Chapter 18 Endocrine System Flashcards
The Nervous and Endocrine System
Work tgt to coordinate functions of all body systems
How does the NS act
Through neurons and secretion of NT
How does the ES act
though hormones produced by cells or endocrine glands
Can a mediator be a hormone and a NT?
Yes, ex. Norepinephrine
Compare NS and ES
NT:
-released locally in response to AP
-Target muscles cells, gland cells, other neurons
-Action occurs within a millisecond and brief
Hormones:
-delivered throughout body and blood
-Acts far from the release
- Onset of action varies from secs to days
-Last longer
General Function of hormones
Regulation of different proccesses (everything in interstitiial fluid)
Exocrine vs Endocrine Glands
Exocrine - secrete products onto an epithelial surface (the outer body)
Endocrine - secrete hormones into interstitial fluid, ends up in the blood stream, cardiovascular system then bind to cell that has their receptor
How Hormones affect target cells
Hormones needs to bind to receptors non covalently
Factors that determine level of activation
-blood levels of hormones
-number of receptors on the cell
-affinity of receptors for its hormones
How can a target cell change to +/- binding
Target calls can change the amount of receptors that are present
Down-regulation - Too much hormones so decrease receptors through endocytosis which degrade them. Lowers sensitivity of cell to hormone
Up-regulation - Defiency in hormones so increase in receptors. Target tissue more sensitive
Circulating hormones
Travel through bloodstream to reach far target cells
Autocrine
hormone acts on the cell that produced it
Paracrine
Affects nearby cells
2 chemical classes of hormones
Lipid soluble hormones
-Steriods
-thyroid hormones
-nitric oxide (vasodilation)
Wate soluble hormones
-Amine hotmones
-peptide/protein hormones
eicosanoid hormones (made from fatty acids)
Lipid soluble hormones
-transported in the blood
-hydrophobic, cant travel in blood easily
-bound to a transport protein (amphipathic): prevents clumping and increases molecule size so less likely to be filtered out by kidneys. Hormone dissociates from transport protein as it approaches target tissue and diffuses into cells.
Action Lipid soluble hormones
- Hormone diffuses INTO CELL
- hormone binds to receptor in the cytoplasm or nucleus
- newly formed mRNA directs synthesis of specific protein on ribosomes
- new proteins alter cells activity
Cell activity changes because of the new proteins
View page 19
Water soluble hormones
hydrophilic - freely travels in blood
Action Water soluble hormones
- Binding of hormones (first messenger) to its receptor activates G protein, which activates adenylate cyclase DOES NOT GO INSIDE THE CELL
- Activated adenylate cyclase converts ATP to cAMP, which serves as a second messenger to activate protein kinases
- Activated protein kinases phosphorylated cellular proteins
- Millions of phosphorylated proteins cause reactions that produce physiological responses
Look at slide 20
Three types of stimulus that trigger hormone secretion
Humoral Stimuli
- Hormone released in direct response to changing levels of certain chemical in blood or body fluids. Environment is read and monitored and hormones are secreted based on the environment they read
Neural Stimuli
-AP trigger the release of hormones from certain glands
Hormonal Stimuli
-Hormone released in response to other hormones
Describe the feedback mechanisms that regulate hormone activity
Most are negative but some are positive feedback systems.
Release is in short bursts with little/ no secretion between bursts
When stimulated an edocrine gland will release its hormone in more frequent bursts increasing the concentration in the blood.
In the absence of stimulation, the blood levels of the hormone decreases
Hypothalamus
Regulates ANS, body temp, thirst, hunger, sexual behaviour, fear, and anger by receiving signals from diff parts of the brain then send signals to the pituitary gland which produces several hormones.
Infundibulum
attatches hypothalamus w the pituitary gland
Anterior pituitary gland
Secrete hormones in response to the hypothalamus hormones that are delivered.
