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ID2 > Exam 2 Falcione stuff > Flashcards

Exam 2 Falcione stuff Flashcards

1
Q

types of antibiotic resistance mechanisms for gram negative organisms

A
  1. loss of porin channels
  2. increased efflux pumps
  3. enzymatic degradation (Beta lactamases, AMEs)
  4. changes in the binding site
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2
Q

define intrinsic resistance

A

bacteria naturally harbor & express the genes in their chromosomes (chromosomal or inherent resistance)

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3
Q

define acquired resistance

A

the bacteria do not naturally harbor in their chromosomes, genes are acquired, typically from other bacteria they encounter

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4
Q

define inducible

A

genes that are typically not being expressed

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5
Q

define constitutive

A

gene that is always on/expressed

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6
Q

E. coli beta lactamases

A

-can produce ESBLs
-some harbor plasmids for the beta lactamase TEM-1

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7
Q

what does TEM-1 do

A

inactivates aminopenicillins but not 1st generation cephalosporins

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8
Q

klebsiella beta lactamases

A

ESBLs, AmpC, KPC/CRE
via MDR plasmids

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9
Q

proteus beta lactamases

A

ESBLs, some harbor plasmids that encode TEM-1

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10
Q

enterobacter, citrobacter, and serratia beta lactamases

A

intrinsic resistance to aminopenicillins, 1st and 2nd Gen Cephs due to AmpC

inducible resistance with 3rd gen Cephs due to mutants constitutively producing high levels of beta lactamase

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11
Q

how many ambler classes are there

A

4

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12
Q

what bacterial pathogens are classified as enterobacterales

A

escherichia, klebsiella, proteus, enterobacter, citrobacter, serratia

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13
Q

enterobacterales grow in what environment

A

they are facultative anaerobes so they can grow/proliferate in aerobic or anaerobic conditions

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14
Q

pseudomonas microbio characteristics

A

gram negative rod arranged in pairs
obligate aerobe
non lactose fermenter
oxidase positive

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15
Q

pseudomonas resistance

A

inherent to many antibiotics
mutation in PBP
BL production
decreased outer membrane porin expression
ESBLs
efflux pump upregulation

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16
Q

anti infectives with spectrum of activity that includes pseudomonas aeruginosa

A

aminoglycosides
aztreonam
cefepime
cefiderocol
ceftazidime
ceftazidime/avibactam
ceftolozane/tazobactam
ciprofloxacin, levofloxacin
delafloxacin
imipenem/cilastatin
imipenem/cilastatin/relebactam
meropenem and meropenem/vaborbactam
piperacillin/tazobactam
polymixin E and polymixin B

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17
Q

acinetobacter drug of choice

A

ampicillin/sulbactam

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18
Q

anti infectives with spectrum of activity that includes anaerobes

A

cephamycins and carbapenems

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19
Q

CDC definition of CRE

A

CRE: members of the enterobacterales order resistant to at least one carbapenem antibiotic or producing a carbapenemase enzyme
*for bacteria that are intrinsically not susceptible to imipenem, resistance to at least one carbapenem other than imipenem is required

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20
Q

______ interact with _____

A

carbapenems interact with valproic acid

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21
Q

which BLIs include a beta lactam structure

A

tazobactam, sulbactam, clavulanate

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22
Q

which BLIs are non beta lactam BLIs

A

avibactam, vaborbactam, relebactam

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23
Q

which anti infectives are distinguished for poor or absent spectrum of activity for gram positive pathogens

A

ceftazidime and aztreonam

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24
Q

which anti infective does not require dose adjustment for renal insufficiency

A

ceftriaxone

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25
Q

beta lactam general mechanism

A

inhibit cell wall synthesis

26
Q

aminoglycoside general mechanism

A

inhibit protein synthesis

27
Q

aminoglycoside chemical component

A

amino sugars with glycosidic links to aminocyclitol

28
Q

how do aminoglycosides inhibit protein synthesis

A

bind to 30S subunit

29
Q

aminoglycosides spectrum

A

greatest utility: therapy of serious systemic infections due to GNRs that can grow aerobically: ex pseudomonas, enterobacterales

less susceptible to aerobic gram + cocci and aerobic gram - cocci

generally resistant to anaerobes, stenotrophomonas, burkholderia

30
Q

aminoglycosides elimination

A

almost entirely as unchanged drug via glomerular filtration: elimination rate increases in proportion with creatinine clearance
**regimen must be adjusted with impaired renal function to avoid nephrotoxicity
**TDM required

31
Q

aminoglycosides pharmacodynamics

A

concentration-dependent killing
post antibiotic effect occurs– permits less frequent administration while still maintaining antibacterial activity

32
Q

what is the most common resistance mechanism of aminoglycosides

A

aminoglycoside modifying enzymes (AMEs)

