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HIV Flashcards

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1
Q

What type of rash is seen in HIV seroconversion?

A

Erythematous, maculopapular rash, mainly on face and trunk +- mucocutaneous ulcers of the mouth, oesophagus or genitals.

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2
Q

Definition of persistent generalised lymphadenopathy

A

Lymphadenopathy that persists for at least 3 months, in at least 2 extra-inguinal sites and is not due to any other cause.
Associated with the early stages of HIV infection.
Mediastinal and intra-abdominal lymphadenopathy are not part of this syndrome- need extra investigations.

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3
Q

Common haematological abnormalities in HIV

A

Lymphopenia
Moderate neutropenia (may be linked to ethnicity)
Normochromic, normocytic anaemai
Thrombocytopenia

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4
Q

Factors associated with increased rate of progression of HIV

A 
Older age
PHI- early onset < 3 weeks and prolonged symptoms > 2weeks
Low baseline albumin
Rapid fall of CD4 count
Route of infection- blood transfusion
Some strains of HIV
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5
Q

Which three cancers are AIDS-defining illnesses?

A

Kaposi’s sarcoma
High-grade B-cell non-Hodgkin’s lymphoma (including primary cerebral lymphoma)
Invasive cervical cancer

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6
Q

How should AIDS-related NHL be managed?

What’s the prognosis?

A

cART + opportunistic infection prophylaxis
Anthracycline-based chemotherapy (+/- intrathecal chemo for those at risk of meningeal relapse)

Durable complete remission in 50-60%

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7
Q

What are the different ways systemic NHL can present?

A

Half present with nodal disease
GI disease
Extranodal disease
‘Primary effusion lymphoma’ (effusions without a nodal mass of disease- associated with KS herpesvirus

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8
Q

What is PCL?

A

Primary cerebral lymphoma.
NHL confined to the craniospinal axis without systemic involvement.
Associated with advanced immunosuppression and poor prognosis.

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9
Q

Commonest causes of cerebral mass lesions in HIV (2)

A

Toxoplasmosis

PCL

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10
Q

Management of PCL

Prognosis

A

Whole brain irradiation + ensure on cART
May use IV chemotherapy for patients with a good performance status.

Poor prognosis. Median survival 1-3 months

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11
Q

Virus that causes KS

How is it transmitted?

A

A gammaherpes virus. KSHV (Kaposi sarcoma herpesvirus)
aka HHV8 (human herpesvirus 8)
Transmitted horizontally and vertically. ?through kissing.

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12
Q

What does KS look like histologically?

Main differential

A

Lots of spindle-shaped cells, with endothelial cells, fibroblasts and inflammatory cells–> form slit-like vascular channels that can look like angiogenesis.

Main differential: bacillary angiomatosis, caused by the rickettsia Bartonella henselae

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13
Q

Commonest sites of visceral disease in KS

A

Pulmonary: life-threatening. Get dyspnoea, dry cough +/- fever. May be haemoptysis. Diffuse reticulonodular disease on CXR.
GI (stomach)

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14
Q

Factors associated with poor risk in KS

A

Tumour-associated oedema or ulceration
Extensive oral KS
GI KS
KS in other non-nodal viscera

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15
Q

Non-AIDS defining malignancies that occur much more commonly in the HIV-positive population

A

Anal cancer (in MSM)]
Hodgkin lymphoma
Multicentric Castleman’s disease
+others

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16
Q

What is MCD

How does it present?

Treatment?

A

Multicentric Castleman’s disease
(rareish) lymphoproliferative disorder related to KSHV

Presents with fever, lymphadenopathy, hepatosplenomegaly and systemic symptoms.

cART + rituximab (anti-CD20) gives good prognosis.

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17
Q

How is PCP stratified?

How is it treated? (first and second line)

A

Mild, moderate or severe, based on PaO2 (>11 = mild, 8-11 = moderate, <8 = severe)

Treatment = high-dose co-trimoxazole for 21 days. Can be given orally if mild disease. Co-trimox can also be used for PCP prophylaxis.
Also glucocorticoids if PaO2 <9.3 (reduces mortality and need for ventilation)

Second line= clindamycin + primaquine/pentamidine

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18
Q

What stain is used to diagnose PCP (in sputum/bronchoalveolar lavage fluid)?

