Page 1 of 1: oncotic pressure???

manipalguy · Credits: 16185 My Scrapbook

albumin contrinutes maximum to oncotic pressure because it has..
1.high MW and low conc
2.low MW and low conc
3high MW and high conc
4. low MW and high conc

manipalguy · Credits: 16185 My Scrapbook

hi nobody for this one ?????

med_00 · Credits: 3666 My Scrapbook

LOW MOL WT AND HIGH CONC

manipalguy · Credits: 16185 My Scrapbook

why do u say this??

shivesh · Credits: 2066 My Scrapbook

oncotic pressure is not the property of mass but concentration ( quantity) .

total mass of albumin = ( molecular weight) * ( no of molecules)

mass is fixed ,so to be a immportant contributor of oncotic pressure it has to have low mol. wt and high concentration ( or more no. of molecules). if it has high mol. wt then no. of mol. will decrease and it wont be an immp. contributor then.

manipalguy · Credits: 16185 My Scrapbook

thanks shivesh for a beautiful explanation.......

josephdhar · Credits: 1655 My Scrapbook

Albumin is the protein of the highest concentration in plasma.

* Single polypeptide, 585 amino acids.
* MW 66,248; IgG is 150,000
* Highly soluble
* Strong negative charge -17
* Manufactured in the liver @ 9-12g/day
* No storage, no reserve
* Rate of production controlled by changes in colliod osmotic pressure and osmolality of extravascular liver space.
* Production can only increase by a factor of 2 or 3.
* Synthesis is increased by insulin / T4 or cortisol.
* Catabolism is at a rate of 9 - 12 g/day by pinoctosis in cells adjacent to the vascular endothelium.
* Albumin is not catabolised in starvation.
* Albumin is an intravascular protein with a concentration of approx 40 g/l.
* Ablumin also exists in the extavascular [interstitial] space. In fact the total extravascular albumin exceeds the total intravascular amount by 30%.
* Albumin leaves the circulation via interstitium to lymph system back to the circulation via thoracic duct.
* Circulation t1/2 is 16 -18 hours.
* 4 - 5% of total intravascular albumin extravascates per hour: this rate of movement is known as the Transcapillary Escape Rate (TER), and this is determined by:

1. Capillary and interstitial free albumin concentration.
2. Capillary permeability to albumin.
3. Movements of solvent / solute.
4. Electrical charges across the capillary wall.
5. Lymph protein content is 80% that of plasma.

Measurement of serum albumin is by using a dye binding technique using bromocresol green or purple: this tends to overestimate albumin concentration when the serum albumin is low - especially when there is increased levels of a or b globulin. Because of this overestimation, is rare to see a serum albumin < 10 - 15g/l.

Why is albumin important?

1. Binding and transport.

2. Maintenance of colloid osmotic pressure.

3. Free radical scavenging.

4. Platelet function inhibition and antithrombotic effects.

5. Effects on vascular permeability.

Binding and transport

There are actually four binding sites on albumin and these have varying specificity for different substances.

Competitive binding of drugs may occur at the same sit or at different sites (conformational changes) [eg. warfarin and diazepam].

The drugs that are important for albumin binding are: warfarin, digoxin, NSAIDS, midazolam, thiopentone.

The relevence of a low albumin and drug binding is unknown.

Osmotic pressure

Albumin is responsible for 75 - 80 % of osmotic pressure.

Starling's equation: Transcapillary Flow = k [(Pcap + p i) - (Pi + p cap )]

Remember that albumin is the main protein both in the plasma and in the interstitium and it is the COP gradient rather than the absolute plasma value that is important: this is what distinguishes hypoalbuminaemia derived from redistribution (capillary leak) from that of pure full body deficiency.

Free Radicals

Albumin is a major source of sulphydryl groups, these "thiols" scavenge free radicals (nitrogen and oxygen species).

Albumin may be an important free radical scavenger in sepsis.

Anticoagulant effects

The anticoagulant and antithrombotic effects of albumin are poorly understood this may be due to binding nitric oxide radicals inhibiting inactivation and permitting a more prolonged antiaggregatory effect.

In diabetes, glycosylated albumin may increase the incidence of thrombotic events and atherosclerosis.

Capillary Membrane Permeability

In sepsis there is an increased rate of albumin loss into the tissues - this is probably related to increased capillary membrane permeability.

What causes serum albumin to decrease?

Plasma albumin concentation = intravascular albumin mass / plasma volume

Decreased plasma albumin:

1. Decreased synthesis.

2. Increased catabolism [ very slow ]

3. Increased loss:

o Nephrotic syndrome
o Exudative loss in burns
o Haemorrhage
o Gut loss

4. Redistribution:

o Haemodilution
o Increased capillary permeability (Increased interstitial albumin)
o Decreased lymph clearance.

