Pharm 2 Exam 4

Front 1

What is the MOA of amphotericin B?

Back 1

Binds to ergosterol component of fungal cell membrane and alters permeability to allow leakage of ions and other intracellular components

Front 2

What is the basis for selective toxicity of amphotericin B?

What can cause cytotoxicity?

Back 2

Greater selectivity for fungal membranes because they contain ergosterol instead of cholesterol;

binding of cholesterol component in mammalian cells

Front 3

What is the MOA of Flucytosine (5FC)?

Back 3

5FC is transported into fungal cells by a perm ease and is then converted to fluorouracil. The metabolite 5-FdUMP is formed and inhibits thymidylate synthetase stopping DNA synthesis

Front 4

What is the basis of selective toxicity of Flucytosine?

Back 4

perm ease affected by this drug is not found in mammalian cells

Front 5

What is the MOA for Azole antifungals (ketoconazole)?

Back 5

Inhibits P450 isoenzyme that converts lanosterol to ergosterol. Inhibition of ergosterol production results in deficient fungal membranes with increased permeability and leakage of cellular components/inhibition of fungal growth

Front 6

What is the MOA for Capsofungin?

Back 6

inhibits synthesis of an essential cell wall component (beta-1,3-D-glucan) in aspergillus species resulting in osmotic fragility and fungal death

Front 7

What is the basis of selective toxicity for Capsofungin?

Back 7

It targets the cell wall, which humans don't have

Front 8

What is the MOA of griseofulvin?

Back 8

Interacts with the fungal cell wall microtubules to disrupt the mitotic spindle and inhibit mitosis.

Front 9

Where does griseofulvin accumulate?

Back 9

in infected keratin-containing tissues creating unfavorable growth conditions

Front 10

What is the basis of selective toxicity for griseofulvin?

Back 10

Targets cell walls, which are not present in humans

Front 11

What is the MOA of Terbinafine?

Back 11

Inhibits squalene epoxidase which is an essential enzyme in fungal sterol synthesis. Produces a deficiency of ergosterol and an accumulation of squalene inside the fungal cell resulting in death.

Front 12

What is the MOA of Nystatin?

Back 12

are polyene abx similar in structure and MOA to amphotericin B (alters cell membrane permeability)

Front 13

What is the basis of selectivity for nystatin?

Back 13

similar to amphotericin B

Front 14

Amphotericin B can be either fungicidal or fungostatic depending on.....

Back 14

tissue concentration achieved and organisms susceptability

Front 15

What is the broadest spectrum anti fungal?

Back 15

amphotericin B

Front 16

What is the DOC (anti fungal) for immunocompromised patients?

Back 16

amphotericin B

Front 17

Is amphotericin B effective against meningitis? What routes of administration are there?

Back 17

achieves nontherapeurtc elves in CSF with/without inflammation however in some cases, IV administration may produce therapeutic levels for cryptococal meningitis

Front 18

What are the indications for the use of the liposomal formulations of Amphotericin B?

Back 18

Patients who cannot tolerate or fail the conventional IV formulation or for renal impairment where unacceptable toxicity occurs.

Includes: invasive aspergillosis, neutropenic pts with fungal infection, candidiasis, etc.

Front 19

What are some advantages to using the liposomal formulation of Amphotericin B?

Back 19

Increased circulation time and reaches higher concentrations in vascularized areas (inflammation, infection, tumors) while being essentially impermeable to normal tissues;

Localizes the drug at disease sites and allows drug levels to be increased several times higher than amounts achieved with free drug from conventional products;

intended to reduce serious renal toxicity by decreasing binding of drug in renal tissues

Front 20

When you are going to use the amphotericin B, what pretreatments would you want to use?

Back 20

NSAIDs, antihistamines, and steroids

Front 21

What is the major toxicity associated with amphotericin B?

Back 21

nephrotoxicity (decreased GFR And creatinine clearance, K+ loss)

Front 22

What is the mechanism of synergism between flucytosine and amphotericin B?

