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148 Cards in this Set
- Front
- Back
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Compare and contrast the general control of body functions by the nervous and endocrine systems.
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Nervous - Electrical neuron impulses; extensive comunication through APs and NT release at system;immediate, short lived responses
Endocrine - organs/tissues positioned that release hormones into ECF; diffuse through blood and affect targets b/c of high affinity receptors; longer effect, generally slower (but can be fast) |
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Distinguish between classical endocrine signaling, paracrine signaling and autocrine signaling.
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Three types of chemical signaling:
Endocrine - circulating hormones in blood, distant target cells Paracrine - affects local cells/nearby target cells Autocrine - affects cell that secreted the hormone |
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What is a hormone? a target cell?
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Hormone - chem. substances produced at one site which cause an effect at a different site in the body; more durable effect to regulate ongoing functions of the body
Target cell - have a receptor in plasma mem/in cell specifically able to recognize and bind to a particular hormone molecule |
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What enables certain cells to respond to a hormone, while others cannot?
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High affinity receptors; hormone-receptor binding
- signal transduction = hormone initiates cascade |
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Identify the major classes of hormones and list several examples of each.
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Biogenic amines - derived from amino acids; (catecholamines, thyroid hormones, serotonin and melatonin , histamine)
Peptides - polypeptides/short ones and glycoproteins/longer ones Lipid derivatives: - steroid hormones from cholesterol (sex hormones, hormones secreted by adrenal cortex, calcitriol) - Eicosanoids from arachidonic acid; with paracrine functions (protaglandins, leukotrienes, thromboxanes, lipoxins) |
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Which class of hormones is derived from cholesterol? from amino acids? from arachidonic acid?
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Cholesterol - steroid hormones (1 of 2 lipid derivatives)
Amino acids - biogenic amines Arachidonic acid - eicosanoids (1 of 2 lipid derivatives) |
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Name the individual amine hormones and identify the amino acid from which each is derived.
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Catecholamines - tyrosine
Thyroid hormones - tyrosine Serotonin and melotonin - tryptophan Hystamine - ? |
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How are hormones transported in the blood? Explain the importance of transport proteins in circulating lipid-soluble proteins.
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- some circulate freely
- lipid soluble bind to transport protein and circulate as hormone-transport protein complexes (thyroid, steroid and peptide hormones) Benefits: longer half life, reserve of hormone in blood to reduce flux, increase in solubility of steroids (lipid soluble hormones) |
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Identify the three types of stimuli that regulate endocrine gland secretion.
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Humoral stimuli - chem changes in blood (ex. parathyroid glands respond to Ca in blood, Pancreas responds to blood glucose w/insulin or glucagon)
Neural stimuli - 1 endocrine tissue: adrenal medula; preganglionic sympathetic fibers stimulate AM to secrete catecholamines (epinepherine and norepinepherine) Hormonal stimuli - one endocrine organ on another (ex. hypothalamus on pituitary gland on thyroid, adrenal cortex, gonads/testes etc) Usu. negative feedback |
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Give an example of negative feedback control of hormone secretion.
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Pancreas - blood glucose up = insulin, less glucagon, causes it to decrease = less insulin, more glucagon
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Which hormones affect their target cells by binding to an intracellular receptor?
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- steroid hormones - diffuse through plasma membrane b/c lipid soluble
- thyroid hormones - carried across membrane by transport protein present in most cells of body - direct gene activation in cytoplasm or nucleoplasm |
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What is the general mechanism through which the hormones that bind to intracellular receptors induce changes in their target cell's metabolism?
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- Steroid and thyroid hormones form hormone-receptor complex in cytoplasm/nucleoplasm
- complex associates w/portion of DNA and alters transcription rate; altered translation = affects protein construction Thyroid hormone - can also bind to mitochondrial receptors and stimulate ATP production (oxidative phosphorylation); increased basal metabolic rate |
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Describe the specific steps in direct gene activatoin by a lipid soluble hormone.
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- steroid and thyroid hormones
- Diffuses/is carried through membrane - Forms hormone-receptor complex in cytoplasm/nucleoplasm - associates w/DNA and alters rate of transcription - protein synthesis rate altered - thyroid hor. can also bind to mitochondrial receptors and affect BMR |
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Where are the receptors for amine and peptide hormones located?
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In cell membrane - hormone never enters cell
- Triggers change in receptor - all biogenic amines (except thyroid hormone) |
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Describe the process of G protein activation ( in your explanation include the role of the hormone, its receptor, GDP, GTP, the alpha subunit, and the By dimer).
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- inactive G protein bound to receptor
- Hormone binds to receptor, triggers change - releases GDP that was bound to alpha subunit of G protein, and binds GTP to the G protein - G protein now activated - alpha subunit dissociates from beta-gamma dimer and slides along membrane - alpha-GTP acts on effector protein in cell during signal transduction |
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Describe the specific steps in the activation of the cAMP second messenger system.
