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First Aid > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Sulfonamides: Examples

A

Sulfadiazine

Sulfamethoxazole (SMX)

Sulfisoxazole

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2
Q

Target: DNA topoisomerases

A

Fluoroquinolones

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3
Q

Fluoroquinolones: Examples

A

Ciprofloxacin

Levofloxacin

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4
Q

Target: Damages DNA

A

Metronidazole

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5
Q

Target: mRNA synthesis (RNA polymerase)

A

Rifampin

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6
Q

Target: Protein Synthesis (50S subunit)

A

Chloramphenicol

Clindamycin

Linezolid

Macrolides

Stretogramins

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7
Q

Macrolides: Examples

A

Azithromycin

Clarithromycin

Erythromycin

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8
Q

Streptogramins: Examples

A

Dalfopristin

Quinupristin

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9
Q

Target: Protein synthesis (30S subunit)

A

Aminoglycosides

Tetracyclines

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10
Q

Aminoglycosides: Examples

A

Amikacin

Gentamicin

Neomycin

Streptomycin

Tobramycin

‘“Mean” (aminoglycosides) GNATS caNNOT kill anaerobes.’

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11
Q

Tetracyclines: Examples

A

Doxycycline

Minocycline

Tetracycline

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12
Q

Target: Peptidoglycan cross-linking (cell wall synthesis)

A

Penicillinase-sensitive penicillins

Penicillinase-resistant penicillins

Antipseudomonals

Cephalosporins

Carbepenems

Monobactams

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13
Q

Penicillinase-sensitive penicillins: Examples

A

Amoxicillin

Ampicillin

Penicillin G, V

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14
Q

Penicillinase-resistant penicillins: Examples

A

Dicloxacillin

Nafcillin

Oxacillin

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15
Q

Antipseudomonals: Examples

A

Piperacillin

Ticarcillin

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16
Q

1st generation cephalosporins: Examples

A

Cefazolin

Cephalexin

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17
Q

2nd generation Cephalosporin: Examples

A

Cefoxitin

Cefaclor

Cefuroxime

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18
Q

3rd generation cephalosporin: Examples

A

Ceftriaxone

Cefotaxime

Ceftazidime

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19
Q

4th generation Cephalosporin: Examples

A

Cefepime

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20
Q

5th generation cephalosporin: Example

A

Ceftaroline

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21
Q

Carbapenems: Examples

A

Doripenem

Ertapenem

Imipenem

Meropenem

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22
Q

Monobactams: Examples

A

Aztreonam

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23
Q

Penicillin G, V: routes of administration

A

Penicillin G (IV and IM)

Penicillin V (oral)

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24
Q

Penicillin G, V: Mechanism

A

Bind penicillin-binding proteins (transpeptidases).

Block transpeptidase cross-linking of peptidoglycan in cell wall.

Activate autolytic enzymes.

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25
Q

Penicillin G, V: Clinical Use

A

Mostly used for gram-positive organisms (S. pneumoniae, S. pyogenes, Actinomyces).

Also used for gram-negative cocci (mainly N. meningitis) and spirochetes (namely T. pallidum).

Bactericidal

Penicillinase sensitive.

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26
Q

Penicillin G, V: Toxicity

A

Hypersensitivity reactions

Hemolytic anemia

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27
Q

Penicillin G, V: Resistance

A

Penicillinase in bacteria (a type of beta-lactamase) cleaves beta-lactam ring.

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28
Q

Amoxicillin, ampicillin: Mechanism

A

Same as penicillin.

Wider spectrum; penicillinase sensitive.

Also combine with clavulonic acid to protect against destruction by beta-lactamase.

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29
Q

Amoxicillin, ampicillin: Clinical use

A

Extended spectrum penicillin: H. influenzae, H. pylori, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci

Ampicillin/amoxicillin HHELPSS kill enterococci.

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30
Q

Amoxicillin, ampicillin: Toxicity

A

Hypersensitivity reactions;

Rash

Pseudomembranous colitis

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31
Q

Amoxicillin, ampicillin: Mechanism of resistance

A

Penicillinase in bacteria (a type of beta-lactamase) cleaves beta-lactam ring.

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32
Q

Penicillinase-resistance penicillins: Mechanism

A

Same as penicillin

Narrow spectrum;

penicillinase resistant because bulky R group blocks access of beta-lactamase to beta-lactam ring.

