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Y4 Obstetrics and Gynaecology > HIV > Flashcards

HIV Flashcards

1
Q

What is HIV ?

A

It is a virus which when left untreated causes acquired immunodeficiency syndrome (AIDS)

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2
Q

What is the life-expectancy of someone with HIV?

A

Someone with treated HIV will have a near normal life expectancy because AIDS is prevented

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3
Q

What is the most common cause of HIV related morbidity & mortality ?

A
  • Late diagnosis - 13% of those in the UK are undiagnosed
  • This means there is time for HIV-related complications to develop
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4
Q

What are the 3 largest groups of people living with HIV in the UK?

A
  1. MSM
  2. Heterosexual people from sub-sahran africa
  3. PWID
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5
Q

What are the most common places in the world affected by HIV ?

A
  • Sub-saharan africa
  • Caribbean
  • South-east asia
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6
Q

What type of virus is HIV and what are the main sub-types

A
  • It is a retrovirus
  • 2 types - HIV-1 (most common globally) & HIV-2 (largely confined to africa)
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7
Q

What is the target sites of HIV virus in the body and what is the relevence of this

A

CD4+ receptors are the target site

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8
Q

What is CD4+ and where is it found ?

A

It is a glycoprotein found on the surfaces mainly of the following cells:

  • T-helper lymphocytes
  • Dendritic cells
  • Macrophages
  • Microglial cells (immune cells in the CNS)
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9
Q

What is the function of CD4+ Th lymphocytes ?

A

CD4+ Th lymphocytes are essential for induction of the adaptive immune response, they recognise MHC2 antigen presenting cells & then activate B cells (these turn into antibodies), macrophaes, & killer T cells. They also release cytokines which tell macrophages & other lymphocytes etc to come over & help

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10
Q

Describe the stages of HIV infection and development into AIDS

A
  • Initial exposure - infection of mucosal CD4+ cell (dendiritic cell), virus is then transported by these cells to regional lymph nodes, infection becomes established within 3 days of exposure (short window to cure patient)
  • Primary infection phase - this is the first 6 months following exposure
  • Asymptomatic phase - this can last ≥ 10years
  • Constitutional symptoms develop just before AIDS
  • Development of AIDS
  • Death - takes 9-11 years without treatment
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11
Q

What effect does HIV infection have on the immune response ?

A
  • Sequestration of cells in lymphoid tissues ==> resulting in reduced circulating CD4+ cells
  • Reduced proliferation of CD4+ cells
  • Reduction CD8+ (cytotoxic) T cell activation - due to dysregulated expression of cytokines (cytokines needed to activate them recall function of CD4+ Th lymphocyte)
  • Reduction in B cells becoming antibodies
  • Chronic Immune Activation

These all lead to incresed susceptibility to infection & infection-induced cancers

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12
Q

What is the normal parameters of CD4+ Th cells and what counts shoud you be worried about getting opportunistic infections ?

A
  • Normal: 500-1600 cells/mm3
  • Risk of opportunistic infections when: <200 cells/mm3
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13
Q

What are the different ways in which HIV infection can be transmitted ?

A
  • Sexual intercourse (vaginal & anal)
  • Mother to child (in utero, during delivery & during breastfeeding)
  • PWID
  • Infected blood products
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14
Q

What are the clinical features of primary HIV infection and when do symptoms/signs usually occur after exposure ?

A

Symptoms usually occur 2-4 weeks after exposure and present with a combination of:

  • Fever
  • Rash (maculopapular)
  • Myalgia
  • Pharyngitis
  • Headache/aseptic meningitis
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15
Q

What is the risk of onward transmission of HIV during the primary infection stage ?

A

Very high - during this period there is uncontrolled viral replication (high HIV levels circulating)

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16
Q

During the primary infection stage of HIV what is happening to the CD4+ count ?

A

It is decreasing whilst the HIV levels are increasing

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17
Q

What clinical features during the asymptomatic stage of HIV infection may someone have ?

