Case Presentation:
Dear Medical Warriors , Here the 61 year old male Presented with Chest wall Pain. We have Updated the X-ray .
Findings on X-ray:
1:Eccentric ill-defined lytic lesion at the left lateral scapula margin.
2: old left proximal humeral fixation and multiple old bilateral rib fractures noted. This may suggest other underlying osseous lesions and subsequent pathological fracture
3: A few other possible lytic lesions eccentrically located within the right proximal humerus medullary cavity.
4: Normal cardiomediastinal contour.
5: Clear Lungs
Dear Medical warriors , Point to be learnt / This case illustrates the importance of the bones as part of your chest x-ray check areas, especially in the setting of pain.
This lesion on its own carries a differential. Given its ill-defined nature, it is probably on the aggressive end of the spectrum (e.g. metastases, myeloma, lymphoma, infection) in an adult. A primary lesion of bone is possible but less likely.
This patient went on to have further cross-sectional imaging, which demonstrated multifocal lytic lesions, predominantly throughout the axial skeleton. The imaging in combination with the patient’s serum results concluded a diagnosis of Multiple Myeloma.
PATHOPHYSIOLOGY involved in Multiple Myeloma :
The development of MM is commonly preceded by MGUS, a premalignant condition that results when plasma cells undergo mutations that restore their capacity for proliferation. In MGUS, these clonal plasma cells take up less than 10% of bone marrow. The serum protein value is less than 3 g/dL and myeloma-related end-organ damage is absent. An intermediate disease stage between MGUS and MM, termed smoldering MM, is characterized by an M protein level of 3 g/dL or more and over 10% clonal plasma cells in bone marrow, but no symptoms of myeloma-related end-organ damage.
A variety of cytogenetic abnormalities are found in MGUS and MM. Approximately half of cases are hyperdiploid, usually with extra copies of the odd-numbered chromosomes. Most of the remainder are nonhyperdiploid and are characterized by a primary translocation involving the Ig heavy-chain gene at 14q32.In addition, virtually all cases involve dysregulation of the cyclin D/retinoblastoma (cyclin D/RB) pathway. This genetic heterogeneity contributes to the rapid emergence of drug resistance in MM.
Increasing evidence suggests that the bone marrow microenvironment of tumor cells plays a pivotal role in the pathogenesis of myelomas.
The pathophysiologic basis for the clinical sequelae of MM involves the skeletal, hematologic, renal, and nervous systems, as well as general processes.
Hematologic Process:
Bone marrow infiltration by plasma cells results in neutropenia, anemia, and thrombocytopenia. M components may interact specifically with clotting factors, leading to defective aggregation
Skeletal Process:
Plasma-cell proliferation causes extensive skeletal destruction with osteolytic lesions, anemia, and 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.
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.
Neurologic Process:
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).
Renal Process:
The most common mechanisms of renal injury in MM are direct tubular injury, amyloidosis, or involvement by plasmacytoma.[13, 14]Renal conditions that may be observed include hypercalcemic nephropathy, hyperuricemia due to renal infiltration of plasma cells resulting in myeloma, light-chain nephropathy, amyloidosis, and glomerulosclerosis.
General Process:
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.
Dear Warriors , We have Updated the Overview of Multiple Myeloma Seperately, Which will Help one in Quick Reference.
