Supportive + ceftriaxone
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27
Q

When would you suspect sepsis in a patient?

A

-Temp <36 or >38
-HR>90
-RR>20
-WBC<4 or >12
with history of infectious source/presumed reason for infection
-Organ dysfunctioneg low bp, low urine output

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28
Q

What is the sepsis 6?

A
  • Blood culture
  • Urine output
  • IV fluids
  • Empirical abx
  • serum lactate
  • high flow o2
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29
Q

List some first line physiological barriers if the innate immune system

A
  • Vomiting
  • Diarrhoea
  • Sneezing
  • Coughing
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30
Q

List some characteristics of the innate immune system

A
  • Fast
  • Non-specific
  • Predictable
  • Non-changing between infections
  • No-memory
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31
Q

What is the man WBC in innate immunity

A

-Neutrophil

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32
Q

How do phagocytes recognise pathogens in innate immunity?

A

-Pathogens have pathogen assiciated molecular patterns which are recognised by pathogen recognition receptors on phagocytes.

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33
Q

What role does complement play in innate immunity?

A
  • Increases opsonisation of pathogens

- Leads to bacterial lysis through membrane attack complex

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34
Q

Name possible causes for decreased phagocytosis

A
  • Asplenic
  • Neutropenia
  • Decreased functioning neutrophils -> chronic granulomatous disease
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35
Q

What is MHC? which cells is it present on? What is their function?

A

Major Histocompatibilty complex

  • MHCI on all nucleated cells -> disinguish self from non self by presenting intracellular peptides to CD8+ T cells
  • MHCII -> only on antigen presenting cells -> Presents peptides from extracellular organisms/debris to CD4+ t cells
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36
Q

Why is MHC described as polymoprhic and what affect does this have in the general population?

A
  • Encoded for by HLA genes of which there are a wide number of variants. Each person has 2 HLA genes producing different alleles amongst different individuals. M
  • MHC in each person can recognise individual number and types of microorganisms meaning susceptibility to infection depends on the MHC molecule present
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37
Q

How does HLA cause problems during organ transplantation?

A

-If the HLA genes upon the transplanted organ does not match the recipient the body will recognise it as foreign and transplant rejection will occur

38
Q

Describe the pathway of activation in response to an extracellular microbe

A

-APC recognises antigen -> phagocytosis -> displays bacterial peptide on MHCII -> Activates CD4+ T cells -> activates B cells and humoral immunity

39
Q

Describe the pathway of activation in response to an intracellular microbe

A

-Intracellular peptides become expressed on MHC I-> recognised by activated CD8+ T cells -> cytotoxic AND expressed on MHCII -> activates CD4+ -> Activate CD8+ cells and B cells

40
Q

Describe the functions of the different classes of antibodies

A
  • IgG -> phagocytosis, complement, neonatal immunity
  • IgM -> non-specific recognition -> complement activation
  • IgE -> Helmonth immunity, mast cell degranulation
  • IgA -> mucous membrane immunity -> most common in body
41
Q

What is a healthcare acquired infection?

A

-Infection which occurs as a consequence of providing/receiving healthcare. Onset must be 48 hours after admission (72 for c.diff)

42
Q

Which two infections are most common HCAI?

A
  • C.diff

- Norovirus

43
Q

Why does MRSA have a high mortality?

A

-Often develops in hard to treat areas such as heart valves

44
Q

Why is c.diff so prevalent in HCAI?

A

-Opportunistic pathogen which can form spores and survive on many surfaces

45
Q

How does norovirus present?

A

-Gastroenteritis (nausea, vomiting, diarrhoea etc)

46
Q

Which groups of people are most likely to get HCAI?

A
  • Elderly
  • Neonates (reduced skin quality and immunity)
  • Smoker
  • Surgical Pts
  • Emergency admission
47
Q

State features of adptive immunity

A
  • Specific
  • Has memory
  • decreased time response to second exposed
  • Slow onset
48
Q

Give 3 examples when Abx are given as a prophylaxis

A
  • Peri-operatively
  • Meningitis contact
  • Asplenic patients/immuodeficiency
49
Q

Give 4 factors which may help you decide what Abx to give

A
  • History of infection eg where did they get it? community vs hosp
  • Severity of infection
  • Resistance of likely organism
  • Immune status of the patient
50
Q

Give 3 influenza-related complications

A
  • Bronchitis
  • Pneumonia
  • Sinusitis
51
Q

Why is influenza A the most severe?

