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Infection > HIV and AIDS > Flashcards

HIV and AIDS Flashcards

1
Q

Immunology of HIV infection

A

Virus has a surface glycoprotein which binds to CD4 glycoprotein on the surface of the host cells
The most important target for the virus is the CD4-bearing lymphocytes which the virus infects and subsequently destroys

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2
Q

What does the progressive destruction of CD4+ lymphocyte population correspond to?

A

Disease progression from HIV infection

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3
Q

What is the normal CD4 lymphocyte count?

A

500-1500 cells/mm^3

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4
Q

A patient is asymptomatic from HIV infection until the CD4 lymphocyte count is at what level?

A

< 200 cells/m^3 - below this level the patient’s risk of opportunistic infection and tumour disease rises dramatically

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5
Q

Patient signs and symptoms which indicate progression of HIV infection

A

Weight loss
Lymphadenopathy
Thrush
Skin and oral disease

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6
Q

When should patients with HIV be started on antivirals?

A

If CD4 < 350

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7
Q

When should PCP prophylaxis for HIV patients be started?

A

When CD4 < 200

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8
Q

Why should a one off cell count not form the basis for treatment of a patient with suspected HIV?

A

The absolute cell count can fall in a healthy patient with an intercurrent infection so treatment should be based on a series of results

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9
Q

What is the HIV viral load like?

A

Initially high during acute infection but usually falls to a low level, only rising again in the later stages of the disease - usually after 6-8 years of infection

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10
Q

How is the HIV viral load quantified?

A

Using PCR assay to measure the number of RNA copies per ml blood, also now used to measure patient response to antiviral treatment

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11
Q

When might a change in antivirals need to be considered?

A

If the viral load is not suppressed to < 40 copies per ml blood with current combination

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12
Q

What factors influence the disease progression of HIV?

A

Age
HLA type
History of seroconversion illness

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13
Q

Rate of progression of HIV if untreated

A

25% to early symptoms after 5 years and 50-70% to severe symptoms and opportunistic infections after 10 years if untreated

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14
Q

What receptor has been studied and is now a target for drug treatment of HIV?

A

Chemokine receptor 5 (CCR-5)

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15
Q

How do HIV infected patients with a single CCR-5 mutation respond to HIV infection compared to others?

A

Appear to have a slower rate of HIV disease progression

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16
Q

Presentation of primary HIV infection

A

Rash
Fever
Pharyngitis
Lymphadeopathy

Similar to glandular fever presentation

May also develop diarrhoea, meningitis or neuropathy

Self-limiting illness

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17
Q

Investigations to be done in primary HIV infection

A

Blood should be taken early in its course and during the convalescent period to test for HIV antibody
HIV viral load testing

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18
Q

What are the typical features of the early and late blood samples taken during a primary HIV infection?

A

Early sample will be antibody negative but antigen positive

Late sample will usually be antibody positive, but this may take up to three months to develop after the illness

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19
Q

HIV viral load testing is sufficiently sensitive to allow detection of

A

HIV during seroconversion and before the development of antibodies

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20
Q

Severe or prolonged seroconversion illness is recognised as

A

a poor prognosticator, correlating to more rapid disease progression

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21
Q

What are the two distinct virus types that HIV can be classified into, and which is more common?

A

HIV 1 and HIV 2

HIV 2 is much less common

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22
Q

Laboratory aspects of HIV infection

A

Causes persistent infection of cells

Easily inactivated by heat, drying and disinfectants

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23
Q

How do HIV 1 and 2 work?

A

Replicate via a DNA intermediate step using the viral enzyme reverse transcriptase
Conversion of RNA to DNA is an error-prone process
The errors cannot be corrected so result in virus diversity
GIV attachments to cells, reverse transcriptase and viral enzymes are all targets for HIV drugs

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24
Q

Main diagnostic method for determining whether a person is infected with HIV

A

combined test for HIV antigen and HIV antibody

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25
Q

How long after exposure might a combined antigen and antibody test take to become positive?

A

Up to 3 months

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26
Q

When should a person be considered infectious?

A

A person positive for HIV antigen/antibody should be considered infectious, but a negative HIV antigen/antibody test does not exclude infection if there may have been exposure in the previous 3 months

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27
Q

What does HIV viral load test do?

