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Pharm 2 > PHARMACOLOGY OF ANTIVIRALS AND ANTIFUNGALS > Flashcards

PHARMACOLOGY OF ANTIVIRALS AND ANTIFUNGALS Flashcards

1
Q
  • Capsid:
A

protein coat surrounding genetic material of a virus

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2
Q
  • DNA polymerase:
A

an enzyme which catalyzes the process of DNA
replication

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3
Q
  • Endocytosis:
A

ingestion/engulfing of materials (e.g. a virus) via the
cell membrane

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4
Q
  • Envelope:
A

outermost lipid (fatty) layer which protects genetic
material when traveling between host cells; only present on some
viruses

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5
Q
  • Host:
A

organism that is infected by a virus

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6
Q
  • Incubation period:
A

time duration between exposure to the virus and
the appearance of symptoms

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7
Q
  • Latency:
A

the ability a pathogenic virus to lie dormant within a cell

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8
Q
  • Neuraminidase:
A

an enzyme found on the surface of influenza virus
which enables the virus to be released from the host cell

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9
Q
  • Nucleocapsid:
A

core of a virus, made up of the genetic material and
the capsid

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10
Q
  • Reverse transcriptase:
A

an enzyme used to generate
complementary DNA (cDNA) from an RNA template (reverse
transcription)

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11
Q
  • RNA polymerase:
A

the enzyme which catalyzes the process of
transcription

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12
Q
  • Transcription:
A

the synthesis of RNA from a DNA template

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13
Q
  • Translation:
A

the synthesis of protein from RNA

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14
Q
  • Virion:
A

a complete and free-living virus particle outside of its host;
the vehicle for transmission of the genome to the next host cell or
organism

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15
Q

What is a Virus?
* “Virus” in Latin means “poison”
* Small, obligate parasites with — genomes
* Viral genomes direct their own replication and the synthesis of other
viral components, using —
- No — of their own
- Not “—” themselves
* Can infect all living organisms; commonly cause — in humans
* — much faster than bacteria
* Much more difficult to — than bacteria

A

DNA or RNA
host cell machinery
metabolic machinery
alive
disease
Reproduces
treat

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16
Q

Characteristics of Viruses
DNA
(3)

A
  • Herpesviruses
    (chickenpox, shingles, cold
    sores, infectious
    mononucleosis)
  • Adenoviruses (sore throat)
  • Papillomaviruses (warts)
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17
Q

Characteristics of Viruses
RNA
(4)

A
  • Orthomyxoviruses
    (influenza)
  • Paromyxoviruses
    (respiratory tract infections)
  • Picornaviruses (colds)
  • Retroviruses (HIV/AIDS)
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18
Q

Virus Life Cycle
General Steps:
(3)

A
  1. Attachment: Polypeptide binding sites (on envelope or
    capsid) interact with host cell receptors
  2. Entry: receptor-virus complex enters host cell (e.g.
    endocytosis)
  3. Replication: utilizing host cell metabolic processes,
    nucleic acids and proteins are synthesized and
    assembled into viral particles
    * Process varies (DNA vs RNA)
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19
Q

Virus Life Cycle
General Replication Differences:
DNA Viruses
(4)

A
  • Viral DNA enters host cell nucleus
  • Host cell’s RNA polymerase
    catalyzes transcription into mRNA
  • Translation of mRNA into virus-
    specific proteins
  • Enzymes for further synthesis of
    viral DNA
  • Structural proteins comprising
    viral coat and envelope
  • Release of complete virions
  • Via budding or host cell lysis
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20
Q

Virus Life Cycle
General Replication Differences:
RNA Viruses
(4)

A
  • Enzymes within virion synthesize
    mRNA from the viral RNA template
    OR viral RNA serves as its own
    mRNA
  • Translation into enzymes
    (including RNA polymerase,
    structural proteins)
  • Assembly of and release similar to
    DNA viruses
  • NOTE: host cell nucleus usually
    NOT involved in viral replication
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21
Q

Virus Life Cycle
General Replication Differences:
Retroviruses (RNA)
(5)

