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228 Cards in this Set
- Front
- Back
What does hormones never do?
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Initiate cellular responses -- they only modulate -speed up or slow down
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What does hormones help the body do?
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1. maintain homeostasis
2. adapt to change 3. perform coordinated complex processes |
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Whats the difference between exocrine and endocrine?
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exocine - secreted into a luman (gland and goes to a specific place)
endocrine- secreted into the blood |
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At what concentration does hormones circulate in the blood?
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very small concentration
|
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What is a primary endocrine gland?
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Its main function is to secrete hormones
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What hormones are made in the adrenal cortex? medulla?
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Cortex -- 1. cortisol, androgens, aldosterone
Medulla - epi and nor |
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What hormones does the placenta secrete?
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1. human chorionic gonadotropin
2. estogen 3. progesterone 4. human placental lactogen |
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Hormones of the thyroid?
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1. T3 2. T4 3. Calcitonin
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What are the 3 main groups of hormones?
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1. amino 2. peptide 3. steroid
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What is the order of organelles that hormones travel to become active?
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Starts as pre-pro then goes to ER to become pro. then to golgi to become active then goes into secretory vessicals
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What is inside the secretory vessicle?
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both the hormone and the copeptide (what was bound to it as pro hormone
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What AA are amino acid hormones derived from?
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Tyrosine
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Whats another name for amine hormones?
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catecholamines
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tyrosine hydroxylase -
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converts tyrosine to DOPA -(this is the rate limiting step to make Epi)
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PNMT-
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coverts NE to E
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What 2 peptide hormones bind to proteins in the blood?
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GH and IGF
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What amine hormone needs to be bound to a protein?
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Thyroid hormones -t3 and t4
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Where is the first enzymatic step to make steroid hormone?
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in the mitochondria
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What are the rate limiting steps to make steroid hormones?
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1. transport of cholesterol into the mito
2. activity of P450 that catalyzes conversion of cholesterol into pregnenolone |
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Give an example of a glucocorticord, mineralocorticoid, androgen that is secreted from the adrenal cortex?
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glucocorticord-- cortisol
mineralocorticoid--aldosterone androgen --DHEA and androstendione |
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What causes receptor down regulation?
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a chonic exposure to a high level of the hormone leads to a lowered max response --diabeties type 2
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Where are catecholamines (amine hormones) released from?
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neurons and adrenal medulla
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What is the pathway from Tyrosine to E with enzymes
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Tyrosine (tyrosine hydroxylase) DOPA, DA, NE (PNMT) E
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What 3 catecholamines are stored in secretory vessicles?
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DA, NE, E
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What are secretory vessicles secreted in response to:?
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Secetogogues that increase intracellular Ca
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What proteins bind to Thyroid hormones?
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thyroxine binding globulin and albumin
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Where is the first step to make steroid hormones from cholesterol?
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in the mitochondria
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What are the rate limiting steps in the formation of steroid hormones?
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1. cholesterol transport to mitochondira
2. activity of P450 - catalyzes conversion of cholesterol to pregnenolone |
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What does enzyme P450 do?
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converts cholesterol into pregnenolone
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Where does the rest of the steps of steroid synthesis take place?
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in the mitochondia or smooth ER
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cholesterol esterase-
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what removes the cholesterol from the LDL
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What is the purpose of the signal peptide?
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to send the protein to the ER
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What is steroidogenesis controlled by?
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trophic hormones that bind G proteins coupled receptors
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What tissues produces steroids? and what steroids?
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adrenal cortex -- aldosterone, cortisol, DHEA
gonads-- testosterone and estradiol |
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Glucocorticoids- example and what they do
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cortisol - increase glucose levels
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mineralocorticolds
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Aldosterone -enhance water and NaCl reabsorption
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What is weaker DHEA or testosterone?
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DHEA
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What is the main estrogen?
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estradiol
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What is a weak estrogen secreted by placenta?
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estriol
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What type of hormones are stored?
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Peptide and amine -- thyroid and steroid diffuse out of cell after synthesis
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How does thyroid and steroid mostly circulate in the blood?
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binded to the plasma binding globulins
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What is actually measured when measuring hormone concentration?
