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DipHIV > Malignancy > Flashcards

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In general local therapies superseded by cART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
Q

Typical presentation of PCNSL?

A

Rarely B symptoms.
Present with mass lesions - neuropsychiatric signs, raised ICP, seizures

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26
Q

Investigations for PCNSL?

A

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

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27
Q

Treatment of PCNSL

A

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

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28
Q

CT findings for PCNSL

A

May show ring enhancement
Diffuse and multi focal supratentorial brain masses
May involve vitreous, retina and optic nerves

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29
Q

What causes PEL?

A

HHV8 protea tumorigenedis by enhanced proliferation and impaired apoptosis in cells with latent gene HHV8 expression

EBV plays an unclear role

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30
Q

Presentation of PEL

A

Commonly - dyspnoea
As a result of pericardial or pleural involvement or abdominal distension from peritoneal involvement

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31
Q

How is PEL diagnosed?

A

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
Q

How to differentiate PEL from other NHL subtype with an effusion

A

No solid LN masses in PEL
HHV8 required for PEL

33
Q

Treatment for PEL

A

Minimal data as low incidence of PEL

cART and CHOP

Advise patients to enter clinical trials

34
Q

Subtypes of plasmablastic lymphoma

A

1 oral mucosa - monomorphic population of plasmablasts with minimal plasmacytic differentiation

  1. More differentiation and usually extra-oral

3rd associated with casteman’s - typically nodal or splenic

35
Q

How is Plasmablastic lymphoma distinguished from immunoblastic variant of DLBCL

A

Immunophrnotyping

Low/absent cd45 and b cell markets
Plasma cell markers always present
Tumours almost always EBV positife

36
Q

Prognosis plasmablastic lymphoma

A

Poor - 5/12 pre HAART
Median survival 24/12

31% 5 year survival

37
Q

Treatment for plasmablastic lymphoma?

A

cART plus systemic anthracycline containing chemotherapy

38
Q

How often should WLWH have smears?

A

Aged 25-65 - yearly

39
Q

Has the incidence of cervical cancer changed with cART?

A

No but reduced incidence of CIN

Incidence increased in lower CD4 counts.
Higher CD4 associated with reduction of incidence and progression of CIN

40
Q

CIN 1

A

Repeat colposcopy 12 months
Unlikely to develop cervical cancer

41
Q

CIN2/3 management

A

Higher chance developing cervical cancer
Therefore treatment offered

42
Q

Risk factors for CIN2/3 treatment failure

A

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
Q

Staging of cervical cancer

A

FIGO criteria

MRI/PET CT for staging

44
Q

Treatment for cervical cancer

A

FIGO IA1 IA2 IB1 - surgery

Anything above that - surgery plus platinum based chemotherapy

45
Q

Pathogenesis of anal cancer

A

HPV infection leading to AIN and ensuing progression from low to high grade dysplasia and subsequently invasive cancer

46
Q

How to diagnose anal cancer

A

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
Q

First line treatment
For Anal Cancer

A

Concurrent chemoradiotherapy (shown to achieve local control and sphincter preservation)
5FU and mitomycin c

48
Q

How has HAART impacted incidence of anal cancer?

A

Increased - people living longer, more chance for HPV to progress

Also improved SURVIVAL

49
Q

Management of relapse of anal Cancer

A

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
Q

Evaluation of response to tx for anal ca

A

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
Q

Screening for AIN

A

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
Q

Diagnosis AIN

A

If symptomatic

Anal smear or anoscopy or proctoscopy with biopsy

53
Q

Treatment low grade AIN

A

Further review in 6-12/12
No immediate treatment

54
Q

Treatment high grade AIN

A

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
Q

OI prophylaxis for those undergoing cancer treatment

A

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
Q

Histology of Hodgkin Lymphoma in PLWH

A

Predominance of mixed cellularity and lymphocyte depleted types with higher percentage of EBV positivity

57
Q

Tests for HL in PLWH

A

Bone marrow biopsy mandatory as higher proportion of BM involvement in PLWH
Whole body PET
Baseline bloods and virology

58
Q

Staging of HL (Ann arbor/Cotswolds)

A
  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
Q

Management of HL in PLWH

A

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
Q

Can AVBD be given with HAART

A

Yes but increased risk of treatment related toxicities

Avoid PI/r - vinblastine mediated neurotoxicity and neutropenia given with ritonavir

61
Q

Second line treatment for HL?

A

Salvage chemo and consolidation with high dose therapy with autologous stem cell rescue

62
Q

OI prophylaxis in HIV associated lymphomas

A

PCP, MAI, fungal infection

63
Q

What should HIV and HL patients requiring blood products be given?

A

Irradiated products

64
Q

What is localised castlemans disease?

A

Usually in young adults
Masses in mediastinum, neck or less commonly intra abdominal
Systemic symptoms rare

65
Q

What is multicentric castlemans?

A

Rare lymphopriferatjve disorder presenting with fevers, anaemia, lymphadenopathy

Multi organ systemic features
More aggressive

66
Q

Symptoms of MCD

A

Malaise, night sweats, rigours, fever, anorexia, weight loss

67
Q

Signs of MCD

A

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
Q

Test findings in MCD

A

Thrombocytopenia, anaemia, hypoalbuminaemia, hypergammaglobulinaemia.
Haemophagocytic lymphohistiocytosus may be present and confirmed on bone marrow

69
Q

MCD originates from…

A

Hhv8 infected extrafollicular B cells

70
Q

PELs originate from..

A

HHV8 infected pre terminally differentiated B cells that have traversed the germinal centre

71
Q

Definition of an MCD ‘attack’

A

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
Q

Things increasing risk of MCD

A

Nadir CD4 >200
Older age
No previous cART
Non caucasian background

73
Q

How to diagnose MCD

A

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
Q

Histological findings in MCD

A

Onion skin appearance and interfollicular plasmablasts that express the HHV8 latent nuclear antigen

Recommended - immunocytochemical staining for HHV8 and IgM lambda

75
Q

Treatment for MCD

A

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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