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Y3M - Infectious Disease > HIV > Flashcards

HIV Flashcards

1
Q

What is HIV?

A

A retrovirus that infects and replicates in CD4+ T-cells and macrophages.

This leads to progressive immune system dysfunction, opportunistic infection and malignancy = AIDS.

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2
Q

How is the virus transmitted?

A

Blood

Sexual fluids

Breast milk

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3
Q

Virus subtypes of HIV.

A

HIV1 global epidemic

HIV2 less pathogenic and predominantly West Africa

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4
Q

Explain pathophysiology of HIV.

A

HIV binds via its GP120 envelope glycoprotein to CD4 receptors on helper T cells, monocytes and macrophages.

These CD4 cells migrate to lymphoid tissue where the virus replicates.

They are released and in turn infect other CD4 cells.

As infection progresses there is depletion and impaired function of CD4 cells leading to impairment of immune function.

HIV encodes via reverse transcriptase which is very error prone and leading to treatment resistance.

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5
Q

Give ways of preventing HIV.

A

Preventing sexual transmission

Post-exposure prophylaxis

Pre-exposure prophylaxis

Preventing vertical transmission

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6
Q

Prevention of sexual transmission of HIV.

A

Condoms

Serosorting if unprotected sex (not very reliable)

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7
Q

Explain post-exposure prophylaxis of HIV.

A

Short-term use of ARVs after potential HIV exposure.

It can be given up to 72h after exposure.

1st line PEP in UK is Truvada (a mix of tenofovir and emtricitabine) and raltegravir for 28 days.

Test for HIV 8-12 weeks after exposure

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8
Q

Explain pre-exposure prophylaxis of HIV.

A

ARV treatment at high risk of acquiring HIV such as serodifferent relationships without suppression of viral load, and condomless anal sex in MSM.

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9
Q

Explain prevention of vertical transmission.

A

All pregnant women with HIV should have commenced ARVs by 24 weeks gestation.

Caesarean delivery is indicated if the viral load > 50 copies/mL.

Neonatal PEP is given from birth to 4ks of age with formula-feeding.

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10
Q

Presentation of early primary HIV infection.

A

80% are symptomatic typically 2-4 weeks after infection.

Flu-like symptoms and an erythematous/maculopapular rash.

Fever, rash, myalgia, pharyngitis, mucosal ulceration, lymphadenopathy and headache/aseptic meningitis.

HIV testing should be offered to anyone regardless of their risk if they show with the symptoms above.

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11
Q

Explain persistant generalised lymphadenopathy in primary HIV infection.

A

Swollen/enlarged lymph nodes > 1cm in two or more non-contiguous sites persisting for over 3 months.

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12
Q

Explain the HIV testing protocol.

A

Any doctor can consent for a HIV test.

Explain the benefits of testing and detail how results will be given.

Written consent is unnecessary.

Arrange a follow-up with a local HIV/GUM service within 2 weeks for patients testing positive for the first time.

You do not have to explicitly ask for permission to test for HIV.

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13
Q

Give ways of testing for HIV.

A

ELISA for HIV antibody and antigen

Rapid point-of-care testing

Viral load

Nucleic acid testing/viral PCR

CD4 count

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14
Q

Explain ELISA testing.

A

Tests for HIV antibody and p24 antigen.

This reduces the window period (aka the time of false-negatives between infection and the production of measurable antigen/antibody) to average around 10 days.

Diagnosis in UK is then confirmed by a confirmatory assay.

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15
Q

Explain rapid point-of-care testing.

A

Immunoassay kit which gives a rapid result from a finger-prick or mouth swab.

Only “CE”-marked kits should be used.

Serological confirmation is needed as well.

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16
Q

Explain viral load testing.

A

This gives a quantification of the HIV RNA.

It is also used to monitor the response to ARVs.

It is not diagnostic due to the possibility of false-positives.

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17
Q

Explain nucleic acid testing/PCR.

A

Qualitative testing for the presence of viral RNA.

IT is used to test for vertical transmission in neonates as placental transfer of maternal antibodies can affect ELISA antibody testing up to 18 months of age.

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18
Q

Explain CD4 count as testing for HIV.

A

This cannot diagnose HIV.

