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Pathopharmacology I > Wk 2 Antivirals > Flashcards

Wk 2 Antivirals Flashcards

1
Q

When do antivirals work?

A

it must get inside the host cells when the virus is still replicating

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2
Q

Often times, the virus has finished…

A

replicating when signs and symptoms develop

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3
Q

Antivirals can also kill…

A

healthy cells

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4
Q

A virus is a __ microbe

A

parasitic

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5
Q

Viruses do not have a __ __ of their own

A

cell wall

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6
Q

How does a virus live?

A

Inserts it’s own DNA or RNA into our cells

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7
Q

List some viruses we are able to treat

A

HSV, HZV, flu, RSV, HIV, CMV, hepatitis

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8
Q

What is acyclovir used to treat?

A

HSV

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9
Q

What are the routes for acyclovir?

A 
oral
tablets
liquid
topical
IV
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10
Q

3 MOA of acycolvir

A

Interferes with nucleic acid synthesis
Prevents virus from binding
Stimulates immune response

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11
Q

Acyclovir side effects

A

Gi distress, renal impairment, seizures, ITP

Tissue necrosis in IV form

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12
Q

The shingles vaccine is a __ vaccine

A

live

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13
Q

What is Shringrix?

A

Herpes zoster vaccine for those over 50

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14
Q

What does oseltamivir do?

A

mostly active against flu A but also some flu B

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15
Q

What is the MOA of oseltamivir?

A

Inhibits neuroamidases

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16
Q

What route is oseltamivir?

A

only PO

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17
Q

What are the side effects of oseltamivir?

A

N/V
seizures
renal impairment

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18
Q

What is ganciclovir?

A

antiviral that treats cytomegalovirus (CMV)

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19
Q

Who is ganciclovir for?

A

Immunosuppressed people like HIV or transplant patients

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20
Q

What is the MOA of ganciclovir?

A

Inhibits DNA polyamerases, stops replication

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21
Q

What routes are ganciclovir?

A

IV and PO

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22
Q

If you crush ganciclovir and get it on your skin, what should you do?

A

wash hands with soap and water

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23
Q

What are the black box warnings for ganciclovir?

A

Hematologic toxicity
Fertility impairment
Fetal toxicity
Carcinogenesis

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24
Q

Who has the highest prevalence of HIV?

A

Black men

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25
Q

What does HIV target?

A

CD4 on t cells

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26
Q

a mutation of __ actually blocks some strains of HIV from entering the cell

A

CCR5

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27
Q

First HIV __ to the cell membraine

A

fuses

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28
Q

Once inside HIV

A

replicates inside the cell and then moves into the nucelus

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29
Q

Final stage of replication, the virus creates

A

HIV protease

30
Q

What re the 7 stages of HIV replication

A 
Binding
Fusion
Reverse transcription
Integration
Replication
Assembly
Budding
31
Q

A TB skin test for a patient with HIV will be…

A

False negative

32
Q

What does HIV use to replicate after it has been integrated into the nucleus?

A

protease

33
Q

What are the hallmarks of HIV infection?

A

Decrease in CD4 t helper cells

Proliferation of HIV particles

34
Q

What is a normal cd4 t cell count?

A

Between 500-1500

35
Q

Early stage of HIV

A

No antibodies
Infectious
Seroconversion - flu like symptoms

36
Q

Clinical latency/chronic HIV

A

Last 3-12 yrs
Asymptomatic or mild symptoms
Stable virus levels

37
Q

Rapid virus production

A

body defenses are less effective and person enters symptomatic stage of HIV, has AIDS

38
Q

AIDS is CD4 count below

A

200

39
Q

Thrush is often seen in the __ phase of HIV

A

acute

40
Q

White lesions on lateral margins of the tongue occur in

A

all stages of HIV infection, oral hairy leukoplakia

41
Q

periodontal disease is common in

A

all stages of HIV

42
Q

What are fungal aids defining illnesses

A

Pulmonary/esophageal candidiasis

Pneumocystitis carinii jiroveci pneumonia

43
Q

What are viral aids defining illnesses

A

CMV

HSV chronic ulcer over a month, pulmonary or esaphageal

44
Q

What are protozoal aids defining illnesses

A

toxoplasmosis
isoporiasis
cryptosporidiosis

45
Q

What are bacterial aids defining illnesses

A

mycobacterium
recurrent pneumonia
salmonella septicemia

46
Q

What are cancerous aids defining illnesses?

A

Kaposi’s sarcoma
Cervical cancer
Lymphomas

47
Q

3 other aids defining illnesses

A

Wasting syndrome
Encephalopathy
AIDS demential complex

48
Q

Why has HIV associated dementia decreased?

A

antiretroviral therapy

49
Q

4 reasons someone who is exposed doesn’t develop HIV

A

Duration/frequency of contact
Concentration of virus
Host immune status
Genetic protective factors - defective ccrd

50
Q

3 methods of transmission

A

unprotexted sex
parenteral
mother-child

51
Q

3 things that further increase risk of HIV

A

oral sex
anal sex
lack of circumcision

52
Q

How long are babies treated after being born for HIV?

A

6 weeks

53
Q

Combination of 3 or 4 drugs to treat HIV is called…

A

HAART - highly active anti retroviral therapy

54
Q

3 reasons to use HAART instead of mono therapy

A

delay or reserve loss of immune function
prplongs life
decreases aids related complications

55
Q

What are the drawbacks of HAART?

A

Expensive
long term side effects
drug interactions
life long

56
Q

CCR5 antagonist

A

Maraviroc

57
Q

Fusion inhibitor

A

Enfurvirtide

58
Q

Protease Inhibitor

A

Lopinavir/Ritonavir

59
Q

Integrase Inhibitor

A

Raltegravir

60
Q

Reverse transcript inhibitors

A

Zidovudine

Efavirenz

61
Q

Zidovudine NRTI side effects

A

Severe anemia and neutropenia

Lactic acidosis in female or obese patients

62
Q

Efavirenz NNRTI side effects

A

Rash, CNS symptoms

Inhibits p450 system drug interactions

63
Q

Reltegravir side effects

A

Well tolerated

Metabolized but UGT caution with other UGT inhibitors

64
Q

Lopinavir/Ritonavir side effects

A

Hyperglycemia, lipodystrphy, hyperlipidemia, bones loss

65
Q

Enfuvirtide side effects

A

sq bidInjection site reactions
Pneumonia
Hypersensitivity

66
Q

Maraviroc side effects

A

Only works with certain strains of HIV, black box liver, drug interaction CYP 3A4. Teach about signs of reaction

67
Q

What is prep?

A

Trivada for those at highest risk of new infection

68
Q

How often are patients on prep followed up with HCP?

A

every 90 days

69
Q

What is pep?

A

Post exposure prophylaxis

70
Q

When should pep be administered?

A

2-3 hours after exposure, effectiveness reduced after 72 hours

71
Q

When is person on pep tested?

A

6 and then 12 weeks after exposure

Pathopharmacology I (33 decks)

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