hodgkins lymphoma Flashcards
What is hodgkins lymphoma
lymphoid neoplasms affecting lymph nodes
Morphology of hodgkins lymphoma
large dysplastic mononuclear and multinucleated cells surrounded by a variable mixture mature non neoplastic inflammatory cells
Hodgkins lymphoma will usually present with
Lymphadenopathy
History of hodgkins
Thomas hodgkin in 1832 following affected lymph glands in postmoterm cases
dOROTHY REED and carl stenberg identified abnormal cell that defines HL in 1898
Diagnostic features of HD
Reed Stenberg cells and its variations in cancerous area
Hodgkins cancerous cells overproduce this cytokine
IL-13
Cancerous R-S cells origin
B origin
Virus that causes HL
EBV
Nucleus in R-S cell
Bi or multinucleate with prominent nucleolus in each nucleus
Other hodgkins cells apart from R-S cells are
Mononucleate
Affected lymph node morphology
Scattered tumour cells mixed with reactive lymphocytes,plasma cells, macrophages,neutrophils,eosinophils, with variable amount of fibrosis
Hodgkin disease sex distributuion
M>F
HL and age
Increased incidence with age, peaks at third decade, then a decline
Classical hodkins dx accounts for what percentage of hodgkins lymphoma
90%
Peak incidence in hodgkins dx
between ages 15-35
and another peak in late life for all subtypes than nodular sclerosis
Nodular sclerosis occurs mostly in
Young adults
Occupational risks foe HL
Wood dust
Benzene exposure
Nitrous oxide as dental anaesthetic
Highest incidence of EB virus association
Mixed cellularity HD
This confers a 5 fold elevated risk of HD
HIV
This karyotype is found rarely in HD
t(14;18)
EBV has its strongest association with
children, elderly with mixed cellularity
This is expressed in R-S cells of patients with HD
bcl-2
Molecular studies for HL
R-S CELLS. Difficult, since R-S cells only make up 2% of total cells in node with HD
Also, point mutations in p53 gene using PCR
What cytokines are present in HD
IL 1-9
TGF-BETA
TNF
TGF-BETA
Produced by eosinophils and is the source of fibrosis in nodular sclerosis
Clinical features of HL
Peripheral lymphadenopathy in 1 or 2 lymph nodes
Spread is contiguous along lymph node
drenching night sweats
fever
weight loss
Alcohol induced pain in lymph nodes
Mediastinal involvement in young adults i.e cough,chest pain, dyspnea
Classification of HL
Nodular lymphocyte HL
Classical HL
Classical HL features
90% OF ALL HL cases
peak incidence 15-35 and a second peak in late life
Rye classification of HL- Classical
Lymphocyte rich
Nodular sclerosisng
Mixed cellularity
Lymphocyte depleted
Morpholy of lymphocyte rich
Small lymphocytes
few eosinophils
R-S cells
mononuclear cells
5%
Nodular sclerosing morphology
lymph nodes divided by broad band of connective tissue into nodules
Nodules contain a mixture of R-S cells, mononuclear H cells,plasma cells,macrphages, eosinophils
70%
Mixed cellularity morphology
R-S cells readily seen
fibrosis
focal necrosis
mononuclear H CELLS, PLASMA CELLS, MACROPHAGES, EOSINOPHILS
20-25%
Lymphocyte depleted morphology
R-S cells
few lymphocytes
Abundant mononuclear Hodgkins cells
less than 2%
Nodular lymphocyte predominant percentage
10%
expresses B cell markers
This type of CLASSICAL HL is present in stage 3-4
Lymphocyte depleted
Basement membrane involvement is common in
Lymphocyte depleted
Relatively more commom in HIV patients is
Lymphocyte depleted
Ann abor staging system
I- disease in only one LN area
II- Dx in 2 or more LN area on same side of diaphragm
III-Dx in LN areas of both sides of diaphragm
3i- involvement of splenic,portal,celiac nodes
3ii- Involvement of para-aortic,iliac, mesenteric nodes
IV-Extensive dx in liver,bone marrow, other extranodal sites
Diagnosis of HD
History/physical exam lymph node biopsy FBC and comment Bone marrow for staging LDH, Uric acid imaging for spleen size Chest Xray for intrathoracic involvement CT
Poor prognosis markers
Males Age greater than 50 Advanced dx Low serum albumin conc anaemia
Chemotherapt
at stage 1A- field radiotherapy and chemotherapy
all other stages - chemotherapy plus adjuvant radiotherapy
Combination therapy for advanced dx
COPP- cyclophosphamide, oncovin, prednisolone, procabazine
ABVD- Andriamycin, Bleomycin, Vincristine, Darcabazine
tREATMENT OF CHOICE
ABVD
Why is ABVD preferred
less toxic
rarely causes sterility
secondary leukemia less
Antibody for relapsed / refractory dx
Brentuximab
How do you evaluate response
Clinical examination and repitition of abnormal exam in initial stages
Evaluate after 3-4 courses of chemo
scan for residual dx
palpate for masses in residual dx
How many ppl with HL can approximately be cured
85%
