Acute Leukemia Flashcards

1
Q

acute leukemia is a ___ expansion of ___ (AML) or ____ (ALL) blasts in the bone marrow.

A

acute leukemia is a clonal expansion of myeloid (AML) or lymphoid (ALL) blasts in the bone marrow.

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2
Q

demographics affected more by AMl vs ALL

A

AML: most adult leukemias.

ALL: most childhood leukemias are ALL. Secondary increase in incidence of ALL inelederly.

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3
Q

associated violaceious rash seen in leukemia

A

leukemia cutis

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4
Q

Why would you mainly see lymphadenopathy in someone with ALL vs AML

A

ALL mostly because lymphadenopathy houses T cells and lymphoid priodcuts. AML is a leukemia of the myeloid line and so you woudn’t expect excess myeloid products to be in the lymph nodes.

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5
Q

general symptoms of leukemia (you can’t really tell the difference between AML or ALL until you run tests,,,except you may lean closer towards ALL if they have lymphadenopathy)

A

on the PE, they may be tachycardic, pale, chest pain, petechiae, ecchymosis and mucosal bleeding. may see splenomegaly or lymphadenoapthy.

they will have a Hx of fatigue, malaise, anorexia, viral-type illness, bruising, bleeding, bone tenderness, infection.

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6
Q

oral characteristic of acute leukmeia

A

gingival hyperplasia

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7
Q

investigations when someone presents with concerning symptoms

A
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8
Q

wats up with this PBS

A

this PBS has a lot of blasts in one area. probably an acute leukemia

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9
Q

characteristic specific featue of AML

A

AML has auer rods. the auer rods are messed up granular material.

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10
Q

which antigens on B cells can point out acute leukemia? T cells? Myeloid? blasts? lymphocytes?

A

B- CD 19, 20, 22

T– 3,7,4, 8

Myeloid: CD13, 33, MPO

blasts: CD34
lymphocytes: tdt

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11
Q

Dx?

A

AML with hyperleukocytosis, the WBCs are over 100.

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12
Q

T/F leukostasis is more common in ALL

A

false. it is more common in AML when peripheral blood WBCs are over 100.

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13
Q

Why does DIC occur in leukemia? what type of acute leukemia is it seen more in?

A

AML?ALL

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14
Q

uric acid crystals are seen in acute leukemia. aka Tumor Lysis Syndrome. What type of acute leukemia is this seen more frequently in?

A
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15
Q

“2 hit” hypothesis of leukemia formation

A

acute leukemia happens because a hematopoietic progenitor is affected by two hits;

  1. proliferative advantage: mutations in genes encoding transcription factors leasds to proliferation faster htan normal
  2. impaired differentiation: mutations in genes that regulate cell division and differentiation
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16
Q
A
17
Q

the ____ internal tandem gene sequence is indicative of higher relapse and decreased survival.

the ____ and ___ mutations confer good prognosis

A

FLT3 internal tandem duplication –
higher relapse, decreased survival

CEBPa and NPM1 mutations confer
good prognosis

18
Q

AML is seen in younger patients. what do you give for the high white blood cell count? what methods of supportive care?

A

-hydroxyurea for high WBC

supportive care: IV fluids, allopurinol to prevent tumour lysis. transfusions and treatment of any infecitons, and aggressively manage DIC.

19
Q

what’re the adverse vs good prognostic factors for ALL (75% of patients are children)

A

Adverse factors: high WBC count over 100. Age under 1 or over 10, phildelphia chromsome seen, or measurable residual disease is + after treatment

good factors: low WBC count. Ages 1-10. hyperdiploid on karyotype and not much measureable residual disease.

20
Q

general treatment of ALL and comp;lications

A
  • induction with multiple drugs in regimen-specfici sequences of dose intensity and time intensity. total 2-3 years of chemotherapy.
    complications: febrile nutropenia, platelet transfusions, RBC transfusions needed, elevated liver enzymes, thrombosis, neuropahty, steroid side effects.

most treatments are only applicable to adults. it’s harder for elderly individuals to tolerate treatment.

21
Q

general mechanism of blinatumomab

A

has CD19 antibodies.can takes cancerous CD19 b cells and bind it to T cell, causing it to get destroyed.

22
Q
A