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In order to maintain homeostasis, what two main systems of the body are responsible for the task of continually receiving, interpreting, and responding to stimuli?
- The nervous system and endocrine systems - coordinate all body systems
- Controlled by mediator molecules
- Nervous: neurotransmitters
- Endocrine: hormones
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hormone
- a mediator molecule secreted from one part of the body that circulates via the body fluids to influence cells in another part of the body
- Typically, secreted into interstitial fluid, then bloodstream till it finds target cell
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The endocrine system
- made up of primary & secondary endocrine organs
- Primary consists of the pituitary, thyroid, parathyroid, adrenal and pineal glands (meaning their primary function is endocrine)
- Secondary are other organs that secrete hormones, but they are not exclusively endocrine glands
- Together with nervous system, coordinate vital body functions to maintain homeostasis
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What are the secondary endocrine organs?
- Hypothalamus, thymus, pancreas, ovaries, testes, kidneys, stomach, liver, small intestine, skin, heart, and placenta
- They have endocrine functions and other functions as well. So not strictly endocrine
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What function do hormones have
- control of composition and voume of internal environment
- regulate metabolism and energy balance
- contraction of smooth and cardiac muscle fibers
- influence glandular secretions
- Integration of growth and development
- reproductive control
- regulation of sleep-wake cycles
- emergency control during physical & mental stress like trauma, starvation, hemorrhage
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recall difference btwn exocrine and endocrine
- Exocrine is secreting products of cells through a duct (tube)
- Endocrine is secreting into fluids
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Control mechanisms of nervous system
- Use neurotransmitters, which are released locally across a synapse
- Targets muscle cells, glands and other neurons
- Onset of action is Milliseconds
- Action duration is also Milliseconds
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Control mechanisms of endocrine systems
- Use hormones; responses are usually distant from the site of release
- Targets cells throughout body; bind to receptors in or on target cells
- Onset of action: Seconds to hours to days
- Action duration: generally longer
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Hormone receptors
- Are simply cellular proteins
- The presence/absence/number of hormone receptors that dictate action of a hormone
- Likewise, Target cells can dictate # of receptors available to bind hormone. They can:
- Up-regulation: increased responsiveness by increasing receptor #'s
- Down-regulation: decreased responsiveness by decreasing receptor #'s
- *therefore,
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circulating hormones
hormones secreted into the interstitial fluid and then into the blood stream, giving them access to the entire body
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paracrines
Hormones secreted into the interstitial fluid that act on neighboring cells
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Autocrines
- Hormones secreted into the interstitial fluid that act on the same cell that secreted it
- therefore the cell can act on itself
- Cancer cells have this ability
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What is one of the main classifications that separates different types of hormones?
- based on their solubility in water or lipids
- recall that a substance can more easily move into a cell if it is small, neutrally-charged OR lipid soluble
- Lipid-soluble hormones or water-soluble hormones
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lipid-soluble hormones
- can freely diffuse into a cell and bind directly to intracellular receptors
- Include steroid hormones, thyroid hormones and nitric oxide
- most of the available lipid-soluble hormone is carried in blood by transport proteins
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What is a "steroid"
- isn't based on what molecule does, but simply on it's shape
- Has a 4 ringed structure
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water-soluble hormones
- freely circulate in the bloodstream; don't need carrier or to be attached to another molecule
- can't pass through cell membrane; must bind to membrane receptors and initiate a change in the cell indirectly
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transport proteins
- proteins which lipid-soluble hormones must bind to in the blood
- By binding, the water solubility of the hormones is increased
- also keep smaller lipid-soluble hormones from getting filters in the kidney and lost in urine
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Lipid-soluble hormone action: explain the process
- Hormone diffuses into the cell through the lipid-bilayer
- If it's the target cell, hormone can bind and create a receptor-hormone complex within the cytosol or nucleus
- This complex can alter the gene expression by "turning" the genes encoded by the cell's DNA "on or off"
- Therefore, depending on type of receptor hormone binds to, can be excitatory or inhibitory in that cell.
- End result is the alteration of cell's activity
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catecholamines
- "-amines" = functional group
- "catecho-" = the ring, or structure, of the molecule
- includes epinephrine, norepinephrine, and dopamine
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Examples of water-soluble hormones:
- amines - epinephrine, norepinephrine, dopamine
- peptides/proteins - insulin, parathyroid hormone
- Eicosanoids - prostaglandins
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Water-soluble hormone action: explain process
- The hormone (1st messenger) attaches to receptors on plasma membrane of target cell
- Receptor-hormone complex activates a G Protein (like a cellular switch "on" or "off")
- G protein activates adenylate cyclase
- Adenylate cyclase converts ATP to cyclic AMP (cAMP) (2nd messenger) in the cytoplasm
- cAMP activates enzymes (protein kinases) which bring about the desired effect within the cell (therefore, 2nd messenger can act as activators, inhibitors or cofactors)
- Ca++ is also a common 2nd messenger
- *recall story about student trying to get friend message, so uses another student to get message to friend in class
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Amines
- water soluble hormones
- include epinephrine, norepinephrine, dopamine
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Can Water-soluble hormone freely enter cell?
