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HIV Flashcards

1
Q

What is HIV?

A

A retrovirus

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2
Q

What is AIDs?

A

Syndrome caused by HIV
Opportunistic infections
AIDs related cancers

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3
Q

Is AIDs preventable?

A

Yes; by early HIV diagnosis and treatment

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4
Q

Is HIV preventable?

A

Yes; there is pre and post exposure prophylaxis

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5
Q

What are the 2 different types of HIV?

A

HIV-2; originated in west africa (known as simian immunodeficiency virus). Noone in Tayside with HIV-2
HIV-1; originated in Central/West African Chimps
HIV-1 group M was responsible for the global pandemic in 1981

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6
Q

What immune cells does HIV target?

A

CD4+ receptors

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7
Q

What are CD4?

A 
Glycoprotein found on the surface of cells including: 
T helper lymphocytes
Dendritic cells
Macrophages
Microglial cells
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8
Q

What is the purpose of CD4+ T helper cells?

A 
Induction of adaptive immune response
Recognition of MHC 2 antigen presenting cells
Activation of B cells
Activation of CD8+ T cells
Cytokine release
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9
Q

What are those with HIV infection susceptible to?

A

Viral infections
Fungal infections
Mycobacterial infection
Infection-induced cancers

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10
Q

What effect does HIV infection have on the immune response?

A

Sequestration of cell in lymphoid tissue (reduced CD4+ T cells circulating)
Reduced proliferation of CD4+ T cells
Reduction in CD8+ T cells (dysregulated expression of cytokines, increasing susceptibility to viral infections)
Reduction in antibody class switching
Chronic immune activation

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11
Q

What is a normal CD4+ T count?

A

500-1600 cells/mm3

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12
Q

What CD4 count correlates with a risk of opportunistic infections?

A

<200

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13
Q

When is HIV viral replication at its highest?

A

Very early and very late infection

New generation every 6-12 hours

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14
Q

When will viral load tend to peak (coincides with lowest CD4 count)?

A

6 weeks

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15
Q

How will HIV spread?

A

Infection of mucosal CD4 cells (langerhans anc dendritic cells)
Transport to regional lymph nodes
Infection established within 3 days of entry
Dissemination of virus

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16
Q

Why is the 72 hour period crucial in the early stages of HIV?

A

You can give post exposure prophylaxis in this time period to prevent HIV progressing

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17
Q

When will symptoms tend to present after infection?

A

2-4weeks

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18
Q

What are the symptoms of HIV infection?

A 
Fever
Rash (maculopapular) 
Myalgia
Pharyngitis
Headache/ aseptic meningitis
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19
Q

What is going on in asymptomatic HIV infection?

A

Ongoing viral replication
Ongoing CD4 count
Ongoing immune activation
Risk of onward transmission if remains undiagnosed

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20
Q

What is an opportunistic infection?

A

An infection caused by a pathogen that does not normally produce disease in a healthy individual
It uses the “opportunity” afforded by a weakened immune system to cause disease

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21
Q

What organism causes pneumocystis pneumonia?

A

Pneumocystis Jiroveci

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22
Q

What is the CD4 threshold for pneumocystis pneumonia?

A

<200

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23
Q

What are the symptoms and signs of pneumocystis pneumonia?

A

Insidious onset
SOB
Dry cough
Exercise desaturation

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24
Q

What can be seen on CXR with pneumocystis pneumonia?