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33
Q

Penicillinase-resistant penicillins: Clinical Use

A

Staph aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

“Use naf (nafcillin) for staph”

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34
Q

Penicillinase-resistant penicillins: Toxicity

A

Hypersensitivity reactions

Intersitital nephritis

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35
Q

Antipseudomonals: Mechanism

A

Same as penicillin.

Extended spectrum.

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36
Q

Antipseudomonals: Clinical use

A

Pseudomonas spp. and gram-negative rods;

susceptible to penicillinase;

use with beta-lactam inhibitors.

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37
Q

Antipseudomonals: toxicity

A

Hypersensitivity reactions

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38
Q

Beta lactamase inhibitors: Examples

A

Clavulonic Acid,

Sulbactam,

Tazobactam.

(CAST).

Often added to penicillin antibiotics to protect the antibiotic from destruction by beta-lactamase.

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39
Q

Cephalosporins (I-V): Mechanism

A

Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases.

Bactericidal

Organisms typically not covered by cephalosporins are LAME: Lysteria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci.

Exception: ceftaroline covers MRSA

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40
Q

1st generation Cephalosporins: Clinical Use

A

Gram-positive cocci

  • Proteus mirabilis*
  • E. coli*
  • Klebsiella pneumoniae* (PEcK)

Cefazolin used prior to surgery to prevent S. aureus wound infections.

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41
Q

2nd generation cephalosporins: Clinical Use

A

Gram positive cocci

  • Haemophilus influenzae*
  • Enterobacter aerogenes*
  • Neisseria spp.*
  • Proteus mirabilis*
  • E. coli*
  • Klebsiella pneumoniae*
  • Serratia marcescens*

HEN PEcKS

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42
Q

3rd generation Cephalosporins: Clinical use

A

Serious gram-negative infections resistant to other beta-lactams

Ceftriaxone: meningitis, gonorrhea, disseminated Lyme disease

Ceftazidime: Pseudomonas

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43
Q

4th generation Cephalosporins: Clinical use

A

Gram negative organisms,

with increased activity against Pseudomonas and gram-positive organisms.

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44
Q

5th generation Cephalosporin: Clinical use

A

Broad gram-positive and gram-negative organism coverage, including MRSA;

does not cover Pseudomonas

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45
Q

Cephalosporins (generations I-V): toxicity

A

Hypersensitivity reactions

Autoimmune hemolytic anemia

Disulfiram-like reaction

Vitamin K deficiency

Exhibit cross-reactivity with penicillins

Increase nephrotoxicity of aminoglycosides

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46
Q

Cephalosporins (generations I-V): Mechanism of Resistance

A

Structure change in penicillin-binding proteins (transpeptidases)

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47
Q

Carbapenems: Mechanism

A

Imipenem is a broad-spectrum, beta-lactamase-resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules. With imipenem, “the kill is lastin’ with cilastatin.”

Ertapenem has limited Pseudomonas coverage

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48
Q

Carbapenems: Clinical use

A

Gram-positive cocci, gram negative rods, and anaerobes.

Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.

Meropenem has a decreased risk of seizures and is stable to dehydropeptidase I.

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49
Q

Carbepenems: Toxicity

A

GI distress

Skin rash

CNS toxicity (seizures) at high plasma levels

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50
Q

Monobactams (Aztreonam): Mechanism

A

Less susceptible to beta-lactamases.

Prevents peptidoglycan cross-linking by binding to penicillin-binding protein

Synergistic with aminoglycosides.

No cross-allergenicity with penicillins.

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51
Q

Monobactams (Aztreonam): Clinical Use

A

Gram-negative rods only – no activity against gram-positives or anaerobes.

For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

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52
Q

Monobactams (Aztreonam): Toxicity

A

Usually nontoxic;

occasional GI upset

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53
Q

Vancomycin: Mechanism

A

Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.

Bactericidal.

Not susceptible to beta-lactamases.

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54
Q

Vancomycin: Clinical Use

A

Gram-positive bugs only – serious, multidrug-resistant organisms, including MRSA, S. epidermidis, sensitive Enteroccocus species, and Clostridium difficile (oral dose for pseudomembranous colitis).

