HIV Flashcards

1
Q

What is meant by a ‘retrovirus’?

A

Once inside the host cell it uses its own reverse transcriptase enzyme to produce DNA from its RNA genome

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2
Q

What HIV group was responsible for the global pandemic in 1981?

A

HIV-1 group M

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3
Q

Where is the CD4 glycoprotein found?

A

Surface of T-helper lymphocytes, macrophages and microglial cells

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4
Q

What cells are the target site for HIV?

A

CD4+ on T-helper lymphocytes

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5
Q

What are the functions of CD4+ T h lymphocytes?

A

Recognise MHC2 antigen presenting cell
Activation of B cells
Activation of cytotoxic T cells (CD8+)
Cytokine release

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6
Q

What is the normal CD4+ Th cell count?

A

500-1600 cells/ mm3

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7
Q

At what CD4+ Th cell count is there a high chance of infection?

A

<200 cells/ mm3

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8
Q

What affects does HIV have on immune resonse? 5 stages

A

Sequestration of cells in lymphoid tissue so reduced circulating CD4+ cells in blood stream
Reduced proliferation of CD4+ cells
Reduced CD8+ T cell activation - increased susceptibility to viruses
Reduced antibody switching
Chronic immune activation - leaky gut

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9
Q

What is the average time to death from HIV with no treatment?

A

9-11 years

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10
Q

How long after exposure to HIV does it take for the infection to become established?

A

3 days

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11
Q

When do the symptoms of the primary HIV infection show?

A

2-4 weeks after infection

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12
Q

What are the symptoms of the primary HIV infection?

A
Fever
Pharyngitis
Aseptic meningitis
Myalgia
Headache
Maculopapular rash on upper body
Often misdiagnosed as cold or flu
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13
Q

What occurs during the asymptomatic phase of HIV infection?

A

Ongoing viral replication, CD4+ count depletion and immune activation

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14
Q

What is an opportunistic infection?

A

Infection caused by a pathogen that does not normally produce disease in a healthy individual

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15
Q

What are examples of opportunistic infections in patients with HIV?

A
Pneumocystic pneumonia (PCP)
Tuberculosis
Cerebral toxoplasmosis
Cytomegalovirus
Skin infections
HIV-associated neurocognitive impairment
Progressive multi-focal leukoencephalopathy
Neurological presentation
HIV associated wasting
Kaposi's sarcoma 
Non-Hodgkin's lymphoma
Cervical cancer
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16
Q

What organism causes pneumocystic pneumonia?

A

Pneumocystis jiroveci (fungi)

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17
Q

At what CD4 count do HIV patients get pneumocystic pneumonia?

A

<200

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18
Q

What are the clinical features of pneumocystic pneumonia?

A

Insidious onset
SOB
Dry cough
Exercise desaturation

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19
Q

What does pneumocystic pneumonia show on CXR?

A

May be normal

Interstitial infiltrates and reticulonodular markings

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20
Q

How can pneumocystic pneumonia be diagnosed?

A
Bronchoalveolar lavage (BAL)
Immunofluorescence +/- PCR
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21
Q

How is pneumocystic pneumonia treated?

A

High dose co-trimoxazole +/- steroid

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22
Q

What organism causes cerebral toxoplasmosis?

A

Toxoplasma gondii

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23
Q

At what CD4 count do patients get cerebral toxoplasmosis?

A

<150

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24
Q

What are the signs and symptoms of cerebral toxoplasmosis?

A
Multiple cerebral abscesses
Headache
Fever
Focal neuro - weaknes
Seizures
Raised ICP
Chorioretinitis
Decreased consciousness
Multiple ring enhancing lesions
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25
Q

What infections does CMV cause?

A

Retinitis (most common)
Oesophagitis
Colitis

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26
Q

Whats does a CMV infection present with?

A
Reduced visual acuity
Floaters in eye
Abdo pain
Diarrhoea
PR bleed
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27
Q

What screening should be done for all patients with a CD4+ of less than 50

A

Ophthalmic screening

28
Q

What sort of skin infections do HIV patients get?

A
Herpes zoster
Herpes simplex
HPV
Pencilliosis
Histoplasmosis
29
Q

What virus causes progressive multifocal leukoencephalopathy?

