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Human Pathophysiology

Answer 1: The identified risk factors for hypothyroidism are iodine deficiency, inflammation of thyroid gland, certain medical treatments such as medications or radiation therapies, and autoimmune diseases such as Hashimoto’s disease. All of them potentially results in to the Hypothyroidism. The iodine deficiency adversely affect the thyroid metabolism as iodine plays a central role in the production of TH so, lack of iodine will lower the production of TH and can cause hypothyroidism. These risk factors can lead to the diagnosis of the patient as due to the deficiency of iodine there are chances of development of goiter, dry skin, and sudden weight gain. These attributes will help the clinician to understand that the patient might have hypothyroidism and he will conduct the appropriate diagnosis assessment. For this, a blood test will be done, to measure the level of TH. The inflammatory response increases the level of TH in case of hypothyroidism. If the results of blood test reveal the high level of TH then, this would confirm that the patient is dealing with hypothyroidism. However, if it is due to autoimmune diseases such as Hashimoto’s diseases then, it leads to show the titer of thyroglobulin (Tg Ab) as well as thyroid peroxidase (TPO Ab) so, detection of them confirms the autoimmune hypothyroidism (McCance, Huether, Brashers & Rote, 2014).

Answer 2: The link between the risk factors, aetiology, and pathophysiology of hypothyroidism can be understood as the risk factors such as deficiency of iodine and autoimmune disease leads to lower the level of TH and this later on in the course of pathophysiology results into the hypothyroidism. This could be understood better as the aetiology of the cognitive hypothyroidism is because of the thyroid aplasia or dysplasia while the acquired hypothyroidism is the result of an autoimmune disease i.e., Hashimoto’s disease in case of hypothyroidism. When, The pathophysiology of hypothyroidism begins, it has been first characterized by a diminution of the generalized myxedema as well as the basal metabolic rate. This leads to fatigue, weight gain, periorbital edema, and cold intolerance. It may later on turn into more rigorous manifestations and this include myxedema coma and myxedematous heart disease, If they are left untreated then can become Life-threatning. Diagnosis could be done as per the identified risk factors, aetiology, followed by the pathophysiology by the detection of serumTH level and by free T4 levels (McCance, Huether, Brashers & Rote, 2014).

Answer 3: In case of primary hypothyroidism, the potential failure of functional thyroid tissue results into decreasing the generation of TH. Because of the lower level of TH there would be no negative feedback of TH on the pituitary gland and without this feedback the secretion of TSH increases. So, what happens exactly is the increase in secretion of TSH might results into the goiter. Later on as the disease processes, there are chances of causes of shrunken fibrotic thyroid this could be non-functional or be with a little function. On the other hand, if focusing on the hypothyroidism that is caused by an autoimmune disease then, this could also potentially result into the enlargement of the thyroid gland independent of the TSH’s actions. This enlargement of the thyroid gland is often because of the deficiency of iodine. The deficiency of iodine results in the congenital hypothyroidism which might also leads to the intellectual disability. While, in case of secondary hypothyroidism, it occurs when the hypothalamus gland fails to produce sufficient thyrotropin-releasing hormone (TRH) or the pituitary gland fails to produce the sufficient amount of TSH. Therefore, this shows the low level of TH. So, this is how the low level of TH along with the inadequate and low level of TSH or TRH leads to secondary hypothyroidism. The secondary hypothyroidism can also be caused by the pituitary adenomas as it tends to compress the pituitary cells that are present in its surrounding. A decrease in the level of both thyroid hormone as well as adrenergic stimulation often leads to bradycardia, this leads to slower the heart rate of the patient. The decrease in the cerebral blood flow results in the cerebral hypoxia and the dilation & pericardial effusion results into the enlarged heart (McCance, Huether, Brashers & Rote, 2014).

Answer 4: Diagnostic strategies: The diagnosis for the hypothyroidism can be done by diagnosing the TSH and T4. This is so because, the thyroid-stimulating hormone (TSH) evaluation is considered as the most sensitive test in order to diagnose hypothyroidism. In case of primary hypothyroidism, when no feedback inhibition of TH on the pituitary gland is shown. In this case the TSH level in the serum remains elevated, while the level of T4 is low. In case of secondary hypothyroidism, both free T4 as well TSH levels are low. So, if the patient’s serum shows high levels of TSH and low level of T4, Primary hypothyroidism can be confirmed. While, if the patient’s serum shows low levels of both TSH as well as of T4, secondary hypothyroidism can be confirmed (McCance, Huether, Brashers & Rote, 2014).

Treatment modalities: Thyroxine, attuned until the level of TSH comes in the midnormal range. There is a wide range of thyroid hormone synthesis have been available, this include artificial synthesis of T4, T3, amalgamation of two synthetic hormones, and shriveled animal thyroid extract. The synthetic T4 hormone is L-Thyroxine and synthetic T3 hormone is liothyronine out of which L-Thyroxine i.e., the synthetic T4 hormone has been preferred mostly.

Myxedema coma can be treated he by following:

  • T4 given IV
  • Corticosteroids
  • Supportive nursing care as per the needs of the patient
  • Adaptation to the oral T4 when the patient become stable.

References for Hypothyroidism 

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2014). Pathophysiology. The biologic basis for disease in adults and children (6th ed.). Elsevier.

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