- because of their limited lipid solubility, they can't freely enter cell
- *recall story of student trying to get message to friend in class. Uses 2nd student to get message to them.
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Water-soluble hormone action: first 2 steps
- 1- The hormone (first messenger) binds to receptor on cell membrane. By forming a receptor-hormone complex, a membrane protein (G protein) is activated.
- The activation of the G protein will then activate the enzyme adenylate cyclase.
- 2- Adenylate cyclase converts ATP into cyclic adenosine monophosphate (cAMP , which is second messenger)
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Water soluble hormone action: 3rd and 4th steps
- 3. cAMP will activate one or more protein kinases
- *remember, kinases phosphorylate (add a phosphate to other molecules)
- 4. In their case, phosphorylated molecules are proteins. Through phosphorylation, some proteins are activated and some are deactivated.
- *There are many different types of kinases, so the effects can be numerous
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Water-soluble hormone action: last step
- to limit the duration of the response, unless new hormone binds to the receptors, the enzyme phosphodiesterase inactivates cAMP
- *Think phospho-"DIE"-sterase
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What other second messengers can there be for water-soluble hormone action
include Ca++ ions and cGMP (cyclic guanosine monophosphate)
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Hormone secretion is signaled and regulated by what different mechanisms
- signals from nervous system
- chemical changes in blood
- levels of other hormones
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What type of feedback system do most hormones work through?
- Negative, few by positive
- Negative feedback = hormone output reverses a particular stimulus
- Positive feedback = hormone output encourages and reinforces the stimulus
- *recall with any feedback system, there must be a receptor for stimulus, interpretation (control) center, and an initiated response
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What factors influence the responsiveness of a target cell to a hormone
- The concentration of hormone
- presence/absence/number of receptors available to bind hormone
- influences of other hormones
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permissive effect
When two hormones are required for desired action
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synergistic effect
when two hormones dictate similar actions and work together to create an even more powerful result
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antagonistic effect
- When two hormones oppose each other
- ex: insulin/glucagon
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hypophysis
- what the pituitary gland was formerly referred to
- pea-shaped gland - anatomically & functionally connected to hypothalamus by the infundibulum
- has two lobes: anterior and posterior
- It's also commonly referred to as the "master glad"; but recall it is controlled by the hypothalamus
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hypothalamus
- the major link btwn the nervous and endocrine systems: received input from several regions in brain
- controls pituitary gland
- *Produces regulating hormones that circulate to adenohypophysis and stimulate it to secrete it's own hormones
- *sends nerve impulses to neurohypophysis which stimulate it to secrete oxytocin and ADH
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infundibulum
a funnel-shaped stalk which connects the pituitary gland to the hypothalamus
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adenohypophysis
- the anterior lobe of the pituitary
- about 75% of pituitary weight - functionally connected to hypothalamus by blood vessels
- The hypothalamus produces regulating hormones to circulate down to anterior lobe & stimulates lobe to secrete it's own hormones
- *"Adeno-" means gland, so the relationship btwn hypothalamus and anterior pituitary is gland to gland
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neurohypophysis
- the posterior pituitary, or second lobe
- functionally connected to hypothalamus by specialized neurosecretory neurons
- to stimulate neurohypophysis, the hypothalamus sends nerve impulses which stimulate it to secrete oxytocin and ADH
- *Does not synthesize any hormones - hormones from this gland are produced by neurosecretory cells in hypothalamus and secreted down axons w vesicles to be stored and later released from posterior pituitary
- *"neuro" refers to the connection btwn posterior lobe & hypothalamus-by neurons
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releasing hormones
- hormones from the hypothalamus
- stimulate the "release" of hormones from the adenohypophysis
- *if releasing is in the name of the hormone, it came from the hypothalamus
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inhibiting hormones
- hormones from the hypothalamus that inhibit the release of hormones from the adenohypophysis
- *used if hypothalamus needs to suppress the action of pituitary
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tropic hormone
- hormones from adenohypophysis that act on other endocrine glands
- *released from one endocrine gland and targets another
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"7 hormones of the adenohypophysis
- hGH = Human growth hormone
- TSH = Thyroid stimulating hormone
- ACTH = Adrenocorticotropic hormone
- FSH = Follicle stimulating hormone
- LH = Lutenizing hormone
- PRL = Prolactin
- MSH = Melanocyte-stimulating hormone
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hGH
- human growth hormone
- stimulated growth of body cells
- Correlates with Growth hormone-releasing hormone (GHRH)
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TSH
- Thyroid stimulating hormone
- Stimulates thyroid gland
- Correlates with thyrotropin-releasing hormone (TRH)
- *thyrotropin = in - only one that has a c is the sex ones. So n is legs closed, c is legs open
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ACTH
- Adrenocorticotropic hormone
- Stimulates cortex of adrenal gland
- Correlates with Corticotropin-releasing hormone (CRH)
- *corticotropin = in - only one that has a c is the sex ones. So n is legs closed, c is legs open
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FSH
- Follicle stimulating hormone
- targets ova/sperm development and production
- Correlates with Gonadotropic-releasing hormone (GnRH)
- *Gonadotropic - ic = legs open.
