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PLE_PHARMA > ANTIBACTERIALS > Flashcards

ANTIBACTERIALS Flashcards

1
Q

BACTERICIDAL vs BACTERIOSTATIC

A
  • BACTERICIDAL
    o can eradicate an infection in the absence of host defense mechanisms
    o kills bacteria
    o Generalization: those that inhibit cell wall synthesis and
    nucleic acid synthesis
  • BACTERIOSTATIC
    o inhibits microbial growth but requires host defense
    mechanisms to eradicate the infection
    o does not kill bacteria
    o Those that inhibit protein synthesis except
    aminoglycosides which are -cidal
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2
Q

o as the plasma level is increased above the MIC, an increasing
proportion of bacteria are killed and at a more rapid rate

WHAT MODE OF ANTIBACTERIAL ACTION?

A

CONCENTRATION-DEPENDENT KILLING ACTION

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3
Q

o efficacy is directly related to time above MIC
o efficacy independent of concentration once the MIC has been
reached
o EXAMPLES: Penicillins, cephalosporins

WHAT MODE OF ANTIBACTERIAL ACTION?

A

TIME-DEPENDENT KILLING ACTION

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4
Q

o seen in aminoglycosides & quinolones
o killing action continues when their plasma levels have
declined below measurable levels
o greater efficacy when administered as single large dose
o toxicity depends on a critical plasma concentration and on
the time such a level is exceeded
▪ shorter with single large dose than multiple small doses
▪ basis for once-daily aminoglycoside dosing protocols

WAHT MODE OF ANTIBIOTIC ACTION?

A

POST-ANTIBIOTIC EFFECT

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5
Q

MOA: * binds to penicillin-binding proteins (PBPs) located in the
bacterial cytoplasmic membrane
* inhibits the transpeptidation reaction that cross-links the
linear peptidoglycan chain constituents of the cell wall

A

BETA-LACTAM ANTIBIOTICS: PENNICILIN

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6
Q

what are 3 mechanisms of resistance development to penicillin?

A
  • Enzymatic hydrolysis of beta-lactam ring by formation of betalactamases
    (penicillinases)
    o EXAMPLE: Staphylococcus aureus
  • Structural change in target PBPs
    o EXAMPLES: MRSA, Pneumococci, Enterococci
  • Changes in the porin structures in outer cell wall impeding access of
    Penicillins to PBPs
    o EXAMPLE: Pseudomonas aeruginosa
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7
Q

Examples od Beta Lactamase Inhibitors? (3)

A

(Clavulanic Acid, Sulbactam,
Tazobactam)

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8
Q

2 notable SE of penicillin?

A

1) Hypersensitivity, cross allergenicity with other penicillins
* 2) Gastrointestinal Upset
* Think first of these two for the SE of pens

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9
Q

DOC for syphilis?
Also for streptococcal, pneumococcal, meningococcal,
G+ bacilli, spirochete infection

A

PENICILLIN G (IV), PENICILLIN V (oral)

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10
Q

Long Actin IM preparations of penicillin?

A

Benzathine Penicillin & Procaine Penicillin

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11
Q

What drug prolongs the effect of penicillin? because the renal tubular secretion is inhibited

A

Probenecid

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12
Q

Penicillins Used for staphylococcal infections

A

Methicillin, nafcillin, oxacillin,
Cloxacillin, dicloxacillin

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13
Q

Penicillin that causes
1. Interstitial nephritis????
2. Neutropenia???

A

Interstitial nephritis (methicillin),
Neutropenia (“N”afcillin)
Methicillin – not clinically used – high SE

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14
Q

Resistant to inactivation by beta-lactamase
(penicillinase) – IMPORTANT!

A

Methicillin, nafcillin, oxacillin,
Cloxacillin, dicloxacillin

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15
Q

Side effect of ampicillin and amoxicillin?

A

Pseudomembranous colitis and Rash (ampicillin)

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16
Q

What penicillin?Greater activity against G(-) infections. Infections due to
Pseudomonas, Enterobacter and Klebsiella

A

Piperacillin, Ticarcillin, Carbenicillin

(antipseudomonals)

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17
Q

Synergistic with aminoglycosides against Pseudomonas

A

Piperacillin, Ticarcillin, Carbenicillin

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18
Q

EXTENDED SPECTRUM PENICILLINS

A

Ampicillin, Amoxicillin

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19
Q

Describe the antimicrobial coverage of extended spectrum
Penicillins (HELPSE):

A

“Amoxicillin HELPS kill Enterococci”

Haemophilus influenzae
Escherichia coli
Listeria monocytogenes
Proteus mirabilis
Salmonella sp.
Enterococci

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20
Q

What are the antipseudomonals penicillins?

