HIV Flashcards

1
Q

In women conceiving on ART, when should CD4 count be monitored?

A

Minimum one Cd4 at baseline and one at delivery

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2
Q

If a woman starts ART in pregnancy, when should CD4 count be monitored

A

As per routine initiation of ART and also at delivery even if starting CD4 is >350

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3
Q

If a newly diagnosed HIV+ woman starts ART in pregnancy, when does she need VL performing?

A

2-4 weeks after starting ARV.
At least 1x per trimester
At 36/40
At delivery

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4
Q

If a woman has started ART in pregnancy but not suppressed VL to <50, what interventions are recommended?

A
Review adherence
Perform resistance tests if appropriate
Consider TDM
Optimise to best regime
Consider intensification
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5
Q

When should pregnant woman (including elite controllers) start ART?

A

Immediately and continue life long

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6
Q

If a pregnant HIV pos woman is not on ART when should she commence it?

A

As soon as she can in 2nd trimester when VL >30,000 copies
As soon as she can in 2nd trimester if VL 30,0000-100,000 HIV copies
In the first trimester if VL >100,000 copies and or CD4 <200
All women should start ARV by 24/40

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7
Q

Which ART regime is recommended for newly diagnosed HIV pos in pregnancy?

A

TDF or abacavir with emtricitabline or lamivudine as nucleoside backbone (truvada or kivexa)
3rd agent- efavirenz or atazanavir (most safety data in pregnancy)
Dolutegravir can be considered after 8/40

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8
Q

Is zidovudine monotherapy recomended in pregnancy?

A

No- only if the woman declines cART and has VL <10,000 HIV RNA copies and is willing to have a caesarean section

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9
Q

Is PI mono therapy recommended in pregnancy?

A

Np

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10
Q

When might a Integrase inhibitor be recommended in as 3rd choice on ART agent in pregnancy?

A

If very high VL >100,000 HIV RNA copies

If CART is failing to suppress the virus

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11
Q

What to give a woman presenting >28/40 pregnant HIV positive with VL unknown or >100,000 RNA copies

A

3 or 4 drug regime that includes raltegravir 400mg bd or dolutegravir 50mg od

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12
Q

How would you manage an untreated woman HIV positive in labour at term?

A

Stat dose of nevi rapine 200mg
Start oral zidovudine 300mg and lamivudine 150mg bd
and Raltegravir 400mg bd
AND RECEIVE IV ZIDOVUDINE FOR DURATION OF LABOUR

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13
Q

What to do if a unbooked woman presents in labour/SROM without documented HIV result

A

Advise them to have an urgent HIV test
If reactive/positive, act upon it immediately
Initiation of interventions to prevent vertical transmission of HIV
Don’t wait for formal serology

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14
Q

What confirmatory tests are needed for hep B/HIV coinfection in pregnancy?

A

Confirm viraemia with HBV DNA, e antigen status, screen for HAV, HDV, HCV
Tests to assess liver inflammation/fibrosis and LFT

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15
Q

What treatment is recommended for HIV/Hep B coinfection in pregnancy

A

TDF and emtricitabine should form the backbone if no CI.

If TDF is not part of ART it should be added

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16
Q

If HIV/Hep B confection, pregnant and not immune to HAV, are vaccines recommended and if so what schedule?

A

Yes- but after first trimester
Normal schedule 0 and 6 m
Unless CD4 <300, give additional dose 0,1,6m

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17
Q

HIV/Hep B coinfection in pregnancy, what is recommended mode of delivery ?

A

NVD if fully suppressed HIV VL (irrespective of hep b VL)

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18
Q

HIV/Hep B or hep C coinfection in pregnancy, does baby need any intervention at birth?

A

Immunisation against hep b with/without immunoglobulin should commence within 24h
Then national infant HBV schedule should be followed

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19
Q

Can ribavirin based DAAs be used in pregnancy for management of HCV infection?

A

No- discontinue immediately.

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20
Q

Can invasive prenatal diagnosis be performed on women who are HIV pos?

A

It should not be done until VL known
Ideally this should be <50 RNA copies/ml
Combined screening test and non invasive prenatal testing- has better sensitivity and specificity and minimises the number needing invasive testing

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21
Q

If HIV pos and not on ART and needing a prenatal invasive diagnostic test what can be done to prevent transmission?

A

Start ART and give raltegravir and a single dose of nevirapine 2-4h prior to the procedure

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22
Q

Can ECV be done in HIV positive women?

A

Yes if VL <50 HIV RNA copies/ml

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23
Q

What mode of delivery is recommended in HIV pos women?

A

If VL <50 at 36/40 and no obstetric CI can have NVD

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24
Q

In what circumstances in an HIV woman might a pre labour c section be recommended?

A

If VL >400 at 36/40

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25
Q

What would be recommended with regards to mode of delivery if HIV positive and VL 50-399 at 36/40?

A

Prelabour c section should be considered

Taking into account length of time on ARV, adherence, obstetric factors and women views

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26
Q

IF HIV positive and SROM and VL <50 what is the time frame ideally required for delivery?

A

Within 24 hours should be the aim.

IF VL <50, immediate induction/augmentation of labour

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27
Q

If HIV positive and SROM and VL <50-399 (or >400) what is recommended with regards to delivery?

A

Immediate C section recommended

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28
Q

HIV positive and SROM <34/40, what intervention is required?

A

Same as per HIV neg
Im steroids
Optimise HIV VL
MDT re timing/mode of delivery

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29
Q

When is IV intrapartum zidovudine recommended in HIV pos women ?

A

If VL >1000 and they present in labour or with SROM or are admitted for PLCS
For untreated women in labour and VL unknown
Can consider if VL 50-1000

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30
Q

Can HIV pos women have a water birth?

A

Yes if VL <50

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31
Q

Does baby need PEPSE if Mum has had ARV in pregnancy and VL <50?

A

YES
2 weeks zidovudine mono therapy recommended if
Mum has been on ART for >10 weeks
2 viral loads >50 during pregnancy 4 weeks apart
Maternal VL <50 at or after 36/40

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32
Q

Does baby need PEPSE if Mum has had ARV in pregnancy and VL <50?

A

Extend to 4 weeks if
not all low risk criteria fulfilled but VL <50 at or after 36/40
If infant born <34/40 but most recent VL <50

Combination PEPSE needed:
If maternal VL >50 on day of birth ?adherence or unknown VL
If resistance to zidovudine

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33
Q

If high risk - Mum HIV and VL >50 at delivery, when does neonatal PEPSE need to be started?

