Hypothalamus and Pituitary Gland
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110 terms
Terms | Definitions |
|---|---|
 Why is the hypothalamus such a huge factor in all endocrine activity? | It basically receives all the signals from cortex, reticular activating substance, thalamus, limbic system, and optic system - and processes information in terms of heat, energy, and autonomic regulation - and signals to antpit and postpit to help control things. |
| The portion of pituitary concerned with water balance - blood volume, thirst, urine output | posterior pituitary |
| The portion of the pituitary concerned with metabolic rate, stress, growth, reproduction and lactation. | anterior pituitary |
| Compare antpit/postpit embryonic development | antpit- Outpocketing of oral cavity endothelium (Rathke's pouch) Postpit - downward extension of brain |
| ***Compare 1. Structure 2. Embryonic development 3. Function 4. How hypothalamus sends signals to it 5. How blood supplies it for anterior and posterior pituitary | 1. ENDOCRINE cells (5 types) for antpit (different hormones), vs. Nervous tissue for postpit 2. Outpocketing of oral cavity endothelium (Rathke's pouch) for antpit while Downward extension of brain for postpit. 3. Growth (GH), Metabolism (TSH), Reproduction (FSH, LH), Milk production (PRL) for antpit. H20 balance (ADH), milk production, labour (OCT) for postpit. 4. Hormonal signals via portal from median eminence for antpit, nerve signals for postpit 5. Venous portal veins from median eminence for antpit, arterial blood feeding terminal axons for postpit. |
| Pituitary embryology 1. Anterior pituitary arises from x that migrated down from the x cavity 2. Posterior pituitary develops from x tissue that extends down from the hypothalamic centers known as the x and x nuclei | Anterior: Glandular epithelial cells that migrated from the oral cavity Posterior: Neural tissue that extended down from the hypothalamic centers (supraoptic and paraventricular nuclei) |
| Sella turcica | Since the sella turcica forms a bony caudal border for the pituitary gland, a pituitary tumor can extend only upward in the rostral direction. This can result in compression of the optic chiasm, which lies on top of the pituitary, enveloping the pituitary stalk. Compression of the optic chiasm can lead to bitemporal hemianopsia, and, when there is no relevant trauma, this clinical finding is pathognomonic for a pituitary tumor. |
| Why do we end up with 5 different types of endocrine cells in the antpit? What must happen for these 5 types to develop? | Cells in anterior pituitary need proper signals to differentiate. 5 types of trophs to begin cell differentiation. |
| What hormone is produced the most in the antpit? | Growth hormone aka somatotropin. About 40%. |
| How to diagnose a pituitary tumor? | Since the sella turcica forms a bony caudal border for the pituitary gland, a pituitary tumor can extend only upward in the rostral direction. This can result in compression of the optic chiasm, which lies on top of the pituitary, enveloping the pituitary stalk. Compression of the optic chiasm can lead to bitemporal hemianopsia, and, when there is no relevant trauma, this clinical finding is pathognomonic for a pituitary tumor |
| Locate the hypothal, neurohypophyseal stalk, and the pituitary gland in this picture |  |
| Big card. Name the 6 major hormones discussed from the Anterior pituitary and the 2 major hormones discussed from the posterior pituitary | Anterior pituitary - growth hormone, thyroid stimulating hormone, prolactin, follicle stimulating hormone, luteinizing hormone, adrenocorticotropic hormone. Posterior pituitary- oxytocin and antidiuretic hormone |
| Basic diagram of antpit/postpit |  |
| Targets all tissues for growth | growth hormone |
| Targets thyroid gland to increase metabolic rate | Thyroid stimulating hormone |
| Targets ovaries and testes. Triggers ovulation and corpus luteum formation in women and testosterone production in men | Luteinizing hormone |
| Targets ovaries and testes. Triggers growth of ovarian follicles and sperm maturation | follicle stimulating hormone |
| Targets adrenal gland to increase cortisol release and increases blood glucose | adrenocorticotropic hormone |
| Does ACTH end up causing lower or higher blood glucose? | Higher |
| Targets breast tissue for lactation | prolactin |
| targets kidney to increase water readsorption | antidiuretic hormone |
