Thyroid Gland Function and Dysfunction

Maintaining optimal tissue metabolism by secreting thyroid hormones.

Stimulates oxygen use in most body cells, influencing metabolism.

Influences body mass & mental function through lipid & carbohydrate metabolism.

Severe developmental issues like mental retardation & dwarfism in fetal/neonatal stages.

Not essential for life, but crucial during early development phases, particularly fetal & neonatal periods.

A condition where the thyroid gland doesn't produce enough thyroid hormone, causing slow metabolism, weight gain, and sensitivity to cold.

A condition where the thyroid gland produces too much thyroid hormone, leading to increased metabolism, weight loss, and nervousness.

A hormone produced by the anterior pituitary gland that stimulates the thyroid gland to produce thyroid hormones.

A regulatory mechanism where high levels of thyroid hormones in the blood inhibit further production of TSH and TRH, preventing excessive thyroid hormone levels.

A hormone produced by the thyroid gland that helps regulate calcium levels in the blood.

A large protein produced by thyroid cells that stores thyroid hormones. It's like a big container for thyroid hormones.

An enzyme that helps attach iodine to thyroglobulin, a crucial step in thyroid hormone production.

A gel-like substance within the thyroid gland that stores thyroid hormones bound to thyroglobulin.

Humans can survive without iodine for up to 2 months before thyroid hormone levels decline because their thyroid glands store it in colloid.

Thyroid hormones are released when the colloid is internalized by the thyrocytes and directed toward lysosomal degradation.

Monoiodotyrosine is the first product formed when thyroid peroxidase reacts with thyroglobulin and adds an iodine atom.

Diiodotyrosine is formed when MIT is further iodinated by thyroid peroxidase, adding another iodine atom.

Two DIT molecules undergo oxidative condensation to form T4 (thyroxine), with the elimination of the alanine side chain from the molecule that forms the outer ring.

T3 (triiodothyronine) is formed by the condensation of MIT and DIT.

T4 is the main thyroid hormone produced, while T3 is a more active form and is converted from T4.

In the liver, kidneys, and other tissues, T4 and T3 undergo deiodination, which means they lose an iodine atom. This process both breaks down the hormones and locally produces T3, considered the primary active form.

While both T4 and T3 circulate, T3 is the major player in the body's response to thyroid hormones. It's the main driver of the hormone's actions on metabolism and other functions.

The amount of thyroid hormones your body produces is controlled by TSH, released from the pituitary gland. More TSH means more thyroid hormones; less TSH means fewer thyroid hormones.

When levels of T4 and T3 in the blood are high, this signals to the pituitary gland to reduce TSH production, preventing an overproduction of thyroid hormones.

While T3 is the main active hormone, T4 also influences thyroid hormone production. Inside the pituitary gland, T4 is converted to T3, enhancing the suppression of TSH.

The inner part of the adrenal gland that secretes catecholamines like epinephrine, norepinephrine, and dopamine.

The outer layer of the adrenal gland that produces steroid hormones, including glucocorticoids and mineralocorticoids.

Steroid hormones produced by the adrenal cortex that regulate carbohydrate and protein metabolism.

Steroid hormones produced by the adrenal cortex that are crucial for maintaining sodium balance and extracellular fluid volume.

Sex hormones like testosterone produced by the adrenal cortex, playing a role in reproductive function.

The adrenal medulla contains two main cell types: epinephrine-secreting and norepinephrine-secreting. Epinephrine-secreting cells are more numerous in humans (90%).

The adrenal cortex is divided into three zones: zona glomerulosa, zona fasciculata, and zona reticularis. Each zone produces different steroid hormones.

The zona glomerulosa is responsible for secreting aldosterone, a hormone that regulates sodium balance.

While all three cortical zones produce corticosterone, cortisol is primarily produced in the zona fasciculata and zona reticularis.

The enzyme required for aldosterone biosynthesis is only found in the zona glomerulosa, making it the sole producer of this hormone.

Norepinephrine, epinephrine, and small amounts of dopamine are produced by the adrenal medulla. Norepinephrine is formed from tyrosine through hydroxylation and decarboxylation, while epinephrine is made by methylating norepinephrine.

In the bloodstream, a majority of dopamine (95%) and norepinephrine/epinephrine (70%) are coupled with sulfate. These sulfate conjugates are inactive and their function is unclear.

Catecholamines have a very short lifespan in circulation, lasting about 2 minutes.

The inner part of the adrenal gland, the adrenal medulla, is responsible for producing catecholamines, primarily norepinephrine and epinephrine.

While their precise function is debated, sulfate conjugates of catecholamines are known to be inactive forms. This means they don't directly participate in the body's usual responses triggered by norepinephrine and epinephrine.