A

JC virus (reactivation of latent infection)

30
Q

At what CD4 count do HIV patients present with progressive multifocal leukoencephalopathy?

A

<100

31
Q

How does progressive multifocal leukoencephalopathy present?

A

Rapidly progressive
Focal neurology
Confusion
Personality change

32
Q

What is HIV associated wasting?

A

Slim’s disease - cachexia

33
Q

What is the aetiology of HIV associated wasting?

A

Metabolic - chronic immune activation
Anorexia
Malabsorption/ diarrhoea
Hypogonadism

34
Q

What virus causes Kaposi’s sarcoma?

A

Human herpes virus 8 (HHV)

35
Q

How can Kaposi’s sarcoma present?

A

Cancer that is:
Cutaneous
Mucosal
Visceral (pulmonary, GI)

36
Q

What is the treatment for Kaposi’s sarcoma?

A

HAART
Liquid nitrogen
Systemic chemotherapy

37
Q

What causes non-Hodgkin’s lymphoma?

A

EBV - burkitt’s lymphoma, primary CNS lymphoma

38
Q

How does non-Hodgkin’s lymphoma present?

A

B symptoms
Bone marrow involvement
Extranodal disease
CNS involvement

39
Q

How is non-Hodgkin’s lymphoma treated?

A

HAART

40
Q

How often are women with HIV screened for cervical cancer?

A

Every year (instead of every 3)

41
Q

Why does psoriasis get worse in HIV?

A

CD8 cells

42
Q

Why does rheumatoid get better in HIV?

A

CD4 cells

43
Q

What are the modes of HIV transmission?

A

Sexual
Parenteral - drug use, infected blood products
Mother to child - in-utero, delivery, breast feeding

44
Q

Why is the rectum vulnerable to HIV?

A

Only 1 cell thick and full of lymphoid tissue

45
Q

How should a baby be delivered if the mother has a detectable viral load?

A

C-section

46
Q

What are the markers for testing HIV?

A

Viral RNA
Antigen (capsule protein p24)
Antibody (envelope proteins gp120)

47
Q

What is the window period of HIV?

A

Have HIV but test negative

48
Q

What is the window period of the 3rd generation HIV antibody tests?

A

20-25 days

49
Q

What is the window period of the 4th generation HIV antibody and antigen tests?

A

14- 28 days

50
Q

What is the rapid antigen test?

A

Fingerprick specimen or saliva

Results in 20-30mins

51
Q

What are the targets for the anti-retroviral drugs?

A
Reverse transcriptase
Integrate
Protease
Entry - fusion and CCR5 receptor
Maturation phase
52
Q

What type of drug is zidovudine?

A

Nucleoside analogue reverse transcriptase inhibitor (NARTI)

53
Q

Is zidovudine useful for asymptomatic patients?

A

No - does not improve survival when used as a monotherapy

54
Q

What does HAART stand for?

A

Highly Active Anti-Retroviral Therapy

55
Q

What is HAART?

A

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

56
Q

What are examples of HAART drugs?

A

Tenofovir
Emtricitabine
Efavirenz

57
Q

What are possible side effects of HAART?

A
GI
Skin - rash, hypersensitivity, Steven-Johnstons
CNS - mood, psychosis
Renal toxicities
Bone - osteomalacia
CVS - increased MI risk
Anaemia
58
Q

What HAART drugs cause GI side effects?

A

Protease inhibitors

Nevirapine

59
Q

What HAART drugs cause skin side effects?

A

Abacavir

Nevirapine

60
Q

What HAART drugs cause CNS side effects?

A

Efavirenz

61
Q

What HAART drugs cause renal side effects?

A

Tenofovir

Atazanavir

62
Q

What HAART drugs cause bone side effects?

A

Tenofovir

63
Q

What HAART drugs cause CVS side effects?

A

Abacavir
Lopinavir
Maraviroc

64
Q

What HAART drugs cause haem side effects?

A

Zidovudine

65
Q

How do HAART drugs interfere with the liver?

A

Protease inhibitors - liver enzyme inhibitors

NNRTIs - liver enzyme inducers