C3 Platelets

Question 1

Formational stages of Platelets

Answer 1

Haemocytoblast->
Myeloid stem cell->
Megakaryoblast->
Promegakaryocyte->
Megakaryocyte: large multi-lobed nucleus –>
Platelets: anucleated parts of megakaryocyte cytoplasm

Question 2

Physical properties of platelets

2. give alterative name
3. What regulates platelet production

Answer 2

Adhesion: ability to stick to the foreign & damaged surface
Aggregation: ability to form a clump
Agglutination: pasting of thrombocytes one with another
2. Thrombocytes
3. Thrombopoietin

Question 3

Describe vascular endothelium and clotting

• what proteins
• what factors
• what mediators produced?

Answer 3

Vascular endothelium: inhibits blood clotting
Surface not conducive to clot formation
Displays membrane proteins that inhibit clotting (heparin like molecules)
Store von Willebrand factor granules: expressed & secreted into circulation or sub-endothelium. (20% made by platelets, rest endothelium)
Makes prostacyclin and NO both inhibit platelet aggregation

Question 4

Describe first response to vascular injury

Answer 4

VASOCONSTRICTION is stimulated (1st response)
Compression of vessel by escaping blood
Injury “chemicals” released by injured cells
Reflexes from adjacent pain receptors

Question 5

Describe Formation of a Platelet Plug

Answer 5

= cascade of platelet activation
Platelets attach to damaged vessel wall to plug it
Platelets produce thromboxane A2
Serotonin/ histamine release enhances vascular contraction
ADP - attracts and stimulates platelets at site ((Adenosine diphosphate (ADP) = platelet agonist: platelet shape change & aggregation + generation of TXA2))
Prostacyclin - inhibits aggregation at other sites
A sharply cut vessel undergoes less spasm, i.e., bleeds longer, than a tore vessel

Question 6

Describe Platelet Plug Formation

Answer 6

Primary haemostasis - platelets aggregate to control blood loss from capillaries, arterioles, & venules If damage is small, platelet plug can arrest bleeding completely by closing minute ruptures in vessels that occur hundreds of times a day
Exposure to collagen & other foreign substances (antigen-Ab complexes, thrombin, proteolytic enzymes, endotoxins, and viruses), platelets undergo dynamic change in appearance and begin the process of adhesion and activation
In adhesion, platelets swell, become sticky and adhere to collagen fibril on the basement membrane - requires von Willebrand factor (vWF) adhere to collagen fibrils on the basement membrane
Activated platelets release granules containing vWF, factor V, PDGF, heparin-neutralizing protein, and ADP (attracts other platelets)

Question 7

Name

1. Intrinsic
2. Extrinsic Coagulation Clotting Pathways

Answer 7

Intrinsic: all components are in the blood (& involved in cascade)
Extrinsic: at least one component from tissue; injury response
- need TF for activation of VIIa
- TF & factor VIIa contact only after injury
- TF-factorVIIa complex also activates factor Xia

Question 8

Name clotting pathways (what molecules are activated)

Answer 8

Platelet cells activated by damage
PF3 and/or TF produced by platelet cells
Factor X activated
prothrombin activator (enzyme) produced
prothrombin conversion-thrombin (another enzyme)
thrombin stimulates: fibrinogen—-> fibrin mesh

Question 9

Describe Intrinsic pathway

Answer 9

W/in damaged vessel
Requires more pro-coagulants (I-XIII) toward PF3 & Factor X (uses all factors)
Allows more “scrutiny” before clotting occurs

Question 10

Describe extrinsic pathway

Answer 10

in outer tissues around vessel (quicker formation of clot: direct activation)
tissue thromboplastin (Tissue Factor) - skips intrinsic steps straight to PF3 and Factor X
allows rapid response to bleeding out of vessel (clot can form in 10 to 15 seconds)

Question 11

Describe Common pathway

Answer 11

Factor X, PF3 (thromboplastin), Factor V, Ca++ –>
prothrombin activator ->
prothrombin converted -> thrombin (active enzyme)
thrombin stimulates: fibrinogen -> fibrin (meshwork)
Ca++ & thrombin -> Factor XIII (fibrin stabilizer)

Question 12

Name drugs

1. promoting haemostasis
2. Drugs preventing clot formation
3. Thrombolytic drugs

Answer 12

1. Pro-coagulants
   Fibrinolysis inhibitors
   Heparin antagonist
2. Anticoagulants
   Antiplatelet drugs
3. (like above also attacking on homeostasis)

Question 13

Define Plasmin

Answer 13

Produced in an inactive form, plasminogen, in the liver.

plasmin degrades fibirn mesh (cuts it)