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Pharma drugs > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Penicillin G, V

MOA

A

> Binds penicillin-binding proteins (transpeptidases) and block them from cross-linking w/ peptidoglycan wall – loss of rigidity, susceptible to rupture.
Activates autolytic enzymes.

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2
Q

Penicillin G, V

Clinical use

A

> Bactericidal, Penicillinase-sensitive.
G(+) organisms (S. pneumoniae, GAS, Actinomyces).
G(-) cocci (N. meningitidis).
Spirochetes (T. pallidum).

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3
Q

Amoxicillin, Ampicillin

MOA

A

> Extended-spectrum, Bactericidal, Penicillinase-sensitive.
Binds to transpeptidases and blocks transpeptidase cross-linking w/ cell wall – susceptible to rupture.
Activates autolytic enzymes.

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4
Q 
Amoxicillin, Ampicillin
Clinical use (HHEELPSS)
A

> H. influenzae, H. pylori, E. coli, Enterococci, L. monocytogenes, Proteus, Salmonella, Shigella.
Combine w/ Clavulanic acid – protect against B-lactamase (co-amoxiclav).

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5
Q

Amoxicillin, Ampicillin

Toxicity

A

Pseudomembranous colitis (ex. C. difficile)

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6
Q

Dicloxacillin, Nafcillin, Oxacillin

MOA

A

> Narrow spectrum, Bactericidal, Penicillinase-resistant.
Binds to pencillin-binding protein and prevents them from cross-linking w/ cell wall – prone to rupture.
Activates autolytic enzymes.

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7
Q

Dicloxacillin, Nafcillin, Oxacillin

[Clinical use, Toxicity]

A

> S. aureus (except MRSA due to altered penicillin-binding protein site).
Toxicity: interstitial nephritis.

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8
Q

Piperacillin, Ticarcillin

MOA

A

> Antipseudomonals, Extended spectrum. Penicillinase-sensitive.
Binds to transpeptidases and prevents them from cross-linking w/ cell wall – prone to rupture.
Activates autolytic enzymes.

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9
Q

Piperacillin, Ticarcillin

Clinical use

A 
Pseudomonas
G(-) rods
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10
Q

Beta-lactamase inhibitors (CAST)

A

Clavulanic acid
Sulbactam
Tazobactam
*Add to penicillin antibiotics

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11
Q

Cephalosporins

MOA

A

> B-lactam drugs – Inhibit cell wall synthesis

*Less susceptible to Penicillinase, unless structural change in binding site.

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12
Q

Cephalosporins

Toxicity

A 
Autoimmune hemolytic anemia.
Vit K deficiency.
Disulfiram-like reactions.
Cross-reaction w/ penicillins.
Inc. nephrotoxicity w/ aminoglycosides.
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13
Q

Cephalosporins don’t cover w/c organisms? (LAME)

A

Listeria
Atypicals (Chlamydia, Mycoplasma)
MRSA (except ceftaroline)
Enterococci

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14
Q

Cephalosporins, gen I

[Drug names, Clinical use]

A

Cefazolin, Cephalexin
>G(+) cocci
>Proteus, E. coli, Klebsiella (PEcK)
*Cefazolin before surgery for S.aureus infections

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15
Q

Cephalosporins, gen II

[Drug names, Clinical use]

A

Cefoxitin, Cefaclor, Cefuroxime.
>G(+) cocci.
>H. influenzae, Enterobacter, Neisseria, Serratia (HENS).
>Proteus, E.coli, Klebsiella (PEcK).
>Cefoxitin is the only one that covers G(+), G(-), and anaerobes.

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16
Q

Cephalosporins, gen III

[Drug names, Clinical use]

A 
Ceftriaxone, Cefotaxime, Ceftazidime.
G(-) resistant to other Beta-lactams.
Can penetrate CSF.
>Ceftriaxone: meningitis, gonorrhea, disseminated Lyme dse.
>Ceftazidime: Pseudomonas
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17
Q

Cephalosporins, gen IV

[Drug names, Clinical use]

A

Cefepime
G(-) organisms.
*Inc. activity vs Pseudomonas, G(+) organisms.

