HIV/AIDS Flashcards

1
Q

What is the role of pharmacists in community and hospital practise?

A
  • Identify and prevent potential drug interactions
  • Help manage medication side effects
  • Understand and optimize management of co-morbidities/conditions
  • Understand the need for uninterrupted supply of antiretroviral therapy (consequences - resistance)
  • Communicate with the patients’ healthcare team (HIV specialist, family doctor, nurse, pharmacist, dietician, social worker, support worker and etc)
  • Understand that YOU are also a part of the patients’ healthcare team
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2
Q

What is HIV?

A

Human Immunodeficiency Virus

  • Retrovirus
  • HIV-1 and HIV-2
  • Chronic infection results in the progressive destruction of CD4+ T lymphocytes (crucial for the normal function of the human immune system)
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3
Q

What is AIDS?

A

Acquired ImmunoDeficiency Syndrome

  • Person is HIV+ AND
  • has a CD4+ cell count below 200 or
  • CD4+ cells account for fewer than 14% of all lymphocytes or
  • Has been diagnosed with one or more of the AIDS-defining illnesses
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4
Q

_____ cells are the target of HIV

A

CD4

-HIV interacts with CD4 receptors, invades - replicates - destroys CD4 cells = CD4 depletion

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5
Q

How are CD4 cells a part of the immune system?

A

CD4 cells direct and activate immune response

-depletion of CD4 = degradation of immune function

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6
Q

What is HAART?

A

Highly Active AntiRetroviral Therapy

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7
Q

What is cART?

A

combination AntiRetroviral Therapy

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8
Q

How many antiretrovirals should HIV patients be taking?

A

3 or more antiretrovirals used in combination for the purpose of minimizing resistance and maximizing antivirologic and immune response

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9
Q

HIV is a chronic viral infection that targets ____ cells and degrades the immune system and without treatment results in death

A

CD4

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10
Q

______ treatment with antiretrovirals decreases mortality and morbidity

A

Combination

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11
Q

Describe the viral transmission of HIV

A

contact with infectious body fluids (i.e. blood, semen, vaginal secretions, breast milk)

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12
Q

Describe the primary HIV infection

A
  • Also called acute HIV infection or acute seroconversion syndrome
  • Symptoms last about 2 weeks and include fever, sore throat, fatigue, weight loss, myalgia, rash, N, V, D, lymphadenopathy, night sweats, aseptic meningitis (fever, headache, photophobia, stiff, neck) may be present in 25% of presenting cases
  • HIV viral load
  • Persistent decrease in CD4 lymphocytes
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13
Q

What is the seroconversion?

A

development of HIV antibody

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14
Q

What is chronic asymptomatic HIV infection?

A

viral replication are more controlled by immune response

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15
Q

Define AIDS

A
  • CD4 cell count < 200 regardless of the presence or absence of symptoms
  • AIDS-defining illness regardless of CD4 cell count
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16
Q

Define Advanced HIV infection

A

CD4 count < 50

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17
Q

What CD4 cell count causes a high risk of opportunistic infections?

A

< 200

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18
Q

What are the main routes of transmission?

A
  • Sex
  • IV drugs
  • Perinatal (mother to child transmission)

Sex, Drugs, and Rock a Bye Baby

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19
Q

What are the 2 most common types of sexual transmission of HIV

A
  • Receptive anal

- Receptive vaginal

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20
Q

What are other types of sexual transmission?

A
  • Insertive anal
  • Insertive vaginal
  • Oral (low risk, Receptive > insertive)
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21
Q

What are some factors that would increase risk of transmission?

A
  • Increased viral load
  • Vaginal bleeding during intercourse
  • Genital ulcers
  • STI
  • Lack of circumcision in males
  • Genetic and host factors
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22
Q

What decreases the risk of transmission?

A
  • Condoms
  • Treatment of STIs
  • Male circumcision
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23
Q

Mother to Child (vertical) transmission:

Overall risk of vertical transmission in _____ of drug therapy and other interventions

A

20-25%

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24
Q

Mother to Child (vertical) transmission:

50-70% of transmission occurs when ?

