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Malignancy Flashcards

1
Q

What causes Kaposi sarcoma?

A

HHV8 (KSHV)

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2
Q

ACTG staging of KS - good risk

A

All of the following

Tumor - confined to skin, LN or minimal oral disease
Immune system - cd4 >150
Systemic illness - performance status >70

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3
Q

KS staging - poor risk

A

Any of the following

Tumour associated oedema or ulceration, extensive oral KS, GI KS, KS in non nodal viscera
Immune - CD4 <150
Systemic - PS <70 or other hiv related illness

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4
Q

Treatment of KS

A

cART plus

1st line Pegylated liposomal doxorubicin 20mg/m2 every 3 weeks

2nd line - paclitaxel every 2 weeks 100mg/m2

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5
Q

Baseline investigation for ?KS

A

Clinical exam
HIV serology
Routine bloods
HHV8 viraemia
Cd4 count
Histology
Whole body CT
Bronchoscopy/endoscopy if any suggestive symptoms

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6
Q

Are there local therapies for KS?

A

Radiotherapy used less now cART is available but may be useful at specific sites
Topical retinoids (not in uk)
Intralesional vinblastine
Cryo

In general local therapies superseded by cART

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7
Q

Who can receive local KS therapies?

A

Symptomatic or cosmetic improvement in early (stage t0) ks

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8
Q

Ongoing KS follow up

A

Depends how serious - if severe hiv related then monthly clinical evaluation, 3/12 radiological evaluation

Bloods, cd4, clinical exam. If symptoms - bronchoscopy, endoscopy, Ct whole body

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9
Q

What constitutes a complete response to KS?

A

Complete resolution with no new lesions for at least 4 weeks. Biopsy needed to confirm resolution in flat pigmented lesions.
Endoscopes must repeated to confirm resolution of previously detected visceral disease

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10
Q

What constitutes partial response to KS?

A

One or more of the following in absence of new cutaneous or visceral lesions, ks associated oedema, 25% increase of any index lesion:
50% decrease in number measurable lesions
Or 50% decrease defined as - 75% nodular lesions become plaques, flattening of 50% lesion, 50% decrease sum of bidimensional diameters of index lesion
Flattening of 50% lesions

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11
Q

What constitutes progressive KS?

A

Any of:
25% increase in size of any index lesion
Appearance of new lesions
Where 25% or more of previously flat lesions become raised
New or increased KS associated oedema

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12
Q

Most common subtypes of aids related non Hodgkin lymphoma

A

Diffuse large B cell lymphoma, burkitt lymphoma/leukaemia

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13
Q

Baseline investigations for DLBCL and BL

A

Bloods - routine plus esr, blood film, g&s, coag, LDH, urate, CRP, immunoglobs, protein electrophoresis, b2 microglobulin.
Hep b, c, cmv, VZV tests
ECG
CXR
Bone marrow
CT NCAP
Pet Ct

LP NOT ROUTINE

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14
Q

Prognostic factors for aggressive NHL?

A

1 point for each -

Age >60
Serum LDH > normal
PS > 1
Stage iii/iv
Extranodal site >1

0-1 low risk
2 low intermediate risk
3 high intermediate risk
4 or 5 high up

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15
Q

Should rituximab be used in treatment of DLBCL?

A

Yes but increased death rate in those with CD4 <50 so need to ensure appropriate antibiotic prophylaxis (fluconazole, aciclovir, septrin, azithromycin), preemptive GCSF, prompt tx of OI

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16
Q

What is the treatment of HIV associated burkitt lymphoma/leukaemia?

A

CODOX-M/IVAC DA-EPOCH
Rituximab should be added

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17
Q

Prevention of secondary CNS lymphoma in those with ARL?

A

Cns relapse less likely if improved control of systemic disease
Those at increased risk - disease in testes, paranasal sinuses, paraspinal disease, breast, renal, epidural space, bone
Also advanced stage, elevated LDH

those with DLBCL at high risk to receive CNS prophylaxis - IT or IV methotrexate

All patients with burkitt lymphoma should be offered prophylactic intrathecal chemo

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18
Q

When does tumor lysis syndrome occur (DLBCL/

A

12-72 hrs after commencement of chemotherapy

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19
Q

What increases risk of tumour lysis syndrome?

A

Elevated LDH and bulky disease (DLBCL) or stage 3/4 disease (BL)

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20
Q

Management of tumour lysis syndrome

A

Aggressive hydration and rasburicase

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21
Q

Should patients on chemotherapy continue their cArt?

A

Yes
May need adjusting if interactions

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22
Q

How is refractory /relapsed aids related lymphoma treated?

A

Offer second line chemotherapy which may contain platinum

For those who respond (CR or PR) should be considered for high dose therapy and autologous stem cell transplant

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23
Q

How is response evaluated for NHL in HIV+patients?