IT is used to monitor immune system function and disease progression in patients with HIV.

<200 cells/mcgL is one of the defining criteria of AIDS.

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19
Q

Prevention of needle stick injury in a patient with HIV.

A

Use safer sharps

Do not recap unprotected medical sharps

When using sharps, ensure there is a disposal container nearby.

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20
Q

Risk of HIV transmission from needle-stick injury from a patient with HIV not on ARVs.

A

1 in 300

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21
Q

Management of needle stick injury exposed to HIV.

A

Ecnourage the wound to bleed, ideally under running water.

Wash with soap and running water, do not scrub.

Seek advice from occy health and infection control regarding source testing and post-exposure prophylaxis.

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22
Q

How can complications of HIV be classified?

A

Into complications of immune dysfunction

Complicating comorbidity

Complications of treatment

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23
Q

Opportunistic disease in HIV.

A

Pneumocystis jirovecii

Candidiasis

Cryptococcus neoformans

Toxoplasma gondii

CMV

Cryptosporidium

Kaposi’s sarcoma

Lymphoma

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24
Q

Presentation of pneumocystis jirovecii in HIV.

A

Progressive SOB on extertion along with malaise and dry cough.

Haemoptysis and pleuritic pain is rare.

On examination there is increased resp rate and often normal breath sounds.

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25
Q

Investigations of pneumocystis jirovecii in HIV.

A

SpO2

CXR shows classically perihilar infiltrates but may be normal.

Induced sputum or BAL with staining or nucleic acid amplification testing (NAAT).

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26
Q

Treatment of pneumocystis jirovecii in HIV.

A

IV co-trimoxazole 21 day course

Steroids in moderate to severe disease

2nd line: clindamycin, pentamidine, atovaquone.

Prophylaxis can be done with co-trixomazole if the patient has a CD4 count <200 cells/microlitre

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27
Q

Explain candidiasis in HIV infection.

A

Oral or oesophageal

There might be pain in the tongue, dysphagia and odynophagia.

It is diagnosed clinically or endoscopically.

IT is the treated with systemic -azoles like fluconazole

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28
Q

What is the most common systemic fungal infection in HIV.

A

Cryptococcus neoformans

Around 5-10% of people without ARV treatment will experience this.

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29
Q

Presentation of Cryptococcus neoformans in HIV.

A

Meningitis, headache, fever.

Might have molluscum-like papules and lung disease.

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30
Q

Investigations of Cryptococcus neoformans in HIV.

A

LP with manometry

CSF stain for CSF/blood cryptococcal antigen

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31
Q

Treatment of Cryptococcus neoformans in HIV.

A

Induction with liposomal amphotericin B (beware AKI and renal tubular damage)

Flucytosine might be beneficial in patients not on ARV therapy.

Maintenance treatment should then be with fluconazole and normalise the ICP with repeat LPs or a shunt if needed.

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32
Q

What is the commonset cause of intracranial mass lesions when the CD4 count is < 200 cells/microlitre?

A

Toxoplasma gondii

33
Q

Presentation of toxoplasmosis.

A

It is a parasite and causes focal neurological signs +/- seizures.

There might be a headache and vomiting, usually secondary to raised ICP.

34
Q

Investigations of toxoplasmosis.

A

Ring-enhancing lesions on MRI with associated oedema.

CSF PCR for Toxoplasma gondii is specific but only moderately sensitive.

Blood serology is not diagnostic as most cases are a reactivation of previous infection.

35
Q

Treatment of toxoplasmosis in HIV.

A

Pyrimethamine, sulfadizine and folinic acid

36
Q

Presentation of CMV in HIV.

A

Retinitis where there is blurry vision and then loss of vision.

Encephalitis

GI disease with oesophagitis and colitis.

Heaptitis

Bone marrow suppression

Pneumonia

37
Q

Diagnosis of CMV.

A

Serial CMV viral load

Retinal lesions suggestive of CMV

GI ulceration

Owl’s eye inclusions on biopsy

38
Q

Treatment of CMV in HIV.

A

Ganciclovir or valganciclovir

Side-effects include rash, diarrhoea and bone myelosuppression

39
Q

What is a common cause of chronic diarrhoea in pre-ARV therapy HIV?

