week 6 Flashcards

1
Q

Clinical presentation of Hodgkin Lymphoma

A
  • Painless lymphadenopathy; most commonly involving supraclavicular or cervical nodes
  • B symptoms: Fatigue, fever, night sweats, weight loss
  • Generalized pruritus
  • Cough, dyspnea, or chest pain (if involving mediastinal nodes)
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2
Q

pancytopenia and Hodgkin Lymphoma

A

Hodgkin Lymphoma can involve the bone marrow extensively which is where RBC, platelets, and WBCs are made. Since the tumor begins taking over the space they are made there is not as much room which causes a decrease.

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3
Q

Explain the relationship between EBV and infectious mononucleosis

A

The structure of the EBV genome is identical in all RS cells in a given case, indicating that infection precedes (and therefore may be related to) transformation and clonal expansion

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4
Q

Characterize EBV, including viral structure, replication, and mode of transmission

A

-Infection with EBV occurs by the oral transfer ofsaliva[13]and genital secretions

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5
Q

role LMP-1 & EBNA-1 play in the pathogenicity of Hodgkin Lymphoma

A

-LMP-1: EBV gene that acts as an oncogene; behaves like a constitutively active CD40 receptor
• CD40 → key recipient of helper T-cell signals that stimulate B-cell growth
• LMP-1 activates the NF-𝞳B & JAK/STAT signaling pathways
○ Occurs autonomously (w/o T-cell or other outside signals)
○ Promotes B lymphocyte survival & proliferation (immortalize)
• LMP-1 prevents apoptosis by activation of Pro-survival BCL-2 proteins
○ Virus “borrows” normal B-cell activation pathways
○ Allows expansion of pool of latently infected cells
-EBNA-2: EBV gene that encodes a nuclear protein that mimics a constitutively active Notch receptor
• EBNA-2 transactivates several host genes, including cyclin D & SRC family of proto-oncogenes

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6
Q

role of Reed-Sternberg cells in the diagnosis of Hodgkin Lymphoma.

A

-distinctive,giant cells; usually derived fromB lymphocytes

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7
Q

clinical significance of bone marrow and liver involvement by Hodgkin lymphoma

A

Lungs, Liver, Bone, or Bone Marrow are the most common sites of extranodal involvement

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8
Q

Ann Arbor staging system used in staging Hodgkin lymphomas

A

• Stage I is involvement of a single lymph node region (I) (mostly the cervical region) or single extralymphatic site (Ie);
• Stage II is involvement of two or more lymph node regions on the same side of thediaphragm(II) or of one lymph node region and a contiguous extralymphatic site (IIe);
• Stage III is involvement of lymph node regions on both sides of the diaphragm, which may include thespleen(IIIs) or limited contiguous extralymphatic organ or site (IIIe, IIIes);
• Stage IV is disseminated involvement of one or more extralymphatic organs.
The absence of systemic symptoms is signified by adding “A” to the stage; the presence of systemic symptoms is signified by adding “B” to the stage. For localised extranodal extension from mass of nodes that does not advance the stage, subscript “E” is added. Splenic involvement is signified by adding “S” to the stage. The inclusion of “bulky disease” is signified by “X”.

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9
Q

signs and symptoms of multiple myeloma

A
Bone pain
Pathologic fractures
Spinal cord compression (from pathologic fracture)
Weakness, malaise
Bleeding, anemia
Infection (often pneumococcal)
Hypercalcemia
Renal failure
Neuropathies
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10
Q

List the potential clinical complications that may occur with multiple myeloma

A

Myeloma kidney syndrome with multiple etiologies
Amyloidosis with light chains
Nephrocalcinosis due to hypercalcemia
Anemia, neutropenia, or thrombocytopenia is due to bone marrow infiltration of plasma cells. Thrombosis and Raynaud phenomenon due to cryoglobulinemia may be present.

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11
Q

significance of pancytopenia in the presentation of multiple myeloma

A

Pancytopenia in multiple myeloma may be attributed to several reasons. Most often it is due to the plasma cell proliferation replacing normal haematopoietic cells. Other causes include fas-ligand mediated apoptosis or cytokine-mediated bone marrow failure or even renal failure induced erythropoietin deficiency

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12
Q

calcium levels in the presentation of multiple myeloma

A

can give rise to neurologic manifestations, such as confusion, weakness, lethargy, constipation, and polyuria, and contributes to renal dysfunction.

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13
Q

significance of the presence of urinary Bence-Jones protein

A

proteins are excreted in the kidney and contribute to a form of renal disease called myeloma kidney

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14
Q

Describe the bone marrow histopathologic findings in multiple myeloma

A
  • bone marrow aspirate demonstrating plasma cells of multiple myeloma
  • blue cytoplasm, eccentric nucleus, and perinuclear pale zone
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15
Q

Explain the significance of the SPEP M-spike in the evaluation of multiple myeloma

A

-SPEP is a useful screening test for detecting M proteins. An M component is usually detected by means of high-resolution SPEP. The kappa-to-lambda ratio has been recommended as a screening tool for detecting M-component abnormalities

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16
Q

Discuss the complications of bone lesions in multiple myeloma

A

leads to pathological fractures; most commonly seen in vertebrae with compression fracture

17
Q

clinical indications for therapy of multiple myeloma and its complications

A

o Bone pain, often in the spine, ribs, or proximal long bones
o Monoclonal immunoglobulin (ie,paraprotein) by serum or urine protein electrophoresis or immunofixation electropheresis
o Clonal plasma cells in the bone marrow or in a tissue biopsy, or both
o Organ damage due to plasma cells (eg, bones, kidneys, hypercalcemia, anemia) or other defined criteria