A

Quantifies the amount of the virus in the blood

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28
Q

When is the viral load high?

A

During the window period of infection when antibody is absent

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29
Q

Main use of HIV viral load

A

monitor effectiveness of antiretroviral therapy

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30
Q

When are tests for viral nucleic acid used?

A

To diagnose infection in babies of HIV-infected women, as the passive maternal antibody can persist for 15 months, making diagnosis using HIV antigen/antibody test difficult

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31
Q

What is involved in HIV resistance testing?

A

Looking for specific nucleic acid changes associated with resistance to the individual antiretroviral agents, aids decision on optimal therapy

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32
Q

What led to the description of the acquired immune deficiency syndrome (AIDS)?

A

In 1981, two previously very rare diseases in young men in the USA - pneumonia and Kaposi’s sarcoma - were noticed to be occurring in homosexual men, indicating that some sort of immunodeficiency was occurring in previously fit homosexual men

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33
Q

How may people are affected by HIV worldwide?

A

34 million, over 90% living in the developing world

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34
Q

How is HIV spread and what are its modes of transmission?

A

Spread by blood and body fluids

Modes of transmission;
sex
blood
mother-to-child

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35
Q

What is the commonest route of transmission of HIV in adults globally?

A

Heterosexual transmission

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36
Q

Modes of transmission relate directly to

A

prevention strategies for transmission

Also relate to groups at high risk for HIV

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37
Q

Examples of groups of people at high risk for HIV infection

A

Homosexual and bisexual men
IVDA
Those who have had sex with someone from a high prevalence area
Recipients of unscreened blood, blood products, tissue or organ (not in the UK)
Sexual contact with a person at risk
Child of HIV-infected mother

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38
Q

What are the risks of transmission of HIV to a healthcare worker following a significant percutaneous exposure, if no preventative action is taken?

A

Approximately 30% for a source positive for hepatitis B surface and E antigens
3% for a source positive for hepatitis C RNA
0.3% for a source positive for HIV

39
Q

Are the risks of transmission greater following percutaneous or mucocutaneous exposure?

A

Mucocutaneous

40
Q

What are the body fluids which should be handled with the same precaution as blood?

A 
CSF 
Pleural, peritoneal and pericardial fluid 
Exudate or tissue fluid from burns or skin lesions 
Breast milk 
Amniotic fluid 
Vaginal secretions
Semen 
Synovial fluid 
Any fluid containing visible blood 
Saliva
41
Q

What immediate actions should be taken after blood/body fluid exposure?

A

Wash off splashes on skin with soap and running water
Encourage bleeding if skin has been broken
Wash out splashes in eyes, nose or mouth
Assessment of risk of virus transmission by someone other than the victim
Report the incident

42
Q

Factors to be considered in risk assessment

A

Source of contamination
Extent of injury and how it was caused
Likelihood of hepatitis B or C or HIV in the source
Hepatitis B vaccination status of the victim

43
Q

By what percentage can combination antiretroviral therapy decrease the risk of HIV infection?

A

80%

44
Q

When should combination antiretroviral therapy be started following possible exposure to HIV?

A

Ideally within 1 hour, but still worthwhile up to 72 hours post-exposure, generally not recommended beyond 72 hours

45
Q

Immunisations available for Hepatitis B

A

Active - recombinant

Passive - hepatitis B immunoglobulin

46
Q

Immunisations available for hepatitis C

A

No vaccine, immunoglobulin or antiviral therapy for post-exposure prophylaxis available

47
Q

When testing an identified source, when should post-exposure prophylaxis for HIV (if indicated) be started?

A

Before the test results

48
Q

Early diagnosis and treatment of hepatitis C is associated with

A

higher likelihood of cure

49
Q

Steps to avoiding exposure to blood-borne viruses in the health care setting

A

Use of good hygiene practices with regular hand washing
Cover existing wounds/skin lesions with waterproof dressings
Take simple protective measures to avoid contamination of person and clothing
Protect mucus membranes
Prevent puncture wounds, cuts and abrasions in presence of blood
Avoid sharps where possible
Use safe procedure for sharps handling and disposal
Clear up spillage of blood and body fluids promptly and disinfect contaminated surfaces
Dispose of contaminated waste safely

50
Q

When should infected pregnant women be started on therapy?

