ANTIFUNGAL, ANTIVIRAL,

AND ANTIPARASITIC DRUGS

Antifungal Drugs
Concepts
• Amphotericin B (polyene)
and azoles (fluconazole
and intraconazole) – major
drugs used in systemic
mycoses
• Interaction with, or blockade
of the synthesis of
ergosterol (essential
component of fungal cell
membranes)  selective
toxicity to fungi
Amphotericin B and Nystatin
• MOA
• Bind to ergosterol  form artificial pores  increased
membrane permeability
• Resistance (rare): decreased level or structural change in
membrane sterols
• PK
• Amp B – given by slow IV infusion, penetrates weakly into CNS,
renal elimination is primarily renal, has long half-life
• Nystatin – too toxic for systemic use; applied locally
Amphotericin B and Nystatin
• Clinical Uses
• Amp B – drug of choice for aspergillosis, systemic candidiasis,
cryptococcal infections, histoplasmosis, mucormycosis, sporotrichosis
• Nystatin – topically applied for treatment of oral or vaginal candidiasis
(swish and spit, swish and swallow)
• Toxicities
• Amp B
• infusion-related effects (hypotension, chills, fever, rigor)
• Give premedications: analgesics, antihistamines, steroids
• Nephrotoxicity (tubular acidosis, electrolyte imbalance, anemia)
• Reduced by full hydration and use of liposomal forms
Azole Antifungals
• MOA
• Interfere with cell membrane synthesis by inhibiting fungal cytochrome
P450 that converts lanosterol to ergosterol
• Resistance: via change in sensitivity of target enzyme or decreased
intracellular accumulation
• PK
• Good oral efficacy; absorption inhibited by antacids
• Fluconazole – only azole that effectively enters CSF; eliminated via the
kidney
• Ketoconazole, itraconazole, voriconazole – metabolized in the liver
Azole Antifungals
• Clinical uses – varied
• Ketoconazole – mucocutaneous candidiasis and
dermatophytosis
• Fluconazole – DOC for esophageal candidiasis, candidemia, and
coccidial infections; also active in cryptococcal meningitis
• Itraconazole – has widest spectrum of the azoles; DOC in
blastomycosis and sporotrichosis
• Voriconazole – for invasive aspergillosis
• Clotrimazole and miconazole – topical
Azole Antifungals
• Toxicities – varied
• GIT distress – most common
• Azoles (esp. ketoconazole) may cause endocrine dysfunction via
inhibition of CYP450s involved in synthesis of cortisol and
testosterone, and drug metabolism
• Voriconazole – associated with visual and hepatic dysfunction;
contraindicated in pregnancy
Flucytosine
• MOA
• Accumulated in the fungi via permease  converted to 5 –
fluorouracil by cytosine deaminase  inhibits thymidylate
synthase
• Resistance: occurs rapidly in fungi deficient in the above
mentioned enzymes
• PK
• Orally active, penetrates most tissues including the CNS
• Eliminated via the kidney  dose reduction required in renal
dysfunction
Flucytosine
• Clinical uses
• Used in combination with Amp B in candidemia or cryptococcal
meningitis
• Toxicities
• Bone marrow suppression
Griseofulvin
• MOA
• Disrupts microtubular functions in dermatophytes
• May inhibit nucleic acid synthesis
• Resistance: inability to accumulate drug
• PK
• Orally active, accumulates in keratin, eliminated via the bile
Griseofulvin
• Clinical uses
• Used for dermatophytes of the skin, hair, and nails
• Toxicities
• GIT irritation, headaches, phototoxicity
• Decreases bioavailability of warfarin
• Causes disulfiram effect with ethanol
Terbinafine
• MOA
• Inhibits squalene epoxidase  increases squalene levels 
inhibit ergosterol synthesis
• PK
• Orally active, accumulates in keratin
• Clinical uses
• Dermatophytoses of skin, hair, and nails
• Toxicities
• GIT irritation, skin rash, headaches, elevation of liver enzymes
Caspofungin (Echinocandins)
• MOA
• Inhibits synthesis of β (1 – 2) glycan (component of fungal cell
wall)
• Clinical uses and toxicity