A

Neonatal PEP should be started within 4 h of birth

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34
Q

When should infant PEPSE be stopped

A

By 4 weeks

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35
Q

Should BCG given to neonate at birth if risk of HIV?

A

Only if low/very low risk HIV transmission and BCG at birth is indicated as per UK guidelines

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36
Q

What is the safest way to feed babies born to HIV + mothers?

A

Formula milk

Free formula provided

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37
Q

When should HIV follow-up be done on baby born to HIV pos mother not breast feeding?

A
In first 48h and prior to discharge
If HIGH risk at 2 weeks
1t 6 weeks
At 12 weeks
HIV ab for seroconversion should be checked at 18-24 m
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38
Q

When should HIV follow-up be done on baby born to HIV pos mother who is breast feeding?

A
In first 48h and prior to discharge
At 2 weeks
Monthly while b/f
At 4 and 8 weeks once stopped b/f
HIV ab for seroconversion should be checked at 18-24 m
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39
Q

What follow-up is required for HIV pos mother postpartum

A

All should be reviewed by member of MDT within 4-6 weeks
MH assessment
Contraceptive needs discussed
Cytology 3/12 postpartum
If newly diagnosed, testing of partner/other children

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40
Q

When should individuals with AIDS defining infection or serious bacterial infection and CD4 <200 start ARV?

A

Within 2 weeks of starting specific antimicrobial chemotherapy

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41
Q

Which ARV therapy is recommended for therapy naive PLWH

A
2 NRTI + 1 PI/r/NNRTI or II
TDF (or TAF) + Emtricitabine + 
Atazanavit/r
Darunavir/r
Dolutegravir/r
Elvitgeravir/c
Raltegravir
Rilpirivine

Alternative Abacavir and lamivudine
+ Efavirenz

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42
Q

When is Abacavir contraindicated?

A

HLA-B-5701 positive

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43
Q

What needs to be considered if using Abacavir and lamivudine as backbone?

A

Viral load

If VL >100,000 only use if in combination with dolutegravir

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44
Q

What do you need to consider if using TDF/emtricitabine/elviteravir

A

Do not use in individuals with Creatinine clearance <70 ml/min
TAF/emtricitabine/elviteravir should not be initiated if cdcl <30ml/min

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45
Q

When is use of RIlpivirine recommended?

A

When baseline VL is 100,000 copies/ml

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46
Q

If there is a risk of prolonged ART interruptions what alternative could be considered?

A

Protease inhibitor/ritonavir booster
- may be considered
May be associated with less frequent selection for drug resistance

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47
Q

What to do if VL 50-200 copies /ml, followed by a undetectable VL?

A

Nothing

Not a cause for clinical concern

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48
Q

What to do if VL >200 copies /ml?

A

Genotypic resistance test

This is indicative of virological failure

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49
Q

Example of NRTIs?

A
ZELAT
Zidovudine
Emtricitabine
Ladivudine
Abacavir
Tenofovir
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50
Q

Examples of NNRTIS

A
NEER
Nevirapine
Efavirenz
Etravirine
Rilpivirine
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51
Q

Examples of integrate inhibitors

A

DR
Dolutegravir
Raltegravir

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52
Q

Examples of Protease inhibitors

A
Boosted with ritonavir (r) or cobisistat (c)
FatLAD
Fosamprenavir (r)
Lopinavir (r)
Atazanavir (r/c)
Darunavir (c/r)
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53
Q

Example of CCR5I

A

Miraviroc

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54
Q

What to do if patient experiences virological failure on first line ART with wild type virus and without emergent resistant mutations

A

Switch to a PI/r or PI/c based cART

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55
Q

When should patients with HIV TB coinfection start ART if CD4 <50?

A

As soon as TB treatment is tolerated and where possible within 2 weeks

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56
Q

When should patients with HIV TB coinfection start ART if CD4 >50?

A

ART can be deferred until between 8 and 12 weeks of TB treatment

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57
Q

What ART regimen should be recommended in HIV/TB coinfection?

A

TDF+ emtricitabine + Efavirenz

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58
Q

Are there any interactions between ARV and Rifampicin to be aware of?

A

Raltegravir should be used with caution with rifampicin

Rifampicin should not be used with Nevirapine or any boosters (cobicistat or ritonavir)

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59
Q

HIV/Hep B coinfection requiring treatment: what to do about ART?

A

Start ARV promptly

Include TDF/TAF and emtricitabine

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60
Q

HIV/Hep B coinfection not requiring treatment: what to do about ART?

A

Start ARV

Include TDF/TAF and emtricitabine

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61
Q

HIV/Hep C coinfection requiring treatment for Hep C: what to do about ART?

A

Start ART before Hepatitis C treatment

If CD4 >500 however can defer ART

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62
Q

When to start ARV in Hepatitis B coinfection?

A

Should be treated with ART inclusive of anti HBV active drugs regardless of CD4

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63
Q

Hep B/HIV coinfection- if emtricitabine/lamivudine resistance- what to do?

A

Can just give TAF/TDF

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64
Q

When should ART be started if KS?

A

ART should be started promptly

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65
Q

When should women with CIN2 /3 start treatment?

A

Promptly

If having chemoradiotherapy for cervical cancer also need opportunistic infection prophylaxis

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66
Q

What needs to be considered in hiv associated malignancy?

A

ART should be started immediately

If starting chemotherapy they should be offered HSV prophylaxis

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67
Q

Which drugs should be avoided if worsening renal function?

A

TDF and atazanavir

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68
Q

Which HIV drugs are preferred if high CVD risk?

A

Avoid miraviroc and abacavir
Alternatives to fosamprevanir and lopinavir/r
Atazanavir is preferred PI
First line therapy is

TDF + emtricitabine +

Dolutegravir /raltegravir/rilpirivine
If VL <100,000

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69
Q

When should efavirenz be stopped promptly?

A
If current or past history of 
Depression
Psychosis
Suicidal ideation 
Attempted suicide
Self harm
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70
Q

Which ART should be avoided if osteoporosis?

A

TDF should be avoided if
>40 with osteoporosis
History of fragility fracture
FRAX >20% - major osteoporotic fracture

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71
Q

What is the res of HIV transmission in anal sex?

A

Receptive 1 in 90

Insertive 1 in 666

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72
Q

What stain is used for diagnosis of PCP?

A

Silver stain

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73
Q

What stain is used for diagnosis of cryptococcal meningitis?

A

India ink stain

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74
Q

Why do G6PD levels need to be taken before administering Cotrimoxazole, dapsone or primaquine?

