BIO 202 CHPT 18 Platelet Form and Function

Extrinsic mechanism

initiated by tissue factor(thromboplastin), released by damaged tissues. Thromboplastin factor III & IV + Ca2 ----> Liver + thrombin/fibrinogen + PF3 = Fibrin.

Intrinsic mechanism

when blood comes in contact with something other than smooth epithelial tissue thus initiating clotting from inside the vessel. Platelets + Factors + Ca2+ + PF3 ----> Liver + thrombin/fibrinogen + PF3 = Fibrin.

Platelet Form

(AKA: Thrombocytes) Cell fragments really: A very small blood cell derived from the fragmented cytoplasm of megakaryocytes in the bone marrow. Platelets participate in coagulation, wound healing, and inflammation. 2nd most abundant formed elements after erythrocytes. However, they are so small they contribute less than WBCs to the blood volume. (r in buffy coat) 25-40% stored in the spleen, released as needed. The rest free in the blood and live for 5-6 days.

Coagulation

(clotting) Do it when you need it, don't when you don't. Complicated process, 30 chemical reactions. Goal: convert plasma protein fibrinogen into fibrin; everything sticks to fibrin: blood cells, platelets, and the goop seals the break.

Hemostasis Mechanisms (3x)

1) Vascular spasm 2) platelet plug formation 3) blood clotting (coagulation)

Fibrin

from fibrinogen, a sticky protein that adheres to the walls of a vessel.

Prostacyclin

A platelet repellant that coats the smooth endothelium and keeps platelets from bursting on healthy tissue.

Thrombosis

Blood clot in a vessel. More likely in veins than in arteries because blood flows more slowly in veins and does not dilute thrombin and fibrin as rapidly.

Megakaryocyte

Enormous cells in the bone marrow that release packets of cytoplasm (platelets) into the circulating blood. Live in bone marrow adjacent to blood sinusoids; gigantic cell with a multilobed nucleus Sprouts long tendrils called Proplatelets.

2 coagulation pathways:

Extrinsic mechanism & Intrinsic mechanism

Thrombocytopenia

Penia = poverty, or deficiency. Anything that interferess with platelet production. Dangerous.

Fibrinolysis

Positive feedback look: Blood clot gradually dissolves as the repairs proceed. Factors & thrombin activate Kallikrein enzyme, activates plasminogen into plasmin (activates more Kallikrein).

Vascular Spasm

Prompt constriction of the broken vessel that buys time for the other two hemostatic mechanisms to come into play.. Triggered by: 1) An injury stimulates pain receptors, causes vessels to constrict. Last only a few minutes, give time for: 2) Injury to the smooth muscle of the blood vessel itself causes a longer-lasting vasoconstriction. 3) Platelets release serotonin, a chemical vasconstrictor.

Procoagulants

REACTION CASCADE Clotting factors that are produced in the liver and are present in the plasma in inactive form, but when on factor is activated, it functions as an enzyme that activates the next one in the pathway (cascade reaction)

clot retraction

Tightening of the fibrin clot. Platelets contain actin and myosin (muscle proteins) which contract and pull the edges of the wound closer together. Occurs over 30-60 minutes after clotting.

inappropriate clot prevention mechanisms:

1) Platelet repulsion 2) Dilution (thrombin might forms in plasma, but in small amounts) As long as blood is moving, not likely to clot. 3) Anticoagulants: present in the plasma suppreses thrombin formaiton. 4) Antithrombin: Produced by the liver, deactivates thrombin before it can act on fibrinogen.

Proplatelets

a megakaryocyte sprouts long tendrils called, that protrude through the endothelium into the blood fo the sinusoid, break off in bits to form the platelets.

Hematoma

bruise or worse. A localize collection of blood within tissued due to leakage from a wall of a blood vessel, producing a bluish discoloration (ecchymosis) and pain. A swelling caused by the collection of blood under the skin or in damaged tissues as a result of an injured or broken blood vessel.

Pulmonary embolism

clot lodge in the lungs and blood cannot circulate freely through the lungs. die of hypoxia.

platelet-derived growth factor

platelet & endothelial cells secret it. stimulates the production of connective tissue cells

Platelet Function

platelets have a greater variety of functions than any of the true blood cells: 1) Secrete vasoconstrictors to slow and reduce blood loss. 2) Stick together as platelet plugs to seal small breaks. 3) secrete procoagulants, clotting factors. 4) Initiate the production of clot dissolving enzymes (for old clots) 5) secrete chemicals that attract neutrophils and monocytes. 6) internalize and destroy bacteria. 7) secret growth factors that stimulate mitosis in fibroblasts and smooth muscle.

Thromboembolism

99% of embolisms represent part of a dislodged thrombus

Embolus

A clot that breaks lose and travels through the bloodstream.

Platelet Plug Formation

A damaged vessel exposes collagen fibers that stimulate the platelets to grow long spiny pseudopods that adhere to the vessel and other platelets. The pseudopods then contract and draw the walls together. the mass of platelets formed is called the Platelet Plug. Not as strong as the following clot, just a temporary stop-gap. ...pressure on a wound does the same thing, constricts the vessel. They undergo degranulation and burst all their chemicals. Postive feedback system.

Hemophilia

A family of hereditary diseases characterized by deficiencies of one factor or another. A deficiency of any clotting factor can shut down the coagulation cascade. Primarily in Males.

Plasmin

A fibrin-dissolving enzyme that breaks up the clot; "the clot buster"

thrombopoiesis

A form of hemopoiesis dedicated to the production of platelets. The liver and kidneys produce enzyme "thrombopoietin" that stimulate some stem cells in the red marrow to produce specialized megakaryoblasts (platelet production line cells).

Heparin

Anticoagulant. An anticoagulant that acts to inhibit a number of coagulation factors, especially factor Xa. Heparin is formed in the liver, or given as injection for treatments.