Hiv

Front 1

transmission of HIV

Back 1

only through contact w/infected body fluids: blood, semen, vaginal secretions, breast milk

Front 2

pathophysiology of HIV

Back 2

RNA virus binds to specific CD4 (T-cells) and chemokine (protein receptors) enter cell

Front 3

Reverse transcriptase

Back 3

enzyme made by retrovirus, assists to make viral DNA from the RNA

Front 4

What happens when viral DNA enters cell

Back 4

It enters cell nucleus and splices itself into genome permanantly

Front 5

What is the consequence of viral DNA integration into genetic structure

Back 5

All daughter cells are infected; Viral DNA will direct cell to make HIV (a new HIV cell)

Front 6

Viremia

Back 6

Large viral levels in the blood usually lasts for 2-3weeks (after initial insult)

Front 7

What happens after viremia

Back 7

A prolonged period (could be to 10-12 yrs) of low viral load

Front 8

What types of cells are infected

Back 8

Cells w/ CD4 receptor sites: CD4 t-cells, lymphocytes, monocytes, astrocytes, oligodendrocytes

Front 9

Healthy/normal T-cells life span

Back 9

about 100 days

Front 10

infected T-cells

Back 10

only about 2 days; viral activity kills about 1 billion T-cells daily

Front 11

Why does invasion of HIV result in immune dysfunction

Back 11

Mostly do to destruction of CD4 T-cells, which are key cells for immune recognition and defense against pathogens

Front 12

Normal T-cell life span

Back 12

100 days

Front 13

infected T-cells life span

Back 13

only about 2 days.
Viral activity destroys about 1 billion T-cells daily

Front 14

Normal T-cell cell count

Back 14

800-1200 cells/μl

Front 15

What are the T-cell levels when immune problems start

Back 15

when levels drop below 500 cells/μl

Front 16

How long does it take for antibodies to become + for HIV

Back 16

approximately 3 wks - 3 mos

Front 17

Acute infection (w/HIV)

Back 17

occurs about 1-3 wks after infection; lasts about 2 wks

Front 18

Clinical manifestations of acute infection

Back 18

Flulike symptoms: fever, swollen lymph glands, sore throat, HA, malaise, nausea, muscle & joint pain, diarrhea, or diffuse rash

Front 19

Early chronic infection (w/HIV)

Back 19

Point when antibodies become positive for infection, 3wks-3mos after infection. It can last for years. Most are not aware of infected status

Front 20

Clinical Manifestations of early chronic infection

Back 20

Generally, pt is asymptomatic, but may display fatigue, HA, low-grade fever, and frequent night sweats

Front 21

Intermediate chronic infection (w/HIV)

Back 21

Generally, years after infection. T-cells drop to 200-500 cells/μl & viral load increases. HIV advances to more active state

Front 22

Clinical manifestations of intermediate chronic infection

Back 22

Thrush, oral hairy leukoplakia, drenching night sweats, severe fatigue, localized infections

Front 23

oral hairy leukoplakia

Back 23

painless lateral lesions on the tongue, Epstein Barre is the etiology

Front 24

Late chronic infection

Back 24

AIDS; CD4 levels drop below 200 cells/μl (immune system greatly compromised); great risk for opportunistic disease

Front 25

Clinical manifestations of AIDS

Back 25

PCP (fungal infection), non productive cough, fever, chills, undx resp failure, possible wasting & dementia

Front 26

Some common opportunistic diseases

Back 26

Pneumocystis jiroveci pneumonia, cryptococcal meningitis, cytomegalovirus retinitis, mycobacterium avium complex, Kaposi sarcoma, influenza

Front 27

CDC criteria for dx of AIDS

Back 27

CD4 T-cell count <200 cells/μl, specific opportunistic infection or cancer, wasting syndrome, AIDS dementia complex

Front 28

HIV testing

Back 28

EIA blood test is done to detect serum antibodies that bind to HIV antigens.

Front 29

Results of EIA test

Back 29

if negative, then reported negative. If positive, the test is repeated, if still positive, a Western blot or immunofluorescence assay is done

Front 30

How often should one be tested for HIV

Back 30

If risky behavior, test should be repeated in 3 wks, 6 wks, then 3 mos

Front 31

window period

Back 31

the time it takes after infection but before antibodies can be detected in the blood

Front 32

How is progression of HIV infection monitored

Back 32

By monitoring CD4 T-cell counts and viral load; abnormal blood tests are common some may reveal neutropenia, thrombocytopenia, and anemia

Front 33

COLLABORATIVE care for HIV pt

Back 33

monitor progression & immune function, initiate & monitor antiretroviral therapy, prevent & detect opportunistic infection, prevent & treat complications of therapy, ongoing health assessment

Front 34

Main goals of drug therapy for HIV

Back 34

decrease viral load, maintain/raise CD4 counts, delay HIV-related symptoms & opportunistic infections

Front 35

action of: Nucleoside reverse transcriptase inhibitors, nonnucleoside transcriptase inhibitors, and nucleotide reverse transcriptase inhibitors

Back 35

work by inhibiting the activity of reverse transcritase (aka inhibit the ability of HIV to make a DNA copy early in replication

Front 36

Action of: protease inhibitors

Back 36

interfere with activity of enzyme protease

Front 37

Action of: Fusion inhibitors (or entry inhibitors)

Back 37

interfere with HIV CD4 receptor site binding and entry into cells

Front 38

combination antiretroviral therapy (ART)

Back 38

three or more drugs from different groups are prescribed at full strength

Front 39

Major advantage of ART?

Back 39

attacks the viral replication in several ways, drug resistance is reduced