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Hormone = 1st messenger; cAMP = 2nd messenger
- Hormone/receptor binding activates G-protein (G-stimulatory alpha subunit) - alpha subunit slides along membrane - activates adenylate cyclase, which makes cAMP from ATP - cAMP activates protein kinase A - protein kinase A is an enzyme that phosphorylates substrates (other enzymes) and has multiple effects in cell; can alter rate of gene transcription by activating transctiption factors |
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Why is cAMP called a "second messenger"?
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1st messenger = hormone
2nd messenger = cAMP relays information inside the cell to activate an enzyme (protein kinase A) |
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What is the effect of activation of phosphodiesterase (PDE) by G-protein inhibitory alpha (Giα) subunits?
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- PDE activated by protein kinase A; rapidly degrades cAMP (no more protein kinase A made)
- Hormones bind to certain receptors associated with inhibitory G proteins - ligand receptor binding = activation of INHIBITORY α-subunit, which also activates PDE - faster cAMP breakdown, reduced enzyme activity |
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Explain why second messenger systems are said to have an amplifying effect?
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- hormones can induce effects at very low levels:
- each cAMP activates thousands of protein kinase A - protein kinase A can activate hundreds of difft. proteins |
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Describe the specific steps in the activation of the PIP2-calcium signal mechanism.
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- it's another system transduction/messenger system
- hormone-receptor binding activates G-protein - alpha subunit dissociates and slides along membrane, activating phospholipase C (PLC) - PLC catalizes hydrolysis of PIP2 into two peices: diacylglycerol (DAG) and IP3 - DAG and IP3 are second messengers that lead to Ca2+ formation in cytoplasm - DAG activates protein kinase C (opens Ca channels and lets it into cell); IP3 (causes Ca release from ER and mitochondria - Ca binds w/proteins, causes effects |
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Name and identify the location of the second messengers of the PIP2-calcium signal mechanism.
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- DAG (diacylglycerol) - opens CA channels in plasma membrane
- IP3 (inositol-1,4,5-triphosphate) - release or Ca from ER and mitochondria |
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Name the two active lobes of the adult pituitary gland. Describe the general histolory and identify the embryologic origins of each.
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Anterior pituitary (adenohypophysis) - larger (3/4 of mass); develops from outpocketing of ectodermal cells from roof of mouth; glandular part; not continuation of brain
Posterior pituitary (neurohypophysis) - from outpocketing of ectodermal cells in embryonic hypothalamus; neuroglial cells (pituicytes), axons, axon terminals of cells w/cell bodies in hypothalamus (in supraoptic and paraventricular nuclei); neurosecretory cells |
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Describe the hypophyseal portal system, noting the general location of each of the three main componenets of the system - ie, the primary capillary plexus, the hypophyseal portal veins, and the secondary capillary plexus.
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- Small bodied neurons secrete releasing/inhititory hormones into primary capilary plexus (in infundibulum/in median eminance)
- blood through hypophyseal portal veins, through secondary capilary plexus to anterior pituitary - affects secretory activity rapidly w/small amts of hormones |
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What is the functional significance of each of the three main components of the hypophyseal portal system?
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Primary capillary plexus - absorbs hormones from hypothalamus
Hypophyseal portal veins - transports blood with hormones in it Secondary capillary plexus - inhibiting/releasing hormones diffuse out of blood into anterior pituitary, |
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What cells create the structural and functional relationship b/w the hypothalamus and the posterior lobe of the pituitary?
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- hypothalamic-hypophyseal tract (bundle of nervous fibers in CNS)
- large neurons of supraoptic and paraventricular nuclei - release ADH and OT (oxytosin) respectively - Hormones in vesicles to axon terminals in posterior pit., released with AP into capillary beds - direct contact |
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What are the hormones associated with the posterior pituitary?
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- antidiuretic hormone (ADH)
- oxytocin (OT) |
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Where are the posterior pituitary hormones synthesized? where are they stored?
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Synthesized - OT +ADH made in large neurons of supraoptic and paraventricular nuclei of hypothalamus (respectively)
Stored - vesicles in axon terminals in the posterior pituitary; released into capillary beds when AP occurs |
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Describe the process through which posterior pituitary hormones are secreted.
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- ADH made in Supraoptic nuclei, OT made in Paraventricular nuclie of hypothalamus
- vesicles transported down axons of cells into posterior pituitary - hormones released from axon terminals when AP fired - released into blood via capillary beds of posterior pituitary |
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Describe the effects of antidiuretic hormone (ADH) on its target cells and tell how its secretion is regulated.
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- Kidneys retain water, less urine
- sudoriferous/sweat glands decrease sweating = increase in blood volume and decrease osmolarity of blood; - arterioles constrict, vasoconstriction increases BP; a vasopressin - Regulated by osmoreceptors in hypothalamus to monitor plasma osmolarity; dehydrated = increased osmolarity = more ADH release; Negative feedback system |
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Describe the effects of ocytocin (OT) on its target cells and tell how its secretion is regulated.
