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Hypothalamus and Pituitary Gland Development

Formation of the Hypothalamus

  • The hypothalamus is small and forms from the alar plates, which create the lateral walls of the diencephalon. A key feature is the hypophyseal sulcus, dividing dorsal and ventral regions.
  • The dorsal region develops into the thalamus, while the ventral region becomes the hypothalamus. This distinction is crucial for understanding brain structure.

Development of the Pituitary Gland

  • Between weeks three to five, an ectodermal protrusion occurs in what is known as stomodeum, leading to a pouch called Rathke's pouch that forms the adenohypophysis (anterior pituitary).
  • Residual cells from Rathke's pouch can lead to cystic tumors like craniopharyngioma, which are slow-growing tumors associated with this embryological structure.

Neurohypophysis Formation

  • The neurohypophysis (posterior pituitary) arises from an infundibular protrusion around week eight, originating from the third ventricle. This process highlights different developmental pathways for each part of the pituitary gland.
  • Key distinctions include that adenohypophysis has a classic glandular structure while neurohypophysis consists mainly of nervous tissue and nerve endings.

Anatomy of the Pituitary Gland

  • The pituitary gland is small (approximately 0.5 cm in height) and located within a bony structure called the sella turcica; its size limits growth, potentially compressing surrounding structures like optic chiasm when hypertrophy occurs.
  • It weighs between 500 to 600 milligrams and has specific vascularization through hypophyseal arteries derived from internal carotid arteries, forming a portal system for hormone transport between hypothalamus and pituitary gland.

Hormonal Functions in Pituitary Gland

  • In contrast to neurohypophysis, which primarily stores and releases hormones, adenohypophysis involves production alongside storage and release processes. This functional difference underscores their distinct roles in endocrine regulation.
  • Acidophilic cells constitute about 50% of adenohypophyseal cells; they produce growth hormone (GH) and prolactin—both significant proteins influencing growth and lactation respectively—highlighting their importance in metabolic functions during development stages.

Hyperprolactinemia and Hormonal Regulation

Causes of Hyperprolactinemia

  • The primary causes of hyperprolactinemia include physiological factors such as pregnancy and lactation, along with nipple stimulation, stress, excessive exercise, and cold exposure which can increase lactotropic cells.

Hormone Production in the Pituitary Gland

  • Gonadotropins are significant hormones produced by the pituitary gland, accounting for 20% of its function; they produce LH (Luteinizing Hormone) and FSH (Follicle-Stimulating Hormone).
  • Corticotropins (10%) produce TSH (Thyroid-Stimulating Hormone), while other important hormones include ACTH (Adrenocorticotropic Hormone).

Anatomical Considerations

  • The anatomical relationship between the pituitary gland and surrounding structures like the cavernous sinuses is crucial; thrombosis in these areas can lead to significant complications including cranial nerve damage.

Hypothalamic Control Mechanisms

  • Understanding the hypothalamus's role is critical; it releases both releasing hormones and inhibiting hormones that regulate pituitary functions.
  • Key inhibitors include somatostatin (which inhibits growth hormone release) and PIF (Prolactin Inhibitory Factor), alongside various releasing hormones like GRH (Growth Releasing Hormone).

Functions of Growth Hormone

  • Growth hormone is primarily stimulated by GRH from the hypothalamus and inhibited by somatostatin. Its main functions include protein production, bone growth stimulation, and lipolysis.
  • Excessive growth hormone leads to acromegaly in adults or gigantism in children due to elevated levels of IGF1 (Insulin-like Growth Factor 1).

Consequences of Growth Hormone Dysfunction

  • Hypofunction results in conditions like hypopituitarism leading to obesity, sarcopenia, and pathological fractures. In children, it may cause dwarfism or hypopituitarism.

Gonadotropins' Role in Sexual Function

  • Gonadotropins play a vital role in sexual health by regulating spermatogenesis in males and menstrual cycles in females. They also contribute to muscle mass maintenance alongside growth hormone.

Understanding Hypogonadism and Thyroid Function

Overview of Hormonal Functions

  • The discussion begins with the roles of testicles and ovaries in producing testosterone, estrogens, and progestogens. It highlights the concepts of hypo- and hyperfunction within these systems.
  • Hyperfunction is noted as less studied and not typically associated with pathological conditions, while hypofunction leads to a condition known as hypogonadism.