Is this combination efficacious for meningitis?

Back 22

Amphotericin B alters the membrane permeability to flucytosine.

yes- effective against cryptococcus neorformans and candidia

Front 23

Are systemic azole antifungals fungicidal or fungistatic?

Are they broad or narrow spectrum?

Back 23

both depending on dose;

Broad spectrum treatment for systemic mycoses

Front 24

Which azole anti fungal is effective against meningitis? What is the route?

Back 24

fluconazole (excellent penetration info CSF)

oral tablets, suspensions or IV injections

Front 25

Why is concurrent use of amphotericin B with azole antifungals contraindicated?

Back 25

azoles contraindicate the actions of amphotericin B

Front 26

What are the indications for which fluconazole is the DOC?

Back 26

cryptococcal meningitis, serious systemic candidiasis (URI, peritonitis, pneumonia), and coccidiodomycosis

Front 27

What are the two serious ADRs associated with itraconazole?

Back 27

Risk of CHF in pts with existing heart disease; hepatic dysfunction

Front 28

Describe the method of pulse dosing of itraconazole for onychomycosis.

Back 28

each pulse is 200mg BID for one week per month;

need 2 for fingernails, 3-4 for toenails (grow slower)

Front 29

Symptoms of endocrine disorders associated with the use of ketoconazole include:

What is the mechanism that causes these symptoms?

Back 29

gynecomastia, impotence, loss of libido, menstrual irregularities;

inhibits gonadal steroid synthesis in humans

Front 30

You don't want to take ketoconazole with things that ____ gastric acidity or with ______ since it is required for dissolution and absorption.

Back 30

decrease, food

Front 31

Ketoconazole can ______ the P450 system and cause....

Back 31

inhibit; toxicity of other drugs

Front 32

Which other azole anti fungal possibly has hepatic effects and needs to be monitored?

Back 32

fluconazole

Front 33

Which other azole anti fungal causes hepatic dysfunction and has strong warnings against liver failure?

Back 33

itraconazole

Front 34

Voriconazole is the first line agent for the treatment of what three conditions?

Back 34

acute invasive aspergillosis * (in pts over 12)

esophageal candidiasis

nonneutropenic pts with candidemia or deep tissue candida infection

Front 35

What are the two indications for Posoconazole?

Back 35

prophylaxis of invasive aspergillosis and candidiasis who are severely immunocompromized;

oropharyngeal candidiasis

Front 36

Echinocandins have potent activity against ____ and ___ except for which 3 species?

Back 36

aspergillosis; candidiasis

candida neoformans, zygomycetes, fusarium

Front 37

Capsofungin is used to treat what 4 conditions?

Back 37

Aspergillosis, esophageal candidiasis, disseminated candida infections, empirical tx of presumed fungal infections in febrile neutropenic patients

Front 38

What is the DOC for secondary prophylaxis of PCP?

Back 38

TMP-SMX DS

Front 39

Is primary prophylaxis (in HIV+ pts) recommended/done for candidiasis, cryptococcosis, and aspergillosis infections?

Back 39

NO

Front 40

What is the strongest recommendation of ART in a TB patient?

Back 40

Pts with CD4 cell counts less than 50 cells/mm and it should be initiated within 2 weeks of starting TB treatment.

Front 41

What are the major toxicities associated with indinavir and what precautions must be taken?

Back 41

acute nephrolitiasis;

ensure adequate hydration, drinking about 1.5L of liquids per 24 hours

Front 42

What is the advantage of using the combination product Combivir compared to dosing with the two individual components? (antiretroviral drug)

Back 42

has synergistic antiretroviral activity and is taken without regard to meals.

Front 43

What is the parameter used to decide whether ART regimens should be modified?

Back 43

regular monitoring of the viral load, CD4+ T cell count and pts clinical condition

Front 44

What are the 6 classic ADRs associated with Antiretroviral agents?

