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Pharmacology 4090 > AMDs > Flashcards

AMDs Flashcards

1
Q

6 groups of AMDs

A

Beta-lactams, aminoglycosides, tetracyclines, sulfonamides, macrolides, fluoroquinolones

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2
Q

Bacteriostatic to bactericidal

A

Can become bactericidal at high enough concentrations

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3
Q

Time-dependent AMDs

A

Efficacy is associated with the length of time the drug concentration stays above the MIC

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4
Q

Concentration-dependent AMDs

A

Efficacy depends on peak concentration

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5
Q

Relationship between resistance and use

A

Positive

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6
Q

Classes of antimicrobial sensitivity

A

Good, variable, moderate, resistance

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7
Q

Are bacteria the same level of sensitivity to all drugs

A

No!

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8
Q

AMD mechanisms

A

Damage membrane s inhibit cell wall synthesis, inhibit protein synthesis, inhibit folic acid synthesis, damage DNA

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9
Q

Serial dilution

A

Keep diluting drug concentration by 50% and then seed with standard amount of bacteria → let grow and assess for cloudiness of tubes

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10
Q

MIC

A

Concentration where there’s no visible growth but some bacteria may be alive

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11
Q

MBC

A

Concentration that sterilized the tube

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12
Q

Kirby-bauer test

A

Paper discs have different drugs and are placed on bacterial lawn to see zone of inhibition

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13
Q

Culture and sensitivity testing

A

Done for life-threatening infections, but takes a long time

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14
Q

Considerations when selecting drugs

A

Bacterial sensitivity, bacteriostatic versus bactericidal, adverse effects, distribution, and cost

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15
Q

Diseases w/ special considerations

A

Osteomyelitis, foreign bodies, abscess, intracellular pathogens, obstructed areas, immunodeficiency

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16
Q

Prophylactic uses of AMDs

A

High risk of infection after trauma, immune or anatomical defects, surgery

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17
Q

AMDs during surgery

A

Want to have adequate levels at the time of incision

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18
Q

Criteria for selecting AMDs

A

Spectrum, mechanism, adverse effects, distribution and elimination, line, cost, route of admin

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19
Q

Health Canada AMD drug categories

A

1,2,3, 4

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20
Q

Category 1

A

Very high importance to human health; life and death situation

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21
Q

Category 2

A

High importance; some alternatives available;drug of choice for serious infections

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22
Q

Category 3

A

Medium importance; not preferred for serious infections

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23
Q

Category 4

A

Low importance; not used in humans

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24
Q

Beta-lactams

A

Penicillins and cephalosporins

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25
Q

Beta-lactam ring

A

In beta-lactams, gives activity, susceptible to temperature changes

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26
Q

Beta-lactamases/penicillinases

A

Enzymes from some bacteria that destroy beta-lactams

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27
Q

Beta-lactam mechanism

A

Bind to and inactivate the transpeptidase enzyme that builds the cell wall → cell lysis

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28
Q

Types of penicillin

A

Narrow spectrum, penicillinase resistant, extended spectrum

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29
Q

Narrow-spectrum penicillin

A

Penicillin G

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30
Q

Penicillinase-resistant penicillin

A

Dicloxacillin

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31
Q

Extended spectrum penicillins

A

Ampicillin, amoxicillin

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32
Q

Targets of penicillin G

A

Gram positive aerobes, anaerobes

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33
Q

Pk of penicillin G

A

Not acid stable so it has to be given parenterally

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34
Q

Target of dicloxacillin

A

Penicillinase-producing staphylococci

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35
Q

Pk of dicloxacillin

A

Acid stable so it can be given orally!

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36
Q

Targets of amoxicillin

A

Gram positive aerobes, gram negative aerobes, and anaerobes

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37
Q

Pk of amoxicillin

A

Acid stable with a very high oral bioavailability

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38
Q

Potentiated penicillin

A

Amoxicillin plus clavulanic acid to resist penicillinases; make the penicillin second line treatment

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39
Q

Distribution of penicillins

A

Everywhere except CNS and prostate

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40
Q

Elimination of penicillins

A

Excreted unchanged in urine, mostly by active secretion

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41
Q

Resistance against penicillins

A

Gram-negative cell wall, acquired penicillinases

42
Q

Adverse effects of penicillins

A

Hypersensitivity (don’t use topically), seizures

43
Q

Cephalosporins

A

Type of beta-lactam with very similar mechanism of action, distribution, elimination, and adverse effects to penicillins

44
Q

Are cephalosporins sensitive to penicillinases?

A

No, but they are sensitive to beta-lactamases

45
Q

Cephalosporin generations

A

1,2,3,4

46
Q

1st generation cephalosporins spectrum and acid stability

A

Identical spectrum to amoxicillin, not acid stable (most)

47
Q

3rd generation cephalosporins spectrum

A

Less effective against gram positive aerobes and anaerobes, but more effective against gram negative aerobes; some can readily cross the BBB

48
Q

Aminoglycosides uses

A

Systemic administration for dangerous gram-negative aerobes, or topical use

49
Q

Most commonly used aminoglycoside

A

Gentamicin - highly ionized so isn’t absorbed orally or topically

50
Q

Aminoglycoside mechanism of action

A

Irreversibly inhibit protein synthesis and cause production of wrong peptides that produce poring → lysis

51
Q

Spectrum of aminoglycosides

A

Gram-negative aerobes, staph, mycoplasma

52
Q

Types of resistance against aminoglycosides

A

Structural (entry requires oxygen-dependent transport so anaerobes are resistant), aminoglycosidases