33
Q

chemical incompatibility with aminoglycosides

A

admixture with penicillins: can cause precipitation and inactivation of both drugs– avoid mixing in same solution or administering via same IV line

34
Q

aminoglycoside drug interactions

A

vancomycin
loop diuretics
polypeptide antibiotics

35
Q

aminoglycoside toxicities

A

nephrotoxicity, ototoxicity, neuromuscular toxicity

36
Q

aminoglycoside dosing strategies

A

high dose, extended interval dosing: effective and may reduce ototoxicity/nephrotoxicity

37
Q

complications of HAP/VAP

A

pleural effusion, empyema, lung abscess, respiratory failure, septic shock

38
Q

what is the site of infection for pneumonia

A

alveoli

39
Q

pathophysiology of HAP

A
  1. bacterial contamination of respiratory secretions from nonsterile oropharynx and nasopharynx
  2. pooling of respiratory secretions normally expelled by changing positions or posture and by coughing
  3. inactivity allows secretions to pool by gravity, interfering with the normal diffusion of oxygen and carbon dioxide in the alveoli
40
Q

definition of HAP

A

pneumonia occurring 48 hours or more after hospital admission – not incubating at time of admission

41
Q

definition of VAP

A

associated with mechanical ventilation pneumonia begins 48 hours after endotracheal intubation

42
Q

when to use 2 antipseudomonal drugs for HAP/VAP

A
  1. risk factors for MDR pseudomonas & GNR: prior IV antibiotics within 90 days, structural lung disease (bronchiectasis, cystic fibrosis)
  2. high quality gram stain from respiratory secretion with numerous & predominant GNRs
  3. patients in ICU with >10% pseudomonas isolates resistant to monotherapy regimen, local ICU antibiogram data unknown
  4. high risk for mortality: ventilator support required for HAP, septic shock
43
Q

when to use MRSA coverage with vancomycin or linezolid for HAP/VAP

A
  1. risks for MRSA: prior IV antibiotics within the past 90 days, hospital unit with >10-20% MRSA, unknown MRSA prevalence in the hospital unit, prior MRSA in a culture or non-culture diagnostic
  2. high risk of mortality: need for ventilator support due to HAP, septic shock
44
Q

which aminoglycosides can be used for pseudomonas

A

tobramycin, amikacin, gentamicin

45
Q

HAP/VAP duration of therapy

A

7 total days empiric + directed

46
Q

which anti infectives are not appropriate for monotherapy for HAP

A

aminoglycosides due to unreliable distribution

47
Q

some inciting events for peritonitis

A
  1. diverticulitis
  2. appendicitis
  3. infections of the liver and biliary system: cholangitis, cholecystitis, liver abscess
48
Q

most common organisms implicated in intra abdominal infections

A
  1. gram positive aerobic cocci: strep, enterococcus, staph
  2. anaerobes: bacteroides, clostridium, prevotella, peptostreptococcus, fusobacterium, eubacterium
  3. facultative and aerobic gram negative: e coli, klebsiella, pseudomonas, proteus, enterobacter
49
Q

duration of therapy for bacteremia for patients who are afebrile, hemodynamically stable, and appropriate source control

A

1 week, & repeat blood cultures unnecessary , & can be treated with oral antibiotics

50
Q

cystitis treatment options

A

nitrofurantoin, TMP/SMZ, fosfomycin

51
Q

pyelonephritis treatment options

A

ciprofloxacin, ceftriaxone, piperacillin/tazobactam, ampicillin

52
Q

cefepime is stable/not stable for what

A

stable for AmpC producing enterobacterales

53
Q

aminopenicilln/BLI is stable/not stable for what

A

activity against Class A BLs and some ESBLs
not KPCs

54
Q

Pip/tazo is stable/not stable for what

A

activity against Class A BLs and some ESBLs
not KPCs

55
Q

ceftazidime is stable/not stable for what

A

vulnerable for AmpC producing enterobacterales

56
Q

ceftolozane/tazobactam is stable/not stable for what

A

activity for cefepime-resistant pseudomonas aeruginosa

57
Q

ceftazidime/avibactam stable/not stable for what

A

Class A (ESBLs and KPC)
Class C (AmpC)
some class D
not MBLs

58
Q

cefiderocol is stable/not stable for what

A

stable for ESBL, AmpC, CRE

59
Q

carbapenems are stable/not stable for what

A

ESBL and AmpC-producing enterobacterales
not MBLs

60
Q

aztreonam is stable/not stable for what

A

is not inactivated by MBLs but can be hydrolyzed by co-produced enzymes such as ESBLs, KPCs: use in combo with ceftazidime/avibactam to protect against other enzymes to allow activity against MBLs

ID2 (13 decks)

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