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- Uterus - mech press. against cervix releases OT, stimulates smooth muscle contraction in uterus wall
- Breasts - mech press from suckling stimulates ejection of milk - Aid in ejaculation of sperm in men - positive feedback system stimulated by mech press! |
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What is a tropic hormone?
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- regulates the activity of another endocrine gland
- also stimulates the gland's growth and development |
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Name the hormones secreted by the anterior lobe of the pituitary and tell which of the secretions are tropic hormones.
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Tropic hormones:
- Thyrotropin/thyroid stimulating hormone (TSH) -Corticotriopin/adrenocorticotropic hormone (ACTH) Gonadotropins: Follicle-stimulating hormone (FSH) and Leuteinizing hormone (LH) Non tropic: - Growth hormone (GH) - Prolactin (PRL) |
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How does the hypothalamus regulate the secretory activity of the anterior pituitary?
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- regulated by hypothalamic releasing/inhibiting hormones (releasing are generally more important)
- negative feedback, indirect effect (whereas posterior has direct effect) - Regulatory hormones secreted by small-bodied neurons in ventromedial hypothalamus - hypophyseal phortal system |
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Describe the effects of thyroid-stimulating hormone (TSH) (thyrotropin) and tell how its secretion is regulated.
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- Targets thyroid gland - it's growth, development, secretion
- TSH regulated by TRH (releasing hormone) secreted by hypothalamus - Thyroid hormone = negative feedback; slows TRH and TSH release |
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Describe the effects of adrenocorticotropic hormone (ACTH) and tell how its secretion is regulated.
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- paptide hormone - targets the adrenal cortex to produce corticosteriods (ex. cortisol)
- Follows circadian rhythms and has pulsatile bursts in its secretion; highest when you wake up; secreted w/starvation, hypoglycemia, surgery, depression, anxiety etc - CRH (a releasing hormone) from the hypothalamus mediates it - negative feedback for CRH= from cortisol (secreted by the adrenal cortex) and possibly ACTH itself |
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Describe the diurnal rhythm of cortocotrophin-releasing hormone (CRH) release.
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- involves circadian rhythms and pulsatile bursts of secretion
- highest when you wake up, decreases throught day, unmeasurable right before you go to sleep - high during stressful stimuli (more stress during the day?) |
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What is the primary function (in males vs. females) of each of the gonadotropins?
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Follicle-stimulating hormone (FSH):
- Females - development of 1 follicle/month; stimulate follicle to release estrogens - Males - testes produce sperm Luteinizing hormone (LH): - Females - works w/FSH and estrogens to mature follicle;triggers ovulation; causes follicle remnent to become corpus luteum (temp. endocrine structure) - Males - Interstitial cells in testis to secrete testosterone; "interstitial cell stimulating hormone" (ICSH) |
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How is gonadotropin secretion regulated?
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- Stimulated by gonadotropin releasing hormone (GnRH)
- present during embryologic growth, not after birth, reappears during puberty - complex negative feedback pathways not well understood |
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At what stage of development does GnRH begin to circulate in measurable quantities in the blood?
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GnRH (gonadotriopin releasing hormone) stimulates gonadotropin (FSH and LH) secretion
- present somewhat in developing foetus - at puberty!!! |
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Describe the effects of growth hormone (somatotropin) on its target cells and tell how its secretion is regulated.
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Indirect - stimulates linear growth; faster protein synthesis, general growth; causes release of insulin-like growth factors (IGFs) from liver and other tissues
Direct - Adipose tissue:increase lipolysis to release fatty acids into blood and spare glucose - liver: increase glycogenolysis, glucos into blood = anti insulin/diabetogenic effect Regulation - hypothalamic releasing and inhibiting hormones (GH-RH) and somatostatin (GH-IH); negative feedback based on level of GH and IGF in blood; secretion is pulsatile Stimulated by exercise, deep sleep, fasting, starvation, decrease in fatty acids/glucose |
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What is the normal biologic role of the insulin-like growth factors (IGFs)?
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- released from liver and other tissues
- increase rate of amino acid uptake and protein synthesis in target cells; anabolic effects Skeletal - linear bone growth Extraskeletal - anabolic; general/somatic grown |
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What conditions result from oversecretion of GH in children? undersecretion of GH in children? what condition results from oversecretion of GH in adults?
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- gigantism
- pituitary dwarfism (associated with TSH and GNRH deficiencies where gonads don't develop properly) - acromegaly - affects hands, feet, face |
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Why is growth hormone said to exert a diabetogenic (or anti-insulin) effect?
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- lipolysis adipose tissue - releases fatty acids into blood to spare glucose
- glycogenesis in liver releases glucose in blood - these mimic the chemistry that exists in a diabetic |
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Describe the effects of prolactin (PRL) on its target cells and tell how its secretion is regulated.
