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43 Cards in this Set
- Front
- Back
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Mcq- features of multiple myeloma |
High blood urea Hypoalbumineamia Thrombocytosis Hypercalcaemia Leucocytosis |
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What is multiple myeloma |
debilitating malignancy that is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia.
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Pathophysiology of multiple myeloma |
MM is characterized by neoplastic proliferation of plasma cells involving more than 10% of the bone marrow Increasing evidence suggests that the bone marrow microenvironment of tumor cells plays a pivotal role in the pathogenesis of myelomas. This discovery has resulted in the expansion of treatment options. |
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What are the characteristics of multiple myeloma |
characterized by a proliferation of malignant plasma cells and a subsequent overabundance of monoclonal paraprotein (M protein). |
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What are the possible aetiologic factors |
Genetic Environmental occupational causes-agriculture, (insecticides, weedicides )food, and petrochemical industries. MGUS, radiation, chronic inflammation, and infection. |
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Processes in which systems give rise to clinical features |
skeletal, hematologic, renal, and nervous systems, |
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What is the range of clinical features |
Signs and symptomsMM can range from asymptomatic to severely symptomatic with complications requiring emergent treatment. MM is often discovered through routine blood screening when patients are being evaluated for unrelated problems. In one third of patients, the condition is diagnosed after a pathologic fracture occurs, usually involving the axial skeleton. So it's more or less presents later.
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What are the processes that lead to bone related symptoms |
Plasma-cell proliferation causes extensive skeletal destruction with osteolytic lesions, anemia, and hypercalcemia. Destruction of bone and its replacement by tumor may lead to pain, spinal cord compression, and pathologic fracture. The mechanism of spinal cord compression symptoms may be the development of an epidural mass with compression, a compression fracture of a vertebral body destroyed by multiple myeloma, or, rarely, an extradural mass. With pathologic fracture, bony involvement is typically lytic in nature. |
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What are the signs and symptoms of bone related problems |
•Bone pain •Pathologic fractures •Spinal cord compression (from pathologic fracture) Hypercalcemia
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What are the haematological processes |
Bone marrow infiltration by plasma cells results in neutropenia, anemia, and thrombocytopenia. M components may interact specifically with clotting factors, leading to defective aggregation. |
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What are the symptoms related to haematological processes |
•Weakness, malaise •Bleeding, anemia •Infection (often pneumococcal)
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What are the other signs and symptoms |
•Renal failure •Neuropathies General processes
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What are the systems that will have significant clinical features |
Eyes Skin Bone Renal
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Eye signs |
Exudative macular detachment, retinal hemorrhage, or cotton-wool spots |
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Findings of dermatology examination |
Pallor from anemia, ecchymoses or purpura from thrombocytopenia; extramedullary plasmacytomas (most commonly in aerodigestive tract but also orbital, ear canal, cutaneous, gastric, rectal, prostatic, retroperitoneal areas) |
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Findings of MSS |
Bony tenderness or pain without tenderness |
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What are the basics of hypercalcemia |
Mechanisms for hypercalcemia include bony involvement and, possibly, humoral mechanisms. Isolated plasmacytomas (which affect 2-10% of patients) lead to hypercalcemia through production of the osteoclast-activating factor. |
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What are the renal processes |
The most common mechanisms of renal injury in MM are direct tubular injury, amyloidosis, or involvement by plasmacytoma |
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What are the renal conditions found in multiple myeloma |
hypercalcemic nephropathy, hyperuricemia due to renal infiltration of plasma cells resulting in myeloma, light-chain nephropathy, amyloidosis, and glomerulosclerosis. |
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What are the neurological processes |
The nervous system may be involved as a result of radiculopathy and/or cord compression due to nerve compression and skeletal destruction (amyloid infiltration of nerves). |
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What are the general processes |