These hormones increase glycogenolysis in liver and muscle, mobilize free fatty acids, elevate plasma lactate, and stimulate the metabolic rate.

Norepinephrine and epinephrine work through these two types of receptors, mediating their diverse effects.

Norepinephrine and epinephrine increase insulin and glucagon release via β-adrenergic receptors, but inhibit their secretion via α-adrenergic mechanisms.

Both hormones increase heart rate and contractility through β1-receptors.

Norepinephrine constricts most blood vessels via α1-receptors, while epinephrine dilates vessels in skeletal muscle and liver via β2-receptors.

The exact role of dopamine in the bloodstream isn't fully understood.

Dopamine causes renal vasodilation, likely by acting on specific dopaminergic receptors in the kidneys.

Dopamine can constrict blood vessels, possibly by triggering the release of norepinephrine.

Dopamine increases the strength of heart contractions (positive inotropic effect) by acting on β1-adrenergic receptors.

Dopamine is produced in the renal cortex, the outer layer of the kidneys.

Cholesterol serves as the fundamental building block for all steroid hormones. It's either produced by the body or obtained from dietary sources like LDL.

Pregnenolone is the initial steroid hormone produced from cholesterol, marking the first step in steroid hormone biosynthesis.

ACTH (Adrenocorticotropic Hormone) stimulates the adrenal cortex to produce steroids, particularly cortisol. It acts via Gs protein and adenylyl cyclase.

The mitochondria play a crucial role in steroid biosynthesis, converting cholesterol to pregnenolone, the first step in the process.

The smooth endoplasmic reticulum (ER) further processes steroid hormones, modifying them into their active forms.

Androgens are hormones like testosterone that exert masculinizing effects. While adrenal androgens have minimal masculinizing effect in normal amounts, excessive secretion can cause significant masculinization.

Adrenal androgen secretion is primarily controlled by ACTH (Adrenocorticotropic Hormone), not by gonadotropins like LH and FSH.

Testosterone, produced by the testes, is the most active androgen. Adrenal androgens have less than 20% of its activity.

In adult males, excess adrenal androgens don't create new masculine features, they merely enhance existing ones.

ACTH directly influences the production of adrenal androgens. Levels of ACTH, controlled by the pituitary gland, regulate the amount of adrenal androgens produced.

Glucocorticoids increase the plasma glucose level by boosting glucose-6-phosphatase activity and promoting hepatic glycogenesis and gluconeogenesis.

Glucocorticoids exert an anti-insulin action in peripheral tissues, hindering glucose uptake and utilization, ultimately worsening diabetes.

Glucocorticoids spare the brain and heart from their anti-insulin effects, ensuring these vital organs have access to extra glucose.

Glucocorticoids raise plasma lipid levels and increase ketone body formation in diabetic patients.

Glucocorticoids increase protein catabolism, breaking down proteins into amino acids for use in gluconeogenesis.

Adrenal insufficiency is marked by an inability to excrete water loads, putting the individual at risk of water intoxication.

Only glucocorticoids are effective in correcting the water excretion deficit seen in adrenal insufficiency.

Patients with adrenal insufficiency who haven't received glucocorticoids may experience high fever ('glucose fever'), collapse, and even death after glucose infusion.

The high fever, collapse, and potential death following glucose infusion in untreated adrenal insufficiency is called 'glucose fever'.

The body's inability to excrete water loads can lead to dangerous water accumulation, making glucose infusion particularly risky for patients with untreated adrenal insufficiency.

A condition caused by prolonged high levels of cortisol in the blood. It leads to characteristic physical changes like weight gain, thin skin, and muscle weakness.

Excess cortisol in Cushing syndrome breaks down proteins, leading to muscle weakness and thin skin.

Excess cortisol causes fat to accumulate in specific areas like the abdomen, face, and upper back, creating a 'buffalo hump'.

Increased cortisol secretion often comes with an increase in adrenal androgens, leading to facial hair growth and acne.

The characteristic 'buffalo hump' is caused by the accumulation of fat in the upper back due to the redistribution of body fat caused by excess cortisol.

Mineralocorticoids like aldosterone promote sodium (Na+) reabsorption from urine, sweat, saliva, and colon, leading to Na+ retention in the extracellular fluid (ECF).

The retention of sodium (Na+) in the extracellular fluid (ECF) due to mineralocorticoids causes an increase in ECF volume.

Under the influence of aldosterone, sodium (Na+) is exchanged for potassium (K+) and hydrogen ions (H+) in the renal tubules, leading to increased potassium excretion (K+ diuresis) and more acidic urine.

Aldosterone's action leads to increased sodium (Na+) reabsorption, potassium (K+) excretion, and increased urine acidity.

Mineralocorticoids increase ECF volume by promoting Na+ reabsorption.