KYJ 45 - Blood Gas series -part 2.
In part one of this series on understanding Blood gases, we reviewed the principle of partial pressure (Dalton's Law).
We also touched on Henry's law that (in part) helps us understand gas dissolving into plasma.
This episode we look at oxygen and CO2 in blood.
Abbreviations
pp= partial pressure
A = Alveoli
a = Arterial
v = Venous (upper case V= ventilation)
p = pressure
O2 = oxygen
CO2 = carbon dioxide
mmHg = millimeters of Mercury
Diffusion = gas particles moving from one area to another eg lungs to blood or blood to cells.
Normal values
The partial pressure (pp) of oxygen in blood varies between arterial and venous blood. When freshly oxygenated in the lungs, arterial blood has a normal value of 80-100 mmHg. In depleted venous blood, the oxygen pressure (tension) is approximately 35-45 mmHg.
Clearly you see that the arterial oxygen tension is more than twice that of venous blood.
The opposite effect happens with Carbon dioxide. Normal tension in arterial blood is 35-45 mmHg, but in venous blood rises to 42-52mmHg. Slightly higher but not as dramatic as the difference in venous vs arterial Oxygen.
For the purpose of this series we will focus on Arterial blood as measured during Arterial Blood Gases.
First Oxygen:
When oxygen is inhaled, it is drawn in with a partial pressure of 159 mmHg (room air 21% of 760 mmHg)
After humidification and mixing with gases inside the lung's alveoli, the partial pressure (pp) has reduced to about 105-110 mmHg. This pressure is abbreviated as pAO2 (uppercase "A" = Alveolar) .
Oxygen diffuses into the blood stream where it dissolves first into plasma exerting pressure in the blood. Any given volume of blood only comes into close contact with alveoli for 0.7 of a second, so time to fully equilibrate gas pressure in both blood and lung is not possible.
Given that blood entering the lung capillaries has a pp oxygen in venous blood of ~40mmHg, the difference in pressure between blood and lung is steep (40 in venous blood vs 105 in alveoli).
Gas diffuses from high pressure to low pressure, so oxygen will migrate from lungs to blood in attempt to balance the pressure.
After a split second, the oxygen pressure in blood has risen from 40 ish to 90 ish, and makes its way back to the left heart to be pumped out to all those starving cells in the body.
At the exodus from the lungs arterial blood has a predictable oxygen tension (paO2) of 80-100mmHg.
Less than 80 is deemed Hypoxaemia. Less than 60 is called Respiratory Failure.
The difference between oxygen pp in alveoli and arterial blood is called the Aa Gradient, and it should be about 7-12 mmHg difference. It slightly increases with age, but a high Aa gradient is an indicator of lung deterioration.
CO2.
CO2 is the waste gas produced by cell metabolism and must be excreted. Most efficiently, carbon dioxide is exhaled. Transported by venous blood, to the lungs, and blown off by breathing. Some is also excreted by kidneys converted into bicarbonate, but let's not get ahead of ourselves.
Diffusion of CO2 from blood into alveoli happens simultaneously with oxygen diffusion.
With almost no measurable CO2 in the air you breathe (shhh don't tell the Greenies) and high CO2 pressure in blood returning to the lungs (42-52), it isn't any surprise that CO2 will diffuse out of the blood and into the lungs to be breathed off. Arterial blood therefore has slightly less CO2 at 35-45mmHg. If CO2 accumulates in our blood, it causes the blood to become acidic (Acidosis). Breathing therefore allows us to maintain a beautiful balance.
We will leave this session here, and tomorrow look at acidosis in greater detail.
Memorise your paO2 80-100
And paCO2 35-45 normal values.
Thursday, 16 January 2014
44 - Understanding Arterial Blood Gases part 1
KYJ 44 understanding Blood gases. Part 1.
In this series of "knowing your jargon (KYJ)", we explore the blood gases, and explain some of the terminology used in interpretation.
We start with some fundamental science and a physics principle called Dalton's Law.
Dalton said that the pressure exerted by a mixture of gases is equal to the sum of all gases in the mix. Air exerts pressure (air pressure).
Air is a mixture of gases, mostly nitrogen (78%) oxygen (21%), and a minute quantity of CO2, argon, xenon, water vapour, and traces of other environmental contaminants make up the last 1%.
