Hematopathology- Wright Flashcards by Catherine Atkinson

What is hematopoesis

Thrombopoesis, Erythropoesis, Leukopoesis (understanding how cells are made)

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What is a blast cell and what is the only place it comes from?

An initial cell only in the bone marrow

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Where are old platelets destroyed?

In the liver

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Erythropoesis is the formation of _____ and becomes a _______- then matures into an erythrocyte

RBCs, reticulocyte

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Platetes are formed from ________

Megakaryoblasts

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Neoplastic cells in the bloodstream

Leukemia

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Neoplastic cells in the lymph system

Lymphoma

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Neoplastic plasma cells

Myeloma

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This type of leukemia is composed of blast cells in the bone marrow

Acute leukemia

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This type of leukemia is composed more of mature precursor cells

Chronic leukemia

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What are some signs and symptoms of leukemia?

Leukocytosis, panncytopenia, bone pain, LAD, splenomegaly

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To make a dx of leukemia, what test should you do to confirm the dx?

Bone marrow bx

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This type of leukemia is the mc leukemia in adults, has circulating blasts >20% (immature myeloid cells) and you’ll see AUER RODS on pathology

AML

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Auer rods should make you think of what?

AML

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AML can lead to these three complications

Anemia, Infection (ABC) and bleeding (low functioning platelets)

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This is the mc CHILDHOOD malignancy between ages 2-5

ALL

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Pathology of this disease confirms lymphoblasts (lymphoid lineage)

ALL

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A good prognosis of ALL is __________ meaning > 50 chromosomes per cell, CD10+ and low WBC count

Hyperdiploid

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A poor prognosis of ALL is ___________, less than 2 years of age or greater than 10 years of age, male gender, and high WBC count > 100,000

hypolipoid

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What is CAR-T therapy

Genetically modified autologous immunotherapy targeting CD-19 where a person’s own T-cells are genetically modified to direct the patient’s T cells against the leukemic cells. However, cytokine release storm occurs in 70-90% of patients. (Used as second or thrid line therapy because of this reason)

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Uncontrolled proliferation of mature and of maturing granulocytes

CML

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Philadelphia chromosome

CML

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Fusion of two genes: BCR and ABL1 resulting in an abnormal chromosome 22

Philadelphia chromosome- CML

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Treatment for CML?

Oral chemo and stem cell transplant if last resort

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Progressive accumulation of functionally incomptent lymphocytes with a blood lymphocyte count of >5,000

CLL

Gingersnap appearance of cells and they are fragile and break during processing so often called smudge cells

CLL

What is the treatment for CLL?

Frequently doesn't need to be treated at the time of dx because it is non-aggressive. Generally will tx based on symptoms or if very severe

Malignant neoplasms derived from B cell progenitors, T cell progenitors, mature B cells, mature T cells, or NK cells

Lymphoma

Presence of REED STERNBERG cells should make you think of what type of cancer?

Hodgkin lymphoma

There are two types of non-hodgkins lymphoma, what are they?

Indolent (slow growing) and aggressive

This type of lymphoma is really common in thin males around the age of 20-30. They may have painless cervical adenopathy or supraclavicular node and sometimes pain in lymph nodes with alcohol consumption

Hodgkin lymphoma

Neoplastic cell=Reed Sternberg cell

Hodgkin lymphoma

Tx for hodgkin lymphoma?

Chemo and rarely surgery

``` Are these aggressive or indolent? • Follicular Lymphoma • Marginal Zone Lymphoma (MALT) • Lymphoplasmocytic Lymphoma • Small Lymphocytic Lymphoma ```

INdolent

``` Are these aggressive or indolent? • Diffuse Large B cell Lymphoma (DLBCL) • Burkitt Lymphoma • Mantle Cell Lymphoma • Peripheral T cell Lymphomas ```

Aggressive

This is an aggressive type of lymphoma that is the mc lymphoma worldwide. It typically presents with a rapidly enlarging symptomatic mass in the neck or abdomen. Can be associated with EBV.

Diffuse Large B Cell Lymphoma

This type of lymphoma has painless peripheral adenopathy and can see it in a lot of nodes but it commonly waxes and wanes but never really goes away.

