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CWSI Flashcards

1
Q

Target of CWSI

A

Penicillin-binding-proteins (PBP)

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2
Q

CMSI are

A

cidal

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3
Q

Peptidoglycan is composed of

A
  1. alternating sugar backbone (NAG and NAM)
  2. chain of four AA extending from backbones (NAM)
  3. peptide bridge that corss-links peptide chains
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4
Q

Last AA on NAM chain, that can be modified for resistance

A

D-alanine

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5
Q

Peptidoglycan

A

assembled in cytoplasm, transported through membrane to cell surface, cross-linking is driven by cleavage of terminal AA (D-alanine)

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6
Q

5 Targets of CWSI

A
  1. Transglycosylation - joining NAG-NAM (performed by PBP)
  2. Transpeptidation- (cross links pentapeptides (performed by PBP)
  3. NAG reduction to NAM
  4. Transport across membrane
  5. AA mimicry - pentapeptide chain
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7
Q

Job of PBP

A

transglycosylation and transpeptidation

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8
Q

inhibits one of the first steps of CWS

A

fosfomycin

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9
Q

MOA of fosfomycin

A

inhibits peptidoglycan synthesis resulting in accumulation of nucleotide precursors and subsequent cell death (acts as PEP to inactivate enzyme) (prevents NAG –> NAM)

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10
Q

MOA of beta-lactams

A

prevent transpeptidation and transglycosylation; beta-lactam ring irreversibly bind to PBP; susceptible to penicillinases

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11
Q

Types of beta-lactams

A

penicillins, cephalosporins, carbapenems, and monobactams

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12
Q

Bactiracin MOA

A

blocks transport of peptidoglycan subunits from cytoplasm to cell exterior; cell-wall subunits accumulate in the cytoplasm and cannot be added to growing chain

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13
Q

Glycopeptides (Vancomycin) MOA

A

bind to D-alanine while subunits are external to the cell membrane but still linked to lipid carrier; binding sterically inhibits the addition of subunits to peptidoglycan backbone

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14
Q

Autolysins

A

cleave peptidoglycan bonds in normal course of cell growth

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15
Q

CWSI require

A

autolysins; cell in GROWING PHASE

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16
Q

CWSI inhibitors can’t be used with

A

protein-synthesis inhibitors (Chloramphenicol) because the cell won’t be growing then

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17
Q

Antagonism for CWSI

A

CWSI + Protein synthesis inhibitor (ex. PCN + choramphenicol)

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18
Q

PBP MOA

A

removes D-alanine to form crosslink w/ nearby peptide

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19
Q

Natural Peniciilin drugs

A
  1. Pen G (IV)
  2. Benzathine PCN (IM)
  3. Procaine PCN G (IM)
  4. Pen V (oral)
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20
Q

Spectrum of natural PCN

A

Best G (+) (especially cocci); some G- and anerobic coverage;
inactivated by beta-lactamases;
no antipseudomonal
elimination- kidney (probenicid reduces elimination);
poor CNS penetration (except inflammation- N. meningitides)

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21
Q

DOC of natural PCN

A

N. meningitides, S. pneumoniae, strep A, B, enterococcus, actinomyces, leptospira, treponema

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22
Q

DOC for syphilis

A

Penicillin

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23
Q

Silver nitrate drops

A

PCN drops in eyes to prevent gonorrhea opthamolgia in newborns

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24
Q

Penicillinase resistant drugs

A

Nafcillin (IM/IV)
Oxacillin (IV/IM, ORAL)
Dicloxacillin (oral)
Methicillin*

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25
Q

Penicillinase resistant drug characteristics

A

lower G+, some G-
resistant to penicillinase
some acid stable and highly protein bound
hepatic metabolism and renal excretion

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26
Q

DOC of penicillinase resistant drugs

A

MSSA (penicillinase producing stap aureus)

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27
Q

Methicillin resistance

A

due to altered PBP; no beta-lactam will work (can’t bind) except for ceftaroline

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28
Q

Only beta-lactam that works against MRSA

A

ceftaroline

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29
Q

Extended spectrum PCN

A 
better G-, less G+
no anti-pseudomonal activity
resistance is frequent
susceptible to beta-lactamases
URINARY EXCRETION
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30
Q

Extended spectrum PCN drugs

A

Ampicillin (oral)

Amoxicillin (oral)

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31
Q

Ampicillin and amoxicillin DOC for

A

Listeria (ampicillin)
H. pylori (amoxicillin in combo)
B. burgdorferi (early; can also use doxycline)

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32
Q

Ampicillin rash

A

generalized, dull red maculopapular rash, usually 3-14 days after starting tx; not allergic and does not preclude future use of PCN; many patients with EBV (mono) develop rash

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33
Q

Antipseudomonal PCN drugs

A

Piperacillin (IV/IM)