Classification of Hypogonadism

  • Hypogonadism can be classified into primary (peripheral damage), secondary (central issues), and tertiary (hypothalamic dysfunction). This classification is crucial for understanding the underlying causes.
  • Primary hypogonadism results from non-functioning testicular or ovarian tissue, leading to elevated LH and FSH levels due to lack of negative feedback.

Causes and Characteristics

  • Various conditions can lead to hypogonadotropic hypogonadism in both men (e.g., delayed puberty syndrome) and women (e.g., anorexia or chronic diseases).
  • The most notable example mentioned is Kallmann syndrome, characterized by anosmia or hearing loss alongside hypogonadotropic features due to hypothalamic damage.

Thyroid Function Insights

  • The role of somatostatin in negative feedback regulation is emphasized, along with the importance of testosterone in males and estrogen/progestogen in females for maintaining hormonal balance.
  • T4's conversion to T3 is discussed; T4 serves primarily as a reserve that must convert peripherally for effective metabolic action across tissues.

Hypothyroidism Types

  • Primary hypothyroidism occurs when there’s direct damage to the thyroid gland itself, often resulting in goiter formation due to inflammation or infiltration.
  • In contrast, secondary hypothyroidism arises from pituitary dysfunction where TSH levels are low; this type does not typically present with goiter.

Common Conditions Related to Thyroid Dysfunction

  • Hashimoto's thyroiditis emerges as the most prevalent cause of primary hypothyroidism globally. Its autoimmune nature contributes significantly to thyroid health issues.
  • A key distinction between primary and secondary hypothyroidism lies in feedback mechanisms: primary shows elevated TSH due to lack of negative feedback while secondary presents low TSH levels linked with pituitary disorders.

Understanding Hyperthyroidism and Adrenal Function

Overview of Hyperthyroidism

  • Hyperthyroidism is more prevalent in women, particularly primary hyperthyroidism, with a ratio of 10:1.
  • The expression of excess thyroid hormone function is termed thyrotoxicosis, which is the typical manifestation of hyperthyroidism.
  • Thyrotoxicosis can lead to increased metabolism, resulting in symptoms such as elevated temperature, tachycardia, sweating, and anxiety.

Causes and Types of Hyperthyroidism

  • The most common cause of primary hyperthyroidism is autoimmune disease, specifically Graves' disease.
  • Secondary hyperthyroidism is typically associated with tumors that produce TSH (Thyroid Stimulating Hormone), such as a thyrotropic adenoma.

Adrenal Gland Functions

  • The adrenal gland has two main parts: the cortex and the medulla. The cortex produces hormones like aldosterone and cortisol.
  • Aldosterone regulates sodium and water reabsorption in the kidneys, maintaining blood pressure and homeostasis.

Cortisol's Role

  • Cortisol acts as a crucial stress hormone that maintains vascular tone; without it, catecholamines cannot function effectively.
  • It serves as a natural anti-inflammatory agent and reduces protein production in immune responses.

Aldosterone Regulation

  • Aldosterone primarily functions through its renin-angiotensin system for regulation; it continues to be produced even when pituitary function fails due to angiotensin stimulation.

Addison's Disease

  • Primary adrenal insufficiency is known as Addison's disease; it results from necrosis or damage to the adrenal glands.
  • In many cases, Addison's disease can be secondary to tuberculosis or associated with hypopituitarism.

Cushing’s Syndrome

  • When suspecting Cushing’s syndrome, it's essential first to rule out exogenous causes like corticosteroid medication use.
  • If not iatrogenic, Cushing’s disease often arises from excessive ACTH production at the pituitary level.

Adenomas and Hormonal Functions

Understanding Adenomas and Hyperfunction

  • The discussion begins with adenoma corticotropo, highlighting that primary hyperfunction is less common. It can arise from adrenal adenomas, adrenal cancer, or adrenal hyperplasia.
  • Cortisol's role in the hypothalamic-pituitary-adrenal (HPA) axis is emphasized, along with prolactin's function in lactation during pregnancy and breastfeeding.

Prolactin and Its Implications

  • Prolactin can inhibit FSH secretion leading to hypogonadism; this condition is termed hyperprolactinemia.
  • Hypoprolactinemia can only be diagnosed under specific conditions such as excessive bleeding post-delivery resulting in a syndrome of Sheehan.

Causes of Prolactin Imbalance

  • The only circumstance for diagnosing hypoprolactinemia early is related to physiological causes or medications affecting dopamine levels.
  • Medications like haloperidol and metoclopramide are noted for increasing prolactin due to dopamine inhibition.

