Antimicrobials Flashcards

1
Q

MOA of PCNs

A

bind PBPs–> inhib. transpeptidation–> inhib. crosslinking of bacterial cell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mech. of Resistance for PNCs

A

penicillinases (B lactamases); structural change in PBP, change in porin structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how do you treat MRSA?

A

vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how do you treat syphillis?

A

PCN G or V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the narrow spectrum PCNs?

A

PCN G and V

*B lactamase sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List the lactams

A

PCNs, cephalosporins, imipenem, meropenem, aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the very narrow spectrum PCNs? what do they treat?

A

methicillin, nafcillin, oxacillin
staph aureus (not MRSA)
*B lactamase resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the broad spectrum PCNs?

A

amoxicillin, ampicillin

tx: gram + cocci, not staph, listeria, E. coli, H influenza, borrelia, H. pylori
* B lactamase sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the extended spectrum PCNs?

A

ticarcillin, piperacillin, azlocillin

tx: gram neg rods, pseudomonas
* B lactamase sensitive
* *synergy with aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how are most PCNs excreted?

A

kidney

*dose reduction in kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What two PCNs are NOT excreted in the kidney?

A

nafcillin, oxacillin (bile excretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

If a person is allergic to one PCN, can you give them a different one?

A

NO, assume allergy to all PCNs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the most unique side effect of PCNs?

A

Jarish-herxheimer rxn - when tx syphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What part of a PCN tends to cause hypersensitivity?

A

sulfur group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a side effect of methicillin?

A

interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a common side effect of PCNs?

A

GI distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do you enhance PCN activity?

A

add Clavulanic acid or sulbactam

they are B lactamase inhib.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what drug increases PCN and cephalosporin concentration?

A

probenecid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the MOA of cephalosporins?

A

same as PCNs: bind PBPs–> inhib. transpeptidation–> inhib. crosslinking of bacterial cell walls
same resistance mech too.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

first generation cephalosporins

A

cefazolin

cePHalexin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are first generation cephalosporins used for?

A
surgical prophylaxis
gram +
E. coli
klebsiella
proteus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

second generation cephalosporins

A

cefotetan, cefaclor,

cefuroxime–> crosses BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are second generation cephalosporins used for?

A

gram neg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

third gen. cephalosporins

A

ceftriaxone, cefotaxime, cefdinir, cefixime, cefoperazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what do you use third gen. cephalosporins for?

A

empirical tx of sepsis and meningitis

NO ACTIVITY AGAINST LAME: listeria, atypicals, MRSA, enterococci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do you treat listeria?

A

amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do you treat atypicals?

A

macrolides or tetracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do you treat enterococci?

A

amoxicillin with aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

4th gen. cephalosporins

A

cefepime IV only!

  • wider spectrum
  • B lactamase resistant
  • *enters CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the mode of excretion for most cephalosporins?

A

Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What cephalosporins are not excreted through the kidney?

A

cefoperazone, ceftriaxone –> bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Cephalosporin Side Effects

A

hypersensitivity, GI distress, Disulfiram-like effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What drug should you use if a pt is allergic to cephalosporins?

A

macrolides (gram+), or aztreonam (gram-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

MOA of imipenem and meropenem?

A

same as PCN but resistant to B lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What doe you use imipenem and meropenem for?

A

gram + cocci, gram - rods, empiric use in nosocomial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What drug must you give with imipenem? Why?

A

cilastatin

prevent kidney from metabolizing it too quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SE of imipenem and meropenem?

A

GI distress, drug fever, CNS

**1/2 of pts have seizures with imipenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

MOA for aztreonam? Use? SE?

A

same as PCNs + B lactamase RESISTANT
ONLY IV
use: gram neg. rods
**no cross allergenicity with cephalosporins and PCNs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MOA vancomycin

A

binds d-ala-d-ala muramyl pentapeptide–> blocks transglycosylation–> prevents elongation of peptidoglycan cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What do you use vancomycin for?

A

MRSA
enterococci
c. diff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the first line tx for C. difficile?

A

metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are VRSA and VRE microbes? how do they develop resistance?

A

vancomycin resistant staph aureus
vancomycin resistant enterococci
*change in muramyl pentapeptide target to d-lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how do you treat VRSA and VRE?

