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RRPA Pathophysiology II > Hematopathology - Wright > Flashcards

Hematopathology - Wright Flashcards

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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
Leukemia Signs and Symptoms
* Leukocytosis (monocyte & lymphocyte elevation) * Pancytopenia * Hypogammaglobulinemia (low proteins to produce healthy immunoglobulins) * Bone pain * LAD * Splenomegaly
26
The onset of leukemia varies. What sx/sxs would you see with acute leukemia?
* Sudden onset of a few months * WBC high (200) - neutrophils * Platelets low (89) * H/H low
27
What sx/sxs would you see with chronic leukemia?
* Incidental diagnosis * Not as many symptoms as acute * Still see anemia, low platelets, no bleeding, no infection
28
Leukemia Dx?
1. MUST do bone marrow biopsy 2. Flow cytometry
29
What is the most common leukemia in adults?
Acute Myeloid Leukemia (AML)
30
Acute Myeloid Leukemia (AML) Dx?
* Circulating blasts \> 20% = DX on bone marrow * **Auer rods** on pathology
31
If you see Auer rods on pathology you should be thinking of what Dx?
Acute Myeloid Leukemia (AML)
32
Complications of Acute Myeloid Leukemia
* Anemia (transfusions, low circulating O2) * Infection (low functioning WBCs) * Bleeding (low functioning platelets)
33
Acute Myeloid Leukemia (AML) Tx?
1. Stem cell transplant (same thing as bone marrow transplant or HCT) - curative 2. High dose Chemotherapy
34
What is the function of a stem cell transplant?
New stem cells are reintroduced and reestablish blood cell production in the bone marrow
35
What is the most common childhood malignancy?
Acute Lymphoblastic Leukemia (ALL)
36
What is peak incidence for Acute Lymphoblastic Leukemia (ALL)?
2-5 y/o
37
Acute Lymphoblastic Leukemia (ALL) Risk Factors
* Genetic component * Down Syndrome
38
What cell lineages comprise Acute Lymphoblastic Leukemia (ALL)?
* B-lineage (85%) * T-lineage (15%) * Uncommon variants/NK-lineage (\<1%)
39
Acute Lymphoblastic Leukemia (ALL) Dx
Pathology confirms lymphoblasts Note: leukemia = problem with _blast_ cells
40
Good prognosis for Acute Lymphoblastic Leukemia (ALL)?
* Hyperdiploid (\>50 chromosomes per cell) * 2-10 y/o * DC10+ * Low WBC count
41
Poor prognosis for Acute Lymphoblastic Leukemia (ALL)?
* **_Hypo_**diploid * \<2 or \>10 y/o * Male * _High_ WBC (\>100k)
42
Tx for higher risk Acute Lymphoblastic Leukemia (ALL) patients?
CAR-T Therapy (usually 2nd or 3rd line therapy)
43
What is CAR-T Therapy?
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
What is Chronic Myeloid Leukemia (CML)?
Uncontrolled proliferation of mature or maturing granulocytes Note: chronic = problem with more mature cells
45
Chronic Myeloid Leukemia (CML) Dx?
_Philadelphia chromosome_ (fusion of **BCR** and **ABL1** genes)
46
T/F Chronic Myeloid Leukemia (CML) has a low progression rate even without treatment
False - without treatment it will progress to a terminal condition (blast crisis)
47
At what age is _Chronic_ Myeloid Leukemia most commonly diagnosed?
* 50 or later * Predominantly in Males
48
Chronic Myeloid Leukemia Tx?
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
What is Chronic Lymphocytic Leukemia (CLL)?
* Progressive accumulation of functionally incompetent lymphocytes * Not as destructive as other leukemias
50
At what age is _Chronic_ Lymphocytic Leukemia (CLL) most commonly diagnosed?
After 70
51
Blood _lymphocyte_ count \>5000 and _Gingersnap appearance_ of cells should make you think of what Dx?
Chronic Lymphocytic Leukemia (CLL)
52
Chronic Lymphocytic Leukemia (CLL) Tx?
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
What are indications for treatment of Chronic Lymphocytic Leukemia (CLL)?
