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Block 3 Pharm > Antibacterials I > Flashcards

Antibacterials I Flashcards

1
Q

transported into the cell by an energy-requiring aerobic process (does not occuranaerobically)
• bind to several ribosomal sites, usually at 30S/50S interface; stops initiation, causes
premature release of ribosome from mRNA, and mRNA misreading
• post-antibiotic effect
• concentration-dependent killing

A

Aminoglycosides

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2
Q

aminoglycoside mechanism

A

binds to several 30S/50S interfce to stop initiation and causes premature release of ribosome from mRNA and mRNA mistreading

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3
Q

How do bacteria resist aminoglycosides?

A

enzymatic modification of the aminoglycosides

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4
Q

more effective against gram-neg. than gram-pos.
• poor activity against anaerobes
• primarily for gram-neg. ‘aerobic’ bacilli, incl. Enterobacteriaceae and Pseudomonas
aeruginosa

A

Aminoglycosides

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5
Q

aminoglycosides are better for gram negative or positive

for anaerobes or aerobes

A

gram negative

aerobes

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6
Q

due to toxicity, use restricted to serious infections in which other agents are unsuitable
• often used in conjunction with other agents (e.g. β-lactams)—- streptomycin

A

aminoglycosides

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7
Q

Gentamicin, tobramycin and amikacin are examples of

A

aminoglycosides

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8
Q

which aminoglycoside is most resistant to bacterial inactivation

A

amikacin

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9
Q

What four bacteria do aminoglycosides work great for

A

P.aeruginoa, Klebsiella, Enterobacter, Serratia

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10
Q

P.aeruginoa, Klebsiella, Enterobacter, Serratia are all suspeptible to what class of drugs

A

aminoglycosides used with B-lactams

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11
Q

How are aminoglycoside metabolized?

A

glomerular filtration

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12
Q

Adverse rxn of aminoglycosides

A

nephrotoxic and ototoxic and is related to dose and duration of therapy. less common is neuromuscular blockade

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13
Q

How are aminoglycosides administered?

A

IV or IM with poor penetration to CSF

*serious infection~~ combined with other antibiotics

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14
Q

MEch of Tetracyclines

A

transported into cell via carrier… binds to 30S ribosomal to stop attachment of aminoacly-tRNA to acceptor site
bacteriostatic

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15
Q

transported into cell via carrier… binds to 30S ribosomal to stop attachment of aminoacly-tRNA to acceptor site
bacteriostatic

A

tetracyclines

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16
Q

Modern tetracyclines such as _____ and ______ have longer 1/2 lives and are more lipophilic

A

minocycline and doxycycline

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17
Q

How does bacteria devo resistance to tetracyclines

A

increased transport of drug out of cells… resistant to one tetracylcine, likely resistant to all of them

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18
Q

Tetracyclines are no longer used bc

A

increased resistance

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19
Q

Preferred agents for rickettsia and chylamydia

A

Tetracyclines

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20
Q

Preferred agent for Mycoplasma and ureplasma and Borrelia (or lymes)

A

tetracyclines

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21
Q

alternative drug for syphilis and gonorrhea

A

tetracyclines

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22
Q

What can tetracyclines be used for

A 
Rickettsia
Chylamydia
Mycoplasma and Ureaplasma
Borrelia
alt for gonorrhea and syphilis
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23
Q

You shouldn’t used antacids with tetracycline because

A

the Ca++ in them will bind to tetracyclines and inhibit absorption

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24
Q

Adverse rxns to tetracyclines

A

GI disturbance, pseudomembranous enterocolitis, Candida superinfection, photosensitive, teeth discoloration, DONT USE IF PREGNANT

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25
Q

Tigecycline mech

A

binds to 30S and blocks aminoacyle-tRNA as well as other unique sites in ribosomes

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26
Q

This tetracycline doesn’t have cross resistance with other antiBacts including tetracyclines

A

Tigecycline

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27
Q

Uses of Tigecycline by SITE

A

skin/skin strucutre infections
complicated intrabdominal infections
Community acquired pneumonia (CAP)

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28
Q

What pathogens are Tigecycline effective for

A 
E.coli, Klebsiella, enterobacter but NOT psuedonomas
Staph (both MSSA and MRSA)
Bacteriodes
Clostridium perfringes
CAP: S. pneumoniae, Haemophilus
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29
Q