All these gases exert their cumulative pressure in the mix that we call Air, but individually these gases all exert their own pressure. This is called Partial Pressure, abbreviated to "pp".
Now air pressure as a whole, or atmospheric pressure is relatively constant at sea level but reduces with altitude. At sea level our atmospheric pressure is 760 mmHg (101.3 KPa).
But if you were at Everest base camp at 5000metres, the air is so thin that atmospheric pressure is about half that at sea level (380 mmHg), and only a third at the summit some 8.3km high.
Now back to Dalton's law. The pressure of a mixed gas is the sum of its parts.
So air pressure (760), is the sum of the pressure of nitrogen, oxygen, argon , CO2 etc.
When we know the percentage of a gas in air, we can calculate its partial pressure. Oxygen makes up 21% ( actually 20.9% but let's not split hairs), of air
If Air is 760mmHg and Oxygen is 21% (or 0.21 of air), then
760 x 0.21 = 159.6
Oxygen at sea level then has a partial pressure of 159.6mmHg.
Expressed as ppO2 = 159.6.
...
Take a sip of your coffee/wine
And do these quick calculations.
...
1. What would the partial pressure of nitrogen (78% of air) be at sea level?
2. What would the partial pressure of Oxygen be at Everest Base Camp?
...
Ok. Answers at the end of this blog session.
Read on:
Now another physics principle is that many gases are soluble in liquids. An excellent example is oxygen and carbon dioxide(CO2).
Ponder the bubbles in your bottle of champagne / soft drink or beer. These are CO2 bubbles coming out of solution and returning to gas. Under pressure the CO2 formed during fermentation (grog) or manufacture (soft drink), dissolves into the liquid. When you pop the top off these beverages, pressure is released and the dissolved gas reforms into bubbles and fizzes or "off gases".
Blood or more correctly, plasma is the same. It dissolves oxygen and CO2 into solution. Of course these gases don't travel in the blood in bubbles do they- they'd get stuck. That is what happens to divers with the bends. But that is another post.
In our next edition we will explore more about oxygen and CO2 gas dissolved in blood.
Answer 1= ppN2 is 600.4 mmHg
Answer 2= ppO2 base camp is only about 80mmHg
In this series of "knowing your jargon (KYJ)", we explore the blood gases, and explain some of the terminology used in interpretation.
We start with some fundamental science and a physics principle called Dalton's Law.
Dalton said that the pressure exerted by a mixture of gases is equal to the sum of all gases in the mix. Air exerts pressure (air pressure).
Air is a mixture of gases, mostly nitrogen (78%) oxygen (21%), and a minute quantity of CO2, argon, xenon, water vapour, and traces of other environmental contaminants make up the last 1%.
All these gases exert their cumulative pressure in the mix that we call Air, but individually these gases all exert their own pressure. This is called Partial Pressure, abbreviated to "pp".
Now air pressure as a whole, or atmospheric pressure is relatively constant at sea level but reduces with altitude. At sea level our atmospheric pressure is 760 mmHg (101.3 KPa).
But if you were at Everest base camp at 5000metres, the air is so thin that atmospheric pressure is about half that at sea level (380 mmHg), and only a third at the summit some 8.3km high.
Now back to Dalton's law. The pressure of a mixed gas is the sum of its parts.
So air pressure (760), is the sum of the pressure of nitrogen, oxygen, argon , CO2 etc.
When we know the percentage of a gas in air, we can calculate its partial pressure. Oxygen makes up 21% ( actually 20.9% but let's not split hairs), of air
If Air is 760mmHg and Oxygen is 21% (or 0.21 of air), then
760 x 0.21 = 159.6
Oxygen at sea level then has a partial pressure of 159.6mmHg.
Expressed as ppO2 = 159.6.
...
Take a sip of your coffee/wine
And do these quick calculations.
...
1. What would the partial pressure of nitrogen (78% of air) be at sea level?
2. What would the partial pressure of Oxygen be at Everest Base Camp?
...
Ok. Answers at the end of this blog session.
Read on:
Now another physics principle is that many gases are soluble in liquids. An excellent example is oxygen and carbon dioxide(CO2).