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55
Q

Vancomycin: Toxicity

A

Well tolerated in general – but NOT trouble free.

Nephrotoxicity,

Ototoxicity,

Thrombophlebitis,

diffuse flushing – red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate).

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56
Q

Vancomycin: Mechanism of resistance

A

Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac.

“Pay back 2 D-Dalas (dollars) for vandalizing (vancomycin).”

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57
Q

Protein synthesis inhibitors: 30S inhibitors

A

A = Aminoglycosides (bactericidal)

T = Tetracylcines (bacteriostatic)

“Buy AT 30, CCEL (sell) at 50.”

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58
Q

Protein synthesis inhibitors: 50S inhibitors

A

C = Chloramphenicol, Clindamycin (bacteriostatic)

E = Erythromycin (macrolides) (bacteriostatic)

L = Linezolid (variable)

“Buy AT 30, CCEL (sell) at 50.”

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59
Q

Aminoglycosides: Mechanism

A

Bactericidal;

irreversible inhibition of initiation complex through binding of the 30S subunit.

Can cause misreading of mRNA.

Also block translocation.

Require O2 for uptake;

therefore ineffective against anaerobes.

“Mean” (aminoglycosides) GNATS caNNOT kill anaerobes.

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60
Q

Aminoglycosides: Clinical use

A

Severe gram-negative rod infections.

Synergistic with beta-lactam antibiotics.

Neomycin for bowel surgery.

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61
Q

Aminoglycosides: Toxicity

A

Nephrotoxicity,

Neuromuscular blockade,

Ototoxicity (especially when used with loop diuretics).

Teratogen

‘“Mean” (aminoglycoside) GNATS caNNOT kill anaerobes.’

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62
Q

Aminoglycosides: Mechanisms of Resistance

A

Bacterial transferase enyzmes inactivate the drug by acetylation, phosphorylation, or adenylation.

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63
Q

Tetracyclines: Mechanism

A

Bacteriostatic;

Bind to 30S and prevent attachment of aminoacyl-tRNA

Limited CNS penetration.

Doxycycline is fecally eliminated and can be used in patients with renal failure.

Do not take tetracyclines with milk (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit drugs’ absorption in the gut.

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64
Q

Tetracyclines: Clinical Use

A

Borrelia burgdorferi, M. pneumoniae.

Drugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia. Also used to treat acne.

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65
Q

Tetracyclines: Toxicity

A

GI distress

Discoloration of teeth and inhibition of bond growth in children

Photosensitivity

Contraindicated in pregnancy

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66
Q

Tetracyclines: Mechanism of Resistance

A

Decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.

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67
Q

Folic acid synthesis (DNA methylation)

A

Sulfonamides

Trimethoprim

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68
Q

Chloramphenicol: Mechanism

A

Blocks peptidyltransferase at 50S ribosomal subunit.

Bacteriostatic

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69
Q

Chloramphenicol: Clinical use

A

Meningitis: Haemophilis influenza, Neisseria meningitis, Streptococcus pneumoniae)

Rocky Mountain spotted fever (Rickettsia rickettsii)

Limited use owing to toxicities but often still used in developing countries because of low cost

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70
Q

Chloramphenicol: Toxicity

A

Anemia (dose dependent),

aplastic anemia (dose independent),

gray baby syndrome (in premature infants becaue they lack liver UDP-glucuronyl transferase)

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71
Q

Chloramphenicol: Mechanism of resistance

A

Plasmid-encoded acetyltransferase inactivates the drug

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72
Q

Clindamycin: Mechanism

A

Blocks peptide transfer (translocation) at 50S ribosomal subunit.

Bacteriostatic

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73
Q

Clindamycin: Clinical Use

A

Anaerobic infects (e.g., Bacteroids spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections. Also effective against invasive group A streptococcal infection.

Treats anaerobic infections above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)

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74
Q

Clindamycin: Toxicity

A

Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea

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75
Q

Linezolid (Oxazolidinones): Mechanism

A

Inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.

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76
Q

Linezolid (Oxazolidinone): Clinical Use

A

Gram-positive species including MRSA and VRE

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77
Q

Linezolid: Toxicity

A

Bone marrow suppression (especially thrombocytopenia),

peripheral neuropathy,

serotonin syndrome

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78
Q

Linezolid: Mechanism of Resistance:

A

Point mutation of ribosomal RNA

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79
Q

Macrolides: Mechanism

A

Inhibit protein synthesis by blocking translocation (“macroslides”); bind to the 23S rTNA of the 50S ribosomal subunit.