A

Grocott methenamine silver stain

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19
Q

Important complication of PCP that worsens prognosis (increased chance esp. if ventilated)

A

Pneumothorax

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20
Q

Presentation of PCP
Examination findings
Radiographic findings

A

Non-productive cough and progressive exertional breathlessness over days/weeks
Chest usually clear on auscultation. Sometimes end-inspiratory crackles.
CXR may be normal. Most common abnormality is perihilar interstitial infiltrates.

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21
Q

First choice drug for PCP prophylaxis

When should primary and secondary prophylaxis be used?

A

Co-trimoxazole

Primary: CD4 <200 or <14% of total lymphocyte count, or with another AIDS-defining illness

Secondary: always after an episode of PCP, but can discontinue if sustained CD4 >200 or UVL

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22
Q

How can pulmonary cryptococcal infection present?

How is it diagnosed?

A

Either as primary cryptococcosis, or as part of disseminated infection with meningitis +- cryptococaemia.
Chest may be clear or have crackles. Many different CXR findings.

Diagnosis by identification of Cryptococcus neoformans in resp secretions

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23
Q

Treatment for pulmonary cryptococcal infection

A

Fluconazole

or liposomal amphotericin and flucytosine.

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24
Q

How does pulmonary histoplasmosis present?
What is found on examination/CXR?
How is it diagnosed?

A

Always as part of disseminated infection. Generally subacute with fever and weight loss. ~1/2 with non-productive cough and dyspnoea.
Examination: hepatosplenomegaly.
CXR: normal or bilateral widespread <4mm nodules.
Diagnosis by identification in BAL fluid.

