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RRPA Pathophysiology II > Hematopathology - Wright > Flashcards

Hematopathology - Wright Flashcards

1
Q

What are the main types of CBCs you can order?

A
  • CBC with no differential (no different types)
  • CBC with automatic differential (computer given count)
  • CBC with manual differential (lab techs manually verify cells present)
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2
Q

What values will you see on a CBC with differential?

A
  • Total WBC (sum of 5 types of WBCs)
  • Hct 3x the value of Hgb
  • Absolute is the actual count of cells (these are what you really want to look at)
  • Note: Platelets and WBCs are x 10^3
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3
Q

What is a bone marrow aspiration?

A
  • Looks at the molecular genetics of a sample of the liquid part of the bone
  • Uses flow cytometry
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4
Q

What is a bone marrow biopsy?

A
  • Looks at the cell constitution of a sample of solid bone marrow
  • Represents all cells
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5
Q

Where are megakaryocytes (precursors to platelets) produced? What do they do?

A

Inside the bone marrow - come from Megakaryoblasts–> Megakaryocyte

Get released into circulation & produce platelets (1,000-3,000)

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6
Q

What is the average lifespan of platelets?

A

8-9 days

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7
Q

Where are old platelets destroyed?

A

spleen and liver

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8
Q

Where are reticulocytes produced? What cells do they come from?

A

Inside the bone marrow

Hematocytoblast –> Proerythroblast –> Reticulocyte

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9
Q

How long does it take for a reticulocyte to mature? What nutrients are vital for this to occur?

A

1-2 days

Need Vit B12 and B9 (folic acid)

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10
Q

What hormone stimulates production of RBCs in the bone marrow?

A

Erythropoetin

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11
Q

Where is erythropoietin produced?

A

Kidneys and liver in response to low O2

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12
Q

Low circulating RBCs in the blood stream means there will be ____(higher/lower) unbound erythropoietin?

A

Higher (erythropoietin is bound by circulating RBCs)

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13
Q

T/F: Disruption of hematopoiesis can be malignant or non-malignant

A

True

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14
Q

What disorders of hematopoiesis are malignant?

A
  • Leukemia
  • Lymphoma
  • Myeloma
  • Myelodysplastic Syndrome
  • Aplastic anemia
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15
Q

What disorders of hematopoiesis are non-malignant?

A
  • Nutritional deficiencies
  • Autoimmune disorders
  • Infectious etiology
  • DIC
  • TTP
  • Hypersplenism
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16
Q

What malignant hematopoiesis disorders are myeloproliferative (over produce)?

A
  • Acute myeloid leukemia
  • Chronic myeloid leukemia
  • Myeloma
  • Essential Thrombocythemia
  • Polycythemia Vera
  • Myelofibrosis
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17
Q

What malignant hematopoiesis disorders are lymphoproliferative?

A
  • Acute lymphoblastic leukemia
  • Chronic lymphocytic leukemia
  • Multiple Myeloma
  • Lymphoma
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18
Q

What are the most common malignant blood disorders?

A
  • Leukemia
  • Lymphoma
  • Myeloma

Note: there can be overlap between leukemia and lymphoma

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19
Q

Leukemia means there are neoplastic cells in the ___?

A

blood stream (CA cells in blood)

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20
Q

Lymphoma means there are neoplastic cells in the ___?

A

lymph system (CA cells in lymph)

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21
Q

Myeloma means there are what type of neoplastic cells?

A

Neoplastic plasma cells (CA plasma cells)

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22
Q

Acute leukemia (within bone marrow) is composed of what type of cells?

A

Blast cells

Note: Acute = problem with immature cells (blasts)

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23
Q

Chronic leukemia (within bone marrow) is composed of more ____ cells?

A

Mature precursor cells

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24
Q

Leukemia Risk Factors

A
  • Radiation
  • Chemotherapy
  • Benzene (second hand smoke, gas, plastics)
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25
Q

Leukemia Signs and Symptoms

A
  • Leukocytosis (monocyte & lymphocyte elevation)
  • Pancytopenia
  • Hypogammaglobulinemia (low proteins to produce healthy immunoglobulins)
  • Bone pain
  • LAD
  • Splenomegaly
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26
Q

The onset of leukemia varies. What sx/sxs would you see with acute leukemia?

A
  • Sudden onset of a few months
  • WBC high (200) - neutrophils
  • Platelets low (89)
  • H/H low
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27
Q

What sx/sxs would you see with chronic leukemia?

A
  • Incidental diagnosis
  • Not as many symptoms as acute
  • Still see anemia, low platelets, no bleeding, no infection
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28
Q

Leukemia Dx?