A
  • Virion contains reverse
    transcriptase enzyme (RNA-
    dependent DNA polymerase) 
    complementary DNA
  • DNA copy integrated into host cell
    genome (“provirus”)
  • Provirus DNA is transcribed into
    new viral genome RNA and mRNA
    for translation into viral proteins
  • Completed viruses released via
    budding
  • NOTE: retroviruses often replicate
    without killing host cell
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22
Q

Herpesviruses
(2)

A
  • DNA viruses
  • Responsible for cold sores, genital ulceration, chickenpox, shingles,
    etc
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23
Q

Herpesviruses
* Eight Types Can Infect Humans:

A
  • Herpes simplex viruses (HSV-1 and HSV-2)
  • Varicella-zoster virus (VZV/HHV-3)
  • Epstein-Barr virus (EBV/HHV-4)
  • Cytomegalovirus (CMV/HHV-5)
  • Herpesvirus type 6 (HBLV/HHV-6)
  • Herpesvirus type 7 (HHV-7)
  • Kaposi’s sarcoma herpesvirus (KSHV/HHV-8)
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24
Q

Herpes Simplex Viruses (HSV-1 &
HSV-2)
* *Manifestations:
* HSV-1
(2)
* HSV-2
(1)

A
  • Primary infection: pharyngitis,
    gingivostomatitis
  • Recurrent infection: herpes labialis
  • Typically genital manifestations
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25
Q

Herpes Simplex Viruses (HSV-1 &
HSV-2)
* Highly Contagious:
(3)

A
  • Transmission via direct contact
  • Sharing food utensils/drinks
  • Oral-genital contact
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26
Q

Herpes Simplex Viruses (HSV-1 &
HSV-2)* HSV Development

A

Exposure
Primary Infection
Latency
Reactivation

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27
Q

Exposure

A

Entry typically via direct contact
with infected person’s:
* Skin
* Mucous membranes
* Bodily fluids

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28
Q

Primary
Infection

A

Clinical illness may occur
Virus travels to nerve
ganglia and establishes
latency

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29
Q

Latency

A

Virus remains inactive/dormant,
but still present within nerve
cells
No symptoms

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30
Q

Reactivation

A

Virus travels to
skin or mucous
membranes:
* Cold sores
* Fever blisters
* Genital
lesions

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31
Q

Herpes Simplex Viruses (HSV-1 &
HSV-2)
* Potential Triggers for Reactivation:
(5)

A
  • Immunosuppression
  • Stress
  • Sunlight
  • Fever
  • Trauma to area of primary infection
  • Dental procedures; extraction
  • Lip injury
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32
Q

Herpes Simplex Viruses (HSV-1 &
HSV-2)
Prodromal symptoms: (3)

A

pain, tingling, burning

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33
Q

Herpes
Simplex
Viruses
(HSV-1 &
HSV-2)
Treatment
(5)

A

Acyclovir (Zovirax)
* Valacyclovir (Valtrex)
* Penciclovir (Denavir)
* Famciclovir (Famvir)
* Docosanol (Abreva)

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34
Q

Herpes
Simplex
Viruses
(HSV-1 &
HSV-2)
Therapeutic management considerations:
(4)

A
  • Primary vs reactivated infection
  • Severity
  • Site of infection
  • Frequency of recurrences
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35
Q

Herpes Simplex Viruses: Therapeutics
Acyclovir (Zovirax)
*Preparation(s)

A

Oral: capsule (200 mg), tablet (400 or 800 mg), suspension (200 mg/5
mL)
Topical: 5% cream, 5% ointment

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36
Q

Herpes Simplex Viruses: Therapeutics
Acyclovir (Zovirax)
Mechanism of Action

A

Converted to acyclovir monophosphate (via thymidine kinase) and
triphosphate (via other enzymes) to target viral DNA synthesis
Monophosphate: incorporates into viral DNA  chain termination
Triphosphate: competitive inhibition and inactivation of viral DNA
polymerase