Bacteriostatic

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80
Q

Macrolides: Clinical Use

A

Atypical pneumonias (Mycoplasma, Chlamydia, Legionella),

STIs (Chlamydia),

gram-positive cocci (streptococcal infections in patients allergic to penicillin), and

B. pertussis

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81
Q

Macrolides: Toxicity

A

MACRO:

Gastrointestinal Motility issues,

Arrhythmia caused by prlonged QT interval, acute Cholestatic hepatitis, Rash, eOsinophilia.

Increases serum concentration of theophylines, oral anticoagulants.

Clarithromycin and erythromycin inhibit cytochrome P-450

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82
Q

Macrolides: Mechanism of Resistance

A

Methylation of 23S rRNA-binding site prevents binding of drug

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83
Q

Trimethoprim: Mechanism

A

Inhibits bacterial dihydrofolate reductase

Bacteriostatic

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84
Q

Trimethoprim: Clinical Use

A

Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP-SMX]), causing sequential block of folate synthesis.

Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis.

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85
Q

Trimethoprim: Toxicity

A

Megaloblastic anemia, leukopenia, granulocytopenia.

(May elleviate with supplemental folinic acid).

TMP Treats Marrow Poorly

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86
Q

Sulfonamides: Mechanism

A

Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic (bactericidal when combined with trimethoprim).

(Dapsone, used to treat lepromatous leprosy, is a closely related drug that also inhibits folate synthesis).

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87
Q

Sulfonamides: Clinical Use

A

Gram-positives, gram-negatives, Nocardia, Chlamydia.

Triple sulfas or SMX for simple UTI.

88
Q

Sulfonamides: Toxicity

A

Hypersensitivity reactions,

hemolysis if G6PD deficient,

nephrotoxicity (tubulointerstital nephritis),

photosensitivity,

kernicterus in infants,

displace other drugs from albumin (e.g., warfarin).

89
Q

Sulfonamides: Mechanism of Resistance

A

Altered enzyme (bacterial dihydropteroate synthase),

decreased uptake, or

increased PABA synthesis.

90
Q

Fluoroquinolones: Mechanism

A

Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV.

Bactericidal

Must not be taken with antacids

91
Q

Fluoroquinolones: Clinical Use

A

Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram-positive organisms.

92
Q

Fluoroquinolones: Toxicity

A

GI upset, superinfections, skin rashes, headache, dizziness.

Less commonly, can cause leg cramps and myalgias.

Contraindicated in pregnant women, nursing mothers, and children <18 years old due to possile damage to cartilage. Some may prolong QT interval. May cause tendonitis or tendon rupture in people >60 years old and in patients taking prednisone.

Fluoroquinolones hurt attachments to your bones.

93
Q

Fluoroquinolones: Mechanism of Resistance

A

Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

94
Q

Daptomycin: Mechanism

A

Lipopetide that disrupts cell membrane of gram-positive coci.

95
Q

Daptomycin: Clinical use

A

S. aureus skin infections (especially MRSA), bacteremia, endocarditis, VRE

Not used for pneumonia (avidly binds to and is inactivated by surfactant).

96
Q

Daptomycin toxicity

A

Myopathy, rhabdomyolysis

97
Q

Metronidazole: Mechanism

A

Forms toxic free radical metabolites in the bacterial cell that damage DNA.

Bactericidal

Antiprotozoal

98
Q

Metronidazole: Clinical Use

A

Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginialis, Anaerobes (Bacteroides, C. difficile).

Use with a proton pump inhibit and clarithromycin for “triple therapy” against H. Pylori.

GET GAP on the Metro with metronidazole! Treats anaerobic infection below the diaphragm vs. clindamycin (anaerobic infections above diaphragm).

99
Q

Metronidazole Toxicity

A

Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alchohol; headache, metallic taste

100
Q

Treatment and prophylaxis for

Mycobacterium tuberculosis

A

Prophylaxis: Isoniazid

Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE for treatment)

101
Q

Treatment and prophylaxis for

Mycobacterium avium - intracellulare

A

Prophylaxis: Azithromycin, rifabutin

Treatment: M. avium-intracellulare is more drug resistant than M. tuberculosis. Azithromycin or clarithromycin + ethambutol. Can add rifabutin or ciprofloxacin.

