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Endo: Posterior Pit
Endocrine System: Posterior Pituitary
| Question | Answer |
|---|---|
| How does anterior and posterior pituitary differ in terms of the characteristics of the hormone releasing cells? | Anterior - release stimulating hormones. Posterior - release neurohypophyseal hormones |
| How does anterior and posterior pituitary differ in term of the control of hormone release? | Both are generally regulated by the hypothalamus. Anterior - through portal vein system. Posterior - in neurosecretory granules along an axon. |
| How does anterior and posterior pituitary differ in term of the hormones that are secreted | Anterior - wide variety of hormones (TSH, FSH, GH, etc.) Posterior - antidiuretic hormones and oxytocin |
| What controls the regulation of both posterior and anterior pituitary? | Hypothalamus |
| What is the median eminence? | Lower border connecting to posterior pituitary |
| What are the structures that make up the anterior pituitary? | Pars distalis, pars intermedia, pars tuberalis |
| What structures make up the posterior pituitary? | Infundibulum, pars nervosa |
| What is the infundibulum? | Infundibular stalk/stem - AKA pituitary stalk |
| What does the infundibulum connect? | Posterior pituitary to median eminence |
| What is the purpose of the infundibulum? | Contains hypophyseal tract that runs from hypothalamic nuclei that synthesize ADH and oxytocin to pars nervosa of posterior pituitary |
| What is the supraoptic nucleus? | Nucleus of the magnocellular secretory cells of the hypothalamus |
| What is the function of the supraoptic nucleus? | Produces mostly ADH |
| What is the paraventricular nucleus? | Nucleus in the hypothalamus |
| What is the function of the paraventricular nucleus? | Produces mostly oxytocin |
| What does the pars nervosa contain? | Herring bodies, pituicytes, and capillary beds |
| What are herring bodies? | AKA neurosecretory bodies. Neurosecretory terminals - representing terminal ends of axons from hypothalamus where hormones are stored |
| What are pituicytes? | Specialized glial cells that assist and support storage and release of neurohypophyseal hormones |
| What is the function of capillary beds? | Site for ADH and oxytocin release |
| Where does the posterior lobe receive blood from? | Inferior hypophyseal artery - a branch of internal carotid artery and psoterior communicating |
| Explain the blood flow in the posterior pituitary | Inferior hypophyseal artery enters posterior lobe and forms capillary plexus to supply it. Small veins arise from the surface of the gland and drain into neighboring dural sinus. Venous blood carries hormones from gland to target cell |
| Venous blood drains into what structure? | Cavernous sinus and internaljugular vein |
| What class of hormones do ADH and oxytocin belong to? | Peptide - because are made from 9 AAs |
| What is ADH also known as? | Vasopressin |
| What is the structure of ADH and oxytocin? | Nonapeptides consisting of 6 AAs with a cysteine-to-cysteine bridge and a 3 AA tail. Structures are nearly identical |
| How are ADH and oxytocin synthesized? | As preprohormone. |
| How is the "pre" cleaved off for ADH and oxytocin? | N-signal peptide, cleaved during cotranslation into ER |
| How is the "pro" cleaved off for ADH and oxytocin | neurophysin I (oxytocin) and II (ADH), cleaved during transport to posterior pituitary |
| What are neurophysins? | Carrier proteins which transport the hormones oxytocin and ADH to posterior pituitary from hypothalamus |
| What is the implication of neurophysins? | Hormones are packaged as part of a precursor molecule consisting of the nonapeptide and a hormone-specific neurophysin. |
| Describe when the hormones would be in their final form, ready to be released | Precursor is packaged in neurosecretory granules and cleaved to products during transport to the posterior pituitary (pars nervosa) |
| Where does synthesis of ADH occur in? | Supraoptic nuclei of hypothalamus |
| Where does synthesis of oxytocin occur in? | Paraventricular nuclei of hypothalamus |
| What does both the paraventricular nuclei and supraoptic nuclei contain? | Large magnocellular neuronal cell bodies |
| Both nuclei of the hypothalamus also contain cell bodies of small (parvocellular) neurons, what are they and what are they released into? | CRH, ADH, TRH into hypothalamo-pituitary portal system |
| What is the function of CRH? | Stimulates release of ACTH |
| What is the function of ADH? | Acts synergistically with CRH to produce ACTH |
| Why does ADH act with CRH to stimulate ACTH? | Because by itself, it is a weak secretagogue |
| What is the function of TRH? | Stimulate release of TSH |
| Where is GHRH produced in? | Arcuate nucleus of hypothalamus |
| Where is PIH made and secreted by? | Made in arcuate nucleus, released by neurosecretory tuberoinfundibulum |
| What is the function of PIH? | Act on D2 receptors of lactotrophs causing inhibition of prolactin secretion |
