Anti-Viral meds

Question 1

What is a virus?

Answer 1

Double or single stranded DNA or RNA enclosed in a protein called capsid

Question 2

Name the components of Influenza

Answer 2

Hemagglutinin (responsible for infecting the cell), Neuraminidase, M2 protein

Question 3

Name the process of the Influenza virus life cycle

Answer 3

1) Attachment (Interaction between hemagglutinin which is found on envelope and binds with silica acid)
2) Penetration into host cell (H+ enters)
3) Uncoating of nucleic acid (Uses RNA dependent RNA polymerase)
4) Replication of nucleic acid
5) Synthesis of viral proteins
6) Assembly of the components
7) Release of new virus by budding or cell lysis (Neuramininidase chops off silica acid)

Question 4

Zanamirvir (Relenza) MOA/Mode

Answer 4

Inhibits viral neuraminidase –> Interfere with release of progeny influenza virus from infected cells

-Inhalation

Question 5

Oseltamivir (Tamiflu) MOA/Mode

Answer 5

Inhibits viral neuraminidase (chopping off) –> Interfere with release of progeny influenza virus from infected cells

-PO (DOC)

-Only given/recommended within 2 days as a prophylaxis

Question 6

Peramirvir (Rapivab) MOA/Mode

Answer 6

Inhibits viral neuraminidase –> Interfere with release of progeny influenza virus from infected cells

-PO

Question 7

Zanamirvir AE/CI

Answer 7

AE:
-Cough
-Headache

CI:
-Milk protein/hypersensitivity
-COPD
-Asthma

Question 8

Oseltamivir (Tamiflu) AE

Answer 8

AE:
-Headache/N/V

Question 9

Peramirvir (Rapivab) AE

Answer 9

AE:Diarrhea

Question 10

Amantadine MOA/AE

Answer 10

MOA: Interferes with M2 protein on influenza A virus
(Also an NMDA Receptor blocker)

-CNS Effects (insomnia, nervousness, light headless)
-GI

Question 11

What is the target of HIV Cells?

Answer 11

CD4 T-Cells

T-Helper cell helps other cells to do a better job

Question 12

Describe the HIV Life cycle

Answer 12

Infection begins with
1) Gp120 binds to CD4 and then after makes a conformational change, and then GP120 can bind to a chemokine receptor CCR5 (or CXCR4)
2) RIP Steps

Question 13

What Inhibits the reverse transcriptase?

Answer 13

Viral DNA is made from RNA in the reverse transcriptase step

-NRTIs (Nucleoside/tide reverse transcriptase inhibitor)

-NNRTIs (New nucleoside reverse transcription inhibitor)

Question 14

What inhibits the Integrase?

Answer 14

Integrates its DNA into our DNA

INSTIs (Integrase strand transfer inhibitors)

Question 15

What inhibits the protease?

Answer 15

mRNA –> Protein –> Virus Assembly. Protease helps assembly virus

PI (Protease Inhibitors)

Question 16

Eufuvirtide

Answer 16

Fusion Inhibitors (GP 41)
-Reserved for people with more complicated HIV cases

Question 17

Maraviroc

Answer 17

Fusion Inhibitors (CCR5) Only

Question 18

Name the NRTI’s? MOA/Class AE/CI

Answer 18

Didanosine
Zidovudine

(SIGNIFICANT MITOCHONDRIAL TOXICITY)

Lamivudine
Abafavir
Tenofovir (Once daily dosing)
Emtricitcitabine (Once daily dosing)

(MINIMAL MITOCHONDRIAL TOXICITY)

“Dine & Bine ending”

MOA:
Competitively inhibit nucleotide binding to reverse transcriptase –>Terminate DNA chain (lacking hook molecule without phosphate to make strand)

nucleotide –> Has phosphate on it
nucleoside –> Prodrug, does NOT have phosphate

CLASS AE:
-Mitochondrial Toxicity (Inhibit DNA dependent DNA polyermase –High affinity for DNA poly)

Pancreatitis
Lactic acidosis
Anemia
Neuropathy (peripheral)

Class AE: Fever compared to other HIV drug classes (no CYP)

Question 19

Abacavir AE

Answer 19

BBW: Hypersensitivity reaction (rash, fever, fatigue)
-Needs HLAB 5701 testing before starting
-Danger with re-challenge

Question 20

Tenofovir AE

Answer 20

Renal/Bone Toxicities ( Need renal dosing)
-New Tenovofir formulation: Tenovofir alfenamide
(TAF): Decrease renal/bone toxicities contrast to old TDF

Question 21

Zidovudine AE

Answer 21

Lipoatrophy
Hepatotixicity or Lactic acidosis (BBW)

Question 22

Other characteristics for Lamivudine, Tenofovir, Emtricitabine

Answer 22

Have activity against HepB
Hepatic flare with acute removal of agents in patients co-infected with hepB
-BBW for HepB exacerbation

Question 23

Didanosine

Answer 23

Pancreatitis
Hepatotoxicity or Lactic acidosis (BBW)

Question 24

Name the NNRTI’s? MOA/AE?

Answer 24

Efavirenz (mixed 3A4 inhibitor/inducer)
Nevirapine (3A4 and 2BG inducer)
Etravirine (3A4 inducer; 2C9, 2C19 inhibitor)
Rilpivirine (none)

“vir” in the name

MOA: Bind directly to RT, cause a conformational change and distrupt catalytic center of RT

AE: Rash (SJS), hepatotoxic (Increase LFT)

Interactions: CYP interactions, Cyp inducers/inhibitors
EXCEPY RILPIRIRINE

Food/AE:
-Efavirenz: needs to be given on empty stomach (High fat calorie diet increase absorption –> Increase AE), CNS symptoms, Teratogenic

-Etravirine and Rilpivirine =take with food to increase absorption

-Nevirapine: take without regards to meal; metabolized with 3A4

Question 25

Name the INSTI’s. MOA/AE?

Answer 25

Raltegravir
Elvitegravir –>(metabolized via 3A4; use with booster (ie. cobicistat) drug that increase effect of other drug ie. blocking metabolism)
Dolutegravir
Bictegravir

MOA: Interfere with with the integration of viral DNA into host DNA

Class AE: Very well tolerated, GIeta

Question 26

Name the PI’s. MOA/AE?

Answer 26

Atazanavir
Darunavir
Ritonavir *
Nelfinavir
Indinavir

Used only as a booster
Navir ever tease a protease

MOA:Block proteolytic cleavage of protein precursors that are necessary for the production of infectious parties

Class AE: Metabolic abnormalities, (less with at)
Hyperlipidemica, hyperglycemia, fat distribution “protease pouch”

AVOID IN PT WITH HISTORY OF CAD/DIABETES

Mechanism: HIV protease has high homology to regions of that regulate lipid metabolism
-Hepatotoxicity

Class interactions: Cyp inhibitors

Atazanacir: Hyperbilirubienmia (inhibitor UDP glycyonyl-transferase)

Characteristcs: Generally boosted with ritonavir or cobicistat; nelfinavir only PI that does not require boosting