Physiological Stimuli for Prolactin Production

  • Physiological factors stimulating prolactin production include gestation, lactation, stress, and nipple stimulation.

Hypothalamic-Pituitary Axis Overview

Origin of Pituitary Gland Components

  • The origin of the adenohypophysis (anterior pituitary) from Rathke's pouch and neurohypophysis (posterior pituitary) from the infundibulum is discussed.

Hormonal Regulation Mechanisms

  • Growth hormone regulation involves positive control by growth hormone-releasing hormone (GHRH) and negative feedback by somatostatin.

Gonadotropins Control

  • Gonadotropins are regulated by gonadotropin-releasing hormone (GnRH), with inhibins providing negative feedback alongside sex hormones like testosterone and estrogen.

Thyroid Function and Feedback Loops

Thyroid Hormone Release Dynamics

  • Thyrotropin-releasing hormone (TRH), while primarily acting on TSH release, also influences prolactin secretion positively.

Corticotropin Regulation

  • Corticotropin-releasing hormone regulates ACTH release; cortisol serves as its negative feedback mechanism.

Catecholamines and Their Pathologies

Medullary Hyperfunction Insights

  • Catecholamine overproduction may result from pheochromocytoma; this tumor type should not be overlooked when discussing medullary hyperfunctions.

This structured summary encapsulates key discussions around hormonal functions, their regulatory mechanisms, pathologies associated with hormonal imbalances, particularly focusing on adenomas' roles within these processes.

Understanding the Endocrine System

Overview of the Endocrine System

  • The endocrine system is described as a vegetative control system, managing major visceral functions through hormonal regulation.
  • Rapid actions are controlled by the autonomic nervous system, while slower processes like metabolism and growth are regulated hormonally.

Hormonal Control Mechanisms

  • Growth and metabolic processes, including lipolysis and muscle loss, are all under hormonal control, primarily managed by the hypothalamus.
  • The hypothalamus acts as a central brain that regulates hormone release from the pituitary gland via releasing and inhibiting factors.

Structure of the Hypothalamus and Pituitary Gland

  • The connection between the hypothalamus and pituitary gland involves a specific venous portal system to ensure targeted hormone delivery.
  • Five groups of hormones are produced at this level: gonadotropins (LH, FSH), growth hormone, thyrotropin (TSH), and corticotropin.

Target Organs for Hormones

  • Gonadotropins target testes and ovaries; TSH targets the thyroid gland; corticotropin affects adrenal glands.
  • Growth hormone influences various tissues without a specific target organ but mediates effects through insulin-like growth factors.

Pathologies Related to Hormonal Imbalances

  • Primary pathologies arise when target organs fail (e.g., testicular damage leading to hypergonadotropic hypogonadism).
  • Thyroid function is crucial; T4 is fully formed in the thyroid while T3 has both thyroidal and peripheral origins. Autoimmune conditions can lead to hyperthyroidism or hypothyroidism symptoms.

Corticotropin's Role in Adrenal Function

  • Corticotropin regulates cortisol production in adrenal glands; secondary adrenal insufficiency typically does not affect aldosterone levels.
  • Prolactin plays a significant role in lactation but also inhibits FSH production, affecting male physiology.

Prolactinemia and Thyroid Function in Women

Prolactinemia Effects

  • Classic symptoms of prolactinemia in women include menstrual dysfunction and hyperproduction of milk.
  • A significant increase in a prolactin-producing adenoma can compress the optic chiasm, leading to pain and bitemporal hemianopsia.

Hypothalamic-Pituitary Axis

  • The hypothalamus-pituitary system regulates peripheral glands, including the thyroid.
  • Understanding thyroid function is crucial for managing both hyperthyroidism and hypothyroidism pharmacologically.

Importance of Thyroid Hormones

  • Thyroid hormones are essential for life; severe hyperthyroidism or hypothyroidism can be fatal.
  • Severe hypoventilation from myxedema leads to dangerously low basal metabolism, while severe hyperthyroidism can cause heart failure and dehydration.

Thyroid Development and Anatomy

Embryological Development

  • The thyroid begins as epithelial proliferation around the third to fifth week of gestation, originating from the floor of the pharynx.
  • It remains connected to the tongue via the thyroglossal duct during migration until it reaches its final position by approximately week seven.