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LH
- Lutenizing hormone
- Maturation of uterine lining, testosterone production, and ovulation
- Correlates with gonadotropic-releasing hormone (GnRH)
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PRL
- Prolactin
- lactation of mammary glands
- Correlates with prolactin-releasing hormone
- (PRH)
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MSH
- Melanocyte-stimulating hormone
- Darkens melanocytes
- Correlates with corticotropin-releasing hormone
- (CRH)
- *corticotropin - in - only one that has a c is the sex ones. So n is legs closed, c is legs open
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TRH
- thyrotropin-releasing hormone
- stimulates pituitary to release TSH
- *thyrotropin - in - only one that has a c is the sex ones. So n is legs closed, c is legs open
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GHRH
- growth hormone-releasing hormone
- stimulates pituitary to release hGH
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CRH
- Corticotropin-releasing hormone
- stimulates pituitary to release ACTH & MSH
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GnRH
- Gonadotropic-releasing hormone
- Stimulates pituitary to release FSH & LH
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PRH
- Prolactin-releasing hormone
- stimulates pituitary to release prolactin
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Factors contributing to disorders of the endocrine system
- having too much or too little (hypo/hypersecretion)
- Can be other causes, but symptoms will be similar to hyper/hyposecretion:
- Ex: insufficient receptors, 2nd messenger defects, faulty receptors, etc.
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Possibilities that can cause hyposecretion
- too little hormone production
- decreased hormone receptors
- second messenger system defects
- lack of hormone precursors
- degraded hormones
- ischemia
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possibilities that can cause hypersecretion
- excessive hormone production
- tumors of endocrine origin - causing excess hormone release. benign or malignant
- Absence of normal feedback mechanisms
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Endocrine disorders of hGH secretion
- pituitary dwarfism
- giantism
- acromegaly
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pituitary dwarfism
- caused by hyposecretion of hGH during childhood
- w/o hGH, epiphyseal plates will close before pt reaches mature level
- deficient growth of tissue will affect all body systems; however child will have normal body proportions
- *not only cause of dwarfism
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giantism
- caused by hypersecretion of hGH during childhood (during pts growth phase)
- overall body proportions will remain consistent, but pt will be very tall
- main cause is tumor of anterior pituitary
- detection and treatment have made giantism fairly rare
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acromegaly
- a disorder caused by excessive hGH during adulthood
- deals with increased density in bone and tissue
- Enlargement and elongation of bones of the face, jaw, cheeks and hands, associated tissues can enlarge causing circulatory, nerve and skin probs.
- The long bones of the extremities are unaffected cause growth plates are already closed
- Commonly causes arthritis and carpal tunnel syndrome due to excess tissue growth
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hypothalamic nuclei
- the nuclei in the hypothalamus which synthesize hormones (oxytocin and ADH) to be sent to the posterior pituitary
- Specifically: paraventricular and
- supraoptic nuclei
- The axons from these nuclei make up hypothalamohypophyseal tract
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oxytocin
- hormone made by paraventricular and supraoptic nuclei in hypothalamus
- targets uterus and breasts after delivery of baby
- In uterus, stimulates contractions THROUGH POSITIVE FEEDBACK
- In breasts, stimulates milk "let down" in response to infant sucking
- *The purpose in men and non-pregnant women is unclear, but thought to promote feelings of sexual pleasure during and after intercourse and encourages emotional bonding btwn mating pair. So some call it the "love hormone"
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vasopressin
- ADH - antidiuretic hormone
- hormone which decreases amount to urine the body produces
- causes arterioles to constrict, thereby increasing blood pressure
- targets ducts in kindey and sweat glands in skin to minimize water loss
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osmoreceptors
found in the hypothalamus, monitor blood osmotic pressure (relates to concentration of blood)
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What happens with high blood osmotic pressure
- The high pressure (meaning high concentrated blood) stimulates hypothalamic osmoreceptors; Which in turn activate the neurosecretory cells that synthesize and release ADH
- Nerve impulses liberate ADH from axon terminals in posterior pituitary into bloodstream
- PRINCIPAL RESULTS:
- Kidneys retain more water, which decreases urine output
- Sudoriferous (sweat) glands decrease water loss by perspiration
- Arterioles constrict, increasing blood pressure
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What happens with low blood osmotic pressure?
