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PR3124 CA2 > Principles of Antimicrobial Use > Flashcards

Principles of Antimicrobial Use Flashcards

1
Q

Septic shock

A

Profound hemodynamic and metabolic abnormalities

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2
Q

TW

A

normal 4-10x10^9/L

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3
Q

neutrophils

A

45-75% normal range (relative to total WBC, most significantly phagocytose bacteria)

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4
Q

CRP

A

normal <10mg/L, infection >40mg/L

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5
Q

Procalcitonin

A

< 0.5ug/L

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6
Q

What does increase in lymphtocyte mostly indicate?

A

TB/ viral infectiom

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7
Q

Which is the most specific biomarker of infection (objective evidence)?

A

procalcitonin helps decide to start/stop abx

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8
Q

Usual sterile sites

A

kidney, bladder, cns, cvs, lower respiratory tract, bone, joint

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9
Q

Most common sites of infection

A

respiratory tract, urinary tract, skin and soft tissue, intra abdominal

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10
Q

Types of combination therapy

A

indifference (most of the time), synergy, antagonism

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11
Q

Benefits of combination therapy

A
  1. Extend spectrum of activity
  2. Achieve synergistic bactericidal effect
  3. Prevent development of resistance
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12
Q

Hospital-acquired pneumonia (combi therapy)

A

Empirical or definitive therapy of polymicrobial infections: piper/tazo + vanco
- extend spectrum of activity

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13
Q

Ventilator associated pneumonia (combi therapy)

A

Empirical therapy to cover all resistant strains of the same org: piper/tazo + cipro, cover Pseudomonas aeruginosa
- extend spectrum of activity

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14
Q

Enterococcus endocarditis (combi therapy)

A

Ampicillin + gentamicin or ampicillin + ceftriaxone

- achieve synergistic bactericidal effect

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15
Q

Why are trimethoprim and sulfamethoxazole combined to be used as co-trimoxazole?

A

Achieve synergistic bactericidal effect

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16
Q

Eg. of combi therapy used for prevention of development of resistance?

A

antimicrobial combinations against M. tuberculosis, HIV

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17
Q

Disadvantages of combination therapy

A
  1. Increased risk of toxicity and allergic reactions
  2. Increased risk of drug interactions
  3. Increased cost
  4. Selection of MDR bacteria
  5. Increased risk of superinfections (2nd infection imposed on earlier one by a different microorg)
  6. Concern for antagonistic effect - more of an issue for antifungals
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18
Q

host factors (9)

A

age, g6pd, pregnancy and lactation, severity of illness, status of host immune function, renal or hepatic impairment, history of allergy and adr, HA-assoc risk factors, recent antimicrobial use

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19
Q

Cross-reactivity present in ADR?

20
Q

Cross-reactivity present in allergy?

21
Q

Cross reactivity between penicillins and cephalosporins or carbapenems is due to?

A

Allergic reaction to abx with similar side chain, not a class effect

22
Q

Shared side chain R1 (clinically relevant cross sensitivity)

A

amoxicillin, ampicillin, cephalexin

ceftriaxone, ceftazidime, cefepime, aztreonam

23
Q

Which cephalosporin has no share side chain R1 with pencillins?

24
Q

Empiric antimicrobial therapy based on

A

clinical presentation of likely site of infection, likely organisms causing infection at that site and likely susceptibility from antibiogram

25
Q

Bactericidal drugs

A

B-lactams, quinolones, aminoglycosides, vancomycin

26
Q

Amp-C

A

Beta-lactamase, can destroy B-lactam rings of cephalosporins (1st-3rd gen)

27
Q

ESBL

A

able to destroy B-lactam rings of 1st-3rd gen cephalosporins
- 4th gen cefepime may be able to retain activity

28
Q

Hepatotoxic antimicrobials

A

pyrizinamide, amoxi/clav

29
Q

Nephrotoxic antimicrobials

A

Aminoglycoside, high dose vancomycin

30
Q

How should you dose aminoglycosides in a renal impaired patient?

A

Require longer time to clear, extend dosing interval

31
Q

Hartford Nomogram/Therapeutic Drug Monitoring of aminoglycosides

A

1st dose of 7mg/kg infusion, take serum conc at a particular time and compare with the graph

32
Q

Aminoglycosides are less effective for?

A

Abscesses (acidic), does not distribute well in acidic envi

33
Q

Concentration-dependent bacterial killing

A

Aminoglycosides, fluoroquinolones

34
Q

Time-dependent bacterial killing with no persistent effect (short half live = 2-3hr)

A

cephalosporins, carbapenems, penicillins

35
Q

Probenecid can be used to

A

block excretion of time-dependent bacterial killing with no persistent effect drugs eg. ceph, pen, carbapenem

36
Q

Time-dependent bacterial killing with persistent effect (long half life or PAE)

A

vancomycin

37
Q

CYP450 inhibitor

A

azole antifungal, macrolides

38
Q

CYP450 inducer

A

rifampicin

39
Q

Aminoglycoside adr monitoring parameters

A

serum creatinine, urine output (renal function)

40
Q

Vancomycin adr monitoring parameters

A

flushing, hypotension, itch (Red Neck Syndrome)

  • SLOW INFUSION: 500MG OVER 1HR
  • PATIENT SHOULD BE LYING DOWN
41
Q

Oral route generally preferred unless

A
  1. GI pathology, absorption provlem
  2. oral dosage form not available eg vanco/aminoglycoside
  3. high tissue conc essential eg endocardititis, meningitis, bone, joint
  4. urgent tx required
  5. pt non-compliance
42
Q

Antimicrobials with good bioavail

A

fluoroquinolones, metroidazole, linezolid, cotrimoxazole

43
Q

IM abx

A

ceftriaxone, streptomycin, penicillin benzathine

44
Q

DDI carbapenem

A

decr conc of valporate, anti-epileptic agent

- if only used for mood stabiliser, therapeutic effect still present

45
Q

Causes of unsatisfactory response

A
  1. Inappropriate diagnosis
  2. Inappropriate choice of agent
  3. Subtherapeutic concentration
  4. Collection of abscesses, need surgery or drainage
  5. Impaired host defense
  6. Superinfection
  7. Toxicity of drug

PR3124 CA2 (6 decks)

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