بوغمه
د ويکيپېډيا لخوا
بوغمه په امريکايي انګريزي کې (Edema) ايډيما او په برتانيوي انګرېزي (Oedema) اوډېما بلل کېږي. پخوا د dropsy ډروپسي يا hydropsy هايډروپسي په نومونو هم پېژندل کېده. بوغمه د بدن په بين البيني فضاګانو کې او يا هم د پوستکي تر لاندې د مايعاتو غيرنورمالې راغونډېدنې ته وايي. په ټولګړي توګه، په نورماله حالت کې د بين البيني مايعاتو کچه د هوميوسټاتيک توازن له مخې برابر ساتل کېږي، نو کله چې په بين البيني فضاګانو کې د حد نه ډېر د مايعاتو ترشح وشي او يا هم د مايعاتو د باندې وېستلو په کړنه کې کوم خنډ پيدا شي بيا نو همدا د بوغمې سبب ګرځي.
نيوليک |
د بوغمې ۵ اهم عاملونه
داسې پينځه عاملونه دي چې په بدن کې د بوغمې د جوړېدنې سبب ګرځېدلای شي.
- د هايډروسټېټيک فشار د لوړوالي په وخت کې، په پښتورګي کې اوبه او سوډيم په بېرته جذبېږي چې همدا بېرته پاتې کېدنه د بوغمې د غبرګون په توګه راڅرګندېږي.[1]
- د وينې په رګونو کې د اونکوټيک فشار د راټيټېدنې په وخت کې.
- د التهاب په وخت کې چې کله د وينې د رګونو شفافيت ډېرېږي نو په دې وخت کې هم بوغمه پېښېدونکې ده.
- د ليمفاوي سيستم له مخې د مايعاتو د وېستلو په لار کې خنډ بوغمې جوړوي.
- ووبونو (انساجو) د اوبو ساتلو په ځانتياو کې بدلونونه هم بوغمه رامېنځ ته کوي.
ميکانيزم
|
د ژباړې لپاره نومېدلي، نور مخونو دلته وګورۍ. |
Generation of interstitial fluid is regulated by the forces of the Starling equation.[2] Hydrostatic pressure within blood vessels tends to cause water to filter out into the tissue. This leads to a difference in protein concentration between blood plasma and tissue. As a result the oncotic pressure of the higher level of protein in the plasma tends to suck water back into the blood vessels from the tissue. It is often not appreciated that the Starling equation does not indicate a balance between these forces. The hydrostatic force must always win, and there must always be leakage of fluid out of the vessel because otherwise there can be no oncotic gradient. Starling's equation states that the rate of leakage of fluid is determined by the difference between the two forces and also by the permeability of the vessel wall to water, which determines the rate of flow for a given force imbalance. Most water leakage occurs in capillaries or post capillary venules, which have a semi-permeable membrane wall that allows water to pass more freely than protein. (The protein is said to be reflected and the efficiency of reflection is given by a reflection constant of up to 1.) If the gaps between the cells of the vessel wall open up then permeability to water is increased first, but as the gaps increase in size permeability to protein also increases with a fall in reflection coefficient.
Changes in the variables in Starling's equation can contribute to the formation of edema either by an increase in hydrostatic pressure within the blood vessel, a decrease in the oncotic pressure within the blood vessel or an increase in vessel wall permeability. The latter has two effects. It allows water to flow more freely and it reduces the oncotic pressure difference by allowing protein to leave the vessel more easily.
A rise in hydrostatic pressure occurs in cardiac failure. A fall in oncotic pressure occurs in nephrotic syndrome and liver failure. An increase in permeability occurs in inflammation. It is commonly taught that these facts explain the occurrence of edema in these conditions. However, it has been known since the 1950s that the situation is more complex and it is still far from completely understood[3].
The variation in hydrostatic pressure in the vessels in the feet as compared to the face is about a metre of water. In the case of human feet, the Starling forces are always a long way out of balance. In severe heart failure the change in central venous pressure is tiny in comparison and cannot explain why edema of the feet develops simply through an effect on capillary leakage. Three other factors may be involved. If the central venous pressure rises to equal that of the thoracic lymph duct then clearance of fluid from the tissue will be impeded (see below). That is to say the edema may actually be caused by a change in output of fluid from the tissue, as much as input to the tissue. Secondly, severe heart failure is one of the most exhausting conditions there is. The sufferers tend to spend what little effort they can make trying to breathe with edematous lungs. They tend to sit up to make breathing easier and their feet hang immobile on the floor. Immobility is perhaps the commonest of all causes of edema, because clearance of fluid via the lymphatics needs muscle action. Thirdly, in severe heart failure endocrine and neural changes alter the way tissues are perfused in ways that are not fully understood.
Although a low plasma oncotic pressure is widely cited for the edema of nephrotic syndrome, most physicians note that the edema may occur before there is any significant loss of protein in the urine or fall in plasma protein level. Fortunately there is another explanation available. Most forms of nephrotic syndrome are due to biochemical and structural changes in the basement membrane of capillaries in the kidney glomerulae, and these changes occur, if to a lesser degree, in the vessels of most other tissues of the body. Thus the resulting increase in permeability that leads to protein in the urine can explain the edema if all other vessels are more permeable as well.
