Homeostasis Principles and Feedback Loops

Maintaining a stable internal environment for normal body function

Mechanism that monitors and adjusts physiological variables to maintain homeostasis

A system's response counteracts the initial change, stabilizing the system.

System's response amplifies the initial change, potentially pushing it further.

Optimal value for a specific physiological parameter (like body temp)

Variables like nutrients, gases, wastes, pH, electrolytes, and temperature, that need to be regulated.

Body's reaction to maintain homeostasis after a change or stress.

Fluid outside of cells, containing sodium, chloride, and nutrients.

A system that regulates a variable by using the output to control the input.

Detects changes in a variable.

Compares the sensor's input to a set point.

Produces a response to bring the variable back to the set point.

Partial pressure of carbon dioxide in the blood.

Partial pressure of oxygen in the blood.

Detect changes in pCO2 and H+ in the brain.

Detect changes in O2, CO2, and H+ in the blood.

Widening of blood vessels to increase blood flow.

Narrowing of blood vessels to decrease blood flow.

Anticipatory response to a changing variable.

Quick response to environmental or internal changes using nerve impulses.

Longer-term responses mediated by hormones as messengers.

Responses that adjust energy balance (deficit/surplus).

Changes in behaviour to cope with environmental changes.

Long-term changes enhancing the organism's ability to cope with stress.

Effectiveness of a control system in maintaining homeostasis.

Consistent effectiveness of a control system.

Low oxygen levels in the body.

Adjusting reference values to maintain tolerance of specific conditions.

Regulated hyperthermia, a normal response to infection.

Control center of the endocrine system, regulating various bodily functions.

Part of the pituitary gland producing hormones.

Part of the pituitary gland storing and releasing hormones.

A network of neurons that connects the anterior and posterior pituitary glands, serving as a critical synapse point for posterior pituitary neurons.

Large neurons with cell bodies in the hypothalamus, whose axons extend to the posterior pituitary, releasing hormones like oxytocin and ADH.

Small neurons in the hypothalamus, responsible for regulating the anterior pituitary gland through hormone release.

Bundle of axons extending from the hypothalamus to the posterior pituitary, carrying hormones for release.

A hormone produced by the hypothalamus and released by the posterior pituitary, regulating water balance in the body.

Specific protein molecules on target cells that bind to ADH, initiating different responses based on receptor type.

Concentration of dissolved substances in the blood, a key factor regulating ADH secretion.

Pressure sensors in the cardiovascular system, detecting changes in blood pressure and influencing ADH release.

A hormone produced by the hypothalamus and released by the posterior pituitary, playing a role in childbirth, breastfeeding, and social bonding.

Muscle-like cells surrounding mammary glands, responsible for contracting to expel milk during breastfeeding.

A condition caused by insufficient ADH production or reduced kidney sensitivity to ADH, leading to excessive urination and dehydration.

A type of diabetes insipidus caused by a deficiency in ADH production by the hypothalamus.

Synthetic versions of ADH, used clinically to treat diabetes insipidus and sometimes to control bleeding.

The process of releasing milk from the breasts, triggered by oxytocin, which causes contractions of myoepithelial cells surrounding milk ducts.

During labor, the stretching of the cervix and vagina releases estrogen, which increases oxytocin sensitivity in the uterus. Oxytocin then causes coordinated contractions, leading to the delivery of the baby. The contractions further stimulate oxytocin release, creating a positive feedback loop.

Crying, particularly in infants, can stimulate the release of oxytocin. While the exact mechanism is not fully understood, this suggests a potential role of oxytocin in social bonding and stress response.

A baby latches onto the nipple, sending signals to the hypothalamus via afferent neurons, which triggers the release of oxytocin from the posterior pituitary gland.

Prolactin, released from the anterior pituitary gland, is responsible for the production of breast milk.

The anterior pituitary gland, a true endocrine organ responsible for producing and releasing crucial hormones that regulate various bodily functions.

Specialized neurons located in the hypothalamus that produce and release hormones that influence the function of the anterior pituitary.

A network of capillaries in the hypothalamus where hypothalamic hormones are secreted.

Specialized non-endocrine cells in the anterior pituitary that support the function of hormone-secreting cells and regulate their activity.

Neurons in the hypothalamus that release peptide hormones, such as releasing and inhibiting factors, which control the secretion of hormones from the anterior pituitary.

A neural pathway that transports dopamine from the hypothalamus to the anterior pituitary, where it inhibits prolactin secretion.