A

Can trigger haemolysis

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75
Q

When is prophylaxis for PCP required?

A

If CD4 is <200

Or they have oral candida/AIDS defining ilness

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76
Q

What is the appearance of cerebral toxoplasmosis on CT?

A

Cerebral abscesses
Ring enhancing lesions at grey/white interface and in deep grey matter of basal ganglia or thalmus
Associated with cerebral oedema/mass effect

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77
Q

When to test baby to HIV positive mum?

A
48 hours
6 weeks, 12 weeks and his ab at 18-24 months
If breast feeding:
48 h
Then monthly until stopped
Then 4, 8 weeks post stopping b/f
18-24 m HIV ab
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78
Q

In 2008, what was the % of undiagnosed HIV in the UK?

A

25% heterosexuals and 47% MSM

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79
Q

What are the preferred treatments for HIV2?

A

Lopinavir/r

Tenfovir and emitricitabine

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80
Q

Which class of ART does HIV2 have innate resistance to?

A

NNRTIs

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81
Q

What follow-up is required for newly diagnosed HIV?

A

2-4 weeks
3m
6m
U&E, LFT, urinalysis
FBC (if on zidovudine or unwell)
CD4 - if <350- every 3m and ay 6m if still <350
If baseline >350, no need to repeat if undetectable VL

VL- measure at 1, 3, 6 months

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82
Q

What would you do if VL not fallen by 10 fold after 1 month in newly diagnosed HIV positive?

A

Repeat again at 2 months

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83
Q

If established on ART, how often does CD4 count need monitoring?

A

If CD4 >200- test 3-6 m
200-350- annual
>350 twice >1 year apart- no more

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84
Q

What to recommend if HIV positive patient is a contact of VZV?

A

Prophylaxis with VZV vaccine or varivax
within 3-5 days of exposure
If CD4 <400 - varicella immunoglobulin should be given within 7-10 days of exposure

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85
Q

Contraindications to live vaccines in HIV?

A

BCG and Typhoid are contraindicated

All replicating live vaccines are contraindicated in pregnancy

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86
Q

Can you give replicating live vaccines in HIV?

A

BCG and typhoid CI.
Only give live vaccines if CD4 >200
i.e. MMR, Varicella, herpes zoster and yellow fever

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87
Q

When does HIV seroconversion usually occur?

A

1-3 weeks after infection.

During this time up to 80% of people have symptoms. These symptoms can last for a few days or a few weeks.

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88
Q

What are the symptoms of HIV seroconversion?

A
Fatigue
Fever
Sore throat
Rash
Headache
Loss of appetite
Aching muscles and joints
Swollen lymph glands
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89
Q

Cause of Kaposi’s sarcoma?

A
HHV8 
Other risk factors:
Immunosuppression
Male 
Caucasian, mediterranean, middle East, Africa
MSM
?non smoking, DM, oral steroids
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90
Q

Advice regarding exposure prone procedures in HCW with HIV?

A

HIV infected HCWs must meet the following criteria before they can perform EPPs:

a) be on effective combination antiretroviral therapy (cART), and
b) have a plasma viral load <200 copies/ml
Or
c) be an elite controller
And
d) be subject to plasma viral load monitoring every three months and
e) be under joint supervision of a consultant occupational physician and
their treating physician, and
f) be registered with the UKAP Occupational Health Monitoring Register
(UKAP-OHR)

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91
Q

what is a late diagnosis of hiv?

A

cd4 <350

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92
Q

why should women who are HIV pos and undetectable be advised not to breast feed even if undetectable?

A

as a immunoglobulins /cd4 in breast milk

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93
Q

why should women who are HIV positive and breast feeding not add in formula/solids?

A

increases risk of transmission because formula can cause gut inflammation?

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94
Q

someone who is newly diagnosed HIV with low cd4 (bbv screen neg) develops transaminitis? what are causes?

A

could be drug related - raletgravir
iris- most likely
if immunosuppressed and exposed to hep c, may not have developed hep c ab and then can reactivate as immune response improves

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95
Q

if reactive HIV POC test what would you advise patient?

A

risk of false positive
around 10% but depends on prevalence of population
need serum sample

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96
Q

When should ARV be started in HIV/Hep C coinfection?

A

Starts ARVS prior to Hepatitis C treatment

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97
Q

What is IRIS?

A
Inflammatory response induced by ARVs
CMV retinitis
HCV
MAC
VZV
TB 
HSV
PML
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98
Q

Which factors might increase risk of HIV transmission?

A
High VL in source
Breaches to mucosa (ulcers/trauma)
Mensutruating
STIs
Ejaculation
Non circumcision
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99
Q

What % of MSM with syphilis are HIV1 coinfected?

A

40%

100
Q

HIV POCT- what advise patient?

A

Different tests
Use oral fluid, finger prick, plamsa, whole blood or urine
In low prevalence setting- false positive relatively higher with poor PPV (number of people with positive test who have disease)

All reactive tests need a confirmatory serum test

101
Q

Zidovudine- side effect

A

Nail pigmentation with zidovudine occurs primarily in black patients.

Reversible and dose-dependent.

? Mechanism

The longitudinal streaks of discoloration seen with zidovudine must be distinguished from the brownish hyperpigmented stripes that are seen in HIV.

Another unusual side effect of zidovudine noted by some is a grayish-black discoloration of the tongue. This is not associated with any toxicity and is asymptomatic.

102
Q

What are HIV clinical indicators for AIDS defining conditions?

A
Tuberculosis 
Pneumocystis
Cerebral toxoplasmosis 
Primary cerebral lymphoma 
Cryptococcal meningitis 
Progressive multifocal leucoencephalopathy
Kaposi’s sarcoma
Persistent cryptosporidiosis
Non-Hodgkin’s lymphoma
Cervical cancer
Cytomegalovirus retinitis
103
Q

Other clinical indicators where HIV testing should be offered?