- Neurosecretory cells release hormones into the primary plexus of the hypopheseal portal sytem
- Hormones go from the primary plexus to the secondary plexus of the hypopheseal portal system
Growth Hormone
Release of growth hormone-releasing hormone (GHRH) from the hypothalamus cause the release of GH.
-promotes growth of skeleton and muscle
-release insulin like growth factor (IGF): promote cell growth and division by increasing uptake of A.A and protein synthesis; inhibit the breakdown of proteins.
IGF
-promote cell growth and division by increasing uptake of A.A and protein synthesis; inhibit the breakdown of proteins
-IGF stimulate breakdown of glycogen to make glucose avail for ATP synthesis.
-Stimulate lipolysis which are fatty acids used for ATP production
Abnormal secretion of GH
Hyposecretion: pituitary dwarfism - short but normal proportions
Hypersecretion: Giantism - abnormally tall but normal proportions
Acromegaly - enlarged bines of hands, feet, and face
Regulation of hGH
- low blood glucose stimulates the release of GHRH
- GHRH stimulates secretion of hGH
- hGH and IGF speed up breakdown of glycogen into glucose
- Blood glucose levels rise to normal
- If blood glucose continues to increase hyperglycemia inhibits release of GHRH
- high blood glucose stimulates release of Growth Hormone Inhibiting Hormone (GHIH)
- GHIH inhibits secretions of hGH.
- low level of hGH and IGFs decrease glycogen break down into glucose
- Blood glucose is normal
- If blood glucose continues to decrease hypoglycemia inhibits release of GHIH
TSH
- Thyrotropin-releasing hormone (TRH) from hypothalamus trigger release of TSH.
- Thyroid gland produces more T3 and T4
Thyroid hormones are involves in the regulation of metabolism
FSH and LH
- Gonadotropin Releasing Hormone (GnRH) from hypothalamus triggers release of FH and LH
- Ovaries and Testes Respond
- Produces more sex hormones and leads to the development of gametes
Prolactin
- Prlactin Releasing Hormone (PRH)and Prolactin Inhibiting Hormone (PIH) control release of prolactin
- Mammary gland responds
- Tgt w progesterone prepares and maintains milk production and secretion
Adrenocorticotropic Hormone (ACTH)
Corticotropin-releasing Hormone (CRH) stimulates release of ACTH
Cause adrenal glands to produce glucocorticoids, cortisol, which provide resistance to stress and act as anti-inflammatory agents
Melanocyte Stimulating Hormone
- CRH stimulate the release of MSH.
- melanocytes and parts of the brain respond
- Melanin is produced which may play a role in certain brain functions. Cause darkening of the skin
Posterior Pituitary Gland
Does not synthesize its own hormones
- Neurosecretory cells synthesize hormones in the hypothalamus.
- Hormones are transported down the axons located in the infundibulum and the posterior pituitary lobe
- Hormones are stored in the posterior pituitary lobe in the axon terminals of neurosecretory cells until they need to be released
- Hormones Oxytocin and ADH are released in the capillary plexus of the infundibular process
Oxytocin (OT)
enhance muscle contraction of the uterus to induce labour and release the placenta. Stimulates ejection of milk from breasts.
Antidiuretic Hormone
Increase blood pressure by keeping water in
-decreasing urine production
-decreasing swear production
-increasing vasoconstriction
Negative Feedback mechanism of ADH
- High blood osmotic pressure stimulates hypothalamic osmoreceptors
- Osmoreceptors activate neurosecretory cells that synthesize and release ADH
- AP liberate ADH from axon terminals in the posterior pituitary into the bloodstream
- Kidneys retain more water which decreases urine output, Sweat glands decrease preparation, arterioles constrict which increases BP
- Low blood osmotic pressure inhibits hypothalamic osmoreceptors
- Inhibition of osmoreceptors reduces or stops ADH secretion
Hyposecretion of ADH
Diabetes Insipidus
-Pee a lot
- Dehydration and thirst
Thyroid Gland
Secrete hormones that affect metabolic rate and calcium levels in body fluids
T thyrocytes
Simple cuboidal epithelium where proteins are stored. Produce T3 and T4
C thyrocytes
Produce calcitonin which activates osteoblasts and inhibits osteoclasts resorption - regulate calcium levels
Thyroid Hormones
T4 is more abundant
T3 is more potent
Number is determined by the amount of tyrosine it has
Function:
(1) oxygen use and basal metabolic rate, (2) cellular metabolism, and (3) growth and development.
