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HEMATOLOGY > Malignancy in Hematology > Flashcards

Malignancy in Hematology Flashcards

1
Q

How to identify NORMAL, more mature NON-lymphoid cells?

A
  • morphology
  • cell surface Ag (glycoprotein A= RED cells)
  • enzyme expression (myeloperoxidase- neutrophils)
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2
Q

How to identify normal, PROGENITOR cells?

A
  1. Immunophenotyping (cell surface Ags)
  2. Cell culture ASSAY
  3. Animal models
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3
Q

What occurs in Malignant Haemopoiesis?

A
  1. incr. no. of ABNORMAL and dysfunctional cells
  2. LOSS of normal activity
    - —-haemopoeisis/ immune function
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4
Q

What causes the prodn of abmormal cells, and thus dysfunctional activity?

A
  1. incr. proliferation
  2. lack of differentiation
  3. lack of maturation
  4. lack of apoptosis
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5
Q

What is the pathophysiology of Acute leukemia?

Give an example of an Acute leukemia.

A
  • proliferation of ABNORMAL progenitors
  • with BLOCK in DIFFERENTIATION/ MATURATION
  • Acute myeloid leukemia
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6
Q

What is the pahtophysiology of Chronic myeloproliferative d.o?

A
  • also PROLIFERATION of abnormal progenitors
  • –NO differentiation/ Maturation block

ex: CHRONIC myeloid leukemia

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7
Q

What causes haematological malignancies?

A
  1. somatic mutation in regulatory genes (DRIVER mutation vs PASSENGER mutation)
  2. usually MULTIPLE hits (more than single event)
  3. genetic, epigenetic, env. interaction
  4. recurrent cytogenic abnormalities (not causal)
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8
Q

What are driver mutations?

A

mutations that provide a selective GROWTH advantage
- thus promotes CANCER development

aka CANCER gene

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9
Q

Is malignant haemopoiesis MONOCLONAL or POLYCLONAL?

A
  • MONOCLONAL
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10
Q

Wht is a clone?

A

popn of cells derived from a SINGLE parent cell
—-parent cell has a driver mutation that is shared with daughter cells

—-clones may diversify; but they contain similar backbone

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11
Q

How to screen kids who develop ACUTE LYMPHOBLASTIC LEUKEMIA?

A

Guthrie cards

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12
Q

What are the haematological malignancies based on ?

A
  1. Lineage (myeloid/ lymphoid)
  2. Developmental stage
  3. Anatomical site
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13
Q

What are the diff. malignancies seen developed in lymphoid lineagee?

A

Acute Lymphoblastic leukemia
>Chronic Lymphocytic Leukemia
>Myeloma

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14
Q

What are the diff. sites of haematological malignancies?

A
  1. blood: LEUKAEMIA

2. Lymph node involvement: LYMPHOMA

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15
Q

AT what sites does chronic lymphocytic leukaemia manifest?

A

in blood and lymph nodes

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16
Q

Where does myeloma manifest?

A

plasma cell malignancy in MARROW

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17
Q

Which is more CLINICALLY aggressive?

A

Acute leukemias and HIGH-grade LYMPHOMAS

—-aggressive due to RAPID progression of SX

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18
Q

What are the histological fts of aggression?

A
  1. large cells with HIGH nuclear-cytoplasmic ratio
  2. Prominent nucleoli
  3. Rapid proliferation
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19
Q

What is Acute lymphoblastic leukaemia a disease of?

A
  • malignant disease of PRIMITIVE lymphoid cell (lymphoblasts)
20
Q

Name the most common childhood cancer.

A

Acute lymphoblastic leukaemia

21
Q

What is the clinical presentation of ALL?

A
  1. Marrow failure (anaemia/ infections/ bleeding)
  2. leukemic efx: high count with OBSTRUCTION of circulation (involves areas OUTSIDE the marrow and blood)—CNS and TESTIS
  3. Bone pain
22
Q

What is seen with Acute Myeloid Leukaemia? And in whom?

A
  • SIMILAR presentation to MARROW failure

- >60 y.o

23
Q

What ivx done for acute leukemia?

A
  1. blood film and COUNT
  2. Coagulation screen
  3. bone marrow aspirate
24
Q

What should be observed on blood film?

