1. Asthma is the acute or chronic obstruction of airflow in the lungs. This relates to changes related to inflammation. The bronchi and bronchioles respond to stimuli with three changes, inflammation of the mucosa with edema, contraction of smooth muscle, and increased secretion of thick mucus in the passages. These changes obstruct airways, partially or totally, and interfere with airflow and oxygen supply.

There are two types of asthma. Extrinsic, involves acute episodes triggered by a Type 1 hypersensitivity reaction to an inhaled antigen. The antigen reacts with immunoglobulin E on the previously sensitized mast cells in the respiratory mucosa, releasing histamine, kinins, prostaglandins, and other chemical mediators, which then cause the inflammation, bronchospasm, edema, and increased mucus secretion. The reaction also stimulates branches of the vagus nerve, causing reflex bronchconstriction. Onset commonly occurs in children. The second type is intrinsic asthma, with onset during adulthood. In this disease, other types of stimuli target hyper responsive tissues in the airway initiating an acute attack.

Internal triggers are respiratory infections, exposure to the cold, exercise, drugs such as aspirin, stress, and inhalation if irritants such as cigarette smoke.

2. Diabetes Mellitus Type 1 is the deficit of insulin resulting from the destruction of the pancreatic beta cells in an autoimmune reaction, resulting in an absolute deficit of insulin in the body and therefore requiring replacement therapy. It is genetic and occurs more frequently in children and adolescents but can occur at any age. The deficit of insulin results in decreased transportation and use of glucose in the cells of the body. Blood glucose levels rise and excess glucose spills into the urine causing increased osmotic pressure in the filtrate and with that polyuria. With the polyuria there is excess loss of fluid and electrolytes. Fluid loss through the urine and high blood glucose draws water from the cells resulting in dehydration.

3. When tissue damage occurs, the damaged mast cells and platelets release histamine, serotonin, prostaglandins, leukotrienes and other chemical mediators into the interstitial fluid and blood. Histamines are released immediately from granules in mast cells and exert their effects at once. Leukotrienes and prostaglandins must be synthesized from arachidonic acid in mast cells before release and are responsible for the later effects, prolonging the inflammation. The rapid release of chemical mediators results in local vasodilatation which causes hyperemia. Capillary membrane permeability increases allowing plasma proteins to move into the interstitial space, diluting any toxic materials at the site. The