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Pharmacology for advance practice nursing 712 > Week 3- Antivirals, vaccines, antiretrovirals > Flashcards

Week 3- Antivirals, vaccines, antiretrovirals Flashcards

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1
Q

Describe viral replication.

A

i) A virus cannot replicate on its own ii) “Obligate intracellular parasites” iii) It must attach to and enter a host cell iv) It then uses the host cell’s energy to synthesize protein, DNA, and RNA v) Viral replication peaks at or before clinical symptoms appear

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2
Q

Why are viruses difficult to kill?

A
  1. Viruses are difficult to kill because they live inside our cells
    1. Any drug that kills a virus may also kill our cells
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3
Q

Describe viral replication steps.

A
  1. Adsorption to and penetration into susceptible cells
  2. Uncoating of viral nucleic acid
  3. Synthesis of early regulatory proteins
  4. Synthesis of RNA or DNA
  5. Synthesis of late structural proteins
  6. Assembly of viral particles
  7. Release from the cell
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4
Q

Describe key characteristics of antiviral drugs.

A
  1. Able to enter the cells infected with virus
  2. Interfere with viral nucleic acid synthesis and/or regulation
  3. Some agents interfere with ability of virus
  4. to bind to cells
  5. Some agents stimulate the body’s immune system
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5
Q

Antiviral Medication Agents- antiviral and antiretroviral

A
  1. Antiviral agents
    1. Used to treat infections caused by viruses containing DNA / RNA
    2. Nucleoside Analogues
    3. Other antivirals for influenza
  2. Antiretroviral agents
    1. Used to treat infections caused by retroviruses e.g. HIV, the virus that causes AIDS
    2. Have RNA uses reverse transcriptase, integrase, and protease to make DNA
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6
Q

Nucleoside Analogues

-Pharmacodynamics

A
  1. Used mainly to treat herpes infection
  2. ALL result in inhibition of DNA synthesis
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7
Q

Nucleoside Analogues

-Different drugs

A
  1. Acyclovir (Zovirax)
    1. Requires activation by thymidine kinase – selectively activated in infected cells
  2. Valcyclovir (Valtrex)
    1. Converted to acyclovir after oral administration
  3. Famciclovir (Famvir)
    1. Converted to active penciclovir which is activated by thymidine kinase in infected cells
  4. Ribavirin (Virazole)
    1. Active against a wide range of DNA and RNA viruses (Influenza A & B, parmyxoviruses, HCV, and HIV
    2. Key role when combined with Interferon for treatment of HCV
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8
Q

Nucleoside Analogues

-Pharmacokinetics

A
  1. Absorption
    1. Acyclovir poorly orally absorbed (15 – 20%)
    2. Famciclovir is absorbed in the intestine for conversion to active form penciclovir
    3. Valacyclovir is a prodrug and is 54% as bioavailable as acyclovir
  2. Metabolism and Excretion
    1. Acyclovir, famciclovir, valacyclovir 90% in urine as unchanged drug
    2. Liver metabolizes the remaining 10%
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9
Q

Nuceloside Analogues

-Pharmacotherapeutics: Precautions and Contraindications

A
  1. Precautions and contraindications
    1. Adjust to Cr Cl if renal impairment
    2. Acyclovir, Valacyclovir, Famciclovir can be used during pregnancy
    3. Acyclovir and Valacyclovir are preferred as most is known
    4. Some acyclovir is excreted in breast milk but low risk
    5. Acyclovir approved for children over 2 years
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10
Q

Nuceloside Analogues

-Pharmacotherapeutics: ADRs

A
  1. Acyclovir: n & v, headache, skin rash, diarrhea – similar for valcylovir but more common
    1. Can cause renal dysfunction – more common in older or renal dysfunction
  2. Famciclovir: headache, dizziness, somnolence, paresthesia
  3. Drug interactions - minimal
  4. Clinical use and dosing – RENAL FUNCTION
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11
Q

Amount of dosages each day

  • Acyclovir
  • Famciclovir
  • Valacyclovir
A
  1. Acyclovir – 3 – 5 times daily
  2. Famciclovir – 2 – 4 times daily
  3. Valacyclovir – 1-2 times daily
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12
Q

Nucleoside Analogues

-Patient Education

A
  1. Food does not alter absorption
  2. Take with a full glass of water
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13
Q

Considerations for Nucleoside Analogues in Primary Care.

