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PHARMACOLOGY > ANTIBIOTICS > Flashcards

ANTIBIOTICS Flashcards

1
Q

vancomycin mechanism of action

A

prevents cell wall synthesis and promotes cell lysis

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2
Q

vancomycin spectrum of activity

A

ONLY gram positive organisms

includes MRSA

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3
Q

pharmacokinetics of vancomycin

A
  • VERY poor oral absorption

- ONLY give PO when treating C. diff

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4
Q

adverse effect of vancomycin

A
  • nephrotoxicity
  • red man syndrome
  • Characterized by flushing, rash, pruritus, urticaria, tachycardia and possibly hypotension
  • Treat symptomatically with anti-histamines
  • SLOW the infusion rate
    1 gram of vancomycin should be given over a minimum of 60 minutes
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5
Q

if a person is allergic to pencillin you give them?

A

cephalosporins

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6
Q

therapeutic index of vancomycin

A

Vancomycin has a narrow therapeutic index

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7
Q

vancomycin monitoring

A
  • Vancomycin levels must be monitored once drug is at steady state
  • Trough levels are preferred
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8
Q

mechanism of action of fosomycin

A

Prevents cell wall synthesis

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9
Q

administration of fosfomycin

A
  • Medication is a powder in a packet

- Educate patient to dissolve powder in water and drink the entire dose

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10
Q

drugs of tetracylines

A

tetracyline
doxycycline
minocycline

doxy and amino are long lasting

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11
Q

tetracylines mechanism of action

A

Inhibits growth of the peptide chain and production of vital proteins

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12
Q

what are the beta-lactam antibiotics (bacteriocidal)

A

penicillins
cephalosporins
carbapenems
monobactams

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13
Q

mechanisms of resistance of tetracycline

A

Increased drug inactivation
Decreased access to the ribosome
↓ accumulation of drug intracellularly

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14
Q

contraindications of tetractclines

A

Pregnancy category D

Do NOT use in children < 8 years old

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15
Q

monitoring/counseling points for taking tetracycline, doxycycline, minocycline

A
  • Do NOT take tetracyclines with diary products, calcium, magnesium or aluminum containing products
  • administer tetracycline 1 hour before or 2 hours after
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16
Q

adverse effects of tetracycline, doxycycline, minocycline

A
  • Discoloration of teeth if taken during pregnancy or childhood
  • Superinfection
  • Photosensitivity
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17
Q

what drugs are macrolides

A
  • Azithromycin
  • Clarithromycin
  • Erythromycin
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18
Q

Mechanism of resistance:
of macrolides (Azithromycin
Clarithromycin
Erythromycin)

A

↓ intracellular concentrations of the drug – efflux pumps

Decrease access to the ribosome

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19
Q

Monitoring/ Counseling Points for macrolide( azithromycin, clarithromycin, erythromycin)

A
  • Avoid combining these agents with other QTc prolonging drugs
  • Take with food to decrease GI upset
  • Ensure erythromycin formulation can be taken with food
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20
Q

Mechanism of action:

clindamycin

A

Inhibits growth of the peptide chain and production of vital proteins

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21
Q

Mechanisms of resistance:

clindamycin

A

↓ intracellular concentrations of the drug – efflux pumps

Decrease access to the ribosome

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22
Q

adverse effect of clindamycin

A

Clostridium difficile

  • Clostridium difficile-associated diarrhea (CDAD)
  • Leads to superinfection of the bowel
  • Characterized by:
    Profuse, watery diarrhea
    10 to 20 stools per day
    Abdominal pain
    Fever
  • Can start as soon as 1 week after antibiotics treatment
  • Educate patients on signs and symptoms of CDAD
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23
Q

mechanism of action linezoid

A
  • Inhibits growth of the peptide chain and production of vital proteins
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24
Q

Spectrum of activity linezoid

A
  • Gram positive organisms only

MRSA
Vancomycin-resistant enterococcus (VRE)

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25
Q

adverse effect of linezolid

A

Thrombocytopenia – typically occurs about 2 weeks after therapy

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26
Q

mechanism of action of tigecycline

A
  • Bind to 30s ribosomal subunit
  • Inhibit binding of transfer RNA to the messenger RNA
  • Inhibits growth of the peptide chain and production of vital proteins
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27
Q

adverse effects of tigecycline

A

Nausea/vomiting
Photosensitivity

Black box warning for increased risk of mortality

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28
Q

Mupirocin

A

Topical antibiotic active against gram positive bacteria

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29
Q

INDICATION OF MUPIROCIN

A

elimination of MRSA

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30
Q

drugs for herpes simplex virus and varicella zoster virus

A

Acyclovir
Valacyclovir
Famciclovir

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31
Q

Famciclovir mechanism of action

A
  • inhibits viral DNA polymerase and prevents replication of viral DNA
  • Blocks further DNA strand growth after being incorporated into viral DNA
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32
Q

whats meant by valacyclovir being a prodrug?

