HIV (Human Immunodeficiency Virus) & AIDS (Acquired Immunodeficiency Syndrome) Flashcards

1
Q

HIV leads to what

A

immunodeficiency

virus incorporates self into host cells to replicate

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2
Q

cmplx of HIV infection

A

AIDS

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3
Q

what virus targets the immune system for HIV

A

retrovirus

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4
Q

how does retrovirus impact DNA

A
  • Usually DNA transcribes into RNA and that forms proteins
  • These viruses take RNA and put it into the DNA of the host (work backwards)
  • results in profound immunosuppression (develop infection & CA easily)
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5
Q

etiology & transmission

A
  • sexually transmitted

- maternal

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6
Q

how is it sexually transmitted

A

semen contains virus & virus carried in blood

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7
Q

how is it transmitted maternally

A
  • in utero
  • labor & delivery (severed blood vessel & baby contacts blood)
  • lactation (through breast milk)
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8
Q

3 stages of HIV

A

1) primary infection
2) latent period
3) overt AIDS

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9
Q

(1) primary infection duration

A

weeks - months

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10
Q

(1) primary infection

A
  • seroconversion
  • high viral load
  • dec CD4 count
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11
Q

pt tests negative for HIV in what stage

A

primary infection (window period – time it takes Abx to form)

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12
Q

seroconversion

A

formation of Abs

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13
Q

(2) latent period

A
  • asympt for years
  • lymphatic tissue damage
  • recurrent respiratory infections
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14
Q

why do recurrent respiratory infections occur in latent period (2)

A

b/c most microbes & viruses enter via inhalation

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15
Q

(3) overt AIDS

A
  • ~10 yr (60-70%): typical progressors
  • ~5 yrs: rapid progressors
  • ~15 yrs: slow progressors
  • long-term non-progressors (2-5%): do not develop AIDS
  • CD4 count below 200 & have an opportunistic infection = AIDS
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16
Q

patho

A
  • targets T helper cells (CD4)
  • also targets macrophages & B cells
  • destroys immune system (new infections occur d/t latent pathogens)
  • many organs affected
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17
Q

if T helper cells (CD4) are damaged, what happens

A

cytokines not generated for immune cells to communicate with e/o –> immune system compromised

18
Q

B cells

A

Responsible for Ab formation, if these are targeted, then Ab formation inhibited

19
Q

Dx

A
  • clinicl presentation
  • ELISA (Ab test) –> Es-linked immunosorbant assay
  • western blot assay
  • PCR (polymerase chain rxn)
  • CD4 counts & viral loads (inversely proportional)
  • quick tests (rapid serum & saliva tests)
20
Q

ELISA (Ab test)

A

Body’s production of Abs measured against entire virus using an enzymatic method

  • if test positive, they confirm w/ Western blot assay
21
Q

Western blot assay

A

Abs produced to a specific part of HIV virus (more specific test)

22
Q

PCR (Polymerase Chain Reaction)

A

Amplifies genetic material and measures viral particle itself (rarely used)

23
Q

CD4 counts & viral loads

A

Surface proteins on T helper cells –> CD4 counts measure the number of T helper cells

(if this is low, then the viral load must be high and vice versa)

24
Q

quick tests: new rapid serum & saliva tests

A

indicates pt might be positive, more specific tests used

  • P24 antigen
25
Q

P24 antigen

A

protein found in the viral core and makes its appearance early (between time of infection and seroconversion, when antibodies are detectable)

26
Q

mnfts

A
  • extensive, involves many body systems
  • recurrent resp infections
  • GI infections
  • NS: dementia, encephalopathy
  • opportunistic CA
27
Q

why do recurrent resp infections occur

A

defense is compromised d/t infection impacting resp tract (ex. TB & pneumonia)

28
Q

why do GI infections occur

A

from normal flora & ingested microbes (in food)

ex. diarrhea, gastroenteritis, etc.

29
Q

why does dementia & encephalopathy occur

A

impaired CNS Fx d/t various infections & virus presence

30
Q

opportunistic CA

A

Malignant cells in early stage controlled by immune system

  • Kaposi’s sarcoma
  • cervical CA
  • Non-Hodgekin’s lymphoma
31
Q

Kaposi’s sarcoma

A

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

32
Q

cervical CA cause

A

d/t HPV infection (compromised defences)

33
Q

Tx

A
  • incurable
  • HAART (Highly-Active Anti-Retroviral Therapy)
  • polypharmacy
34
Q

what drugs used

A

antiviral agents (at least 3) – each target diff steps

35
Q

what antivirals used

A
  • reverse transcriptase inhibitors
  • protease inhibitors
  • entry inhibitors
  • integrase inhibitors
36
Q

reverse transcriptase inhibitors

A

inhibit the viral RNA replicating into DNA, and the multiplication of the virus

37
Q

protease inhibitors

A

inhibits the enzyme that breaks down proteins –> proteases break up polypeptides in host cells

38
Q

entry inhibitors

A

inhibit entry into the host cell

if the virus cannot get into the cell then it cannot damage it

39
Q

integrase inhibitors

A

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

40
Q

functions of antivirals

A

A) Prevents virus from entering host cell
B) Presents virus from integrating RNA into DNA
C) Prevents virus from dividing