Hyperthyroidism: Nursing process (ADPIE)

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Suzanne Benoit is a 45-year-old female client who presents to her primary care clinic with a report of insomnia, anxiety, and unintentional weight loss. She states she hasn’t felt like herself for the past few weeks, and reports occasional episodes of heart palpitations and hand tremors that she initially thought might be manifestations of panic attacks. After an examination by her physician and a review of laboratory results, Suzanne is diagnosed with primary hyperthyroidism.  

Hyperthyroidism is a condition in which the thyroid gland produces and releases excess thyroid hormones. Now, hormonal production is normally regulated by the hypothalamus, which is located at the base of the brain. When the hypothalamus detects low blood levels of thyroid hormones, it releases thyrotropin-releasing hormone, or TRH for short. TRH then stimulates the anterior pituitary gland to release thyroid-stimulating hormone, or TSH, which in turn stimulates hormone production by the thyroid gland, a butterfly-shaped gland located in the neck. The thyroid gland is made up of thousands of thyroid follicles, which release two iodine-containing thyroid hormones, triiodothyronine or T3, and thyroxine or T4, into the bloodstream. These hormones then get picked up by nearly every cell in the body. Once inside the cell, T­4 is mostly converted into T3, which is the active form, and it can exert its effect. T3 speeds up the cell’s basal metabolic rate by stimulating protein synthesis, and burning up more energy in the form of sugars and fats. Other effects of thyroid hormones include increasing the cardiac output, stimulating bone resorption, as well as heat production and activating the sympathetic nervous system, which is responsible for our ‘fight-or-flight’ response.

Now, hyperthyroidism occurs when there’s too much thyroid hormone, leading to a hypermetabolic state, in which cellular reactions are happening faster than normal. Hyperthyroidism is usually either primary or secondary. In primary hyperthyroidism, the problem is an overactive thyroid gland. Okay, the most common primary cause is Graves disease, an autoimmune disorder where autoantibodies bind to and activate TSH receptors, which ultimately stimulates the thyroid gland to produce excess thyroid hormones. Another primary cause is toxic nodular goiter, where one or more follicles autonomously start generating lots of thyroid hormone. Next is a hyperfunctioning thyroid adenoma, where the follicular cells start growing uncontrollably, forming a benign tumor that produces excess thyroid hormones. In addition, anytime the thyroid gets damaged or inflamed, like in thyroiditis, there can be a large release of thyroid hormones. On the other hand, in secondary hyperthyroidism, the underlying problem is in the anterior pituitary gland that’s releasing too much TSH. One cause of secondary hyperthyroidism is a TSH-secreting tumor in the anterior pituitary gland, which stimulates a healthy thyroid to produce too much thyroid hormone. Finally, there’s exogenous hyperthyroidism, which is caused by the excessive intake of exogenous thyroid hormones, like the medication levothyroxine