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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
beta lactam general mechanism
inhibit cell wall synthesis
26
aminoglycoside general mechanism
inhibit protein synthesis
27
aminoglycoside chemical component
amino sugars with glycosidic links to aminocyclitol
28
how do aminoglycosides inhibit protein synthesis
bind to 30S subunit
29
aminoglycosides spectrum
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
aminoglycosides elimination
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
aminoglycosides pharmacodynamics
concentration-dependent killing post antibiotic effect occurs-- permits less frequent administration while still maintaining antibacterial activity
32
what is the most common resistance mechanism of aminoglycosides
aminoglycoside modifying enzymes (AMEs)
33
chemical incompatibility with aminoglycosides
admixture with penicillins: can cause precipitation and inactivation of both drugs-- avoid mixing in same solution or administering via same IV line
34
aminoglycoside drug interactions
vancomycin loop diuretics polypeptide antibiotics
35
aminoglycoside toxicities
nephrotoxicity, ototoxicity, neuromuscular toxicity
36
aminoglycoside dosing strategies
high dose, extended interval dosing: effective and may reduce ototoxicity/nephrotoxicity
37
complications of HAP/VAP
pleural effusion, empyema, lung abscess, respiratory failure, septic shock
38
what is the site of infection for pneumonia
alveoli
39
pathophysiology of HAP
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
definition of HAP
pneumonia occurring 48 hours or more after hospital admission -- not incubating at time of admission
41
definition of VAP
associated with mechanical ventilation pneumonia begins 48 hours after endotracheal intubation
42
when to use 2 antipseudomonal drugs for HAP/VAP
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
when to use MRSA coverage with vancomycin or linezolid for HAP/VAP
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
which aminoglycosides can be used for pseudomonas
tobramycin, amikacin, gentamicin
45
HAP/VAP duration of therapy
7 total days empiric + directed
46
which anti infectives are not appropriate for monotherapy for HAP
aminoglycosides due to unreliable distribution
47
some inciting events for peritonitis
1. diverticulitis 2. appendicitis 3. infections of the liver and biliary system: cholangitis, cholecystitis, liver abscess
48
most common organisms implicated in intra abdominal infections
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
duration of therapy for bacteremia for patients who are afebrile, hemodynamically stable, and appropriate source control
1 week, & repeat blood cultures unnecessary , & can be treated with oral antibiotics
50
cystitis treatment options
nitrofurantoin, TMP/SMZ, fosfomycin
51
pyelonephritis treatment options
ciprofloxacin, ceftriaxone, piperacillin/tazobactam, ampicillin
52
cefepime is stable/not stable for what
stable for AmpC producing enterobacterales
53
aminopenicilln/BLI is stable/not stable for what
activity against Class A BLs and some ESBLs not KPCs
54
Pip/tazo is stable/not stable for what
activity against Class A BLs and some ESBLs not KPCs
55
ceftazidime is stable/not stable for what
vulnerable for AmpC producing enterobacterales
56
ceftolozane/tazobactam is stable/not stable for what
activity for cefepime-resistant pseudomonas aeruginosa
57
ceftazidime/avibactam stable/not stable for what
Class A (ESBLs and KPC) Class C (AmpC) some class D not MBLs
58
cefiderocol is stable/not stable for what
stable for ESBL, AmpC, CRE
59
carbapenems are stable/not stable for what
ESBL and AmpC-producing enterobacterales not MBLs
60
aztreonam is stable/not stable for what
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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