Lecture 2- Exam 1 Flashcards
1
Q
Means “poison” in latin:
A
Virus
2
Q
Small obligate parasites with DNA or RNA genomes:
A
Virus
3
Q
Viral genomes direct their own replication and the synthesis of other viral components, using ____ machinery
A
host cell
4
Q
T/F: Viruses have machinery of their own.
A
False- No metabolic machinery
5
Q
T/F: Viruses are alive:
A
False- not alive
6
Q
What are more difficult to treat? Viruses or bacteria?
A
Viruses
7
Q
T/F: Influenza as a virus cannot cause any type of stomach flu or stomach bug
A
True
8
Q
What type of infection does the influenza virus cause?
A
respiratory
9
Q
Antiviral drugs have limited:
A
selective toxicity
10
Q
Describe two ways why antiviral drugs have limited selective toxicity:
A
- Viruses use host cell machinery, so very few unique targets
- Most drugs block steps that take place within cells, increasing chances for cell toxicity
11
Q
Most antivirals are considered ____, because they can’t actively kill the virus (as the virus is not living)
A
viruSTATIC
12
Q
List some drug targets of antivirals:
A
- attachment (virals attachment to host cell)
- uncoating of virus
- viral DNA/RNA synthesis
- viral assembly
- budding/release
- stimulate/ assist immune system
13
Q
Give an example of an antiviral that targets the viral attachment stage:
A
Enfuvirtide (anti-HIV drug)
14
Q
Describe the mechanism of action for Enfuvirtide:
A
blocks folding of gp41 protein & prevents fusion of virus with host cell membrane
15
Q
Describe the mechanism of action for the anti-flu drug Amantadine:
A
Blocks M1 receptor , preventing detection of pH outside virus (uncoating of virus stage)
16
Q
What is the primary target for most antivirals?
A
Viral DNA/ RNA synthesis
17
Q
List some examples of antivirals stimulating/assisting the immune system: (4)
A
- Natural human peptides
- Interferons
- Immunoglobulin
- Monoclonal antibodies
18
Q
Natural humans peptides, Interferons, Immunoglobulins, and Monoclonal antibodies are all examples of:
A
stimulating/assisting immune system
19
Q
Is HSV a DNA or RNA virus?
A
DNA
20
Q
How is HSV spread?
A
direct contact (due to viral shedding from saliva or blood)
21
Q
When HSV infection occurs through broken skin and inoculates nerve tissue this is known as:
A
primary infection
22
Q
Herpes viruses remain ___ for long periods of time without reproducing and avoid the immune response
A
latent
23
Q
What can serve to reactivate latent HSV?
A
- immune deficiency states
- stress
- irritating agents
24
Q
List some dental scenarios that may reactive a latent herpes virus:
A
- Trauma to area of primary infection
- Dental procedures/ extraction
- Lip injury
25
What are the prodromal symptoms of HSV?
1. Pain
2. Tingling
3. Burning
26
What type of tissue does HSV occur on?
Keratinized tissue
27
Herpes Simplex Labials =
Cold sore - HSV type 1
28
What percent of HSV type 1 occurs as "genital herpes"
3%
29
Herpes Simplex Genitalis =
Genital herpes- HSV type 2
30
What percentage of HSV type 2 occurs as "oral herpes"
30%
31
In the herpes virus, the virus ascends in the ____ nerve and survives/persists
trigeminal
32
The herpes virus "hides" from immune system in nerve cell bodies of ____
ganglia
33
What are reactivation triggers for HSV?
1. UV light
2. Friction/ Trauma
3. Fever/Illness
4. Stress
5. Steroids
6. Immunosupressants
34
What nerve and what ganglion are involved in the latent stage of herpes virus?
Trigeminal nerve; Gasserion ganglion
35
Prodromal HSV symptoms typically occur about ____ before an outbreak
24 hours
36
The management approach of HSV-1 is dependent on:
1. Primary HSV-1 infection or reactivation
2. Severity of symptoms
3. Site of infection (mucosal vs. disseminated disease)
4. Frequency of recurrences
37
Systemic agents used for HSV-1:
1. Acyclovir
2. Famciclovir
3. Valcyclovir
38
_____ & ____ have better oral bioavailability than _____ (for HSV)
Fam & Val ; Acyclovir
39
Between Famciclovir, Acyclovir, and Valacyclovir, which is the most effective against HSV?
Acyclovir
40
Although Acyclovir is the most effective drug against HSV, what is the downfall?