A

Persistent lymphadenopathy

Alos multiple niggly things which are easily overlooked:

  • Mucosal candidiasis
  • Sebhorrhoeic dermatitis
  • Diarrhoea
  • Fatigue
  • Worsening psoriasis
  • Parititis
  • STI’s
  • Hep B or C
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18
Q

During the asymptomatic phase of HIV infection what is happening to the CD4+ counts and HIV viral load ?

A
  • CD4+ counts still decreasing
  • HIV viral load increasing
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19
Q

Following the asymptomatic phase patients develop aids related complex - symptomatic HIV infection, what are the symptoms which patients presnet with?

A

Constitutional symptoms:

  • Fever
  • Night sweats
  • Diarrhoea decreased weight
  • Minor opportunisitic infections e.g. oral candida, hairy leukoplakia, herpes zoster, recurrent HSV, regular infections
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20
Q

What is AIDS charactersied by ?

A
  • Being HIV positive & having an indicator disease i.e. opportunistic infection
  • CD4+ count is also usually < 200 cells/mm3
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21
Q

Define what an opportunisitic infection is

A

This is an infection caused by a pathogen that does not normally produce disease in a healthy individual

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22
Q

What is by far the most common opportunisitc infection seen in HIV?

A

Pneumocystis pneumonia

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23
Q

What is the causative organism of Pneumocystis pneumonia ?

A

Pneumocystis jiroveci

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24
Q

Under what CD4+ count does a patient become susceptable to Pneumocystis pneumonia infection?

A

< 200

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25
Q

What are the signs/symptoms of Pneumocystis pneumonia infection?

A
  • SOB & dry cough over a number of weeks
  • Excercise desaturation - O2 sats <88% during exercise
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26
Q

How is Pneumocystis pneumonia diagnosed ?

A

BAL & Sputum immunofluorescence (gained via cough or broncoscopy) +/- PCR

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27
Q

What is the treatment of high Pneumocystis pneumonia infection ?

A

High dose co-trimoxazole +/- steroid (prednisolone) if severe hypoxia

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28
Q

What prophylatic treatment can be given to prevent further attacks of Pneumocystis pneumonia and when is this given ?

A

If CD4+ count < 200 then given low dose co-trimoxazole after 1st attack until CD4+ count is > 200

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29
Q

If a HIV +ve patient has cough, fever, night sweats or weight loss, what do they have until proven otherwise ?

A

TB

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30
Q

How is active TB diagnosed ?

A

CXR + multiple sputum samples for TB microscopy & culture

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31
Q

What is latnet TB infection ?

A

This is where you’ve been infected with TB but do not have any symptoms

32
Q

What investigations should be done for someone at risk of having latent TB i.e. those who have been in close contact of a person with pulmonary or laryngeal TB ?

A
  • 1st line = mantoux test if +ve then
  • 2nd line = assess for active TB
33
Q

What is the main CNS pathogen affecting AIDS patients ?

A

Cerebral toxoplasmosis

34
Q

What is the causative organism of cerebral toxoplasmosis ?

A

Toxoplasma gondii

35
Q

What are the signs/symptoms of cerebral toxoplasmosis ?

A
  • Headache
  • Fever
  • Focal neurology
  • Seizures
  • Reduced consciousness
  • Raised ICP
36
Q

What is the characteristic appearance seen on CT scan of cerebral toxoplasmosis ?

A

Multiple cerebral abcesses

37
Q

At what CD4+ count should you be worried about CMV infection ?

A

<50

38
Q

How can CMV infection present in HIV patients ?

A
  • Reduced visual acuity
  • Floaters
  • Abdo pain, diarrhoea, PR bleeding

Because it can cause retinitis, colitis and oesophagitis

39
Q

Why is opthalmic screening required for all individuals with a CD4+ count <50 ?

A

This is because CMV infection can lead to blindness

40
Q

Go over some of the skin infections which might make you think someone has HIV

A
  1. Herpes Zoster - Multidermatomal, Recurrent
  2. Herpes Simplex - Extensive, Hypertrophic, Aciclovir resistant not responding to tx
  3. Human papilloma virus - Extensive, Recalcitrant, Dysplastic
  4. Weird/wonderful infections - Penicilliosis, Histoplasmosis
41
Q

When HIV becomes disseminated throughout the body it also invades the brain & replicates causing inflammation & damage resulting in cognitive behavioural and motor difficulties, what is this condition called and what HIV virus causes this ?