A

Normal
Interstitial infiltrates
reticulonodular markings

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25
How is pneumocystis pneumonia diagnosed?
BAL and immunofluorescence | +/- PCR
26
What is the treatment of pneumocystis pneumonia?
High dose co-trimoxazole +/- steroid
27
Is prophylaxis given for pneumocystis pneumonia?
Yes; if CD4 count <200 start low dose co-trimoxazole
28
In terms of TB and HIV, what is more common in HIV+ individuals?
``` Symptomatic primary infection Reactivation of latent TB Lymphadenopathies Miliary TB Extrapulmonary TB Multi-drug resistant TB Immune reconstitution syndrome ```
29
What is the issue with HIV with concurrent TB?
Drug-drug interactions between antiretrovirals and TB drugs
30
Which organism causes cerebral toxoplasmosis?
Toxoplasma gondii
31
What is the CD4 threshold for cerebral toxoplasmosis?
<150
32
What can cerebral toxoplasmosis cause?
Reactivation of latent infection | Multiple cerebal abscess - chorioretinitis
33
What are the sy/si of cerebral toxoplasmosis?
``` Headache Fever Focal neurology Seizures Reduced conciousness Raised ICP ```
34
What is the CD4 threshold for CMV?
<50
35
What can CMV cause?
Retinitis Colitis Oesophagitis
36
What is the presentation of CMV?
``` Reduced visual acuity Floaters Abdo pain Diarrhoea PR bleeding ```
37
What is the guidelines surrounding ophthalmic screening in HIV?
All individuals with a CD4 <50 should receive ophthalmic screening
38
How will herpes zoster present in HIV +ve patients?
Multidermatomal | Recurrent
39
How will herpes simplex present in HIV +ve patients?
Extensive Hypertrophic Aciclovir resistant
40
How will HPV present in HIV +ve patients?
Extensive Recalcitrant Dysplasitc
41
What organism causes HIV assoc neurocognitive impairment?
HIV-1
42
What is the CD4 threshold for HIV assoc neurocognitive impairment?
Any | Increased incidence with increased immunosuppression
43
What is the presentation of HIV assoc neurocognitive impairment?
Reduced short term memory | Motor dysfunction
44
What organism causes Progressive Multifocal Leukoencephalopathy (PML)?
JC virus
45
What is the CD4 threshold for PML?
<100
46
What is the presentation of PML?
Rapidly progressing Focal neurology Confusion Personality changes
47
What are common opportunistic infections seen in HIV?
``` Pneumocystis pneumonia TB Cerebral toxoplasmosis CMV Herpes zoster Herpes simplex HPV PML ```
48
Apart from HIV assoc neurocognitive impairment and PML how can HIV present neurologically?
``` Distal sensory polyneuropathy Mononeuritis multiplex Vacuolar myelopathy Aseptic meningitis GBS Viral meningitis (CMV, HSV) Cryptococcal meningitis Neurosyphilis ```
49
What is the aetiology behind HIV assoc wasting?
``` Metabolic (chronic immune activation) Anorexia (multifactorial) Malabsorption Diarrhoea Hypogonadism ```
50
What causes Kaposi's Sarcoma?
HHV 8
51
What is the pathogenesis of kaposi's sarcoma?
Vascular tumour
52
What is the CD4 threshold for kaposi's sarcoma?
Any | Increased incidence with increased immunosuppression
53
What is the presentation of kaposi's sarcoma?
Cutaneous Mucosal Visceral; pulmonary, GI
54
What is the treatment of Kaposi's Sarcoma?
HAART Local therapies Systemic chemo if visceral
55
What virus causes non-hodgkin's lymphoma in HIV +ve patients?
EBV (also assoc with burkitt's lymphoma and primary CNS lymphoma)
56
What is the presentation of non-hodgkin's lymphoma?
``` More advanced B symptoms Bone marrow involvement Extranodal disease Increased CNS involvement ```
57
What is the CD4 threshold for non-hodgkin's lymphoma?
Increased incidence with increased immunosuppression
58
What organism causes cervical cancer in HIV?
HPV Persistence of HPV infection Rapid progression to severe dysplasia and invasive disease
59
Who should HIV testing be offered to in terms of cervical dysplasia?
HPV disease Recalcitrant warts High grade; CIN, VIN, AIN, PIN
60
What symptoms are generally present in the "asymptomatic" period of HIV?
``` Mucosal candidiasis Seborrhoeic dermatitis Diarrhoea Fatigue Worsening psoriasis Lymphadenopathy Parotitis Epidemiologically linked conditions; STIs, hep B, hep C ```
61
What are the haematological manifestations of HIV?
Anaemia (up to 90%) | Thrombocytopenia (ITP)
62
What are the AIDs related cancers?
Kaposi's sarcoma Non-hodgkin's lymphoma Cervical cancer; VIN, CIN2 or higher
63
What is the main mode of HIV transmission?
Sexual; 95% 53% in MSM 42% men and women