A
  • reduction in NORMAL
  • presence of ABNORMAL
  • —note the BLASTS with a HIGH nuclear:cytoplasmic ratio
25
Q

What could be invx with bone marrow sampling?

A
  • Morphology
  • Immunophenotyping
  • cyto/molecular genetics (diagnostic UTILITY and PROGNOSTIC significance)
  • Trephine
26
Q

How tell AML apart from ALL?

A

by immunophenotyping

— replaced cytochemistry as a diagnostic tool

27
Q

What does immunophenotyping seek?

A

(by flow-cytometry) —lineage-specific proteins on cell surface

28
Q

What is trephine?

A
  • the analysis of a PIECE pf a bone

- allows better assessment of cellularity and HELPFUL when aspirate is sub-optimal

29
Q

What is the treatment for ALL like?

A
  1. lasts up to 2-3 years
  2. diff. phases of rx (varying intensity)
  3. targeted rx for diff. subsets
30
Q

What is the rx for AML like?

A
  • normally intensive
  • 2-4 cycles of CHEMO (5-10 days of chemo followed by 2-4 weeks of recovery)
  • prolonged hospitalisation
  • target rx
31
Q

What is a Hickman-Line?

A
  • long, flexible, plastic tube inserted underneath the CHEST wall skin
    > into the large vein draining INTO the heart
    —allows the delivery of medication
32
Q

What are the issues with marrow suppression?

A
  1. Anaemia
  2. Neutropenia (Infections/ severity and duration)
  3. Thrombocytopenia
33
Q

What are neutropenic pts predisposed to?

A
  • gram (-)ve bacteria

- –may cause fulminant LIFE threatening sepsis

34
Q

Risk of thrombocytopenia.

A

BLEEDING

  • purpura
  • petechiae (plt <20 x10)
35
Q

What are the complications of rx?

A
  • N.V
  • hair loss
  • liver, renal dysfxn
  • tumor lysis syndrome (1st course of rx)
  • INFECTION
  • later: loss of fertility/ cardiomyopathy with anthracyclines)
36
Q

What is tumor lysis syndrome?

A
  • the mass breakdown of tumor cells, results in a huge spike in K+, uric acid
  • drop in calcium levels
37
Q

What are the symptoms of tumor lysis syndrome?

A
  1. palpitations
  2. seizures
  3. DARK urine, reduced output and flank pain
  4. Nausea (with/without vomitting)
  5. lack of appetite
  6. numbness/ hallucinations
  7. muscle cramps/ spasms

—left untreated> KIDNEY FAILURE and DEATH

38
Q

What should be done as soon as a chemo pt develops a fever?

A
  • neutropenic fever

- give EMPIRICAL treatment with BROAD spectrum antibiotics (cover gram (-)ve)

39
Q

What does it mean if there is PROLONGED neutropenia with a PERSISTING fever unresponsive to anti-bacterial agents?

A

FUNGAL infection

40
Q

What protozoan infection maybe seen with chemo?

A

PJP

41
Q

What kind of infections are common in individuals?

A

bacterial is COMMON

—-but they are v. susceptible to FUNGAL

42
Q

Define acute leukemia.

A
  • excess of BLASTS (>20%) in either the peripheral blood or bone marrow !

—–rapid, progressive clonal malignancy of the marrow or blood with maturation defects.

43
Q

Characteristic presentation for AML subgroups.

A
  • gum hypertrophy

- DIC

44
Q

How effective if rx for leukaemia?

A
  • MANY go into REMISSION (<5% marrow blasts with recovery of NORMAL haemopoiesis)
  • —remissions not durable for some types of leukaemia (many RELAPSE)

—some die of rx-related toxicity

45
Q

What are other options for treamtment of leukaemia?

A
  1. targeted rx (Molecular targeting- with KINASE inhibitors; Acute lymphocytic leukaemia wuth PHILADELPHIA chromosome)
  2. allogenic stem cell transplant
46
Q

What makes AML (acute promyelocytic leukaemia) associated with another particular disorder.

A
  • specific chromosomal translocation
    t(15:17)
  • a.w DIC
47
Q

What is immunotherapy about?

A
  • egineering T-cells to ATTACK leukaemic cells

CAR T-CELL therapy

HEMATOLOGY (20 decks)

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