A
  • It has multiple host species meaning it can be easily transferred
  • Expresses the most antigenic drift and shift
52
Q

Describe the life cycle of influenzae virus

A

1) Entry into cell as haemagglutinin binds to sialic acid on host membrane and initiates receptor mediated endocytosis
2) Endosomal vesicle has low pH and triggers fusion of the endosomal membrane with the viral membrane. Also triggers M2 ion channel to open.
3) H+ enters viral core through M2 and uncoating is initiated. Virl proteins are released into the cell
4) Transcription of viral components via RNA polymerase and viral particles are assembled into a new virus
5) New virus buds out of cell taking host cell membrane with it in order to evade the immune system. During budding haemagglutinin binds to sialic acid again but it is cleaved via neuroamidase caused its release

53
Q

Describe the possible RX of influenza infection

A
  • Vaccination produces Abs to Haemagglutinin
  • M2 inhibitors prevent the viral proteins from being uncoated and preleased into cell eg amantidine/rimantidine
  • Neuroamidase inhibitors which prevents new viruses from budding out of the cell eg Oseltamivir/zanamivir
54
Q

Give some ADRs of amantidine and Osetlamivir

A
  • Amantidine -> (dopamine agonist) CNS excitability, irritability, GI disturbances, Hypotension
  • Oseltamivir -> GI disturbances, headache, nosebleed
55
Q

When is oseltamivir recommended for use by NICE?

A

-Complicated influenza with onset within 48 hours

56
Q

Give the most likely causative organisms of meningitis inthe following age groups:

i) neonates
ii) 2-5 years
iii) 5-30 years
iv) 30+

A

i) E.coli/L.monocytogenes
ii) H.Influenzae
iii) N. Meningitidis
iv) S.Pneumoniae

57
Q

Which part of the brain does encephalitis affect? What type of organism classically causes encephalitis? Which viruses are associated with temporal, spinal cord and brainstem encephalitis?

A
  • Brain parenchyma (rather then the meninges)
  • Viruses
  • Temporal = herpes, SC = polio, brainstem = rabies
58
Q

Describe the pathogenesis and presentation of malaria

A
  • Bitten by females anopheles bacteria infected with a protozoan known as plasmodium
  • Protozoa infect liver cells and form schizonts (mature parasite with many infective offspring) -> Rupture -> Merozoites infect RBC and matures to form schizont -> ruptures RBC -> Enters a cycle and leads to haemolytic anaemia
  • Presents with jaundice, fever/chills, myalgia, headache
59
Q

What are the v strains of plasmodium which cause malaria and which is most severe?

A
  • Falciparum (severe)
  • Vivax
  • Ovale
  • Malariae
60
Q

Quinines are often prescribed for malarial infections, in who have you to be careful in prescribing quinines?

A

-People with G6PD deficiency

61
Q

What is the pathogenesis enteric fever? How does it present?

A
  • Feacal-oral spread of the organism salmonella typhi/paratyphi which produces endotoxin and invasins allowing direct epithelial damage of bowels. Infect peyers patches in ileum
  • Constipation, severe cramps, vomiting
62
Q

Give 3 causes of travellers diarrhoea

A

-E.coli, Campylobacter, Salmonella typhi, shigella

63
Q

What is antgenic drift and shift?

A
  • Drift is small mutations which continually occur from person to person
  • Shift is complete change in viral protein composition -> can lead to virulent subtypes
64
Q

How is HIV spread?

A

-Sexual, sharing needles, vertical, medical

65
Q

Describe what happens to the viral load and CD4+ count during infection

A

1) Acute infection occurs with high viral load and body attempts to mount a response but it is not enough to clear infection -> initial flu-like symptoms but viral load decreased
2) Latent infection for 2-10 years with a gradual decrease in CD4+ count as infected cells die and a slow rise in viral load. the bone marrow begins to produce more and CD4 count begins to rise again
3) Viral load increases and symptomatic infection occurs as the viral load outweights the CD4+ cells -> Pneumonias, candida etc
4) AIDS as viral load high and CD4 very low -> kaposis sarcoma, PJP, TB etc

66
Q

What are the main ways bacteria travel from surfaces to cause infection?

A
  • Invasion
  • Migration
  • Innoculation
  • Haematogenous
67
Q

Define hypersensitivity

A

-Antigen-specific immune responses which are either inappropriate or excessive and result in damage to the host

68
Q

What is t1 hypersensitivity?