64
What are factors that increase the transmission risk of HIV sexually?
Anoreceptive sex Trauma Genital ulceration Concurrent STI
65
How can HIV be transmitted parenterally?
PWID Infected blood products Iatrogenic
66
How can HIV be passed from mother to child?
``` In utero/ trans placental Delivery Breast feeding 1 in 4 at risk babies become infected 1 in 3 HIV+ infants will die before first birthday ```
67
What is the total number of people living with HIV in the UK?
104,000 Prevalence is 1.6/1000 7% undiagnosed
68
Which group is highest risk for HIV in the UK?
MSM
69
Who should be tested for HIV?
Universal testing in high prevalence areas Opt-out testing in certain clinical settings Screening in high risk groups Testing in the presence of clinical indicaors
70
What is universal testing for HIV?
In high prevalence areas in the UK (>0.2%), HIV testing is recommended to all general medical admissions and all new patients registering at GP
71
Which services are involved in out-out HIV testing?
``` Termination of pregnancy services GUM clinics Drug dependence services Antenatal services Assisted conception services ```
72
Which high risk groups are screened for HIV?
``` MSM Female partners of bisexual men PWID Partners of people living with HIV Adults from endemic areas Children from endemic areas Sexual partners from endemic areas History of iatrogenic exposure in endemic area ```
73
What are high prevalence areas for HIV?
Sub-saharan africa Caribbean Thailand
74
When should HIV testing be performed under clinical grounds?
When HIV falls within the DD, a HIV test should be performed regardless of risk factors
75
How can consent be obtained for a HIV test?
Explain to patient they are being offered a HIV and why Benefits of testing; improve long term health, protect partner(s) How and when receive results Reassure re: confidentiality
76
How is a HIV test taken?
Document consent or refusal Obtain venous sample for serology Request via ICE Ensure pathway in place for retrieving and communicating result If incapacitated: only take if in patients best interest, consent from relative not required, if safe wait until patient regains capacity
77
What marker of HIV is used by labs to detect infection?
Antibodies take 3 months | So we now look for p24 markers
78
What is a 3rd generation HIV test?
HIV1 and HIV2 antibodies; detects IgG and IGM Very sensitive/ specific in established infections Window period; 20-25 days
79
What is a 4th generation HIV test?
Combined antibody and antigen (p24) Shortens window period Window period; 14-28 days
80
Describe a 4th generation test and a window period?
A negative 4th generation test performed at 4 weeks following an exposure is highly likely to exclude HIV infection
81
What is a rapid HIV test?
Finger Prick blood specimen or saliva Results within 20-30 mins 3rd gen (Ab only) or 4th gen (Ab/Ag)
82
Advantages of rapid HIV test?
``` Simple No lab No venipuncture No anxious wait Reduce follow up Good sensitivity ```
83
Disadvantages of rapid HIV test?
``` Expensive Quality control Poor predictive value in low prevalence settings Not suitable for high volume Not so reliable in early infection ```
84
What should you do when someone first presents with HIV?
``` Staging infection Opportunistic infections OI prophylaxis Psychological/ emotional support Education HIV treatment Mode of acquisition STI screening Partner notification Prevention medicine/ vaccinations Prevention of onward transmission ```
85
What should be sent in someone with HIV who tests positive for rectal chlamydia?
LGV serology
86
What conditions commonly co-exist with HIV?
``` Hep b/c Syphilis STI Schistosomiasis TB ```
87
What are the targets for antiretroviral drugs?
``` Reverse transcriptase Integrase Protease Entry; fusion and CCR5 receptor Maturation ```
88
What is HAART - exam q?
A combination of 3 drugs from at least 2 drug classes to which the virus is susceptible
89
What is the purpose of HAART?
Reduce viral load to undetectable Restore immunocompetence Reduce morbidity and mortality
90
Describe the HIV replication cycle?``
1: fusion of HIV to the host cell surface 2: HIV RNA , reverse transcriptase, integrase and other viral proteins enter the host cell 3: Viral DNA is formed by reverse transcriptase 4: viral DNA is transported across the nucleus and integrates into the host DNA New viral RNA is used as genomic RNA and to make viral proteins 6: new viral RNA and proteins move to cell surface, and a new, immature HIV forms 7: virus is released. Viral protease cleaves new polyproteins to create mature infectious virus