• Administered IV for management of invasive aspergillosis and
systemic candidiasis
• Cause mild infusion-related reactions and headache
• Other examples: micafungin, anidulafungin
ANTIFUNGAL DRUG INTERACTIONS
• Ketoconazole and related drugs inhibit CYP450-mediated
metabolism of:
• Cyclosporine
• Didanosine
• Lovastatin
• Phenytoin
• Quinidine
• Verapamil
• Warfarin
ANTIFUNGAL DRUG INTERACTIONS
• Oral absorption of azoles may be impeded by PPIs, H2-receptor
blockers, and other antacids
• Griseofulvin increases metabolism of warfarin
Antiviral Drugs
Concepts
• Antivirals act at several stages of viral replication, but inhibit nucleic
acid or late protein synthesis
• Many are antimetabolites that resemble naturally occurring
compounds
• Some require phosphorylation by viral or host cell kinases prior to
exerting their antiviral actions
Major Sites of Drug Action on Viral Replication
 Summary of Antivirals and Antiretrovirals
Antivirals Antiretrovirals
Antiherpes CMV Antihepatitis Anti-influenza NRTIs NNRTIs Protease Entry
inhibitors Inhibitors
Acyclovir Ganciclovir IFN-α Amantadine Abacavir Delavirdine Atazanavir Enfuvirtide
Valacyclovir Valganciclovir Adefovir- Rimantadine Didanosine Efavirenz Darunavir Maraviroc
(prodrug) Cidifovir dipivoxil Oseltamivir Emtricitabine Etravirine Fosamprenavir
Penciclovir Foscarnet Lamivudine Zanamivir Lamivudine Nevirapine Idinavir
Famciclovir Ribavirin Stavudine Nelfinavir
(prodrug) Tenofovir Ritonavir
Zalcitabine Saquinavir
Zidovudine Tipranavir
Acyclovir
• MOA
• Monophosphorylated by viral thymidine kinase  further phosphorylated by host
kinases to the nucleotide  effects: substrate and inhibitor of viral DNA polymerase,
and causes chain termination when incorporated into DNA
• Resistance
• Most resistant strains of herpes are deficient in thymidine kinase
• Others have decreased sensitivity of DNA polymerase to inhibition
• PK
• Acyclovir – orally active, but with very short half life (requires multiple dosing)
• Eliminate mainly by renal excretion
• Topical and IV forms are available
Acyclovir
• Clinical uses
• Treatment of mucocutaneous and genital HSV, prophylaxis in immunocompromised
patients, and varicella zoster infections
• Toxicities
• GIT distress and headache (common)
• IV use – crystalluria, delirium, tremor, seizures
• NOT hematotoxic
• Newer forms
• Famciclovir and Valcyclovir
• Longer duration of action; Not active against TK- strains of HSV
• Penciclovir
• Used topically; does not cause chain termination*
ANTIMICROBIAL AND ANTIVIRAL
PROPHYLAXIS
• Acyclovir – effective prophylaxis against recurrent genital herpes infections
• Other non-surgical prophylactic antimicrobial regimen with established
efficacy include prevention of:
• Endocarditis – amoxicillin or ampicillin
• Recurrent otitis media – amoxicillin
• Rheumatic fever – penicillin G
• Tuberculosis – isoniazid or rifampicin
• AIDS patients
• Pneumocyctis carinii pneumonia and Toxoplasma encephalitis – trimethoprim-
sulfamethoxazole
• Mycoplasma avium-intracellulare - rifabutin
Ganciclovir
• MOA
• Viral-specific enzymes (phosphotransferases) initiate
bioactivation; further phosphorylation occurs via host kinases
• Nucleotide inhibits viral DNA polymerase, but DOES NOT cause
chain termination
• Resistance: via decreased viral phosphotransferases or changes
in DNA polymerase
Ganciclovir
• PK
• Usually given IV; intraocular implants may be given for CMV
retinitis
• Eliminated by the kidney  dose adjustment
• Clinical uses
• Prophylaxis and treatment of CMV infections
• Toxicities
• Hematotoxicity
• Neurotoxicity (seizures in overdose)
Foscarnet
• MOA
• Inhibits viral RNA and DNA polymerases, but is not an antimetabolite (no
bioactivation)
• Resistance: via mutations in polymerase genes
• PK
• Administered IV