Ticarcillin (IV/IM)

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34
Q

Antipseudomonal PCN drug properties

A

bacteria covered by extended spectrum (good G-) + additional enteric Gram (-) (proteus, enterobacter, providencia and serratia);
major use: pseudomonas aeurginosa
susceptible to beta-lactamase
only available in combo with B-lactamase inhibitors
parenteral
renal excretion

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35
Q

DOC for antipseudomonal PCN drugs

A

P. aeruginosa (in combo w/ aminoglycoside to avoid resistance)

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36
Q

Beta-lactamase inhibitors

A

clavulanic acid
Sulbactam
Tazobactam

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37
Q

Beta-lactamase inhibitors used with

A

ampicillin, amoxicillin, ticarcillin, piperacillin

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38
Q

role of beta-lactamase inhibitors

A

block penicillinase activity; extend spectrum of drug

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39
Q

PCN resistance

A
  1. Penicillinase
  2. altered PBP
  3. autolytic enzymes not active (not growing)
  4. lack of cell wall/not peptidoglycan cell wall (mycoplasma; chlamydia)
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40
Q

what bacteria have penicillinase activity

A

Staphylcocci and other Gram-negative

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41
Q

Tranpeptidase

A

PBP

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42
Q

Toxicity of PCN

A
  1. ALLERGY (safest drug besides this)
  2. electrolyte imbalance
  3. GI
  4. Superinfections
43
Q

Hypersensitivity drugs

A

PCN, sulfa, cephalosporins, etc.

44
Q

Pharmacokinetics of PCN

A 
good tissue penetration
poor CNS penetration
mostly renal elimination (extended spectrum is urinary)
filtration and tubular excretion
probenecid inhibits renal elimination
45
Q

Probencid

A

inhibits renal elimination; increases half-life of PCN

46
Q

Benzathine Penicillin

A

longest acting, low blood levels

47
Q

Pen G

A

mild/moderate infections

48
Q

Pen G DOC

A

rheumatic fever, syphilis

49
Q

Excretion of PCN

A

most rapidly excreted by kidney; most is tubular secretion (can be partially blocked by probenecid)

50
Q

Cephalosporins MOA

A

activate cell wall autolytic enzymes through blocking terminal cross-linking of peptidoglycan (PBP)

51
Q

Advantage of cephalosporins over penicillins

A

7-methyl group that increases resistance to beta-lactamases

52
Q

1st generation cephalosporins (narrow spectrum) drugs

A

cefazolin (IV/IM)

Cephalexin (oral)

53
Q

1st gen properties

A

good G+
moderate G - (e. coli, klebsiella, proteus)
MSSA susceptible
Resistant (entercocci, MRSA, s. epidermis)
Alternative for PCN-allergic individuals
increased beta-lactamase resistance
Renal excretion

54
Q

DOC for surgical prophylaxis

55
Q

2nd gen cephalosporin drugs (intermediate spectrum)

A

Cefaclor (oral)
Cefuroxime (IV/IM)
Cefprozil (oral)

56
Q

2nd gen properties

A

lower G+, somewhat increase G-
no antipseudomonal activity
mostly renal excretion
VERY SIMILAR TO FIRST GEN EXCEPT SOME MORE G-

57
Q

All cephalosporins lack activity against

A

enterococci, listeria, MRSA

58
Q

DOC of 1st gen cepahlosporin

A

E. coli, Klebsiella, proteus; cefazolin for surgical prophylaxis

59
Q

DOC of 2nd gen cephalosporin

A

E. coli, Klebsiella, proteus, moraxella

60
Q

Only 2nd gen ceph that can cross BBB

A

cefuroxime

61
Q

3rd gen ceph drugs

A

Ceftriaxone (IV/IM)
Ceftaxime (IV/IM)
Ceftazidime (IV/IM)
Cefixime (oral)

62
Q

Ceftriaxone

A

CNS penetration, N. gonorrhea

63
Q

Cefotaxime

A

CNS penetration

64
Q

Ceftazidime

A

P aeruginosa (if ticarcillin or piperacillin can’t be used)

65
Q

Cefixime

A

gonorrhea, but ceftriaxone IM is better

66
Q

3rd gen ceph properties

A

less active against G+
much more active against Enterobacteriaceae (penicillinase producing)
Kidney excretion

67
Q

Ceftriaxone contraindication

A

neonates or jaundiced; bilirubin displacement

68
Q

4th gen ceph drug

A

Cefepime (BROAD SPECTRUM)

69
Q

4th gen ceph properties (cefepime)

A

better G+
ANTIPSEUDOMONAL
renal excretion
BROADEST COVERAGE: enterobacter, MSSA< pseudomonas
empirical therapy when Beta-lactamases are anticipated