53
Q

Main adverse effects of aminoglycosides

A

Mephrotoxicity and ototoxicity

54
Q

Nephrotoxicity from aminoglycosides

A

Every patient will have some renal damage but it usually isn’t a problem unless they are dehydrated, have renal disease, or are elderly

55
Q

Washout period

A

Give single dose of aminoglycosides and let concentrations fall over the day

56
Q

Ototoxicity from aminoglycosides

A

Damage to cranial nerve 8 and hair cells that can cause permanent, high-frequency hearing loss but the vestibular system is okay

57
Q

Susceptibility to ototoxicity

A

Inherited susceptibility for severe hearing loss, most people will just have a little

58
Q

Tetracycline mechanism of action

A

Reversible inhibit bacterial protein synthesis (bacteriostatic)

59
Q

Tetracycline spectrum

A

Basically all atypical bacteria

60
Q

Atypical bacterial infections

A

Rickettsia, chlamydia, mycoplasma

61
Q

Tetracycline distribution

A

Water-soluble don’t readily enter cells or CNS, lipid-soluble (doxycycline) enters cells

62
Q

Doxycycline

A

Lipid-soluble tetracycline important for intracellular pathogens

63
Q

Tetracycline elimination

A

Water-soluble are excreted in urine and metabolized in liver, lipid-soluble are entirely metabolized in liver and secreted in bile

64
Q

Resistance to tetracyclines

A

Efflux pump; can be overwhelmed by high topical doses

65
Q

Adverse effects of tetracyclines

A

Renal damage, photosensitivity, incorporation into teeth and bones

66
Q

What line are tetracyclines?

A

First!

67
Q

Effectiveness of sulfonamides alone

A

Largely ineffective

68
Q

Diaminopyrimidine inhibitors

A

Trimethoprim (TM)

69
Q

Potentiated sulfonamides

A

Trimethoprim plus sulfonamides (TMS or co-trimoxazole)

70
Q

Are sulfonamides bactericidal or bacteriostatic

A

Bactericidal

71
Q

Mechanism of action of sulfonamides

A

Competitively Inhibit dihydropteroate synthetase, which helps synthesize folic acid from PABA

72
Q

Mechanism of action of trimethoprim

A

Competitively inhibit dihydrofolate reductase, which helps synthesize topic acid later in the pathway

73
Q

Why potentate sulfonamides are more effective

A

You competitively inhibit 2 of the enzymes in the pathway and resistance to both of these enzymes is less common

74
Q

Why sulfonamides are ineffective with pus

A

Pus has a lot of PABA so they will be outcompeted

75
Q

Spectrum of sulfonamides

A

Atypical bacteria; can also be used against lower UTI infections

76
Q

Distribution of sulfonamides

A

To all tissues

77
Q

Elimination of sulfonamides

A

Some excreted unchanged in urine, some metabolized in liver; metabolites accumulate in kidneys

78
Q

Resistance to sulfonamides

A

Can acquire different dihydropteroate synthetase or dihydrofolate reductase enzymes

79
Q

Adverse effects of sulfonamides

A

Hypersensitivity and renal damage

80
Q

Most recent class of AMDs

A

Fluoroquinolones

81
Q

Most common fluoroquinolone

A

Ciprofloxacin

82
Q

Fluoroquinolone mechanism of action

A

Damage DNA by inhibiting DNA gyrases and topoisomerases

83
Q

Spectrum of fluoroquinolones

A

Gram negative aerobes, staph, and some atypical (no anaerobes)

84
Q

Pharmacokinetics of fluoroquinolones

A

Oral bioavailability ~100%, very long half-life, concentrates in lung, renal excretion

85
Q

Adverse effects of fluoroquinolones

A

Severe cartilage damage, tendon rupture, reduction of seizure threshold, phototoxicity

86
Q

Resistance to fluoroquinolones

A

Mutations in DNA gyrases and topoisomerases that stop fluoroquinolones from binding

87
Q

Fluoroquinolone line

A

Only second

88
Q

Macrolides mechanism of action

A

Inhibit protein synthesis reversibly

89
Q

Pharmacokinetics of macrolides

A

Penetrate cells easily, concentrate in lung, older have very short half-life while newer have very long, erythromycin can inhibit p450 enzymes

90
Q

Erythromycin

A

Oldest macrolide

91
Q

Spectrum of erythromycin

A

Closest to broad spectrum: gram positive aerobes, anaerobes, some gram negative aerobes, some atypical

92
Q

Spectrum of newer macrolides

A

Mostly gram negative aerobes, somewhat affects everything else (good for community-acquired bacterial pneumonia)

93
Q

Macrolide resistance

A

Very effective macrolide efflux pump

94
Q

Adverse effects of macrolides

A

Tissue irritation, vomiting because erythromycin stimulates motilin receptors

95
Q

Divalent cations

A

Inhibit oral absorption of tetracyclines

96
Q

Spectrum of chloramphenicol

A

Broad

97
Q

Routes of admin of chloramphenicol

A

Basically all

98
Q

Distribution of chloramphenicol

A

All except prostate

99
Q

What tissue chloramphenicol penetrates best

A

Cornea

100
Q

Major adverse effect of chloramphenicol

A

Fatal aplastic anemia

101
Q

Mechanism of action of chloramphenicol

A

Inhibits protein synthesis (bacteriostatic)

102
Q

When to use chloramphenicol

A

In fatal or crippling infections where there are no other options

Pharmacology 4090 (11 decks)

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