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Pathophys Ex 1 > Hematopathology- Wright > Flashcards

Hematopathology- Wright Flashcards

1
Q

What is hematopoesis

A

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

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2
Q

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

A

An initial cell only in the bone marrow

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3
Q

Where are old platelets destroyed?

A

In the liver

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4
Q

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

A

RBCs, reticulocyte

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5
Q

Platetes are formed from ________

A

Megakaryoblasts

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6
Q

Neoplastic cells in the bloodstream

A

Leukemia

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7
Q

Neoplastic cells in the lymph system

A

Lymphoma

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8
Q

Neoplastic plasma cells

A

Myeloma

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9
Q

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

A

Acute leukemia

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10
Q

This type of leukemia is composed more of mature precursor cells

A

Chronic leukemia

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11
Q

What are some signs and symptoms of leukemia?

A

Leukocytosis, panncytopenia, bone pain, LAD, splenomegaly

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12
Q

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

A

Bone marrow bx

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13
Q

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

A

AML

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14
Q

Auer rods should make you think of what?

A

AML

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15
Q

AML can lead to these three complications

A

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

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16
Q

This is the mc CHILDHOOD malignancy between ages 2-5

A

ALL

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17
Q

Pathology of this disease confirms lymphoblasts (lymphoid lineage)

A

ALL

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18
Q

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

A

Hyperdiploid

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19
Q

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

A

hypolipoid

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20
Q

What is CAR-T therapy

A

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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21
Q

Uncontrolled proliferation of mature and of maturing granulocytes

A

CML

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22
Q

Philadelphia chromosome

A

CML

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23
Q

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

A

Philadelphia chromosome- CML

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24
Q

Treatment for CML?

A

Oral chemo and stem cell transplant if last resort

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25
Q

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

A

CLL

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26
Q

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

A

CLL

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27
Q

What is the treatment for CLL?

A

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

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28
Q

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

A

Lymphoma

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29
Q

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

A

Hodgkin lymphoma

30
Q

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

A

Indolent (slow growing) and aggressive

31
Q

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

A

Hodgkin lymphoma

32
Q

Neoplastic cell=Reed Sternberg cell

A

Hodgkin lymphoma

33
Q

Tx for hodgkin lymphoma?

A

Chemo and rarely surgery

34
Q 
Are these aggressive or indolent? 
• Follicular Lymphoma
• Marginal Zone Lymphoma (MALT)
• Lymphoplasmocytic Lymphoma
• Small Lymphocytic Lymphoma
35
Q 
Are these aggressive or indolent? 
• Diffuse Large B cell Lymphoma (DLBCL)
• Burkitt Lymphoma
• Mantle Cell Lymphoma
• Peripheral T cell Lymphomas
A

Aggressive

36
Q

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.

A

Diffuse Large B Cell Lymphoma

37
Q

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.

A

Follicular lymphoma

38
Q

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

A

Burkitt Lymphoma

39
Q

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?

A

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

40
Q

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

A

Mantle cell lymphoma

41
Q

What is a marginal zone?

A

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

42
Q

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

A

Marginal zone lymphoma

43
Q

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

A

Marginal zone lymphoma

44
Q

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

A

Lymphoplasmacytic Lymphoma

45
Q

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

A

Multiple myeloma

46
Q

CRABS

A

Calcemia, renal dysfunction, Anemia, bone lesions

Multiple myeloma

47
Q

M-Spike on SPEP

A

Multiple myeloma

48
Q

Bence jone protein in urine

A

Multiple myeloma

49
Q

Lytic lesions (punched out) on skeletal imaging

A

multiple myeloma

50
Q

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

A
  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)
51
Q

Tx for multiple myeloma?

A

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

52
Q

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

A

Myelodysplastic syndrome

53
Q

What is primary hemostasis?

A
  • 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
54
Q

What is secondary hemostasis?

A
  • 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
55
Q

Hemostasis can occur due to what three things?

A
  1. Platelet dysfunction
  2. Increased platelet destruction
  3. Decreased platelet production
56
Q

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

A

Immune Thrombocytopenic Purpura

57
Q

What are some sx/sxs of ITP

A

petechia, purpura, bleeding

58
Q
  • Antibody mediated destruction of platelets
  • Acquired with use of heparin
  • Antibody platelet factor 4 and heparin which triggers thrombosis
A

Heparin Induced Thrombocytopenia

59
Q

• 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

A

TTP (Thrombocytic Thrombocytopenic Purpura)

60
Q

What is the pentad of symptoms of TTP?

A

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

61
Q

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

62
Q

• 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

A

Hemolytic Uremic Syndrome

63
Q
  • Shiga toxins are produced by Shigella dysenteriae and some serotypes of Escherichia coli
  • Renal dysfunction more common than with TTP
64
Q
  • Dysfunction of platelets and coagulation cascade

* Activation of clotting and fibrinolytic system (bleeding and clotting at the same time)

65
Q

What are the tree causes of disorders of secondary hemostasis?

A

VWF, Hemophilia A, Hemophilia B, hypercoag states

66
Q
  • Deficiency of Von Willebrand factor (carrier for factor VIII)
  • Most common inherited bleeding disorder
  • Most cases are autosomal dominant
A

Von Willebrand Disease

67
Q

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

A

Von Willebrand Dz

68
Q

This disease is due to deficiency of factor 8

A

Hemophilia A

69
Q

This disease is due to deficiency of factor 9

A

Hemophilia B

70
Q

This disease has elevated PTT with normal PT and bleeding time

A

Hemophilia A

Pathophys Ex 1 (4 decks)

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