Mod8-Obj4&5: 6 Hormones of the endocrine system (control and function) Flashcards
The endocrine system is a three-tiered axis
Involves the release of hormones from the hypothalamus (hypothalamic releasing and release inhibiting hormones), the pituitary gland (anterior and posterior) and hormones releasing from various target hormones
Posterior pituitary hormones
The hypothalamas synthesis two hormones that are transported in vesicles down the axons of the hypothalamic-hypophyseal tract to the posterior pituirary where they are released into the blood stream
- Antidiuretic hormone (ADH)
- Oxytocin
Release of antidiuretic hormones (ADH)
ADH is a peptide hormone that is released from the posterior pituitary in response to changes in the solute concentration of blood plasma.
Changes in osmolarity are detected by…
Osmoreceptors in the hypothalamus
If solute conc of blood plasma is high, ADH will be synthesised and released as follows:
- Osmoreceptors are depolarised and transmit impulses to hypothalamic neurons to “turn on” the synthesis ADH
- The ADH is packaged into vesicles in the hypothalamus and transported along the nerve axons (hypothalamic-hypophyseal tract) to the posterior pituitary)
- Conduction of action potentials to nerve terminals in the posterior pituitary causes the release of ADH into the blood stream, where it can be transported to the kidneys.
(Release of ADH may also be triggered by low blood pressure (baroreceptor reflex), haemmorrhage, drugs and diuretics and inhibited by alcohol
Effect of ADH on urine formation
Once at the kidneys, ADH promotes the reabsoption of water, thus decreasing urine output. By keeping water in the body, which is reabsored into the blood stream, solutes are ‘diluted’, resulting in a decrease in solute concentration of blood plasma
Hyposecretion of ADH
Damage to the cells in the hypothalamus that produce ADH by head injury, can result in decrease in the amount of ADH synthesised and released
Hyposecretion of ADH: Diabetes insipidus
A disorder that results from the insufficient secretion of ADH and results in excessive urination (polyuria) due to water not being absorbed by the kidney.
-Treatment involves daily administration of ADH
Hypersecretion of ADH: Syndrome of inappropriate ADH secretion (SIADH)
Is a condition that results when too much ADH is secreted.
-Can be a result of a tumour, head injury or after neurosurgery.
SIADH results in excessive water retention which can cause weakness, muscle cramps, nausea, high blood pressure and fatigue
-Treatment involves water restriction and use of diuretics (promots urine formation and water loss)
Oxytocin
Oxytocin is released from the posterior pituitary and regulated by positive feedback in response to uterine contraction during childbirth and contraction of the mammary lobules of the breast during breastfeeding
During breastfeeding
- Suckling action of the infant stimulates nerve endings
- Neural pathways carry the stimulus to the hypothalamus (producing oxytocin)
- Oxytocin is transported in vesicles down the axons of the hypothalamic-hypophyseal tract to the posterior pituitary
- Depolarisation of the axon terminals in the posterior pituitary causes the release of oxytocin into the blood stream
- Oxytocin then stimulates the contraction of the mammary lobules in the breast (causing milk let down)
- As the infant recieves milk, it will continue the suckling action, which continues to stimulate the hypothalamus and the synthesis and release of oxytocin in a positive feedback loop
Anterior pituitary hormones
The anterior pituitary synthesises and releases seven hormones under the control of the hypothalamic release and release inhibiting hormones
- ) Growth hormone (GH)
- ) Thyroid stimulating hormone (TSH)
- ) Andrenocorticotropic hormone (ACTH)
- ) Follicle stimulating hormone (FSH)
- ) Luentinizing hormone (LH)
- ) Prolactin (PL)
- ) Melanocyte stimulating hormone (MSH)
Anterior pituitary hormones activate…
The second messenger cAMP (except GH) at their target organs. TSH, ACTH, FSH and LH are all tropic hormones, which are hormones that regulate the secretory action of another endocrine gland
Growth hormone (GH)
- Secreted by the anterior pituitary and controlled by two hormones (transported from the hypothalamus along the hypophyseal portal system)
1. ) Growth hormone releasing horme (GH-RH) stimulate secretion of GH from the anterior pituitary
2. ) Growth release-inhibiting hormone (somatostatin) inhibit secretion of GH from the anterior pituitary
Secretion of GH across the lifespan
Highest level of GH secretion occurs during adolescence and is decreased in the elderly
GH effects growth and metabolism
- The liver is the primary target of growth hormone. GH affects liver metabolism and induces the production of another endocrine hormone. IGF-1 increases bone and cartilage growth
- Stimulates cell division in bone and skeletal muscle for growth and maintenance of body tissues
- Promotes protein synthesis and fat usages
Hyposecretion of GH in children
May be as a result of a defect in the release of GH-RH or somatostatin from the hypothalamus, or a failure of the anterior pituitary. Genetic link, a brain tumour in the pituitary gland, an absent pituitary gland or a head injury are potential causes of pituitary dwarfism in children
Hyposecretion of GH in infants
Reduced rate of growth
- Treatment may involve the administration of GH or drugs to induce GH secretion.
