Antimicrobials

Question 1

Pencillin G, V

Answer 1

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

Question 2

Penicillinase-sensitive penicillins.

Answer 2

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

Question 3

Penicillinase-resistant penicilins

Answer 3

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

Question 4

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

Answer 4

Clavulanic acid, sulbactam, tazobactam.

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

Question 5

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

Answer 5

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)

Question 6

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

Answer 6

Cefazolin, cephalexin

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

Question 7

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

Answer 7

Cefaclor, cefoxitin, cefuroxime

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

Question 8

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

Answer 8

Ceftriaxone, cefotaxime, ceftazidime

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

Question 9

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

Answer 9

Cefepime

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

Question 10

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

Answer 10

Ceftaroline

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

Question 11

Carbapenems

Answer 11

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

Question 12

Monobactams (aztreonam)

Answer 12

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

Question 13

Vancomycin

Answer 13

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

Question 14

Aminoglycosides

Answer 14

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.

Question 15

Tetracyclines

Answer 15

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

Question 16

Chloramphenicol

Answer 16

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

Question 17

Clindamycin

Answer 17

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.

Question 18

Oxazolidinones (linezolid)

Answer 18

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.

Question 19

Macrolides

Answer 19

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.

Question 20

Sulfonamides

Answer 20

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

Question 21

Dapsone

Answer 21

MOA: Similar to sulfonamides (but structurally distinct)

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

Adverse Effects: Hemolysis if G6PD deficient

Question 22

Trimethoprim

Answer 22

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.

Question 23

Fluoroquinolones

Answer 23

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

Question 24

Daptomycin

Answer 24

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

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

Adverse Effects: Myopathy, rhabdomyolysis.

Question 25

Metronidazole

Answer 25

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

Question 26

Prophylaxis and treatment for M tuberculosis

Answer 26

Prophylaxis: Isoniazid Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol

Question 27

Prophylaxis and treatment for M avium - intracellulare

Answer 27

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

Question 28

Treatment of M leprae

Answer 28

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

Question 29

Rifamycins

Answer 29

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.

Question 30

Isoniazid

Answer 30

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

Question 31

Pyrazinamide

Answer 31

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

Question 32

Ethambutol

Answer 32

MOA: ↓ carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase Use: M tuberculosis Advers Effects: Optic neuropathy (red-green color blindness)

Question 33

Streptomycin

Answer 33

MOA: Interferes with 30S component of ribosome. Use: M tuberculosis (2nd line) Adverse Effects: Tinnitus, vertigo, ataxia, nephrotoxicity

Question 34

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

Answer 34

Amoxicillin

Question 35

Prophylaxis after exposure to gonorrhea

Answer 35

Ceftriaxone

Question 36

Prophylaxis for a history of recurrent UTIs

Answer 36

TMP-SMX

Question 37

Prophylaxis after exposure to meningococcal infection

Answer 37

Ceftriaxone, ciprofloxacin, or rifampin

Question 38

Prophylaxis for pregnant woman carrying group B strep

Answer 38

Intrapartum penicillin G or ampicillin

Question 39

Prophylaxis for prevention of gonococcal conjunctivitis in newborn

Answer 39

Erythromycin ointment

Question 40

Prophylaxis for prevention of postsurgical infection due to S aureus

Answer 40

Cefazolin

Question 41

Prophylaxis for strep pharyngitis in child with prior rheumatic fever

Answer 41

Benzathine penicillin G or oral penicillin V

Question 42

Prophylaxis for exposure to syphilis

Answer 42

Benzathine penicillin G

Question 43

Treatment of MRSA

Answer 43

Vancomcyin, daptomycin, linezolid, tigecycline, ceftaroline

Question 44

Treatment of VRE

Answer 44

Linezolid and streptogramins (quinupristin, dalfopristin)

Question 45

Treatment of multi-drug resistant P aeruginosa, Acinetobacter baumannii

Answer 45

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

Question 46

Amphotericin B

Answer 46

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

Question 47

Nystatin

Answer 47

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

Question 48

Flucytosine

Answer 48

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

Question 49

Azoles

Answer 49

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).

Question 50

Terbinafine

Answer 50

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

Question 51

Echinocandins

Answer 51

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)

Question 52

Griseofulvin

Answer 52

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

Question 53

Treatment of toxoplasmosis

Answer 53

Pyrimethamine

Question 54

Treatment of Trypanosoma brucei

Answer 54

Suramin and melarsoprol

Question 55

Treatment of T cruzi

Answer 55

Nifurtimox

Question 56

Treatment of leishmaniasis

Answer 56

Sodium stibogluconate

Question 57

Anti-mite/louse therapy

Answer 57

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)"

Question 58

Chloroquine

Answer 58

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

Question 59

Treatment of P falciparum

Answer 59

Artemether/lumefantrine or atovaquone/progaunil. For life-threatening malaria, use quinidine in US or artesunate

Question 60

Antihelminthic therapy

Answer 60

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

Question 61

Oseltamivir, zanamivir

Answer 61

MOA: Inhibit influenza neuraminidase → ↓ release of progeny virus Use: Treatment & prevention of influenza A & B

Question 62

Acyclovir, famciclovir, valacyclovir

Answer 62

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

Question 63

Ganciclovir

Answer 63

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.

Question 64

Foscarnet

Answer 64

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

Question 65

Cidofovir

Answer 65

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)

Question 66

NRTIs

Answer 66

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

Question 67

NNRTIs

Answer 67

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

Question 68

Protease inhibitors

Answer 68

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)

Question 69

Integrase inhibitors

Answer 69

Raltegravir, elvitegravir, dolutegravir MOA: Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase. Toxicity: ↑ creatine kinase

Question 70

Enfurvitide

Answer 70

MOA: Binds gp41, inhibiting HIV viral entry Toxicity: Skin reaction at injection sites

Question 71

Maraviroc

Answer 71

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

Question 72

Interferons (MOA & Adverse Effects)

Answer 72

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

Question 73

IFN-α (Uses)

Answer 73

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

Question 74

IFN-β (Uses)

Answer 74

Multiple sclerosis

Question 75

IFN-γ (Uses)

Answer 75

Chronic granulomatous disease

Question 76

Ribavirin

Answer 76

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

Question 77

Sofosbuvir

Answer 77

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

Question 78

Simpeprevir

Answer 78

MOA: HCV protease inhibitor; prevents viral replication Use: Chronic HCV in combinationg with ledipasvir (NS5A inhibitor) Adverse Effects: Photosensitivity reactions, rash