A

it is converted to acyclovir after absorption from the GI tract

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33
Q

adverse effect of acyclovir

A
  • IV therapy

– phlebitis, nephrotoxicity

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34
Q

Monitoring/ Counseling Points

for acyclovir

A
  • Oral administration requires three to five doses daily
  • Prevent nephrotoxicity:

Hydrate patient
Decrease other nephrotoxic medications

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35
Q

topical drugs for herpes labialis (cold sores)

A
  • penciclovir cream

- docosanol cream

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36
Q

drugs for cytomegalovirus

A

Ganciclovir
Valganciclovir
Cidofovir
Foscarnet

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37
Q

mehcanisms of actions for Ganciclovir and Valganciclovir

A
  • Inhibits viral DNA polymerase

- Blocks further DNA strand growth after being incorporated into viral DNA

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38
Q

what does it mean for Valganciclovir to be a prodrug?

A

After absorption from the GI tract it is converted to ganciclovir

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39
Q

adverse effects of ganciclovir

A
  • Agranulocytosis
  • Thrombocytopenia
  • Reproductive toxicity
  • Nausea
  • Liver dysfunction
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40
Q

monitoring/ counseling points for ganciclovir

A

Monitor white blood cell count, platelets, liver function tests, serum creatinine (Scr)
Avoid use in pregnancy
Avoid pregnancy for 90-days following therapy

Handle with caution. Should be treated as a cytotoxic drug

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41
Q

mechanism of action of cidofovir

A
  • inhibits viral DNA polymerase

- Inhibits viral DNA strand growth after being incorporated

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42
Q

adverse effect of cidofovir

A

nephrotoxicity

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43
Q

monitoring/ counseling points of cidofovir

A
  • Prevention of nephrotoxicity:

Hydrate patient with IL NS prior to dose
Avoid other nephrotoxic medications

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44
Q

foscarnet mechanism of action

A
  • Inhibits viral DNA polymerase and reverse transcriptase

- Inhibits synthesis of viral nucleic acids

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45
Q

foscarnet adverse effects

A

nephrotoxicity

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46
Q

prevention of nephrotoxicty

A

Hydrate patient with IL NS prior to dose

Avoid other nephrotoxic medications

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47
Q

mechanism of action of interferon-alfa

A
  • Interferon alfa binds to the host cell membranes
  • Binding to the host cell membrane inhibits viral entry into the cell
  • Interferon alfa stimulates cell to turn on genes for antiviral proteins
  • Antiviral proteins block viral reproduction
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48
Q

clinical effects of interferon-alfa

A
  • 30 to 40% response rate with sustained virologic response (SVR)
  • Up to 50% of patients with - - SVR will relapse
  • SVR is maintained only in 5-15% of patients
  • Best effects when combined with another agent
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49
Q

mechanism of actions: nucleoside analogs

A
  • Inhibits viral DNA strand growth after being incorporated
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50
Q

mechanism of actions of ribavirin

A

Interferes with RNA metabolism needed for viral replication

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51
Q

ribavirin is used in combination with inteferon BUT NEVER used as……

A

monotherapy for HCV

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52
Q

adverse effects for ribavarin

A
  • Hemolytic anemia (10%)
    ( Develops in 1 to 2 weeks of therapy )
  • Fetal injury
    ( Contraindicated during pregnancy )
  • Pancreatitis
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53
Q

prevention with vaccination is…..

