Recent from talks
Carcinoid syndrome
Knowledge base stats:
Talk channels stats:
Members stats:
Carcinoid syndrome
Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to neuroendocrine tumors (formerly known as carcinoid tumors). The syndrome is caused by neuroendocrine tumors most often found in the gut releasing biologically active substances into the blood causing symptoms such as flushing and diarrhea, and less frequently, heart failure, vomiting and bronchoconstriction.
The carcinoid syndrome occurs in approximately 10% of all neuroendocrine tumors or about 30–40% of more advanced/well developed neuroendocrine tumors. The biologically active substances that are released by the tumors cause the symptoms of the carcinoid syndrome. These substances act on the vessels to produce the symptoms of the carcinoid syndrome.
Less common symptoms include malabsorption (leading to pellagra), fatigue, muscle loss, and cognitive impairment. Late complications may include mesenteric and retroperitoneal fibroses as well.
The carcinoid syndrome occurs secondary to neuroendocrine tumors. These tumors occur mostly in the gut and less commonly in the lungs, but may also occur in other places in the body such as the pancreas, kidneys, and other organs. Neuroendocrine tumors produce several biologically active substances, mainly amines and peptides. There are over 40 substances known to be secreted by these tumors but the exact effect of each and their contribution to the carcinoid syndrome is unknown. The most common substances found to be released and contribute to the syndrome include serotonin, histamine, tachykinins, kallikrein, and prostaglandins with the greatest contribution appearing to be from serotonin. The symptoms of the carcinoid syndrome result from the action of these substances largely on the blood vessels. These biologic substances are often metabolized and inactivated by the liver in a process known as first pass metabolism. This is why carcinoid syndrome most often occurs in patients whom the neuroendocrine tumor has metastasized to the liver, which allows the substances to bypass the first pass metabolism. Neuroendocrine tumors arising in the bronchi may be associated with manifestations of carcinoid syndrome without liver metastases because their biologically active products reach the systemic circulation before passing through the liver and being metabolized.
Tryptophan metabolism is altered in the carcinoid syndrome. With neuroendocrine tumors, there is a shift in conversion of tryptophan to serotonin from the normal 1% to as high as 70%. Increased amounts of serotonin lead to increased gut motility causing the diarrhea seen in carcinoid syndrome. Increased amounts of serotonin can also cause the flushing seen as the main symptom of carcinoid syndrome. Tryptophan is also needed for niacin synthesis which can be a cause for pellagra associated with carcinoid syndrome. In the pulmonary neuroendocrine tumors or metastases, histamine release and kallikrein metabolism are the vasoactive mediators of flushing and the other symptoms of carcinoid syndrome.
Carcinoid crisis is an extreme exacerbation of the carcinoid syndrome. This results from excessive release of amines by the neuroendocrine tumors. It is largely a result of stressful procedures such as anesthesia, surgery, or radiation treatment. Symptoms of carcinoid crisis include flushing, hypotension, arrhythmia and bronchospasm.
Carcinoid heart disease is the result of valvular damage related to the vasoactive substances released by the neuroendocrine tumor reaching the right side of the heart. This mainly affects the right side of the heart unless there is anomalous circulation (i.e. patent foramen ovale) because the lungs will metabolize the substances released by the tumor similar to how the liver will. After initial tissue injury around the valves, plaque will develop and fibrosis will occur, possibly mediated by excess serotonin.
With a certain degree of clinical suspicion, the most useful initial test is the 24-hour urine levels of 5-HIAA (5-hydroxyindoleacetic acid), the end product of serotonin metabolism. Chromogramin A, a glycoprotein released by neuroendocrine tumors, can be used to detect non-secreting tumors.
Hub AI
Carcinoid syndrome AI simulator
(@Carcinoid syndrome_simulator)
Carcinoid syndrome
Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to neuroendocrine tumors (formerly known as carcinoid tumors). The syndrome is caused by neuroendocrine tumors most often found in the gut releasing biologically active substances into the blood causing symptoms such as flushing and diarrhea, and less frequently, heart failure, vomiting and bronchoconstriction.
The carcinoid syndrome occurs in approximately 10% of all neuroendocrine tumors or about 30–40% of more advanced/well developed neuroendocrine tumors. The biologically active substances that are released by the tumors cause the symptoms of the carcinoid syndrome. These substances act on the vessels to produce the symptoms of the carcinoid syndrome.
Less common symptoms include malabsorption (leading to pellagra), fatigue, muscle loss, and cognitive impairment. Late complications may include mesenteric and retroperitoneal fibroses as well.
The carcinoid syndrome occurs secondary to neuroendocrine tumors. These tumors occur mostly in the gut and less commonly in the lungs, but may also occur in other places in the body such as the pancreas, kidneys, and other organs. Neuroendocrine tumors produce several biologically active substances, mainly amines and peptides. There are over 40 substances known to be secreted by these tumors but the exact effect of each and their contribution to the carcinoid syndrome is unknown. The most common substances found to be released and contribute to the syndrome include serotonin, histamine, tachykinins, kallikrein, and prostaglandins with the greatest contribution appearing to be from serotonin. The symptoms of the carcinoid syndrome result from the action of these substances largely on the blood vessels. These biologic substances are often metabolized and inactivated by the liver in a process known as first pass metabolism. This is why carcinoid syndrome most often occurs in patients whom the neuroendocrine tumor has metastasized to the liver, which allows the substances to bypass the first pass metabolism. Neuroendocrine tumors arising in the bronchi may be associated with manifestations of carcinoid syndrome without liver metastases because their biologically active products reach the systemic circulation before passing through the liver and being metabolized.
Tryptophan metabolism is altered in the carcinoid syndrome. With neuroendocrine tumors, there is a shift in conversion of tryptophan to serotonin from the normal 1% to as high as 70%. Increased amounts of serotonin lead to increased gut motility causing the diarrhea seen in carcinoid syndrome. Increased amounts of serotonin can also cause the flushing seen as the main symptom of carcinoid syndrome. Tryptophan is also needed for niacin synthesis which can be a cause for pellagra associated with carcinoid syndrome. In the pulmonary neuroendocrine tumors or metastases, histamine release and kallikrein metabolism are the vasoactive mediators of flushing and the other symptoms of carcinoid syndrome.
Carcinoid crisis is an extreme exacerbation of the carcinoid syndrome. This results from excessive release of amines by the neuroendocrine tumors. It is largely a result of stressful procedures such as anesthesia, surgery, or radiation treatment. Symptoms of carcinoid crisis include flushing, hypotension, arrhythmia and bronchospasm.
Carcinoid heart disease is the result of valvular damage related to the vasoactive substances released by the neuroendocrine tumor reaching the right side of the heart. This mainly affects the right side of the heart unless there is anomalous circulation (i.e. patent foramen ovale) because the lungs will metabolize the substances released by the tumor similar to how the liver will. After initial tissue injury around the valves, plaque will develop and fibrosis will occur, possibly mediated by excess serotonin.
With a certain degree of clinical suspicion, the most useful initial test is the 24-hour urine levels of 5-HIAA (5-hydroxyindoleacetic acid), the end product of serotonin metabolism. Chromogramin A, a glycoprotein released by neuroendocrine tumors, can be used to detect non-secreting tumors.