Back 44

lactic acidosis, hepatomegaly with steatosis, hyperglycemia, rash, hyperlipidemia, GI intolerance

Front 45

What are the three major characteristics of all preferred ART Regimens?

Back 45

use at least 3 drugs; use a combination of drugs with different MOAs, and are class sparing

Front 46

What is the spectrum of activity of Griseofulvin?

Back 46

fungistatic

Front 47

What are the indications for Griseofulvin?

Back 47

only active aginst dermatophytes (trichophytan, microsporum and epidermophyton) and in the treatment of severe tinea infections that dont respond to other antifungals

Front 48

What are some ADRs with Griseofulvin

Back 48

GI distress, photosensitivity, possible antabuse reaction with alcohol

Front 49

What are some symptoms of an Antabse reactioin?

Back 49

tachycardia and flushing

Front 50

How may the oral absorption of Grisofulvin be enhanced?

Back 50

Using ultra-fine crystalline preps and eating with high fat meals

Front 51

Where does Griseofulvin distribute to?

Back 51

keratinized tissues (skin, hair, nails)

Front 52

How long must therapy with griseofulvin be continued for?

Back 52

until normal tissue replaces infected tissue (weeks to months)

Front 53

What is the current clinical use of amantadine and rimantadine?

Back 53

against influenza A virus

Front 54

What is the oral availability for ACY (acyclovir) and DHPG (gangciclovir)?

Back 54

poor

Front 55

Describe how Acyclovir is given via IV to avoid nephrotoxicity.

Back 55

Given by a slow infusion over at least 1 hour with adequate hydration. Make sure to establish sufficient urine flow over the 1st 2 hours post-infusion

Front 56

How does the spectrum of activity for gangciclovir differ from acyclovir?

Back 56

the same but also effective against CMV

Front 57

What is the boxed warning for gangciclovir and what are the resulting hematological effects?

Back 57

myelosuppression. Monitor for neutropenia, anemia and thrombocytopenia

Front 58

What is the action and indication for penciclovir dermatological cream?

Back 58

Antiviral activity against HSV-1 and HSV-2; indicated for treatment of recurrent herpes labialis in adults (cold sores)

Front 59

What is the DOC for tx of PCP pneumonia?

Alternate agent (mod-severe)?
Alternate agent (mild-mod)?

Back 59

TMP-SMX, IV pentamidine, atovaquone

Front 60

What is the DOC for post-exposure primary prophylaxis?

Back 60

varicella-zoster immune globulin ASAP for at least 3 weeks

Front 61

What is the DOC for varicella infection?

Back 61

acyclovir

Front 62

What is the spectrum of activity for Terbinafine?

Back 62

fungicidal

Front 63

What are the indications for Terbinafine?

Back 63

tx of onychomycosis of the toenail or fingernail due to dermatophytes (superior to griseofulvin)

Front 64

What are the ADR of Terbinafine?

Back 64

GI distress, ageusia, asx elevation of liver enzymes, less commonly neutropenia, derm eruptions and ophthalmic complaints

Front 65

How may oral absorption of terbinafine be enhanced?

Back 65

take with food to increase bioavailability

Front 66

How do the distribution properties of terbinafine relate to the clinical uses?

Back 66

highly lipophilic with slow elimination from skin and adipose tissue

Front 67

How long must therapy of terbinafine be continued?

Back 67

treatment can last weeks to months

Front 68

What are the three preparations of ciclopirox and what are their indications?

Back 68

Cream/lotion= tinea infections;

shampoo=seborrheic dermatitis

nail lacquer= nail infections

Front 69

What are the preparations of nystatin and what are they used for?

Back 69

Topical (cream, ointment, powder)= superficial cutaneous candida;

Oral (swish and swallow)= oral/mucous membrane candidiasis

Oral tablet= intestinal candida

Vaginal tablet= vulvovaginal candidiasis

Front 70

What are the preparations and clinical uses of Clotrimazole?

