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Clinical Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Cidal

A

Kill target organism. No not need host defense to make it work. Concentration dependent

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2
Q

Static

A

stop growth and replication. rely on pts immune system to work. Time dependent

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3
Q

Bacteria have this, we do not

A

a cell wall! This is key to drug targeting.

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4
Q

Penicillins, how do they work?

A

Cell wall inhibitors. Degrade the peptidoglycan wall of the pathogen. Penicillins are Cidal and Bind to PBP to inhibit the cross-linking of peptidoglycan units. They only work on actively proliferating cells!

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5
Q

PCN Gram activity

A

Good G+, little G- because they cannot penetrate the outer membrane of G-

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6
Q

PCN side effects

A

anaphlaxis- rare but when it happens it is severe. 10% of pts allergic to PCN will also react to cephalosporin, but its ok to give ceph if all they have get with PCN is a rash. 100% of its with mono will develop a PCN rash.

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7
Q

PCN preg category

A

B

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8
Q

PCN G

A

Natural penicillin, came from a mold. It is semi bulk, cannot get through porins. It is IV only, and is the DRUG OF CHOICE FOR SYPHILIS!

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9
Q

PCN V

A

Natural penicillin, only orally active. Cannot fit through porins, is semi-bulky.

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10
Q

Antistaphylococcal PCN

A

these are resistant to penicillinase. These are used for treating Methicillin sensitive S. Aureus (MSSA). Can penetrate the CNS only if there is active inflammation there. So this is a narrow- spectrum drug.

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11
Q

Aminopenicillin drugs

A

ampicillin, ampicillin/sulbactam, amoxicillin, amoxicillin/clavulanic acid

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12
Q

Aminopenicillin gram activity

A

G+ and a little G- (more than PCN because these are smaller and can fit through more porins)

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13
Q

Aminopencillin use

A

WHEN GIVEN WITH BETA-LACTAMASE INHIBITORS can be used fro MSSA.

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14
Q

Ampicillin use

A

IV for meningitis

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15
Q

Amoxicillin use

A

its absorbed better than ampicillin. Used for almost everything.

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16
Q

B-lactamases

A

kill the b-lactam ring of the antibiotic. these are acquired by bacteria through plasmid transfer/conjugation –> antibiotic resistance.

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17
Q

B-lactamase inhibitors

A

keep b-lactameses busy and away from the antibiotics. Must be given with smaller sized abx whose bulkiness does not protect them from b-lactamases.

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18
Q

antipseudomonal drugs

A

piperacillin, ticarcillin, carbenicillin. Piperacillin is most Potent.

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19
Q

antipseudomonal gram activity

A

Improved G- activity, decreased G+ activity

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20
Q

when do you use an antipseudomonal?

A

treats P. aeruginosa (green skin infection!) and will treat MSSA if combined with a beta-lactamase inhibitor. Used empirically to create hospital acquired infections (nosocomial)

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21
Q

pereracillin/tazobactam

A

an antipseudomonal + b-lactamse inhibitor to treat MSSA

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22
Q

monobactams- how do they work?

A

cell wall inhibitors

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23
Q

Aztreonam

A

a monobactam that can be given even if a pt is allergic to penicillins!

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24
Q

monobactam gram activity

A

only G- rods

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25
Q

Aztreonam pregnancy category

A

B

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26
Q

Cephalosporins, how do they work?

A

Cell wall inhibitors. Cidal. Have the same mechanism as PCN. They are resistant to pencillinases, but there are now cephalosporinases….

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27
Q

1st generation cephalosporin drugs

A

Cephalexin and cefazolin

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28
Q

1st generation cephalosporin activity

A

good G+ and MSSA coverage. PEK G- coverage. No anaerobic coverage

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29
Q

PEK G-

A

P. mirablis

E. coli

K. pneumo

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30
Q

2nd generation cephalosporin drugs

A

cefuroxime, cefaclor, cefoxitin, cefotetan

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31
Q

2nd gen cephalosporin activity

A

Good G+ and MSSA coverage. HENPEK G- coverage. IV will cover B. fragilis (an anaerobe)..

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32
Q

HENPEK G-

A

H. flu

Enterobacter aerogenes

Neisseria

P. mirablis

E. coli

K. pneumo

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33
Q

cefotetan side effects

A

a disulfiram-like reaction and bleeding disorder

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34
Q

3rd generation cephalospirin drugs

A

cefdinir, ceftriaxone, ceftazidime

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35
Q

3rd gen ceph activity

A

variable G+, good G-. will cover p.aeruginosa, but resistance is becoming an issue. will also cover lyme disease

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36
Q

ceftriaxone

A

used to treat goborrhea. Not renally eliminated. good bone and BBB penetration.