A

Assess response halfway through treatment - clinical evaluation, Ct scan, bone marrow

PET CT at least 4-6 weeks after last chemo 8-12 weeks after last radiotherapy

Follow up 3/12ly first year, 4-6/13ly 2nd and 3rd year, 6/12 up to 5 years

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24
Q

I what is a PCNSL?

A

Non Hodgkin lymphoma confined to cranio-spinal axis.

Characteristically is DLBCL or immunoblastic NHL

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25
Typical presentation of PCNSL?
Rarely B symptoms. Present with mass lesions - neuropsychiatric signs, raised ICP, seizures
26
Investigations for PCNSL?
MRI brain with GAD, CT CAP, LP when safe, serum LDH Brain biopsy only confirmatory test EBV intumour cells a universal feature of hiv associated PCNSL
27
Treatment of PCNSL
In normal pop iv methotrexate and cytatabin I’m HIV+patients iv methotrexate only most utilised Whole brain radiotherapy may also be used for symptom control Everyone to start cART
28
CT findings for PCNSL
May show ring enhancement Diffuse and multi focal supratentorial brain masses May involve vitreous, retina and optic nerves
29
What causes PEL?
HHV8 protea tumorigenedis by enhanced proliferation and impaired apoptosis in cells with latent gene HHV8 expression EBV plays an unclear role
30
Presentation of PEL
Commonly - dyspnoea As a result of pericardial or pleural involvement or abdominal distension from peritoneal involvement
31
How is PEL diagnosed?
Cytology of fluid Morphologically- cells large, round to irregular nuclei, conspicuous nucleoli, may have appearance of immunoblasts, plasmablasts and/or anaplastic Immunohistostaining for LANA-1 expression is standard for detecting HHV8
32
How to differentiate PEL from other NHL subtype with an effusion
No solid LN masses in PEL HHV8 required for PEL
33
Treatment for PEL
Minimal data as low incidence of PEL cART and CHOP Advise patients to enter clinical trials
34
Subtypes of plasmablastic lymphoma
1 oral mucosa - monomorphic population of plasmablasts with minimal plasmacytic differentiation 2. More differentiation and usually extra-oral 3rd associated with casteman’s - typically nodal or splenic
35
How is Plasmablastic lymphoma distinguished from immunoblastic variant of DLBCL
Immunophrnotyping Low/absent cd45 and b cell markets Plasma cell markers always present Tumours almost always EBV positife
36
Prognosis plasmablastic lymphoma
Poor - 5/12 pre HAART Median survival 24/12 31% 5 year survival
37
Treatment for plasmablastic lymphoma?
cART plus systemic anthracycline containing chemotherapy
38
How often should WLWH have smears?
Aged 25-65 - yearly
39
Has the incidence of cervical cancer changed with cART?
No but reduced incidence of CIN Incidence increased in lower CD4 counts. Higher CD4 associated with reduction of incidence and progression of CIN
40
CIN 1
Repeat colposcopy 12 months Unlikely to develop cervical cancer
41
CIN2/3 management
Higher chance developing cervical cancer Therefore treatment offered
42
Risk factors for CIN2/3 treatment failure
CD4 <200, high VL, non use of HAART Compromised margins on excisional specimen are frequently seen in WLWH and are a risk factor for tx failure
43
Staging of cervical cancer
FIGO criteria MRI/PET CT for staging
44
Treatment for cervical cancer
FIGO IA1 IA2 IB1 - surgery Anything above that - surgery plus platinum based chemotherapy
45
Pathogenesis of anal cancer
HPV infection leading to AIN and ensuing progression from low to high grade dysplasia and subsequently invasive cancer
46
How to diagnose anal cancer
EUA and biopsy in all suspected cases CT CAP for ?mets and MRI pelvis for LN and tumour extension PET can have false positives in PLWH
47
First line treatment For Anal Cancer
Concurrent chemoradiotherapy (shown to achieve local control and sphincter preservation) 5FU and mitomycin c
48
How has HAART impacted incidence of anal cancer?
Increased - people living longer, more chance for HPV to progress Also improved SURVIVAL
49
Management of relapse of anal Cancer
22-25% in general population have persisting primary or recurrent disease Treated with salvage surgery - abdominoperineal excision of rectum and anal canal with pedicle flap and colostomy If metastatic disease or local relapse following salvage surgery can sometimes try palliative chemo - best supportive care may be more appropriate
50
Evaluation of response to tx for anal ca
6-8 weeks after completion - clinical exam, MRI pelvis and EUA Review every 3-6/12 for 2yes then 6-12 mon this for 5 years
51
Screening for AIN