| Targets breasts and uterus to increase lactation and uterine contraction | oxytocin |
| Oxytocin and vasopressin/ADH are synthesized where? | In the cell bodies of neurosecretory neurons of the paraventricular and supraoptic hypothalamic nuclei |
| How are oxytocin and vasopressin/ADH transported to posterior pituitary? | These hormones travel down the hypothalamic posterior pituitary stalk and are stored in terminal axons in the posterior pituitary. |
| How are oxytocin and vasopressin/ADH triggered for release into bloodstream? | Action potentials initiated in hypothalamic nuclei trigger release of hormones into venous bloodstream. |
| Explain general mechanism of posterior pituitary hormone synthesis and release | Oxytocin and Vasopressin are synthesized in the PVN and SON hypothalamic nuclei -These hormones travel down and are stored in terminal axons in the posterior pituitary -Action potentials initiated in hypothalamic nuclei trigger release of hormones into venous bloodstream |
| Are postpit hormones secreted into arterial or venous blood? | venous |
| Anterior pituitary hormones are synthed where? Where are they stored? | Hormones synthesized and stored in anterior pituitary itself (5 cell types synthesize the 6 hormones) |
| How are hormones from anterior pituitary released after synthesis? | Release of hormones regulated primarily by 1. hypothalamic hormone release (+ or -) and 2. feedback regulation from target gland hormones |
| Of the 5 cell types that synth the 6 hormones in antpit. What cell type makes 2? | Gonadotroph derived cells that make FSH and LH |
| Synth, storage, release of hormones from anterior pituitary | Hormones synthesized and stored in anterior pituitary itself (5 cell types synthesize the 6 hormones) -Release of hormones regulated primarily by hypothalamic hormone release (+ or -) and feedback regulation from target gland hormones |
| What's different about locations for synthesis, storage, and release between postpit and antpit hormones? | Antpit = Hormones synthesized and stored in anterior pituitary itself (5 cell types synthesize the 6 hormones) -Release of hormones regulated primarily by hypothalamic hormone release (+ or -) and feedback regulation from target gland hormones Postpit - Oxytocin and Vasopressin are synthesized in the PVN and SON hypothalamic nuclei -These hormones travel down and are stored in terminal axons in the posterior pituitary -Action potentials initiated in hypothalamic nuclei trigger release of hormones into venous bloodstream |
| Negative feedback between hypothalamus, pituitary, and peripheral gland 1. Ultrashort loop definition 2. Short loop definition 3. Long loop definition | Big picture - Hypothalamus makes Xreleasing hormone that tells pituitary to make Xtropic hormone that tells peripheral gland to make X. 1. Ultra short loop : When high levels of a hormone negatively regulate the hormone itself. High X releasing hormone will negatively regulate production of X releasing hormone 2. Short loop: When the product of one hormone negatively regulates the hormone itself. For example, X tropic hormone is stimulated by X releasing hormone. High levels of X tropic hormone will inhibit release of X releasing hormone. 3. Long loop: when the final hormone produced can regulate most stages of the pathway. So hormone X will negatively regulate X tropic hormone at pituitary, negatively regulate X releasing hormone at hypothalamus, and can positively stimulate a hypothetical X inhibiting hormone. |
| ***Probably an exam essay-Explain the production of an anterior pituitary hormone, how it gets into the portal system, and how can the portal system allow for negative feedback? |  1. Hypophysiotropic hormones (releasing and inhibiting) produced by neurosecretory neurons in the hypothalamus enter the hypothalamic capillaries. 2. The hypothalamic capillaries rejoin and form the hypothalamic hypophyseal portal system to anterior pituitary 3. Arterial blood enters at the hypothalamic capillaries, with venous blood constituting the pathways to pituitary. 4. The hypophysiotropic hormones leave blood from capillary and go into anterior pituitary, which controls anterior pituitary hormone release. When stimulated to release by a hypothalamic releasing hormone, the antpit will secrete the hormone into the capillary 5. The anterior pituitary capillaries rejoin to form a vein that exits at the bottom of the antpit, and thus this distributes everything to system circulation. Because substances in one vascular bed can go directly to each other, this gives valveless 2 way communication. |
