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MD1 SF3 - EXAM 2 > VIH-SIDA > Flashcards

VIH-SIDA Flashcards

1
Q

What is HIV?

A

human immunodeficiency virus —> Virus de l’immunodéficience humaine

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2
Q

What does it mean to be seropositive for HIV?

A

To be infected with HIV —> antibodies present

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3
Q

What is an opportunistic infection?

A

Infection that happens in someone who is immunocompromised… would not happen if pt wasn’t immunocompromised

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4
Q

What is AIDS?

A

Acquired immunodeficiency syndrome —> syndrome d’immunodéficience acquise

  • extreme form of HIV infection that manifests by a severe immunodeficiency —> makes pts susceptible to opportunistic infections and certain cancers
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5
Q

What does the décompte de CD4 measure?

A

Degré de dommage fait au système immunitaire par le VIH

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6
Q

What is the décompte lymphocytaire?

A

Dénombrement des différents lymphocytes dans une prise de sang… low # = sign of immunodeficiency

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7
Q

What is the charge virale?

A

number of copies of HIV in the blood per PCR

measures the potential that HIV has to destroy the immune system

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8
Q

What is génotypage?

A

Détection des mutations de résistance aux différents antirétroviraux sur les gènes du virus

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9
Q

What is reconstitution immunitaire?

A

augmentation du nombre de CD4 et CD8 et la proportion de cellules naïves suivant l’initiation du traitement antirétroviral

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10
Q

The history of VIH/SIDA: (11 dates)

A

1908 —> HIV in humans… derived from SIV in chimpanzees

1959 —> first seropositive serum in the Congo and first dead pt (UK marine)

1968 —> first dead pt in US

1981 —> CDC link between PCP/Kaposi in young gay men, initially named GRID before identifiable in other at risk groups

1982 —> renamed AIDS, discovery of transmission through blood (hemophiliacs and blood transfusions), first cases in Africa

1983 —> virus isolated from ganglia.. doctors think its the origin for AIDS (LAV: lymphadenopathy-associated virus)

1985 —> Americans discover virus HTLV-III but it was actually the same virus discovered in 1983 LAV, first dx testing and start of all blood being tested in Canada

1986 —> LAV renamed HIV

1987 —> first antiretroviral Rx commercialized (AZT)

1996 —> HAART treatment established (combination of 3 antiretroviral drugs becomes standard)

2008 —> Nobel Prize in Medicine given to Françoise Barré-Sinoussi et Luc Montagnier for discovery of HIV

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11
Q

How has HIV come to exist?

A

SIV in chimps transmitted to humans during hunting probably in the early 20th century —> transmission of SIV to HIV —> HIV then transmitted between humans

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12
Q

What has contributed to the dissemination of HIV in Africa? (4)

A
  1. injections given without sterilizing needles
  2. urbanization, development of road systems
  3. inequality between men and women
  4. sex work
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13
Q

What has contributed to the dissemination of HIV in Western countries? (4)

A
  1. change in sexual behaviour (multiple partners, no protection) in the 70s –> sexual liberation movement
  2. sexual tourism
  3. gay community
  4. use of IV drugs (the needles not the drugs)
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14
Q

What has happened to HIV in recent years?

A

Since 1998, dim. of incidence by 40%

Since 2004, dim. of deaths by 60%

Why?

  • Treatment is more accessible, change in behaviour towards at risk and seropositive individuals, access to prevention services, and education
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15
Q

What was the objective set by the UN in 2014 for 2020?

A

90-90-90

  • 90% of seropositive pts know they’re seropositive
  • 90% of patients currently being treated
  • 90% of treated pts have their disease under control

95-95-95 by 2030

Sadly this is not yet the case globally or in Canada

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16
Q

How can we attain this objective?

A

Intensify measures already put in place and take charge of poverty, lack of education, gender inequality, sexual violence

17
Q

Epidemiology in Canada:

A
18
Q

How is HIV transmitted?

A

Sexually:

  • Anal sex is the highest risk: higher vascularization and lymphatic cells in anal mucosa and its more fragile
  • Heterosexual insertive sex is the least at risk

Use of IV drugs

Vertical transmission: mom —> child

Transmitted through blood and its byproducts

19
Q

What are the two steps for HIV screening?

A
  1. détection d’anticorps (ELISA): simple, fast, sensible, accurate, cheap
    • We now use 4th generation tests that detect antibodies and Ag p24 (acute infection marker —> detectable in first weeks of infection)
  2. detection of proteins (Western blot):
    • Test de confirmation
    • Very complex
    • Requires the LSPQ
20
Q

What is the pathogenesis of HIV?

A

It is a retrovirus

  • Single strand RNA virus
  • Tropisme pour cellules sanguines
  • Transcription en ADN par transcriptase inverse
  • Intégration par l’intégrase dans le génome de la hôte
  • Long period between infection and clinical manifestations
  • Associated with an acquired immunodeficiency
21
Q

What is the primo-infection?

