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Adv Patho > Leukocyte Disorder > Flashcards

Leukocyte Disorder Flashcards

1
Q

Leukocyte Disorder Type- Too Few

A

Leukopenia - Neutropenia (most common cause)/
Agranulocytosis (baso/eosino/neutrophils)
-Etiology -
-decreased production or activity
due to aplastic anemia or drugs,
-decreased survival due to infectious processes, immune or splenic destruction
-acquired clinical states.

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2
Q

Leukocyte Disorder Types- Too Many

A

Leukocytosis
Lymphocytosis
Lymphoid Neoplasms and leukemias (many)

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3
Q

Too many - Leukocytosis

A 
Etiology - Increased cell activity
Release fro bone marrow
Demargination from vessel walls
Reactive inflammatory states.
 *Cytokines stimulates release of WBCs from bone marrow. Macrophages circulate into tissue and when activated, they're stimulated to divide.
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4
Q

Too many - Lymphocytosis - Infectious Mono

A

Etiology - Epstein Barr infection of B-cells
Patho - Infected B cells secrete antibodies (heterophil antibodies diagnostic for mono - spot test_
-Antibodies produced against EBV (memory B cells for life)
-Tc and K control EBV.Tc particular to EBV called atypical lymphocytes and diagnostic of mono.

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5
Q

Too Many - Lymphocytosis - Infectious Mono - clinical manifestation

A
  • Leukocytosis with atypical lymphocytes
  • Lymphadenopathy
  • Splenomegaly
  • Infection by EBV risk for autoimmune disease and neoplasm
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6
Q

Too Many - Lymphoid Neoplasms & Leukemias - General info

A

Derived from neoplastic proliferation of B, T, or NK lymphocytes.

  • most are of B cell origin
  • WHO classifies on cell origin, differentiation, clinical features, and genotype.
  • Myeloid Neoplasms arise from hematopoietic stem cells
  • Leukemia tumors involve bone marrow.
  • Clinical manifestations are similar as they can spill into each other.
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7
Q

Lymphoid neoplasms and leukemias - General Characteristics (know)

A

-Uncontrolled proliferation of a single progenitor cell (gene mutation to one cell proliferates and accumulates).
-Decreased production and function of normal hematopoietic cells.
-Acute lymphomas and leukemias-
undiff or immature cells
(blast cell from myeloid or lymphoid lines, cells not functional, differentiation blocked).
-Chronic lymphomas and leukemias-
cell differentiated, mature but do not functional normally.

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8
Q

Lecture info on lymphoid neo & leukemias

A

Leukemia

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9
Q

Lymphoid Neoplasms - general clinical manifestation (know)

A
  1. Spleno and Hepatomegaly & lymphadenopathy
  2. Lymphedema
  3. Constitutional symptoms (B symptoms)
    - Fatigue, fever, night sweats, wt loss.
    - Increased metabolic active cells and cytokine release (action of IL-1 & TNFa).
  4. Susceptible to infection and immune disorder (no tolerance to self antigen, lymphocytes dysfunctional).
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10
Q

Lecture on clinical manifestation Lymphoid Neoplasms

A
  • TNFa and IL 1 lead to systemic symptoms (B symptoms).
  • When immune systems activated (B & T cells), it activates inflammatory system (IL1 an TNFa).
  • Proliferation decreases production and prolix of T & B cells leading to infection susceptibility.
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11
Q

Luekemias - general clinical manifestation (know)

A
  1. elevated WBC 15-150K - spills into blood leading to elevated WBC
  2. Neutropenia (stem cell suppression)
  3. Anemia
  4. Thrombocytopenia
  5. Bone pain (due to marrow pressure)
  6. Spleno/hepatomegaly & lymphadenopathy
  7. B symptoms or constitutional - (fever, wt loss, night sweats, fatigue).
  8. Cytokines/TNF can decrease production of erythropoietin.
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12
Q

Lymphoid Neoplasm - Hodgkins Lymphoma

A
  • Arises from germinal cancer B cells
  • Epi - one for common in young adults, another form common >50.
  • Etiology - preceding infection (mostly EBV), immunodeficiency
  • Patho - Mutant B cell in single node and spreads (initial involvements typically above diaphragm).
  • Spreads to spleen, liver, bone marrow.
  • Extranodal involvement uncommon.
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13
Q

Lymphoid Neoplasm - Hodgkins Lymphoma - clinical manifestation

A

In addition to General manifestations:

  • Reed-Sternberg giant cells (seen in background of non-neoplastic inflam. cells).
  • Painless, enlarged nodes
  • Staged I-IV (stage I-II 90% survival, III-IV 60-70%
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14
Q

Lymphoid Neoplasm - Non-Hodgkins Lymphoma

A
  • Tumor composed of neoplastic lymphoid cells (occur 3X > Hodgkins).
  • Epi - Age >50, men>women (6-8%)
  • Etiology - HIV/AIDS, EBV, Hep C, immunosuppression, herbicides/chemicals
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15
Q