| Hormonal control of anterior pituitary hormone secretion | Hormones (stored in median eminence of hypothalamus) regulating the anterior pituitary are releasing hormones (RHs) or inhibiting hormones (IHs) of pituitary secretion that travel down portal venous system |
| Neural control of posterior pituitary secretion | Hypothalamic nerve impulse travels down axon into posterior pituitary. Hormones go from terminal end of axon into postpit capillary and leave via venous circulation |
| Why do we say that arterial blood feeds posterior pituitary while anterior pituitary receives venous blood? |  Venous blood draining median eminence supplies anterior pituitary (Hypothalamic-hypophyseal portal vein) Arterial blood feeds posterior pituitary |
| *How is blood circulation to hypothalamus and pituitary different from the rest of the brain? | Blood supply outside the blood brain barrier. Allows for negative feedback and regulation Arteries go into median eminence and posterior pituitary into capillaries Veins come from antpit and postpit |
| What important about low pressure in hypothalamic hypophyseal portal system? | low pressure because it's valveless, basically allows 2 way communication across the capillaries. |
| Site of hormone synthesis 1. Antpit 2. Postpit | 1. 5 types of endocrine cells in anterior pituitary 2. Hypothalamus (ADH, OCT) in neurons of Paraventricular and supraoptic nuclei |
| How hypothalamic hormones are stored for 1. antpit 2. post pit | 1. Releasing and inhibiting hormones in median eminence 2. ADH, OCT, stored in terminal axons in posterior pituitary |
| How hypothalamus sends a signal to 1. ant pit 2. post pit | 1. Nerve impulse->median eminence->hormone signal released into portal vein->anterior pit 2. Nerve impulse down axon to posterior pit |
| How signal from hypothalamus generates action in 1. antpit 2. postpit | 1. Neurocrine signal to anterior pituitary->endocrine signal to multiple tissues of body 2. ADH, OCT released from terminal axon->neurocrine signal to kidney, mammary gland |
| Important Factor in Stimulating Growth and Regulating Metabolism | growth hormone |
| Does growth hormone control most of the growth in the body? | It's an important factor, but don't forget Other factors in growth: Genetics Diet Freedom from chronic disease or environmental stress Normal Hormonal Milieu |
| Why doesn't growth hormone have as much as an effect on adults as it does on kids? | In children, GH increases length and strength of long bones by acting on epiphyseal growth plates -In adults, GH can increase thickness and strength of membraneous bones (hands, feet, skull), but not long bones (cartilage on either side of epiphyseal line gives way to bone, fuses) |
| In children, GH increases length and strength of long bones by acting on x | In children, GH increases length and strength of long bones by acting on epiphyseal growth plates |
| In adults, GH can increase thickness and strength of X bones but not X bones. | In adults, GH can increase thickness and strength of membraneous bones (hands, feet, skull), but not long bones (cartilage on either side of epiphyseal line gives way to bone, fuses) |
| Why is Barry Bonds likely to be suspected of GH even though GH loses most of its effects on adults? | Because GH in adults affects membranous bones like hands, feet, and skull - Barry Bonds would likely have those parts be bigger. They usually don't change size once done growing, but in Barry's case - they are larger than in previous years |
| Growth of long bones - general sentence |  Cartilage (chondrocytes) is replaced with bone. |
| GH controls growth and proliferation of tissues and metabolism regulation, but in general, these are the three major effects in terms of protein, fat, carbohydrates. | Increase protein stores, burn fat stores, conserving carbohydrate stores. |
| Growth hormone effect on metabolism 1. Plasma glucose 2. Plasma FFA 3. Plasma amino acids 4. Plasma urea | 1. Increase 2. Increase 3. Decrease 4. Decrease |
| Growth hormone effect on muscle 1. Glucose uptake 2. Amino acid uptake 3. Protein synthesis 4. lean body mass | 1. Decrease 2. Increase 3. Increase 4. Increase |
| Growth hormone effect on adipose tissue 1. Glucose uptake 2. Lipolysis 3. Adiposity | 1. decrease 2. increase 3. decrease |