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- protein hormone
- development of mammary glands of breast; initiate/maintain milk production - regulation not well understood: only hormone regulated by an inhibitory hormone (dopamine) from hypothalamus and some other parts of brain - levels rise/fall in women based on ovulation, rise b4 menses |
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Up-regulation
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more hormone receptors, so cell is more sensitive to the hormone
target cell regulates its response this way |
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Down regulation
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fewer hormone receptors, so cell is less sensitive to the hormone
target cell regulates its response this way |
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Protein kinase A
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- part of cAMP cascade
- activated by cAMP - enzyme that phosphorylates substrates |
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Protein kinase C
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- part of PIP-calcium signal mechanism
- activated by DAG - lets Ca into cell (opens Ca channels) - Ca binds with calmodulin and has various effects |
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Calmodulin
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Ca2+ binds to this as part of the PIP-calcium signal mechanism
- an intracellular protein - forms calcium calmodulin (regulates smooth muscle contraction etc) |
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Adenohypophysis
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- another word for anterior pituitary
- the larger part that forms the glandular part of the pituitary |
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Neurohypophysis
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Another word for posterior pituitary
- made up of axon and axon terminals |
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infundibulum
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the stalk of the pituitary, that goes through the dura mater
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Phospholipase C (PLC)
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- in PIP-calcium signal mechanism
- the alpha subunit from the G protein activates it - it catalyzes hydrolysis of PIP2 into DAG and IP3, which both help increase the amount of CA in the cell |
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hypophysis
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another word for the pituitary gland
2 lobes controls a lot of endocrine functions |
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protein kinase
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an enzyme that phosphorylates substrates
- type a works as part of the cAMP cascade - type c is activated by DAG in the PIP-calcium signal mechanism and lets Ca into cell by opening the channels in the plasma membrane |
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osmoreceptor
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a receptor (in this case, in the hypothalamus), that monitors changes in plasma osmolarity
- activates neurosecretory cells of hypothalamus when osmolarity increases, in order to increase ADH secretion by post. pituitary |
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Vaopressin
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- another name for ADH (antidiuretic hormone)
- called this because ADH causes vasoconstriction of vascular smooth muscle which causes BP to increase |
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Releasing hormone
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- how hypothalamus controls anterior pituitary hormone secretion
- generally the more common/important one - secreted by small bodied neurons in ventromedial hypothalamus (travel thru hypophyseal portal system) |
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Inhibiting hormone
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- how hypothalamus controls anterior pituitary hormone secretion
- generally the less common/important one - secreted by small bodied neurons in ventromedial hypothalamus (travel thru hypophyseal portal system) |
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Neurosecretory cells
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- communicate w/posterior pituitary
- supraoptic and paraventricular nuclei in hypothalamus make ADH and OT, transport down hypothalamic-hypophyseal tract - hormones released from vesicles in axon terminals when AP occurs (released into blood stream) - part of direct contact |
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hypothalamo-pituitary (HPA) axis
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- the hypothalamus and pituitary gland
- control a large variety of endocrine organs and functions |
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signal transduction
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- the signal is converted across the membrane from one form to another
- G proteins are involved in signal transduction for all second messenger systems |
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gonadotrophs
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- secrete gonadotropins:
-- Follicle-stimulating hormone (FSH) -- luteinizing hormone (LH) - affects gonads - secretes a tropic hormone |
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corticotrophs
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- Secrete corticotropin/adrenocorticotropic hormone (ACTH)
- affects adrenal gland - secretes a tropic hormone |
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thyrotrophs
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- secrete thyrotropin/thyroid-stimulating hormone (TSH)
- affects thyroid - secretes a tropic hormone |
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lactotrophs
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- secrete prolactin (PRL)
- secrete one of 2 anterior pituitary hormones that is not tropic |
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somatotrophs
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- secrete growth hormone (GH or hGH)
- secrete one of 2 anterior pituitary hormones that is not tropic |
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glycogenolysis
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- the breakdown of glycogen
- a direct mechanism of GH action - occurs in liver - releases glucose into blood, causes diabetogenic effect |
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lipolysis
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- the breakdown of lipids
- a direct mechanism of GH action - occurs in adipose tissue - releases fatty acids into blood, glucose sparing effect |
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Distinguish between endocrine and exocrine glands.
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Endocrine - secrete hormones, don't have ducts
Exocrine - glands with ducts, secrete products into the area where there ducts come out (ex. sweat, salivary, mammary, etc) |
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Name the two types of endocrine cell of the thyroid gland, and identify the secretory product of each.
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- Follicular cells - synthesize thyroid hormones (thyroxine/T4 the inactive one and triiodothyronine/T3 the active one)
- Parafollicular cells/"C cells" - produce calcitonin |
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Name the two hormones that are collectively referred to as "thyroid hormones". Which of the two is the main hormone secretion of the follicular cells?
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- Thyroxine (T4) - 90%, but inactive, circulates in the blood and converted when needed
- triiodothyronine (T3) - 10%, but biologically active - both synthesized by follicular cells of the thyroid |
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Where is thyroglobulin synthesized? From what amino acid is it derived?
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-glycoprotein synthesized in follicular cell and packaged into vesicle; released into colloid
- amino acids and thyroxine, an iodine containing protein derived from tyrosine |
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What is the role of thyroid peroxidase?