Follicular lymphoma

This is a highly aggressive B cell neoplasm that comprises of 30% of pediatric lymphomas in the US. Typically endemic in Africa and can be associated with HIV

Burkitt Lymphoma

Patients with burkitt can have a high propensity for tumor lysis syndrome (like cytokine storm) and you might commonly see what lab result because of it?

Hyperuricemia (put lots of people on allopurinol because of it)

This lymphoma can involve any region of the GI tract and nuclear staining for D1 is present in 95% of cases

Mantle cell lymphoma

What is a marginal zone?

Type of slow growing non-Hodgkin lymphoma that develop from B cells

Extranodal marginal zone lymphoma of mucosa associated lymphoid tissue (MALT lymphoma)

Marginal zone lymphoma

This type of lymphoma is frequently due to chronic gastritis from H.pylori infections and arrises from tissue in the stomach. Also common in Hispanics

Marginal zone lymphoma

This lymphoma is associated with IgM monoclonal gammopathy and smudge cells can be pressent

Lymphoplasmacytic Lymphoma

Neoplastic proliferation of plasma cells producing an monoclonal immunoglobulin and proliferation of plasma cells causes skeletal destruction with osteolytic lesions, osteopenia, and/or pathologic fracture

Multiple myeloma

CRABS

Calcemia, renal dysfunction, Anemia, bone lesions Multiple myeloma

M-Spike on SPEP

Multiple myeloma

Bence jone protein in urine

Multiple myeloma

Lytic lesions (punched out) on skeletal imaging

multiple myeloma

These two things are needed to make the diagnosis of multiple myeloma

1. Clonal bone marrow plasma cells greater than or equal to 10% or bx proven bony or soft tissue plasmacytoma 2. PLUS presence of related organ impairment or tissue impairment (CRABS)

Tx for multiple myeloma?

Non-curable but a stem cell transplant can prolong life (an attempt to buy time)

Heterogrnous group of malignant hematopoietic stem cell disorders characterized by dysplastic and ineffective blood cell production

Myelodysplastic syndrome

What is primary hemostasis?

* Primary hemostasis refers to the initial steps in clot formation, which mostly rely on vessel wall and platelet function * Disorders of primary hemostasis often present with mucocutaneous bleeding or petechiae

What is secondary hemostasis?

* Secondary hemostasis refers to the subsequent formation of the fibrin- based clot, which mostly relies on coagulation factors * Disorders of secondary hemostasis present with deep tissue hematomas or joint bleeding

Hemostasis can occur due to what three things?

1. Platelet dysfunction 2. Increased platelet destruction 3. Decreased platelet production

This is when there is an antibody destruction of platelet and can also be known as ITP

Immune Thrombocytopenic Purpura

What are some sx/sxs of ITP

petechia, purpura, bleeding

* Antibody mediated destruction of platelets * Acquired with use of heparin * Antibody platelet factor 4 and heparin which triggers thrombosis

Heparin Induced Thrombocytopenia

• Deficiency of the ADAMTS13 protease, which results in accumulation of very long von Willebrand factor multimers on the endothelial surface that are capable of binding platelets

TTP (Thrombocytic Thrombocytopenic Purpura)

What is the pentad of symptoms of TTP?

Fever, thrombocytopenia, renal failure, neuro changes, microangiopathic anemia (hemolytic)

• Abnormalities in the vessel wall of arterioles and capillaries lead to microvascular thrombosis

TTP

• Abnormalities in the vessel wall of arterioles and capillaries lead to microvascular thrombosis – similar to TTP • Complement-induced damage to the endothelium from shiga toxin

Hemolytic Uremic Syndrome

* Shiga toxins are produced by Shigella dysenteriae and some serotypes of Escherichia coli * Renal dysfunction more common than with TTP

HUS

* Dysfunction of platelets and coagulation cascade | * Activation of clotting and fibrinolytic system (bleeding and clotting at the same time)

DIC

What are the tree causes of disorders of secondary hemostasis?

VWF, Hemophilia A, Hemophilia B, hypercoag states

* Deficiency of Von Willebrand factor (carrier for factor VIII) * Most common inherited bleeding disorder * Most cases are autosomal dominant

Von Willebrand Disease

This disease will have an elevating bleeding time and PTT with a normal PT

Von Willebrand Dz

This disease is due to deficiency of factor 8

Hemophilia A

This disease is due to deficiency of factor 9

Hemophilia B

This disease has elevated PTT with normal PT and bleeding time

Hemophilia A