Pulmonary Embolism
Pulmonary embolism (PE) involves occlusion of a pulmonary artery by an embolus, most often a thrombus, obstructing blood flow to the lungs. Impairment of pulmonary circulation leads to severe ventilation-perfusion mismatching of the lungs, terminating in hypoxemia and respiratory failure. Most PEs are sequelae of Deep Vein Thrombosis (DVT), resulting from the breakage and propagation of a venous thrombus formed within the extremities to a pulmonary artery.As DVT commonly precedes PE, risk factors for PE overlap with risk factors for DVT. These include a sedentary lifestyle, prior surgery, trauma, history of DVT, and hypertension. A sedentary lifestyle and lack of movement are critical modifiable risk factors for PE. Immobility reduces the rate of leg muscle contraction, enhancing thrombus formation in vessels of the calves that may propagate to the lungs. Thus, physical activity is essential in preventing PE. Complications
Diseases of arterial occlusion may progress into life-threatening conditions with improper prevention or management. Myocardial infarction, gangrene, and ischemic stroke are among the complications of severe arterial occlusion. Myocardial Infarction
A myocardial infarction (MI), or heart attack, arises from complete occlusion of a coronary artery. The most frequent cause of MI is the rupturing of an atherosclerotic plaque formed in CAD. Plaque rupture exposes the subendothelial matrix beneath the plaque, initiating thrombus formation within the vasculature. The thrombus deposits on the ruptured plaque to completely block the coronary artery, halting oxygen supply to cardiomyocytes. Under hypoxia, cardiomyocytes perform anaerobic respiration, producing more lactate. With blocked coronary circulation, lactate clearance from cardiomyocytes is also hindered.
Many common anti-allergy medications are useful because they reduce the mast cells ability to react to histamine.At least one clinical study suggested that nifedipine, a calcium channel blocker used to treat high blood pressure, may reduce mast cell degranulation in patients with urticaria pigmentosa. A 1984 study by Fairly et al. included a patient with symptomatic urticaria pigmentosa who responded to nifedipine at dose of 10 mg po tid. However, nifedipine has never been approved by the FDA for treatment of urticaria pigmentosa. Another mast cell stabilizer Gastrocrom, a form of cromoglicic acid has also been used to reduce mast cell degranulation. Epidemiology
Urticaria pigmentosa is a rare disease, affecting fewer than 200,000 people in the United States. See also
Urticaria
Dermatographic urticaria
Generalized eruption of cutaneous mastocytosis (adult type)

References
Further reading
Alto WA, Clarcq L (June 1999). "Cutaneous and systemic manifestations of mastocytosis". Am Fam Physician. 59 (11): 3047–54, 3059–60. PMID 10392589. == External links ==