A

key

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54
Q

types of influenza vaccines

A
  • Inactivated influenza vaccine

- Live-attenuated vaccine

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55
Q

vaccine contraindications of everyone 6 months and older

A
  • Prior history of anaphylactic reaction to influenza vaccine
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56
Q

Patients at high risk for influenza complications:
Children < 5 years
Pregnant women
Adults > 65
People living in long-term care facilities
American Indians or Alaskan Natives

A

Confirmed history of Guillain-Barre syndrome occurred within 6 weeks following previous vaccination and LOW risk for influenza complication

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57
Q

neuraminidase inhibitors drugs

A

Oseltamivir
Zanamivir
Peramivir

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58
Q

mechanisms of actions of neuraminidase ( Oseltamivir, Zanamivir. Peramivir ) inhibitors

A

Inhibit neuraminidase

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59
Q

adverse effects of Oseltamivir

A
  • Nausea

- Delirium or abnormal behavior in children

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60
Q

monitoring/ counseling point of oseltamivir

A

take with food to decrease nausea

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61
Q

respiratory syncytial virus (RSV)

A
  • Ribavirin (inhaled)

- Palivizumab

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62
Q

indications of respiratory syncytial virus (RSV)

A

Prevention of RSV in premature infants or children with chronic lung disease

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63
Q

AIDS is defined by:

A
  • CD4 counts below a certain level

- Contracting an AIDS defining illness

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64
Q

without CD4 helper T cells, the immune system experiences .

A

progressive decline

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65
Q

CD4 helper T cells are required for

A

production of antibodies by B lymphocytes, and activation of cytotoxic T cells.

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66
Q

HIV replication cycle

A

Co-receptors CCR5

HIV lipid bilayer fuses with the host cell membrane. Viral RNA is released into the cell.

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67
Q

Reverse transcriptase converts

A

single-strand DNA to double-strand

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68
Q

HIV DNA is integrated into host cell DNA by what enzyme

A

integrase

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69
Q

HIV RNA is transcribed into DNA by

A

reverse transcriptase

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70
Q

Protease cleaves large?

A

viral polyproteins.

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71
Q

Mutations may lead to

A

drug resistance

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72
Q

Higher viral loads increase the chance of

A

developing resistance

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73
Q

To combat resistance:

A
  • Treat HIV infection with multiple agents

- Ensure compliance with HAART therapy

74
Q

what are the 5 classes of antiretroviral drugs

A
  1. Reverse transcriptase inhibitors
  • Nucleoside/nucleotide reverse transcriptase inhibitors
  • Non-nucleoside reverse transcriptase inhibitors
    2. Integrase strand transfer inhibitors
    3. Protease inhibitors
    4. Fusion inhibitors
    5. Chemokine receptor 5 (CCR5) antagonists
75
Q

ALL clinicians should check drug-drug interactions before ?

A

administering HAART therapy

76
Q

Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTI)

A

DO NOT USE AS MONOTHERAPY

77
Q

mechanism of action of Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTI)

A

Incorporated into the DNA strand and cause strand termination

78
Q

adverse effects of abacavir

A

Associated with mitochondrial toxicity:

  • Lactic acidosis
  • Hepatic steatosis
  • Pancreatitis
  • Myopathies
  • GI upset
79
Q

Monitoring/ Counseling for NRTI

A

MUST check if patient has genetic variation *HLA-B5701

80
Q

Non-nucleoside Reverse Transcriptase Inhibitors (NNRTI)

A

Used in combination with NRTIs

81
Q

mechanisms of actions of Non-nucleoside Reverse Transcriptase Inhibitors (NNRTI)

A

Terminates DNA strand formation

82
Q

adverse effects of Non-nucleoside Reverse Transcriptase Inhibitors (NNRTI)

A
  • Rash
    can be life-threatening, counsel patient to seek medical advice immediately if rash occurs
  • CNS symptoms
  • Hepatotoxicity
83
Q

Protease Inhibitors (PI)

A

MUST be used in combination with other antiviral medications

84
Q

Mechanism of action: protease inhibitors (PI)

A
  • Inhibits the HIV protease enzyme
  • Prevents maturation of the HIV virus
  • Immature HIV virus is non-infectious
85
Q

drug-drug interactions of protease inhibitors (PI)

A
  • all protease inhibitors inhibit certain CYP enzymes

- Some protease inhibitors (PI) can therefore increase serum concentrations of other protease inhibitors

86
Q

Ritonavir

A

often combined with other drugs for this purpose – RITONAVIR BOOSTING

87
Q

adverse effects of protease inhibitors (PI)

A
  • Hyperglycemia/ diabetes
  • Lipodystrophy
  • Hyperlipidemia
    ↑ LFTs (Liver Function Test)
    ↑ risk of bleeding in patients with hemophilia
88
Q