Back 70

OTC cream or solution= tinea infections

OTC intravaginal cream= VVC

Rx buccal tablet= tx and prophylaxis of oropharyngeal candidiasis

Front 71

What are the preparations and clinical uses of Miconazole?

Back 71

Intravaginal cream and suppository= VVC

topical cream= cutaneous candidiasis

Front 72

What is the clinical use of Butoconazole?

Back 72

VVC

Front 73

What is the DOC for trichomoniasis? What infections can Trich cause?

Back 73

Metronidazole;

vaginitis, NG urethritis, prostatitis

Front 74

What is the preferred regimen of Metronidazole for use against trichomonas?

What is the alternative regimen

Back 74

2g PO single dose;

500mg BID x 7 days

Front 75

If treatment failure occurs with metrondiazole, what do you want to do?

what do you want to take metronidazole with and what do you want to avoid?

If you are allergic to metronidazole, what do you want to do?

Back 75

tx with a single 2 g dose once daily x 5 days;

food; alcohol;

desensitize the pt

Front 76

What is the proposed MOA of mebendazole?

Back 76

selectively and irreversibly inhibits glc uptake in susceptible adult intestinal-dwelling helminthes; also a spindle poison that induces chromosome nondisjunction

Front 77

What is mebendazole indicated for?

Back 77

pinworms (worms in general)

Front 78

When treating a pt with pinworms with mebendazole, what other things must be taken into consideration?

Back 78

repeat dosing may be needed adn may need to treat family members in close contact. Also hygiene precautions need to be taken to prevent reinfection

Front 79

What organisms are susceptible to acyclovir?

Back 79

HSV-1/2, varicella and ebstein barr

Front 80

Why is CMV resitant to acyclovir?

Back 80

it lacks a specific viral thymidine kinase

Front 81

What are the 4 groups of patients for whome ART is recommended regardless of CD4 cell count?

Back 81

pregnancy, Hx of an AIDS-defining illness, HIV-associated nephropathy, HIV/hepatitis B coinfection

Front 82

What is the CD4+ t cell count associated with the strongest ART recomendation?

Back 82

<350 cells/mm3

Front 83

What are the specific toxicities associated with Zidovudine?

Back 83

myelosuppression, neutropenia, severe anemia

Front 84

What is the resulting drug interaction of Zidovudine with ganciclovir?

Back 84

additive hematology toxicity

Front 85

What is the major boxed warning for nevirapine?

Back 85

severe, life-threatening skin reactions (steven-johnson syndrome, Toxic epidermal necrolysis) and potentially fatal hepatotoxicity

Front 86

State what effect the following drugs have on the P450 system:

Nevirapine-
Saquinavir-
Ritonavir-

Back 86

induces;

inhibits;

strong inhibitor

Front 87

Which ART drug inhibits the P450 system but is also a substrate for the enzyme (3A4) so induces of 2A4 may decrease the concentration of this drug?

Back 87

saquinavir

Front 88

When using Zidovudine during pregnancy, what is the route of administration and when is it given?

Back 88

IV; at onset of labor until delivery

Front 89

When using Zidovudine in the infant, what is the route of administration and what are the treatment recommendations?

Back 89

Oral; 2x daily as soon after birth as possible (within 6-12 hours) and continues for up to 6 weeks

Front 90

For the post-exposure prophylaxis of HIV, what is the duration of all regiments used?

What is the basic regimen?

What is a reason for using the expanded regimen?

What is the preferred expanded regimen?

Back 90

4 weeks;

ZDV + lamivudine;

for exposures posing an increased risk of transmission or where resistance to one or more of the agents is known or suspected;

basic regimen plus lopinavir/ritonavir

Front 91

What is the DOC for primary prophylaxis of Pneumocystic jirovecci pneumonia?

What are the alternative regimens?

