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Pathology > White Blood Cell Disorders > Flashcards

White Blood Cell Disorders Flashcards

1
Q

Signs + symptoms of infectious mononucleosis.

A
  • fever
  • sore throat
  • pharyngitis
  • generalized lymphadenopathy
  • hepatosplenomegaly
  • (antibody + T cell response)
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2
Q

Cause of infectious mononucleosis?

A

-Typically EBV
can also be CMV.

Serologically: EBV –> heterophile positive
CMV heterophile negative

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3
Q

What does mono mainly infect in the body, and then how does our body respond?

A
  • oral mucosa –> Pharyngitis
  • liver –> elevating liver enzymes, causing hepatomegaly
  • B cells
    Response:
  • Cytotoxic T cells (increase) cause T cell hyperplasia in lymph causing general lymphadenopathy
  • T cell hyperplasia in PALS causing splenomegaly
  • high WBC count with atypical lymphocytes n the blood
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4
Q

How can you distinguish Hodgkins and non-hodgkins histologically?

A

Hodgkins –> Reed-sternberg giant cells (neoplastic cells)

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5
Q

What are the 3 main neoplastic proliferations of white blood cells?

A

1) Lymphoid neoplasms
2) Myeloid neoplasms
3) Histiocytic

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6
Q

What are the 3 main groups of myeloid neoplasms?

A

1) Acute myelogenous leukaemia
2) Chronic myeloproliferative disorders
3) Myelodysplastic syndromes

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7
Q

Explain pathophysiology of acute myeloid leukaemia?

A

Genetic mutation causing a “maturation block” that interferes with the differentiation of early myeloid cells, thus leads to accumulation of myeloid blast cells in the bone marrow.

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8
Q

How can acute promyelocytic leukaemia be distinguished from acute monocytic and acute megakaryoblastic leukaemia?

A

Acute promyelocytic leukaemia has myeloperoxidase (MPO) in it’s cytoplasm.

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9
Q

How is acute promyelocytic leukemia treated?

A

All-trans-retinoic acid (ATRA) is given. It binds to altered receptors causing myeloblasts to mature, and eventually die (lifespan 6 hrs), clearing the tumour quite quickly.

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10
Q

How are lymphoblasts differentiated from myeloblasts and mature lymphocytes?

A

Lymphoblasts have a positive nuclear stain for TdT (DNA polymerase)

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11
Q

What type of cells are involved in chronic lymphocytic leukemia (CLL)?

A

Neoplastic proliferation of naive B cells.

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12
Q

Complications of CLL:

A
  • hypogammaglobulinemia –> infections
  • autoimmune hemolytic anemia
  • transformation to diffuse large B-cell lymphoma (Richter transformation)
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13
Q

What is the Richter transformation? Which disease states can it occur in?

A

The transformation to diffuse large B-cell lymphoma.
Can occur in:
- CLL (chronic lymphoid leukemia)
- hairy cell leukaemia

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14
Q

What type of cell(s) are involved in hairy cell leukaemia?

A

Neoplastic proliferation of mature B cells

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15
Q

What type of leukaemia is the most common in adults?

A

CLL (chronic lymphocytic leukemia)

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16
Q

In what leukemia do you find “dry tap” from the bone marrow aspiration?

A
  • Hairy cell leukemia
  • myelofibrosis
    Due to marrow fibrosis.
17
Q

What do you clinically find in hairy cell leukaemia?

A
  • massive splenomegaly
  • pancytopenia
  • dry tap in marrow aspiration
  • NO lympadenopathy!! (vs CLL, where there is)
  • (+) For TRAP (tartrate resistant acid phosphatase)
18
Q

What are Pautrier microbabscesses? What condition do you find them in?

A

They are little aggregations of neoplastic cells in the epidermis.
Found in mycosis fungoides (leukaemia)

19
Q

What can mycosis fungoides progress to?

A

Sezary syndrome (T cell leukaemia)

20
Q

What are cells (+) for in hairy cell leukaemia?

A

TRAP

21
Q

What does TRAP (+) indicate?

A

Hairy cell leukaemia

22
Q

What is the leukamoid reaction?

A

Increase in WBCs due to infection.

Looks like it mimics CML

23
Q

How can you distinguish CML and leukamoid reaction?

A

CML is:

  • negative for LAP stain
  • high basophils
  • presence of t(9;22), the Philadelphia chromosome
24
Q

How do you treat CML?

A

Tyrosine kinase inhibitor

imatinab

25
Q

What does CML present with? What can it progress to?

A
  • Massive splenomegaly
  • Increased WBCs, mainly basophils

Can progress to:

  • AML (2/3s of cases)
  • ALL (1/3)
26
Q

What is polycythemia?

What is absolute and relative polycythemia?

A

Polycythemia is disease state with high hematocrit.

Absolute polycythemia = increase in RBCs causing the increase in Ht

Relative polycythemia = decrease in volume of plasma

27
Q

What is polycythemia vera?

A

Neoplastic proliferation of mature myeloid cells, with high RBCs mainly, but also high granulocytes and platelets.

28
Q

Signs + symptoms for polycythemia vera?

A
  • headache + blurry vision
  • flushed skin/face (high RBC)
  • risk of venous THROMBOSIS!! (hepatic v., portal v., dural sinus)
  • itching (after bath from high mast cells)
29
Q

Treatment for polycythemia vera?

A
  • phlebotomy

- hydroxyurea

30
Q

What is hydroxurea used to treat?

A
  • sickle cell anemia
  • polycythemia vera (PV)
  • CML
  • cervical cancer
31
Q

What type of mutation is present in polycythemia vera?

A

JAK-2 kinase mutation

32
Q

Explain EPO production in reactive polycythemia

A

High EPO from ectopic production. Due to renal cell carcinoma

33
Q

What is myelofibrosis?

A

Neoplastic proliferation of mature myeloid cells, especially megakaryocytes.
They overproduce PDGF (platelet derived growth factor) and cause marrow fibrosis.

34
Q

Clinical/histo signs of myelofibrosis?

A
  • splenomegaly
  • tear drop RBCs
  • nucleated RBCs
  • immature granulocytes
35
Q

What condition do you find tear drop RBCs?

A

Myelofibrosis

Pathology (13 decks)

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