A
  1. MUST do bone marrow biopsy
  2. Flow cytometry
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29
Q

What is the most common leukemia in adults?

A

Acute Myeloid Leukemia (AML)

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30
Q

Acute Myeloid Leukemia (AML) Dx?

A
  • Circulating blasts > 20% = DX on bone marrow
  • Auer rods on pathology
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31
Q

If you see Auer rods on pathology you should be thinking of what Dx?

A

Acute Myeloid Leukemia (AML)

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32
Q

Complications of Acute Myeloid Leukemia

A
  • Anemia (transfusions, low circulating O2)
  • Infection (low functioning WBCs)
  • Bleeding (low functioning platelets)
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33
Q

Acute Myeloid Leukemia (AML) Tx?

A
  1. Stem cell transplant (same thing as bone marrow transplant or HCT) - curative
  2. High dose Chemotherapy
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34
Q

What is the function of a stem cell transplant?

A

New stem cells are reintroduced and reestablish blood cell production in the bone marrow

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35
Q

What is the most common childhood malignancy?

A

Acute Lymphoblastic Leukemia (ALL)

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36
Q

What is peak incidence for Acute Lymphoblastic Leukemia (ALL)?

A

2-5 y/o

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37
Q

Acute Lymphoblastic Leukemia (ALL) Risk Factors

A
  • Genetic component
  • Down Syndrome
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38
Q

What cell lineages comprise Acute Lymphoblastic Leukemia (ALL)?

A
  • B-lineage (85%)
  • T-lineage (15%)
  • Uncommon variants/NK-lineage (<1%)
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39
Q

Acute Lymphoblastic Leukemia (ALL) Dx

A

Pathology confirms lymphoblasts

Note: leukemia = problem with blast cells

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40
Q

Good prognosis for Acute Lymphoblastic Leukemia (ALL)?

A
  • Hyperdiploid (>50 chromosomes per cell)
  • 2-10 y/o
  • DC10+
  • Low WBC count
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41
Q

Poor prognosis for Acute Lymphoblastic Leukemia (ALL)?

A
  • Hypodiploid
  • <2 or >10 y/o
  • Male
  • High WBC (>100k)
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42
Q

Tx for higher risk Acute Lymphoblastic Leukemia (ALL) patients?

A

CAR-T Therapy (usually 2nd or 3rd line therapy)

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43
Q

What is CAR-T Therapy?

A

Where an individual’s T cells are genetically modified to directly target against leukemic cells. These cells are then infused back into the patient. Theoretically this should last forever since it is training the immune system

Result = very low recurrence

44
Q

What is Chronic Myeloid Leukemia (CML)?

A

Uncontrolled proliferation of mature or maturing granulocytes

Note: chronic = problem with more mature cells

45
Q

Chronic Myeloid Leukemia (CML) Dx?

A

Philadelphia chromosome (fusion of BCR and ABL1 genes)

46
Q

T/F Chronic Myeloid Leukemia (CML) has a low progression rate even without treatment

A

False - without treatment it will progress to a terminal condition (blast crisis)

47
Q

At what age is Chronic Myeloid Leukemia most commonly diagnosed?

A
  • 50 or later
  • Predominantly in Males
48
Q

Chronic Myeloid Leukemia Tx?

A
  1. Technically curable with stem cell transplant (usually do not have to do if controlled with PO chemo)
  2. Chemotherapy PO - can manage dz but NOT curable
49
Q

What is Chronic Lymphocytic Leukemia (CLL)?

A
  • Progressive accumulation of functionally incompetent lymphocytes
  • Not as destructive as other leukemias
50
Q

At what age is Chronic Lymphocytic Leukemia (CLL) most commonly diagnosed?

51
Q

Blood lymphocyte count >5000 and Gingersnap appearance of cells should make you think of what Dx?

A

Chronic Lymphocytic Leukemia (CLL)

52
Q

Chronic Lymphocytic Leukemia (CLL) Tx?

A

Considered non-curable but treatable

  1. Stem cell transplant considered a risky option
  2. Not many CLL pts need Tx - Does not require Tx at the time of diagnosis
  3. Transforming more active form of dz (anemia, thrombocytopenia, neutropenia, hospitalization for PNA, splenomegaly, LAD)
53
Q

What are indications for treatment of Chronic Lymphocytic Leukemia (CLL)?

A

Active disease:

  • progressive marrow failure
  • progressive or massive splenomegaly
  • progressive symptomatic LAD
  • progressive lymphocytosis
  • constitutional symptoms
54
Q

What are lymphomas?

A

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

55
Q

Signs and Symptoms of Lymphoma?