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37
Q

Herpes Simplex Viruses: Therapeutics
Acyclovir (Zovirax)
Dosing (Adult)

A

Primary infection: acyclovir 400 mg PO 3x/day OR 200 mg PO 5x/day x 7-
10 days
Recurrent: Acyclovir 400 mg PO 3x/day x 5 days OR (if topical) Apply to
affected area topically 5x/day x 4 days
*Requires renal dose adjustment

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38
Q

Herpes Simplex Viruses: Therapeutics
Acyclovir (Zovirax)
Drug-Drug
Interaction(s)

A

Tizanidine

39
Q

Herpes Simplex Viruses: Therapeutics
Acyclovir (Zovirax)
Adverse Effects

A

GI upset, malaise; Local pain (topical)

40
Q

Valacyclovir (Valtrex)
*Preparation(s)

A

Oral: tablets (500 mg or 1000 mg)

41
Q

Valacyclovir (Valtrex)
Mechanism of
Action

A

Prodrug which is rapidly converted to acyclovir
[See acyclovir MOA]

42
Q

Valacyclovir (Valtrex)
Dosing (Adult)

A

Primary infection: valacyclovir 1 gram PO twice daily x 7-10 days
Recurrent: valacyclovir 2 grams PO 2x/day x 1 day
*Requires renal dose adjustment

43
Q

Valacyclovir (Valtrex)
Drug-Drug
Interaction(s)

A

Tizanidine

44
Q

Valacyclovir (Valtrex)
Adverse Effects

A

GI upset, headache

45
Q

Valacyclovir (Valtrex)
Miscellaneous

A

Following maternal administration of valacyclovir, acyclovir is detectable in cord
blood and amniotic fluid; Pregnancy Category B
Higher than serum concentrations present in breast milk (caution)

46
Q

DDIs: Acyclovir and Valacyclovir
Oral acyclovir and oral valacyclovir are weak –inhibitors
May increase serum concentration of —
Risk Rating:

A

CYP1A2
tizanidine
D  Consider therapy modification

47
Q

If therapy cannot be modified, monitor for increased adverse
reactions of tizanidine
(3)

A
  • Hypotension
  • Bradycardia
  • Drowsiness
48
Q

Thymidine Kinase

A
  • Phosphorylates thymidine and other nucleoside
    analogs
  • Herpesviruses have their OWN viral thymidine kinase
    (TK) enzyme which works much more efficiently than
    human TK
  • Preferentially phosphorylates antiherpetic drugs (e.g.
    acyclovir)
  • Human cellular TK is much less likely to be able to
    activate antiherpetic drugs
  • Drug remains inactive in normal uninfected cells
  • Effective HSV treatment with minimal side effects to
    the host
  • Viral thymidine kinase is the key to selective toxicity
49
Q

Penciclovir: Efficacy

A
  • Penciclovir 1% cream vs. matching
    placebo cream
  • 3,057 immunocompetent patients
    initiated treatment
  • Penciclovir: n = 1,516
  • Placebo: n = 1,541
  • Penciclovir recipients’ lesions healed
    31% faster than placebo patients
  • HR 1.31; 95% CI (1.20 to 1.42); P=
    0.0001)
  • Significant benefit when initiated in
    both early (p = 0.001) and later (p =
    0.0055) stages
  • Effective at speeding healing and
    pain relief by ~1 day
50
Q

Orthomyxoviruses
(3)

A
  • RNA viruses
  • Responsible for causing influenza
  • Four generate infect vertebrates
51
Q
  • Four generate infect vertebrates
A
  • Influenza A (most virulent, “seasonal flu”)
  • Influenza B (“seasonal flu”)
  • Influenza C (milder)
  • Influenza D (infect swine, cattle, sheep – NOT humans)
52
Q

Influenza A
* Divided into subtypes based
on surface proteins:
(2)
* Subtypes N1 - N11
* Subtypes known to infect
humans:
(2)
* Known to cause …