• Undergoes renal elimination
Foscarnet
• Clinical uses
• Prophylaxis and treatment of CMV infections
• Active against ganciclovir-resistant CMV strains and TK- strains
of HSV
• Toxicities
• Nephrotoxicity, genitourinary ulceration, neurotoxicity (seizures in
overdose)
Other Antiherpetic Drugs
• Cidofovir • Fomivirsen
• Antimetabolite; on nonviral • Antisense nucleotide that binds
bioactivation, it inhibits DNA to mRNA of CMV, inhibiting early
polymerases of HSV, CMV, protein synthesis
adenovirus, and papillomavirus • Injected intravitreally for CMV
• Markedly nephrotoxic retinitis
• Vidarabine
• Antimetabolite active against
HSV, VZV, and CMV
• Mainly used topically due to
severe neuro- and hepatotoxicity
Nucleoside Reverse Transcriptase Inhibitors
• MOA
• Phosphorylated by viral and host kinases to nucelotides  inhibit HIV
reverse trancriptase and cause chain termination in viral DNA
• Resistance: via mutation at several sites of the pol gene that encodes
reverse transcriptase
• Drugs and pharmacokinetics
• Zidovudine (ZDV) – prototype; others – didanosine (ddI), zalcitabine
(ddC), lamivudine (3TC), stavudine (d4T), abacavir
• Most have good oral bioavailability and are eliminated via metabolism
and/or renal elimination
Nucleoside Reverse Transcriptase Inhibitors
• Clinical uses
• Standard components of anti-HIV drug regimens (usually 2 NRTIs + PI)
• Zidovidine (with or without other anti HIV drugs) – used as prophylaxis in
needlestick accidents and to reduce vertical transmission in pregnancy
• Lamivudine – used with IFN-α or as individual agent in hep B infection
• Toxicities
• Bone marrow suppression (zidovudine)
• Peripheral neuropathy (zalcitabine and stavudine)
• Severe hypersensitivity (abacavir)
• Lactic acidosis (NRTIs in general)
Nonnucleoside Reverse Transcriptase Inhibitors
• MOA:
• Do not require bioactivation; directly and allosterically inhibit
viral RNA polymerases
• Resistance occurs rapidly if used as single agents (via mutation
of reverse transcriptase)
• Cross-resistance with nucleoside inhibitors does not occur
Nonnucleoside Reverse Transcriptase Inhibitors
• Drugs and toxicities
• Nevirapine – severe hypersensitivity reactions
• Delavirdine – skin rash and teratogenicity
• Efavirenz – neurotoxicity, hyperlipidemia, teratogenicity
Protease Inhibitors
• MOA
• Inhibit aspartate protease (cleaves precursor proteins needed
for producing mature HIV virions)
• Resistance: via point mutations in the protease gene
• Cross-resistance between PIs in incomplete
• Clinical uses
• Used in anti-HIV regimens that usually include two RTIs
Protease Inhibitors
• Drugs and toxicities
• Idinavir – hematotoxicity and nephrotoxicity
• Ritonavir – nausea, diarrhea, inhibition of metabolism of many
drugs, including other PIs
• Saquinavir – neutropenia
• Nelfinavir – diarrhea and hypersensitivity
• PIs as a class – disorders of carbohydrate and lipid metabolism
Enfuvirtide
• MOA
• Synthetic peptide that binds to he gp41 subunit of the viral
envelope protein  blocks fusion of the virus with cellular
membranes
• No cross resistance with other anti-HIV drugs
• Resistance may occur via mutations in the env gene
Enfuvirtide
• Clinical use and toxicity
• Given via SQ route and with othe anti-HIV agents in patients with
persistent HIV replication despite ongoing therapy
• Adverse effects:
• Injection site reactions
• Increased incidence of bacterial pneumonia
 Miscellaneous Antivirals
Drugs Clinical Use Mechanisms of Action Toxicities
Amantadine Influenza A Prevents viral fusion GIT distress, dizziness,
and uncapping slurred speech
Oseltamivir, Influenza A and B Inhibit neuraminidase
Zanamivir and impede viral
release
Interferon-α Hepatitis viruses (A, B, C), Interferes with viral RNA Neutropenia, fatigue,
