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HIV Flashcards

1
Q

What is HIV?

A

Retrovirus
HIV-2 originated in West African Sootey mangabey
Less virulent
HIV-1 originated in Central/West African chimpanzees: HIV1 group M responsible for global pandemic

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2
Q

What is the target site for HIV?

A

CD4+ receptors

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3
Q

What cells are CD4+ receptors found on?

A

T helper lymphocytes
Dendritic cells
Macrophages
Microglial cells

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4
Q

What do CD4+Th lymphocytes do?

A 
Essential for induction of adaptive immune response 
Recognition of MHC2 APC
Activation of B cells
Activation of cytotoxic CD8+ T cells
CK release
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5
Q

What effect does HIV infection have on immune response?

A

Sequestration of cells in lymphoid tissues
-Reduced circulating CD4+ cells
Reduced proliferation of CD4+ cells
Reduction CD8+ (cytotoxic) T cell activation
-Dysregulated expression of cytokines
-Increasing susceptibility to viral infections (including HIV)
Reduction in antibody class switching
-Reduced affinity of antibodies produced
Chronic Immune Activation (microbial translocation)

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6
Q

What does HIV increase susceptibility to?

A

Viral infections
Fungal infections
Mycobacterial infections
Infection-induced cancers

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7
Q

At what CD4+Th count is there a risk of opportunistic infection?

A

<200cells/mm3

Normal is 500-1600

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8
Q

Describe HIV viral replication

A

Rapid in very early and very late infection

New generation every 6-12hours

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9
Q

How does HIV spread in the body?

A

Infection of mucosal CD4 cell (Langerhans/dendritic)
Transport to RLNs
Infection established within 3 days of entry
Dissemination of virus

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10
Q

When is the usual onset of HIV?

A

2-4wks after infection

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11
Q

What are the common symptoms of primary HIV infection?

A 
Fever
Rash (maculopapular)
Myalgia
Pharyngitis
Headache/aseptic meningitis
Up to 80% present with symptoms
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12
Q

What happens during the asymptomatic HIV infection?

A

Ongoing replication
Ongoing CD4 count depletion
Ongoing immune activation
Risk of onward transmission if remains undiagnosed

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13
Q

What is an opportunistic infection?

A

An infection caused by a pathogen that does not normally produce disease in a healthy individual. It uses the “opportunity” afforded by a weakened immune system to cause disease

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14
Q

What organism causes pneumocystis pneumonia?

A

Pneumocystis jiroveci

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15
Q

What are the symptoms and signs of pneumocystis pneumonia?

A

Insidious onset
SOB
Dry Cough
Exercise desaturation

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16
Q

How is pneumocystis pneumonia diagnosed?

A

CXR: May be normal, interstitial infiltrates, reticulonodular markings
BAL and immunofluorescence +- PCR

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17
Q

What is the treatment and prophylaxis for pneumocystis pneumonia?

A

Rx- High dose co-trimoxazole (+- steroid)

Proph: Low dose co-trimoxazole

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18
Q

What tuberculosis infections/conditions are more common in HIV+ than HIV- individuals?

A 
Symptomatic primary infection
Reactivation of latent TB
Lymphadenopathies
Miliary TB
Extrapulmonary TB
Multi-drug resistant TB
Immune reconstitution syndrome
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19
Q

What organism causes cerebral toxoplasmosis?

A

Toxoplasma gondii

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20
Q

What happens in cerebral toxoplasmosis?

A

Reactivation of latent infection

Multiple cerebral abscess (chorioretinitis)

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21
Q

What are the symptoms/signs in cerebral toxoplasmosis?

A 
Headache
Fever
Focal neurology
Seizures
Reduced consciousness
Raised intracranial pressure
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22
Q

What does CMV cause?

A

Retinitis, colitis, oesophagitis

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23
Q

How does CMV present?

A 
Reduced visual acuity
Floaters
Abdo pain
Diarrhoea
PR bleeding
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24
Q

What skin infections can be due to HIV?

A

Herpes Zoster: Multidermatomal, Recurrent
Herpes Simplex: Extensive, Hypertrophic, Aciclovir resistant
Human papilloma virus: Extensive, Recalcitrant, Dysplastic
Penicilliosis
Histoplasmosis

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25
Q

What causes HIV-associated neurocognitive impairment?

A

HIV-1

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26
Q

How does HIV-associated neurocognitive impairment present?

A

Reduced STM

+- motor dysfunction

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27
Q

What causes progressive multifocal leukoencephalopathy?

A

JC virus

Reactivation of latent infection

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28
Q

How does progressive multifocal leukoencephalopathy present?

A

Rapidly progressing
Focal neurology
Confusion
Personality change

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29
Q

What are some other neurological presentations of HIV?

A 
Distal sensory polyneuropathy
Mononeuritis multiplex
Vacuolar myelopathy
Aseptic meningitis
Guillan-Barre syndrome
Viral meningitis (CMV, HSV)
Cryptococcal meningitis
Neurosyphilis
30
Q

What causes HIV-associated wasting aka Slim’s Disease?

A

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

31
Q

What causes Kaposi’s sarcoma?

A

Human herpes virus 8 (HHV8)

32
Q

What is the basic pathology of Kaposi’s sarcoma?

A

Vascular tumour

33
Q

How does Kaposi’s sarcoma present?

A

Cutaneous
Mucosal
Visceral- pulmonary, GI

34
Q

What is the treatment for Kaposi’s sarcoma?

