principles of antimicrobial use Flashcards

(80 cards)

1
Q

4 steps in systematic approach

A
  1. confirm presence of infection
  2. identification of pathogens
    ^ both for confirming indication of antibiotic
  3. selection of antimicrobial and regimen
    ^ choice, route, dose, duration
  4. monitoring response
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2
Q

how to confirm is presence of infection

A
  • look at risk factors
  • subjective evidence
  • objective evidence
  • whats the possible site of infection
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3
Q

what are possible risk factors for infection

A

1.disruption of natural barriers
eg break in skin or mucous membrane eg ulcer
or damaged cilia or resp tract
ANY disruption to host immune system innate or adaptive

  1. age , very old or very young
  2. immunosuppression
    eg malnutrition, acquired or hereditary ( hiv/aids)
    drugs eg chemo or immunosuppresants , steroids
  3. alterations in normal flora
    eg use of ab - clear susceptible bacteria but stronger bact grows
    or uncontrolled blood sugar - nutrients for bact to grow
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4
Q

what are localised subjective evidence of infection

think location wise

A

git - diarrhea, nausea, vomitting, abdominal distension
resp tract - cough , sputum
uti - frequency , urgency, dysuria
purulent discharge - in wound, urethal or vaginal
pain and inflamation @ site , eythema, swelling , warmth

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5
Q

why is pus a sign of infection

A

pus > wbc > there to rescue during infection

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6
Q

what are systemic subjective evidence of infection

A
fever , chills, rigors
malaise - general tiredness 
palpitations 
sob 
mental status changes 
weakness
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7
Q

vital signs indicating infection IMPT

objective evidence

A
  1. fever > 38 deg
    - may be masked by use of antipyretics,
    panadol, nsaids, ibuprofen or aspirin
  2. hypotension SBP < 100MMhG
  3. tachypnea resp rate > 22bpm
  4. heart rate > 90bpm
  5. mental status esp in elderly, drop is glasglow coma scale
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8
Q

non infectious causes of fever (5)

A
cancer 
autoimmne disease 
intracranial hemrrhage 
drug fever - could be hypersensitivity but reduces when drug removed 
hyperthyroidism
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9
Q

which drugs often cause drug fever

A

blactams, antiepileptic or anticonvulsants, allopurinol

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10
Q

lab tests indicating infection

A

acute phase reactants - conc inc during inflammation
1. elevated or depressed Total white
normal 4-10 x 10^9 /L

  1. inc neutrophils normal 45-75%
  2. inc CRP c reactive protein , normal < 10, infection> 40
  3. inc ESR , erythrocyte sedimentation rate ESR ( more useful for bone and joint infection not rlly for general infection
  4. inc procalcitonin
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11
Q

whats an impt consideration for objective infection

A

compare against baseline values

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12
Q

procalcitonin guide for starting ab

A

conc 1 or more microgram/L - AB stronly encouraged
0.5 to < 1 - ab encouraged
0.25 to < 0.5 AB discouraged
<0.25 AB strongly discouraged

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13
Q

what to consider for renally impaired patients and their procalcitonin levels

A

procalcitonin excreted renally so there could be continued inc in the levels, so compare with baseline levels

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14
Q

if blood sample taken for calculation of procalcitonin concentration at early stage of episode , when to take the second reading

A

obtain a second procalcitonin concentration 6-12 hr later

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15
Q

procalcitonin guidelines for stopping AB

A
  • inc from peak conc & 0.5 or more - change ab
  • dec < 80% from peak conc & 0.5 or more - cont AB
  • dec 80% or more from peak conc & 0.25 to 0.5 - stop AB
  • conc < 0.25 - stop AB strongly encouraged
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16
Q

objective evidence from radiological imaging

A

tissue changes ,
collections,
abscess, - pus collection
obstructions - disruption = higher chance of growth

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17
Q

which are the common sites of infection

A

uti, rti , ssti and intra abdominal

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18
Q

why is it impt to send pretreatment cultures and not follow up culture

A

could result in false negatives bc empiric therapy could have killed the pathogen
- could leave behind other pathogens that are not the causative ones

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19
Q

likely contaminant from blood culture

A

staphylococcus epidermis , bacillus spp.

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20
Q

likely coloniser from urine culture

A

yeast

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21
Q

what to consider when choosing the antimicrobial regimen

A

purpose - empiric, definitive or prophylaxis
which route, dose, dosing and duration
consider host and drug factors too

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22
Q

differentiate between prophylaxis, empiric and definitive

A

empiric:
- microbio results not out yet
- use ab based on clinical presentation of likely infection site, likely organism at the site and likely susceptibility from antibiogram

definitive

  • when microbio test results avail
  • culture-directed therapy

prophylaxis
- ab given to prevent infection

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23
Q

eg of prophylaxis situations

A

surgical prophylaxis

or post exposure prophylaxis eg for hiv or std to remove microorganism and prevent infection

