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Repro > HIV 1 > Flashcards

HIV 1 Flashcards

1
Q

What can HIV lead and two and what are the two things that causes

A

AIDS - acquired immunodeficiency syndrome

opportunistic infections
AIDS related cancers

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2
Q

AIDS related conditions are the single highest predictor for what

A

of mortality in HIV

1/4 of deaths caused by late diagnosis - too late for effected treatment

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3
Q

when can AIDS be prevented

A

early HIV dx

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4
Q

What happens to LE of a person with HIV

is HIC preventable

A

near normal LE

yes

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5
Q

Is HIV the same as AIDs

A

No
HIV can lead to AIDS
but HIV does not equal AIDS

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6
Q

how is HIV transcribed

A

retrovirus

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7
Q

what is the difference between HIV2 and HIV 1

A

HIV 2- less virulent - less likely to get AIDS

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8
Q

what is CD4
why is it important in HIV
where is found

A

glycoprotein on the surface of cells
CD4 receptors are the target site for HIV
T helper cells (aka CD4 cells),
dendritic cells, macrophages, microglial cells

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9
Q

What do CD4 T lymphocytes do

A

essential for induction of adaptive immune response

recognise MHC2 APC
activation of B cells
activation of CD8 cells
cytokine release

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10
Q

what effect does HIV response have on immune response (5)

A

sequestration of cells in lymphoid tissue - reduce circulating CD4 cells

reduced prolif of CD$ cells

reduced CD8 cell activation - increased susceptibility of viral infections

reduction in antibody switching class

chronic immune activation - loss of lymphoid tissue in the gut - bacteria gets into blood - other systems are activated

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11
Q

what does the effect of HIV infection on the immune system lead to

A

susceptibility to viral/fungal/mycobacterial infections, infection-induced cancer

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12
Q

normal range of CD4 cells

risk of opportunistic infections

A

500-1600cells/mm3
<200cells/mm3

however 200-500 may still get opportunistic infections

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13
Q

HIV viral replication - when

new generation when

A

rapid replication in very early and late infection

new gen every 6-12 hours

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14
Q

average time to eat without treatment is what

A

9-11 years

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15
Q

process of infection from first intro to the spread

A

infection of mucosal CD4 cells (langerhans and dendritic)
transport to regional Los
infection established within 3 days of entry [can intervene with prophylaxis at this point)
replication and dissemination of virus

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16
Q

primary HIV infection
how many present with symptoms

how long after infection

symptoms

transmission risk

diagnosis rate

A

up to 80% present with symptoms

2-4 weeks after

fever, rash (maculopapular), myalgia, pharyngitis, headache/aseptic meningitis

high risk of transmission

often go undx

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17
Q

after the primary infection of HIV what stage does the infection enter

what is happening during this phase

risk of transmission

A

asymp HIV infection

ongoing viral replication, ongoing CD4 count depletion, ongoing immune activation

risk of onward transmission if remains undx

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18
Q

definiton of opportunistic infections

A

an infection caused by a pathogen that does not normally produce disease in a healthy individual - uses the opportunity of a weakened immune system to cause disease

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19
Q

pneumocystis pneumonia caused by what

CD4 count

symptoms

signs

CXR

dx

treatment

prophylaxis

A

pneumocysic jiroveci (fungal)

<200

insidious onset, SOB, dry cough

exercise desaturation - sats go down

may be normal. interstitial infiltrates, reticulonodular markings

BAL and immunflouresence +/- PCR

high dose co-trimoxazole (+/- steroid)

low dose co trimoxazole if just CD4 count low

20
Q

what is commoner in HIV + patients connected to TB

what should you be aware of in someone who has both

A 
symptomatic primary infection 
reactivation of latent TB
lymphadenopathies
military TB
extra pulmonary TB
multi drug resistant TB
immune reconstitution syndrome - immune system is activated but is very very aggressive

drug - drug interactions

21
Q 
cerebral toxoplasmosis organism 
CD4
what does HIV cause
symptoms/signs 
on MRI/XR
A

toxoplasma gondii

<150

reactivation of latent infection, multiple cerebral abscesses, choriorentitis

headache, fever, focal neurology, seizures, reduced consciousness, raised inter cranial pressure

ring enhancing lesions

22
Q 
cytomegalovirus organism 
CD4
what does HIV do and what does it lead to 
presentation 
screening
A

CMV

<50

reactivation of latent infection which can cause retinitis, colitis, oesophagitis

reduced visual acuity, floaters, abode pain, diarrhoea, PR bleeding

ophthalmic screening for all indivduals with CD <50

23
Q

HIV and skin infections

A

herpes zoster - multi dermal and recurrent

herpes simplex - extensive, hypertrophic (warty/tumour like), acyclovir resistant

HPV - extensive, recalcitrant, dysplastic

pencilliosis, histoplasmosis

24
Q

HIV assoc neurocognitive impairment organism
CD4
presentation
why?