A
  1. Don’t cure but shorten the duration, decrease the severity, and reduce incidence of sequelae
  2. HSV – Genital herpes
  3. Herpes zoster (shingles)
    1. Within 3 days
  4. Varicella (chicken pox)
    1. 20 years and older or immunocompromised (24 hours)
  5. Gingivostomatitis in children
  6. Selection is based on cost and convenience
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14
Q

Describe influenza. Type A compared to Type B.

A
  1. Serious respiratory tract infection
  2. Major cause of morbidity and mortality worldwide
  3. 3 – 11% of the population in the US is affected.
  4. Caused by influenza viruses, which are highly variable and undergo constant evolution (mutation)
    1. Type A – more infectious than B
    2. Type B
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15
Q

What are classifications of anti-virals used for influenza?

A
  1. Adamantanes
  2. Neuraminidase Inhibitors
  3. Cap-dependent endonuclease inhibitors
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16
Q

Antivirals for Influenza

-Adamantanes

A
  1. Adamantanes
    1. Amantadine and rimantadine effective against Influenza A – HIGH levels of resistance (99%)
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17
Q

Antivirals for Influenza

-Neuraminidase Inhibitors

A
  1. Oseltamivir (Tamiflu)
  2. Zanamivir (Relenza)
  3. Peramivir (Rapivab) (2014)
  4. Active against both A and B
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18
Q

Neuraminidase Inhibitors

-Pharmacodynamics/MOA

A
  1. Prevent viral replication by interfering with neuraminidase, an enzyme needed for enabling a virus to leave the infected host cell.
  2. Prevents viral spread across respiratory track mucous membranes.
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19
Q

Neuraminidase Inhibitors

-Oseltamivir, zanamivir, baloxavir, and peramivir

A
  1. Should be started within 48 hours of onset of symptoms
  2. Can be used for prophylaxis (osteltamivir and zanamivir)
  3. CDC - Seasonal Influenza (Flu) - Antiviral Medications: Summary for Clinicians
  4. Know guidelines for treatment and prophylaxis
  5. Know guidelines for who are recommended for antiviral treatment
  6. Shorten the duration of illness (1-2 days)
  7. Mitigate severity
  8. Decrease viral shedding and spread
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20
Q

Antivirals for influenza

-Cap-dependent endonuclease inhibitor

A
  1. Cap-dependent endonuclease inhibitor
    1. Interferes with viral RNA transcription and blocks virus replication
    2. Baloxavir (Xofluza) A & B (2018)
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21
Q

Differentiate between vaccination and immunization.

A
  1. Vaccination: act of administering a vaccine
  2. Immunization: development of immunity to a pathogen
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22
Q

What is a vaccine?

A
  1. Suspension with antigenic molecules derived from a microorganism given to stimulate an immune response to an infectious disease
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23
Q

Describe 4 different types of vaccines.

A
  1. Weakened or killed microbe
  2. Inactivated toxins
  3. Toxoids derived from microbes
  4. Immunologically active surface markers extracted or copied from microbes
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24
Q

Define Herd Immunity.

A
  1. A high level of immunization in a population results in protection of another unvaccinated population
25
Q

What are contraindications to vaccination?

A
  1. Previous anaphylactic reaction to that specific vaccine
  2. Previous anaphylactic reaction a specific vaccine component
  3. Moderate to severe illness, with or without fever
  4. Live virus is contraindicated during pregnancy or for those who are severely immunocompromised
26
Q

What is a preservative found in vaccines?

A
  1. Thimerosol: mercury-based preservative
27
Q

Define Live Attenuated Vaccine. Contraindications. Give examples.

