1. Drugs Affecting Blood

2. three important dysfunctions of blood
thrombosis, bleeding, and anemia. Thrombosis--the formation of an unwanted clot within the blood vessels or heart.
Bleeding disorders involving failure of hemostasis are less common than thromboembolic diseases and include hemophilia and vitamin K deficiency.
Anemias caused by nutritional deficiencies can be treated with either dietary or pharmaceutical supplementation.

3. NORMAL RESPONSE TO VASCULAR TRAUMA
Physical trauma to the vascular system, such as a puncture or cut, initiates a complex series of interactions between platelets, endothelial cells, and the coagulation cascade. This results in the formation of a platelet-fibrin plug.

4. A. Formation of a clot
Clot formation requires platelet activation and aggregation, followed by formation of thrombin.

5. Role of platelets
Platelets respond to vascular trauma by "activation" processes, which involve three steps: adhesion to the site of injury, release of intracellular granules, and aggregation of the platelets.

7. Role of fibrin
Local stimulation of the coagulation cascade by factors released from the injured tissue and platelets results in the formation of thrombin (Factor II). In turn, thrombin, a serine protease, catalyzes the conversion of fibrinogen to fibrin, which is incorporated into the plug.

8. Thrombus versus embolus
A clot that adheres to a vessel wall is called a thrombus, whereas an intravascular clot that floats within the blood is termed an embolus. Thus, a detached thrombus becomes an embolus.

9. Fibrinolysis
During platelet plug formation, the fibrinolytic pathway is locally activated. Plasminogen is enzymatically processed to plasmin (fibrinolysin) by plasminogen activators present in the tissue. Plasmin interferes in clot propagation and dissolves the fibrin network as wounds heal.

11. ANTICOAGULANTS
Heparin is an injectable, rapidly-acting anticoagulant that is often used acutely to interfere with the formation of thrombi.

12. Mechanism of action
Heparin acts indirectly by binding to antithrombin Ill to cause a rapid anticoagulant effect.
Maximal anticoagulation occurs within minutes after intravenous heparin injection

13. Therapeutic uses
Heparin limits the expansion of thrombi by preventing fibrin formation.
Heparin is the major antithrombotic drug for the treatment of deep vein thrombosis and pulmonary embolism.
It decreases the incidence of recurrent thromboembolic episodes. Clinically, heparin is used prophylactically to pre- vent postoperative

14. Pharmacokinetics
Absorption: Heparin must be given parenterally either in a deep subcutaneous site or intravenously, because the drug does not readily cross membranes.

15. Fate:
In the blood, heparin binds to many proteins that neutralize its activity and can cause resistance to the drug. Although generally restricted to the circulation, heparin is taken up by the reticuloendothelial system and undergoes depolymerization to inactive products.

16. Adverse effects: Bleeding complications: Hypersensitivity reactions:
Thrombocytopenia:

17. DRUGS USED TO TREAT BLEEDING
Bleeding problems may have their origin in naturally occurring pathologic conditions such as hemophilia, or as a result of fibrinolytic states that may arise after gastrointestinal surgery or prostatectomy.

18. Vitamin K
That vitamin K1 administration can stem bleeding problems due to the oral anticoagulants,
The response to vitamin K is slow, requiring about 24 hours; thus if immediate hemostasis is required, fresh frozen plasma should be infused.

19. AGENTS USED TO TREAT ANEMIA
Anemia is defined as a below-normal plasma hemoglobin concentration resulting from a decreased number of circulating red blood cells or an abnormally low total hemoglobin content per unit of blood volume.
Anemia can be caused by chronic blood loss, bone marrow abnormalities, increased hemolysis, infections, malignancy, endocrine deficiencies, and a number of other disease states.

20. Iron
Folic acid
Cyanocobalamin (vitamin B12)

21. vitamin B12
Deficiencies of vitamin B12 can result from either low dietary levels or, more commonly, from poor absorption of the vitamin due to the failure of gastric parietal cells to produce intrinsic factor (as in pernicious anemia) or to a loss of activity of the receptor needed for intestinal uptake of the vitamin.

22. vitamin B12
Nonspecific malabsorption syndromes or gastric resection can also cause vitamin B12 deficiency. The vitamin may be administered orally (for dietary deficiencies), or intramuscularly or deep subcutaneously

23. vitamin B12
Therefore, megaloblastic anemia should not be treated with folic acid alone, but rather with a combination of folate and vitamin B12.