- Admistration would be required every 3-7 days, depending on the extent
Hyposecretion of GH in adults
May occur after surgery for the removal of a pituitary tumour or a traumatic head injury.
- Link between deficient GH and cardiovascular complications
- May exhibit a decrease in body mass and bone density
- Treatment involves GH replacement therapy
Hypersecretion of GH
Commonly due to the presence of a tumour that prevents the release of somatostatin from the hypothalamus. The secretion of GH from the anterior pituitary is not regulated properly by the hypothalamus, resulting in excess being released in the blood stream.
-Stimulates the liver to produce IGF-1, increasing soft and bony tissue growth in the body
Hyersecretion of GH in childhood
Rapid growth occurs resulting in pituitary gigantism
-If left untreates, usually results in cardiovascular complications that can be fatal
Hypersecretion of GH in adults
- acromegaly,* as a result of a tumour
- Increase in the size of hands and feet over several years, enlargement of the brow and mandible.
- Will continue to develop including skin tags, increase in the size of body organs, deepening voice, enlargement of the tongue and sleep apnea.
- Treatment involves surgical removal of tumour and suppression of GH secretion from anterior pituitay using a synthetic (artificial) form of somatiostatin
Adrenocorticotropic Hormone (ACTH)
Synthesis and secreted by the anterior pituitary.
- Secretion of ACTH is stimulated by corticotropin-releasing hormone (CRH) from the hypothalamus (daily rhythm)
- CRH peak early just before waking, but may be altered by external/internal changes (fever).
Secretion of ACTH into the blood stream stimulates the adrenal gland to release…
- Corticosteroid hormones (glucocorticoids, i.e. cortisol) from the adrenal cortex
- Small amounts of aldosterone (mineralcorticoids) from the adrenal cortex
(controlled by negative feedback, whereby cortisol acts on the anterior pituitary and hypothalamus to reduce the secretion of ACTH from the anterior pituitary and the release of CRH from the hypothalamus)
Hypersecretion of ACTH
hypersecretion of hormones from the adrenal gland (cortisol, adrenaline, aldosterone) which have a range of physiological effects
Gonadotrophins
The anterior pituirary synthesis and secretes two gonadotrophins into the blood stream:
- Follicle stimulating hormone (FSH)
- Lutenizing hormone (LH)
Stimulated by hypothalamic gonadotropin-releasing hormone (GnRH)
Gonadotrophins (FSH)
Protein hormone that stimulates gamete production in males and females.
- In women, FSH promotes development of follicles in the ovaries and in combination with LH, the secretion of estrogen (prominant in the ovarian cycle)
- In males, FSH stimulates the maturation of sperm in the testes. +Inhibited by inhibin, a hormone released by the testes and ovaries
Gonadotrophins (LH)
Promotes the production of gonadal hormones
- -Estrogen and progesterone* in females (required for ovulation)
- Testosterone in males (maturation of sperm)
Prolactin
Peptide hormone synthesised in lactotropes in the anterior pituitary
- Secretion is normally inhibited by dopamine which is released by the hypothalamus.
- Release is stimulates in response to prolactin releasing factors and thyrotropin releasing hormone from the hypothalamus
Positive feedback of prolactin
The level of prolactin circulating in the blood slowly begins to rise towards the end of pregnancy due to estrogen.