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25
Treatment for pulmonary histoplasmosis
Liposomal amphotericin Itraconazole is an option for milder disease.
26
How is CMV pneumonitis diagnosed?
Characteristic intranuclear and intracytoplasmic inclusions in BAL fluid cells or lung tissue.
27
How does pulmonary KS present? | What factor strongly predicts its presence?
Non-specific cough and progressive dyspnoea. Sometimes haemoptysis. Palatal KS strongly predicts the presence of pulmonary and/or foregut disease.
28
Which parts of the thorax can KS involve? What are the radiological findings.
The airways, lung parenchyma, pleura and mediastinal lymph nodes. Interstitial or nodular infiltrates and alveolar consolidation. Pleural effusion in 40% and hilar/mediastinal lymphadenopathy in ~25%.
29
Treatment of pulmonary KS
cART can induce remission- used in addition to chemotherapy.
30
Is lung cancer more common in HIV-infected smokers than HIV -ve?
Yes. 2-4 times mroe common. Presentation is usually with disseminated disease.
31
What is non-specific pneumonitis? How is the diagnosis made? How is it treated?
Non-infectious pneumonitis that often mimics PCP. Tends to occur at higher CD4 counts than PCP. Diagnosis by transbroncial, VATS or open-lung biopsy. Most episodes are self-limiting. Prednisolone may be beneficial.
32
How does lymphocytic interstitial pneumonitis present? How is it diagnosed? How is it treated?
Slow progressive dyspnoea and cough, more commonly in HIV-infected children. Clinical resembles idiopathic pulmonary fibrosis. CXR: bilateral reticulonodular infiltrates, or like PCP. Diagnosis via biopsy Treatment with cART
33
Lung conditions more common in HIV
``` Various infections Lung cancer COPD Pulmonary arterial hypertension Pneumothorax (always exclude PCP!) ```
34
Probability of latent TB activation in the HIV-uninfected and infected populations
Uninfected: ~10% lifetime risk Infected: 10% risk per annum (therefore 20-40 times more likely to develop active TB)
35
Differences in CXR features of TB in HIV -ve and +ve individuals What other features are also more common in HIV+ve
HIV -ve: upper zone cavitatory disease HIV +ve: pulmonary infiltrates, mediastinal lymphadenopathy, pleural effusions. More common also non-pulmonary, disseminated and multi-organ involvement.
36
What are the standard diagnostic tests for pulmonary TB? Why are these less good in HIV? How can this be improved??
AFB smear and culture HIV: more likely to be AFB sputum smear-negative. Culture of other samples e.g. blood/urine = good as disseminated and non-pulmonary disease is more common
37
Which anti-TB drug interacts with antiretrovirals and how? What is an alternative drug? Which ARVs should be avoided during therapy with these drugs?
Rifampicin: CYP450 inducer--> can lead to treatment failure and HIV drug resistance. Rifabutin = alternative, but more expansive. PIs (protease inhibitors) as these interact with both, but in different ways
38
How much of an effect does cART have on risk of development of active TB?
60-90% risk reduction in the development of active TB, but even with high CD4 and UVL, individuals are still at considerably higher risk than the greater population
39
What is IRIS? | What makes IRIS more likely to happen?
Immune reconstitution inflammatory syndrome When drug therapy e.g. for TB leads to worsening of existing disease or the reveal of new conditions. More likely if low baseline CD4 or disseminated TB (can also occur in HIV-ve)
40
What conditions can IRIS mimic? | it is a diagnosis of exclusion!
Adverse drug reactions Progressive disease due to resistance Inadequate drug levels due to malabsorption Drug-drug interactions or non-adherence Alternative diagnoses e.g. lymphoma/other infections.
41
What are the standard diagnostic tests for LTBI?
Tuberculin skin test and blood interferon gamma release assays- these become more problematic as a persons CD4 count falls
42
AIDS-defining conditions affecting the GI tract
``` Oesophageal candidiasis CMV (other than liver, spleen and lymph nodes) Cryptosporidiosis for >2 month TB MAI Recurrent salmonella septicaemia Microsporidium Kaposi sarcoma Burkitt's lymphoma Immunoblastic lymphoma ```
43
Treatments for oesophageal candidiasis
Oral fluconazole or itraconazole If can't swallow: IV amphotericin B or caspofungin
44
Opportunistic oesophageal infections in HIV | What are their treatments?
Candida HSV- IV aciclovir CMV- IV ganciclovir, and screen for retinal disease (HSV and CMV usually only at CD4 <100)
45
Causes of nausea and vomiting in HIV
Now most commonly cART associated, or associated with non-adherence. Opportunistic infections Tumours (incl KS and lymphoma) HIV-related CNS infection
46
Appearance of CMV oesophagitis
Discrete ulceration with rolled edges, resembling a carcinoma
47
What are microsporidium? When does chronic diarrhoea due to these occur? How is it diagnosed?
Obligate intracellular parasites. Cysts are ingested from contaminated water. Causes mild-moderate watery, non-bloody diarrhoea Most commonly in CD4 <100 Stool examination with specific fluorescent stains
48
What does cryptosporidium cause in the immunocompetent? and in the immunocompromised?