A

TCP: Takes Care of Pseudomonas

Ticarcillin Carbenicillin Piperacillin

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21
Q

What are the diseases associated with Pseudomonas?

A

Pneumonia
Sepsis
Ecthyma gangrenosum,
UTI,
DM,
Otitis externa, Mucopolysaccharidoses –
Cystic Fibrosis, Osteomyelitis,
Nosocomial infection (HAP and VAP)
Skin infection (in burns and hot tub folliculitis)

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22
Q

**Bactericidal; mostly IV; all have renal excretion

what drug class?

A

CEPHALOSPORINS

**Bactericidal; mostly IV; all have renal excretion
EXCEPT Cefoperazone and Ceftriaxone **

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23
Q

Which microbes are covered by the spectrum of activity of first
generation cephalosporins?

A

PEcK FIRST
Proteus mirabilis
Escherichia coli
Klebsiella pneumoniae

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24
Q

How do you remember first generation cephalosporins?

A

FIRST GENERATION CEPHALOSPORINS
FADer, help me FAZ my PHarmacology boards!

CeFADroxil
CeFAZolin
CePHapirin
CePHalexin
CePHalothin
CePHradine

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25
Q

Which microbes are covered by the spectrum of activity of
second generation cephalosporins?

A

HEN PEcKS

Haemophilus influenzae
Enterobacter aerogenes
Neisseria spp.
Proteus mirabilis
Escherichia coli
Klebsiella pneumoniae
Serratia marcescens

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26
Q

How do you remember second generation cephalosporins?
SECOND GENERATION CEPHALOSPORINS

A

In a FAMily gathering, you see your
FOXy cousin wearing a FUR coat and drinking TEA.

CeFAMandole, CeFOXitin,
CeFURoxime, CefoTEtan

FAC! LORA the PROfessional AZhOLE is still on the FONe.

CeFAClor, LORAcarbef, CefPROzil,
CefmetAZOLE, CeFONicid

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27
Q

ANTI-PSEUDOMONAL CEPHALOSPORINS?

A

ANTI-PSEUDOMONAL CEPHALOSPORINS
Ceftazidime Cefepime Cefoperazone

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28
Q

General Mnemonics in classifying the generation of the cephalosphorin

A

1st Generation: Starts with CEPH. Including DRO+ZOL. (CefaDROxil and
CefaZOLin) they start in CEF but are 1st gen

2nd Generation: Starts with CEF. Doesn’t end in -ONE and -IME, plus LORA
ceFU!!!! (dapat with feelings na parang inaaway mo si LORA!
(LORAcarbef and Cefuroxime)

3rd Generation: Starts with CEF. Ends in -ONE and -IME. Plus Moxi Dinir,
Ditoren, Buten.

4th Generation: Cefipime, Cefipirome

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29
Q

First Generation Ceph used in surgical prophylaxis?

A

CEFAZOLIN

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30
Q

What generation? Cefazolin, Cefadroxil, Cephalexin,
Cephalothin, Cephapirin, Cephradine

A

First Generation

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31
Q

What generation?
Cefaclor, Cefamandole, Cefmetazole, Cefonicid, Cefuroxime,
Cefprozil, Ceforanide, Cefoxitin, Cefotetan, Loracarbef

A

Second

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32
Q

what second gen ceph causes a disulfiram reaction?

A

Cefamandole,
Cefotetan

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33
Q

2nd Gen Ceph that has Improved action against
pneumococcus and H. influenzae

A

Cefuroxime

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34
Q

Second gen ceph that has Good activity against B. fragilis
(abdominal and pelvic infections) (2)

A

Cefotetan and cefoxitin

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35
Q

What generation?

Cefoperazone, Cefotaxime, Ceftazidime, Ceftizoxime,
Ceftriaxone, Cefixime, Cefpodoxime Proxetil, Cefdinir,
Cefditoren Pivoxil, Ceftibuten, Moxalactam

A

Third Generation Ceph

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36
Q

What generation has this use:

Decreased gram-positive coverage. Increased gramnegative
activity (Pseudomonas, Bacteroides), against
Providencia, Serratia, Neisseria, Haemophilus

A

Third Gen

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37
Q

DOC for Gonorrhea? (2)

A

Ceftriaxone and Cefixime

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38
Q

Third Gen Ceph that causes DISULFIRAM REACTION?