- The release of prolactin (anterior pituitary) is continued by the stimulus of an infant suckling the nipple
- Causing a positive feedback loop the continues the secretion of prolaction, allowing lactation to occur
Thyroid stimulating Hormone (TSH)
Produced in the anterior pituitary and secreted in response to the release of thyrotropin releasing hormone (TRH) from the hypothalamus
- TSH stimulates the normal development and secretory activity of the thyroid gland (secretes its own hormones)
- Rise in T3 (triiodothyronine) and T4 (thyroxine) in blood levels inhibit the release of TRH (hypothalamus) and TSH (anterior pituitary) via negative feedback
Thyroid Gland
Located at the front of the neck
- secretes T3 and T4 (thyroid hormone) from specialised cells called follicular cells
- The follicular cells perform all the functions required to secrete thyroid hormones, including trapping iodine, which has a role in synthesis of thyroid hormones.
- Parafollicular cells secrete calcitonin
Thyroid Hormone (TH)
- Stimulates growth in conjunction with growth hormone
- Increases the basal (resting) metabolic rate through cellular metabolism, heat production and myocardiarial (heart) contractility
- Promotes development of the skeletal and nervous systems in the fetus and infants
Calcitonin
Synthesised in the parafollicular cells
- Inhibits the release of calcium from the bone matrix
- Stimulates calcium uptake and incorporation into bone matrix
- Calcitonin is an agonist to the parathyroid hormone*
Hypothyroidism may be a result of:
- Defects in normal functioning
- Inadequate TRH release or TSH secretion
- Inadequate dietary iodine
- Surgical removal of part or all of the thyroid gland
Results of hyposecretion of TH
Overall metabolic rate of the body is reduced.
- Individuals will feel cold, have dry skin and puffy eyes, as well as feel lethargic and sluggish
- Subject to weight gain
- In infants profound physical and mental retardation is evident
Hypersecretion of TH
Hyperthyroidism is usually the result od overstimulation of the thyroid gland
- Graves disease involves the immune system producing an antibody the stimulates the action of TSH (overstimulatinf the thyroid gland)
- More common in women than men
Results of hyper secretion of TH
- Increased metabolic rate
- Weight loss, rapid pulse, nervousness
- Protruding eyeballs (exophthalmia)
Goitre
Hypersecretion and hyposecretion of the thyroid hormone can result in an enlarged thyroid gland=goitre
Calcium
- Found in the skeleton and extracellular fluid
- Excess calcium can be taken up by the bone and released when blood calcium levels are low
Esesential in a number of body functions including;
- Blood clotting
- The excitability of nerve and muscle cell membranes (synapse)
- Muscle contraction
Calcium levels are regulated by a number of hormones;
- ) Calcitonin
- ) Parathyroid hormone
- ) Vitamin D (calcitriol)
Parathyroid hormone (PTH)
- Found in the posterior aspect of the thyroid gland
- -Calcium homeostasis*
- PTH is released in response to a drop in blood calcium levels
PTH functions to maintain increase blood calcium levels to maintain homeostasis by:
- Stimulating osteoclast activity to digest bone
- Enhancing the reabsorption of calcium at the kidneys
- Promoting the activation of vitamin D to increase the uptake of calcium from the digestive tract
Hyperparathyroidism
Usually due to a tumour, usually results in the over production and secretion of PTH
can cause:
- Hypercalcaemia
- Softening of bones and deformities
- Depression of the nevous system
- Formation of kidney stones
- Cardiac arrhythmias
Hypoparathyroidism
Too little PTH being produced, may be a result of the presence of a tumour, surgical removal of parathyroid gland or a deficiency in magnesium
May result in:
- Hypcalcaemia
- Cardiac arrhythmia (abnormal heart beat)
- Tingling sensations
- Tetany (twitching muscles)
- Respiratory paralysis
- Death
Insulin
Allows the transport of glucose into cells for the production of ATP.
