Primary Overt Hypothyroidism

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The main treatment for hypothyroidism is synthetic thyroid hormone in pill form to replace what’s missing. Depending on the reason for the slow thyroid, adding more iodine to the diet and generally eating a healthy diet can help.

Physical assessment reveals intermittent heart palpitations with strong carotid and radial pulses, brisk deep tendon reflexes, 1+ non-pitting edema of bilateral ankles, hair thinning, onycholysis, orbital lid lag and an enlarged neck with positive audible bruit. Mrs. J.P. denies pain upon palpation of neck as slight thyroid enlargement is noted. Orders to perform complete blood count (CBC), complete metabolic panel (CMP), thyroid stimulating hormone (TSH), thyroxine index, free (T4), triiodothyroine (T3), and pregnancy test result in abnormal values including:

Thyrotoxicosis is a clinical condition caused by excess circulating serum thyroxine (T4), triiodothyronine (T3), or both with suppression of thyroid-stimulating hormone (TSH). A negative feedback loop involving the hypothalamus, pituitary, and thyroid gland regulates the production and release of thyroid hormones. (Fig. 1) The hypothalamus releases thyroid-releasing hormone (TRH), stimulating the pituitary gland to release TSH, in turn stimulating the thyroid gland to release T4 and T3. Enhanced production of T4 and T3

Taking L-thyroxine is the main treatment mechanism; therefore, medication compliance is the one of the most important part in education. The clinical effect of L-thyroxine may include normalizing abnormalities associated with hypothyroidism. Optimal treatment of hypothyroidism may lead to improvement of various symptoms. In neuropsychological aspect, patients may show improved motor skills, myopathy and depression. With treatment, patient’s overall energy level may enhance constipation symptoms may improve and weight problem may lessen if thyroid balance was a main contributor. It has been shown that treatment of hypothyroidism would also improve lipid profiles in patients (Roe, 2015).

Primary hypothyroidism is “caused by the inability of the thyroid gland to make T3 and T4” (Hurd, 2006). It is the inability to make and retain sufficient amounts of T3 and T4, the common thyroid hormones. Secretions are controlled by a negative feedback mechanism, which controls the thyroid-stimulating hormone (TSH) from the pituitary, which then stimulates T3 and T4 secretions (Wiersinga, 2014). Normal functions of the thyroid hormones are to maintain the basal metabolic rate, stimulate oxygen consumption, absorb carbohydrates from the intestines, regulate lipid metabolism, as well as activating the next phase of the hair growth cycle (Melmed, 2011)(Contreras-Jurado, 2015).

The thyroid which is a butterfly shaped gland situated between your voice box and collarbones and no bigger than your thumb, influences practically every process in your body. It produces hormones that regulate metabolism and energy. The rate in which the brain, heart, liver, and other organs function is influenced by the thyroid gland. Hypothyroidism as characterized by the medical dictionary; is deficient activity of the thyroid gland. Also, called underactive thyroid, hypothyroidism is an endocrine disorder where the thyroid gland does not produce enough thyroid hormones to address the body’s need.

The differential diagnosis for Mary is hypothyroidism as her TSH was 6.5 mIU/l, along with antithyroid antibodies: 1:1,800. The pathophysiology entails having the thyroid hormone imbalance which results in the signs and symptoms of fatigue, cold intolerance, a crenulated tongue, headaches, and periorbital swelling. According to Garber et al. (2012), primary hypothyroidism differential diagnosis is made by the TSH, along with the T4 levels which is addressed by ensuring euthyroid state. There is a need to ensure that there is a balance between hyperthyroidism and hypothyroidism. This is called the euthyroid state where the TSH that should be between TSH 0.35 to 5.5 mIU per L. Levothyroxine is the medication that is used to replenish a hypothyroidism

The thyroid gland is an organ located in the neck on either side of the trachea. It secrets thyroxine, triiodothyronine, and calcitonin. It releases hormones that control your metabolism, breathing, heart rate, nervous system, weight, body temperature, and many other functions in the body. Hyperthyroidism is a condition in which the thyroid gland is overactive and the body’s processes speed up and you may experience anxiety, nervousness, hand tremor, rapid heartbeat, excessive sweating, weight loss, and sleep problems.

