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YEAR 3 HAEMATOLOGY > Lymphoid malignancies > Flashcards

Lymphoid malignancies Flashcards

1
Q

what is used to diagnose a leukaemia?

A

Biopsy (bone marrow, lymph node)

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2
Q

how Is staging done?

A

thorugh clinical examination and imaging (CT) - this tells us WHERE it is = location and extent, prognosis, influences tx.

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3
Q

what are the types of lymphorpoliferative disorders?

A

Acute lymphoblastic leukaemia (ALL)
Chronic lymphocytic leukaemia (CLL)
Hodgkin lymphoma
Non-Hodgkin lymphoma (NHL) -High-grade (diffuse large B-cell lymphoma), Low-grade (follicular, marginal zone)

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4
Q

ALL (Acute lymphoblastic leukamia) - what is it?

A

Cancerous disorder of lymphoid progenitor cells, Usually in the bone marrow but they can go anywhere.
Normal = Immature, rapidly proliferating cells that differentiate into lymphocytes
Leukaemia = No differentiation. Instead, rapid, uncontrolled growth and accumulation.

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5
Q

75% of cases occur in people of what age group?

A

children below the age of 6. present with a 2-3 wk hx of bone marrow failure or bone/joint pain.

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6
Q

RF’s of ALL

A

Increasing age, Increased white cell count, Cytogenetics/molecular genetics t(9;22); t(4;11), Slow/poor response to treatment

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7
Q

what is a TYPICAL ALL hx?

A

17m, 1 month impaired vision in both eyes, 1/2 stone weight loss, dypnoea on minimal exertion

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8
Q

general features of acute leukaemia?

A

BONE PAIN, INFECTION, SWEATS, dyspnoea, fever, pale, splenomegaly, lymphadenopathy, purpura, bleeding gums, fatigue

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9
Q

TYPICAL ALL Ix and results

A

FBC = low Hb, raised WCC, low platelets. Bone marrow shows 90% B-Lymphoblasts, BONE MARROW FAILURE WITH RAISED WCC

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10
Q

what are the characteristics of ALL cells? And what do they express?

A

large, EXPRESS CD19!!!, cd34 and tdt

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11
Q

Tx of ALL…

A

chemo to obtain remission, consolidation therapy, CNS directed tx, maintainance of tx for 18 months, Allogenic Stem cell transplantation may be used if risk is high.

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12
Q

ALL tx newer therapies…

A

bi-specific t-cell engagers e.g.blinatumab, CAR (chimeric antigen receptor T-cells) - this is where healthy t cells are harvested, made to express a specific receptor for cd19 on leukaemia cells then reinfused into the pt.

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13
Q

KEY SIDE EFFECTS OF T CELL IMMUNOTHERAPY

A

cytokine release syndrome (fever, hypotension, dyspnoea)

Neurotoxicity (confusion, normal conscious level, seizure, headache, focal neurology, coma)

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14
Q

prognosis of ALL

A

adults and children = 90% remission rate.

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15
Q

how is ALL different to CLL?

A

the abnormal cells are mature - they usually resemble normal, well behaved lymphocytes (grow slowly, carry many of the normal markers which b lymphocytes have)

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16
Q

what lymphocyte count is required to be diagnostic of CLL?

A

> 5

17
Q

epidemiology

A

> 1700 new cases CLL per year in the UK, Commonest leukaemia worldwide, 2 males: 1 female, Occasionally familial, Rare in far East – this likely indicates a Geographic/ ethnic role in pathogenesis.

18
Q

CLL sy/sx

A

of asymptomatic. Frequent findings: bone marrow failure (anaemia, thrombocytopenia), lymphadenopathy, splenomegaly, fever and sweats. Less common: hepatomegaly, infetions, weight loss.

19
Q

what are associated ifndings with CLL?

A

immune paresis (loss of normal immungoglobulin production), Haemolytic anaemia

20
Q

Outline BINET STAGING for CLL…

A

A = <3 lymph nodes, B = >3 lymph nodes, C = B + anaemia or thrombocytopenia (6yr survival)

21
Q

what are the indications for tx of CLL?

A

progressive bone marrow failure, huge lymphadenopathy, progressive splenomegaly, lymphocyte doubling time <6 months, systemic sy, autoimmune cytopenias.

22
Q

CLL Tx

A

often do nothing. Cytotoxic chemotherapy e.g. fludarabine, bendamustine
Monoclonal antibodies e.g. Rituximab, obinatuzumab
Novel agents - Bruton tyrosine kinase inhibitor eg ibrutinib, PI3K inhibitor eg idelalisib, BCL-2 inhibitor eg venetoclax.

23
Q

what are poor prognostic markers for CLL?

A

Advanced disease (Binet stage B or C), Atypical lymphocyte morphology, Rapid lymphocyte doubling time (<12 mth), CD 38+ expression, Loss/mutation p53; del 11q23 (ATM gene), Unmutated IgVH gene status

24
Q

what is the Px of a LYMPHOMA?

A

lymphadenopathy/ hepatosplenomegaly
Extranodal disease
“B symptoms” = fever, drenching night sweats, unexplained weight loss over the last 6 months.
bone marrow involvement

25
Q

DEFINE LYMPHOMA

A

cancers of lymphoid origin, px with enlarged lymphnodes, extranodal involvement, bone marrow involvement and systemic sy (weight loss, fever, night sweats, pruritus, fatigue)

26
Q

how are lymphomas staged?

A

lymphnode biopsy, ct scan, bone marrow aspirate and trephine.

27
Q

what is stage a and b?

A

a = absence of b symptoms, b = fever, night sweats, weight loss.
1- localized - single lymph node, 2 - 2 or more lymph node regions above the diapragm, 3 - 2 or more lymph node regions below the diaphragm, 4 - widespread disease effecting multpile organs.

28
Q

NON-HODGKIN LYMPHOMA - how is it classified?

A

Cancer of lymphoid origin, all lymphomas besides Hodgkin’s lymphoma.
Classified according to: lineage (B-cell or T-cell) = Majority are B-cell in origin (90%)
”Grade” = High-grade vs low-grade

29
Q

in terms of GRADE of disease - what is low grade lymphoma?

A

Indolent, often asymptomatic

responds to chemotherapy but incurable

30
Q

in terms of GRADE of disease - what is high grade lymphoma?

A

Aggressive, fast-growing
Require combination chemotherapy
Can be cured

31
Q

Diffuse B-cell lymphoma

A

Commonest subtype of lymphoma (of any kind)

High-grade lymphoma

32
Q

follicular lymphoma

A

2nd commonest subtype of lymphoma
Low-grade lymphoma
Like CLL, leave alone if not causing problems – “watch and wait”

33
Q

how are both tx?

A

chemotherapy and anti-CD20 monoclonal antibody

34
Q

what virus is HODGKINS LYMPHOMA associated with?

A

association with Epstein Barr virus; familial and geographical clustering

35
Q

Tx of HODGKINS LYMPHOMA…

A 
Combination chemotherapy (ABVD) +/- radiotherapy
Monoclonal antibodies (anti-CD30)
Immunotherapy (checkpoint inhibitors)
PET scanning central to assessment of response to treatment

YEAR 3 HAEMATOLOGY (17 decks)

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