A
  • Constitutional symptoms “B symptoms”
  • LAD
  • Splenomegaly
  • Anemia, thrombocytopenia, neutropenia
  • Hypercalcemia
  • Hyperuricemia
  • Elevated LDH
  • M spike on SPEP
56
Q

The major difference between Hodgkin Lymphoma and Non-Hodgkin Lymphoma is the presence of what cells on Bx of lymph?

A

Hodgkin Lymphoma = presence of Reed Sternberg cells

57
Q

Is Hodgkin Lymphoma or Non-Hodgkin Lymphoma more common?

A

Non-Hodgkin Lymphoma

58
Q

Hodgkin Lymphoma epidemiology and Sx/Sxs?

A
  • Male
  • Peak incidence 20-50
  • Painless cervical adenopathy
  • Constitutional symptoms
  • Pruritus
  • Pain in lymph nodes w/ alcohol consumption
59
Q

What lymph nodes are most commonly involved in Hodgkin Lymphoma?

A

Mediastinal and neck nodes

Note: Extranodal involvement is rare (blood or bone involvement)

60
Q

What are the Indolent Lymphomas for Non-Hodgkin?

A
  • Follicular Lymphoma
  • Marginal Zone Lymphoma (MALT)
  • Lymphoplasmocytic Lymphoma
  • Small Lymphocytic Lymphoma
61
Q

What are the Aggressive Lymphomas for Non-Hodgkin?

A
  • Diffuse Large B cell Lymphoma (DLBCL)
  • Burkitt Lymphoma
  • Mantle Cell Lymphoma
  • Peripheral T Cell Lymphomas
62
Q

Diffuse Large B Cell Lymphoma is the most common lymphoma worldwide. What is the epidemiology, Sx, and Prognosis?

A
  • Male
  • Median age of 64
  • Sx: Typically present with rapidly enlarging symptomatic mass
  • Prog: 60% present with advanced stage dz - Curable in about half w/ current therapy
63
Q

Follicular Lymphoma is the most common Non-Hodgkin Lymphoma. What are the Sx and Prognosis?

A
  • Sx: Painless peripheral adenopathy
  • Waxes and wanes - but never completely goes away
  • No other organ involvement, constitutional symptoms, or elevated LDH

Prog: May have waxing and waning symptoms for 5 years before Dx

Can progress to diffuse large B cell or Burkitt lymphoma

64
Q

What is Burkitt Lymphoma? Epidemiology/Etiology?

A
  • Highly aggressive B cell neoplasm
  • 30% of pediatric lymphomas
  • Endemic form seen in Africa - present w/ jaw or facial bone tumor
  • Immunodeficiency associated form seen in HIV positive patients
  • High propensity for tumor lysis syndrome
65
Q

What is Mantle Cell Lymphoma?

A
  • Can involve any region of the GI tract
  • Occasionally presenting as lymphomatous intestinal polyposis
66
Q

Nuclear staining for cyclin D1 should make you think of what Dx?

A

Mantle Cell Lymphoma

67
Q

What is Marginal Zone Lymphoma?

A

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

68
Q

What is the frequent cause of Marginal Zone Lymphoma?

A
  • Chronic gastritis from H. pylori infections
  • Arises is a number of epithelial tissues including the stomach
69
Q

Lymphoplasmacytic Lymphoma (Waldenstrom macroglobulinemia) is associated with what monoclonal gammopathy?

A

IgM monoclonal gammopathy

Note: no lytic lesions noted

70
Q

Raynaud phenomenon (poor circulation - fingertips turn white) and Smudge cells should make you think of what Dx?

A

Lymphoplasmacytic Lymphoma

71
Q

Non-Hodgkin Lymphoma involves discontinuous groups of lymph nodes that are?

A

Not amendable to surgical excision for cure

72
Q

Non-Hodgkin Lymphoma Sx?

A
  • Extranodal involvement is possible
  • Spleen often involved
  • Painless LAD - neck (also inguinal and axillary)
  • Constitutional Sx in 20%
73
Q

What is Multiple Myeloma

A

Neoplastic proliferation of plasma cells producing a monoclonal immunoglobulin –> causes skeletal destruction

74
Q

Signs and Symptoms of Multiple Myeloma?

A
  • Anemia
  • Hypercalcemia
  • Renal dysfunction
  • M-Spike on SPEP
  • Bence Jones protein in UPEP
  • Lytic lesions on skeletal imaging (“punched out”)
75
Q

M-Spike on SPEP and Bence Jones proteins should make you think of what Dx?

A

Multiple Myeloma

76
Q

What are the variations of Multiple Myeloma?

A
  • MGUS
  • Smoldering
  • Myeloma with amyloidosis
77
Q

What 2 things must you have in order to have a Dx of Multiple Myeloma?

