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Breast Cancer Metastasis
Secondary breast cancer, also called metastatic breast cancer, occurs when the disease spreads from the breast to elsewhere in the body. Some patients will have their first diagnosis of breast cancer only to discover that it has spread and is in fact metastatic breast cancer. Many women who are diagnosed with secondary cancer have had breast cancer at a previous time. Secondary cancer is caused by cancerous cells breaking away from their first place of infection to travel via the bloodstream to other parts of the body. Obviously metastatic breast cancer is serious and harder to fight because the disease is not confined simply to the breast.
When metastatic cancer develops, the most likely places it will spread to are the liver, lungs, bones and the brain. But because this type of cancer spreads, it does not mean it will necessarily spread to most or all of these places.
Because every woman is unique, those who develop metastatic breast cancer will have their own set of symptoms. These are determined by the location of the secondary cancer. If in the bones, the symptoms will usually mean aches and pains in the bones and particularly so when moving. It can also be difficult to sleep.
Epidemiology
The pain in cancer patients is usually multifactorial, may arise from the process itself, treatment side effects or both. For these reasons the approach and management of this symptom should be multidisciplinary. Pain syndrome occurs either by local proliferation or tumor invasion of a metastatic tumor from a distance. With metastatic bone pain often reflects the presence of a tumor in breast, thyroid, prostate, kidney, lung or adrenal.
Physiology of bone pain
Bone pain is associated with tissue destruction by osteoclast cells. Normally, osteoclastic bone resorption are in balance with bone formation mediated by osteoblasts. In neoplastic osteolytic activity is increased and there are substances such as cytokines, local growth factors, peptides similar to parathyroid hormone and prostaglandins. Autacoids are also released other owners as potassium ions, bradykinin and osteoclast activating factors. These tissue substances play an important role in sensitizing the neural tissue against chemical and thermal stimuli, lower thresholds for discharge of the neuronal membrane, produce exaggerated responses to stimuli above the threshold and result in discharges of tonic impulses normally silent nociceptors. This phenomenon is called peripheral sensitization and primary hyperalgesia and is understood as events occurring within the ranks of the injured tissue and stimulate peripheral nociceptors (C fibers and A delta fibers) translating pain. In bone tissue of the sensory receptors are located primarily in the periosteum, whereas the bone marrow and bone cortex are insensitive. This phenomenon of peripheral sensitization results in abnormal sensitivity to pressure surrounding skin (allodynia and hyperalgesia), pain in muscles, tendons, joints and deep tissues in contact with bone. This is limited to ensure that the peripheral ends have a greater capacity for alarm response to injury.
The constant presence of harmful process, stimulating nociceptive receptors gives the introduction of a subacute pain that tends to be chronic with the growth of bone metastases. These stimuli lead to another prevalent phenomenon called central sensitization important which includes abnormal amplification of incoming sensory signals to the central nervous system, particularly the spinal cord. The phenomenon occurs because of the persistent input stimulus through the fibers C. This spinal cord triggers a temporary increase in the power of silent synaptic terminals. In this process plays an important role of glutamate receptor N-methyl-D-aspartate (NMDA). The resulting amplification of the signal generated in the postsynaptic neuron sends a message to the brain which is interpreted as pain. In short central sensitization amplifies the sensory effects of both peripheral nociceptive inputs (C fibers of pain) and non-nociceptive fibers (A of touch).
In practice the two phenomena come together in the genesis of metastatic bone pain and peripheral sensitization occurs acutely metastatic lesions to appear nociceptors and translate the information conveyed through the afferent myelinated A-delta or unmyelinated C fibers to the spinal cord where the information is modulated by various systems. With the set up process subacute begins the process of central sensitization which sensory synapses begin to activate silent. And there is a state of increased central perception. By becoming chronic pain phenomenon becomes even more complex because all that is in contact with the area of injury becomes a powerful generator of pain. The touch, muscle movement or joint pain result, manifesting the phenomena of allodynia and hyperalgesia much more marked.
