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Human Phys - TEST II prep.doc

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Human Kinetics
HK 2810
Coral Murrant

Human Physiology TEST II FALL 2003 1. Feedback control is critical in the regulation of estrogen secretion in women. Diagram the control of estrogen production in the middle of the follicular phase of the ovarian cycle. Explain why follicle stimulating hormone and luteinizing hormone levels drop during this part of the phase. Answer: follicular phase: primordial follicle  primary follicle  secondary follicle  ovulation Cerebral cortex and limbic system send input on hypothalamus, and hypothalamus release GnRH to anterior pituitary to release LH and FSH to body (works on gonad). Thecal cell has Rc for LH, so in response to LH, it releases androgen, progesterone and estrogen, while Granulosa cell releases aromatase, growth factors (protein, activin, and inhibin) in response to FSH and LH. Aromatase converts androgen from thecal cell to estrogen. Estrogen from theca cell and from aromatase activity work on development and maturation of endometrium and oogenesis(developing ovum). Growth factors also help oogenesis and endometrium proliferation. Activin has positive feedback on anterior pituitary while inhibin and proteins have negative feedback on anterior pituitary. Initial release of estrogen has positive feedback on local system. Heightened level of estrogen increases LH Rc on thecal cell(more sensitive to LH  more estrogen, progesterone and androgen  development of endometrium, oogenesis), increases FSH Rc on granulosa cells(more sensitive to FSH  more aromatase activity  more estrogen  development of endometrium, oogenesis, and more FSH Rc on granulosa cell) and increases estrogen Rc on both cells (more sensitive to estrogen).To prevent the positive feedback from getting out of control, there is a central negative feedback. Hypothalamus and anterior pituitary reduce their hormonal release in response to increased E level (less GnRH, LH, FSH release). The heightened levels of estrogen due to local positive feedback are exerting a greater inhibitory effect on GnRH, LH, and FSH release thus their level will drop. 2. High blood glucose affects both alpha and beta cells of the pancreas. Identify the resulting hormonal release and the hormonal actions on the liver in order to restore blood glucose back to normal Answer: When the [glucose]pl increases, alpha cell releases less glucagons, and beta cell releases more insulin to stimulate uptake of glucose into the cell. In response to decreased glucagon level… In Liver- decreased glucose release  decreased G6Phosphatase (G6P glucose), increased glucokinase (glucose  G6P) Less glycogenolysis  decreased glycogen phosphorylase (glycogen  G1P), increased glycogen synthase (G1P  glycogen) Less gluconeogenesis  increased glucokinase, phosphofructokinase, and pyruvate dehydrogenase In adipocyte – decrease lipolysis (decreased FFA synthase) Net effect is to keep energy stores in storage by releasing less glucose  reduce blood glucose In response to increased insulin level In liver – increased glycogen synthesis  increased glycogen synthase, and dcreased gluycogen phosphorylase Increased glucose uptake  increased glucokinase, and decreased G6Phosphatase T/G synthesis (increased glycolysis)  increased glucokinase, phosphofructokinase, pyruvate dehydrogenase, acetyl CoA carboxylase, and FFA synthase In adipocyte – increased T/G synthesis  increased Acetyl CoA carboxylase, and FFA synthase Decreased FFA release In Skeletal muscle – increased glucose uptake (increased GLUT4 in response to increased insulin level)  increased hexokinase Increased glycogen synthesis  increased glycogen synthase Increased glycolysis  increased phosphofructokinase, and pyruvate dehydrogenase Net effect is to put energy into storage by taking up blood glucose  reduce blood glucose 3. Identify the secretion of the exocrine pancreas and their physiological importance. Discuss the regulation involved in their access to the small intestine at the appropriate time Answer: Exocrine pancreas is important in digestion and composed of two parts which are pancreatic duct cells (aqueous), and acinar cells (enzymatic component). Pancreatic duct cell secretes bicarbonate in response to secretin from S cell(SI), CCK from I cell(SI) and Ach from PNS innervation to buffer acid from chyme in small intestine Secretin increase cAMP to increase H+K+ ATPase on basolateral side (to hyperpolarize the cell) and to increase open time of Cl- channel on luminal side CCK and Ach increases [Ca2+] to activates K+ channel (to hyperpolarize cell)  Cl- and HCO3- flux out (electrogradient) Enzymatic component – acinar cells Protease (trypsinogen, chymotrypsin, procargboxypeptidase, and proelastase)- all in proenzyme form(for protection) which then activated by trypsin (trypsinogen enterokinase  trypsin). This positive feedback is then controlled by limited amount of trypsinogen Alpha amylase (same one as secreted in salivary gland) to digest starch 1 Lipase – Triacylglyceride hydrolase(glycerol+ 3FFA), CE hydrolase(cholesterol + free FFA), phospholipase A2 (cleave FFA at C2 site of phospholipids) to digest lipid Ribonuclease and deoxyribonuclease (RNA and DNA) Pancreatic acinar cells are stimulated by gastrin (G cell in stomach) and CNS innervation and then release enzymes into common bile duct rindt above the sphincter of Oddi. Sphincter of Oddi opens when acid is present in duodenum which means the chyme has moved to intestine (2 stage of intestinal phase). Acid in duodenum stimulates CCK release from I cell (SI), and CCK causes relaxation of sphincter of Oddi to release enzyme and bicarb into the small intestine to begin digesting and buffering the acidity from the chyme. 