A

CEFOPERAZONE

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39
Q

What Third Gen Ceph?

All have renal excretion except (2)

A

Cefoperazone and
Ceftriaxone

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40
Q

What Third Gen Ceph?

All penetrate BBB except (2)

A

Cefoperazone and
Cefixime

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41
Q

What Third Gen Ceph?

Has very good CNS penetration

A

Ceftriaxone

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42
Q

What 3rd Gen ceph?

Has very good action on pseudomonas

A

Ceftazidime

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43
Q

What 3rd Gen Ceph?

Most active against Penicillin
resistant S. pneumoniae (2)

A

Ceftriaxone and Cefotaxime

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44
Q

Cefepime, Ceftaroline (5th in other references), Cefpirome

What Generation?

A

4th

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45
Q

MOA: Binds to penicillin-binding proteins. Inhibits
transpeptidation in bacterial cell walls.

A

MONOBACTAM: Aztreonam

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46
Q

is the silver bullet. It is design for gram negative
rods. Pseudomonas is a gram-negative rod.

A

AZTREONAM

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47
Q

MOA: Binds to penicillin-binding proteins. Inhibits
transpeptidation in bacterial cell walls.

A

CARBAPENEMS: IMIPENEM-CILASTATIN, ERTAPENEM, MEROPENEM,
DORIPENEM

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48
Q

CARBAPENEMS:

All are active against Pseudomonas and
Acinetobacter EXCEPT ?

A

ERTAPENEM

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49
Q

CARBAPENEMS:

inhibits renal metabolism (Hydrolysis) of
imipenem by Dihydropeptidase (thus given together)

A

CILASTATIN

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50
Q

Most important mechanism of carbapenem resistance?

A

Production of carbapenemases (carbapenem-hydrolyzing
enzymes) is the most important mechanism of carbapenem
resistance

Other methods of resistance: Porins, efflux pumps, mutations in
penicillin-binding proteins

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51
Q

Inhibits inactivation of Penicillins by bacterial betalactamase
(penicillinase)

give 3 drugs?

A

Clavulanic acid, Sulbactam, Tazobactam

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52
Q

Most active against plasmid encoded beta lactamases
(Gonococci, Streptococci, E coli and H. Influenzae)

Not good inhibitor of inducible chromosomal beta
lactamases (Enterobacter, Pseudomonas, Serratia)

A

Clavulanic acid, Sulbactam, Tazobactam

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53
Q

MOA: Inhibits cell wall synthesis by binding to the D-Ala-DAla
terminus of peptidoglycan → inhibit
transglycosylation → prevent elongation and crosslinking
of peptidoglycan chain

A

Vancomycin, Teicoplanin, Dalbavancin, Telavancin

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54
Q

NOTABLE SIDE EFFECT ODF VANCOMYCIN?

A

Red Man syndrome

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55
Q

VANCOMYCIN:
VRSA and VRE are due to

A

due to D-Ala-D-Lactate formation

Must knows:
● Vancomycin – D-Ala-D-Ala (Dala Dala niya yung Vanco!). Redman
syndrome
● Baci(+)racin – For gram (+), (+)oxic, (+)opical use

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56
Q

MOA: Interferes with a late stage in cell wall synthesis in
gram-positive organisms

A

PEPTIDE ANTIBIOTICS: BACITRACIN

Must knows:
● Vancomycin – D-Ala-D-Ala (Dala Dala niya yung Vanco!). Redman
syndrome
● Baci(+)racin – For gram (+), (+)oxic, (+)opical use

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57
Q

MOA: Blocks incorporation of D-Ala into the pentapeptide
side chain of the peptidoglycan

A

Cycloserine

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58
Q

MOA: Binds to cell membrane
causing depolarization
and rapid cell death

A

DAPTOMYCIN

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59
Q

MOA: Cationic detergents.
Attach to and disrupt
bacterial cell membrane,
bind and inactivate
endotoxin. Bactericidal.

A

POLYMYXIN B,
Polymyxin E

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60
Q

MOST NOTBALE SIDE EFFECT OF DAPTOMYCIN?

A

Myopathy
Monitor Creatine
Phosphoki nase weekly

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61
Q

What drug?

