KYJ38 - Intrinsic Coagulation System. 4 of 7.
This is the 4th post in a series on Coagulation factors.
In the first three episodes we looked at the Tissue Factor Activation pathway- otherwise known as the Extrinsic pathway.
This edition of a KYJ looks at the initiation of the Intrinsic pathway, or more recently known as the Contact Activation.
Let's start with blood or more specifically Plasma.
Plasma is a cocktail of salts, glucose and proteins. Many of the proteins in plasma serve a role in coagulation, and to date, we have discussed Tissue factor 3, VonWillebrand Factor and the plasma Factors 7, 10, 2, and 1.
Well as you guessed, the numbers in between are all involved in the intrinsic pathway. Let's start with the contact (intrinsic) activation of the coagulation cascade.
If blood comes into contact with a negatively charged surface such as glass, foreign objects, bacteria, or Tissue factors released by damaged cells, it initiates the contact activation pathway.
It starts when a protein called "High-molecular-weight kininogen" (HMWK), (also known as the Williams-Fitzgerald-Flaujeac Factor ) that shares a role in both the coagulation system as well as the kinin-kallikrein system, is activated by a negatively charged contact.
Additionally, a factor called Hageman Factor (Factor XII) And another protein called Prekellikrein (PK) also activates , and together the three proteins activate Factor 12 into Factor XIIa.
Hageman Factor was named in 1955 after a Railway worker was found to be deficient in Factor XII. His blood simply wouldn't coagulate in a glass test tube. Deficiency of factor XII is a rare genetic disease and can be considered a form of a Haemophilia. The genetic link was discovered when some family members also were found to be deficient in this liver manufactured protein.
Are you developing an understanding as to why chronic liver failure patients develop clotting and coagulation disorders??
More on this system in our next edition.
Tuesday, 14 January 2014
37 - Coagulation Factors part 3 of 7
KYJ37- Series part 3- Coagulation.
Summarising Coagulation : the solidification of liquid blood into
A solid gel is called Coagulation. It starts with either an injury to a vessel wall , or blood coming into contact with a negatively charged surface eg Bacteria, tissue injuries.
In the first two episodes we looked at the extrinsic pathway (vessel wall injury) and simplified the steps and coagulation factors (F):
F3 activates F7
F7 activates F10
F10 activates F2 (prothrombin into Thrombin)
Easy to remember if we say this simple math equation.
3+7=10 (2 Easy). A euphemism for the steps.
The activation of F10 was described as the beginning of the what is called the "Common Pathway", so named because both the extrinsic and intrinsic coagulation paths lead to the activation of F10 (Factor X).
So let's kick of from the Thrombin (factor IIa) the activated form of a Factor II.
Thrombin is a protein enzyme which is pivotal in the clotting cascade. Thrombin (FIIa) converts a plasma protein called Fibrinogen (Factor I) into the end product of coagulation, Fibrin (Factor Ia).
Fibrin are fine strands of fibres or strands which bond together in plasma to form a mesh like net.
This mesh wraps itself around and through platelets that aggregate at the site of the injured blood vessel. They sort of weave the platelet clot into a tight stable clump called a Fibrin Clot. The net like mesh further traps blood cells and more platelets together causing solidification of the blood.
Ultimately, all coagulation pathways lead to this final process of a Fibrinogen being converted (activated) into Fibrin.
Look at any scab or clot and what you are looking at is blood cells, platelets, and solidified plasma (Fibrin).
The whole process started with the exposure of blood to Tissue a Factor (FIII) and it finished with Factor I activated.
In our next edition, we will look at Factor 12 and the initiation of the Contact Pathway (Intrinsic) ,
Summarising Coagulation : the solidification of liquid blood into
A solid gel is called Coagulation. It starts with either an injury to a vessel wall , or blood coming into contact with a negatively charged surface eg Bacteria, tissue injuries.
