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Heam Onc > Oncology > Flashcards

Oncology Flashcards

1
Q

Leukemia

A
  1. Proliferation of Lymphoid/Myeloid –>
    a. Blasts (immature cells with punched out nuclei) in acute, while mature in chronic setting
    b. Bone marrow involvement is > 20% –> pancytopenias
    c. Blood spillage of WBC –> inc. TLC
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2
Q

leukeMoid reaction

A

cMl v/s acute inflammatory reaction:

  1. Both have inc. TLC count with Neutrophilia and left shift i.e. Bands
  2. LR has inc. LAP score
  3. CML has t(9;22 BCR-ABL) mutation and Basophilia with low LAP score.
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3
Q

Hodgkin’s Lymphoma

A
  1. EBV
  2. CD20 -ive, but B cell origin of Reed Sternberg cells. can lead to fibrosis due to cytokines leak.
  3. No leukemia phase
  4. CD15, CD30 +ive
  5. A lymphocytic mix can cause IL5 –> Eosinophilia.
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4
Q

Non-Hodgkin’s Lymphoma

A
  1. CD20 +ive, CD30-, CD15-, B cell origin except for Adult - T Cell leukemia/lymphoma and T-ALL (Acute Lymphoblastic Lymphoma)
  2. HIV and Autoimmune association
  3. Can occur leukemia phase
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5
Q

Myelophthisic anemia v/s Pancytopenias

A

Metastasis, fibrosis, TB —> Bone marrow invasion —> Leuko-erythroblastosis i.e. immature Granulocytes with left shift plus reticulocytes of a teardrop shape.
Aplastic anemia or pancytopenias do not give Leuko-erythroblastosis.

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6
Q

Lymphoma

A
  1. only lymphoid lineage is involved sparing myeloid cells

2. Reticuloendothelial system is involved sparing blood.

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7
Q

Non-Hodgkin’s Lymphoma (size and type)

A
  1. Small cell –> Folliculo Man-Co Mar
  2. Intermediate –> Burkitt
  3. Large –> DLBCL
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8
Q

Follicular Lymphoma

A
  1. CD20 +
  2. t(14;18) –> Translocation of heavy chain Ig @ 14 to BCL-2 site @ 18 –> overexpression of BCL-2 –>overstabalization of mitochondrial memb –> no cytochrome C release –> No apoptosis.
  3. Rx: Ritux –> CD20 antibody
  4. Reactive V/S follicular lumphoma:
    a. Destruction of normal LN architecture
    b. NO tingible macrophages
    c. Monoclonality
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9
Q

Mantle (corona region) Lymphoma

A
  1. CD 20+
  2. t(11;14) –>Translocation of heavy chain Ig @ 14 to Cyclin D1 site @ 11 –> increase in promotion of G1 to S phase of cells
  3. CD 5+
  4. This is Mantle Co so coexpress CD 20 and CD 5 to gather
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10
Q

Marginal zone lymphoma

A
  1. CD 20+
  2. Linked to chronic inflammation
  3. eg. MALToma
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11
Q

Burkitt Lymphoma

A
  1. CD20+, asso. with EBV
  2. t(8;14) –> Translocation of heavy chain Ig @ 14 to c-myc site @ 8 –> c-myc is a transcription activator. other mutaions are t(8;2), t(8;22)
  3. African type involve jaw
  4. Sporadic type involve abdomen
  5. Starry sky appearance –> Lymphocytes with interspaced macrophages.
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12
Q

n-myc mutations are in

A
  1. Neuroblastoma

2. Small cell carcinoma of lung

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13
Q

DLBCL

A
  1. CD 20+

2. most common

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14
Q

AML (Acute Myeloblastic Leukemia)

A
  1. Acute –> Acute clinical picture
  2. Myeloblasts > 20% in bone marrow
  3. MPO (Myeloperoxidase) + in cytoplasm –> Auer rods
  4. Myelodysplastic syndrome is a risk factor
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15
Q

