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Step 1 2019 First Aid Flashcards > Micro FA p.187 - 204 Antimicrobials > Flashcards

Micro FA p.187 - 204 Antimicrobials Flashcards

1
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5
Q

MoA of Penicillin

A

D-Ala-D-Ala structural analog
Bind penicillin-binding proteins (transpeptidases)
Block transpeptidase cross-linking of peptidoglycan in cell wall.

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6
Q

Clinical use of penicillins

A

gram ⊕ organisms (S pneumoniae, S pyogenes, Actinomyces).
Also used for gram ⊝ cocci (mainly N meningitidis) and spirochetes (mainly T pallidum).

(Bactericidal for gram ⊕ cocci, gram ⊕ rods, gram ⊝ cocci, and spirochetes. )

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7
Q

Adverse effects of penicillins

A

Hypersensitivity reactions, direct Coombs ⊕ hemolytic anemia, drug-induced interstitial nephritis

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8
Q

How do bact form resistence to penicillin?

A

β-lactamase cleaves the β-lactam ring. Mutations in PBPs.

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9
Q

Penicillinase sensitive penicillins ex.

A

Amoxicillin, ampicillin; aminopenicillins

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10
Q

MoA of Penicillinase sensitive penicillins, what do you combine it with

A

Same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against destruction by β-lactamase.

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11
Q

Amoxicillin has greater ____ ________than ampicillin.

A

AmOxicillin has greater Oral bioavailability than ampicillin.

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12
Q

Clinical use of penicillinase sensitive penicillins

A

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

Coverage: ampicillin/amoxicillin HHELPSS kill enterococci.

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13
Q

SE/ Penicillinase sensitive penicillins

A

Hypersensitivity reactions, rash, pseudomembranous colitis

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14
Q

How does bact form resistence vs amoxicillin (et al)

A

Penicillinase (a type of β-lactamase) cleaves β-lactam ring.

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15
Q

Ex of penicillinase resistant penicillins

A

Dicloxacillin, nafcillin, oxacillin.

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16
Q

MoA of penicillinase resistant penicillins

A

Same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.

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17
Q

Clinical use of penicillinase resistant penicillins

A

S aureus (except MRSA).

“Use naf (nafcillin) for staph.”

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18
Q

SE/ of Dicloxacillin, Nafcillin, etc

A

Hypersensitivity reactions, interstitial nephritis.

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19
Q

Mech of resistance of penicillinase resistant penicillins

A

MRSA has altered penicillin-binding protein target site

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20
Q

Ex of antipseudomonal penicillins

A

Piperacillin, ticarcillin.

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21
Q

Clinical use of piperacillin

A

Pseudomonas spp. & G- rods

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22
Q

MoA of Cephalosporins

A

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

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23
Q

Organisms typically not covered by 1st–4th generation cephalosporins are

1.

2.

3.

4.

A

Organisms typically not covered by 1st–4th generation cephalosporins are LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci.

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24
Q

1st gen cephalosporins used for?

ex/ of Rx

A

1st generation (cefazolin, cephalexin)—gram ⊕ cocci, Proteus mirabilis, E coli, Klebsiella pneumoniae.

1st generation—⊕ PEcK

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25
Q

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

A

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

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26
Q

Clinical use of 2nd gen cephalosporins
ex/ of Rx?

A

2nd generation (cefaclor, cefoxitin, cefuroxime, cefotetan)—gram ⊕ cocci, H influenzae, Enterobacter aerogenes, Neisseria spp., Serratia marcescens, Proteus mirabilis, E coli, Klebsiella pneumoniae.

2nd graders wear fake fox fur to tea parties. 2nd generation—HENS PEcK.

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27
Q

Ex of 3rd gen cephalosporins?

A

ceftriaxone, cefotaxime, cefpodoxime, ceftazidim

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28
Q

Which gen of cephalosporins can cross brain barrier

A

3rd gen

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29
Q

Which cephalosporin is used for meningitis, gonorrhea, and disseminated Lyme disease?