Consequences of decreased plasma albumin

1. Decreased ligand binding.

2. Decreased plasma colloid pressure: decreased colloid oncotic pressure, and oedema formation.

The formation of oedema is determined by:

The rate of fluid flux

The clearance of fluid by lymphatics.

* In critical illness, there is a stronger correlation between colloid oncotic pressure and Total protein than with albumin.
* In these patients the decreased albumin is compensated for by an increase in acute phase proteins.
* Unquestionably there is increased leakage of albumin and this drags fluid with it .
* Lymphoid function is important - if it is overwhelmed by increased capillary permeability or fluid flux then oedema will occur.
* It is likely that lymphoid dysfunction plays a significant role in oedema formation in critical illness. ?? do free radicals cause this lymphoid dysfunction?

Bottom line: low serum albumin does not necessarily mean low plasma oncotic pressure.
Disease processes associated with Hypoalbuminaemia
Malnutrition

Serum albumin does not appear to decrease in starvation.

The body maintains the serum albumin at the expense of muscular protein:

Decreased synthesis increased redistribution decreased catabolism.

Bottom line: decreased albumin in adults is a marker of associated disease not a feature of isolated protein-energy malnutrition.
Liver Dysfunction

Albumin is a poor marker of liver dysfunction; Prothrombin time is more reliable.
Renal disease

Albumin loss occurs in nephropathies (nephrotic syndrome).

There is a small loss of albumin in dialysis circuits.
Pre-Eclampsia

In normal pregnancy there is an increase in plasma volume. In PET there is a paradoxical decrease in plasma volume and capillary leak syndrome.

Stress response

Interleukins cause a marked decease in synthesis of plasma proteins other than albumin.

In fact Albumin and Transferrins decrease in the stress response, a process often termed "negative acute phase proteins".

IL6 directly decreases the expression of albumin messenger RNA.

Overall, the picture in the stress response is:

1. Initial decrease in albumin associated with increase in acute phase proteins.

2. Subsequent global increase in hepatic protein synthesis; including albumin.

Burns

There is massive protein loss from the burn site & increased vascular permeability & decreased albumin synthesis & protein losing nephropathy.

Trauma

Increased redistribution and transcapillary escape of albumin.

Surgery

Decreased serum albumin preoperatively is an independent indicator of poor outcome.

Sepsis

SIRS - associated with increased capillary permeability, due to the effects, amongst others, of bacterial endotoxin and cytotoxic T cells.

In sepsis there is a profound reduction in plasma albumin associated with marked fluid shifts.

Albumin as a prognostic index

Low albumin is associated with dozens of diseases.

Controversy regarding whether or not albumin is a good indicator of prognosis in critical illness. One recent study suggests:

"In patients with acute and chronic illness serum albumin concentration is inversely related to risk of death. A systematic review of cohort studies meeting specified criteria estimated that for each 2.5 g/l decrement in serum albumin concentration the risk of death increases by between 24% and 56%."

Journal of Clinical Epidemiology 1997; 50; [snip]-703.

Following serum albumin levels may be of value - intial decrease associated with deterioration, later gradual increase signifies recovery in process.

Correcting Hypoalbuminaemia

Low serum albumin concentrations are the consequence of a disease process and successful treatmen of the underlying disease should result in a gradual return to normal serum albumin concentrations.

Studies have not shown that the theraputic "normalisation" of albumin levels in critically ill patients is beneficial. Indeed the Cochrane group's recent "meta" analysis suggests a higher mortality rate in critically ill patients treated with albumin.

Previous strategies have involved administering albumin to decrease the loss of intravascular volume by enhancement of collloid oncotic effect. However, in sepsis, 2/3 of administered albumin has been shown to extravascate within 4 hours of administration.

Debunked Myths (by randomised controlled trials):

* The use of 20% albumin and frusemide to reduce oedema in SIRS.
* The administration of albumin following paracentesis for ascites.
* The use of replacement albumin in nephrotic syndrome.

It is very questionable whether or not albumin should remain the colloid of first choice in paediatric practice.

Commercially available albumin is fractionated in ethanol and purified and heat treated for 10 hours at 60 degrees celcius.

This process:

Probably alters the charge on albumin - making it more permeable.

Contains significant quantities of residual ions - aluminium and vanadium.

aungnyein · Credits: 561 My Scrapbook

Plasma half-life of albumin is 21 days.

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