- Is secreted and synthesised by the B cells in the pancreas, where it is stored until its secretion is triggered by a rise in blood glucose levels
- Pancreas also syntheses and secretes glucagon from a cells. Secretion is triggered by a fall in BGLs and aims to mobilise the body’s energy stores
Insulin and Glucose Uptake
- ) Insulin binds to a recptor on the surface of the cell
- ) Insulin-receptor complex triggers a signalling pathway inside the cell that moves the insulin responsive glucose transport units to the plasma membrane of the cell
- ) Glucose transport units, transport glucose across the plasma membrane into the cell where it can be used to make ATP, thus lowering blood glucose levels
- ) Excess glucose can be stored as glycogen in adipose and liver cells
Glucagon
Released from a cells of the pancrease when the BGL s are low to promote the breakdown of our energy stores in muscle and liver cells.
-The breakdown products can be used to make glucose and therefore ATP
The major target of glucagon is the liver where it promotes…
- ) The breakdown of stored glycogen to glucose, known as glucogenolysis
- ) The production of glucose from amino acids and fatty acids, known as gluconeogenisis
* -*The release of these products into the blood increases BGL
Homeostatic imbalances of insulin
A chronic disorder of carbohydrate, protein and fat metabolism is Diabetes Mellitus (DM). DM occurs when not enough insulin is synthesised, or secreted (hyposecretion) from the pancreas or the insulin that is secreted from the pancreas is defective (hypoactivity)
Two types of DM
- ) Type 1 DM: absolute lack of insulin due to destruction of B cells by the body’s own immune system
- ) Type 2 DM: occurs when there is hyposecretion of the insulin or it is hypoactive
Hyperglycaemia
Hyperglycaemia is characterised by a consistently high BGL due to
an inability of cells to take glucose from the blood
- Indicates that the individual has diabetes or is not managing the condition correctly
- Excess glucose removed from the blood at the kidneys and excreted in urine, eventually leads to dehydration, through increased water loss
There are a number of consequences of uncontrolled DM and these include:
- peripheral neuropathy loss of sensory function of peripheral nerves, particularly in the feet
- ) Nephropathy: kidney disease
- ) Vascular complications: interfere with the circulation of blood around the body
- ) Increased chance of infections as microbes like sugar
Hypoglycaemia
Due to the presence of a tumor in the B cells of the pancreas causing hypersecretion of insulin
The adrenal glands
Is two endocrine glands in one consisting of the adrenal cortex and the adrenal medulla
The adrenal cortex
The adrenal cortex consists of three layers of glandular tissue and is responsible for the synthesis and secretion of the corticosteroids, cortisol & aldosterone
The adrenal medulla
The adrenal medulla consists of nervous tissue that secretes the catecholamines, adrenalin & noradrenalin, in response to the sympathetic nervous system
Function of cortisol (glucocorticoid)
Cortisol is released from the adrenal cortex and is known as a glucocorticoid due to its effects on glucose metabolism
- Helps to maintain blood glucose levels by accelerating the rates of glucose synthesis and glycogen formation, influencing energy metabolism within body cells
- Can increase BP as it can activate vasoconstrictors to return BP to normal
- Released during the stress response
Regulation of cortisol release
Cortisol is released from the adrenal cortex in response to stimulation by ACTH (anterior pituitary)
- Release of ACTH is controlled by both corticotropin-releasing hormone (CRH) and negative feedback
When cortisol levels are high…
The released ACTH and CRH is inhibited, thus inhibiting the release of cortisol
- Cortisol peaks just prior to awakening and is at its lowest in the evening (before bed)
Amount of cortisol
- The amount of cortisol released from theadrenal cortex is increased in response to stressors
- Ideal amounts of cortisol promote normal energy metabolism
- Too much cortisol has significant anti-inflammatory effects
Hypersecretion of cortisol
The oversecretion of cortisol can be due to the presence of a tumor (or brain injury) on the adrenal cortex, anterior pituitary or in the hypothalamus
- Cushing syndrome is used when the hypersecretion is being stimulated by ACTH from the anterior pituitary
Cushing disease characteristics
- Moon face and buffalo hump
- Depressed cartilage and bone formation (fractures)