Very short half-life; would have to dose 3-5x daily
41
Valacyclovir is Acyclovir with an extra ____ on it, that allows it to evade some of the first pass metabolism and gives it a longer half-life
Valine
42
HSV medications are categorized as:
DNA nucleoside analogs
43
Drugs that are structural analogs of nucleosides (building blocks of DNA & RNA)
DNA nucleoside analogs
44
HSV medications (DNA nucleoside analogs) are good antiviral drugs because they block:
viral nucleic acid synthesis
45
DNA Nucleoside Analogs are selectively toxic prodrugs meaning they only work on viruses with:
viral thymidine kinase
46
What is the key to selectivity for DNA nucleoside analogs (HSV Antivirals)
Thymidine Kinase
47
DNA Nucleoside analogs changes nucleosides into ____ by adding ____
NucloeTIDES; adding 1st phosphate
48
What are the main side effects seen with HSV medications?
GI upset & Headache
49
Herpesvirus antivirals are "selectively toxic" because the drug is phosphorylated by kinase only, meaning the drug is activated in:
infected cells ONLY
50
Nucleoside antiviral drugs require initial phosphorylation by:
VIRAL thymidine kinase
51
Viral thymidine kinase works ____ than host cell thymidine kinase
100x faster
52
With herpesvirus antivirals, the false nucleotide :
stops DNA polyemerase/synthesis
53
What adds the first phosphate when talking about nucleoside antiviral drugs?
VIRAL thymidine kinase
54
What is the typical dosing for an adult taking Acyclovir for a primary infection?
200mg 5x/day for 7-10 days
or
400mg 3x/day for 7-10 days
55
What is the typical dosing for an adult taking Acyclovir for a reactivated infection?
400mg 3x/day for 5 days
56
When might a dose adjustment need to occur with Acyclovir?
When a patient has renal dysfunction
57
What is the target of Acyclovir?
VIral DNA synthesis
58
Adverse effects of Acyclovir include:
GI upset & Malaise
59
What is the primary drug interaction to be aware of when prescribing acyclovir?
Tizanidine (muscle relaxer)
60
What is another name for Acyclovir?
Zovirax
61
What is another name for Valacylovir?
Valtrex
62
Acyclovir + _____ = Valacyclovir
valine
63
T/F: Valacylovir itself does not have antiviral activity, however it is a prodrug which is rapidly converted to acyclovir (the active form)
True
64
Dosing for an adult taking Valacyclovir for a PRIMARY herpetic infection:
Valacyclovir: 1 gram twice daily for 7-10 days
65
Dosing for an adult taking valacyclovir for a recurrent herpetic outbreak:
Valacyclovir: 2 grams by twice daily for 1 day
66
Drug-drug interactions for valacyclovir:
Tizanidine
67
Adverse effects for Valacyclovir:
GI upset & Headache
68
Oral acyclovir and oral valacyclovir are weak _____ inhibitors
CYP1A2
69
Acyclovir and Valacyclovir may increase serum concentration of ____ (a drug)
Tizanidine (Zanaflex)
70
Another name for Famciclovir:
Famvir
71
Famiciclovir is a prodrug which is rapidly converted to:
Penciclovir
72
Dosing of Famiciclovir for an adult with a primary herpetic infection:
Famciclovir: 250 mg 3x/ day or 500mg 2x per day for 7-10 days
73
Dosing of Famiciclovir for an adult with recurrent herpetic outbreak:
1500mg single dose
74
Drug-drug interactions with Famiciclovir=
minimal
75
Adverse effects of famiciclovir:
Nausea & Headache
76
Topical agents for herpes labials are ____ effective than oral agents
less
77
HIV attacks and destroys the immune system especially ____ cells.
CD4 T-cells
78
HIV is a ____ ___virus
RNA retrovirus
79
The host cell for the flu is a _____ cell
The host cell for HSV is a ____ cell
The host cell for HIV is a _____ cell.
Respiratory; nerve; T-cells
80
HIV is a (DNA/RNA) virus
RNA virus!
81
HIV virus is a RNA retrovirus that transforms its RNA to DNA, _____ the natural process
reversing
82
Oral complications of HIV such as oral candidiasis, oral hairy leukoplakia, oral kapok's sarcoma and oral viral infections (HSV) are associated with:
low CD4 counts
83
List some oral complications of HIV:
1. oral candidiasis
2. oral hairy leukoplakia
3. oral kaposi's sarcoma
4. oral viral infections (HSV)
5. ulcerative disease
6. malignancy
7. dental caries, gingivitis, periodontitis
8. more severe manifestations of periodontal disease (linear gingival erythema, necrotizing ulcerative gingivitis, & necrotizing ulcerative periodontitis)
84
HIV is associated with a lot of ____ infections, and the more these infections occur, this is a sign of disease infection
opportunistic infections
85
Normal CD4 count =
over 1000
86
We monitor HIV patients with their ____ count, which is a way to help determine if the antivirals that they are on are effective or if we need to add on antibiotics for opportunistic infections
CD4
87
If a patients CD4 count drops below ____ we will start prophylacting them
below 200
88
If a patients CD4 count drops below 200 we will start prophylactics drugs to prevent:
Pneumocystis Jiroveci pneumonia (PCP; PJP)
89
Once a patients CD4 count drops below 200 we will prescribe daily:
Bactrim (1 DS tablet everyday) until the patients CD4 count is maintained above 200 for several months
90
If you look at a patients medication list and they are taking a daily Bactrim, this is a good sign that the patient is:
immunosupressed
91
If a patients CD4 count drops below 100, we will prescribe a daily Bactrim to prevent: (what disease do we need to worry about with a patients counts this low)
Toxoplasmosis
92
If a patients CD4 count drops below 50, what should we worry about?