A
  • Hemagglutinin (HA or H)
  • Subtypes H1 - H18
  • Neuraminidase (NA or N)
  • Hemagglutinin subtypes:
    H1, H2, and H3
  • Neuraminidase subtypes:
    N1 and N2

global
influenza pandemics

53
Q

Influenza A and B
(4)

A
  • Cause acute viral respiratory disease or “seasonal flu”
  • Affect individuals of all ages worldwide
  • Primarily respiratory droplet transmission person-to-person
    (sneezing, coughing, etc.)
  • Some airborne and indirect contact transmission
  • Incubation period: average ~2 days (range 1-4 days)
54
Q

Influenza A and B
* Manifestations (not comprehensive):
(2)

A
  • Fever, nonproductive cough, myalgia, malaise, chills, sore
    throat, nausea, congestion, headache, fatigue
  • Varies based on infecting strain and severity
55
Q

Influenza A and B
* Management:
(2)

A
  • Oseltamivir (Tamiflu)
  • Baloxivir marboxil (Xofluza)
56
Q

Influenza A and B
* Therapeutic management considerations:
(3)

A
  • Treatment vs. post-exposure prophylaxis
  • Severity
  • Onset of symptoms (48-hour window)
57
Q

Retroviruses
(2)

A
  • RNA viruses
  • Responsible for causing acquired immunodeficiency syndrome
    (AIDS), T-cell leukemia
58
Q
  • Retroviruses with implications in Dentistry
  • HIV-1
    (2)
  • HIV-2
    (2)
A
  • Most common; higher rate of transmission
  • Worldwide
  • Also causes immune suppression; less virulent
  • Endemic in West Africa
59
Q

Human Immunodeficiency Virus
(HIV)
* Virus that causes HIV infection
(2)

A
  • If left untreated, may caused AIDS (most advanced stage)
  • Attacks and destroys immune system’s CD4 T-cells
60
Q

Human Immunodeficiency Virus
(HIV)* Manifestations:
* Acute: (7)
* Range of severity
* Median duration:

A

fever, fatigue, myalgia, skin rash (commonly with
trunk involvement), headache, pharyngitis, cervical
adenopathy

~14 days

61
Q

HIV Transmission
(4)

A
  • Anal or vaginal intercourse
  • Oral sexual activity
  • Exposure to infected blood
  • Sharing of needles or syringes (injecting drugs,
    tattooing, etc)
  • Accidental percutaneous injury
  • Pregnancy, childbirth, or breastfeeding
62
Q

Post-Exposure Prophylaxis (PEP)
Treatment to prevent HIV infection following potential exposure
Indications:
(2)
Administer ASAP - Ideally within – hours of exposure
Example regimens:
* Bictegravir + TAF + Emtricitabine
* Dolutegravir + TAF + Emtricitabine
* Dolutegravir + TDF + Emtricitabine

A
  • Occupational exposure
  • Non-occupational exposure:

72

63
Q

Pre-Exposure Prophylaxis (PrEP)

A
  • Preventative strategy to prevent transmission of HIV for those who
    are at high risk but are currently HIV negative
64
Q

Pre-Exposure Prophylaxis (PrEP)
* Risk Factors (NOT comprehensive):
(3)

A
  • Those in a sexual relationship with HIV-positive partner
  • Drug-using behaviors
  • Recent sexually transmitted infections (e.g. syphilis, gonorrhea)
65
Q

Pre-Exposure Prophylaxis (PrEP)
* Pre-treatment evaluation and testing:
(2)

A
  • HIV, HBV, STI testing
  • Renal function, osteoporosis, lipid testing
66
Q

Pre-Exposure Prophylaxis (PrEP)
* Example Regimens:
(2)

A
  • Tenofovir disoproxil fumarate-emtricitabine
  • Tenofovir alafenamide-emtricitabine
67
Q

Reduction of HIV Transmission
(6)

A

Antiretroviral
Therapy (ART)
and Viral
Suppression
Post-exposure
prophylaxis
Pre-exposure
prophylaxis
(PrEP)
Testing and early
diagnosis
Safe sex
practices
Avoid sharing
needles/syringes

