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Repro and Sexual Health > HIV > Flashcards

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
Q

How is pneumocystis pneumonia diagnosed?

A

BAL and immunofluorescence

+/- PCR

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26
Q

What is the treatment of pneumocystis pneumonia?

A

High dose co-trimoxazole +/- steroid

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27
Q

Is prophylaxis given for pneumocystis pneumonia?

A

Yes; if CD4 count <200 start low dose co-trimoxazole

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28
Q

In terms of TB and HIV, what is more common in HIV+ individuals?

A 
Symptomatic primary infection 
Reactivation of latent TB
Lymphadenopathies
Miliary TB
Extrapulmonary TB
Multi-drug resistant TB
Immune reconstitution syndrome
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29
Q

What is the issue with HIV with concurrent TB?

A

Drug-drug interactions between antiretrovirals and TB drugs

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30
Q

Which organism causes cerebral toxoplasmosis?

A

Toxoplasma gondii

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31
Q

What is the CD4 threshold for cerebral toxoplasmosis?

A

<150

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32
Q

What can cerebral toxoplasmosis cause?

A

Reactivation of latent infection

Multiple cerebal abscess - chorioretinitis

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33
Q

What are the sy/si of cerebral toxoplasmosis?

A 
Headache
Fever
Focal neurology
Seizures
Reduced conciousness
Raised ICP
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34
Q

What is the CD4 threshold for CMV?

A

<50

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35
Q

What can CMV cause?

A

Retinitis
Colitis
Oesophagitis

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36
Q

What is the presentation of CMV?

A 
Reduced visual acuity
Floaters
Abdo pain 
Diarrhoea
PR bleeding
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37
Q

What is the guidelines surrounding ophthalmic screening in HIV?

A

All individuals with a CD4 <50 should receive ophthalmic screening

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38
Q

How will herpes zoster present in HIV +ve patients?

A

Multidermatomal

Recurrent

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39
Q

How will herpes simplex present in HIV +ve patients?

A

Extensive
Hypertrophic
Aciclovir resistant

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40
Q

How will HPV present in HIV +ve patients?

A

Extensive
Recalcitrant
Dysplasitc

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41
Q

What organism causes HIV assoc neurocognitive impairment?

A

HIV-1

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42
Q

What is the CD4 threshold for HIV assoc neurocognitive impairment?

A

Any

Increased incidence with increased immunosuppression

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43
Q

What is the presentation of HIV assoc neurocognitive impairment?

A

Reduced short term memory

Motor dysfunction

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44
Q

What organism causes Progressive Multifocal Leukoencephalopathy (PML)?

A

JC virus

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45
Q

What is the CD4 threshold for PML?

A

<100

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46
Q

What is the presentation of PML?

A

Rapidly progressing
Focal neurology
Confusion
Personality changes

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47
Q

What are common opportunistic infections seen in HIV?

A 
Pneumocystis pneumonia
TB
Cerebral toxoplasmosis
CMV 
Herpes zoster
Herpes simplex 
HPV 
PML
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48
Q

Apart from HIV assoc neurocognitive impairment and PML how can HIV present neurologically?

A 
Distal sensory polyneuropathy
Mononeuritis multiplex
Vacuolar myelopathy
Aseptic meningitis 
GBS
Viral meningitis (CMV, HSV)
Cryptococcal meningitis
Neurosyphilis
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49
Q

What is the aetiology behind HIV assoc wasting?

A 
Metabolic (chronic immune activation) 
Anorexia (multifactorial) 
Malabsorption
Diarrhoea
Hypogonadism
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50
Q

What causes Kaposi’s Sarcoma?

A

HHV 8

51
Q

What is the pathogenesis of kaposi’s sarcoma?

A

Vascular tumour

52
Q

What is the CD4 threshold for kaposi’s sarcoma?

A

Any

Increased incidence with increased immunosuppression

53
Q

What is the presentation of kaposi’s sarcoma?

A

Cutaneous
Mucosal
Visceral; pulmonary, GI

54
Q

What is the treatment of Kaposi’s Sarcoma?

A

HAART
Local therapies
Systemic chemo if visceral

55
Q

What virus causes non-hodgkin’s lymphoma in HIV +ve patients?

A

EBV (also assoc with burkitt’s lymphoma and primary CNS lymphoma)

56
Q

What is the presentation of non-hodgkin’s lymphoma?