A

just before or during birth process/delivery

*in utero transmission is rare

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25
Q

Mother to Child (vertical) transmission:

Can virus be transmitted in breast milk?

A

you betcha

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26
Q

Mother to Child (vertical) transmission:
In HIV patients who have babies, it is recommended that they exclusively ________ _____ their baby if have clean water available to do so

A

formula feed

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27
Q

Mother to Child (vertical) transmission:

How do we prevent this?

A
  • Treat mother with antiretroviral therapy DURING pregnancy (may want to delay initiation until after the first trimester)
  • Antiretroviral treatment DURING labor & delivery and TO BABY post delivery
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28
Q

What drug is given to mother during labour & delivery

A

IV Zidovudine

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29
Q

What drug is given to baby for first 6 weeks?

A

Oral Zidovudine

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30
Q

Mother to Child (vertical) transmission:

May require C-section if ?

A

viral load too high (>1000 copies/mL)

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31
Q

Describe IV transmission

A
  • IV injection with used needles and other injection paraphernalia
  • Needle stick injuries (occupational & non-occupational)
  • Mucosal exposure to blood
  • Recipient of blood products
  • Recipient of organ transplant
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32
Q

How can you decrease the risk of parenteral transmission ?

A
  • Free needle exchange programs
  • Not sharing injection parphernalia
  • Sterilize equipment (bleach)
  • Safe disposing of used paraphernalia
  • Use of Post Exposure Prophylaxis (PEP)
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33
Q

What 4 treatment strategies are known to prolong survival?

A
  • ART
  • PCP prophylaxis
  • MAC prophylaxis
  • Care by a healthcare team specializing in HIV
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34
Q

List the stages of HIV infection

A

Stages of HIV infection include transmission, primary infection, chronic infection

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35
Q

HIV is transmitted through 3 main exposure routes, what are they?

A
  • sexual
  • parenteral
  • perinatal
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36
Q

What methods can decrease the risk of transmission?

A

condom use, not sharing IV drug equipment and treatment during pregnancy

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37
Q

List the 9 steps of HIV viral entry/replication

A

1) Binding
2) Fusion
3) Uncoating
4) Reverse Transcription
5) Genome Integration
6) Genome Replication
7) Protein Synthesis
8) Protein Cleavage
9) Virus Assembly and spread

*slide 20

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38
Q

What are ARV’s known as?

A

Birth control for HIV

  • Prevents new infectious virus from being made IF taken daily and able to achieve and maintain therapeutic blood levels.
  • If ARV stopped or missed, nothing preventing for new virus being made
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39
Q

___ is like an intruder in a factory

A

HIV

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40
Q

Describe how HIV enters

A

HIV enters the CD4 factor, hijacks the production line to make viral components instead of CD4 components resulting in thousand/millions of new virus

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41
Q

List the 6 classes of antiretrovirals

A

1-Nucleoside/tide Reverse Transcriptase Inhibitors (NRTIs) “nukes”
2-Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) “non-nukes”
3-Protease Inhibitors (PIs)
4-Integrase Strand Transfer Inhibitors (INSTIs)
5-Fusion Inhibitors
6-CCR5 Receptor Antagonists

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42
Q

see slide 23

A

okay

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43
Q

What is an STR?

A

Single tablet regimens (has 3 antiretrovirals in a single pill)

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44
Q

Cobicistat acts as a _____

A

booster

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45
Q

Antiretrovirals work at different parts of the HIV life cycle to _____ _______

A

disrupt replication

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46
Q

Currently there are __ classes of antiretrovirals with different mechanisms of action

A

6

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47
Q

Many antiretrovirals available and can exist as single entity, single tablet regimen or co-formulated products but need at least _ antiretroviral drugs used in combination (low dose booster does not count)

A

3

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48
Q

Goals of therapy for HIV treatment

A
  • Reduce HIV-associated morbidity and prolong the duration and quality of survival
  • Restore and preserve immunologic function using antiretroviral therapy
  • Maximally and durably suppress plasma HIV viral load
  • Prevent HIV transmission
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49
Q

What are the 2 markers of disease progression?

A

1) Virus (viral load) - HIV RNA in blood
- Average viral burden (without therapy) is 30,000 to 50,000 RNA copies/mL but huge range
- Lives in/targets the lymphoid cells (CD4+, T cells)
- High capacity for replication and subsequent destruction of CD4+ cells (up to 1 billion per day)

2) CD4+ T cell lymphocyte counts and percentage
- Normal CD4+ count in non-HIV patient = 800-1050
- The average rate of decline of CD4 cells is about 50 cell/year after first year of infection
- Increased risk of morbidity at 200 cells
- <50 cells medium survival = 12-18 months without treatment

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50
Q

Benefits of starting ART earlier rather than later

A
  • increase potency, durability, simplicity, safety of current regimens
  • decrease emergence of resistance
  • decrease toxicity with earlier therapy
  • increase subsequent treatment options
  • risk of uncontrolled viremia at all CD4+ cell count levels
  • decrease transmission
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51
Q

Describe the patient evaluation prior to initiation of HAART

A

Physical:

  • Evidence of symptomatic HIV disease
  • Evidence of opportunistic infections
  • Infections, weight loss, fevers, malaise, diarrhea, cognitive problems, neuropathy, visual problems, oral lesions, skin rashes or lesions, and any chronic complaints

Psychosocial:
-Substance abuse, housing, access to medications, psychiatric

Laboratory:
-CD4+ count, VL, serology for Hepatitis A, B, C toxoplasmosis, CBC, Chemistry, BUN, CSR, s-glucose, LFTs, cholesterol

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52
Q

What test is done before Abacavir can be administered?

A

HLA *B5701
-for Abacavir associated hypersensitivity reaction (fever, rash, fatigue, nausea, vomiting, respiratory symptoms, headache, arthralgia, increased CK, increased LFTs) - can be life-threatening

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53
Q

List 2 boosters

A

Low dose Ritonavir or Cobicistat

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54
Q

Describe the 3 types of regimens

A
  • 2 NRTIs and 1 NNRTI
  • 2 NRTIs and 1 PI
  • 2 NRTIs and INSTI
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55
Q

We want to individualize regimen based on what?

A
  • HIV characteristics (genotype for drug resistance)

- Patient (co-morbidiites, side effect profile, preference)

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56
Q

Describe the recommended initial regimen for most people with HIV (INSTI-based)

A

INSTI-based:

1) Raltegravir & Tenofovir DF or AF + Emtricitabine
2) Dolutegravir & Tenofovir DF or AF + Emtricitabine
3) Dolutegravir & Abacavir + Lamivudine
4) Elvitegravir/Cobicistat/Tenofovir DF or AF/Emtricitabine
* Only for patients who are HLA B5701 negative

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57
Q

________ and ________ can be used interchangeably for each other

*if you develop resistance for one, can’t use the other

A

Emtricitabine and Lamivudine

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58
Q

Describe the recommended initial regimen for certain clinical situations with HIV (NNRTI-based)

A

1) Efavirnez/Tenofovir DF/Emtricitabine
2) Efavirnez + Tenofovir AF/Emtricitabine
3) Rilpivirine/Tenofovir DF or AF/Emtricitabine (if VL < 100 000 and CD4 > 200)

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59
Q

Describe the recommended initial regimen for certain clinical situations with HIV (INSTI-based)

A

Raltegravir + Abacavir/Lamivudine

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60
Q

Describe the recommended initial regimen for certain clinical situations with HIV (PI-based)

A

1) Atazanavir + Ritonavir or Cobicistat once daily
&
TDF or TAF/Emtricitabine

2) Darunavir + Ritonavir
Or
Darunavir/Cobicistat
&amp;
Abacavir/Lamivudine

3) Darunavir/Cobicistat
&
TDF or TAF/Emtricitabine

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61
Q

DF

A

Disoproxil Fumarate

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62
Q

AF

A

Alafenamide

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63
Q

_______ can only be used if HLA B5701 negative

A

Abacavir

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64
Q

______ should not be used in patients who require > 20 mg omeprazole/equivalent per day

A

Atazanavir

65
Q

What are some factors to consider for selection of ARVs

A
  • drug resistance
  • viral load
  • CD4 count
  • HLA B5701
  • co-morbidities
  • genetic predisposition
  • drug interactions
  • pill burden
  • patient preference
  • side effect profile
  • ability to swallow/formulation (liquid/crush/split)
66
Q

List 2 advantages of INSTI (integrase strand transfer inhibitors)

A
  • NNRTI and PI options preserved for future use

- Less negative effects on lipids

67
Q

List advantages/disadvantages of Raltegravir

INSTI (integrase strand transfer inhibitors)

A

Advantage: Not metabolized through CYP and less likely to have drug interactions

Disadvantage:

  • BID dosing
  • Low genetic barrier to develop drug resistance (single key mutation wipes out activity)
68
Q

List advantages/disadvantages of Elvitegravir

INSTI (integrase strand transfer inhibitors)

A

Advantage: Once daily dosing and available as STR (single tablet regimen)

Disadvantage:

  • Needs booster (Cobicistat)
  • Potential for CYP drug interactions
  • Low genetic barrier to developing drug resistance
  • Only available as STR (*guidelines for renal insufficiency)
69
Q

List advantages/disadvantages of Dolutegravir

INSTI (integrase strand transfer inhibitors)

A

Advantage:

  • Once daily dosing
  • Highest genetic barrier of INSTI class

Disadvantage:

  • UGT substrate; potential for drug interactions
  • Oral absorption can be reduced by simultaneous administration with products containing polyvalent cations (Ca, Mg, Al, Fe)
70
Q

List advantages of protease inhibitors

A
  • Higher genetic barrier for resistance - multiple mutations to cover resistance
  • PI resistance uncommon with failure (boosted PIs)
71
Q

List disadvantages of protease inhibitors

A
  • Metabolic complications (fat maldistribution, dyslipidemia, insulin resistance)
  • Gastrointestinal adverse effects
  • Greater potential for drug interactions (CYP450) especially with Ritonavir (boosted regimens)
72
Q

List advantages of NNRTIs (non-nucleoside reverse transcriptase inhibitors)

A
  • Less dyslipidemia and fatmaldistribution then PI based regimen
  • Long half-life
  • PI and INSTI options preserved for future use
73
Q

List disadvantages of NNRTIs (non-nucleoside reverse transcriptase inhibitors)

A
  • Low genetic barrier (single mutation can confer class resistance)
  • Skin rash
  • Hepatotoxicity (Nevirapine)
  • CNS effects (Efavirenz)
  • Potential for CYP450 drug interactions
  • Transmitted resistance to NNRTis more common than resistance to PI
74
Q

List 2 side effects of ALL NRTIs

A

-Lactic acidosis and hepatic steatosis
Rare: higher incidence with older/no longer used compared to newer NRTIs
-Lipodystrophy (a change in body fat distribution)
Uncommon: significantly higher incidence with older/no longer used NRTIs

75
Q

Describe Lipodystrophy

A
  • Mechanism not understood
  • May be associated with dyslipidemia, insulin resistance, lactic acidosis
  • Switch to other agents may slow progression
76
Q

List adverse effects of Abacavir (NRTI)

A
  • Hypersensitivity reaction 3-8%, can be fatal. HLA *B5701 testing prior to treatment (next to zero risk if negative, don’t use if positive)
  • Headache
  • GI intolerance.
77
Q

List adverse effects of Tenofovir (NRTI)

A
  • Headache
  • GI intolerance
  • Renal impairment (use with caution in patients with pre-existing impairment or risk of renal impairment)
  • Usually well tolerated
78
Q

List adverse effects of Zidovudine (NRTI)

A
  • Headache
  • GI intolerance
  • Bone marrow suppression
  • Lipoatrophy
79
Q

List adverse effects of Emtricitabine, Lamivudine (NRTI)

A
  • GI intolerance
  • headache
  • potential hyperpigmentation in patients with darker complexions or ethnicities
80
Q

Adverse effects of Raltegravir (INSTIs)

A
  • insomnia
  • headache
  • nausea
  • fatigue
  • creatine kinase (CK) elevation
  • rhabdomyolysis (dark urine in the absence of dehydration - indicative of rhabdomyolysis
81
Q

Adverse effects of Elvitegravir (INSTIs)

A
  • nausea
  • diarrhea
  • headache
82
Q

Adverse effects of Dolutegravir (INSTIs)

A
  • nausea
  • diarrhea
  • headache
  • insomnia
83
Q

Monitoring for INSTIs

A

if symptoms of rhabdomyolysis/myositis (unexplained muscle pain, tea coloured urine) check serum CK levels

84
Q

Adverse effects of ALL PIs

A
  • Hyperlipidemia (differs between different PIs and also related to amount of Ritonavir)
  • Insulin resistance and diabetes
  • Lipodystrophy
  • Elevated liver function tests
  • Drug-drug interactions
85
Q

Adverse effects of Atazanavir (PI)

A

Hyperbilirubinemia (may manifest as jaundice/scleral icterus)

Tell patient to watch for yellowness of skin or eyes

86
Q

Adverse effects of Darunavir (PI)

A

Rash, food requirement, GI intolerance

87
Q

Adverse effects of Lopinavir/ritonavir (PI)

A
  • GI intolerance
  • diarrhea
  • dyslipidemia
88
Q

Adverse effects of Ritonavir (PI)

A
  • GI intolerance
  • hepatitis/elevated liver enzymes
  • diarrhea
89
Q

Ritonavir is only used for _______ other PIs at 100-200 mg/day

A

boosting

90
Q

Adverse effects of Efavirenz (NNRTI)

A
  • CNS/neuropsychiatric: feeling of dissociated, disconnected, nightmares, vivid dreams, insomnia, depression, “fuzzy feeling”, “hung-over”, impaired concentration, agitation, euphoria
  • Onset: first day - 6 weeks
  • Incidence: 50% (but need to discontinue in about 2%)
  • Usually SE get better over time (6 weeks)
  • Take at HS “sleep through the side effect”, on an empty stomach (avoid elevated levels)
  • Patient counselling and support is important

*Teratogenic in nonhuman primates

91
Q

Adverse effects Nevirapine (NNRTI)

A

Hepatotoxicity (may be severe and life-threatening)

  • Increased risk in women CD4 > 250 and men CD4 > 400
  • Greatest risk during the first 6 weeks
  • Symptoms: often non-specific, including fatigue, malaise, anorexia, nausea, jaundice
  • Rash
92
Q

Monitoring of Nevirapine? (NNRTI)

A
  • Transaminases (baseline, at 2 weeks, 4 weeks then monthly for first 18 weeks)
  • Rash
93
Q

_______ is an example of a second generation NNRTI

A

Etavirine

94
Q

Describe the MOA of Etavirine (second generation NNRTI)

A

binds to reverse transcriptase and inhibits replication

95
Q

Dose of Etavirine (second generation NNRTI)

A

200mg BID (or if no significant mutations then 400mg once daily)

96
Q

Place in therapy of Etavirine (second generation NNRTI)?

A

Treatment experienced patients with resistance to other classes of ARVs including NNRTIs

97
Q

Adverse drug reactions of Etavirine (second generation NNRTI)

A
  • rash
  • nausea
  • less CNS effects (vivid dreams, dizziness) than with Efavirenz
98
Q

MOA of CCR5 receptor antagonists

A

binds to CCR5 co-receptor of CD4 cell preventing entry into cell

PREVENTS ENTRY INTO CELL

99
Q

CCR5 receptor antagonists:

indication ?

A

treatment experienced patients with resistance to other classes of ARBs

100
Q

CCR5 receptor antagonists:

Requires _____ test (not available locally)

A

tropism

101
Q

CCR5 receptor antagonists:

Only effective if ??

A

virus uses CCR5 EXCLUSIVELY (won’t work if CXCR4 or both CCR5 and CXCR4)

102
Q

CCR5 receptor antagonists:

Side effects ?

A

cough, rash, upper respiratory infection, fever

103
Q

Give an example of a fusion inhibitor

A

Enfuvirtide (T-20)

this is the only injectable antiviral at this point !!

104
Q
Fusion Inhibitors (ex. Enfuvirtide T-20):
MOA
A

binds to gp41 and prevents fusion of viral and cellular membranes

105
Q
Fusion Inhibitors (ex. Enfuvirtide T-20):
Route and frequency?
A

SC injection BID

106
Q
Fusion Inhibitors (ex. Enfuvirtide T-20):
Place in therapy ?
A

Treatment experienced patients with resistance to other classes of ARVs

107
Q

Fusion Inhibitors (ex. Enfuvirtide T-20):

SE ?

A
  • local injection site reaction is common (95%)
  • pruritis
  • pain/discomfort
  • nodule/cyst formation
  • induration
  • ecchymosis
108
Q

Is anyone on a Fusion Inhibitors (ex. Enfuvirtide T-20): in manitoba?

A

No:

  • no one wants to inject themselves if they don’t have to
  • BID dosing
  • lots of adverse reactions
109
Q

List advantages of Triumeq (Dolutegravir/Abacavir/Lamivudine)

-a STR

A
  • Single tablet regimen
  • Less negative lipid effects compared to PI and NNRTI classes
  • Potentially higher genetic resistance compared to other INSTI and NNRTI
  • No pharmacoenhancer - less potential for drug interactions
  • No food requirement for absorption (good for homeless ppl who may not have access to food)
110
Q

List disadvantages of Triumeq (Dolutegravir/Abacavir/Lamivudine)

-a STR

A

-Need B5701 test result prior to use due to Abacavir
-If taken on empty stomach, space apart from polyvalent cation containing products (Mg, Ca, Fe including multivitamins or oral antacids)
(space apart 2hrs before or 6hrs after)

  • not worried about calcium in dietary products
  • more concerned with the high concentration present in medicines
111
Q

Stribild
Genvoya
(only differ between salt of Tenofovir)

Advantages?

A

Less negative lipid effects compared to PI and NNRTI classes

112
Q

Stribild
Genvoya
(only differ between salt of Tenofovir)

Disadvantages?

A
  • Potential drug interactions w Cobicistat boosting
  • Food requirement for optimal absorption
  • Lower genetic barrier to drug resistance than PI class
  • Co-formulated w Tenofovir DF or AF
    • Cannot start in patients with renal insufficiency CrCl < 70 for TDF
    • Cannot start in patients with renal insufficiency CrCl < 30 for TAF
113
Q

Advantages of:

Darunavir (boosted with Ritonavir or Cobicistat and 2 NRTIs)

A
  • no evidence of PI resistance mutations with virology failure when used as the initial PI
  • HIGHEST genetic barrier to drug resistance
114
Q

Disadvantages of:

Darunavir (boosted with Ritonavir or Cobicistat and 2 NRTIs)

A
  • Rash
  • Negative lipid effects (compared to INSTI)
  • Pill burden greater than NNRTI or INSTI regimen (2-3 pills/day)
  • Food requirement for optimal absorption
  • Potential drug interactions with Ritonavir or Cobicistat boosting
  • GI intolerance due to Ritonavir or Cobicistat
115
Q

Advantages of:

2 Pill Regimen:
Dolutegravir + Tenofovir DF or AF/Emtricitabine

A
  • Higher genetic barrier to drug resistance compared to NNRTi and INSTi classes; comparable to PI class
  • Can use if unknown or positive HLA B5701 status
  • NO booster = less potential drug interactions with CYP 3A4 drugs
  • NO food requirement for absorption
  • Can crush, split to administer
116
Q

Disadvantages of:

2 Pill Regimen:
Dolutegravir + Tenofovir DF or AF/Emtricitabine

A
  • 2 pills
  • Drug interactions with divalent cations - space apart or take w food
  • Interacts with metformin (increases serum levels)
  • Dolutegravir - higher reports of insomnia (7%) compared to other INSTIs
117
Q

List some short term ADRs

A
  • N, V, D
  • headache
  • rash/allergies
  • CNS effects (dizzy, drowsiness, vivid dreams, headache)
118
Q

List some long term ADRs

A
  • Bone marrow suppresion
  • Mitochondrial toxicity
  • Metabolic complications
  • Nephrotoxicity
  • Hepatotoxicity
119
Q

How can we manage GI side effects

A
  • Take w food if possible
  • HS dosing
  • Antiemetics (Dimenhydrinate, metoclopramide, ondansetron/granisetron)
  • Consider dietary issues
  • Antidiarrheals (loperamide, calcium carbonate, pancreatic enzymes, codeine)
120
Q

3-5% of HIV patients develop ______

A

diabetes

121
Q

Diabetes:

Onset ?

A

weeks to months

122
Q

Type __ DM = insulin resistance & decreases insulin production

A

2

123
Q

Risk factors for HIV patients developing diabetes?

A
  • underlying hyperglycemia

- family history

124
Q

All ____ associated with hyperglycemia

A

PIs

125
Q

How do we manage Hyperglycemia?

A
  • Diet & Exercise
  • Consider switching of PI based regimen
  • Treatment with oral hypoglycemics
  • Monitor FPG @ baseline, 3-6 months, then annually, and A1C)
126
Q

Onset of hyperlipidemia?

A

3 months

127
Q

Describe the order in which agents have highest chance of causing hyperlipidemia?

A

Boosted PI > NNRTI > INSTI

128
Q

Consequences of hyperlipidemia?

A

CV disease, Pancreatitis

129
Q

Management of hyperlipidemia in those with HIV

A
  • minimize CVD risks (ex. smoking)
  • pharmacologic treatment with either Atorvastatin 10 mg daily, Pravastatin 20 mg daily, or Rosuvastatin
  • Statin x 4 months then add vibrate if needed
130
Q

Monitoring of hyperlipidemia?

A

lipid profile @ baseline, 3-6 months after initiation then at least annually

131
Q

List 2 potential consequences of antiretroviral interactions

A

1) Decreased antiretroviral activity
- Risk of sub therapeutic drug levels, inadequate viral suppression, resistance, disease progression

2) Increased risk of toxicity
- May lead to morbidity, non-adherence, drug discontinuation

132
Q

List 1 desirable drug interaction for HIV patients

A

Exploiting drug interaction to enhance/improve therapy

  • Ritonavir and Covicistat strong inhibitor of CYP450 3A4
  • Ritonavir used at low dose 100-200 mg/day to “boost” concomitant PI serum levels
  • Cobicistat used at 150 mg
  • Higher trough levels
  • Allows for less frequent dosing
133
Q

Describe the interaction between:

Antacids (PPIs, and H2B) and Atazanavir

A

significant decrease in Atazanavir bioavailability - pH dependent (max 20mg opemrazole equivalent daily)

134
Q

Describe the interaction between:

Boosted PI and Statin

A

increased statin levels and effect - may need to decrease dose

135
Q

Describe the interaction between:

HIV meds and products with divalent cations

A

Chelation Ca, Fe, Al, Mg

136
Q

Describe the interaction between:

HIV meds and integrase inhibitors

A

space apart 2 hours before or 6 hours after or give with food

137
Q

Describe the interaction between:

Warfarin & Etravirine

A

May cause elevated levels leading to toxic adverse effects

Etravirine inhibits warfarin metabolism

138
Q

Describe the interaction between:

Ritonavir/Cobicistat & Steroids (ex. fluticasone)

A
  • increases fluticasone plasma concentration and decreases plasma cortisol concentration
  • Recommend Beclomethasone

**Key point: do not withhold/delay systemic steroid for treatment of acute disease - asthma or COPD

139
Q

Describe the interaction between:

Ritonavir/Cobicistat & Statins

A

-increases plasma concentrations of atorvastatin and increases risk of myopathy and rhabdomyolysis

Manage: use lowest dose possible and monitor for signs & symptoms of myopathy and rhabdomyolysis (muscle pain, tenderness, weakness) and consider monitoring CK levels if signs or symptoms appear

140
Q

What is the optimal response with HAART?