The low pressure (low concentration, or dilute) inhibits hypothalamic osmoreceptors, which reduces or stops ADH secretion
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What specific target tissues does ADH act on?
- kidneys - influencing the collecting tubules (ducts) to increase water reabsorption
- sudoriferous (sweat) glands
- smooth muscle cells of blood vessels - increased BP by constricting arterioles
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diabetes insipidus
- most common condition related to ADH
- Two physiological types:
- *Either form has same effect: pt will not reabsorb water and therefore secrete large volumes of very dilute urine - from 1-1.5 liters (normal) to >2.5+ per day
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Two types of diabetes insipidus
- neurogenic = insufficient production or secretion of ADH
- nephrogenic = diminished renal response to ADH that was produced
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diabetes insipidus vs diabetes mellitus
- *"insipidus" = tasteless - urine is very dilute
- "mellatis" = sweet - urine is sweet
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thyroid gland
- has two lateral lobes, connected in middle by "isthmus" bridge
- sores 100-day supply of secretory products
- located inferior to larynx, specifically the thyroid cartilage (adams apple)
- butterfly shaped
- thyroid follicles make up most of gland, they secrete 2 hormones: T4 & T3
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thyroid follicle
- small spherical sacs which make up the thyroid
- main functional unit of thyroid gland
- each follicle consists of a central lumen, surrounded by wall of follicular cells (these cells change shape when stimulated to produce hormone)
- Secrete 2 hormones: T3 & T4
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TGB
- Thyroglobulin ~ is a protein synthesized inside thyroids follicular cells (bordering cells)
- consists of approx 5000 amino acids, which more than 100 are the amino acid tyrosine
- *"bin" - making Thyroid hormone from ingredients in the bin
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C cells
- also called parafollicular cells
- a scattered group of cells surrounding each follicle
- *on the outside of each follicle - so in betwn follicles
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How is T3 & T4 made from TGB
- to synthesize the thyroid hormones, TGB is released into the lumen of thyroid follicles
- Within TGB, 1 or 2 iodine atoms attach to each tyrosine molecule
- The tyrosine molecules then link to form thyroid hormone, containing either 3 or 4 atoms of iodine
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So how are the thyroid hormones synthesized and put into circulation?
- When needed, TGB moves into follicular cells, and digestive enzymes cleave T3 and T4 from the TGB molecule
- T3 and T4 are lipid soluble, so they can diffuse through the plasma membrane and bind to the carrier protein thyroxin-binding globulin (TBG) in the blood
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T4
- thyroxin (tetraiodothyronine)
- (tetra = 4)
- T4, hormone secreted by thyroid
- *prefix describes # of iodine molecules
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T3
- Triiodothyronine
- *prefix describes # of iodine molecules
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What stimulates the hypothalamus to secrete TRH & Whats the result
- TRH = thyrotropin-releasing hormone
- low T3 and T4 levels OR low metabolic rate stimulates release of TRH
- this results in the anterior pituitary producing TSH (thyroid-stimulating hormone) which is released into the blood and binds to TSH receptors in follicular cells, stimulating secretion of T3 & T4 into blood
- Elevated T3 inhibits release of TRH and TSH (negative feedback)
- *Most of the T4 released is converted to the more potent T3
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Required steps for T3 & T4 synthesis
- Iodine trapping
- Synthesis of TBG
- Oxidation of iodide
- Iodination of tyrosine
- Coupling of T1 and T2 to make T3 and T4
- Pinocytosis and digestion of colloid
- Secretion of thyroid hormones
- Transport of T3 and T4 in the blood
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Iodine trapping
- First required step in T3 & T4 synthesis
- Iodine circulates in blood as iodide ( I- )
- Iodide is actively transported into the follicular cells
- Because of this process the thyroid gland contains most of the iodide in body
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synthesis of TGB
- TGB (thyroglobulin) is a glycoprotein produced by follicular cells
- it contains large numbers of the amino acid tyrosine
- Tyrosine is the site on the TGB molecule that will bind with iodine
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Oxidation of iodide
Before iodide can bind to tyrosine, it must be oxidized and combine with another iodide to form an iodine molecule ( I2 )
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Iodination of tyrosine
The side chain of tyrosine may pick up one (T1) or two (T2) iodine molecules
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Coupling of T1 and T2 to make T3 and T4
As one of the last steps, two tyrosine molecules are joined to form either T3 (T1+ T2) or T4 ( T2 + T2)
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Pinocytosis and digestion of colloid
Once synthesized, the iodine-containing TGB reenters the follicular cells and digestive enzymes break down the molecule, releasing the formed T3 and T4
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Secretion of thyroid hormones
T3 and T4 are lipid soluble, so they freely pass the cell membrane into the interstitial fluid and into the blood
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Transport of T3 and T4 in the blood
- Once in bloodstream, 99% of secreted hormone binds to transport proteins, mainly TBG (thyroxine-binding globulin)
- NOT TO BE CONFUSED WITH TGB
*most body cells have receptors for T 3 & T 4, so the actions are quite broad
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Thyroid hormone actions:
- regulate oxygen use
- increase basal metabolic rate
- increase protein synthesis
- increase carb and fatty acid catabolism
- increase reactivity of nervous system by increasing sensitivity to epinephrine and norepinephrine
- Control tissue growth and development along with hGH
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importance of thyroid hormone: increasing BMR
- BMR = basal metabolic rate
- the rate of oxygen consumption while awake, at rest and fasting.