Active disease: * progressive marrow failure * progressive or massive splenomegaly * progressive symptomatic LAD * progressive lymphocytosis * constitutional symptoms
54
What are lymphomas?
Malignant neoplasms derived from B or T cell progenitors, mature B or T cells, or NK cells
55
Signs and Symptoms of Lymphoma?
* Constitutional symptoms "B symptoms" * LAD * Splenomegaly * Anemia, thrombocytopenia, neutropenia * Hypercalcemia * Hyperuricemia * Elevated LDH * M spike on SPEP
56
The major difference between Hodgkin Lymphoma and Non-Hodgkin Lymphoma is the presence of what cells on Bx of lymph?
Hodgkin Lymphoma = presence of **Reed Sternberg** cells
57
Is Hodgkin Lymphoma or Non-Hodgkin Lymphoma more common?
Non-Hodgkin Lymphoma
58
Hodgkin Lymphoma epidemiology and Sx/Sxs?
* Male * Peak incidence 20-50 * Painless cervical adenopathy * Constitutional symptoms * Pruritus * _Pain in lymph nodes w/ alcohol consumption_
59
What lymph nodes are most commonly involved in Hodgkin Lymphoma?
Mediastinal and neck nodes Note: Extranodal involvement is rare (blood or bone involvement)
60
What are the Indolent Lymphomas for Non-Hodgkin?
* Follicular Lymphoma * Marginal Zone Lymphoma (MALT) * Lymphoplasmocytic Lymphoma * Small Lymphocytic Lymphoma
61
What are the Aggressive Lymphomas for Non-Hodgkin?
* Diffuse Large B cell Lymphoma (DLBCL) * Burkitt Lymphoma * Mantle Cell Lymphoma * Peripheral T Cell Lymphomas
62
Diffuse Large B Cell Lymphoma is the most common lymphoma worldwide. What is the epidemiology, Sx, and Prognosis?
* 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
Follicular Lymphoma is the most common Non-Hodgkin Lymphoma. What are the Sx and Prognosis?
* 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
What is Burkitt Lymphoma? Epidemiology/Etiology?
* 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
What is Mantle Cell Lymphoma?
* Can involve any region of the GI tract * Occasionally presenting as lymphomatous intestinal polyposis
66
_Nuclear staining for cyclin D1_ should make you think of what Dx?
Mantle Cell Lymphoma
67
What is Marginal Zone Lymphoma?
Extranodal marginal zone lymphoma of _mucosa_ associated lymphoid tissue (MALT lymphoma)
68
What is the frequent cause of Marginal Zone Lymphoma?
* Chronic gastritis from *H. pylori infections* * Arises is a number of epithelial tissues including the stomach
69
Lymphoplasmacytic Lymphoma (Waldenstrom macroglobulinemia) is associated with what monoclonal gammopathy?
**IgM** monoclonal gammopathy Note: no lytic lesions noted
70
_Raynaud phenomenon_ (poor circulation - fingertips turn white) and _Smudge cells_ should make you think of what Dx?
Lymphoplasmacytic Lymphoma
71
Non-Hodgkin Lymphoma involves discontinuous groups of lymph nodes that are?
Not amendable to surgical excision for cure
72
Non-Hodgkin Lymphoma Sx?
* Extranodal involvement is possible * Spleen often involved * Painless LAD - neck (also inguinal and axillary) * Constitutional Sx in 20%
73
What is Multiple Myeloma
Neoplastic proliferation of _plasma_ cells producing a monoclonal immunoglobulin --\> causes skeletal destruction
74
Signs and Symptoms of Multiple Myeloma?
* Anemia * Hypercalcemia * Renal dysfunction * **M-Spike** on SPEP * **Bence Jones** protein in UPEP * Lytic lesions on skeletal imaging ("punched out")
75
_M-Spike_ on SPEP and _Bence Jones_ proteins should make you think of what Dx?
Multiple Myeloma
76
What are the variations of Multiple Myeloma?
* MGUS * Smoldering * Myeloma with amyloidosis
77
What 2 things must you have in order to have a Dx of Multiple Myeloma?