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24
Q

what happens if overtreat

A

ab associated toxicity
c difficile - diarrhea
resistance = inc cost

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25
guidelines for which to choose
narrowest spectrum dose individualised shortest duration
26
t/f active antimicrobials shld be administered as soon as possible for severly ill patients
true
27
3 diff outcomes of combination therapy
indifference - combo of A and B slightly better synergy - combo is much more effective antagonism - combo gives a worse effect
28
which combination for hospital acquired pneumonia
piperacillin-tazobactam + vancomycin
29
which combination for ventilator associated pneumonia
piperacillin-tazobactam + ciprofloxacin to cover pseudomonas aeruginosa
30
which combi for entercoccus endocarditis
ampicillin + gentamicin/ ceftriaxone
31
whats another ab combination that has synergistic bactericidal effect
trimethoprim + sulfamethoxazole
32
why use combi treatment
for empiric treatment | following antibiogram combine to get as close to 100% coverage as possible
33
disadvantages of combination therapy
- risk of toxicity and allergic reactions - ddi risk - inc cost - selection pressure - inc risk of superinfections ( 2nd infection superimposed on the orignal infection cause by another microroganism resistant to the initial treatment used ) - antagonistic effect use
34
eg of antagonistic combination
in treatment of aspergillus, combination of amphotericin and itraconazole
35
which ab avoided in children generally
tetracyclines ( discolouration ) | fluoroquinolones - cause joint athropathy in animals
36
why g6pd deficiency is concern for ab
concern about hemolysis of rbc
37
which ab to avoid if g6pd deficiency present
sulfonamides nitrofurantoin fluoroquinolones ( inconsistent data )
38
what causes cross reactivity between penicillins, cephalosporins and carbapenems
``` similar side chain not class effect ```
39
drugs safe for pregnancy
blactams and macrolides
40
avoid in pregnancy
aminoglycosides co-trimoxazole fluoroquinolones tetracyclines
41
causes nephrotoxicity
aminoglycosides, high dose vancomycin
42
causes hepatoxicity
pyrazinamide | amoxicillin-clav ( augmentin )
43
if immunocompromised use what and give examples
bactericidal growth - kills bact eg blactams, guinolones, aminoglycosides, vanco
44
t/f if immunocompromised give broader spectrum coverage
true
45
covers esbl producing enterobacterales
5th gen cephalosporins
46
covers amp-c producing enterobacterales
4th gen cephalosporins onwards
47
impt consideration for amp c producing
may appear sensitive because inherently able to product amp c upon exposure to 3rd gen so must be careful bc could be induced to produce amp c and become resistant during treatment - for sick patients use carbapenams to treat
48
unable to reach adaqueate csf conc
gen 1 and 2 cephalo aminoglycosides macrolides clindamycin
49
used for csf
``` meropenam peniciilins ceftriaxone cefepime ceftazidime vancomycin ( option for mrsa, give intrathecal) ```
50
why is daptomycin not for pneumonia
inactivated by lung surfectant
51
why aminoglycosides not for abscesses
acidic environmetn
52
which drugs for prostatitis and why
ciprofloxacin and co-trimoxazole bc distribute well into prostate
53
concentration dependant pkpd meaning and examples of drug like this
rate and extent of killing is related to the ab conc = higher conc = more rapid and extensive killing grps : aminoglycosides and fluoroquinolones
54
what is the dosing strategy for conc dependant pkpd
optimise peak - MIC ratio peak is 8-10x above mic high auc/mic ratio or cmax /mic - larger doses at extended intervals eg once daily aminoglycoside dosing
55
for conc dependant killing would u choose 250mg q12h or 500mg q24h
to achieve high peak, give less frequency for better bacterial kill based on pkpd, choose 500mg q24h higher cmax/mic ratio
56
what is pae and what does this mean
post antibiotic effect | dosent matter if trough is below mic
57
why is once daily dosing given instead of multiple daily dose for aminoglycoside
- conc dependant killing - pAE - prevents adaptive resistance = prevents selection of more resistant mutants - less nephrotoxicity - save cost
58
describe time dependant bacteria killing with no persistent effect aka short half life
rate and extent of killing to do with amt of time ab conc is above the mic
59
time dependant killing for which classes
pencillins , cephalosporins and carbapenems
60
dosing strategy for time dependant killing
optimise %T>MIC 40-70% of dosing interval shld be above mic - more frequent administration - iv infusion or intermittent infusion
61
what is used to block excretion of drugs
probenacid
62
describe time dependant bact killing with persistent effect aka long half life or PAE
rate and extent of killing related to overall drug exposure AUC vs MIC
63
classes that experience the time dependant killing w persistent half life
vanco
64
dosing strategy for time dependant killing with persistent half life
optimise AUC : MIC ratio auc : dose/clearance eg vanco target for 400-600 for MRSA
65
give 500mg q12 or 1g q24 for vanco
1g q24hr bc auc = dose/cl and for same patient both have same total dose so reducing adm freq = save cost
66
when to give iv
hospitalised, severe inf | when need high blood conc
67
when to avoid oral
gi pathology suitable oral antibiotic not avail ( eg aminogly) high tissue conc needed eg endocarditis or meningitis , bone or joint urgent treatment non compliance
68
antimicrobes with good oral bio
fluoroquinolones metronidazole linezolid co-trimoxazole
69
im examples
im ceftriaxone IM streptomycin Im benzathine penicillin
70
topical eg
clotrimazole pessaries for vaginal candidiasis
71
aerosolised or nebulised drug eg
nebulised colistin for mdr pseudomonas aeruginosa pneumonia
72
drug that could cause collateral damgage
fluoroquinolones | - can select for resistant bacteria or other resistance patient wasnt even exposed to
73
what cannot be use d with carbapenams
valproate | - bc wanna keep high conc but ddi reduces the conc
74
which class cant be used with cyp450 inhibitbors
azole antifungals and macrolides
75
which class cant be used with cyp450 inducers
rifampicin
76
adr for aminoglycoside to monitor for
serum creatinine , urine output
77
adr for vancomycin
flushing , hypotension, itch , red man syndrome | slow infusion start 500mg over 1 hr and monitor
78
what to consider when modifying therapy
if can narrow, do that if can use oral do that stop if completed duration
79
what could cause unsatisfactory response
- inappropriate diagnosis - resistance - non compliance - renal function - ddi - collections or abscess- needing surgery or drainage - immune response - superinfection - toxicity
80
how long to given empiric treatment for
48 to 72 hrs to work