Antimicrobials Flashcards

1
Q

Pencillin G, V

A

MOA: Prototype β-lactam antibiotics. D-Ala-D-Ala structural analog. Bind PBPs (transpeptidases). Block transpeptidase cross-linking of peptidoglycan cell wall. Activate autolytic enzymes.

Use: Mostly used for gram ⊕ organisms (S pneumoniae, S pyogenes, Actinomyces). Also used for gram ⊕ cocci, gram ⊕ rods, gram ⊖cocci, and spirochetes. Penicillinase sensitive.

Adverse Effects: Hypersensitivity reactions, direct Coombs ⊕ hemoltyic anemia.

Resistance: Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring

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2
Q

Penicillinase-sensitive penicillins.

A

Amoxicillin, ampicillin, aminopenicillins

MOA: Wider spectrum. Also combine with clavulanic acid to protect against destruction against β-lactamase.

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

Adverse Effects: Hypersensitivity reactions; rash; pseudomembrane colitis.

Resistance: Pencillinase in bacteria cleaves β-lactam ring

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3
Q

Penicillinase-resistant penicilins

A

Dicloxacillin, nafcillin, oxacillin

MOA: Narrow spectrum; penicillinase resistant because bulky R rings blocks access of β-lactamases to β-lactam ring

Use: S aureus (except MRSA; resistant because of altered penicillin-binding protein target site)

Adverse Effects: Hypersensitivity reactions, interstitial nephritis

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4
Q

What are examples of β-lactamase inhibitors? How do they work?

A

Clavulanic acid, sulbactam, tazobactam.

Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamases

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5
Q

Cephalosporins (MOA, Adverse Effects, and Mechanism of Resistance)

A

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

Adverse Effects: Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency. Exhibit cross-reactivity with penicillins. ↑ nephrotoxicity of aminoglycosides

Resistance: Structural change in penicillin-binding proteins (transpeptidases)

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6
Q

What are the 1st generation cephalosporins and what are they used for?

A

Cefazolin, cephalexin

Use: Gram ⊕ cocci, Proteus mirabilis, E coli, Klebsiella pneumoniae. Cefazolin used before surgery to prevent S aureus wound infections

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7
Q

What are the 2nd generation cephalosporins and what are they used for?

A

Cefaclor, cefoxitin, cefuroxime

Use: Gram ⊕ cocci, H influenzae, Enterobacter aerogenes, Neisseria spp., Serratia marcescens, Proteus mirabilis, E. coli, Klebsiella pneumoniae

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8
Q

What are the 3rd generation cephalosporins and what are they used for?

A

Ceftriaxone, cefotaxime, ceftazidime

Use: Serious gram ⊖ organisms resistant to other β-lactams
Ceftriaxone: meningitis, gonorrhea, disseminated Lyme disease
Ceftazidime: Pseudomonas

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9
Q

What are the 4th generation cephalosporins and what are they used for?

A

Cefepime

Use: Gram ⊖ organisms with ↑ activity against Pseudomonas and gram ⊕ organisms

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10
Q

What are the 5th generation cephalosporins and what are they used for?

A

Ceftaroline

Use: Broad gram ⊕ and gram ⊖ organisms, including MRSA; does not cover Pseudomonas.

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11
Q

Carbapenems

A

Imipenem, meropenem, ertapenem, doripenem

MOA: Imipenem is a broad-spectrum, β-lactamase-resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehyropeptidase I) to ↓ inactivation of drug in renal tubules.

Use: Gram ⊕ cocci, gram ⊖ rods, and anaerobes. Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.

Adverse Effects: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels

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12
Q

Monobactams (aztreonam)

A

MOA: Less susceptible to β-lactamases. Prevents peptidoglycan cross-linking by binding to PBP 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins.

Use: Gram ⊖ rods - no activity against gram ⊕ rods or anaerobes. For penicillin-allergic patients ad those with renal insufficiency who cannot tolerate aminoglycosides.

Adverse Effects: Usually nontoxic; occasionally GI upset

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13
Q

Vancomycin

A

MOA: Inhibits cell wall peptidogylcan formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal against most bacteria (bacteriostatic against C difficile). Not susceptible to β-lactamases.

Use: Gram ⊕ bugs only - serious, multidrug-resistant organisms including MRSA, S epidermidis, sensitive Enterococcus species, and C difficile

Adverse Effects: Well tolerated in general. Nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing.

Mechanism of Resistance: Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac

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14
Q

Aminoglycosides

A

Gentamicin, neomycin, amikacin, tobramycin, streptomycin

MOA: Bactericidal; irreversible inhibition of initiation complex through binding of 30S subunit. Can cause misreading of mRNA. Also block translocation. Require O2 for uptake; therefore ineffective for anaerobes.