A mechanism where the hormones released from the pituitary gland or peripheral organs regulate the release of stimulatory hormones from the hypothalamus, creating a balance in the endocrine system.

Hormones secreted from peripheral endocrine glands act on both the hypothalamus and the anterior pituitary to regulate the release of stimulatory hormones.

Anterior pituitary hormones exert a direct regulatory effect on the hypothalamus.

Thyroid hormones produced by the thyroid gland, essential for metabolism and growth.

High levels of T3 and T4 in the blood inhibit TSH secretion, preventing overproduction of thyroid hormones.

Overactive thyroid gland, produces excessive T3 and T4, leading to symptoms like weight loss and rapid heartbeat.

Underactive thyroid gland, produces insufficient T3 and T4, leading to symptoms like fatigue and weight gain.

Follicle Stimulating Hormone and Luteinizing Hormone, released by the anterior pituitary, regulate gonadal function in both males and females.

Gonadotropin Releasing Hormone, released by the hypothalamus, stimulates FSH and LH release from the anterior pituitary.

FSH stimulates follicle growth, while LH triggers ovulation and corpus luteum formation.

Hormones produced by ovaries, involved in regulating menstrual cycles and pregnancy.

Stress hormone produced by the adrenal cortex, helps regulate blood sugar and reduce inflammation.

High levels of cortisol in the blood inhibit ACTH secretion, preventing overproduction of cortisol.

Synthetic ACTH, used to diagnose adrenal insufficiency by stimulating cortisol production.

ACTH stimulates cortisol synthesis by activating melanocortin receptors and the cAMP pathway, contributing to adrenal cortex growth and maintenance.

Chronic administration of glucocorticoids suppresses ACTH secretion, leading to adrenal atrophy due to the loss of ACTH's trophic action.

Growth hormone stimulates growth by promoting IGF-1 production, which mediates anabolic functions. It also regulates metabolism.

GH secretion is stimulated by GHRH and inhibited by somatostatin. IGF-1 and somatostatin provide negative feedback on GH production.

Lack of GH leads to pituitary dwarfism. It can be treated with GH therapy.

Excess GH results in gigantism in children and acromegaly in adults.

Prolactin controls milk production by stimulating breast milk manufacture. It also plays a role in breast development during pregnancy.

Prolactin secretion is normally inhibited by dopamine. Suckling, estrogen and dopamine antagonists stimulate prolactin release.

Prolactin levels increase during pregnancy due to estrogen's effect, preparing for lactation after birth.

Bromocriptine, a dopamine agonist, is used to reduce excessive prolactin secretion.

The process of creating melanin, a pigment responsible for skin, hair, and eye color, stimulated by melanocyte-stimulating hormone (MSH).

G-protein coupled receptors on melanocytes that bind to MSH and activate cAMP synthesis, leading to melanin production.

A mechanism where hormones produced by target organs influence the production of tropic hormones by the pituitary gland and hypothalamus, regulating hormone levels.

A feedback loop where the target organ's hormone inhibits the anterior pituitary's production of the tropic hormone.

Feedback loop where the target organ's hormone inhibits both the anterior pituitary and hypothalamus.

The posterior pituitary composed of neural tissue, storing and releasing hormones produced by the hypothalamus.

A butterfly-shaped organ in the neck consisting of two lobes connected by an isthmus. Its basic unit is the thyroid follicle, a spherical structure with follicular cells surrounding a colloid-filled lumen.

Thyroid follicular cells synthesise and iodinate thyroglobulin, the precursor to thyroid hormones T3 and T4, within the follicle lumen.

An inactive form of thyroid hormone, produced in small amounts by the thyroid and during peripheral T4 metabolism. It has no physiological role and is cleared from circulation.

The process where the inactive thyroid hormone T4 is converted to the active form T3 by deiodinase enzymes in peripheral tissues.

Enzymes that regulate thyroid hormone activity by removing iodine atoms from T3 and T4, leading to activation or inactivation.

A low-affinity deiodinase found in tissues with high blood flow. It converts T4 to T3 (activation) and T4 to rT3 (deactivation).

A high-affinity deiodinase found in the brain and pituitary gland. It converts T4 to T3 (activation) to maintain local T3 levels.

A deiodinase that inactivates thyroid hormones, converting T4 to rT3 and T3 to T2, both inactive forms.

