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Pharmacology II > Antimicrobials > Flashcards

Antimicrobials Flashcards

Antifungals/Antiparasitics/Antivirals

1
Q

Fungal infections

A

most commonly superficial involving the skin but if systemic can be severe and life-threatening (often affecting immunocompromised patients)

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2
Q

Amphotericin B MOA

A

a polyene (produced by Streptomyces nodosus) that is a lipophilic rod-like molecule that disrupts fungal cell wall synthesis by binding to sterols, primarily ergosterol, leading to the formation of pores in the cell membrane resulting in K+ leaking out of the cell and causing death

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3
Q

Amphotericin B spectrum of activity

A

used to treat severe invasive fungal infections with the widest spectrum of activity of all antifungals

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4
Q

Amphotericin B pharmacokinetics

A

used IV which has wide tissue distribution with rapid onset of action and is not dependent on the organism’s growth rate, has poor oral absorption and little CSF penetration - narrow therapeutic index

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5
Q

Amphotericin B adverse effects

A

reversible nephrotoxicity due to a dose-dependent decrease in GFR and vasoconstriction of afferent renal arterioles, infusion-related reactions (fever and rigors), nausea/vomiting, reversible anemia, phlebitis, and renal tubular acidosis with wasting of K+, Mg2+, and HCO3-

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6
Q

Amphotericin B contraindications

A

use with cyclosporine, tacrolimus, aminoglycosides can exacerbate nephrotoxicity, pre-existing renal insufficiency, intravascular volume depletion - hypotension

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7
Q

Flucytosine (5-FC) MOA

A

synthetic pyrimidine analog that inhibits thymidylate synthase and incorporates into fungal RNA disrupting nucleic acid and protein synthesis

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8
Q

Flucytosine spectrum of activity

A

used in combination with amphotericin B (synergistic) to treat systemic mycoses and meningitis caused by cryptococcus and candida species and in combination with itraconazole to treat chromoblastomycosis infections (not used as monotherapy due to high resistance)

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9
Q

Flucytosine resistance mechanism

A

fungi decrease the level of enzymes that are targeted by flucytosine

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10
Q

Flucytosine pharmacokinetics

A

has good oral absorption and penetrates CSF, dose adjustment required for renal impairment

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11
Q

Flucytosine adverse effects

A

most common are GI upset, N/V, and diarrhea, also reversible neutropenia, thrombocytopenia, dose-related bone marrow suppression, reversible hepatic dysfunction,

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12
Q

Ketoconazole MOA

A

an imidazole that inhibits C-14 alpha-demethylase decreasing synthesis of ergosterol thereby disrupting membrane structure

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13
Q

Ketoconazole spectrum of activity

A

used topically and orally to treat Candida, Histoplasma, Blastomyces, and Coccidioides infections

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14
Q

Ketoconazole contraindications

A

use with Amphotericin B and in pregnancy

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15
Q

Ketoconazole pharmacokinetics

A

requires gastric acid for dissolution and absorption (can’t be used with antacids, H2-histamine blockers, and PPIs), metabolized by CYP450 in the liver - low levels found in urine (cannot treat mycotic UTIs), does not penetrate CSF, inhibits human gonadal and adrenal steroid hormone synthesis

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16
Q

Ketoconazole resistance mechanism

A

mutations in the C-14 alpha-demethylase gene resulting in decreased binding of the drug and some strains have developed the ability to pump drug out of the cell

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17
Q

Ketoconazole adverse effects

A

Gi upset most common, hepatitis (monitor LFTs), gynecomastia, decreased libido, menstrual irregularities due to endocrine effect

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18
Q

the Imidazoles

A

ketoconazole, miconazole, and clotrimazole

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19
Q

the Triazoles

A

fluconazole, itraconazole, voriconazole, and posaconazole

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20
Q

Fluconazole MOA

A

a triazole that inhibits the synthesis of cell membranes via inhibition of C-14-alpha-demethylase, a fungal CYP450 enzyme similar to ketoconazole, however, it does not interfere with mammalian CYP450 enzymes involved in the synthesis of steroid hormones

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21
Q

Itraconazole MOA

A

a triazole that inhibits the synthesis of cell membranes via inhibition of C-14-alpha-demethylase, a fungal CYP450 enzyme similar to ketoconazole, however, it does not interfere with mammalian CYP450 enzymes involved in the synthesis of steroid hormones

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22
Q

Fluconazole spectrum of activity

A

used to treat Candida, Cryptococcus neoformans, and Coccidiomycosis infections (no activity against aspergillus)