Use: Severe gram ⊖ rod infectons. Synergistic with β-lactam antibiotics. Neomycin for bowel surgery

Adverse Effects: Nephrotoxicity, neuromuscular blockade, ototoxicity, teratogen.

Resistance: Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

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15
Q

Tetracyclines

A

Tetracycline, doxycycline, minocycline

MOA: Bacteriostatic; bind 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 with milk, antacids, or iron-containing preparations because divalent cations inhibit drug gut absorption.

Use: Borrelia burgdorferi, M pneumoniae. Drugs’ ability to accumulate intracellularly make them effective against Rickettsia and Chlamydia. Also used to treat acne.

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

Resistance: ↓ uptake or ↑ efflux out of bacterial cells by plasmid-encoded transport pumps

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16
Q

Chloramphenicol

A

MOA: Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic.

Use: Meningitis (H influenzae, N meningitidis, S pneumoniae) and Rocky Mountain spotted fever (Rickettsia rickettsii)

Adverse Effects: Anemia (dose-dependent), aplastic anemia (dose-independent), gray baby syndrome (in premature infants because they lack liver UDPGT

Resistance: Plasmid-encoded acetyltransferase inactivates the drug

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17
Q

Clindamycin

A

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

Use: Anaerobic infections (Bacteroides spp, Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections. Also effective against invasive group A streptococcal infection.

Adverse Effects: Pseudomembrane colitis, fever, diarrhea.

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18
Q

Oxazolidinones (linezolid)

A

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

Use: Gram ⊕ species including MRSA and VRE

Adverse Effects: Bone marrow suppression (especially thrombocytopenia),peripheral neuropathy, serotonin syndrome.

Resistance: Point mutation of ribosomal RNA.

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19
Q

Macrolides

A

Azithromycin, clarithromycin, erythromycin.

MOA: Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.

Use: Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STIs (chlamydia), gram ⊕ cocci (streptococcal infections), and B pertussis.

Adverse Effects: GI motility issues, Arrhythmia caused by prolonged QT interval, acute cholestatic hepatitis, rash, eosinophilia. Increases concentration of theophyline, oral anticoagulants. Clarithromycin and erythromycin inhibit cytochrome P-450.

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

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20
Q

Sulfonamides

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

MOA: Inhibit dihydropteroate synthase, thus inhibiting folate synthesis. Bacteriostatic (bactericidal when combined with trimethoprim)

Use: Gram-⊕, gram ⊖, Nocardia, Chlamydia, SMX for simple UTI

Adverse Effects: Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (interstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (eg. warfarin)

Resistance: Altered enzyme (bacterial dihydropteroate synthase), ↓ uptake, or ↑ PABA synthesis

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21
Q

Dapsone

A

MOA: Similar to sulfonamides (but structurally distinct)

Use: Leprosy (lepromatous and tuberculoid), Pneumocystis jiroveii prophylaxis

Adverse Effects: Hemolysis if G6PD deficient

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22
Q

Trimethoprim

A

MOA: Inhibits bacterial dihydrofolate reductase. Bacteriostatic.

Use: Used in combination with sulfonamides, causing sequential block of folate synthesis. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pnuemonia treatment and prophylaxis, toxoplasmosis prophylaxis.

Adverse Effects: Bone marrow suppression (megaloblastic anemia, leukopenia, granulocytopenia). May alleviate with supplemental folic acid.

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23
Q

Fluoroquinolones

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enxoacin

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

Contraindications: Must not be taken with antacids. Pregnant, nursing women, and children and in patients taking prednisone.

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

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24
Q

Daptomycin

A

MOA: Lipopeptide that disrupts cell membrane of gram ⊕ cocci.

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

Adverse Effects: Myopathy, rhabdomyolysis.

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25
Q

Metronidazole

A

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

Use: Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C difficile). Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H pylori.

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

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26
Q

Prophylaxis and treatment for M tuberculosis

A

Prophylaxis: Isoniazid

Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol

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27
Q

Prophylaxis and treatment for M avium - intracellulare

A

Prophylaxis: Azithromycin, rifabutin

Treatment: More drug resistant than M tuberculosis. Azithromycin or clarithromycin +/ ethambutol. Can add rifabutin or ciprofloxacin.

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28
Q

Treatment of M leprae

A

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

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29
Q

Rifamycins

A

Rifampin, rifabutin

4 Rs: RNA polymerase inhibitor, Ramps up microsomal cytochrome P-450, Red/orange body fluids, Rapid resistance if used alone.

MOA: Inhibit DNA-dependent RNA polymerase

Use: Mycobacterium tuberculosis; delay resistance to dapsone when used for leprosy. Used in meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenza type B.

Adverse Effects: Minor hepatotoxicity and drug interactions (↑ cytochrome P-450); orange body fluids (nonhazardous side effect). Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.

