Břišní tuk a lymfatický systém

Formování postavy

• Mazání Ryor mořské řasy - rozmíchat s vodou "blátíčkem"
• Prohřívací zábal
• Lymfodrenáž
• 10 týdnů - 9 kjg dole, 12 cm úbytek v pase

• Manželka p. Kopsy po porodu, sdělení 2022

• Kazuistiky cca 3 po porodu se selháním lymfat. syst.

• p. Ing. Kopsa , sdělení 2022

• 2 letý kluk s prim. lymfedémem
• Matka až po 2. porodu projev prim. lymfedmu také

• p. Ing. Kopsa , sdělení 2022

• Námět na studii
• Lymfodrenáže na obezitu ženám po porodu a vliv na redukci hmotnosti

• p. Ing. Kopsa , sdělení 2022

• Fibrotizace tkání - byla v ruce
• Cvičila a dělala ML - zbavila se i po 8 letech zfibrotizovaných tkání
• Opakované fyzické manipulace s firbotickou tkání - může vymizet

• p. Ing. Kopsa , sdělení 2022

• Doplatky dle typu návleku a stroje

Lymfatická insufficience jako obezita

• Jedna z možných teorií obezity
• Zhoršená lymfatická drenáž podporuje rozvoj obezity
• Otázka je jak velký faktor u koho to je
• Ps.: po sexu dojde k výraznému objemu břicha u něktrých žen

Transudation or fluid filtration

• Through the serosal covering of organs positioned within the pericardial, pleural and peritoneal spaces provides a second route for interstitial fluid removal in healthy organs. The factors governing filtration across the serosal barrier are approximated by a modified form of the Starling-Landis equation where interstitial fluid pressure acts to drive fluid flow out of the organ and interstitial COP acts to restrain that flow (97, 98). In both the heart and liver, increases in venous and microvascular pressures result in increases in interstitial fluid pressure and, thus, serosal transudation (97, 98). These findings are consistent with the clinical observations of pericardial effusion and ascites associated with pulmonary hypertension and right-sided heart disease (99–101).

In response to chronic edemagenic challenges, the permeability of the serosal surface can change over time. Following 5–6 weeks of caudal vena caval hypertension in dogs, the fluid and protein permeabilities of the hepatic serosal surface significantly decreased leading to significant decreases in serosal transudation and ascites volume (27).Edema: Causes, Mechanisms, and Consequences
Interstitial edema, the accumulation of excess fluid in the interstitial space, can lead to a number of negative consequences depending on the organ system involved. In addition to increasing oxygen diffusion distance within tissues, edema affecting the lung, heart and intestine impairs the organ's mechanical and physiological function (102–104). Interstitial edema in organs like the brain, intestines and kidney, where volume expansion is constrained, can lead to the development of compartment syndrome with resultant impairment of blood flow and organ failure (105). For the same reason, intestinal edema can also prevent surgical closure of an open abdomen. Pulmonary edema increases the work of breathing and carries the added risk of alveolar flooding.
Classically, interstitial edema forms as a result of some combination of increased microvascular pressure, decreased plasma COP, increased microvascular permeability and decreased lymphatic drainage. The effect of the first three of these factors is to increase the rate of microvascular filtration into the interstitial space as can be appreciated in the Starling-Landis equation (1). As discussed above, inhibition of lymphatic drainage caused by lymphatic obstruction or elevated lymphatic outflow pressure does not necessarily promote interstitial edema formation. However, it does magnify the impact of other edemagenic insults such as elevated microvascular pressure (58, 106).
Microvascular fluid pressure acts to promote microvascular filtration and is commonly increased in association with venous hypertension resulting from venous thrombosis or cardiac dysfunction. It is also increased by the arteriolar dilation that occurs in maldistributive shock associated with inflammation and sepsis. Plasma COP opposes microvascular fluid pressure and acts to restrain filtration, therefore decreased plasma COP due to hypoproteinemia/hypoalbuminemia also leads to greater filtration. This increase in filtration can have a broader impact than the easily recognized effects on lungs and skin. Hypoproteinemia in dogs has been shown to cause myocardial edema and impaired diastolic function (107). Intravenous administration of isotonic crystalloid solutions to normal subjects thus promotes interstitial edema formation by simultaneously increasing microvascular pressure via blood volume expansion and decreasing plasma colloid osmotic pressure via dilution.
Microvascular filtration can also be increased as a result of increases in the permeability of the microvascular barrier to either fluid or protein (1, 108–110). The permeability of the microvascular barrier to both is actively regulated at the level of the vascular endothelium and the glycocalyx layer located on the endothelial surface (111, 112). Numerous inflammatory mediators increase microvascular permeability leading to increased microvascular filtration and interstitial edema formation (111, 112).
https://www.frontiersin.org/articles/10.3389/fvets.2020.609583/full