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18
Q

Cephalosporins, gen V

[Drug names, Clinical use]

A

Ceftaroline
Broad G(+/-) coverage
Includes MRSA
*Doesn’t include Pseudomonas

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19
Q

Carbapenems

Drug names

A

Imipenem, Meropenem, Ertapenem, Doripenem

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20
Q

Carbapenems

MOA

A

Inhibit cell wall synth by binding to penicillin-binding proteins (same MOA as penicillin).
>Imipenem: broad spectrum, Penicillinase-resistant; Administer w/ Cilastatin (inhibits renal dehydropeptidase I) – dec. inactivation in renal tubules.

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21
Q

Carbapenems

Clinical use

A

G(+) cocci, G(-) rods, anaerobes.

>Only use in life-threatening infections or if other drugs failed – major side effects

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22
Q

Carbapenems

Toxicity

A

CNS toxicity (seizures)
GI distress, skin rash
*Meropenem has less risk of seizure and more stable to dehydropeptidase I

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23
Q

Vancomycin

MOA

A

> Binds to D-ala D-ala of cell wall precursors – inhibits cell wall peptidoglycan formation.
Resistant bacteria have D-ala D-lac modification.

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24
Q

Vancomycin

Clinical use

A

G(+) only.

Includes MRSA, S. epidermidis, Enterococcus, C. difficile

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25
Q

Vancomycin

Toxicity

A

Generally well-tolerated.
Nephrotoxic, ototoxic.
*Thrombophlebitis – Red man syndrome: diffuse flushing due to nonspecific mast cell degranulation (pretreat w/ slow-infusing antihistamines).

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26
Q 
Aminoglycosides
Drug names (GNATS)
A

Gentamicin, Neomycin
Amikacin, Tobramycin
Streptomycin

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27
Q

Aminoglycosides

MOA

A

Bactericidal.
>Binds to 30s subunit – inhibits initiation complex – inhibits transcription of bacterial mRNA, causes misreading of mRNA.
>Needs O2 for uptake (useless w/ anaerobes).

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28
Q

Aminoglycosides

Clinical use

A 
Severe G(-) rod infections.
Synergistic w/ Beta-lactams
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29
Q

Aminoglycosides

Toxicity

A

Nephrotoxicity, Ototoxicity.
Neuromuscular blockade.
Teratogen.

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30
Q

Tetracyclines

Drug names

A

Tetracycline
Doxycycline
Minocycline

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31
Q

Tetracylines

[MOA, don’t give with what]

A

> Binds 30s subunit – prevents attachment of new AA-tRNA – inhibits protein elongation.
*CI w/ milk (Ca2+), Antacids (Ca2+, Mg2+), or iron-containing preparations (Fe2+) – divalent ions inhibit absorption.

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32
Q

Tetracyclines

[Clinical use, CI]

A

Borrelia, M. pneumoniae.
Rickettsia, Chlamydia (accumulates intracellularly).
Contraindicated in pregnancy.

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33
Q

Clindamycin

MOA

A

Bacteriostatic.

Blocks peptide transfer (translocation) at 50s subunit – blocks transfer of peptidyl-tRNA to P site.

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34
Q

Clindamycin

Clinical use

A

Anaerobic (Bacteroides, C. perfringens).
Aspiration pneumonia, lung abscesses, oral infections.
Invasive GAS infection.
*Treats anaerobic infxns ABOVE diaphragm (vs. metronidazole)

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35
Q

Clindamycin

Toxicity

A

Pseudomembranous colitis (C. difficile overgrowth)

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36
Q

Linezolid

[MOA, clinical use, toxicity]

A

Binds to 50s – no initiation complex – inhibits protein synthesis.
For G(+), MRSA, VRE.
Toxicity: bone marrow suppression, peripheral neuropathy, serotonin syndrome.

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37
Q

Macrolides

Drug names

A

Azithromycin
Clarithromycin
Erythromycin

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38
Q

Macrolides

MOA

A

Bacteriostatic.

Binds 23s rRNA (50s) – blocks translocation – inhibits protein synthesis.