- When need for ATP increases, use of all nutrients increases
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importance of thyroid hormone: stimulating synthesis of additional sodium-potassium pumps
- Is a major action with a cascade of effects
- With the increase in the Na/K pumps, the demand for ATP is greater
- At ATP is produced, calories are used, and more heat is produced (exothermic)
- This is how thyroid hormones help a person regulate their normal body temp
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importance of thyroid hormone:
*increasing protein synthesis
*increasing fatty acid & glucose catabolism
*decreasing blood cholesterol
- Increasing protein synthesis encourages growth
- Fatty acids and glucose are used to synthesize ATP
- Reduces blood cholesterol by increasing cholesterol excretion
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importance of thryoid hormone:
*increasing the effects of nor/epinephrine
*Accelerating body growth
- Increasing efforts of epinephrine/norepinephrine enhances the sympathetic nervous response (heart rate, force of heart contraction, and BP)
- Accelerating body growth, especially during fetal life and adolescence, by working synergistically w hGH and insulin to develop the skeletal and nervous systems
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goiter
- an enlargement of the thyroid
- found in pts with hypothyroidism, hyperthyroidism, and euthyroidism (normal thyroid function)
- *In many countries, goiter is due to iodine deficiency. Rare in US cause of "iodized" salt
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What happens with hypothyroidism
- low basal metabolic rate
- cold intolerant
- constipation
- decreased respiratory rate
- bradycardia
- weight gain
- lethargic
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What happens with hyperthyroidism
- hight basal metabolic rate
- heat intolerant
- diarrhea
- increased respiratory rate
- tachycardia
- weight loss
- anxious
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Congenital hypothryoidism
- hypothyroid disorder with occurs in childhood
- formerly called cretinism (= idiot-ism)
- In addition to common hypothyroidism, pt demonstrates low growth rate (dwarfism) & mental retardation, due to the decreased synergistic relationship btwn thyroid hormones and hGH.
- Result is decrease in development of nervous and skeletal systems
- "congenital" = your born w it
- can be treated
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Myxedema
- hypothyroid disorder which occurs in adulthood
- insufficient thyroxin
- has similar symptoms to congenital hypothyroidism, w/o CNS & skeletal issues
- Pts aren't mentally retarded but do show some diminished intelligence
- pts gain weight easily
- have abnormal "edema"
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Graves disease
- most common form of hyperthyroidism
- autoimmune disease resulting in excess thyroid hormone secretion due to the production of antibodies that act like TSH
- Peculiar trait is exophthalmos, which is a condition that causes the eyes to protrude or bulge
- *the antibodies act as "Ghosts" robbing a grave
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What controls our calcium levels & what do we use it for?
