3 Anti Microbials Flashcards

1
Q

What are the common “Natural Penicillins”?

A
  • Penicllin G (IV,IM)
  • penicillin V (PO)
    • Narrow; Gram(+) cocci, Mostly Streptococci
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2
Q

Common anti-staphylococcal penicillins?

A
  • Oxacillin (IV, IM)
  • Dicloxacillin (PO)
  • Nafcillin (IV, IM)
    • Narrow
    • Gram (+) cocci
    • Staphylococci
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3
Q

Common Aminopenicillins?

A
  • Ampicillin (PO, IV, IM)
  • amoxicillin (PO)
    • Extended
    • Gram (+)/(-)
      • (-): E.coli, H. influenzae, P. mirabilis
      • (+): Listeria, enterococci
    • Enterococci (primary target)
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4
Q

1st generation cephalosporins.

A
  • Cefazolin (IV, IM)
  • Cephalexin (PO; keflex)
    • Gram (+)
    • some effect on gram (-)
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5
Q

2nd generation cephalosporins.

A
  • Cefoxitin
  • Cefuroxime
    • somewhat active against gram (-). mostly active agaisnt Bacteroides fragilis
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6
Q

3rd generation cephalosporins.

A
  • Ceftriaxone (IV, IM)
    • choice drug for gonorrhea.
  • ceftazidime (IV, IM)
    • less active against gram (+)
    • good against gram (-)
      • Klebsiella, enterobacter, proteus, serratia, haemophilus
        *
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7
Q

Carbapenems

A
  • Imipenem (IV)
  • Meropenem (IV)
  • Ertapenem (IV, IM)
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8
Q

Glycopeptides common drugs

A
  • Vancomycin (PO, IV)
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9
Q

Common Beta-lactamase inhibitors

A
  • Amoxicillin-clavulanic acid [augmentin] (PO)
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10
Q

Common Fluoroquinolones.

A
  • Ciprofloxacin (PO, IV, topical)
  • levofloxacin (PO, IV, topical)
  • Moxifloxacin (PO, IV, topical)
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11
Q

Common aminoglycosides

A
  • Gentamicin (PO, IV)
  • Tobramycin (IV, IM, INH, topical)
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12
Q

Common tetracyclines

A
  • Doxycycline (PO, IV)
  • Minocycline (PO, IV)
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13
Q

Common macrolides

A
  • Azithromycin (PO, IV, topical)/ Z-pack or zithromax.
  • Clarithromycin (PO)
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14
Q

Common lincosamides

A
  • Clindamycin ( PO, IV, IM, topical)
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15
Q

Common Antivirals

A
  • Acyclovir (PO, IV, topical)
  • Oseltamivir (PO/tamiflu)
  • zanamivir
  • amantadine
  • rimantadine
  • valacyclovir
  • ganciclovir
  • valganciclovir
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16
Q

Common Antifungals

A
  • Fluconazole/diflucan (PO, IV)
  • Amphotericin B (IV)
  • itraconazole
  • voriconazole
  • caspofungin
  • micafungin
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17
Q

What are the goals of prophylactic therapy?

A
  • prevent infection, or dangerous disease in those who are alredy infected.
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18
Q

An 18 y/o female is admitted to the hospital with a diagnosis of meningococcal meningitis. She lives in the dorms and is only one month into her freshman year of college. What type of therapy should be given to her roommate?

A

Prophylactic therapy to prevent infection due to the close contact.

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19
Q

What is pre-emptive therapy?

A

Early targeted therapy in high risk patients who are asymptomatic but have been infected.

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20
Q

An 8 y/o male presents to the ED with a perforated appendix. Why would you initiate antibiotics pre-operatively?

A

Antibiotics are initiated pre-operatively to reduce the risk of intra-abdominal abscess and/or surgical wound infection.

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21
Q

What is empiric therapy?