1. Clonal bone marrow _plasma_ cells \> 10% or Bx proven bony or soft tissue plasmacytoma **PLUS** 2. Presence of related organ or tissue _impairment_ (anemia, hypercalcemia, renal insufficiency, bone lesions, \>60% plasma cells)
78
Multiple Myeloma Laboratory Findings
* M-Spike Elevated Immunoglobulin: * IgM, IgA, IgG * -Elevated Kappa or lambda * Heavy or light chain
79
Multiple Myeloma Prognosis?
* Non-curable * Without therapy pts will die w/i 6 months * Stem cell transplant - option to prolong event
80
What is Myelodysplastic Syndrome?
* Heterogeneous group of malignant hematopoietic stem cell disorders * Ineffective blood cell production (inadequate or abnormal cells)
81
Myelodysplastic Syndrome causes _reduction_ in production of cells or _reduction_ in function of existing cells resulting in?
* Anemia * Thrombocyto**_penia_** * Leuko**_penia_**
82
Myelodysplastic Syndrome Epidemiology, Dx, and Prognosis
* Males * \>65 * Dx: \< 20 % blasts * Prog: 6 - 54 month survival
83
Brief Summary of the Hemostasis pathway
1. Platelet plug formation 2. Propagation/ Coagulation Cascade 3. Termination of blotting 4. Fibrinolysis (removal of clot)
84
What are _primary_ disorders of hemostasis?
Refers to the _initial_ steps in clot formation - mostly rely on vessel wall and platelet function
85
Patients with disorders of primary hemostasis often present with?
Bleeding or petechiae
86
What are _secondary_ disorders of hemostasis?
Refers to _subsequent_ formation of the fibrin-based clot - mostly relies on coagulation factors
87
Patients with disorders of secondary hemostasis often present with?
Deep tissue hematomas or joint bleeding
88
What is Immune Thrombocytopenic Purpura (ITP)?
Antibody mediated destruction of platelets
89
Immune Thrombocytopenic Purpura Sx?
* Petechia * Purpura * Bleeding
90
Heparin Induced Thrombocytopenia is when Heparin triggers antibody mediated destruction of platelets. What specific antibody triggers thrombosis?
Antibody platelet Factor 4
91
What is Thrombotic Thrombocytopenic Purpura?
Abnormalities in the vessel wall of arterioles and capillaries lead to microvascular thrombosis
92
A deficiency of the ADAMTS13 protease should make you think of what Dx?
Thrombotic Thrombocytopenic Purpura
93
What does a deficiency of the ADAMTS13 protease result in?
Accumulation of very long von Willebrand factor multimers on the endothelial surface - capable of binding platelets
94
What is Hemolytic Uremic Syndrome (HUS)?
* Abnormalities in the vessel wall of arterioles and capillaries - lead to microvascular thrombosis * Complement-induced damage to endothelium from _shiga toxin_
95
What are shiga toxins produced by?
* **Shigella dysenteriae** * Some serotypes of E. coli
96
If a patient is septic with E. coli, has a UTI, and then renal dysfunction develops you should be thinking of what Dx?
Hemolytic Uremic Syndrome
97
What is Disseminated Intravascular Coagulation (DIC)?
* Dysfunction of platelets and coagulation cascade * Activation of clotting and fibrinolytic system
98
Causes of DIC?
* Obstetric conditions (placental abruption, retained fetus, septic abortion, amniotic fluid embolism) * Infection-sepsis * Carcinomas (pancreas, prostate, lung) * Massive trauma
99
Von Willebrand Dz is the most common _inherited_ bleeding disorder. Most cases are?
Autosomal dominant
100
What lab values would you see for Von Willebrand Dz?
* **Bleeding Time Elevated** * **PTT Elevated** * PT normal
101
What lab values would you see for Hemophilia A?
* Bleeding Time normal * **PTT Elevated** * PT normal
102
Hemophilia A patients are deficient in what clotting factor?
Factor VIII
103
Hemophilia B patients are deficient in what clotting factor?
Factor IX
104
What is a hypercoaguable state?
* 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
What is the most common inherited hypercoaguable state disorder?
Factor V Leiden mutation

RRPA Pathophysiology II (16 decks)

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