Kaposis sarcoma, papillomatosis and DNA synthesis mental confusion,
cardiomyopathy
Ribavirin Respiratory syncytial virus, Inhibits viral DNA Myelosuppression,
Hanta and Lassa viruses, polymerases and end- teratogenicity
hepatitis C capping of viral RNA
HIGHLY ACTIVE ANTIRETROVIRAL THERAPY
(HAART)
• Combination anti-HIV protocol; commonly involve 2 NRTIs + PI
• Slows development of resistance and reverses the decline in CD4
cells that occurs during disease progression
• Decreases viral RNA load (sometimes to undetectable levels) and
reduces rate of opportunistic infections
• Cessation of therapy in AIDS patients usually results in re-
emergence of detectable viral RNA
Newer HIV Drugs
• Maraviroc
• Entry inhibitor; acts as antagonist to the CCR5 receptor; used
orally and is a substrate of CYP3A4; can cause cough, diarrhea,
muscle and joint pain, and increases hepatic transaminases

• Raltegravir
• Integrase inhibitor; metabolized by glucuronidation
 Summary of Antivirals and Antiretrovirals
Antivirals Antiretrovirals
Antiherpes CMV Antihepatitis Anti-influenza NRTIs NNRTIs Protease Entry
inhibitors Inhibitors
Acyclovir Ganciclovir IFN-α Amantadine Abacavir Delavirdine Atazanavir Enfuvirtide
Valacyclovir Valganciclovir Adefovir- Rimantadine Didanosine Efavirenz Darunavir Maraviroc
(prodrug) Cidifovir dipivoxil Oseltamivir Emtricitabine Etravirine Fosamprenavir
Penciclovir Foscarnet Lamivudine Zanamivir Lamivudine Nevirapine Idinavir
Famciclovir Ribavirin Stavudine Nelfinavir
(prodrug) Tenofovir Ritonavir
Zalcitabine Saquinavir
Zidovudine Tipranavir
Antiparasitic Drugs
 Antimalarial Drugs
Drug Mechanisms of Action Clinical Uses Toxicities
Chloroquine Heme accumulation; Prophylaxis and GIT distress, skin rash, and, at
resistance via efflux treatment in chloroquine- high doses, neuropathy,
transporters sensitive regions retinopathy, auditory
dysfunction, psychosis
Atovaquone Inhibit mitochondrial Chloroquine-resistant Rash, cough, GIT effects;
+ proguanil electron transport and folate malaria avoid in pregnancy and in
metabolism severe renal dysfunction

Medications that can be used for the treatment of malaria in pregnancy include
chloroquine, quinine, atovaquone-proguanil, clindamycin, mefloquine (avoid in 1st
trimester), sulfadoxine-pyrimethamine (avoid in 1st trimester) and the artemisinins.
 Antimalarial Drugs
Drug Mechanisms of Action Clinical Uses Toxicities
Mefloquine1 Chemically related to Chloroquine-resistant GIT effects, skin rash, and
chloroquine, but with malaria headache; avoid if with history
unknown MOA of seizures
Primaquine Forms redox compounds Plasmodium vivax and P GIT effects, pruritus,
that cause cellular oxidation ovale headache,
methemoglobinemia; avoid in
G6PD deficiency
Quinine Blocks DNA replication and Chloroquine-resistant Cinchonism, quinidine-like
transcription to RNA Plasmodium falciparum cardiotixicity, blackwater fever;
avoid in pregnancy and G6PD
deficiency
1Mefloquine is a drug of choice for prophylaxis in chloroquine-resistant regions; doxycycline and atovaquone-proguanil (Malarone) are
also used and have activity in malaria caused by mefloquine-resistant falciparum malaria
Examples of Modern Medicines Derived from Plant
Sources
Medicine Common Scientific Indication Mechanism of action
name of name of
plant plant
Warfarin Sweet clover Melilotus Prevention of deep vein thrombosis Inhibits vitamin K epoxide reductase
silage and pulmonary embolism component 1 of vitamin K to its active form
Artemisinin Qinghaosu Artemisia Treatment of chloroquine-resistant Inhibition of a parasite Ca+ dependent
annua falciparum malaria ATPase
Paclitaxel Pacific yew Taxus Treatment of breast cancer Binds with tubulin and inhibits its
brevifolia polymerization into microtubules, causing
arrest at metaphase
