HIV Flashcards

1
Q

What does HIV cause?

A

The Acquired Immunodeficiency Syndrome (AIDS)

+ Opportunistic infections
+ AIDS-related cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the single highest predictor of mortality in AIDS?

A

AIDS-related conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What proportion of deaths in AIDS are caused by a late diagnosis?

A

1/4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

People with HIV have a ‘near-normal’ life expectancy

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

HIV infection is not preventable

A

FALSE - it is preventable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of virus is HIV?

A

A retrovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where did HIV 2 originate?

A

West Africa – Sootey mangabey (simian immunodeficiency virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Is HIV 1 or 2 less virulent?

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where did HIV 1 originate?

A

Central/West African chimpanzees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What was responsible for the global pandemic starting in 1981?

A

HIV 1 group M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the target site for HIV?

A

CD4+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CD4 (Cluster of Differentiation) is a glycoprotein found on the surface of a range of cells. Give examples of such cells.

A
  • T helper lymphocytes (“CD4+ cells”)
  • Dentritic cells
  • Macrophages
  • Microglial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are CD4+ Th Lymphocytes essential for?

A

The induction of the adaptive immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What roles in particular do CD4+ Th Lymphocytes carry out to achieve their aim of adaptive immune response induction?

A
  • Recognition of MHC2 antigen-presenting cell
  • Activation of B-cells
  • Activation of cytotoxic T-cells (CD8+)
  • Cytokine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List conditions that people with HIV have susceptibility to.

A
  • Viral infections
  • Fungal infections
  • Mycobacteria infections
  • Infection induced cancers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What effect does HIV infection have on immune response?

A
  • Cessation of cells in lymphoid tissue
  • Reduced proliferation of CD4+ cells
  • Reduction of CD8+ T cell activation
  • Reduction in antibody class switching
  • Chronic immune activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens to CD4+ cells in AIDS?

A

They essentially just stop replicating and die.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe microbial translocation.

A

Because the gut is full of lymphoid tissue, it is attacked first.

It can then no longer protect itself, and bits of bacterial cells leak across the gut.
this leads to chronic immune activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the normal parameters for CD4+ Th cells?

A

500-1600 cells/mm3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What level of CD4+ Th cells confers risk for opportunistic infections?

A

<200 cells/mm3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When does rapid replication of the HIV virus occur?

A

In very early and very late infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How often is there a new generation?

A

Every 6-12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the average time to death without treatment?

A

9-11 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Outline how infection goes from initial infection to dissemination.

A
  • Infection of mucosal CD4 cell.
  • Transport to regional lymph nodes.
  • Infection established within 3 days of entry.
  • Dissemination of virus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name 2 examples of mucosal CD4+ cells.

A

Langerhans and dendritic cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Up to what % present with symptoms?

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

When is the average onset of sx of primary HIV infection?

A

2-4 weeks after infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the primary symptoms of a HIV infection?

A
  • Fever.
  • Rash (maculopapular).
  • Myalgia.
  • Pharyngitis.
  • Headache/aseptic meningitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What can a primary HIV infection often be mistaken for?

A

Glandular fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the danger with primary HIV infection?

A

There is a very high risk of transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What happens during the asymptomatic phase of HIV infection?

A
  • Ongoing viral replication.
  • Ongoing CD4 count depletion.
  • Ongoing immune activation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is there a risk of during the asymptomatic stage of HIV?

A

Onward transmission if remains undiagnosed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the definition of ‘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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the causative organism in Pneumocystis Pneumonia?

A

Pneumocystis jiroveci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the causative organism in Pneumocystis Pneumonia?

A

Pneumocystis jiroveci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What symptoms are associated with Pneumocystis Pneumonia?

A
  • Insidious onset.
  • SOB.
  • Dry cough.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What symptoms are associated with Pneumocystis Pneumonia?

A
  • Insidious onset.
  • SOB.
  • Dry cough.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the MAIN sign associated with Pneumocystis Pneumonia?

A

Exercise desaturation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How may Pneumocystis Pneumonia appear on CXR?

A
  • May be normal.
  • Interstitial infiltrates, reticulonodular markings.

(looks a bit like cardiac failure, but without cardiac enlargement)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What methods are used to diagnose Pneumocystis Pneumonia?

A

BAL and immunofluorescence +/- PCR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How is Pneumocystis Pneumonia treated?

A

With high dose co-trimoxazole (+/- steroid).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the prophylactic treatment of Pneumocystis Pneumonia?

A

Low dose co-trimoxazole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the relationship between HIV and TB.

A

EPIDEMIOLOGICAL SYNERGY!

People who are HIV + are more likely to get TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What organism is associated with cerebral toxoplasmosis?

A

Toxoplasma gondii (associated with cat litter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the CD4 threshold for cerebral toxoplasmosis?

