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NUR 326-Pathopharm > Antivirals/HIV > Flashcards

Antivirals/HIV Flashcards

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?

A

HIV protease

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
Q

Event: Body forms anti-HIV antibodies

Significance:

A

Antibodies are a marker of infection but it is not protective

26
Q

Event: Progressive destruction of Helper T cells

Significance:

A

Compromised cell-mediated immunity

27
Q

Event: Immune defense collapse

Significance:

A

Opportunistic infection, neoplasms

28
Q

Why is HIV such a problem?

A

Decreases the number of CD4 and T Helper cells

HIV replicates prolifically

Completely overwhelms the body’s defenses

29
Q

Stage 1

A

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
Q

Stage 2

A

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
Q

Stage 3

A

Symptomatic HIV Infection
AIDS
-CD4 cells fall below 200 cells/mm
-Without treatment, people typically survive 3 years

32
Q

Initial Symptoms of HIV

A

Sore throat
Fever
Muscle Aches
Night sweats
Fatigue
Mouth ulcers
Chills
Swollen lymph nodes
Rash

33
Q

Diagnosis of AIDS

A
  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
Q

What manifestation is linked to a higher risk of progression to AIDS

A

Oral manifestations
-Seen with falling CD4+ counts

35
Q

Examples of oral manifestations

A

Oral hairy leukoplakia

periodontal disease

36
Q

HIV-Associated Dementia

A

“AIDS dementia complex”

Symptoms:
-poor concentration
-forgetfulness
-changes in behavior
-difficulty word finding
-depression
-motor/speech/balance/visual problems

37
Q

How is HIV transmitted?

A

-Sex without a condom
-Passed from mother to baby
-Sharing equipment
-Contaminated blood transfusion or organ transplant

38
Q

Why doesn’t everyone who is exposed develop HIV?

A

-Duration and frequency of contact
-Volume, virulence, and concentration of virus
-Host immune status
-Genetic protective factors

39
Q

Drug to treat individuals with HIV

A

Antiretroviral therapy (ART)
-NRTIs
-Given in PAIRS with other NRTIs most commonly

40
Q

Most common ART

A

Dual nucleoside and a third agent from other class

41
Q

NRTI MOA

A

Inhibits reverse transcriptase
-Thus blocking the HIV retrovirus to incorporate its RNA into the host cell’s DNA

42
Q

NRTI Adverse Effects

A

peripheral neuropathy, pancreatitis,
lipoatriphy, hepatic steatosis

43
Q

ART Principals

A

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
Q

True/False

A low CD4 and high viral load is healthy

A

False

Measured in drop of blood:
CD4 cells should be high
Viral load is better low

45
Q

What is PrEP used for?

A

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
Q

What is PEP used for?

A

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

NUR 326-Pathopharm (24 decks)

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