HIV and AIDS Flashcards

1
Q

HIV and AIDS

A
  • chronic, progressive retroviral infection (prognosis gets better, but most ppl w HIV will develop AIDS, takes ~10 yrs)
  • HIV leads to immunodeficiency
  • complx of HIv results in AIDS
  • retrovirus targets immune system (Th cells destroy defenses)
  • no cure
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2
Q

how does HIV lead to immunodeficiency?

A

virus incorporates itself into host cell to replicate (happens to target immune cells = ID)

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3
Q

discuss how the retrovirus targets the immune system

A
  • usually DNA transcribes into RNA and that forms proteins, but here the viruses take RNA and put it into DNA of the host
  • this results in profound immunosuppression -> develop CA and infections very readily
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4
Q

etiology

A
  • HIV-1 and HIV-2 (strains of virus)

- 3 stages: primary infection, latency, overt AIDS (8-12 yrs)

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5
Q

transmission

A
  • sexual (semen can contain virus)
  • contaminated blood, blood products, organs
  • placenta, delivery (severed bv and baby is in contact
  • lactation (through breast milk)
  • needle stick injury (0.3% risk if precautions taken)
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6
Q

how do you determine the degree of risk with a needle stick injury?

A

viral load, depth, and site of injury

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7
Q

primary infection

A
  • wks to months
  • window period and seroconversion
  • increased viral load (# of viral particles)
  • decreased CD4 count
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8
Q

window period

A
  • time it takes for Abs to form

- dependent on microbe, individual, and dx test

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9
Q

seroconversion

A

formation of Abs

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10
Q

CD4

A
  • cluster of differentiation 4
  • surface protein on T helper cells, macrophages, and some epithelial cells
  • CD4 count is an indirect measure of the # of T cells
  • can’t be used for dx in primary stage
  • CD4 and viral load are inversely proportionate
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11
Q

latency

A
  • could be asympt for yrs
  • lymphadenopathy
  • recurrent resp infections
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12
Q

why do you have recurrent resp infections in the latency stage?

A

bc its through this system that most microbes and viruses enter via inhalation, but are usually fought off by a functioning immune system

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13
Q

overt AIDS

A
  • typically 60-70% of cases in 10 yrs (typical progressors)
  • ~5yrs = rapid progressors
  • ~15 yrs = slow progressors
  • long term non-progressors (2-5%) -> don’t develop AIDS
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14
Q

patho

A
  • targets T helper cells (CD4)
  • targets macrophages and B cells (Ab formation inhibited)
  • destroys immune system -> decreased immunity and defenses -> many new systemic infections and via latent pathogens
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15
Q

what happens when the virus targets T helper cells (CD4)?

A

responsible for cell-mediated response, if these cells are damaged then cytokines aren’t generated for immune cells to communicate with each other and the immune system is compromised

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16
Q

diagnosis

A
  • presentation and labs
  • ELISA
  • western blot assay
  • PCR
  • CD4 counts and viral loads (viral load not recommended for screening or dx)
  • newer blood and saliva tests (P24 antigen)
17
Q

ELISA

A
  • serology, Ab test
  • Enzyme Linked Immunosorbant Assay
  • body’s prod of Abs measured against entire virus using an enzymatic method
  • if it’s positive, you confirm using a western blot
18
Q

western blot assay

A
  • Abs prod to a specific part of the HIV virus

- more specific test

19
Q

PCR

A
  • polymerase chain reaction
  • amplifies genetic material and measures the viral particle itself
  • not a routine test, but a research test
20
Q

P24 antigen

A

protein found in viral core and makes its appearance early (between infection and seroconversion, when Abs are detectable)

21
Q

manifestations

A
  • many, systemic
  • opportunistic infections that impact the resp tract, GI, nervous system
  • opportunistic CA (Kaposi’s sarcoma, cervical CA, non-Hodgkin’s lymphoma)
22
Q

how do opportunistic infections impact the resp tract?

A

defense compromised so recurrent infection can not be prevented
ex.)TB and pneumonia

23
Q

how is the GI system impacted?

A

infections from normal flora and ingested microbes

ex.) diarrhea

24
Q

how is the nervous system impacted?

A

dementia, encephalopathy (impairment of CNS fx d/t various infections and the presence of the virus)

25
Q

opportunistic CA

A

malignant cells in the early stage are controlled by the immune system

26
Q

Kaposi’s sarcoma

A

mesenchyme origin (non-epithelial) -> arises in endothelial cells (lining bv), forms malignant lesions (appear in skin, mucosa of mouth, lymph nodes)

27
Q

why might you be at risk for cervical CA?

A

d/t HPV infection

28
Q

treatment

A
  • no cure

- HAART

29
Q

HAART

A
  • Highly Active Anti-Retroviral Therapy
  • therapy targets reverse transcription used by the virus
  • at least 3 antivirals are used -> each target a different step
30
Q

what are examples of antivirals that can be used in HAART?

A
  1. reverse transcriptase inhibitors
  2. protease inhibitors
  3. entry inhibitors
  4. integrase inhibitors
31
Q

entry inhibitors

A

inhibit entry into host cell, if the virus cannot get into the cell it can’t damage it

32
Q

integrase inhibitors

A

enzyme inhibited -> prevents the viral particle from integrating its RNA into the host’s DNA

33
Q

reverse transcriptase inhibitors

A

inhibit viral RNA replicating DNA and the multiplication of the virus

34
Q

protease inhibitors

A

inhibits the enzyme that breaks down proteins -> protease breaks up polypeptides in host cells