Running Head: Anorexia Nervosa anorexia Nervosa

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ANOREXIA NERVOSA

Anorexia Nervosa

Anorexia Nervosa

Introduction

Anorexia nervosa is a serious progressive disorder associated with high chronicity and a mortality rate of 5-10%. Herzog DB, Dorer DJ, Keel PK, Selwyn SE, Ekeblad ER, Flores AT et al. Recovery, and relapse in anorexia, and bulimia nervosa: a 7.5-year follow-up study. The factors that determine the course and outcome of anorexia nervosa are unknown, and management requires a long-term perspective. Usually, the reason for hospitalization is a combination of a life-threatening complication such as electrolyte imbalance, severe weight loss, bradycardia, hypothermia, hypoproteinemia, edema and dehydration, and the need to reverse the course of the disease. However, patients characteristically maintain poor insight and refuse to seek help. Even for those who do, the initial response to treatment may not be long- lasting. Thirty to fifty percent of patients relapse, and 75% of relapses occur in the first year after discharge. (Groot 1998)

Pathophysiology

The bronchi and bronchioles are very responsive to irritants, leading to contraction of the smooth muscle (bronchoconstriction), inflammation with edema (swelling), and increased secretion of thick mucous. These changes can block the airways, totally or partially, and interfere with the air flow and oxygen supply. In extrinsic asthma, the allergic reaction causes release of chemical mediators like histamine that causes the bronchospasms, edema and increased mucous secretion. This reaction also stimulates the vagus nerve, causing a reflex bronchoconstriction. The second stage of the allergic reaction occurs a few hours later. During this stage, the increased leukocytes (white blood cells) release additional chemical mediators that cause tissue damage. Left untreated, frequented and prolonged attacks can lead to chronic asthma later in life. The mechanisms behind intrinsic attacks are not fully understood.

Partial obstruction of the smaller airways results in air trapping with hyperinflation of the lungs. Air passes into the areas distal to the obstruction (alveoli), but are only partially exhaled. Since exhalation is a passive process, less force is available to move air out, and forced expiration often collapses the bronchial wall, creating a further barrier to exhalation. The residual volume (air left in the lungs after exhalation) increases and as a result. It becomes harder to inhale fresh air or to cough to effectively remove the mucous. To better understand this air trapping, try this experiment. Take several breaths and exhale only partially before inhaling again. After a few breaths you will see how hard it is to inhale, or to cough. This is what an asthma attack feels like.

Total obstruction of the airway results when mucous plugs completely block the airflow in an already narrowed passage. This leads to atelectasis (collapse of the alveoli). The air left in the alveoli diffuses out and is not replaced. This could lead to collapse of the lung. Both a partial and total obstruction will lead to hypoxia. Oxygen levels are further depleted by the increased demand by the muscles of respiration and by the stress of the individual fighting for air. Hypoxemia causes vasoconstriction if the pulmonary blood vessels, slowing blood flow and increasing the workload on ...
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