A

Known as HIV-associated neurocognitive impairment caused by HIV-1

42
Q

What is the CD4+ threshold where HIV-associated neurocognitive impairment occurs ?

A

Any CD4+ count - its prevelence increasing with increasing immunosuppression (lower counts)

43
Q

What are the presenting features of HIV-associated neurocognitive impairment ?

A

Reduced short term memory +/- motor dysfunction (dementia & encephalopathy symptoms as these are the neurocognitive conditions essentially being caused by the HIV)

44
Q

What is progressive multifocal leukoencephalopathy ?

A

Progressive multifocal leukoencephalopathy (PML) is a rare and often fatal viral disease characterized by progressive damage (-pathy) or inflammation of the white matter (leuko-) of the brain (-encephalo-) at multiple locations (multifocal).

45
Q

What CD4+ counts should you worry about progressive multifocal leukoencephalopathy development ?

A

<100

46
Q

What is the causative organism of progressive multifocal leukoencephalopathy ?

A

JC virus

47
Q

What are the presenting features of progressive multifocal leukoencephalopathy ?

A
  • Rapidly progressing
  • Focal neurology
  • Confusion
  • Personality change
48
Q

List some of the other neurological manifestations of HIV besides PML and HIV-associated neurocognitive impairment

A
  • Distal sensory polyneuropathy
  • Mononeuritis multiplex
  • Vacuolar myelopathy
  • Aseptic meningitis
  • Guillan-Barre syndrome
  • Viral meningitis (CMV, HSV)
  • Cryptococcal meningitis
  • Neurosyphilis
49
Q

If a patient presents with meningitis and you cannot find the cause what may you consider testing for ?

A

HIV

50
Q

What is HIV associated wasting and the potential causes of it ?

A

It is weight loss of at least 10%

Has multiple aetiologies:

  • Metabolic (chronic immune activation) ==> increased resting energy ependiture
  • Anorexia (multifactorial e.g. painful oral, oesophageal complications)
  • Malabsorption/diarrhoea
  • Hypogonadism (decreased testosterone ==> decreased muscle mass etc)
51
Q

What are the 3 main AIDS related cancers ?

A
  1. Kaposis sarcoma
  2. Non-hodgkins lymphoma
  3. Cervical cancer
52
Q

Are kaposis sarcomas common in HIV patients now ?

A

They are much less common now, but did affect upto 40% pre-ART era

53
Q

What is the causative organism of kaposis sarcoma ?

A

Human herpesvirus 8

54
Q

What is the CD4+ count threshold for risk of development of kaposis sarcoma ?

A

Any, the incidence increases with increased immunosuppression

55
Q

Describe the presenting features of a kaposis sarcoma

A
  1. Cutaneous: Usually appears as spots on the skin (lesions) esp on the legs and face, which may be purple, red or brown (can appear anywhere)
  2. Mucosal: It can also develop on mucosal surfaces affecting the mouth & throat
  3. Visceral: The pulmonary (causing blockage or SOB) and GI tracts (causing abdo pain & diarrhoea) may also be affected

Note - you can get other features of cancer e.g. weight loss, haemoptysis, blood in stool, fatigue, anaemia

56
Q

What is the treatment of kaposis sarcoma ?

A
  • Optimise HAART +/- interferon-alpha
  • May need topical retinoids, cryotherapy or radiotherapy for skin lesions
  • Chemo may also be needed
57
Q

What is non-hodgkins lymphoma ?

A

This is a cancer which starts in lymphocytes (mainly B-cell lymphocytes)

58
Q

Infection with what is a risk factor for future non-hodgkins lymhoma development ?

A

EBV

59
Q

What is the CD4+ threshold for risk of non-hodgkins lymphoma development ?

A

Any, increases incidence with increasing immunosupression

60
Q

What are the presenting features of non-hodkins lymphoma ?

A
  • Lymphadenopathy
  • Fever
  • Night sweats
  • Fatigue, easy bruising, frequent infections

If affecting the abdomen - swelling or pain in abdo, loss of apetite

If affecting the chest - coughing, SOB, chest pain

If affecting the brain - headache, trouble thinking, focal neurology, personality change, seizures

If affecting the skin - appears as itchy red or purple bumps/lumps under the skin

61
Q

How is non-hodkins lymphoma diagnosed ?