A

Bacterial pneumonia
Aspergillosis
Aseptic meningitis/encephalitis
Cerebral abscess
Space occupying lesion of unknown cause Guillain–Barré syndrome
Transverse myelitis
Peripheral neuropathy
Dementia
Leucoencephalopathy
Severe or recalcitrant seborrhoeic dermatitis Severe or recalcitrant psoriasis Multidermatomal or recurrent herpes zoster
Oral candidiasis
Oral hairy leukoplakia
Chronic diarrhoea of unknown cause
Weight loss of unknown cause
Salmonella, shigella or campylobacter Hepatitis B infection
Hepatitis C infection
Anal cancer or anal intraepithelial dysplasia Lung cancer
Seminoma
Head and neck cancer
Hodgkin’s lymphoma
Castleman’s disease
Vaginal intraepithelial neoplasia
Cervical intraepithelial neoplasia Grade 2 or above
Any unexplained blood dyscrasia including: • thrombocytopenia
• neutropenia
• lymphopenia
Infective retinal diseases including herpesviruses and toxoplasma
Any unexplained retinopathy
Lymphadenopathy of unknown cause Chronic parotitis
Lymphoepithelial parotid cysts
Mononucleosis-like syndrome (primary HIV infection)
Pyrexia of unknown origin
Any lymphadenopathy of unknown cause
Any sexually transmitted infection

104
Q

What are symptoms of neurotoxicity with efavirenz?

A

Symptoms of CNS toxicity
Dizziness, irritability, headache, diminished concentration, euphoria, vertigo and depression, insomnia, nervousness, suicidal ideation, psychosis

Sleep disturbance (somnolence, insomnia and vivid or abnormal dreams) -nearly half of cases.

2% of subjects report more serious neurological effects, including delusion, paranoia, depersonalization, hallucinations, anxiety, aggressive behaviour, abnormal thinking, mania and severe depression.

Mechanisms - ?disturbances in brain mitochondrial function

105
Q

Which ARV causes hyperbilirubinaemia and kidney stones?

A

Atazanavir

106
Q

Which ARV causes CV problems eg MI and stroke?

A

Abacavir (and PIs)

107
Q

Which ARV causes high cholesterol?

A

Efavirenz

108
Q

Which ARV can cause SJS and TEN and liver problems?

A

Nevirapine

109
Q

What are commonest causes of community acquired bacterial pneumonia in HIV positive?

A

Strep pneumonia and Haemophilus influenza (same as general population.)

S aureus and pseudomonas aerginosa are more common in HIV pos than HIV neg

110
Q

Allergy to Darunavir?

A

Darunavir is a PI
Darunavir contains a sulfonamide moiety. She patients may have sulfonamide allergy.

Also can't have
Amprenavir 
Darunavir 
Delavirdine
Fosamprenavir
Tipranavir
111
Q

What is the BASHH guidance for follow up HIV testing post PEPSE?

A

Follow-up HIV testing at 8–12 weeks post-exposure

112
Q

Why might you need to come off efavirenz safely?

A

It has a long half life so if stop all ARV at same time, risk of monotherapy and therefore resistance.
Advised to put patient on a PI for 1/12 (PI monotherapy is ok as there is a high barrier to resistance)

113
Q

Level of evidence for PEPSE where risk >1 in 1000

A

Level 1C

We recommend the use of PEPSE where there is a significant risk of HIV transmission (risk >1/1000)

114
Q

Level of evidence for PEPSE regimen where risk >1 in 1000

A

Level 1B

Truvada and raltegravir as the regimen of choice for PEPSE

115
Q

Level of evidence for f/u testing post PEP

A

Level 1C

We recommend follow-up HIV testing at 8-12 weeks after exposure

116
Q

How is chickenpox transmitted (VZV)

A

Chickenpox is highly infectious and can be transmitted by respiratory droplets and aerosols up to 48 hours prior to the onset of the rash.

117
Q

Complications of VZV?

A

Complications may include severe cutaneous rashes, secondary bacterial infections, visceral involvement (e.g. pneumonia, hepatitis), and neurological disease (meningitis, encephalitis, myelitis).

All adults with chickenpox, and especially pregnant women, are at risk of VZV pneumonia.

118
Q

Complications of VZV or HZV in pregnancy?

A

Occasionally, infection in pregnancy leads to fetal injury (congenital varicella syndrome).

119
Q

Complications of shingles HZV

A

Shingles is usually self-limiting, although persistent debilitating pain is a frequent complication, particularly in the elderly (post-herpetic neuralgia, PHN); eye involvement may lead to permanent visual impairment.

120
Q

Can varicella vaccines causes latent infection?

A

The vaccine strain can establish latent infection in some vaccine recipients, and can reactivate to cause shingles,

121
Q

CI to varicella vaccine

A

Contraindications include pregnancy and significant immunocompromise.
HIV don’t give is cd4 <200 as live vaccine

122
Q

Who should receive shingles vaccine?

A

In the UK, shingles vaccination is recommended for adults without a history of immunodeficiency aged 70 years,

‘catch- up’ programme currently targets those aged 70–79 years.

Contraindications include pregnancy and breast feeding and significant immunocompromise.

123
Q

What are recommendations for HIV positive adults with ?hx of chickenpox or shingles

A

VZV IgG testing to determine susceptibility to primary infection and reactivation

124
Q

What if HIV positive and bloods are VZV seronegative for IgG?

A

If CD4 cell count >200 cells/μL and preferably on ART

two doses of the chickenpox vaccine
3 months apart

Serological testing for evidence of VZV IgG seroconversion should be performed 4–6 weeks after the second vaccine dose

125
Q

What if HIV positive and bloods are VZV seropositive for IgG?

A

We recommend VZV IgG seropositive patients who have a CD4 cell count >200/μL and preferably are established on ART be offered one dose of the shingles vaccine in line with national age- related indications- but may benefit from shingles vaccination from the age of 60 years

126
Q

If HIV positive and given replicating VZV and develop rash/other sx, what is recommendation?

A

Report and seek medical evaluatio

May be offered appropriate antiviral therapy against VZV if required

127
Q

HIV positive and contact of VZV?

A

We recommend that following a significant exposure to VZV, the VZV IgG status of the HIV- positive contact be ascertained regardless of vaccination history (although prophylaxis should not be delayed waiting for the results)

VZV IgG seronegative patients be considered for post- exposure prophylaxis and monitored closely for symptoms to facilitate prompt institution of antiviral therapy

128
Q

HIV positive- CD 4 <200, exposed to VZV and seronegative what would recommend?

A

If CD4 <200 cells/μL give VZIG and antiviral prophylaxis

Aciclovir (800 mg qds / valaciclovir (1 g tds) starting from day 7 after exposure and continuing for 7 days

129
Q

HIV positive- CD 4 <400, exposed to VZV and seronegative what would recommend?

A

If CD4 <400 cells/μL:
PEP with VZIG within 7 days and not later than 10 days after exposure

If no PEP, antiviral prophylaxis

Aciclovir (800 mg qds / valaciclovir (1 g tds) starting from day 7 after exposure and continuing for 7 days

130
Q

HIV positive- CD 4 >400, exposed to VZV and seronegative what would recommend?