General pathophysiologic processes include hyperviscosity syndrome. This syndrome is infrequent in MM and occurs with overproduction of IgG1, IgG3, or IgA. Sludging in the capillaries can result in purpura, retinal hemorrhage, papilledema, coronary ischemia, or central nervous system (CNS) symptoms (eg, confusion, vertigo, seizure). Cryoglobulinemia causes Raynaud phenomenon, thrombosis, and gangrene in the extremities. |
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Cardiology and abdomen examination |
Cardiomegaly Hepatosplenomegaly |
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Characteristics of those with MM and Amyloidosis |
•Shoulder pad sign•Macroglossia•Typical skin lesions•Post-proctoscopic peripalpebral purpura (eyelid purpura may also follow coughing, vomiting, the Valsalva maneuver, or forced expiration during spirometric testing)•Carpal tunnel syndrome•Subcutaneous nodules
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Standard investigative workup for those suspected of having MM |
•Serum and urine assessment for monoclonal protein (densitometer tracing and nephelometric quantitation; immunofixation for confirmation)•Serum free light chain assay (in all patients with newly diagnosed plasma cell dyscrasias)•Bone marrow aspiration and/or biopsy•Serum beta2-microglobulin, albumin, and lactate dehydrogenase measurement•Standard metaphase cytogenetics•Fluorescence in situ hybridization•Skeletal survey•MRI
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What are the routine laboratory investigations |
•Complete blood count and differential•Erythrocyte sedimentation rate•Comprehensive metabolic panel (eg, levels of total protein, albumin and globulin, BUN, creatinine, uric acid)•24-hour urine collection for quantification of the Bence Jones protein (ie, lambda light chains), protein, and creatinine clearance; proteinuria greater than 1 g/24 hr is a major criterion•C-reactive protein•Serum viscosity in patients with CNS symptoms, nosebleeds, or very high M protein levels
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What are the findings in blood |
anemia, thrombocytopenia, or leukopenia. differential may show pancytopenia. The reticulocyte count is typically low. Peripheral blood smears may show rouleau formation. |
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What are the imaging studies |
•Simple radiography for the evaluation of skeleton lesions; skeletal survey, including the skull, long bones, and spine•MRI for detecting thoracic and lumbar spine lesions, paraspinal involvement, and early cord compression•PET scanning in conjunction with MRI potentially useful
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Findings |
Q |
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What are the treatment options |
There is currently no cure for MM. However, advances in therapy, such as autologous stem cell transplantation, radiation, and surgical care in certain cases, have helped to lessen the occurrence and severity of adverse effects of this disease and to manage associated complications. Chemotherapy and immunosuppression. |
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What are the concerns in doing imaging studies |
Consider the risk of acute kidney injury, especially in the setting of contrast medium injection for imaging studies. Take care to limit patients’ exposure and maintain hydration |
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What is expected in ESR |
The erythrocyte sedimentation rate (ESR) is typically increased. |
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What can be seen in coagulation studies |
They can be abnormal |
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What are the components of a comprehensive metabolic panel that has to be done |
• Total protein, albumin, and globulin • Blood urea nitrogen (BUN) and creatinine • Uric acid (will be elevated if the patient has high cell turnover or is dehydrated) |
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What are the expected findings in chemical studies |
azotemia hypercalcemia an elevated alkaline phosphatase level hypoalbuminemia |
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What is the significance of high LDH |
A high lactate dehydrogenase (LDH) level is predictive of an aggressive lymphomalike course. |
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What is the place of SPEP |
screening test for detecting M proteins. An M component is usually detected by means of high-resolution SPEP. In 25% patients May protein cannot be detected by SPEP.
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What is the diagnostic criterian for M proteins |
An M-component serum concentration of 30 g/L is a minimal diagnostic criterion for MM. |
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Can routine urinalysis be used to detect Bence Jones protein |
No we can't. a 24-hour urinalysis by means of UPEP or immunoelectrophoresis may be required. |
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What other things we can look for in 24h urine collection |
UPEP or immunoelectrophoresis can also be used to detect an M component and kappa or lambda light chains. |
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Y |
The most important means of detecting MM is electrophoretic measurement of immunoglobulins in both serum and urine. |
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What is the place of Beta 2 microglobulin |
Beta-2 microglobulin is a surrogate marker for the overall body tumor burden. The level of beta-2 microglobulin is increased in patients with renal insufficiency without MM, which is one reason that it is a useful prognosticator in MM |
