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Repro and Sexual Health > HIV: Pathophysiology and Presentation > Flashcards

HIV: Pathophysiology and Presentation Flashcards

1
Q

what type of virus is HIV?

A

retrovirus

- when it makes DNA it uses reverse transcriptase (instead of transcriptase)

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2
Q

2 types of HIV?

A

HIV-1 = from central/west afrivan chimps, transferred to humans and main cause of infection and global pandemic in 80s

HIV-2 = from west african sootey mangabey, not as significant

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3
Q

main target of HIV?

A

CD4+ receptors

- glycoprotein found on surface of T helper cells (CD4 cells), dendritic cells, macrophages and microglial cells

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4
Q

what do CD4 T helper cells do?

A

essential for induction of adaptive immune response

  • recognition of MHC2 antigen-presenting cell
  • activation of B cells
  • activation of cytotoxic T-cells (CD8)
  • cytokine release
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5
Q

how does HIV affect immune response?

A

sequestration of cells in lymphoid tissues
- reduced CD4 cells
reduced proliferation of CD4 cells
reduction of 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

effect of reduced immune response?

A

susceptibility to viral, fungal and mycobacterial infection and infection induced cancers

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7
Q

normal and risky CD4 cell parameters?

A

normal = 500-1600 cells/mm3

risk of opportunistic infection = <200 cells/mm3

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8
Q

how fast does HIV replicate?

A

rapid replication in very early and very late infection

new generation every 6-12 hours

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9
Q

how does CD4 cell count and rate of HIV RNA copies made per hour progress?

A

CD4 count
- drops dramatically over first 6 weeks, then recovers slightly over next few weeks, then declined at a lower rate over following years (asymptomatic infection)

HIV RNA
- increases rapidly up to 6 weeks, then decreases a bit over next 3 weeks, then gradually increase over following years, increase rapidly again over final years of life

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10
Q

initial infection of HIV?

A

infection of mucosal CD4 cell (langerhans and dendritic cells)
transport to regional lymph nodes
infection established within 3 days of entry
after 3 days, virus disseminates to all tissues

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11
Q

post exposure time window where you can prevent the virus with treatment?

A

3 days

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12
Q

features of primary HIV infection?

A 
onset 2-4 weeks after infection
fever
rash (maculopapular)
myalgia
pharyngitis 
headache/aseptic meningitis 
- basically flu like illness
 very high risk of transmission at this stage
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13
Q

asymptomatic phase of HIV infection?

A

after primary infection when CD4 cell count has recovered slightly
asymptomatic but not latent
ongoing viral replication and CD4 count depletion
ongoing imune activation
risk of onward transmission if remains undiagnosed

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14
Q

what is the definition of apportunisitic infection?

A

an infection caused by a pathogen that does not normally produce disease in a health individual
infection only occurs in a weakened immune system

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15
Q

what organism causes pneumocystis pneumonia (PCP)?

A

pneumocystis jiroveci

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16
Q

CD4 threshold in PCP?

A

<200

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17
Q

symptoms of PCP?

A

insidious onset
SOB
dry cough
exercise desaturation (become tachycardic and sats plummet after 5 mins exercise)

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18
Q

CXR findings in PCP?

A

may be normal
interstitial infiltrates, reticulonodular shadowing
can resemble heart failure more than a pneumonia

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19
Q

diagnosis of PCP?

A

BAL and immunoflourescence +/- PCR

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20
Q

how is PCP managed?

A

high dose co-trimoxazole +/- steroid

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21
Q

PCP prophylaxis?

A

low dose co-trimoxazole

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22
Q

relationship between TB and HIV?

A

epidemiological synergy

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23
Q

features of TB which are more common in HIV sufferers?

A 
symptomatic primary infection
reactivation of latent TB
lymphadenopathy
miliary TB
extrapulmonary TB
multi-drug resistant TB
immune reconstitution syndrome (immune system wakes up and goes on the attack)
24
Q

what is cerebral toxoplasmosis?

A

reactivation of latent infection causing multiple cerebral abscess (chorioretinitis)

25
Q

what causes cerebral toxoplasmosis?

A

toxoplasma gondii

in people with CD4 < 150

26
Q

symptoms of cerebral toxoplasmosis?

A 
headache
fever
focal neurology
seizures
reduced consciousness
raised ICP
27
Q

what causes cytomegalovirus in HIV?

A

reactivation of latent infection in CD4<50

can be retinitis, colitis, oesophagitis

28
Q

symptoms of CMV in HIV?

A

reduced visual acuity
floaters
abdo pain
PR bleeding

29
Q

what skin infections are common in HIV?

A

herpes zoster (recurrent and multidermatomal)
herpes simplex (extensive, hypertorpic and aciclovir resistant)
HPV (extensive, recalcitrant and dysplastic)
wierd things like penicillosis and histoplasmosis

30
Q

features of HIV associated neurocognitive impairment?

