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antivirals Flashcards

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1
Q

Capsid

A

Capsid: protein coat surrounding genetic material of a virus

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2
Q
  • DNA polymerase:
A
  • DNA polymerase: an enzyme which catalyzes the process of DNA
    replication
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3
Q
  • Endocytosis:
A
  • Endocytosis: ingestion/engulfing of materials (e.g. a virus) via the
    cell membrane
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4
Q
  • Envelope:
A
  • Envelope: outermost lipid (fatty) layer which protects genetic
    material when traveling between host cells; only present on some
    viruses
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5
Q
  • Incubation period:
A
  • Incubation period: time duration between exposure to the virus and
    the appearance of symptoms
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6
Q
  • Latency:
A
  • Latency: the ability a pathogenic virus to lie dormant within a cell
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7
Q
  • Neuraminidase:
A
  • Neuraminidase: an enzyme found on the surface of influenza virus
    which enables the virus to be released from the host cell
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8
Q
  • Nucleocapsid:
A
  • Nucleocapsid: core of a virus, made up of the genetic material and
    the capsid
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9
Q
  • Reverse transcriptase:
A
  • Reverse transcriptase: an enzyme used to generate
    complementary DNA (cDNA) from an RNA template (reverse
    transcription)
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10
Q
  • RNA polymerase:
A
  • RNA polymerase: the enzyme which catalyzes the process of
    transcription
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11
Q
  • Transcription:
A
  • Transcription: the synthesis of RNA from a DNA template
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12
Q
  • Translation:
A
  • Translation: the synthesis of protein from RNA
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13
Q
  • Virion:
A
  • Virion: 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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14
Q

What is a Virus?
* genomes?
* Viral genomes direct their own?
* metabolic machinery
* alive?
* Can infect all ?
* Reproduction rate?
* tx dif?

A

What is a Virus?
* “Virus” in Latin means “poison”
* Small, obligate parasites with DNA or RNA genomes
* Viral genomes direct their own replication and the synthesis of other
viral components, using host cell machinery
* No metabolic machinery of their own
* Not “alive” themselves
* Can infect all living organisms; commonly cause disease in humans
* Reproduces much faster than bacteria
* Much more difficult to treat than bacteria
Pellett PE, et al. Basics of virology. Handb Clin Neurol. 2014.

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15
Q

viral structures?

A
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16
Q

DNA viruses for this class

A
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17
Q

RNA viruses for this class

A
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18
Q

DNA vs RNA life cycles

A
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19
Q

Virus Life Cycle General Steps:
1. Attachment:
2. Entry:
3. Replication:

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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20
Q

DNA Viruses life cycle
* Viral DNA enters?
* Host cell’s enzyme used?
* Translation?
* what is made?
* Release of?
* end resullts

A
  • Viral DNA enters host cell nucleus
  • Host cell’s RNA polymerasem catalyzes transcription into mRNA
  • Translation of mRNA into virus- specific proteins: Enzymes for further synthesis of
    viral DNA and Structural proteins comprising viral coat and envelope
  • Release of complete virions
  • Via budding or host cell lysis
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21
Q

RNA Viruses life cycle
* mRNA production?
* Translation into?
* Assembly of and release?
* NOTE:

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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22
Q

Retroviruses (RNA)
* Virion contains ?
* DNA copy?
* Provirus DNA is?
* Completed viruses released?
* NOTE:

A

Retroviruses (RNA)
* 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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23
Q

Common Viral Drug Targets

A
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24
Q

Herpesviruses
* genome?
* Responsible for?
* Eight Types Can Infect Humans:

A
  • DNA viruses
  • Responsible for cold sores, genital ulceration, chickenpox, shingles,
    etc.
  • Eight Types Can Infect Humans:
  • 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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25
Herpes Simplex Viruses (HSV-1 & HSV-2) * *Manifestations
26
hsv 1 and 2 spread
Highly Contagious: * Transmission via direct contact * Sharing food utensils/drinks * Oral-genital contact
27
hsv development cycle
28
hsv exposure
29
hsv primary infection
30
hsv latency
31
hsv reactivation
32
hsv triggers for reactivation
33
prodromal symptoms of hsv reactivation
pain, tingling, burning
34
hsv tx agents
35
hsv Therapeutic management considerations:
* Primary vs reactivated infection * Severity * Site of infection * Frequency of recurrences
36
acyclovir preps for hsv oral cap, tablet, suspension and ointment
37
acyclovir moa
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
38
acyclovir rx for adults (recurrent and primary infections) | adjusted for?
39
acyclovir interactions
tizanidine
40
acyclovir adrs
GI upset, malaise; Local pain (topical)
41
valcyclovir preps
Oral: tablets (500 mg or 1000 mg)
42
valcyclovir moa
Prodrug which is rapidly converted to acyclovir [See acyclovir MOA]
43
valcyclovir dosing (primary and recurrent infections) | adjust for?
44
valcyclovir interaction
tizanidine
45
valcyclovir Adverse Effects
GI upset, headache
46
maternal use of valcyclovir
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)
47
DDIs: Acyclovir and Valacyclovir
48
penciclovir prep
1% external cream
49
penciclovir moa
50
penciclovir dosing
51
penciclovir ddi
minimal
52
# penciclovir adr
Erythema, headache
53
maternal penciclovir
not used
54
famciclovir preps
Oral: tablets (125, 250, and 500 mg) *Tablets contain lactose
55
famciclovir moa
Prodrug which is rapidly converted to active penciclovir [See Penciclovir MOA]
56
famciclovir dosing (primary and recurrent infections) | adjust for?
57
famciclovir ddis
minimal
58
# famiciclovir adrs
Nausea, headache
59
famciclovir in pregnancy
60
Docosanol preps
10% external cream
61
docosanol moa
62
docosanol dosing
63
# docosanol ddi
none
64
docosanol adrs
well tolerated
65
Thymidine Kinase role and selectivity with rx
66
Penciclovir: Efficacy
Penciclovir: Efficacy * 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
67
acyclovr suspensionexample rx
68
valacyclovir recurrence example rx
69
penciclovir example rx
70
famciclovir recurrence example rx
71
Orthomyxoviruses * genome * Responsible for? * Four generates
* RNA viruses * Responsible for causing influenza * Four generate infect vertebrates * Influenza A (most virulent, “seasonal flu”) * Influenza B (“seasonal flu”) * Influenza C (milder) * Influenza D (infect swine, cattle, sheep – NOT humans)
72
Influenza A * Divided into subtypes based on? * Subtypes known to infect humans: * Known to cause ?
73
Influenza A and B * Cause? * Affect who? * transmission? * Incubation period:
* 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)
74
Influenza A and B * Manifestations (not comprehensive):
* Fever, nonproductive cough, myalgia, malaise, chills, sore throat, nausea, congestion, headache, fatigue * Varies based on infecting strain and severity
75
flu A and B drugs
* Oseltamivir (Tamiflu) * Baloxivir marboxil (Xofluza)
76
Therapeutic management considerations of flu A and B:
* Treatment vs. post-exposure prophylaxis * Severity * Onset of symptoms (48-hour window)
77
Oseltamivir prep | oral ans suspension
78
Oseltamivir dosing | tx and prevention,adjust for?
79
# Oseltamivir moa
80
Oseltamivir ddi
minimal
81
Oseltamivir adr
gi, headache
82
Oseltamivir maternal
Oseltamivir phosphate and its active metabolite oseltamivir carboxylate cross the placenta. Use during pregnancy and breastfeeding is acceptable. Limited excretion into breast milk
83
Neuraminidase Inhibitors diagrammed
84
Baloxavir marboxil prep
single tablet pack (40 or 80 mg)
85
Baloxavir marboxil moa
86
Baloxavir marboxil dosage | tx and prophy
87
Baloxavir marboxil ddi
88
Baloxavir marboxil adrs
gi upset
89
Baloxavir marboxil pregnancy
Pregnancy: No adverse events in animal reproduction studies; minimal data; not recommended Unknown if excreted in breast milk
90
endonuclease inhibitors diagrammed
91
oseltamavir example rx
92
Baloxavir marboxil example rx
93
Retroviruses