Ponder the bubbles in your bottle of champagne / soft drink or beer. These are CO2 bubbles coming out of solution and returning to gas. Under pressure the CO2 formed during fermentation (grog) or manufacture (soft drink), dissolves into the liquid. When you pop the top off these beverages, pressure is released and the dissolved gas reforms into bubbles and fizzes or "off gases".
Blood or more correctly, plasma is the same. It dissolves oxygen and CO2 into solution. Of course these gases don't travel in the blood in bubbles do they- they'd get stuck. That is what happens to divers with the bends. But that is another post.
In our next edition we will explore more about oxygen and CO2 gas dissolved in blood.
Answer 1= ppN2 is 600.4 mmHg
Answer 2= ppO2 base camp is only about 80mmHg
Tuesday, 14 January 2014
43- Troponin and the Sarcomeres
KYJ-43 Troponin.
Let's zoom down deep
Into a muscle cell.
The muscle cell of Striated muscle (striped muscle) has molecular structures called Sarcomeres.
These are strands of proteins wrapped around each other that physically shorten in length when electrically stimulated. The two primary filaments are called Actin (thin filaments) and Myocin (thick filaments).
These Sarcomeres may number in the thousands inside each muscle cell.
Binding these Sarcomeres together is a protein glue called Troponin. Think of it as cheese melted on a pizza gooing all the other stuff together.
There are three types of troponin. They are called T, C and I. All striped muscle including cardiac muscle and skeletal muscle has Troponin C. But types of Troponin I and T are specific to cardiac muscle cells.
If a heart muscle cell is injured or damaged, this troponin leaks out of the damaged cell, and stains the interstitial fluid surrounding the cell. It leaches into the lymphatic system which drains eventually into the blood stream.
If detected in the blood (on blood tests) it is a direct indicator that cardiac muscle injury/ damage has occurred.
Normal blood troponin is functionally zero- ie, troponin is an intramuscular substance, not an intravascular substance. That said, a tolerance of less than 0.04 mcg/L is considered ok.
If Troponin I&T are elevated >0.04 then this is highly suggestive of cardiac damage, and one of three diagnostic criteria for myocardial infarction. The other two criteria being ST elevation on ECG, and or a pain history that sounds cardiac typical.
Troponin can take 4-6 hours to reach the blood, and up to 12 hours to peak during a cardiac episode. Once elevated, can be present in blood for 5-14 days.
The I-Stat point of care blood test is a common method to test for troponin at the bedside, and in around 10 mins can support a diagnosis of MI.
For those with an unclear ECG based diagnosis, the patient can be admitted onto a ward for serial enzymes at 6 and 12 hours or 4 and 9 hours post onset of pain.
Because of troponin's ability to linger in the blood, it is a handy test for those patients that state they had chest pain yesterday or last week.
It is, to date, our most sensitive blood test for MI diagnosis.
Let's zoom down deep
Into a muscle cell.
The muscle cell of Striated muscle (striped muscle) has molecular structures called Sarcomeres.
These are strands of proteins wrapped around each other that physically shorten in length when electrically stimulated. The two primary filaments are called Actin (thin filaments) and Myocin (thick filaments).
These Sarcomeres may number in the thousands inside each muscle cell.
Binding these Sarcomeres together is a protein glue called Troponin. Think of it as cheese melted on a pizza gooing all the other stuff together.
There are three types of troponin. They are called T, C and I. All striped muscle including cardiac muscle and skeletal muscle has Troponin C. But types of Troponin I and T are specific to cardiac muscle cells.
If a heart muscle cell is injured or damaged, this troponin leaks out of the damaged cell, and stains the interstitial fluid surrounding the cell. It leaches into the lymphatic system which drains eventually into the blood stream.
If detected in the blood (on blood tests) it is a direct indicator that cardiac muscle injury/ damage has occurred.
Normal blood troponin is functionally zero- ie, troponin is an intramuscular substance, not an intravascular substance. That said, a tolerance of less than 0.04 mcg/L is considered ok.
If Troponin I&T are elevated >0.04 then this is highly suggestive of cardiac damage, and one of three diagnostic criteria for myocardial infarction. The other two criteria being ST elevation on ECG, and or a pain history that sounds cardiac typical.
Troponin can take 4-6 hours to reach the blood, and up to 12 hours to peak during a cardiac episode. Once elevated, can be present in blood for 5-14 days.
