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167 Cards in this Set
- Front
- Back
4 layers of dig. syst
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Mucosa, submucosa, muscularis externa, serosa
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layers of the mucosa
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mucous membrane - epithelial layer
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Four functions of dig syst
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Motility – Secretion – Digestion – Absorption
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Motility
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Two types propulsive and mixing
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Fat Digestion Yields
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Fatty acids and monoglycerides
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absorption
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Small units resulRng from digesRon, along with water, vitamins, and electrolytes are transferred from digesRve tract lumen into blood or lymph
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Bilary system
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Liver and gallbladder
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Mucosa
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Endocrine, exocrine, has GALT, and thin layer of sm muscle the muscularis mucosa
• Lines lumen of digestive tract • Highly folded surface greatly increases absorptive area • Three layers • Modified for secreRon and absorption • Contains – Exocrine gland cells – secrete digestive juices – Endocrine gland cells – secrete blood‐borne gastrointestinal hormones – Epithelial cells – specialized for absorbing digestive nutrients – Lamina propria • Houses gut‐associated lymphoid Rssue (GALT) – Important in defense against disease‐causing intesRnal bacteria – Muscularis mucosa • Sparse layer of smooth muscle |
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Submucosa
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allows stretch, has submucosal plexus (nerves), has big lymph and BV.
• Thick layer of connective tissue • Provides digestive tract with distensibility and elasticity • Contains larger blood and lymph vessels • Contains nerve network known as submucosal plexus |
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Muscularis Externa
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• Major smooth muscle coat of digesRve tube • In most areas consists of two layers – Circular layer • Inner layer • ContracRon decreases diameter of lumen – Longitudinal layer • Outer layer • ContracRon shortens the tube • ContracRle acRvity produces propulsive and mixing movements • Myenteric plexus – Lies between the two muscle layers
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serosa
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• Secretes serous fluid – Lubricates and prevents fricRon between digesRve organs and surrounding viscera • ConRnuous with mesentery throughout much of the tract – Acachment provides relaRve fixaRon – Supports digesRve organs in proper place while allowing them freedom for mixing and propulsive movements
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Digestive motility and secretion are regulated by
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Autonomous smooth muscle function – Intrinsic nerve plexuses – Extrinsic nerves – Gastrointestinal hormones
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short reflex pathway
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receptors in dig. tract - intrinsic nerve plexuses - sm. muscle, exocrine, endocrine
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long relex pathway of dig tract.
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external influences - extrinsic autonomic nerves - sm. muscle, exocrine, endocrine
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swallowing center in the brain
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Swallowing center inhabits respiratory center in brain stem
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gastric emptying process
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1) peristalsis starts in upper fundus and goes down 2) becomes stronger as it goes to thick antrum which pushes chyme forward 3) few mL pushed into duodenum (stronger pushes = more out) 4) when peristalsis reaches pyloric sphincter it closes tight and the chyme moving forward bounces off and tosed backwards mixing
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factors that control gastric emptying
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Amount of chyme in stomach is main factor in strength, in duodenum fat, acid and hypertonicity, and distension inhibit stomach emptying
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Three types of gastric exocrine secretory cells
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Mucous cells - Line gastric pits and entrance of glands Chief cells • Secrete pepsinogen – Parietal (oxyntic) cells secrete HCl and intrinsic factor
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Two distinct areas of gastric mucosa that secrete gastric juice
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Oxyntic mucosa • Lines body and fundus – Pyloric gland area (PGA) • Lines the antrum
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diagram stomach and the gastric pits and cell found in each area
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PGA - only G and D cells Oxyntic mucosa: surface epi., mucosa cells, chief cells, parietal cells, Enterochrmaffin-like cells
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Parietal Cell
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HCl Secretion activates pepsinogen to pepsin, breakdown of connective tissue and muscle fibers – Denatures protein – Along with salivary lysozyme, kills most of the microorganisms ingested with food
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Chief cells
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pepsinogin which is activated by H+ and can autocatayze
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Phases of Gastric Secretion
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cephalic, gastric and intestinal Cephalic phase – increased HCl and pepsinogen in response to stimuli in the head before food reaches stomach • Gastric phase – Begins when food actually reaches the stomach – protein increases gastric secretions • Intesnal phase – Inhibitory phase – Helps shut off flow of gastric juices as chyme begins to empty into small intestine
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Gastric Mucosal Barrier
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Enables stomach to contain acid without
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What digestion occurs in the stomach
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Carbs continue in the body, and protein dig, begins in antrum.