Integrase Strand Transfer Inhibitors

A

Used in combination with other antiviral drugs

89
Q

Mechanism of action: Integrase Strand Transfer Inhibitors

A

Inhibits the enzyme integrase

Prevents HIV from inserting its viral DNA into the host cell DNA

90
Q

adverse effects for dolutegravir (integrease stand transfer inhibitor)

A

↑ LFTs

  • Insomnia
  • Headache
  • Diarrhea/nausea
91
Q

monitoring/counseling for dolutegravir (integrease stand transfer inhibitor)

A

DDI interaction with drugs containing calcium, iron or magnesium

– give dolutegravir 2 hours before these agents

92
Q

what is dolutegravir

A

an Intergrease Stand Transfer Inhibitor (INSTI)

93
Q

HIV Fusion Inhibitors

A

Enfuvirtide

94
Q

usage of Enfuvirtide

A

treatment-resistant HIV-1

95
Q

mechanism of action of enfuvirtide

A

Blocks entry of HIV into CD4 cells

96
Q

adverse effects of enfuvirtide

A
  • Injection site reactions (98%), especially in first week of treatment
  • Pneumonia
  • Hypersensitivity reactions
    ( If this develops, discontinue therapy and never use again)
97
Q

what is maraviroc (CCR5 ANTAGONIST) used for?

A

treatment-resistant HIV-1 in patients ≥ 16 years old

98
Q

Pathophysiology of maraviroc

A

Some HIV strains require CCR5 binding to access the host cell = CCR5 tropic

99
Q

mechanism of action of maraviroc

A

Prevents HIV from binding to the host cell

100
Q

maraviroc requires genetic testing to identify if…

A

patient’s strain of HIV is CCR5 tropic

101
Q

adverse effects of maraviroc

A

Upper respiratory tract infections

↑ LFTs

102
Q

intial therapy for HIV

A

always a multi-drug regimen

INSTI + 2 NRTI

103
Q

Laboratory Tests and Resistance for HIV

A
  • CD4 T cell count - how much immunocompetency is left

- Viral Load - magnitude of viral replication

104
Q

pre-exposure prohylaxis (PrEP) for hiv is rommended for

A

patients at high-risk of HIV transmission:

105
Q

Post-exposure Prophylaxis

A
  • Goal to start therapy AS SOON AS POSSIBLE (1 to 2 hours)

- Therapy can be started up to 72 hours after exposure

106
Q

Non-occupational exposure

of post- exposure prophylaxis

A
  • Unprotected intercourse, sharing needles, sexual assault

- 28-day HAART regimen

107
Q

occupational exposure

of post- exposure prophylaxis

A
  • Accidental needle stick, blood or body fluid splashes

- 28-day HAART regimen

108
Q

what is selective toxicity

A

ability of a drug to injure a target organism without injuring other cells or organisms inclose contact with the target
( Kill bacteria, don’t kill host )

109
Q

Narrow spectrum of antimicrobial drugs

A

active against a few different microbial species

110
Q

Broad spectrum of antimicrobial drugs

A

= active against wide range of different microbial species

111
Q

Bactericidal effects of antimicrobial drugs

A

kill bacteria

112
Q

Bacteriostatic effects of antimicrobial drugs

A

slow bacterial growth

113
Q

How do bacteria develop resistance to antibiotics?

A

Bacteria may become resistant to antimicrobials over time and with repeat exposure
( Acquired resistance )

114
Q

Resistance to one drug or class may confer

A

resistance to other drug classes as well

115
Q

Spontaneous mutation method of bacterial resistance to antimicrobial drugs

A
  • random changes in bacterias DNA

- Spontaneous mutations confer resistance to one drug

116
Q

spontaneous mutations confer

A

confer resistance to one drug

117
Q

Conjugation method of bacterial resistance to antimicrobial drugs

A
  • Extrachromosomal DNA is transferred from one bacteria to another
  • Primarily occurs in gram negative organisms
  • Confers resistance to multiple drugs
118
Q

Reduction of Drug Concentration at its Active Site

mechanisms of bacteria resistance

A
  • Decrease active uptake of the drug

- Increase active export of the drug

119
Q

Alteration of Drug Target Molecules

mechanisms of bacteria resistance

A

If a drug binds to a certain site on the ribosome, the bacteria will change the shape of the ribosome

120
Q

Antagonist Production

mechanisms of bacteria resistance

A

-bacteria produce a compound that antagoizes the drugs action

121
Q

Drug Inactivation

mechanisms of bacteria resistance

A

Produce enzymes that breakdown the drug

122
Q

The more antimicrobials are used more often,

A

the faster resistant organisms will emerge. Need to be judicious with use.