A

<150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Outline 2 important features of cerebral toxoplasmosis in HIV.

A
  • REACTIVATION OF LATENT INFECTION

- MULTIPLE CEREBRAL ABSCESSES (chorioretinitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Outline the signs and symptoms of cerebral toxoplasmosis.

A
  • Headache.
  • Fever.
  • Focal neurology.
  • Seizures.
  • Reduced consciousness.
  • Raised intracranial pressure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What organism is responsible for cyclomegalovirus?

A

CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the CD4 threshold for Cyclomegalovirus?

A

<50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What can CMV virus also cause?

A
  • Retinitis
  • Colitis
  • Oesophagitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How may CMV infection present?

A
  • Reduced visual acuity
  • Floaters
  • Abdo pain, diarrhoea, PR bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is therefore mandatory for all individuals with CD4<50?

A

Ophthalamic screening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Herpes zoster is _____ dermatomal and _________

A

Multi

Recurrent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Herpes simplex is hypertrophic

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Herpes simplex is resistant to acyclovir

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What organism is responsible for HIV associated neurocognitive impairment?

A

HIV - 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the CD4 threshold for HIV associated neurocognitive impairment?

A

Any

Increased incidence with increased immunosuppression though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does HIV associated neurocognitive impairment present with?

A

Reduced short term memory +/- motor dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the causative organism in Progressive Multifocal Leukoencephalopathy?

A

JC virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the CD4 threshold for the development of Progressive Multifocal Leukoencephalopathy?

A

<100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How does Progressive Multifocal Leukoencephalopathy present?

A
  • Rapidly progressing focal neurology.
  • Confusion.
  • Personality change. (causes demyelination)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is cachexia in HIV known as?

A

‘Slims’ disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Slims disease has multiple causes, list some of these.

A
  • Metabolic – chronic immune activation.
  • Anorexia – multifactorial.
  • Malabsorption/diarrhoea.
  • Hypogonadism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What organism is responsible for AIDS related Kaposi’s sarcoma?

A

Human herpes virus 8 (HHV 8).

65
Q

In the pre-ART era, what % of people with AIDS developed Kaposi’s sarcoma?

A

Up to 40%

66
Q

What is Kaposi’s sarcoma?

A

A vascular tumour

67
Q

What is the CD4 threshold for Kaposi’s sarcoma?

A

Any – but increased incidence with increased immunosuppression.

68
Q

How does Kaposi’s sarcoma present?

A

As spongy raised nodules or papules (vascular tumours) on CUTANEOUS, MUCOSAL and VISCERAL (ie. pulmonary, GI) surfaces.

69
Q

How is Kaposi’s sarcoma treated?

A
  • If just on skin – treating HIV with HAART should help.
  • Local therapies.
  • Systemic chemotherapy.
70
Q

What organism is responsible for AIDS related non-hodgkins lymphoma?

A

EBV (Burkitt’s lymphoma, primary CNS lymphoma).

71
Q

What is the CD4 threshold for AIDS related non-hodgkins lymphoma?

A

Any - but incidence increases with immunosuppression

72
Q

How does non-hodgkins lymphoma present?

A
  • More advanced B symptoms
  • Bone marrow involvement
  • Extranodal disease
  • ↑ CNS involvement
73
Q

How is non-hodgkins lymphoma treated?

A

As for HIV, with the addition of HAART

74
Q

What organism is responsible for AIDS related cervical cancer?

A

HPV

75
Q

What is the difference between HPV infection in people with HIV compared to non-affected individuals?

A
  • Persistence of HPV infection.

* Rapid progression to severe dysplasias and invasive disease.

76
Q

How often should women with HIV be screened for HPV

A

Every year, rather than every 3 years

77
Q

Now, all MSM <45 are vaccinated against HPV due to risk of anal cancers

A

TRUE

78
Q

HIV testing should be offered to all complicated HPV disease, give examples?

A
  • Recalcitrant warts

* High grade CIN, VIN, AIN, PIN

79
Q

List some non-opportunistic symptoms/sources of symptoms in HIV.

A
  • Mucosal candidiasis
  • Seborrhoeic dermatitis
  • Diarrhoea
  • Fatigue
  • Worsening psoriasis (as this is CD8-mediated)
  • Lymphadenopathy
  • Parotitis
  • Epidemiologically linked conditions
  • STIs
  • Hepatitis B
  • Hepatitis C
80
Q

What can haematological manifestations be caused by?

A
  • HIV.
  • Opportunistic infections (MAI).
  • AIDS-malignancies.
  • (HIV drugs)
81
Q

What is the CD4 threshold of haem manifestations?

A

Any

82
Q

ANAEMIA AFFECTS UP TO 90% of people with AIDS

A

TRUE

83
Q

What % of all HIV infections in the UK does sexual transmission account for?

