HIV Flashcards

1
Q

Where is HIV most prevalent

A

Sub Saharan Africa

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2
Q

How does PCP present?

A

Pneumocystis pneumonia - often associated with hiv - reasonably unwell for sometime - then suddenly well

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3
Q

What type of infections are lies to be seen late on in someone who is immunosupressed

A

Fungal eg yeast mould

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4
Q

What is teh likely outcome of HIV

A

Death is probably if diagnoses lat/untreated

In ppl diagnosed early - can live a normal life with period of chronic infection

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5
Q

Which group is HIV most oprevelant

A
Men who have sex with men
• 101,000 total – Men 69%,  Women 31%
• UK – 1.1/1,000 
• Leicester – 3.8/1,000 
• MSM – 46% (58/1000) 
• Heterosexuals
– 54%
– Overall UK rate: 1/1000
– >1/2 are black African
HIV acquisition by risk group (2014)
• Men:  22/1000 • Women:  42/1000
• People who inject drugs (PWID) – 3.8/1000
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6
Q

Describe viral structure

A
1) Genome - RNA or DNA
• Single-stranded (ss)
• Double-stranded (ds) 
2) Capsid – protein shell, protects the
genome 
• Helical (rod-shaped or coiled) 
• Icosahedral (spherical or symmetric)
3) Lipid envelope – present or absent
• Derived from host cell membranes
• Contains virus-specific proteins (antigens) 
4) Replication strategy
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7
Q

What are the properties of HIV?

A
• Human Immunodeficiency Virus – discovered in 1984
• Retrovirus (“backwards”) 
– ssRNA -> DNA -> ssRNA
• Infects cells with CD4
surface receptor
– T-helper lymphocytes (predominant) – (Monocytes / macrophages)
• HIV replicates inside cells
Destroys the cell 
Causes inflammation 
Spreads to / infects more cells
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8
Q

Describe HIV reproduction

A

1) free virus
2) binding and fusion - virus binds to a CD4 molecule and one of 2 coreceptos (CCR5 or CXCR4) receptor molecules are common on cell surface. Virus then fuses with cell
3) infection - virus penetrates cell. Contents emptied into cell
4) reverse transcription - single strands of viral RNA are converted into dsDNA by the reverse transcriptase enzyme
5) Integration - Viral DNA is combines with the cells own DNA by the integrate enzyme
6) Transcription - when the DNA in infected cll divides, the viral dna is read and long protein chains are made
7) Assembly - sets of viral proteins chains come together
8) Budding - immature virus pushes out o the cell, taking come cell membranes with it
9) immature virus breaks fre of the infected cell
10) maturation - protein chains in the new viral particle are cut bu the protease enzyme into individual roteins that combine to make a working virus

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9
Q

How is HIV transmitted

A

Contact of infected bodily
fluids with mucosal tissue / blood / broken skin
Sexual contact, transfusion, contaminated needles, peripheral transmission (transplacental, delivery through an infected birth canal, breast milk)
*Medical procedures
• Blood/blood-products, skin grafts,
organ donation

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10
Q

Describe thr progression of the viral load and CD4 count

A

Primary infecton/seroconversion - viral load high, CD4 count starts to recover - May have symptoms but they settle down, antibodies produced and viral load decreases a lot but infection not cleared from blood

Latent infection - viral gradually increase, cd4 slowly go down

Symptomatic infection - C44 count decreasing, viral load high

Sever infection/AIDS - Viral load high,cd4 very low, risk of PCP, fungal, viral infections

See slide

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11
Q

What does HIv have similar presentation to

A

Glandular fever - HIV in early stages may not be identified

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12
Q

What actors affect HIV transmission

A

• Type of exposure
– type of sexual act
– transfusion vs needlestick (healthcare worker accidentally pricks with infected needle) vs mucous membrane
• Viral level (viral load) in blood
– Transmission unlikely if undetectable VL
• Condom use
• Breaks in skin or mucosa
– other STI (Inflammation of genital tract)
– sexual assault

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13
Q

How can HIv be lived with

A
• Life expectancy and quality of life now excellent 
• General pop: 80yrs (approx) 
• HIV +ve: 78yrs
– Early detection / good CD4 
– Treatment 
– Adherence- take treatment (ppl might struggle with dealing with diagnosis or stigma
– Healthy living
• Smoking, alcohol, metabolic problems
• Late detection = worse prognosis
(x10   Increase risk death in 1st year)
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14
Q

What are diagnostic tests for HIV

A
• Blood tests - Serology
– HIV antigen (Ag) – viral protein
– HIV antibody (Ab) – immunoglobulin;
immune response to antigen 
– Current test: detects both Ag and Ab 
– +ve in 4 weeks 
– Result on same day 
– May get false negative result
• Blood tests 
– PCR:
– Polymerase chain reaction
– Detects HIV nucleic acid
– Highly sensitive
– Detects very early infection (few days)
– Expensive; results slow (up to 1 week)
– Not used for initial HIV testing
– Used for follow-up / treatment response
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15
Q

What are other “rapid” diagnostic tests for HIV

A
• “Rapid” tests – low cost, <1hr
– Usually detect HIV antibody 
– Blood test (finger-prick) 
– Oral (saliva) 
– In-Home tests 
– Postal testing

• If negative – accurate
• May get false positive result
– Need to confirm with serology

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16
Q

Who should be tested

A

When not sure whatsgoing on
• Everyone! (If rate >2/1000 in population)
• Resp: bacterial pneumonia / TB
• Neuro: meningitis/dementia
• Derm: Severe psoriasis 0 recurrent multi-dermal shingles
• Gastro: Chronic diarrhoea/weight loss ?cause
• Haem: any unexplained blood abnormality
• Onc: lymphoma, anal cancer
• Gynae: Cervical intrapithelial neoplasia (CIN)
• Any STI/ Hep B/ HepC

17
Q

What strategies would you use to treat and reduce the prevalence of HIV>?

A

Anti-retroviral drugs

18
Q

What are the aims of HIV treatment

A
  • Undetectable HIV viral load
  • Reconstitute CD4 count /immune system - takes years to restore cd4 cells if low
  • Reduce general inflammation
  • Reduce risk of transmission
  • Good quality of life
  • Normalise lifespan
19
Q

When should you start treatment?

A

CD4<350
Primary HIV infection
Any AIDS-defining illness

  • other blood borne infection
  • cancer/lymphoma
  • recent transmission to others
  • patient choice

Now treat everyone asa regardless of cd4

20
Q

What ARV drugs ae given

A

Nucleoside reverse transcriptase inhibitor + Non-NRTI OR Protease inhibitor + Integrase inhibitor

21
Q

Why 3 drugs?

A
  • Millions of rounds of viral replication each day
  • Virus mutuates (changes/adapts) every 2- 3 rounds
  • Resistance to drugs develops in days
  • 1 drug – resistance develops quickly
  • 3 drugs – harder to develop resistance
  • Patient must keep taking drugs
22
Q

What strategies would you use to treat and reduce the prevalencee of HIV/

A
  • Increase condom usage • Prevention of mother-to-child transmission
  • ARV treatment as prevention
  • Medical circumcision
  • Post-exposure prophylaxis (PEP)
  • Pre-exposure prophylaxis (PrEP)
  • Combine the above
  • ?future vaccine
23
Q

What ethical dilemmas need to be considered in HIV?

A
• Psychological impact of diagnosis 
• Dealing with stigma 
• Patient confidentiality vs:
– Health of mother
– Health of unborn child
– Health of sexual contact (husband)
– Health of older child
– Risk to patients / staff at workplace