L27+HIV/AIDS Flashcards

1
Q

Initial HIV infection symptoms

A

asymptomatic

sore throat, LAD, mimics Mono

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2
Q

During which stage of infection is there a high risk of transmission?

A

Early stages when the patient is unaware

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3
Q

Average time from HIV infection to AIDS if left untreated

A

8 years

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4
Q

Main symptoms of Acute HIV infection

A
Mouth sores
Thrush
Fever
Weight loss
Myalgia
Hepatosplenomegaly
HA, neuropathy
LAD
Rash
N/V
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5
Q

When is Stage 3 HIV (AIDS) diagnosed?

A

severe damage to the immune system= CD4 <200

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6
Q

Examples of AIDS defining conditions

A
Kaposi's sarcoma (HHV-8)
Pneumocystis pneumonia (PJP)
MAC infection, TB
Invasive cervical cancer
CMV retinitis
Chronic intestinal Cryptosporidiosis
Candidiasis
Encephalopathy
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7
Q

4 HIV disease course classes

A
  1. Fast: <3 years to AIDS
  2. Average: ~10 years
  3. Long term non-progressors >10 years, <5% of cases
  4. Elite controllers: don’t become infected. RARE AF
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8
Q

HIV virus

A

dsRNA genome
Enveloped
Reverse transcriptase: RNA dependent DNA polymerase inserts DNA copy into human genome, establishes latency

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9
Q

HIV-1

A

Wide spread form, more common

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10
Q

HIV-2

A

Form found in West Africa
less easily transmitted, and has a slower progression
resistant to NNRTI antiretrovirals

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11
Q

How did we get AIDs originally?

A

Zoonotic: Primates: Simian Immunodeficiency Virus

entered into human population in Africa at least 3 times

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12
Q

How long has AIDs been around

A

Found in human sera as early as the 1950s in retrospective studies

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13
Q

Which cells does HIV-1 infect?

A

Infection of cells with CD4 and chemokine co-receptor molecule displayed:
Th, Monocytes, Macrophages

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14
Q

Cytopathic effects of HIV

A
Th cell loss 
immunosuppression
mechanism is uncertain:
1. Direct virus killing
2. Apoptosis of immune cells
Formation of "swarms"
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15
Q

Why do you have to use combination therapy for HIV treatment?

A

Mutates rapidly, prevents swift virus inhibition of antivirals
monitor viral load frequently to ensure virus hasn’t mutated

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16
Q

Labs of primary infection:

A

High CD4 count
High HIV RNA copies
Viremia

17
Q

Labs of clinical latency:

A

CD4 count declines over time
Viremia sharply declines to 0
HIV RNA copies drop and then level off (don’t get to 0)

18
Q

Labs of reactivation: constitutional symptoms

A

Lower CD4+ (~300)

Rising HIV RNA and viremia

19
Q

Labs of reactivation: opportunistic diseases and/or death

A

Few/No CD4+

Very high HIV RNA and viremia

20
Q

Detection of HIV

A

HIV antibody: 2 steps

  1. EIA screen
  2. Confirm (+) results with Western blot
21
Q

Direct tests of HIV detect

A

presence of virus RNA or protein antigens
Nucleic acid test
PCR: antigen p24, RNA genome

22
Q

How is donated blood screened for HIV?

A

Nucleic acid test, as to avoid antibody response lag

23
Q

Rapid HIV tests

A

OraQuick Rapid HIV-1/2 Antibody test
takes 20 minutes
identify infected and prevent transmission (doesn’t account for antibody lag though)

24
Q

Classes of antiretroviral agents

A
***use in combination***//***not curative***
Reverse transcriptase inhibitors:
1. Nucleoside analogs
2. Non-nucleoside inhibitors
Protease inhibitors
-stop maturation of viral assembly
Fusion-penetration inhibitors
25
Q

Viral load tests reveal

A

amount of HIV in blood as copies per milliliter
limit: minimum 50 copies/ml to be detected
run frequently during early treatment, during effective treatment viral counts are low
watch trends

26
Q

HIV-associated neurocognitive disorder

A

idk neuro symptoms, brain fog, impacts cognitive function

might not be able to comply with complex drug regimen

27
Q

who ain’t contagious?

A

viral suppression state

U=U

28
Q

PrEP

A

pre-exposure prophylaxis for healthy individuals at high risk

29
Q

What’s gonna mess up this HIV situation

A

Opioid epidemic: neeeedles