A

Acquisition and dissemination

Virus is quite homogeneous

Tropism for peripheral mononucleated cells

Haute virémie

CD4s lower transitionally

1-6 weeks after initial infection

Sx similar to viral infection in 90% of pts: fever, rash, headaches, pharyngitis, myalgia, generalised adénopathies —> 1-3 weeks

The more severe the symptoms, the less favourable the progression is

Ag p24 is detectable

22
Q

What is latency phase 1?

A

CD4 > 500 cells/cubic mm

Equilibrium between the virus and immune system

Not much virus found in peripheral mononucleated cells

Have attained the “set point”

Charge virale baisse et se maintient quelques années

BUT activité intense dans les centres germinatifs des ganglions —> production de bcp de virus et anticorps (> billion a day)

23
Q

What is latency phase 2?

A

CD4 between 200 and 500 cells/cubic mm

Ganglia start to deteriorate

Dim. de capacité des centres germinatifs à contrôler le virus

Aug. de la quantité de virus dans les ganglions et cellules mononuclées

AUGMENTATION DE LA VIRÉMIE

24
Q

Clinical aspects of latency phase:

A

Pts usually asymptomatic or general sx (fatigue, fever, night sweats, generalized adenopathies)

Immune system starts to show its weaknesses: candidose orale, leucoplasie chevelue de langue, zona, herpès, autres infections non opportunistes sont plus fréquents (ex: pneumonie)

Usually around 8-10 years

Pts become a “transmission reservoir”

The risk of developing AIDS without treatment increases by 4-10% per year gone untreated

25
Q

What is AIDS?

A

CD4 < 200 cells/cubic mm

Dissolution des centres germanatifs

Uncontrollable multiplication of the virus

Virémie très élevée et virus est très hétérogène

26
Q

Clinical manifestations of AIDS:

A

Same manifestations as latency phase plus:

  • réactivations d’infections latentes (CMV, toxoplasmosis, tb)
  • opportunistic infections (ex: Pneumonie à Pneumocystis jirovecii)
  • certain forms of cancer more likely to develop (ex: Kaposi sarcoma)
27
Q

What are the goals of treatment of HIV and AIDS?

A

Améliorer l’état clinique

Dim. mortalité et increase life expectancy

Améliorer qualité de vie

Rendre charge virale indétectable —> dim. transmission

Augmenter CD4/reconstitution du système immunitaire

28
Q

What are the 4 principal classes of antiretroviral medications?

A
  1. INTIs —> inhibiteurs nucléosidiques de la transcriptase inverse
  2. INNTIs —> inhibiteurs non nucléosidiques de la transcriptase inverse
  3. IIs —> inhibiteurs de l’intégrase
  4. IPs —> inhibiteurs de la protéase

Not really used (inhibiteurs de l’entrée) —> inhibiteur de fusion, antagonistes du CCR5

29
Q

In 2021, how is HIV treated?

A

Treat early to preserve reservoirs… tx is offered to all pts, independent of stage of illness

Tx also dim. chronic inflammation associated with premature ageing and CV disease

Sticking with treatment is extremely important

Treating using a tritherapy method (HAART)

30
Q

What is tritherapy?

A

2 antiretrovirals from the same class (INTIs) combined with an antiretroviral from another class (IP or INNTI)

Virus genotype guides tx decisions

3 Rx must be started at the same time to prevent resistance from developing

31
Q

How is HIV prevented?

A

Avoid at risk contact (blood/unprotected sex)

Avoid contact between muqueuses/open wounds and blood, vaginal secretions, and sperm/semen

32
Q

When is transmission of HIV basically non-existent?

A

Indetectable for > 6 mths when tested > 1 time = intransmissible

If pt sticks with the treatment plan and their viral load is undetectable more than once and they have no genital lesions/STIs —> they can have unprotected sex within a monogamous couple

33
Q

What is PrEP?

A

Pre-exposure prophylaxis

Used in high risk pts HARSAs, drug users, sex workers

  • Take 2 antiretroviral drugs once daily continuously (pt without HIV)
  • Important reduction in transmission but condom should still be used

Mothers are treated when pregnant/breastfeeding to reduce chances of vertical transmission to newborn (breastfeeding is usually recommended against)

34
Q

What is prophylaxie post-exposition?

A

Given to pts after possible exposition to HIV/AIDS

Combination of 3 antiretroviral Rx to diminish risk of acquiring HIV (earlier is better… should be in first hours after exposure)

35
Q

What are some future challenges?

A

Prevent transmission —> dim. new infections

Increase treatment in Canada and globally

Treat ageing population with HIV

Control resistance to Rx

Stop stigmatization against and work towards better education

MD1 SF3 - EXAM 2 (12 decks)

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