A

94%

84
Q

What % of new infections in the UK does this account for?

A

96%.

  • Sex between men (51%).
  • Sex between women (45%).
85
Q

What factors increase the risk of sexual transmission of HIV?

A
  • Anoreceptive sex. (the anus has lots of CD4 cells)
  • Trauma.
  • Genital ulceration.
  • Concurrent STI.
86
Q

What type of cells are plentiful in the anus?

A

CD4

87
Q

Outline the ways in which there is parental transmission of HIV.

A
  • Injection drug use (sharing ‘works’).
  • Infected blood products.
  • Iatrogenic.
88
Q

When may mother-to-child transmission of HIV occur?

A
  • In utero/trans-placental.
  • During delivery.
  • During breastfeeding.
89
Q

What proportion of at-risk babies will become infected with HIV?

A

1 in 4

90
Q

What proportion of HIV+ infants will die before their first birthday if untreated?

A

1 in 3

91
Q

In the UK, what is the risk of MTCT in the uk i) overall ii) when viral load undetected at delivery?

A

i) 1.2%.

ii) <0.1%.

92
Q

How many MSM have AIDS?

A

1 in 20

93
Q

How many MSM have AIDS in London?

A

1 in 8

94
Q

Who is the risk group with the highest proportion of HIV in the UK?

A

MSM (1:26 outside London and 1:8 in London).

95
Q

What % of individuals living with HIV in the UK are undiagnosed?

A

17%

96
Q

Who is most likely to be undiagnosed with HIV?

A

Heterosexual men

97
Q

Who are most likely to present late with HIV?

A

Heterosexual men

98
Q

HIV in PWID’ is UNCOMMMON

A

TRUE

99
Q

Where is universal screening of HIV done?

A

In high prevalence areas

100
Q

Testing in the UK is done in the presence of clinical indicators

A

YES

101
Q

When is universal screening recommended?

A

In high prevalence areas in the UK, where local prevalence is >0.2% (2/1000).

102
Q

In universal testing, who are HIV tests recommended to?

A
  • All general medical admissions.

* All new patients registering at a GP.

103
Q

Tayside’s prevalence is <0.2% (~1.5/1000), so universal testing is not recommended.

A

TRUE

104
Q

Outline 5 situations where an op-out service for HIV testing is offered.

A
  • TOP service
  • GUM clinics
  • Drug dependancy services
  • Antenatal service
  • Assisted conception service
105
Q

Name 3 areas of high HIV prevalence.

A
  • Sub-Saharan Africa
  • Caribbean
  • Thailand
106
Q

What groups of people are offered HIV screening tests?

A
  • MSM
  • Females with bisexual partners
  • PWID
  • People with HIV + partners
  • Adults from endemic areas
  • Children from endemic areas
  • Sexual partners from endemic areas
  • History of iatrogenic exposure in endemic areas
107
Q

How do you obtain consent for a HIV test?

A
  1. Explain to patient they are being offered an HIV test and why (normalise)
  2. What the benefits of testing are
    (Improve long term health + Protect partner(s))
  3. How and when they can expect to receive results
  4. Reassure re: confidentiality
  5. Written information can be made available
108
Q

How should you, as a clinician, go about taking a HIV test?

A
  1. Document consent (or refusal).
  2. Obtain VENOUS sample for serology.
  3. Request via ICE (accelerate if clinically indicated).
  4. Ensure pathway in place for retrieving and communicating result
109
Q

What should you do if a patient is incapacitated but you want to do a HIV test?

A
  • Only test if in patient’s best interest.
  • Consent from relative not required.
  • If safe, wait until patient regains capacity.
  • Obtain support from HIV team if required.
110
Q

Which markers of HIV are used by labs to detect infection?

A
  • RNA
  • Capsule protein p24
  • Envelope proteins gp120
111
Q

What do HIV antibody tests detect?

A

HIV-1 and HIV-2 antibody  detect IgM and IgG

112
Q

When are antibody tests very sensitive/specific?

A

In established infection

113
Q

What is the average window period of antibody tests?

A

average of 20-25 days.

114
Q

What is the average window period of antibody tests?

A

Average of 20-25 days.

115
Q

What do 4th generation HIV tests test for?

A

Combined antibody and antigen (p24).

116
Q

By how much do 4th generation tests shorten the window period?

A

By ~5 days.

117
Q

Outline the variation quoted in the window period.

A

14-28 days.

Variability between assays.
Variability between labs.

118
Q

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

A

TRUE

119
Q

How is a rapid HIV test (POCT) done?

A

Fingerprick specimen or saliva.

120
Q

How long do results take for a POCT?

A

20-30 mins

121
Q

What are the 2 categories of POCT?

A

3rd generation – Ab only.
or
4th generation – Ab/Ag

122
Q

Outline the advantages of POCT.

