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Reproduction/Sexual Health > HIV > Flashcards

HIV Flashcards

1
Q

Types of HIV

A

HIV1 (M responsible for epidemic)
HIV2
Geographical variation - recombinant

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2
Q

Surface antigens and receptors that bind HIV to host cell

A

GP120 and GP41
CC45 and CD4

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3
Q

How does HIV infect and then dissemninate virus?

A

Infection of mucosal CD4+ cell (Langerhans and Dendritic cells)

Transport to regional lymph nodes and into gut lymphoid tissue

Infection established within 3 days of entry

Dissemination of virus

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4
Q

Why is neuro disease common in HIV?

A

Microglial cells have CDD4+ on surface which is target site for the virus

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5
Q

How does HIV infection affect immune response?

A

Reduced circulating CD4+ cells

Reduced proliferation of CD4+ cells

Reduction CD8+ (cytotoxic) T cell activation
- Dysregulated expression of cytokines

Reduction in antibody class switching
- Reduced affinity of antibodies produced

Chronic Immune Activation (microbial translocation)

Susceptible to: viral, fungal, parasitic, mycobacterial, infection rel cancer

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6
Q

WHich immune response do HIV+ pts retain?

A

Antibacterial response
(unless severely immunocompromised)

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7
Q

When are people at highest risk of opportunistic infections?

A

CD4+ Th cells <200 cells/mm3

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8
Q

How long do HIV+ people live without tretament?

A

Avg 9-11 years post-diagnosis

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9
Q

Most common pres of HIV

A

Onset average 2-4 weeks after infection (up to 3 months)]
Looks like non-specific viral infection

Combination of:
Fever
Rash (maculopapular)
Myalgia
Pharyngitis
Headache/aseptic meningitis

High risk of this transmission at this point

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10
Q

Features of asymptomatic HIV

A

Ongoing viral replication

Ongoing CD4 count depletion

Ongoing immune activation

Risk of onward transmission

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11
Q

Define opportunistic infection

A

infection caused by a pathogen that does not normally produce disease in a healthy individual

e.g. mycobacterium TB, CMVr, cerebral toxo, pneumocystic jiv

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12
Q

Clinical presentation of PCP

A

Symptoms:
Insidious onset
SOB
Dry cough

Signs:
exercise oxygen desaturation
might be normal chest/ diffuse crackles

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13
Q

Features of PCP on CXR

A

CXR:
May be normal
Interstitial infiltrates
Reticulonodular markings

Looks a bit like HF except HF normal size

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14
Q

Diag and management of PCP

A

Diagnosis: BAL and immunofluorescence +/- PCR

Treatment: high dose co-trimoxazole (+/- steroid)

Prophylaxis: low dose co-trimoxazole

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15
Q

WHat TB infections are HIV pts mor likely to get?

A

Reactivation of latent
Symptomatic primary infection
Drug resistance
Extra-pulmonary
etc etc

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16
Q

Clinical pres of cerebral toxo

A

CD4 threshold: <150

Reactivation of latent infection
→ multiple cerebral abscess
→ (Chorioretinitis)

Presentation:
Headache
Fever
Focal neurology
Seizures
Reduced consciousness
Raised ICP

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17
Q

Ring enhancing lesions in a pt with HIV?

A

Cerebral toxo

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18
Q

Clinical pres of CMV in HIV

A

CD4 threshold: <50

Reactivation of latent infection
→ retinitis, colitis, oesophagitis

Presentation:
Reduced visual acuity
Floaters
Abdo pain, diarrhoea, PR bleeding

Screened ophtho with CD4+ <50

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19
Q

Clinical pres of HIV assoc neurocog impairment (AIDS rel dementia)

A

CD4 threshold: ↑ incidence with ↓CD4 (incr with longer disease presence)

Presentation:
Reduced short term memory
+/- motor dysfunction
Brain atrophy on MRI

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20
Q

Clin pres of PML

A

Caused by JC virus
CD4 threshold: <100

Presentation:
Rapidly progressing
Focal neurology
Confusion
Personality/behaviour change

21
Q

3 main skin infections assoc with HIV

A

Extensive, treatment resistent, hypertrophic, dysplastic versions of each virus:

Herpes zoster
HSV
HPV (also assoc cervical cancer)

22
Q

Clinical pres of HIV wasting/Slim’s disease

A

Severe cachexia
Metabolic (chronic immune activation)
Anorexia (multifactorial)
Malabsorption/diarrhoea
Hypogonadism

