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NUR 326 > HIV > Flashcards

HIV Flashcards

(58 cards)

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1
Q

If a bacteria produces beta – lactamase, will antibiotics kill them?

A

No

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2
Q

Peak

A

Highest concentration of med in patient

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3
Q

IV peak

A

15 to 30 minutes after administration

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4
Q

trough

A

Lowest concentration of med, impatient

30 minutes prior to next admin dose

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5
Q

Virus

A

Parasitic microbe

no cell wall of their own, lives by inserting on RNA/DNA into a healthy cell

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6
Q

How do antivirals kill viruses?

A

By inhibiting their ability to replicate

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7
Q

HIV

A

Human immunodeficiency virus

Retrovirus that destroys CD4 T cells

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8
Q

Aids

A

acquired immune deficiency syndrome

Late stage of HIV

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9
Q

CD4 count in AIDS

A

<200 cells

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10
Q

What ethnic group has the highest prevalence of HIV/aids?

A

South Africa

Black men

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11
Q

Highest transmission of HIV/aids

A

Men to men sex

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12
Q

Stages of HIV/aids

A

Binding
Fusion
Reverse transcription
Integrase
Replication
Assembly
Budding

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13
Q

Binding stage of HIV

A

Virus binds to CD4 cell receptor

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14
Q

Fusion stage of HIV

A

virus fuses with surface T cell receptors CD4, and CCR5

Can insert self into cell

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15
Q

Reverse transcription stage of HIV

A

viral RNA to DNA
Enter cell nucleus

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16
Q

integrase stage of HIV

A

Viral DNA into CD4 cell

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17
Q

replication stage of HIV

A

Virus assembles new proteins

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18
Q

Assembly stage of HIV

A

Protease released to break up chains to make mature, HIV into immature

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19
Q

budding stage of HIV

A

HIV attacks other cells

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20
Q

what is the effect when HIV invades CD4 cell becomes part of DNA?

A

Patient is infected for life

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21
Q

what is the effect when the virus proliferates infected cells and sheds particles?

A

Virus in blood and body fluids

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22
Q

what is the effect of the body forming HIV antibodies?

A

Antibody is marker of infection, not protective

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23
Q

what is the effect of progressive destruction of helper T cells?

A

Compromised cell mediated immunity

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24
Q

what is the effect of immune defense collapse?

Study These Flashcards
A

Opportunistic infection
Neoplasms

25
normal CD4 count
500 to 1500
26
CD4 count of opportunistic infections
Less than 500
27
acute early infection
Rapid replication – present in blood/fluids
28
is HIV detectable in acute early infection?
Not detectable by labs – no antibodies yet No symptoms
29
when does HIV become infectious?
Seroconversion – antibodies detectable 3 weeks – 6 months flu, mono like symptoms (1-4 weeks, then disappear)
30
clinical latency – chronic
3 to 12 years, still active Virus levels stabilized – body is fighting virus Asymptomatic or mild symptoms
31
rapid virus production
Decreased CD4 T cell count Viral load increases Antiviral fight decreases Patient enters AIDS
32
Oral symptoms of HIV
higher risk of progression to AIDS Seen with decreased CD4 counts types: fungal, viral, bacterial, cancerous
33
oral candidiasis symptoms
Acute stages Lesions in oral cavity Bleeds with scraping Pain with eating and swallowing
34
herpes simplex symptoms
Clusters of vesicles
35
Oral hairy leukoplakia
Nonmovable lesions on lateral part of tongue All stages Not painful, asymptomatic Caused by Epstein-Barr virus
36
periodontal disease
rapid or linear Very little plaque build up Rapid loss of bone, soft tissue
37
A I DS defining illness
CD4 count >200 cells, or one of illnesses Opportunistic infections Fungal, viral, protozoa, bacterial, cancers
38
Kaposi’s sarcoma
Can be late stages of HIV/AIDS Red, blue, purple lesions in mouth Hard palate – most common
39
lymphoma
Undifferentiated non-Hodgkin’s disease Firm, painless
40
AIDS dementia complex sx
Poor concentration, mental slowness Forgetfulness, memory loss Changes in behavior Difficulty word finding Depression, withdrawal from activities Motor/speech/balance/visual problems
41
can HIV be spread by hugging, or exchanging saliva or sweat?
No
42
risk behaviors
Men to men sex Injection drug use Heterosexual contact Mother to baby transmission Blood transfusions
43
factors of exposure to HIV
Duration and frequency of contact Volume, virulence, and concentration of virus Host immune status – compromised/not Genetic protective factors
44
HIV transmission
unprotected sex with HIV infected partner Sexual – semen, vaginal secretions Parenteral – blood Mother to child – pregnancy, birth, breast-feeding
45
sexual transmission
Unprotected, HIV, infected partner
46
increased risk of sexual transmission
Being receiver of semen Unprotected, anal or oral sex Multiple partners STI Lack of circumcision Alcohol and drug use
47
parenteral transmission
Needle/syringe sharing between IV drug users Blood or blood products Healthcare exposure to blood, body fluids, puncture wounds
48
mother to child transmission
Pregnancy Delivery Breast-feeding
49
what increases the risk with mother to child transmission?
Lack of awareness of HIV status Lack of prevention services
50
Pharmacology goals for HIV
Delay or reverse loss of immune function Decreased AIDS related complications Prolong life
51
drawbacks of med therapy for HIV
Expensive Serious, long-term side effects Drug interactions Lifelong Not a cure
52
recipients of ART
any person living with HIV Pregnant women who are HIV positive
53
preexposure prophylaxis
Use of antiretroviral meds Detailed, sexual and drug history – determine risk Determine potential barriers to adherence of daily med regimen Condom used encouragement
54
Post exposure prophylaxis
based on exposure and barriers Treatment for non-occupational and healthcare providers ART therapy for 28 days HIV testing initially, 6 and 12 weeks after exposure
55
what is the most common risk behavior?
Men to men sex
56
integrase
enzyme that creates a viral DNA copy and is inserted into the genetic material of the infected cell
57
protease
enzyme that is responsible for the virus particles that are released to attack, replicate and release more virus
58
reverse transcriptase
enzyme that’s converts viral RNA to DNA

NUR 326 (32 decks)

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