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PHRM 865 > Vanco + GP Agents - SOA > Flashcards

Vanco + GP Agents - SOA Flashcards

1
Q

What is the mechanism of action of vancomycin?

A

Vancomycin inhibits cell wall synthesis during the second stage by binding to D-ala-D-ala of the cell wall precursors. This prevents cross-linking and further elongation of peptidoglycan.

Which then weakens the cell wall and makes it prone to lysis.

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2
Q

What is the mechanism of resistance to vancomycin?

A

The D-ala-D-ala binding site gets mutated into D-ala-D-lactate – which vancomycin does not bind to.

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3
Q

What kind of activity does vancomycin display?

A
  • slow bactericidal
  • time-dependent
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4
Q

What is the general SOA of vancomycin?

A
  • Many GP aerobes and anaerobes
  • NO ACTIVITY against GN aerobes nor anaerobes
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5
Q

Which target organisms does vancomycin have activity against?

A
  • PRSP
  • MSSA
  • MRSA
  • C. diff
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6
Q

What is the drug of choice for MRSA?

A

vancomycin

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7
Q

What route of administration of vancomycin is used when treating C. diff?

A

Oral

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8
Q

What are the pharmacokinetic characteristics of vancomycin?

A
  • negligible oral absorption
  • widely distributed into tissues and fluid (including adipose)
  • variable CSF penetration
  • takes an hour to distribute
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9
Q

How is vancomycin eliminated?

A
  • Vancomycin is eliminated unchanged by the kidneys via glomerular filtration.
  • Half-life increases and renal function decreases

Half-life in ESRD patients approaches 7-14 days

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10
Q

When should peak concentrations of vanc be drawn for therapeutic monitoring?

A

One hour after the end of the infusion

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11
Q

What is vancomycin clinically useful for?

A
  • MRSA
  • C. diff
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12
Q

What are the adverse effects from vancomycin?

A
  • Red-Man Syndrome
  • Nephrotoxicity - reversible
  • ototoxicity - irreversible
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13
Q

How is Red-Man Syndrome from vancomycin administration provoked?

A
  • The reaction is related to the rate of vancomycin infusion.
  • Infusing faster than 15 mg per minute causes the release of histamine and other vasodilating substances.
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14
Q

How can Red-Man Syndrome from vancomycin administration be avoided?

A
  • Vancomycin doses of 1 gram should be infused over at least one hour
  • Larger doses should be infused over 90 to 120 minutes

Premedication with antihistamines or corticosteroids can alleviate the reaction

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15
Q

What are the risk factors for developing nephrotoxicity and ototoxicity from vancomycin?

A
  • underlying renal insufficiency
  • prolonged therapy or high doses
  • high serum vanc concentrations
  • concomitant use of other ototoxins or nephrotoxins
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16
Q

What is the mechanism of action of Synercid?

quinpristin + dalfopristin

A
  • Synercid inhibits protein synthesis by binding to 50S ribosomal subunits
  • each agent alone is bacteriostatic, but the combination can provide a bactericidal effect
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17
Q

What are the mechanisms of resistance against Synercid?

A
  • alteration of ribosomal binding site – coded by erm
  • enzymatic inactivation
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18
Q

What is the general spectrum of activity of Synercid?

A

Really only used for GP

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19
Q

What target organisms does Synercid have activity against?

A
  • PRSP
  • VRE faecium
  • MSSA
  • MRSA
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20
Q

How is Syndercid eliminated?

quinpristin + dalfopristin

A
  • Both agents are converted to active metabolites by CYP enzymes that are then eliminated by hepatic clearance or biliary elimination. Small portion undergoes urinary elimination.

  • Dose adjustment is suggested for hepatic insufficiency and unnecessary for renal insufficiency
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21
Q

What is Synercid clinically useful for?

A

VRE faecium bacteremia

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22
Q

What drugs does Synercid interact with?

Synercid is a CYP3A4 inhibitor

A
  • Statins (HMG-CoA reductase inhibitors)
  • Immunosuppressants (cyclosporine, tacrolimus)
  • Carbamazepine
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23
Q

What are the adverse effects from Synercid?

A
  • venous irritation/phlebitis
  • myalgias, arthralgias
  • GI
  • rash
24
Q

How can venous irritation/phlebitis be avoided when administering Synercid?

A

Use a central vein

25
Q

List the oxazolidinones:

A
  • linezolid
  • tedizolid
26
Q

What is the mechanism of action of linezolid and tedizolid?

A
  • Linezolid and tedizolid inhibit protein synthesis by binding to 50S ribosomal subunit near the 30S interface
  • bacteriostatic
27
Q

What is the mechanism of resistance to the oxazolidinones?

linezolid, tedizolid

A

Alteration of ribosomal subunit – rare for these agents

28
Q

What is the general SOA of linezolid and tedizolid?

A

Gram positive and nothing else really

29
Q

What target organisms do linezolid and tedizolid have activity against?

A
  • PRSP
  • MSSA
  • MRSA
  • VISA
  • VRSA
  • VRE faecium and faecalis

  • VISA = vancomycin intermediate staph aureus
  • VRSA = vancomycin resistant staph aureus
  • VRE = vancomycin resistant enterococci
30
Q

Describe the absorption of linezolid and tedizolid:

A
  • linezolid is rapidly and completely absorbed after oral administration with an oral BA of 100%
  • tedizolid BA = 91%
30
Q

How is linezolid used clinically?

A

Linezolid is a first-line option for VRE

  • pt can’t be on an SSRI
  • pt platelets need to be > 50k
30
Q

How are linezolid and tedizolid eliminated?