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Stomach absorption
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No food or water, but alcohol and asprin.
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Small IntesJne
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• Site where most digesJon and absorpJon take place • Three segments – Duodenum – Jejunum – Ileum • MoJlity includes – SegmentaJon – MigraJng moJlity complex
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segmentation
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– Primary method of moJlity in small intesJne
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What initiates segmentation of the sm int. and what is the rate
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pacemaker cells which produce BER. Look up the rate
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Migrating motility complex
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sweeps intestines clean between meals
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Control of ileocecal valve/sphincter
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gastrin relaxes it.
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Secretion by the sm int.
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Juice secreted do not contain any digestive enzymes – Synthesized enzymes act within brush‐border membrane of epithelial cells • Enterokinase • Disaccharidases • aminopeptidases
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What is happening in general with digestion in the small intestine?
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Pancreatic enzymes continue carbohydrate and protein – Brush‐border enzymes complete digestion of carbohydrates and protein – Fat is digested entirely within small intestine lumen by pancreatic lipase
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how much does the surface area increase due to folds and villi in the sm int
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600X
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general info about absorption in the small intestine
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absorbs almost everything presented to it – Most occurs in duodenum and jejunum – Adaptations that increase small intestine’s surface area • Inner surface has permanent circular folds • Microscopic finger‐like projections called villi • Brush border (microvilli) arise from luminal surface of epithelial cells – Lining is replaced about every three days – Products of fat digestion undergo transformations that enable them to be passively absorbed • Eventually enter lymph
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Where does fat digestion take place
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exclusively in the small intestine
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where are the villi
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on the surface of the rings in the sm int.
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what forms the brush border
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the microvilli on the epithelial cells of the sm int.
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Makeup of the villus
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epi cells, mucus cells, capillaries, and a central lacteal, provided blood by an arteriole and drained by and drains to a venule.
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lacteal
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lymphatic capillary that absorbs dietary fats in the villi of the small intestine.
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Pancreas
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Elongated gland located behind and below the
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Exocrine secretion by pancreas controlled by
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secretin and CCK.
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Proteolytic enzymes from the pancreas
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Trypinogen, Chymotrypsinogen, procarboxypeptidase
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carbolytic enzymes
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Pancreatic and salivary amylases – Converts polysaccharides into the disaccharide
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Cells of pancreas
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Duct cells - secrete aqueous NaHCO3, Acinar cells - secrete digestive enzymes Islets of Langerhans - make insulin, and glucagon
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Response to acid in duodenum
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duodenal mucosa (s cells in crypts) releases secretin into blood which stims pancreatic duct cells to secrete bicarb.
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Hormonal response to fat and protein in duodenum
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CCK released from mucosal epi. pancreatic acinar cells to secrete dig. enzymes
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Crypts of Lieberkuhn
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also house antimicrobial stuff like lysozyme.
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production and recycling of bicarb and H+
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Cl-, CO2 and water come in from blood into stomach parietal cells. CO2 and water with and Carbonic anhydrase makes bicarb and H+, bicarb leaves parietal cells to go back to the blood and ends up in pancreatic duct cell and is secreted with a Na+ into duodenum. They all react in the duodenum and NaCl and CO2 and H2O are made which are taken back up by the intestinal epithelial cells to be recycled
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Liver
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• Largest and most important metabolic organ in the body • Body’s major biochemical factory • Importance to digesMve system – secreMon of bile salts
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diagram liver blood flow
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Hepatic portal vein forms from small venules coming from dig syst. which then drains into the liver before going into primary circulation where it is purified. It also mixes with arterial blood that comes from hepatic artery. Reforms hepatic vein to go to the inferior vena cava.