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the free H --what is maintained at a set point
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What serves as a reservior for the steroid and thyroid hormones?
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H:BG
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What 2 things must be working to have a hormone response?
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receptor and hormone
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Sensitivity of a hormone -defined as
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[H] that creates the half max response
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A more sensitive receptor would shift to the ___
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Left -- less hormone needed to create the same response
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Which way does receptor down regulaton shift the hormone concentration Hormone effect graph"?
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decreases the hormone effect -- so shifts it down
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Receptor sensitivity may change due to __ and shift the graph__ in the case of diametes
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1. genetics 2. inhibitors 3. activators
shifts graph to the right -requires more hormone for the same response |
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How does receptor down regulation work?
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The chronic exposure to the target hormone decreases the number of receptors on the cell
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What type of hormones lead to generation of second messengers like cAMP, cGMP, Ca++, activation of kinases leading to P of proteins?
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Both peptide and catacholamines
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What hormones are in blood attached to binding proteins?
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all steroid, thyroid and GH
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What 3 major tissues/organs make and store energy?
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liver, muscle, fat
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intermediary metabolism-
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sum of anabolism and catabolism
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Anabolism -When does anabolism occur?
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build up of moleculesduring the absorptive phase -- requires energy
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Catabolism - when?
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the break down of larger molecules - releases energy --during post absorptive phase or fasting
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glycogenesis -
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Glucose to glycogen
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Where does gluconeogensis happen?
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liver and sometimes kidney
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What 3 tissues participate in intermediary metabolism?
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liver, muscle and fat
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What does lipolysis start with and then produce?
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TG --> Glycerol 3P and 2 FA
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What is ketogensis? where does it happen?
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FFA to Ketones in liver
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Where is insulin produced?
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Beta cells in pancreas
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What hormone levels increase when fasting?
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glucagon, epi, GH, and cortisol -- all act to increase blood glucose
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Fasting causes what in respect to innervation of liver and adipose tissue?
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Increases the activity of the sympathetic nerves in liver and adipose
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What is the storage form of fat muscle, and liver tissue?
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fat- fat
muscle - muscle glycogen liver- glycogen |
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When is the absorptive phase?
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Lasts 4 hours after eating
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What are the insulin opposing hormones? and where are they produced
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GH (anterior pit), cortisol (adrenal cortex), epi (adrenal medulla), and glucagon (pan - alpha cells)
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What is the main energy source ffor all cells during absorptive phase?
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Glucose
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What dictates the metabolic events during absorptive phase?
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Insulin
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What are 3 effects of insulin?
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1. decreases sympathetic activity
2. increases digestion 3. stimulates anabolic events in liver, muscle, and fat |
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What tissues are insulin dependent?
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muscle and fat - requires GLUT 4
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What GLUT does the liver have? How does glucose in liver still depend on insulin?
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Liver =GLUT2
Insulin still increases the glucose uptake in liver by increasing glucose kinase (glucose --> G6P |
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Why is the increased activity of glucose kinase help to bring more glucose into the cell?
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Lowers the concentration of glucose so more will flow in
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What is excess glucose changed into in the liver? - where does it travel and then what is it changed into ?
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VLDL - exported to the blood and then hydrolyzed into monoglycerides and FFA
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VLDL is hydrolyzed to what? by what? and where?
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VLDL changed into FFA and monoglycerides by LPL at the adipocyte capillaries
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After the formation of FFA where do they go? and form/
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FFA then enters the adipocyte and combine with glycerol phosphate to form fat
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When the fat cells uptakes excess glucose what forms?
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fat --TG
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What is the final location of absorbed triglycerides in plasma chylomicrons?
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follow the same path as VLDL and goes to form fat (TG) in adipocytes
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What is LPL activated by and when?
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Insulin the absorptive phase (4 hours after eating)
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What is the path of absorbed amino acids?
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go to make new protein
stored energy as protein in muscle |
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What does LPL do?
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strips a TG from the VLDL and then breaks it down into FFA and 2 glycerols
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What carries the TGs from the liver to the fat cells?
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VLDL and chylomicrons
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Post absorptive phase-when? enzymes?
