HIV Flashcards
If a bacteria produces beta – lactamase, will antibiotics kill them?
No
Peak
Highest concentration of med in patient
IV peak
15 to 30 minutes after administration
trough
Lowest concentration of med, impatient
30 minutes prior to next admin dose
Virus
Parasitic microbe
no cell wall of their own, lives by inserting on RNA/DNA into a healthy cell
How do antivirals kill viruses?
By inhibiting their ability to replicate
HIV
Human immunodeficiency virus
Retrovirus that destroys CD4 T cells
Aids
acquired immune deficiency syndrome
Late stage of HIV
CD4 count in AIDS
<200 cells
What ethnic group has the highest prevalence of HIV/aids?
South Africa
Black men
Highest transmission of HIV/aids
Men to men sex
Stages of HIV/aids
Binding
Fusion
Reverse transcription
Integrase
Replication
Assembly
Budding
Binding stage of HIV
Virus binds to CD4 cell receptor
Fusion stage of HIV
virus fuses with surface T cell receptors CD4, and CCR5
Can insert self into cell
Reverse transcription stage of HIV
viral RNA to DNA
Enter cell nucleus
integrase stage of HIV
Viral DNA into CD4 cell
replication stage of HIV
Virus assembles new proteins
Assembly stage of HIV
Protease released to break up chains to make mature, HIV into immature
budding stage of HIV
HIV attacks other cells
what is the effect when HIV invades CD4 cell becomes part of DNA?
Patient is infected for life
what is the effect when the virus proliferates infected cells and sheds particles?
Virus in blood and body fluids
what is the effect of the body forming HIV antibodies?
Antibody is marker of infection, not protective
what is the effect of progressive destruction of helper T cells?
Compromised cell mediated immunity
what is the effect of immune defense collapse?
Opportunistic infection
Neoplasms
normal CD4 count
500 to 1500
CD4 count of opportunistic infections
Less than 500
acute early infection
Rapid replication – present in blood/fluids
is HIV detectable in acute early infection?
Not detectable by labs – no antibodies yet
No symptoms
when does HIV become infectious?
Seroconversion – antibodies detectable
3 weeks – 6 months
flu, mono like symptoms (1-4 weeks, then disappear)
clinical latency – chronic
3 to 12 years, still active
Virus levels stabilized – body is fighting virus
Asymptomatic or mild symptoms
rapid virus production
Decreased CD4 T cell count
Viral load increases
Antiviral fight decreases
Patient enters AIDS
Oral symptoms of HIV
higher risk of progression to AIDS
Seen with decreased CD4 counts
types: fungal, viral, bacterial, cancerous
oral candidiasis symptoms
Acute stages
Lesions in oral cavity
Bleeds with scraping
Pain with eating and swallowing
herpes simplex symptoms
Clusters of vesicles
Oral hairy leukoplakia
Nonmovable lesions on lateral part of tongue
All stages
Not painful, asymptomatic
Caused by Epstein-Barr virus
periodontal disease
rapid or linear
Very little plaque build up
Rapid loss of bone, soft tissue
A I DS defining illness
CD4 count >200 cells, or one of illnesses
Opportunistic infections
Fungal, viral, protozoa, bacterial, cancers
Kaposi’s sarcoma
Can be late stages of HIV/AIDS
Red, blue, purple lesions in mouth
Hard palate – most common
lymphoma
Undifferentiated non-Hodgkin’s disease
Firm, painless
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
can HIV be spread by hugging, or exchanging saliva or sweat?
No
risk behaviors
Men to men sex
Injection drug use
Heterosexual contact
Mother to baby transmission
Blood transfusions
factors of exposure to HIV
Duration and frequency of contact
Volume, virulence, and concentration of virus
Host immune status – compromised/not
Genetic protective factors
HIV transmission
unprotected sex with HIV infected partner
Sexual – semen, vaginal secretions
Parenteral – blood
Mother to child – pregnancy, birth, breast-feeding
sexual transmission
Unprotected, HIV, infected partner
increased risk of sexual transmission
Being receiver of semen
Unprotected, anal or oral sex
Multiple partners
STI
Lack of circumcision
Alcohol and drug use
parenteral transmission
Needle/syringe sharing between IV drug users
Blood or blood products
Healthcare exposure to blood, body fluids, puncture wounds
mother to child transmission
Pregnancy
Delivery
Breast-feeding
what increases the risk with mother to child transmission?
Lack of awareness of HIV status
Lack of prevention services
Pharmacology goals for HIV
Delay or reverse loss of immune function
Decreased AIDS related complications
Prolong life
drawbacks of med therapy for HIV
Expensive
Serious, long-term side effects
Drug interactions
Lifelong
Not a cure
recipients of ART
any person living with HIV
Pregnant women who are HIV positive
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
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
what is the most common risk behavior?
Men to men sex
integrase
enzyme that creates a viral DNA copy and is inserted into the genetic material of the infected cell
protease
enzyme that is responsible for the virus particles that are released to attack, replicate and release more virus
reverse transcriptase
enzyme that’s converts viral RNA to DNA
