HIV/AIDS Flashcards

1
Q

HIV

A

human immunodeficiency virus

retrovirus that destroys CD4+ T cells
HIV1 and HIV2

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2
Q

AIDS

A

acquired immune deficiency syndrome
*HIV progresses into AIDS

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3
Q

how is HIV transmitted?

A
  1. sexual: semen, vaginal secretions
  2. parenteral: blood
  3. mother to child: pregnancy, birth, breastfeeding
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4
Q

risk factors for development of HIV

A

-men having sex with men
-IV drug use
-heterosexual contact
-mother-to-child (perinatal)
-blood transfusions
+ unknowns!

(black, South Africa)

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5
Q

why doesn’t everyone who is exposed develop an active HIV infection?

A

-duration + frequency of contact
-volume, virulence, concentration of virus
-host immune fxn
-genetic protective factors

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6
Q

CCR5

A

protein on CD4+ cells

defective CCR5 can block entry of HIV

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7
Q

with sexual transmission, what increases the risk of developing HIV?

A

-unprotected ANAL sex (higher risk of bleeding)
-receiver of semen
-multiple partners
-STIs
-uncircumcised
-alcohol and drug use
-uses sex in trade for drugs and $$

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8
Q

with parenteral transmission, what increases the risk of developing HIV?

A

-sharing of needle between IDUs
-blood
-health care exposure to blood, body fluids, needles/sharps
*puncture high risk
*splash of blood less of a risk

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9
Q

mother to child HIV transmission

A

pregnancy, delivery, breastfeeding

increased risk when mom doesn’t know she has HIV and isn’t being treated

C-section common, unless low viral levels, possible vaginal delivery

HIV mom should be treated, then baby once born

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10
Q

non-movable white stripes of the side of tongue

A

oral hair leuoplakia

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11
Q

what are white stripes/patches that can be scraped off, bleed, that can be painful?

A

thrush

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12
Q

antiretrovirals

A

HAART (ART): highly active (antiretroviral therapy)

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13
Q

why do we use HAART instead of mono therapy?

A

reduce risk of drug-resistant HIV

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14
Q

goals/benefits of HAART

A

-delay or reverse loss of immune fxn
-decrease AIDS-related complications
-prolong life

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15
Q

drawbacks of HAART

A

-expensive
-long-term SE
-serious drug interactions
-must be taken for life

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16
Q

who should receive ART?

A

anyone with HIV & all pregnant HIV+ women

*still infectious when taking therapy
*pt must be motivated to adhere to med

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17
Q

pre-exposure prophylaxis (PrEP)

A

*truvada (NRTI) - taken before exposure for high risk pt’s
*can reduce risk of HIV transmission by > 90%

-determine barriers
-obtain sexual and drug use history
-teach condom use

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18
Q

when and why do you need to follow up with a HCP for PrEP?

A

follow up every 90 days for HIV testing, screening for acute infections, and assessing risk behaviors

*possibly prescribe other meds

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19
Q

post-exposure prophylaxis (PEP)

A

-recommendations based on exposure and barriers
-treatments for non-occupation and HCP
-ART for 28 days
-HIV testing at 6 and 12 weeks after exposure

20
Q

how does HIV work?

A
  1. HIV targets CD4+ T helper cell and binds to it
  2. HIV on CD4+ cell then fuses with cell membrane and enters host cell
  3. once inside, viral RNA –> viral DNA (transcriptase)
  4. viral DNA is inserted into the infected cell’s genetic material (integrase) and hijacks cell
  5. (protease) releases particles within the virus that attack, replicate and release more HIV
21
Q

HIV1

A

has a very high mutation rate
more resistant to drugs

22
Q

HIV invades CD4+ cells and becomes part of that cell DNA. what does this mean regarding the infection status of the infected person?

A

individual infected for life

23
Q

virus proliferates in infected cells and shed virus particles. where is the virus present?

A

virus is present in the blood and bodily fluids

proliferates RAPIDLY

24
Q

body forms anti-HIV antibody. what is important to know about this antibody?

A

antibody is a marker of infection BUT is NOT protective

25
Q

progressive destruction of helper T cells means

A

compromised cell-mediated immunity

26
Q

immune defense collapses

A

opportunistic infection, neoplasms

completely overwhelms body’s defense

27
Q

T/F: reactivity of a PPD skin test in someone with HIV could result in a false negative

A

TRUE

don’t have T helper cells to have the normal immune response

28
Q

CD4+ T helpers cells: normal amount

A

500-1500

<500 = opportunistic infections occur

29
Q

early infection (acute)

A

-rapid replication
-not detected in labs
-no symptoms
-contagious

large amounts in body, may be asymptomatic or develop flu-like symptoms

30
Q

early infection (acute): seroconversion

A

when sufficient antibodies are detected in the blood (HIGH levels of HIV in genital fluids)
~3 weeks to 6 months

flu-like symptoms for several weeks
highly contagious

31
Q

clinical latency

A

HIV reproduces at low levels, still active (body fighting infection)

-lasts for 3-12 years
-asymptomatic or mild symptoms

32
Q

rapid virus production

A

-persistent drop in CD4+ T cell count (<200 = AIDS)
-antiviral fight becomes less effective
-viral load increases

33
Q

oral manifestations of HIV

A

fungal (oral candidiasis)
viral (herpes simplex, oral hair leukoplakia)
bacterial (periodontal disease)
cancerous

34
Q

oral candidas (thrush)

A

fungal

seen in early infection/acute

bleed when scraped
pain with eating and swallowing

35
Q

herpes simplex

A

viral

blistered vesicles, clustered, painful, rupture

heal within 7 - 10 days

*acyclovir: shorten healing time

36
Q

oral hairy leukoplakia

A

triggered by Epstein Barr virus
hairy, white-like lesions on lateral parts of tongue
non-movable

occurs in ALL stages of HIV

cannot be scraped off or painful- doesn’t require treatment

37
Q

periodontal disease

A

bacterial
*sudden onset
*rapid loss of bone and soft tissue
*can be painful If nerves are exposed

2 types:
1. linear gingival erythema
2. necrotizing ulcerative periodontitis (rapid-severe)

38
Q

fungal AIDS-defining illnesses

A
  1. candidiasis (pulmonary, esophageal)
  2. pneumocystis (carinii) jiroveci PNA
39
Q

viral AIDS-defining illnesses

A
  1. cytomegalovirus
  2. herpes simplex (both) –> chronic ulcer >1 month (pulmonary/esophageal)
40
Q

protozoal AIDS-defining illnesses

A
  1. toxoplasmosis
  2. isosporiasis
  3. cryptosporidiosis (intestinal)
41
Q

bacterial AIDS-defining illnesses

A
  1. mycobacterium (TB, avium)
  2. PNA, recurrent
  3. salmonella septicemia, recurrent
42
Q

cancers: AIDS-defining illnesses

A
  1. kaposi’s sarcoma
  2. cervical cancer (invasive)
  3. lymphomas
43
Q

karposi’s sarcoma

A
44
Q

other: AIDS-defining illnesses

A
  1. wasting syndrome
  2. encephalopathy
  3. AIDS dementia complex (can cross BBB)
45
Q

karposi’s sarcoma

A

purple/blue/red lesions on oral mucous membranes

late stage HIV or AIDS

sudden onset

46
Q

lymphoma

A

lesions are firm, painless swellings