Back 91

TMP-SMZ;

dapsone, dapsone plus pyrimethamine (plus leucovorin), Aerosolized pentamidine or atovaquone

Front 92

What other parasitic infection is covered by the DOC for the treatment of PCP pneumonia? (TMP-SMZ)

Back 92

toxoplasmosis

Front 93

What is the regimen used for prophylaxis of PCP and toxoplasmosis when tolerance to TMP-SMZ occurs?

Back 93

dapsone + pyrimethamine + leucovorin

Front 94

What is the DOC for the tx of toxoplasmosis?

Back 94

pyrimethamine plus sulfadiazine plus leucovorin

Front 95

Why is leucovorin included in the treatment for toxoplasmosis?

Back 95

to prevent megaloblastic anemia effects that can occur from the pyrimethamine

Front 96

What is the major toxicity of sulfadiazine and what precaution must be taken?

Back 96

neutropenia, interstitial nephritis, crystalluria and nephrolitiasis.

drink 2-3L of fluid/day to decrease risk of crystalluria

Front 97

What is the alternative regimen for toxoplasmosis (for those allergic to sulfas)

Back 97

pyrimethamine plus leucovorin plus clindamycin

Front 98

What is the MOA for pyrimethamine?

Back 98

inhibits dihydrofolate reductase preventing the conversion of dihydrofolate to the active form tetrahydrofolate. Activity is highly selective for DHFR from plasmodium or toxoplasma parasites

Front 99

What is the clinical uses for pyrimethamine?

Back 99

chemoprophylaxis of malaria; and as part of the treatment for toxoplasmosis

Front 100

What are some precautions that need to be taken when using pyrimethamine?

Back 100

may cause folate deficiency (give leucovorin), may also precipitate hemolytic anemia in G6PD deficient patients

Front 101

What is the DOC for esophageal candidiasis?

Back 101

fluconazole

Front 102

What is the DOC for oropharyngeal candidiasis?

Back 102

fluconazole

Front 103

What is the DOC for cryptococcal meningitis?

Back 103

amphotericin B plus flucytosine

Front 104

What is the DOC for aspergillosis?

Back 104

voriconazole

Front 105

For the treatment of TB in HIV patients, what are the induction phase drugs and how long are they used?

How about the continuation phase?

Back 105

8 weeks; INH, RIF (or RBN), PZA and EMB;

18 weeks; either INH and RIF (or RBN) every day (((OR))) INH and RIF 3x weekly

Front 106

Is the use of DOT strongly recommended for HIV pts undergoing tx for TB?

Back 106

YES

Front 107

What is the preferred rifamycin drug used when a protease inhibitor-based ART regimen is to be used? Why?

Back 107

Rifabutin; less potent 3A4 inducer

Front 108

What is the preferred agent for the primary prophylaxis of mycobacterium avium complex in adults with HIV?

Back 108

clarithromycin (or azithro)

Front 109

What is the the preferred agent for the treatment of an active MAC infection?

Back 109

clarithromycin with ethambutol. Addition of rifabutin may be considered (but need to think about DIs)

Front 110

What is the recommendations for the primary prophylaxis of CMV?

Back 110

not generally recommended

Front 111

What is the treatment of CMV retinitis?

Back 111

ganciclovir intraocular impant and valganciclovir PO

Front 112

What are the disadvantages of the ganciclovir ocular implant?

Back 112

cannot prevent CMV infection in the contralateral eye or systemic infection which is why concurrent PO treatment is needed

Front 113

What are some alternative therapies for treatment of cytomegalovirus?

Back 113

IV ganciclovir, foscarnet, or cidofovir

Front 114

What are the dosing recommendations for cidofovir and why?

Back 114

once weekly;has a very long intracellular half-life

Front 115

What major ADR is associated with cidofovir? What precautions are needed to be taken?

Back 115

nephrotoxicity (dose-limited);

adequate hydration with NS and concurrent probenecid (along with avoiding other nephrotoxic drugs)

Front 116

What is the DOC for secondary prophylaxis of CMV?