A

Provides therapy to a symptomatic patient without identification of the infecting organism. (consider more broad class, until identification)

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22
Q

A 50 y/o male presents to his PCP with dyspnea, fever, and cough. Community-acquired pneumonia is suspected and his physician initiates appropriate therapy to cover the most likely infecting organisms. This describes what type of therapeutic approach?

A

empiric therapy

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23
Q

Definitive therapy

A

Identification of the organism. Antibiotics are targeted at the susceptibility and duration for the proper length. As both susceptibility (concentration) and time affect the organism.

24
Q

›A 45 y/o female, undergoing 3x weekly dialysis, presents with fever and fatigue. Blood cultures reveal gram-positive cocci on gram stain and Staphylococcus is suspected. After sensitivity determined, antibiotics are appropriately adjusted to the most narrow-spectrum coverage. The switch that was made, is indicative of what type of new therapy?

A

Definitive therapy.

25
Q

Post-Treatment Suppressive Therapy

A

Antimicrobial coverage at lower dose when the infection has not been completely eradicated.

26
Q

›A 75 y/o male presents to his PCP for follow-up of prosthetic hip joint infection. Review of his drug list reveals continued low dose antimicrobial therapy. Hip prosthesis was unable to be removed and replaced during hospitalization. In order to prevent infection until the hip can be removed, what is the best type of therapy approach?

A

Post-treatment suppressive therapy.

27
Q

What are common structures you should expect to find in Gram(+) bacteria/cellular envelope?

A
  • Capsule: immunogenic/antiphagocytic
  • Surface proteins: antiphagocytic/ immunogenic
  • Teichoic acid: attach peptidoglycan layers. Lipoteichoic: anchors peptidoglycan layer to lipid membrane.
  • Peptidoglycan layer: rigid structural support of cell. Protects from osmotic damage
  • Cytoplasmic Membrane: membranous matrix for enzymes in final stages of cell wall synthesis.
28
Q

What should you expect to find in the cell membrane/envelope of Gram (-) bacteria?

A
  • Capsule: antiphagocytic and immunogenic
  • Outer membrane: hydrophobic phospholipid bilayer, LPS with endotoxin A
  • Porin: transporter across the outer membrane to the periplasmic space.
  • Peptidoglycan layer: very small thin layer of peptidoglycan
  • Inner membrane layer: membranous matrix for enzymes and the final stages of the cell wall synthesis.
29
Q

Susceptible

A

Likely to inhibit pathogenic microorganisms

30
Q

Intermediate susceptibility

A

Effective at higher doses, more frequent administration or in a specific body location.

31
Q

Resistant susceptibility

A

Not effective at inhibiting the growth of microorganisms.

32
Q

Minimum inhibitory concentration (MIC)

A
  • The lowest concentration of medication that will inhibit microbial growth.
    • standards established by Clinical/Laboratory Standards Institute (CLSI)
33
Q

What are the common types of susceptibility testing?

A
  • Dilution Test
  • Disk Diffusion
  • Gradient Diffusion
34
Q

Describe the process of the Dilution “susceptibility” Test

A
  1. Isolate bacterial strain colonies
  2. Combine multiple cultures and incubate.
  3. Add broth to tubes, with proper dilution and inoculate bacteria.
  4. Plate the combined/diluted bacterial test tubes and let growth occur.
  5. REplace cultures to test tube.
    1. MIC is the lowest concentration of antiobiotic that prevents growth.
    2. Essentially dilute down the antibiotic dosage systematically until you can compare two vials (one with growth and the other without growth)
35
Q

Narrow-spectrum antibiotics

A

Act on a single or limited group of microorganisms

36
Q

Extended-spectrum antibiotics

A

Act on Gram (+) bacteria with some extension into Gram (-) bacteria

37
Q

Broad-spectrum antibiotics

A

Active on a wide variety of bacterial species. Both Gram (+)/(-)

38
Q

Bacteriostatic

A

Ability to stop growth of bacteria. Helps limit infection by reducing the replication.

39
Q

Concentration dependent bacteriocidal.