A
  1. Live microbes that have been weakened or made avirulent
  2. Avoid in pregnancy or immunocompetent or exposure to same
  3. Immune response more similar to natural infection
  4. Examples: Measles, mumps, rubella (MMR), live attenuated influenza (intranasal)
28
Q

Define Inactivated/killed Vaccine. Give examples.

A
  1. Whole microbes that have been killed or specific pieces of microbe (e.g. polysaccharide coat of a virus)
  2. Examples: Inactivated polio virus (IPV), Trivalent or quadrivalent influenza vaccine, human papilloma virus (HPV), hepatitis B
29
Q

Define Toxoid Vaccine. Give examples.

A
  1. Made from endotoxins and exotoxins from bacteria
  2. Bacterial toxins undergo chemical treatment to render them nontoxic
  3. Antibodies are produced to protect
  4. Examples: Tetanus toxoid, diphtheria toxoid (Td)
30
Q

What can we do to promote vaccine rates?

A
  1. Educate, spend time talking about the disease and vaccine
31
Q

What are the adult immunization rates for pneumococcal and influenza?

A

50-60%

32
Q

Vaccina recommendations and contraindications for pregnant patients.

A
  1. Pregnancy – no live vaccines, ok in 2nd and 3rd trimester but not more than 2 weeks prior to EDC. Encourage influenza / Tdap.
33
Q

What are adverse effects of vaccines?

A
  • Local reactions
  • Arthus reactions: Type III sensitivities – local reaction of entire thigh or deltoid
  • Fever >38C or 100.4F – more common with whole pertussis vs. acellular and live virus
  • Guillain Barre Syndrome – review – influenza, old Hepatitis B, menningococcal
34
Q

Describe the overview of HIV replications.

A
  1. Entry
    1. Binding of HIV receptors (chemokine receptors) on surface of CD4 cell- results in membrane fusion
    2. CCR5 Antagonists
    3. Fusion inhibitors
    4. Post attachment inhibitors
  2. Reverse Transcription
    1. Reverse transcriptase, protease, integrase enzymes: RNA to DNA
    2. Nucleoside /Nucleotide reverse transcriptase inhibitors (NRTI / NtRTI)
    3. Nonnucleoside reverse transcriptase inhibitors (NNRTI)
  3. Integration
    1. Enzyme integrase inserts viral DNA
    2. Integrase Strand Inhibitors (INSTIs)
  4. Replication
    1. Viral DNA forms long polypeptide chains that will become the viral protein and enzymes
    2. No meds inhibit this step
  5. Assembly
    1. Proteins and enzymes mover into cells outer member and assemble into a new non infectious HIV particle /bud
    2. No meds inhibit this step
  6. Budding and Maturation
    1. Viral but is released, viral enzyme protease cuts long HIV polyprotein chains into small mature infectious viral particle
    2. Protease inhibitors.
35
Q

Describe the life cycle of the HIV/AIDs virus.

A
  1. HIV enters the body
  2. Outer glycoprotein binds to CD4 receptors
  3. 95% of newly infected use CCR5 to enter
  4. Use CXCR 4 in advanced disease
  5. Early stage = 10 billion virions per day
  6. Initially killed by cytotoxic T lymphocytes or undergo apoptosis (programmed death) but viruses in macrophages and T lymphocytes in lymph nodes are protected
36
Q

Discuss the different ways of HIV/AIDs transmission.

A
  1. Sexual – anal and vaginal receptive or insertive intercourse most common
  2. Parenteral – blood, blood products, drug use (up to 42 days on a syringe)
  3. Perinatal
  4. Increased probability if at a time of high viral replication, uncircumcised, lesions, concomitant STI
  5. Do not seroconvert (Undergo a change from a seronegative to a seropositive condition) until 4 – 12 weeks post exposure / infection
  6. 95% within 6 months
37
Q

Differentiate between HIV and AIDs.

A

HIV is the virus that causes AIDs. People with HIV do not always have AIDs. AIDs is sometimes referred to as “late stage HIV” or “advanced HIV disease”

38
Q

Define a retrovirus.