| Growth hormone effect on kidney/pancreas/intestines/islet cells/parathyroids/skin/connective tissue/bone/heart/lungs 1. protein synthesis 2. DNA/RNA synthesis 3. cell size and cell number 4. organ size 5. organ function | 1. increase 2. increase 3. increase 4. increase 5. increase |
| Growth hormone effect on chondrocytes 1. amino acid uptake 2. protein synthesis 3. DNA/RNA synthesis 4. chondroitin sulfate 5. collagen 6. cell size and number 7. linear growth | 1. increase 2. increase 3. increase 4. increase 5. increase 6. increase 7. increase |
| **Gigantic growth hormone regulation diagram** 1. Major inputs to hypothalamus for GH 2. Minor inputs to hypothalamus for GH 3. Somatostatin 4. GHRH 5. GH effect on liver and IGF-I production 6. GH effect on metabolic actions unrelated to growth such as fat breakdown/glucose uptake by muscles/ glucose output by liver |  |
| *****Does growth hormone increase or decrease tissue response to insulin, why? | Decreases tissue response to insulin, this is so that GH can keep a supply of glucose in circulation for BRAIN rather than having insulin promote uptake into cells. This happens usually in starvation response. |
| How does GH function to increase protein stores? | Increase Amino acid uptake, transcription, ribosomal assembly, protein synthesis Decreases protein catabolism |
| How does GH function to burn fat stores? | Increase mobilization of fatty acids from adipose tissue, FFA in blood increase oxidation of FFA->A-CoA energy in tissues |
| How does GH function to conserve carbohydrate stores? | Maintain glucose in blood and glycogen stores decrease burning glucose for energy ***decrease tissues response to insulin (insulin resistance) |
| If you wanted to have glucose uptake into cells, would you want insulin, growth hormone, or both? | insulin only. GH decreases tissue response to insulin |
| Insulin's effects on muscle | increase glucose uptake and increase synthesis of protein and glycogen |
| Insulin's effects on liver | increase glucose uptake and increase synthesis of protein and glycogen |
| Insulin's effects on adipose tissue | Increase glucose uptake and increase synthesis of fatty acids |
| Would you see insulin secretion when blood glucose is high or low? | high |
| Would you see growth hormone secretion when blood glucose high or low? | GH secretion peaks during periods when blood GLU may fall, to oppose INS-mediated GLU uptake and maintain blood GLU for CNS. |
| Explain when GH would be secreted to counteract insulin's effects? | GH secretion peaks during periods when blood GLU may fall, to oppose INS-mediated GLU uptake and maintain blood GLU for CNS |
| Insulin secretion peaks after x to promote uptake, anabolism | Insulin secretion peaks after glucose absorption to promote uptake, anabolism |
| Compare insulin secretion to GH secretion. If you were to draw a graph of the level's of each over an entire day, what would they look like? | Insulin is secreted only after glucose intake, or a meal - so, you see really only 1 big peak, indicating a high insulin concentration after the meal But for GH, is actually peaks up and down because it's made during sleep, exercise, and stress. This allows a healthy kind of insulin resistance to protect blood glucose levels. You see high peaks of GH secretion when working out and during deep sleep. |
| If you eat a protein rich meal, how would insulin and GH react? | both GH and insulin secreted. GH stimulated by protein intake, and opposes insulin to prevent hypoglycemia |
| If you eat a carbohydrate rich meal full of noodles and bread, what would levels of insulin and GH be? | Insulin increased, growth hormone suppressed. Insulin action goes unopposed. Carbs means sugars. You want high insulin at this time |
| If you fast for awhile, what happens to levels of insulin and GH? | insulin decreases and growth hormone rises to enhance lipolysis and decrease glucose uptake to maintain blood glucose for CNS |
| Explain the dawn phenomenon of GH secretion and how this affects insulin and diabetes | Dawn phenomenon -a natural GH surge followed by cortisol spikes at 12-3 am. This impairs insulin sensitivity because GH decreases insulin response Thus, the impaired insulin secretion and sensitivity means that around 4-8am, you're going to have a high blood sugar. When you eat breakfast, insulin secretion stimulated, finally counterbalances the natural GH surge, and lowers blood glucose. Thus, diabetics who naturally have a high blood sugar, should focus on having breakfast to get a jump start on insulin secretion |