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39
Q

Macrolides

Clinical use

A

Atypical pneumonias (Mycoplasma, Chlamydia, Legionella).
STI (chlamydia).
G(+) cocci (streps allergic to Penicillin).
B. pertussis.

40
Q

Macrolides

Toxicity (MACRO)

A 
Motility (GI) issues
Arrhythmia
Cholestatic hepatitis
Rash
Eosinophilia
41
Q

Trimethoprim

[MOA, clincal use]

A

> Inhibits bacterial dihydrofolate reductase; combined w/ sulfonamides.
For UTI, Shigella, Salmonella.
For P. jirovecii pneumonia prophylaxis and tx; Toxoplasmosis prophylaxis.

42
Q

Sulfonamides

MOA

A

Bacteriostatic. Inhibit folate synthesis. Compete w/ PABA to bind and inhibit dihydropteroate synthase.

43
Q

Sulfonamides

Clinical use

A

G(+/-)
Nocardia, Chlamydia
UTI (SMX)

44
Q

Sulfonamides

Toxicity

A

Hemolysis if G6PD deficient.
Nephrotoxic.
Photosensitivity.
Displaces other drugs from albumin (warfarin).

45
Q

Fluoroquinolones

Drug names

A

Ciprofloxacin, Norfloxacin
Levofloxacin, Ofloxacin
Moxifloxacin, Gemifloxacin
Enoxacin

46
Q

Fluoroquinolones

MOA

A

Bactericidal.
Inhibits prokaryotic topoisomerase II (DNA gyrase), topoisomerase IV.
*Don’t take w/ antacids

47
Q

Fluoroquinolones

Clinical use

A

G(-) rods of UT/GIT (Pseudomonas)

Neisseria

48
Q

Fluoroquinolones

Contraindications

A

> Pregnant women, Nursing mothers, Kids below 18 – possible cartilage damage.
Elderly over 60 y.o, prednisone-takers – tendonitis, tendon-rupture.

49
Q

Metronidazole

MOA

A

Bactericidal, Antiprotozoal.

>Forms toxic free radical metabs – DNA damage.

50
Q

Metronidazole

Clinical use

A

> Antiprotozoal: Giardia, Entamoeba, Trichomonas, Gardnerella.
Anaerobes: Bacteroides, C. difficile.
Triple therapy vs H.pylori (if w/ Pen allergy).
*Anaerobic infxns below diaphragm (vs. clindamycin).

51
Q

Rifampin, Rifabutin

[MOA, clinical use]

A

> Inhibits DNA-dependent RNA polymerase.
For M. tuberculosis, meningococcal prophylaxis, prophylaxis for contacts of pts w/ Hib.
Monotherapy leads to rapid resistance.

52
Q

Rifampin, Rifabutin

Toxicity

A

Orange body fluids.

Rifabutin favored in pts w/ HIV infection (less CYP450 stimulation).

53
Q

Isoniazid

[MOA, clinical use, toxicity]

A

> Inhibits mycolic acid synthesis.
For M. tuberculosis; can be used as solo prophylaxis against TB.
Neurotoxicity (give vit B6), hepatotoxicity.

54
Q

Pyrazinamide

[MOA, clinical use, toxicity]

A

MOA uncertain.
For M. tuberculosis
Toxicity: Hyperuricemia, hepatotoxicity

55
Q

Ethambutol

[MOA, clinical use, toxicity]

A

> Blocks arabinosyl transferase – inhibits carb polymerization of mycobacterial wall.
For M. tuberculosis.
Optic neuropathy (red-green color blindness).

56
Q

Drugs against MRSA organisms

A

Vancomycin, Daptomycin
Linezolid, Tigecylcine
Ceftaroline

57
Q

Drugs against VRE organisms

A

Linezolid

Streptogramins (quinupristin, dalfopristin)

58
Q

Tx for Multidrug-resistant P. aeruginosa

A

Polymyxins B and E (colistin)

59
Q

Amphotericin B

MOA

A

Binds ergosterol in fungal membranes – forms membrane pores – electrolytes leak out

60
Q

Amphotericin B

Clinical use

A

> Systemic mycoses.
Cryptococcus, Histoplasma, Blastomyces, Coccidioides, Candida, Mucor.
Supplement K and Mg (altered renal tubule permeability)

61
Q

Amphotericin B

Toxicity

A

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

62
Q

Nystatin

[MOA, clinical use]

A

> Binds to ergosterols in fungal membranes and creates pores – electrolyte leakage.
*Topical use only (too toxic for systemic).
For oral candidiasis (“swish and swallow”), diaper rash, vaginal candidiasis.