A

HAART
Local therapies
Systemic chemotherapy

35
Q

What causes Non-Hodgkins lymphoma?

A

EBV (Burkitt’s lymphoma, primary CNS lymphoma)

36
Q

How does Non-Hodgkins lymphoma present?

A 
More advanced
B symptoms
Bone marrow involvement
Extranodal disease
Increased CNS involvement
37
Q

What should be offered to all with complicated HPV disease?

A

HIV testing

38
Q

How can cervical cancer present?

A

Recalcitrant warts

High grade CIN, VIN, AIN, PIN

39
Q

What are the clinical features of non-OI symptomatic HIV?

A 
Mucosal candidiasis
Seborrhoeic dermatitis
Diarrhoea
Fatigue
Worsening psoriasis
Lymphadenopathy
Parotitis
Epidemiologically linked conditions: STIs, Hepatitis B, Hepatitis C
40
Q

What are some haematologic manifestations of HIV?

A

Anaemia

Thrombocytopenia

41
Q

What are the modes of transmission of HIV?

A

Sexual
Parenteral
Mother to Child

42
Q

What factors increase transmission risk of HIV in sex?

A

Anoreceptive sex
Trauma
Genital ulceration
Concurrent STI

43
Q

How does parenteral transmission of HIV occur?

A

Injection drug use (sharing ‘works’)
Infected blood products
Iatrogenic

44
Q

How does MTCT of HIV occur?

A

In utero/trans-placental
Delivery
Breast-feeding

45
Q

What is the sex ratio of HIV?

A

2.1:1 M:F

46
Q

What risk group has the highest proportion of HIV in the UK?

A

MSM

47
Q

What services include an opt-out HIV test?

A 
TOP services
GUM
Drug dependency services
Antenatal services
Assisted conception services
48
Q

What high risk groups should regular HIV screening be carried out on?

A 
MSM
Female partners of bisexual men
IVDU
Partners of people living with HIV
Adults, children, sexual partners, and people with history of iatrogenic exposure from/in an endemic area
49
Q

What are the high prevalence areas of HIV?

A

Sub-Saharan Africa
Caribbean
Thailand

50
Q

When HIV falls within the DDx what should be performed regardless of risk factors?

A

HIV test

Risk assessment not necessary

51
Q

What is important when taking an HIV test of an incapacitated person?

A

Only test if in patients best interest
Consent from relative not required
If safe, wait until patient regains capacity
Obtain support from HIV team if required

52
Q

Which markers of HIV are used by labs to detect infection?

A 
RNA (viral genome)
Envelope proteins (gp120)
Capsule protein (p24)
53
Q

What do 3rd generation HIV tests detect?

A

HIV 1+2 antibody
IgM
IgG

54
Q

What is the window period of 3rd generation HIV tests?

A

Avg. 20-25 days

55
Q

What do 4th generation HIV tests detect?

A

Combined antibody and antigen (p24)

56
Q

What is the window period of 4th generation HIV tests?

A

14-28 days

57
Q

What is the recent infection testing algorithm?

A

Can be used to identify if an infection occurred within the preceding 4-6months

58
Q

How does RITA work?

A

Measure different types of antibodies or strength of antibody binding- HIV1, subtype B

59
Q

What are the targets for anti-retroviral drugs?

A 
Reverse transcriptase
Integrase
Protease
Entry: fusion, CCR5 receptor
Maturation
60
Q

What was shown to have in vitro activity against HIV?

A

Nucleotide analogues reverse transcriptase inhibitors (NRTI) e.g. zidovudine

61
Q

What is highly active anti-retroviral therapy (HAART)?

A

A combination of three drugs from at least 2 drug classes to which the virus is susceptible

62
Q

What is most important in preventing drug resistance in HIV?

A

Adherence

63
Q

What are the S/Es of HAART?

A

GI S/Es (protease inhibitors), transaminitis, fulminant hep (nevirapine, most others)
Skin: rash, HS, SJS (abacavir, nevirapine)
CNS: mood, psychosis (efavirenz)
Renal: proximal renal tubulopathies (tenofovir, atazanavir)
Bone: osteomalacia (tenofovir)
CVS: increased MI risk (abacavir, lopinavir, maraviroc)
Haematology: anaemia (zidovudine)

64
Q

What enzymes do protease inhibitors interact with?

A

Liver enzyme inhibitors

65
Q

What enzymes do NNRTIs interact act with?

A

Liver enzyme inducers

66
Q

Describe partner notification and disclosure in HIV

A

Voluntary process- may takes weeks, months, years

Duty of care to a known third party

67
Q

How can you prevent onward HIV sexual transmission?

A 
Condom use
HIV treatment
STI screening and treatment
Sero-adaptive sexual behaviours 
Disclosure 
Post-exposure prophylaxis
Pre-exposure prophylaxis
68
Q

What are conception options for an HIV+ male, HIV- female?

A

Timed unprotected sex with HAART

Treatment as Prevention

69
Q

What are conception options for an HIV+ female, HIV-male?

A

? Self-insemination
Timed unprotected sex with HAART
Treatment as Prevention

70
Q

How can you prevent mother to child transmission?

A 
HAART during pregnancy
Vaginal delivery if undetected viral load
Caesarean section if detected viral load
4/52 PEP for neonate
Exclusive formula feeding

Reproduction (40 decks)

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