A

Before the third trimester

51
Q

When is the three drug combination adjusted?

A

If viral load is not adequately suppressed after 4-6 weeks of therapy

52
Q

Current life expectancy of patients diagnosed at age 20 with CDF counts of;
< 100
100-200
> 200

A

< 100 - 52 years old

100-200 - 62 years old

> 200 - 70+ years old

53
Q

How long is HIV treatment?

A

Lifelong

54
Q

Once the virus penetrates the host cell, what happens?

A

It releases RNA which must be converted to DNA to allow incorporation into the host genome - this process is known as reverse transcriptase

55
Q

What was the first group of drugs with activity against HIV?

A

Nucleoside reverse transcriptase inhibitors

  • zidovudine
  • didanosine
  • zalcitabine
  • lamivudine
  • stavudine
  • abacavir
56
Q

What is the possible consequence of nucleoside reverse transcriptase inhibitors therapy?

A

They are nucleoside analogues which interfere with the function of many healthy host cells, including marrow cells, so marrow toxicity is a frequently encountered adverse effect

57
Q

What was the first drug to be licensed for HIV treatment?

A

Zidovudine

58
Q

When is zidovudine particularly useful?

A

In reducing transmission of infection from mother to infant during pregnancy and in stopping the development of AIDS dementia

59
Q

In what time would patients taking zidovudine monotherapy develop resistant strains of HIV?

A

Within 18 months of starting treatment

60
Q

What class of drugs is currently used as first line treatment in combination with nucleoside analogues?

A

Non-nucleoside reverse transcriptase inhibitors

61
Q

How do non-nucleoside reverse transcriptase inhibitors work?

A

Act on the reverse transcriptase enzyme at a different site from the nucleoside analogues, sometimes better tolerated

62
Q

What is the commonest side effect of the non-nucleoside reverse transcriptase inhibitor efavirenz?

A

Vivid dreams/nightmares

63
Q

How do protease inhibitors work?

A

Inhibit the virus protease enzyme which cleaves polyproteins into proteins which are required for viral maturation - most potent group of antivirals

64
Q

Why might the benefit of protease inhibitors be short-lived if given alone?

A

Resistance can develop

65
Q

What is a possible side effect of protease inhibitor use?

A

Raised cholesterol levels occur in many patients taking this group of drugs, can have implications for development of premature vascular disease

66
Q

How do integrase inhibitors work?

A

Act by preventing viral DNA integration into the CD4+ cell chromosome

67
Q

Give an example of an integrase inhibitor

A

Raltegravir

68
Q

How do chemokine receptor antagonists work?

A

Act by interfering with the interaction between HIV and CCR-5

69
Q

How do fusion inhibitors work?

A

Inhibit the attachment of the virus to host cells, preventing virus entry into cells and viral replications, have to be administered as injections currently

70
Q

When do most clinicians introduce three drugs in treatment of HIV?

A

When patients develop symptoms or laboratory markers which suggest disease progression

71
Q

What current techniques and development should make it possible in the future to know which drugs the virus will respond to before treatment is started and which ones it is resistant to after treatment fails?

A

Laboratory techniques which allow the analysis of HIV for detection of the genetic mutations associated with resistance to reverse transcriptase inhibitors or protease inhibitors

72
Q

Why is compliance important in HIV treatment?

A

Poor drug compliance and intermittent dosing will promote viral resistance.
Studies show that patients need to be > 95% compliant to achieve the optimum effect of their drug regime

73
Q

Side effects of HIV drugs

A 
Lipodystrophy (stavudine, AZT) 
Anaemia (AZT)
Pancreatitis (esp didanosine)
Neuropathy (esp stavudine)
Hepatitis (esp nevirapine)
Drug interactions (protease inhibitors and NNRTIs)
74
Q

What is lipodystrophy?