63
Q

Flucytosine

[MOA, clinical use, toxicity]

A

> Inhibits DNA and RNA synthesis (Uracil on fungal mRNA converted to 5-FU by cytosine deaminase).
For systemic mycoses (combined w/ AmphoB) – Cryptococcal meningitis.
Toxicity: Bone marrow suppression

64
Q

Azoles

Drug names

A

Clotrimazole, Fluconazole
Itraconazole, Ketoconazole
Miconazole, Voriconazole

65
Q

Azoles

MOA

A

Inhibit 14-alpha-demethylase (CYP450) – inhibits conversion of lanosterol to ergosterol (inhibit ergosterol synthesis).
*Ergosterol needed for fungal cell membrane

66
Q

Azoles

Clinical use

A

Local mycoses, less serious systemic mycoses.
>Fluconazole: cryptococcal meningitis in AIDS, candidal infections.
>Itraconazole: Blastomycoses, Coccidioides, Histoplasma.
>Clotrimazole, Miconazole: topical.

67
Q

Azoles

Toxicity

A 
Testosterone synthesis inhibition (ketaconazole, gynecomastia).
Liver dysfunction (inhibit CYP450).
68
Q

Terbinafine

[MOA, clinical use, toxicity]

A

> Inhibits squalene epoxidase – no lanosterol (ergosterol) synthesis.
For dermatophytes (onchymycosis).
Toxicity: taste disturbance, hepatotoxicity, GI upset.

69
Q

Echinocandins

[Names, MOA, use, toxicity]

A

Anidulafungin, Capsofungin, Micafungin.
>Inhibits B-glucan synth – inhibits fungal wall synth.
>For invasive aspergillosis, Candida.
>Toxicity: flushing (histamine release).

70
Q

Griseofulvin

[MOA, use, toxicity]

A

> Interferes w/ microtubule function; disrupts mitosis.
Oral tx of superficial infxns (dermatophytes).
Toxicity: carcinogenic, teratogenic, induces CYP450 and warfarin metab.

71
Q

Chloroquine

[MOA, use, toxicity]

A

> Blocks plasmodium Heme polymerase – blocks detoxification of heme into hemozoin – heme accumulates – toxic to plasmodia.
For Plasmodium (except P. falciparum w/c is often resistant).
Toxicity: retinopathy, pruritus

72
Q

Antiprotozoan therapy

Toxoplasmosis, T. brucei, T. cruzi, Leishmaniasis

A

> Toxoplasmosis: Pyrimethamine + Sulfadiazine.
T. brucei: Suramin (acute, blood-borne) and Melarsoprol (chronic, CNS penetration).
T. cruzi: Benznidazole, Nifurtimox.
Leishmaniasis: AmphoB, Sodium stibogluconate.

73
Q

Antihelminthic therapy

A 
Mebendazole
Pyrantel pamoate
Ivermectin
Diethylcarbamazine
Praziquantel
74
Q

Oseltamivir, Zanamivir

[MOA, use]

A

> Inhibit influenza neuraminidase – dec. release of viral progeny.
Tx and prevention of Influenza A and B

75
Q

Acyclovir, Famciclovir, Valacyclovir

[MOA, use, toxicity]

A

> Requires phosphorylation by viral thymidine kinase.
Inhibits viral DNAp by chain termination – inhibits viral replication.
For HSV, VZV; weak against EBV, nonactive against CMV.
Tox: obstructive crystalline nephropathy, ARF – hydrate well.

76
Q

Ganciclovir

[MOA, use, toxicity]

A

> Inhibits viral DNAp by chain termination.
For CMV.
Toxicity: leukopenia, neutropenia, thrombocytopenia, renal toxicity

77
Q

Foscarnet

MOA

A

> Viral DNAp/RNAp inhibitor, HIV reverse transcriptase inhibitor.
Binds to pyrophosphate-binding site.
*Doesn’t need phosphorylation by viral kinases.