- Thyroid - C Cells (parafollicular cells) AND
- Parathyroid - Parathyroid hormone
- Stored in bone matrix, need a little in blood/extracellular space for blood clot & muscle contraction
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thyrocalcitonin
- more commonly called calcitonin
- produced by C cells in the thyroid
- high blood calcium stimulates C cells to secrete calcitonin
- decreases calcium by:
- decreasing action of osteoclasts (thereby promoting calcium & phosphate storage in bone matrix)
- decreases amount absorbed by GI tract
- increase amount of calcium in urine
- ** think calci-TONE-in; tone DOWN calcium levels
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parathyroid glands
- small, round masses of tissue attached to the posterior surface of the lateral lobes of thyroid
- Typically there are 4: two parathyroid glands attached to each lobe (one superior and one inferior)
- contain chief (principal) cells which produce and secrete PTH
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Actions of PTH
- parathyroid hormone
- Stimulated when blood calcium levels are LOW; brings it up by:
- Stimulating osteoclastic activity
- increases levels of calcitriol (active form of Vit D) in GI tract
- Decreasing amount of calcium lost in urine
- also decreases blood phosphate levels
- *think of "para" - for = lets get calcium for our neighbors and friends
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Compare the actions of the parathyroid hormone and calcitonin
- they are antagonists
- PTH's goal is to increase blood calcium levels
- Calcitonin wants to lower calcium levels
- This is how the body maintains normal calcium, phosphate, and magnesium homeostasis
- *Parathyroid hormone vs. calcitonin made in the Parafollicular cells
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Adrenal Glands
- Two total: each located superior to each kidneys
- two regions: the adrenal cortex and the adrenal medulla
- Produce steroid hormones that regulate glucose and electrolyte levels
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adrenal medulla
- the innermost region of adrenal glands
- Secretes epinephrine and some norepinephrine
- Innervated & controlled by sympathetic preganglionics
- Acts similar to a sympathetic postganglionic neuron; secretes "-pinephrine" as hormone (instead of neurotransmitter)
- Job is to duplicate and prolong the sympathetic response
- Contain chromaffin cells
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What is the effect of the adrenal medulla releasing epinephrine/norepinephrine as a HORMONE (instead of neurotransmitter; as the medulla tends to act sympathetic postganglionic)
- similar to sympathetic effects;
- slower onset but last longer
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chromaffin cells
- of the medulla
- controlled by sympathetic preganglionic neurons from CNS
- This is why medullary response is very fast
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Adrenal cortex
- of the adrenal glands
- has 3 functional zones: zona glomerulosa, zona fasciculata, zona reticularis
- produce the "cortical" hormones
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zona glomerulosa
- most superficial zone of the adrenal cortex
- secretes mineralocorticoids
- *"The earth is Gloreous" - live on top, made of minerals
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mineralocorticoids
- a cortical hormone secreted by the zona glomerulosa
- help control water and electrolyte (Na+ and K+) balance
- *Job is to keep blood volume and BP homeostasis
- Aldosterone is main mineralocorticoid
- "mineral" = controls minerals; "corticoids" = comes from cortex
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aldosterone
- plays largest role of mineralocorticoids
- Job is to raise blood volume & BP
- Conserves Na+ & H2O through reabsorption in kidneys
- Promotes the excretion of H+ and K+ from kidneys into urine
- *the increased water reabsorption results in blood volume and BP increase
- *"Where's Aldo?" - earth needs water
- Controlled by RAAS
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zona fasciculata
- middle zone of adrenal cortex
- secretes glucocorticoids
- *you stuff your Face with Glucose suger behind a mask
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glucocorticoids
- secreted from the zona fasciculata of the adrenal cortex
- primary glucocorticoid is cortisol
- functions to regulate glucose availability and metabolism
- "gluco-" = controlling glucose; "corticoids" = from cortex
- *because of sugar, you need cortisol diet
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zona reticularies
- most deep zone of adrenal cortex
- produces and secretes gonadocorticoids;
- *basements are rectangular, and that's the bedrooms are for sex
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gonadocorticoids
- weak androgens
- small amounts are secreted in both male and females
- In males, converted to testosterone
- In females, converted to testosterone and finally estrogen (also contribute to libido)
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androgens
- masculinizing steroid hormones from adrenal cortex
- contribute to development of secondary sex characteristics
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What is the sequence for release of "cortical" hormones?
- Hypothalamus secretes CRH (Corticotropin-releasing hormone)
- This stimulates the pituitary to release ACTH
- This, in turn, stimulates release of the "cortical" hormones
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RAAS
- Renin-angiotensin-aldosterone system
- controls the secretion of aldosterone - whose job is to raise Blood volume & BP
- Stimulated by decrease in BP by all or one:
- decrease in blood volume
- dehydration
- Na+
- Hemorrhage