The I-Stat point of care blood test is a common method to test for troponin at the bedside, and in around 10 mins can support a diagnosis of MI.
For those with an unclear ECG based diagnosis, the patient can be admitted onto a ward for serial enzymes at 6 and 12 hours or 4 and 9 hours post onset of pain.
Because of troponin's ability to linger in the blood, it is a handy test for those patients that state they had chest pain yesterday or last week.
It is, to date, our most sensitive blood test for MI diagnosis.
42- the Reticuloendothelial System
KYJ42- Reticuloendothelial system.
If you are one of those nurses who learned stuff once upon a time for exams, then forgot most of it, then we are probably kindred spirits.
The numbers of times I have learned, forgotten and relearned stuff is astounding, so you are not alone.
I once learned, forgot and relearned about the Reticuloendothelial System (RES) and thought I would do a simple KYJ on it.
Let's start by saying it is no longer called the Reticuloendothelial system any more. The new name is the Mononuclear Phagocyte System (MPS).
The new name is helpful, because it offers an inkling into its function.
The MPS is part of our greater immune system. It is responsible for removing dead and dying cells and debris resulting from an immune response and programmed cell deaths (apoptosis). For an example. A few posts ago we spoke about bilirubin and it's precursor being the natural death of Red Blood Cells. The MPS has s role in the mopping up of this cell debris.
Reflecting on our greater immune system we can use the analogy of a cake.
The cake is made up of many ingredients. So too is our immune system.
Consisting of proteins in plasma (antibodies and complement proteins), and white blood cells (macrophages, monocytes, basophils, mast cells, lymphocytes, eosinophils, phagocytes, neutrophils)
These ingredients all bring a different function to the fight against disease, cell death, pathogens, and allergens.
That part of our immune system that physically digests the foreign and dead cells. Is what we formerly called the Reticuloendothelial system.
Specifically monocytes.
These cells are types of white blood cell (leukocyte). Their role is uniquely different to lymphocytes and granulocytes. Where lymphocytes manufacture chemicals to kill nasties, but monocytes actually engulf and digest particles like "The Pacman". Monocytes, are the largest of all the white blood cells and it is perhaps surprising to note that more than half of all the monocytes live in the spleen. Monocytes have an innate ability to migrate out of the blood stream and into tissues. They do this in response to chemical signals released by damaged or infected tissues. When they migrate to the site of infection they change form and become macrophages- a type of phagocyte (phago= to eat, cyte=cell).
Macrophages are the largest of the phagocytes, and are thus named- macro=big, phage=eater.
If you are one of those nurses who learned stuff once upon a time for exams, then forgot most of it, then we are probably kindred spirits.
The numbers of times I have learned, forgotten and relearned stuff is astounding, so you are not alone.
I once learned, forgot and relearned about the Reticuloendothelial System (RES) and thought I would do a simple KYJ on it.
Let's start by saying it is no longer called the Reticuloendothelial system any more. The new name is the Mononuclear Phagocyte System (MPS).
The new name is helpful, because it offers an inkling into its function.
The MPS is part of our greater immune system. It is responsible for removing dead and dying cells and debris resulting from an immune response and programmed cell deaths (apoptosis). For an example. A few posts ago we spoke about bilirubin and it's precursor being the natural death of Red Blood Cells. The MPS has s role in the mopping up of this cell debris.
Reflecting on our greater immune system we can use the analogy of a cake.
The cake is made up of many ingredients. So too is our immune system.
Consisting of proteins in plasma (antibodies and complement proteins), and white blood cells (macrophages, monocytes, basophils, mast cells, lymphocytes, eosinophils, phagocytes, neutrophils)
These ingredients all bring a different function to the fight against disease, cell death, pathogens, and allergens.
That part of our immune system that physically digests the foreign and dead cells. Is what we formerly called the Reticuloendothelial system.
Specifically monocytes.
These cells are types of white blood cell (leukocyte). Their role is uniquely different to lymphocytes and granulocytes. Where lymphocytes manufacture chemicals to kill nasties, but monocytes actually engulf and digest particles like "The Pacman". Monocytes, are the largest of all the white blood cells and it is perhaps surprising to note that more than half of all the monocytes live in the spleen. Monocytes have an innate ability to migrate out of the blood stream and into tissues. They do this in response to chemical signals released by damaged or infected tissues. When they migrate to the site of infection they change form and become macrophages- a type of phagocyte (phago= to eat, cyte=cell).