A

-Immediate reaction eg allergies to infectious agents, driven by IgE and TH2 cells

69
Q

What is t2 hypersensitivity?

A

-Antibody mediated response to a tissue or cellular component 5-12 hours after exposure (IgG or IgM)

70
Q

What is t3 hypersensitivity?

A

-Immune complex mediated response to soluble antigen which causes immune complexes to de deposited in the tissues eg SLE, poststreptococcal glomerulonephritis

71
Q

What is t4 hypersensitivity?

A

-Cell mediated response to self antigen or infectious agent 24-48 hours after exposure eg transplant rejection

72
Q

What is anaphylatic shock?

A

-Systemic activation of mast cells causing hypotension/circulatory collapse, generalised urticaria, angioedema and breathing difficulty

73
Q

What is the sensitisation and effector phase of allergy?

A
  • Sensitisation refers to the first encounter with antigen -> no response but antibody made
  • Effector is second encounter with same angitgen produces a response
74
Q

How does adrenaline work in anapylaxis?

A

-Reverses peripheral vasodilation, reduces oedema, reverses bronchospasm, increased force of myocardial contraction. inhibits mast cell activation

75
Q

Define the terms endemic disease, outbreak, epidemic and pandemic

A
  • Endemic is the usual background rate of a disease
  • Outbreak is two or more cases related in time and place
  • Epidemic is infection greater then the usual background rate
  • Pandemic is a very high rate spreading across many places
76
Q

How can evolution of pathogens cause new outbreaks?

A
  • New virulence factor
  • New resistance
  • New antigens
77
Q

What interventions can be put in place to stop outbreaks?

A
  • Vaccinations
  • Appropriate antibacterial use
  • Appropriate PPE in clinical settings
  • Good housing and sanitation
78
Q

What is the danger of herd immunity?

A

-If not enough people become vaccinated it may just delay the age of onset

79
Q

Give 3 benefits of antimicrobial stewardship

A
  • Decreased emergence of resistant bacteria
  • Decrease economic cost
  • Minimise toxicity and ADRs due to shortened course
80
Q

What 3 types of interventions can be used in antimicrobial stweardship?

A
  • Persuasion eg education
  • Restriction eg on fomulary
  • Structural eg rapid lab tests on orgamisms
81
Q

What is the basic reproduction number?

A

-The average number of cases one case will generate over its infectious period in an otherwise uninfected, non immune population

82
Q

Why do infections often occur aside chronic disease?

A
  • Change in the structure/function of affected organ(s)
  • Changes in interaction between patient and pathogen
  • Altered presence of microbiota
  • Consequences of treatment
83
Q

What 2 organisms are associated with COPD?

A
  • Haemophilus Influenza

- Pseudomonas Areuginosa

84
Q

Why are diabetic patients more prone to infections?

A
  • Hyperglycaemia favours the growth of microorganisms
  • Hyperglycaemia/acidosis impair immunity
  • Microvascular insult impairs perfusion favouring infection
  • Diabetic neuropathy leads to decreased sensation to the skin including cuts, abrasions and ulcers -> may become infected
85
Q

Why are people with CF prone to infection?

A
  • Decreased ability to clear organisms from lungs due to defective mucociliary esculator
  • Viscous mucus traps microbes which multiply
86
Q

What infection are people with CF prone to?

A

-Mucoid pseudomonas aeruginosa

87
Q

What infections are diabetics prone to getting?

A
  • UTIs

- Cellulitis or skin infections

88
Q

What is an immunocomprimised host?

A

-A person who’s immune system is unable to respond appropriately and effectively to infectious microbes leading to increasing frequency and severity of infections

89
Q

What is a primary immunodeficiency? Who do they most commonly present in? When do the symptoms become evident?

A
  • An intrinsic defect eg gene disorder which causes the immune system to function inappropriately
  • Males under 20 years
  • In the first few months of life
90
Q

If a person has an antibody deficiency, what infections are they prone to?

A

-Recurrent bacterial infections

91
Q

What is chronic granulomatous disease?

A

-Primary phagocutic disease where neutrophils are unable to produce the oxidative burst needed to clear infections leading to prolonged infections

92
Q

A T cell deficiency would lead to increased susceptibility to which infections?

A

-Viruses

PPE (15 decks)

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