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

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30
Q

Isoniazid

A

MOA: ↓ synthesis of mycolic acids. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolites.

Use: M tuberculosis (only agent used as solo prophylaxis, also used as monotherapy for latent TB)

Adverse Effects: Hepatotoxicity, P-450 inhibition, drug-induced SLE, vitamin B6 deficiency (peripheral neuropathy, sideroblastic anemia). Administer with vitamin B6

Resistance: Mutations leading to underexpression of KatG

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31
Q

Pyrazinamide

A

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

Use: M tuberculosis

Adverse Effects: Hyperuriemia, hepatotoxicity

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32
Q

Ethambutol

A

MOA: ↓ carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

Use: M tuberculosis

Advers Effects: Optic neuropathy (red-green color blindness)

33
Q

Streptomycin

A

MOA: Interferes with 30S component of ribosome.

Use: M tuberculosis (2nd line)

Adverse Effects: Tinnitus, vertigo, ataxia, nephrotoxicity

34
Q

Prophylaxis for patients with high risk for endocarditis and undergoing surgical or dental procedures

A

Amoxicillin

35
Q

Prophylaxis after exposure to gonorrhea

A

Ceftriaxone

36
Q

Prophylaxis for a history of recurrent UTIs

A

TMP-SMX

37
Q

Prophylaxis after exposure to meningococcal infection

A

Ceftriaxone, ciprofloxacin, or rifampin

38
Q

Prophylaxis for pregnant woman carrying group B strep

A

Intrapartum penicillin G or ampicillin

39
Q

Prophylaxis for prevention of gonococcal conjunctivitis in newborn

A

Erythromycin ointment

40
Q

Prophylaxis for prevention of postsurgical infection due to S aureus

A

Cefazolin

41
Q

Prophylaxis for strep pharyngitis in child with prior rheumatic fever

A

Benzathine penicillin G or oral penicillin V

42
Q

Prophylaxis for exposure to syphilis

A

Benzathine penicillin G

43
Q

Treatment of MRSA

A

Vancomcyin, daptomycin, linezolid, tigecycline, ceftaroline

44
Q

Treatment of VRE

A

Linezolid and streptogramins (quinupristin, dalfopristin)

45
Q

Treatment of multi-drug resistant P aeruginosa, Acinetobacter baumannii

A

Polymyxins B and E (colistatin) (Bind to, disrupt, and interfere with permeability of cytoplasmic membrane)

46
Q

Amphotericin B

A

MOA: Binds ergosterol; forms membrane pore that allows leakage of electrolytes

Use: Serious, systemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Histoplasma, Candida, Mucro. Intrathecally for fungal meningitis Suppmement K+ and Mg2+ because of altered renal tubule permeability.

Adverse Effects: Fever/chills, hypotension, nephrotoxicity, arrhythmias, anemia IV phlebitis. Hydration ↓ nephrotoxicity. Liposomal amphotericin ↓ toxicity

47
Q

Nystatin

A

MOA: Binds ergosterol; forms membrane pores that allow leakage of electrolytes. Topical use only as too toxic for systemic use.

Use: “Swish and swallow” for oral candidiasis; topical for diaper rash or vaginal candidiasis

48
Q

Flucytosine

A

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

Use: Systemic fungal infections (especially meningitis caused by Cryptococcus) in combination of amphotericin B

Adverse Effects: Bone marrow suppression

49
Q

Azoles

A

Clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, voriconazole

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

Use: Local and less serious systemic mycoses.
Fluconazole: Chrnic suppression of cryptococcal meningitis in AIDS patients and candidal infection of all types
Itraconazole: Blastomyces, Coccidioides, Histoplasma
Clotrimazole & miconazole: Topical fungal infections

Adverse Effects: Testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450).

50
Q

Terbinafine

A

MOA: Inhibits the fungal enzyme squalene epoxidase

Use: Dermatophytoses (especially onychomycosis - fungal infection of finger or toe nails)

Adverse Effects: GI upset, headaches, hepatotoxicity, taste disturbance

51
Q

Echinocandins

A

Anidulafungin, caspofungin, micafungin

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

Use: Invasive aspergillosis, Candida.

Adverse Effects: GI upset, flushing (by histamine release)

52
Q

Griseofulvin

A

MOA: Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissue (nails)

Use: Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm)

Adverse Effects: Teratogenic, carcinogenic, confusion, headaches, ↑ cytochrome P-450 and warfarin metabolism

53
Q

Treatment of toxoplasmosis

A

Pyrimethamine

54
Q

Treatment of Trypanosoma brucei

A

Suramin and melarsoprol

55
Q

Treatment of T cruzi

A

Nifurtimox

56
Q

Treatment of leishmaniasis

A

Sodium stibogluconate

57
Q

Anti-mite/louse therapy

A

Permethrin (blocks Na+ channels → neurotoxicity)
Malathion (acetylcholinesterase inhibitor)
Lindane (Blocks GABA channels → neurotoxicity)

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

“Prevent Mite/Louse with PML (permethrin, malathion, lindane) because they NAG you (Na+, acetylcholinesterase, GABA)”

58
Q

Chloroquine

A

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

Use: Treatment of plasmodial species other than P falciparum.