A

linezolid and streptogramins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is vancomycin delivered?

A

IV

orally only for colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

SE of vancomycin?

A

Red man syndrome (histamine induced vasodilation)
ototoxicity
nephrotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

MOA of aminoglycosides

A

inhibits initiation of protein synthesis (30S subunit)–> BACTERIOSTATIC
can also cause misreading of genetic code-> BACTERIOCIDAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Name the aminoglycosides

A

gentamycin, tobramycin, amikacin, streptomycin

48
Q

What do you use aminoglycosides for?

A

TB, bubonic plague, tularemia
gram neg rods: pseudomonas
CANT BE USED ON ANAEROBES

49
Q

Excretion of aminoglycosides?

A

water soluble–> KIDNEY

50
Q

Side effect of aminoglycosides?

A

nephrotoxicity, ototoxicity, neuromuscular blockade

51
Q

What is neomycin and what is it known for?

A

aminoglycoside in neosporin, known for contact dermatitis (hypersensitivity)

52
Q

How are aminoglycosides given?

A

1xday dosing: bacteriocidal so only need a spike once a day

decreases SE

53
Q

aminoglycosides resistance?

A

conjugating enzymes–> eliminates it too fast to be effective

54
Q

MOA of chloramphenicol?

A

inhibits peptides transferase (50S)

bacteriostatic

55
Q

What is chloramphenicol used for?

A

backup for salmonella, b. fragillis, rickettsia, bacterial meningitis

56
Q

Where is chloramphenicol broken down?

A

LIVER; does reduction in liver dysfunction and in neonates

INHIBITS CYP450

57
Q

SE of chloramphenicol?

A

dose dependent bone marrow suppression (hypersensitivity), grey baby syndrome and kernicterus

58
Q

Resistance of chloramphenicol?

A

changes in peptidyl transferase

59
Q

Macrolides MOA?

A
inhibit translocation (50S) 
**inhib. CYP450
60
Q

Names of Macrolides?

A

erythromycin, azithromycin, clarithromycin, clindamycin

61
Q

What are the Macrolides used for?

A

gram pos. cocci: staph aureus and anaerobes
also goes into bones for osteomyelitis
atypicals (chlamydia, mycoplasma, ureaplasma)
legionella
campylobacter
mycobacteria avium-intracellular

62
Q

SE of Macrolides?

A

GI distress, reversible deafness

63
Q

how do you treat macrolide resistant s. pneumo?

A

telithromycin

64
Q

Macrolides resistance?

A

methylation of rRNA by methyltransferase of bug–> unable to recognize binding site

65
Q

Tetracylines MOA?

A
inhibits elongation (30S)
bacteriostatic
66
Q

What abx cannot be used in pregnant women?What do you use tetracyclines for?

A

aminoglycosides, fluoroquinolones, sulfonamides, tetracylcines

67
Q

What do you use tetracyclines for?

A

chlamydia, mycoplasma, H. pylori, rickettsia, borrelia burgdorferi, brucella, vibrio, treponema

68
Q

name the tetracyclines

A

doxycycline, minocycline, demeclocycline

69
Q

what do you use doxycycline for?

A

prostatitis

70
Q

what do you use minocycline for?

A

gingivitis

71
Q

what do you use demeclocycline for?

A

SIADH (blocks ADH receptors)

72
Q

SE of tetracyclines

A

tooth enamel dysphagia, decreased bone growth, phototoxicity, GI distress, superinfection with candidiasis, vestibular dysfunction

73
Q

tetracycline resistance

A

pumps drugs out of cells

74
Q

excretion of tetracyclines

A

most through kidneys, doxycyline goes through liver

75
Q

What is unique about the tetracyclines in regard to divalent cations?

A

they are chelators

so they shouldn’t be taken with food or with vitamins

76
Q

streptogramins moa?

A

inhibit elongation 50S by blocking acceptor site and decreases release of completed peptide

77
Q

what are the streptogramins?

A

quinipristin and dalfopristin

78
Q

What do you use streptogramins for?

A

VRE and VRSA

79
Q

Linezolid MOA?

A

inhibits initiation (50S)

80
Q

What do you use Linezolid for?

A

VRE, VRSA, drug resistant pneumococci

81
Q

SE of Linezolid?