| What triggers a hormone transport from hypothalamus to posterior pituitary? | Same stimuli that causes hormone synthesis |
| How long does it take for hormones to be transported inside neurosecretory granules? | Can take several days |
| How does transport of hormones occur by? | Via anterograde axonal transport using microtubule tracks |
| Where are the hormones stored? | Secretory granules in magnocellular axon terminals in the posterior pituitary |
| What are the terminals that store hormones called? | Herring bodies |
| What stimulates the release of hormones? | Same stimuli that cause hormone synthesis and transport |
| What does stimulation of magnocellular neurons lead to? | Increased transcription, mRNA content, and hormone synthesis; propagation of action potentials down the magnocellular axons to the pituitary |
| What is the implication of increased synthesis? | Stimulates increased transport down hypophyseal tract |
| What is the implication of propagation of action potentials? | Leads to calcium influx into axon terminals, fusion of neurosecretory vesicles with membrane, and release of hormones into blood |
| There seems to be a synchronicity between synthesis, transport, and release, why is it that there isn't always a balance of hormones then? | The timing of each events differs and the changes in the content of stored hormones. EX) certain events like dehydration can deplete ADH which would normally be enough to last 2 months but dehydration would deplete it down to only 2 weeks worth, |
| Describe the hypothalamus control release of hormones from pituitary gland | Hypothalamic neurons synthesize oxytocin and ADH which are transported down the axons of the hypothalamic-hypophyseal tract to posterior pituitary where they are stored in axon terminals. Action potentials arrive at the terminals for their release |
| What does ADH's two names tell you? | Two names relate to its function. ADH - antidiuretic, Vasopressin - vasoconstrictor |
| What is the function of an antidiuretic? | Promotes water reabsorption at level of kidney |
| What is the function of vasopressin? | Constricts arterioles which raises peripheral vascular resistance to raise blood pressure |
| What is vasopressin also known as and why? | Arginine vasopressin as it contains arginine in most species |
| What stimulates synthesis/release of ADH? | Increased ECF osmolarity and reduced plasma volume |
| Why would increased ECF osmolarity stimulate synthesis/release of ADH? | Increased solute concentration - not enough water/too much solute in the blood. ADH would respond to the hypertonicity. |
| Why would reduced plasma volume stimulate synthesis/release of ADH? | To prevent effects of further blood volume loss |
| What kind of receptors respond to an increase in plasma osmotic pressure? | Osmoreceptors in hypothalamus |
| What kind of receptors respond to a reduced plasma volume? | Baroreceptors in the veins, atria, and carotid sinus |
| Explain the role osmoreceptors have, in regards to ADH | Expand when blood plasma is more dilute and contract with higher concentrations. This sends an afferent neural signal to be sent to hypothalamus which increases/decreases ADH secretion from posterior pituitary to return blood concentration to normal |
| How much of an increase or decrease in osmolarity will alter ADH secretion? | 1% |
| In regards to the BBB, where are osmoreceptors found in? | Outside BBB |
| What is the implication of osmoreceptors being outside the BBB? | Don't effectively enter cells. Respond largely to sodium and anions which creates an osmotic gradient that pulls water from osmoreceptors |
| What happens when dehydrated osmoreceptors cells shrink? | Opens cation channels and causes depolarization |
| What happens to hypothalamic osmoreceptors when there is an increase in ECF osmolality? | They shrink as water diffuses out? |
| What is the implication of osmoreceptors shrinking? | Opens cation channels, leading to depolarization |
| What is the implication of depolarization? | Release of glutamate at magnocellular neurons and activation of hypothalamic thirst centers |
| What is the implication of activation of hypothalamic thirst centers? | Drinking to decrease ECF osmolality |
| What is the implication of release of glutamate at magnocellular neurons? | Magnocellular neurons (mostly SON, some PVN) are stimulated |
| What is the implication of stimulated magnocellular neurons? | ADH synthesis, transport, and release |
| ADH synthesis, transport, and release leads to increased levels of ADH. At what level are antidiuretic effects seen and/or vasoconstrictive effects? | Low levels - only antidiuretic. High levels - antidiuretic and vasoconstrictive effect |
| What is the implication of antidiuretic effects? | Leads to water reabsorption → decreased ECF osmolality and increased BP |
| What is the implication of vasoconstriction? | Increased BP |
