Question

For the essay that you pick, if there is a relevant pathway to outline, YOU M NEXT PAGE MARKED PATHwAY" UST OUTLINE THE PATHWAY ON and then attempt to answer the problem. NO OUTLINE-NO POINTS the next Dr. Frankenstein and are analyzing a series of anti-hemostatic/hemostatic agents to bring back the "DEAD(ie. ZOMBIES) and a way to kill them. Your administering the drug, you slash their wrists and also do isolated damage to the blood vessinnetunica intimal damage on y and observe how well their blood clots at the cellularand bi chemical level. victims are a pool of hungry and poor college students pon administration of the drug BBA#3, you observe the following Blood clotting in response to the both types ofdamage was never initiated. Plese identifyand xpla all of the potential actions of BBA 3 (BE SPECIFIC AND DETAILED DOWN TO THE MOLECULAR LEVEL) A) U of the drug-BBM4 et observethe following. Blood clotting developed in both of the cle took twice as long to dissolve. At the time of this experiment, your victim was lsuffering from sccondary polyeythemi)and ir seemea that twice the number of platelets could occupy the sime an space as a normal pe r Plea e dentify and explain all of the potential actions of BBA#4 on this SPECIFIC atint, QBE SPECIFIC AND DETAILED DOWN TO THE MOLECULAR LEVED)

Answer 1

A. The drug has property of platelet aggregation inhibition

It irreversibly inhibits the enzyme cyclo-oxygenase, which leads to reduction in thromboxane synthesis in platelets and prostacyclin in vascular endothelial cells.

Trombone is released by activated platelets during hemostasis and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation. This is achieved by activating the thromboxane receptor, which results in platelet-shape change, activation of integrins, and degranulation. Circulating fibrinogen binds these receptors on adjacent platelets, further strengthening the clot. Thromboxane A2 is also a vasoconstrictor

Thus the absence of thromboxane can lead to uncontrolled bleeding by way of failure of primary democratic plug formation by injury to endothelial and lack of fibrin stabilisation of the clot

B. This drug reversibly binds on plasminogen. This reduces conversion of plasminogen to plasmin, preventing fibrin degradation and preserving the framework of fibrin's matrix .

Thus this drug prolongs clot dissolution

As more platelets are present in this patient may trigger a DIC like reaction