A

If CD4 cell counts >400 cells/μL:
Varivax vaccine within 3 and up to 5 days after exposure
2nd dose- >3 months

131
Q

Can you give antivirals and VZV vaccine together?

A

No
VZV replicating vaccines are not given treatment doses of antiviral drugs with anti-herpetic activity (e.g. aciclovir) at the time of vaccination and for 4 weeks subsequently as it may reduce vaccine immunogenicity

132
Q

How common are strokes/TIA in HIV?

A

0.5-8% of HIV positive

133
Q

What are vascular risk factors that increase risk of stroke in HIV pos?

A

HIV is hypercoaguable state

RFs-
smoking
high BP
Hyperlipidaemia
Cocaine/alcohol- nacres risk of thrombotic stroke

Cerebral vasculitis from syphilis, VZV may cause cerebral thrombosis

134
Q

Face-to-face provision of HIV test results is strongly encouraged for

A

ward-based patients
patients more likely to have an HIV-positive result
those with mental health issues or risk of suicide
English is a second language
young people under 16 years
those who may be highly anxious or vulnerable

135
Q

Refusal of testing by a competent young person

A

Legal advice should be sought about whether to apply to the court if testing is thought to be in the best interests of a competent child who refuses.

136
Q

What to tell children about having an HIV test

A

A developmentally and age-appropriate explanation of the test should be given to children
Does not necessarily mean using the term HIV.

1) Older children (> 11 yo) should be asked to give consent for an HIV test.
2) Younger children (5-10 yo) can be told they are being tested for a ‘bug’ in the blood.
3) Pre-school children and infants do not need any formal explanation of why they are having a blood test.

137
Q

Refusal of testing by parents of a non-competent child or young person

A

If in the best interests –
consider involving other members of the multidisciplinary team
an independent advocate or named/designated doctor for child protection before seeking legal advice.
This also applies if both a young person with capacity and their parents refuse testing.

138
Q

What to do if source patient in a needlestick injury is HIV pos or other HIV risk exposure

A

The source patient’s consent to testing must always be gained.
Consent from the patient should be obtained from a healthcare worker other than that who sustained the injury.
If the rationale for testing is explained, it is unusual for consent to be refused.
If the patient does not wish to know the result the option of testing without any documentation should be considered.

139
Q

HIV testing and insurance?

A

Questions regarding whether an individual has ever had an HIV test or a negative result should not be asked.

Applicants should declare any positive results if asked as would be the case with any other medical condition

140
Q

In which cases is HIV testing universally recommended?

A
  1. GUM or sexual health clinics
  2. antenatal services
  3. termination of pregnancy services
  4. drug dependency programmes
  5. healthcare services for those diagnosed with tuberculosis, hepatitis B, hepatitis C and
    lymphoma.
141
Q

HIV test should be considered in the following settings where diagnosed HIV prevalence in the local population?

A

Where diagnosed HIV prevalence in the local population (PCT/LA) exceeds 2 in 1000 population

  1. all men and women registering in general practice
  2. all general medical admissions.
142
Q

HIV testing should be also routinely offered and recommended to the following patient?

A
  1. all patients presenting for healthcare where HIV, including primary HIV infection, enters the differential diagnosis (see table of indicator diseases and section on primary HIV infection)
  2. all patients diagnosed with a sexually transmitted infection
  3. all sexual partners of men and women known to be HIV positive
  4. all men who have disclosed sexual contact with other men
  5. all female sexual contacts of men who have sex with men
  6. all patients reporting a history of injecting drug use
  7. all men and women known to be from a country of high HIV prevalence (>1%*)
  8. all men and women who report sexual contact abroad or in the UK with individuals from countries of high HIV prevalence.*
143
Q

HIV testing should also be routinely performed in the following groups in accordance with existing Department of Health guidance

A
  1. blood donors
  2. dialysis patients
  3. organ transplant donors and recipients.
144
Q

How often to offer an HIV test?

A
  1. all individuals who have tested HIV negative but where a possible exposure has occurred within the window period
  2. men who have sex with men (MSM) – annually or more frequently if clinical symptoms are suggestive of seroconversion or ongoing high risk exposure
  3. injecting drug users – annually or more frequently if clinical symptoms are suggestive of seroconversion (see section on primary HIV infection)
  4. antenatal care – women who refuse an HIV test at booking should be re-offered a test, and should they decline again a third offer of a test should be made at 36 weeks. Women presenting to services for the first time in labour should be offered a point of care test (POCT).
145
Q

Should pregnant women be offered a second HIV test in pregnancy?

A

In areas of higher seroprevalence, or where there are other risk factors, women who are HIV negative at booking may be offered a routine second test at 34–36 weeks’ gestation as recommended in the BHIVA pregnancy guidelines

146
Q

How common is seborrhoeic dermatitis in HIV?

A

Occurs in 85%
May be first indicator
Severity/increased recurrences if CD4 count low
Related to infection with pittosporum app, increased sebum and genetic predisposition

147
Q

Treatment of seborrhoeic dermatitis?

A

Topical antifungals/steroids eg miconazole/hydrocortisone
Scalp- tar shampoo, salicylic acid, ketoconazole
Severe disease- systemic triazoles eg itraconazole

148
Q

What is hep B vaccine schedule if HIV positive and not on ARV?

A
Hep B vax pro 40 mcg
or Engerix B (double dose) 40 mcg
or fendrix 20 mcg
4 doses
0, 1 m, 2m, 6m
149
Q

Can ultra rapid Hepatitis B vaccine course be given in HIV positive patients?

A

ultra-rapid vaccination course (0, 7, 21 standard dose) be considered only in selected patients with CD4 cell counts >500 cells/μL
If imperative need to ensure rapid completion of vaccination and/or where compliance with a full course is doubtful
We recommend against using high-dose vaccination in an ultra-rapid schedule due to the lack of safety data

150
Q

If primary vaccine hep B course in HIV pos and HBsAb levels <10 IU/L at 6 weeks, what is recommended?

A
three further vaccine 
monthly intervals
high dose (40 μg) with Engerix B or HBvaxPRO 
standard dose (20 μg) with Fendrix 

We suggest that revaccination with Fendrix may be preferred in non-responders

revaccination of non-responders may be
delayed until the viral load is suppressed on ART and the CD4 cell count has increased >350

151
Q

If after primary vaccine for hep B in HIV, HBsAb levels ≥10 but <100 IU/L, what is recommended?

A

one booster dose

152
Q

How often should hepbsAb level be measured in HIV positive patients who are vaccinated?