| A study found that after injecting a hyperosmotic solution into blood vessels that perfused with the hypothalamus produced antidiuresis effect, what is the implication of this? | ADH-secreting magnocellular neurons themselves are the osmoreceptors |
| What is the problem with the ADH-secreting magnocellular neurons being osmoreceptors? | They are inside BBB and can't respond quickly to small changes in osmolality in circulation even though they have osmoreceptor characteristics |
| After finding the improbability of the ADH-secreting magnocellular neurons being the main osmoreceptors, what did scientists find? | Circumventricular organ called the organ vasculosum of the lamina terminalis and areas adjacent to the hypothalamus near the anterior wall of the 3rd cerebral vesicle, which lacks BBB, as main brain osmoreceptors |
| What kind of baroreceptors detect reduced plasma volume? | Atrial (cardiopulmonary) stretch receptors, carotid sinus and aortic arch stretch receptors |
| At what blood volume is it an especially strong stimulus for ADH? | 15-25% or more |
| At 15-25% or more decrease in blood volume, what is the rate of ADH secretion? | As high as 50X normal |
| What kind of pressure does atrial (cardiopulmonary) stretch receptors detect? | Low pressure |
| Where are cardiopulmonary receptors found? | Atria of heart and veins that lead to the right side of the heart |
| What are the veins that lead to the right side of the heart? | Inferior and superior vena cava |
| What nerve are afferent signals from the atrial stretch receptor carried by? | Vagus |
| What kind of pressure do aorta and carotid sinus stretch receptors detect? | High pressure |
| What nerve are afferent signals from aorta and carotid artery carried by? | Glossopharyngeal and vagus |
| What veins lead to the right atrium of the heart? | Vena cava |
| What veins lead to the left atrium of the heart? | Pulmonary veins |
| Describe the distribution of low pressure baroreceptors | Junction of right atrium with vena cava flows into right atrium which flows into right ventricle. Junction of left atrium with pulmonary veins flows into left atrium which flows into left ventricle |
| Describe the distribution of high-pressure baroreceptors for the carotid | Goes from carotid sinus(at junction of common carotid) branches into internal and external carotid artery which goes to the head. Afferent signals come from sinus nerve attached to carotid body which then becomes glossopharyngeal to go to brain |
| Describe the distribution of high pressure baroreceptors of aortic arches | Aorta arch branches into brachiocephalic artery and left subclavian artery to go to brain. Afferent signals come from recurrent branch of left (on left subclavian) and right (on brachiocephalic) vagus nerves to travel to brain |
| Which nerve functions as an afferent to both low pressure and high pressure stimuli? | Vagus nerve |
| When there is normal filing of the atria, what kind of signals does the afferent vagal fibers send? | Inhibition of hypothalamic control of ADH production and release because there is a normal level of pressure |
| What is low blood volume called? | Hypovolemia |
| What can cause hypocvolemia? | Hemorrhage, dehydration |
| What is the implication of hypovolemia? | Decreases both atrial filing and stretch receptor stimulation |
| What is the implication of decreased atrial filing and stretch receptor stimulation? | Decreases firing rate to hypothalamus, removing inhbition of ADH production and release. Also sensitizes magnocellular neurons to osmoreceptor input |
| What is the implication of high blood pressure? | Sends action potentials via CN IX (carotid) and X (aortic) to hypothalamus - inhibiting hypothalamic control of ADH |
| What is the relationship between blood pressure, stretch, and action potentials? | Low blood pressure → less stretch →fewer action potentials → removal of inhibition of ADH production and release. High blood pressure →more stretch →more action potentials →inhibition of ADH production and release |
| How does ADH accomplish its antidiuretic effect? | Increases water reabsorption by increasing permeability of the collecting ducts of the kidney to water |
| What would happen if there was no ADH? | Collecting ducts reabsorb very little water, resulting in water loss |
| What part of the nephron does ADH have its biggest effect on? | Last part of the nephron, before urine is collected by ureter. Cortical collecting ducts and outer/inner medullary collecting duct |
| What is the antidiuretic mechanism? | V2 receptors on tubular cells which respond to ADH, leading to a reaction that results in reabsorption of water |
| Describe the structure of tubular cells | Have extracellular V2 receptors and cytoplasmic vesicles containing type 2 aquaporins |
| What are aquaporins? | Water channels that allow movement of water from the tubular lumen back to the blood stream |
| What is the implication of aquaporins? | Reabsorption or recovery of water |
