Thyroid Gland Function and Disorders

This assignment delves into the intricate workings of the thyroid gland and its production of vital hormones. It outlines the physiological roles of these hormones and examines the consequences of imbalances, such as hyperthyroidism and hypothyroidism. The document explores the causes, symptoms, and treatment options for these conditions, providing a comprehensive understanding of thyroid function and related disorders.

Human Biology: Endocrine System 1
Human Biology: Endocrine System
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Human Biology: Endocrine System 2
Human Biology: Endocrine system
Thyroid gland and homeostasis:
In the homeostatic condition of the thyroid gland has an inherent relationship with the
hypothalamus and the pituitary gland [1]. In homeostasis, the thyroid gland is essentially
regulated or controlled by the hypothalamus [1, 2, 3]. Several stimuli of the central nervous
system (CNS) acting for the modification of the activity of the endocrine system are primarily
carried out by the changes occurring in the rate of secretion from the pituitary gland [1, 2, 3].
The control of the hypothalamus on the thyroid gland is, however, an often debated aspect and
research is striving to establish a definite and plausible explanation for the hypothalamic control
of the thyroid [1, 2, 3]. It is known that the hypothalamus controls the secretion of trophic
hormones via a vital involvement of the hypothalamo-hypophysial portal vessels of the
hypothalamus [3]. The evidence of the extent to which the thyroid gland is under the control of
the hypothalamus is a constantly researched topic [1, 2, 3]. Several studies have indicated two
salient observations: a) There is a significant reduction in the thyroid activity following an
interruption in the vascular relationship between the hypothalamus and the anterior pituitary b)
Electrolytic lesions of the hypothalamus cause a marked decrease in thyroid activity in animal
models [3].
Thyroid hormone
The hormonal secretion of the thyroid gland is an important contributor in the rate of metabolism
and the cardiovascular functionality [1, 2, 3]. In pathological conditions, the thyroid hormone is
aberrant and displays anomalous values [1, 2, 3]. These effects of thyroid hormone are directly
ascribed to the functions of the thyroid hormones on peripheral organs including the heart [1, 2,
3]. Tissues of the skeletal muscle etc are metabolically active and the effect of the thyroid

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hormone is profound in these tissues [1, 2, 3]. There are several underlying cellular mechanisms
that define the influence of the thyroid hormone on metabolic functions [1, 2, 3]. In conditions of
hyperthyroidism and hypothyroidism, there is a marked influence on several metabolic functions
and tissue functions [1, 2, 3]. Recent research has indicated that the thyroid hormone regulates
the molecular processes in metabolically active tissues via the brain which is an important target
tissue of the thyroid hormone [1, 2, 3].
In the diagnosis of anomalies in the thyroid gland, thyroid hormone levels are tested [4, 5]. The
levels of free thyroxin (T4) and serum triiodothyronine (T3) are measured in order to diagnose
abnormalities [4, 5]. The normal levels are T4 – 0.7 – 1.9 μg/dl i.e. 4.6 – 12 and T3 – 80-180
ng/dl respectively [4, 5]. In Helen’s case, the level of T4 is 15.2 μg/ dl and the level of T3 is
194.6 ng/ dl, which is significantly higher than the normal serum levels of the hormones [4, 5].
Helen, presumably, has hyperthyroidism [4, 5]. However, a proper diagnosis has to be carried
out in order to ascertain that [4, 5].
Thyroid hormones are essential for the normal growth of individuals [6]. It is also an essential
contributor in the regulation of metabolism in adult humans [5, 6]. The status of the thyroid
hormone in the body largely dictates the metabolism level, energy usage, and body weight
regulation in humans [5, 6]. Excess presence of thyroid hormones in the body leads to the
condition of hyperthyroidism [5, 6]. In hyperthyroidism, the individual experiences elevated
metabolism rates, excessive loss of weight, increased energy expenditure etc [5, 6]. In certain
cases, the occurrence of increase in gluconeogenesis and lipolysis is also likely [5, 6]. On the
contrary, hypothyroidism is a condition of lowered levels of thyroid hormones leading to
remarkable reduction in metabolism, fatigue, increase in weight, loss of activity, decrease in

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expenditure of energy etc [5, 6]. Conversely to hyperthyroidism, there is a reduction in the
overall rate of lipolysis and gluconeogenesis [5, 6].
Relationship between the hypothalamus, pituitary gland and the thyroid
hormones
There is an inherent connection between the hypothalamus and the pituitary glands in the
functionality of the thyroid hormones [6]. Hypothalamus is a primary organ in the neurological
system and is responsible for the regulation of endocrine organs such as the pituitary [6]. In the
neuroendocrine system, the hypothalamus, pituitary gland, and the thyroid gland form an axis
which is responsible for the regulation of metabolic functions [6].
Hypothalamus-pituitary-thyroid axis
The hypothalamus-pituitary-thyroid (HPT) axis is crucial for the maintenance of homeostatic and
normal physiological levels of thyroid hormones which are indispensible in most biological
processes in the body [7, 8]. A few of the essential biological functions include development of
brain, regulation of activities of the brain, food ingestion, functioning of the liver, metabolism,
and expenditure of energy in adults [7, 8]. The HPT axis controls the release of the thyroid
hormones T3 and T4. The thyrotropin releasing hormone (TRH) is responsible for the release of
thyroid stimulating hormone (TSH) [7, 8]. HPT axis is critical for the regulation of the basal
rates of metabolism and thus, the overall expenditure of energy [7, 8]. Thyrotropin-release
hormone (TRH) plays a vital role in the central regulation of the HPT axis [7, 8]. TRH is
responsible for synthesising, releasing, and the biological activity of TSH [7, 8]. The