In the first two episodes we looked at the extrinsic pathway (vessel wall injury) and simplified the steps and coagulation factors (F):
F3 activates F7
F7 activates F10
F10 activates F2 (prothrombin into Thrombin)
Easy to remember if we say this simple math equation.
3+7=10 (2 Easy). A euphemism for the steps.
The activation of F10 was described as the beginning of the what is called the "Common Pathway", so named because both the extrinsic and intrinsic coagulation paths lead to the activation of F10 (Factor X).
So let's kick of from the Thrombin (factor IIa) the activated form of a Factor II.
Thrombin is a protein enzyme which is pivotal in the clotting cascade. Thrombin (FIIa) converts a plasma protein called Fibrinogen (Factor I) into the end product of coagulation, Fibrin (Factor Ia).
Fibrin are fine strands of fibres or strands which bond together in plasma to form a mesh like net.
This mesh wraps itself around and through platelets that aggregate at the site of the injured blood vessel. They sort of weave the platelet clot into a tight stable clump called a Fibrin Clot. The net like mesh further traps blood cells and more platelets together causing solidification of the blood.
Ultimately, all coagulation pathways lead to this final process of a Fibrinogen being converted (activated) into Fibrin.
Look at any scab or clot and what you are looking at is blood cells, platelets, and solidified plasma (Fibrin).
The whole process started with the exposure of blood to Tissue a Factor (FIII) and it finished with Factor I activated.
In our next edition, we will look at Factor 12 and the initiation of the Contact Pathway (Intrinsic) ,
36- Coagulation series part 2 of 7
KYJ Series part 2 on Coagulation Factors.
In series 1, we reviewed the initiation of the Tissue Factor (extrinsic) pathway of coagulation. It used to be called extrinsic meaning external stimuli, because the cascade is initiated when Tissue Factor (Factor III) is exposed through vessel wall injury.
This session carries on with where we left off. Factor VII .
Factor VII circulates in the blood in an inactive form. It is manufactured by the liver using Vitamin K, a fat soluble nutrient found in leafy Green vegetables.
FVII is activated by tissue factor and vonWillebrand factor released by the endothelium and damaged vessel walls. Here it becomes factor VIIa.
Now this activated FVIIa causes a conversion of the first factor of the Common Pathway. So called because this is where the Tissue factor (extrinsic) initiation of coagulation converges with the contact activation (intrinsic pathway (another post)).
This first factor of the Common pathway is :
Factor X (Stuart-Prower factor), named after two people who suffered a form of factor X deficiency in the 20s and 30s.
Like FVII, Factor X is a liver synthesised protein enzyme also manufactured from Vit K. It circulates in blood doing nothing until it comes into contact with activated FVII (FVIIa) , then it activates to form Factor Xa.
This activation now stimulates the conversion of prothrombin (Factor II) into Thrombin, it's activated form (FIIa).
Let's summarise :
Injury to vessel
FIII exposed to plasma
FVII activates
FVIIa converts FX to FXa
FXa activates FII (prothrombin)
Into Factor IIa (Thrombin).
Perhaps you wondered how Warfarin (Coumadin) works to
Inhibit coagulation.
Well this drug and others like it inhibit the Vit K initiated synthesis of factors VII, X and Prothrombin (FII).
We are almost there with this arm of the coagulation cascade and the Extrinsic pathway factors.
Stay tuned for our next edition of KnowingYourJargon .
In series 1, we reviewed the initiation of the Tissue Factor (extrinsic) pathway of coagulation. It used to be called extrinsic meaning external stimuli, because the cascade is initiated when Tissue Factor (Factor III) is exposed through vessel wall injury.
This session carries on with where we left off. Factor VII .
Factor VII circulates in the blood in an inactive form. It is manufactured by the liver using Vitamin K, a fat soluble nutrient found in leafy Green vegetables.
FVII is activated by tissue factor and vonWillebrand factor released by the endothelium and damaged vessel walls. Here it becomes factor VIIa.