| *****Essay question on exam - We see how GH counterbalances the effects of insulin, but GH can't function without insulin. Why is this? What role does insulin play that is critical for GH growth signalling to occur? | You need to remember the IGF/IGFBP pathway for this one. IGF= insulin like growth factor IGFBP = insulin like growth factor binding protein GH stimulates IGF (aka somatomedins), but IGF remains bound to IGFBP when insulin concentration low. This helps prevent overaction of GH if no insulin. However, when insulin is high, this tells the body to switch from insulin to GH signaling. It does this because rise in insulin inhibits IGFBP formation in liver. Thus GH will stimulate IGF synthesis, and high insulin will decrease IGFBP synthesis - so you get some free floaty IGF's hanging around. These IGF's go and bind to receptors and initiate growth signaling response. Thus, insulin is the key to inhibiting IGFBP which blocks GH signaling. |
| One of the primary ways in which doctors analyze growth hormone levels | levels of IGF |
| Why don't GH or insulin alone stimulate growth but both together do? | You need to remember the IGF/IGFBP pathway for this one. IGF= insulin like growth factor IGFBP = insulin like growth factor binding protein GH stimulates IGF (aka somatomedins), but IGF remains bound to IGFBP when insulin concentration low. This helps prevent overaction of GH if no insulin. However, when insulin is high, this tells the body to switch from insulin to GH signaling. It does this because rise in insulin inhibits IGFBP formation in liver. Thus GH will stimulate IGF synthesis, and high insulin will decrease IGFBP synthesis - so you get some free floaty IGF's hanging around. These IGF's go and bind to receptors and initiate growth signaling response. Thus, insulin is the key to inhibiting IGFBP which blocks GH signaling. |
| Would you see growth in Isolated cells cultured outside the body + GH? | no, b/c no insulin |
| Would you see growth in Cells within a living system (normal IGF/insulin)+ GH ? | yes, normal growth |
| Would you see growth in Individuals with normal/high GH + low IGF | yes, but retarded growth such as African pygmies |
| Growth hormone shows both direct effects and indirect effects due to modification of other things. What are the things that indirectly regulate GH activity? | 1. Direct effect of receptor binding causes metabolic changes 2. Indirect effects mediated by insulin, IGFBP, and IGF insulin inhibits IGFBP --> gives free IGF IGFBP (liver, other tissues) blocks IGF but gives it stability until insulin comes along IGF (liver, other tissue) - GH stimulates IGF synth, thus binding to receptor, thus growth effects |
| Why do we need IGFBP? | Because it confers stability to IGF and allows prolonged time of action. |
| Review this - GH secretion and negative feedback regulation diagram - identify short, long loops |  |
| 3 GH abnormalities 1.Acromegaly 2.Dwarfism 3.Panhypopituitarism What are they? How to diagnose? Treatment? | 1.Acromegaly - sustained GH secretion due to somatotroph tumor Diagnose if person still has elevated GH even when given tons of glucose or IGF - which negatively regulates GH production Treat with surgery or somatostatin analogues 2. Dwarfism - Too little secretion of GH, can be treatable and/or cured with GH treatment. If you have dwarfism with elevated GH: then you have impaired insulin or IGF 3. Panhypopituitarism: anterior pituitary is f'd up. Can be a side complication of acromegaly where a tumor grows inside - but it can destroy the gland too and impair anterior pituitary function |
| Acromegaly 1. what? 2. how to diagnose? 3. treatment? 4. Other subtypes? | Acromegaly - sustained GH secretion due to somatotroph tumor Diagnose if person still has elevated GH even when given tons of glucose or IGF - which negatively regulates GH production Treat with surgery or somatostatin analogues Gigantism - where GH causes increase in both bone length and bone thickness before adolescence |
| where GH causes increase in both bone length and bone thickness before adolescence | gigantism / acromegaly |
| Is caused by hyposecretion of GH. Is generally treatable and cured with HGH treatment. Has a subtype with elevated GH: impaired INS/IGF | dwarfism |
| Impaired function of anterior pituitary on a broad scale. | panhypopituitarism |
| Prolactin 1. Does it increase during pregnancy? 2. What maintains elevated prolactin? 3. Negatively regulates this hormone 4. What is the main function of prolactin? | 1. yes, 20 fold elevation 2. nursing 3. Prolactin negatively regulates dopamine 4. Stimulate original differentiation of breast tissue, expansion during pregnancy, and milk production |