  • More rapidly
    bactericidal than
    Vancomycin
  • Inactivated by
    pulmonary surfactants
    so cannot be used
    against pneumonia
A

DAPTOMYCIN

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62
Q
  • Proteus and Neisseria
    are resistant
  • For Topical use only (to
    limit toxicity)
  • *Both are Preg Cat C

what drug?

A

POLYMIXIN B AND E

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63
Q

MOA: MOA: Inactivates the enzyme UDP-Nacetylglucosamine-
3-enolpyruvyltransferase
which is important in peptidoglycan synthesis
(very early stage of bacterial cell wall synthesis)
USE: Uncomplicated UTI; safe for pregnant
patients; renal excretion; resistance emerges
rapidly

A

FOSFOMYCIN

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64
Q

Which antibiotics are considered drugs of last resort?

A

I” AM your Last Shot at Victory”

Imipenem
Amikacin
Meropenem
Linezolid
Streptogramins
Vancomycin

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65
Q

What are the protein synthesis inhibitors?

A

“AT CELLS”

Aminoglycosides
Tetracyclines
Chloramphenicol (HNBS)*
Erythromycin (Macrolides)
Lincosamides (Clindamycin)
Linezolid
Streptogramins

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66
Q

All bacterial protein synthesis inhibitors are bacteriostatic except ???, ???, ???
to the
following bugs: Hemophilus, Neisseria, Bacteroides and Streptococcus
pneumoniae.

A

Aminoglycosides, Streptogramins, and Chloramphenicol

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67
Q

(+)/(-) Mycoplasma pneumoniae,Chlamydia, Rickettsia
and Vibrio, and other atypical organisms

WAHT DRUG?

A

Tetracycline, Doxycycline, Minocycline,
Tigecycline, Demeclocycline, Lymecycline
(All are Preg Cat D)

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68
Q

WHat tetracycline is used in SIADH?

A

Demeclocycline

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69
Q

What tetracycline is used in CAP and Bronchitis; Lyme disease

A

Doxycycline

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70
Q

Most notable SE of Tetracycline

A

GI disturbance, Teratogen (tooth enamel dysplasia/
discoloration),

MNEMONICS:
T = TeTracyclines
Block aTTachment of T-RNA to acceptor site
Teeth-racycline = tooth enamel dysplasia / discoloration

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71
Q

Mechanism of resistance to tetracycline?

A

Resistance:
* 1) Development of efflux pumps for active extrusion
of tetracyclines
* 2) Formation of ribosomal protection proteins that
interfere with tetracycline binding

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72
Q
  • Derivative of: MINOCYCLINE
  • Broadest spectrum + longest t½ (30-
    36hrs)
  • Given IV only and is unaffected by
    common tetracycline resistance
    mechanisms.

what drug?

A

TIGECYCLINE

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73
Q

Inhibits transpeptidation (catalyzed by
peptidyl transferase)

What drug?

A

Chlorampenicol

74
Q

Most notable SE of chlorampenicol?

A

Aplastic anemia
(idiosyncratic), Gray baby syndrome,

75
Q

Mechanism of resistance to chlorampenicol?

A

Resistance is due to the formation of
acetyltransferase that inactivates drug

76
Q

is a bacteriostatic antibiotic but is
bactericidal to the ff: Hemophilus influenza, Neisseria,
Bacteroides and Streptococcus pneumoniae.

A

Chlorampenicol

77
Q

is the way to metabolize chloramphenicol

A

Glucoronidation

premature neonates are deficient in hepatic
glucuronosyltransferase

78
Q

characterized by decreased red
blood cells, cyanosis and
cardiovascular collapse
* Characteristic ashen gray skin

A

Gray baby syndrome

79
Q

Drug class?

ERYTHROMYCIN, AZITHROMYCIN, CLARITHROMYCIN,
TELITHROMYCIN, ROXITHROMYCIN

A

Macrolides

80
Q

Most notable SE of MACROLIDES?

A

Gastrointestinal upset, QT prolongation,
Cholestatic hepatitis,

81
Q

All macrolides inhibit CYP450 EXCEPT

A

Azithromycin

82
Q

What macrolide has Biliary excretion?

A

Erythromycin

83
Q

What macrolide has hepatic and urinary excretion?

