Angina : Definition: Angina is chest pain or discomfort that occurs when an area of the heart is deprived of oxygen. It is typically described as a crushing or squeezing sensation in the chest and may radiate to the jaw, shoulders, arm or back. It is usually a symptom of underlying heart disease, such as coronary artery disease. Angina can be classified into two i.e Stable Angina and Unstable Angina
Stable Angina - Usually results from atherosclerotic plaques in the coronary arteries. Acute attacks of stable angina should be managed with (1) Nitrates - Glyceryl trinitrate, Isosorbide dinitrate
(2) Antiplatelet drugs - Aspirin
(3) Calcium-channel blockers - Verapamil , Diltiazem,Nifedipine, nicardipine, amlodipine, and felodipine
(4) Other antianginal drugs - Nicorandil and Ivabradine
Unstable Angina - usually due to plaque rupture and may occur either in patients with a history of stable angina or in those with previously silent coronary artery disease. Unstable angina (UA) (also "c
Coagulation (clotting) : Coagulation (clotting) is the process by which blood changes from a liquid to a gel. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin. Disorders of coagulation are disease states which can result in bleeding (hemorrhage or bruising) or obstructive clotting (thrombosis). Coagulation is highly conserved throughout biology; in all mammals, coagulation involves both a cellular (platelet) and a protein (coagulation factor) component. The system in humans has been the most extensively researched and is the best understood.
Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the vessel. Exposure of blood to the space under the endothelium initiates two processes: changes in platelets, and the exposure of sub endothelial tissue factor to plasma Factor VII, which ultimately leads to fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Additional coagulation factors or clotting factors beyond Factor VII, respond in a complex cascade to form fibrin strands, which strengthen the platelet plug