Question

how endocrine/lymphatic system affected by COPD. write in 400 words

Answer 1

The number of lymph vessels and nodes in patients with COPD increases, as does the concentration of chemokine ligand 21 (CCL21), expressed by endothelial lymph cells and one of the G-protein-coupled receptor (GPCR) subtypes A, and its chemokine ligand receptor 7 (CCR7) on activated dendritic cells. This approach increases the number of chemokine scavenger 6 (D6) receptors synthesised by endothelial cells to maintain the gradient of the CCL21 chemoattractant, promote the migration of the CCR7 receptor, and tag the immune cells.

Lymphangiogenesis is directly associated with disease severity and can be measured in 1 s by the value of the forced expiratory volume (FEV1). In patients with COPD, lymphatic nodes undergo hypertrophy, particularly at the level of the bronchi up to the bronchioles. It is possible to find calcified lymph nodes or nodes that have been invaded by adipose tissue in the caudal section of the trachea .

Via phagocytosis, dendritic cells (specialising in the capture of antigens) can internalise an antigen and process the antigen for presentation to T lymphocytes (in lymph nodes) or retain the antigen on their surface in a native form accessible to B lymphocytes (in lymph nodes) unique to that antigen. Their name (dendritic cell) derives from the branched form they believe is unique.

Recognition of antigen occurs by particular receptors (pattern recognition receptor, PRR; toll-like receptor, TLR). The lymphatic follicle can be stimulated by traditional dendritic cells (DCs) to develop alpha/beta lymphotoxins, which will then cause the dendritic-follicular cell to present the antigen to B-cell lymphocytes.

It is no longer known that chronic obstructive pulmonary disease (COPD) affects only the lungs and airways but also the rest of the body. A variety of endocrine disorders are found in the systemic forms of COPD, such as those affecting the pituitary, thyroid, gonads, adrenals and pancreas. The mechanisms by which COPD changes endocrine function are not fully known, but probably include hypoxaemia, hypercapnia, systemic inflammation and administration of glucocorticoids. Via several mechanisms, including decreased protein anabolism, increased protein catabolism, nonenzymatic glycosylation and activation of the rennin-angiotensin-aldosterone system, altered endocrine function can exacerbate the clinical manifestations of COPD. Systemic symptoms of endocrine disorders include breathing regulation abnormalities, decreases in respiratory and limb-muscle mass and function, impaired respiratory mechanics, impaired heart function, and fluid balance disorders. Research on endocrine manifestations of COPD includes molecular biology methods, integrative physiology and clinical trials that are regulated.