A

Clarithromycin

84
Q

MEchanism of resistance of MACROLIDES

A

Resistance is due to development of efflux pumps and
production of methylase enzyme

85
Q

What drug?

has a good pharmacokinetic profile.
has a tremendous 4-day half-life and has
a high volume of distribution. It is greater in tissue
macrophage than the plasma level.

A

Azithromycin

86
Q

WHAT MACROLIDE?

Highest Vd and slowest elimination???

Used for macrolide-resistance???

A

Azithromycin

Telithromycin

87
Q

What drug class?
Clindamycin, Lincomycin

A

LINCOSAMIDES

88
Q

Most notable SE of LINCOSAMIDES?

A

Can cause Pseudomembranous colitis (C. difficile
overgrowth

(CLINDAMYCIN AND LINCOMYCIN)

89
Q

Mechanism of resistance of LINCOSAMIDES?

A

Resistance is due to methylation of binding sites and
enzymatic inactivation

90
Q

??? for anaerobic infections ABOVE the diaphragm.

??? for anaerobic infections BELOW the diaphragm.

A

CLINDAMYCIN for anaerobic infections ABOVE the diaphragm.
* METRONIDAZOLE for anaerobic infections BELOW the diaphragm.

91
Q

WHAT DRUG?

Binds to the 23S ribosomal RNA of 50S subunit

A

OXAZOLIDINONE: LINEZOLID, TEDIZOLID

92
Q

What drug is used?

Drug-resistant gram-positive cocci such as Staphylococci
and Enterococcus (MRSA, VRSA, VRE), Listeria,
Corynebacteria

A

OXAZOLIDINONE: Linezolid, Tedizolid

From the parent compound name, meron sila lahat ZOLID

93
Q

Binds 50S subunit. Bactericidal.

what drug?

A

STREPTOGRAMIN: Quinupristin-Dalfopristin

94
Q

What drug class?

Gentamicin, Tobramycin

A

AMINOGLYCOSIDES

95
Q

Most notable SE of Streptogramins: Quinupristin-Dalfopristin

A

severe Arthralgia-myalgia
syndrome

96
Q

Multi Drug-Resistant Tuberculosis (2nd line drug)

A

AMIKACIN

97
Q

WAHT AMINOGLYCOSIDES?

Synergistic with: Beta-lactams
* LEAST RESISTANCE but
* NARROWEST therapeutic window

A

AMIKACIN

98
Q

Uses: Tuberculosis, Tularemia, Bubonic plague, Brucellosis,
Enterococcal endocarditis
SE Additional: Teratogen (congenital deafness), Injection
site reactions

what drug?

A

Streptomycin

99
Q

Most ototoxic Aminoglycoside

A

KANAMYCIN

100
Q

What aminoglycoside?
Uses: Drug-resistant gonorrhea, Gonorrhea in penicillinallergic
patients
SE Additional: Anemia

A

Spectinomycin

101
Q

has the narrowest therapeutic window among
aminoglycosides

A

Amikacin

102
Q

What drug class?

bind to the 30S ribosomal subunit and interfere with protein synthesis:
o block formation of the initiation complex
o cause misreading of the code on the mRNA template
o inhibit translocation

A

Aminoglycosides

103
Q

MEchanism of resistance of aminoglycosides

A
  • plasmid-mediated formation of inactivating enzymes (group
    transferases)
104
Q

Resistance to streptomycin mechanism?

A

resistance to STREPTOMYCIN develops due to changes in the
ribosomal binding site

105
Q

What are the aminoglycosides?

A

AminOglycosides require O2 for transport.
They won’t work under anaerobic conditions.

“Mean GNATS canNOT kill anaerobes.”

Gentamicin
Neomycin
Amikacin
Tobramycin
Streptomycin

Nephrotoxicity
Ototoxicity
Teratogen

106
Q

AMINOGLYCOSIDES:
o MOST OTOTOXIC: ?? and ??
o MOST VESTIBULOTOXIC: ??? and ???

A

o MOST OTOTOXIC: kanamycin, amikacin
o MOST VESTIBULOTOXIC: tobramycin, gentamicin
o cumulative ototoxicity when used with loop diuretics

107
Q

Most nephrotoxic aminoglycoside? (2)

A

tobramycin, gentamicin

108
Q

Aminoglycosides associated with skin reactions?

A

Neomycin and Streptomycin

109
Q

MOA: Inhibits translocation process during protein
synthesis; an antibiotic isolated from the
fermentation broth of Fusidium coccineum;
used as topical antimicrobial against most
common skin pathogens including S. aureus

waht drug?