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37
Q

4th generation cephalosporin drugs

A

cefepime

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38
Q

cefepime activity

A

Good G+ and G-, MSS and P.aeruginosa. it is consistently useful in enterobacter and serratia.

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39
Q

5th generation cephalosporin drug

A

ceftaroline

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40
Q

5th generation cephalosporin activity

A

Good G+, MSSA, S. pneumo. Similar to vanco+ ceftriaxone efficacy.

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41
Q

Vancomycin, how does it work?

A

Cidal. Inhibits cell wall construction by preventing glycosylatyion (prevents glycan units)

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42
Q

Vancomycin activity

A

good G+ and MRSA. treats c.diff when given orally (2nd line tx).

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43
Q

Vanco side effect

A

red man syndrome can happen when you give it infusion too rapidly. this is from a histamine release.

44
Q

Vancomycin pregnancy category

A

C

45
Q

Tetracyclines, how do they work?

A

They are protein synthesis inhibitors (remember that human ribosomes are similar to bacterial ribosomes). They reversibly bind to the 30S ribosomal subunit, inhibiting protein synthesis of the bacteria. They are Static.

46
Q

Tetracycline drugs

A

tetracycline, doxycycline, minocycline

47
Q

Tetracycline activity

A

G+, G-, some atypical, some anaerobes.

48
Q

When would you use tetracycline drugs?

A

Known for treatment of rikettsial diseases like Lyme and Rocky mountain spotted fever. Also common in acne tx.

49
Q

tetracycline pregnancy category

A

D

50
Q

Tetracycline side effects

A

GI upset, growth issues, tooth discoloration and enamel dysplasia and sun sensitivity.

51
Q

Macrolides, how do they work?

A

Static. protein synthesis inhibitor, bind irreversibily to the 50S subunit on the bacterial ribosome.

52
Q

Macrolide activity

A

Good G+ and atypical coverage

53
Q

Macrolide drugs

A

erythromycin, azithromycin, clarithromcin. (Erythromycin is poorly absorbed)

54
Q

When would you use azithromycin?

A

chlamydia, and walking pneumonia (DOC)

55
Q

Macrolide drug side effects

A

N/V/D, QT prolongation –> arrhythmia

56
Q

Clindamycin, how does it work?

A

Protein sythesis inhibitor that has the same mechanism of action as Macrolide drugs. It can be static or cidal, depending on the organism.

57
Q

Clindamycin activity

A

G+ and anaerobes

58
Q

Clindamycin pregnancy category

A

B

59
Q

Most likely abx to result in c.diff

A

Clindamycin

60
Q

Aminoglycosides, how do they work?

A

Protein synthesis inhibitors. Cidal. Bind to 30S ribosomal subunit irreversibly. Used in conjunction with b-lactams or vancomycin.

61
Q

Aminoglycoside drugs

A

gentamycin, tobramycin, amikacin

62
Q

Aminoglycoside activity

A

Only tx aerobic G+/-

63
Q

Aminoglycoside pregnancy category

A

C/D

64
Q

Aminoglycoside side effects

A

ototoxicity and nephrotoxicity.

65
Q

Fluoroquinolones, how do they work?

A

DNA replication inhibitors. All interfere with topoisomerases. Gen 1 and 2 work better on TOPO II, Gen 3 and 4 work better on TOPO IV.

66
Q

TOPO II

A

A DNA gyrase, nicks the strand, allows uncoiling, then re-seals.

67
Q

TOPO IV

A

cuts 2 strands instead of 1, releasing the daughter strand as well.

68
Q

Fluoroquinolone first gen

A

Nalidixic acid –> quinolone.

69
Q

Fluoroquinolone 2nd gen drug

A

Ciprofloxacin

70
Q

Ciprofloxacin activity

A

It has atypical coverage, G+ cocci, and G-rods

71
Q

3rd generation Fluoroquinolone drug

A

levofloxacin

72
Q

Levofloxacin activity

A

atypicals, G+ cocci, G-rods, and activity against s.pneumo. Its a respiratory Fluoroquinolone.

