HIV/AIDS Flashcards

1
Q

Tx of Candida Infections in AIDS

A

-fluconazole

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2
Q

Fluconazole Dose for Candida Infections

A

100-200 mg daily until resolved then PRN

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3
Q

Primary Prophylaxis Drug for Pneumocystis Pneumonia

A

-TMP/SMX

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4
Q

Primary Prophylaxis Alternatives for Pneumocystis Pneumonia

A
  • clindamycin + pyrimethamine
  • atovaquone
  • pentamidine
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5
Q

Long Term Management of Pneumocystis Pneumonia

A

ongoing secondary prophylaxis

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6
Q

Primary Prophylaxis for Toxoplasmosis gondii

A

-TMP/SMX

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7
Q

Treatment of Toxoplasmosis gondii

A
  • sulfadiazine: wt based dose qid

- pyrimethaine: high loading dose then 50-75 mg daily

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8
Q

Long Term Management of Toxoplasmosis

A

-secondary prophylaxis and ongoing suppressive therapy

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9
Q

Primary Prophylaxis for Cryptococcal Infections

A

primary prophylaxis not indicated

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10
Q

Cryptococcus Treatment

A

-liposomal amphotericin

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11
Q

AEs of Amphotericin

A
  • HoTN
  • fever/rigors
  • anemias
  • low Mg, low K
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12
Q

Amphotericin Toxicities

A
  • renal dysfunction

- marrow suppression

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13
Q

Long Term Management of Cryptococcus

A
  • consolidation: fluconazole 400 mg daily x8 wks

- secondary prophylaxis: fluconazole 1 year

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14
Q

Cytomegalovirus Prophylaxis

A

-not used b/c of therapy toxicity

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15
Q

Cytomegalovirus Treatment

A

-ganciclovir or valganciclovir

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16
Q

Mycobacterium Avium Intercellulare Primary Prophylaxis

A

azithromycin 1200 mg/wk

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17
Q

Treatment of Mycobacterium Avium Intercellulare

A

-azithromycin 600 mg/day PO
-plus ethambutol
+/- rifampin or rifabutin

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18
Q

Primary Goals of Opportunistic Infection Therapy

A
  • reduce HIV associated morbidity
  • prolong the duration and quality of survival
  • preserve and restore immunologic function
  • maximally and durably suppress HIV
  • prevent future transmissions
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19
Q

Drawbacks of Early Therapy

A
  • unknown long term ARV-related toxicities
  • life long tx and pill fatigue = non-adherence
  • costs to the pt and the healthcare system
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20
Q

What conditions might favor earlier treatment?

A
  • pregnancy
  • HIV associated nephropathy
  • HBV-HIV or HCV-HIV co-infection
  • acute or recent infx
  • HIV associated dementia
  • AIDS defining condition
  • lower CD4 <200
  • acute opportunistic infxs
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21
Q

When should deferral of therapy be considered?

A
  • significant adherence barriers (clinical, personal, psychosocial)
  • serious comorbidity: incurable CA, end stage liver dz, life expectancy shorter than time for QOL benefits
  • long term non-progressor
  • elite controller
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22
Q

MOA NRTIs

A
  • drugs compete with nucleotides
  • terminate viral DNA chain
  • block HIV replication
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23
Q

How are NRTIs administered?

A

PO

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24
Q

What is the bioavailability of NRTIs?

A
  • variable

- not affected by food

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25
How are NRTIs excreted?
renally cleared
26
MOA of N-NRTIs
- binds non-competitively adjacent to active site | - prevents HIV RNA conversion to proviral DNA
27
How are N-NRTIs administered?
PO
28
What is the bioavailability of N-NRTIs?
- very good | - increased with food
29
How are N-NRTIs metabolized?
- extensive hepatic metabolism | - many drug-drug interactions due to CYP450
30
MOA of Protease Inhibitors
-blocks process that stimulates viral maturation
31
How are PIs administered?
PO
32
How are PIs metabolized?
- extensive hepatic metabolism | - many drug-drug interactions due to CYP450
33
What do all preferred HIV treatment regimens have?
TWO NRTIs
34
Emtricitabine-Tenofovir (Truvada) AEs
- fatigue - cramps - elevated creatine kinase - hypophosphatemia
35
Emtricitabine-Tenofovir (Truvada) Toxicities
- renal insufficiency (Fanconi's syndrome) | - changes in bone density
36
Emtricitabine-Tenofovir (Truvada) Lab Follow-up
- renal function | - DEXA scan
37
Lamivudine-Abacavir (Epzicom) Toxicities
- hypersensitivity reaction | - may have additive effects if combined w/ other meds with overlapping AEs
38
Lamivudine-Abacavir (Epzicom) Pre-treatment Lab and Why It Is Done
- HLA B5701 | - if positive, 50-50 chance for severe hypersensitivity reaction
39
Lamivudine-Abacavir (Epzicom) Lab Follow-up
- hepatic function | - renal function
40
NNRTI Efavirenz (Sustiva) AEs
- vivid dreams, insomnia, depression - rash - increased LFTs - dizziness - high triglycerides
41
NNRTI Efavirenz (Sustiva) Toxicities
- hepatitis | - hepatic necrosis
42
NNRTI Efavirenz (Sustiva) Metabolism
-inducer/inhibitor of CYP450
43
When should NNRTI Efavirenz (Sustiva) be taken?
-take on empty stomach qHS to reduce AEs
44
NNRTI Rilpivirine (Edurant) AEs
- depression - insomnia - HA - rash
45
NNRTI Rilpivirine (Edurant) Toxicities
- QT prolongation - dyslipidemia - increased LFTs
46
NNRTI Rilpivirine (Edurant) Metabolism
hepatic via CYP3A4
47
How should NNRTI Rilpivirine (Edurant) be taken?
-with food b/c it needs an acidic environment to be absorbed
48
What is contraindicated with NNRTI Rilpivirine (Edurant)?
taking PPIs (can cause therapeutic failure)
49
INSTI Raltegravir (Isentress) AEs
- elevated BGs, including lipase and ALT | - myopathy
50
INSTI Raltegravir (Isentress) Lab Follow-up
- blood glucose - CK - LFTs
51
How is INSTI Raltegravir (Isentress) dosed?
- PO tablet | - must be BID (2 pills @ once may cause therapeutic failure)
52
INSTI Elvitegravir (Vitekta) AEs
- well tolerated | - N/D
53
INSTI Elvitegravir (Vitekta) Lab Follow-up
fasting lipid panel
54
How should INSTI Elvitegravir (Vitekta) be taken?
- oral tablet once daily | - WITH food and a PK booster (blocks metabolism of elvitegravir so it stays in body longer)
55
What is a PK booster (eg Cobicistat/Tybost)?
- pharmacokinetic enhancer: blocks metabolism of a drug so it stays in body longer - NO antiviral properties
56
Cobicistat/Tybost AEs
- nausea, loose stool | - elevated SCr, cholesterol and triglyceride
57
INSTI Dolutegravir (Tivicay) AEs
- well tolerated - HA - hyperglycemia - elevated lipase and transaminases
58
INSTI Dolutegravir (Tivicay) Lab Follow-up
- blood glucose (HbA1c) | - CK
59
How should INSTI Dolutegravir (Tivicay) be taken?
- PO once daily - may take w/o food - does not require a PK booster
60
PI Atazanavir (Reyataz) AEs
- rash | - hyperbilirubinemia
61
PI Atazanavir (Reyataz) Toxic Effects
- AV block - nephrolithiasis - elevated transaminases
62
PI Atazanavir (Reyataz) Lab Follow-up
- fractionated bilirubin | - LFTs
63
How should PI Atazanavir (Reyataz) be taken?
- once daily - take w/ food (needs acidic enviro to be absorbed) - needs PK booster
64
PK Booster Ritonavir (Norvir) AEs
- HA - N/V/D - taste perversion - elevated CK - hyperglycemia - elevated LFTs - hyperlipidemia
65
PK Booster Ritonavir (Norvir) Lab Follow-up
- LFTs - fasting lipids and BGs - possible EKG
66
PI Darunavir (Prezista) AEs
- rash (SJS) - diarrhea - hypercholesterolemia/TGs - hyperglycemia
67
PI Darunavir (Prezista) Lab Follow-up
- LFTs - fasting lipid panel - BGs
68
How should PI Darunavir (Prezista) be taken?
- qday or BID - take with food - always take with PK booster
69
Are there major drug interactions with NRTIs?
- not really - all but one (abacavir) are renally cleared) - dose adjust all except abacavir for renal impairment/failure
70
Are there major drug interactions with N-NRTIs?
- YES! | - varying CYP450 influences (+ or -)
71
What drugs are contraindicated with N-NRTIs?
- dexamethasone - PPIs - certain anticonvulsants (phenytoin, CBZ, etc)
72
Are there major drug interactions with PIs?
- YES - all PIs have extensive CYP450 interactions - LOTS of contraindications with commonly used medications
73
What drugs are contraindicated with PIs?
- alprazolam, triazolam - simvastatin, lovastatin - all ergot alkaloids - amiodarone, propafenone - salmeterol - caution with fluticasone, ethinyl estradiol, warfarin
74
What lab monitoring should be done with ARVTx?
- absolute CD4 count should be stable or improved | - viral load should decrease
75
Based on lab values, when is tx considered a failure?
VL > 400 copies/mL @ 24 weeks | OR VL > 48-75/mL @ 48 weeks
76
What factors can contribute to ARV resistance?
- improper administration - improper absorption (delayed or malabsorption) - improper storage - missing doses - wide variability or inconsistent dosing schedule