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Between meals - decreased insulin and increased glucagon, GH, epi, and cortisol
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How does the body maintain glucose levels?
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by gluconeogensis and having non CNS cells use FFA and ketones-- glucose sparing
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What can be used as energy for CNS?
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ketones and glucose -- FFA can not cross the blood brain barrier
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What is glucagons main target?
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the liver
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How does the 4 insulin antagonist hormones work together?
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each hormone works on a different pathway
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Why is cortisol needed?
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to upregulate uptake of epi
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FFA are turned into what in the post absorptive phase? where?
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Ketone bodies in the liver
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What is the final product of glycogen break down in skeletal? why/
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lactic acid or pyruvate -- because no G6Pase -- an enzyme in glycolysis
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TG is broken down in to? by what? where?
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TG - FFA and glycerol3P Hormone sensitive lipase - in the fat cell
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What inhibits HSL?
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insulin
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What is limited at the start of fasting?
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protein catabolism -- strategy the body uses to withstand a long fast
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What is the cause of cushions syndrome?
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increased cortisol
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Diabetes Mellitus --
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a condition which insulin production 1 or function 2 is imparied
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What is an effect of diabetes?
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hungry cells because the glucose cant be taken in - so high blood glucose
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What are some symptoms of diabetes?
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polyuria, polyphagia, polydepisa, weight loss, blurry vision, numbness,
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Type 1 diabetes-
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due to beta cell destruction by auto immune disease - normal or super sensitive insulin function
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Type 1.5 diabetes-
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delayed onset of type 1
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Type 2 diabetes-
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insulin insensitivity-receptor problem, genetics, obesity, normal or high insulin levels in plasma, leads to beta cell exhaustion
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Gestational diabetes0
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pregnant women - like type 2 insulin resistance
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If you have a GH secreting hormone what effect on blood glucose?
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increases it
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Does cushings syndrome cause higher or lower blood glucose?
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Cushings = cortisol secreting tumor =higher blood glucose
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What is one mandated activity for diabetes patients? Why?
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excercise - contraction of skeletal muscle can stimulate translocation of vesicles with GLUT4 to plasma membrane -feeds into the same pathway as insulin
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What diabetic symptoms could excercise aleaveate?
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problems due to hyperglycemia
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What is the pathway that excercise feeds into called?
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Contraction induced signals
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How does our body control food intake and weight? where?
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through central integrating center located in hypothalamus
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Short term control of weight and food intake includes-
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ghrelin - from stomach stimulates hunger center in hypothalamus
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What hormones stimulate the satiety center as short term control?
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glucose, insulin, and gut hormones
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How does the body do long term control of body weight and food intake?
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fat inhibits appetite by secreting leptin
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What does CRH inhibit? What is CRH?
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CRH is from the hypothalamus and stimulates the secretion of ACTH- adrenocorticotropic hormone --CRH inhibits the hunger center
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What nervous system does fasting stimulate? eating
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Eating- parasympathic - rest and digest
Fasting sympathic |
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Where is the hypothalamus, posterior pituitary, and anterior pituitiary derivered from?
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hypothalamus - embryonic brain tissue
posterior pituitary-embryonic brain tissue anterior pituitiary-roof of the mouth |
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What tissue types is the pituritary a hybrid of?
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endocrine tissue (anterior) and neural (posterior)
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How does the anterior pituitary receive the releasing hormones from the hypothalamus?
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through the hypothalamic pituitary portal system --hormones released from hypo and travel to median eminence, travel through capillaries to AP
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How does the posterior receive blood?
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directly arterial blood supply
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At what concentrations are the hypothalamus hormone levels in portal vessel? systemic circulation?
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portal - pM to nM
systemic - not dectable |
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What is the only pituitary hormone under chronin inhibition? how are others controlled
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prolactin others by negative feedbakc
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What increases the size of the target tissue of anterier pituitary hormones?
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if you increase the AP hormones
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Sheehan's syndrome --
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blockage in the hypothalamic portal vessel from mother who just delivered baby -lots of blood loss vessel collapse
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Why does prolactin only have negative feed back?