Back 116

valganciclovir

Front 117

What is the MOA for Zanamavir?

Back 117

selective inhibition of influenza virus neuraminidase.

Front 118

What is the function of viral neuraminidase?

Back 118

allows viral release from infected cells, prevents virus aggregation and decreases viral inactivation by mucus

Front 119

What are the indications for zanamavir?

Back 119

uncomplicated acute illness due to influenza A or B in pts >7 years old who have had sx less than 2 days

Front 120

Which antiviral is also used for prevention of influenza illness in pts over 5 years old?

Back 120

zanamavir

Front 121

What is the route of administration of zanamavir?

What is the dose and course of treatment?

Back 121

oral inhalation using a diskhaler devise

2 inhalations BID x 5 days

Front 122

When is Zanamavir treatment not recommended?

Back 122

in pts with underlying airway disease due to risk of severe bronchospasm

Front 123

What is the MOA of Oseltamavir?

Back 123

Oral prodrug which is converted by hepatic esterases to the active agent in vivo (oseltamivir carboxylate) which then inhibits viral neuraminidase altering virus partical release and aggregation

Front 124

What are the indications for Oseltamavir?

Back 124

Type A and B influenza infections in pts over 1 year of age who have had sx for less than 2 days

Front 125

What is the route of administration for Oseltamavir?

Back 125

oral suspension

Front 126

What are the major toxicities/ADRs with Oseltamavir?

Back 126

N/V/D

Front 127

What are the 4 major goals of ART therapy

Back 127

reduction of HIV-related morbidity/mortality and to increase duration/QOL;

Restoration and preservation of immunologic fxn;

Maximal and durable suppression of viral load (goal=to suppress to undetectabe levels after 3-6 mo of tx);

Prevent HIV transmission

Front 128

What is the spectrum of antiviral activity for Ribavirin?

Back 128

active vs RSV and some activity vs Influenza A and B (low efficacy when given PO)

Front 129

What are the indications of Ribavirin?

Back 129

Tx of severe lower respiratory tract infections due to RSV in hospitalized infants and young children (not adults!)

Front 130

What is the method of administration of Ribavirin?

Back 130

Aerosol given via a generator, mechanically-ventilated through ET tube, via oxygen hood/tent/face mask

Front 131

What are some serious problems that result from the mode of administration of Ribavirin?

Back 131

Drug precipitation in ET tube and ventilators has caused inadequate ventilation and gas exchange with sudden deterioration of respiratory function;

is also absorbed systemically and accumulates in RBCs decreasing their half-life to 40 ays

Front 132

Ribavirin is contraindicated in which patients?

What are precautions that need to be taken?

Back 132

Pregnant women and male partners of pregnant women.

Child-bearing aged women must use effective contraception during therapy and for 6 mo post-tx

Front 133

What toxicity can Ribavirin cause in caregivers with reactive airway diseases?

Back 133

bronchospasm and chestpain

Front 134

What is the MOA for palivizumab?

Back 134

monoclonal Ab that neutralizes and has fusion-inhibitor activity against RSV and inhibits RSV replication

Front 135

What are the indications for Palivizumab?

Back 135

prevention of serious lower resp tract disease caused by RSV in high risk ped patients (premies, bronchopulm dysplasia pts, hemodynamically significant congestive heart disease pts)

Front 136

What is the dosing of Palivizumab?

Back 136

15 mg/kg once a month during RSV season IM in anterolateral thigh

Front 137

What are the toxcities associated with Efavirenz (given once daily)?

Back 137

Rash, CNS/Psych symptoms, Teratogenicity in pregnancy, other symptoms (diarrhea, fever, and cough in ped pts)

Front 138

What are some symptoms of acute primary HIV infections?

Back 138

fever, lymphadenopathy, pharyngitis, rash, myagia/arthralgia, diarrhea (similar to flu, mono, etc and even asx)

Front 139

What is the first step in the MOA of Acyclovir?