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- After Iodine trapped, passed into colloid through apical border
- TPO catalyzes oxication of iodide into iodine at apical border of follicular cells - now iodine can join onto the tyrosines all along the thyroglobulin - also catalyzes iodination of tyrosine all along the thyroglobin into DIT (w/2 iodines) and MIT (w/1 iodine) |
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Where does thyroglobulin become iodinated?
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- in the colloid
- catalyzed by TPO (thyroid peroxidase) - at follicle cell-colloid junction - turns into di-iodotyrosine/DIT w/ 2 iodines and monoiodotyrosine/MIT w/1 iodine |
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Describe the process of thyroid hormone synthesis and release.
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- Iodine trapped into cell (na+/I- pump)
- Thyroglobulin synthesized in follicular cell - iodid oxidized into iodine as it passes through apical surface into colloid (enzyme=thyroid peroxidase) - Tyrosine along thyroglobulin iodized into MIT (T1) and DIT (T2) (enzyme=thyroid peroxidase/TPO) - T2+T2 = T4(thyroxine); T1 + T2 = T3 (triiodothyonine) - Back into follicular cell, fuses w/lysosome; cleaves off T3 and T4 from thyroglobulin, and I to recycle - Thyroid hormones released into bloodstream |
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How is thyroid hormone (TH) secretion regulated?
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- Primary regulator = TSH secreted by ant. pituitary
- TSH speeds up TPO (thyroid peroxidase, the iodide oxidating/tyrosine iodizing enzyme) - speeds up iodine trapping - several days, increased thyroglobulin production - Negative feedback - more T3 + T4 = less TRH (hypothalamus) + TSH (ant. pituitary) - colloid stores lengthen time for deficiency to appear |
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What effects does thyroid hormone have on metabolism?
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- increase BMR; calorigenic effect
- increased: use of glucose and O2 for ATP, synthesis of Na/K ATPase pumps, body temp for calorigenic effect, protein synthesis, tissue growth, lipolysis, cholesterol excretion - to support this, also increased: HR, cardiac output, respiration, substrate circulation (fatty acids for ATP production), tissue growth and dev. |
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What is the role of thyroid-binding globulin?
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- (TBG) - carrier protein increases half life
- provides circulating pool - must measure thyroid hormone and TBG clinicaly for thyroid level |
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What hormone prevents high blood calcium levels?
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Calcitonin (CT)
- antagonist to parathyroid hormone - produced by thyroid gland |
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Describe the effects of calcitonin (CT) and tell how its secretion is regulated.
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Effects: inhibits osteoclasts (less bone resorption), stimulates osteoblasts (better uptake of Ca salts into bone matrix), increase rate of Ca excretion by kidneys
Regulation - negative feedback; antagonist to parathyroid hormone |
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What hormone prevents low blood calcium levels?
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- Parathyroid hormone (PTH)
- antagonist to calcitonin (produced by thyroid) - produced by parathyroid glands |
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Normally, how many parathyroid glands does each human have? Where are they located?
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- 4 glands
- posterior surface of the thyroid - very tiny, hard to see |
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Identify the specific cells of the parathyroid gland that synthesize and secrete PTH.
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- Cheif cells/principle cells
- not the oxyphil cells |
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Describe the effects of PTH on its target cells.
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- increase osteoclast activity (more bone resorption)
- more Ca2+ and Mg2+ reabsorption by kidneys - more conversion in kidneys of vit D to active form of calcitriol (blood ca needed for muscle contraction, axon terminals for NT exocyosis, cofactor for blood clotting etc) |
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Tell how PTH (parathyroid hormone) secretion is regulated.
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- regulated by negative feedback
- Calcitonin (CT) secreted by thyroid is its antagonist |
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What are the potential deleterious effects of abnormally high blood calcium levels (hypercalcemia)?
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- caused by hyperparathyroidism
- fatigue, muscle weakness, confusion, abnormal reflexes - brittle bones, osteoperosis!!! - nausia/vomiting from CNS disruption - body considers skeletal system as repository for Ca |
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What are the potential deleterious effects of abnormally low blood calcium levels (hypocalcemia)?
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- caused by hypoparathyroidism
- nervous system more excitable b/c resting membrane potentials disrupted - creates tetany/muscle spasams; fatal if affects diaphragm and respiratory muscles |
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Where are the adrenal glands located?
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- suprarenal glands, right above kidneys
- at level of floating ribs - nestled b/w ribcage and diaphragm |
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Identify and locate the 2 major structural and functional regions of each adrenal gland.
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Adrenal cortex - superficial region; develops from mesoderm, secretes corticosteroids
Adrenal medula - inner, develops from ectoderm, secretes catecholamines, stimulated by preganglionic fibers of SNS |
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What is the main secretory product of each of the 3 secretory zones of the adrenal cortex?
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Zona glomerulosa - secretes mineralocorticoids (regulate electrolyte conc)
Zona fasciculata - secretes glucocorticoids Zona reticularis - secretes gonadocorticoids (esp androgens) |
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Identify and locate the 3 secretory zones of the adrenal cortex, superficial to deep.
