Haemostasis and blood coagulation 2 Flashcards
Describe Thromboembolic conditions.
Thrombi and Embolic
1. An abnormal clot that develops in blood vessel is called Thrombus (clotting without injury)
freely flowing clots (unbound) are known as embolic
THE EMBOLIC ORIGINATING:
a) in left side of the heart & large arteries= can block arteries or arterioles in the brain,
kidneys, or elsewhere.
- b) in the venous system or right side of the heart = flow into lungs = pulmonary arterial
embolism
the causes of thromboembolic conditions.
Roughened endothelial surface of a vessel—due to arteriosclerosis, infection, or
trauma (likely to initiate clotting process)
b) Very slow blood flow where small quantities of thrombin and other procoagulants are
always being formed.
THE USE OF TISSUE PLASMINOGEN ACTIVATOR IN TREATING INTRAVASCULAR CLOTS
- Genetically engineered tissue plasminogen activator (t-PA) is available.
- When delivered to an area with a thrombus, it is effective in activating plasminogen to
plasmin, which in turn can dissolve some intravascular clots.
Femoral Venous Thrombosis
Blood stasis (due to immobility of patients confined to bed; practice of propping theknees up with pillows) →Intravascular clotting
1. Femoral Venous Thrombosis:
* These clots grow in slow moving venous blood, full length of leg veins, even up into
common iliac vein and inferior vena cava.
Massive pulmonary Embolism
A large part of the clot disengages from its attachments to the vessel wall →flows through
venous blood →right side of the heart → pulmonary arteries → massive blockage of the
pulmonary arteries.
- If both pulmonary arteries are occluded at the same time = immediate death ensues.
- If only one pulmonary artery is blocked:
a) death may not occur, OR
b) the embolism may lead to death a few hours to several days later due to further clot growth - However, t-PA therapy can be a lifesaver.
- Disseminated Intravascular Coagulation:
circulation→ disseminated intravascular coagulation (DIC).
* DIC results from the presence of large amounts of traumatized or dying tissue in the body
that releases great quantities of tissue factor into the blood.
- Frequently, the clots are small but numerous, and they plug a large share of the small
peripheral blood vessels. - This process occurs especially in patients with widespread septicemia, in which circulating
bacteria or bacterial toxins (esp. endotoxins), activate the clotting mechanisms. - The plugging of small peripheral vessels greatly diminishes delivery of oxygen and other
nutrients to the tissues→ circulatory shock. - septicemic shock is lethal in 35% to 50% of patients.
- Effect of DIC, patients begin to bleed= due to so many of the clotting factors being removed
by the widespread clotting → too few procoagulants remain to allow normal hemostasis of the
remaining blood
The delay of coagulation processes in some thromboembolic conditions is due to ———–being developed
anticoagulation
Most clinically useful anticoagulants are:
- Heparin—Intravenous Anticoagulant
- Coumarins as Anticoagulants
Heparin the intravenous anticoagulant
Injection of about 0.5 to 1 mg/kg of body weight→ ↑s blood-clotting time from about 6 minutes
(normal time) to 30 or more minutes.
* This change in clotting time occurs instantaneously → immediately preventing or slowing
further development of a thromboembolic condition.
Anticoagulants for Clinical Use
* The action of heparin lasts about 1.5 to 4 hours.
* The injected heparin is destroyed by an enzyme in the blood known as heparinase.
Coumarins as Anticoagulants.
- Coumarin, such as warfarin, given to a patient→ ↓s active prothrombin and factors VII, IX, and
X. - Warfarin causes this effect by inhibiting the enzyme VKORC1.
- VKORC1 enzyme converts inactive, oxidized form of vitamin K to its active, reduced form.
- So, inhibition of VKORC1 by warfarin→ ↓s active form of vitamin K in the tissues → this
decrease inactivates coagulation factors.
Anticoagulants for Clinical Use - After administration of an effective dose of warfarin, the coagulant activity of the blood
decreases to about 50% of normal by the end of 12 hours and to about 20% of normal by the
end of 24 hours. - Normal coagulation usually returns 1 to 3 days after discontinuing coumarin therapy
Prevention of Blood Coagulation Outside the Body
Substances that ↓ [calcium ions] in the blood → can prevent blood.
coagulation outside the body.
Example:
a) Soluble oxalate compound mixed with sample of blood →causes precipitation of
calcium oxalate from the plasma → ↓ [calcium ions] → blockage of blood
coagulation.
b) Citrate anticoagulants
Fibrinolysis breaks up clots
- Cross-linked stable fibrin traps RBCs and WBCs as well as platelets in a newly
formed thrombus. - After plug formation, fibrinolysis (the breakdown of stable fibrin) breaks up the
clot in a process known as thrombolysis. - Fibrinolysis begins with the conversion of plasminogen to plasmin, catalyzed by
tissue-plasminogen activator (t-PA) or urokinase-plasminogen activator (u-PA). - The tissue plasminogen activator is produced by the endothelial cells.
- The presence of fibrin greatly accelerates the conversion of plasminogen to
plasmin.
Enzyme that breaks down both fibrin and fibrinogen?
Plasmin
The system that regulates fibrinolysis at several levels using both inhibitors and enhancing mechanisms?
Cardiovascular system