A

HIV 1
any increased incidence with increased immunosuppression
reduced short term memory +/- motor dysfunction
CD4 present of microglial cells

25
Q

progressive multifocal leukoencephalopathy organism
what does HIV do
CD4
presentation

A

JC virus

reactivation of latent infection

<100

rapidly progressing
lesions - focal neurology
confusion
personality change

26
Q

neurological presentations with HIV

why

A 
distal sensory polyneuropathy
mononeuritis multiplex
vacuolar myelopathy
aseptic meningitis 
GBS
viral meningitis (CMV, HSV)
cryptococcal meningitis 
neurosyphilis

related to the viral replication rather than the immunosuppression

27
Q

HIV associated wasting

causes

A

slims disease

metabolic (chronic immune activation)
anorexia - multifactorial
malabsorption/diarrhoea
hypogonadism

28
Q 
AIDS released kaposi;s sarcoma 
organism 
pathology
CD4
presentation 
rx
A

human herpes virus 8
more common in MSM

vascular tumour

any increased incidence with increased immunosuppression

cutaneous, mucosal, visceral (pulmonary, GI)

HAART, local therapies, systemic chemo ofr visceral

29
Q 
non hodgkins lymphoma 
organism 
CD4
presentation
dx
rx
prognosis
A

EBV
increase incidence with increase immunosuppression

more advanced, B symptoms, bone marrow involvement, extranodal disease, increase CNS involvement

as for HIV

as for HIV add HAART

approaching HIV -

30
Q

cervical cancer organism
testing
screening

A

HPV
persistence of HPV infection

rapid progression to severe dysplasia and invasive disease

HIV testing should be offered to all complicated HPV disease

women with HIV are screened every year instead of every 3 years

31
Q

Non symptomatic HIV symptoms

A 
mucosal candidiasis 
secorrhoeic derm
diarrhoea 
fatigue
worsening psoriasis 
lymphadenopathy
parotitis
STIs, Hep B, Hep C
32
Q

haematological manifestations caused by what

CD4

(2)

A

HIV, opportunistic infections, AIDS malignancies, HIV drugs

any increased incidence with increased immunosuppression

anaemia (affect up to 90%)
thrombocytopenia (CD4 300-600)

33
Q

modes of HIV transmission sexual

what increases risk

A

94% of all infections
between 51%
man to woman 45%

anoreceptive sex
trauma
genital ulceration
concurrent STI

34
Q

tranmission parenteral

A

injection drug use
infected blood products
iatrogenic

35
Q

transmission mother to child
how

how many will become infected

mortality

risk

A

in utero/placental
delivery
breast feeding

1/4 babies at risk

1/3 HIV + babies will die before their 1st birthday if untreated

risk 1.2% but <0.1% if viral load undetectable at delivery

36
Q

epidemiology of HIV

A

MSM larges risk group
hetero men most likely to be undx and present late

HIV in people who inject drugs is uncommon

37
Q

who is tested

A

universal testing in high prevalence areas

opt out in certain clinical settings - TOP, GUM, drug dependency, antenatal, assisted conception

screening of high risk groups - MSM, female partners of bisexual men, people who inject drugs, partners of HIV+, adults from endemic areas, children from endemic areas, sexual partners form endemic areas, history of iatrogenic exposure in an endemic area
testing in the presence of clinical indicators

38
Q

endemic areas

A

sub saharan africa
thailand
carribbean

39
Q

testing on clinical grounds

A

when HIV falls into differential disgnosis list - test regardless of risk factors

40
Q

how to take a HIV test

if incapacitated

A

consent, obtain venous sample for serology

only test if in patients best interest, consent form relative not required, if safe wait till patient regains capacity, obtain support from HIV team if required

41
Q

what markers of HIV are used in the lab to detect infection

A

Viral RNA
capsule protein - p24
antibody

42
Q

3rd gen test

A

HIV 1 and 2
detect IgM, IgG
very sensitive/specific in established infection
window period - 20-25 days

43
Q

4th gen test

A 
combined antigen (p24) and antibody
shortens window period by 5 days
the one which is used in tayside
44
Q

rapid HIV tests

A

POCT
finger prick specimen of saliva
results within 20-30 mins
3rd gen (Ab) 4th (Ab/Ag)

45
Q

advantages of using POCT

disadvantages

A

simple, no lab, no wait up, good sensitivity

expensive, quality control, poor positive predictive value, can’t be relied on in early infection

46
Q

RITA is what

A

incidence testing
used to identify if an infection occurred within the preceding 4-6 months

large margin of error

47
Q

home sampling which is available online

A

finger prick/saliva

Repro (56 decks)

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