- Inhibition of inflammation and depression of the immune system (infections)
- Changes in cardiovascular, neural and gastrointestinal function
Hyposecretion of cortisol
Can be due to a tumour or injury to either the adrenal cortex, anterior pituitary or hypothalamus
- Addison’s disease is caused by either the destruction of the adadrenal gland by the body’s own immune system, or trauma/haemorrhage of the adrenal gland
- Regulation of the levels of each hotmone, is not regulate by negative feedback
Clinical features of a reduction of cortisol (Addison’s disease)
- Decrease in glucose and Na+ levels
- Weight loss
- Severe dehydration
- Hypotension
Aldosterone (mineralcorticoid)
Released by the adrenal cortex
- Important in regulating electrolyte levels in the ECF, particularly Na+ and K+
- Stimulated by a decrease in blood volume and pressure and an increase in blood K+ levels
- NOT UNDER PITUITARY CONTROL
Secretion of aldosterone
- Stimulates the conserveation of Na+ and the elimination of K+
- More Na+ are reabsorbed by the kidneys, sweat glands, salivary glands and pancreas to prevent loss of Na+ in urine, sweat, saliva and digestive secretions respectively
- Water is reabsorbed, increasing blood volume and pressure
Hypersecretion of aldosterone
Due to tumors on the adrenal cortex or other conditions associated with fluid and electrolyte balance
- NOT UNDER THE CONTROL OF THE PITUIRARY GLAND
- Development of hypertension and oedema due to excessive Na+ and therefore water reabsorbtion
- Depletion of K+ leading to the abnormal functioning of neurons and muscles (K+ is essential in the resting membrane potential of cells)
Hyposecretion of ACTH
Results in a resuction in the amount of these hormones being released
Adrenalin
The adrenal medulla synthesis and secretes the catecholamines, adrenalin & noradrenalin
- Under the control of the SYMPATHETIC DIVISION
Function of adrenalin and noradrenalin
Secreted (slowly) and bind to the adrenergic receptors (a & B) on cells
- In response to stimulation by sympathetic nervous system, i.e.) during the short term stress response, secretion is increased to accelerate the utilisation of cellular energy and mobilise energy reserves
- Additionally secreted in response to ACTH from the anterior pituitary
Adrenalin and noradrenalin hormones…
- Breakdown glycogen stores to glucose for ATP production in skeletal muscle and neural tissue
- Increase fatty acid production (from adipose tissue) for use in ATP production
- Stimulat B1 receptors in the heart to increase heart rate and force of contraction
- constrict blood vessels for diversion of blood to brain, heart and skeletal muscles
- Are involved in the stress response
The stress response
Also known as the general adaptation syndrome (GAS)
Three phases
- Alarm phase
- Resistance phase
- Exhaustion phase
The stress response: The alarm phase
Essentially mobilises the energy reserves and prepares the body for the fight or flight response
The stress response: Resistance phase
Dominated by cortisol
- Maintains the energy demands of the body
The stress response: The exhaustion phase
When the resistance phase ends and homeostatic regulation breaks down, the exhaustion phase begins
- Multiple organ systems will begin to fail as the high energy demands of the body cannot be met, resulting in death
The stress response results in:
- Mobilisation of energy stores from the liver and fat
- Increased heart rate and blood pressure
- Constriction of blood vessels to shunt blood to skeletal muscles and away from other organs
- Bronchiole dilation
- Increased metabolic rate
The short-term stress response
Activated by the sympathetic nervous system
- Secretes adrenalin and noradrenalin and is fast and short lived
The long term stress response (chronic)
Involves the release ACTH, the secretion of cortisol & aldosterone
- Accumulative and prolonged stress can lead to severe complication
Long term release of cortisol and aldosterone will:
- Effect kidney function due to increase Na+ and water retention (aldosterone): increased blood volume and blood pressure
- Increased blood glucose levels to maintain the energy demands of the body
- Suppress the immune system, making an individual more prone to illness
- Long term stress can lead to severe illness or can even be fatal
Erythropoietin
Is a glycoprotein hormone that is secreted by the kidneys in response to a drop in RBC
- Signals the bone marrow to increase RBC production (erythropoiesis)
- Too little erythropoietin, may result in anaemia