102
Q

Treatment and prophylaxis for

Mycobacterium leprae

A

Prophylaxis: N/A

Treatment: Long-term treatment with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form.

103
Q

Rifamycins: Examples

A

Rifampin

Rifabutin

104
Q

Rifamycin: mechanism

A

Inhibits DNA-dependent RNA polymerase

Rifampin’s 4 R’s:

RNA polymerase inhibitor

Ramps up microsomal cytochrome P-450

Red/orange body fluids

Rapid resistance if used alone

Rifampin ramps up cytochrome P-450, but rifabutin does not.

105
Q

Rifamycins clinical use

(Rifampin, rifabutin)

A

Mycobacterium tuberculosis; delay resistance to dapsone when used for leprosy.

Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B.

106
Q

Rifamycins: Toxicity

(Rifampin, rifabutin)

A

Minor hepatotoxicity and drug interactions (increase cytochrome P-450); orange body fluids.

Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.

107
Q

Rifamycins: Mechanism of resistance

(Rifampin, rifabutin)

A

Mutations reduce drug binding to RNA polymerase. Monotherapy rapidly leads to resistance.

108
Q

Isoniazid: Mechanism

A

Decrease synthesis of mycolic acids

Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite.

109
Q

Isoniazid: Clinical Use

A

Mycobacterium tuberculosis

The only agent used as solo prophylaxis against TB.

Different INH half-lives in fast versus slow acetylators.

110
Q

Isoniazid: Toxicity

A

Neurotoxicity, hepatotoxicity.

Pyridoxine (vitamine B6) can prevent neurotoxicity

INH Injures Neurons and Hepatocytes

111
Q

Isoniazid: Mechanism of Resistance

A

Mutations leading to underexpression of KatG (bacterial catalase-peroxidase needed to convert INH to active metabolite).

112
Q

Pyrazinamide: Mechanism

A

Mechanism Uncertain

Pyrazinamide is a prodrug that is converted to the active compound pyrazinoic acid.

113
Q

Pyrazinamide: Clinical Use

A

Mycobacterium tuberculosis

114
Q

Pyrazinamide: Toxicity

A

Hyperuricemia

Hepatotoxicity

115
Q

Ethambutol: Mechanism

A

Decrease carbohydrate polymerization of mycobacterium cell wall by blcoking arabinosyltransferase

116
Q

Ethambutol: Clinical Use

A

Mycobacterium tuberculosis

117
Q

Ethambutol: Toxicity

A

Optic neuropathy (red-green color blindness). Pronounce “eyethambutol”)

118
Q

Antimicrobial prophylaxis:

High risk for endocarditis and undergoing surgical or dental procedures

A

Amoxicillin

119
Q

Antimicrobial prophylaxis:

Exposure to gonorrhea

A

Ceftriaxone

120
Q

Antimicrobial prophylaxis:

History of recurrent UTIs

A

TMP-SMX

121
Q

Antimicrobial prophylaxis: Exposure to meningococcal infection

A

Ceftriaxone, ciprofloxacin, or rifampin

122
Q

Antimicrobial prophylaxis:

Pregnant woman carrying group B strep

A

Penicillin G

123
Q

Antimicrobial prophylaxis:

Prevention of gonococcal conjunctivitis in newborn

A

Erythromycin ointment

124
Q

Antimicrobial prophylaxis:

Prevention of postsurgical infection due to S. aureus

A

Cefazolin

125
Q

Antimicrobial prophylaxis:

Prophylaxis of strep pharyngitis in child with prior rheumatic fever

A

Banzathine penicillin G or oral penicillin G

126
Q

Antimicrobial prophylaxis:

Exposure to syphilis

A

Benzathine penicillin G

127
Q

Prophylaxis in HIV patients:

CD4 < 200 cells/mm3

A

Prophylaxis: TMP-SMX

Infection: Pneumocystis pneumonia

128
Q

Prophylaxis in HIV patients:

CD4 < 100 cells/mm3

A

Prophylaxis: TMP-SMX

Infection: Pneumocystis pneumonia and toxoplasmosis

129
Q

Prophylaxis in HIV patients:

CD4 < 50 cells/mm3

A

Prophylaxis: Azithromycin or clarithromycin

Infection: Mycobacterium avium complex

130
Q

Treatment of MRSA

A

Vancomycin

Daptomycin

Linezolid

Tigecycline

Ceftaroline

131
Q

Treatment of VRE

A

Linezolid and streptogramins (quinupristin, dalfopristin)

132
Q

Treatment for multidrug-resistant Pseudomonas aeruginosa

A

Polymixins B and E (colistin)

133
Q

Treatment for multidrug-resistant Acinetobacter baumannii

A

Polymixins B and E (colistin)

134
Q

Amphotericin B: Mechanism

A

Binds ergasterol (unique to fungi); forms membrane pores that allow leakage of electrolytes

Amphotericin “tears” holes in the fungal membrane by forming pores.

135
Q

Amphotericin B: Clinical Use

A

Serious, systemic mycoses

Cryptococcus (amphotericin B with/without flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor.

Intrathecally for fungal meningitis.

Supplement K+ and Mg2+ becaues of altered renal tubule permeability.

136
Q

Amphotericin B: Toxicity

A

Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (“amphoterrible”).

Hydration decreases nephrotoxicity.

Liposomal amphotericin decreases toxicity.

137
Q

Nystatin: Mechanism

A

Same as amphotericin B. Topical use only as too toxic for systemic use.

Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes.

138
Q

Nystatin: Clinical Use

A

“Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.

139
Q

Flucytosine: Mechanism

A

Anti-fungal

Inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase

140
Q

Flucytosin: Clinical Use

A

Systemic funal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B.

141
Q

Flucytosine: Toxicity

A

Bone marrow suppression

142
Q

Azoles: Examples

A

(Anti-fungals)

Clotrimazole

Fluconazole

Itraconazole

Ketoconazole

Miconazole

Voriconazole

143
Q

Azoles: Mechanism

A

Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.

144
Q

Azoles: Clinical Use

A

Local and less serious systemic mycoses. Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infection sof all types.

Itraconazole for Blastomyces, Coccidioides, Histoplasma.

Clotrimazole and miconazole for topical fungal infections.

145
Q

Azoles: Toxicity

A

Testosterone synthesis inhibition (gynecomastia, especially with ketoconazole),

liver dysfunction (inhibits cytochrome P-450)

146
Q

Terbinafine: Mechanism

A

Inhibits the fungal enzyme squalene epoxidase

147
Q

Terbinafine: Mechanism

A

Dermatophytoses (especially onchymomycosis–fungal infection of the finger or toe nails).

148
Q

Terbinafine: Toxicity

A

GI upset, headaches, hepatotoxicity, taste disturbance

149
Q

Echinocandins: Examples

A

Anidulafungin

Caspofungin

Micafungin

150
Q

Echinocandins: Mechanism

A

Inhibit cell wall synthesis by inhibiting synthesis of beta-glucan

151
Q

Echinocandins: Clinical Use

A

Invasive aspergillosis, Candida

152
Q

Echinocandins: Toxicity

A

GI upset,

flushing (by histamine release)

153
Q

Griseofulvin: Mechanism

A

Anti-fungal

Interferes with microtubule function; disrupts mitosis

Deposits in keratin-containing tissues (e.g., nails)

154
Q

Griseofulvin: Clinical Use

A

Anti-fungal

Oral treatment of superficial infections;

Inhibits growth of dermatophytes (tinea, ringworm)

155
Q

Griseofulvin: Toxicity

A

Teratogenic

Carcinogenic

Confusion

Headaches

Increased cytochrome P-450 and warfarin metabolism

156
Q

Treatment for toxoplasmosis

A

Pyrimethamine

157
Q

Treatment for Typanosoma brucei

A

Suramin and melarsoprol

158
Q

Treatment for Trypanosoma cruzi

A

Nifurtimox

159
Q

Treatment for leishmaniasis

A

Sodium stibogluconate

160
Q

Anti-mite/louse therapy

Used to treat scabies (Sarcoptes scabei) and lice (Pediculus and Pthirus)

A

Permethrin (blocks Na+ channels -> neurotoxicity)

Malathion (acetylcholinesterase inhibitor)

Lindane (blacks GABA channels -> neurotoxicity)

161
Q

Chloroquine: Mechanism

A

Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.