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production of bile salts are done by what cells
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Hepatocytes produce the salts from cholesterol or recycled from salts in hepatic circulation. Builds up and is stored in gall bladder.
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Bile made up of
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• Bile salts • Cholesterol • Lecithin • Bilirubin
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Ways to break up fat globules for digestion
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Bile salts have negatively charged hydrophobic portion (carboxyl at end of glycine or taurine chain) and a lipid soluble part made from cholesterol. They adsorb on the exterior and segmentation breaks up droplets into smaller portions which the salts keep from sticking back together. End up about 1mm which is still too small for digestion. Micelle formation
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micelle formation
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Cholesterol and lecithin adds to droplet with bilesalts. Becomes about 10nm
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Digestion and absorption of carbs
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Amylase makes disaccharides, which are broken down into single monosaccharides through diff pathways done on brush border which also bring them into the cell. Galactose and glucose have a Na+ cotransport (sodium and energy dependent secondary active tranport). Fructose comes into cell through passive facilitated diffusion.
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protein and small peptide absorption and digestion
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pepsin in stomach then pancreatic enzymes in sm int. break down the protein. AAs absorbed by Na+and energy dependent absorption. AA transport out on the basal side due to high concentration inside into lumen of the villus which then diffuses into the capillary. Small peptides broken down by aminopeptidases on brush border or intracellular aminopeptidases
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Fat absorption and digestion
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large globs - bile salts chelest. and emulsify to micelles. - lipase turns triglyc. to monoglyc. and fatty acids on interior of micelles. Micelle hits epi surface, dumps monoglyc. and FFAs into cell. Then makes triglyc. from mono and FFAs. aggregagte and coated with lipoprotein to make chylomicron. - basal memb. exocyt. chylomicrons - go to lacteals and lymph.
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longitudinal fibers in L.int.
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tinae coli
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gastrocolic reflex - definition and what hormone causes it
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– Mediated from stomach to colon by gastrin and by autonomic nerves – Most evident after first meal of the day – Often followed by urge to defecate
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Mass movements
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massive movements that move stuff to end of L.int.
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Defecation reflex
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rectal stretch receptors stimmed by distension, internal anal sphincter relaxes, rectum and sigmoid colon to contract more. If external anal sphincter relaxed defecation occurs.
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Gastrointestinal Hormones
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Gastrin, CCK, GIP,
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Gastrin
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stimulated by protein in stomach, inhibited by acid in stomach. Increases HCl and pepsinogen secr. Ups gastric and ileal motility, relaxes ileocecal sphincter, induces mass movements in colon, • Helps maintain well‐developed, functionally viable digestive tract lining (mucosal lining of stomach and small intestine)
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Secretin
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Stims bicarb release by pan. duct cells, inhibits gastric emptying, stims bicarb rich bile release, Along with CCK, is trophic to exocrine pancreas
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CCK (Cholecystokinin)
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motility, panc enz. secretion, contract gallbladder, relax sphincter of Oddi,
– Functions • Inhibits gastric motility and secretion • Stimulates pancreatic acinar cells to increase secretion of pancreatic enzymes • Causes contraction of gallbladder and relaxation of sphincter of Oddi (sphincter for gallbladder duct) • Along with secretin, is trophic to exocrine pancreas • Implicated in long‐term adaptive changes in proportion of pancreatic enzymes in response to prolonged diet changes • Important regulator of food intake |
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GIP
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Glucose dependent insulinotrophic peptide – Made in duodenum Stimulates insulin release by pancreas
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External work
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Energy expended when skeletal muscles are contracted to move external objects or to move body in relaNon to the environment
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Internal work
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All other forms of biological energy expenditure that do not accomplish mechanical work outside the body – Skeletal muscle acNvity used for purposes other than external work (postural maintenance contracNons, shivering) – All the energy‐expending acNviNes that go on conNnuously just to sustain life
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eating control centers in brain and effect of leptin on these centers
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2 regions in the hypothalamus in the arcuate nucleus: one for satiety which secretes melanocortins, one for appetite secretes neuropeptide Y to increase food intake. Leptin inhibits NP-Y and stims melanocortins
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ghrelin
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hunger hormone produced in the stomach regulated by feeding status stims NP-Y neurons
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Peptide YY3‐36
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signals satiety – Produced by small and large intestines – important mealtime terminator
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Lateral hypothalamus area (LHA)
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secretes orexins • Strong stimulators of food intake
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Hypothalamic Paraventricular nucleus (PVN) and eating
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Releases neuropepNdes that decrease food intake
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Parathyroid Hormone
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increases in plasma calcium through action at bone, GI Tract & kidney. • Requires Active Vitamin D for optimal affects.
