hiv Flashcards

1
Q

What is HIV?

A

Human immunodeficiency virus
Mutates readily- as reverse transcriptase doesn’t proof read

AIDS- acquired immunodeficiency syndrome

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2
Q

How is HIV transmitted?

A

Sexual contact
Blood-blood contact
Infected blood products
In utero
Breast milk

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3
Q

What are the types of HIV?

A

HIV 1- more common (3 main subtypes- M, N, O)
HIV 2- less easily transmitted/pathogenic (stays confined to West Africa)

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4
Q

What is the structure of HIV?

A

Envelope glycoproteins
Lipids from host cell
Nuclear capsid containing single stranded RNA
Reverse transcriptase
Protease

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5
Q

How does HIV infect?

A

1. gp120 binds to CD4 positive cells and CCR5/CXCR4 which triggers internalisation of virus into cell

2. RNA is reverse transcribed into DNA which is incorporated into genome

3. Protective environment and new copies of virus (budding to infect other cells)

Pts w CCR5 mutations are resistant to HIV

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6
Q

How does the virus vary during infection?

A

EARLY
-targets CCD5
-macrophage tropic, low cytopathic, more transmissible

LATE
-targets CXCR4
-T-cell tropic, high cytopathic, less transmissible

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7
Q

What are some oral manifestations of HIV?

A

Thrush
Erythematous candidosis
Gingival erythema
Hairy oral leukoplakia*

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8
Q

What are drug targets?

A

1. Fusion inhibitors
2. NRTIs (nucleotide reverse transcriptase inhibitor- chain terminator)
3. NNRTIs
4. Integrase inhibitors
5. Protease inhibitors
6. CCR5 entry inhibitors

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9
Q

What is the treatment for HIV?

A

HAART
Highly active antiretroviral therapy

First line-
2 NRTIs eg. Zidovudine and lamivudine
+ 1 NNRTI/PI/II eg. Nevirapine

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10
Q

What are side effects to HIV drugs?

A

Headaches
Nausea
Anaemia
Neutropenia
Lactic acidosis
Lipoatrophy
Peripheral neuropathy
Rashes
Stevens Johnson syndrome
Teratogenecity
Lipodystrophy

RESISTANCE

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11
Q

How should you manage a HIV pt?

A

Normal infectious control

If at risk- Occu health for prophylactic HAART and HIV testing

If needle stick- PEP administration ASAP and continual HIV testing

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12
Q

How is HIV tested?

A

ELISA
detects antibodies
6–12 weeks after infection so 3 months most reliable
Babies may have false +ve due to cross placental antibodies so PCR

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13
Q

Why is diagnosis important?

A

15% undiagnosed

If diagnosed late
-more likely to die
-transmission to others

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14
Q

What are indicator illnesses for HIV?

A

Kaposis sarcoma
Severe/recalcitrant seborrhoeic dermatitis
Multidermatomal/recurrent herpes zoster
Oral candidiasis
Oral hairy leukoplakia
Head and neck cancer
Hodgkin’s lymphoma
Castlemans disease
Lymphadenopathy (unknown cause)
Chronic parotitis
Lymphoepithelial parotid cysts

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15
Q

Why is oral candidiasis an indicator illness?

A

Unusual in healthy people
But VERY prevalent in HIV

Risk factors- antibiotics/immunocompromisation

ADVANCED INDICATOR

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16
Q

Why is shingles an indicator illness?

A

Reactivation of varicella zoster virus
Dermatomal distribution
Painful blistering rash, malaise

Risk factors- age, immunocompromisation

17
Q

How do we test for HIV?

A

Verbal consent
Send clotted blood to lab
4th generation test (antibody/antigen, window period 1 month, costs <£5)
Confirmatory test 99.9% accurate

18
Q

What do you do if the pt is HIV +ve?

A

Call specialist for advice

Result
-YOU give the result
-face to face
-confidential environment

Contact tracing is done by specialist service

19
Q

What are other ways to test?

A

Point of care test
HIV RNA PCR

20
Q

What does Kaposis sarcoma look like?

A

Red-brown-purple lesion
Can be multiple
Can be in mouth
HHV8
Spindle cells on biopsy
Needs referral to oncology

ADVANCED INDICATOR

21
Q

What is hairy oral leukoplakia?

A

EBV
White patches can’t be scraped off
On tongue

ADVANCED INDICATOR

22
Q

Is herpes simplex virus an indicator illness?

A

In hiv
-more severe
-more frequent
-outbreaks last longer
-may also have genital herpes

ADVANCED INDICATOR

23
Q

How is HIV managed?

A

HAART
Highly active antiretroviral therapy
3+ drugs
Act on different points of HIV replication cycle

24
Q

How does HAART work?

A

Within CD4 cell
Drug blocks receptor to prevent virus binding (fusion/entry inhibitor)
Prevent transcription of viral RNA into viral DNA (NRTI)
Prevents viral DNA to be integrated into host DNA (Integrase inhibitor)
Repackaging of new virus is prevented (protease inhibitor)

25
Q

Why is HIV resistant to drugs?

A

50% mutation every time virus replicates
1-5 billion mutations/day

26
Q

Why are therapeutic drug levels important?

A

1. Non adherence- missing 1 or 2 doses can cause resistance
2. Drug-drug interaction- sub therapeutic levels