Antivirals/HIV Flashcards

(46 cards)

1
Q

Why are there only a few antivirals?

A
  1. Often the virus has finished replicating by the time S&S develop
  2. Antivirals only work during cell replication
  3. Viruses live inside the body’s cells, so the drugs that kill a virus could also kill healthy cells
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2
Q

How do antivirals kill viruses?

A

Inhibit their ability to replicate
-Allows the body’s immune system to destroy the virus

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3
Q

Antiviral used to suppress replication of:

HSV 1 (oral)
HSV 2 (genital)
VZV (herpes zoster and varicella/chickenpox)

A

acyclovir

Used for BOTH initial and recurrent infection (may require MULTIPLE TREATMENTS)

Reduces viral shedding and decreases local symptoms

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4
Q

MOA of acyclovir

A

Works in 3 ways:

-Interferes with viral nucleic acid synthesis, its regulation or both (DNA and RNA)

-Prevents virus from binding to cells so VIRUS CAN NOT GET INTO CELLS thus preventing viral replication

-Stimulates the body’s immune system to kill the virus

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5
Q

Acyclovir Routes

A

Routes: Oral, tablet and liquid, topical cream and ointment, IV

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6
Q

Acyclovir

AE and considerations

A

AE: GI distress, renal impairment, seizures, ITP

Considerations:
-IV form: tissue necrosis if not IV is not patent
-Decreases symptom severity and frequency of outbreaks, NOT a cure
-May require multiple treatments

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7
Q

Antiviral drug for “the flu”

A

oseltamivir

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8
Q

oseltamivir

MOA and route

A

MOA: inhibit neuraminidase in influenza viruses

Mostly active against influence A, some action against influenza B

Route:ONLY PO

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9
Q

oseltamivir

Indications and AE

A

Indications:
-Used for prophylaxis and to treat active disease (48H of symptom onset)
-most often given to the elderly/immunocompromised after known exposure to influenza A or B
-CDC approved April 2009 for treatment of H1N1 (swine flu)

AE: nausea and vomiting, seizures, renal impairment

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10
Q

Antiviral to treat cytomegalovirus (CMV)

A

ganciclovir

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11
Q

ganciclovir

MOA and indications

A

MOA: inhibits viral DNA polymerase resulting in change termination

Indications: CMS
Patients typically include: immunocompromised, AIDS, immunosuppressed, transplant patients

Controls but doesn’t cure

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12
Q

ganciclovir

Route and considerations

A

Route: IV and PO

Considerations:
Black box warning: hematologic toxicity, fertility impairment, fetal toxicity, carcinogenesis

Teratogenic in pregnant patients

Do NOT give with imipenem/cilastatin→ seizure potential

Watch kidneys if given with other nephrotoxic drugs

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13
Q

HIV (Human Immunodeficiency Virus

A

A retrovirus that destroys CD4 and T cells

HIV 1- discovered first and is most prevalent

HIV 2-less pathogenic and confined to West Africa

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14
Q

AIDS (Acquired Immune Deficiency Syndrome)

A

Caused by HIV

Typically UNTREATED HIV infection turns to AIDs in 8-10 years

Severe immune system dysfunction is present when AIDS occurs

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15
Q

Epidemiology of HIV

A

South Africa has the highest prevalence of HIV

76% of adults and adolescents with HIV are men
-Black men have the highest rate of new infections
-Men who have sex with men accounts for most new and existing HIV infections

New cases among women are increasing

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16
Q

What is a retrovirus?

A

A type of virus that uses an enzyme, reverse transcriptase, to translate its genetic information into DNA

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17
Q

4 pathophysiology components of retrovirus

A
  1. Cannot replicate outside living host cells
  2. Contains only RNA; no DNA
  3. Destroys the body’s ability to fight infections
  4. Infects CD4 cells-the primary target of HIV infection
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18
Q

Which viral enzyme assists the viral DNA copy to be inserted into the genetic material of the infected cell?

A

HIV integrase

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19
Q

Which viral enzyme is responsible for the virus particles that are released to attack, replicate, and release more viruses?