Vincristine Periwinkle Vinca rosea Treatment of numerous types of Binds with tubulin and inhibits its
cancer polymerization into microtubules, causing
arrest at metaphase
Quinine Cinchona Cinchona Alternative treatment of severe Inhibits hemozoin biocrystallization in heme
bark officinalis malaria in combination with other detoxification pathway, which facilitates the
antimalarials aggregation of cytotoxic heme
Metformin French lilac Galega Treatment of type 2 diabetes Reduction of hepatic glucose production and
officinalis mellitus and polycystic ovary renal glucogenesis
syndrome
GLUCOSE-6-PHOSPHATE DEFICIENCY
• Common X-linked enzymopathy  susceptible to attacks of acute
hemolysis if exposed to chemicals that cause oxidative stress
• Most prevalent in males of African, Asian, or Mediterranean descent
• Antimalarial drugs to be avoided are chloroquine, primaquine, and
quinine
• Considered safe antimalarials in G6PD deficiency: halofrantrine, artemisinine
derivatives, proguanil, atovoquon
• Other drugs to be avoided:
• α-methyldopa, chloramphenicol, dimercaprol, enalapril, hydralazine,
hydrofurantoin, norfloxacin, procainamide, probenecid, quinidine, antibacterial
sulfonamides
Drugs for Specific Protozoal Infections
Infection Primary Drug(s) Comments
Amebiasis Metronidazole Diloxanide (or iodoquinol) can be used for noninvasive intestinal
disease
Giardiasis Metronidazole “Backpacker’s diarrhea” may not be treated
Leishmaniasis Stibogluconate Metronidazole, pentamidine, and polyenes are back-up drugs
Pneumocystis TMP – SMX Aerosolic pentamidine is also prophylactyic, but the IV form is needed;
atovaquone is also active
Trichomoniasis Metronidazole Treat both sexual partners
Toxoplasmosis Pyrimethamine + Clindamycin is a back-up drug if sulfonamides are contraindicated
sulfadiazine
Trypanosomiasis Melarsoprol African forms
Nifurtimox American forms
HELMINTHIC INFECTIONS
• Over 1 billion worldwide estimated to be infected with intestinal nematodes
• About 500 million suffer from tissue nematode infections
• US – pinworm infections are common; hookworm and threadworm infection
are endemic in southern states
• Southeast Asia and Indian subcontinent – trematodes (flukes)
• Most world regions – cestodes (tapeworm)
 Drugs for Nematode Infections
Drug Infections Characteristics and Comments
Albendazole Co-DOC for most nematodes Inhibits microtubule assembly in worms
Dimethylcarbamazine DOC for filariasis Reactions to parasite proteins include fever, rashes, joint
pain, and ocular dysfunction
Ivermectin DOC for threadworm GABA receptor activation leads to paralysis and expulsion
of worms
Mebendazole DOC for whipworm; co-DOC for Inhibits microtubule synthesis in worms; avoid in
hookworm, pinworm, and roundworm pregnancy
Piperazine Back-up drug for roundworm GABA receptor activation leads to paralysis and expulsion
of worms
Pyrantel pamoate Co-DOC for hookworm and roundworm Nicotinic receptor activation leads to a depolarization
paralysis of worms
Thiabendazole DOC for larva migrans Toxicity includes gastrointestinal distress, cholestasis,
leukopenia, CNS effects, and reactions to dying parasites
 Drugs for Trematode and Cestode Infections
Drug infections Characteristics and Comments
Bithionol DOC for sheep liver fluke Causes tinnitus, headache, phototoxicity, GIT distress,
and leukopenia
Metrifonate Bilharziasis Inhibits acetylcholinesterase of parasites
(schistosomiasis)
Praziquantel DOC for most flukes and Increases Ca2+ influx causing parasite contraction then
co-DOC for most relaxation; causes headache, dizziness, malaise, and GIT
tapeworms distress
Albendazole DOC for cysticercosis and See previous table
hydatid disease
Niclosamide Co-DOC for most Uncouples oxidative phosphorylation; causes headache,
tapeworms GIT distress, rashes, and fever
THANK YOU!!!