Not recommended in current guidelines - current treatments aren’t good enough to make screening worthwhile, tx can be uncomfortable have side effects and don’t always stop AIN from recurring
52
Diagnosis AIN
If symptomatic Anal smear or anoscopy or proctoscopy with biopsy
53
Treatment low grade AIN
Further review in 6-12/12 No immediate treatment
54
Treatment high grade AIN
Options - surgery to remove lesions that cover a small area, cream eg Aldara or 5FU 2-3x week for 4/12, ablative therapies In many cases the problem recurs as tx doesn’t get rid of HPV
55
OI prophylaxis for those undergoing cancer treatment
CD4 changes can be unpredictable with chemo and radiotherapy so OI considered regardless of CD4 KS treated by doxorubicin or paclitaxel not at increased risk so standard guidelines should be followed 1/12 after the end of chemo or radiotherapy repeat CD4 and reconsider Prophylaxis for - PCP <200 or at risk fluconazole 50mg qds for everyone HSV/VZV prophylaxis NTM prophylaxis if detectable VL cd4 <50 or risk of dropping below 50
56
Histology of Hodgkin Lymphoma in PLWH
Predominance of mixed cellularity and lymphocyte depleted types with higher percentage of EBV positivity
57
Tests for HL in PLWH
Bone marrow biopsy mandatory as higher proportion of BM involvement in PLWH Whole body PET Baseline bloods and virology
58
Staging of HL (Ann arbor/Cotswolds)
1. Single LN or lymphoid structure 2. 2 or more LNs same side diaphragm 3. LN groups both sides diaphragm IV. Extranodal sites beyond those designated ‘e’ X - bulky disease >10cm Or >1/3 widening of mediastinum at t5-6 E - Extranodal extension contiguous or proximal to known nodal site of disease A/B - absence of B symptoms
59
Management of HL in PLWH
Less risky strategies used as precise Ed higher risk with HIV and less good-risk disease in PLWH ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) Number of cycles and addition of radiotherapy depend on risk factors and stage of disease Early favourable ABVD X2-4 + IFRT 20-30 Early unfavourable ABVD x4 + ifrt 30 Advanced stage - ABVD x6-8 +/- RT
60
Can AVBD be given with HAART
Yes but increased risk of treatment related toxicities Avoid PI/r - vinblastine mediated neurotoxicity and neutropenia given with ritonavir
61
Second line treatment for HL?
Salvage chemo and consolidation with high dose therapy with autologous stem cell rescue
62
OI prophylaxis in HIV associated lymphomas
PCP, MAI, fungal infection
63
What should HIV and HL patients requiring blood products be given?
Irradiated products
64
What is localised castlemans disease?
Usually in young adults Masses in mediastinum, neck or less commonly intra abdominal Systemic symptoms rare
65
What is multicentric castlemans?
Rare lymphopriferatjve disorder presenting with fevers, anaemia, lymphadenopathy Multi organ systemic features More aggressive
66
Symptoms of MCD
Malaise, night sweats, rigours, fever, anorexia, weight loss
67
Signs of MCD
Widespread lymphadenopathy Often accompanied by one or more of- hepatosplenomegaly, ascites, oedema, pulmonary and pericardial effusions May present with pancytopenia, renal or respiratory failure Polyneuropathy and leptomeningeal and CNS infiltration with central pontine myelinolisis as well as myaesthenia Gravis. PEL can also develop in presence of MCD
68
Test findings in MCD
Thrombocytopenia, anaemia, hypoalbuminaemia, hypergammaglobulinaemia. Haemophagocytic lymphohistiocytosus may be present and confirmed on bone marrow
69
MCD originates from…
Hhv8 infected extrafollicular B cells
70
PELs originate from..
HHV8 infected pre terminally differentiated B cells that have traversed the germinal centre
71
Definition of an MCD ‘attack’
Fever, raised CRP and 3 of the following symptoms - Peripheral lymphadenopathy, splenomegaly, oedema, pleural effusion, ascites, cough, nasal obstruction, xerostomia, rash, CNS symptoms, jaundice, autoimmune haemolytic anaemia
72
Things increasing risk of MCD
Nadir CD4 >200 Older age No previous cART Non caucasian background
73
How to diagnose MCD
Ct NCAP to identify lymphadenopathy, organ involvement and direct tissue sampling Definitive diagnosis by LN biopsy HHV8 viral load may aid in diagnosis and monitoring response to treatment (cut off >1000)
74
Histological findings in MCD
Onion skin appearance and interfollicular plasmablasts that express the HHV8 latent nuclear antigen Recommended - immunocytochemical staining for HHV8 and IgM lambda
75
Treatment for MCD
Rituximab first line CHOP chemotherapy should be added to this for aggressive disease In relapse - rituximab based therapy

DipHIV (19 decks)

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