123
Q

Broad-spectrum are less likely to cause resistance than narrow spectrum

A

false. Broad-spectrum are more likely to cause resistance than narrow spectrum since they affect more bacteria

124
Q

Resistant organisms are especially common in

A

hospitals.

Hospital Acquired Infections (HAI)
Very difficult to treat due to limited antimicrobial options

125
Q

does antimicrobial directly cause changes to bacterial DNA?

A

Antimicrobials do not directly cause changes to bacterial DNA that make them resistant. They promote resistance via “survival of the fittest”

126
Q

If some bacteria are resistant

A

antimicrobials create a more favorable environment for them to grow

127
Q

what is a superinfection

A

New infection that appears during a course of antibiotic treatment for a different infection.

128
Q

Superinfections are more common with what spectrum antimicrobials

A

broad- spectrum

129
Q

Goal of antimicrobial therapy =

A

produce maximal antibiotic effects while minimizing harm to the patients

130
Q

Three key principles of selecting antimicrobials

A
  • Identification of the infecting organism
  • Organism susceptibility to the drug
  • Host factors – site of infection, immunocompetence, etc.
131
Q

what is empiric therapy of antimicrobial

A

starting the antimicrobial treatment before the infecting organism can be identified =

132
Q

Empiric therapy may use what spectrum antibitics

A

broad-spectrum antibiotics.

After the organism is identified the therapy can be de-escalated

133
Q

Most infections will have a ‘first-choice’ drug to treat it; however, a patient may not be able to take the ‘first-choice’ drug from a number of reasons such as

A

allergies or inability for drug to penetrate the site of infection

134
Q

abcess and antibiotics

A

Abscesses _ must be drained first, antibiotics will not penetrate them

= Foreign bodies _ very difficult to treat

135
Q

Dose of antibiotic must be optimized to:

A
  • Achieve maximum concentrations of antibiotic at site of infection
  • Maintain concentrations for longest possible duration
  • Goal is typically 4 to 8 times the MIC of the organism
136
Q

Duration of antibiotic therapy depends on the type of infection

A
  • Patients MUST take the full course of antibiotics

- Patients must be educated not to stop antibiotic early since this leads to increased risk of resistance

137
Q

Why would multiple antibiotics be used at once?

A
  • Empiric therapy for a severe infection
  • Mixed infections
  • Preventing resistance
  • Decreased toxicity
  • Enhanced antibacterial action
138
Q

When should antimicrobial prophylaxis be used?

A
  • Surgery
  • Bacterial endocarditis
  • Neutropenia
  • Recurrent urinary tract infections
139
Q

What are ways in which antibiotics are misused

A
  • Treatment of a VIRAL infection
  • Treatment of fever with unknown origin
  • Improper dosage
  • Lack of source control (eg. undrained abscess or no removal of necrotic tissue)
140
Q

What antibiotics are included in the beta-lactam class?

A
  • Penicillins
  • Cephalosporins
  • Carbapenems
  • Monobactams
141
Q

are beta-lactam antibiotics bacteriostatic or bacteriocidal?

A

bactericidal,

142
Q

Penicillin Mechanism of Action

A

Inhibits actions of transpeptidases
Increases actions of autolysins
Weakens the structure of the cell wall → cell lysis

143
Q

penicillin weakens what?

A

the structure of the cell wall = cell lysis

144
Q

what does penicillin bind to

A

Penicillins bind to penicillin-binding proteins (PBPs) on the cell membrane

145
Q

penicillin does not penetrate what system?

A

DOES NOT PENETRATE CNS. eyes or joints well. unless inflammation is present

146
Q

since 90% of penicillin is excreted by kidneys, doses must be…..

A

doses MUST be reduced in patients with renal impairment

147
Q

common adverse effects of penicillin

A
  • Allergic reaction
  • Rash
  • Neurotoxicity
148
Q

List the narrow spectrum penicillins and their route of administration.

A

pencillin G

Sodium IV
Potassium IV
Procaine IM
Benzathine IM

149
Q

Penicillinase-Resistant Penicillins

A
  • Nafcillin
  • Oxacillin
  • Dicloxacillin

(not effective agaisnt methicillin-resistant MRSA)

NARROW SPECTRUM

150
Q

How does broad spectrum penicillin differ from penicillin G?