A
  • Simple to use.
  • No lab required.
  • No venepuncture required.
  • No anxious wait.
  • Reduce follow-up.
  • Good sensitivity.
123
Q

What are the disadvantages of POCT?

A
  • Expensive ~£10
  • Quality control
  • Poor positive predictive value in low prevalence settings
  • Not suitable for high volume
  • Can’t be relied on in ?early infection
124
Q

What can RITA be used for?

A

To identify if an infection has occurred within the preceding 4-6months.

125
Q

What do RITA do?

A

Measure different types of antibodies or strength of antibody binding.

126
Q

What is the largest downfall of RITA?

A

Have a large margin of error

127
Q

Essentialy, what does RITA do?

A

This tests the antibody binding strength, and can tell you if an infection might be recent.

128
Q

What are the advantages of RITA?

A
  • Surveillance.
  • Local epidemiology.
  • Assess HIV testing programmes.
  • Inform partner notification.
  • Safer sex advice.
  • Interpretation of CD4.
129
Q

What are the disadvantages of RITA?

A
  • Accuracy.
  • Patient distress.
  • Criminalisation.
130
Q

What is CD4 a marker of?

A

How well the immune system is working

131
Q

What is there an increased risk of the more the CD4 count falls?

A

Opportunistic infection

132
Q

Outline the potential targets for anitviral drugs.

A
  • Reverse transcriptase.
  • Integrase.
  • Protease.
  • Entry – fusion, CCR5 receptor.
  • Maturation.
133
Q

What drugs have in-vitro effects against HIV?

A

Nucleoside analogues reverse transcriptase inhibitors (NRTI), e.g. zidovudine

134
Q

Dual NRTI therapy reduced mortality by 33%

A

TRUE

135
Q

The HIV virus is goof at developing resistance

A

TRUE

136
Q

What is HAART defined as?

A

A combination of three drugs from at least 2 drug classes to which the virus is susceptible.
(ie. drugs which work at two different points in the cycle)

137
Q

What is the purpose of HAART?

A
  • Reduce virus load to undetectable.
  • Restore immunocompetence.
  • Reduce morbidity and mortality.
  • Minimise toxicity (maximise tolerability).
138
Q

What is key to preventing drug resistance in HIV?

A

ADHERENCE
ADHERENCE
ADHERENCE

139
Q

Outline some key factors in an anti-viral wish list.

A
  • Tolerability.
  • Low toxicity.
  • Low pill burden.
  • Low dosing frequency.
  • Minimal drug-interactions.
  • High barrier to resistance.
140
Q

Generally, protease inhibitors are what?

A

Potent liver enzyme inhibitors

141
Q

Generally, NNRTI’s are potent what?

A

Liver enzyme inducers

142
Q

Some drugs require pharmacological boosting (with potent liver enzyme inhibitors)

A

TRUE

143
Q

Look at notes for HAARTS toxicity

A

Many HAART drugs cause side effects in different body systems

144
Q

Partner notification and disclosure of HIV is a _________ process

A

Voluntary

145
Q

What strategies may be used to encourage partner notification?

A
  • Partner referral.
  • Provider referral.
  • Conditional referral.
146
Q

Outline some barriers to partner notification and disclosure.

A
  • Fear (rejection, isolation, violence)
  • Confidentiality
  • Stigma
147
Q

What is stigma?

A

The shame or disgrace attached to something regarded as socially unacceptable

148
Q

How can sexual transmission of HIV be prevented?

A
  • Condom use
  • HIV treatment
  • STI screening and treatment
  • Sero-adaptive sexual behaviours
  • Disclosure
  • Post-exposure prophylaxis
  • Pre-exposure prophylaxis
149
Q

THERE IS NO RISK OF TRANSMISSION BY CASUAL/HOUSEHOLD CONTACT!!!!

A

True

150
Q

What are the conception options in a HIV+ male and HIV- female?

A
  • Treatment as prevention.

* PreP in female partner.

151
Q

What are the conception options in a HIV+ female and HIV- male?

A
  • Self-insemination.
  • Treatment as prevention.
  • PreP in male partner.
152
Q

What should be given during pregnancy to prevent mother to child transmission?

A

HAART

153
Q

How should baby be delivered if there is i) an undetected ii) a detected viral load?

A

i) Vaginal delivery.

ii) Caesarean section.

154
Q

What should be given to a neonate is their mother is HIV+?

A

4/52 PEP.

155
Q

What should be baby be fed with if its mother is HIV +?

A

Exclusive formula feeding

156
Q

What is the risk of MTCT in UK/Ireland?

A

<1%

157
Q

What is the risk of MTCT if viral load is undetected at delivery?

A

<0.1%

158
Q

HIV testing must be UPSCALED to reduce the undiagnosed fraction.

A

True