Human Biology: Endocrine System 5
hyperphysiotropic TRH neurons present in the hypothalamic paraventricular nucleus (PVN) are
responsible for the central regulation of the HPT axis [7, 8].
Physiology
The HPT axis is a feedback system and is composed of multiple loops [10]. The control of the
feedback loop lies with the thyrotropic hormones [9]. Any up-regulation or decrease in the HPT
axis or hormonal levels is directly fed back to the system for review of the HPT functionality
[10]. In pathologies, there is an anomalous functionality in the HPT feedback system [10]. The
TSH gene and anomalies resulting after the translation of the gene, leading to the production of
the protein may result in hyperthyroidism and hypothyroidism [10].
Hyperthyroidism and HPT axis
It is established in research that the HPT axis is primarily responsible for the activities of the
thyroid hormone in adults [9]. Typically, the metabolic rate and the heart rate are the parameters
that are affected most importantly [9]. In conditions of homeostasis, the metabolic rate is
normally enhanced by the thyroid hormone [9]. The thyroid hormones T3 and T4 are critical
contributors to the growth of the individual [9]. In hyperthyroid individuals, the rate of
metabolism is increased abnormally [9]. The most important occurrence in hyperthyroidism is
tachycardia which is the occurrence of abnormally rapid heart rate [9]. The most common
symptoms associated with hyperthyroidism are fatigue, tremors, sleeplessness or disturbed
sleeping patterns, polydipsia, perspiration, loss of weight, anxiety etc [9]. Generally, in the
diagnosis of diseases related to thyroid level irregularities, thyroid stimulating hormone (TSH)
and free thyroxine (FT4) are the key components of thyroid function tests [9].
The HPT axis has a direct association with these two vital components of diagnostic thyroid tests
[9]. The functionality of the thyroid hormones is affected along with de-alignment of the HPT

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axis in hyperthyroid individuals [9]. Helen, in this case, displays several of the symptoms of
hyperthyroidism [9]. She has lost weight significantly without the loss of energy expenditure as
she is able to perform her regular exercise of walking [9]. There is, additionally, an increase in
her energy levels and she feels inclined to taking up running [9]. Such an observable increase in
energy levels along with increase in temperature is a clear sign of hyperthyroidism [9].
Hypothyroidism
Hypothyroidism is the converse of hyperthyroidism and thus, naturally, the signs and
physiological symptoms of hypothyroidism are quite the opposite of those of hyperthyroidism
[10]. Typically, the absence of thyrotropic function and the functionality of pituitary gland result
in hypothyroidism [10]. In hypothyroidism, there is a notable reduction in the expenditure of
energy along with the development of brachycardia or slowness of heart rate [10]. The individual
additionally experiences fatigue and weight gain [10]. Evidently, there is a stark reduction in the
rate of metabolism in the individual [10].
References
1. Fekete, C. & Lechan, R.M. (2014). Central Regulation of Hypothalamic-Pituitary-Thyroid
Axis under physiological and pathophysiological conditions. Endocr Rev, 35(2), 159-194.

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2. Warner, A. & Mittag, J. (2012). Thyroid hormone and the central control of homeostasis. J
Mol Endocrinol, 49, 29-35
3. Brown-Grant, K. (1960). The hypothalamus and the thyroid gland. Br Med Bull, 16(2), 165-
169
4. Bechtold, D.A. & Loudon, A.S.I. (2007). Hypothalamic thyroid hormones: mediators of
seasonal physiology. Endocrinology, 148, 3605–3607.
5. Mullur, R., Liu, Y., & Brent, G.A. (2014). Thyroid hormone regulation of metabolism.
Physiol Rev., 94(2), 355-382
6. Reichlin S. (1989). TRH: historical aspects. Ann NY Acad Sci, 553, 1–6
7. Boler, J., Enzmann, F., Folkers, K., Bowers, C.Y., & Schally, A.V. (1969). The identity of
chemical and hormonal properties of the thyrotropin releasing hormone and pyroglutamyl-
histidyl-proline amide. Biochem Biophys Res Commun, 37, 705–710
8. Lechan, R.M., Hollenberg, A., & Fekete, C. (2009). Hypothalamic-pituitary-thyroid axis:
organization, neural/endocrine control of TRH. In: Squire LR, editor. , ed. Encyclopedia of
Neuroscience. Oxford, UK: Academic Press, 75–87
9. Leo, S.D., Lee, S.Y., & Braverman, L.E. (2016). Hyperthyroidism. Lancet, 388(10047), 906-918
10. Chakera, A.J., Pearce, S.H.S., & Vaidya, B. (2012). Treatment of primary hypothyroidism: current
approaches and future possibilities. Drug Des Devel Ther, 6, 1-11
11. Beck-Peccoz, P. & Mariotti, S. (2016). Physiology of the hypothalamic-pituitary-thyroid axis.
Thyroid Disease Manager.