What are the subequent steps that form the ACY-triphosphates?

Back 139

acyclovir is a synthetic acyclic guanosine analog that is posphorylated in the viral-infected cell by the viral enzyme thymidine kinase;

monophosphate form is converted by host cell to the diphosphate and triphosphate forms. ACYTP competes with the endogenous substrate deoxyguanosine triphosphate as the substrate for viral DNA polymerase

Front 140

What is the basis for selective toxicity of acyclovir?

Back 140

reaction occurs 100x more rapidly inside the virus-infected cell that non-infected host cells

Front 141

What are the effects of Acyclovir on viral DNA polymerase?

Back 141

ACYTP is incorporated into the viral DNA causing premature chain termination; ACYTP inactivates viral DNA polymerase but is less reactive towards the host DNA polymerase

Front 142

What is the first step of the MOA of ganciclovir?

What occurs in CMV-infected cells?

What are the subsequent steps that form the final product?

Back 142

Prodrug which is converted intracellularly to an active triphosphate form.

A viral protein kinase is responsible for the initial phosphorylation of ganciclovir and the subsequent phosphorylation steps to the active form.

same as acyclovir (?-look up)

Front 143

What are the effects of ganciclovir on DNA polymerase?

Back 143

competitive inhibition of viral DNA polymerase and direct incorporation into viral DNA which terminates DNA elongation

Front 144

What is the active drug produced from famciclovir?

Back 144

penciclovir

Front 145

What are the indications (4) for acyclovir?

Back 145

Initial and recurrent mucosal and cutaneous HSV1/2 and VAV infections in immunocompromised pts;

severe initial genital herpes in immunocompetent pts;

initial and recurrent genital herpes in adults (PO);

Acute tx of herpes zoster in immunocompetent adults (PO)

Front 146

How is the oral availability of Famciclovir different from the active drug penciclovir?

Where does the conversion of the prodrug form occur?

Back 146

is well absorbed;

liver and gut wall

Front 147

Famciclovir (and active drug) are indicated for...

Back 147

acute treatment of herpes zoster, genital herpes in immunocompetent pts, and recurrent mucocutaneous HSV infections in HIV-infected pts

Front 148

What is the active drug produced from Valacyclovir?

Back 148

acyclovir

Front 149

How is the oral availability different in valacyclovir compared to acyclovir?

Back 149

PO availability increases 3-5x resulting in increased acyclovir concentrations

Front 150

What are the indications for valacyclovir (and active drug form)?

Back 150

acute tx of herpes zoster, genital herpes in immunocompetent pts, recurrent mucocutaneous HSV infections in HIV-infected pts

Front 151

What is the major clinical uses of Foscarnet sodium?

Back 151

CMV retinitis in AIDS pts, tx of acyclovir-resistant or ganciclovir-resistant mucocutaneous herpes virus infections in immunocompromised pts

Front 152

What is the 3rd line tx for CMV retinitis in AIDS pts?

Back 152

cidofovir

Front 153

What are the two boxed warnings for Foscarnet?

Back 153

renal dysfunction and seizures

Front 154

What are the two boxed warnings for Cidofovir?

Back 154

nephrotoxicity and neutropenia

Front 155

What is the major risk factor for developing seizures when using foscarnet?

Back 155

low serum calcium

Front 156

Why does hypocalcemia occur when using foscarnet?

What are some symptoms?

Back 156

chelation of divalent cations may cause the hypocalcemia;

perioral tingling, numbness/paresthesias in lower extremities and seizures

Front 157

What precautions must be taken when giving Cidofovir to prevent nephrotoxicity?

Back 157

give via a slow IV infusion with probenecid and IV saline prehydration

Front 158

What are the major clinical uses of ophthalmic antiherpetic agents (Trifluridine)

Back 158

Primary keratoconjunctviitis and recurrent epithelial keratitis due to HSV1/2, epithelial keratitis that has not repsonded to topical idoxuridine or when ocular toxicity or hypersensitivity to this drug occurs, and in kids over 6 for tx of corneal inflammation due to HSV

Front 159

What are the major boxed warnings associated with abacavir?