A

caused by HIV1 and reduced CD4

causes reduced short term memory +/ motor dysfunction

31
Q

what is progressive multifocal leukoencephalopathy?

A

reactivation of latent JC virus (john cunningham virus)
causes rapidly progressing focal neurology and confusion and personality change (in frontal lobe involvement)
occurs when CD4 < 100

32
Q

other neurological presentations in HIV?

A 
distal sensory polyneuropathy
mononeuritis multiplex
vascular myelopathy
aseptic meningitis
GBS
viral meningitis
cryptococcal meningitis
neurosyphilis
33
Q

what causes wasting in HIV?

A

metabolic (chronic immune activation)
anorexia
malabsorption/dairrhoea (gut gets leaky)
hypogonadism

34
Q

AIDS related cancers?

A

kaposi’s sarcoma

non-hodgkins lymphoma

cervical cancer

35
Q

how is kaposi’s sarcoma managed?

A

HAART (if just cutaneous)
local therapies
systemic chemo (if visceral)

36
Q

features of kaposi’s sarcoma?

A
  • vascular tumour caused by human herpes virus

- can be cutaneous, mucosal or visceral (pulmonary, GI)

37
Q

features of non-hodgkins lymphoma?

A 
caused by EBV
usually more advanced at presentation
B symptoms
bone marrow involvement
extranodal disease
increased CNS involvement
38
Q

how is non-hidgkins lymphoma managed?

A

same as in non HIV

add HAART

39
Q

features of cervical cancer?

A

due to HPV

rapid progression to severe dysplasia and invasive disease

40
Q

non infectious features of HIV?

A 
mucosal candidiasis (thrush)
seborrhoeic dermatitis
diarrhoea
fatigue
worsening psoriasis
lymphadenopathy 
parotitis
epidemiologically linked conditions (STIs, hepatitis B/C)
41
Q

haematological manifestations of HIV?

A

caused by the HIV virus, infections, AIDs malignancies and HIV drugs and reduced CD4

cause anaemia and thrombocytopaenia (ITP)

42
Q

modes of transmission of HIV?

A 
sexual transmission (95%)
- more common transmission in anal sex, trauma, genital ulceration and concurrent STI

parenteral transmission (IV drug use, blood products, iatrogenic)

mother to child (in utero, delivery or breast feeding)

43
Q

4 senarios for HIV testing?

A

universal testing in high prevelence areas (not available in many places)
opt out testing in certian clinical settings (sexual health clinic, drug services etc)
screen high risk groups
test in presence of clinical indicators

44
Q

where is opt out HIV testing done?

A 
abortion services
GUM clinics
drug dependency services
antenatal services
assisted conception services
45
Q

high risk groups who may be screened?

A

homosexual men
female partners of bisexual men
IV drug users
people from endemic areas

46
Q

when is testing done on clinical grounds?

A

whenever HIV falls within differentials a test should be done regardless of risk factors (e.g psoriasis not getting any better with treatment)

47
Q

how is consent obtained for HIV test?

A

explain that theyre being tested for HIV and why
what the benefits of testing are
how and when they get results
reassure confidetiality

48
Q

process of taking an HIV test in a patient?

A

document consent or refusal
obtain venous sample for serology
request via ICE (accelerate is clinically indicated)
ensure pathway in place for retrieving and communicating result

49
Q

process of testing if patient is incapacitated?

A

only test if in patient’s best interest
consent from relative not needed
if its safe, wait until patient regains capacity
obtain support from HIV team if needed

50
Q

which HIV markers are used in testing?

A

viral RNA
antigen (p24)
antibody

51
Q

how does viral load, p24 and antibody change over time?

A

viral load and p24 have same pattern but viral load higher

  • rapidly increase then decrease over first 3 months
  • then very gradually decrease over following years
  • then both increase in last years of life

antibody increases very rapidly around 3 month mark, remains high for duration of disease then decreases at end of life

52
Q

describe 3rd generation HIV antibody test

A

measures HIV1 and HIV2 antibody
detects IgM and IgG
very sensitive/specific in established infection
20-25 day window period

53
Q

describe 4th generation HIV test

A

combined antibody and antigen (p24)
shortens window
variation in quoted window (14-28 days)

54
Q

significance of window period?

A

negative test during window period (e.g 4th gen test at 14 days) doesnt rule out infection but negative test at 4 weeks does rule it out

55
Q

what is POCT?

A

rapid HIV test
fingerprick blood specimen or saliva
results within 20-30 mins
3rd or 4th generation

56
Q

advantages of POCT?

A 
simple
no lab required
no venepuncture needed
no anxious wait
reduce follow up
good sensitivity
57
Q

disadvantages of POCT?

A

expensive (£10 per test)
quality control
poor positive predictive value in low prevalence settings
not suitable for high volume or early infection

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