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Parathyroid Gland
A gland that regulates calcium levels, It is located on or near the thyroid capsule (region of the thyroid gland) sometimes within the thyroid gland.
It may also be found outside their normal anatomic site – between the hyoid bone in the neck and mediastinum.
Smallest endocrine gland in the body
TRUE
TRUE OR FALSE
Most people have 4 parathyroid glands but some have 8 or as few as 2.
Parathyroid Hormone (PTH)
Secreted by the chief cells of parathyroid glands as a Polypeptide, it increases blood calcium levels by promoting bone resorption, activating vitamin D, and stimulating intestinal calcium absorption.
If Calcium Levels Decrease, PTH is released
Oxyphil cells
Cells of no known function
Parathormone or Parathyrin
Other name of Parathyroid hormone
84
How many Amino acids do Parathyroid Hormone contain.
FALSE
TRUE OR FALSE
Parathyrin acts to decrease calcium concentration, whereas calcitonin acts to increase the concentration of calcium (Ca2+) in the blood.
4 minutes
PTH approximate Half-life
9.4 kDa
PTH Molecular Mass
PTH Regulation of Serum Calcium
Bone- enhances the release of calcium from the large reservoir contained in the bones.
Kidney- enhances active reabsorption of calcium and magnesium from distal tubules and the thick
ascending limb.
Intestine via Kidney- enhances the absorption of calcium in the intestine by increasing the production of
activated vitamin D.
PTH Regulation of Serum Phosphate
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney which means more phosphate is excreted through the urine.
PTH role in Vit D synthesis
PTH increases the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol to 1,25 dihydroxycholecalciferol, the active form of vitamin D.
Hyperparathyroidism
Excessive production of parathyroid hormone leading to hypercalcemia, with primary, secondary, and tertiary forms having different causes and effects.
Primary Hyperparathyroidism
Physiologic effect lies with the PT gland
Most common cause of hypercalcemia
Due to the presence of a functioning parathyroid adenoma
Accompanied with phosphaturia
If it is undetected, severe demineralization may occur
Secondary Hyperparathyroidism
Develops in response to serum calcium
There is diffuse hyperplasia of all 4 glands
The patient develops severe bone disease
Causes: vitamin D deficiency and chronic renal failure
Tertiary Hyperparathyroidism
It occurs when patients with secondary hyperparathyroidism
Develop autonomous function of the hyperplastic parathyroid glands or of a parathyroid
adenoma
The phosphate levels are normal to high; calcium phosphates in soft tissue
Hypoparathyroidism
Individuals are unable to maintain calcium concentration in blood without calcium supplementation
Due to accidental injury to the PT glands during thyroid or neck surgery, removal of the glands with
thyroid glands, or idiopathic atrophy
Other cause: autoimmune parathyroid destruction
Adrenal Gland
Endocrine glands located atop the kidneys
In humans, the right suprarenal gland is triangular shaped, while the left suprarenal gland is semilunar shaped.
Comprising the adrenal cortex (Outer and Yellow) and adrenal medulla (Dark Mahogany), responsible for releasing hormones in response to stress.
Suprarenal Glands
Other name of Adrenal Gland
Functions of Adrenal Glands
They are chiefly responsible for releasing hormones in response to stress.
through the synthesis of corticosteroids such as cortisol and catecholamines such as epinephrine.
The adrenal glands affect kidney function through the secretion of aldosterone, a hormone involved in
regulating the osmolarity of blood plasma.
Adrenal Corterx
Outer region of the adrenal gland secreting the steroid hormone.
Major site of steroid hormone production.
Zona Glomerulosa
Most Superficial Cortical Layer
Mineralocorticoids (Aldosterone)
Zona fasciculate
Middle cortical layer
Glucocorticoid (Cortisol)
Zona reticularis
Deepest cortical layer
weak androgens
Mineralocorticoids
The primary mineralocorticoid is aldosterone (most potent – electro regulating hormone).
Its secretion is regulated by the oligopeptide angiotensin II (angiotensin II is regulated by angiotensin I, which in turn is regulated by renin).
Aldosterone effects on metabolism
It increases urinary excretion of potassium ions
It increases interstitial levels of sodium ions
It increases water retention and blood volume
Primary hyperaldosteronism (Conn’s disease)
Caused by Aldosterone-secreting adrenal adenoma
Symptoms: HPN, hypokalemia, mild hypernatremia and metabolic alkalosis.
Secondary hyperaldosteronism
Occurs as a result of excessive production of rennin
Bartter’s syndrome (Bumetanide-sensitive chloride channel mutation)
Elevated concentrations of Aldosterone and rennin
Gitelman’s syndrome (Thiazide-sensitive transporter mutation)
Increased aldosterone
Liddle’s syndrome (pseudohyperaldosteronism)
resembles primary aldosteronism
clinically but aldosterone level is low and absence of HPN
Hypoaldosteronism
Due to destruction of the adrenal glands and deficiency of glucocorticoid.