A large glycoprotein produced by follicular cells, serving as a scaffold for thyroid hormone synthesis. It contains tyrosine residues that are iodinated and coupled to form T4 and T3.

A mechanism by which thyroid epithelial cells actively take up iodide (I-) from the blood. This ensures a sufficient supply of iodine for thyroid hormone synthesis.

An enzyme on the apical membrane of follicular cells. It catalyzes the iodination of tyrosine residues in thyroglobulin to form thyroid hormones.

A gel-like substance within the thyroid follicles, where thyroid hormones are synthesized and stored in thyroglobulin. It's taken up by follicular cells through endocytosis.

The primary carrier protein in the blood for transporting thyroid hormones. It binds mainly to T4 but also to T3.

Thyroid-stimulating hormone (TSH) released from the anterior pituitary stimulates all aspects of thyroid hormone synthesis and release, including iodine uptake, thyroglobulin production, and thyroid hormone release.

Therapeutic substances that block the activity of deiodinase enzymes, potentially used for managing thyroid hormone-related disorders.

A clinical condition characterized by low levels of active T3, often in critical illness or cancer. It can result from increased DIO3 activity.

T3 and T4 increase the speed of energy use in the body by influencing carbohydrate, fat, and protein metabolism. They increase the activity of enzymes involved in cellular respiration and energy production, leading to higher caloric burn.

T3 and T4 increase the uptake and utilization of glucose by enhancing the expression of glucose transporters (GLUT1 and GLUT4), allowing cells to absorb more glucose. They also stimulate glycogenolysis and gluconeogenesis, increasing blood glucose levels for energy.

T3 and T4 stimulate the breakdown of fats (lipids) by increasing the expression of lipases. This releases fatty acids and glycerol into the bloodstream for energy production.

T3 and T4 influence protein synthesis and breakdown. They can enhance protein synthesis in tissues like muscle, but also increase protein breakdown in some contexts, leading to balanced protein turnover.

T3 and T4 are crucial for brain development, growth, and maturation. They promote growth hormone and stimulate maturation of the CNS, including the formation of myelin.

T3 and T4 promote bone growth by regulating the activity of growth plates, stimulating osteoblast proliferation, and facilitating chondrocyte maturation. They also enhance the effects of growth hormone on bone and cartilage.

T3 and T4 increase the responsiveness to catecholamines, such as adrenaline and noradrenaline, by increasing the number of receptors.

Increased levels of T3 and T4 increase the BMR, leading to higher oxygen consumption, heat production, and energy expenditure.

T3 and T4 influence the cardiovascular and respiratory system by altering the expression of calcium channels in the sarcoplasmic reticulum and enhancing the sensitivity of adrenoreceptors.

T3 and T4 increase the number of adrenergic receptors, enhancing the effects of catecholamines within the autonomic nervous system.

Medicines that block the synthesis of thyroid hormones (T3 and T4) in the thyroid gland.

Commonly used thioureylene drugs for hyperthyroidism, often used first due to their effectiveness.

Another thioureylene drug used for hyperthyroidism, often switched to when patients experience skin rash from Carbimazole/Methimazole.

The phenomenon where high iodine concentrations temporarily inhibit thyroid hormone production and release.

A radioactive isotope of iodine used to treat hyperthyroidism by selectively destroying thyroid cells.

A compound that can temporarily block thyroid hormone release, often given alongside iodine.

Drugs that block beta-adrenergic receptors, reducing the effects of adrenaline and noradrenaline.

A commonly used beta-blocker for hyperthyroidism, helping to manage symptoms like rapid heartbeat and tremors.

An autoimmune disorder where the immune system attacks the thyroid gland, causing hypothyroidism.

An enlarged thyroid gland, often associated with iodine deficiency.

A condition characterized by a low number of granulocytes (white blood cells that fight infection), which can be a side effect of some medications.

Damage to the liver, which can be a potential side effect of some medications.

A large protein found in the thyroid follicular colloid, serving as a scaffold for thyroid hormone (TH) synthesis. It contains tyrosine residues that are iodinated to form MIT and DIT, essential intermediates in TH production.

An enzyme located at the interface of thyroid follicular cells and colloid, responsible for oxidizing iodine and attaching it to tyrosine residues within thyroglobulin.

A tyrosine residue in thyroglobulin iodinated at position 3 on its ring.

A tyrosine residue in thyroglobulin iodinated at positions 3 and 5 on its ring.