| How does ADH binding to V2 cause an increased movement of water from urine back to bloodstream? | ADH binding to V2 receptors on tubular cells causes activation of adenylyl cyclase →increased cAMP →PKA activation →insertion of aquaporins into the tubular cell membrane →increased movement of water from urine back to bloodstream |
| How long does the reaction to reabsorb water from kidneys take? | 5-10 minutes - the same in the absence of ADH to reverse reaction |
| How does ADH exert its vasoconstrictive effects? | V1 receptors on arterioles and arteries which are activated by high concentrations of ADH |
| Which V1 receptor exerts vasoconstrictive effects? | V1a |
| What does v1b activate? | ACTH release |
| What are the two mechanisms by which ADH can increase blood pressure? | Increasing water concentration increases blood volume and pressure. Vasoconstriction constricts blood vessels to increase blood pressure. |
| What are paraneoplastic syndromes? | Syndrome that is the consequence of a neoplasm that is mediated by an immune response against a tumor |
| What would happen to blood sodium levels if a tumor was secreting ADH? | Decrease because ADH works to reduce the amount of sodium by reabsorbing water |
| What would happen to plasma osmolality if a tumor was secreting ADH? | Decrease because ADH works to reduce hypotonicity by reabsorbing water |
| What would happen to urine osmolality if a tumor was secreting ADH? | Increase because ADH works to reduce hypertonicity so less outflow of water which means urine osmolality would have more solutes |
| What is the function of oxytocin? | Stimulate uterine contractions and milk let-down from mammary glands |
| What are the two stimuli for oxytocin production/release? | Ferguson reflex and milk let-down reflex |
| How does a ferguson reflex stimulate oxytocin production and release? | Distention of vagina and pressure on cervix during labor to stimulate uterine contractions |
| How does milk let-down reflex stimulate oxytocin production and release? | Baby suckling at breast to stimulate milk let down |
| What is the effect of the Ferguson reflex on sensory neurons? | Distention of uterine wall and vagina + pressure on cervix causes increased firing of sensory neurons |
| For the Ferguson reflex, what pathway do sensory neurons travel in? | Relayed in spinal cord to ascending somatosensory pathway |
| How does afferent signals from the spinal cord stimulate production and release of oxytocin? | Afferent signals stimulate magnocellular neurons (mostly paraventricular) leading to increased production and release of oxytocin |
| What kind of feedback system is oxytocin, in regards to uterine contractions? | Positive feedback. Increased pressure on cervix or vaginal wall → oxytocin production/release →uterine contractions →increased pressure on cervix or vaginal wall |
| What pathway does the mechanism for milk release travel through | Suckling innervates mechanoreceptors around areolar region which follows the spinothalamic tract |
| Explain the pathway for oxytocin release? | 1st neuron travels through Lissauer's tract before synapsing with 2nd order neurons (tract cells) in posterior dorsal horn which then decussate via anterior white commissure to anterolateral corner and ascend to the hypothalamic nucleus to 3rd neuron |
| What role does PIH have? | Prolactin inhibitory hormone - inhibits prolactin so won't produce milk |
| Explain how prolactin also has mild milk secretion | Inhibits release of PIH →removing inhibition of prolactin cells release in anterior pituitary → release of prolactin stimulates mild secretion |
| How does oxytocin stimulate uterine contractions? | Binds to oxytocin receptors that are upregulated on uterine smooth muscle towards end of pregnancy |
| What kind of signaling pathway does oxytocin follow for uterine contractions? | Oxytocin receptors are G-protein linked which stimulate a PLC signal transduction cascade that ends in increased intracellular calcium levels and muscle contractions |
| How does oxytocin stimulate milk secretion? | Oxytocin binds to myoepithelial cells that line the ducts of the breast, causing them to contract and expel milk from alveoli into ducts and subareolar sinuses that empty through a nipple pore |
| What kind of pathway does oxytocin follow for milk secretion? | Oxytocin receptors are G-protein linked which stimulate PLC signal transduction cascade that ends in increased calcium levels and myoepithelial cell contraction increasing pressure on alveoli for milk ejection |
| What are other functions of oxytocin? | Increased feeling of openness, empathy, and profoundly positive feelings; sexual arousal; vasopressin-like effects, and more |
| What drug is known for its oxytocin effects of profoundly positive feelings, openness, and empathy? | Ecstacy - MDMA |
| Why does oxytocin have vasopressin-like effects? | Because they're structurally similar |
| What is the clinical correlation for oxytocin? | Induce labor and potential use in couples therapy, PTSD, depression, autism |
Created by:
nnguyen44
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