Drug to tx E.coli, Klebsiella, enterobacter but NOT psuedonomas

A

Tigecycline

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30
Q

Drug that can tx bacteriodes and Clostridium perfringes

A

Tigecycline

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31
Q

Tetracycline that can take care of both MSSA and MRSA

A

Tigecycline

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32
Q

Adverse affects of Tigecycilne

A

nausea and vomit and cant use with antacids

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33
Q

interferes with binding of aminoacyl-tRNA to 50S subunit and inhibits peptide bond
formation (blocks peptidyl transferase)

A

Chloramphenicol

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34
Q

Mech of Cloramphenicol

A

fucks with binding of amino-tRNA to 50s and inhibits peptide bond formaiton

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35
Q

administration of tigecycline

A

iv only

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36
Q

alternative for Pen G sensitive syphilis and uncomplicated gonhorea

A

Doxycycline and minocycline

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37
Q

Tricycline least sensitive for Ca++ antiacids

A

Doxycycline

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38
Q

most lipophilic tetracycline thats used prophylactictly for N. Meningitis

A

Minocycline

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39
Q

1/2 life of minocycline

A

11-26 hours

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40
Q

1/2 for doxycycline

A

24 hours

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41
Q

Uses of Chloramphenicol

A

broad spectrum but VERY serious side effects

42
Q

Major used of Chloramphenicol

A

alternative tx of meningitis in B lactam allergic pts
brain abscesses
severe slamonella infections

43
Q

Drug of choice for rickettsia in children

A

doxycycline

44
Q

Used to tx chronic granulomatois, bacterial ophthalmic issues

A

Chloramphenicol

45
Q

Chloramphenicol is toxic because

A

Bone marrow depression (most common effect and limits its use to life-threatening
infections); can progress to a fatal aplastic anemia

46
Q

Bone marrow depression (most common effect and limits its use to life-threatening
infections); can progress to a fatal aplastic anemia

A

Chloramphenicol

47
Q

What causes Grey baby syndrome

A

high level of unmetabolized Chloramphenicol

48
Q

Adverse affects of chloramphenicol

A

Grey baby/aplastic anemia/ optic neuritis/ enterocolitis

~~ binds to mitochondrial 70S

49
Q

3 key macrolides

A

Azithromycin, Clarithromycin, Erythromycin

50
Q

Mech of macrolides

A

bind to 50S and block protein synthesis by blocking translocation

51
Q

Macrolides are bacteriostatic or bacteriacidal

A

bacteriostatic

52
Q

Bacteria devo resistance to chloramphenicol via:

A

CAT: acetylated by bacteria

53
Q

When is the activity of macrolides reduced

A

when pH is below 7

54
Q

Resistance to macrolides

A

they methylate the 23S of teh 50S and inhibit binding or drug efflux

55
Q

Macrolide for gram-pos.

→ e.g. Streptococcus, only some Staphylococcus (MSSA)

A

Erythromycin

56
Q

Uses of Erythromycin

A

gram +streptococcus and some staph

57
Q

Macrolide for Chlamydia, mycoplasma, Legionella and Bordetela

A

Erythromycin

58
Q

What bacteria does Erythormycin tx

A

Chlamydia, mycoplasma, Legionella and Bordetela

59
Q

Toxicity of Erythromycin

A

inhibits CYP3A4, increase risk of arrhthymias and cardiac arrest and nausea

60
Q

What macrolide inhibits CYP3A4

A

Erythromycin

61
Q

alternative to erythromycin for treatment of: pharyngitis, respiratory infections

A

Clarithromycin

62
Q

Clarithromycin tx the same bacteria as Erythromycin as well as

A

H. influenza, Moraxella, penicillin-resistant Strep.pneumoniae, Helicobacter pylori

63
Q

Tx H. influenza, Moraxella, penicillin-resistant Strep.pneumoniae, Helicobacter pylori

A

Clarithromycin

64
Q

Macrolide to tx atypical mycobacterial infections

A

Clarithromycin

65
Q

Adverse rxn of Clarithromycin

A

less GI issues then Erythro but INCREASED cardiovascular risk (longer QT interval)

66
Q

less GI issues then Erythro but INCREASED cardiovascular risk (longer QT interval)

A

Clarithromycin

67
Q

Macrolide for respiratory infections such as S.penumonai, H.influenza, mycoplasm

A

Azithromycin

68
Q

Used to be 1st line for chlamydia and N. gonorrheoae

A

Azithromycin

for gonorrhea, use ceftriaxone + azithromycin

69
Q

Is Azithromycin used for Helicobacter?