162
Q

Chloroquine: Clincal Use

A

Treatment of plasmodial species other than P. falciparum (frequency of resistance in P. falciparum is too high). Resistance due to membrane pump that decreases inctracellular concentration of drug. Treat P. falciparum with artemether/lumefantrine or atovaquane/proguanil. For life-threatening malaria, use quinidine in U.S. (quinine elsewhere) or artesunate.

163
Q

Chloroquine: Toxicity

A

Retinopathy;

Pruritis (especially in dark-skinned individuals)

164
Q

Anti-helminthic therapy

A

Mebendazole

pyrantel pamoate

ivermectin

diethylcarbamazine

praziquantal

165
Q

Inhibitors of Influenza neuraminidase

  1. Examples
  2. Mechanism
  3. Clinical use
A

Examples: Oseltamivir, Zanamivir

Mechanism: Inhibit influenza neuraminidase, decreasing release of progeny virus

Clinical Use: Treatment and prevention of both influenza A and B

166
Q

Guanasine analogs: Examples

A

Acyclovir

Famiciclovir

Valacyclovir

167
Q

Acyclovir, famiciclovir, valacyclovir: Mechanism

A

Guanosine analogs

Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells -> few adverse effects.

Triphosphate formed by cellular enzymes.

Preferentially inhibit viral DNA polymerase by chain termination.

168
Q

Acyclovir, famiciclovir, valacyclovir: Clincial Use

A

HSV and VSZV.

Weak activity against EBV.

No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis.

Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV.

Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.

169
Q

Acyclovir, famiciclovir, valacyclovir: Toxicity

A

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated

170
Q

Acyclovir, famiciclovir, valacyclovir: Mechanism of resistance

A

Mutated viral thymidine kinase

171
Q

Ganciclovir: Mechanism

A

5’-monophosphate formed by a CMV viral kinase.

Guanosine analog.

Triphosphate formed by cellular kinases.

Preferentially inhibits viral polymerase by chain termination.

172
Q

Gancyclovir: Clinical Use

A

CMV, especially in immunocompromised patients.

Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability.

173
Q

Ganciclovir: Toxicity

A

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

174
Q

Ganciclovir: Mechanism of resistance

A

Mutated viral kinase

175
Q

Foscarnet: Mechanism

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor. Binds to pyrophosphate-binding site of enzyme. Dose not require activation by viral kinase.

Foscarnet = pyrofosphate analog

176
Q

Foscarnet: Clinical use

A

CMV retinities is immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV.

177
Q

Foscarnet: Toxicity

A

Nephrotoxicity, electrolyte abnormalites (hypo- or hypercalcemia, hypo- or hyperphosphatemia, hypokalemia, hypomagnesemia) can lead to seizures.

Foscarnet is a pyrophosphate analog and can chelate calcium. Foscarnet-induced renal wasting of magnesium may lead to hypomagnesemia and a reduction in the release of parathyroid hormone, which contributes to the hypocalcemic state. Both hypocalcemia and hypomagnesemia can promote seizures.

178
Q

Foscarnet: Mechanism of resistance

A

Mutated DNA polymerase

179
Q

Cidofovir: Mechanism

A

Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.

180
Q

Cidofovir: Clinical Use

A

CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life.

181
Q

Cidofovir: Toxicity

A

Nephrotoxicity (coadminister with probenecid and IV saline to decrease toxicity)

182
Q

HAART therapy

A

3 drugs to prevent resistance

2 Nucleoside Reverse Transcriptase inhibitors

AND

Non-nucleoside reverse transcriptase inhibitor

or

Protease inhibitor

or

Integrase Inhibitor

183
Q

Protease inhibitors: Examples

A

All end in -navir

“Navir (never) tease a protease”

Atazanavir

Darunavir

Fosamprenavir

Indinavir

Lopinavir

Ritonavir

Saquinavir

184
Q

Protease inhibitors: Mechanism

A

Assemply of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

Ritonavir can “boost” other drug concentrations by inhibiting cytocrhome P-450.

All protease inhibitors end in -navir.

185
Q

Protease inhibitors: Toxicity

A

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy

Nephropathy, hematuria (indinavir)

Rifampin (a potent CYP/UGT inducer) contraindicated with protease inhibitors because it can decrease protease inhibitor concentration.