Why is rechallenge contraindicated?

Back 159

hypersensitivity reactions (fever, skin, rash, NVD, etc), lactic acidosis, severe hepatomegaly with steatosis;

severe outcomes (hypotension, hepatic failure and renal failure), anaphylaxis or death can occur

Front 160

What are class sparing regimens/what is the idea behind it?

Back 160

Idea is that if you use only 2 of the 3 classes of hte preferred regimen, you have 'spared' one class in this category and you can use the spared one in the next regimen because resistance wont have been developed

Front 161

What are preferred regimens (definition)?

Back 161

treatments that have been shown to have optimal and durable virologic efficacy, have favorable tolerability and toxicity profiels are easy to use

Front 162

Why can viral load serve as a marker for improved clinical outcome due to ART?

Back 162

trials have shown a significant association between a decrease in plasma viremia and improved clinical outcome

Front 163

Viral load reduction to below limits of assay detection in an ART-naive pt usually occurs within the first _____ weeks of therapy.

Back 163

12-24

Front 164

What levels are generally very high in acute HIV infections?

Back 164

HIV RNA

Front 165

You can dx an HIV infection even though there are no Abs formed against the virus in early infections by testing for...

Back 165

HIV RNA

Front 166

What are the two major toxicities associated with didanosine?

Back 166

pancreatitis and fatal lactic acidosis

Front 167

Which drugs have significant DIs with didanosine and what occurs?

Back 167

Ketoconazole;

Ribavirin (increases intracellular levels of active metabolite of didanosine)

Tenofovir (increases didanosine levels)

Front 168

Didanosine is formulated as a ________ bead that degrades in acid and needs to be taken on a......

Back 168

delayed-release capsule/enteric coated;

empty

Front 169

Intrapartum IV zidovudine is recommended for all HIV-infected pregnant women regardless of.....

Back 169

their antepartum regimen to reduce perinatal transmission of HIV

Front 170

For women who are receiving a stavudine-containing antepartum regimen, this drug should be ______ during labor while IV zidovudine is being administered.

Back 170

discontinued

Front 171

For women who have received antepartum ARV drugs but have suboptimal viral suppression near delivery, what is recommended?

Back 171

C-section

Front 172

If the confirmatory HIV test is positive in a women who had an unknown status at presentation of labor, what do you want to do?

Back 172

give infant ARV drugs for 6 weeks

Front 173

ART Regimen #1 contains what 2 classes of drugs?

What drugs were specified in the notes?

What class does this spare?

Back 173

one NNRTI and two NRTI's;

efavirenz plus tenofovir/emtricitabine;

PIs

Front 174

Tenofovir is a...... (ART drug class)......

Back 174

nucleotide RTI

Front 175

Emtricitabine is a ......(ART drug class).........

Back 175

nucleoside RTI

Front 176

ART regimen #4 contains which drug classes?

What drugs were specified in the notes?

What classes does this spare?

Back 176

INSTI plus 2 NRTIs;

Raltegravir plus tenofovir/emtricitabine;

NRTIs and NNRTIs

Front 177

In boosted regimens, Ritonavir is used at a lower dose that is not antiretroviral but is at a level that does what? This is so that.....

Back 177

inhibits the P450 system; it blocks the metabolism of another PI drug so the combined use results in a 20x increase in plasma levels

Front 178

ART Regimens #2 and #3 contain which drug classes?

Which 2 regimens were listed in the notes?

What classes were spared?

Back 178

Ritonavir boosted PI plus NRTIs;

Ritonavir-boosted atazanavir plus tenofovir/emtricitabine;
Ritonavir-boosted darunavir plus tenofovir/emtricitabine;

NNRTIs