A

Ceftriaxone

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30
Q

Which cephalosporin is used for Pseudomonas?

A

Ceftazidime—Pseudomonas

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31
Q

4th gen cephalosporins used for? ex?

A

—gram ⊝ organisms, with  activity against Pseudomonas and gram ⊕ organisms.

ex/ cefepime

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32
Q

unlike 1st–4th generation cephalosporins, ceftaroline covers ____, and ______ ________

and does not cover ___________.

A

unlike 1st–4th generation cephalosporins, ceftaroline covers MRSA, and Enterococcus faecalis—does not cover Pseudomonas.

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33
Q

SE/ Cephalosporins

A

Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency.

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34
Q

Cephalosporins increase what toxicity of aminoglycosides?

A

Inc nephrotoxicity of aminoglycosides.

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35
Q

Ex of β-lactamase inhibitors

A

Clavulanic acid, Avibactam, Sulbactam, Tazobactam

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36
Q

List antibiotic/B lactamase (-)’r combos (4)

A

amoxicillin-clavulanate, ceftazidime-avibactam, ampicillin-sulbactam, piperacillin-tazobactam)

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37
Q

List Carbapenems

A

Doripenem, Imipenem, Meropenem, Ertapenem (DIME antibiotics are given when there is a 10/10 [life-threatening] infection).

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38
Q

Imipenem is always administered with? MoA of that rx?

A

Imipenem always administered with cilastatin (inhibitor of renal dehydropeptidase I) to dec inactivation of drug in renal tubules.

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39
Q

Clinical use of carbapenems

A

Gram ⊕ cocci, gram ⊝ rods, and anaerobes.

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40
Q

Meropenem has a dec risk of _______ and is stable to ___________.

A

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

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41
Q

SE// of Carbapenems

A

GI distress, rash, and CNS toxicity (seizures) at high plasma levels.

Carbapenems Cause a bad rash

C- CNS

CARBa-penems - GI

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42
Q

Mech of resistance of carbapenems?

A

Inactivated by carbapenemases produced by, eg, K pneumoniae, E coli, E aerogenes.

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43
Q

Which antibiotic is synergistic with aminoglycosides?

A

Aztreonam

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44
Q

MoA of monobactams?

A

Less susceptible to β-lactamases. Prevents peptidoglycan cross-linking by binding to penicillinbinding protein 3.

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45
Q

What are monobactam used for clinically?

A

Gram ⊝ rods only—no activity against gram ⊕ rods or anaerobes.

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46
Q

MoA of Vancomycin?

A

Inhibits cell wall peptidoglycan formation by binding D-Ala-D-Ala portion of cell wall precursors. Bactericidal against most bacteria

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47
Q

Clinical use of Vancomycin?

A

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

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48
Q

SE/ of Vancomycin

A

Well tolerated in general—but NOT trouble free. Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing—red man syndrome A (largely preventable by pretreatment with antihistamines and slow infusion rate), drug reaction with eosinophilia and systemic symptoms (DRESS syndrome).

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49
Q

Mech of resistance against Vanco?

A

Occurs in bacteria (eg, Enterococcus) via amino acid modification of D-Ala-D-Ala to D-Ala-D-Lac. “If you Lack a D-Ala (dollar), you can’t ride the van (vancomycin).”

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50
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A
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51
Q

All protein synthesis inhibitors are bacteriostatic, except ______ (bactericidal) and ______(variable).

A

All are bacteriostatic, except aminoglycosides (bactericidal) and linezolid (variable).

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52
Q

Give ex of aminoglycosides?

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

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53
Q

MoA of Aminoglycosides?

A
  • Bactericidal; irreversible inhibition of initiation complex through binding of the 30S subunit.
  • Can cause misreading of mRNA.
  • Also block translocation.
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54
Q

Aminoglycosides require ___ for uptake; therefore ineffective against _____.