A
  • Both agents are eliminated by both renal and non-renal routes
  • Linezolid is removed by hemodialysis
  • Neither drug requires dose adjustment in renal dysfunction
31
Q

What are the potential drug interactions with the oxazolidinones?

linezolid and tedizolid

A
  • Oxazolidinones are very weak inhibitors of monoamine oxidase (MAO)
  • Could cause serotonin syndrome in patients taking SSRIs

As long as you monitor for serotonin syndrome, it should be fine

32
Q

What are the adverse effects from linezolid and tedizolid?

A
  • thrombocytopenia and anemia
  • CNS - headache, peripheral and optic neuropathy
  • GI

  • thrombocytopenia and anemia are more common if treatment lasts longer than 2 weeks. They are reversible after d/c of therapy
  • peripheral and optic neuropathy were only studied in linezolid and they are more common after 28 days of tx
33
Q

What kind of drug is daptomycin?

A

lipopeptide

34
Q

What is the mechanism of action of daptomycin?

lipopeptide

A
  • Daptomycin causes membrane depolarization by inserting lipophilic tail into cell wall which ultimately leads to inhibition of protein, DNA, and RNA synthesis –> cell death
  • Displays rapid concentration-dependent bactericidal activity
35
Q

What is the mechanism of resistance against daptomycin?

lipopeptide

A
  • Rare, but altered cell membrane binding due to loss of a membrane protein
36
Q

What is the general SOA of daptomycin?

A

Gram positive aerobes

37
Q

Which target organisms does daptomycin have activity against?

A
  • PRSP
  • MSSA
  • MRSA - not used for this
  • VRE (faecium and faecalis)
  • VISA
  • VRSA
38
Q

How is daptomycin eliminated?

A
  • Daptomycin is excreted primarily by the kidneys
  • Dosage adjustments are required in the presence of renal insufficiency
39
Q

When would daptomycin be used clinically?

A

Daptomycin would be used for serious infections from resistant GP bacteria when vanc and/or linezolid can’t be used.

Dapto should NOT be used for pneumonia bc it is inactivated by pulmonary surfactant

40
Q

What drug interactions can occur with daptomycin?

A

Concomitant use with statins may lead to increased incidence of myopathy.

Use together with caution or temporarily d/c statin while on dapto

41
Q

What are the adverse effects from daptomycin?

A
  • myopathy and CPK elevation
  • acute eosinophilic pneumonia
  • injection site rxn
  • rash
42
Q

List the lipoglycopeptides:

A
  • telavancin
  • dalbavancin
  • oritavancin
43
Q

What is the mechanism of dalbavancin?

lipoglycopeptide

A
  • works just like vancomycin
  • Inhibits cell wall synthesis during the second stage by binding to D-ala-D-ala of the cell wall precursors. This prevents cross-linking and further elongation of peptidoglycan.
44
Q

What is the mechanism of action of telavancin and oritavancin?

lipoglycopeptides

A
  • Inhibits cell wall synthesis during the second stage by binding to D-ala-D-ala of the cell wall precursors. This prevents cross-linking and further elongation of peptidoglycan.
  • They also bind to bacterial membranes and insert their lipophilic tails into the cell wall to cause depolarization, leakage, and cell death.

They have the mechanisms of vancomycin and daptomycin

45
Q

What is the mechanism of resistance against the lipoglycopeptides?

telavancin, dalbavancin, oritavancin

A

Mutation of D-ala-D-ala to D-ala-D-lactate

46
Q

What is the general SOA of the lipoglycopeptides?

A

Gram-positive aerobes

47
Q

What target organisms do the lipoglycopeptides have activity against?

telavancin, dalbavancin, oritavancin

A
  • PRSP
  • MSSA
  • MRSA
  • some VRE
  • VISA
  • VRSA (oritavancin only)
48
Q

What PK parameter best predicts efficacy of the lipoglycopeptides?

A

AUC/MIC

They display concentration-dependent bactericidal activitiy

49
Q

How is telavancin eliminated?

dose adjustments?

A
  • Telavancin is excreted by the kidneys
  • Dosage adjustments are suggested in renal dysfunction
50
Q

How is dalbavancin eliminated?

half-life, dose adjustments?

A
  • Dalbavancin is excreted in the feces and urine.
  • Half-life of 346 hours
  • Dosage adjustments of dalbavancin are suggested in patients with severe renal dysfunction who are not receiving HD

None of the lipoglycopeptides are removed by HD

51
Q

How is oritavancin eliminated?

half-life? dosage adjustment?

A
  • unknown
  • half-life is 245 hours
  • no dosage adjustments are required in renal or hepatic insufficiency
52
Q

When would the lipoglycopeptides be used clinically?

A

Only where vancomycin, linezolid/tedizolid, AND daptomycin can’t be used.

almost never used

53
Q

What are the adverse effects of the lipoglycopeptides?

mainly telavancin

A
  • Nephrotoxicity
  • QTc prolongation
  • taste disturbances
  • adverse developmental outcomes –> BBW

Pregnancy test needed before use in women of childbearing age

54
Q

What are the risk factors for developing nephrotoxicity from telavancin?

A
  • comorbidities predisposing to renal dysfunction
  • receiving other nephrotoxins
  • patients > 65 years old

  • comorbidities = renal disease, diabetes, CHF, HTN
  • nephrotoxins = NSAIDs, loop diuretics, ACE inhibitors

PHRM 865 (22 decks)

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