78
Q

Foscarnet

[Clinical use, toxicity]

A

> CMV retinitis in IC patients when ganciclovir fails.
Acyclovir-resistant HSV.
Toxicity: nephrotoxic, electrolyte abnormalities can lead to seizures (Ca, PO, K).

79
Q

HAART therapy for HIV consists of what 3 types of drugs?

A

2 NRTI

1 NNRTI / Protease inhibitor / Integrase inhibitor

80
Q 
Protease inhibitors (-navir)
Drug names (at least 3)
A

Atazanavir, Darunavir
Fosamprenavir, Indinavir
Lopinavir, Ritonavir
Saquinavir

81
Q

Protease inhibitors

MOA

A

> HIV-1 protease (pol gene) cleaves polypeptide provirus into functional parts.
Protease inhibitors prevent this maturation of new viruses.

82
Q

Protease inhibitors

Toxicity, CI

A

Hyperglycemia, lipodystrophy.
Nephropathy, hematuria (indinavir).
*Contraindicated w/ Rifampin – can decrease protease inhibitor concentrations.

83
Q 
NRTIs
Drug names (at least 3)
A

Abacavir (ABC), Didanosine (ddl)
Emtricitabine (FTC), Lamivudine (3TC)
Stavudine (d4T), Tenofovir (TDF)
Zidovudine (ZDV, formerly AZT)

84
Q

NRTIs

MOA

A

> Inhibits HIV-DNA synthesis from RNA template by terminating DNA chain elongation.
Competitive RT inhibitors.
*Nucleosides need to be phosphorylated (Tenofovir is the only nucleotide).
*ZDV can be used in pregnancy to dec. fetal transmission.

85
Q

NRTIs

Toxicity

A

Bone marrow suppression
Lactic acidosis (nucleosides)
Anemia (ZDV)
Pancreatitis (didanosine)

86
Q 
NNRTIs
Drug names (3)
A

Delavirdine
Efavirenz
Nevirapine

87
Q

NNRTIs

MOA

A

> Allosteric RT inhibitors, terminates DNA chain elongation of HIV-DNA.
*Don’t require phosphorylation to be active or compete w/ nucleotides

88
Q

NNRTIs

Toxicity (esp Efavirenz), CI

A

Rash, hepatotoxicity.
>Efavirenz: vivid dreams, CNS sx
>CI in pregnancy: Efavirenz, Delavirdine

89
Q 
Fusion inhibitors (Efuvirtide, Maraviroc)
[MOA]
A

> Efuvirtide: binds gp41 – inhibits viral entry.
Maraviroc: binds CCR5 co-receptor on T cells and monocytes – inhibits interaction w/ gp120 (inhibits viral attachment).

90
Q

Interferons (alpha, beta, gamma)

Clinical use

A

> IFN-alpha: chronic hep B and C, Kaposi sarcoma, hairy cell leukemia, condyloma accuminata, RCC, malignant melanoma.
IFN-beta: multiple sclerosis.
IFN-gamma: CGD.

91
Q

Ribavirin

[MOA, use, toxicity]

A

> Inhibits IMP dehydrogenase – inhibits guanine synthesis.
For chronic HCV, also RSV.
Toxicity: hemolytic anemia, severe teratogen.

92
Q 
Integrase inhibitors (-gravir)
Drug names
A

Dolutegravir

Raltegravir

93
Q

Integrase inhibitors

MOA

A

Inhibits HIV-DNA integration into host genome

94
Q

Chloramphenicol

MOA

A

Bacteriostatic.

>Blocks peptidyltransferase at 50s subunit – blocks growing peptide from attaching to AA in A site.

95
Q

Chloramphenicol

Use, toxicity

A

> Meningitis (H. influenza, N. meningitides, S. pneumonia).
Rocky Mountain Spotted Fever (R. rickettsi).
Limited use due to Toxicity: anemia, aplastic anemia; gray baby syndrome (prematures lack liver UDP-glucuronyl transferase).

Pharma drugs (12 decks)

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