AML - M3 type

A

Acute Pro-Myeloblastic Leukemia

  1. t(15;17) –> Retinoic Acid Receptor (RAR) fussion —> Mal maturation —> Blasts accumulation
  2. Have Auer rods
  3. cause DIC
  4. Rx: Tretinoin i.e. All Trans-Retinoic Acid (ATRA)
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16
Q

AML - M5 type

A

Acute Monoblastic Leukemia

1. Give gum hypertrophy

17
Q

AML - M7 type

A

Acute Megakaryoblastic Leukemia

  1. Exclusively lacks MPO
  2. Asso with Down Syndrome < age 5 years.
18
Q

ALL (Acute Lymphoblastic Leukemia)

A
  1. Lymphoblasts > 20% in bone marrow
  2. tDt+
  3. Asso with Down syndrome > age 5 years
19
Q

B-ALL

A
  1. tDt +
  2. CD 10-20 +
  3. t(12;21) Good prognosis
  4. t(9;22) Bad prognosis
20
Q

T-ALL

A
  1. tDt+
  2. CD 1-9 +
  3. Give mediastinal mass so we call it “Acute Lymphoblastic Lymphoma”
  4. Acco with Down, Patau, Ataxia telengectasia, Bloom, Fanconi
  5. May spread to CNS and testes.
21
Q

Myeloproliferative Disorders.

A
  1. Chronic Myeloid Lineage Proliferation —> Inc TLC —> Hypercellular Bone marrow with neoplastic WBC involvement of Myeloid lineage —> Can give either Marrow fibrosis with pancytopenias OR transformation into Acute Leukemias
  2. Types:
    a. Polycythemia vera
    b. CML
    c. Essential thrombocythemia
    d. Myelofibrosis
22
Q

Polycythemia Vera

A
  1. All 3 myeloid lineage cells increase while most prominent are RBCs
  2. JAK-2 Kinase mutation
  3. Hyperviscosity syndrome (inc hematocrit), Plethora, Itching after hot shower (inc Basophils), Erythromelalgia (microthrombi), Peptic ulcers (inc Histamine), Gout (high turnover)
  4. Rx: Phlebotomy or Hydroxyurea
  5. Ruxoli-tinib for hydroxyurea resistant cases
23
Q

CML (Chronic Myeloid Leukemia)

A
  1. t(9;22) BCR-ABL mutation —> Philadelphia chromosome —> Inc tyrosine kinase activity
  2. Granulocytes proliferation, especially Basophils and Metamyelocytes.
  3. Rx: Imatinib (tyrosine kinase blocker)
  4. Phases are:
    a. Chronic: stable phase
    b. Accelarated: When becoming symtomatic e.g. splenomegally
    c. Blast: Transform into AML or ALL
24
Q

Essential thrombocythemia

A
  1. JAK-2 mutation —> inc platelets —> overfunction can cause thrombosis or under function can cause bleeding.
25
Q

Myelofibrosis

A
  1. JAK-2 mutation of megakaryocytes —> inc PDGF —> fibroblasts proliferation –> marrow fibrosis –> erythroleukoblastosis
  2. Cause hepatosplenomegaly due to secondary extramedullary hematopoiesis. V/S aplastic anemia which does not cause any extramedullary erythropoiesis or erythroleukoblastosis.
  3. Teardrop cells and dry tap
  4. Inc infections, thrombosis or bleeding
  5. Rx: Ruxoli-tinib
26
Q

Chronic Leukemia

A
  1. Mature WBCs
  2. Myeloid –> CML
  3. Lymphoid –> B v/s T cells
  4. B lymphocyte:
    a. Naive –> CLL
    b. Mature –> Hairy cell leukemia
  5. T lymphocytes:
    a. Node –> Adult - T Cell leukemia/lymphoma
    b. Skin –> Mycosis fungoides
    c. Blood –> Sezary syndrome
27
Q