A

guided by the initial HBsAb level (measured
after completion of the primary vaccine course

Usually yearly HBsAb screening

Longer intervals (i.e. 2–4 years) if initial HBsAb levels >100 IU/L, CD4 cell counts >350 cells/μL, and viral load suppression on ART

153
Q

HIV pos, exposed to Hepatitis B

A

No prophylaxis required if evidence of current/ past HBV infection

Vaccinated patients with initial HBsAb >10 IU/L - 1 booster dose and if the CD4 cell count is <200 cells/μL also receive HBIg

Non-responders to previous HBV vaccination (initial HBsAb <10 IU/ L)–> booster vaccine and HBIg regardless of CD4 cell count

Patients who have not been vaccinated or ? vaccination history should be offered a rapid vaccine course (0, 1, 2 months; see above for dosing) and also receive HBIg regardless of CD4 cell count

When indicated, two doses of HBIg should be given 1 month apart

Post-exposure prophylaxis should be given within 7 days of exposure

We suggest that prophylaxis beyond 7 days (up to 6 weeks after exposure) may be considered

154
Q

Which is the screening test antenatally for hepatitis B?

A

HepBsag- looking for active infection

155
Q

Which is the screening test in SH for hepatitis B?

A

Hep B Core ab IgG

hepBcab

156
Q

Which HBV genotype is highest risk for HCC?

A

Genotype C

157
Q

PREP baseline tests required?

A
HIV testing with ag/ab
Hep B
Hep C
Syphilis serology
GC/CT
Renal funciton- egFR
PT
Urinalysis
158
Q

Risk of HIV transmission in IV drug use (Sharing equipment)

A

1 in 149 per exposure from a known HIV positive individual not on ART

159
Q

Complications of PCP?

A

Systemically unwell- weight loss, cough
SOB (initially on ecxertion, then on rest)
PNEUMOTHORAX- may need chest drain
Respiratory failure

160
Q

Prophylaxis for PCP- when offered in HIV?

A

Recommended if CD4 <200

1st line cotrimazole 480-960mg daily
Alternatives- dapsone +pyrimethamine + folinic acid

Continue until CD4 >200 for 3 months

161
Q

Prophylaxis for Toxoplasma- when offered in HIV?

A

Recommended if CD4 <200 and positive serology

1st line cotrimazole 480-960mg daily
Alternatives- dapsone +pyrimethamine + folinic acid

Continue until CD4 >200

162
Q

Prophylaxis for mycobacterium avium- when offered in HIV?

A

Recommended if CD4 <50

1st line: azithromycin 1250mg weekly

Discontinue if CD4v >50 for 3 months

163
Q

PEP in HIV positive patients for

- diphtheria, h. influenzae, meningococcus, pertussis

A

Offer abx and vaccination if contacts

164
Q

Prophylaxis if HIV pos and contact of HAV

A

Offer HAV if HAV IgG negative

If CD4 <200, offer HAV immunoglobulin within 14 days

165
Q

Prophylaxis if HIV pos and contact of Hep B?

A

Determine Hep B immunity
If suboptimal - offer booster

Non immune- rapid vaccine
Hep B immunoglobulin regardless of CD4

166
Q

Prophylaxis if HIV pos and contact of measles

A

Request measles igG
If IgG positive and CD4 >200 do nothing
If cd4 <200- give immunoglobulin (even if
measles immunity)

If IgG negative and Cd4 >200, give measles vaccine within 3 days or immunoglobulin within 6 days

167
Q

If immunocompromised and given oral polio by mistake, what can you do?

A

Give polio HNIG

168
Q

Contact of VZV and HIV positive?

A

Prophylaxis with VZV- chickenpox/varivax vaccine within 3-5 days
If CD4 <400- give varicella immunoglobulin within 7-10 days of exposure

169
Q

Why do you need to give ART first in HIV/Hep C confection?

A

Immune recovery if CD4 <350 (or 350-500)

The start anti HCV rx

170
Q

How long do you treat HCV with DAAs?

A

Total 48 weeks

171
Q

When diagnosed with HIV, what hepatitis serology needs to be done?

A
HCV ab
Screen HepA ing
HepBsAg (annual)
HepCab
Hepsab
172
Q
If HIV positive and 
HepBcab positive
HepBsag negative
HepBsAb negative
AST and ALT raised
A

?occult

Need to check HepB RNA

173
Q

Who do you need to check HDV ab on?

A

All who are HepBSag positive

If HDV ab positive check RNA

174
Q

If someone has raised transaminases what do you need to consider?

A

Hep B, Hep C

If negative consider HEV

175
Q

What is recommended ART regimen for Hep B, HIV coinfection?

A

TDF/ FTC

176
Q

How common in oral candida in HIV?

A

seen in 90%

177
Q

How does oral candida present?

A

White plaques/red patches

Angular chelitis

178
Q

Treatment of oral candida?

A

Fluconazole 50-100mg 7-14 days
Itraconazole 100-200mg 7-14 days

Prophylaxis - fluconazole 50mg daily

179
Q

Apthous ulcers- treatment

A
Vesicular
Can be necrotic
Lidocaine 5%
Hydrocortisone tablets held on lesions
If severe prednisolone 40-60mg
180
Q

Complications of oral HSV in HIV?

A

Keratitis
Oesophagitis
Meningitis

181
Q

Treatment of oral HSV in HIV?

A

400mg Aciclovir 5 x day for 10/7

or 1000mg bd Valaciclovir

182
Q

Presentation of CMV oral ulcers in HIV

A

Deep necrotic red/white ulceration

Arise when CD4 <50 cells/ul

183
Q

Prevalence of CMV oral ulcers in HIV?

A

90% in HIV MSM

184
Q

Presentation of oral hairy leukoplakia?

A
White adherent corrugated lesion
Found in the mouth
EBV
NOT PREMALIGNANT
Associated with increase progression to AIDS
185
Q

Presentation/rx of oesophageal candida?

A

CD4 <200
Oral candida association
Painful to swallow
Treat with fluconazole 100-200mg 10-14 days

186
Q

How to treat salmonella in HIV?

A

Needs treating in PLWH- severity, high relapse, high risk of dissemination
Ciprofloxacin 750mg bd

187
Q

Treatment of CMV retinitis?

A

CD4

188
Q

Causes of bacterial pneumonia in HIV?

A

AS in general population
Strep pneumoniae
Haemophilus influenza

(staph aureus and pseudomonas aeriginosa -commoner than HIV neg)

189
Q

Treatment of bacterial pneumonia in PLWH?