A

FUSIDIC ACID or
Na FUSIDATE
(Group: Fusidane)

110
Q
  • weakly acidic compounds that have a common chemical nucleus
    resembling p-aminobenzoic acid (PABA)

what drug class?

A

SULDONAMIDES

111
Q

Short Acting Sulfonamides? (3)

A

Sulfacytine
Sulfisoxazole
Sulfamethizole

112
Q

Intermediate Acting Sulfonamides? (4)

A

Sulfadiazine
Sulfamethoxazole
Sulfapyridine
* Trimethoprim

113
Q

Long Acting Sulfonamides?

A

Sulfadoxine
* Pyrimethamine

114
Q
  • structurally similar to folic acid
  • weak base that is trapped in acidic environments
  • reaches high concentrations in prostatic and vaginal fluids

What sulfonamides?

A

TRIMETHOPRIM

115
Q

MOA of ANTIFOLATES:
o bacteriostatic inhibitors of folic acid synthesis
o competitive inhibitors of dihydropteroate synthase

waht drug?

A

Sulfonamides

S for S = Synthase for Sulfonamide;
Don’t forget: when used alone they are bacteriostatic. What used together
they act bactericidal

116
Q

MOA: o selective inhibitor of bacterial dihydrofolate reductase

A

TRIMETHOPRIM

117
Q

Mechanism of resistance to Anti FOlates?

A

● plasmid-mediated and results from:
o decreased intracellular accumulation of the drugs
o increased production of PABA by bacteria
● decrease in the sensitivity of dihydropteroate synthase to

118
Q

Commonly used in UTI as well as P. jiroveci pneumonia?

A

Co-Trimoxazole

119
Q

Used in burn infections, displaces protein binding of other drugs/bilirubin

A

Silver Sulfadiazine, Mafenide Acetate

120
Q

OTHER SULFONAMIDES AND ANTIFOLATE DRUGS:

only for lower UTI

A

SULFISOXAZOLE

121
Q

DOC for Toxoplasmosis

A

SULFADIAZINE-PYRIMETHAMINE

122
Q

2nd line agent for malaria

A

SULFADOXINE-PYRIMETHAMINE

123
Q

used for lower UTI, may be safely given to
patients with sulfonamide allergy

A

TRIMETHOPRIM

124
Q

co-administered with Leucovorin to limit
bone marrow toxicity

A

PYRIMETHAMINE

125
Q
  • caused by increased levels of unconjugated bilirubin
  • due to immaturity of fetal blood brain barrier
  • histopathology
    o bilirubin deposits in subcortical nuclei and basal ganglia
  • clinical presentation
    o hypo/hypertonia, lethargy, high-pitched cry, opisthotonos
A

Kernickterus

126
Q

MOA: * interfere with bacterial DNA synthesis by inhibiting:
o Topoisomerase II (DNA Gyrase) in gram-negative organisms
* prevents relaxation of supercoiled DNA
o Topoisomerase IV in gram-positive organisms
▪ interferes with the separation of replicated
chromosomal DNA during cell division

A

QUINOLONES

127
Q

What generation of Quinolones?

o Nalidixic acid, Cinoxacin, Rosoxacin, Oxolinic acid
o Urinary tract infections

A

First

128
Q

What generation of Quinolones?
o Ciprofloxacin, Ofloxacin, Norfloxacin, Lomefloxacin, Enoxacin
o gram negatives, gonococci, gram positive cocci and Mycoplasma

A

Second

129
Q

What gen of quinolones?

o Levofloxacin, Gemifloxacin, Moxifloxacin, Sparfloxacin, Grepafloxacin,
Gatifloxacin, Pazufloxacin, Tosufloxacin, Balofloxacin
o less gram negative and more gram positive activity,
streptococci and enterococci

A

Third

130
Q

What generation of quinolones?

o Trovafloxacin, Alatrofloxacin, Prulifloxacin, Clinafloxacin
o broad spectrum, including anaerobes

A

4TH GENERATION

*WITH INCREASING GENERATION, INCREASING GRAM POSITIVE
ACTIVITY (unlike cephalosporins where increasing generation leads to
increasing gram negative activity)

131
Q

General properties of quinolones: good oral bioavailability, high
Vd, t½ 3-8hrs, absorption is impeded by antacids, elimination is
via kidneys by tubular secretion (may compete with probenecid
for excretion) EXCEPT for

A

Moxifloxacin

132
Q

What generation of Quinolones cause QTc prolongation?