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calcitonin
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no known effects from deficiencies Some of Parathyroid Hormone effects, less potent.
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Distribution Calcium in Body
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• Plasma – 8.6 – 10.6 mg/dl. 1000 mg total content in plasma. • If plasma concentration falls below 7 mg/dl increase membrane excitability. Loss of selective permeability, and tetany in skeletal muscles • Bone - 1 x 10^6 mg or 1 kg 1. Soluble, rapidly mobilized Ca pool 2. Stable, slowly mobilized Ca pool
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Bone
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Collagen and Protein Matrix in which Calcium, Phosphate, and Hydroxide (Hydroxyapatite Crystals) deposited.
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Osteocyte
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osteoblast that is surrounded by formed bone. Cells no longer have the ability to lay down new bone.
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Osteoclast
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Bone Dismantling. Cells, which differentiate from macrophages, responsible for bone breakdown – release of Calcium and Phosphate from bone into blood.
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Balance between Osteoblast and Osteoclast activity
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determines if there is net bone Accresion or net Bone Dismantling,
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Greater Osteoblast Activity
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Decrease Plasma Ca & PO4 & Bone Formation (Accresion)
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Greater Osteoclast Activity (Dismantling)
cause and effect |
stimmed by PTH stimming OPGL and RANKL production by osteoblasts.
OPG inhibits. Increase Plasma Ca & PO4. |
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Sources of Vitamin D
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• Sunlight acting on Dihydrocholesterol Precursor to Vit D Inactive Vit D • Diet – fortified milk, cereals, etc.
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Formation of either Inactive or Active Vitamin D determined by hydroxylation where, and done where
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• Inactive Vitamin D – precursor hydoxylated at #1 & #24 positions • Active Vitamin D (Calcitriol) – precursor hydroxylated at #1 & #25 positions. • Conversion of Inactive Vit D to Calcitriol occurs in Kidney
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Calcitriol formed when
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• Ca and P04 plasma levels are low. • Parathyroid Hormone levels increase • Low levels of Calcitriol, stimulate conversion of Inactive Vit D to Calcitriol
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Actions of Active Vitamin D
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Net Effects: Increase both Plasma Ca and P04 from Bone, Increase Ca and PO4
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osteoblast signaling
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1. Bone Dismantling through Osteoprotegerin Ligand (OPGL) –directly binds to receptors on osteoclasts stimulating bone dismantling (increases alkaline phosphatase activity stimulates breakdown of bone mineral) 2. Inhibition of Bone Dismantling by Osteoprotegerin (OPG) – binds to OPGL & prevents OPGL preventing OPGL stimulation of osteoclast activity. (Sex steriods, estrogen and testosterone, increase the synthesis and secretion of OPG by osteoblasts, reducing OPGL stimulation of osteoclasts. Therefore, sex steriods, shift balance in favor of bone accresion.)
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Ca homeostasis requires
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both Calcitriol and Parathyroid Hormone.
