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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lymphoma

A
  1. only lymphoid lineage is involved sparing myeloid cells

2. Reticuloendothelial system is involved sparing blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Non-Hodgkin’s Lymphoma (size and type)

A
  1. Small cell –> Folliculo Man-Co Mar
  2. Intermediate –> Burkitt
  3. Large –> DLBCL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Marginal zone lymphoma

A
  1. CD 20+
  2. Linked to chronic inflammation
  3. eg. MALToma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

n-myc mutations are in

A
  1. Neuroblastoma

2. Small cell carcinoma of lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DLBCL

A
  1. CD 20+

2. most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Myelofibrosis
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
Chronic Leukemia
1. Mature WBCs 2. Myeloid --> CML 3. Lymphoid --> B v/s T cells 3. B lymphocyte: a. Naive --> CLL b. Mature --> Hairy cell leukemia 4. T lymphocytes: a. Node --> Adult - T Cell leukemia/lymphoma b. Skin --> Mycosis fungoides c. Blood --> Sezary syndrome
27
CLL (Chronic Lymphocytic leukemia)
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
Hairy cell leukemia
1. Form hairy cytoplasmic projections 2. + 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
Adult - T Cell leukemia/lymphoma
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
Mycosis fungoides (cutaneous T cell lymphoma)
1. CD4 + in skin 2. localized rash, plaques, nodules 3. Pautrier microabscess
31
Sezary syndrome
CD4 + cells in blood with cerebriform nuclei
32
Langerhans cell histiocytosis
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
EPO producing tumors
1. Renal cell carcinoma 2. Hepatocellular carcinoma 3. Hydronephrosis
34
Myelodysplastic syndrome
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
Monoclonal gammopathy of undetermined significance (MGUS)
1. Asymptomatic i.e. no CRAB, MONOclonal expansion of plasma cells and only forming M spike.
36
Waldenstrom macroglobulinemia (WSMG)
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
Multiple Myeloma
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
Bortezomib
Inhibits catalyzing site of Proteasome leading to accumulation of misfolded proteins and apoptosis of cells