A young male patient who has no prior history of HSV infection
develops painful pustular lesions o his genitalia and severe dysuria
with a mucoid discharge characteristic of herpetic urethritis. Acyclovir
is prescribed for his condition.
Which of the following statements about acyclovir and its use in this
patient is accurate?
A. Acyclovir must be administered intravenously in herpetic urethritis
B. Dose-dependent bone marrow suppression is anticipated with the use of
acyclovir
C. Once-daily dosing with acyclovir is effective in genitourinary herpes
infections
D. Thymidine kinase-deficient strains of HSV are resistant to acyclovir
E. To prevent crystalluria, this patient should be administered mannitol
parenterally
Influenza vaccines are contraindicated in patients with egg
allergy. In such cases, prophylaxis against influenza A and B
can be provided by which of the following?
A. Amantadine
B. Foscarnet
C. Oseltamivir
D. Ribavirin
E. Valacyclovir
A 37-year-old female patient who has been treated for Hodgkin’s
disease is cellularly immunodeficient. She develops symptoms of
headache, confusion, nausea, and vomiting. Spinal fluid findings
include increased intracranial pressure, pleocytosis, increased
protein, decreased glucose, and budding encapsulated fungal cells. A
preliminary diagnosis of fungal meningitis is made and CSF analysis
demonstrates polysaccharide antigen of Cryptococcus neoformans.
Which of the following statements about the management of this
patient is accurate?
A. Amphotericin B (intrathecal) must be administered in all cases of
crytococcal meningitis
B. The antifungal drug treatment of choice is monotherapy with flucytosine
at maximally tolerated doses
C. In patients with mild disease (spinal fluid antigen titer < 1:28) oral
fluconazole for 12 weeks is an effective treatment regimen
D. Ketoconazole has synergistic effects with amphotericin B in the
treatment of fungal meningitis due to Cryptococcus neoformans
E. Terbinafine is highly effective in fungal meningitis, as it readily enters the
CSF
If amphotericin B is used in this patient, its potential
nephrotoxic effects include azotemia, hypokalemia,
hyposthenuria, nephrolithiasis, acute tubular necrosis, and
renal failure. Nephrotoxicity of amphotericin B can be reduced
by the use of which of the following?
A. Antihistamines
B. Hydrocortisone
C. Ibuprofen
D. Liposomal formulations
E. Meperidine
A 30-year-old male with AIDS has a CD4+ count of 200/μL and a viral
RNA load of 70,000 copies/mL. His highly active antiretroviral therapy
(HAART) includes zidovudine, didanosine, and ritonavir. He has
several episodes of oral candidiasis that have been managed by
treatment with ketoconazole. Oral trimethoprim-sulfamethoxazole
(TMP-SMX) has been prescribed for prophylaxis against
Pneumocyctis carinii pneumonia. He is also taking dronabinol to
improve appetite and decrease nausea.
In terms of toxicities he is likely to be experiencing, which of
the following pairs of drug: adverse effect is accurate?
A. Didanosine: hemolysis in G6PD deficiency
B. Dronabinol: bone marrow suppression
C. Ritonavir: inhibition of drug-metabolizing enzymes
D. TMP-SMX: pancreatitis
E. Zidovudine: gynecomastia
If this AIDS patient could not tolerate TMP-SMX because he
was allergic to sulfonamides, which of the following drugs
would provide effective prophylaxis against Pneumocystis
carinii pneumonia?
A. Ampicillin
B. Clarithromycin
C. Nystatin
D. Pentamidine
E. Rifabutin
Which of the following is the optimal drug treatment for
hepatic amebiasis?
A. Diloxanide furoate
B. Metronidazole
C. Metronidazole plus a luminal amebicide
D. Pyrantel pamoate
E. Tetracycline
A person is advised to take 100 mg doxycycline daily while
visiting a foreign country. This regimen will be an effective
prophylaxis against which of the following?