CLL (Chronic Lymphocytic leukemia)

A
  1. Co-express CD23, 20 and CD 5 plus Smudge cells on a peripheral blood smear. Del of 13q is the main mutation.
  2. If invades nodes –> called “ Small Lymphocytic Lymphoma (SLL)”. and give generalized lymphadenopathy.
  3. Richter transformation: SLL —> DLBCL
  4. Cause low IgG –> infections and Autoimmune diseases –> hemolytic anemia.
28
Q

Hairy cell leukemia

A
  1. Form hairy cytoplasmic projections
    • for TRAP
  3. Get trap in the wrong place –> Red pulp of spleen –> splenomegaly & in bone marrow –> dry tap
  4. Do not cause lymphadenopathy.
29
Q

Adult - T Cell leukemia/lymphoma

A
  1. HTLV - 1 virus associated
  2. Hepatomegaly, adenopathy.
  3. Hypercalcemia (due to punched-out lytic lesions of bone) + Rash (which differentiate it from MM).
30
Q

Mycosis fungoides (cutaneous T cell lymphoma)

A
  1. CD4 + in skin
  2. localized rash, plaques, nodules
  3. Pautrier microabscess
31
Q

Sezary syndrome

A

CD4 + cells in blood with cerebriform nuclei

32
Q

Langerhans cell histiocytosis

A
  1. Proliferative disorder of dendritic langerhans cells.
  2. Presentation:
    a. Child with rash and lytic bone lesions, lytic skull lesions
    b. Recurrent otitis media with mastoid bone involvement
  3. Immature dentritic cells can not activate T cells.
  4. Co express S-100 and CD1a.
  5. Birbeck granules (tennis rackets).

Letterer-Siwe: <2 year old, malignant, multiple organ involvement

Hand-Schuller-Christian: >3 year old.

Eosinophilic granuloma: Benign, skin is NOT involved, pathological fractures with eosinophilic granulomas.

33
Q

EPO producing tumors

A
  1. Renal cell carcinoma
  2. Hepatocellular carcinoma
  3. Hydronephrosis
34
Q

Myelodysplastic syndrome

A
  1. Defect in the maturation process of all myeloid lineage
  2. De novo mutation or environmental exposure via chemo, radiation, or substance.
  3. Risk of transformation to AML
  4. Pseudo-Pelger-Huet anomaly: Bilobed neutrophils, mostly seen after chemo.
35
Q

Monoclonal gammopathy of undetermined significance (MGUS)

A
  1. Asymptomatic i.e. no CRAB, MONOclonal expansion of plasma cells and only forming M spike.
36
Q

Waldenstrom macroglobulinemia (WSMG)

A
  1. Asymptomatic i.e. no CRAB, MONOclonal expansion of plasma cells and forming M spike due to IgM and leading to hyperviscosity syndrome e.g. Raynaud phenomenon, blurred vision.
37
Q

Multiple Myeloma

A
  1. Symptomatic MONOclonal expansion of plasma cells in bone marrow and producing IgG (55%) OR IgA (25%).
    A bone marrow invasion of >30% of plasma cells is diagnostic.
    C: hyperCalcemia
    R: Renal involvement
    A: Anemia
    B: Bone lytic lesions
  2. Give M spike
  3. Most common cause of death is infections (due to Ig loss via kidneys).
  4. Can give the followings:
    a. Primary amyloidosis ( in kidneys, heart, tongue, and look apple green with Congo red.
    b. Plasma cells –> IL 1 and 6 –> inc RANK activation of osteoclasts –> lytic bone lesions –> hypercalcemia
    c. Renal failure due to hypercalcemia, inc light chain filtration (Bence Jones Protein) and amyloidosis.
    d. Rouleaux formation
38
Q

Bortezomib

A

Inhibits catalyzing site of Proteasome leading to accumulation of misfolded proteins and apoptosis of cells

Heam Onc (4 decks)

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