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Stimulus for PTH secretion
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decreasing Ca++ levels
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Effect in the drop of phosphate on PTH secretion
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does nothing
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Sites of Action: PTH
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Kidney, Intestine & Bone
• Kidney Inactive Vit D to Calcitriol, reabsorb Ca and decrease reabsorb PO4 • (Note: Mass action of decrease in plasma PO4 on soluble fraction of bone release of Ca and PO4 from bone.) Intestine - absorb Ca & PO4 (Maximal absorption of ingested Ca and PO4 requires active Vit D) Bone • Stimulates synthesize & release of RANKL (Receptor Activator of NF-kB ligand) & Osteoprotegrin (OPG) when • Ca low increase RANKL over OPG. • Increase RANKL stimulate conversion of Macrophages osteoclasts bone dismantling over accresion increase both plasma Ca and plasma PO4. |
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Net Effect: PTH
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Increases Ca and PO4.Ca increases more than PO4 because of kidney
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Regulation of Plasma Phosphate
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• Parathyroid Hormone does not directly regulate Plasma PO4 • Plasma PO4 regulated through action of Calcitriol. • Stimulus: Decreases Plasma PO4 stimulate conversion of Inactive Vit D Calcitriol. • Action Calcitriol on PO4: • Increases absorption of PO4 from GI Tract • Increases reabsorption of PO4 from Kidney • Stimulates Osteoclast activity increase rate of bone dismantling increase plasma PO4.
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Link between Neural & Endocrine Regulation
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link between Hypothalamus and Posterior Pituitary is Direct Neural. Posterior Pituitary contains nerve terminals of neurons originating in Hypothalamus
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Vascular Link between Hypothalamus and Anterior Pituitary
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via Hypothalamic Hypophyseal Portal System (HHPS)
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List pit hormones their effects and what stimulates them from the hypothalamus
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Growth Hormone (GH) or Somatotropin
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(ADH) or Vasopressin
cells and cause for stimulus receptor types and each of their effects |
Stim for ADH secretion increase in osmol. by Receptors in supraoptic nucleus. 2. Decrease in circulating blood volume leads increase ADH secretion. inhibitory afferent input from volume (stretch) receptors at the junction of the pulmonary veins and left atrium to the supraoptic neurons (disinhibition by decreasing circulating blood volume). • Action – Stims insertion of (Aquaporins). Constricts afferent and efferent arterioles. Reduction vasa recta blood flow which conserves medullary gradient by reducing vascular removal of the kidney medullary osmotic gradient.
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Overview of Feedback Control of Hypothalamic Neurosecretion and Anterior Pituitary Hormone Secretion
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What causes the death of the corpus luteum
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PGF2alpha
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Gigantism
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Proportional Growth of Skeletal and Muscle Tissue
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Excess Growth Hormone Post Puberty
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Acromegaly – Growth of Soft Cartilaginous Tissue – Enlarged, Protruding Cheek Bones; Enlarged, Protruding Sternum and Ribs; Enlarged hands and Feet
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glycerol absorption
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too big to get through cell membranes
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Deficiency Growth Hormone Prior to Puberty
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Dwarfism – small body, poor muscle dev., subcut. fat because deficiency of Growth Hormone, or normal Growth Hormone but lack of Growth Hormone receptors, or normal Growth Hormone but low levels of IGF-1 (liver hormone that stims cell growth and inhibits apoptosis).
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African Pigmy
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Normal GH levels but lower than normal IGF-1 levels
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Thyroid Gland & Thyroid Hormones
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Permissive, regulates metabolism, enzymes and (oxid. phosphor.) PRL and GH need normal levels. Thyroxine ( T3 – Active Form; T4 – Inactive or Prohormone) 5/27/08 4 Broad Range of General Metabolic Effects • Permissive Action – Establishes metabolic conditions for synthesis and action other hormones. • Regulates Metabolism • Stimulates mitochondrial oxidative phosphorylation. Required for normal energy production. • Stimulates normal synthesis of enzymes and proteins. • Required Normal Growth and Development • Prolactin and Growth Hormone both require normal levels of T3. • Pre and postnatal neural development requires normal levels of T3. • Bone Growth
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T4
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Tetraiodothyronine – Inactive or Prohormone. 80% hormone produced & secreted by Thyroid Follicles is T4.
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T3
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Triiodothyronine – Active Hormone. 20% hormone produced & secreted by Thyroid Follicles is T3. • Inactive T4 converted to Active T3 in the Liver.
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Three Steps in the Synthesis of Thyroid Hormones
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1. Uptake of Iodine from the Blood by the Follicle Cells & conversion to iodine to iodide by peroxidase enzyme within Follicle Cells. 2. Iodination of tyrosine within thyroglobulin molecule - occurs within the Lumen of the Follicle. Iodination produces two products: • Monoiodotyrosine (MIT) & Diiodotyrosine (DIT). 3. Coupling within the Lumen of the Follicle of MIT + DIT T3, and DIT + DIT T4
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Long Loop Negative Feedback of T3
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• T3 inhibits TSHRH by Neurosecretory Neurons in Hypothalamus • T3 inhibits the Synthesis and Secretion of TSH by Thyrotrophs in Anterior Pituitary
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Hypothyroidism
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lack of or low levels of T3.
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cretinism
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poor neurological development if low levels of T3 before and in first few years of life.
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adult hypothyroidism
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Myxedema in Adult + decrease contractility, decrease responsiveness to sympathetic activity , decrease ability to mobilize lipid stores + other effects
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Causes of Hypothyroidism
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no Iodine, inability to synthesize T3 & T4, no Negative Feedback on TSHRH & TSH secretions. TSH stimulates follicle hypertrophy get Goiter (Grossly enlarged Thyroid Gland producing mass in the front of the neck. Or no Receptors in the Follicles of the gland so won't respond to TSH. No negative feedback to Hyp. and Ant. Pit. by T3 High Levels of TSHRH & TSH but no Goiter. Also may lack TSHRH receptors in Ant, Pit. Thyrotrophs.
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How would you expect circulating levels of TSHRH and TSH to change in absence of TSHRH receptors?
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Hypersecretion of TSHRH, TSH or T3 –T4 Secreting Tumors
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Excess T3 – T4 is an emergency – increase sensitivity of norepi. and epi. leads to cardiac arrhythmias, very high BP, stroke.
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Hyperthyroidism
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Graves Disease - Immune system synth. of (TSI) Same affects as TSH but nofeedback which leads to const. stim. of T3 and T4 production. Question: What would you expect to happen to the levels of TSHRH and TSH in the presence of TSI? Would you expect a goiter?
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Exophthalmos
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protruding eyeballs (Fig. 19-5 textbook) as a consequence of high levels of TSI because of accumulation of mucopolysaccharide behind the eye. Edema around eyes. Lid retraction drying of the cornea.
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Adrenal Cortex & Adrenal Steroid Hormones
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Mineralocorticoid is Aldosterone Glucocorticoid is Cortisol and Sex Steroids – Estrogen and Testosterone
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Mineralocorticoids
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Aldosterone (Synthesis and release stimulated by Angiotensin)
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Glucocorticoids
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Cortisol - • imp. for normal gluc. levels. Only hormone stim. synth. of new gluc. through the conversion of AA
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Dehydroepiandrosterone (DHEA)
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in males Adrenal cortex source of estrogens (cortex possesses enzyme to convert testosterone to estradiol. Testes very little of the enzyme)
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Females: Adrenal cortex source of testosterone (enzyme converts testosterone to estradiol much lower concentration (not as active) in adrenal cortex than in ovaries)
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Effects of insulin.
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Insertion of transport prot. called gluc 4 in muscle. absence of insulin gluc. absorb into skel. muscle is sig. impaired. Stims. conv. of gluc.to glyc. Stims adipocytes to produce glycerol from glucose to remake triglyc. from fatty acids.
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insulin stims adipocytes to produce glycerol from glucose to remake triglycerides from fatty acids.
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intracellular lipase (hormone sensetive lipase)
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Responds to glucagon to break up fat for energy
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ENDOCRINE 3
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Somatostatin GHIH
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stimmed by IGF-1
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Draw the feedback control loop on slide 2 of endo 3
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Excess Growth Hormone Prior Puberty & Prior to Closure of the Growth Plates in the Long Bones
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gigantism
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Excess Growth Hormone Post Puberty
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Acromegaly – Growth of Soft Cartilaginous Tissue – Enlarged, Protruding Cheek Bones; Enlarged, Protruding Sternum and Ribs; Enlarged hands and Feet (Fig. 18-14)
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Deficiency Growth Hormone Prior to Puberty
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Dwarfism – small body size, may have poor muscle development, subcutaneous fat – baby fat (pudgy). • occurs because of deficiency Growth Hormone, or normal Growth Hormone but lack of Growth Hormone receptors, or normal Growth Hormone but low leves of IGF-1.
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why is a pygmy small
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Normal GH levels but lower than normal IGF-1 levels
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Broad Range of General Metabolic Effects of thyroid hormone
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• Permissive Action – Establishes metabolic conditions for synthesis and action other hormones. • Regulates Metabolism • Stimulates mitochondrial oxidative phosphorylation. Required for normal energy production. • Stimulates normal synthesis of enzymes and proteins. • Required Normal Growth and Development • Prolactin and Growth Hormone both require normal levels of T3. • Pre and postnatal neural development requires normal levels of T3. • Bone Growth
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Three Steps in the Synthesis of Thyroid Hormones – T3 & T4
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1. Uptake of Iodine by the Follicle Cells & conversion to iodine to iodide by peroxidase . 2. Iodination of tyrosine within thyroglobulin - occurs within the Lumen of the Follicle. Iodination produces two products: • Monoiodotyrosine (MIT) & Diiodotyrosine (DIT). 3. Coupling within the Lumen of the Follicle of MIT + DIT T3, and DIT + DIT T4
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Long Loop Negative Feedback of thyroid hormone. Which one and the process
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• T3 inhibits TSHRH by Neurosecretory Neurons in Hypothalamus • T3 inhibits the Synthesis and Secretion of TSH by Thyrotrophs in Anterior Pituitary
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Hypothyroidism in adult and children and affects.
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kids - Cretinism – poor neuro. dev.if low T3 in first few years of life.
Adult - Myxedema, decreased contract., decreased respons. to symp. activity, decrease mobilize lipid stores + other effects |
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Cause of Hypothyroidism
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• Also may have lack of TSHRH receptors in Anterior Pituitary Thyrotrophs.
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Absence of Iodine in diet
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Cause of Hypothyroidism - can't make T3 & T4 no Negative Feedback on TSHRH & TSH High TSHRH and TSH. • TSH stimulates follicle hypertrophy Goiter
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Lack of Receptors in the Follicles of the Thryoid Gland
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Cause of Hypothyroidism - unresponsive to TSH no neg. feedback to Hyp. and Ant. Pit. by T3. High TSHRH & TSH but No Goiter because no stim. of thyroid follicles.
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How would you expect circulating levels of TSHRH and TSH to change in absence of TSHRH receptors?
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Hypersecretion of TSHRH, TSH or T3 –T4 Secreting Tumors
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Large excess T3 – T4 is a major medical emergency – increase sensitivity of norepinephrine and epinephrine leads to fatal cardiac arrhythmias, very high blood pressure, stroke.
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Hyperthyroidism
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Immune system synthesis of Thyroid Stimulating Hormone Immunoglobulin (TSI) • Same affects as TSH but TSI not under feedback control leads to constant stimulation of Thyroid and T3 and T4 production.
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What would you expect to happen to the levels of TSHRH and TSH in the presence of TSI? Would you expect a goiter?
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Exophthalmos
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protruding eyeballs (Fig. 19-5 textbook) as a consequence of high levels of TSI because of accumulation of mucopolysaccharide behind the eye. Edema around eyes. Lid retraction drying of the cornea.
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Inability Synthesize or Secrete Corticoids
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Addison’s Disease • no Aldosterone • Can't maintain NA+ H2O balance. inadequate volume regulation. • Reduced secretion H+ and K+. • Death from reduced capacity for Gluconeogenesis • can't get glucose under stress or when low. • reduced activity of Glucagon – mobilization of glucose dependent on glucocorticoids.
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Excess Cortisol
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Cushing’s Disease • Decrease fat in limbs but more in trunk and face – moon face. • Muscle and bone Wasting.
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Two Functions of the Gonads
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Gametogenic Function Endocrine Function
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Spermatogenesis
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Sertoli Cells in seminiferous tubules
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Sperm are stored
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in Epididymis, and early segments of the Vas Deferens.
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Cells of Leydig
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between the Sertoli cells in the wall of the seminiferous tubules. Leydig Cells synthesize and secrete Testosterone.
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Theca and Granulosa Cells
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in the wall of the Ovarian Follicle synthesize and secrete Estrogens and Progestins.
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Three Levels in Classification of Gender
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genetic, gonadal, and phenotypic • Genetic Sex – Presence of X or Y sex chromosome. • Gonadal Sex – Presence of Ovaries or Testes. • Genital Sex (Phenotypic Gender) – Presence of Female or Male External Reproductive Structures
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Maleness – Requires
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Y Chrom.& Functioning SRY Which controls dif. of gonads to testes. (codes for signaling molecule). Need X chromosome for full diff. (1)synth. testosterone; (2) T recept (3) enzymes to convert T to DHT (4) Mullarian Inhibiting Substance (MIS)
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Femaleness –
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When no Y chrom., or non-funct. SRY or absence of any coding for functional maleness
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hormones prepuberty
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everything low and constant
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Puberty Male
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GNRH –pulsatile throughout
FSH and LH puls. with FSH higher Test. high and constant. |
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Puberty Female
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GNRH –cycling monthly FSH & LH – cycling monthly with LH higher before ov.
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Changes in Secretion of CRH and ACTH
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increasedadrenal sex steroid secretions leads to increased hair growth in both males and females observed at onset of Puberty. Other secondary sex characteristics observed with onset of puberty produced by gonadal testosterone and estrogens.
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Change in Feedback Regulation of GNRH. FSH & LH Secretions, and Sex Steroid Secretions
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Pub. changes Sex Ster. Synth.and Secretion, and Dev. of Prim. and Sec. Sex Char. • Decrease responsiveness of GNRH, and FSH & LH to negative feedback from estrogens leads to increase GNRH, FSH and LH, Secr. • Change from constant, low GNRH secretion to pulsatile secr. in male and cyc. secr. in female. • Increase resp. of gonads to FSH and LH increase T in males and E2 in females • Change to postpubertal higher & pulsatile testosterone secretion, & monthly cyclical changes in estrogens and progesterone secretions.
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Secondary male Sex Characteristics
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• Male Pattern Hair Growth • Bone Growth and Closure of the Growth Plates • Increase Protein Synthesis Increase Muscle Mass • Decrease in Body Fat and Increase Lean Body Mass • Increase RBC Production – Male Hemoglobin and Hematocrit greater than Female. • Increase in VLDL and Decrease Synthesis LDL and HDL • Enlargement of Larynx and Thickening Vocal Cords Deepening Voice
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Effects of Estrogen and Progesterone Synthesized and Secreted by Cells within the Ovaries
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Reproductive Structures • Breast Development including development of Ductile System • Enlargement of the Labia • Changes in Lining and Secretions of the Vagina Oogenesis – Formation of the Follicles, Initiates the 2nd meiotic division of the ova, and ovulation. Secondary Sex Characteristics • Stimulation of Hair Growth • Bone Growth and Earlier (compared to male) Closure Growth Plates • Promotes Female Distribution of Fat – subcutaneous fat storage. • Decreases Sensitivity of Tissues to Insulin – Diabetogenic Effect
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oogenesis
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completion of first meiotic division
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