Macrophages are the largest of the phagocytes, and are thus named- macro=big, phage=eater.
41- Coagulation part 7 of 7
KYJ 41- Coagulation series part 7.
Rob's Pizza analogy
Factors 8, 5 and 13.
As we draw to the end of our marathon series on coagulation, we must address the coagulation factors that have been missing from previous discussion.
In earlier sessions we discussed that:
9 activates to 9a under the influence of 11a.
9a then binds with 10 using calcium. Where calcium is the glue, Factor 8 is the protein that allows 10 to activate.
The same relationship occurs between factor 10a and 2. Using calcium, prothrombin (F2) is activated to become Thrombin, but there must be Factor 5 present for this reaction to occur.
Thrombin (2a) is like a Food processor . It chops fibrinogen in the plasma (factor 1) in to tiny strands called Fibrin. These fibrin strands use Factor 13 to weave and inter tangle with the platelet plug, and stabilise the thrombus.
Think of a block of cheese (fibrinogen) being placed into a food processor (Thrombin), turned on (Calcium and Factor 5) and it comes out grated (Fibrin).
Now, sprinkled on the pizza (platelets plug) the cheese is all loose.
It is grilled in the pizza oven (Factor 13). And the cheese melts into and forms a topping on the pizza (Stabilised Thrombus).
So where did the Cheese come from?? Well it was once Milk (factor 9a) using rennet (factor 8) separated in to curds (10) and with calcium gummed together to set into cheese (10a).
Without milk or rennet you can't have cheese. Without cheese you can't make pizza.
Rob's Pizza analogy
Factors 8, 5 and 13.
As we draw to the end of our marathon series on coagulation, we must address the coagulation factors that have been missing from previous discussion.
In earlier sessions we discussed that:
9 activates to 9a under the influence of 11a.
9a then binds with 10 using calcium. Where calcium is the glue, Factor 8 is the protein that allows 10 to activate.
The same relationship occurs between factor 10a and 2. Using calcium, prothrombin (F2) is activated to become Thrombin, but there must be Factor 5 present for this reaction to occur.
Thrombin (2a) is like a Food processor . It chops fibrinogen in the plasma (factor 1) in to tiny strands called Fibrin. These fibrin strands use Factor 13 to weave and inter tangle with the platelet plug, and stabilise the thrombus.
Think of a block of cheese (fibrinogen) being placed into a food processor (Thrombin), turned on (Calcium and Factor 5) and it comes out grated (Fibrin).
Now, sprinkled on the pizza (platelets plug) the cheese is all loose.
It is grilled in the pizza oven (Factor 13). And the cheese melts into and forms a topping on the pizza (Stabilised Thrombus).
So where did the Cheese come from?? Well it was once Milk (factor 9a) using rennet (factor 8) separated in to curds (10) and with calcium gummed together to set into cheese (10a).
Without milk or rennet you can't have cheese. Without cheese you can't make pizza.
40 - Coagulation part 6 of 7
KYJ40-Series on Coagulation part 6- the role of calcium.
As a young ICU nurse in a big tertiary hospital more than 20 years ago, we had these blokes (4) who were burned in a caravan fire, all came into our unit. It was one of the most interesting (physiology) experiences of my life. The daily grind of bathing these guys, drug paralysed, sedated and fully ventilated became monotonous and the relentless surgeries, skin harvests and grafts made one wing of our ICU look nothing short of a macabre scene from some horror movie.
Daily these blokes seemed to return from theatre, and the dressing of choice was a product called Kaltostat. A calcium rich mesh that filled with blood oozing from graft sites, and became a clot.
Two points will be addressed in today's post. The first is the difference between a clot and a thrombus, the second is the role of calcium in this dressing and in the coagulation system in general.
First the Jargon. Clot vs Thrombus.
When platelets stick to the damaged inside wall of a vessel. This is called Platelet Adhesion.
When platelets stick to each other like a snow flakes in a snow ball, this is called Platelet Aggregation.
