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Pharmacology Exam 3 > Ch.31: Antibiotics (Vickroy) > Flashcards

Ch.31: Antibiotics (Vickroy) Flashcards

1
Q

shared side effect of macrolides

A

GI effects

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2
Q

shared side effect of aminoglycosides

A

renal toxicity

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3
Q

shared side effect of aminopenicillins

A

GI effects

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4
Q

beta lactam abx include:

A

penicillins**
cephalosporins**
monobactams
carbapenems

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5
Q

properties of beta lactam abx

A
  • widely used
  • good safety profile
  • good efficacy
  • resistance a problem
  • contain a beta-lactam ring that confers antibacterial activity, hydrolytic instability, and microbial resistance**
  • acidic
  • prone to hypersensitivity rxn
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6
Q

beta-lactam MOA

A

cell wall inhibitors: irreversible inhibit enzymes that crosslink peptidoglycan polymers in the cell wall, which weakens cell walls and they eventually burst. Also inhibit penicillin binding proteins

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7
Q

killing by beta-lactams is time or conc.-dependent?

A

time

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8
Q

spectrum of beta-lactams

A

mainly gram + ; minimal broad-spec activity

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9
Q

Pharmacokinetics of beta-lactams

A

Oral absorption
Rapid kidney clearance
Does NOT cross BBB
Not well bound to plasma proteins

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10
Q

3 mechs. of beta-lactam resistance

A

1) prod. of beta-lactamase
2) changes in penicillin-binding-proteins
3) impenetrable membrane pores

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11
Q

procaine penicillin MOA***

A

forms moderately insoluble salt to allow penicillin to have a slower release and longer duration of action

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12
Q

penicillins drug interactions

A

phenylbutazone
sulfonamides
salicylates
barbiturates

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13
Q

5 subgroups of penicillins. Which are broad spectrum?

A

1) natural
2) beta-lactamase resistant
3) Aminopenicillins (broad spec)
4) Extended-spectrum (broad spec)
5) Augmented (broad spec)

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14
Q

International Units

A

amt of a substance that is based on biological activity rather than mass.

  • there is no equivalence between IU measurements for different antimicrobial agents
  • 1 mg of penicillin G procaine = 1009 IU ***
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15
Q

augmented penicillins are a combination of:

A

broad spectrum agent + beta-lactamase inhibitor

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16
Q

cephalosporins are very similar to penicillins. Name a difference

A

Cephalosporins have a longer duration of action

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17
Q

difference between earlier and later generations of cephalosporins

A

earlier have less broad-spec activity, less resistant ot beta-lactamase, less expensive, etc.

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18
Q

cephalexin is what generation?

A

1st

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19
Q

ceftiofur is what gen?

A

3rd

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20
Q

cephalexin features of note

A
  • 1st gen. cephalosporin
  • dogs only
  • tx for pyoderma
  • good oral bioavailability
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21
Q

ceftiofur features of note

A
  • 3rd gen. cephalosporin
  • dogs and food animal
  • give IM or SC
  • good tissue distr.
  • scrutinized in LA!
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22
Q

ELDU of cephalosporins allowed in minor species?

A

yes (not in major species)

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23
Q

cephalosporins have cross-hypersensitivity with penicillins?

A

Y

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24
Q

which has longer duration of action: ceftiofur or cephalexin?

A

ceftiofur

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25
Q

imipenem features of note

A
  • in carbapenem class
  • expensive**
  • effective against anaerobes and G+ aerobes
  • shouldn’tbe used in resistant classes
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26
Q

Are cell wall inhibitors effective against intracellular organisms?

A

N

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27
Q

do cell wall inhibitors cross BBB?

A

N

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28
Q

common use of penicillins

A

UTI

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29
Q

aminoglycosides bactericidal/static? conc/time-dependent?

A

cidal (conc.-dependent)

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30
Q

aminoglycosides chem. properties**

A
  • highly water soluble
  • organic bases
  • structurally diverse
  • due to these properties, they have limited scope of cross-resistance*
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31
Q

Aminoglycosides MOA

A
  • irreversible inhibition of protein synthesis

- must be transported into orgs. by transporter since not lipid soluble

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32
Q

aminoglycosides spectrum

A

G -

ineffective against anaerobes

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33
Q

aminoglycosides are synergistic with:**

A

beta-lactams (against Gram - bacteria)

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34
Q

trough conc.

A

lowest conc. obtained before next dose of drug is given

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35
Q

aminoglycosides pharmacokinetics

A
  • not orally absorbed**
  • distr. in ECF
  • renal elimination
  • peak conc. correlate with antimicrobial efficacy
  • trough conc. correlate with organ toxicity (higher trough conc. = higher toxicity)
36
Q

predominant organs for aminoglycoside toxicity***

A

renal cortex

inner ear

37
Q

mech. of resistance to aminoglycosides

A
  • inc. enzymatic degradation
  • dec. memb. transport
  • altered ribosomal binding site
38
Q

signs of aminoglycoside toxicity

A
  • nephrotoxicity**
  • ototoxicity (irreversible)
  • neuromuscular weakness (reversible)
  • anaphylactoid rxns
39
Q

aminoglycoside contraindications

A

renal dz, dehydration, NM disorders, etc.