23
Q

Clinical pres of Kaposi’s sarcoma

A

Caused by HSV
Pathology: vascular tumour in viscera/skin

CD4 threshold: Any. ↑ incidence with ↑ immunosuppression

Presentation:
Cutaneous
Mucosal
Visceral – pulmonary, GI

24
Q

Management of Kaposi’s

A

Anti-retrovirals
Local therapies
Systemic chemotherapy if visceral

25
Q

Clinical pres of non-Hodgkins in HIV

A

CD4 threshold: ↑ incidence with ↑ immunosuppression

Presentation:
More advanced B symptoms
Bone marrow involvement
Extranodal disease
↑ CNS involvement

26
Q

Non-AIDS symptoms of HIV

A

Mucosal candidiasis
Seborrhoeic dermatitis
Diarrhoea
Fatigue
Worsening psoriasis (CD8 rel)
Improvement of RA (CD4 rel)
Lymphadenopathy
Parotitis
Epidemiologically linked conditions (STIs and heps)
Also neuro manifesttations e.g. polyneuropathy

27
Q

Haem manifestations in HIV

A

Leuko/lymphopenias (due to ↓ CD4)
Thrombocytopenia (HIV infects megakaryocytes)

28
Q

Factors incr transmission risk in sex

A

Anoreceptive sex
Trauma
Genital ulceration
Concurrent STI e.g. rectal chlamydia

29
Q

Types of parenteral transmission

A

Injection drug use (not v common anymore)
Infected blood products
Iatrogenic

30
Q

Features of vertical MtC transmission

A

May be:
In utero/trans-placental
Delivery
Breast-feeding

If no management:
1 in 4 babies infected
more likely if mother seroconverts while pregnant

31
Q

Who should be tested for HIV?

A

Universal testing in high prevalence areas

Opt-out testing in certain clinical settings

Screening of high risk groups

Testing in the presence of “clinical indicators”

32
Q

Where is HIV testing opt out?

A

TOP
Sexual health
Addiction/subs misuse
Antenatal
Assisted conception

33
Q

High risk groups in HIV

A

MSM
Female partners of MSM
People from endemic areas >1%
Incarcerated people
Trans women
PWID
Partners of HIV+

34
Q

Which markers are tested in HIV?

A

Viral RNA (pcr is expensive)
p24 (comes positive after RNA)
Antibody (only pos after 3 months/seroconversion)

35
Q

When are most HIV cases tested best?

A

4th generation Ab/Ag laboratory test 99% sensitive at 45 days

36
Q

What is a rapid HIV test?

A

Fingerprick blood specimen or saliva

Results within 20-30 minutes

3rd generation (Ab only) or 4th generation (Ab/Ag)

37
Q

When do you treat HIV+ people?

A

Immediately
Don’t wait for low CD4

38
Q

Define HAART

A

a combination of 3 drugs from at least 2 drug classes to which the virus is susceptible

test for resistnace initially

function
Reduce viral load to undetectable levels
Restore immunocompetence
Reduce morbidity and mortality
Prevets onward transmission

39
Q

Rifampicin in HIV?

A

NO

40
Q

What’s the main solution to ARV resistance?

A

ARV adherence

41
Q

Prognosis of HIV

A

Young people started on HAART with CD4 >500 may have a longer life expectancy than HIV negative counterparts

Though if poorly managed people have fewer good health years

42
Q

DD interactions of HIV drugs

A

Protease inhibitors are generally potent liver enzyme inhibitors
Some drugs require pharmacological boosting (with potent liver enzyme inhibitors)
NNRTIs are generally potent liver enzyme inducers

Some ARVs are victim to DDIs

43
Q

When is someone HIV+ unable to transmit the virus?

A

CD4+ under 200 (lab says 30)

44
Q

How do people tend to take PrEP?

A

Usually everyday
If sex event e.g. use in lead up and afterwards

45
Q

Features of PEP

A

Within 72h of sexual/occ exposure
Combination ART taken for 4 weeks
Unlicensed

46
Q

Prevention of vertical transmission

A

HAART during pregnancy
Vaginal delivery if undetected viral load
Caesarean section if detected viral load
2-4/52 PEP for neonate
Exclusive formula feeding though there are some mothers breastfeeding in Tayside under caution

47
Q

What is the risk of MTCT/vertical transmission?

A

<1% risk of MTCT in UK/Ireland
<0.1% risk of MTCT if VL undetected at delivery

48
Q
A

Reproduction/Sexual Health (9 decks)

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