A

Aminoglycosides require O2 for uptake; therefore ineffective against anaerobes.

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55
Q

Clinical use of aminoglycosides

A

Severe gram ⊝ rod infections. Synergistic with β-lactam antibiotics

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56
Q

What aminoglycoside is used for bowel surgery?

A

Neomycin

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57
Q

SE of Aminoglycosides

A

Nephrotoxicity, Neuromuscular blockade (absolute contraindication with myasthenia gravis), Ototoxicity (especially with loop diuretics), Teratogenicity.

also dec Mg2+ in the body

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58
Q

Ex of tetracyclines

A

Tetracycline, doxycycline, minocycline

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59
Q

MoA of tetracyclins?

A

Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA

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60
Q

Doxycycline is _____ eliminated and can be used in patients with ____ _______.

A

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

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61
Q

Can’t take tetracyclins with what?

A

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

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62
Q

Clinical use of tetracyclins?

A

Borrelia burgdorferi, M pneumoniae. Drugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia.
Doxycycline effective against community-acquired MRSA.

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63
Q

SE/ of Tetracyclins

A

GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.

Tetracyclin - severe nephrotox

TEETHracyclins

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64
Q

Mech of resistance of tetracyclins

A

Dec uptake or inc efflux out of bacterial cells by plasmid-encoded transport pumps.

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65
Q

MoA of Tigecyclin

A

Tetracycline derivative. Binds to 30S, inhibiting protein synthesis. Generally bacteriostatic.

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66
Q

Clinical use of Glycylcyclines?

A

Broad-spectrum anaerobic, gram ⊝, and gram ⊕ coverage.
Multidrug-resistant organisms (MRSA, VRE) or infections requiring deep tissue penetration.

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67
Q

MoA of Chloramphenicol

A

Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic

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68
Q

Clinical use of chloramphenicol?

A

Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and rickettsial diseases (eg, Rocky Mountain spotted fever [Rickettsia rickettsii]).

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69
Q

SE of Chloramphenicol

A

Anemia (dose dependent), aplastic anemia (dose independent), grey baby syndrome

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70
Q

Why does admin of chloramphenicol in premature infants lead to grey baby syndrome?

A

because they lack liver UDP-glucuronosyltransferase

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71
Q

Mech of resistance vs chloramphenicol

A

Plasmid-encoded acetyltransferase inactivates the drug

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72
Q

Clindamycin MoA

A

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

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73
Q

Clinical use of clindamycin?

A

Anaerobic infections (eg, Bacteroides 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, and Metronidazole below diaphragm

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74
Q

_______ treats anaerobic infections above the diaphragm vs ________ anaerobic infections below diaphragm.

A

Clindamycin treats anaerobic infections above the diaphragm vs metronidazole (anaerobic infections below diaphragm).

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75
Q

SE/ of Clindamycin

A

Pseudomembranous colitis (C difficile overgrowth), fever, diarrhea

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76
Q

MoA of Linezolid.

A

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

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77
Q

Use of Linezolid?

A

Gram ⊕ species including MRSA and VRE

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78
Q

SE/ of Linezolid

A

BOne marrow suppression (especially thrombocytopenia), peripheral NEuropathy, Serotonin syndrome (due to partial MAO inhibition).

Linezolid is bad for BONES

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79
Q

Mech of resistance of Linezolid

A

point mutation of ribosomal DNA

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80
Q

Macrolide MoA

A

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

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81
Q

Clinical use of Macrolides

A

Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STIs (Chlamydia), gram ⊕ cocci (streptococcal infections in patients allergic to penicillin), and B pertussis.

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82
Q

SE of Macrolides

A

MACRO: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT interval, acute Cholestatic hepatitis, Rash, eOsinophilia

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83
Q

Macrolides Inc serum conc of ___________ & ____ _____________

A

Theophylline & oral anticoagulants

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84
Q

Which macrolides (-) Cyt p450?