Mycobacterium avian complex (MAC)
93
If a patients CD4 count drops below 50, we worry about them contracting MAC. What would we prescribe prophylactically?
Once weekly Azithromycin 1200mg
94
If a patient reports to clinic and is taking once weekly Azithromycin (1200mg) this is a very good indication of:
an extremely weak immune system
95
HIV medication targets include:
1. Fusion inhibitors
2. Reverse Transcriptase inhibitors
3. Integrase inhibtors
4. Protease inhibitors
96
NRTI's =
Nucleoside Reverse Transcriptase inhibitors
97
____# of NRTI's are always used together (the backbone of therapy)
Two
98
List some examples of NRTIs (HIV therapy)
1. Abacavir (Ziagen, ABC)
2. Lamivudine (Epivir, 3TC)
3. Tenfovir (Viread, TDF)
99
NNRTI's=
Non-nucleoside reverse transcriptase inhinitors
100
HIV drug - incorporated into viral DNA and stops further transcription of DNA
- interrupt the virus from duplicating
- Nucleoside analogs converted by host cell thymidine kinase to nucleotides
Nucleoside Reverse Transcriptase Inhibitors (NTRI's)
101
HIV drug- directly binds/ blocks reverse transcriptase enzyme:
NNRTI (Non-nucleoside Reverse Transcriptase Inhibitor)
102
What is the main disadvantage of NNRTI's to treat HIV?
Highest incidence of resistance (~18%); 1 in 5 after first year
103
NNRTI's are non-nucleoside reverse transcriptase inhibitors meaning they bind reverse transcriptase directly and inhibit it which stops it from taking:
Viral RNA to Viral DNA
104
Two examples of NNRTI's to treat HIV:
1. Efravirenz (Sustiva, EFV)
2. Rilpivirine (Edurant, RPV)
105
NNRTI's are _____ inducers
CYPP450
106
What are the advantages of Non-nucleoside reverse transcriptase inhibitors (NNRTI)?
1. Daily dosing (long half lives)
2. No interference with food
3. Do not increase TG; less severe side effects vs. PI's
4. Can use in renal disease
107
HIV drug- blocks last stage of virus production (new protein production)
- Prevents HIV assembly
- All are CYP3A4 substrates
Protease inhibitors
108
The protease inhibits bind to _____ and inhibit it from the crucial element of viral assembly that it has
HIV protease
109
The side effect that is most strongly attributed to protease inhibitors includes:
metabolic side effects including:
- insulin resistance
- hyperglycemia
- diabetes
- hyperlipidemia
- lipodystrophy
- hepatotoxicity
- increased risk of bleeding
- PR interval prolongation
110
One side effect from a dental perspective to be aware of is that if a patient is on a protease inhibitor, they have an:
increased risk of bleeding
111
Protease inhibits (PIs) are often boosted meaning:
we add on CYP3A4 inhibitors
112
Strong inhibitors of ____ are added to boos levels of PI's/ NNRTI's
CYP3A4
113
HIV drug that - binds integrate enzyme; blocks viral DNA integration into host cell
Integrase Strand Transfer Inhibitors (INSTI's)
114
Why are most HIV patients starting on therapy prescribed an INSTIs?
1. High efficacy
2. Low adverse effect profile
3. Minimal drug interactions
115
Dolutegravir (Tivicay, DTG) & Bictegravir (Biktarvy) are examples of:
Integrase Strand Transfer Inhibitors (INSTIs)
116
Describe initial HIV treatment:
Combination of INSTI + 2 NRTIs is the preferred method for most patients
117
What is described as the "backbone" for initial HIV treatment?
2 NRTIs + 1 INSTI
118
For initial HIV treatment, it is important to prescribe ____ drugs from at least _____ different classes of medication
3 drugs; 2 classes
119
What is considered the FIRST- LINE treatment variation for initial HIV treatment?
2 NRTIs + 1 PI
120
A 3 drug regiment for healthcare personnel with a percutaneous, mucous membrane, or non intact skin exposure to body fluids of concern (blood or blood tinged fluids) if source patient is, or is spec'd to be, HIV-infected:
PEP
121