Structural Characteristics

  • By week 11, key features such as follicle formation and colloid production mark the onset of fetal thyroid function.
  • Parafollicular cells (C cells), which produce calcitonin, originate from the ultimobranchial body during embryonic development.

Anatomical Features of the Thyroid Gland

Location and Structure

  • The thyroid gland is butterfly-shaped, weighing between 25 to 30 grams, located between cervical vertebrae C5 and C1.
  • It has three lobes: two classical lobes (left and right), with a pyramidal lobe often present on the left side in over 75% of individuals.

Clinical Relevance

  • Growth or fibrosis of the thyroid can lead to dysphagia (difficulty swallowing) due to compression on surrounding structures like the trachea and esophagus.

Surgical Considerations Related to Thyroid Anatomy

Surgical Risks

  • The recurrent laryngeal nerve runs near the thyroid gland; damage during surgery can lead to vocal cord complications requiring immediate reoperation.

Increasing Incidence of Thyroid Surgery

  • There has been a rise in thyroid surgeries globally due to increased incidence rates linked with environmental factors like radiation exposure since events like Chernobyl.

Physiological Functions of Thyroid Hormones

Hormonal Production

  • The primary role of the thyroid is metabolic regulation through hormone production—specifically T3 (triiodothyronine) and T4 (thyroxine).
  • Notably, only 20% of T3 is produced directly by the thyroid; most is converted from T4 within tissues.

Understanding Thyroid Hormones and Their Metabolism

Half-life of T4 and T3

  • The half-life of T4 ranges from 4 to 7 days, while T3 has a much shorter half-life of about 18 hours. However, T3 is three times more potent than T4.
  • Approximately 80% of the body's T3 is produced through the conversion of T4 via deiodinases, primarily occurring in peripheral tissues.

Role of Deiodinases

  • There are different types of deiodinases: D1 and D2 produce active T3, while D3 converts it into inactive reverse T3 (rT3).
  • rT3 is generated when there is a need to decrease basal metabolic rate, particularly in critical or chronically ill patients.

Clinical Implications of Reverse T3

  • In critically ill patients or those with chronic debilitating diseases, decreased production of normal T3 leads to increased levels of rT3.
  • Normal thyroid-stimulating hormone (TSH) levels can still be present despite high rT3 levels due to feedback inhibition on the hypothalamus-pituitary axis.

Euthyroid State in Illness

  • A patient with normal TSH but low active T3 may be classified as "euthyroid sick," indicating they are not producing enough active hormone due to their illness.
  • This state often occurs during prolonged starvation or critical illnesses like sepsis or COVID-19, where metabolism needs to be conserved.

Effects on Metabolism and Hormonal Activity

  • The body reduces metabolism by converting more active hormones into inactive forms (like rT3), which helps preserve muscle mass and energy reserves.
  • Understanding the role of thyroid hormones in various tissues is crucial; for instance, free T3 rather than total T3 provides better clinical insights since total values can fluctuate significantly based on transport proteins.

Importance of Free Thyroid Hormones

  • Free forms of thyroid hormones (especially free T4 and free T3) are responsible for physiological actions; excess can lead to thyrotoxicosis.
  • Thyroid hormones enhance catecholamine activity leading to positive effects such as increased heart rate and lipolysis. They also play a vital role in mental development during childhood.

Impact on Other Body Systems

  • Increased thyroid hormone levels promote carbohydrate absorption in the intestines and influence lipid metabolism by stimulating LDL receptor formation.
  • Hypothyroidism can lead to dyslipidemia due to reduced hormonal activity affecting lipid processing.

Understanding Thyroid Hormone Production

The Role of Colloids and Blood Vessels in Hormone Formation

  • The colloid is essential for hormone formation, requiring a connection to blood vessels to obtain iodine, the base of thyroid hormones. Each thyroxine can carry one or two iodine atoms, with a maximum of two being crucial for exams.

Functional Unit: The Thyroid Follicle

  • The thyroid follicle serves as the functional unit where each thyrocyte begins synthesizing hormones that are later transported back into the thyrocyte and released into the bloodstream.

Importance of Parafollicular Cells

  • Surrounding the follicles are parafollicular cells (C cells) responsible for producing calcitonin, which plays a significant role in certain diseases, including medullary cancer where calcitonin acts as an important tumor marker.

