BS

Question 1

primary hemostasis

Answer 1

platelet plug formation at the site of vascular injury. (platelets are exposed to collagen, etc at injury site; leads to adherence, activation, aggregation of platelets; vWF assists platelets in adherence and bridges them together at site of injury)

Question 2

secondary hemostasis

Answer 2

coagulation. conversion of fibrinogen to a fibrin clot.

Question 3

vascular constriction in the clotting cascade

Answer 3

part of primary hemostasis. contraction of vascular smooth muscle in response to injury to slow blood flow to the area. occurs while platelet plug is forming.

Question 4

conversion of prothrombin to thrombin in the clotting cascade

Answer 4

part of the common pathway. factor Xa converts prothrombin to thrombin. effects: activates fibrinogen to fibrin; positive feedback activation of intrinsic pathway; activates platelets

Question 5

conversion of fibrinogen to fibrin in clotting cascade

Answer 5

part of the common pathway. catalyzed by thrombin. effects: activated platelets have a binding site for fibrinogen which helps form bridges between aggregating platelets.

Question 6

formation of the platelet plug

Answer 6

primary hemostasis secondary to vessel injury. consists of platelets, vWF, Fibrinogen. temporary fix until “proper clot” forms

Question 7

formation of a blood clot

Answer 7

platelet plug solidified by conversion of fibrinogen into fibrin. less temporary than platelet plug; prevents rebleeding.

Question 8

fibrous organization of clot

Answer 8

fibrin cleaved into fibrin molecules; fibrin monomers crosslink to form net-like mesh that encases RBCs to prevent further spillage.

Question 9

development of a blood clot

Answer 9

fibrinogen and other clotting components freely exist in circulation. without regulatory mechanisms, thrombin would continue to form clots everywhere. 3 major regulators control clot formation: antithrombin III, protein C, protein S.

Question 10

sequence of events in blood clotting

Answer 10

1. injury to the blood vessel wall or to the blood induces the formation of prothrombin activator.
2. prothrombin activator catalyzes the change of prothrombin to thrombin.
3. thrombin changes fibrinogen to fibrin, which mix w RBCs, platelets, and plasma to form clot.
4. clot retraction

Question 11

clot retraction

Answer 11

assisted by platelets, expresses serum. plasma can clot, serum cannot.

Question 12

lysis of blood clots

Answer 12

plasmin cleaves fibrin resulting in breakup of the clot and creating fibrin products that inhibit thrombin.

Question 13

major components of hemostasis

Answer 13

platelets, endothelial cells (lining the blood vessels), other tissue-factor bearing cells, and the coagulation factors (which are plasma proteins)

Question 14

intrinsic pathway

Answer 14

requires negatively charged collagen inside the damaged endothelium to activate factor XII, which activates XI, then IX, then VIII, then leads to the common pathway

Question 15

extrinsic pathway

Answer 15

initiated when factor VII contacts tissue factor released into the circulation from injured endothelium (a call for help from the injured tissue). this starts the common pathway by activating factor X with factor V, then factor II (prothrombin to thrombin), then factor I (fibrinogen to fibrin)

Question 16

antithrombin

Answer 16

anticoagulant protein. produced in the liver. protease inhibitor: physically blocks the action of factor Xa and thrombin as well as factors IX and XI in the intrinsic pathway. activity enhanced when bound to heparin

Question 17

protein S

Answer 17

anticoagulant protein. produced in the liver, vitamin K dependent. w/ cofactor protein C, inhibits factor Va and VIIIa. this protein “exposes” the site so that protein C can cleave the activated factor

Question 18

plasminogen

Answer 18

promotes clot degradation. proenzyme that is cleaved to form plasmin, the main enzyme of fibrinolysis. activated plasmin digests fibrin, thus dissolving the clot.

Question 19

tissue factor pathway inhibitor

Answer 19

protects against excessive coagulation. plasma protein secreted by endothelial cells. check and balance of the coagulation pathway. regulates max thrombin production.

Question 20

clotting factors that are vitamin K dependent

Answer 20

II, VII, IX, X

Question 21

anticoagulation factors

Answer 21

protein C, protein S, warfarin interferes w vitamin K atiity and therefore messes up clotting

Question 22

viral hemorrhagic fever

Answer 22

associated w zoonotic viruses. prodrome of fever, myalgias, malaise. pts develop vascular damage, petichiae, and local hemorrhage. shock, multifocal hemorrhaging, and neuro signs predict a poor prognosis. related to increased vascular permeability and disseminated intravascular coagulation. vascular abnormalities may be d/t circulating virus antibody complexes which mediate compliment activation & release of vasoactive amines (the reason for this is unclear).