91
What are the 7 HIV drug classes?
Non-nucleoside reverse transcriptase inhibitors Nucleoside reverse transcriptase inhibitors Protease inhibitors Fusion inhibitors CCR5 antagonists Integrase strand transfer inhibitors Post-attachment inhibitors
92
What is the mode of action of NNRTIs and NRTIs?
Block conversion of HIV RNA to HIV DNA
93
What is the mode of action of protease inhi1bitors?
Block protease which prevents new HIV from becoming mature and therefore able to infect other CD4 cells
94
What makes up truvada?
Emtricitabine Tenofovir Both NRTIs
95
What is truvada used for?
PrEP
96
What is a common single tablet co-formulation used in HIV?
Tenofovir (NRTI) Emtricitabine (NRTI) Efavirenz (NNTRI)
97
What adhernace is required to prevent resistance in HIV?
95%
98
What helps to prevent HIV resistance?
``` Adherence Lifestyle Tolerability Pharmacokinetics Drug-drug interaction Treatment interruptions ```
99
What would make the perfect ARV?
``` Tolerability Low toxicity Low pill burden Low dosing frequency Minimal drug-interactions High barrier to resistance ```
100
What are the GI side effects of HAART (commonly protease inhibitors)?
Transaminitis | Fulminant hepatitis
101
What are common skin side effects of HAART (abacavir, nevirapine)?
Rash Hypersensitivity SJS
102
What are common CNS side effects of HAART (efavirenz)?
Mood - suicidal ideation n Psychosis Insomina
103
What are common renal side effects of HAART (tenofovir, atazanavir)?
Proximal renal tublopathies
104
What are common bone side effects of HAART (tenofovir)?
Osteomalacia
105
What are common CVS side effects of HAART (abacavir, lopinavir, maraviroc)?
Increased MI risk
106
What are common haematological side effects of HAART (zidovudine)?
Anaemia | Majority of people with HIV have anaemia be that due to HIV itself or the drug
107
Describe the effect of HAART on liver enzymes?
Protease inhibitors are potent liver enzyme inhibitors NNRTIs are potent liver enzyme inducers Some drugs require pharma boosting with potent liver enzyme inhibitors
108
What is the issue with hep C and TB co-infections?
Drug interactions with hepatitis and TB treatment
109
What vaccines are given to those with HIV?
Hep A/B Flu Pneumococcus HPV
110
Is partner notification voluntary?
Yes
111
What are the different methods of partner notification?
Partner referral Provider referral Conditional referral
112
What are barriers to PN and disclosure?
Fear; rejection, isolation, violence Confidentiality Stigma
113
How does stigma manifest?
Discrimination | Ostracism
114
How can onward HIV transmission be prevented?
``` Condom use HIV treatment STI screening and treatment Sero-adaptive sexual behaviours; risk of transmission lower when receptive anal sex in MSM Disclosure PEP PrEP ```
115
When can PEP be taken?
72 hours after expsoure
116
What is the guidelines surrounding reproduction with HIV positive male or females?
Treatment as prevention; if either partner has an undetectable viral load then it CANNOT be transmitted...adding PrEP will make no difference
117
How can mother to child transmission of HIV be prevented?
``` HAART during pregnnacy Vaginal delivery if undetected viral load C section if detected viral load 4/52 PEP for neonate Exclusive formula feeding ```
118
When is viral load measured in pregnant women to help determine vaginal or c section?
36 weeks
119
What is the risk of MTCT is viral load undetectable at birth?
<0.1% risk
120
What are the HIV prevention strategies?
``` Needle exchange Testing and treatment for STIs Condom programmes PEPSE Circumcision PrEP Treatment as prevention ```
121
What is the UN AIDs target for 2020?
90-90-90 90% aware of HIV status 90% on HIV treatment 90% virally suppressed
122
What is the risk reduction of HIV transmission when PrEP is used?
86% efficacy
123
What is the PrEP eligibility criteria?
High risk for HIV; HIV+ partner with detectable viral load OR MSM who have UPAI > 2 partner in 12/12 and likely to do so again in next 3/12 OR confirmed bacterial rectal STI in last 12/12 Patient eligibility: Aged >16 AND can commit to 3/12'ly follow up AND willing to stop is eligibility criteria no longer apply AND resident in Scotland

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