PAS hematology slides Flashcards

1
Q

Bone marrow biopsy in ALL shows ?

A

> 20% Lymphoblasts

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2
Q

ALL remission rate ?

A

> 85%

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3
Q

Relapse rate in ALL ?

A

High -> SCT

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4
Q

Bone marrow biopsy in AML ?

A

> 20 % myeloblasts

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5
Q

Auer rods are seen in ?

A

AML ( it helps to deffrentiate it AML from ALL)

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6
Q

AML M3 ( ApML )

A

High risk of DIC : All trans retinoic acid and Arsenic trioxide.

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7
Q

AML type M5

A

High risk of Lukostasis ( leukopheresis)

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8
Q

Most common chronic lukemia in adults ?

A

CLL ( impaired maturation of Lymphoblasts to Lymphocytes).

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9
Q

CLL pathophysioloy ?

A
  • delayed apoptosis of Lymphocytes.
    *
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10
Q

What is the cause of infection in CLL ?

A

Hypogamaglobulinemia

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11
Q

Most common presenation of CLL?

A

Lymphadenopathy

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12
Q

What is the cause of hemolysis in CLL

A

Autoimmune hemolysis ( direct coomb test positive)
elevated LDH

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13
Q

Smudge cell is a Hallmark of

A

CLL

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14
Q

Bone marrow biopsy in CLL ?

A

Not required

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15
Q

What are the mutations significant for poor prognosis in CLL?

A

*ZAP-70+
*del(17p)
*del(11q)

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16
Q

Myeloid erythroid ratio in CML ?

A

3:1

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17
Q

Blasts in CML chronic vs blast phase

A

> 20 blast
<10 chronic

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18
Q

Lymphomas comprise what % of all malignancies ?

A

3

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19
Q

What are Hodgkin’s Cells ?

A

Mononuclear malignant B cells.

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20
Q

Immunological markers of Hodgkin’s Lymphoma ?

A

CD15 and CD13 positive.

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21
Q

Popcorn cells are seen in ?

A

Nodular Lymphocyte predominat Hodgkins Lymphoma.

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22
Q

Non Hodgkin’s Lymphoma Low grade is common in __ and high grade in ___?

A

Adults high grade, clinically indolent
Peads low grade clinically agressive.

23
Q

Median age of NHL

A

10 and increases with age

24
Q

What percentage of low grade transforms to high grade in NHL?

A

30%

25
Q

Echymosis is seen in what type of Lymphoma

A

NHL

26
Q

Jaundice is seen in what type of Lymphoma ?

A

HL

27
Q

ABVD can result in ?

A

Temporary oligospermia

28
Q

R-CHOP for NHL how many cycles ?

A
  • 8 cycles of 21 days blocks.
    *Rituximab, cyclophosphamide, Hydroxydaunorubicin, Vincristine, Prednisolone
29
Q

HL prognosis ?

A

HL 5-year survival
Stage 1 & 2 = 90%
Stage 3 = 84%
Stage 4 = 65%

30
Q

NHL prognosis ?

A

Low-grade NHL: Median survival 8-10 years
High-grade NHL: 40% 5-year survival

31
Q

What is the primary vs secondary dichotomy in MDS ?

A

Primary = 90%
Secondary = 10%

32
Q

symptoms in MDS ?

A

It depends on the affected myeloid cell line.

33
Q

Bone marrow in MDS may ?

A

Howell- Jolly bodies
Pappenhimer bodies.

34
Q

What is the MDS dx criteria ?

A

The diagnosis of MDS is made based on the presence of:
one or more cytopenia’s,
≥10 percent of nucleated cells in at least one lineage that are morphologically dysplastic,
<20 percent blasts forms in blood and bone marrow,
and/or characteristic cytogenetic or molecular findings,
without evidence of an alternate cause of these findings

35
Q

What is the drug of choice for MDS patients with 5q deletion?

A

Lenalidomide

36
Q

In splenic sequestration hypovolumic shock occurs ?

A

Within hours due to rapid drop in circulating blood volume.

37
Q

What are the prenatal screening in Sickle cell carriers children

A

Chorionic villus sampling before 15 weeks of gestation. after 15 weeks Amniocentesis.

38
Q

Golf ball like RBC’s are seen in

A

HbH disease ( aplha thalasemia 3 gene mutation)

39
Q

Target cells are seen in ?

A

All thalasemias.

40
Q

Transferin saturation in Hemochromatosis ?

A

HIgh ( Low rules out it)

41
Q

Iron overload symptoms starts when?

A

total body iron
reaches 10-20 g

42
Q

mutation in Type 1 Hereditary Hemochromatosis? (classic )

A

C282Y mutation; autosomal recessive
1:8 carrier frequency in N. Europe

43
Q

mutation in Type 2 Hereditary Hemochromatosis? (Juvenile Hemochromatosis)

A

Mutation in HJV gene; autosomal
recessive

44
Q

Type 4 Hereditary Hemochromatosis?

A

“Ferroportin disease”
* Autosomal dominant mutation in
SLC40A1 gene

45
Q

Total body iron

A
  • Women = 2 to 3 g
  • Men = 3 to 4 g
46
Q

How to diagnose Protein C and S deficiency ?

A

*Low Protein C antigen or low Protein S antigen
* Functional assays for either protein

47
Q

What is the cause of Factor V laden ?

A

Point mutation in F5 gene, autosomal dominant condition. Most common in general population.

48
Q

Prothrombin G20210A Mutation

A

It is the second most common inherited thrombophelia

49
Q

Anti-phosphospholpid syndrome is associated to what gene ?

A

HLA-DR7 association

50
Q

What is the normal function of anti-beta2-glycoprotein 1?

A

inhibit plate aggregation. But defects triggers clotting in antiphospholipd syndrome.

51
Q

In anti-phospholipid syndrome ?

A
  • C3 and C4 decreased and aPTT increased.
52
Q

In arterial thrombosis only test for

A

APS

53
Q

In venous thrombosis test for ?

A

Factor V Leiden
APS
Antithrombin deficiecny
Protein C and S
Prothrombin G20210A mutation