A

Clarithromycin Erythromycin

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85
Q

Mech of resistance vs macrolides

A

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

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86
Q

MoA of Polymyxins

A

Cation polypeptides that bind to phospholipids on cell membrane of gram ⊝ bacteria. Disrupt cell membrane integrity –> leakage of cellular components–> cell death

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87
Q

Clinical use of Polymyxins

A

Salvage therapy for multidrug-resistant gram ⊝ bacteria (eg, P aeruginosa, E coli, K pneumoniae)

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88
Q

Polymyxins tox

A

Nephrotoxicity, neurotoxicity (eg, slurred speech, weakness, paresthesias), respiratory failure.

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89
Q
A
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90
Q

Ex of Sulfonamides?

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine.

91
Q

MoA of Sulfonamides

A

Inhibit dihydropteroate synthase, thus inhibiting folate synthesis.

92
Q

Are Sulfonamides bacteriostatic or cidal?

A

Bacteriostatic (bactericidal when combined with trimethoprim).

93
Q

Use of Sulfonamides

A

Gram ⊕, gram ⊝, Nocardia. TMP-SMX for simple UTI.

94
Q

SE of Sulfonamides

A

Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, Stevens-Johnson syndrome, kernicterus in infants, displace other drugs from albumin (eg, warfarin)

95
Q

Mech of resistance of Sulfonamides

A

Altered enzyme (bacterial dihydropteroate synthase), dec uptake, or inc PABA synthesis

96
Q

Clinical use of Dapsone

A

Leprosy (lepromatous and tuberculoid), Pneumocystis jirovecii prophylaxis, or treatment when used in combination with TMP.

97
Q

SE/ of Dapsone

A

Hemolysis if G6PD deficient, methemoglobinemia, agranulocytosis.

98
Q

SE of Trimethoprim

A

Hyperkalemia (high doses), megaloblastic anemia, leukopenia, granulocytopenia, which may be avoided with coadministration of leucovorin (folinic acid).

99
Q

Mech of Trimethoprim

A

Inhibits bacterial dihydrofolate reductase. Bacteriostatic

100
Q

Use of Trimethoprim?

A

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

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

101
Q

Ex of Flouroquinolones

A

Ciprofloxacin, enoxacin, norfloxacin, ofloxacin; respiratory fluoroquinolones—gemifloxacin, levofloxacin, moxifloxacin

102
Q

Mech of Flouroquinolones

A

Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV. Bactericidal. Must not be taken with antacids.

103
Q

Clinical use of Flouroquinolones

A

Gram ⊝ rods of urinary and GI tracts (including Pseudomonas), some gram ⊕ organisms, otitis externa

104
Q

SE/ of Flouroquinolones

A

GI upset, superinfections, skin rashes, headache, dizziness. Less commonly, can cause leg cramps and myalgias

105
Q

Flouroquinolones contraindicated in?

A

Contraindicated in pregnant women, nursing mothers, and children < 18 years old due to possible damage to cartilage. Some may prolong QT interval.

106
Q

SE/ of Flouroquinolones in ppl >60 yrs and in pt taking prednisone

A

May cause tendonitis or tendon rupture in people > 60 years old and in patients taking prednisone.

107
Q

Mech of resistance of flouroquinolones

A

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

108
Q

Daptomycin MoA

A

Lipopeptide that disrupts cell membranes of gram ⊕ cocci by creating transmembrane channels

109
Q

Clinical use of Daptomycin

A

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

110
Q

Why can’t Daptomycin be used in pneumonia?

A

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

111
Q

SE/ of Daptomycin

A

Myopathy, rhabdomyolysis.

112
Q

MoA of Metronidazole?

A

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

113
Q

Clinical use of Metronidazole?

A

Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C difficile). - Can be used in place of amoxicillin in H pylori “triple therapy” in case of penicillin allergy.

114
Q

SE/ of Metronidazole

A

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

115
Q
A
116
Q

Rifamycins

A

Inhibit DNA-dependent RNA polymerase.