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because DA goes straight to prolactin - no intermediate
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Sheehans syndrome would do what to the anteteior pituitary levels?
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decrease all except prolactin
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Primary disfunction of homeostatic hormonal regulation --
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happens with the target h
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Tertiary disfunction?
Secondary/ |
Happens with hypothalamus
2- anterier pituitary |
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What is the posterier pituitary composed of?
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axons and terminals of neurons that are originiated from the SON and PVN --the cell bodys (somas) are in hypothalamus
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Where are posterior pituitary hormones released? stored? created?
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directly into venous circulation -stored in the posterier pit - created in the hypothalamus
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What are SON and PVN?
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Dendrites in the hypothalamus responding to stimulus
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What hormones are made in posterier?
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ADH and oxytocin
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What is the infundibulum?
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Connects the hypothalamus to pituitary. - where the axons to the pp are found
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What does oxytocin do?
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stimulats smooth muscle growth and modulates the activity of many neurons - helps facilitate species propagation
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What does the release of PP hormones require?
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an Action potential in the hypothalus to get release
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How many effects can the hypothalamic pituitary axis produce from 1 signal?
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Same signal can stimulate secretion from both PP and AP through 2 distinctly different pathways ex- oxytocin and prolactin
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What needs to happen to get milk synthesis and ejection?
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Anterior P - stops producing DA because its inhibitory so more prolactin is now there -- PP - neurons signal to secrete more oxytocine
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What type of hormone is somatostain?
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PEPTIDE
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What is the only nonpeptide regulatory protein?
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DA
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What are the 3 pillars that are involved in balancing physiology? how?
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1. thyroid- metabolic rate
2. adrenal - restores homeostasis after physiological stress 3. sex - development and maintance |
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Where is thyroid? what is beside it/
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beside trachea - just below larnx - contains 4 parathyroid glands
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what does the parathyroid do/
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secrete PTH- increases plasma Ca and decreases PO4
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Where is the site of thyroid hormone synthesis?
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a single layer of follicular cells that surround a pool of colloid --hormones made in the lumen of the follicular cell
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When the thyroid is hyperactive what happens?
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the colloid increases and you get a goiter
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What are the 3 steps in TH synthesis?
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1. addition of I to tyrosine residues in thyroglobulin in luman
2. coupling to make TH on thyroglobulin 3. cleaving TH from thyroglobulin and send it back to the follicular cell |
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Where is thyroglobulin (TG) made? and then sent to?
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made in the follicular cell and then sent to the follicular cell lumen wo I can bind to it
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How does I get into the follicular cell? what type of transporter?
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I comes from the circulation - and then is symported with Na in a 2ndary active transporter
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What is a 2ndary active transporter-
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doesnt directly use ATP - uses the energy from some other process
|
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What does the conjugation of I into tyrosine residues of TG produce?
|
MIT - monoiodotyrosine or DIT - diiodontyrosine
|
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How does MIT or DIT produce T3 or T4?
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Either MIT and DIT form T3 or 2 DIT form T4
|
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How are T3 and T4 secreted back into the follicular cell?
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with the TG still attached
|
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Which is stronger T3 or T4? What is secreted more? whos half life is longer?
|
T3 - much more potent
T4 is secreted more T4 lasts longer |
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What converts T4 to T3? where?
|
deiodinase in the liver and target cells
|
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Where are Thyroid receptors found?
|
in most cells in the body
|
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What does TH do?
|
1. increase BMR main function
2. increase sympathetic responses - beta adrenergic responses - increases epi so increased heart rate |
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What are THs required for?
|
neuron development and function --formation of nerve terminals and synpases
--increases GH secretions -normal reproduction in adults --proper nerve/muscle reflexes --normal recognition |
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Would plasma TSH levels of a subject with inactive thyroid receptors be higher or lower?
|
higher - because your taking away the negative feedback
|
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What is the most obvious thing that indicates a thyroid dysfunction?
|
a goiter -but a goiter could be caused by something else too
|
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When does a goiter form?
|
When chronically stimulated by TSH/TSH like substances - the thyroid glands (coloid) increases
|
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hyperplasia- define - what does it cause
|
increase in the number of cells
causes a goiter |
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What does colliod droplets contain in follicular cell?
