Oncotic pressure

Gum-Saline. Gum is a galactoso—gluconic acid having molecular weight of approximately 1500. First used (16) in kidney perfusion experiments, gum—saline enjoyed great popularity as a plasma expander starting from the end of World War I. The aggregation state of gum depends on concentration, pH, salts, and temperature, and its coUoid oncotic pressure and viscosity are quite variable. Conditions were identified (17) under which the viscosity would be the same as that of whole blood. 

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... 

In arterioles, the hydrostatic pressure is about 37 mm Hg, with an interstitial (tissue) pressure of 1 mm Hg opposing it. The osmotic pressure (oncotic pressure) exerted by the plasma proteins is approximately 25 mm Hg. Thus, a net outward force of about 11 mm Hg drives fluid out into the interstitial spaces. In venules, the hydrostatic pressure is about 17 mm Hg, with the oncotic and interstitial pressures as described above thus, a net force of about 9 mm Hg attracts water back into the circulation. The above pressures are often referred to as the Starling forces. If the concentration of plasma proteins is markedly diminished (eg, due to severe protein malnutrition), fluid is not attracted back into the intravascular compartment and accumulates in the extravascular tissue spaces, a condition known as edema. Edema has many causes protein deficiency is one of them. 

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... 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

A value of greater than or equal to 1.1 g/dL (greater than or equal to 11 g/L) identifies portal hypertension as the cause of the ascites with 97% accuracy.22,30 In portal hypertension the ascitic fluid is low in albumin this balances the oncotic pressure gradient with the hydrostatic pressure gradient of... 

Colloids Resuscitation fluids that restore and/or increase the intravascular oncotic pressure. 

The primary disadvantage is the large volume necessary to replace or augment intravascular volume. Approximately 4 L of normal saline must be infused to replace 1 L of blood loss. In addition, dilution of colloid oncotic pressure leading to pulmonary edema is more likely to follow crystalloid than colloid resuscitation. 

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... 

Haemoglobin, described in Section 5.3.1.3, is the most well known but it is just one of a number of carrier proteins present in blood. Albumin is quantitatively the most abundant protein in plasma. It is synthesized in the liver and circulates with a half life of about 3 weeks before being degraded or eliminated. Albumin has two very important functions to fulfil. First, it makes a significant contribution to the oncotic pressure of the blood and so influences the distribution of fluid between the intracellular and... 

Albumin has a molecular mass of approximately 66 000 and is synthesized at a rate of about 12 g, equal to 3% of total body albumin, per day to replace that which is degraded or lost. Impaired albumin synthesis and therefore a low plasma albumin concentration, is a hallmark of chronic liver disease. Several functions can be ascribed to albumin including osmotic (oncotic) pressure regulation of the plasma and a non-specific transport protein for ligands such as calcium, fatty acids, drugs and bilirubin. 

Considering that LEH is still in a developmental phase, it is imperative that each batch of LEH is fully characterized for physicochemical and biological properties. Typically, lipid content, particle diameter, oxygen affinity, hemoglobin, methemoglobin, carbonyl-hemoglobin, oncotic pressure, viscosity, endotoxin, and osmolality are determined by conventional methods. Several issues that need specific attention in the case of LEH are as follows ... 

Weil MH, Henning RJ, Puri VK. Colloid oncotic pressure clinical significance. Crit Care Med 1979 7 113. 

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. 

Plasma substitutes/expanders are high molecular weight substances when infused intravenously into blood stream retain fluid in the vascular compartment and exert oncotic pressure. But before infusing into the blood stream, the following requirement may be present. 

Should have same oncotic pressure with plasma. 

It is a polypeptide and exerts oncotic pressure similar to albumin. It remains in circulation for 12 hours and is slowly excreted by the kidney. It does not interfere with blood grouping and cross matching. 

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. 

The author proposed that raised arterial pressure, which is an adverse effect of high dose glucocorticoid treatment, and low oncotic pressure due to a low protein plasma concentration in a patient with nephrotic syndrome, could have increased trans-synovial fluid flow at a lower arterial pressure than normal. 

The most 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, or abnormalities in the blood oncotic pressure. Salt and water retention with edema formation often occurs when diminished blood delivery to the kidney is sensed as insufficient "effective" arterial blood volume. Judicious use of diuretics can mobilize interstitial edema fluid without significant reductions in plasma volume. However, excessive diuretic therapy in this setting 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 condition. 

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... 

The liver does not synthesise enough albumin and does not metabolise aldosterone. A lack of albumin in the vascular space reduces colloid oncotic pressure and water flows out of the blood vessels to form tissue oedema or ascites (oedema in the peritoneal cavity). Water oozing from the pulmonary arteries causes pulmonary oedema. 

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