117
Q

Clinical use of Rifamycins

A

Mycobacterium tuberculosis; delay resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H influenzae type b.

118
Q

SE/ of Rifamycins

A

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

119
Q

In patients with HIV, which rifamycin do we use?

A

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

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

120
Q

What is the mech of resistance of Rifamycins?

A

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

121
Q

Rifampin’s 4 R’s:

A
  • RNA polymerase inhibitor
  • Ramps up microsomal cytochrome P-450
  • Red/orange body fluids
  • Rapid resistance if used alone
122
Q

MoA of Isoniazid

A

dec synthesis of mycolic acids.

123
Q

_____ ____________ (encoded by _____) needed to convert INH to active metabolite

A

Bacterial catalaseperoxidase (encoded by KatG) needed to convert INH to active metabolite

124
Q

Only agent used as solo prophylaxis vs TB

A

Isoniazid

125
Q

Monotherapy for latent TB

A

Isoniazid

126
Q

SE of Isoniazid

A

Hepatotoxicity, P-450 inhibition, drug-induced SLE, anion gap metabolic acidosis, seizures (in high doses, refractory to benzodiazepines).

127
Q

What vitamin do we co-administer with Isoniazid?

A

Give vitamin B6 bc it can lead to vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia),

128
Q

MoA of Pyrazinamide

A

Pyrazinamide is a prodrug that is converted to the active compound pyrazinoic acid. Works best at acidic pH (eg, in host phagolysosomes).

129
Q

SE/ of Pyrazinamide & what disease?

A

Used for TB; hyperuricemia, hepatoxicity

130
Q

MoA of Ethambutol

A

dec carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

131
Q

Ethambutol SE/

A

Optic neuropathy (red-green color blindness, may be reversible). Pronounce “eyethambutol.

132
Q

Streptomycin MoA and use

A

Interferes with 30S component of ribosome.

2nd line Tx for TB

133
Q

Streptomycin Tox

A

tinnitus, vertigo, ataxia, nephrotox

134
Q

Prophylaxis - Exposure to meningococcal infection

A

Ceftriaxone, ciprofloxacin, or rifampin

135
Q

High risk for endocarditis and undergoing surgical or dental procedures prophylaxis

A

Amoxicillin

136
Q

History of recurrent UTIs - prophylaxis

A

TMP-SMX

137
Q

Malaria prophylaxis for travelers

A

Atovaquone-proguanil, mefloquine, doxycycline, primaquine, or chloroquine (for areas with sensitive species)

138
Q

Pregnant woman carrying group B strep

A

intrapartum penicillin G/ ampicillin

139
Q

Prevention of gonococcal conjunctivitis in newborn

A

Erythromycin ointment on eyes

140
Q

Prevention of postsurgical infection due to S aureus

A

Cefazolin

141
Q

Prophylaxis of strep pharyngitis in child with prior rheumatic fever

A

Benzathine penicillin G or oral penicillin V

142
Q
A
143
Q

MRSA Tx

A

vancomycin, daptomycin, linezolid, tigecycline, ceftaroline, doxycycline.

144
Q

VRE Tx

A

linezolid, tigecycline, and streptogramins (quinupristin, dalfopristin).

145
Q

Multidrug-resistant P aeruginosa, multidrug-resistant Acinetobacter baumannii

A

polymyxins B and E (colistin).

146
Q
A
147
Q
A
148
Q

MoA of Amphotericin B

A

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

149
Q

Use of Amphotericin

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+ because of altered renal tubule permeability.

150
Q

Tox of Amphotericin B, how to reduce it?

A

Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (“amphoterrible”).
Hydration dec nephrotoxicity.
Liposomal amphotericin dec toxicity.

151
Q

Use of Nystatin

A

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

152
Q

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

A

Flucytosine

153
Q

SE/ of Flucytosine

A

Bone marrow suppression.

154
Q

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

A

Azoles - Clotrimazole, fluconazole, isavuconazole, itraconazole, ketoconazole, miconazole, voriconazole.

