Capillary oncotic pressure

Edema formation in patients with nephrotic syndrome is primarily related to renal sodium and water retention. A decrease in capillary oncotic pressure does not appear to play a major role until the serum albumin concentration falls to less than 2 g/dL. This is explained by the fact that both capfllary and interstitial oncotic pressure decrease proportionately above a serum albumin concentration of 2 g/dL, and thus the transcapUlary oncotic gradient is not significantly altered. ... 

Glomerular filtration rate (GFR) is the volume of plasma-like fluid that is filtered per unit time across the glomerular capillary membranes to enter the tubular space. Filtrate formation is driven by the net filtration pressure that is equal to the capillary hydrostatic pressure diminished by the sum of capillary oncotic... 

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... 

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... 

Mobilization of edemas (A) In edema there is swelling of tissues due to accumulation of fluid, chiefly in the extracellular (interstitial) space. When a diuretic is given, increased renal excretion of Na and H2O causes a reduction in plasma volume with hemoconcentra-tion. As a result, plasma protein concentration rises along with oncotic pressure. As the latter operates to attract water, fluid will shift from interstitium into the capillary bed. The fluid content of tissues thus falls and the edemas recede. The decrease in plasma volume and interstitial volume means a diminution of the extracellular fluid volume (EFV). Depending on the condition, use is made of thiazides, loop diuretics, aldosterone antagonists, and osmotic diuretics. 

Q4 If protein is lost from the body, for example because of kidney disease, or there is a reduction in the synthesis of plasma protein, for example in starvation, the balance of fluid loss and gain in the capillaries is altered. Reduction in plasma protein reduces the oncotic pressure and reduces the return of fluid from the tissues back to the capillaries. So fluid accumulates in the tissues and forms oedema. 

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. 

The reverse flux of fluid from the interstitial to the vascular space (14) is caused by increased interstitial fluid pressure (12) and increased plasma protein concentration (oncotic pressure), hyperosmotemia, or both depending upon the intensity (above or below 50 -peak capacity) and duration of the exercise. Increased interstitial hydrostatic pressure and increased plasma osmotic pressures retard the fluid shift from plasma to the interstitium. Equilibrium is reached when interstitial pressure balances capillary filtration pressure (24). After cessation of exercise, restitution of plasma volume takes 40-60 minutes (21,22) unless significant dehydration is present. The immediate post-exercise hyperosmotemia, the relative hyperproteinemia, and the reduction in systemic blood pressure contribute to the restoration of plasma volume. The reduction in blood pressure, which produces a fall in local hydrostatic pressure within the capillaries of the previously active muscle, is probably the single most important factor. 

However, the significance of the decreased colloidosmotic (oncotic) pressure is not as great as has been hitherto assumed. Nevertheless, when the hydrostatic pressure is raised at the same time, incongruity between these two Starling forces is created, and fluid escapes into the abdominal cavity. This process is greatly furthered by the disparity between lymph production and lymph transport. Tliese mechanical factors (s. tab. 16.3) may effect the formation of ascites, yet they cannot produce large quantities of ascitic fluid. Such a development, however, can be expected if the capillary permeability is additionally heightened due to toxic or inflammatory causes. 

Pccap = glomerular-capillary hydrostatic pressure IIbc - oncotic pressure in Bowman s capsule Pbc = hydrostatic pressure in Bowman s capsule Ifccap - oncotic pressure in the glomerular capillary... 

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. 

Pulmonary edema may result from the failure of any of a number of homeostatic mechanisms. The most common cause of pulmonary edema is an increase in capillary hydrostatic pressure because of left ventricular failure. Excessive fluid administration in compensated and decompensated heart failure patients is the most frequent cause of iatrogenic pulmonary edema. Besides hydrostatic forces, other homeostatic mechanisms that may be disrupted include the osmotic and oncotic pressures in the vasculature, the integrity of the alveolar epithelium, interstitial pulmonary pressure, and the interstitial lymph flow. The edema fluid in cardiogenic pulmonary edema contains a low amount of protein, whereas noncardiogenic pulmonary edema fluid has a high protein concentration. This indicates that noncardiogenic pulmonary edema results primarily from disruption of the alveolar epithehum. The reader is referred to Chap. 28 for a detailed discussion of this topic. 

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). 

The presence of blood protein molecules, such as albumins and globulins, are critical factors in maintaining the proper fluid balance between cells and extracellular space. Proteins are present in the capillary beds, which are one-cell-thick vessels that connect the arterial and venous beds, and they cannot flow outside the capillary beds into the tissue because of their large size. Blood fluid is pulled into the capillary beds from the tissue through the mechanics of oncotic pressure, in which the pressure exerted by the protein molecules counteracts the blood pressure. Therefore, blood proteins are essential in maintaining and regulating fluid balance between the blood and tissue. The lack of blood proteins results in clinical edema, or tissue swelling, because there is insufficient pressure to pull fluid back into the blood from the tissues. The condition of edema is serious and can lead to many medical problems. 

The effective osmotic pressure of the blood across capillary walls. The greatest contribution to the colloid osmotic pressure comes from plasma proteins, which, unlike the plasma ions, cannot move through the capillary walls. The oncotic pressure balances the effect of capillary blood pressure which tends to force water into the interstitial spaces. 

The primary functions of albumin are to help maintain the osmotic (oncotic) transmural pressure differential that ensures proper mass exchange between blood and interstitial fluid at the capillary level and to serve as a transport carrier molecule for several hormones and other small biochemical constituents (such as some metal ions). The primary function of the globulin class of proteins is to act as transport carrier molecules (mostly of the a and p class) for large biochemical substances, such as fats (lipoproteins) and certain carbohydrates (muco- and glycoproteins) and heavy metals (mineraloproteins), and to work together with leukocytes in the body s immune system. The latter function is primarily the responsibflity of the y class of immunoglobulins, which have antibody activity. The primary function of fibrinogen is to work with thrombocytes in the formation of a blood clot — a process also aided by one of the most abundant of the lesser proteins, prothrombin (MW 62,000). 

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