A

(Third and Fourth Gen)

133
Q

Most active agent against Gram
Negative organisms esp.
Pseudomonas

A

CIPROFLOXACIN

134
Q

WHAT QUINOLONES:
Does not achieve adequate plasma
levels for use in systemic infections

A

Norfloxacin

135
Q

QUINOLONE:

Drug vs C. trachomatis

A

Ofloxacin

136
Q

Quinolones:

Newest members of this family and are
considered to have the broadest
spectrum of activity with increased
activity against anaerobes ang
atypical agents.

A

Moxifloxacin
Gemifloxacin

137
Q

Quinolones

used for CAP caused by Chlamydia, Mycoplasma
and Legionella “THE ATYPICALS”
superior activity against G(+) bacteria
including S. pneumoniae ;

A

Levofloxacin

138
Q

Used as alternatives to Ceftriaxone and Cefixime in
gonorrhea

A

Third Gen Quinolones

Levofloxacin
Moxifloxacin

139
Q

Third Gen QUinolones: FQ elimination is via kidneys by tubular secretion (may
compete with probenecid for excretion)

A

Moxifloxacin

140
Q

Notable SE of Trovafloxacin?

A

Hepatotoxicity

141
Q

Mechanism of resistance to fluproquinolones?

A
  • decreased intracellular accumulation of the drug via the
    production of efflux pumps
  • changes in porin structure
  • changes in the sensitivity of the target enzymes via point
    mutations in the antibiotic binding regions
142
Q

MOA: Reactive reduction by ferredoxin forming free radicals
that disrupt electron transport chain. Bactericidal

A

Nitroimidazole (Antiprotozoal)

Metronidazole, Tinidazole, Secnidazole

143
Q

DOC for amoebiasis, giardiasis &
Pseudomembranous colitis

A

METRONIDAZOLE

144
Q

MOA: Forms multiple reactive intermediates when acted upon
by bacterial nitrofuran reductase →
disrupt protein, RNA and DNA synthesis. Bactericidal

A

NITROFURANTOIN

145
Q

USed in Uncomplicated Urinary tract infections (EXCEPT
Proteus and Pseudomonas)

A

Nitrofurantoin

146
Q

Inhibits Staphylococcal isoleucyl tRNA synthetase.
Bactericidal.
Uses Gram positive cocci including methicillin-susceptible
and MRSA, for minor skin infections such as Impetigo

A

Mupirocin

147
Q

Which anti-TB drugs are hepatotoxic?

A

ISO a Red PYRe! (I saw a red fire!)

Isoniazid < Rifampin < Pyrazinamide

148
Q

All can be used for ACTIVE TB. ??? and ??? can
be used for LATENT TB.

A

ISONIAZID AND RIFAMPICIN

149
Q

MOA Inhibits mycolic acid synthesis. Bactericidal.

A

ISONIAZID

150
Q

SE of Isoniazid?

A

Hepatitis, Neurotoxicity

151
Q

IN Isoniazid, we can prevent neurotoxcity by co-administering waht?

A

Pyridoxine (vitamin B6)

152
Q

M OA: Inhibits DNA-dependent RNA polymerase → inhibits
RNA production. Bactericidal.

A

Rifampicin (Rifampin), Rifabutin, Rifapentine, Rifaximin

153
Q

Side effect: Red-orange Body Fluids, Light chain proteinuria,
Skin rash, Thrombocytopenia, Nephritis, Hepatotoxicity,
Flulike Syndrome, Anemia, Cholestasis

A

Rifampicin

154
Q

The 4 Rs of Rifampicin?

A

The Rs of Rifampicin
RNA polymerase inhibitor
Red-orange body fluids
Rapid development of resistance
Revs up cytochrome P450 (inducer)

155
Q

is a Rifampin derivative that is not
absorbed in the GIT, and so is used for the prevention
of hepatic encephalopathy, for treatment of traveler’s
diarrhea, (off-label use: for IBS and
Pseudomembranous colitis)

A

RIFAXIMIN

156
Q

is equally effective as anti-mycobacterial
agent with less drug interaction and it is the preferred
anti-TB for AIDS patients

A

RIFABUTIN

157
Q

MOA: Unknown. Converted to active pyrazinoic acid under
acidic conditions of macrophage lysosomes.
Bacteriostatic but can be bactericidal on actively
dividing mycobacteria.