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23
Q

Fluconazole pharmacokinetics

A

available orally and IV and not dependent on gastric acid for absorption, has good CSF penetration, requires dose adjustment for renal impairment

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24
Q

Fluconazole adverse effects

A

nausea, vomiting, rashes, alopecia, rare hepatitis, teratogenic

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25
Q

Fluconazole contraindications

A

in pregnancy (teratogenic)

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26
Q

Itraconazole MOA

A

a triazole that inhibits the synthesis of cell membranes via fungal CYP450 inhibition similar to ketoconazole, however, it does not interfere with mammalian CYP450 enzymes involved in the synthesis of steroid hormones

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27
Q

Itraconazole spectrum of activity

A

broad spectrum of activity and is the drug of choice for the treatment of histoplasmosis, blastomycosis, Coccidioidomycosis, and sporotrichosis infections

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28
Q

Itraconazole pharmacokinetics

A

has good oral bioavailability but requires gastric acid for absorption (no IV formulation available), metabolized in the liver, does not require dose adjustment for renal impairment, does not penetrate CSF well

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29
Q

Itraconazole adverse effects

A

nausea, vomiting, rash, headache, hypertension, hypokalemia, edema, rare hepatitis, alopecia with chronic therapy, teratogenic

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30
Q

Itraconazole contraindications

A

in pregnancy (teratogenic), in patients with CHF or history of CHF

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31
Q

Caspofungin MOA

A

an echinocandins that inhibits B(1,3)-D-glucan synthase which is an enzyme involved in fungal wall synthesis

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32
Q

Caspofungin spectrum of activity

A

used to treat Candida glabrata infections and azole-resistant Candida esophagitis, used second line to treat invasive aspergillus infections (not active against Zygomycetes and Cryptococcus neoformans), has poor CNS penetration

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33
Q

Caspofungin adverse effects

A

generally well tolerated, only thing is histamine infusion reaction which can be pretreated with diphenhydramine

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34
Q

Caspofungin drug interactions

A

use with cyclosporine, tacrolimus, and rifampin

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35
Q

DOC for treatment for invasive aspergillus infections

A

Voriconazole

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36
Q

Nystatin MOA

A

a polyene that binds to ergosterol and disrupts fungal cell wall synthesis leading to the formation of pores in the cell membrane resulting in K+ leaking out of the cell and causing death

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37
Q

Nystatin clinical indications

A

used topically (powder, cream, ointment) or as an oral suspension to treat fungal skin/vaginal/mouth infections

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38
Q

Nystatin pharmacokinetics

A

too toxic for systemic use (never used IV), not absorbed from the GI tract

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39
Q

Griseofulvin MOA

A

inhibits mitosis by interfering with microtubules

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40
Q

Griseofulvin clinical indications

A

used to treat dermatophytic nail infections due to accumulation in keratin-containing tissues - treatment may be required for 6-12 months

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41
Q

Griseofulvin drug interactions

A

induces CYP450 and increases the rate of metabolism of other drugs including warfarin

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42
Q

Itraconazole drug interactions

A

warfarin, statins, and phenytoin

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43
Q

Ketoconazole drug interactions

A

cyclosporine, phenytoin, tolbutamide, warfarin, and rifampin

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44
Q

Terbinafine MOA

A

inhibits cell wall synthesis by inhibiting fungal squalene epoxidase decreasing the synthesis of ergosterol

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45
Q

Terbinafine clinical indications

A

DOC for treatment of onychomycosis and dermatophytic infections due to accumulation in skin, nails, and fat

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46
Q

Terbinafine contraindications

A

in nursing mothers due to accumulation in breast milk

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47
Q

Terbinafine adverse effects

A

hepatotoxicity - needs LFTs at baseline

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48
Q

DOC for the treatment of Coccidioidomycosis

A

Fluconazole or Itraconazole, if severe/disseminated then Amphotericin B

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49
Q

DOC for the treatment of Histoplasmosis

A

Itraconazole

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50
Q

DOC for the treatment of Blastomycosis

A

Itraconazole

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51
Q

DOC for the treatment of Aspergillus

A

1st line = Voriconazole, then Posaconazole, then Caspofungin, and then Amphotericin B

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52
Q

DOC for the treatment of Zygomycetes

A

1st line = Posaconazole, then Amphotericin B

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53
Q

Metronidazole MOA

A

contains a nitro group that serves as an electron acceptor and forms toxic metabolites that disrupt DNA helical structure leading to cell death when activated by anaerobes

