IC7 PR3151 Principles of antimicrobial use Flashcards
what is the systematic approach to abx use
1) confirm the presence of inf
2) determine pathogen
3) select antimicrobial
4) monitoring
what to do in step 1 of abx use
CONFIRM presence of infection:
1) risk factors
2) subjective
3) objective
4) potential site of infection
what are the risk factors for infection
1) age
2) immunosuppression
3) disruption of protective barriers
4) alterations to host flora
what are some examples of pyretic drugs
thyroid medications
anti-epileptics
beta-lactams
what are some subjective signs of infection
systemic and localised signs
Localised symptoms
* Diarrhoea, nausea, vomiting, abdominal distension
* Cough, purulent sputum
* Dysuria, frequency, urgency
* Pain and inflammation at site of infection – erythema, swelling, warmth
* Purulent discharge (wound, vaginal, urethral)
Systemic symptoms
* Feverish, chills, rigors
* Malaise
* Palpitations
* Shortness of breath
* Mental status changes
* Weakness
what are some objective signs of an infection?
vital signs
- fever > 38
- SBP < 100
- RR > 22
- HR >90
- glascow coma scale
lab tests
- TW
- neutrophils
- CRP
- ESR
- procalcitonin
radiology
what is the TW suggestive of an infection?
10 x 10^9 /L
what is the neutrophil count suggestive of an infection
> 75%
what is the CRP suggestive of an infection?
> 40mg/L
what is the procalcitonin suggestive of an infection?
> 0.5micrograms/L
difference between pathogen, coloniser and contaminant
provide some examples of the latter 2.
pathogen
- invade tissue and cause host immune response
- may be picked up from external environment or from the normal flora
coloniser
- from natural host flora but does not cause immune response
e.g., yeast
contaminant
- from external sources
e.g., s epidermis and bacillus from blood samples
how to find the difference between pathogen, coloniser and contaminant
1) single or mix growth?
2) signs and symptoms
3) consider whether the pathogen is usually found at the site of infection
4) consider epidemiology and likelihood of cause of disease
5) signs of tissue invasions
6) isolated from a single cell culture?
what are the 3 steps to antimicrobial selection?
organism, host (patient), and drug factors
benefits of combination therapy
increase the spectrum of activity, reduce incidence of resistance, synergistic effect
what is one example of synergistic effect
ampicillin + gentamicin OR ceftriaxone for enterococcal species
which penicillins have similar r1 side chains
pencillin G and V
which penicillins vs cephalosporins have similar r1 side chains
ampicillin vs cefalexin
which cephalosporins have similar r1 side chains
ceftriaxone vs cefepime
ceftazidime vs aztreonam
what is the rate of cross reactivity in penicillins vs cephalosporins and carbepenems
<2 and <1% respectively
(penicillin allergy history and management) what to use if patient has a severe immediate penicillin allergy
OKAY:
- non beta lactam antibiotics
- aztreonam
NOT OKAY
- non cross rxt cephalosporins abx can still be used but with close monitoring
- penicillins and cross rx cephalosporins unless (1) skin prick / intradermal followed by drug challenge OR (2) desensitisation
(penicillin allergy history and management) what to use if patient has a NON-severe immediate penicillin allergy
OKAY:
- non beta lactam
- aztreonam
- carbapenems
- non cross rx cephalosporins
NOT OKAY
- penicillins and cross rx cephalosporins unless (1) skin prick / intradermal followed by drug challenge OR (2) desensitisation
(penicillin allergy history and management) what to use if patient has a severe delayed (type 4) penicillin allergy
OKAY:
- non beta lactam
- aztreonam
NOT OKAY
- penicillin carbapenem cephalosporins
- avoid desensitisation
(penicillin allergy history and management) what to use if patient has a non severe delayed (type 4) penicillin allergy
OKAY:
- non beta lactam
- aztreonam
- carbapenems
- cephalosporins
- can consider penicillins with close monitoring
what are the antibiotics with good csf penetration
linezolids, penicillins, 3-5 gen cephalosporins, meropenem, vancomycin, aztreonam
what are abx with poor csf penetration
1-2 gen cephalosporins, aminoglycosides, macrolides, lincosamides
what are the different types of killing for antibiotics
time dependent
conc dependent
exposure dependent
what are the qualities of conc dependent killing? list benefits and examples
high doses with extended intervals, e.g., one single extended dose.
e.g., aminoglycossides
- reduces cost
- reduce the chance of resistance
- reduce nephrotoxicity as the tubules are already saturated.
- post antibiotic effect (pae)
aminoglyclosides target cmax/mic
8-10
recall hartford nomogram for gentamicin
dosing:
if TBW <30% IDW: use TBW
if TBW > 30% IDW: use adjBW
adjBW = 0.4*(TBW-IBW)+IBW
gentamicin dosing
5-7mg/kg
once-daily dosing
peak: 16-24mg/ml
trough <1 mg/ml
time dependent killing qualities
time > mic should be 40-70%
in cases where the pt is critically ill or there is poor concentration at the target site:
time > MIC should be 4-5x at 5-100 percent of the dosing interval
examples of drugs with concentration dependent killing
fluroquinolones
ahminoglycosides
metronidazole
examples of drugs with time dep killing
CCP - M
beta lactams: carbapenem, cephalospor, penicillin, monobactams
examples of drugs with AUC dependent killing
CLMT V
clinda
linezolid
macrolide
tetracycline
vancomycin
vancomycin AUC/MIC dosing
400-600
fluoroquinolones dosing
gram (+) auc/mic >30
gram (-) auc/mic > 125, cmax/mic: 8-12
strategies to improve time depedent killing
1) block excretion via probenecid
2) increase frequency of admin
3) continuous infusion (iV)
MINDME for ABX stewardship
Microbiology guided
Indication is evidence-based
Narrow spectrum
Dose is appropriate
Minimise duration of therapy
Ensure monotherapy