Abnormal removal of interstitial fluid is caused by failure of the lymphatic system. This may be due to obstruction from, for example, pressure from a cancer or enlarged lymph nodes, destruction of lymph vessels by radiotherapy, or infiltration of the lymphatics by infection (such as elephantiasis). It is most commonly due to a failure of the pumping action of muscles due to immobility, most strikingly in conditions such as multiple sclerosis, or paraplegia. Lymphatic return of fluid is also dependent on a pumping action of structures known as lymph hearts. It has been suggested that the edema that occurs in some people following use of aspirin-like cyclo-oxygenase inhibitors such as ibuprofen or indomethacin may be due to inhibition of lymph heart action.
In myxedema and a variety of other rarer conditions edema is due to an increased tendency of the tissue to hold water within its extracellular space. In myxedema this is because of an increase in hydrophilic carbohydrate-rich molecules (perhaps mostly hyaluronan) deposited in the tissue matrix. Edema forms more easily in dependent areas in the elderly (sitting in chairs at home or on aeroplanes) and this is not well understood. Estrogens alter body weight in part through changes in tissue water content. There may be a variety of poorly understood situations in which transfer of water from tissue matrix to lymphatics is impaired because of changes in the hydrophilicity of the tissue or failure of the 'wicking' function of terminal lymphatic capillaries.
ځانګړو غړو ته اړونده بوغمه
د بدن د ځينو ځانګړو غړو د التهاب په وخت کې بوغمه رامېنځ ته کېدلای شي، لکه د ستوني د التهاب، د پلو التهاب او يا د پانکراس التهاب دا ټول بوغمه رامېنځ ته کوي. د بدن ځينې نور غړي د ووبونو د خاص ميکانيزم له مخې بوغمه کېږي. په ځانګړو غړو کې د بوغمې بېلګې:
-
- مغزي بوغمه په ماغزو کې د سلولونو د خارجي مايع د راغونډېدلو په پايله کې رامېنځ ته کېږي. دا د زهرجن او غيرنورمال ميټابوليک دريځ او حالتونو لکه د سيسټېميک لوپس ناروغۍ په وخت کې هم راپېښېدلای شي. داسې حالت په ناروغ کې سربدالي او بې هوشي رامېنڅ ته کوي.
- د سږو بوغمه هغه وخت پېښېږي کله چې د سږو د وينې په رګونو کې فشار جګېږي. د وينې په رګونو کې د فشار د لوړوالي سبب د وينې د بهېدو په بهير کې خنډ او بنديز دی. چې د سږو د وريدونو له لارې د خنډونو او بنديزونو د ليرې کولو لپاره فشار جګېږي. او بل سبب يې د زړه ا کيڼ بطن د ناسوبوالي له امله هم راپېښېږي. دا ډول بوغمه په لوړو سطحو کې او د کيميايي زهرجنو توکيو د تنفس کولو په سبب هم مېنځ ته راځي. د سږو د بوغمې د راپېښېدلو سره د ناروغ ساه لنډه لنډه کېږي. همدا راز په ناروغ کې د سږو په پوښل شوې پرده يا پليورا کې هم اوبلنه ماده راغونډېدلی شي.
-
- کله چې د سترګو قرنيې د ګلاوکوما په ناروغۍ اخته وي نو په هغو سترګو کې بوغمه هم راپېښېدلی شي، د کانجنکټيواټېس يا کيراټايټس او يا هم د سترګو د عمليات نه وروسته هم بوغمه رامېنځ ته کېږي.
د بوغمې سببونه د بدن يوه غړي پورې نه دي محدوده او په عام ډول ټول بدن بدن کې هم د ګڼو غړيو بوغمن کېدلو امکان هم شته. د ساري په توګه د زړه د حاد ناسوبوالي په نتيجه کې د سږو بوغمه، په پليورا کې د اوبلنې مادې راغونډېدنه، د نس ډډ بډ والی، او د بدن د خارجي اعضاؤ بوغمې ډېر راپېښېږي، چې په دغو ټولو کې د بدن د باندنيو غړو بوغمه، ناروغ ته د ډېره جدي روغتيايي ستونزه نه ده.[4]
Common appearances of cutaneous edema are observed with mosquito bites, bee stings (wheal and flare), and skin contact with certain plants such as Poison Ivy or Western Poison Oak,[5] the latter of which are termed contact dermatitis.
بوغمه په بوټو کې
بوغمه په بوټو کې هم پېښېږي او دا د بوټو په اورګانونو کې هغه غځېدلی پړسوب دی چې په اصلي توګه د ډېرو اوبو د راغونډېدنې په سبب رامېنځ ته کېږي. دا چې سلولي دېوال د ارتجايي سلولوز نه جوړ شوی نو په همدې دليل د ډېرو اوبو راغونډېدنه سلولوز د اوبو د فشار په سمت ټېلوهي او په بوټي کې ځرګنده بوغمه ښکاري.
سرچينې
- ↑ Kumar, Abbas, Fausto (1999). Pathologic Basis of Disease, 7th edition, 122, China: Elsevier Saunders.
- ↑ Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch, Elsevier/Saunders. ISBN 1-4160-2328-3.
- ↑ Renkin EM. (1994) Cellular aspects of transvascular exchange: a 40-year perspective. Microcirculation 1(3):157-67.
- ↑ Cho S, Atwood J (2002). "Peripheral oedema". Am J Med 113 (7): 580–6. DOI:10.1016/S0002-9343(02)01322-0.
- ↑ C.Michael Hogan (2008) "Western poison-oak: Toxicodendron diversilobum", GlobalTwitcher, ed. Nicklas Strömberg