A

increased coverage of gram negative bacteria

151
Q

Are broad spectrum penicillin affected by beta-lactamases?

A

inactivated by beta-lactamase enzymes

152
Q

what are the broad spectrum penicillins

A
  • Ampicillin IV/PO

- Amoxicillin PO

153
Q

what are the extended spectrum penicillins

A

Piperacillin

154
Q

extended spectrum penicillin are…

A

Highly susceptible to beta-lactamases

155
Q

what bacterias do extended spectrum penicillin cover

A
  1. Gram positive organisms
  2. Gram negative organisms
    - PSEUDOMONAS aeruginosa
  3. Anaerobic organisms
156
Q

WHAT ARE Beta-lactamase inhibitor

A

drug that inhibits beta-lactamase enzymes.

tazobactam
sulbactam
clavulanate

157
Q

Piperacillin combined with

A

tazobactam

158
Q

Ampicillin combined with

A

Sulbactam

159
Q

Amoxicillin combined with

A

Clavulanate

160
Q

what is anaphylaxis?

A

an immediate allergic reaction mediated by IgE.

treatment = epinephrine

  • often associated with airway swelling, hypotension and cardiovascular collapse
161
Q

If a patient is allergic to penicillin, they are considered allergic to…

A

ALL penicillins

162
Q

Most patients will be able to take cephalosporins since there is only a ~1% risk of cross-reactivity BUT

A
  • If reaction is mild = give cephalosporins

- If reaction is severe (anaphylaxis) = do NOT give cephalosporins, select alternative agent

163
Q

are cephalosporins bactericidal or bacteriostatic

A

bactiricidal

164
Q

cephalosporins are more resistance to

A

beta-lactamase enzymes

165
Q

How are cephalosporin antibiotics categorized?

A

Note that not all cephalosporins are equally susceptible to beta-lactamase enzymes.

  • 1st generation tend to be the most susceptible to beta-lactamase enzymes
  • the fifth generation are the most resistant.

Beta-lactam antibiotics;
- chemical structure composed of a beta-lactam ring with varying side chains

166
Q

what generation of cephalosporins are more resistant

A

5th generation are more resistant.

1st generations are most susceptible

167
Q

Which generations of cephalosporins can be used to treat CNS infections?

A

3-5

168
Q

Which generations have the most gram negative coverage?

A

2-5

169
Q

Which generations have the leastgram negative coverage?

A

1

170
Q

Describe the pharmacokinetics of cephalosporins?

A

Poor oral absorption; most agents are given IV

171
Q

What is the drug-drug interaction between ceftriaxone and calcium?

A
  • Precipitates can form
  • Do NOT reconstitute or mix ceftriaxone with calcium-containing solutions
  • Do NOT administer through the same line at the same time
172
Q

List the carbapenem antibiotics.

A
  • Imipenem/ cilastin
  • Meropenem
  • Doripenem
  • Ertapenem
173
Q

What bacteria do carbapenem antibiotics cover?

A

Broad-spectrum of antimicrobial activity
- gram positive (no MRSA)
- Gram negative
Anaerobes

174
Q

carbapenem MRSA or no MSRA

A

no MSRA

175
Q

carbapenems relation with beta-lactase enzymes

A

Very resistant to beta-lactamase enzymes

176
Q

What serious adverse effect is associated with meropenem and Imipenem/cilastin?

A

seizure

177
Q

What are monitoring/counseling points for beta-lactam antibiotics?

A

Monitor for

  • Clinical signs of improvement
  • Allergic reactions
  • Signs of worsening or new infections
  • Adverse effects including seizure
  • Ensure patient completes and appropriate course of therapy
    Dose adjustments for renal impairment
178
Q

Imipenem has DDI with…………. and can……… of valproic acid

A

valproic acid, decrease levels

179
Q

What type of antibiotic is aztreonam?

A

Unique type of beta-lactam called a monobactam

180
Q

When is aztreonam the drug of choice?

A

Drug of choice for gram negative coverage in a patient with a penicillin allergy

181
Q

What types of bacteria does aztreonam cover?

A

ONLY gram negative organisms, including Pseudomonas

182
Q

mechanism of actions of macrolides

A

inhibits growth of the peptide chain and production of vital proteins

PHARMACOLOGY (7 decks)

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