A

Refer to haem - bloods, marrow & node biopsy

62
Q

What are the causative infections which greatly increase the risk of cervical cancer ?

A

HPV 16&18

63
Q

What should be offered to all patients with complicated HPV disease i.e:

  • Resistant/difficult to treat warts
  • High grade CIN
A

HIV testing

64
Q

What haematological manifestations may HIV patients present with ?

A
  • Anaemia - affects upto 90%
  • Thrombocytopenia (low platelets)
65
Q

What should patients with thombocytopenia be tested for ?

A

HIV

66
Q

What are the targerts for anti-retroviral drugs used in HIV treatment ?

A
  • Reverse transcriptase
  • Integrase
  • Protease
  • Entry - Fusion, CCR5 receptor
  • Maturation
67
Q

Why was mono&dual anti-retroviral therapy ineffective in HIV treatment ?

A

Because HIV is very good at developing resistance

68
Q

What is used to treat HIV and what is it

A

HAART therapy

This is a combination of ≥ 3 drugs from at least 2 classes to which the virus is susceptible

69
Q

What is the common intital HAART regime ?

A

2 NRTI’s + either a protease inhibitor or a non-NRTI

70
Q

List all the classes of anti-retroviral drug classes which can be used in HIV treatment

A
  • NRTI’s - abacavir, zidovudine, tenofovir,
  • Protease inhibitors - atazanavir, lopinavir
  • Integrease inhibitors
  • Non-NRTI’s - nevirapine, efavirenz
  • CCR5 antagnosits - maraviroc
71
Q

State which of the following side effects are caused by which anti-retroviral drug/drug class:

  • GI side-effects
  • Skin: rash, hypersensitivity, Stevens-Johnsons
  • CNS side-effects: mood, psychosis
  • Renal toxicity: proximal renal tubulopathies
  • Bone: osteomalacia
  • CVS: increased MI risk
  • Haematology: anaemia
  • GI: transaminitis, fulminant hepatitis
A
  • GI side-effects (protease inhibitors)
  • Skin: rash, hypersensitivity, Stevens-Johnsons (abacavir, nevirapine)
  • CNS side-effects: mood, psychosis (efavirenz)
  • Renal toxicity: proximal renal tubulopathies (tenofovir, atazanavir)
  • Bone: osteomalacia (tenofovir)
  • CVS: increased MI risk (abacavir, lopinavir, maraviroc)
  • Haematology: anaemia (zidovudine)
  • GI: transaminitis, fulminant hepatitis (nevirapine, most others)
72
Q

How soon should partner notification be completed by i.e. telling someone they could have transmitted onto

A

Ideally within 3 months - but may be persued further if there is clear timelines

73
Q

Due you have a duty of care to a known 3rd party in terms of partner notification?

A

Yes

74
Q

What steps should be taken to prevent onward HIV sexual transmission ?

A
  • Condom use
  • HIV treatment
  • STI screening and treatment
  • Sero-adaptive sexual behaviours
  • Disclosure
  • Post-exposure prophylaxis (PEP)
  • Pre-exposure prophylaxis (PREP)
75
Q

Is there any risk of onward HIV transmission from casual/household contact?

A

No

76
Q

For couples where one of them is HIV +ve what can be done to prevent onward transmission when trying to concieve ?

A

HIV+ male, HIV- female:

  • Treatment as Prevention
  • PreP in female partner

HIV+ female, HIV- male:

  • ? Self-insemination
  • Treatment as Prevention
  • PreP in male partner

If whoever is infected have a viral load which is undetectable for > 6 months then the risk is minuscule of transmitting the virus

77
Q

How is mother to child onward HIv transmission prevented during and after pregnancy ?

A
  • HAART during pregnancy
  • Vaginal delivery if undetected viral load
  • Caesarean section if detected viral load
  • 4/52 PEP for neonate
  • Exclusive formula feeding is the best way to feed

Y4 Obstetrics and Gynaecology (63 decks)

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