Thyroiditis, from the word, means inflammation of the thyroid gland, which, therefore, points to a previous insult the thyroid tissue which triggers an inflammatory process which ends up destroying the thyroid parenchyma cells. The damaged cells release the synthesized TH into the bloodstream thereby causing hyperthyroidism. Often, this condition is transient, and remission occurs after the eradication of the triggering agent. Thyroiditis seen in postpartum women is linked to lymphocytic infiltration of the thyroid gland, initiation of an autoimmune reaction and destruction to the thyroid cells. With the unchecked destruction of the thyroid cells, a hypothyroid state develops. A compensatory regeneration of the thyroid parenchyma leads to a remission in up to 80% of the individuals CITATION Sha11 \l 1033 (Sharma, Aronow, Patel, Gandhi, & Desai, 2011).
Another form of thyroiditis is the painful subacute thyroiditis. This condition is associated with viral infection and is the primary cause of thyroid pain. The main symptoms of this disease are thyroid pain and neck swelling. In some patients, both symptoms may present. 50% of the affected individuals present with signs and symptoms of thyrotoxicosis which progress to hypothyroidism after several weeks. Remission occurs in almost all patients. The main laboratory findings in these patients are C-reactive protein and erythrocyte sedimentation rate that are both markedly elevated CITATION Sha11 \l 1033 (Sharma, Aronow, Patel, Gandhi, & Desai, 2011).
Clinical Presentation of Hyperthyroidism
Thyroid hormone is catabolic in nature. Therefore, increased production of this hormone into the bloodstream puts the body at a stressed and hypermetabolic state. Various organ systems are affected by this abnormality and therefore the presenting symptoms point towards the affected system. Some of the symptoms that usually present in hyperthyroidism or thyrotoxicosis are palpitations, anxiety, abnormal circadian rhythm, polydipsia, tremors, weight loss, and fatigue.
Effects on various organ systems
Cardiovascular system
Thyroid hormone presents with both inotropic and chronotropic effects. These effects can be caused by either direct action of the hormone, or secondary to the increased production of catecholamines. The thyroid hormones also increase the number and sensitivity of beta-adrenergic receptors, thereby, propagating its adverse effects on the cardiovascular system. Moreover, TH leads to a proliferation of heavy chains of the alpha-myosin subtype in the cardiac cells, enhancing cardiac muscle contractility CITATION Bar10 \l 1033 (Barett, Barman, Boitano, & Brooks, 2010).
Nervous System
Increased TH and the resultant production of catecholamines lead to brain hyperactivity and hypersensitivity of neurons. This effect presents with shortened reaction time of stretch reflexes, anxiety, tremors and increased alertness, restlessness and irritability. The overall consumption of glucose by the brain matter remains unaffected. Thyrotoxicosis also affects the reticular activating system, either through its direct action of the TH or via catecholamines. The resultant effect is altered circadian rhythm, whereby, the sleep is affected CITATION Guy \l 1033 (Hall, 2010).
Endocrine system
The main endocrine gland affected is the adrenal gland. High TH levels lead to overstimulation of the adrenals and, therefore, increased activity of catecholamines. Epinephrine and norepinephrine have a direct effect on the various body systems since they are hypermetabolic in nature. However, in hyperthyroidism, the levels of the catecholamines are usually normal. Therefore, the resultant hypermetabolic effects have been attributed to a suspected synergistic action of the TH and catecholamines. TH has been shown to increase the number and the sensitivity of beta-adrenergic receptors, thus, making the body more responsive to catecholamines. Beta-blockers like propranolol are administered to patients with thyrotoxicosis CITATION Leo16 \l 1033 (Leo, Lee, & Braverman, 2016).
Musculoskeletal System
Hyperthyroidism leads to thyrotoxic myopathy that presents with muscle weakness. The cause of the muscle weakness has been attributed to the increased protein breakdown in muscles due to the catabolic effect of TH CITATION Bar10 \l 1033 (Barett, Barman, Boitano, & Brooks, 2010).
