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Pharmacology Unit 1 > Antivirals > Flashcards

Antivirals Flashcards

1
Q

what are the five major classes of antiretroviral medications for HIV

A
  1. nucleoside reverse transcriptase inhibitors (NRTI’s)
  2. non-nucleoside reverse transcriptase inhibitors (NNRTI’s)
  3. protease inhibitors (PI’s)
  4. Entry inhibitors
  5. Integrase inhibitors
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2
Q

MOA for NRTI’s?

A

viral DNA chain termination via inhibition of reverse transcriptase enzyme

serve as analog “posers”

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3
Q

Tenofovir

  1. class?
  2. specific side effects?
A
  1. NRTI’s

2. nephrotoxicity

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4
Q

Abacavir

  1. class?
  2. specific side effects?
A
  1. NRTI’s

2. hypersensitivity rxns

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5
Q

Lamivudine/emtricitabine

  1. class?
  2. specific side effects?
A
  1. NRTI’s

2. few, generally well-tolerated

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6
Q

Zidovudine

  1. class?
  2. specific side effects?
  3. PEARLS?
A
  1. NRTI’s
  2. anemia
  3. used in pregnant women
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7
Q

NRTI class side effects?

A

lactic acidosis (much less with new agents)

GI side effects

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8
Q

MOA for NNRTI’s?

A

bind directly to reverse transcriptase and inhibit its action

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9
Q

Efavirenz

  1. class?
  2. specific side effects?
A
  1. NNRTI’s
  2. CNS symptoms; vivid dreams, drowsiness
    Teratogenic
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10
Q

Etravirine

  1. class?
  2. specific side effects?
A
  1. NNRTI’s

2. rash, increased LFTs

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11
Q

Rilpivirine

  1. class?
  2. specific side effects?
A
  1. NNRTI’s

2. rash, QT prolongation

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12
Q

MOA of protease inhibitors (PIs)?

A

bind within active pocket of protease, inhibiting binding of virus

minimize cross-reaction between drugs in the same class

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13
Q

Ritonavir Boosting

  1. Ritonavir at ___ doses enhances blood levels of other PIs when given together
  2. MOA?
A
  1. low doses

2. P4503A4 inhibition in gut and liver, P-glycoprotein inhibition

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14
Q

Cobiscistat

  1. function?
  2. PEARLS?
A
  1. pharmacokinetic enhancer

2. similar to ritonavir but NO antiretroviral therapy

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15
Q

PI class toxicities; what two main categories?

A
  1. GI = N/V, diarrhea

2. Metabolic toxicities = dyslipidemia, hyperglycemia, lipodystrophy

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16
Q

what are the 3 steps of HIV entry?

A
  1. specific binding of HIV gp120 to CD4 molecule
  2. Conformational change followed by co-receptor binding (CCR5 or CXCR4)
  3. Exposure of gp41 that mediates fusion of viral and cell membranes
17
Q

Enfurvirtide

  1. MOA?
  2. PEARLS?
  3. side effects?
A
  1. blocks gp41
  2. injectable, only oral form of HIV treatment
  3. local injection sight reaction, increased rate of bacterial pneumonia, hypersensitivity
18
Q

Maraviroc

  1. MOA?
  2. side effects?
  3. PEARLS?
A
  1. CCR5 antagonist as HIV uses CCR5 as a co-receptor necessary to enter T-cells
  2. hepatotoxicity, upper respiratory infections, rash, MSK symptoms
  3. can test for co-receptor; CCR5 vs. CXCR4
19
Q
  1. MOA of integrase inhibitors?

2. adverse reactions?

A
  1. Inhibit enzyme which is necessary for viral insertion into human DNA genome
  2. nausea, headache, diarrhea, pyrexia, myopathy and rhabdomyolysis
20
Q

Raltegravir, Elvitegravir, Dolutegravir

what class of drugs?

A

Integrase inhibitors

21
Q

antiretroviral therapy (ART) is recommended for ____ HIV-infected patients to ____ disease progression

A
  1. all HIV-infected patients

2. reduce risk of disease progression

22
Q

2 basics of HAART?

A
  1. Combination therapy - at least 3 active agents

2. Utilization of multiple classes

23
Q

why is Hepatitis C Virus the most genetically diverse virus?

A

Variability in RNA sequence

24
Q

what is the important predictor of poor IFN treatment in HCV?

A

genotype

25
Q

true or false?

sustained virologic response is NOT equivalent to a cure?

A

FALSE, it is!

26
Q

Sofosbuvir, Paritaprevir

  1. class?
  2. MOA?
  3. HCV genotypes active across?
  4. toxicity concerns?
A
  1. NS5B polymerase inhibitors
  2. inhibitor of NS5B, RNA-dependent RNA polymerase and competes with natural viral nucleotide to cause chain termination
  3. ALL!
  4. relatively safe; fatigue, HA, GI, anemia possible
27
Q

Ledipasvir, Daclatasvir, Ombitasvir, Elbasvir, Velapatasvir

  1. class?
  2. MOA?
  3. Toxicity concerns?
A
  1. NS5A inhibitors (HCV)
  2. inhibits HCV NS5A, viral phosphoprotein required for viral replication
  3. relatively safe; fatigue, headache, GI side effects possible
28
Q

Grazoprevir, Simeprevir, Boceprevir, Telaprevir

  1. class?
  2. MOA?
  3. toxicity concerns?
A
  1. NS3/4A protease inhibitors
  2. prevent viral maturation through inhibition of protein synthesis
  3. slightly variable depending on the agent;
    possibly anemia, rash, itching, GI side effects, drug interactions
29
Q

Acyclovir

  1. class?
  2. MOA?
  3. spectrum?
  4. RoA?
  5. toxicity?
A
  1. guanosine nucleoside antivirals
  2. competes with DNA analogous to cause viral chain termination
  3. herpes simplex 1+2. varicella-zoster
  4. IV, PO, topical
  5. CNS (malaise, headache, confusion), N/V, diarrhea, renal dysfunction
30
Q

Ganciclovir

  1. spectrum?
  2. RoA?
  3. toxicity?
A
  1. HSV, VZV, and CMV
  2. IV/PO but poor bioavailability with PO
  3. myelosuppresion, CNS toxicity (headache, seizure, confusion), hepatotoxicity, GI intolerance
31
Q

Foscarnet

  1. MOA?
  2. PEARLS?
  3. Adverse effects?
A
  1. directly inhibits herpesvirus DNA polymerase or HIV reverse transcriptase
  2. active against acyclovir and ganciclovir resistant viruses
  3. dose-limiting nephrotoxicity, electrolyte/metabolic abnormalities, CNS side effects, myelosuppression
32
Q

Influenza

  1. class/drug of choice?
  2. names?
  3. spectrum?
  4. MOA?
  5. side effects?
A
  1. neuramindase inhibitors
  2. Oseltamivir (Tamiflu), Zanamivir (Relenza), Peramivir (Rapivab)
  3. influenza A and B
  4. inhibits viral neuraminidase which is critical in penetration of respiratory tract mucus and in release of virus from infected cells
  5. GI (N/V, diarrhea), neuropsychiatric (agitation, anxiety, altered mental status)

Pharmacology Unit 1 (5 decks)

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