A

Cryptosporidium

40
Q

Presentation of Cryptosporidium in HIV.

A

Acute or sub-acute non-bloody, watery diarrhoea.

Cholangitis and pancreatitis

41
Q

Investigations of Cryptosporidium in HIV.

A

Stool microscopy - the oocyst excretion is intermittent so multiple samples will be needed.

PCR

Enzyme immunoassay

Direct fluorescent antibody.

42
Q

Treatment of Cryptosporidium in HIV.

A

Supportive

ARV therapy

43
Q

What is the most common tumour in HIV and AIDS defining?

A

Kaposi’s sarcoma

44
Q

What is Kaposi’s sarcoma caused by?

A

Kaposi sarcoma herpes virus (human herpesvirus 8)

45
Q

Presentation of Kaposi’s sarcoma.

A

Cutaneous or mucosal lesions, patch, plaque or nodular.

Visceral disease is less common.

46
Q

Diagnosis of Kaposi’s sarcoma.

A

Histology

47
Q

Treatment of Kaposi’s sarcoma.

A

ARV therapy

Intralesional retinoids or vinblastine

Radiotherapy for cosmetological reasons and pain.

Chemo + ARV therapy in advanced disease.

48
Q

What types of Lymphoma might develop in HIV?

A

Diffuse large B-cell lymphoma

Burkitt’s lymphoma

Primary CNS lymphoma

49
Q

Presentation of lymphoma in HIV.

A

Depends upon the area of involvement.

Includes lymphadenopathy, cytopenia, and CNS symptoms.

50
Q

Treatment of lymphoma in HIV.

A

Combined ARV therapy and chemo.

Rituximab can be used in non-CNS disease.

Whole-brain radiotherapy for CNS disease if there is excess toxicity with chemo.

51
Q

Which comorbidities are common to be complicated by HIV?

A

Cardiovascular disease

Bone disease

TB

Hep B

Hep C

52
Q

Explain CVD and HIV.

A

There is an increased risk of CVD in HIV.

Younger age, normotensive and no DM with HIV have a higher risk of CVD than completely healthy.

53
Q

Contributing factors causing CVD in HIV.

A

Dyslipidaemia due to ARV therapy.

Acceleration of pro-atherosclerotic inflammatory processes by HIV.

54
Q

Contributing factors to bone disease in HIV.

A

There is an increased risk of low BMD and fragility fractures in HIV.

This is because of side effects to ARV therapy, increased prevalence of risk factors such as poor nutrition, smoking, alcohol and low vit D levels.

55
Q

TB and HIV.

A

All patients with TB and HIV need ARV therapy.

Consider Truvada + efavirenz as 1st line in the UK

56
Q

Treatment of HIV + Hep B.

A

ARV therapy including antivirals with anti-HBV activity like tenofovir + emtricitabine.

57
Q

Treatment of HIV + Hep C.

A

Assess all with HIV for HCV treatment.

Pegylated interferon efficacy is less with HIV due to low CD4 count.

Aim for CD4 > 500 cells/microlitre with ARV therapy first.

58
Q

When is ARV therapy (ART) indicated?

A

In everyone with HIV regardless of their CD4 count.

59
Q

What are the aims of ART?

A

Reduce the HIV viral load to a level of undetectability by standard lab techniques.

This leads to immunological recovery, reduced clinical progression and reduced mortality.

This gives a normal life expectancy, this does not come necessarily with a normal life quality however due to possible side effects of drugs.

60
Q

Mechanisms of action of ARTs.

A

CCR5 antagonists - inhibits entry of the virus into the cell.

Nucleoside and non-nucleoside reverse transcriptase inhibitors (NRTI and NNRTIs). - They inhibit reverse transcriptase and the conversion of viral RNA into DNA.

Protease inhibitors (PIs) - Inhibits protease which is an enzyme involved in the maturation of virus particles.

Integrase strand transfer inhibitors (INSTIs) - inhibits integrase and prevent HIV DNA integrating into nucleus.

Pharmacokinetic enhancers/boosters - increase the effectiveness of ART allowing lower doses

61
Q

Explain management before initiating ART.

A

Counselling

Screen for infections and malignancy.