A

PYRAZINAMIDE

158
Q

Also known as “sterilizing agent” used during the first
2 months of therapy
* Most hepatotoxic anti-TB drug

A

PYRAZINAMIDE

159
Q

MOA: Inhibits arabinosyl transferases involved in the
synthesis of arabinogalactan in mycobacterial cell wall.
Bacteriostatic.

A

Ethambutol

160
Q

SE: Visual disturbances (decreased visual acuity, red-green
color blindness, retrobulbar neuritis, retinal damage),
Headache, Confusion, Hyperuricemia, Peripheral
neuritis

A

Ethambutol

161
Q

perform what examination before starting antimycobacterial therapy?

A

Perform baseline ophthalmologic examination before
starting antimycobacterial therapy

162
Q

MOA Inhibit protein synthesis by binding to S12 ribosomal
subunit. Bactericidal.

A

STREPTOMYCIN

163
Q

MOA Inhibition of folic acid synthesis. Bacteriostatic.
Uses: Leprosy, PCP pneumonia (backup)

A

DAPSONE, ACEDAPSONE (Sulfones)

164
Q

Most active drug against M. leprae

A

DAPSONE

165
Q

is a repository form of dapsone which has
drug action that can last for several months

A

ACEDAPSONE

166
Q

Binds to guanine bases in bacterial DNA. Bactericidal

A

CLOFAZIMINE

167
Q

Interferes with microtubule function. Inhibits
synthesis and polymerization of nucleic acids.
Fungistatic.

A

GRISEOFULVIN

168
Q

Interfere with ergosterol synthesis by inhibiting fungal
squalene oxidase. Fungicidal.

A

Terbinafine, Butenafine, Naftifine

169
Q

MOA Binds to ergosterol in fungal cell membranes, forming
artificial pores. Fungicidal.
Uses: Candidiasis (Oropharyngeal, Esophageal, Vaginal)

A

POLYENE:

Nystatin, Natamycin

170
Q

MOA Inhibit fungal P450-dependent enzymes blocking
ergosterol synthesis. Fungistatic.
Uses:Mucocutaneous candidiasis, Dermatophytosis,
Seborrheic dermatitis, Pityriasis versicolor

A

Clotrimazole, Miconazole, Ketoconazole, Butoconazole, Econazole,
Sulconazole, Oxiconazole, Terconazole, Tioconazole

171
Q

MOA Binds to ergosterol in fungal cell membranes, forming
artificial pores. Fungicidal.
Uses: Systemic fungal infections (Aspergillus, Blastomyces,
Candida albicans, Cryptococcus, Histoplasma, Mucor)

A

Amphotericin B

172
Q

Has the WIDEST antifungal spectrum

A

AMPHOTERICIN B

173
Q

MOA: Accumulated in fungal cells by the action of permease and
converted by cytosine deaminase to 5-FU, which inhibits
thimidylate synthase. Fungistatic.

Uses Cryptococcosis, Systemic candidal infections,
Chromoblastomycosis

A

Flucytosine

174
Q

MOA: Inhibit fungal P450-dependent enzymes blocking
ergosterol synthesis. Fungistatic.
* SE: Gastrointestinal disturbances (vomiting, diarrhea), Rash and
Hepatotoxicity

A

AZOLES

175
Q

narrow spectrum azole that is Used Chronic mucocutaneous candidiasis, Dermatophytosis

A

KETOCONAZOLE

176
Q

AZOLE

Uses: Cryptococcal meningitis (treatment and prophylaxis)
Candidiasis (esophageal, oropharyngeal, vulvovaginitis),
Coccidioidomycosis

A

Fluconazole [D],

177
Q

Alternative to Amphotericin B in the treatment of
C. neoformans
* As effective as Amphotericin B in candidemia

A

FLUCONAZOLE

178
Q

Alternative to Amphotericin B in the treatment of
C. neoformans
* As effective as Amphotericin B in candidemia

A

POSACONAZOLE

179
Q

Broad spectrum azole, Poor CNS Penetration

A

ITRACONAZOLE

180
Q

MOA Inhibits â-glucan synthase decreasing fungal cell wall
synthesis
Uses: Disseminated and mucocutaneous candidiasis, Salvage
therapy for invasive aspergillosis

A

ECHINOCANDIN:

Caspofungin, Anidulafungin, Micafungin

181
Q
A

PLE_PHARMA (16 decks)

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