A
  • Bacteria killing medication based on drug concentration.
  • Rate and extent of killing is proportional to the concentration of the drug.
40
Q

Time-dependent bactericidal medication

A
  • Bacterial killing that continues as long as the concentration is at or above the MIC.
  • Must be within the serum and not localized to the tissue (less effective)
41
Q

What would be the most effective way to kill enterococci?

A

Synergism of Penicillin and Gentamicin. Incorporates specific aspects of each medication to induce bacterial killing.

42
Q

What sites within bacteria are significantly different when compared to human cells?

A
  1. Cell wall
  2. Ribosomes
  3. Nucleic Acids
  4. Cell membrane

all differ in bacteria when compared to humans.

43
Q

What anitbiotics are grouped into break down of cell walls?

A
  • ß-lactams
    • ​Penicillins
    • Cephalosporins
    • Carbapenems
    • Monobactams
  • bacitracin
  • vancomycin
  • daptomycin
44
Q

What is the mechanism of action of the ß-lactam cell wall inhibitors?

A
  • Time-dependent (long course of medication)
  • Acts on penicillin-binding proteins (PBP)
    • ​analog to D-Ala-D-Ala
45
Q

What is the effect of Beta-lactam drugs acting on the cell wall?

A

B-lactams bind to penicillin-binding proteins which inhibits the ability of transpeptidation. The last step of cell wall synthesis.

46
Q

Common adverse effects of penicillins?

A
  • NVD
  • Pseudomembranous colitis.
  • Allergic reaction/anaphylaxis.
47
Q

What is an important component found in beta-lactamase inhibitor drugs?

A
  • Clavulanic acid.
    • used for treatment of B-lactam resistant pathogens.
    • therefore allowing for prolonged activity of beta-lactam to penetrate/inhibit cell wall synthesis.
48
Q

Vancomycin: MOA, Spectrum, Adverse Effects.

A
  • MOA: inhibit cell wall synthesis with high binding affinity to “D-Ala-D-Ala”
  • Spectrum: gram (+) with inclusion of resistant microbe. C. difficile
  • Adverse effects: red-man syndrome (massive histamine release), Ototoxicity, nephrotoxicity.
49
Q

What is the MOA of fluoroquinolones?

A
  • Concentration-dependent
  • Acts on bacterial DNA gyrase and topoisomerase IV
    • Prevents relaxation and promotes positive supercoils
50
Q

What are the adverse effects of Fluoroquinolones?

A
  • GI distress
  • CNS problems
  • Photosensitivity
  • Achilles tendon rupture.
51
Q

What is the spectrum for fluoroquinolones?

A
  • Broad-gram (-)
    • S. aureus, but not the MRSA strand.
  • Limited coverage of streptococcus species.
52
Q

How can translation be inhibited via medications?

A
  • Prevent formation of the initiation complex.
  • Incorporate amino acids.
  • Induce formation of a peptide bond.
  • Inhibit translocation.
53
Q

Aminoglycosides: MOA, Adverse Effects, Spectrum.

A
  • MOA: concentration dependent. Binds 30S subunit preventing formation of initiator complex leading to misreading of mRNA/
  • Adverse effects: ototoxicity, nephrotoxicity
  • Spectrum: Aerobic gram (-) bacteria.
54
Q

Tetracycline: MOA, Adverse effects, Spectrum.

A
  • MOA: bacteriostatic. Binds 30S and prevents tRNA from reaching “A” site.
  • Adverse effects: photosensitivity, teeth discoloration
  • Spectrum: Broad gram (-)/(+).
    • Rickettsia, coxiella burnetii, borrelia burgdorferi (Lyme’s disease)
55
Q

Macrolides: MOA, Adverse effects, Spectrum

A
  • MOA: bacteriostatic. 50S subunit preventing translocation.
  • Adverse effects: arrythmia, QT prolong.
  • Spectrum: aerobic gram (+), some gram (-)