Now this activated FVIIa causes a conversion of the first factor of the Common Pathway. So called because this is where the Tissue factor (extrinsic) initiation of coagulation converges with the contact activation (intrinsic pathway (another post)).
This first factor of the Common pathway is :
Factor X (Stuart-Prower factor), named after two people who suffered a form of factor X deficiency in the 20s and 30s.
Like FVII, Factor X is a liver synthesised protein enzyme also manufactured from Vit K. It circulates in blood doing nothing until it comes into contact with activated FVII (FVIIa) , then it activates to form Factor Xa.
This activation now stimulates the conversion of prothrombin (Factor II) into Thrombin, it's activated form (FIIa).
Let's summarise :
Injury to vessel
FIII exposed to plasma
FVII activates
FVIIa converts FX to FXa
FXa activates FII (prothrombin)
Into Factor IIa (Thrombin).
Perhaps you wondered how Warfarin (Coumadin) works to
Inhibit coagulation.
Well this drug and others like it inhibit the Vit K initiated synthesis of factors VII, X and Prothrombin (FII).
We are almost there with this arm of the coagulation cascade and the Extrinsic pathway factors.
Stay tuned for our next edition of KnowingYourJargon .
35- Coagulation series 1 of 7
KYJ Series Part1-Coagulation factors.
I've posted before about the differences between clotting and coagulation. In summary, clotting is the clumping of platelets and coagulation is the solidification of fluid blood into a solid jelly.
The subject of this mini- series of posts is Coagulation, and specifically the different proteins that cause it to happen.
There are 14 factors involved in the complex cascade that we know of as coagulation. Most of them have funky names that honour people in history who had a deficiency or a discovery of one or more factors, or some complicated chemical name. But all coag factors have a Roman numeral name , and it is these that I will refer to most.
Most nurses will remember the old intrinsic and extrinsic coagulation pathways, from 1st or 2nd year of their studies. This old theory has since been replaced by a similar "contact activation vs common coagulation pathways"
This series will tackle this as simply as possible.
Start off with the following basics:
A blood vessel is lined by dynamic cells (endothelium) that produce many substances that repel platelets, constrict vessels, and inhibit solidification of blood.
If damaged, the underlying collagen surface of the vessel is exposed, and attracts platelets to stick to the injured vessel wall. This exposed collagen also initiates the first steps of the coagulation cascade.
Here we start.
Damaged endothelium, allows platelets to stick because a substance in the collagen called Tissue factor (factor III) attracts platelets and his starts the cascade.
Enter another substance secreted by endothelium. Endothelium makes and stores von Willebrand factor (vWF). Von Willebrand factor is secreted from the endothelial cell both into the plasma and also under the endothelial layer into the subendothelial matrix. It is a large protein that acts like glue sticking platelets to one another and to the subendothelial matrix at an injury site.
The other major function of vWF is to act as a carrier protein for factor VIII (antihaemophilic factor). More on this factor in another post.
So vonWillebrand Factor (vWF) allows platelets to stick to their mates- this is called platelet aggregation and when this happens, the platelet undergoes activation and the result is a fragile and unstable clot.
The unstable clot is called a Primary platelet plug, because it aims to plug the hole in the vessel wall at the site of endothelial injury.
To stabilise and strengthen the clot, plasma is activated to form strands of insoluble fibrin, which wraps around the clot like a mesh, and traps more platelets, and blood cells floating past.
The activation of plasma takes place by the release of the tissue factor (factor III) and vWF now joining with a plasma protein called proconvertin (factor VII).
This chemical cocktail activates Factor VII into VIIa . The little "a" means activated.
This is the contact activation or (extrinsic) pathway under way.
In our next part we will
Look at the role of activated factor VII (FVIIa), and the solidification of plasma.
Summary:
Vessel injury exposes FIII to platelets and plasma.
Platelets respond by using vWF to stick together.
Plasma responds by activating FVII.