When platelets release substances to signal new tissue to grow eg- (Platelet Derived Growth Factor (PDGF)), or to signal other platelets to come (Thromboxane A2, ADP), or to initiate the coagulation cascade (PGI and calcium, factor V and VIII). This is all collectively called Platelet activation.
All these processes (adhesion, aggregation and activation) occur in the intravascular space. Ultimately this leads to a plug of solid matter at the site of vessel injury. This is called a thrombus.
When a thrombus breaks away from its attachment on a vessel wall and travels in the blood stream, it is called an embolus or embolism.
A clot is a thrombus, but outside the blood vessel.
A scab is a dehydrated or dried clot- usually over an external wound. The active mushy slough at the base of the scab and the wound bed is often active platelets, releasing PDGF stimulating the growth of new granulation tissue .
Now let's focus on Calcium.
Fundamentally a positively charged ion (cation) abbreviated to Ca++ .
Calcium is present in plasma, and interstitial fluid, but also specialised granules inside platelets called Delta granules. When a platelet is activated it releases the contents of its Delta granules which among other chemicals, includes Calcium onto its surface and into the surrounding plasma.
Factoid: sleeping (dormant) plasma coagulation factors like 7,9,10 and prothrombin(F2), are all negatively charged proteins. They therefore readily accept a positive charged particle to bind with. Calcium does this.
It is like the glue that makes factor 7 activate Factor 10.
It is the glue that activates 9 to 9a, and the glue that activates 10 to 10a, and the glue which converts (2) prothrombin into (2a) thrombin.
In a simplified way, think of calcium a positively electrically charged particle that "electrically" flicks a switch to start these protein chemical reactions.
Now back to my burns patient covered in calcium rich impregnated gauze mesh; do you appreciate Kaltostat and products like it a little more?
As a young ICU nurse in a big tertiary hospital more than 20 years ago, we had these blokes (4) who were burned in a caravan fire, all came into our unit. It was one of the most interesting (physiology) experiences of my life. The daily grind of bathing these guys, drug paralysed, sedated and fully ventilated became monotonous and the relentless surgeries, skin harvests and grafts made one wing of our ICU look nothing short of a macabre scene from some horror movie.
Daily these blokes seemed to return from theatre, and the dressing of choice was a product called Kaltostat. A calcium rich mesh that filled with blood oozing from graft sites, and became a clot.
Two points will be addressed in today's post. The first is the difference between a clot and a thrombus, the second is the role of calcium in this dressing and in the coagulation system in general.
First the Jargon. Clot vs Thrombus.
When platelets stick to the damaged inside wall of a vessel. This is called Platelet Adhesion.
When platelets stick to each other like a snow flakes in a snow ball, this is called Platelet Aggregation.
When platelets release substances to signal new tissue to grow eg- (Platelet Derived Growth Factor (PDGF)), or to signal other platelets to come (Thromboxane A2, ADP), or to initiate the coagulation cascade (PGI and calcium, factor V and VIII). This is all collectively called Platelet activation.
All these processes (adhesion, aggregation and activation) occur in the intravascular space. Ultimately this leads to a plug of solid matter at the site of vessel injury. This is called a thrombus.
When a thrombus breaks away from its attachment on a vessel wall and travels in the blood stream, it is called an embolus or embolism.
A clot is a thrombus, but outside the blood vessel.
A scab is a dehydrated or dried clot- usually over an external wound. The active mushy slough at the base of the scab and the wound bed is often active platelets, releasing PDGF stimulating the growth of new granulation tissue .
Now let's focus on Calcium.
Fundamentally a positively charged ion (cation) abbreviated to Ca++ .
Calcium is present in plasma, and interstitial fluid, but also specialised granules inside platelets called Delta granules. When a platelet is activated it releases the contents of its Delta granules which among other chemicals, includes Calcium onto its surface and into the surrounding plasma.
Factoid: sleeping (dormant) plasma coagulation factors like 7,9,10 and prothrombin(F2), are all negatively charged proteins. They therefore readily accept a positive charged particle to bind with. Calcium does this.
It is like the glue that makes factor 7 activate Factor 10.
It is the glue that activates 9 to 9a, and the glue that activates 10 to 10a, and the glue which converts (2) prothrombin into (2a) thrombin.
In a simplified way, think of calcium a positively electrically charged particle that "electrically" flicks a switch to start these protein chemical reactions.
