Thyroid Hormone Physiology Review

Thyroid Hormone - Physiology Review

• Thyroid hormones, T3 and T4, are produced by follicle cells in the thyroid gland.
• T4 is the dominant form, accounting for 90% of secreted thyroid hormone.
• T4 has a longer half-life than T3.
• Initially, T4 is more abundant, but it's converted to T3 as it travels to target cells.
• T3 is the more biologically active form, having a stronger effect on metabolic processes.

Physiological Effects

• Thyroid hormones regulate protein production by influencing transcription.
• They stimulate the body's metabolic rate, speeding up chemical reactions for energy production.

Feedback and Regulation of T3/T4

• TRH (Thyrotropin-releasing hormone) from the hypothalamus triggers TSH (Thyroid-stimulating hormone) release from the anterior pituitary gland.
• TSH stimulates thyroid function, increasing T3 and T4 production, follicle growth, and gland size.
• High levels of T3 and T4 in the bloodstream inhibit TRH and TSH release, maintaining a healthy range of hormone levels. This is a negative feedback loop.

TRH and TSH

• TRH (Thyrotropin-releasing hormone) is secreted by the hypothalamus.
• TSH (Thyroid-stimulating hormone) is produced by the anterior pituitary gland.
• TSH acts directly on the thyroid gland to promote T3 and T4 production.

Hyperthyroidism

• Hyperthyroidism is when the body's tissues are exposed to excessive thyroid hormone.
• Causes of hyperthyroidism include primary problems in the thyroid gland itself or secondary problems due to excessive TSH release from the anterior pituitary.
• Common causes include: genetic predisposition, thyroiditis, toxic nodular or multinodular goiter, thyroid adenomas, or thyroid cancer.

Pathophysiology of Hyperthyroidism

• Primary hyperthyroidism: The thyroid gland is overly active, leading to increased T3 and T4 production, and TSH suppression (negative feedback).
• Secondary hyperthyroidism: An overactive pituitary gland releases excessive TSH, stimulating the thyroid to produce excess T3 and T4.

Clinical Consequences of Hyperthyroidism

• Increased metabolic rate, leading to weight loss, heat intolerance, and increased energy expenditure.
• Increased neuromuscular activity: tremors, restlessness, rapid heartbeat, and anxiety.
• Increased SNS (sympathetic nervous system) activity: rapid heartbeat, increased blood pressure, anxiety, and excessive sweating.
• Goiter: An enlarged thyroid gland, often associated with secondary hyperthyroidism, caused by the consistent stimulation.

Graves' Disease

• An autoimmune disorder where the body mistakenly attacks the thyroid gland, producing antibodies (TSI) mimicking TSH's actions.
• TSI overproduction leads to overstimulation of the thyroid gland, increased T3 and T4 production, and suppressed TSH levels.
• Clinical consequences include symptoms of hyperthyroidism, such as: Increased metabolic rate, tremors, rapid heartbeat, and anxiety, along with specific symptoms like goiter or vision issues (exophthalmos and ocular tissue issues).

Hypothyroidism

• Hypothyroidism occurs when the thyroid gland isn't functioning properly, resulting in low levels of T3 and T4.
• Causes include loss of thyroid tissue, iodine deficiency, congenital lack of thyroid tissue, Hashimoto's thyroiditis and secondary hypothyroidism.

Primary Hypothyroidism

• Problems originating in the thyroid gland itself, such as loss of thyroid tissue, iodine deficiency, or congenital lack of thyroid tissue.

Hashimoto's Thyroiditis

• An autoimmune condition where the immune system attacks the thyroid gland, decreasing hormone production.

Secondary Hypothyroidism

• Problems within the pituitary gland, such as pituitary tumor, stroke to hypothalamus or pituitary, or postpartum pituitary necrosis.

Clinical Consequences of Hypothyroidism

• Decreased metabolic rate, leading to weight gain, fatigue, cold intolerance, and slowness of movement.
• Decreased neuromuscular activity: generalized fatigue, decreased reflexes and slowness of movements.
• Decreased SNS activity: reduced heart rate, blood pressure, along with potential depression.
• Myxedema: swelling due to water retention in tissues.

Cortisol - Physiology Review

• Cortisol, the primary glucocorticoid, regulates glucose metabolism and has anti-inflammatory effects, crucial for survival during stress.
• Cortisol is secreted by the adrenal cortex, located near the kidneys.

Physiological Effects of Cortisol

• Cortisol regulates glucose metabolism.
• It elevates blood glucose levels through decreasing glucose uptake in tissues and increasing gluconeogenesis.
• It promotes protein breakdown in muscles and collagen; this provides amino acids for gluconeogenesis.
• It stimulates fat breakdown and promotes fat deposition in the face and trunk.
• It suppresses the immune response.

Feedback and Regulation of Cortisol

• The hypothalamus releases CRH (corticotropin-releasing hormone).
• CRH stimulates ACTH (adrenocorticotropic hormone) release from the anterior pituitary gland.
• ACTH stimulates cortisol production by the adrenal cortex.
• High cortisol levels inhibit CRH and ACTH release (negative feedback).

Hypercortisolism

• Excess cortisol in the body, caused by primary adrenal cortex overactivity (Cushing syndrome) or secondary pituitary gland overactivity (Cushing disease).
• Causes can also include ectopic production from other tumors.
• Etiologies: includes adrenal adenomas and carcinomas, non-adrenal tumors, and cortisol-like medications like hydrocortisone and prednisone.

Pathophysiology of Hypercortisolism

• Primary hypercortisolism: The adrenal cortex produces too much cortisol, and ACTH levels are usually suppressed.
• Secondary hypercortisolism: The pituitary gland excessively releases ACTH encouraging the adrenal cortex to produce excessive cortisol.

Clinical Consequences of Hypercortisolism

• Hyperglycemia, weight gain (especially in the face and trunk), thinning extremities, muscle weakness, skin changes, and osteoporosis, blood pressure increase, and increased susceptibility to infections.
• Increased SNS (sympathetic nervous system) activity leading to symptoms like increased heart rate, blood pressure, and anxiety.

Hypocortisolism (Addison Disease)

• Insufficient cortisol production by the adrenal cortex.
• This can be due to adrenal cortex atrophy, destruction (e.g., autoimmune destruction), or issues with the anterior pituitary.
• Pathophysiology differs in primary and secondary hypocortisolism
• Primary hypocortisolism is adrenal-based: decreased cortisol production due to adrenal cortex damage.
• Secondary hypocortisolism is pituitary-based: insufficient ACTH (anterior pituitary hormone) leading to reduced cortisol production.

Clinical Consequences of Hypocortisolism

• Hypoglycemia, decreased SNS activity (low blood pressure, reduced heart rate), and dehydration.
• Also includes impaired functioning of the kidneys in relation to sodium and water retention and processing.
• Hyperpigmentation, sometimes in creases and areas exposed to the sun or high friction.

This quiz reviews the physiology of thyroid hormones, focusing on the roles of T3 and T4 in the body. Learn about their production, physiological effects, and the feedback regulation mechanism that maintains hormonal balance. Ideal for students looking to understand endocrine system functions.