It does get exciting from here on in.
I've posted before about the differences between clotting and coagulation. In summary, clotting is the clumping of platelets and coagulation is the solidification of fluid blood into a solid jelly.
The subject of this mini- series of posts is Coagulation, and specifically the different proteins that cause it to happen.
There are 14 factors involved in the complex cascade that we know of as coagulation. Most of them have funky names that honour people in history who had a deficiency or a discovery of one or more factors, or some complicated chemical name. But all coag factors have a Roman numeral name , and it is these that I will refer to most.
Most nurses will remember the old intrinsic and extrinsic coagulation pathways, from 1st or 2nd year of their studies. This old theory has since been replaced by a similar "contact activation vs common coagulation pathways"
This series will tackle this as simply as possible.
Start off with the following basics:
A blood vessel is lined by dynamic cells (endothelium) that produce many substances that repel platelets, constrict vessels, and inhibit solidification of blood.
If damaged, the underlying collagen surface of the vessel is exposed, and attracts platelets to stick to the injured vessel wall. This exposed collagen also initiates the first steps of the coagulation cascade.
Here we start.
Damaged endothelium, allows platelets to stick because a substance in the collagen called Tissue factor (factor III) attracts platelets and his starts the cascade.
Enter another substance secreted by endothelium. Endothelium makes and stores von Willebrand factor (vWF). Von Willebrand factor is secreted from the endothelial cell both into the plasma and also under the endothelial layer into the subendothelial matrix. It is a large protein that acts like glue sticking platelets to one another and to the subendothelial matrix at an injury site.
The other major function of vWF is to act as a carrier protein for factor VIII (antihaemophilic factor). More on this factor in another post.
So vonWillebrand Factor (vWF) allows platelets to stick to their mates- this is called platelet aggregation and when this happens, the platelet undergoes activation and the result is a fragile and unstable clot.
The unstable clot is called a Primary platelet plug, because it aims to plug the hole in the vessel wall at the site of endothelial injury.
To stabilise and strengthen the clot, plasma is activated to form strands of insoluble fibrin, which wraps around the clot like a mesh, and traps more platelets, and blood cells floating past.
The activation of plasma takes place by the release of the tissue factor (factor III) and vWF now joining with a plasma protein called proconvertin (factor VII).
This chemical cocktail activates Factor VII into VIIa . The little "a" means activated.
This is the contact activation or (extrinsic) pathway under way.
In our next part we will
Look at the role of activated factor VII (FVIIa), and the solidification of plasma.
Summary:
Vessel injury exposes FIII to platelets and plasma.
Platelets respond by using vWF to stick together.
Plasma responds by activating FVII.
It does get exciting from here on in.
Saturday, 4 January 2014
Why shouldn't we put Oxygen on chest pain patients
WHY NO OXYGEN ON MY CHEST PAIN PATIENT???
I've received an email from a follower to cover the oxygen on a chest pain issue from a Why we don't use oxygen any more on AMI patients.
I'll start by saying... Do what your policies /protocols say, and if they are wrong, lobby to have them changed.
Second what I'm summarising here is a distillation of literature that spans papers back to 1964.
Cabello, J. et.al. (2010). Oxygen therapy for acute myocardial infarction (Review). The Cochrane Library
http://www.thecochranelibrary.com/details/file/742697/CD007160.html
Burls et al 2011
Emergency med Journal did a meta analysis.
http://www.medscape.com/viewarticle/752314
Beazley et al 2007 who looked at
Historical perspectives
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809170/
And the article that probably started the debate early in 1900, yes 113 years ago...
Steele's article in the BMJ claiming oxygen relieved Angina.
And it does. No one is disputing this. It is like saying Crack makes you High, but does it mean that it is the right thing to use??
Oxygen in the blood of a MI / chest pain patient is (more often than not) in sufficient saturations (94-99%).
Pain is caused by a narrowing, vasospasm or clot blockage to a coronary vessel feeding oxygenated blood to a chunk of heart muscle.
