Plasma oncotic pressure

Oedema refers to an accumulation of interstitial fluid to a point where it is palpable or visible. In general this point is reached with a fluid volume of 2-3 liters. Oedema formation is the result of a shift of fluid into the interstitial space due to primary disturbances in the hydraulic forces governing transcapillary fluid transport and of subsequent excessive fluid reabsorption by the kidneys. Deranged capillary hydraulic pressures initiate oedema formation in congestive heart failure, and liver cirrhosis whereas a deranged plasma oncotic pressure... 

Albumin 18-20 Maintains plasma oncotic pressure transports small molecules Dehydration, anabolic steroids, insulin, infection Overhydration, edema, kidney insufficiency, nephrotic syndrome, poor dietary intake, impaired digestion, burns, congestive heart failure, cirrhosis, thyro id/adrena / pitu itary hormones, trauma, sepsis... 

Patients with renal diseases leading to the nephrotic syndrome often present complex problems in volume management. These patients may exhibit fluid retention in the form of ascites or edema but have reduced plasma volume due to reduced plasma oncotic pressures. This is very often the case in patients with "minimal change" nephropathy. In these patients, diuretic use may cause further reductions in plasma volume that can impair GFR and may lead to orthostatic hypotension. Most other causes of nephrotic syndrome are associated with primary retention of salt and water by the kidney, leading to expanded plasma volume and hypertension despite the low plasma oncotic pressure. In these cases, diuretic therapy may be beneficial in controlling the volume-dependent component of hypertension. 

Liver disease is often associated with edema and ascites in conjunction with elevated portal hydrostatic pressures and reduced plasma oncotic pressures. Mechanisms for retention of Na+ by the kidney in this setting include diminished renal perfusion (from systemic vascular alterations), diminished plasma volume (due to ascites formation), and diminished oncotic pressure (hypoalbuminemia). In addition, there may be primary Na+ retention due to elevated plasma aldosterone levels. 

Although hyperlipidemia may be partly reversed by the increase of plasma oncotic pressure with dextran infusion, decreased albumin and plasma oncotic pressure cannot fully explain nephrotic hyperlipidemia. In analbuminemic rats, lipid changes are different from those in nephrotic subjects (D4). There may be a direct causal link between proteinuria and lipid abnormalities because a 1 -acid glycoprotein isolated from urine of nephrotic patients may correct the impaired lipolysis of nephrotic rats (SI 6, K12). Thus, impaired lipoprotein metabolism may be caused by the loss of some regulatory substance into urine due to increased glomerular permeability. 

Albumin is the main plasma protein, with a molecular weight of about 69 kDa, and is important for normal plasma oncotic pressure and the transport of many biologically active substances, including free fatty acids, phospholipids (e.g., lysophosphatidic acid), prostanoids, heavy metals, steroid hormones, and vitamins. Albumin-bound lysophosphatidic acid serves as a survival factor for cultured mouse proximal tubular cells (L4). Lysophosphatidic acid is an exquisitely potent inhibitor of apoptosis, comparable with growth factors, for example, EGF. The influence of lysophosphatidic acid on the survival of tubular cells depends on the activation of phophatidylinositol 3-kinase (PI3K) with subsequent activation of Akt and pp70s6k. pp70s6k is a rapamycin-inhibited kinase, which plays an important role in the cellular proliferation. Lysophosphatidic acid also serves as a proliferation factor of mouse proximal tubular cells. Further albumin-bound factors important for the survival of the proximal tubular cells are phosphatidic acid... 

When oedema fluid collects in the tissues of the skin, it gives a puffy look to the skin of the face. In the lung, the capillaries run close to the alveoli, and reduction in plasma oncotic pressure can result in fluid accumulation in the alveolar wall and in the alveoli. This fluid increases the diffusion distance for oxygen between blood and alveolar air and acts as a diffusion barrier, reducing gas exchange. If severe, lung (pulmonary) oedema can result in development of abnormal blood gas concentrations. Treatment of pulmonary oedema is critical as it can develop into a life-threatening situation. 

The main function of albumin in the plasma is to provide colloid osmotic pressure. It is of major importance in maintaining blood volume and in the exchange of fluid between blood and the tissues. Heavy proteinuria may involve the loss of >3.5 g of albumin per day and this, in turn, causes a reduction in plasma oncotic pressure. When plasma oncotic pressure is reduced, fluid is not completely reabsorbed from the tissues at the venous end of capillaries. The fluid is retained within the tissues, causing oedema. The effects of gravity on fluid accumulation in the body causes oedema to be more marked in the lower body than in the upper parts, so oedema is often noticed first around the ankles. 

Mohsenin, V. Gonzales, R.R. (1984) Tissue pressure and plasma oncotic pressure during exercise. J. Appl. Physiol. Respirat. Environ. Exercise Physiol. 56, 102-108. 

Albumin Maintains plasma oncotic pressure. Transports fat-soluble substances, e.g. bilirubin, drugs Reduced levels Low levels cause ascites and increase free plasma concentration of albumin-bound drugs, e.g. oestradiol, phenytoin Albumin is a useful clinical indicator of the liver s synthetic function. The liver produces and exports up to 12 g of albumin per day. Low levels are also seen in malnutrition, hypercatabolism and nephrotic syndrome. Half-life of 20 days, therefore indicator of chronic liver disease... 

There are a number of other factors that contribute to the formation of ascites, the main one being hypoalbuminaemia. This is associated with chronic liver disease, resulting in reduced plasma oncotic pressure and hence the leakage of plasma into the peritoneal... 

Maintains plasma oncotic pressure transports small molecules... 

Stein HD. Dextran-40, acute renal failure, and elevated plasma oncotic pressure. N Engl J Med 1988 318(4) 253. 

One precaution when using colloids is that the plasma total solids or total protein concentration is no longer a useful guide to plasma oncotic pressure (Bumpus et al 1998). 

Altered plasma oncotic pressure increased Altered renal blood flow decreased... 

Osmotic balance across the plasma membrane is regulated by the concentration of proteins (albumin more than globulins). Relative dehydration would increase plasma oncotic pressure and capillary absorption of water and water-soluble molecules. Phenol is soluble in water, and its absorption rate could be accelerated by the slightest dehydration. 

Albumin Liver M.W. 66,000 15-19 days N 3.5-5.0g/dl Mild 2.8-3.5 g/dl Moderate 2.1-2.7 g/dl Severe <2.1 g/dl Transports many endogenous and exogenous ligands, major determinant of plasma oncotic pressure. Large body pool and long half-life makes it a poor index of acute malnutrition... 

Hypoallniiniiiaemia. The effective blood volume is reduced because the hypoalbuminaemia lowers the plasma oncotic pressure. This disrupts the normal exchange of solutes and lluid in the capillary bed resulting in unsatisfactory circulation of the blood and ECF. Hypoalbuminaemia occurs when synthesis is inadequate due to liver disease (pp.. 50-.51) or when losses exceed the liver s synthetic capacity as occurs in the nephrotic syndrome (p. 44). 

Albumin Is the main determinant of plasma oncotic pressure. 

The proteins in plasma include enzymes, transport proteins, hormones, clotting factors and antibodies. Collectively they are responsible for the plasma oncotic pressure. Electrophoretically the proteins can be classified into a number of different fractions ... 

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