Iodine Uptake Mechanism

  • Iodine uptake occurs through the sodium-iodide symporter (NIS), which facilitates iodine entry into thyrocytes. Excessive iodine can temporarily block oxidation processes, known as the Wolff-Chaikoff effect. This will be revisited later in detail.

Transport and Oxidation of Iodine

  • Once inside the thyrocyte, iodine is expelled into the colloid via pendrin protein for oxidation by thyroid peroxidase (TPO). A deficiency in pendrin can lead to conditions like hypothyroidism and hearing loss due to its presence in vestibular and cochlear cells.

Synthesis of Thyroglobulin

  • In addition to iodine transport, TPO also catalyzes iodination reactions necessary for forming mono-iodotyrosine (MIT) and di-iodotyrosine (DIT) from tyrosine residues within thyroglobulin after it is synthesized in the Golgi apparatus and secreted into colloid via exocytosis.

Organification Process

  • During organification, MIT or DIT combines with additional iodines facilitated by TPO to produce T3 (triiodothyronine) or T4 (thyroxine). This process is critical for proper hormone synthesis within thyroid follicles.

Coupling Phase of Hormone Formation

  • The coupling phase involves combining MIT with DIT to form T3 or linking two DIT molecules to create T4; this step remains dependent on TPO activity ensuring effective hormone production before release into circulation through endocytosis from thyrocytes.

Release Mechanism of Thyroid Hormones

  • After synthesis and coupling, hormones are released from vesicles via endocytosis back into circulation; this marks a crucial transition from intracellular processing to systemic availability of thyroid hormones like T3 and T4 needed by various body systems.

Understanding Thyroid Hormone Synthesis

Mechanism of T4 and T3 Production

  • The synthesis of T4 is crucial, especially when considering patients who have T4 activity but are not producing it in the thyroid. This indicates they may be taking thyroid hormone supplements.
  • Upon release, both T3 and T4 hormones are liberated from the vesicles; however, mono-iodinated and di-iodinated forms do not get released immediately as they undergo deiodination for recycling within the process.

Physiological Importance of Iodine in Thyroid Function

  • The iodine absorption process occurs in the thyroid follicle, which is a functional unit that interacts with blood vessels to absorb iodine effectively.
  • The sodium/iodine symporter (NIS) plays a vital role by facilitating the simultaneous transport of sodium and iodine into thyroid cells.

Steps in Thyroid Hormone Synthesis

  • After iodine uptake, oxidation occurs through thyroperoxidase, which is essential for iodination. This step also involves synthesizing thyroglobulin within the Golgi apparatus.
  • Thyroglobulin is secreted into colloid where it combines with oxidized iodine to form mono-iodotyrosine (MIT) and di-iodotyrosine (DIT), marking critical steps in organification.

Organification Process

  • Organification involves attaching one or two iodine molecules to tyrosine residues on thyroglobulin, leading to MIT and DIT formation. This process can be inhibited by excess iodine intake due to Wolff-Chaikoff effect.

Final Steps of Hormone Release

  • Following organification, coupling occurs where MIT and DIT combine to form T3 or T4. A single MIT with a DIT yields T3 while two DIT yield T4.
  • Once synthesized, these hormones are endocytosed back into cells where they are released into circulation. Notably, 100% of T4 is produced in the thyroid while only 20% of T3 originates there.

Reutilization of Iodine

  • Unused mono and di iodides undergo internal deiodination allowing for recycling within new cycles of hormone production.

Pharmacological Implications

  • Thionamides like methimazole block oxidation processes crucial for hormone synthesis; understanding this mechanism aids in treating hyperthyroidism effectively.

Understanding the Parathyroid Glands and Calcium Regulation

Anatomy of the Parathyroid Glands

  • The parathyroid glands are located behind the thyroid gland, with their anatomical positioning crucial for understanding their function. They embrace the trachea, highlighting their close relationship with surrounding structures.
  • There are typically four parathyroid glands: two superior (from the fourth pharyngeal pouch) and two inferior (from the third pharyngeal pouch), each weighing approximately 25 to 30 milligrams.
  • The superior parathyroid glands receive blood supply from the superior thyroid arteries, while the inferior ones are supplied by branches from the subclavian artery, specifically from a thyrotracheal branch.