When cardiac blood flow reduces, the cells suffer Ischaemia (hypoxia) not due to lack of oxygen in the blood, but lack of flow to tissue (perfusion).
The thought originally was improve O2 in blood, and we prove O2 cell delivery in what little perfusion we have. But it doesn't work.
It doesn't work.!!
When you increase O2 concentration in blood it dissolves more oxygen in plasma (Pa02). It doesn't carry more on haemoglobin. And high plasma concentrations (pressures) of oxygen exert a vasoconstrictor effect on coronary arteries.
Doesn't that seem dumb to you? In Angina, or AMI, aren't we trying to improve blood flow?!!
Effect 2
Oxygen molecules when released to previously ischaemic cardiac tissue cause physical damage to the cardiac cell membranes. This Oxidative burst results in the overproduction of oxygen free radicals. Hydrogen Peroxide, superoxide dismutase, singlet oxygen, to name a few. These substances are the route cause of the cell damage that occurs when we dissolve the clot or give GTN restoring blood flow. This lipid peroxidation of the cell membranes is called Reperfusion Injury. It destabilises action potentials in the cardiac mass , which leads to reperfusion arrhythmias.
So in a nut shell organisations are scrambling to change policies to ensure clinicians only use oxygen on patients in shock or those with desaturation. If sats are <94% Use oxygen, but if not, they don't need it, and it is probably doing damage.
ILCOR and our own Australian Resuscitation Council are on it with guideline changes in 2010 as a result of Cabello's work.
The giants of the cardiac world Am Heart Assn , Australian Heart Foundation has given it the tick!
Queensland Health is on it with policy written categorically stating to only oxygenate to maintain O2 above 93%. (PCCM 2011 page 80)
For more than 45 years we have known that oxygen delivery on chest pain patients is potentially damaging. Use it judiciously.
I've received an email from a follower to cover the oxygen on a chest pain issue from a Why we don't use oxygen any more on AMI patients.
I'll start by saying... Do what your policies /protocols say, and if they are wrong, lobby to have them changed.
Second what I'm summarising here is a distillation of literature that spans papers back to 1964.
Cabello, J. et.al. (2010). Oxygen therapy for acute myocardial infarction (Review). The Cochrane Library
http://www.thecochranelibrary.com/details/file/742697/CD007160.html
Burls et al 2011
Emergency med Journal did a meta analysis.
http://www.medscape.com/viewarticle/752314
Beazley et al 2007 who looked at
Historical perspectives
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809170/
And the article that probably started the debate early in 1900, yes 113 years ago...
Steele's article in the BMJ claiming oxygen relieved Angina.
And it does. No one is disputing this. It is like saying Crack makes you High, but does it mean that it is the right thing to use??
Oxygen in the blood of a MI / chest pain patient is (more often than not) in sufficient saturations (94-99%).
Pain is caused by a narrowing, vasospasm or clot blockage to a coronary vessel feeding oxygenated blood to a chunk of heart muscle.
When cardiac blood flow reduces, the cells suffer Ischaemia (hypoxia) not due to lack of oxygen in the blood, but lack of flow to tissue (perfusion).
The thought originally was improve O2 in blood, and we prove O2 cell delivery in what little perfusion we have. But it doesn't work.
It doesn't work.!!
When you increase O2 concentration in blood it dissolves more oxygen in plasma (Pa02). It doesn't carry more on haemoglobin. And high plasma concentrations (pressures) of oxygen exert a vasoconstrictor effect on coronary arteries.
Doesn't that seem dumb to you? In Angina, or AMI, aren't we trying to improve blood flow?!!