A

IV cefuoroxime 1.5 g tds

and macrolide eg clarithromycin 500mg bd

190
Q

Investigation and treatment of PCP?

A

Night sweats, weight loss, cough/sob
CXR- bibasal perihilar interstitial infiltrates,
CT- ground glass
Rx- clotrimoxazole 120mg /kg or dapsone

191
Q

Investigation and treatment of TB?

A

Pleuritic chest pain
Haemoptysis
Weight loss

AFB- 2 sputum
CXR- UL cavity changes
Rx- isoniazid, rifampicin, ethambutol, pyrazinamide

192
Q

Which group of ARV can cause insulin resistance?

A

PIs

193
Q

What derangement of lipids can be seen with HIV?

A

Raised triglycerides
Raised cholesterol
Low LDL

194
Q

Side effects of azoles

A

Low cortisol and low testosterone

195
Q

Electrolyte disturbances with drugs- raised K

A

cotrimoxazole

Trimethoprim

196
Q

HIV nephropathy - investigations

A
Heavy proteinuria
Low albumin
Oedema
Lipids raised
BP normal
197
Q

Electrolyte disturbances with drugs- low Ca

A

Tenofovir
Foscarnet
Ketoconazole

198
Q

HIV nephropathy - treatment?

A

ARV

Avoid nephrotoxic trigs - eg TDF and PI

199
Q

Immune mediated renal disease - HIV

What are associations?

A

Hep B and hep C
Light proteinuria
microhaematuria
Treat with ARV

200
Q

HIV - CV complications

A

Infective endocarditis

201
Q

Which valve is affected by infective endocarditis in HIV and which infections implicated?

A

Tricuspid valve

step viridians, staph A, candida

202
Q

Which ARVs cause cardiac complications?

A

Zidovudine, foscarnet cause cardiomyopathy
Ganciclovir, interferon- dysrrythmia
Cotrimoxazole- conduction defect

203
Q

Reactive arthritis - HIV

A

Lower limb and peripheral joints
Leucocytes and glucose in synovial fluid
Rx- NSAIDs

204
Q

What is persistent generalised lymphadenopathy in HIV?

A
2 extra inguinal LN sites
>3/12
symmetrical
LN >1cm
Non tender
205
Q

Kaposi’s sarcoma- how does it present?

A

Pigmented macules/papules/plaques
YEllow halo
On face, nasal margin, end of nose, eyelid
33% have red purple lesion on hard palate

206
Q

How much more common is KS in HIV?

A

500 x

207
Q

Diagnosis of KS?

A

biopsy or HHV8 VL

208
Q

Treatment of KS?

A

80% improve with ART
Cryotherapy
Radiotherapy
Chemotherapy if prognosis poor

209
Q

Treatment of Castleman’s disease

A

rituximab

210
Q

What is castlemans disease?

A

HIV associated malignancy
Recurrent increase in LN
HHV8
High VL

211
Q

Cause of Non hodgkins lymphoma?

A

12 x more likely in HIV
Monoclonal B cells- large B cells
Burketts/non Burketts
Systemic lymphoma

212
Q

Diagnosis of Non hodgkins lymphoma?

A

Biopsy
MRI/CT to stage
Toxoplasma serology

213
Q

treatment of Non hodgkins lymphoma?

A

ART
CHOP
Radiotherapy

214
Q

Which 3 types of cancer are AIDS defining?

A

High grade B-cell non-Hodgkin’s lymphoma (NHL) including primary cerebral lymphoma
Kaposi sarcoma (KS)
Invasive cervical cancer

215
Q

How common is high grade B-cell NHL in PLWH?

A

60-100 times more frequently in people with HIV than in the matched general population

216
Q

What is associated with primary effusion lymphoma in HIV?

A

KS herpesvirus, (a gamma-2 herpesvirus,) is the causative agent of

  • KS
  • Primary effusion lymphoma
  • A plasma cell variant of multicentric Castleman’s disease.

Primary effusion lymphoma may present with effusions (pleural, pericardial or ascites) without any nodal mass of disease is associated with KS herpesvirus

217
Q

Treatment of Non Hodgkin’s lymphoma?

A

Intravenous combination chemotherapy
Intrathecal chemotherapy (for those at risk of meningeal relapse)
ART
Opportunistic infection prophylaxis - PCP, MAC and antifungal.

This management approach will result in durable complete remission in about 60% of patients who will in effect be cured of their NHL.

218
Q

Define Primary cerebral lymphoma?

A

Primary cerebral lymphoma is defined as lymphoma that is confined to the cranio-spinal axis without systemic involvement.

In the context of HIV infection, it occurs in patients with advanced immunosuppression and has a particularly poor prognosis. The incidence of PCL has declined since the introduction of ART

219
Q

What are commonest causes of cerebral SOL in HIV?

A

Toxoplasmosis and PCL are the most common causes of cerebral space occupying lesions in HIV

220
Q

At what CD4 count and toxoplasma and Primary cerebral lymphoma seen in HIV?

A

Both toxoplasmosis and PCL occur at low CD4 counts (<50 cells/ µ L) and present with headaches and focal neurological deficits.

221
Q

What is the aetiology of primary cerebral lymphoma?

A

The detection of Epstein–Barr virus (EBV) DNA in the cerebrospinal fluid (CSF) by polymerase chain reaction (PCR) in patients with PCL has become established as a diagnostic test with a high sensitivity and specificity.

222
Q

How common is primary cerebral lymphoma in PLWH?

A

1000x

223
Q

How to differentiate between cerebral toxoplasma and PCL?

A

Clinical and radiological features may aid differential diagnosis but are not definitive.

Toxoplasma- fever (PCL and PML don’t)

Over 85% patients with cerebral toxoplasmosis will respond clinically and radiologically to 2 weeks of anti-toxoplasma therapy.

EBV DNA in the CSF by PCR in patients with PCL has become established as a diagnostic test with a high sensitivity and specificity.

F-fluorodeoxyglucose-positron emission tomography (FDG-PET) helps differentiate between PCL and cerebral toxoplasmosis.

224
Q

Where in the brain does toxoplasma affect?

A

Basal ganglia and brainstem

225
Q

Where in the brain does primary CNS lymphoma affect?

A

periventricular/anywhere

226
Q

Where in the brain does PML (progressive multifocal leukoencephalopathy) affect?

A

parietal lobe/white matter

227
Q

Which infection causes KS?

A

KS is caused by infection with a gammaherpesvirus
named either Kaposi sarcoma herpesvirus (KSHV)
or human herpesvirus 8 (HHV8).
This virus which resembles EBV is transmitted horizontally. Highest levels of KSHV are found in saliva.