Digestive System
TH is calorigenic in nature. This hormone leads to increased absorption of carbohydrates from the gastrointestinal tract and also gluconeogenesis through glycogenolysis, lipolysis and muscle breakdown. Hyperthyroidism, therefore, leads to increased postprandial glucose levels which also drop rapidly CITATION Guy \l 1033 (Hall, 2010).
Diagnosis
The initial test on a patient suspected to have hyperthyroidism is TSH levels assays. Hyperthyroidism is diagnosed if the TSH are undetectable. In Graves disease, thyroid stimulating immunoglobulins are detected.
Treatment Modalities
Treatment of hyperthyroidism depends on the determination of the etiology and severity of the condition. Other factors considered in the choice of the mode of therapy are the age, comorbidities, goiter size and the preference of the patient. Management of hyperthyroidism is directed towards the reduction of the hypermetabolic state, side effects, and also preventing the conversion to a hypothyroid state. Below is a review of the treatment modalities CITATION Sha11 \l 1033 (Sharma, Aronow, Patel, Gandhi, & Desai, 2011).
Beta Blockers
These drugs help by giving quick relief to symptoms caused by catecholamines. These include nervousness, palpitations, heat intolerance, sweating, and tremors. Propranolol, a nonselective beta-blocker, is most commonly used due to its action on hypermetabolism. Calcium channel blockers like Diltiazem can be administered patients who are intolerant to beta-blockers, in the management of palpitations CITATION REI05 \l 1033 (REID & STEPHEN, 2005).
Iodides
These prevent the peripheral activation of T4 to T3 and also inhibit the release of TH. They are used as adjuncts in patients who are unresponsive to beta-blockers, and to reduce vascularity in preparation for thyroid surgery. Prolonged usage of iodides may cause a paradoxical surge in TH. Therefore, iodides are not used routinely. Organic iodides are preferred to inorganic iodides CITATION REI05 \l 1033 (REID & STEPHEN, 2005).
Antithyroid Drugs
These drugs suppress the production of TH by interfering with iodine organification. The primary agents used are Propylthiouracil and Methimazole. Remission occurs in up to 60% of the patients on this treatment for two years. However, a relapse can also occur on up to 50% of the individuals who had initially responded. Methimazole is used in non-pregnant individuals while propylthiouracil is used in pregnancy due to its low incidence of teratogenicity CITATION Sha11 \l 1033 (Sharma, Aronow, Patel, Gandhi, & Desai, 2011).
Radioactive Iodine
This method is the treatment of choice in patients with graves disease or nodular goiter. This preference is attributed to its cheapness, ease of administration, effectiveness and safety profile. Women in the fertile age are usually not administered this drug due to the suspicion of teratogenicity. High doses are administered in toxic adenomas and toxic nodular goiter due to their radio-resistance CITATION Leo16 \l 1033 (Leo, Lee, & Braverman, 2016).
Surgery
Radioactive iodine has replaced this modality and, therefore, reduced its usage considerably. Subtotal thyroidectomy is the surgical therapy of choice since it reduces the chance of conversion to hypothyroid state. Total thyroidectomy carries a significant risk of injury to the recurrent laryngeal nerve and hyperparathyroidism. It is, therefore, reserved for patients with large goiters and severe disease CITATION Sha11 \l 1033 (Sharma, Aronow, Patel, Gandhi, & Desai, 2011).
New Possibilities
Some of the new modalities under investigation include thyroid artery embolization, plasmapheresis, Endoscopic subtotal thyroidectomy, and percutaneous injection of ethanol into toxic thyroid nodules. Autotransplantation of cryopreserved thyroid tissue is another modality under investigation CITATION Leo16 \l 1033 (Leo, Lee, & Braverman, 2016).
Prognosis
The prognosis of a hyperthyroid patient used is dependent on the modality of treatment administered. Some complications are irreversible, thereby, increasing the morbidity and mortality rate of the affected patient. There is increased the risk of thromboembolism, obesity, and atherosclerosis. Therefore, continuous screening is adv...
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