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STEP > ID 17 > Flashcards

ID 17 Flashcards

1
Q

Cephalosporins as a class..

A

beta lactase that are less susceptible to penicillinases.

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2
Q

organisms not covered by 1st-4th generation cephalosporins? exception?

A 
LAME
Listeria
Atypicals (chlamydia, mycoplasma)
MRSA
Enterococci 
Exception: ceftaroline (5th generation cephalosporin, which covers MRSA)
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3
Q

1st gen cephalosporins?

A

Cefazolin

Cephalexin

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4
Q

1st gen cephalosporin use?

A

Proteus
E coli
klebsiella

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5
Q

other use for cefazolin?

A

prior to surgery to prevent s aureus wound infections

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6
Q

2nd gen cephalosporins?

A

Cefaclor
Cefoxitin
Cefuroxime

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7
Q

2nd gen cephalosporin use?

A 
H influenza
Enterobacter aerogenes
Neisseria
Serratia
Proteus
E coli
Klebsiella
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8
Q

3rd gen cephalosporins?

A

Ceftriaxone
Cefotaxime
Ceftazidime

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9
Q

ceftazidime uses..

A

pseudomonas

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10
Q

ceftriaxone uses..

A

meningitis
gonorrhea
disseminated lyme disease

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11
Q

4th generation cephalosporins…

A

cefepime

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12
Q

cefepime uses…

A

gram negatives with increased activity against pseudomonas

gram positives

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13
Q

cephalosporin AE’s

A

1) hypersensitivity reactions
2) AIHA
3) disulfiram-like reaction
4) vitamin K deficiency
5) cross-reactivity with penicillins
6) increase nephrotoxicity of aminoglycosides

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14
Q

carbapenems

A

imipenem
meropenem
ertapenem
doripenem

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15
Q

imipenem as a drug and caveat

A

1) broad spectrum, b-lactamase resistant.

2) always administered with cilastatin

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16
Q

what is cilastatin? why do you give it with imipenem?

A

1) inhibitor of renal dehydropeptidase I

2) decreases inactivation of drug in renal tubules.

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17
Q

meropenem benefits

A

1) Decreased seizure risk

2) stable to dehydropeptidase I

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18
Q

carbapenem uses

A

Gram positive cocci
gram negative rods
anaerobes

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19
Q

Carbapenem AE’s

A

1) CNS toxicity, seizure
2) skin rash
3) GI distress

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20
Q

benefits of aztreonam

A

1) less susceptible to beta-lactamases

2) no cross-allergenicity with penicllins

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21
Q

aztreonam mechanism

A

Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3.

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22
Q

aztreonam has activity against

A

only gram negative rods

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23
Q

aztreonam uses?

A

penicillin-allergic patients and those with renal insufficiency who can’t tolerate ahminoglycosides.

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24
Q

vancomycin characteristics

A

1) bactericidal against most bacteria, except c diff

2) not susceptible to beta-lactamses

25
Q

vancomycin uses..

A

*only gram positives–serious multidrug-resistant organisms like enterococcus, MRSA, C diff, S epidermidis

26
Q

vanco AE’s

A

1) nephrotoxic
2) ototoxic
3) thrombophlebitis
4) diffuse flushing/red man syndrome

27
Q

how do you prevent red man syndrome?

A

Pretreat with antihistamines + slow infusion rate.

28
Q

vanco resistance mechanism

A

amino acid modification of D-ala D-ala to D-ala D-lac

29
Q

bactericidal protein synthesis inhibitor?

A

ahminoglycosides, linezolid is variable

30
Q

peptidyl transferase function

A

Forms peptide bonds between adjacent amino acids using tRNAs during translation.

31
Q

amino glycoside mechanism

A

1) irreversible inhibition of initiation complex through 30s binding
2) can cause misreading of mRNA
3) also block translocation

32
Q

antibiotic used for bowel surgery?

A

neomycin

33
Q

amino glycoside use?

A

severe gram negative rods. synergistic with beta-lactams

34
Q

other aminoglycoside AE?

A

neuromuscular blockade

35
Q

main concern for ototoxicity with ahminoglycosides?

A

when combined with loop diuretics

36
Q

amino glycoside mechanism of resistance?

A

acetylation, phosphorylation, or adenylation

37
Q

other things that interact with tetracyclines?

A

iron-containing preparations

38
Q

tetracycline for use in renal failure?

A

doxycycline (fecally eliminated)

39
Q

tetracyclines and CNS penetration?

A

limited

40
Q

why are tetracyclines good at treating rickettsia and chlamydia?

A

can accumulate intracellularly

41
Q

MOA of resistance to tetracyclines?

A

Decreased uptake or increased efflux out of bacterial cells by *plasmid encoded transport pumps.

42
Q

chloramphenicol mechanism?

A

Blocks peptidyltransferase at 50S ribosomal subunit.

43
Q

chloramphenicol uses

A

RMSF

Meningitis

44
Q

Why are premies at increased risk of chloramphenicol induced aplastic anemia?

A

they lack UDP-glucoronyl transferase.

45
Q

chloramphenicol MOA of resistance

A

Plasmid-encoded acetyltransferase inactivates the drug.

46
Q

clindamycin MOA

A

blocks peptide transfer (*translocation) at 50S ribosomal subunit.

47
Q

other clindamycin use…

A

invasive group A strep infection

48
Q

clindamycin vs. metronidazole uses

A

clindamycin for anaerobes above the diaphragm, metro for below diaphragm

49
Q

linezolid drug class

A

oxazolidinones

50
Q

linezolid MOA

A

Inhibit protein synthesis by binding to 50s subunit and preventing formation of the initiation complex.

51
Q

linezolid AE’s

A

1) bone marrow suppression (especially thrombocytopenia)
2) peripheral neuropathy
3) serotonin syndrome

52
Q

Linezolid MOA of resistance

A

point mutation of ribosomal RNA

53
Q

where do macrolides bind to?

A

23S rRNA of 50S ribosomal subunit

54
Q

CYP450 inhibitor macrolides?

A

clarithromycin and erythromycin

55
Q

macrolide MOA of resistance?

A

methylation of 23s rRNA binding site prevents drug binding.

56
Q

macrolides AE’s

A 
gastrointestinal motility issues
arrhythmia/QT prolongation
acute cholestatic hepatitis
rash
eosinophilia
57
Q

migratory thrombophlebitis?

A

Vein inflammation related to recurrent thrombus formation in different locations.

58
Q

How does migratory thrombophlebitis present?

A

Redness and tenderness on palpation of extremities.

59
Q

phlebitis

A

vein inflammation

STEP (85 decks)

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