20
Q

HIV targets CD4 on:

A

T lymphocytes, monocytes, macrophages

21
Q

What is the primary target of HIV protease?

A

Helper T lymphocytes

22
Q

Seven stages of HIV life cycle

A
  1. Binding
  2. Fusion
  3. Reverse transcription
  4. Integration
  5. Replication
  6. Assembly
  7. Budding
23
Q

Event: HIV invades CD4+ cells and becomes a part of cell DNA

Significance:

A

The individual is infected for life

24
Q

Event: Virus proliferates in infected cells and sheds virus particles

Significance:

A

Virus present in blood and body fluids

25
Event: Body forms anti-HIV antibodies Significance:
Antibodies are a marker of infection but it is not protective
26
Event: Progressive destruction of Helper T cells Significance:
Compromised cell-mediated immunity
27
Event: Immune defense collapse Significance:
Opportunistic infection, neoplasms
28
Why is HIV such a problem?
Decreases the number of CD4 and T Helper cells HIV replicates prolifically Completely overwhelms the body's defenses
29
Stage 1
Early infection (Acute) -Rapid replication -Not detectable by traditional lab tests (no symptoms) -Infectious Seroconversion -Antibodies are detectable -Flu-like symptoms for several weeks HIGHLY INFECTIOUS
30
Stage 2
Clinical Latency (Chronic) -Virus levels have stabilized -Body is fighting infection -Lasts 3-12 years -Asymptomatic or mild symptoms Rapid virus production -Persistent drop in CD4 and T cell count -Antiviral fight becomes less effective -Viral load increases
31
Stage 3
Symptomatic HIV Infection AIDS -CD4 cells fall below 200 cells/mm -Without treatment, people typically survive 3 years
32
Initial Symptoms of HIV
Sore throat Fever Muscle Aches Night sweats Fatigue Mouth ulcers Chills Swollen lymph nodes Rash
33
Diagnosis of AIDS
1. Must have an AIDs-defining condition -Kaposi's Sarcoma -Wasting syndrome -Cancers -Pervasive candidiasis 2. CD4 count less than 200 cell/mm regardless if an AIDs-defining condition is present
34
What manifestation is linked to a higher risk of progression to AIDS
Oral manifestations -Seen with falling CD4+ counts
35
Examples of oral manifestations
Oral hairy leukoplakia periodontal disease
36
HIV-Associated Dementia
"AIDS dementia complex" Symptoms: -poor concentration -forgetfulness -changes in behavior -difficulty word finding -depression -motor/speech/balance/visual problems
37
How is HIV transmitted?
-Sex without a condom -Passed from mother to baby -Sharing equipment -Contaminated blood transfusion or organ transplant
38
Why doesn't everyone who is exposed develop HIV?
-Duration and frequency of contact -Volume, virulence, and concentration of virus -Host immune status -Genetic protective factors
39
Drug to treat individuals with HIV
Antiretroviral therapy (ART) -NRTIs -Given in PAIRS with other NRTIs most commonly
40
Most common ART
Dual nucleoside and a third agent from other class
41
NRTI MOA
Inhibits reverse transcriptase -Thus blocking the HIV retrovirus to incorporate its RNA into the host cell's DNA
42
NRTI Adverse Effects
peripheral neuropathy, pancreatitis, lipoatriphy, hepatic steatosis
43
ART Principals
Start AS SOON AS POSSIBLE after diagnosis GOAL: Decrease viral load to undetectable level Treatment guided by CD4 count, viral load, and patient preferences
44
True/False A low CD4 and high viral load is healthy
False Measured in drop of blood: CD4 cells should be high Viral load is better low
45
What is PrEP used for?
Pre-exposure prophylaxis -Use of antiretroviral medications -Detailed sexual and drug use history to determine risk -Determine potential barriers -Condom use -Can reduce risk of HIV transmission by greater than 90%
46
What is PEP used for?
Post-exposure prophylaxis -Recommendations based on exposure and barriers -Treatments include ART for 28 days -HIV testing initially and at 6-12 weeks after exposure