- (Notice they all cause loss in BP & blood volume)
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Basic summary of the process resulting in release of Aldosterone
- Low BP stimulates juxtaglomerular cells in kidneys to secrete the enzyme renin
- Renin circulates in blood & converts angiotensinogen into angiotensin I
- As angiotensin I circulates to lungs, the enzyme ACE converts angiotensin I to angiotensin II
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-ogen
- refers to molecule that is not activated yet
- When activated, becomes a biologically active molecule
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renin
- secreted by juxtaglomerular cells in the kidney; which are stimulated by low BP
- This circulates in the blood and converts angiotensinogen into angiotensin I
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angiotensinogen
- a plasma protein produced in the liver
- *-ogen = inactive
- converted into angiotensin I by the enzyme renin
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Angiotensin I
circulates in blood till it comes into contact with an enzyme in the lungs called ACE
then it is converted into angiotensin II
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ACE
- angiotensin-converting enzyme
- when it comes into contact with angiotensin I, it converts it into angiotensin II
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angiotensin II
- has 2 main actions to increase blood pressure :
- stimulates vasoconstriction
- stimulates the release of aldosterone from adrenal cortex (which then circulates to kidneys
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cortisol
- main glucocorticoid
- is a person's anti-hypoglycemic hormone
- will do whatever it can to keep glucose levels up; even if it means gluconeogenesis
- *Main stress hormone
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effects of cortisol
- regulate metabolism
- gluconeogenesis
- anti-inflammatory effects
- Resist stress (extremes)
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gluconeogenesis
- the formation of new glucose
- takes place when we haven't had any carbohydrates
- Goes to other body sources to get nutrients & forms glucose-like-stuff
- does this by promoting breakdown of proteins (typically muscle) and triglycerides from adipose tissue to form glucose
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Anti-inflammatory effects of cortisol
- very powerful anti-inflammatory
- works by suppressing inflammation
- *side effect is suppressing immune system
- therefore, having high levels of cortisol lowers immune defense
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Disorders of Adrenal cortex
- Cushing disease/syndrome
- addison disease
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disease vs syndrome
- Disease relates to a certain CAUSE of a condition
- Syndrome relates to a GROUP of symptoms that looks like the disease
- *Ex: A person with Cushings syndrome has symptoms that look like Cushings disease; yet they don't have the disease, there is another reason for their symptoms
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Cushing disease/syndrome
- Caused by hypersecretion of cortisol OR ACTH-secreting tumor causing excess of cortisol
- Results:
- High blood glucose
- Immune suppression and poor wound healing
- High BP
- Body fat redistribution = moon face, buffalo hump (fat pads on shoulders) and a hanging abdomen
- *basically, body breaks down fats and redistributes it to the core of body. Big trunk, tiny extremities
- **Cortisol is CRUSHING me w too much sugar and water!!
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Addison disease
- Results from hyposecretion of cortisol and aldosterone
- Caused by autoimmune destruction of adrenal cortex
- Symptoms:
- low blood glucose
- Low Na+
- high K+
- Low BP
- *your really wanting to "Add" sugar and water to Kool-aid, but you can't
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Pheochromocytoma
- an adrenal medulla disorder involving a benign tumor of the chromaffin cells
- results in hypersecretion of epinephrine & norepinephrine
- Causes prolonged sympathetic fight or flight response:
- high heart rate
- high BP
- increased metabolism (weight loss)
- anxiety/nervousness
- hyperglycemia
- sweating and headaches
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Pancreas
- Has both endocrine and exocrine cells; 99% of cells are exocrine
- therefore, main function is digestion
- Exocrine cells are arranged in clusters called acini
- Endocrine cells are among acini are clusters islets of Langerhans
- Located posterior & inferior to stomach-spleen is located by tail of pancreas
-
acini
- provide the exocrine function of pancreas
- clusters of cells making up outside layer - form majority of pancreas
- produce digestive enzymes that are secreted into the small intestine
-
islets of Langerhans
- contain 4 different types of endocrine cells
- also called pancreatic islets
- tiny clusters of cells found in middle of pancreas
- cells: alpha, beta, delta, and F cells
-
Glucagon vs insulin
are antagonist
-
Alpha cells
- type of endocrine cells making up 17% of pancreatic islets
- secrete glucagon - raise blood sugar:
- Increases blood glucose levels
- Acts on hepatocytes to convert glycogen to glucose - released into blood raises glucose levels to normal
- *stimulated by low blood glucose levels
- **if blood glucose continues to rise, hyperglycemia inhibits release of glucagon
-
-
Beta cells
- type of endocrine cell making up 70% of pancreatic islets
- secrete insulin - lowers blood sugar
- Speeds conversion of glucose to glycogen & get it out of blood stream
- accelerates facilitated diffusion of glucose into cells by making transporters to cross membrane
-
What all does insulin do?