186
Q

Nucloside/Nucleotide Reverse Transcriptase Inhibitors: Examples

A

Abacavir (ABC)

Didanosine (ddl)

Emtricitabine (FTC)

Lamuvidine (3TC)

Stavudine (d4T)

Tenofovir (TDF)

Zidovudine (ZDV, formerly AZT)

187
Q

NRTIs: Mechanism

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Tenofovir is a nucleoTide; the others are nuceosides and need to be phosphorylated to be active.

ZDV is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission.

Have you dined (vudine) with my nuclear (nucleosides) family?

188
Q

NRTIs: Toxicity

A

Bone marrow supprssion (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), anemia (ZDV), pancreatitis (didanosine)

189
Q

NNRTIs: Examples

A

Delavirdine

Efavirenz

Nevirapine

190
Q

NRTIs: Mechanism

A

Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.

191
Q

NNRTIs: Toxicity

A

Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy.

192
Q

Ingegrase Inhibitors: Example(s)

A

Raltegravir

193
Q

Integrase inhibitor: Mechanism

A

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase.

194
Q

Integrase inhibitor: Toxicity

A

Increases creatinine kinase

195
Q

Fusion inhibitors: Examples

A

Enfuvirtide

Maraviroc

196
Q

Enfuvirtide: Mechanism

A

Fusion inhibitor

Binds gp41, inhibiting viral entry

197
Q

Enfuvirtide: Toxicity

A

Skin reaction at injection sites

198
Q

Maraviroc: Mechanism

A

Fusion inhibitor

Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120

199
Q

Interferons: Mechanism

A

Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties

200
Q

Interferon alpha: Clinical Use

A

Chronic heptatis B and C

Kaposi sarcoma

Hairy cell leukemia

Condyloma acuminatum

Renal cell carcinoma

Malignant melanoma

201
Q

Interferon Beta: Clinical Use

A

Multiple sclerosis

202
Q

Interferon gamma: Clinical Use

A

Chronic granulomatus disease

203
Q

Ribavarin: Mechanism

A

Hepatitis C therapy

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase

204
Q

Ribavarin: Clinical Use and toxicity

A

Chronic HCV, also used in RSV (palivizumab preferred in children)

Toxicity: hemolytic anemia; severe teratogen

205
Q

Simeprevir: Mechanism

A

Hepatitis C Therapy

HCV protease inhibitor; prevents viral replication

206
Q

Simeprevir: Clinical Use and Toxicity

A

Clinical Use: Chronic HCV in combination with ribavirin and peginterferon alfa.

Do not use as monotherapy

Toxicity: Photosensitivty reactions, rash

207
Q

Sofosbuvir: Mechanism

A

Hepatitis C therapy

Inhibits HCV RNA-dependent RNA polymerase acting as a chain terminator

208
Q

Sofosbuvir: Clinical Use and Toxicity

A

Clinical Use: Chronic HCV in combination with ribavirin, =/- pegineterferon alfa.

DO not use as monotherapy.

Toxicity: fatigue, headache, nausea

209
Q

Disinfection: definition

A

Reduction of pathogenic organisms to safe levels

210
Q

Sterilization: definition

A

Inactivation of self-propogating biological entities

211
Q

Autoclave

A

Pressurized steam at >120 degrees C.

May be sporicidal

212
Q

Alcohols

A

Denature proteins and disrupt cell membranes.

Not sporicidal.

213
Q

Chlorhexidine

A

Denatures proteins and disrupts cell membranes.

Not sporicidal.

214
Q

Hydrogen peroxide

A

Free radical oxidation

Sporicidal

215
Q

Iodine and iodophors

A

Halogenation of DNA, RNA, and proteins

May be sporicidal

216
Q

Antibiotics to avoid in pregnancy

A

Sulfonamides: Kernicterus

Aminoglycosides: Ototoxicity

Fluoroquinolones: Cartilage damage

Clarithromycin: Embryotoxic

Tetracyclines: Discolored teeth, inhibition of bone growth

Ribavarin (antiviral): Teratogenic

Griseofulvin (antifungal): Teratogenic

Chloramphenicol: Gray baby syndrome

SAFe Children Take Really Good Care

First Aid (4 decks)

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