54
Q

Metronidazole spectrum of activity

A

active against amebiasis, giardiasis, trichomoniasis, and anaerobic bacteria, considered tissue agent and co-administered with luminal agent Paromomycin

55
Q

Metronidazole pharmacokinetics

A

metabolized in liver and accumulates in patients with severe hepatic disease, excreted in urine

56
Q

Metronidazole adverse effects

A

GI upset, metallic taste, seizures, neuropathy, disulfiram effect with alcohol

57
Q

Griseofulvin contraindication

A

use with alcohol

58
Q

Metronidazole contraindications

A

in pregnancy, breastfeeding, and in recent use with disulfiram

59
Q

Alternatives to Metronidazole

A

tinidazole, ornidazole, and nitazoxanide

60
Q

Trimethoprim-Sulfamethoxazole (TMP-SMX) MOA

A

combination of TMP-SMX provides sequential and synergistic blockade of folate pathway which leads to the inhibition of thymidine synthesis

61
Q

TMP-SMX spectrum of activity

A

active against Cyclospora and Isospora infections

62
Q

TMP-SMX adverse effects

A

rash, SJS, kernicterus, hemolysis in G6PD deficiency, bone marrow suppression, anemia, renal impairment, and hepatotoxicity

63
Q

TMP-SMX contraindications

A

caution in patients with renal disease, contraindicated in newborns (<2 months) and pregnancy

64
Q

TMP-SMX drug interactions

A

warfarin, phenytoin, and methotrexate

65
Q

Albendazole MOA

A

binds to microtubules in intestinal and tegmental worms and larvae impairing glucose uptake, leading to glycogen depletion, degeneration of ER and mitochondria, release of lysosomes, and depletion on ATP/energy causing helminth/worm death

66
Q

Albendazole spectrum of activity

A

broadly effective against nematode infections (roundworms)

67
Q

Albendazole adverse effects

A

headache, elevated LFTs, rarely GI upset and alopecia, and very rarely liver failure, myelosuppression, and seizures, teratogenic

68
Q

Albendazole contraindication

A

in pregnancy (teratogenic)

69
Q

Pyrantel Pamoate MOA

A

causes the release of acetylcholine and inhibits cholinesterase, acts as a depolarizing neuromuscular blocker, and spastic paralysis and release of helminths

70
Q

Pyrantel Pamoate spectrum of activity

A

alternative to albendazole therapy for the treatment of Enterobius vermicularis (pinworms) infections, however, not preferred agent

71
Q

Pyrantel Pamoate adverse effects

A

rare headache, dizziness, and GI distress

72
Q

Praziquantel MOA

A

increases cell permeability to Ca2+ in schistosomes causing strong contractions and paralysis of helminth musculature which leads to detachment, dislodgement, and death

73
Q

Praziquantel spectrum of activity

A

active against cestodes (tapeworms) and trematodes (flukes and Schistosoma)

74
Q

Praziquantel adverse effects

A

abdominal pain, dizziness, and drowsiness (CNS side effects such as headache and seizures in patients with cerebral cysticercosis from the death of the parasites)

75
Q

Praziquantel pharmacokinetics

A

extensively metabolized by CYP3A4, avoid co-administration with CYP inducers

76
Q

Ivermectin MOA

A

binds to and activates glutamate-gated chloride channels in invertebrate nerve and muscle cells causing hyperpolarization and death of the helminth, does not cross the BBB

77
Q

Ivermectin spectrum of activity

A

active against strongyloidiasis and onchocerciasis (river blindness) and used topically for treatment of head lice

78
Q

Ivermectin adverse effects

A

neurotoxicity (CNS depression, ataxia) from activation of GABA-ergic synapses and some cutaneous effects

79
Q

Ivermectin contraindications

A

in pregnancy and meningitis

80
Q

Oseltamivir MOA

A

inhibitor of neuraminidase which is an enzyme essential for cleaving the virus from the host cell and allowing the spread of the virus from cell to cell

81
Q

Oseltamivir spectrum of activity

A

effective in decreasing Influenza A and B viral load and shortening the course of disease by 1-2 days if administered within 48 hours of symptoms onset, also can be administered prophylactically

82
Q

Oseltamivir pharmacokinetics

A

administered orally and is a prodrug that is hydrolyzed in the liver to its active form, required dose adjustment in renal impairment

83
Q

Oseltamivir adverse effects

A

most commonly nausea and/or vomiting (recommend taking with food to minimize GI effects)

84
Q

Patients considered high risk for influenza complications

A

children < 2 years old or adults > 65 years old, persons with comorbidities or who are immunocompromised, pregnant women, persons morbidly obese, nursing home residents or residents of chronic care facilities