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Zona glomerulosa
Zona fasciculata Zona reticularis |
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What is the principle mineralcorticoid secreted by the adrenal cortex?
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Aldosterone
- mainly enhances Na reabsorption/K excretion in kidney |
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Describe the effects of Aldosterone on its target cells.
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(a mineralcortitoid secreted by adrenal cortex)
- Enhance Na+ reabsorption/K+ excretion by kidney - targets cells in distal part of renal tubule - increases transcription of Na/K ATPases, to increase Na reabsorption - also influences sweat gland, salivary glands, digestive - to get more Na, and thus more H2O reabsorption (if ADH is present) |
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Tell how aldosterione secretion is regulated (four ways).
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- Renin-angiotensin aldosterone mechanism (RAAS): renen released in kidney when low BP/volume or low blood osmolarity; thru cascade brings blood presss and volume back up
- Plasma conc of Na and K: dec Na/inc K (= when low BP) stimulate aldosterone secretion in Zona glomerulosa cells - ACTH - during periods of stress CRH from hypothalamus = increase in adrenocorticotropic hormone from Ant. pituitary = small inc. in aldosterone - Atrial natriuretic peptide (ANP): secreted by atrial cells of heart (inc, Na secretion in urine); inhibits RAAS/renin realease and aldosterone sec from adrenal cortex |
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Describe the steps in the renen-angiotnsin cascade.
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- Decreasd BP, volume
- Kidney stimulated to produce renin and liver to produce antiotensin (inactive) - renin catalyzes rxn converting angiotensin to angiotensin I - ACE (angiotensin converting enzyme) in lungs converts Antiotensin I to Antiotensin II - Angiotensin II stimulates: adrenal cortex to secrete more aldosterone, vasoconstriction - Aldosterone = increased Na+ and H2O reabsorption in kidney - increased blood pressure and volume |
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How does angiotensin II (AT II) contribute to the homeostasis of blood volume and blood pressure?
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- part of renin-angiotensin cascade
- stimulates vasoconstriction - stimulates adrenal cortex to secrete aldosterone - aldosterone enhances Na reabsorption and H2O reabsorption (when present with ADH): this absorption happens b/c it increases transcroption of Na/K ATPases inside liver cells |
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Name the glucocorticoid hormone secreted by the adrenal cortex.
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- Cortisol
- generally a glucose sparing effect to sustain blood glucose durin prolonged stress b/c brain needs the glucose |
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Describe the effects of cortisol (glucocorticoid hormone from adrenal cortex) on its target cells.
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- glucose sparing, diabetogenic effect: breakdown of protein in musc cells, lipolysis, more glucose uptake
- enhanced epinephrine's effects on BP - much greater lipolytic effect - inhibit collagen synthesis as a backbone for bones (can make bones brittle) - strong anti-inflammatory effect by inhibiting leukocytes - cortisol + GH = a lot more lypolysis |
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Tell how cortisol (glucocorticoid hormone from adrenal cortex) secretion is regulated.
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- hypothalamic-pituitary-adrenal cortex axis (HPA)
- CRH secretion from hypothalamus, and ACTH from hypothalamus normally stimulate adrenal cortex to produce cortisol: modulated w/negative feedback to both the hypothalamus and pituitary - regulation follows diurnal pattern of secretion of CRH, only a few min afterwards; pattern overridden durin acute stress by sympathetic nervous system to make more cortisol |
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What are the potential side-effects of abnormally high and/or prolonged glucocorticoid exposure?
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- Brittle bones: inhibits collagen synthesis (which forms backbone for Ca-Phosphate to be laid down in bone cells) = too much cortisol makes brittle bones
- Infection and poor wound healing: Strong anti-inflammatory effect by inhibiting leukocytes = decreased wound healing and resistance to infection - Decreased muscle: glucose sparing effect results in protein being broken down in muscle cells - High BP: increases epinepherine's effects on BP - can lead to hypertension b/c it raises HR, contractility and vasoconstriction etc. - Obesity: stimulates appetitie |
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What are the principle gonadocorticoids secreted by the adrenal cortex?
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- androgens (male sex hormones)
- weak, so must be converted to stronger sex hormones elsewhere to have much effect |
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What seems to be the biological role of the adrenal sex hormones?
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- role not well understood
- Weak; must be converted to other sex hormones to have much effect - can be converted to testosterone and estrogen - more production in late childhood - puberty? - sex drive in adult women? |
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Name the individual steriod hormones.
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- one of two lipid derivatives (other is eicosanoids)
- sex hormones - hormones secreted by adrenal cortex - calcitriol |
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Identify the secretion for each of the steroid hormones.
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- sex hormones - gonads
- hormones secrete by adrenal cortex (mineralcorticoids/aldosterone, glucocorticoids/cortisol, gonadocorticoids/androgens) - calcitriol - active form of Vit. D; converted in kidneys (stimulated by parathyroid hormone/PHT) |
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Review the ways in which the hypothalamus contributes to the homeostasis of body systems.
