Edema pathophysiology

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

Cellular pathophysiology of asthma. Top, Cross-section of the normal airway and the asthmatic ain/vay. Mediators released during the inflammatory process associated with asthma cause bronchoconstriction, mucus secretion, and mucosal inflammation and edema. These changes reduce the size of the airway lumen and increase resistance to airflow, which leads to wheezing and shortness of breath. Bottom, The multitude of inflammatory cells (macrophages, eosinophils, mast cells, neutrophils) and neurotransmitters implicated in asthma pathophysiology. 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

Despite intensive study, the pathophysiology of idiopathicedema (fluctuating salt retention and edema) remains obscure. Some studies suggest that intermittent diuretic use may actually contribute to the syndrome. Idiopathic edema should probably be managed with moderate salt restriction alone if possible. 

The pathophysiology of IR injury in the lung involves increased leakage from the pulmonary microvasculature leading to interstitial and alveolar edema, excessive infiltration of polymorphonuclear cells into the lung, tissue inflammation, and apoptosis (de Perrot et al. 2003). 

Pathophysiologically, the pronounced ADC decline during ischemia occurs at the same time as anoxic depolarization. Anoxic depolarization is the consequence of energy failure with secondary failure of ion pumps (in particular Na+/K+-ATPase), which are necessary to maintain ion gradients over cell membranes. The resulting influx of Na+-ions is accompanied by a water shift from the extra- to the intracellular space (cytotoxic edema) without a net uptake of water (Fig. 7.1). 

Related to the post-traumatic microvascular damage is the pathophysiological process of vasogenic brain edema that represents a disruption of blood-brain barrier integrity, resulting in sodium and protein accumulation and osmotic fluid expansion of the brain extracellular space. Clinically, this is reflected by an increase in intracranial pressure which, if unchecked, can cause secondary compressive injury to vital brain structures. 

The pathophysiology of scleritis is complex and not fully understood.The main dysfunction is thought to be the deposition of immime complexes in the vasculature of the sclera and episclera, creating a vasculitis. This leads to edema and inflammatory cell infiltration of the sclera and episclera, which in turn cause disorganization and destruction of the collagen lamellae. However, not all presentations of scleritis demonstrate the same pathology. 

Blei, A.T. Pathophysiology of brain edema in fubninant hepatic failure, revisited. Metab. Brain Dis. 2001 16 85-94... 

IsraUi ZH, Hall WD. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review of the literature and pathophysiology. Ann Intern Med 1992 117(3) 234-42. 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

These processes can be complemented and enhanced by the liberation of biologically active cellular mediators from intracellular compartments or from the cell membrane. Thus, it is understandable that PFTs provoke inflammatory lesions and acute organ dysfunction in vitro and in vivo, and are lethal in experimental animals. When perfused through an isolated lung, PFTs provoke profound pathophysiological alterations in the pulmonary microvasculature and cause irreversible pulmonary edema. The underlying mechanisms are complex, but include a direct toxic action on endothelial cells, and the pro-... 

The pathophysiology of both TOS and EMS involves an immunological component. Generally, early skin biopsies in both TOS and EMS showed edema and inflammatory infiltrates. Inflammatory lesions of arteries and cardiac neural structures in both EMS and TOS patients were primarily composed of lymphocytes. Persistent elevated levels in the serum level of the soluble fraction of IL-2 receptor were noted in both EMS and TOS patients, suggesting chronic immune activation. 

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