228
Q

What is the route of transmission for KS?

A

kissing

229
Q

Major differential diagnosis for KS?

A

The major clinical differential diagnosis is bacillary angiomatosis caused by the rickettsia Bartonella henselae and this is best excluded by biopsy

230
Q

What are the most common sites of visceral involvement by KS?

A

lungs and stomach.

231
Q

What are GI associations with KS?

A

Gastrointestinal lesions are usually asymptomatic but may bleed or cause obstruction. The diagnosis is usually confirmed at endoscopy

232
Q

How much more common is cancer in PLWH than general population?

A

2-3 x more common in HIV

Cancers associated with oncogenic viral infections
eg anal cancer HPV
Hodgkin’s disease- EBV
Hepatocellular cancers- hepatitis

However, some cancers with no known viral aetiology such as seminoma and non-small cell lung cancers also occur significantly more commonly in people living with HIV.

233
Q

Can NHL be cured?

A

The treatment of systemic AIDS related NHL results in durable complete remission in about 60% of cases

234
Q

Examination newly diagnosed HIV pos

A
Physical exam
Weight
Height
BMI
BP
Waist circumference
235
Q

Ix for newly diagnosed HIV pos

A
Confirmatory test HIV1/2
Test for primary HIV (avidity)
VL
Drug resistance
CD4
HepA ing
Hep B
Hep B ab
STI
Measles/varicella ab
FBC
U+E
LFT
Bone profile
Dip urine
Ur pr/cr ratio if pos
HLA B5701
Viral tropism if considering CCR5 inhibitor
QRrisk if over 40
FRAX- ver 50/postmenopausal/high risk
?IGRA (TB)

Smear- women
Rubella

236
Q

What additional considerations in first 3 months for newly diagnosed HIV?

A
MH
Neurocognitive problems
Social hx
Employment
Immigration status
237
Q

ARV treatment failure?

A

Inadequate response to initial regimen with
-Less than a 1 log reduction in VL by week 4 on therapy
-OR failure to suppress VL to <50 copies/ml within 4-6 months of initiation of therapy
Or
-Persistent viral load rebound where previously <50 copies/ml and either low-level viraemia >50 and <400 copies/ml or sustained viral load rebound to >400 copies/ml

238
Q

HIV transmitted drug resistance ARV

A

Global prevalence of HIV drug resistance (HIVDR) is rising, mainly due to resistance to NNRTI drugs

239
Q

Which ARV are less prone to resistance?

A

Newer ARVs and drug classes, such as the integrase inhibitor, dolutegravir, have much higher genetic barriers to resistance.

And PIs?

240
Q

Mutations that confer resistance to ARV?

A

For some drugs, such as the NRTI lamivudine and all NNRTIs, just one mutation – notably the M184V or K103N mutations – can result in high-level drug resistance.

K65R and M184V can confer resistance to 2 drugs in PREP

K103N is the most common resistant mutation to NNRTIs- can cause efavirenz or nevirapine failure

241
Q

Types of resistance testing in HIV?

A

Genotypic resistance testing

Genotype tests look at the specific genetic sequence within the viral DNA to assess whether there has been any change in structure compared to a ‘wild type’ virus (a viral sample with no genetic mutations or drug resistance). This type of test will detect specific mutations within the genetic structure of the virus.

Phenotypic resistance testing

Phenotype tests look at the impact of mutations on resistance in practice. They test the dose of antiretroviral drugs needed in order for viral replication to stop (testing each drug separately).

242
Q

What drives HIV drug resistance?

A

Patient factors- not taking their drugs as prescribed, increasing their risk of developing drug resistant mutations.

Programme factors- challenges arising from the delivery of HIV treatment programmes

Drug stock-outs, where people cannot get their drugs because the pharmacy doesn’t have their treatment,

Drug and treatment regime factors

Regime and drug-specific factors refer to the selection of ARV that may increase or decrease the likelihood of HIVDR, with different types of drugs and drug classes having varying genetic barriers to resistance

NNRTI-based treatment regimens are still commonly prescribed as first-line treatment , and while these drugs are effective, they are more susceptible to drug resistance over other treatment regimens – such as boosted PI-based or integrase-based regimes.

Providing treatment in one single-pill fixed-dose means people are more likely to adhere to their drug taking regime; it also makes it easier for drug procurement.

Sub-optimal prescribing of ARVs, such as single tablet nevirapine or zidovudine for pregnant women, as well as use of just one of two types of drug for HIV therapy also increase the risk of HIVDR as they allow for mutations to occur in the presence of drugs already in the body.

Viral factors

Virus-related factors refer to resistance that arises by nature of the HIV type or subtype that may affect a drug regime. For example, HIV-2 is intrinsically resistant to NNRTIs, so people with this strain of HIV should not have NNRTIs included in their regime.

Also, some evidence suggests that thymidine analog mutations – caused by the drugs zidovudine and stavudine – may develop more quickly in people with HIV subtype C. These cannot be helped on their own, but if the healthcare provider is aware, they can control the progressions of drug resistance by addressing other drivers.

243
Q

Types of HIV drug resistance?

A

Transmitted HIVDR (TDR) – occurs when an uninfected, treatment-naïve person is infected with a drug-resistant strain of HIV from someone with HIVDR mutations.

Acquired HIVDR (ADR) – occurs when a treatment-experienced person living with HIV develops drug mutations in the presence of ART as a result of sub-optimal treatment adherence, treatment interruptions, inadequate drug concentrations in the body, or the use of suboptimal drugs and combinations.

Pre-treatment HIVDR (PDR) – HIVDR that is detected at the time of first-line ART initiation or re-initiation, that could be due to transmitted drug resistance, or HIVDR acquired as a result of previous ARV exposure, such as mothers and children in prevention of mother-to-child transmission programmes (PMTCT).

244
Q

HIV dug resistance

A

PrEP is not directly linked to the emergence of HIVDR
But regular testing for HIV while on PrEP is important to ensure that people aren’t inadvertently taking suboptimal HIV treatment should they become HIV-positive while on PrEP.

245
Q

HIV risk of transmission?

A

Risk that source is HIV positive x risk per exposure

eg. receptive UPAI with ?HIV source in london

Risk= 12.5/100 (prevalence in london) x 1/65 (risk HIV UPAI Rec)

= 12.5/6500= 1/520

246
Q

Which ARV are enzyme inducers and can’t give with contraception?

A

NEAR

Nevirapine
Efavirenz
Atazanavir
Ritonavir