Adverse Effects: Retinopathy; pruritis

Resistance: Membrane pump that ↓ intracellular concentration of drug

59
Q

Treatment of P falciparum

A

Artemether/lumefantrine or atovaquone/progaunil.

For life-threatening malaria, use quinidine in US or artesunate

60
Q

Antihelminthic therapy

A

Mebendazole (microtubule inhibitor), pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel

61
Q

Oseltamivir, zanamivir

A

MOA: Inhibit influenza neuraminidase → ↓ release of progeny virus

Use: Treatment & prevention of influenza A & B

62
Q

Acyclovir, famciclovir, valacyclovir

A

MOA: 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.

Use: HSV and VZV. Weak activity against EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. No effect on latent forms of HSV or VZV.
Valacyclovir: Prodrug of acyclovir, better oral availability
Famciclovir: Herpes zoster

Adverse Effects: Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated

Resistance: Mutated viral thymidine kinase

63
Q

Ganciclovir

A

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

Use: CMV, especially immunocompromised patients. Valganciclovir (prodrug of ganciclovir) has better oral bioavailability.

Adverse Effects: Bone marrow suppression (leukopenia, neutropenia), thromboctopenia), renal toxicity. More toxic to host enzymes than acyclovir.

Resistance: Mutated viral kinase.

64
Q

Foscarnet

A

MOA: Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor. Binds to pyrophosphate-binding site of enzyme. Does not require any kinase activation.

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

Adverse Effects: Nephrotoxicity, electrolyte abnormalities (hypo- or hypercalcemia, hypo- or hyperphosphatemia, hypokalemia, hypomagnesmia) can lead to seizures.

Resistance: Mutated DNA polymerase

65
Q

Cidofovir

A

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

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

Adverse Effects: Nephrotoxicity (coadministered with probenecid and IV saline to ↓ toxicity)

66
Q

NRTIs

A

Abacavir (ABC), didanosine (ddI), emtricitabine (FTC), lamivudine (3TC), stavudine (d4T), tenofovir (TDF), zidovudine (ZDV)

MOA: Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DA Chain (lack a 3’ OH group). Tenofovir is a nucleotide and the others are nucleosides (need to be phosphorylated to be active)

Use: HAART; ZDV can be used for general prophylaxis and during pregnancy to ↓ risk of fetal transmission

Toxicity: Bone marrow suppression (can be reversed with G-CSF and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), anemia (ZDV), pancreatitis (ddI).

Contraindications: Abacvir if patient has HLA-B*5701 mutation

67
Q

NNRTIs

A

Delavirdine, Efavirenz, Nevirapine

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

Toxicity: Rash and hepatotoxicity.
Efavirenz: Vivid dreams and CNS symptoms
Delavirdine & efavirenz: Contraindicated in pregnancy

68
Q

Protease inhibitors

A

Atazanavir, darunavir, fosamprenavir, indinavir, lopinavir, ritonavir, saquinavir

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

Toxicity: Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy (Cushing-like syndrome).
Indinavir: Nephropthy, hematuria

Contraindications: Rifampin (decreases protease inhibitor concentration)

69
Q

Integrase inhibitors

A

Raltegravir, elvitegravir, dolutegravir

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

Toxicity: ↑ creatine kinase

70
Q

Enfurvitide

A

MOA: Binds gp41, inhibiting HIV viral entry

Toxicity: Skin reaction at injection sites

71
Q

Maraviroc

A

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

72
Q

Interferons (MOA & Adverse Effects)

A

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

Adverse Effects: Flu-like symptoms, depression, neutropenia, myopathy

73
Q

IFN-α (Uses)

A

Chronic HBV and HCV, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma

74
Q

IFN-β (Uses)

A

Multiple sclerosis

75
Q

IFN-γ (Uses)

A

Chronic granulomatous disease

76
Q

Ribavirin

A

MOA: Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase

Use: Chronic HSV; also used in RSV

Adverse Effects: Hemolytic anemia; severe teratogen

77
Q

Sofosbuvir

A

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

Use: Chronic HCV in combination with ribavirin, +/- peginterferon-α

Adverse Effects: Fatigue, headache, nausea

78
Q

Simpeprevir

A

MOA: HCV protease inhibitor; prevents viral replication

Use: Chronic HCV in combinationg with ledipasvir (NS5A inhibitor)

Adverse Effects: Photosensitivity reactions, rash