155
Q

Tx for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types

A

Fluconazole

156
Q

Blastomyces, Coccidioides, Histoplasma, Sporothrix schenckii - Which azole can be used for them?

A

Itraconazole

157
Q

Which azoles for Topical fungal infections

A

Clotrimazole and miconazole

158
Q

Voriconazole used for?

A

for Aspergillus and some Candida

159
Q

Isavuconazole for ?

A

Serious Aspergillus/ Mucor

160
Q

SE/ of azoles

A

Testosterone synthesis inhibition (gynecomastia, especially with ketoconazole), liver dysfunction (inhibits cytochrome P-450).

161
Q

Inhibits the fungal enzyme squalene epoxidase.

A

Terbinafin

162
Q

Clinical use of Terbinafine

A

Dermatophytoses

163
Q

SE of Terbinafine

A

GI upset, headaches, hepatotoxicity, taste disturbance.

164
Q

Inhibit cell wall synthesis by inhibiting synthesis of β-glucan.

ex?

A

Echinocandins

Anidulafungin, caspofungin, micafungin

165
Q

The flushing that is a SE of Echinocandins is caused by ?

A

Histamine release

166
Q

Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (eg, nails).

A

Griseofulvin

167
Q

SE of Griseofulvin

A

Teratogenic, carcinogenic, confusion, headaches, disulfiram-like reaction, Inc cytochrome P-450 and warfarin metabolism.

168
Q

Rx for (toxoplasmosis),
(Trypanosoma brucei), (T cruzi),
(leishmaniasis).

A

Pyrimethamine (toxoplasmosis), suramin and melarsoprol (Trypanosoma brucei), nifurtimox (T cruzi), sodium stibogluconate (leishmaniasis).

169
Q

Permethrin

A

Permethrin (inhibits Na+ channel deactivation –> neuronal membrane depolarization),

170
Q

Malathion MoA

A

malathion (acetylcholinesterase inhibitor),

171
Q

Lindane - MoA and used for?

A

lindane (blocks GABA channels Ž neurotoxicity). Used to treat scabies (Sarcoptes scabiei) and lice (Pediculus and Pthirus).

PML (Pesty Mites and Lice) with PML (Permethrin, Malathion, Lindane), because they NAG you (Na, AChE, GABA blockade).

172
Q

What rx? Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to _____ species

A

Chloroquine;

Plasmodia

173
Q

Which species of Plasmodium can one not use Chloroquine for?

A

P falciparum (frequency of resistance in P falciparum is too high).

174
Q

Resistance to chloroquine - mech?

A

Resistance due to membrane pump that dec intracellular concentration of drug. Treat P falciparum with artemether/lumefantrine or atovaquone/proguanil

175
Q

Chloroquine Tox

A

Retinopathy; pruritus

176
Q

Helminth Tx

A

Pyrantel pamoate, Ivermectin, Mebendazole, Praziquantel, Diethylcarbamazine.

Helminths get PIMP’D.

177
Q

MoA of Mebendazole & Praziquantel?

A

Mebendazole (microtubule inhibitor), Praziquantel (inc Ca2+ permeability, inc vacuolization),

178
Q
A
179
Q
A
180
Q

Inhibit influenza neuraminidase –> dec release of progeny virus.

A

Oseltamivir, zanamivir

181
Q

Use of Oseltamivir, zanamivir

A

Treatment and prevention of both influenza A and B. Beginning therapy within 48 hours of symptom onset may shorten duration of illness

182
Q

inhibit viral DNA polymerase by chain termination

A

Acyclovir, famciclovir, valacyclovir

183
Q

How is Acyclovir (etc) activated? why does it not affect uninfected cells?

A

Guanosine analogs. Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells –> few adverse effects. Triphosphate formed by cellular enzymes

184
Q

Use of Acyclovir, Famciclovir, etc

A

HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSVinduced mucocutaneous and genital lesions as well as for encephalitis

185
Q

Tx for herpes zoster?

