T8

Question 1

antifungal classes

Answer 1

azoles
polyene
echinocandin

Question 2

azole antifungals

Answer 2

imidazoles
triazoles

Question 3

imidazole
triazole

Answer 3

topical
IV/PO

Question 4

azoles MOA

Answer 4

inhibit 14-a-sterol demethylase, key enzyme in ergosterol synthesis
when this is inhibited, a toxic 14-a-methysterol placed in cell wall

Question 5

azoles side effects

Answer 5

GI upset

Question 6

azoles toxicity

Answer 6

elevated liver enzymes
QT prolongation
voriconazole - blurred vision and changes in color vision in approx 30%
itraconazole - BBW for QT prolongation, heart failure, negative inotropic effects and drug interactions

Question 7

azoles considerations

Answer 7

itraconazole, voriconazole, and fluconazole contraindicated in pregnancy

numerous drug interactions
-common inhibitors and substrates for a variety of CYP enzymes

Question 8

polyene MOA

Answer 8

amphotericin B forms aggregates that bind and extract ergosterol from the fungal cell wall which compromises membrane structure

Question 9

polyene considerations

Answer 9

broadest spectrum
IV only, poor oral absorption
“Amphoterrible” - infusion related toxicity and renal toxicity limit utility
-lipid formulation reduce risk of renal toxicity

Question 10

echinocandin MOA

Answer 10

inhibit glucan synthase complex which is required to maintain the structural integrity of the cell

Question 11

echinocandin considerations

Answer 11

only available in IV
well tolerated (minor GI upset, flushing)
all contraindicated in pregnancy

Question 12

antiviral targets

Answer 12

cell entry
uncoating
transcription
translation of viral proteins
posttranslational modifications
assembly of virion componenets
release

Question 13

herpes viruses

Answer 13

HSV 1 - oral herpes “cold sores”
HSV 2 - genital herpes

Varicella-Zoster Virus
varicella = chick pox
zoster = shingles

Cytomegalovirus (CMV)
most often affects immunosuppressed patients

Question 14

guanine nucleoside analogs MOA

Answer 14

require three phosphorylation steps for activation -> triphosphorylation

triphosphate active metabolite is then incorporated into replicating viral DNA

inhibits viral DNA polymerase and halts viral DNA synthesis

Question 15

guanine nucleoside analogs side effects

Answer 15

usually well tolerated
may cause headache, diarrhea, nausea

Question 16

guanine nucleoside analogs toxicity

Answer 16

nephrotoxicity (acyclovir)
neutropenia (ganciclovir/valganciclovir)

Question 17

guanine nucleoside analogs treatment considerations

Answer 17

topical, oral, IV
begin therapy as soon as possible after symptom onset but ideally within 72 hours
poor oral bioavailability -> reformulated as prodrugs and/or available IV

Question 18

anti-influenza M2 protein inhibitors MOA

Answer 18

inhibit M2 protein and uncoating of the viral RNA within infected host cells, thus preventing its replication

Question 19

anti-influenza M2 protein inhibitors indications

Answer 19

influenza A prophylaxis and/or treatment

Question 20

anti-influenza M2 protein inhibitors side effects

Answer 20

nausea, loss of appetite, insomnia, and difficulty concentrating

Question 21

anti-influenza M2 protein inhibitors considerations

Answer 21

only available as oral formulations - tablet, capsule, or syrup
should be started within 48 hours of symptom onset or as soon as possible after known exposure

Question 22

neuraminidase inhibitors MOA

Answer 22

inhibit the release of replicated viruses from the host cell thereby halting the spread of infection

Question 23

neuraminidase inhibitors indications

Answer 23

influenza A and B prophylaxis and/or treatment

Question 24

neuraminidase inhibitors side effects

Answer 24

nausea, vomiting, headache
inhaled: cough, bronchospasm, and throat irritation

Question 25

neuraminidase inhibitors considerations

Answer 25

should be started within 48 hours of symptom onset or as soon as possible after known exposure duration of 5 days for treatment and 7 days for prophylaxis (except IV which is a one dose treatment)

Question 26

baloxivir marboxil MOA

Answer 26

interferes with viral RNA transcription and blocks virus replication

Question 27

baloxivir marboxil indications

Answer 27

influenza A and B prophylaxis and/or treatment

Question 28

baloxivir marboxil side effects

Answer 28

nausea, diarrhea, headache

Question 29

antiretroviral drugs MOA

Answer 29

each of the antiretroviral classes inhibit a key step in the HIV lifecycle due to resistance mechanisms, drug regimens target multiple steps in this pathways

Question 29

baloxivir marboxil considerations

Answer 29

should be started within 48 hours of symptom onset or as soon as possible after known exposure single dose oral treatment

Question 30

antiretroviral drugs side effects

Answer 30

fever, fatigue, nausea, vomiting, diarrhea

Question 31

antiretroviral drugs considerations

Answer 31

hypersensitivity reactions (DRESS and SJS) protease inhibitors have MANY drug interactions due to CYP3A4 induction or inhibition

Question 32

antiretroviral drugs goals of treatment

Answer 32

suppress virus replication as much as possible for as long as possible undetectable viral load within 24 weeks of starting treatment three different antiretroviral drugs simultaneously for initial treatment and two to three drugs for the remaining duration of treatment

Question 33

prophylactic treatment approaches PrEP

Answer 33

PREP - pre exposure prophylaxis -used to prevent HIV infection in those who are currently HIV negative but at increased risk of exposure used continuously for prevention

Question 34

prophylactic treatment approaches PEP

Answer 34

PEP - post exposure prophylaxis treatement after potential HIV exposure to stop the virus from replication must be started within 72 hours of exposure (pref within 24 hours) three different antiretroviral drugs simultaneously for 28 days

Question 35

hepatitis B life cycle

Answer 35

chronic liver caused by hepatitis B virus bloodborne transmission vaccine preventable

Question 36

hepatitis B treatment considerations

Answer 36

treatment is NOT curative, but medications can be used indefinitely combination therapy may be needed to achieve viral suppression sudden discontinuation or interruption can cause acute exacerbation of hepatitis

Question 37

hepatitis C life cycle

Answer 37

chronic lover disease caused by HepC virus NOT vaccine preventable

Question 38

hepatitis C MOA

Question 39

hepatitis C treatment regimens

Answer 39

treatment is curative -> combination therapy required for 8-12 weeks

Question 40

hepatitis C treatment considerations

Answer 40

well tolerated with headache and fatigue as the most common side effects always check for HBV co-infection prior to initiating treatment -HBV reactivation may occur when HBC treatment is started -related to altered immune response and opportunity for HBV replications

Question 41

antifungals

Answer 41

Primarily impacting those who are immunocompromised or immunosuppressed Discovery and development of drugs that target the pathogen without posing significant toxicity to the host is challengin