Formation, storage, and release of Thyroid hormones
- Iodid trapping: t thyrocytes trap iodide ions by transporting them from blood into their cytosol. Thyroid gland contains most of the iodide in the body.
- Synthesis of thyroglobulin: Made while trapping iodide. Then vesicles filled w TGB undergo exocytosis to go to the lumen of the thyroid follicle.
- Oxidation of iodide: negative iodide ions must be oxidized so that it can bind w tyrosine. As they oxidize they go to the lumen of the follicle.
- Iodination of tyrosine: As iodide atoms form, they react w tyrosines that are part of the TGB molecule. The binding of a tyrosin determines the number.
Binding of iodide and tyrosine forms a colloid
- Coupling of T1 and T2. During the last step in the synthesis of thyroid hormone, two T2 molecules join to form T4, or one T1 and one T2 join to form T3.
- Pinocytosis and digestion of colloid. Droplets of colloid reenter T thyrocytes by pinocytosis and merge with lysosomes. Digestive enzymes in the lysosomes break down TGB, cleaving off molecules of T3 and T4.
- Secretion of thyroid hormones. Because T3 and T4 are lipid-soluble, they diffuse through the plasma membrane into interstitial fluid and then into the blood. T4 normally is secreted in greater quantity than T3, but T3 is several times more potent. Moreover, after T4 enters a body cell, most of it is converted to T3 by removal of one iodine.
- Transport in the blood. More than 99% of both the T3 and the T4 combine with transport proteins in the blood, mainly thyroxine-binding globulin (TBG).
hyperthyroidism
Graves disease
-autoimmune that produce antibodies that mimic TSH
Iodine deffiency
Goiter
Control of Thyroid hormone secretion
When levels drop
- Anterior pituitary secretes TSH
- T thyrocytes produce T3 and T4
- Elevated levels inhibit the production of Thyroid releasing hormone and TSH.
View table 18.
parathyroid Gland
release PTH which increases osteoclast resorption which releases calcium and phosphate from bone into blood.
-raises blood calcium levels
-promotes the formation of calcitriol which enhances the absorption of calcium and magnesium by interstitial cells.
blood calcium homeostasis
When blood calcium levels high
- C thyrocytes secrete calcitonin
- inhibits osteoclast resorption which decreases blood calcium levels
When blood calcium levels low
- Parathyroid secretes PTH
- increases osteoclast resorption increasing blood calcium levels
- PTH also stimulates kidney to produce calcitriol
- Calcitriol stimulates increased absorption of calcium which increases blood calcium levels as well
Hypoparathyroidism
Low levels of calcium, magnesium, and phosphate: results in twitches, spasms
Hyperparathyroidism
High levels of calcium, phosphate, magnesium: Excessive bone resorption so that bones become soft and easily fractured
Pancreatic islets
Alpha cells - glucagon
Beta cells - insulin
Acini
Exocrine function of the pancreas
-produce digestive enzymes and buffer
Glucose Homeostasis
- Low blood glucose
- Aphha cells produce glucagon which convert glycogen into glucose
- Glucose released by hepatocytes raises blood glucose levels to normal
- High blood glucose
- Beta cells secrete insulin which speed the breakdown of glucose into glycogen
- Blood glucose decreases to normal
Diabetes Mellitus
Type 1: Unable to produce insulin
Type 2: Decreased sensitivity to insulin due to reduces insulin receptors on target cells
The signs and symptoms of diabetes include increased thirst, frequent urination, increased hunger, fatigue, unexplained weight loss, blurred vision, irritability, slow-healing cuts and sores, frequent infections, and ketone bodies in the urine. Because body cells can’t use glucose to produce energy, they break down fats into fatty acids and glycerol. The further metabolism of fatty acids produces ketone bodies. As the ketone bodies build up, the blood pH falls (becomes more acidic). This condition is called ketoacidosis and can result in death if not treated quickly.
