Disorders of White Blood Cells and Lymphoid Tissues Flashcards

1
Q

leukopenia

A

A low level of white blood cells in the blood, which can interfere with the ability to fight infection.

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2
Q

anemia

A

a condition marked by a deficiency of red blood cells or of hemoglobin in the blood, resulting in pallor and weariness.

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3
Q

thrombocytopenia

A

a condition of low platelets in the blood

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4
Q

neutropenia

A

a condition of low neutrophils in the blood, thus leaving the body more susceptible to infection and inflammation.
This might happen due to an infection, but can result from cancer treatment. Avoiding infection is very important.

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5
Q

lymphomas

A

lymphomas are cancers of the lymph nodes.

a diverse group of solid tumors composed of neoplastic lymphoid cells.

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6
Q

leukemia

A

malignant neoplasms of cells originally derived from hematopoietic precursor cells. Characterized by diffuse replacement of the bone marrow with unregulated, proliferating, immature neoplastic cells.

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7
Q

plasma cell/multiple myeloma

A

A cancer of plasma cells.
The plasma cells are a type of white blood cell in the bone marrow. With this condition, a group of plasma cells becomes cancerous and multiplies. The disease can damage the bones, immune system, kidneys, and red blood cell count.

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8
Q

Contrast non-Hodgkin lymphoma & Hodgkin lymphoma by where they ARISE IN THE BODY.
which possesses Reed Sternberg cells?

A

NON Hodgkin’s lymphoma:
arise from the lymphocytes (extra-nodal sites) , alterations in the developmental process of the cells.

HODGKIN’S lymphoma:
a specialized form of lymphoma that features a Reed-Sternberg cell (large, atypical, mononuclear tumor cell), arises in a single node or chain of nodes.

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9
Q

Which of the 2 is more susceptible to radiation & chemotherapy?

List clinical symptoms and signs for both.

A

Hodgkin’s lymphoma is more susceptible to radiation and chemotherapy.

clinical Sx/Sx: non-Hodgkin's 
painless lymphadenopathy (starting) 
fever, night sweats, unintentional weight loss, susceptibility to infections (advanced) 

clinical Sx/Sx: Hodgkin’s
painless enlargement of a node or single group of nodes, typically above the level of the diaphragm, mediastinal masses, chest discomfort (cough/dyspnea), fevers, chills, night sweats, weight loss.
fatigue and anemia indicate advanced disease/disease spread

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10
Q

and typical course of treatment for Hodgkin’s and non-Hodgkin’s

A

TX: Non-Hodgkin’s:
early stage: localized radiation
later stage: combo of chemo, biotherapy, and adjuvant radiation

TX: Hodgkin’s:
early stage: localized radiation
later stages: combo of radiation, biotherapy and chemotherapy.

CORRECT STAGING IS CRITICAL TO GET EFFECTIVE TREATEMENT

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11
Q

recall the Ann Arbor staging for lymphomas

A

stage I: involvement of a single lymph node region or of a single extra lymphatic organ or site

stage II: involvement of two or more lymph node regions on the same side of the diaphragm or localized involvement of an extra lymphatic organ or site

stage III: involvement of lymph node regions or structures on both sides of the diaphragm

stage IV: diffuse or disseminated involvement of one or more extra lymphatic organs,
or either:
isolated extra lymphatic organ involvement without adjacent regional lymph node involvement, but with disease in distant sites
involvement of the liver, bone marrow, pleura or cerebrospinal fluid

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12
Q
  1. Regarding acute leukemias- which predominant cell types are involved (hint: ALL & AML) and underlying physiology of why the patient presents with symptoms
A

ALL: neoplasms in lymphoblasts
physiology: acute lymphoblastic leukemia is caused by a series of acquired genetic aberrations. Malignant transformation usually occurs at the pluripotent stem cell level, although it sometimes involves a committed stem cell with more limited capacity for self-renewal. Abnormal proliferation, clonal expansion, aberrant differentiation, and diminished apoptosis (programmed cell death) lead to replacement of normal blood elements with malignant cells.

AML: neutrophils, monocytes, macrophages
physiology: acute myeloid leukemia is caused by a series of acquired genetic aberrations. Malignant transformation usually occurs at the pluripotent stem cell level, although it sometimes involves a committed stem cell with more limited capacity for self-renewal. Abnormal proliferation, clonal expansion, aberrant differentiation, and diminished apoptosis (programmed cell death) lead to replacement of normal blood elements with malignant cells.

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13
Q

explain the tumor lysis syndrome in relation to ALL and AML treatment

A

tumor lysis syndrome is when there is a massive necrosis of malignant cells in the initial phase of chemo. This can lead to life-threatening metabolic disorders such as hyperkalemia and others, causing the potential for acute renal failure.

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14
Q

regarding chronic myeloid leukemia, describe pathogenesis, clinical signs, and treatment

A

chronic myeloid leukemia develops from a disorder of the pluripotent hematopoietic progenitor cell. Philadelphia chromosome is where you can see the first indication of the cancer.

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15
Q

chronic myeloid leukemia–treatment

A

treatment: to get the hematologic response better (characterized by normalized blood counts), to get a cytogenic response by reduction/elimination of the Philadelphia chromosome from the bone marrow, to get a molecular response.
only curative tx is bone marrow transplant

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16
Q

chronic myeloid leukemia–clinical signs

A

clinical signs come in three stages:
a chronic phase–nonspecific symptoms, leukocytosis is most characteristic lab finding, anemia and thrombocytopenia develop.
a short accelerated phase–enlargement of the spleen and progressive symptoms.
a terminal blast crisis phase–the disease evolves to acute leukemia and is characterized by an increasing number of myeloid precursors, especially blast cells, in the blood.

17
Q

describe bone marrow transplant (autologous vs. allogenic)

A

autologous bone marrow transplant: An autologous stem cell transplant uses healthy blood stem cells from your own body to replace your diseased or damaged bone marrow
SELF TO SELF

allogenic bone marrow transplant: Allogeneic: Allo means other. The stem cells in allogeneic transplants are from a person other than the patient, either a matched related or unrelated donor.

18
Q

describe the risks and complications with autologous vs. allogenic bone marrow transplants

A

autologous:
rejection of new cells (mediated by T cells)

allogenic:
graft versus host disease (where the body attacks the new cells–nausea, vomiting, SOB, cough, etc. are symptoms)

risk of death with both
also risk of new cancers, organ damage, infections and more.