It is also associated with enzyme 21-hydroxylase deficiency.
Symptoms: hyperkalemia and metabolic acidosis.
Glucocorticoids
Hormones produced in the adrenal cortex, like cortisol, influencing metabolism, immune response, and stress adaptation.
Its secretion is regulated by the hormone ACTH from the anterior pituitary.
TRUE
TRUE OR FALSE
Glucocorticoids are high in early morning (6-8am), lowest at night (10-12am).
Cortisol effects in Metabolism
It stimulates the release of amino acids from the body
It stimulates lipolysis, the breakdown of fat
it stimulates gluconeogenesis, the production of glucose from newly-released amino acids and lipids – resulting in hyperglycemia (anti-insulin effect)
It increases blood glucose levels in response to stress, by inhibiting glucose uptake into muscle and fat cells
It strengthens cardiac muscle contractions
It increases water retention
It has anti-inflammatory and anti-allergic effects
Androstenedione (Andro)
An androgenic steroid produced by the testes, adrenal cortex, and ovaries, serving as a precursor to testosterone and other androgens, as well as the parent structure of estrone.
Hypercorticolism (Cushing’s syndrome)
Is cause primarily by excessive production of cortisol and ACTH
Signs and symptoms: weight gain but with thin extremities (buffalo hump), hyperglycemia, thinning of the skin, poor wound healing, HPN, decreased WBC
Primary Hypocorticolism (Primary Adrenal Insufficiency)
Due to decreased cortisol production – 90% destruction of the adrenal cortex, Aldosterone deficiency, excess ACTH release
Disorders: Addison’s disease – hypotension, Hyponatremia, hyperkalemia, hyperpigmentation and darkening of the skin
Secondary and Tertiary Hypocorticolism
Due to hypothalamic-pituitary insufficiency with loss of ACTH.
No problem with mineralocorticoid secretion; absence of hyperpigmentation.
Androgens
Produce as by-product of cortical synthesis that are regulated by ACTH.
They circulate bound to steroid hormone binding globulin (SHBG).
Testosterone
A hormone with a wide variety of effects, ranging from enhancing muscle mass and stimulation of cell growth to the development of the secondary sex characteristics.
Dihydrotestosterone (DHT)
A metabolite of testosterone, and a more potent androgen than testosterone in that it binds more strongly to androgen receptors.
Androstenedione (Andro)
An androgenic steroid produced by the testes, adrenal cortex, and ovaries. While androstenediones are converted metabolically to testosterone and other androgens, they are also the parent structure of estrone.
Dehydroepiandrosterone (DHEA)
The primary precursor of natural estrogens, also known as dehydroisoandrosterone or dehydroandrosterone, produced by the reticularis and sulfated by SULT2A1 by the action of sulfotransferase.
Adrenal Medulla
It is located at the center of the gland, being surrounded by the adrenal cortex.
consisting of hormone-producing chromaffin cells that secrete epinephrine (adrenaline), norepinephrine (noradrenaline), and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons.
the principal site of the conversion of the amino acid tyrosine into the catecholamines epinephrine, norepinephrine, and dopamine.
Epinephrine (Adrenaline / Secondary Amine)
A hormone and neurotransmitter
Most abundant medullary hormone
Called the “flight and fright hormone” because it is released in response to physiologic (injuries) or
psychological (stress, anxiety) threats.
Released in response to stress.
Functions of Epinepherine
increasing heart rate
constricting blood vessels
dilating air passages
mobilizing glucose for energy (Glycogenolysis)
"On the kidney"
The term adrenaline is derived from the Latin roots ad- and renes and literally means ?
Catecholamine
What is the Chemical property that makes epinephrine a monoamine produced only by the adrenal glands from the amino acids phenylalanine and tyrosine?
Norepinephrine (Noradrenaline / Primary Amine)
A catecholamine acting as a hormone and neurotransmitter
involved in the fight-or-flight response, increasing heart rate, glucose release, and oxygen supply to the brain.
Noradrenergic
Areas of the body that produce or are affected by norepinephrine are described as
An increase in norepinephrine from the sympathetic nervous system increases the rate of contractions
Role of norepinephrine as neurotransmitter
dopamine β-hydroxylase
Norepinephrine is synthesized from dopamine by
noradrenegic neurons in the locus coeruleus
Norepinephrine is released to the CNS and Sympathetic Nervous System by?
The binding to adrenergic receptors
The actions of norepinephrine are carried out via
Dopamine
A catecholamine produced from 3,4-dihydroxyphenylalanine (DOPA), mainly found in the brain, influencing attention and responses.
Enkephalin
Produced by chromaffin cells, regulating pain perception.
Pheochromocytoma
Tumors of the adrenal medulla or sympathetic ganglia leading to catecholamine overproduction, causing symptoms like tachycardia, tightness of chest, pallor and sweating.
Neuroblastoma
A malignant condition in children associated with excessive norepinephrine production under extreme stress.