Blood Transfusions and Coagulation/Thrombolysis Flashcards
What is the difference between blood grouping vs. crossmatching?
Blood Grouping = determining red cell antigens in blood of donor and recipient – look for agglutination (clumping of cells in the presence of an antibody) – we use this to determine the red cell compatability between donor and patient
Cross-matching – mix donor and recipient blood outside of the body – indicates that the donor blood is incompatable for the patient- it ensures that there was no error in ABO grouping of donor or recipient – and it also ensures that recipient has no naturally occurring or immune antibodies active against donors cells.
Describe how the blood is grouped into A, B or O type
A type - has ‘A’ antigens on the surface
B type - has ‘B’ antigens on the surface
AB type - has ‘A and B’ antigens on the surface
and O type- does not have antigens on its surface
What is the Rhesus system for classifying blood type?
They are either negative or positive for the rhesus antigen (most often rhesus antigen ‘D’) - these are also found on the surface of RBCs
If you are blood type ‘A negative’ what antibodies do you possess?
you have
- ‘B’ antibodies
If you are blood type ‘AB positive’ what antibodies do you posess?
- you do not posses any antibodies against blood
If you are blood type “O negative” what antibodies do you produce?
- ‘A’ antibodies
- ‘B’ antibodies
- *this is the universal donor - will not produce a reaction in anyone*
Why do we have antibodies against other blood types?
we encounter small amounts of Type A or B in food/bacteria
Do rhesus negative blood types have antibodies against it?
NO - neither Rh positive, nor negative blood types have antibodies against this
UNLESS
unless you come across it somehow during life (like a mother with an infant) - you don’t expect to come across it under normal conditions
Do we donate whole blood in blood transfusions?
NO we filter out the red cells from plasma and platelets - really we just want the red cells and plasma, we don’t want the WBC because that leads to immune garbage
Why might the O negative blood type NOT be considered a universal donor?
Because the sample would also contain the antiA or antiB antibodies. We try to filter them out of the blood, but ultimately it depends on the titres
Why might a mother reject her fetus based on blood type? Why is there no risk of this in the first pregnancy?
If the mother is rh negative and the fetus is positive, she creates antibodies against this …. with the next pregnancy she has the antibodies, baby could be born with jaundice and face anaemic death
What is an autologous transfusion?
Donate your own blood weeks before a surgery - therefore there is no risk aassociated with blood borne viruses like AIDS
What is haemostasis?
the maintanence of blood in a fluid/clot free state
Haemostasis induces a rapid formation of a localized haemostatic plug at the site of vascular injury - this is a well regulated process
What is a Thrombos?
it is the inappropriate activation of the normal haemostatic process (blood clot formation) within the vascular system
- it has the potential to block the blood flow to the vital areas
What does a Thrombus contain?
it consists of fibrin, red blood cells, and platelets
What do you call a thrombus that breaks loose and travels to organs?
an Embolus
If an embolus moves to the heart, what occurs?
an
Acute Myocardial Infarction (AMI= heart attack)
what occurs if the embolus moves to your brain?
Thrombotic stroke or Transient ischemic attach (TIA)
What if the embolus moves to your legs?
peripheral arterial disease - causes claudication
In the venous system, what happens if an embolus moves to your legs, or your lungs?
In the venous system of legs = DVT
in the venous lungs = pulmonary embolism
How do we treat an arterial thrombus vs. a venous thrombosis?
arterial = platelet inhibitors
venous = anti-coagulents
*though it’s not as if only platelets are at play in arteries and only coagulents are effecting the veins- it’s a matter of which is more dominantly effecting. You can remmber which is which by remembring that platelets are more likely to be activated by the sheer strain and quick movement of the blood in the arteries as opposed to the relatively relaxed venous system
What is Virchow’s Triad?
thrombosis is caused by abnormalities in one or more of the following
1) quality of the vessel wall (endothelial cell injury?)
2) nature of the blood flow (stasis/tubulence)
3) composition of the blood (hypercoagulable or thrombophilia)
What can cause arterial thrombosis?
a common cause of arterial thrombosis is atrial fibrillation - causes disturbed blood flow or
arterial thrombosis can follow a rupture of atheroma (antherothrombosis)
How many plasma proteins are involved in the coagulation cascade?
11 plasma proteins in the cascade - most factors are protease enzymes (an enzyme that cleaves a protein at a specific residue)
What are the alternative names for
Factor 1
Factor 2
Factor 3
of the coagulation cascade?
1= fibrinogen
2= prothrombin
3= tissue factor or throboblastin
What are the first steps of the extrinsic coagulation cascade?
- small amounts of tissue factor is realeased by damaged endothelial cells or exposed at the site of injury
- TF activates factor VII in the plasma
- TF enables the conversion of Factor VII to activated Factor VII (FVIIa)
What is the first step of the instrinsic coagulation cascade?
contact with a synthetic or chaged surface causes the activation of a different coagulation factor (Factor XII) = activation converts it to FXIIa an active protease
Where do the extrinsic and intrinsic coagulation cascades meet?
They meet when they activate Factor X - after that it is a common pathway
What does the Final Common Pathway consist of in the coagulation cascade
it results in the conversion of the plasma preprotein, fibrinogen, to fibrin polymer or clot
What factor feedsback and accelerates the conversion of Factor VII to it’s activated form?
Factor 10a feedsback and accelerates it’s formation
Without calcium present, what reaction cannot take place?
Factor 10a cannot convert prothrombin to thrombin
Thrombin has many roles in the coagulation cascade- name them all
1) thrombin (when in the presence of calcium) will convert fibrinogen to fibrin
2) it activates factor 13 allowing it to crosslink fibrin clots
3) activates Factor 5 and accelerates the action of Factor 10
4) Generates more factor 7 - positive feedback loop
5) it is also a potent activator of platelet aggregation
What controls coagulation?
The activation of FXa by TF- FVIIa is almost immediately inhibited by tissue factor pathway inhibitor (TFPI) - which is a naturally occuring anticoag. protein that directly inactivates coagulation factor Xa and produces feedback inhibition of the factor VIIa/tissue factor catalytic complex
*ultimately it’s a ballance between Tissue factor and TFPI that determines whether coagulation will proceed
What naturally occuring inhibitors are there for Factor X and Factor II?
- Anti-Thrombin III
- Heparin
- Thrombomodulin
What factors are involved in the intrinsic pathway?
Factors XII, XI, IX, VIII, and X as well as prekallikrein, HK, calcium, and platelet phospholipids
What cofactors are necessary for the proper function of the coagulation cascade?
- calcium and phospholipid for the tenase and prothrombinase complexes
- negatively charged phospholipids
- calcium mediates the binding of coagulation factors
- calcium - for the Vitamin K dependent coagulation factors
Why is Vitamin K an essential component in coagulation?
Vitamin K acts as a catalyst for the maturation of coagulation cascade factors in formation
What factors favor thrombosis?
- blood stasis allows accumulation of HMWK etc.
- the release of tissue factor- activates cascade
- exposed collagen- binds plasma and platelets adhere
- Thrombin - converts fibrinogen to polymeric fibrin
What factors inhibit thrombosis?
- antithrombin
- PGI2 and NO
What is the last step in the coagulation cascade?
- enzymatic cleavage of soluble plasma fibrinogen (Factor I to Factor Ia)
fibrin spontaneoulsy polymerizes and results in the formation of a permanent fibrous plug - and induces further platelet recruitement