A 
More advanced
B symptoms
Bone marrow involvement
Extranodal disease
Increased CNS involvement
57
Q

What is the CD4 threshold for non-hodgkin’s lymphoma?

A

Increased incidence with increased immunosuppression

58
Q

What organism causes cervical cancer in HIV?

A

HPV
Persistence of HPV infection
Rapid progression to severe dysplasia and invasive disease

59
Q

Who should HIV testing be offered to in terms of cervical dysplasia?

A

HPV disease
Recalcitrant warts
High grade; CIN, VIN, AIN, PIN

60
Q

What symptoms are generally present in the “asymptomatic” period of HIV?

A 
Mucosal candidiasis
Seborrhoeic dermatitis
Diarrhoea
Fatigue
Worsening psoriasis
Lymphadenopathy
Parotitis
Epidemiologically linked conditions; STIs, hep B, hep C
61
Q

What are the haematological manifestations of HIV?

A

Anaemia (up to 90%)

Thrombocytopenia (ITP)

62
Q

What are the AIDs related cancers?

A

Kaposi’s sarcoma
Non-hodgkin’s lymphoma
Cervical cancer; VIN, CIN2 or higher

63
Q

What is the main mode of HIV transmission?

A

Sexual; 95%
53% in MSM
42% men and women

64
Q

What are factors that increase the transmission risk of HIV sexually?

A

Anoreceptive sex
Trauma
Genital ulceration
Concurrent STI

65
Q

How can HIV be transmitted parenterally?

A

PWID
Infected blood products
Iatrogenic

66
Q

How can HIV be passed from mother to child?

A 
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
Q

What is the total number of people living with HIV in the UK?

A

104,000
Prevalence is 1.6/1000
7% undiagnosed

68
Q

Which group is highest risk for HIV in the UK?

A

MSM

69
Q

Who should be tested for HIV?

A

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
Q

What is universal testing for HIV?

A

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
Q

Which services are involved in out-out HIV testing?

A 
Termination of pregnancy services
GUM clinics
Drug dependence services
Antenatal services
Assisted conception services
72
Q

Which high risk groups are screened for HIV?

A 
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
Q

What are high prevalence areas for HIV?

A

Sub-saharan africa
Caribbean
Thailand

74
Q

When should HIV testing be performed under clinical grounds?

A

When HIV falls within the DD, a HIV test should be performed regardless of risk factors

75
Q

How can consent be obtained for a HIV test?

A

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
Q

How is a HIV test taken?

A

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
Q

What marker of HIV is used by labs to detect infection?

A

Antibodies take 3 months

So we now look for p24 markers

78
Q

What is a 3rd generation HIV test?

A

HIV1 and HIV2 antibodies; detects IgG and IGM
Very sensitive/ specific in established infections
Window period; 20-25 days

79
Q

What is a 4th generation HIV test?

A

Combined antibody and antigen (p24)
Shortens window period
Window period; 14-28 days

80
Q

Describe a 4th generation test and a window period?

A

A negative 4th generation test performed at 4 weeks following an exposure is highly likely to exclude HIV infection

81
Q

What is a rapid HIV test?

A

Finger Prick blood specimen or saliva
Results within 20-30 mins
3rd gen (Ab only) or 4th gen (Ab/Ag)

82
Q

Advantages of rapid HIV test?

A 
Simple
No lab
No venipuncture
No anxious wait
Reduce follow up
Good sensitivity
83
Q

Disadvantages of rapid HIV test?

A 
Expensive
Quality control
Poor predictive value in low prevalence settings
Not suitable for high volume
Not so reliable in early infection
84
Q

What should you do when someone first presents with HIV?

A 
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
Q

What should be sent in someone with HIV who tests positive for rectal chlamydia?

A

LGV serology

86
Q

What conditions commonly co-exist with HIV?

A 
Hep b/c 
Syphilis
STI
Schistosomiasis
TB
87
Q

What are the targets for antiretroviral drugs?

A 
Reverse transcriptase
Integrase
Protease
Entry; fusion and CCR5 receptor
Maturation
88
Q

What is HAART - exam q?

A

A combination of 3 drugs from at least 2 drug classes to which the virus is susceptible

89
Q

What is the purpose of HAART?

A

Reduce viral load to undetectable
Restore immunocompetence
Reduce morbidity and mortality

90
Q

Describe the HIV replication cycle?``

A

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
Q

What are the 7 HIV drug classes?

