Platelets - formation, action and inhibition Flashcards
a thrombus
clot blocking a blood vessel
when collagen is exposed due to endothelial damage platelets stick to it when this happens platelets get activated and release chemical that calls on more platelets - what is this molecule
thromboxane A2 (TxA2)
Haemostasis is a protective mechanism whereby blood flow is arrested by localised vasoconstriction and through the initiation of a blood clot through the clotting cascade. Effective haemostasis will thus help prevent significant blood loss through breaches in blood vessels due to damage in the blood vessel wall
ontop of platelets fibrin proteins sticks platelets together forming the clot
the fibrin will trap what cells in it
RBC - THIS PROCESS REPEATS CAUSING A CLOT OR A THROMBUS
cox inhtiobrs stop thrombus forming by stopping TxA2 what is an example of this
aspirin - platelets won’t stick together and clot won’t be formed
side effect is accessive bleeding
what cells are your smallest blood cells at 2-4micrometres and are colourless
platelets
platelet granules are unique among secretory vesicles in both content and their life cycle there are two types what are they
dense granules and alpha granules
what are dense granules
darker
these contain high concentrations of low molecular weight compounds that potentiate platelet activation ( contains phospholipids, triglycerides, cholesterol, ATP, ADP , serotonin( 5HT which obtain while passing through GIT))
what are alpha granules
concentrate large polypeptides that contribute to both primary and secondary homeostasis containing secreted proteins such as clotting factors and PDGF
normal platelet count
150000-400000 per mm^3
life span of platelet
8-12 days average 10
platelets are destroyed by tissue macrophages in the spleen
a bigger spleen ( splenomegaly ) reduced platelet count so removal of the spleen …( splenectomy- remove spleen)
increase platelet count
where does thrombopoiesis occur
bone marrow
also lungs
haemocytoblast- magakaryoblast - promegakaryocte - megakaryocte - platelets
what is the coagulation triad - the triangle of death
coagulation proteins ( hyper coagulation) platelts ( stasis of blood flow) endothelium ( endothelia injury)
the intrinsic pathway contains what factors
12,11,9,8
extrinsic is Tf and 7
protein S acts where
factor 8
protein c acts where
factor 5
dmaged blood vessel lead to release of clotting factors covering prothrombin to thrombin then fibrinogen to fibrin leading to development of a clot
platet bound by the three receptors ……
platelet granules relates relaxing ADP, ATP and serotonin , causing additional platelet aggregation and activation. Phospholipase c is activated by platelet causing calcium release leading to phospholipase A2 activation leading to TXa production as well as platelet surface changing and activating thrombin all increasing platelet activation and aggregating
GP1b
GPV
GPIX
Moa of clopidogrel - anti-platelet ( prevent heart attack and strokes)
selectively inhibits ADP binding to P2Y12 receptor on the platelet thereby inhabiting platelet aggregation - irreversible
Moa of aspirin
blocks prostacyclin synthesis - non selective COX-1 inhibitor inhibiting platelet aggregation for about 7-10 days
What is the clotting factor that activates platelets
vWF
Which cytosolic component of platelets is responsible for ADP release?
dense granules
How are platelets destroyed by the body after circulating for 8-12 days?
Phagocytosis by macrophages in the spleen
Which cell is responsible for platelet production?
Megakaryoblasts
The key function of platelet induced clotting is to…
- …form a platelet plug
- …inhibit Tissue Factor release
- …promote fibrin formation
- …prevent atherosclerosis
1 and 3
The primary factors that propagate platelet clot formation are:
ADP and Thromboxane A2
What is the precursor molecule to Thromboxane A2?
Prostaglandin H2
What is the primary target of the drug Aspirin in order to prevent clot formation?
COX1
What is the mechanism of action of the drug clopidogrel bisulphate?
ADP receptor antagonist