A
  1. Clonal bone marrow plasma cells > 10% or Bx proven bony or soft tissue plasmacytoma

PLUS

  1. Presence of related organ or tissue impairment (anemia, hypercalcemia, renal insufficiency, bone lesions, >60% plasma cells)
78
Q

Multiple Myeloma Laboratory Findings

A
  • M-Spike

Elevated Immunoglobulin:

  • IgM, IgA, IgG
  • -Elevated Kappa or lambda
  • Heavy or light chain
79
Q

Multiple Myeloma Prognosis?

A
  • Non-curable
  • Without therapy pts will die w/i 6 months
  • Stem cell transplant - option to prolong event
80
Q

What is Myelodysplastic Syndrome?

A
  • Heterogeneous group of malignant hematopoietic stem cell disorders
  • Ineffective blood cell production (inadequate or abnormal cells)
81
Q

Myelodysplastic Syndrome causes reduction in production of cells or reduction in function of existing cells resulting in?

A
  • Anemia
  • Thrombocytopenia
  • Leukopenia
82
Q

Myelodysplastic Syndrome Epidemiology, Dx, and Prognosis

A
  • Males
  • >65
  • Dx: < 20 % blasts
  • Prog: 6 - 54 month survival
83
Q

Brief Summary of the Hemostasis pathway

A
  1. Platelet plug formation
  2. Propagation/ Coagulation Cascade
  3. Termination of blotting
  4. Fibrinolysis (removal of clot)
84
Q

What are primary disorders of hemostasis?

A

Refers to the initial steps in clot formation - mostly rely on vessel wall and platelet function

85
Q

Patients with disorders of primary hemostasis often present with?

A

Bleeding or petechiae

86
Q

What are secondary disorders of hemostasis?

A

Refers to subsequent formation of the fibrin-based clot - mostly relies on coagulation factors

87
Q

Patients with disorders of secondary hemostasis often present with?

A

Deep tissue hematomas or joint bleeding

88
Q

What is Immune Thrombocytopenic Purpura (ITP)?

A

Antibody mediated destruction of platelets

89
Q

Immune Thrombocytopenic Purpura Sx?

A
  • Petechia
  • Purpura
  • Bleeding
90
Q

Heparin Induced Thrombocytopenia is when Heparin triggers antibody mediated destruction of platelets. What specific antibody triggers thrombosis?

A

Antibody platelet Factor 4

91
Q

What is Thrombotic Thrombocytopenic Purpura?

A

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

92
Q

A deficiency of the ADAMTS13 protease should make you think of what Dx?

A

Thrombotic Thrombocytopenic Purpura

93
Q

What does a deficiency of the ADAMTS13 protease result in?

A

Accumulation of very long von Willebrand factor multimers on the endothelial surface - capable of binding platelets

94
Q

What is Hemolytic Uremic Syndrome (HUS)?

A
  • Abnormalities in the vessel wall of arterioles and capillaries - lead to microvascular thrombosis
  • Complement-induced damage to endothelium from shiga toxin
95
Q

What are shiga toxins produced by?

A
  • Shigella dysenteriae
  • Some serotypes of E. coli
96
Q

If a patient is septic with E. coli, has a UTI, and then renal dysfunction develops you should be thinking of what Dx?

A

Hemolytic Uremic Syndrome

97
Q

What is Disseminated Intravascular Coagulation (DIC)?

A
  • Dysfunction of platelets and coagulation cascade
  • Activation of clotting and fibrinolytic system
98
Q

Causes of DIC?

A
  • Obstetric conditions (placental abruption, retained fetus, septic abortion, amniotic fluid embolism)
  • Infection-sepsis
  • Carcinomas (pancreas, prostate, lung)
  • Massive trauma
99
Q

Von Willebrand Dz is the most common inherited bleeding disorder. Most cases are?

A

Autosomal dominant

100
Q

What lab values would you see for Von Willebrand Dz?

A
  • Bleeding Time Elevated
  • PTT Elevated
  • PT normal
101
Q

What lab values would you see for Hemophilia A?

A
  • Bleeding Time normal
  • PTT Elevated
  • PT normal
102
Q

Hemophilia A patients are deficient in what clotting factor?

A

Factor VIII

103
Q

Hemophilia B patients are deficient in what clotting factor?

104
Q

What is a hypercoaguable state?

A
  • An increased risk for thromboembolism
  • 50% of thrombotic events with an inherited thrombophilia are associated with the additional presence of an acquired risk factor
105
Q

What is the most common inherited hypercoaguable state disorder?

A

Factor V Leiden mutation

RRPA Pathophysiology II (16 decks)

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