A

bone marrow suppression

82
Q

Fluoroquinolones MOA?

A

inhib. NA synthesis by inhib. topoisomerase 2 and 4 (DNA gyrase)

83
Q

Name the Fluoroquinolones?

A

norfloxacin, ciprofloxacin, ofloxacin

84
Q

What do you use Fluoroquinolones for?

A

UTI, STD (chlamydia, gonorrhea), skin and soft tissue infection with gram neg., shigella, salmonella, E. coli, campylobacter, drug resistant pneumo

85
Q

Why do you have to take Fluoroquinolones without food?

A

it binds to iron and calcium which inhibits its absorption

86
Q

Excretion of Fluoroquinolones

A

kidney

87
Q

SE of Fluoroquinolones

A

tendonitis, tendon rupture, phototoxicity, rash, CNS effects (increase QT interval, Seizures with IV), contraindicated in kids and preg

88
Q

MOA of sulfonamides?

A

inhib. dihydropteroate synthetase (indirectly inhib. NA synth.)

89
Q

SE of sulfonamides?

A

hypersensitivity, Stevens-Johnson syndrome (aka exfoliating dermatitis), hemolysis in G6PD deficiency, phototoxicity

90
Q

MOA of trimethoprim and pyrimethamine?

A

inhib. dihydrofolate reductase (also in humas) - indirectly inhib NA synth.

91
Q

How does trimethoprim and pyrimethamine have anti-neoplastic activity?

A

because its inhib. dihydrofolate reductase, which is in the microbe and human!

92
Q

SE of trimethoprim and pyrimethamine?

A

bone marrow suppression

*worrisome because it is used for tx in HIV pts and can worsen leukoplakia

93
Q

What is trimethoprim-sulfamethoxazole used for?

A

nocardia, listeria, gram neg. and gram pos., pneumocystis jiroveci (prophylaxis in HIV)

94
Q

Pyrimethamine-sulfadiazine use?

A

toxoplasma gondii (prophylaxis in HIV)

95
Q

Metabolism of trimethoprim and pyrimethamine?

A

acetylation by liver, excreted in kidney–> can cause kidney stones because its conjugate is less water soluble

96
Q

Why do trimethoprim and pyrimethamine cause drug interactions?

A

high protein binding, causes kernicterus in neonates

97
Q

Metronidazole MOA?

A

produces free radicals, bactericidal

98
Q

What is Metronidazole used for?

A

drug of choice for giardia, trich, entamoeba, C. diff, gardernella, H. pylori

99
Q

SE of Metronidazole?

A

metallic taste!

disulfiram-like effect

100
Q

What combos are usually used for H. pylori?

A

BMT= bismuth + metronidazole + tetracycline OR

clarithromycin + amoxicillin + omeprazole

101
Q

Antitubercular drugs

A

isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin

102
Q

How do you prevent resistance in antitubercular drugs?

A

combination therapy

103
Q

isoniazid MOA?

A

cell wall synth inhib. - mycolic acid synth.

104
Q

isoniazid is a prodrug, what allows it to become activated?

A

conversion by catalase

105
Q

isoniazid resistance?

A

if the microbe is missing the catalase gene

106
Q

isoniazid use?

A

mycobacterium only

107
Q

SE of isoniazid?

A

hepatitis, peripheral neuritis, sideroblastic anemia (B6 def., increased iron), SLE, hemolysis in G6PD def.

108
Q

Rifampin MOA?

A

inhib. DNA dependent RNA polymerase (transcription)

109
Q

SE of Rifampin?

A

hepatitis, induction of P450, red-orange metabolites in urine, saliva, tears

110
Q

Ethambutol MOA?

A

inhib. cell wall synth. by blocking arabingalactan

111
Q

SE of Ethambutol?

A

dose dependent optic neuritis –> loss of color vision

112
Q

Pyrazinamide MOA?

A

UNKOWN, prodrug

113
Q

SE of Pyrazinamide?

A

hepatitis, hyperuricemia

114
Q

Streptomycin MOA?

A

inihib protein synthesis

115
Q

SE of Streptomycin?

A

deafness, vestibular dysfunction, nephrotoxicity, neuromuscular blockade vie decreased ach release