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- regulates temp, blood osmolarity, hunger etc
- the link b/w nervous and endocrine system - has internal receptors, and also has info relayed to it from cerebral cortex, thalamus, visual system etc - regulates commands through pituitary and ANS neurons |
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What is the result of severe hypothyroidism in infants?
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- cretinism - mental retardation; short disproportionate body, thick tongue and neck.
- treatable/preventable, but non-reversable |
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Basal metabolic rate (BMR)
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- measured at rest when you haven't eaten for 8-12 hrs
- baseline/lowest level of metabolism - Thyroid hormone increases BMR |
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calorigenic effect
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- caused by thyroid hormone
- increased expenditure of calories, higher BMR |
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calcitriol
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- active form of Vit D
- converted in kidneys - stimulated by parathyroid hormone (as a way to increase blood Ca)... |
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Describe the relationship between the adrenal medulla and the autonomic nervous system.
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Embryologically chromaffin cells of the AM are like the nervous system; arise from same tissue as sympathetic gangila (looks like they'll be post ganglionic cells)
Functionally are endocrine cells - receive direct innervation frrom preganglionic fibers of sympathetic ANS - stress = AP = preganglionic sympathetic fibers = adrenal medula = catecholamines |
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Identify the hormone-producing cells of the adrenal medula.
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- Chromaffin cells - large densly packed around blood vessels
- innervated by sympathetic ANS - secrete epinepherine and norepinepherine |
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Identify the major secretions of the adrenal medula.
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Catecholamines: epinepherine and norepinepherine (4:1 ratio)
- mimic effects of sympathetic nervous system but longer |
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Which of the two secretions of the adrenal medula accounts for the greater proportion of the medullary secretions?
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- epinepherine (by exocytosis into blood)
- more than norepinepherine - 4:1 ratio - Both are catecholamines for short term stress |
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Describe the effects of the two secretions of the adrenal medula.
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Epinepherine and norepinepherine
- increase: BP through HR/contractility and vasoconstriction; respiration rate; bronchodilation; glycogenolysis; blood glucose levels; fatty acid mobilization from adipose tissue - decrease: degestive activity; urine output - reroute blood to essential organs |
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Tell how the secretion of the two hormones of the adrenal medula is regulated.
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Primarily regulated by sympathetic portion of ANS
- so controlled by CNS - some negative feedback from itself, but not as important than cerebral control |
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There are two general receptor types for the catecholamines (i.e. alpha and beta) and subclasses of each type. Review the major locations of each of these receptors. p. 536
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B1 - heart; also kidneys and adipose tissue
B2 - lungs; blood vessels serving heart; liver; skeletal muscle B3 - Adipose tissue Alpha1 - all sympathetic target organs except heart; blood vessels serving most of body Alpha2 - membrane of adrenergic axon terminals, pancreas, platelets |
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There are two general receptor types for the catecholamines (i.e. alpha and beta) and subclasses of each type. Describe the general effect of the hormones on their target cells. p.536
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B1 - (binding increases HR and renin release in kidneys)B2 - (inhibitory - dilates vessels/bronchioles, relaxes digestive, uterus and urinary muscle walls)
B3 - ( stimulates lypolysis) Alpha 1 - (constricts vessels/organ sphyncters, dilates pupils) Alpha2 - (inhibits NE release from terminals, and insulin secretion from pancreas; promotes clotting) |
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Identify the 3 phases of the physiological stress response (i.e. the general adaptation syndrome identified by selye) and describe the physiological changes that are likely to occur in each stage.
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Alarm - fight/fligh; dominated by catecholamines (NE and epinepherine)
Resistance - dominated by cortisol, caused by prolonged stress, immune function decreases Exhaustion - adrenal glands atrophied, death follows (seen in swimming rats) |
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What are the insulin-secreting cells of the pancreatic islets?
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Beta cells - 75% of cell population
- antagonist to alpha cells which secrete glucagon - part of the pancreas |
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What cells of the pancreatic islets secrete glucagon?
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- Alpha cells - 15% of cells
- antagonist to beta cells which secrete insulin |
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Describe the effects of insulin and glucagon.
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Insulin - decreases flood glucose levels
- increase: glycogenesis in liver and skeletal musc; amino acid uptake and protein synthesis; lipogenesis; ATP production; tryglyceride synthesis in liver; glucose uptake by muscle cells, CT and adipose tissue Decrease: blood glucose; gluconeogenesis; glycogenolysis - Glucagon - increase blood glucose thru 2nd messenger systems Increase: glycogenolysis and gluconeogenesis in liver for glucose release; lypolysis in adipose tissue |
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Describe how insulin and glucagon secretion is regulated.
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Insulin - secreted in response to: high blood glucose, high argenine and lucine (AAs), high fatty acids, parasympathetic nervous system
Inhibited: sympthetic n.s.; decrease in glucose Glucagon - stimulated by low blood glucose, sympathetic N.S., high AAs in blood Inhibited:negative feedback; rising blood glucose, GH-IH (somatostatin) |
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Why are insulin and glucagon described as antagonists?