Lymphoid Neoplasm - Non-Hodgkins

A
  • Patho - T or B cell gene mutation during develop or differentiation.
  • Dx and classif. require test to determine lineage and maturity.
  • Manifestations of disease dependent on which T or B cell gene affected.
  • Widely disseminated by diagnosis time.
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16
Q

Clinical differences between hodgkin and non- (KNOW)

A

Kumar p 442
Hodgkin:
1. Localized to single axial group (cervical, mediastinal, para-aortic)
2. Orderly spread (contiguous)
3. Mesenteric nodes and Waldeyer ring rarely invovled.
4. Extranodal involvement uncommon
Non-Hodgkin:
1. Frequent involvement of peripheral nodes.
2. Non -contiguous spread
3. Mesenteric nodes and Waldeyer ring involvement
4. Extranodal involvement common.

17
Q

Lymphoid Neoplasm - Multiple Myeloma

A

Etiology - gene mutation translocation of plasma B cells (myeloma plasma cells)
Epi - adults 50-60, black males
Risk factors - Farmers, cosmetologists, radiation, herpes virus, petrochemical workers.

18
Q

Lymphoid Neoplasm - Multiple myeloma - Pathophys

A
  • Myeloma plasm cells accumulate in bone marrow (characteristic).
  • Fibroblasts and macrophages in marrow produce IL6, causing plasma cell proliferation.
  • Lymph node involvement + extranodal sites
  • Cells produce excessive # of immunoglobulin (IgG or IgA).
  • It is a mutated immnunoglobulin (called Serum M protein) decreasing production of normal immunoglobulin.
19
Q

Lymphoid Neoplasm - Multiple myeloma - Pathogenesis

A

Myeloma plasma cells secrete osteoclast-secreting factors that lead to bone destruction and reabsorption and replace normal bone marrow.

20
Q

Lymphoid Neoplasm - Multiple Myeloma - clinical manifestation

A

In addition to general manifestations:

  • Punched out bone and bone pain.
  • HyperCa+ and fractures
  • Increased infection
  • Pancytopenia
  • Blood smear - myeloma cells
  • Renal insufficiency due to Bence-Jones proteins.
21
Q

Leukemia - Acute Lymphoctic Leukemia (ALL)

A

-Etiology - genetic alteration, virus, radiation
-Epi - up to young adults, peaks age 4, older adults
-Pathogenesis - Pre B or Pre T cell mutation (80% B cell origin) Express ALL antigen
-Pre B cell involvement - Marrow overproduction and proliferation of undiff B-lymphoblasts.
Inflitrate live, spleen, lymph node.
-If Pre T cell has left to thymus, then T-lymphoblasts proliferation takes place there (do not mature and differentiate).

22
Q

Leukemia - Acute Lymphocytic Leukemia (ALL) - clinical manifestations

A

In addition to general manifestations:

  • Rapid onset of symptoms
  • Blood smear - lymphoid blast cells, few mature leukocytes, anemia
  • Thrombocytopenia
  • Bone marrow - high number of blast cells
  • Bone Pain
  • Liver/spleen/lymph node enlargement
23
Q

Leukemia - Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Lymphoma

A
  • Etiology - gene mutation with no link to radiation, virus, or chemicals.
  • Epi - age 50-60, Western world, males
  • Patho - Neoplasm of MATURE B cells.Mature B cell proliferates and accumulates but cannot differentiate into plasma cell.
24
Q

Leukemia - Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Lymphoma - clinical manifestations

A
  • Develops slowly. Asymptomatic for long time.
  • Blood smear - B cells in marrow. WBC 200K, small round lymphocytes easily disrupted called –Smudge cells (*characteristic!!).
  • Hypogammaglobulinemia - increased risk infection
  • Anemia, thrombocytopenia
  • Lymphadenopathy/splenomegaly in60% of cases.
25
Q

Leukemia - Acute Myelogenous Leukemia

A
  • Etiology - toxins, chemo, radiation, chromosomal mutations, myelodysplastic syndrome.
  • Epi - > age 60 (about 50%)
  • Patho - abnormal proliferation of myeloid stem cell or myeloid precursor cells.
  • Arrested cellular differentiation.
  • Clinical manifestations - bone marrow smear >20% early myeloid cells (*characteristic!!)
  • Blood smear - Increased blast or promyelocyte cells. Decreased WBC, RBC, Platelet cells.
26
Q

Leukemia - Chronic Mylelogenous Leukemia

A
  • Etiology - acquired genetic alteration (95% due to mutation of Philadelphia chromosome *characteristic!!! or BCR-ABL).
  • Epi - Age 25-60, peak 40-50
  • Patho - Immature granulocytes but more mature than in AML.
  • Clinical Manifestation:
    1. Blood smear - leukocytosis>abnormal granulocytes
    2. Bone marrow - increase neoplastic granulocyte precursors
    3. Splenomegaly
    4. Increased hematopoieses - extra medullary hematopoesis
    5. Stages - chronic/stable, accelerated, acute/blast crisis

Adv Patho (11 decks)

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