A

Loss of subcutaneous fat from the face and limbs with redistribution to the breasts and abdomen, significantly altering the patient’s appearance

75
Q

Side effects of nucleoside reverse transcriptase inhibitors

A

Marrow toxicity
Neuropathy
Lipodystrophy

76
Q

Side effects of non-nucleoside reverse transcriptase inhibitors

A

Skin rashes
Hypersensitivity
Drug interactions

77
Q

Side effects of protease inhibitors

A

Drug interaction
Diarrhoea
Lipodystrophy
Hyperlipidaemia

78
Q

Side effects of integrase inhibitors

A

Rashes

79
Q

Challenges of HIV care

A 
Ageing population 
Osteoporosis 
Cognitive impairment 
Malignancy 
Cerebrovascular disease 
Renal impairment 
Ischaemic heart disease 
Diabetes mellitus
80
Q

HIV prevention

A 
Behaviour change 
Condoms 
Education 
Circumcision 
Treatment 
Pre-exposure prophylaxis 
Post-exposure prophylaxis for sexual exposure
81
Q

Skin manifestations of HIV

A 
Seborrheic dermatitis 
Molluscum contagiosum 
Shingles 
Recurrent varicella zoster virus 
Recurrent genital, perianal or oral herpes, often severe and extensive
82
Q

Oral manifestations of HIV

A

Oral hairy leukoplakia (OHL)

Oral candidiasis

83
Q

Tumours associated with HIV

A

Kaposi’s sarcoma

Lymphoma

84
Q

Features of Kaposi’s sarcoma

A

Vascular tumour arising from endothelium
Develops in multifocal way
No obvious spread through blood or lymphatics
Skin is commonest site, also occurs on hard palate, in gut and in bronchi

85
Q

Cause of Kaposi’s sarcoma

A

Herpes virus - Kaposi’s associated virus (KAV)

86
Q

Transmission of KAV

A

Probably sexual or through close contact

87
Q

Treatment of Kaposi’s sarcoma

A

Effective HIV antiviral treatment can often lead to resolution

88
Q

Common sites of Lymphoma in HIV

A

B cell lymphoma at many unusual sites e.g. gut and soft tissue, cerebral lymphoma is the most commonly seen

89
Q

Prognosis of lymphoma in HIV

A

Extremely poor as most patients are intolerant of chemotherapy, best approach may be to use highly active antiretroviral therapy in combination with chemotherapy

90
Q

Features of primary HIV infection

A

Asymptomatic

Acute retroviral syndrome

91
Q

Features of HIV clinical stage 1

A

Asymptomatic

Persistent generalised lymphadenopathy

92
Q

Features of HIV clinical stage 2

A 
Moderate unexplained weight loss, < 10% of presumed or measured body weight 
Recurrent RTI e.g. sinusitis, tonsillitis
Herpes zoster infection 
Angular cheilitis 
Recurrent oral ulceration 
Papular pruritic eruptions 
Seborrheic dermatitis 
Fungal nail infections
93
Q

Features of HIV clinical stage 3

A

Unexplained severe weight loss > 10% presumed or measured body weight
Unexplained chronic diarrhoea for > 1 month
Unexplained persistent fever for > 1 month
Persistent oral candidiasis
Oral hairy leukoplakia
Pulmonary tuberculosis
Severe presumed bacterial infections
Acute necrotising ulcerative stomatitis, gingivitis or periodontitis
Unexplained anaemia
Neutropenia
Chronic thrombocytopenia

94
Q

Features of HIV clinical stage 4

A 
HIV wasting syndrome 
Pneumocystis pneumonia 
Recurrent severe bacterial pneumonia 
Chronic HSV infection 
Oesophageal candidiasis 
Extrapulmonary TB 
Kaposi sarcoma
Cytomegalovirus infection 
CNS toxoplasmosis 
HIV encephalopathy 
Cryptococcosis extrapulmonary 
Disseminated non-TB mycobacteria infection 
Progressive multifocal leukoencephalopathy 
Candida of the trachea, bronchi or lungs 
Chronic cryptosporidiosis
Chronic isosporiasis 
Disseminated mycosis 
Recurrent non-typhoidal salmonella bacteraemia 
Lymphoma 
Invasive cervical carcinoma 
Atypical disseminated leishmaniasis 
Symptomatic HIV associated nephropathy/cardiomyopathy 
Reactivation of American trypanosomiasis

Infection (14 decks)

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