| Negatively regulates dopamine | prolactin |
| Stimulate original differentiation of breast tissue, expansion during pregnancy, milk production | prolactin |
| Explain why prolactin negatively regulates dopamine. | Dopamine is an inhibitory of pituitary secretion of prolactin. It's usually the only thing besides prolactin long loop negative feedback. Prolactin however, itself negatively regulates it. |
| stimulated by suckling, sexual intercourse (in males and females); emotional distress can inhibit its secretion | oxytocin |
| Oxytocin is stimulated by x, x (in males and females); and can be inhibited in secretion if you are x. | stimulated by suckling, sexual intercourse (in males and females); emotional distress can inhibit OCT secretion |
| Functions of oxytocin 1. Help express x proteins in breast 2. Stimulates this in ducts 3. uterus? 4. Discoveries found in ovary and testes show that | Functions: 1. to help express milk proteins in the breast 2. 'letdown' of milk into ducts 3. OCT stimulate contraction of the uterus (may help in childbirth) 4. OCT and OCT receptors found in ovary and testis; likely local (but unclear) effects in reproduction |
| Why would having an emotionally stressed mother be bad for a baby's nutrition? | emotional stress impairs mother's ability to breastfeed by f'ing up hypothalamus signalling for oxytocin and prolactin. |
| Secreted in order to conserve water at the kidney | ADH/vasopressin |
| Stimulated by small changes in blood osmolality, hypovolemia, hypotension | ADH/vasopressin |
| Hypovolemia | Too low blood plasma volume - ADH would be secreted. |
| Combined with ADH release, what's another way the body signals to increase plasma volume? | increased thirst and water ingestion |
| ***Specific mechanism of ADH action. ADH helps reabsorb water, but how? Draw a diagram of this pathway. What's the key receptor to remember here? |  |
| In a nutshell, ADH increases water reabsorption by attaching to a x receptor and activates a x to cause the insertion of x into the apical membrane. H20 then moves in through this in response to an osmotic gradient and can move out through x and x in the basolateral membrane | |
| Production of large amounts of dilute urine | diabetes insipidus |
| Frequent need to drink water and urinate | diabetes insipidus |
| ADH can be misregulated in three ways 1. Diabetes insipidus 2. Alcohol 3. Syndrome of inappropriate ADH secretion (SIADH) Explain what causes ADH dysregulation in each | 1. Diabetes insipidus Production of large amounts of dilute urine Frequent need to drink water and urinate --Central Diabetes Insipidus ADH production impaired or absent in posterior pituitary Can treat with ADH --Nephrogenic Diabetes Insipidus Impaired ADH action at collecting tubules of kidney (breakdown anywhere in G-protein/cAMP/PKA/aquaporin cascade) ADH treatment ineffective, can treat with drugs 2. Alcohol - Confuses osmoreceptors in hypothalamus, decreases ADH secretion, leading to dehydration and increased urine production 3. Syndrome of inappropriate ADH secretion (SIADH) Too much ADH is produced, regardless of plasma osmolality Treat with limitation of water intake, ADH inhibitors |
| Diabetes insipidus 1. What is it? 2. Central diabetes insipidus 3. Nephrogenic diabetes insipidus | 1. Production of large amounts of dilute urine Frequent need to drink water and urinate 2. Central Diabetes Insipidus ADH production impaired or absent in posterior pituitary Can treat with ADH 3. Nephrogenic Diabetes Insipidus Impaired ADH action at collecting tubules of kidney (breakdown anywhere in G-protein/cAMP/PKA/aquaporin cascade) ADH treatment ineffective, can treat with drugs |
| ADH production impaired or absent in posterior pituitary. Can treat with ADH | Central diabetes insipidus |
| Impaired ADH action at collecting tubules of kidney (breakdown anywhere in G-protein/cAMP/PKA/aquaporin cascade) ADH treatment ineffective, can treat with drugs | Nephrogenic diabetes insipidus |
| Confuses osmoreceptors in hypothalamus, decreases ADH secretion, leading to dehydration and increased urine production | alcohol |
| Too much ADH is produced, regardless of plasma osmolality Treat with limitation of water intake, ADH inhibitors | Syndrome of inappropriate ADH secretion (SIADH) |
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