A

Type of virus that inserts a copy of its RNA genome into the DNA of a host cell that it invades, thus changing the genome of that cell.

39
Q

History of HIV and AIDs.

A
  1. First recognized in 1981 – 35 million have died
  2. HIV is a retrovirus – able to create DNA copies of their RA genome, thus reversing the usual flow of genetic information
  3. Pathophysiology is related to loss of CD4+ cells critical to maintain cell mediated immune function.
  4. HIV – 1 retrovirus, HIV- 2 less common
  5. HIV -2 endemic to West Africa and is zoonotic (pathogen jumps from animal to human). Transmitted from Sooty mangabey (Primate)
    1. Related to eating bush meat and keeping pets
40
Q

Describe screenign and diagnostics for HIV/AIDs.

A
  1. Routine screening is recommended for all adolescents and adults 15 – 65 years of age (younger and older if at risk)
  2. Routine screening for all pregnant women
  3. HIV Enzyme Linked Immunoabsorbant Assay (ELISA): GOLD STANDARD
  4. Rapid Test e.g. OraQuick – at home testing
  5. 2012 FDA approves in home test kit
  6. Confirmatory test: Western Blot ****Gold standard
  7. Diagnostics used to assess HIV progression to AIDS
    1. CD4+ T cell counts and percentage
    2. HIV RNA plasma concentration (viral load)
    3. ART is recommended for all viremic patients with established HIV infection, regardless of CD 4 count
    4. ART prevents HIV transmission
41
Q

Describe treatment goals for HIV/AIDs.

A
  1. Treatment goals
    1. Improve quality of life
    2. Obtain maximal and durable suppression of HIV
    3. Prevent vertical HIV transmission
    4. Prolong survival
    5. Reduce HIV related mortality
    6. Reduce transmissibility of HIV
    7. Restore and preserve immunologic function
42
Q

When should antiretroviral therapy (ART) be initiated?

A
  1. ART is recommended for all viremic patients with established HIV infection, regardless of CD 4 count
  2. ART prevents HIV transmission
  3. Previously the threshold for initiating ART was CD4 cell count of <= 350 per mm3
43
Q

What is the gold standard test for HIV/AIDs?

A
  1. HIV Enzyme Linked Immunoabsorbant Assay (ELISA): GOLD STANDARD
  2. Confirmatory test: Western Blot ****Gold standard
44
Q

Seven classes of antiretrovirals.

A
  1. Nucleoside (NRTI) / Nucleotide (NtRTI) Reverse Transcriptase Inhibitor (NUKES)
  2. Nonnucleoside Reverse Transcriptase Inhibitor (NNRTI) (NONNUKES)
  3. Protease Inhibitor (PI)
  4. Integrase Strand Transfer Inhibitors (INSTI)
  5. CCR5 Inhibitors
  6. Fusion Inhibitors (ENTRY INHIBITORS)
  7. Post attachment Inhibitors (MONOCLONAL ANTIBODIES)
45
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class

-Nucleoside (NRTI) / Nucleotide (NtRTI) Reverse Transcriptase Inhibitor (NUKES)

A
  1. Nucleoside (NRTI) / Nucleotide (NtRTI) Reverse Transcriptase Inhibitor (NUKES)
    1. Inhibits reverse transcriptase from synthesizing viral DNA
    2. NtRTIs are already chemically activated, NRTI’s must undergo chemical changes to activate
    3. INHIBITS ENYZMES REQUIRED FOR REPLICATION
46
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class

-Nonnucleoside Reverse Transcriptase Inhibitor (NNRTI) (NONNUKES)

A
  1. Nonnucleoside Reverse Transcriptase Inhibitor (NNRTI) (NONNUKES)
    1. Inhibits reverse transcriptase by binding to the center of the enzyme
    2. INHIBITS ENYZMES REQUIRED FOR REPLICATION
47
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class

-Protease Inhibitor (PI)

