Functions of the Thyroid Gland

Why This Matters

The thyroid gland is your body's metabolic thermostat—a small, butterfly-shaped structure that punches way above its weight in physiological importance. In Anatomy and Physiology II, you're being tested on how endocrine feedback loops work, how hormones interact with target tissues, and what happens when these systems fail. The thyroid is the perfect case study because its hormones touch nearly every organ system: cardiovascular, nervous, skeletal, and metabolic pathways all depend on proper thyroid function.

Understanding thyroid functions means grasping negative feedback mechanisms, hormone synthesis pathways, and the clinical consequences of hyper- and hypofunction. When you see exam questions about basal metabolic rate, thermogenesis, or calcium homeostasis, the thyroid is often the answer. Don't just memorize that T3 and T4 exist—know why they matter, how they're regulated, and what breaks when levels are abnormal. That's the difference between recognition and real understanding.

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Hormone Production and Regulation

The thyroid produces two main categories of hormones with distinct functions. Understanding their synthesis and regulation is fundamental to grasping thyroid physiology—and it's a favorite topic for exam questions on endocrine feedback loops.

Thyroxine (T4) and Triiodothyronine (T3) Synthesis

• T4 is the primary hormone produced (about 90%)—it serves as a prohormone that converts to the more active T3 in peripheral tissues
• Iodine and tyrosine are the essential building blocks; iodine deficiency directly impairs hormone synthesis, leading to goiter formation
• TSH from the anterior pituitary regulates production via a classic negative feedback loop—high T3/T4 suppresses TSH release

Calcitonin Production

• Calcitonin lowers blood calcium by inhibiting osteoclast activity, the cells responsible for bone resorption
• Parafollicular cells (C cells) produce calcitonin—distinct from the follicular cells that make T3/T4
• Works antagonistically with PTH from the parathyroid glands to maintain calcium homeostasis within the narrow physiological range

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Metabolic Regulation

Thyroid hormones are the master regulators of metabolism. They increase oxygen consumption and ATP production at the cellular level, which cascades into effects on every macronutrient pathway.

Basal Metabolic Rate Control

• Thyroid hormones increase BMR by upregulating $Na^+/K^+$-ATPase activity in cells, consuming more ATP and generating heat
• Hyperthyroidism causes elevated BMR—patients experience weight loss despite increased appetite; hypothyroidism causes the opposite
• Direct clinical application: TSH and T4 levels are first-line tests when patients present with unexplained weight changes

Carbohydrate Metabolism

• Increases intestinal glucose absorption and promotes glycogenolysis in the liver, raising blood glucose availability
• Enhances insulin sensitivity in peripheral tissues, facilitating glucose uptake into cells
• Thyroid dysfunction mimics diabetes—hypothyroidism can cause insulin resistance; hyperthyroidism can unmask latent diabetes

Fat Metabolism

• Stimulates lipolysis (breakdown of triglycerides into fatty acids and glycerol) for energy production
• Regulates cholesterol levels by increasing LDL receptor expression on hepatocytes, promoting cholesterol clearance
• Hypothyroidism causes hypercholesterolemia—this is why lipid panels are often abnormal in untreated thyroid disease

Protein Synthesis

• Promotes amino acid uptake into cells and stimulates ribosomal protein synthesis for tissue growth and repair
• Essential for muscle maintenance—thyroid hormones support positive nitrogen balance in healthy individuals
• Imbalances cause opposite effects: hyperthyroidism leads to muscle wasting (catabolism exceeds synthesis); hypothyroidism impairs repair

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Cardiovascular and Thermoregulatory Effects

Thyroid hormones directly affect the heart and blood vessels while also controlling heat production. These effects are mediated by increased expression of beta-adrenergic receptors and enhanced catecholamine sensitivity.

Heart Rate and Blood Pressure Regulation

• Increases cardiac contractility and heart rate by upregulating beta-1 adrenergic receptors on cardiomyocytes
• Affects vascular resistance—T3 causes vasodilation in peripheral vessels, which can lower diastolic pressure
• Clinical red flag: new-onset atrial fibrillation in older adults should prompt thyroid function testing

Body Temperature Control

• Drives thermogenesis through increased cellular oxygen consumption and metabolic heat production
• Cold intolerance signals hypothyroidism—patients lack sufficient hormone to generate adequate heat
• Heat intolerance and sweating characterize hyperthyroidism—excess metabolic activity produces too much heat

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Growth, Development, and Neural Function

Thyroid hormones are critical during developmental windows and continue supporting neural function throughout life. Deficiency during critical periods causes irreversible damage.

Growth and Skeletal Development

• Essential for linear growth in children by synergizing with growth hormone to promote epiphyseal plate activity
• Promotes skeletal maturation through effects on osteoblast activity and bone matrix formation
• Congenital hypothyroidism (cretinism) causes growth stunting and intellectual disability if untreated—newborn screening is mandatory

Nervous System Function

• Critical for CNS myelination during fetal and early postnatal development; deficiency causes permanent cognitive deficits
• Regulates neurotransmitter synthesis affecting mood, cognition, and mental processing speed in adults
• Depression and anxiety are common in thyroid disorders—always consider thyroid function in psychiatric presentations

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Quick Reference Table

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Self-Check Questions

1. Which two thyroid functions both depend on increased cellular oxygen consumption, and how do their clinical manifestations differ?

2. Compare and contrast the roles of calcitonin and T3/T4—how do their target tissues, cell origins, and physiological effects differ?

3. A patient presents with weight gain, cold intolerance, and depression. Which specific thyroid functions are impaired, and what would you expect their TSH level to be?

4. Why does congenital hypothyroidism cause permanent intellectual disability while adult-onset hypothyroidism causes reversible cognitive symptoms?

5. If an FRQ asks you to explain how the thyroid maintains metabolic homeostasis, which three macronutrient pathways should you discuss, and what is the common mechanism linking them?