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HIV Antivirals Flashcards

1
Q

What are CD4 cells, where are they located and why do I care about them?

A
  • immune cells in lymph tissue that keep our body healthy

- HIV uses CD4 cells to replicate

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2
Q

3 things HIV attacks?

A
  • CD4 cells
  • Macrophages
  • Microglial cells
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3
Q

Which cell that is attacked by HIV is in the CNS and acts a reservoir for HIV?

A

microglial cells

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4
Q

3 stages of HIV

A
  • acute (flu like sxs)
  • latency
  • AIDS diagnosis
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5
Q

What does a person have to have to be in AIDS stage of HIV?

A

CD4 count <200

OR

Aids defining illness

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6
Q

What is the normal CD4 count in a healthy person?

A

800-1200 cells/mm3

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7
Q

HIV is _____ prone

A

error prone

-mutates frequently

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8
Q

What is the plasma life of HIV?

A

6 hours

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9
Q

What is the relationship between viral load and drug resistance?

A

increase viral load = increase mutations = increase drug resistance
-every time it replicates it can have more mutations

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10
Q

What is a steady state of HIV viral load?

A

1,000 - 100,000 viron/ml

  • requires frequent replication
  • 1/2 of HIV virons in plasma are lost every 6 hours
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11
Q

What is the HIV life cycle?

A
  • attach to CD4 cell at CCR5 or CXCR4 receptors
  • gain entry
  • viral RNA –> viral DNA due to enzyme reverse transcriptase
  • viral DNA –> enter CD4 cell nucleus due to enzyme integrase
  • Integrate into machinery of CD4 cell
  • CD4 cells makes viral DNA (transforms what CD4 cell does)
  • Protease enzyme cuts HIV chain into small pieces that combine to form a new working virus
  • HIV virons bud off, travel, and infect new CD4 cells
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12
Q

What are the 6 types of HIV antiviral drugs that fall into 2 broad categories ?

A
  1. CCR5 antagonist
  2. Fusion inhibitors
  3. Nucleoside reverse transcriptase inhibitor
  4. Non-nucleoside reverse transcriptase inhibitor
  5. Integrase inhibitor
  6. Protease inhibitor
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13
Q

What are the 2 broad categories of HIV antiviral drugs?

A
  1. block viral entry into cell

2. inhibit enzymes required for HIV replication

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14
Q

What is CCR5 and what does it bind to?

A

CCR5 is 1 of 2 co-receptors on the surface of CD4 cells that binds to GP120 on the HIV molecule

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15
Q

What does it mean to be R5 trophic?

A

HIV is usually R5 trophic

–> HIV usually binds to CCR5 in early infection not CXCR4

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16
Q

What does it mean to be “dual trophic” ?

A

GP120 on HIV virus can switch from binding to CCR5 or CXCR4

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17
Q

In order for Maraviroc to work what do HIV patients have?

A

R5 trophic strain of Hiv!

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18
Q

How does Marovic work ?

A
  • BLOCK ENTRY into CD4 cell

- blocks ability for coreceptor CCR5 to bind to GP120

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19
Q

Who should use maraviroc? (3)

A
  • HIV naive
  • treatment resistant
  • R5 Trophic strain of HIV
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20
Q

Maraviroc side effects

A

mild, CV risks

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21
Q

How do Fusion inhibitors work?

A

block entry into the CD4 cell by inactivating GP41

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22
Q

What is GP41?

A

Protein on HIV surface that is a transmembrane complex

-binds to CD4 causing fusion of HIV lipid bilayer to CD4

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23
Q

What is Enfuviritide (Fuzeon, T20) mechanism of action?

A
  • block HIV from entering CD4 cell by binding to GP41

- GP41 becomes rigid and unable to fuse to fuse lipid bilayers

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24
Q

Enfuviritide (Fuzeon, T20) route?

A

sub Q injection 2x/day (BID)

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25
Enfuviritide (Fuzeon, T20) Cost
$52,000 annually
26
Enfuviritide (Fuzeon, T20) Adverse Effects
- 98% people get reaction @ injection site: | - -pain, tenderness, erythema, induration, nodules, cystitis, pruritis, echimosis
27
Enfuviritide (Fuzeon, T20) patient teaching?
- rotate injection site - avoid deep injection --> to decrease adverse effects
28
Enfuviritide (Fuzeon, T20) indication for use?
used when resistant to other drugs | --> b/c of side effects last ditch effort
29
What is the function of nucleotide/nucleoside reverse transcriptase inhibitor?
(when virus enters CD4 it comes in as RNA andmust be changed to DNA by copying itself from single strand DNA to double strand DNA) - inhibit creation of viral DNA by substituting a useless nucleotide in strand of base pairs and prevents future base pairs being added into strand - Inhibit enzyme reverse transcriptase
30
What is the first line treatment regimen for HIV?
2 NNRTI + 1 other drug
31
Adverse effects of all NRTI?
- Lactic Acidosis (nausea, anorexia, fatigue, hyperventilation) - Severe hepatomegaly with fatty liver
32
What is Zidovdine (AZT)?
- NRTI , block reverse transcriptase enzyme | - 1st HVI drug on the market
33
Zidovdine (AZT) side effects?
anemia, neutropenia -- damage to bone marrow
34
What is Abacavir (Zigen, ABC)?
-NRTI, block reverse transcriptase
35
What do you have to test for with Abacavir (Zigen, ABC)?
-genetic variant HLA-B5701 | if + can't use the drug due to hypersensitivity rxn
36
What are the 2 NRTI's to know?
Zidovdine (AZT) | Abacavir (Zigen, ABC)
37
How does a Non nucleotide Reverse Transcriptase inhibitor (NNRTI) fxn?
- bind to active center of reverse transcriptase enzyme causing direct inhibition - -> puts a cog in wheel and not allowing enzyme to do what it is supposed to do
38
Which HIV drug class reacts with CYP450?
NNRTI (Efavirenz/Sustiva)
39
Adverse effect of all NNRTI?
rash, hypersensitivity (Stevens Johnson Syndrome)
40
What cells does Efavirenz(Sustiva) target?
crosses blood brain barrier targeting microglial cells
41
What class of drugs does Efavirenz(sustiva) fall under?
NNRTI
42
How do integrase inhibitors function?
-prevent HIV genetic material from being integrated into the DNA of CD4 cell (HIV RNA in CD4 cell --> RNA-- > DNA--> now DNA can't integrate into CD4 machinery
43
What class of drugs does Raltegravir fall in?
integrase inhibitor
44
When do you use Raltegravir?
-1st line of defence
45
Adverse effects from Raltegravir?
1st line of defense, well tolerated - increase liver enzymes rare: Hypersensitivity rxn
46
How do protease inhibitors fxn?
-prevents protease enzyme from cutting HIV polyprotein into smaller sections of viron (HIV hijacked CD4 --> RNA-->DNA -> machinery--? can't use replicated virons to spread virus) -keeps HIV cell inactive and useless
47
If resistant to 1 protease inhibitor.....
-if resistant to one protease inhibitor, reistant to others
48
Drug drug interactions with protease inhibitors?
- decrease effectiveness of beta blockers | - no statin drugs
49
Adverse effects of protease inhibitors
-increase liver enzymes -decrease cardiac conduction (watch with betablockers) -increase risk of cardiovascular diease METABOLIC SYNDROME: -hyperglycemia (secondary DM) -lipodystrophy -hyperlipidemia
50
Pharmacokinetic enhancers- 2 boosters to know?
Rotonavir (Norvir) | Cobicistat (Tybost)
51
How do boosters work?
synergistic effect with HIV meds
52
what is rotonavir (norvir)?how does it work?
booster that used in low doses with other drugs will increase level of other drug
53
what is Cobicistat (Tybost)? how does it work?
- booster - blocks CYP450 3A4 enzymes - -> increase concentration of certain antiviral drugs
54
What happens is HIV patient develops resistance to HIV med?
change all the drugs in the regimen
55
How does CD4 count effect treatment?
-treat all patients regardless of CD4 count
56
What is the goal of HIV treatment?
-reach undetectable level (20-75/ml)
57
What levels are needed to be considered unable to transmit HIV?
-if undetectable for 6months won't transmit HIV
58
What is general treatment regimen for HIV?
- treat with 3-4 drugs from at leas 2 classes to prevent drug resistance - 2NRTI+ 1 other
59
Most drug drug interactions are with.....
CYP450 pathway
60
Drug therapy for HIV patients includes what 3 things:
- treat HIV virus - Treat HIV med side effects - treat for preventing opportunistic infections
61
What is HAART?
Highly Active AntiRetroviral Therapy
62
When do we give HIV meds to pregnant people?
- while preg - during L&D - 6 months after for baby
63
Preferred delivery method for HIV + women?
-C section @ 38 weeks especially for over 1000 copies/mL
64
Transmission rate from mom to baby if use right treatment/delivery method?
0%
65
What is PREP?
-preexposure prophylaxsis
66
Who should take PREP?
-high risk populations(sex services, drug users)
67
Effectiveness of PREP?
decrease risk by 44-73%
68
What is the 1 PREP med approved by FDA?
Triveda
69
How often take Triveda (Prep)?
``` 1 tablet daily or episodic recommendation (not official rec so use caution with advising this) ```
70
what is PEP?
Post Exposure Prophylaxis
71
When to use PEP?
- one time treatment after exposure | - most effective within 1-2 hours up to 72 hours post exposure
72
How long do you take PEP after exposure?
3 drug regimen for 28 days
73
In addition to taking PEP after exposure also test. When is testing frequency?
-test for HIV antibodies @ time of exposure, 6 weeks, 12 weeks, 6 mo + test source individual
74
What do HIV labs tell us?
where patient is in disease
75
CD4 count vs Viral load, what do they mean, which are you using to determine drug therapy?
CD4 = track left, will see come back up after treatment @ different rates Viral Load= how fast it is progressing, use this to determine drug therapy** -should see dramtic decrease within 6 weeks
76
What is a high CD4 count
>100,000
77
Labs for HIV to test for what 3 things for which meds to use?
- drug resistance - genetic variance (Abacavir) - CCR5 trophism (Maraviroc)
78
Pneumocycstis Jeroveci Pneumonia (PCP) prophylaxsis
TMP/SMX DS
79
CMV retinitis prophylaxis
Valganciclovir or Ganciclovir implant
80
Mycobacterium Avium Complex prophylaxis
Azithromycin
81
Candidiasis prophylaxis
Clotrimazole Troche
82
HSV prophylaxis
Acyclovir or Gancyclovir
83
Cryptococcal Meningitis prophylaxis
fluconazole or itraconazole

Pharm 313 (26 decks)

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