A
  1. Protease Inhibitor (PI)
    1. Used with a pharmacokinetic enhancer (booster) e.g. cobacistat or ritonavir
    2. Inhibits HIV proteases which prevents formation of smaller functional proteins, virions produced are not infectious.
    3. INHIBITS ENYZMES REQUIRED FOR VIRAL REPLICATION
48
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class

-Integrase Strand Transfer Inhibitors (INSTI)

A
  1. Integrase Strand Transfer Inhibitors (INSTI)
    1. Inhibits the enzyme integrase which inserts HIV into the DNA of T cells thus stopping viral replication.
    2. INHIBITS ENYZMES REQUIRED FOR VIRAL REPLICATION
49
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class

-CCR5 Inhibitors

A
  1. CCR5 Inhibitors
    1. Drug binds with CCR5 preventing HIV virus to enter the T cells
    2. BLOCK ENTRY OF THE VIRUS INTO THE CELL
50
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class

-Fusion Inhibitors (ENTRY INHIBITORS)

A
  1. Fusion Inhibitors (ENTRY INHIBITORS)
    1. Prevents HIV envelope from fusing with the cell membrane of T-cells, preventing the virus from entering and replicating
    2. SubCut and $$$$$
    3. BLOCK ENTRY OF THE VIRUS INTO THE CELL
51
Q

Mechanism of action (Pharmacodynamics) of specific antiretroviral class
-Post attachment Inhibitors (MONOCLONAL ANTIBODIES)

A
  1. Post attachment Inhibitors (MONOCLONAL ANTIBODIES) – IV, used when resistant to other ARVs, prevents virus from entering cell.
52
Q

Antiretroviral therapy (ART) Considerations.

A
  1. Patients will be taking for a longer time
  2. Many combinations
  3. Improvement in # pills and frequency
  4. Significant adverse effects, drug interactions, and morbidity related to CV, bone, and kidney disease.
  5. Treatment for ART Naïve Patients
53
Q

What are some non-pharmacological treatments for HIV/AIDs?

A
  1. Nonpharmacological management
    1. Multidisciplinary approach
    2. Lifetime
    3. Patient adherence
    4. Nutritional and dietary counseling
    5. Mental health
    6. Other lifestyle risks
54
Q

What are drug regimens for pre-exposure prophylaxis for HIV/AIDs?

A
  1. Tenofovir disoproxil fumarate/ emtricitabine (2 NRTI): Truvada (30@ $1900)
  2. Tenofovir alafenamide / emtricitabine (2 NRTI): Descovy
  3. Alternate dosing includes an option to start daily PreP prior to a discrete period of risk (e.g. vacation) one week before (male patient) or three weeks before (female partner) and continued for one month after

OR

  1. On demand (event driven) therapy with loading dose (two tablets ) taken 2 – 24 hours before, daily during event of sexual activity, and two days after.
55
Q

What drug regimen is used for post-exposure prophylaxis for HIV/AIDs?

A
  1. Tenovir disoproxil fumarate and emtricitabine (2 NTRIs)

With

  1. Raltegravir or dolutegravir (INSTI)
56
Q

What is the mainstay of antiretroviral treatment for experienced patients?

A
  1. Ongoing viral replication will eventually lead to resistance to prescribed medication
  2. No consistency on when to change therapy
  3. COMPLEX!!!
57
Q

When potentially exposed to HIV when should the ELISA be completed?

A

-Initial visit, re-test one month and three months later

58
Q

What are the primary options for initial antiretroviral treatment?

A

NRTI combinations for initial treatment

  • PRIMARY OPTION is 2 NRTIs with and INSTI
  • Biktarvy (bictagravir (INSTI) with emtricitabine and tenofovir alafenamide (NRTIs) (one tablet daily) Feb 2018
  • Monitor liver and renal function
  • $3500 for a 30 day supply
59
Q

General guidelines for ART.

  • Typical classes of drugs used.
  • Considerations prior to initiation.
A

***Initial treatment= 2 NRTI and a NNRTI or PI or INSTI

***Do a pregnancy test before initiating

***Single tablets help adherence

Pharmacology for advance practice nursing 712 (24 decks)

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