Clinical features of AIDS Flashcards

1
Q

what causes the immune dysfunction in HIV infection?

A

-loss of functional CD4 lymphocytes-> loss of memory CD4 cells, and inability to modulate new cell-mediated and antibody-mediated immune response

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2
Q

what happens with CD8 cells in HIV infection?

A

eventual loss of CD8 cytotoxic cells and ability to mount T cell mediated responses against opportunistic infections

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3
Q

what happens with B cells in HIV infection?

A

polyclonal activation (non-antibody specific) of B cells with inability to mount new antibody responses

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4
Q

diagnosis of infection

A

based on demonstrating antibody to multiple HIV antigens: gp120/160 + gp41 or P24

  • must have BOTH, one + one
  • shown on western blot
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5
Q

what is the sensitivity and specificity of HIV testing?

A

HIV serology + WB-> >99%

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6
Q

why can’t test for seroconversion in HIV?

A

may not take place for 6-12 weeks

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7
Q

what is the “gold standard” for diagnose and monitor HIV infection?

A

HIV RNA level

  • follow effectiveness of therapy
  • indicated breakthrough of virus
  • predicts diagnosis in combination with CD4 levels
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8
Q

what is a full blown AIDS CD4 count level?

A

below 200/ml

-long lasting fever, fatigue, weight loss, diarrhea

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9
Q

what is the strongest indicator or disease progression?

A

CD4 count

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10
Q

in HIV infection, what do the lymphoid tissue show?

A

loss of T-cells (particularly peyer’s patches) and expansion of B cell area (b/c of polyclonal acitvation) and generalized lymphadenopathy

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11
Q

what is found in the follicular mantle cells in early infection?

A

marked follicular hyperplasia, viral particles

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12
Q

in later stages, what to the lymph nodes show signs of?

A

“burn out” pattern: loss of most lymphoid elements

  • chronic inflammation leads to cell loss, fibrosis
  • infected tissue may show formation of lymphocyte syncytial (giant cells) with the X4 type of virus
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13
Q

what is infection of the CNS associated with?

A

subacute meningoencephalitis with chronic inflammatory infiltrate with microglial nodules and multinucleated giant cells

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14
Q

what are some complications to HIV?

A

Kaposi’s sacroma (proliferating mesenchymal spindle cells that form blood vessels) and AIDS associated B cell lymphomas

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15
Q

what are two IMPORTANT facts with the pathology of those with AIDS?

A
  1. ) infections in patients with AIDS don’t present in typical manner, present in atypical manner with fewer symptoms
  2. )serology not helpful in diagnosing-> unable to mount an antibody response
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16
Q

what can present at time of transmission?

A

constitutional symptoms-> fever, malaise, rash

17
Q

what is acute retroviral syndrome?

A

high levels of viral replication, viremia, widespread seeding of lymphoid tissue (controlled by host antiviral immune response)

18
Q

when are antibodies not yet detectable?

A

seroconversion may not take place for 6-12 weeks, “window

when antibodies not detectable

19
Q

what do initial drop in viral titers correspond with?

A

development of specific anti-HIV cell mediated immunity

20
Q

a patient can remain well during what period?

A

period in which his/her immune function undergoes slow deterioration with gradual loss of CD4 cells and immune dysregulation
(can last several years)

21
Q

what is a predictor of progression of the disease?

A

level of steady state viremia

22
Q

what do concurrent infection appear to do with this disease?

A

accelerate the disease process by activating the immune system and causing increased proliferation of virus

23
Q

what do patients suffer from with HIV infection of microglial cells?

A

CNS dementia

-virus carried to brain by infected macrophages

24
Q

associated neoplastic conditions?

A

Kaposi’s sarcoma, Hodgkin’s disease and lymphoma

25
Q

Opportunistic infections with HIV?

A
Candidiasis
Pneumocytis
Cryptococcus
GI infection: Giardia, entamoeba, cryptosporidiosis 
Mycobacterium avium, 
Pneumocystis j.
CVM
26
Q

what can give overwhelming viral infections?

A

CMV, herpes zoster

27
Q

reactivation of latent infections?

A

toxoplasmosis, TB, herpes zoster

28
Q

AIDS associated cancers

A

Kaposi’s sarcoma
non-Hodgkin’s lymphoma
invasive carcinoma of uterine cervix (assoc. HPV)

29
Q

Kaposi’s sarcoma

A
  • more common in homosexual/bisexual males
  • associated with HHV8 infection
  • more aggressive than other cancers
  • involves skin, mucous membranes, GI tract
  • proliferation of endothelial cells, smooth muscle cells, pericytes
  • inefficient vascular formation with blood-filled channels
30
Q

non-Hodgkin’s lymphoma

A

highly aggressive
B cell origin, polyclonal B cell activation
extra nodal sites, brain
EBV in 30%

31
Q

what causes the lack of immune response in this disease?

A
  1. immune exhaustion
  2. lack of T helper cells
  3. immune escape by virus
  4. host genetic factors
32
Q

what is the problem with virus specific antibodies

A

how to promote anti-viral response in people without the destruction of HIV-specific CD4 cells in the process

33
Q

what is the major focus of HIV eradication and therapy?

A

prevention

HAART minimizes viral load but does not eliminate the virus

34
Q

what kind of vaccine might be helpful more than antibody mediated responses?

A

vaccines that stimulate cell-mediated responses

35
Q

complications to HAART therapy?

A
lipoatrophy, lipoaccumulation, elevated lipids
insulin resistance
peripheral neuropathy
premature cardiovascular disease
renal, hepatic dysfunction