Effect 2
Oxygen molecules when released to previously ischaemic cardiac tissue cause physical damage to the cardiac cell membranes. This Oxidative burst results in the overproduction of oxygen free radicals. Hydrogen Peroxide, superoxide dismutase, singlet oxygen, to name a few. These substances are the route cause of the cell damage that occurs when we dissolve the clot or give GTN restoring blood flow. This lipid peroxidation of the cell membranes is called Reperfusion Injury. It destabilises action potentials in the cardiac mass , which leads to reperfusion arrhythmias.
So in a nut shell organisations are scrambling to change policies to ensure clinicians only use oxygen on patients in shock or those with desaturation. If sats are <94% Use oxygen, but if not, they don't need it, and it is probably doing damage.
ILCOR and our own Australian Resuscitation Council are on it with guideline changes in 2010 as a result of Cabello's work.
The giants of the cardiac world Am Heart Assn , Australian Heart Foundation has given it the tick!
Queensland Health is on it with policy written categorically stating to only oxygenate to maintain O2 above 93%. (PCCM 2011 page 80)
For more than 45 years we have known that oxygen delivery on chest pain patients is potentially damaging. Use it judiciously.
Friday, 3 January 2014
34- Respiratory Failure 1 and 2
KYJ34 - Resp Failure 1 & 2.
Today's post is really very simple, yet complicated by jargon by the medical world.
What is your concept of Respiratory Failure?
For many nurses, the notion of RF is a simple one defined by its title. Remember "respiration" is all about the exchange of gases.
So respiratory failure is a failure to maintain normal blood gas- ultimately, normal oxygen levels.
Hence, the definition of Respiratory Failure is a patient with PaO2 < 60mmHg (normal is 80-100)
Now once RF is determined, type 2 respiratory failure includes an altered Carbon Dioxide (PaCO2) level in and a reduced pH of arterial blood.
Specifically PaCO2 > 50mmHg ( normal is 35-45)
and
Lower pH than 7.35 (acidosis).
Functionally, a type 1 RF is a fairly acute condition like pneumonia, Pulmonary Oedema, PE, asthma, or low oxygen environments like high altitude climbers.
Type 2 RF, is seen in patients with chronic lung diseases like Mesothelioma, emphysema, COPD, and lung cancers. These patients invariably started with Hypoxaemia, (the diagnostic criteria for RF) but their pathology, affects the excretion of CO2, and drop in pH in addition to the Hypoxaemia (PaO2 <60).
Recap-
RF1= low oxygen in blood
RF2= low oxygen in blood
and high CO2 (hypercapnoea)
and Low pH (acidosis)
What to do-- oxygenate.
Remember hypoxia kills, hypercapnoea happens!
Today's post is really very simple, yet complicated by jargon by the medical world.
What is your concept of Respiratory Failure?
For many nurses, the notion of RF is a simple one defined by its title. Remember "respiration" is all about the exchange of gases.
So respiratory failure is a failure to maintain normal blood gas- ultimately, normal oxygen levels.
Hence, the definition of Respiratory Failure is a patient with PaO2 < 60mmHg (normal is 80-100)
Now once RF is determined, type 2 respiratory failure includes an altered Carbon Dioxide (PaCO2) level in and a reduced pH of arterial blood.
Specifically PaCO2 > 50mmHg ( normal is 35-45)
and
Lower pH than 7.35 (acidosis).
Functionally, a type 1 RF is a fairly acute condition like pneumonia, Pulmonary Oedema, PE, asthma, or low oxygen environments like high altitude climbers.
Type 2 RF, is seen in patients with chronic lung diseases like Mesothelioma, emphysema, COPD, and lung cancers. These patients invariably started with Hypoxaemia, (the diagnostic criteria for RF) but their pathology, affects the excretion of CO2, and drop in pH in addition to the Hypoxaemia (PaO2 <60).
Recap-
RF1= low oxygen in blood
RF2= low oxygen in blood
and high CO2 (hypercapnoea)
and Low pH (acidosis)
What to do-- oxygenate.
Remember hypoxia kills, hypercapnoea happens!
Thursday, 2 January 2014
33- Blood and it's products
KYJ 33- Blood products
When they bleed, why not just give them blood?