Breast Cancer Metastasis
Secondary breast cancer, also called metastatic breast cancer, occurs when the disease spreads from the breast to elsewhere in the body. Some patients will have their first diagnosis of breast cancer only to discover that it has spread and is in fact metastatic breast cancer. Many women who are diagnosed with secondary cancer have had breast cancer at a previous time. Secondary cancer is caused by cancerous cells breaking away from their first place of infection to travel via the bloodstream to other parts of the body. Obviously metastatic breast cancer is serious and harder to fight because the disease is not confined simply to the breast.
When metastatic cancer develops, the most likely places it will spread to are the liver, lungs, bones and the brain. But because this type of cancer spreads, it does not mean it will necessarily spread to most or all of these places.
Because every woman is unique, those who develop metastatic breast cancer will have their own set of symptoms. These are determined by the location of the secondary cancer. If in the bones, the symptoms will usually mean aches and pains in the bones and particularly so when moving. It can also be difficult to sleep.
Epidemiology
The pain in cancer patients is usually multifactorial, may arise from the process itself, treatment side effects or both. For these reasons the approach and management of this symptom should be multidisciplinary. Pain syndrome occurs either by local proliferation or tumor invasion of a metastatic tumor from a distance. With metastatic bone pain often reflects the presence of a tumor in breast, thyroid, prostate, kidney, lung or adrenal.
Physiology of bone pain
Bone pain is associated with tissue destruction by osteoclast cells. Normally, osteoclastic bone resorption are in balance with bone formation mediated by osteoblasts. In neoplastic osteolytic activity is increased and there are substances such as cytokines, local growth factors, peptides similar to parathyroid hormone and prostaglandins. Autacoids are also released other owners as potassium ions, bradykinin and osteoclast activating factors. These tissue substances play an important role in sensitizing the neural tissue against chemical and thermal stimuli, lower thresholds for discharge of the neuronal membrane, produce exaggerated responses to stimuli above the threshold and result in discharges of tonic impulses normally silent nociceptors. This phenomenon is called peripheral sensitization and primary hyperalgesia and is understood as events occurring within the ranks of the injured tissue and stimulate peripheral nociceptors (C fibers and A delta fibers) translating pain. In bone tissue of the sensory receptors are located primarily in the periosteum, whereas the bone marrow and bone cortex are insensitive. This phenomenon of peripheral sensitization results in abnormal sensitivity to pressure surrounding skin (allodynia and hyperalgesia), pain in muscles, tendons, joints and deep tissues in contact with bone. This is limited to ensure that the peripheral ends have a greater capacity for alarm response to injury.
The constant presence of harmful process, stimulating nociceptive receptors gives the introduction of a subacute pain that tends to be chronic with the growth of bone metastases. These stimuli lead to another prevalent phenomenon called central sensitization important which includes abnormal amplification of incoming sensory signals to the central nervous system, particularly the spinal cord. The phenomenon occurs because of the persistent input stimulus through the fibers C. This spinal cord triggers a temporary increase in the power of silent synaptic terminals. In this process plays an important role of glutamate receptor N-methyl-D-aspartate (NMDA). The resulting amplification of the signal generated in the postsynaptic neuron sends a message to the brain which is interpreted as pain. In short central sensitization amplifies the sensory effects of both peripheral nociceptive inputs (C fibers of pain) and non-nociceptive fibers (A of touch).
In practice the two phenomena come together in the genesis of metastatic bone pain and peripheral sensitization occurs acutely metastatic lesions to appear nociceptors and translate the information conveyed through the afferent myelinated A-delta or unmyelinated C fibers to the spinal cord where the information is modulated by various systems. With the set up process subacute begins the process of central sensitization which sensory synapses begin to activate silent. And there is a state of increased central perception. By becoming chronic pain phenomenon becomes even more complex because all that is in contact with the area of injury becomes a powerful generator of pain. The touch, muscle movement or joint pain result, manifesting the phenomena of allodynia and hyperalgesia much more marked.