73
Q

4th gen Fluoroquinolone drug

A

Moxifloxacin

74
Q

Moxifloxacin activity

A

atypicals, G+ cocci, G-rods, and activity against s.pneumo. Addition of anaerobe activity. Its a respiratory Fluoroquinolone. The only one excreted in bile, all others are renally excreted.

75
Q

Fluoroquinolone activity, general

A

All have good gut activity and in general are good for UTI.

76
Q

General Fluoroquinolone precautions/side effects

A

N/V/D, Drug interactions (its a cytochrome inhibitor), headache, dizziness, QT prolongation (Moxi>levo> cipro), photosensitivity, tendon rupture in elderly. Not recommended in kids, unless its a complicated UTI or CHF pt with p.aeruginosa infection.

77
Q

Sulfonamides, how do they work

A

Static. Interfere with folic acid synthesis, which is needed for bacterial DNA synthesis. These are often COMBINED with trimethoprim or pyrimethamine, which block a step downstream in bacterial folate synthesis. THis provides synergism of drug activity.

78
Q

When would you use a sulfonamide?

A

to treat MRSA. To treat prophylactively for PCP (opportunistic pneumonia). To treat a UTI caused by e.coli.

79
Q

Sulfonamide drug

A

sulfamethaxazole/trimethoprim–> bactrim

80
Q

Sulfonamide side effects

A

crystalluria, rashes, kericterus of newborn. Don’t give if pt has a known G6PD deficiency. Watch out for drug interactions, it easily displaces other protein bound drugs.

81
Q

Sulfonamide pregnancy category

A

B. If mom is near delivery it is a D because of Kericterus in newborn.

82
Q

Metronidazole, how does it work?

A

Cidal. Treats anaerobes and protozoa.

83
Q

When would you use Metronidazole?

A

used in vaginal yeast infection.s First line of treatment for C.diff.

84
Q

Metronidazole side effects

A

Disulfiram-like reaction, no EtOH while taking.

85
Q

Metronidazole pregnancy category

A

B

86
Q

Nitrofurantoin, how does it work?

A

Cidal. It is metabolized really fast and renal excreted, so only gets to function in the lower UTI.

87
Q

When would you use nitrofurantoin?

A

For a lower UTI. CrCl needs to be > 60 ml/min, otherwise can get toxicity.

88
Q

Antifungals, general

A

keep in mind that these are hard to kill without harming the host because we are both eukaryotes. The thing we do target on these is their chitin cell wall.

89
Q

Amphotericin B

A

An anti fungal that inserts itself into the fungal membrane, creating leaky pores. Can be static or cidal.

90
Q

When would you use amphotericin b?

A

in a life-threatening systemic fungal infection. It is broad spectrum, but is toxic and renal damage is common –> renal failure.

91
Q

Ketoconazole

A

its a fungistatic, it inhibits the fungus’s CYP450 enzymes, which prevents them from making ergosterol.

92
Q

When would you use ketoconazole?

A

its used topically. Its not that good, because it lacks specificity for fungi vs. humans.

93
Q

ketoconazole pregnancy category

A

C when taken orally

94
Q

amphotericin B pregnancy category

A

B

95
Q

Fluconazole

A

its a fungistatic, has the same MOA as ketoconazole, but it is better because it is more selective for the fungi. Unlike Itraconazole, you do not need an acidic environment for it to work.

96
Q

Fluconazole pregnancy category

A

C

97
Q

Itraconazole

A

Fungistatic, same MOA as ketoconazole but has better selectivity. You need a high stomach acid in order for it to be absorbed.

98
Q

Itraconazole side effects

A

Has a BLACK BOX warning for QT prolongation –> arryhtmias –> CHF

99
Q

Itraconazole pregnancy category

A

C

100
Q

Voriconazole

A

an anti fungal that is better than amphotericin b for aspergillosis. Drug interactions with this are common. Pts can have auditory and visual hallucinations if trough levels are too high

101
Q

Voriconazole pregnancy category

A

D

102
Q

Posaconazole

A

an anti fungal used in prevention of candida and aspergillus infections in immunocompromised patients.

103
Q

Posaconazole pregnancy category

A

C

104
Q

terbinafine

A

an anti fungal that is used topically, especially for nail infections.

105
Q

Griseofulvin

A

an antifungal, used for topical infections. Need to take with a Greasy fatty meal in order for it to be absorbed. Usually takes 6-12 months of tx.

Clinical Pharmacology (6 decks)

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