* RNA viruses * Responsible for causing acquired immunodeficiency syndrome (AIDS), T-cell leukemia * Retroviruses with implications in Dentistry * HIV-1: Most common; higher rate of transmission, Worldwide * HIV-2: Also causes immune suppression; less virulent, Endemic in West Africa
94
Human Immunodeficiency Virus (HIV)
95
Oral Care challenges for the HIV Patient
96
Oral Complications of HIV | what is seen with low cd4 counts
97
Opportunistic Infections of HIV | cd4 levels for prophy, preffered agents
98
HIV Transmission
* 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
99
HIV Post-Exposure Prophylaxis (PEP) | timeframe
100
HIV PEP regimens
101
HIV PrEP | pre tx testing
Preventative strategy to prevent transmission of HIV for those who are at high risk but are currently HIV negative Pre-treatment evaluation and testing: * HIV, HBV, STI testing * Renal function, osteoporosis, lipid testing
102
HIV PrEP regimens
* Tenofovir disoproxil fumarate-emtricitabine * Tenofovir alafenamide-emtricitabine
103
Reduction of HIV Transmission strategies
104
undetectable HIV means?
untransmissable
105
HIV Life Cycle steps
1. Binding 2. Fusion 3. Reverse Transcription 4. Integration 5. Replication 6. Assembly 7. Budding
106
binding anf fusion of hiv | what rx's stop these stages
107
reverse transcription of hiv
108
integration hiv
109
replication, assembly, and budding of hiv | inhibitory rx?
110
Antiretroviral Therapy The routine use of a combination of HIV medication classes to? * Recommended for? *cure? * Potential for?
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
111
goals of ART
* Reduce morbidity and mortality associated with HIV * Restore and preserve immunologic function * Suppress plasma HIV viral load * Prevent HIV transmission
112
HIV Drug Classes
*** 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
113
NRTIs and NNRTIs moa diagrammed
114
NRTIs * Nucleoside reverse Transcriptase Inhibitors names
* 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)
115
NRTI moa
block and prevent reverse transcriptase enzyme from accurately copying its RNA into complementary DNA( cDNA
116
Abacavir-Lamivudine-Zidovudine (Trizivir) moa
block and prevent reverse transcriptase enzyme from accurately copying its RNA into complementary DNA( cDNA
117
Tenofovir alafenamide-Emtricitabine (Descovy) moa
block and prevent reverse transcriptase enzyme from accurately copying its RNA into complementary DNA( cDNA
118
Tenofvoir disoproxil fumarate-Emtricitabine (Truvada) moa
block and prevent reverse transcriptase enzyme from accurately copying its RNA into complementary DNA( cDNA)
119
NRTI adrs | common and serious adrs
* 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
120
NRTI contraindications
* Abacavir and moderate or severe hepatic insufficiency
121
NRTI ddi
minimal * Tenofovir products and high-dose or multiple NSAIDs  May enhance nephrotoxic effects of tenofovir * Category D: Consider Therapy Modification
122
NNRTIs * Non-nucleoside reverse transcriptase inhibitors names
* Doravirine (Pifeltro) *** Efavirenz (Sustiva)** * Etravirine (Intelence) * Nevirapine (Viramune) *** Rilpivirine (Edurant)**
123
NNRTIs moa
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
124
Efavirenz (Sustiva) moa
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
125
Rilpivirine (Edurant) moa
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
126
nnrtis adr | common ones, sedation? serious adr?
127
Rilpivirine must be administered with?
Rilpivirine must be administered with a full meal to increase absorption (better absorbed with acids)
128
Rilpivirine* PLUS ddi
129
Efavirenz or Etravirine ddi
130
Protease Inhibitors (PIs) diagrammed
131
Protease Inhibitors (PIs) * MOA:
* MOA: block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
132
Protease Inhibitors and P450
* CYP3A4 substrates * Often “boosted” by pharmacokinetic enhancers
133
protease inhibitors adrs
134
oral adverse effects of : * Atazanavir, Ritonavir, Fosamprenavir
* Fosamprenavir - Perioral numbness (lips), taste changes * Atazanavir - Dental (tooth) pain, taste changes * Ritonavir - Taste changes
135
Protease Inhibitors * Examples:
-vir suffix *** Atazanavir (Reyataz) * Atazanavir-Cobicistat (Evotaz) * Darunavir (Prezista) * Darunavir-Cobicistat (Prezcobix) * Fosamprenavir (Lexiva)** * Indinavir (Crixivan) * Lopinavir-Ritonavir (Kaletra) * Nelfinavir (Viracept) * Saquinavir (Invirase) * Tipranavir (Aptivus)
136
Atazanavir (Reyataz) moa
block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
137
Atazanavir-Cobicistat (Evotaz) moa
block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