Now back to my burns patient covered in calcium rich impregnated gauze mesh; do you appreciate Kaltostat and products like it a little more?
39 - coagulation series 5 of 7
KYJ39- Intrinsic Coagulation part 5.
I was over viewing the coagulation cascade that we have covered in our first 4 episodes, and also the process yet to cover, when it dawned on me that coagulation is much like the startup sequence of an aircraft. Flick that switch, twist that knob, push this button, then shift that lever. It happens with all the precision of a skilled pilot.
The intrinsic (contact activation) pathway started with Factor 12 (FXII or Hageman Factor) becoming activated by a blood contaminant, bacteria or tissue injury.
The process in now underway. Activated Hageman factor (FXIIa) catalyses the activation of factor XI (Plasma Thromboplastin). There is not much to
Be said for FXI, except that it is another liver produced protein which circulates in plasma as a dormant sleeper, and woken up by activation of Hageman Factor.
Once activated Thromboplastin, switches on factor 9 (Factor IX) also called Christmas Factor. We discussed this briefly in an earlier post (KYJ 28) if you missed it click to http://KnowingYourJargon.blogspot.com
Now Factor 9 is activated which activates Factor 10.
12 - 12a - 11 - 11a - 9 - 9a - 10 - 10a.
Do you get a sense that one inactive protein is activated, which switches on or activates the next in a "dominoes" effect like cascade. It is literally a chain reaction.
Now we have covered all the coagulation factors that are called Serine proteases. This means that they act as enzymes (*ases) that activate other chemical reactions.
This post brings the Intrinsic and extrinsic pathway to a common point- Factor X.
The X Factor is therefore the start of what is called the Common Pathway.
Let's summarise:
Injured vessel releases tissue factor (F3)
F3 converts F7 to activate F10.
Or
Tissue injury allows F12 to activate, converting F11, converting F9 activating F10.
Now the pathway to clotting is the same.
Factor 10 activates F2 (prothrombin to Thrombin),
which activates Factor 1 (fibrinogen into Fibrin clots)
...
The coagulation factors that have not been covered yet include Factors 5, 8, 13, and the proteins S, C, Z and of course Calcium (Factor 4).
Stay tuned and we will fill in the gaps in the next episode.
I was over viewing the coagulation cascade that we have covered in our first 4 episodes, and also the process yet to cover, when it dawned on me that coagulation is much like the startup sequence of an aircraft. Flick that switch, twist that knob, push this button, then shift that lever. It happens with all the precision of a skilled pilot.
The intrinsic (contact activation) pathway started with Factor 12 (FXII or Hageman Factor) becoming activated by a blood contaminant, bacteria or tissue injury.
The process in now underway. Activated Hageman factor (FXIIa) catalyses the activation of factor XI (Plasma Thromboplastin). There is not much to
Be said for FXI, except that it is another liver produced protein which circulates in plasma as a dormant sleeper, and woken up by activation of Hageman Factor.
Once activated Thromboplastin, switches on factor 9 (Factor IX) also called Christmas Factor. We discussed this briefly in an earlier post (KYJ 28) if you missed it click to http://KnowingYourJargon.blogspot.com
Now Factor 9 is activated which activates Factor 10.
12 - 12a - 11 - 11a - 9 - 9a - 10 - 10a.
Do you get a sense that one inactive protein is activated, which switches on or activates the next in a "dominoes" effect like cascade. It is literally a chain reaction.
Now we have covered all the coagulation factors that are called Serine proteases. This means that they act as enzymes (*ases) that activate other chemical reactions.
This post brings the Intrinsic and extrinsic pathway to a common point- Factor X.
The X Factor is therefore the start of what is called the Common Pathway.
Let's summarise:
Injured vessel releases tissue factor (F3)
F3 converts F7 to activate F10.
Or
Tissue injury allows F12 to activate, converting F11, converting F9 activating F10.
Now the pathway to clotting is the same.
Factor 10 activates F2 (prothrombin to Thrombin),
which activates Factor 1 (fibrinogen into Fibrin clots)
...
The coagulation factors that have not been covered yet include Factors 5, 8, 13, and the proteins S, C, Z and of course Calcium (Factor 4).
Stay tuned and we will fill in the gaps in the next episode.
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