anti parasite drugs; antivirals

Question 1

chloroquine MOA

Answer 1

blocks detoxification of heme into hemozoin. heme accumulates and is toxic to plasmodia

Question 2

chloroquine use

Answer 2

treast plasmodial species other than P. falciparum. doesn’t work for P falciparum becasue of a membrane pump that decreases the intracellular concentration of the drug (falciparum should be treated with artemether/lumefantrine or atovaquone/proguanil).

Question 3

chloroquine toxicity

Answer 3

retinopathy, pruritis,

Question 4

zanamivir: mechanism and clinical use

Answer 4

inhibits flu neuraminidase: decreases the release of progeny virus.
used to treat and prevent flu A and B
oseltamivir also works this way

Question 5

ribavirin: mechanism and clinical use

Answer 5

inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase.
used for RSV and hepC

Question 6

ribavirn: toxicity

Answer 6

hemolytic anemia, severe teratogen

Question 7

acyclovir: others, mechanism

Answer 7

others includ famciclovir, valacyclovir. this drug is monophosphorylated by HSV/VSV thymidine kinase and not phosphorylated in uninfected cells, so there are few adverse effects. it is a guanosine analog that inhibits viral DNA pol by chain termination.

Question 8

acyclovir: use, considerations

Answer 8

used for HSV and VZV; weakly useful against EBV. no activity against CMV. no effect on latent forms of HSV and VZV. valacyclovir is a prodrug of acyclovir with better oral availability

Question 9

toxicity and resistance for acyclovir

Answer 9

can cause crystalline nephropathy and acute renal failure. resistance by mutated viral thymidine kinase.

Question 10

ganciclovir mechanism

Answer 10

5’ monophsphate formed by a CMV viral kinase. this is a guanosine analog. it preferentially inhibits viral DNA pol.

Question 11

ganciclovir use and resistance

Answer 11

CMV, esp. in immunocompromised pts. valganciclovir is a prodrug with better oral availability. resistance by mutated CMV DNA pol or lack of a viral kinase

Question 12

gancyclovir toxicity

Answer 12

leukopenia, neutropenia, thrombocytopenia, renal toxicity. more toxic than acyclovir

Question 13

foscarnet: mechanism

Answer 13

viral DNA pol inhibitor that binds to the pyrophospate binding site of the enzyme. doesn’t require viral kinase activation. resistance by mutated DNA pol.

Question 14

foscarnet use

Answer 14

CMV retinitis in immunocompromised when ganciclovir fails. good for asyclovir resistant HSV.

Question 15

toxicit of foscarnet

Answer 15

nephrotoxic

Question 16

cidofovir mechansim

Answer 16

preferentially inhibits viral DNA pol. doesn’t require phosphorylation by a viral kinase.

Question 17

cidofovir use

Answer 17

CMV retinitis in immunocompromised pts; acyclovir resistant HSV. long half life.

Question 18

toxicity of cidofovir

Answer 18

nephrotoxicity. coadminister with pronebecid (incr. uric acid excretion in urine) and IV saline to decr. toxicity