A

Famciclovir

186
Q

Which guanosine analog has best oral availability?

A

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

187
Q

SE of Acyclovir

A

Obstructive crystalline nephropathy and acute kidney injury if not adequately hydrated.

188
Q

Mech of resistance of Acyclovir

A

mutated viral thymidine kinase

189
Q

Ganciclovir MoA

A

5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase.

190
Q

Use of Ganciclovir?

A

CMV, esp in immunocompromised

191
Q

prodrug of Ganciclovir? advantage?

A

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

192
Q

SE of Ganciclovir?

A

Bone marrow suppression (leukopenia, neutropenia, thrombocytopenia), renal toxicity. More toxic to host enzymes than acyclovir.

193
Q

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.

A

Foscarnet

194
Q

How does Foscarnet bind/activate?

A

Binds to pyrophosphate-binding site of enzyme. Does not require any kinase activation.

195
Q

Use of Foscarnet?

A

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV

196
Q

Tox of Foscarnet?

A

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

197
Q

Preferentially inhibits viral DNA polymerase

A

Cidofovir

198
Q

Use of Cidofovir?

A

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

199
Q

SE of Cidofovir?

A

Nephrotoxicity

200
Q

How to avoid nephrotox of Cidofovir?

A

(coadminister with probenecid and IV saline to dec toxicity).

201
Q

Mech of NRTIs

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group)

202
Q

Which NRTI is a nucleotide? what’s the advantage?

A

Tenofovir is a nucleoTide; the others are nucleosides. All need to be phosphorylated to be active

203
Q

What drug is used to decrease fetal transmission?

A

ZDV can be used for general prophylaxis and during pregnancy to dec risk of fetal transmission

204
Q

Abacavir contraindicated when?

A

Abacavir contraindicated if patient has HLA-B*5701 mutation due to inc risk of hypersensitivity.

205
Q

Which NRTI is assoc with pancreatitis?

A

Didanosine

206
Q

How do you treat the SE of NRTIs?

A

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin)

207
Q

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

A

Delavirdine Efavirenz Nevirapine

208
Q

SE/ of NNRTIs?

A

Rash and hepatotox

209
Q

What do protease inhibitors do?

A

Assembly 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.

210
Q

Which protease inhibitor inhibits cyt p450?

A

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

211
Q

Tox of Protease inhibitors in gen?

A

Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy (Cushing-like syndrome).

212
Q

Tox of Indinavir?

A

Nephropathy, hematuria, thrombocytopenia

213
Q

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase - ex?

A

Dolutegravir Elvitegravir Raltegravir

214
Q

What lab parameter is inc by integrase (-)’rs?

A

Inc CK

215
Q

What does Enfurviritide bind to? What does that accomplish?

A

Binds gp41, inhibiting viral entry.

216
Q

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

A

Maraviroc

217
Q

Inhibits NS5A, a viral phosphoprotein that plays a key role in RNA replication, unknown exact mechanism?

A

Ledipasvir & Ombitasvir

(-) NS5A = -asvir

218
Q

Tox of Ledipasvir Ombitasvir?

A

headache diarrhea

219
Q

Inhibits NS5B, an RNA-dependent RNA polymerase acting as a chain terminator. Prevents viral RNA replication.

A

NS5B - Buvirs

Sofosbuvir
Dasabuvir

220
Q

Inhibits NS3/4A, a viral protease, preventing viral replication.

A

Grazoprevir
Simeprevir

221
Q

Tox of Grazoprevir, Simeprevir

A

Grazoprevir: Photosensitivity reactions, rash. Simeprevir: Headache, fatigue

222
Q

What enzyme is inhibited by Ribavirin?

A

IMP DH

223
Q

Tox of Ribavirin?

A

Hemolytic anemia, severe teratogen

224
Q
A

Step 1 2019 First Aid Flashcards (63 decks)

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