Physiological Functions of Parathyroid Hormone (PTH)

  • The primary role of parathyroid hormone is to regulate calcium levels in the body. It is essential for maintaining calcium homeostasis and is produced in response to low serum calcium levels.
  • Normal serum calcium levels range between 8.4 and 10 mg/dL. Hypocalcemia is classified as mild when between 8.0 and 8.4 mg/dL, moderate below 8.0 mg/dL, and severe when under 7.5 mg/dL.
  • PTH secretion increases when calcium levels drop; it acts on renal tubules to enhance calcium reabsorption while decreasing phosphate reabsorption, thus preventing further drops in serum calcium.

Mechanisms of Action of PTH

  • PTH stimulates bone resorption when calcium levels are low, releasing both calcium and phosphorus into circulation which can lead to osteodystrophy if chronically elevated.
  • In normal conditions, PTH promotes bone formation; however, excessive PTH leads to increased bone resorption instead of formation due to its hyperactive state.
  • When functioning normally within physiological ranges, PTH supports bone health by facilitating proper mineralization but can cause detrimental effects like renal osteodystrophy if overproduced due to chronic kidney disease.

Interaction with Vitamin D

  • In conjunction with its actions on kidneys and bones, PTH also enhances calcitriol production in proximal renal tubules—calcitriol being an active form of vitamin D that significantly aids dietary calcium absorption.
  • Calcitriol's synthesis involves converting inactive vitamin D (25-hydroxyvitamin D from liver metabolism) into its active form through processes regulated by PTH in renal proximal tubules.

This structured overview provides a comprehensive understanding of how parathyroid glands function within human physiology concerning calcium regulation and highlights critical interactions between hormones involved in maintaining mineral balance.

Understanding the Role of Calcitriol in Renal Health

The Impact of Renal Function on Calcitriol Production

  • A renal patient with a clearance below 50 experiences reduced calcitriol formation, leading to decreased intestinal absorption of calcium and phosphorus (90% dependent on calcitriol).
  • As calcitriol levels drop due to renal impairment, hypocalcemia occurs, prompting an increase in parathyroid hormone (PTH) levels.

PTH's Response to Calcium Levels

  • PTH regulates calcium reabsorption in the distal tubule while decreasing phosphate reabsorption, maintaining normal serum calcium levels.
  • PTH also stimulates the formation of calcitriol by acting on alpha-hydroxylase in the proximal tubule.

Consequences of Decreased Calcitriol

  • With insufficient calcitriol production from kidney failure, calcium absorption declines, leading to increased PTH secretion as a compensatory mechanism.
  • If renal function is severely compromised (e.g., clearance at 20 or 30), even elevated PTH cannot effectively regulate calcium levels.

Bone Resorption and Hyperparathyroidism

  • Elevated PTH leads to bone resorption for calcium release, which can result in hyperparathyroidism and subsequent bone matrix loss.
  • Normally, PTH promotes bone formation; however, during hypocalcemia with excess PTH, it causes bone resorption instead.

The Role of Calcitonin

  • Calcitonin counteracts the effects of PTH by inhibiting calcium reabsorption and promoting its deposition into bones.
  • In cases of hypocalcemia, calcitonin activity is suppressed; it primarily functions during hypercalcemia.

Hyperparathyroidism and Its Implications

Understanding Primary Hyperparathyroidism

  • The most common cause of elevated parathyroid hormone (PTH) is autoimmune conditions, while adenomatous tumors can also lead to primary hyperparathyroidism.
  • Primary hyperparathyroidism typically results in mild hypercalcemia, characterized by calcium levels between 10 and 11.9 mg/dL, which may not present significant symptoms but can lead to kidney stones.
  • Surgical intervention is often required for treatment, focusing on the removal of the adenoma responsible for excessive PTH production.

Effects of Excessive PTH

  • Excess PTH increases gastric acid secretion and can contribute to ulcer disease; surgical correction usually resolves these issues.

Paraneoplastic Hypercalcemia

  • Extraglandular production of PTH can occur in certain cancers, such as squamous cell lung cancer, leading to paraneoplastic hypercalcemia through a variant known as PTH-related peptide (PTHrP).

Severe Hypercalcemia Causes

  • The leading cause of severe hypercalcemia (levels above 14 mg/dL) is paraneoplastic hypercalcemia. It’s crucial to understand this relationship for effective diagnosis and treatment.

Role of Calcitriol and Calcium Homeostasis

  • PTH regulates calcitriol formation, which aids in maintaining normal calcium levels by enhancing intestinal absorption. It also controls tubular reabsorption of calcium and phosphate, playing a vital role in bone health and overall calcium homeostasis.