A

Non-nucleoside reverse transcriptase inhibitors
Nucleoside reverse transcriptase inhibitors
Protease inhibitors
Fusion inhibitors
CCR5 antagonists
Integrase strand transfer inhibitors
Post-attachment inhibitors

92
Q

What is the mode of action of NNRTIs and NRTIs?

A

Block conversion of HIV RNA to HIV DNA

93
Q

What is the mode of action of protease inhi1bitors?

A

Block protease which prevents new HIV from becoming mature and therefore able to infect other CD4 cells

94
Q

What makes up truvada?

A

Emtricitabine
Tenofovir
Both NRTIs

95
Q

What is truvada used for?

A

PrEP

96
Q

What is a common single tablet co-formulation used in HIV?

A

Tenofovir (NRTI)
Emtricitabine (NRTI)
Efavirenz (NNTRI)

97
Q

What adhernace is required to prevent resistance in HIV?

A

95%

98
Q

What helps to prevent HIV resistance?

A 
Adherence 
Lifestyle
Tolerability 
Pharmacokinetics
Drug-drug interaction 
Treatment interruptions
99
Q

What would make the perfect ARV?

A 
Tolerability
Low toxicity
Low pill burden
Low dosing frequency
Minimal drug-interactions
High barrier to resistance
100
Q

What are the GI side effects of HAART (commonly protease inhibitors)?

A

Transaminitis

Fulminant hepatitis

101
Q

What are common skin side effects of HAART (abacavir, nevirapine)?

A

Rash
Hypersensitivity
SJS

102
Q

What are common CNS side effects of HAART (efavirenz)?

A

Mood - suicidal ideation n
Psychosis
Insomina

103
Q

What are common renal side effects of HAART (tenofovir, atazanavir)?

A

Proximal renal tublopathies

104
Q

What are common bone side effects of HAART (tenofovir)?

A

Osteomalacia

105
Q

What are common CVS side effects of HAART (abacavir, lopinavir, maraviroc)?

A

Increased MI risk

106
Q

What are common haematological side effects of HAART (zidovudine)?

A

Anaemia

Majority of people with HIV have anaemia be that due to HIV itself or the drug

107
Q

Describe the effect of HAART on liver enzymes?

A

Protease inhibitors are potent liver enzyme inhibitors
NNRTIs are potent liver enzyme inducers
Some drugs require pharma boosting with potent liver enzyme inhibitors

108
Q

What is the issue with hep C and TB co-infections?

A

Drug interactions with hepatitis and TB treatment

109
Q

What vaccines are given to those with HIV?

A

Hep A/B
Flu
Pneumococcus
HPV

110
Q

Is partner notification voluntary?

A

Yes

111
Q

What are the different methods of partner notification?

A

Partner referral
Provider referral
Conditional referral

112
Q

What are barriers to PN and disclosure?

A

Fear; rejection, isolation, violence
Confidentiality
Stigma

113
Q

How does stigma manifest?

A

Discrimination

Ostracism

114
Q

How can onward HIV transmission be prevented?

A 
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
Q

When can PEP be taken?

A

72 hours after expsoure

116
Q

What is the guidelines surrounding reproduction with HIV positive male or females?

A

Treatment as prevention; if either partner has an undetectable viral load then it CANNOT be transmitted…adding PrEP will make no difference

117
Q

How can mother to child transmission of HIV be prevented?

A 
HAART during pregnnacy
Vaginal delivery if undetected viral load
C section if detected viral load
4/52 PEP for neonate
Exclusive formula feeding
118
Q

When is viral load measured in pregnant women to help determine vaginal or c section?

A

36 weeks

119
Q

What is the risk of MTCT is viral load undetectable at birth?

A

<0.1% risk

120
Q

What are the HIV prevention strategies?

A 
Needle exchange
Testing and treatment for STIs
Condom programmes
PEPSE
Circumcision 
PrEP
Treatment as prevention
121
Q

What is the UN AIDs target for 2020?

A

90-90-90
90% aware of HIV status
90% on HIV treatment
90% virally suppressed

122
Q

What is the risk reduction of HIV transmission when PrEP is used?

A

86% efficacy

123
Q

What is the PrEP eligibility criteria?

A

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

Repro and Sexual Health (77 decks)

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