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- act against eachother and block eachother's actions
- insulin lowers blood glucose, glucagon raisese it - stimulated by opposite things |
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What are the 3 cardinal signs of diabetes mellitus?
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Polyuria - excess urine
Polydipsia - excessive thirst Polyphagia - excessive hunger |
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Physiologically speaking, why do the 3 cardinal signs of diabetes mellitus occur?
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Polyuria - too much glucose for kidney to reabsorb; some is in urine; decrease in osmotic press; water flows down the press gradient and is peed out
Polydipsia - because you're peeing a lot, you loose more water Polyphagia - although their is glucose in the blood, your cells do not have the ability to take it up, so basically they are starving in a period of abundance |
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Compare and contrast type 1 and type 2 diabetes.
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Type 1 - IDDM/juvinile onset; caused by autoimmunie beta cell destruction; usu presents w/acidosis and ketosis; insulin therapy required; risk doesn't increase with obesity
Type II - NIDDM; more common; caused by insulin resistance; presents in a mild form first, with normal or elevated glucose levels; can be helped w/lifestyle changes; usu. appears in ppl over 40 and overweight |
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Name the male and female sex hormones.
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Ovaries - estrogens, progesterone, inhibin (inhibits FSH secretion)
Testes - testosterone, inhibin (inhibits FSH secretion) |
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What are the general effects (in males vs. females) of the sex hormones?
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Females - maturation of sex organs, appearance of female secondary sex characteristies; sustain pregnancy, mammary glands
Male - maturation of male reproduc. organds; male secondary sex characteristics; sperm production; sex drive/libido |
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Identify the hormone secreted by the pineal gland.
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Melatonin
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Describe the general effects of melatonin.
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- secreted by pineal gland
- inhibits GnRH release esp during childhood (high in kids, drops @ puberty) - BP rise and fall - sleep/wake cycle - core body temp - time in REM vs. nonREM sleep - when old, low amts, so hard to sleep |
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Describe how melatonin secretion is regulated.
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- secreted by pineal gland
- diurnal pattern - lowest @ noon, hightest @ night - input from visual pathways, allows it to figgure out duration and intensity of light |
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Locate and describe the function of the thymus gland.
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- in thorax, deep to sternum
- produces peptide hormones (thymopoietins and thymosins) - large in kids, then fades away/shrivels - key role in T lymphocyte development |
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What is arachadonic acid?
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- eicosanoids (a class of paracrine hormones) are derived from it
- it is a fatty acid cleaved from phospholipids of plasma mem. - Procudes Leukotrienes, Thromboxanes and other prostaglandins |
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Identify the 2 main pathways of arachodonic acid metabolism.
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- cyclooxygenase (COX) pathway
- 5-lipoxygenase pathway |
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What families of biologically active producs is/are generated by each of the pathways?
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- cyclooxygenase (COX) pathway - Prostaglandins and thromboxanes
- 5-lipoxygenase pathway - leukotrienes |
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Leukotrienes (LT)
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- formed from Arachodonic acid by 5-lipoxygenase pathway
- an eicosanoids (class of paracrine hormones) - allergic and inflammatory responses - sustains inflammatory condition in some patients |
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Thromboxanes (TXA)
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- formed from Arachodonic acid by cyclooxygenase pathway
- an eicosanoids (class of paracrine hormones) - blood clotting - blood homeostasis |
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Prostaglandins (PG)
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- formed from Arachodonic acid by cyclooxygenase pathway
- an eicosanoids (class of paracrine hormones) - produced by every tissue of body - mediate inflammatory response - vasoconstriction/dilation: important for regulating blood flow @ tissue level |
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Polyuria
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Excess urine
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Polydipsia
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Excess thirst
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Polyphagia
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Excess hunger/appetite
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hypoglycemia
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low blood glucose
- stimulates glucagon |
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hyperglycemia
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high blood glucose
- stimulates insulin |
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Cyclooxygenase (COX)
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- the pathway that forms PGH2 from Arachodonic acid
- then forms Thromboxanes and prostaglandins from PGH2 - a pathway of arachadonic acid metabolism |
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5-lipoxygenase
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- a patheway of arachadonic acid metabolism
- this pathway produces leukotrienes |
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Exophthalamos
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abnormal protrusion of the eyeball
thyroid orbitopathy is the most common cause |
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Describe how the hypothalamus/pituitary gland/adrenal glands (i.e., the HPA axis) work together to mediate the body's response to stress.
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Short term: Stress; hypothalamus stimulated; preganglionic sympathetic fibers go to adrenal medula; NE and epinephrine released
Long term: stress; hypothalamus stimulated; CRH/corticotropin releasing hormone secreted; anterior pituitary secretes ACTH into blood; adrenal cortex secretes mineralcorticoids(aldosterone) and glucocorticoids (cortisol) |