Baseline tests - CD4, viral loads, FBC, LFTs, electrolytes, crea, pregnancy test and viral genotype for drug resistance.

Review usual medication for possible interactions.

62
Q

Explain counselling in HIV.

A

HIV transmission and sexual health.

Explain the benefits of therapy, stress that it is not a cure.

That is it important with life-long adherence to medication.
Explain that resistance can emerge.

Explain the side effects of treatment

The necessary monitoring

And that full disclosure to family members is important.

63
Q

What is the usual treatment to start off with in a new HIV infection?

A

Two NRTI (called NRTI backbone) + one of;

Ritonavir-boosted protease inhibitor

NNRTI

Integrase inhibitor

64
Q

What are the 1st line drugs commonly used in the UK?

A

NRTI backbone with tenofovir and emtricitabine or abacavir and lamivudine.

and one of the following;

Protease inhibitiors such as Atazanavir or darunavir

NNRTI such as Rilpivirine or Efavirenz

Integrase inhibitor such as dolutergravir, elvitegravir and raltegravir.

65
Q

Side-effects of NRTI backbone.

A

GI disturbance

Anorexia

Pancreatitis

Hepatic dysfunction

Decreased BMD

Avoid abacavir if high risk of CVD

Avoid tenofovir if eGFR < 30

66
Q

SEs of protease inhibitors.

A

Hyperglycaemia

Insulin resistance

Dyslipidaemia

Jaundice

Hepatitis

67
Q

SEs of NNRTIs.

A

CNS toxicity

Association with suicidality

Rash

GI disturbance

Be careful with these drugs in depression and anxiety.

68
Q

SEs of integrase inhibitor.

A

Rash

GI disturbance

Insomnia

69
Q

How is monitoring done in ARV therapy?

A

Adherence is monitored

Adverse effects of the medicine

Viral load to check for the response of treatment.

CD4 counts to guide prophylaxis of opportunistic disease.

70
Q

Complications of poor adherence in HIV.

A

Can lead to drug resistance

Disease progression

Death

71
Q

Explain assessment of adherence in HIV.

A

Ask about it in a non-judgemental way.

Do not put any blame on the person.

Explain why you are asking about it.

Is it due to practical issues or due to healthcare beliefs?

What would your patient want help with?

72
Q

Baseline investigations for all patients newly diagnosed with HIV.

A

Confirmatory HIV test

CD4 count

HIV viral load

HIV resistance profile

HLA B*5701 status

Serology for syphilis, hep B, hep C and hep A.

Toxoplasma IgG, Measles IgG, Varicella IgG, Rubella IgG

FBC, U&Es, LFTs, bone profile and lipid profile.

Schistosoma serology if the patient has spent over a month in sub-Saharan Africa.

Women should have annual cervical cytology screening.

73
Q

Additional testing done in HIV diagnosis.

A

TB and MAI culture

Fungal culture and PCR, fungal stains.

Cryptococcal antigen

Toxoplasma PCR

Viral PCR for EBV, CMV, HSV, VZV and JC

74
Q

What should patients with a CD4 <200 be prescribed?

A

Co-trimoxazole 480mg PO OD as primary prophylaxis agaisnt PCP.

75
Q

What should patients with a CD4 count < 50 be prescribed?

A

Azithromycin 1250mg PO once weekly as prophylaxis against MAI (Mycobacterium avian intracellulare infection)

76
Q

What else should be performed in patients with a CD4 count < 50.

A

Referred to opthalmology for dilated fundoscopy to look for evidence of intra-ocular infections such as CMV retinitis

77
Q

Vaccinations done in HIV.

A

Hep B and A and pneumococcus

Annual flu

Polio

Tetanus

Diphteria

Avoid live vaccines

78
Q

HIV and cervical smears

A

Yearly cervical smears are required for women. HIV predisposes to developing cervical HPV infection and cervical cancer so female patients need close monitoring to ensure early detection of these complications.

79
Q

HIV and CVD

A

HIV infection increases the risk of developing cardiovascular disease.

Patients with HIV have close monitoring of cardiovascular risk factors and blood lipids and appropriate treatment (such as statins) to reduce their risk of developing cardiovascular disease.

Y3M - Infectious Disease (21 decks)

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