85
Q

Acyclovir MOA

A

activated by viral thymidine kinase (TK) into acycloGTP (a guanosine analog) which inhibits viral DNA polymerase and terminates viral transcription

86
Q

Acyclovir spectrum of activity

A

active against Herpes simplex viruses (HSV) 1 and 2 and Varicella-zoster (VZV) which causes chickenpox and zoster, no activity against CMV or latent Herpes viruses

87
Q

Acyclovir pharmacokinetics

A

administered orally or through IV and metabolized by the kidneys, has poor oral bioavailability so requires frequent dosing, requires dose adjustment in renal impairment

88
Q

Acyclovir adverse effects

A

generally well tolerated, more side effects with IV administration - most common is GI upset, nephrotoxicity due to IV acyclovir crystallization in renal tubules causing obstruction, and neurotoxicity causing lethargy, confusion, and delirium

89
Q

Valacyclovir MOA

A

a valine ester of acyclovir and prodrug that is hydrolyzed by first-pass metabolism in the intestine and liver with a 99% conversion rate to acyclovir, requires less frequent dosing in comparison to acyclovir (but 5x more expensive)

90
Q

Valacyclovir spectrum of activity

A

active against Herpes simplex viruses (HSV) 1 and 2 and Varicella-zoster (VZV) which causes chickenpox and zoster, no activity against CMV or latent Herpes viruses

91
Q

Valacyclovir adverse effects

A

same adverse effects as acyclovir but headache more common with valacyclovir

92
Q

Famciclovir MOA

A

metabolized to penciclovir via phosphorylation by viral thymidine kinase (TK) in infected cells which activates it where it then selectively inhibits viral DNA polymerase by termination of transcription

93
Q

Famciclovir adverse effects

A

same as acyclovir

94
Q

Famciclovir spectrum of activity

A

same as acyclovir

95
Q

Acyclovir resistance mechanism

A

mutation or loss of viral thymidine kinase (TK) which is the first step in the phosphorylation of acyclovir with 6-8% incidence in immunocompromised hosts

96
Q

Foscarnet MOA

A

inorganic pyrophosphate analog that directly inhibits DNA polymerase by reversibly blocking the pyrophosphate binding site of viral DNA polymerase (does not require activation by viral TK)

97
Q

Foscarnet spectrum of activity

A

active against CMV retinitis and mucocutaneous acyclovir-resistant HSV in immunocompromised patients and VZV infections

98
Q

Foscarnet pharmacokinetics

A

available only in IV form and requires dose adjustment for renal impairment

99
Q

Foscarnet adverse effects

A

GI upset, electrolyte abnormalities including hypokalemia, hypocalcemia, hypomagnesemia, and hypophosphatemia, also reversible nephrotoxicity worsened by concomitant use of nephrotoxic agents (Amphotericin B, cyclosporine, tacrolimus, and aminoglycosides)

100
Q

Interferons MOA

A

host cytokines (proteins) with complex antiviral, immunomodulatory, and anti-proliferative activities thought to induce gene transcription of host cell enzymes that inhibit viral RNA, increase phagocytic activity of macrophages, and increase cytotoxicity of lymphocytes for target cells

101
Q

Interferons clinical indications

A

used to treat HBV and HCV as part of a combination but rarely used as first-line choice

102
Q

Interferons adverse effects

A

flu-like symptoms shortly after admin, mood disorders, depression, somnolence, confusion, profound fatigue, weight loss, seizures, myelosuppression, rash, cough, myalgia, alopecia, tinnitus, reversible hearing loss, retinopathy, pneumonitis, cardiotoxicity, and autoimmune reaction

103
Q

Interferons pharmacokinetics

A

administered IV or subcutaneously, no oral formulation, require dose adjustment with renal disease (if CrCl < 10)

104
Q

Goals of HBV antiviral treatment

A

suppression of HBV DNA levels, seroconversion of HBeAg-positive to HBeAg-negative, loss of HBsAg detection, and decrease the risk of liver damage due to necrosis, failure, and hepatocellular carcinoma

105
Q

Lamivudine MOA

A

cytosine analog that works to inhibit viral DNA synthesis by inhibiting HBV DNA polymerase, also works against HIV reverse transcriptase

106
Q

Lamivudine clinical indications

A

used to treat chronic Hep B infections and may be used in combination with other Hep B antivirals in the treatment of HIV-HBV co-infections, requires HIV testing prior to treatment initiation