68
Q

HIV Life Cycle
(7)

A
  1. Binding
  2. Fusion
  3. Reverse Transcription
  4. Integration
  5. Replication
  6. Assembly
  7. Budding
69
Q

Antiretroviral Therapy (ART)
(4)

A
  • The routine use of a combination of HIV medication classes to
    treat or prevent HIV
  • Recommended for all patients with HIV, regardless of CD4
    count
  • NOT a cure
  • Potential for resistance; adherence is KEY
70
Q

ART
* Goals:
(4)

A
  • Reduce morbidity and mortality associated with HIV
  • Restore and preserve immunologic function
  • Suppress plasma HIV viral load
  • Prevent HIV transmission
71
Q

HIV Drug Classes
(9)

A
  • Nucleoside Reverse Transcriptase Inhibitors (NRTI)
  • Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTI)
  • Protease Inhibitors (PI)
  • Integrase Strand Transfer Inhibitors (INSTI)
  • Fusion Inhibitors
  • CCR5 Antagonists
  • Attachment Inhibitors
  • Post-Attachment Inhibitors
  • Capsid Inhibitors
72
Q

NRTIs
* Nucleoside reverse Transcriptase Inhibitors
* MOA:

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA( cDNA)

73
Q

NRTIs
Adverse Effects:
(2)

A
  • Common: N/V/D, upset stomach, headache
  • Serious: bone marrow suppression (and associated increased risk of
    bleeding or oral ulcers), peripheral neuropathy, pancreatitis,
    lipoatrophy, hepatic steatosis, lactic acidosis
74
Q

NRTIs
* Contraindications:

A
  • Abacavir and moderate or severe hepatic insufficiency
75
Q

NRTIs
* DDIs: Minimal

A
  • Tenofovir products and high-dose or multiple NSAIDs  May enhance
    nephrotoxic effects of tenofovir
  • Category D: Consider Therapy Modification
76
Q

NRTIs
* Examples:

A
  • Abacavir (Ziagen)
  • Abacavir-Lamivudine (Epzicom)
  • Abacavir-Lamivudine-Zidovudine (Trizivir)
  • Didanosine (Videx)
  • Emtricitabine (Emtriva)
  • Lamivudine (Epivir)
  • Stavudine (Zerit)
  • Tenofovir alafenamide-Emtricitabine (Descovy)
  • Tenofovir disoproxil fumarate (Viread)
  • Tenofvoir disoproxil fumarate-Emtricitabine (Truvada)
  • Zidovudine (Retrovir)
  • Zidovudine-Lamivudine (Combivir)
77
Q

NNRTIs
* Non-nucleoside reverse transcriptase inhibitors
* MOA:

A

block and prevent reverse transcriptase enzyme from accurately
copying its RNA into complementary DNA (cDNA)
* Binding occurs in a pocket further away from active site

78
Q

NNRTIs
* Adverse Effects:
(3)

A
  • Common: rash, GI upset, elevated liver enzymes, metabolic changes
    (cholesterol)
  • Sedation (benzodiazepines, barbiturates, opioids, etc) used in dental procedures
    may need adjustment if liver toxicity is present
  • Serious: QT prolongation and neurologic/psychiatric side effects with efavirenz
    and rilpivirine
79
Q
  • Rilpivirine must be administered with a full meal to
A

increase absorption

80
Q

NNRTIs
* Examples:
(5)

A
  • Doravirine (Pifeltro)
  • Efavirenz (Sustiva)
  • Etravirine (Intelence)
  • Nevirapine (Viramune)
  • Rilpivirine (Edurant)
81
Q

Protease Inhibitors (PIs)
* MOA:

A

block protease enzyme to prevent new (immature) HIV from
becoming a mature virus that can infect other CD4 cells
* CYP3A4 substrates
* Often “boosted” by pharmacokinetic enhancers

82
Q

PIs
* Adverse Effects:
(2)

A
  • Many are agent-specific
  • Class effects: insulin resistance, hyperglycemia, diabetes, hyperlipidemia,
    lipodystrophy, hepatotoxicity, increased risk of bleeding, PR interval
    prolongation
83
Q

