Chapter 11 Flashcards
1
Q
Hodgkin’s Lymphoma
A
- represents about 30% of malignant lymphoma
- can occur across the lifespan
- Higher incidence in males with a worse prognosis
- about a 5 year survival rate in 85% of treated hodgkins
2
Q
Pathogenesis of Hodgkin’s Lymphoma
A
- malignant disorder of the lymph nodes
- characterized by reed-sternberg cells
- originates from B cells in germinal centers of lymph nodes
- usually metastasizes along contiguous lymphatic pathways
3
Q
Reed-Sternberg characteristics
A
- epstein barr virus frequently found in genome of transformed reed-sternberg cells
- usually present in single node or localized node chain
- constitute about 2% of cells in lymph node tumor
4
Q
Types of Hodgkins
A
- rare lymphocyte predominance type (5%)
- classical type (cHD)(95%)
5
Q
Clinical manifestations of Hodgkin’s Disease
A
- depend on origin site and dissemination stage ( early stages are often asypmtomatic)
- painless lymphadenopathy (abnormally sized lymph nodes)
- possibly with fever, night sweats, pruritus (itching), weight loss, malaise (discomfort)
- lymph node enlargement above diaphragm, cervival nodes are the most common site
- nodes below the diaphragm less common primary site
- disease spreads from site of origin to other lymph nodes/lymphatic tissue
6
Q
Prognosis of Hodgkins Disease
A
- Ann Arbor staging system
- uses presence/absence of certain clinical systems AND locations of affected nodes
- 4 stages and 4 modifying characteristics
7
Q
Treatment of Hodgkins Disease
A
- stages dictate treatment modality
- localized tumor: radiation therapy
- Disseminated disease: chemotherapy
8
Q
Non Hodgkin’s Lymphoma
A
- do not have Reed - Sternberg Cells
- Majority arise from lymph nodes, but can originate in any lymphoid tissue
- 95% occur in older adults
- Most arise from B cells, T cells, or NK cells
9
Q
Types of Non Hodgkin’s
A
- indolent: longer survival times
- Aggressive: disseminated at presentation, generally poor prognosis
10
Q
Pathogenesis of Non Hodgkins
A
- tumor cells derived from single mutant precursor cell and are clonal
- Viruses suspected in development of some lymphomas
- 5 year survival rate 50%
11
Q
Clinical Manifestations of Non Hodgkins
A
- painless lymphadenopathy, fever, night sweats, weight loss, malaise, puritus
- extranodal involvement occurs early
- may present with infiltrative disease of the skin, GI tract, bone, or bone marrow
12
Q
Complications of Non Hodgkins
A
- two very serious: superior vena cava obstruction, spinal cord compression
- other complications: infection, bone, metastasis, joint effusions
13
Q
Staging of Non Hodgkins
A
uses same staging system as hopkins
14
Q
Treatment of Non Hodgkins
A
- radiation
- chemotherapy
- tissue specific therapies: monoclonal antibodies & BMT
- treatment determined by stage
15
Q
Hairy Cell Leukemia
A
- rare chronic type of leukemia
- 2% of adult leukemia but highly treatable
- B cell phenotype
- Peculiar cells with hair like projections on their surface
16
Q
Pathogenesis & Clinical Manifestations of Hairy Cell Leukemia
A
- hairy cells in peripheral blood
- reduced numbers in granulocytes, platelets, red blood cells
- splenomegaly (90%) (enlarged slpeen)
17
Q
Treatment of Hair Cell Leukemia
A
- begins when patient is symptomatic (enlarged spleen, recurrent infection, bleeding disorder, anemia)
- CR rate of 80% with appropriate chemotherapy protocol
18
Q
Multiple Myeloma (Plasma Cell Myeloma)
A
- malignant disorder of mature, antibody secreting B lymphocytes (plasma cells)
- occurs exclusively in adults
- men > women
19
Q
Pathogenesis of Multiple Myeloma
A
- malignant plasma cells invade bone and form multiple tumor sites
- may also target other tissues (lymph nodes, liver, spleen, kidneys)
- abnormalities in chromosome structure/number
20
Q
Clinical Manifestations of multiple Myeloma
A
- diagnosis based on monoclonal antibody peak, presence of Bence Jones Protein, Hypercalcemia, evidence of bone lesions
- bone marrow biopsy confirms diagnosis
21
Q
Bence Jones Protein
A
malignant plasma cells produce light chain antibody fragments that accumulate in blood and urine; can accumulate in kidneys and damage them
22
Q
Bone marrow Biopsy
A
- plasma cells occupt 20% to 95% of bone
- minimum of 10% to 15% for diagnosis
23
Q
Monoclonal gammopathy of undermined significance (MGUS)
A
-test for the presence of an abnormal protein (paraprotein) in the blood.
24
Q
Signs and Symptoms of Multiple Myeloma
A
- protein in urine
- high serum calcium levels
- first symptom usually bone pain
- anemia
- recurrent infections
- bleeding tendencies
- renal insufficiency (50% of cases)
- Honeycomb appearance in bones
25
Treatment of Multiple Myeloma
- stem cell transplant
- pharmacologic management for renal dysfunction and bone pain
- Antineoplastic agents
- chemo
26
Chronic Lymphoid Leukemia
- accounts for 30% of all leukemia cases in US
- 95% malignant B Cell precursors
- 5% associated with more aggressive T cell transformation
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27
Symptoms of CLL
- fatigue, weight loss, anorexia
| - increased susceptibility to infections
28
Pathogenesis and Clinical Manifestations of CLL
- malignant lymphocytes invade lymphoid tissue and bone marrow; disrupts function
- CLL cells characterized by defective apoptosis and longer lifespan
- derived from mature peripheral B cells
29
Complete Remission (CR)
- return to normal hematopoiesis with normal red cell, neutrophil, and platelet count; no detectable neoplastic cells
- not a cure
30
Chemotherapy treatment phases
- remission induction: eliminate all detectable neoplastic cells and achieve CR
- Post remission or consolodation: begins after CR is attained to eliminate any undetected cells that may have escaped initial induction-phase treatment
- Remission maintenance: used to manage some neoplasms to prolong the remission interval
31
Leukocytosis and Steroids
glucocorticoids cause an increase in WBC count, primarily PMNs