138
Darunavir (Prezista) moa
block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
139
Darunavir-Cobicistat (Prezcobix) moa
block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
140
Fosamprenavir (Lexiva) moa
block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
141
Darunavir ddi with:
142
Atazanavir ddi with:
143
Fosamprenavir ddi with:
144
INSTIs moa diagrammed
145
# Integrase stand transfer inhibitors INSTIs moa
block integrase enzyme, preventing insertion of HIV viral DNA into the DNA of the host CD4 cell, thus preventing replication
146
INSTIs general adrs
* Generally well tolerated * Increased weight gain, insomnia, dizziness
147
INSTIs adrs for dentistry
* Osteopenia/osteoporosis * Xerostomia (dry mouth) * Oral ulcers, mucosal irritation * Altered taste * Increased risk of bleeding
148
INSTIs: DDIs * Raltegravir PLUS:
* Proton pump inhibitors= may increase concentrations of raltegravir * Category B: No Action Needed
149
INSTIs * Examples: * suffix?
**-gravir suffix** * * Cabotegravir (Apretude) *** Dolutegravir (Tivicay)** * Raltegravir (Isentress) * Elvitegravir (within combination products) * **Bictegravir (within combination products)**
150
Dolutegravir (Tivicay) moa
block integrase enzyme, preventing insertion of HIV viral DNA into the DNA of the host CD4 cell, thus preventing replication
151
Bictegravir (within combination products) moa
block integrase enzyme, preventing insertion of HIV viral DNA into the DNA of the host CD4 cell, thus preventing replication
152
backbone hiv therapy
153
Other Drug Classes for HIV
* CCR5 Antagonists * Attachment Inhibitors * Post-Attachment Inhibitors * Capsid Inhibitors
154
Pharmacokinetic Enhancers moa
155
Pharmacokinetic Enhancers general adrs
gi upset
156
Pharmacokinetic Enhancers dentistry related adrs | which specific PK enhancer?
* Ritonavir: Metallic or bitter taste, oral ulcers or inflammation, perioral numbness/tingling, increased bleeding risk (if DDI with anticoagulants) * Dry mouth
157
Pharmacokinetic Enhancers examples
* Ritonavir (Norvir) * Cobicistat (Tybost)
158
Ritonavir (Norvir) moa
block CYP3A4, increase rx concentration (decreases amoutn rx used= lower toxiciity)
159
* Cobicistat (Tybost) moa
block CYP3A4, increase rx concentration (decreases amoutn rx used= lower toxiciity)
160
Pharmacokinetic Enhancers diagrammed
161
Ritonavir ddis with:
162
# Cobicistat ddis with:
163
most common signle tab regimens for HIV
164
Bictegravir-TAF-Emtricitabine MOA's
Bictegravir: INSTI TAF-Emtricitabine: NRTI
165
Dolutegravir-Abacavir-Lamivudine moa's
Dolutegravir- INSTI Abacavir- NRTI Lamivudine- NRTI
166
Dolutegravir-Lamivudine moa's
Dolutegravir- INSTI Lamivudine- NRTI
167
hsv tx agents
168
* Oseltamivir (Tamiflu) * Baloxivir marboxil (Xofluza)
flu A and B drugs
169
* 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)
NRTIs * Nucleoside reverse Transcriptase Inhibitors names
170
* Doravirine (Pifeltro) *** Efavirenz (Sustiva)** * Etravirine (Intelence) * Nevirapine (Viramune) *** Rilpivirine (Edurant)**
NNRTIs * Non-nucleoside reverse transcriptase inhibitors names
171
*** Atazanavir (Reyataz) * Atazanavir-Cobicistat (Evotaz) * Darunavir (Prezista) * Darunavir-Cobicistat (Prezcobix) * Fosamprenavir (Lexiva)** * Indinavir (Crixivan) * Lopinavir-Ritonavir (Kaletra) * Nelfinavir (Viracept) * Saquinavir (Invirase) * Tipranavir (Aptivus)
Protease Inhibitors * Examples:
172
* Cabotegravir (Apretude) *** Dolutegravir (Tivicay)** * Raltegravir (Isentress) * Elvitegravir (within combination products) * **Bictegravir (within combination products)**
INSTIs * Examples:
173
* Ritonavir (Norvir) * Cobicistat (Tybost)
Pharmacokinetic Enhancers examples
174
what can these formulations be used for?
HIV PEP regimens
175
# mechanism of what rx? block and prevent reverse transcriptase enzyme from accurately copying its RNA into complementary DNA( cDNA
NRTI moa
176
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
NNRTIs moa
177
* MOA: block protease enzyme to prevent new (immature) HIV from becoming a mature virus that can infect other CD4 cells
Protease Inhibitors (PIs) * MOA:
178
block integrase enzyme, preventing insertion of HIV viral DNA into the DNA of the host CD4 cell, thus preventing replication
# Integrase stand transfer inhibitors INSTIs moa
179
Pharmacokinetic Enhancers moa
180
what HIV rx is both a PI and a PK enhancer?
ritonavir

pharm 2 (20 decks)

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