Adrenal glands
produce epinephrine and norepinephrine
Adrenal Gland Medulla
- NT from hypothalamus trigger adrenal medulla to release hormones epinephrine and norepinephrine
- They cause the fight or flight response
Fight or flight response
-Increased HR and force of contraction
-constriction of blood vessels
-decrease in digestive activities
-dilation of blood vessels of heart, lungs, brain, and skeletal muscle
-conversion of glycogen into glucose in the liver
-dilation of air ways
-decrease blood flow to kidneys, leading to decrease in urine output, water retention and elevates BP
Stress Response
- Fight or flight: short lives and is initiated by AP from the hypothalamus
- Resistance Reaction: Long lasting and helps body continue fighting a stressor long after the fight or flight response is gone. Initiated by hormones released by the hypothalamus.
- Exhaustion: Body runs out of resources and cannot sustain the resistance. Body becomes depleted.
Stress response resistance reaction
See pg 103 FIGURE 18.19
Ovaries
Secrete:
Estrogen: Which maintains enlargement of breast and widening of the hips
Inhibin: Inhibits FSH
Progesterone: Prepares mamillary glands for lactation
relaxin: Helps dilate the uterine cervix during labour and delivery
Testes
Secrete:
Testosterone: Regulates descent of testes and sperm production
Inhibin: Inhibits FSH secretion
Pineal Gland
Secrete melatonin which is involved in the circadian rhythm
Thymus
T lymphocyte development and activation and in various responses of the immune system
Heart
Release Atrial Natriuretic Peptide in response to high BP
Kidney
Release erythropoietin in response to hypoxia
Adrenal Gland Cortex
three dif hormones
1. Glucocorticoids - include cortisol
2. mineralocorticoids - maintain blood volume and electrolyte levels
3. Androgen - role in male features
Glucocorticoids
Provide resistance to stress by:
-promoting protein and fat breakdown for ATP
-gluconeogenesis - conversion of AA and fats to glucose
-enhancing vasoconstriction which increases BP
have anti-inflammatory and immune impression effects as they delay tissue repair
Cushings syndrome
Hypersecretion of glucocorticoids
Regulation of Glucocorticoid levels
- Low levels in blood cause neurosecretory cells in the hypothalamus to release cortotropin-releasing hormone (CRH)
- Corticotropin-releasing hormone (CRH) stimulates the anterior pituitary to release ACTH.
- ACTH stimulates the adrenal cortex to release glucocorticoids
- Increases glucocorticoid levels in blood
Mineralocorticoids
regulate homeostasis of sodium, potassium and water
-the main hormone is aldosterone: which promotes sodium absorption, thereby promoting water absorption
Regulates blood volume and BP
Regulation of aldosterone: renin angiotensin aldosterone pathway
REFER TO SLIDE 94
Regulation of Aldosterone:
Renin-angiotensin-aldosterone (RAA) pathway
The RAAS is stimulated by a decrease in blood volume and/or blood pressure
◦ Low BP stimulates juxtaglomerular cells in the kidney to secrete the enzyme
renin
◦ Renin converts the plasma protein angiotensinogen (produced in the liver)
into angiotensin I.
◦ As angiotensin I circulates to the lungs, an enzyme called angiotensin
converting enzyme (ACE) converts angiotensin I to angiotensin II
◦ Angiotensin II stimulates the adrenal cortex to secrete aldosterone (salt and
H20 resorption indirectly increases BP), and it is a potent vasoconstrictor
(which directly increases BP