A

NOPE

70
Q

Adverse rxn of azithromycin

A

less GI then erythromycin, fewer drug interations and slight QT prolonged

71
Q

which macrolide has long 1/2 of 3 days and is more acid stable

A

azithromycin

72
Q

Mech of Clindamycin

A

binds to 50S ribosomal subunit,

blocks translocation along ribosomes

73
Q

Uses of Clindamycin

A

most gram-pos. cocci and many anaerobes incl. Bacteroides fragilis

74
Q

most gram-pos. cocci and many anaerobes incl. Bacteroides fragilis

A

Clindamycin

75
Q

What do we NOT use Clindamycin for?

A

hospital aquired MRSA

76
Q

What limits our use of Clindamycin

A

serious colitis

77
Q

Adverse rnxs of Clindamycin

A

Antibiotic associated enterocolitis
GI and diarrhea
hepatotoxic

78
Q

Mech of Linezolid

A

interferes with protein synthesis: binds to 50S ribosomal subunit, interfering with formation of 70S initiation complex

79
Q

Uses of Linezolid

A

VRE
MRSA and MSSA
Group A and B strep
S. pneumonia (even if its multidrug resistant)

80
Q 
What can treat all of these
VRE
MRSA and MSSA
Group A and B strep
S. pneumonia (even if its multidrug resistant)
A

Linezolid

81
Q

Linezolid is _______ for staph and enterooccus

A

Bacteriostatic

82
Q

This drug is a non-selective inhibitor of MAO

A

Linezolid

83
Q

Sides of Linezolid

A

non-selective inhibitor of MAO (many possible drug interactions, avoid foods with
tyramine), bone marrow suppresion, superinfection, enterocolitis

84
Q

inhibit folate synthesis in bacteria by competitive inhibition of dihydropteroate synthase

A

Sulfonamides

85
Q

______ is necessary co-factor for key rxns in all cells and bacteria make their own

A

folate

86
Q

humans are different from bacteria in regards to folate bc

A

we get it from diet, they make it, thus its a good target for therapies

87
Q

Sulfonamides work by:

A

inhibiting folate synthesis in bacteria… done via competitive inhibition of dihydropteroate synthase

88
Q

Main uses of sulfonamides

A

UTI

89
Q

most common: sulfamethoxazole given with trimethoprim is used for

A 
urinary tract infections 
bacillary dysentery (Shigella) 	typhoid fever (Salmonella typhi)
90
Q

Used to tx
UTIs
Bacillary dynsteary or Shigella
typhoid fever

A

Sulfamethoxazole + trimethoprim

91
Q

Used to tx burn pts

A

silver sulfadiazine

92
Q

Two sulfonamide drugs

A

sulfamethoxazole

silver sulfadiazine

93
Q

Adverse rxns of sulfonamides

A

CYP2C9 inhibitors

renal damage dt cystalluria, rashes or hypersensitive

94
Q

CYP2C9 inhibitors

renal damage dt cystalluria, rashes or hypersensitive

A

sulfonamides

95
Q

inhibits folate synthesis in bacteria by competitively inhibiting dihydrofolate
reductase

A

Trimethoprim

96
Q

Trimpethoprim mechanism

A

inhibits folate synthesis by competitively inhibiting dihyrofolate reductase

97
Q

How is trimethoprim more specific for bacteria then humans

A

while humans have dihydrofolate reductase, it is 100,000-fold less sensitive to trimethoprim than is the bacterial enzyme

98
Q

Adverse rxn to trimethoprim

A

nausea, vomiting, diarrhea, rashes
• eosinophilia, neutropenia, bone marrow suppression
inhibits CYP2C9, causing increased levels of warfarin, etc.

99
Q

most often in conjunction with sulfamethoxazole to have bactericidal affects

A

Trimethoprim

100
Q

urinary infections (Enterobacteriaceae and coagulase-negative Staphylococcus)
• upper respiratory tract and ear infections (H. influenzae, Moraxella, S. pneumoniae)
• also for Pneumocystis jiroveci (carinii), Salmonella, Shigella,

A

Trimethoprim

101
Q

Drug choice based on

A

susceptibility of the pathogen site of infection, drug penetration emergence of resistance superinfection with another organism

102
Q

Four categories of antibacterials use

A
  1. Prophylactic
  2. Empiric
  3. Pathogen-directed
  4. Susceptibility-guided

Block 3 Pharm (19 decks)

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