- Accelerated facilitated diffusion of glucose into cells (increases # of transport proteins)
- Speed conversion of glucose into glycogen
- Increases uptake of amino acids by cells to increase protein synthesis
- Speeds up synthesis of fatty acids
- Decreases gluconeogenesis
-
Delta Cells
- type of endocrine cell making up 7% of pancreatic islets
- secrete somatostatin:
- Acts to inhibit release of insulin and glucagon
- *Your gonna Die
-
F cells
- type of endocrine cell making up 6% of pancreatic islets
- secrete pancreatic polypeptide
- inhibits somatostatin (digestion)
- * Fatty needs a diet
-
hypoinsulinism
can be lack of production or lack or response to insulin, or both
-
diabetes mellitus
- most common disorder affecting insulin production
- results in person not producing enough insulin, or they don't respond well to minimal or moderate amount they do produce
-
Type I diaetes
- also called juvenile-onset & insulin dependent
- typically occurs in younger population
- results in complete loss of beta cells
- Genetically influenced but environmentally induced
- Autoimmune antibody against beta cells resulting in their destruction
- With loss of beta cells, pt doesn't have insulin to help facilitate diffusion of glucose
-
Type II
- Also adult-onset & non-insulin dependent
- more genetically influence than type I
- Pt still produce insulin, but either don't produce enough or don't effectively utilize what they do produce; OR BOTH
- One of leading causes is obesity
-
decreased insulin sensitivity
- happens when individuals overeat = continually giving pancreas a carb challenge
- Pancreas must secrete insulin to assist w transport of glucose out of blood and into cells; if this happens too much, body may respond by "down-regulating" insulin receptors
- So even though insulin is present, body isn't responding in normal faction & more glucose stays in blood stream
-
metabolic syndrome
- a cluster of hyperlipidemia, obesity, hypertension, and insulin resistance
- Most medical scientist would reclassify type II diabetes as part of this
-
hyperinsulinism
- most common in diabetic pts that take too much insulin compared to their caloric intake
- Low glucose causes increased amount of epinephrine, glucagon, and hGH (causing anxiety, sweating, tremors, increased HR, hunger, and weakness)
- Brain cells deprived of glucose, so mental disorientation, convulsions, and unconsciousness can occur
- can result in "insulin shock"
-
diabetic coma
- the pts glucose is critically high
- commonly occurs in hypoinsulinism
- pt doesn't have or take enough insulin or meds to match their food intake
-
ketoacidosis
- occurs with a complete lack of insulin involving type I diabetics
- Pt doesn't have any available glucose due to complete lack of insulin
- Therefore, they utilize fatty acids for their energy source
- The byproducts from fatty acid metabolism are ketoacids (simply called ketones)
- The overproduction of ketones (cause they have NO insulin) causes a persons pH to drop and become acidic
- *person with type II produces enough insulin to not completely rely on fatty acid metabolism for ATP
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gonads
- ovaries in women, testes in men
- organs responsible for gamete production
- also have endocrine function
- in response to FSH and LH from pituitary, gonads produce various hormones:
- ovaries produce estrogen and progesterone
- testes produce testosterone
-
Gonadal hormone functions
- the development and maintenance of the secondary sex characteristics and fertility
- *secondary sex characteristics are those that are present during and after puberty
-
Estrogens and progesterone
- regulate the female reproductive cycle
- Maintain pregnancy
- breast development and maturation
- widening of the hips
- adipose tissue deposition in the breasts and around the hips
-
Testosterone
- sperm production (spermatogenesis)
- hair growth patterns
- increased skeletal and muscular growth
- voice changes
-
Pineal gland
- attached to top of the third ventricle; is part of the epithalamus
- produces and secretes the hormone melatonin
- *I'm going to "Pin" you down in bed so you will sleep
-
melatonin
- hormone which is believed to assist with the setting of the daily biological clock by:
- promoting sleepiness
- Controls seasonal and daily cycles
- More is released during darkness than light
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Thymus gland
- located in the mediastinum (behind sternum and btwn lungs)
- important for immune system
- secretes thymosin
-
Thymosin
along with other related hormones, secreted from the thymus gland and encourages the maturation of T-lymphocytes (T cells)
-
T Cells
a type of white blood cells (lymphocyte) that destroys microorganisms and foreign substances through direct cellular contact or by recruiting other white cells
-
stressor
- anything that disrupts normal homeostasis
- Ex: chemicals, psychological stress, heat, cold, confinement, injury, hemorrhage, etc.
- *can be helpful in some situations; it heightens responsiveness and helps increase concentration = eustress
- *stress that has negative effect is called distress, is always harmful
-
GAS
- general adaption syndrome
- also called the "stress response"
- the body's response to emergency or stressful situations, real or imagined
- *the idea that a variety of stressors would invoke a very similar response, regardless of stressor type. The common effects, controlled mainly by hypothalamus, were termed the "stress response"
- **The goal is to maintain homeostasis
-
Three stages of GAS
- fight - or - flight
- resistance reaction
- exhaustion
-
Fight or flight stage of stress response
- initiated by hypothalamus - stimulated the adrenal medulla by sympathetic nervous system
- body is trying to quickly activate mechanisms to allow immediate physical response:
- provided large amts of glucose and oxygen
- mental alertness
- increased blood flow to essential organs
-
resistance action
- initiated by hypothalamus by secreting the releasing hormones: ACTH, hGH and TSH
- Since this is a hormonal response instead of neural, can allow body to fight stressor longer after fight/flight diminishes
- The hormones:
- increase BP, glycogen and protein catabolism, lipolysis, and sodium/water retention
- decreases inflammation, wound healing and immune response
-
exhaustion stage of stress response
- the body's resources have depleted and resistance reaction can't be maintained
- Prolonged exposure to resistance response causes immune suppression, muscle wasting, ulceration of GI tract, failure of pancreatic cells and depletion of K+
- Common relationship with chronic diseases
- Death is a potential severe consequence
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