PIs
* Oral adverse effects:
(3)

A
  • Fosamprenavir - Perioral numbness (lips), taste changes
  • Atazanavir - Dental (tooth) pain, taste changes
  • Ritonavir - Taste changes
84
Q

Protease Inhibitors
* Examples:

A
  • Atazanavir (Reyataz)
  • Atazanavir-Cobicistat (Evotaz)
  • Darunavir (Prezista)
  • Darunavir-Cobicistat (Prezcobix)
  • Fosamprenavir (Lexiva)
  • Indinavir (Crixivan)
  • Lopinavir-Ritonavir (Kaletra)
  • Nelfinavir (Viracept)
  • Saquinavir (Invirase)
  • Tipranavir (Aptivus)
85
Q

INSTIs
* Integrase stand transfer inhibitors
* MOA:

A

block integrase enzyme, preventing insertion of HIV viral DNA into the
DNA of the host CD4 cell, thus preventing replication

86
Q

INSTIs
* Adverse Effects:

A
  • Generally well tolerated
  • Increased weight gain, insomnia, dizziness
  • Pertinent adverse effects related to dentistry:
  • Osteopenia/osteoporosis
  • Xerostomia (dry mouth)
  • Oral ulcers, mucosal irritation
  • Altered taste
  • Increased risk of bleeding
87
Q

INSTIs: DDIs

A
  • Raltegravir PLUS:
  • Proton pump inhibitors (omeprazole, pantoprazole, etc)  may
    increase concentrations of raltegravir
  • Category B: No Action Needed
88
Q

INSTIs
* Examples:

A
  • Cabotegravir (Apretude)
  • Dolutegravir (Tivicay)
  • Raltegravir (Isentress)
  • Elvitegravir (within combination products)
  • Bictegravir (within combination products)
89
Q

Other Drug Classes
* CCR5 Antagonists
* Example:
* Attachment Inhibitors
* Example:
* Post-Attachment Inhibitors
* Example:
* Capsid Inhibitors
* Example:

A

Maraviroc (Selzentry)
Fostemsavir (Rukobia)
Ibalizumab-uiyk (Trogarzo)
Lenacapavir (Sunlenca)

90
Q

Pharmacokinetic Enhancers
* MOA:

A

Inhibit enzymes (CYP3A4) that metabolize other antiretroviral drugs
to “boost” concentrations and effectiveness
* ↑ concentration, ↑ PK profile, ↑ effectiveness
* Allows for ↓ doses used and ↓ associated drug toxicity

91
Q

Pharmacokinetic Enhancers
* Adverse Effects:

A
  • Common: GI upset
  • Pertinent adverse effects in dentistry:
  • Ritonavir: Metallic or bitter taste, oral ulcers or inflammation, perioral numbness/tingling,
    increased bleeding risk (if DDI with anticoagulants)
  • Dry mouth
92
Q

Pharmacokinetic Enhancers
* Examples:

A
  • Ritonavir (Norvir)
  • Cobicistat (Tybost)
93
Q

Single-Tablet Regimens
* Examples:

A
  • Bictegravir-TAF-Emtricitabine (Biktarvy)
  • Darunavir-Cobicistat-TAF-Emtricitabine (Symtuza)
  • Dolutegravir-Abacavir-Lamivudine (Triumeq)
  • Dolutegravir-Lamivudine (Dovato)
  • Dolutegravir-Rilpivirine (Juluca)
  • Doravirine-TDF-Lamivudine (Delstrigo)
  • Efavirenz-TDF-Emtricitabine (Atripla)
  • Elvitegravir-Cobicistat-TAF-Emtricitabine (Genvoya)
  • Elvitegravir-Cobicistat-TDF-Emtricitabine (Stribild)
  • Rilpivirine-TAF-Emtricitabine (Odefsey)
  • Rilpivirine-TDF-Emtricitabine (Complera)
94
Q
A

Pharm 2 (13 decks)

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