|
T3 or T4 with bound TG
|
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How does TH increase BMR?
|
by stimulating moblization of energy substrates, O2 consumption, and Na/K ATPase activity
|
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What could hyperthyroidism be caused by?
|
A TSH secreting tumor
|
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Grave's Disease -
|
presence of immunoglobulins that bind and activate TSH receptors -which leads to high TH and then lower levels of actual TSH but still have goiter b/c of immunoglobins
|
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What does a thryrotrope do/
|
produces TSH
|
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What is a cause of hypothyroidism?
|
death of thyrotropes -- you cant make TSH so thyroid atrophys without stimulation
|
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Does chronic I deficiency result in a goiter?
|
Yes - Low TH removes neg feedback and increases TSH
|
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What can thyroiditis cause? lead to?
|
causes slow or rapid inflammation of the thyroid gland -- eventually hypothyridism
|
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What is another name for hyperthyroidism?
|
Thyrotoxicosis
|
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What are some symptoms of hyperthyroidism?
|
exopthalmos (grave's diease--eyes) fine tremor,tachycardia, weight loss, heat intolenance
|
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symptoms of hypothyroidism-
|
cretinism for congenitial deficiency, growth stunt, cold intoleance, bradycardia, weight gain
|
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What is the effect of defective TH receptors?
|
cannot activate TH receptors on TSH or TRH - so increase in TH and increase in TSH -- but you would have the symptoms of hypo because TH cant do anything bc of defective receptors
|
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What secretes catacholamines? What are they?
|
sympathetic nervous system and adrenal medulla -- epi and nor
|
|
What does the adrenal cortex secrete? function?
|
cortisol - increase blood glucose, anti inflam, anti immune and anti stress
|
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What is the adrenal gland a hybrid of?
|
endocrine cortex and neural medulla
|
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Where is the adrenal glands?
|
superior pole of the kidney
|
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How is blood supplied to the adrenal glands/
|
1st to the cortex (outside) then medulla
|
|
What kind of nerves are supplied to the medulla?
|
modified ganglion of the sympathetic nervous system
|
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What are the different layers of the adrenal cortex glands and what do they secrete?
|
OUTER
1.Zona glomeralosa- Aldosterone 2.Zona fasciculate - Cortisol and androgens 3. Zona Reticularis - androgens(DHEA) and cortisol INNER |
|
What do all things secreted from cortex have in common?
|
All steroid hormones
|
|
What does the medulla secrete
|
amine hormones - Epi and Nor the catachoamines
|
|
What is the rate limiting step of forming Epi/
|
Tyrosine to DOPA by tyrosine hydrolase
|
|
What happens with DHEA levels with aging?
|
they decrease - some take as antiaging supplement
|
|
What are adrenal steriods derived from? rate limiting step?
|
cholesterol = conversion of cholesterol to prenenolone by P450 located in inner mit membranne
|
|
What do both epi and cortisol protect the body from?
|
stress - maintain plasma glu levels
|
|
What does cortisol do normally? at high levels?
|
maintains glu levels by gluconeogensis and lipolysis
high levels -- stimulates protein breakdown |
|
Why give pregnant women who are goin to have a premie a cortisol shot?
|
to stimulate lung maturation---surfactant production
|
|
What is the active form of cortisone?
|
hydrocortisone
|
|
When is cortisol levels the highest? how does the pattern change when stressed? a ACTH secreting tumor?
|
when you first wake = stressed =same pattern but highre
ACTH tumor - flat line |
|
What are some therapeutic uses of cortisol?
|
1. bee stings
2. arthritis 3. prevent rejection of organ transplant |
|
Why would you have hyposection of cortisol?
|
autoimmune destruction of adrenal cortex -- loss of both aldosterone and cortisol
|
|
Addison's Disease -
|
destruction of adrenal cortex - hypotension, hypoglycemia, fatigue, and weakness
|
|
What causes impaired cortisol secretion?
|
congenital adrenal hyperplasia -- cant convert cholesterol to cortisol
|
|
Cushings syndrome caused by? symptoms?
