Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3124 ca2 > principles of antimicrobial use > Flashcards

principles of antimicrobial use Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how to confirm is presence of infection

A
  • look at risk factors
  • subjective evidence
  • objective evidence
  • whats the possible site of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why is pus a sign of infection

A

pus > wbc > there to rescue during infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are systemic subjective evidence of infection

A 
fever , chills, rigors
malaise - general tiredness 
palpitations 
sob 
mental status changes 
weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which drugs often cause drug fever

A

blactams, antiepileptic or anticonvulsants, allopurinol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

whats an impt consideration for objective infection

A

compare against baseline values

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

objective evidence from radiological imaging

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which are the common sites of infection

A

uti, rti , ssti and intra abdominal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

likely contaminant from blood culture

A

staphylococcus epidermis , bacillus spp.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

likely coloniser from urine culture

A

yeast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

eg of prophylaxis situations

A

surgical prophylaxis

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what happens if overtreat

A

ab associated toxicity
c difficile - diarrhea
resistance = inc cost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

guidelines for which to choose

A

narrowest spectrum
dose individualised
shortest duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

t/f active antimicrobials shld be administered as soon as possible for severly ill patients

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 diff outcomes of combination therapy

A

indifference - combo of A and B slightly better
synergy - combo is much more effective
antagonism - combo gives a worse effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which combination for hospital acquired pneumonia

A

piperacillin-tazobactam + vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

which combination for ventilator associated pneumonia

A

piperacillin-tazobactam + ciprofloxacin to cover pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

which combi for entercoccus endocarditis

A

ampicillin + gentamicin/ ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

whats another ab combination that has synergistic bactericidal effect

A

trimethoprim + sulfamethoxazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

why use combi treatment

A

for empiric treatment

following antibiogram combine to get as close to 100% coverage as possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

disadvantages of combination therapy

A
  • 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
Q

eg of antagonistic combination

A

in treatment of aspergillus, combination of amphotericin and itraconazole

35
Q

which ab avoided in children generally

A

tetracyclines ( discolouration )

fluoroquinolones - cause joint athropathy in animals

36
Q

why g6pd deficiency is concern for ab

A

concern about hemolysis of rbc

37
Q

which ab to avoid if g6pd deficiency present

A

sulfonamides
nitrofurantoin
fluoroquinolones ( inconsistent data )

38
Q

what causes cross reactivity between penicillins, cephalosporins and carbapenems

A 
similar side chain 
not class effect
39
Q

drugs safe for pregnancy

A

blactams and macrolides

40
Q

avoid in pregnancy

A

aminoglycosides
co-trimoxazole
fluoroquinolones
tetracyclines

41
Q

causes nephrotoxicity

A

aminoglycosides, high dose vancomycin

42
Q

causes hepatoxicity

A

pyrazinamide

amoxicillin-clav ( augmentin )

43
Q

if immunocompromised use what and give examples

A

bactericidal growth - kills bact

eg blactams, guinolones, aminoglycosides, vanco

44
Q

t/f if immunocompromised give broader spectrum coverage

A

true

45
Q

covers esbl producing enterobacterales

A

5th gen cephalosporins

46
Q

covers amp-c producing enterobacterales

A

4th gen cephalosporins onwards

47
Q

impt consideration for amp c producing

A

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
Q

unable to reach adaqueate csf conc

A

gen 1 and 2 cephalo
aminoglycosides
macrolides
clindamycin

49
Q

used for csf

A 
meropenam 
peniciilins 
ceftriaxone 
cefepime 
ceftazidime 
vancomycin ( option for mrsa, give intrathecal)
50
Q

why is daptomycin not for pneumonia

A

inactivated by lung surfectant

51
Q

why aminoglycosides not for abscesses

A

acidic environmetn

52
Q

which drugs for prostatitis and why

A

ciprofloxacin and
co-trimoxazole
bc distribute well into prostate

53
Q

concentration dependant pkpd meaning and examples of drug like this

A

rate and extent of killing is related to the ab conc
= higher conc = more rapid and extensive killing

grps : aminoglycosides and fluoroquinolones

54
Q

what is the dosing strategy for conc dependant pkpd

A

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
Q

for conc dependant killing would u choose 250mg q12h or 500mg q24h

A

to achieve high peak, give less frequency
for better bacterial kill based on pkpd, choose 500mg q24h
higher cmax/mic ratio

56
Q

what is pae and what does this mean

A

post antibiotic effect

dosent matter if trough is below mic

57
Q

why is once daily dosing given instead of multiple daily dose for aminoglycoside

A
  • conc dependant killing
  • pAE
  • prevents adaptive resistance
    = prevents selection of more resistant mutants
  • less nephrotoxicity
  • save cost
58
Q

describe time dependant bacteria killing with no persistent effect aka short half life

A

rate and extent of killing to do with amt of time ab conc is above the mic

59
Q

time dependant killing for which classes

A

pencillins , cephalosporins and carbapenems

60
Q

dosing strategy for time dependant killing

A

optimise %T>MIC
40-70% of dosing interval shld be above mic
- more frequent administration
- iv infusion or intermittent infusion

61
Q

what is used to block excretion of drugs

A

probenacid

62
Q

describe time dependant bact killing with persistent effect aka long half life or PAE

A

rate and extent of killing related to overall drug exposure AUC vs MIC

63
Q

classes that experience the time dependant killing w persistent half life

A

vanco

64
Q

dosing strategy for time dependant killing with persistent half life

A

optimise AUC : MIC ratio
auc : dose/clearance
eg vanco target for 400-600 for MRSA

65
Q

give 500mg q12 or 1g q24 for vanco

A

1g q24hr bc
auc = dose/cl and
for same patient both have same total dose so reducing adm freq = save cost

66
Q

when to give iv

A

hospitalised, severe inf

when need high blood conc

67
Q

when to avoid oral

A

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
Q

antimicrobes with good oral bio

A

fluoroquinolones
metronidazole
linezolid
co-trimoxazole

69
Q

im examples

A

im ceftriaxone
IM streptomycin
Im benzathine penicillin

70
Q

topical eg

A

clotrimazole pessaries for vaginal candidiasis

71
Q

aerosolised or nebulised drug eg

A

nebulised colistin for mdr pseudomonas aeruginosa pneumonia

72
Q

drug that could cause collateral damgage

A

fluoroquinolones

- can select for resistant bacteria or other resistance patient wasnt even exposed to

73
Q

what cannot be use d with carbapenams

A

valproate

- bc wanna keep high conc but ddi reduces the conc

74
Q

which class cant be used with cyp450 inhibitbors

A

azole antifungals and macrolides

75
Q

which class cant be used with cyp450 inducers

A

rifampicin

76
Q

adr for aminoglycoside to monitor for

A

serum creatinine , urine output

77
Q

adr for vancomycin

A

flushing , hypotension, itch , red man syndrome

slow infusion start 500mg over 1 hr and monitor

78
Q

what to consider when modifying therapy

A

if can narrow, do that
if can use oral do that
stop if completed duration

79
Q

what could cause unsatisfactory response

A
  • inappropriate diagnosis
  • resistance
  • non compliance
  • renal function
  • ddi
  • collections or abscess- needing surgery or drainage
  • immune response
  • superinfection
  • toxicity
80
Q

how long to given empiric treatment for

A

48 to 72 hrs to work

3124 ca2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions