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Pharm 313 > HIV Antivirals > Flashcards

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
Q

Enfuviritide (Fuzeon, T20) Cost

A

$52,000 annually

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26
Q

Enfuviritide (Fuzeon, T20) Adverse Effects

A
  • 98% people get reaction @ injection site:

- -pain, tenderness, erythema, induration, nodules, cystitis, pruritis, echimosis

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27
Q

Enfuviritide (Fuzeon, T20) patient teaching?

A
  • rotate injection site
  • avoid deep injection

–> to decrease adverse effects

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28
Q

Enfuviritide (Fuzeon, T20) indication for use?

A

used when resistant to other drugs

–> b/c of side effects last ditch effort

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29
Q

What is the function of nucleotide/nucleoside reverse transcriptase inhibitor?

A

(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
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30
Q

What is the first line treatment regimen for HIV?

A

2 NNRTI + 1 other drug

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31
Q

Adverse effects of all NRTI?

A
  • Lactic Acidosis (nausea, anorexia, fatigue, hyperventilation)
  • Severe hepatomegaly with fatty liver
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32
Q

What is Zidovdine (AZT)?

A
  • NRTI , block reverse transcriptase enzyme

- 1st HVI drug on the market

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33
Q

Zidovdine (AZT) side effects?

A

anemia, neutropenia – damage to bone marrow

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34
Q

What is Abacavir (Zigen, ABC)?

A

-NRTI, block reverse transcriptase

35
Q

What do you have to test for with Abacavir (Zigen, ABC)?

A

-genetic variant HLA-B5701

if + can’t use the drug due to hypersensitivity rxn

36
Q

What are the 2 NRTI’s to know?

A

Zidovdine (AZT)

Abacavir (Zigen, ABC)

37
Q

How does a Non nucleotide Reverse Transcriptase inhibitor (NNRTI) fxn?

A
  • 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
Q

Which HIV drug class reacts with CYP450?

A

NNRTI (Efavirenz/Sustiva)

39
Q

Adverse effect of all NNRTI?

A

rash, hypersensitivity (Stevens Johnson Syndrome)

40
Q

What cells does Efavirenz(Sustiva) target?

A

crosses blood brain barrier targeting microglial cells

41
Q

What class of drugs does Efavirenz(sustiva) fall under?

A

NNRTI

42
Q

How do integrase inhibitors function?

A

-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
Q

What class of drugs does Raltegravir fall in?

A

integrase inhibitor

44
Q

When do you use Raltegravir?

A

-1st line of defence

45
Q

Adverse effects from Raltegravir?

A

1st line of defense, well tolerated

  • increase liver enzymes
    rare: Hypersensitivity rxn
46
Q

How do protease inhibitors fxn?

A

-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
Q

If resistant to 1 protease inhibitor…..

A

-if resistant to one protease inhibitor, reistant to others

48
Q

Drug drug interactions with protease inhibitors?

A
  • decrease effectiveness of beta blockers

- no statin drugs

49
Q

Adverse effects of protease inhibitors

A

-increase liver enzymes
-decrease cardiac conduction (watch with betablockers)
-increase risk of cardiovascular diease
METABOLIC SYNDROME:
-hyperglycemia (secondary DM)
-lipodystrophy
-hyperlipidemia

50
Q

Pharmacokinetic enhancers- 2 boosters to know?

A

Rotonavir (Norvir)

Cobicistat (Tybost)

51
Q

How do boosters work?

A

synergistic effect with HIV meds

52
Q

what is rotonavir (norvir)?how does it work?

A

booster that used in low doses with other drugs will increase level of other drug

53
Q

what is Cobicistat (Tybost)? how does it work?

A
  • booster
  • blocks CYP450 3A4 enzymes
  • -> increase concentration of certain antiviral drugs
54
Q

What happens is HIV patient develops resistance to HIV med?

A

change all the drugs in the regimen

55
Q

How does CD4 count effect treatment?

A

-treat all patients regardless of CD4 count

56
Q

What is the goal of HIV treatment?

A

-reach undetectable level (20-75/ml)

57
Q

What levels are needed to be considered unable to transmit HIV?

A

-if undetectable for 6months won’t transmit HIV

58
Q

What is general treatment regimen for HIV?

A
  • treat with 3-4 drugs from at leas 2 classes to prevent drug resistance
  • 2NRTI+ 1 other
59
Q

Most drug drug interactions are with…..

A

CYP450 pathway

60
Q

Drug therapy for HIV patients includes what 3 things:

A
  • treat HIV virus
  • Treat HIV med side effects
  • treat for preventing opportunistic infections
61
Q

What is HAART?

A

Highly Active AntiRetroviral Therapy

62
Q

When do we give HIV meds to pregnant people?

A
  • while preg
  • during L&D
  • 6 months after for baby
63
Q

Preferred delivery method for HIV + women?

A

-C section @ 38 weeks especially for over 1000 copies/mL

64
Q

Transmission rate from mom to baby if use right treatment/delivery method?

A

0%

65
Q

What is PREP?

A

-preexposure prophylaxsis

66
Q

Who should take PREP?

A

-high risk populations(sex services, drug users)

67
Q

Effectiveness of PREP?

A

decrease risk by 44-73%

68
Q

What is the 1 PREP med approved by FDA?

A

Triveda

69
Q

How often take Triveda (Prep)?

A 
1 tablet daily or
episodic recommendation (not official rec so use caution with advising this)
70
Q

what is PEP?

A

Post Exposure Prophylaxis

71
Q

When to use PEP?

A
  • one time treatment after exposure

- most effective within 1-2 hours up to 72 hours post exposure

72
Q

How long do you take PEP after exposure?

A

3 drug regimen for 28 days

73
Q

In addition to taking PEP after exposure also test. When is testing frequency?

A

-test for HIV antibodies @ time of exposure, 6 weeks, 12 weeks, 6 mo + test source individual

74
Q

What do HIV labs tell us?

A

where patient is in disease

75
Q

CD4 count vs Viral load, what do they mean, which are you using to determine drug therapy?

A

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
Q

What is a high CD4 count

A

> 100,000

77
Q

Labs for HIV to test for what 3 things for which meds to use?

A
  • drug resistance
  • genetic variance (Abacavir)
  • CCR5 trophism (Maraviroc)
78
Q

Pneumocycstis Jeroveci Pneumonia (PCP) prophylaxsis

A

TMP/SMX DS

79
Q

CMV retinitis prophylaxis

A

Valganciclovir or Ganciclovir implant

80
Q

Mycobacterium Avium Complex prophylaxis

A

Azithromycin

81
Q

Candidiasis prophylaxis

A

Clotrimazole Troche

82
Q

HSV prophylaxis

A

Acyclovir or Gancyclovir

83
Q

Cryptococcal Meningitis prophylaxis

A

fluconazole or itraconazole

Pharm 313 (26 decks)

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