|
caused by - hypersection of cortisol - hypertension, muscle weakness, immunosuppressive,
|
|
What does high concentrations of cortisol do?
|
stimulates protein degradation and inhibits bone formation and stimulates bone resorption (can lead to osteoprosis
|
|
What molecules could causes a growth stunt?
|
high glucocorticoids
|
|
What is congenital adrenal hyperplasia?
|
A definciency in 21 alpha OHase which changes cholesterol to cortisol - so the ACTH increases which increases DHEA
|
|
What hormones increase during stress?
|
Aldsterone- retain Na
,ADH - retain h20 GH- mobilze stored energy epi and nor -pain killing glucagone- increase blood glucose |
|
What hormones decrease during stree?
|
insulin and reproductive
|
|
What are the primary reproductive organs? another name? What happens here?
|
gonads -ovaries and testes - gametogeneisis and steroid hormone production
|
|
What are accessory reproductive organs?
|
duct systems and related secretory glands - gamete transport or storage -- can be internal or external genetials
|
|
What are the major steroids from testes and ovaries?
|
testosterone and estradiol
|
|
What tissues secrete estrogens?
|
ovaries, fat, and placent
|
|
What tissues secrete testosterone?
|
testes and non gonadal tissue
|
|
What is more potent that testosterone? the enzyme?
|
DHT formed from testosterone by 5alpha reductase
|
|
What converts testosterone to estradiol?
|
armatase
|
|
Name the cell types in meiosis in males in order
|
Spermatogonium, Primary spermatocyte, Secondary spermatocyte, spermatids, sperm
|
|
How long does it take to make 1 sperm from the begininng?
|
60 days
|
|
At what cell stage does the sperm become haploid?
|
Spermatid
|
|
What happens at puberty to signal spermatogenesis?
|
awakening of the hypothalamic axis - anterior pit secretes GH and enlarges testes
|
|
How many sperm do you get out of spermatogenesis?
|
4
|
|
What are women born with? at what stage are that arrested? When are they arrested until
|
A fixed number of oocytes arrected at prophase 1 until puberty
|
|
What is the first phase of spermogenisis?
|
mitosis
|
|
At birth how many oocytes? puberty?
|
400,000 and continuely die off 200,000
|
|
What stage is an ovulated egg in?
|
Secondary oocyte arrested at metaphase 2
|
|
When can nondisjunction happen?
|
during M1 or M2
|
|
Name the disorder
XO 21 tri XXY |
XO - Turners syndrome
21 tri - downs syndrome XXY - Kleinefelts |
|
XO -
|
female but no 2ndary sex characterists and will not go through puberty
|
|
XXY -
|
Kleinefelts - functioning male but infertile
|
|
When does sex determination happen/
|
5-10 weeks
|
|
-Thalidomide-
|
sold to prevent morning sickness-but it produced teratogen a exogenous chemical that can disrupt a growing fetus - no arms
|
|
Sex differentiation involves -
|
transformation of mullerian ducts (female) or wolffian(male) ducts to either male or female
|
|
How does males break the female default?
|
by producing SRY gene on the Y chromosome
|
|
What does SRY od? what is it/
|
formation of testes through the wolffian duct -- its is a transcription factor that breaks M cycle
|
|
testes secrete-- and they do?
|
testosterone and MIH - together inhibit female and stimulate formation of male
|
|
What is testosterone to by? and then what does it do?
|
testosterone to DHT by 5alpha reductase -- induces differentiation of urogenital sinus to male
|
|
What binds to androgen receptors?
|
both T and MIH
|
|
What is the main hormone that is responsible for forming male external genitalia?
|
DHT
|
|
What causes the testes to decend?
|
Testosterone
|
|
What causes androgen insensitivity?
|
defective androgen receptors - neither T or DHT can activate the receptors --still has SRY
|
|
What will form with androgen insensitivity?
|
the testes b/c you still have SRY and the hormones from testes will be secreted but will have no function
|
|
What hormones will still have function in androgen insensitivity?
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MIH - so no internal gental b/c you have MIH which stops female and no DHT or test functioning
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What inhibits LH?
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Testosterone
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