A protein located on the basalateral surface of thyroid follicular cells, transporting iodine into the cell against its concentration gradient, using energy provided by the Na+/K+ ATPase pump.

An ion exchanger located on the apical membrane of thyroid follicular cells, moving iodine from the cell into the follicular lumen in exchange for chloride ions.

A nuclear receptor protein that binds to thyroid hormone (T3 or T4), triggering a cascade of transcriptional events to regulate gene expression.

The major isoform of the THRa receptor, expressed in various tissues like the heart, skeletal muscle, and brain. It plays a crucial role in regulating metabolism, cardiac function, and muscle development.

An isoform of the TRB receptor, expressed in tissues like the liver, brain, and kidneys. It's essential in regulating TH action in the liver and central nervous system.

A specific DNA sequence in the promoter region of target genes recognized by the TR-RXR heterodimer. This binding triggers either activation or repression of gene transcription.

Proteins bound to TR-RXR in the absence of thyroid hormone, repressing gene expression through interactions with histone deacetylases (HDACs).

Proteins recruited to TR-RXR in the presence of thyroid hormone, promoting gene expression through interactions with histone acetyltransferases (HATs).

A nuclear receptor that heterodimerizes with TR, creating the active form of the receptor that binds to TREs. Retinoic acid, a vitamin A derivative, binds to RXR.

The wide-ranging effects of thyroid hormone on various metabolic processes, including cellular differentiation, development, metabolism, heart function, and brain function.

These receptors are located in heart muscle and are activated by epinephrine and norepinephrine. This activation leads to an increase in intracellular cAMP, a second messenger that triggers a cascade of events ultimately increasing heart rate and contractility.

The production and release of thyroid hormones (T3 and T4) is tightly regulated by a feedback loop involving the hypothalamus, pituitary gland, and thyroid gland. This ensures optimal levels of thyroid hormones are maintained for metabolism, growth, and development.

This hormone is released from the hypothalamus and stimulates the pituitary gland to release TSH (thyroid-stimulating hormone).

Released from the anterior pituitary gland, TSH acts on the thyroid gland to stimulate the production and release of T3 and T4.

High levels of T3 and T4 in the blood inhibit the release of TRH from the hypothalamus and TSH from the pituitary gland, preventing overproduction of thyroid hormones.

Iodine is essential for the synthesis of T3 and T4. The thyroid gland uses iodine from the bloodstream to produce these hormones. A deficiency in iodine can lead to hypothyroidism.

The most common cause of hyperthyroidism. It is an autoimmune disorder where the body's immune system attacks the thyroid gland, causing it to produce excessive thyroid hormones.

Treatment involves reducing the activity of the thyroid gland. Treatment options include surgery (partial/complete removal of the gland), medications (antithyroid drugs), and radioactive iodine therapy.

These are antithyroid drugs that inhibit the synthesis of thyroid hormones by blocking the enzyme thyroid peroxidase, which is crucial for the iodination of tyrosine in thyroglobulin.

These medications are sometimes used in the treatment of hyperthyroidism, but they are not effective for all patients. They can work by interfering with the uptake of iodine by the thyroid gland.

These medications block the effects of epinephrine and norepinephrine on the heart and other tissues, helping to alleviate some of the symptoms of hyperthyroidism.

A hormone that stimulates the growth, development, and activity of its target gland.

Goitre can be caused by various factors, including iodine deficiency, Graves disease, Hashimoto's thyroiditis, and thyroid nodules.

Thyroid Stimulating Hormone (TSH) promotes thyroid hormone production. In iodine deficiency, TSH levels rise due to lack of negative feedback from T3, leading to goitre.

A type of goitre where the entire thyroid gland is uniformly enlarged.

A type of goitre characterized by one or more nodules (lumps) within the thyroid gland.

Goitre associated with hyperthyroidism, meaning the thyroid gland produces excessive hormones.

Goitre that doesn't affect thyroid hormone levels. Commonly caused by iodine deficiency.

A severe neurodevelopmental disorder caused by mutations in the MCT8 gene, leading to impaired T3 transport into the brain.

During childbirth, the stretching of the cervix and vagina releases estrogen. This hormone increases the uterus's sensitivity to oxytocin, which then causes coordinated contractions. These contractions further stimulate the release of more oxytocin - a positive feedback loop.

A mechanism where the hormones released from the pituitary gland or peripheral organs regulate the release of stimulatory hormones from the hypothalamus. This creates a balance in the endocrine system.