Leukemia & Lymphoma Flashcards

1
Q

Leukemia

A
• A group of malignant disorders affecting the blood and blood‐forming tissues of:
– Bone marrow 
– Lymph system 
– Spleen
• Occurs in all age groups
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2
Q

Leukemia

A

• Results in an accumulation of dysfunctional cells because of a loss of regulation in cell division
• Fatal if untreated
– Progressive

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3
Q

Leukemia: Etiology and Pathophysiology

A

• No single causative agent
• Most from a combination of factors
– Genetic and environmental influences

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4
Q

Leukemia: Etiology and Pathophysiology

A
• Associated with the development of leukemia 
– Chemical agents
– Chemotherapeutic agents
– Viruses
– Radiation
– Immunological deficiencies
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5
Q

Leukemia: Classification; Acute vs. Chronic

A

• Acute versus chronic
– Cell maturity
• Acute: clonal proliferation of immature hematopoietic cells
• Chronic: mature forms of WBC; onset is more gradual
– Nature of disease onset

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6
Q

Leukemia: Classification; Type of WBC

A
• Type of white blood cell (WBC)
– Acute lymphocytic leukemia (ALL)
– Acute myelogenous leukemia (AML)
• Also called acute non‐lymphoblastic leukemia (ANLL)
– Chronic myelogenous leukemia (CML) 
– Chronic lymphocytic leukemia (CLL)
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7
Q

Acute Myelogenous Leukemia (AML)

A
• One quarter of all leukemias
– 85% of the acute leukemias in adults
• Abrupt, dramatic onset
– Serious infections, abnormal bleeding
• Uncontrolled proliferation of myeloblasts 
– Hyperplasia of bone marrow and spleen
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8
Q

Acute Lymphocytic Leukemia (ALL)

A
  • Most common type of leukemia in children
  • 15% of acute leukemia in adults
  • Immature lymphocytes proliferate in the bone marrow
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9
Q

Acute Lymphotytic Leukemia (ALL): S&S

A
• Signs and symptoms may appear abruptly 
– Fever, bleeding
• Insidious with progressive 
– Weakness, fatigue
• Central nervous system manifestations
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10
Q

Chronic Myelogenous Leukemia (CML)

A

• Excessive development of mature neoplastic granulocytes in the bone marrow
– Move into the peripheral blood in massive numbers
– Ultimately infiltrate the liver and spleen

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11
Q

Chronic Myelogenous Leukemia

A

• Philadelphia chromosome
– Genetic marker
• Chronic, stable phase followed by acute, aggressive (blastic) phase

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12
Q

Chronic Lymphocytic Leukemia (CLL)

A

• Production and accumulation of functionally inactive but long‐lived, mature‐appearing lymphocytes
• B cell involvement
• Lymph node enlargement is noticeable throughout the body
– ↑ incidence of infec􏰀on

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13
Q

Chronic Lymphocytic Leukemia (CLL): Complications

A

• Complications from early‐stage CLL is rare
– May develop as the disease advances
– Pain, paralysis from enlarged lymph nodes causing pressure

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14
Q

Leukemia: Clinical Manifestations

A

• Relate to problems caused by
– Bone marrow failure
• Overcrowding by abnormal cells
• Inadequate production of normal marrow elements
• Anemia, thrombocytopenia, ↓ number and functi􏰀on of
WBCs

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15
Q

Leukemia: Clinical Manifestations

A

• Relate to problems caused by
– Leukemic cells infiltrate client’s organs
• Splenomegaly
• Hepatomegaly
• Lymphadenopathy
• Bone pain, meningeal irritation, oral lesions (chloromas)

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16
Q

Leukemia: Diagnostic Tests

A
• To diagnose and classify
– Peripheral blood evaluation 
– Bone marrow evaluation
• To identify cell subtype and stage
– Morphological, histochemical, immunological, and cytogenic methods
17
Q

Leukemia: Complications

A
  • Opportunistic infections, including pneumonia
  • Sepsis
  • Congestiveheartfailure
  • Hemorrhage
  • Liverfailure
  • Renalfailure
  • CNS depression and coma
18
Q

Lymphoma

A
  • Malignant neoplasms originating in the bone marrow and lymphatic structures
  • Result in the proliferation of lymphocytes
19
Q

Lymphoma: Two major types

A

• Two major types of lymphomas
– Hodgkin’s disease
– Accounts for 15% of all lymphomas
– Non‐Hodgkin’s lymphoma (NHL)

20
Q

Lymphoma: Risk Factors

A
  • Auto immune disease (e.g.,rheumatoid arthritis)
  • Exposure to pesticides, chemical solvents, dyes
  • Exposure to some viral infections such as Epstein‐Barr virus
  • Immunodeficiency states such as AIDS, congenital immunodeficiency, or chronic immunosuppression by medications
  • Prior exposure to chemotherapy or radiation therapy
21
Q

Hodgkin’s Disease

A
• Malignant condition 
• Characterized by
– Proliferation of abnormal giant, multinucleated cells
• Reed‐Sternberg cells
– Located in the lymph nodes
22
Q

Hodgkin’s Disease: Etiology and Pathophysiology

A
• Cause remains unknown
• Several key factors play a role
– Infection with Epstein‐Barr virus 
– Genetic disposition
– Exposure to occupational toxins
23
Q

Hodgkin’s Disease: Etiology and Pathophysiology

A

• Normal structure of lymph nodes is destroyed by hyperplasia of monocytes and macrophages
• Main diagnostic feature
– Presence of Reed‐Sternberg cells in lymph node biopsy specimens

24
Q

Hodgkin’s Disease: Etiology and Pathophysiology

A

• Believed to arise in a single location – Spreads in adjacent lymphatics
– Eventually infiltrates other organs
• Lungs, spleen, liver
• Two‐thirds of clients are affected first in the cervical lymph nodes

25
Q

Hodgkin’s Disease: Etiology and Pathophysiology

A

• Disease begins above the diaphragm
– Remains confined to lymph nodes for a variable amount of time
• Originating below the diaphragm
– Frequently spreads to extra‐lymphoid sites such as the liver

26
Q

Hodgkin’s Disease: Clinical Manifestations

A

• Insidious onset
• Enlargement of cervical, axillary, or inguinal lymph nodes
• May experience
– Weight loss, fatigue, weakness, fever, chills, tachycardia, night sweats

27
Q

Hodgkin’s Disease: Clinical Manifestations

A
• B symptoms (fever, night sweats, weight loss) correlate with a worse prognosis
• Alcohol‐inducedpain
• Generalized pruritus without lesions
• Mediastinal node involvement
– Cough, dyspnea, stridor, dysphagia
• Advanced cases
– Hepatomegaly, splenomegaly
– Anemia
28
Q

Hodgkin’s Disease: Diagnostics

A
  • Peripheral blood analysis
  • Lymph node biopsy
  • Bone marrow examination
  • Radiological evaluation