70
Q

5th gen ceph drug

A

Ceftaroline

71
Q

Ceftaroline (5th gen) properties

A

no antipseudomonal activity
active against G+/G-
renal excretion
MRSA and VRSA coverage; only beta-lactam active against MRSA (can bind to PBP2A with high affinity)

72
Q

DOC for cephalosporins

A

moraxella (2nd/3rd gen)
N. gonorrhea (cetriaxone, cefixime)
E.coli, Klebsiella, Proteus (1st/2nd gen)- UTI
Salmonella- 3rd gen
PCN resistant strep pneumonia (cetriaxone)
Borellia- ceftriazone (late disease)

73
Q

Borellia tx

A

Early: amoxicillin, doxycycline
Late: cetriaxone

74
Q

Toxicity of cephalosporins

A 
superinfection
DISULFIRAM-LIKE RXN
ALLERGY (don't give if PCN allergy)
positive Coomb's test
Diarrhea
DOSE DEPENDENT RENAL TUBULAR NECROSIS (synergistic nephrotoxicity with aminoglycosides)
75
Q

Monobactam drug

A

Aztreonam (IM/IV)

76
Q

Aztreonam (monobactam) properties

A

similar to 3rd gen ceph
relatively resistant to beta-lactamases
Spectrum: AEROBIC GRAM - (including pseudomonas)
no activity against G+ or anaerobes
renal excretion
no cross-sensitivity to beta lactams (good alternative for PCN allergic people)

77
Q

Side effects of aztreonam

A

phlebitis, skin rash, abnormal liver function

78
Q

Aztreonam not effective against

A

G+ or anaerobes

79
Q

Aztreoname spectrum

A

G- aerobes only

80
Q

Good alternative for penicillin allergic pt. w/ gram-negative infection

81
Q

Carbapenem drugs

A

Imipenem + cilastin (primaxin) (IV)
meropenem (IV)
ertapenem (IV/IM)

82
Q

Carbapenem indications

A

organisms resistant to other antimicrobias and for MIXED AEROBC/ANAEROBIC infections; one of best classes for broad spectrum coverage

83
Q

Imipenem administration

A

must be given with cilastin: imipenem is inactivated in renal tubule by dihydropeptidase, which results in low urinary concentrations

84
Q

Cilastin

A

dihydropeptidase inhibitor; given with imipenem

85
Q

Imipenem and Meropenem

A

highly stable against beta-lactamases (including extended spectrum lactamases)
broad spectrum activity (anaerobes, G+, G-, rods)
Pseudomonas may develop resistance rapidly (use with aminoglycosdie) renal excretion

86
Q

Broadest coverage of beta-lactams

A

carbapenems

87
Q

Causes seizures

88
Q

Ertapenem

A

stable against beta-lactamses
Spectrum: G+, G0 and anerobic (Enterobacter)
IV/IM
Should not be used for pseudomonas

89
Q

DOC of imipenem or meropenem

A

Serratia, Enterobacter (beta-lactamase producing)

90
Q

Pseudomonas drug order

A

anti-pseudomonal PCN –> Cefepime (4th gen) –> Aztreonam –> Imipenem/meropenem

91
Q

non-beta lactam ICWS

A

vancomycin
Fosfomycin
Bacitracin

92
Q

MOA of vancomycin

A

prevents transpeptidation by binding to D-ala; bactericidal

93
Q

Resistance to vancomycin

A

mutation of D-ala site

94
Q

DOC of vancomycin

A

PCN and MRSA infections; G+ infections to allergic patients;

Superinfections (Oral): staph, c. diff

95
Q

Vanco is only effective against

96
Q

VRE

A

vancomycin resistant enterococci (drug of last resort)

97
Q

Adverse effects of vancomycin

A

OTOTOXIC, NEPHROTOXIC, RED MAN SYNDROME, thrombophlebitis at injective site

98
Q

red man syndrome

A

Rxn to vancomycin; flushing from histamine release

99
Q

Fosfomycin MOA

A

analog of PEP (prevents NAG to NAM reduction); early inhibitor of CWS

100
Q

Fosfomycin properties

A

Spectrum: G+/G-
oral; excreted by kidney
used for uncomplicated UTI’s
Synergism: beta-lactam, aminoglycoside or fluorquinolone

101
Q

Synergism of fosmomycin

A

beta-lactam, aminoglycoside or fluorquinolone

102
Q

Bacitracin MOA

A

interferes with final dephosphorylation step in phospholipid carrier cycle; can’t tranport NAG-NAM across inner membrane

103
Q

Bacitracin properties

A

parenteral (rare) and TOPICAL
Spectrum: G+
Used in combo with neomycin and polymyxin (G-) (neosporin)
Nephrotoxicity in parenteral

Pharm exam 2 (6 decks)

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