107
Q

Lamivudine pharmacokinetics

A

has good oral bioavailability and requires dose adjustment in renal impairment (if CrCl < 50)

108
Q

Lamivudine adverse effects

A

generally well tolerated, can cause headache, dizziness, pancreatitis, and rarely lactic acidosis and severe hepatomegaly

109
Q

Entecavir MOA

A

phosphorylated to guanosine triphosphate (GTP) and competitively inhibits HBV DNA polymerase

110
Q

Entecavir clinical indications

A

used to treat chronic Hep B infections and weakly active against HIV (not recommended for use in HIV-HBV co-infections without a fully suppressive anti-HIV regimen as it may cause resistance to lamivudine), also not preferred for lamivudine-resistant HBV strains

111
Q

Entecavir pharmacokinetics

A

requires dose adjustment in renal impairment (CrCl < 50)

112
Q

Entecavir adverse effects

A

may cause increased ALT levels, mild GI upset, mild hyperglycemia, headache, and rarely lactic acidosis and hepatomegaly

113
Q

Tenofovir MOA

A

inhibits replication of HBV by inhibiting HBV DNA polymerase, also works against HIV reverse transcriptase

114
Q

Tenofovir clinical indications

A

used to treat chronic Hep B infections and may be used in patients who have had prior treatment or developed drug resistance, preferred if there is lamivudine resistance, HIV testing required prior to treatment initiation

115
Q

Tenofovir pharmacokinetics

A

2 formulations are available: tenofovir disoproxil fumarate and tenofovir alafenamide (associated with less renal and bone toxicity), dose adjustment is required in renal impairment (CrCl < 50)

116
Q

Tenofovir adverse effects

A

GI upset, rash, hypercholesterolemia, decreased bone mineral density, and rarely lactic acidosis and hepatomegaly

117
Q

Black Box Warning for anti-hep B therapy discontinuation

A

severe acute exacerbations of hepatitis have been reported in hepatitis B virus-infected patients who have discontinued anti-hep B therapy (must monitor liver function closely for several months in patients who discontinue therapy to avoid this)

118
Q

Goal of chronic HCV treatment

A

eradicate the virus where the response to therapy is measured by looking at the sustained virologic response (SVR) which is determined by measuring HCV RNA (quantitative assay) and eradication = undetectable RNA levels after 12 weeks of therapy

119
Q

Ribavirin MOA

A

inhibits guanine nucleotide synthesis thereby inhibiting viral transcription and RNA replication

120
Q

Ribavirin clinical indications

A

used for the treatment of Hep C (oral administration in combo with interferon) and also may be used for the treatment of severe pediatric RSV infections (aerosol)

121
Q

Ribavirin adverse effects

A

hemolytic anemia

122
Q

Ledipasvir MOA

A

direct-acting antiviral that inhibits NS5A protein which plays a role in both Hep C viral replication and viral assembly

123
Q

Ledipasvir pharmacokinetics

A

administered orally in combination with other direct-acting antivirals and also available in combination treatment with sofosbuvir, increased gastric pH levels may decrease absorption

124
Q

Ledipasvir adverse effects

A

generally well tolerated, expensive

125
Q

Sofosbuvir MOA

A

direct-acting antiviral that inhibits NS5B protein which plays a role in both Hep C viral replication and viral assembly

126
Q

Sofosbuvir pharmacokinetics

A

administered orally in combination with ledipasvir and/or protease inhibitors, expensive

127
Q

Sofosbuvir adverse effects

A

generally well tolerated but may cause fatigue, headache, and insomnia, if used with amiodarone can cause symptomatic bradycardia and a fatal cardiac arrest

128
Q

Sofosbuvir contraindications/drug interactions

A

use with rifampin, rifapentine, carbamazepine, phenytoin, phenobarbital, oxcarbazepine, and tipranavir/ritonavir (used for HIV)

129
Q

Ledipasvir-Sofosbuvir clinical indications

A

administered orally as a single combination tablet with or without ribavirin for treatment of hepatitis C depending on the patient

130
Q

Ledipasvir-Sofosbuvir adverse effects

A

generally well tolerated but can cause fatigue, headache, and insomnia

131
Q

Ledipasvir-Sofosbuvir contraindications

A

avoid in patients with severe renal impairment (CrCl < 30) and coadministration with amiodarone due to symptomatic bradycardia and fatal cardiac arrest

132
Q

Ledipasvir-Sofosbuvir drug interactions

A

potential drug interactions due to the presence of Sofosbuvir

Pharmacology II (5 decks)

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