Normally causes acute attacks of diarrhoea. | If CD4 <100, can cause severe chronic diarrhoea, with nausea, malabsorption and anorexia--> weight loss.
49
Commonest cause of cryptosporidial infection. Treatment
Normally contaminated water (stopped by boiling) No treatment reliably eradicates it. Best therapy = cART
50
CD4 for CMV colitis Classic presentation Complications Management
<50 Bloody diarrhoea and typical colitis appearance at endoscopy Can lead to perforation or toxic dilatation Treatment: forscarnet or ganciclovir. Exclude active retinal infection. cART!
51
What is an important differential for RUQ pain in HIV? How does it appear? CD4 count? What is it almost always associated with?
AIDS-related sclerosing cholangiits Appears pathologically and radiologically identical to idiopathic sclerosing cholangitis: irregular dilatation and narrowing of intrahepatic and extrahepatic ducts caused by areas of fibrosis. CD4 <100 Almost always associated with microsporidium, cryptosporidium or CMV infection
52
How does MAI classically present?
Severe abdominal pain- sometimes associated with massive enlargement of intra-abdominal lymph nodes. Raised alkaline phosphatase Anaemia Fever
53
Neurological opportunistic infections in HIV
Toxoplasma gondii (abscesses and encephalitis) Cryptococcus neoformans (meningitis) JC virus (PML) CMV- retinitis, encephalitis, cauda equina, vasculitic neuropathy TB- meningitis, abscesses
54
CNS tumours associated with HIV
PCNSL (primary CNS lymphoma) | Metastatic systemic lymphoma
55
HIV-related neurological disorders (not infectious or malignant)
HAND - HIV associated neurocognitive disorders Vacuolar myelopathy Peripheral neuropathy (distal sensory peripheral neuropathy) Polymyositis
56
Organisms causing neurological immune reconstitution syndromes in HIV
Cryptococcus PML TB HIV
57
What percentage get neurological features in seroconversion? | Examples of these features
10% (cf 70% get a glandular fever like illness) ``` Aseptic meningitis Meningoencephalitis GBS Transverse myelitis Cauda equina etc. ```
58
Commonest cause of meningitis in HIV | What does the CD4 count have to be for this?
Cryptococcus neoformans | CD4 <200
59
What does the CD4 count generally have to be for neurological complications of CMV? Treatment of CMV encephalitis
<50 Ganciclovir +- forscarnet
60
CSF findings in cryptococcal meningitis
Cell count, protein and glucose may be normal, but often get raised opeing pressure due to blockage of CSF resorption across arachnoid vill by Cryptococcus.
61
Treatment of cryptococcal meningitis
2-weeks of liposomal amphotericin B +- flucytosine, then 6 weeks of fluconazole. Manage raised ICP by repeated lumbar puncture or lumbar drain.
62
Treatment for toxoplasmosis
Dexamethasone if significant mass effect on scans/raised ICP | Co-trimoxazole
63
Presentation of PML How is it diagnosed? Treatmnet
Slowly evolving focal neurological deficits: hemiparesis, visual field defects, language problems, incoordination. Sometimes dementia Not raised ICP. Diagnosis by isolating JC virus DNA on CSF PCR. May be reduced sensitivity if on cART. Treat with cART
64
Risk factors for HAND
Older age, female gender, current/previous low CD4 (<100), high viral load, co-morbid conditions e.g. anaemia, co-infection with hep C, IVDU
65
What is DSPN? | How is it treated?
Distal sensory peripheral neuropathy (now quite rare) Anticonvulsants (gabapentin, pregabalin, carbamazepine), antidepressants (amitriptyline), opiates (oxycodone). Consider vasculitis + optimise HTN/high cholesterol etc.
66
How does antiretroviral toxic neuropathy present?
Similar to DSPN, but often more painful.
67
How does neurological IRIS present? | How is it managed?
Presents as encephalitis-like syndrome or with headache, seizures + focal deficits. Controversial. Standard = treat infection if present + dexamethasone for mass effect/oedema.
68
Retinal findings in non-infectious HIV retinopathy | What are these a result of?
Cotton wool spots Microaneurysms Retinal haemorrhages Direct result of HIV itself (don't occur with cART)
69
CD4 count for CMV retinitis Locations of CMV retinitis that really risk visual loss Treatment
Approx <100 Risky if close to macula or optic nerve Intraocular ganciclovir or foscarnet injections, or 6-month ganciclovir implant in the affected eye. But then need oral maintenance therapy unless CD4 >100 for >3 months
70
How can HSV affect the eye? CD4 for this Treatment
HSV keratitis- can permanently affect vision if central cornea involved HSV retinitis- acute retinal necrosis (appears white on fundoscopy) Can occur at higher CD4 than CMV and in the immunocompetent. Keratitis: topical aciclovir ointment Retinitis: Intravitreal foscarnet + 7 days IV aciclovir
71
How can VZV affect the eye in HIV?
``` HZO Cerebral vasculitis- CN palsies Keratitis Uveitis Necrotizing retinitis- can cause one similar to HSV or much worse w. similar treatment but v poor prognosis ```
72
CD4 for retinal Toxoplasmosis | Management
CD4 <150 Same as for cerebral disease: sulfadiazine + pyrimethamine Also check for CNS disease and continue prophylaxis until CD4 >200
73
Malignancies that can occur in the eye in HIV
Kaposi sarcoma (usually regresses with cART) Lymphoma SCC of the conjunctiva

Urology & GUM (3 decks)

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