Blood is a cocktail of substances. Water, cells, salts and proteins.
Cells carry oxygen (red cells) , fight infection (white cells) and stop bleeding by forming clots (platelets).
Because capillaries are prone to leaking certain salts and proteins hold water inside the blood vessel (albumen). These large molecules of albumen can't fit through the small holes in the capillary walls, and attract water, so by staying in the vessel this holds volume.
Another role of albumen is as a carrier of chemicals bound to the protein. Many drugs, bilirubin and hormones are transported on blood bound or plasma proteins.
Other proteins help fight infection. These are called antibodies or Immunoglobulins, and they are created by white blood cells after an exposure to a wild pathogen or vaccine .
Finally a class of proteins called coagulation factors aid in the clotting process ( collectively these proteins are called factors. There are 13 of them). Ultimately these factors are activated by damage to a vessel wall, and result in the formation of insoluble strands of solid matter called fibrin, or a fibrin clot.
Once blood is donated at a blood bank (volume 500 ml) it is spun into it's separate parts.
The factors ( factor 1, 8 and 13) can be are separated off and frozen , this is called cryoprecipitate (Cryo for short), or Anti-haemophilic factor (AHF). Additionally factor 8 (VIII) can be further isolated.
The rest of the plasma is fresh frozen and hence called FFP.
Usually the FFP is thawed and given neat, but some people have allergic reactions to some of the Coagulation Factors , especially 1, 8 and 13, (cryo) so they cleave this off and deplete the FFP to make it safer for people likely to have a transfusion reaction. Some proteins are more allergenic.
This type of FFP is called cryodepleated FFP.
They harvest the red cells for people needing a haemoglobin transfusions, eg bleeding post op, or trauma, anaemic people. This blood product is called "packed cells".
White cells are binned (they would attack the person getting a transfusion) .
Platelets are kept in a separate bag alive (they die in 8 days).
Quick overview video I posted on the Subject.
When they bleed, why not just give them blood?
Blood is a cocktail of substances. Water, cells, salts and proteins.
Cells carry oxygen (red cells) , fight infection (white cells) and stop bleeding by forming clots (platelets).
Because capillaries are prone to leaking certain salts and proteins hold water inside the blood vessel (albumen). These large molecules of albumen can't fit through the small holes in the capillary walls, and attract water, so by staying in the vessel this holds volume.
Another role of albumen is as a carrier of chemicals bound to the protein. Many drugs, bilirubin and hormones are transported on blood bound or plasma proteins.
Other proteins help fight infection. These are called antibodies or Immunoglobulins, and they are created by white blood cells after an exposure to a wild pathogen or vaccine .
Finally a class of proteins called coagulation factors aid in the clotting process ( collectively these proteins are called factors. There are 13 of them). Ultimately these factors are activated by damage to a vessel wall, and result in the formation of insoluble strands of solid matter called fibrin, or a fibrin clot.
Once blood is donated at a blood bank (volume 500 ml) it is spun into it's separate parts.
The factors ( factor 1, 8 and 13) can be are separated off and frozen , this is called cryoprecipitate (Cryo for short), or Anti-haemophilic factor (AHF). Additionally factor 8 (VIII) can be further isolated.
The rest of the plasma is fresh frozen and hence called FFP.
Usually the FFP is thawed and given neat, but some people have allergic reactions to some of the Coagulation Factors , especially 1, 8 and 13, (cryo) so they cleave this off and deplete the FFP to make it safer for people likely to have a transfusion reaction. Some proteins are more allergenic.
This type of FFP is called cryodepleated FFP.
They harvest the red cells for people needing a haemoglobin transfusions, eg bleeding post op, or trauma, anaemic people. This blood product is called "packed cells".
White cells are binned (they would attack the person getting a transfusion) .
Platelets are kept in a separate bag alive (they die in 8 days).
Subscribe to:
Posts (Atom)