40
Q

Tetracyclines bacteristatic or cidal?

A

static

41
Q

Tetracyclines MOA

A

REVERSIBLE inhibition of protein synthesis (but have to be actively transported into cells)

42
Q

Tetracyclines acid or base?

A

Both! (Amphoteric compounds)

43
Q

name 2 aminoglycosides

A

gentamicin, amakacin

44
Q

Tetracyclines well absorbed orally?

A

Y

45
Q

Tetracyclines spectrum

A

G+, G- anaerobes, mycoplasms

46
Q

Mechs. of tetracycline resistance

A
  • altered transporter
  • active excretion
  • enzymatic degradation
  • assoc. with cross-resistance to aminoglycosides and sulfonamides*
47
Q

Tetracycline toxicity

A

(can be substantial)

GI, superinfections, pain, arrhythmias, teeth/bone discoloration, nephrotoxic, etc.

48
Q

Tetracycline pharmacokinetics

A
  • well absorbed orally
  • can be highly protein bound
  • distr. well into most tissues
  • renal elimination
49
Q

tetracycline and Ca

A

-avoid adding it to anything with Ca (binds Ca and causes precipitates)

50
Q

Name 2 tetracyclines

A

tetracycline

doxycycline

51
Q

Doxy features ofnote

A
  • long-acting*
  • lipophilic
  • don’t give w/o water
  • irritant if given IM or SC
  • tx for Ehrlichiosis
52
Q

What should you monitor during extended use of tetracycline

A

hepatic and renal fx

53
Q

Name 2 macrolides

A

erythromycin

azithromycin

54
Q

macrolides basic chemical properties

A
  • contain lactone ring
  • basic
  • highly lipid soluble
55
Q

Macrolides MOA

A

REVERSIBLE inhibition of protein synthesis

-accumulated by neuts

56
Q

macrolides bacteriostatic or cidal?

A

static (cidal at high dose)

57
Q

macrolides spectrum

A

G+
G-
intracellular organisms (because lipophilic)**

58
Q

Pharmacokinetics (PK) of macrolides

A
  • well absorbed all routes
  • distr. widely
  • mixed elimination via kidney, liver, biliary
59
Q

macrolides toxicity

A

GI (can be fatal in horses!)

60
Q

resistance to macrolides

A
  • strong cross resistance

mech: alteration of ribosomal binding sites

61
Q

which has less GI effects: erythromycin or azithromycin?

A

azithromycin

62
Q

chem. properties of phenicols

A
  • bases
  • lipophilic
  • good distr. into tissues and fluids (including milk, fetus**)
63
Q

Name 2 phenicols

A

chloramphenicol

Florfenicol

64
Q

chloramphenicol MOA

A

reversible inhibitor of protein synthesis

65
Q

chloramphenicol toxicity***

A

GI
reduced liver metabolism
bone marrow depression–> never use in food animals!!***

66
Q

PK of chloramphenicol

A
  • absorbed all routes
  • widespread tissue distr.**
  • hepatic elimination
  • species-dependent half-life
67
Q

Can florfenicol be used in food animal?***

A

yes

68
Q

sulfonamides acids/bases?

A

acids

69
Q

sulfonamides MOA

A

interfere with folic acid form. for purine synthesis (a DNA precursor)

70
Q

sulfonamides bacteriostatic or cidal?

A

static

71
Q

sulfonamides spectrum

A

G+

G-

72
Q

resistance to sulfonamides

A

-fairly widespread, limits effectiveness

73
Q

PK of sulfonamides

A
  • well absorbed in GIT
  • wide distr.
  • mixed elimination
74
Q

4 groups of sulfonamides and uses

A

standard (systemic infections)
highly water soluble (UTI)
poor water soluble (topical or GI infections)
potentiated (most widely used; uses a bactericidal combo of sulfonamides)

75
Q

potentiated sulfonamides MOA

A

interferes with folic acid metabolism, which ultimately prevents DNA synthesis

76
Q

main side effect of sulfonamide**

A 
renal crystalization (esp. older agents)
-hydrate to avoid
77
Q

Name a sulfonamide potentiated agent

A

sulfamethoxine + trimethoprim

78
Q

sulfonamides drug interactions

A
  • prolongs duration of action of drugs that use the same carriers
  • antagonized by PABA
79
Q

fluoroquinolones MOA

A

inhibits DNA gyrase (topoisomerase II)

80
Q

fluoroquinolone action time or conc. based?

A

conc. More specifically, it is dependent on the area under the plasma conc-time curve above MIC.

81
Q

are fluoroquinolones effective against anaerobes?**

A

No

82
Q

fluoroquinolones side effects

A

nephrotoxicity at high dose

GI

83
Q

fluoroquinolones contraindications

A

pregnancy
chondrotoxicity/tendonopathy*
off label use in food animals

84
Q

fluoroquinolones drug interaction

A

antacids, NSAIDs,sucralfate

85
Q

Name a fluoroquinolone

A

enrofloxacin

Pharmacology Exam 3 (11 decks)

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