During periods of stable biochemical and clinical findings, control of serum TSH once a year is appropriate. Interpretation of TSH monitoring can provide challenges to FNP, usually resulting from tests showing a persistently elevated TSH with normal or raised FT4 levels. This situation usually arises from poor compliance with medication and patients taking their levothyroxine only in the few days in the run-up to their scheduled blood test. Routine follow-up is thus important and having a structured follow up system to ensure compliance may be useful (Roe, 2015).

Goitre which is related with hypothyroidism or hyperthyroidism may be present with symptoms of the primary disorder.

The hormones regulate your metabolism, including the production of energy, hormones, tissue growth, elimination of waste products, and the distribution of nutrients in the blood. “Hyperthyroidism can affect all of your body functions.  It causes the body’s normal rate of functioning to speed up.  This can result in physical, behavioral, and emotional changes.  Untreated hyperthyroidism can lead to serious medical problems.  Hyperthyroidism cannot be prevented, but it is generally treatable and rarely fatal.” (Colonial Healthcare, 2018, para. 2). For nursing implication there isn’t anything to be aware of considering it is only known to be caused from hereditary factors. “Thyroid storm is most commonly associated with underlying Graves' disease, although has been reported with autonomous thyroid nodular disease.” (Carroll, 2014, para. 1) “The interference of thyroid hormones in this system and in cardiovascular events has been studied in recent years. However, the mechanisms involved in vascular, purinergic, and oxidative changes in thyroid disorders are not completely understood.” (Jucimara Baldissarelli, 2018, p.

The thyroid gland is prone to several distinct problems, some of which are extremely common. These problems can be broken down into those concerning the production of hormone (too much, or too little), those due to increased growth of the thyroid, causing compression of important neck structures or simply appearing as a mass in the neck[1]. Subclinical hypothyroidism is diagnosed when person has: No symptoms or mild symptoms of hypothyroidism, a mildly high thyroid-stimulating hormone (TSH) level, and a normal thyroxine (T4) level[2]. Subclinical hyperthyroidism is defined by low or undetectable serum thyroid-stimulating hormone levels, with normal free thyroxine and total or free triiodothyronine (T3) levels[3]. People with subclinical hyperthyroidism may

The diagnosis of primary hypothyroidism is made by measurement of increased levels of TSH (thyroid stimulating hormone) and decreased levels of TH (thyroid hormone including total T, and both total and free T4)(McCance & Huether, 2014, p. 729). Thyroid disorders are detected by testing TSH, T4, and T3 levels in the blood. A decrease of thyroid hormone causes the pituitary gland to produce more TSH, which increase levels in the bloodstream in an attempt to encourage thyroid hormone production. This rise

Thyroid hormones (L-thyroxine). Hypothyroidism is classically treated by oral replacement with synthetic L-thyroxine (levothyroxine). Normalization of TSH levels using levothyroxine therapy can ameliorate the effects of comorbidities in older adults (Hennessey, 2015). It has been shown then there is no added benefit in using combination therapy of levothyroxine and liothyronine (another synthetic thyroid hormone supplement) (Kraut, 2015). L-thyroxine (levothyroxine) monotherapy has become the mainstay of treating hypothyroidism and allows more desirable therapy (Jonklaas, 2014). Patients whose serum TSH levels exceed 10 mIU/L are at increased risk for heart failure and cardiovascular mortality, and should be considered for treatment with L-thyroxine (Garber, 2012). L-thyroxine is peripherally converted to free-triiodothyronine (FT3), the active form of thyroid hormone. It has a half-life of 6 days and is typically administered as a once-daily dose of 1.6 µg/kg