CHAPTER 21: ANTICOAG/PLATELETS INTRO TERMS

Question 1

Hemostasis

Answer 1

process of slowing/stopping flow of blood to initiate wound healing

Question 2

thrombosis

Answer 2

formation of an UNWANTED clot within a blood vessel
- most common abnormality of hemostasis

Question 3

Thrombotic Disorders

Answer 3

• acute MI
• deep vein thrombosis (DVT)
• pulmonary embolism (PE)
• acute ischemic stroke

Question 4

Anticoagulants and Fibrinolytics

Answer 4

drugs used for treating thrombotic disorders

Question 5

Bleeding Disorders caused by

Answer 5

defects in hemostasis that lead to INC susceptibility to bleeding

Question 6

Thrombus vs Embolus

Answer 6

thrombus: clot that adheres to vessel wall

embolus: intravascular clot that floats in blood

detached thrombus becomes an embolus

Question 7

Arterial Thrombosis

Answer 7

occurs in medium-sized vessels, consists of a platelet-rich clot

Question 8

Venous Thrombosis

Answer 8

triggered by blood stasis or inappropriate activation of coagulation cascade

• clot rich in FIBRIN and fewer platelets

Question 9

why are thrombi and emboli dangerous?

Answer 9

they both may occlude/block blood vessels are deprive tissues of oxygen and nutrients

Question 10

Platelets without vascular injury

Answer 10

• absence of injury, platelets circulate freely bc balance of chemical signals indicate there is no damage to vascular system
• prostacyclin inc, cAMP inc, Ca2+ dec and no platelets aggregate

Question 11

platelet responding to vascular injury: initial recognition of injury

Answer 11

• injury detected in endothelial cells, dec prostacyclin levels which decreases cAMP
• dec in cAMP then leads to inc in Ca2+ released

Question 12

platelet responding to vascular injury: chemical mediators

Answer 12

• platelets now bind to the collagen
• starts sending out chemical mediators in granules (like storage vacuoles)
  chem mediators: ADP/serotonin/thrombin/thromboxane A2
• trigger activation of thromboxane A2 synthesis and the GP IIb/IIIa receptors that were inactive before
• now fibrinogen binds to the receptors on the platelets and links other platelets together to form clot

Question 13

fibrinogen
- what is it
- how does it work

Answer 13

• soluble plasma glycoprotein (GP)
• binds to IIb/IIIa rec on two separate platelets
• result in platelet aggregation once their receptors are activated

Question 14

fibrinogen vs chemical mediators

Answer 14

chemical mediators call the platelets over to the site and activation of the receptors lets the clot form so fibrinogen can link the platelets

Question 15

Formation of Clot and Fibrinolysis

Answer 15

• stim coagulation cascade by tissue factors released from injured tissues and mediators on surface of platelets

this forms thrombin (factor IIa) a serine protease

Question 16

Thrombin in formation of a clot

Answer 16

thrombin catalyzes hydrolysis of fibrinogen to fibrin (which is in the clot)

• cross-links fibrin strands, stabilizes clot, forms hemostatic platelet-fibrin plug

Question 17

Fibrinolytic Pathway
- how does it work
- what is plasmin/ its purpose

Answer 17

• locally activated
• plasminogen enzymatically processed to plasmin by plasminogen activators in tissue

plasmin limits growth of clot and dissolves fibrin network as the wound heals