A. Ascariasis (roundworm infection)
B. Malaria
C. Tapeworm infection
D. Sexually transmitted infections
E. Trypanosomiasis (sleeping sickness)
ANSWERS
A young male patient who has no prior history of HSV infection
develops painful pustular lesions o his genitalia and severe dysuria
with a mucoid discharge characteristic of herpetic urethritis. Acyclovir
is prescribed for his condition.
Which of the following statements about acyclovir and its use in this
patient is accurate?
A. Acyclovir must be administered intravenously in herpetic urethritis
B. Dose-dependent bone marrow suppression is anticipated with the use of
acyclovir
C. Once-daily dosing with acyclovir is effective in genitourinary herpes
infections
D. Thymidine kinase-deficient strains of HSV are resistant to acyclovir
E. To prevent crystalluria, this patient should be administered mannitol
parenterally
Influenza vaccines are contraindicated in patients with egg
allergy. In such cases, prophylaxis against influenza A and B
can be provided by which of the following?
A. Amantadine
B. Foscarnet
C. Oseltamivir
D. Ribavirin
E. Valacyclovir
A 37-year-old female patient who has been treated for Hodgkin’s
disease is cellularly immunodeficient. She develops symptoms of
headache, confusion, nausea, and vomiting. Spinal fluid findings
include increased intracranial pressure, pleocytosis, increased
protein, decreased glucose, and budding encapsulated fungal cells. A
preliminary diagnosis of fungal meningitis is made and CSF analysis
demonstrates polysaccharide antigen of Cryptococcus neoformans.
Which of the following statements about the management of this
patient is accurate?
A. Amphotericin B (intrathecal) must be administered in all cases of
crytococcal meningitis
B. The antifungal drug treatment of choice is monotherapy with flucytosine
at maximally tolerated doses
C. In patients with mild disease (spinal fluid antigen titer < 1:28) oral
fluconazole for 12 weeks is an effective treatment regimen
D. Ketoconazole has synergistic effects with amphotericin B in the
treatment of fungal meningitis due to Cryptococcus neoformans
E. Terbinafine is highly effective in fungal meningitis, as it readily enters the
CSF
If amphotericin B is used in this patient, its potential
nephrotoxic effects include azotemia, hypokalemia,
hyposthenuria, nephrolithiasis, acute tubular necrosis, and
renal failure. Nephrotoxicity of amphotericin B can be reduced
by the use of which of the following?
A. Antihistamines
B. Hydrocortisone
C. Ibuprofen
D. Liposomal formulations
E. Meperidine
A 30-year-old male with AIDS has a CD4+ count of 200/μL and a viral
RNA load of 70,000 copies/mL. His highly active antiretroviral therapy
(HAART) includes zidovudine, didanosine, and ritonavir. He has
several episodes of oral candidiasis that have been managed by
treatment with ketoconazole. Oral trimethoprim-sulfamethoxazole
(TMP-SMX) has been prescribed for prophylaxis against
Pneumocyctis carinii pneumonia. He is also taking dronabinol to
improve appetite and decrease nausea.
In terms of toxicities he is likely to be experiencing, which of
the following pairs of drug: adverse effect is accurate?
A. Didanosine: hemolysis in G6PD deficiency
B. Dronabinol: bone marrow suppression
C. Ritonavir: inhibition of drug-metabolizing enzymes
D. TMP-SMX: pancreatitis
E. Zidovudine: gynecomastia
If this AIDS patient could not tolerate TMP-SMX because he
was allergic to sulfonamides, which of the following drugs
would provide effective prophylaxis against Pneumocystis
carinii pneumonia?
A. Ampicillin
B. Clarithromycin
C. Nystatin
D. Pentamidine
E. Rifabutin
Which of the following is the optimal drug treatment for
hepatic amebiasis?
A. Diloxanide furoate
B. Metronidazole
C. Metronidazole plus a luminal amebicide
D. Pyrantel pamoate
E. Tetracycline
A person is advised to take 100 mg doxycycline daily while
visiting a foreign country. This regimen will be an effective
prophylaxis against which of the following?
A. Ascariasis (roundworm infection)
B. Malaria
C. Tapeworm infection
D. Sexually transmitted infections
E. Trypanosomiasis (sleeping sickness)