A

Decrease viral load
Increase CD4 count

*requires adherence

141
Q

When should you monitor HIV RNA viral load?

A
  • At baseline and 2-8 weeks after treatment or change in therapy (should be minimum decrease of 1 log10 copies/mL
  • Repeat every 3-4 months on stable ART

*Goal is to reduce HIV VL < 20 copies/mL

142
Q

When should you monitor CD4+ T cell count?

A
  • At baseline and every 3-4 months

- May decrease frequency if on stable suppressive ART

143
Q

When should you monitor CBC?

A
  • At baseline

- Repeat every 3-4 months

144
Q

When should you monitor electrolytes?

A
  • At baseline

- Repeat every 3-4 months

145
Q

When should you monitor liver function, LFTs, and albumin?

A
  • At baseline and at 4-6 weeks

- Repeat every 3-4 months on stable ART

146
Q

When should you monitor Kidney function, BUN, S-Cr?

A
  • At baseline

- Repeat every 3-4 months on stable ART

147
Q

What should you monitor for glucose intolerance?

A

monitor blood glucose and A1C

148
Q

What should you monitor for lipids?

A

total cholesterol, LDL, HDL, Triglycerides

149
Q

What should you monitor for fat redistribution?

A
  • no routine tests

- some measure waist to hip ratio

150
Q

What should you monitor for lactic acidosis?

A

If symptoms - monitor lactic acid levels, some monitor anion gap

151
Q

List 3 Limitations to treatment safety and efficacy

A

1) Adherence
2) Drug interactions
3) Adverse effects

152
Q

When should we switch/modify treatment? (4)

A

1) Virologic failure
2) Toxicity
3) Difficulty adhering to the regimen
4) Current antiretroviral regimen is suboptimal

153
Q

What defines virologic failure?

A

The failure to achieve a viral load < 50 copies/mL by 48 weeks or any sustained return of the viral load to > 50 copies/mL

154
Q

Causes of virologic failure?

A
  • Incomplete adherence
  • Inadequate antiretroviral potency
  • The development of drug resistance
  • Failure of the drugs to reach the target site
155
Q

Describe enhancing adherence (patient-focused)

A
  • Treat depression & substance abuse
  • Social support
  • Determine patient readiness
  • Involve patient in selection and scheduling
  • Educate about ADRs
156
Q

Describe enhancing adherence (treatment focused)

A
  • Simplify regimen
  • Individualize regimen
  • Offer medication “run through”
  • Offer adherence aids (calendars, beepers, pill organizers, bubble packing)
  • Manage ADRs aggressively
157
Q

Describe a Medication run through (NOT A RUN DOWN JIM LOL)

A

Discuss how they think it would be fit into their daily life:

  • time of day
  • If best taken with food and how much
  • Ensure they have uninterrupted access to their meds

Trouble shooting tips:
-What to do if they are late taking a med, forget taking, vomit or are travelling with medication

158
Q

What is PrEP and describe it.

A

Pre-Exposure Prophylaxis:

  • to prevent acute formation of the virus
  • 2 drugs
  • Use antiretroviral medication PRIOR to exposure to HIV to protect against infection
  • Currently only Tenofovir DF/Emtricitabine approved for use in Canada as daily oral therapy
159
Q

What is PEP and describe it.

A

Post Exposure Prophylaxis:

  • 3 drugs
  • Use of the combination of 3 antiretrovirals AFTER potential exposure to HIV
  • Initiation within 72 hours (ASAP)
  • Starter kits in ERs
  • 28 day treatment