4. Describe how water and the ions Na+, K+, Cl-, and Ca2+ are absorbed in the small intestine. Discuss the role that an increase in parathyroid hormone plays, if any, in altering the absorption of the ions. Answer: On basolateral side there are Na+/K+ ATPase to pump Na+ out of the epithelial cell and to pump K+ into the cell from ISS. The Na+ concentration established by ATPase then pulls Na+ back to the cell (with amino acid, glucose, & galactose). Since there are higher [Na+] in ISS, via drive from electrogradient, Cl- diffuse into ISS via paracellular pathway down its concentration gradient. Water follows Na+, therefore to ISS where [Na+] is higher. As water moves from luminal side to ISS, K+ concentration outside the cell increases. Since there is lower [K+] in ISS, K+ passively diffuse into ISS (via paracellular pathway)down its concentration gradient. nd Ca2+ diffuses into the cell via facilitated diffusion(channel) from the lumen, and binds Calbindin which inhibits Ca2+ from performing 2 messenger activity. Then Ca2+ inside is transported out to ISS via H+/Ca2+, Na+/Ca2+ exchanger .Also as water leaves the lumen, Ca2+ gets concentrated in luminal side, and passively diffuse between cells down its concentration gradient. Increased PTH activates 1-alpha- hydroxylase which converts 23-OH-D to 1,25-(OH)2-D. 1,25-(OH)2-D is vitamin D derivative so it gets into the cell and binds nuclear membrane Rc and induce change in genetic expression (increased protein synthesis). It results in increased Ca2+ channel on luminal side, H+/Ca2+ & Na+/Ca+ exchanger, and calbindin in the cell which aids in Ca2+ absorption 5. You are at the Keg following your physiology test and the waiter has just delivered the huge plate of chicken wings you ordered. Before you begin to eat, the cephalic phase of gastic acid regulation has already begun. Describe the regulation of acid production in the stomach during this phase. Explain how this activity would affect blood insulin levels? Answer: Cephalic phase begins in presence of thoughts, smell, sight and taste of food and feed-forward to prepare digestive system Signals from CNS feed onto pancreatic acinar cell for enzymatic secretion and also enteric plexus via vagus nerve. When it reaches enteric plexus, it stimulates G cells to release gastrin, parietal cells to release HCl, ECL cells to release histamine, and inhibit D cell from releasing somatostatin. Gastrin is gastric hormone which can work both in endocrine and in paracrine. Gastrin stimulates intestinal motility and acinar cell enzymatic secretion via endocrine and stimulates ECL cell for histamine release and parietal cell for HCl secretion via paracrine. All this activity results in lowering pH in stomach and this is detected by chemoRc and this Chemo Rc sends sensory afferent to enteric plexus to stimulate G, ECL, and parietal cells more, and also stimulate chief cell to secrete pepsinogen. Since low pH has been established by HCl secretion, it is then converted to active pepsin which works as protease. But in absence of food, it doesn’t digest anything. Presence of digestive enzyme in the blood such has gastrin stimulates beta cell to secrete insulin (feed-forward) to prepare for increased blood glucose level that will occur once you begin eating 6. Describe the process by which parathyroid hormone regulates high plasma calcium back to normal Answer: In response to high [Ca2+]pl, chief cell in parathyroid decreases PTH release into the body. In response to decreased PTH, bone decrease osteoclast activity therefore build bone instead of reabsorbing it  decreased [Ca2+]pl, [Pi]pl. Kidney then increase Ca2+ excretion and decrease Pi excretion which then results in decreased in [Ca2+]pl, but increased [Pi]pl. Since 1-alpha-hydroxylase is activated by PTH, there are less 1- alpha-hydroxylase activated, and as a result, there will be less 1,25 (OH)2 D present in plasma. Decreased 1,25(OH)2D then increase Ca2+ excretion and decrease in Pi excretion in Kidney (decreased [Ca2+]pl, increased [Pi]pl) and decrease osteoclast activity to decrease bone reabsorption therefore increase bone formation (decrease in both [Ca2+]pl, [Pi]pl). In small intestine, 1,25(OH)D decrease Ca2+ and Pi absorption therefore decrease both [Ca2+]pl, [Pi]pl. As a result, you have decreased Ca2+ in blood and sustained level of Pi FALL 2004 7. List the secretions of the stomach and the cell types responsible for these secretions (marks will be deducted for listing cell types and secretion not found in stomach). Describe how the low pH environment being promoted in the cephalic phase of digestion affects the paracrine and endocrine relationships between these cells Answer: Stomach secretion Columnar epithelial cells and mucous cells secrete mucous for lubrication and bicarb for protection of stomach wall. Parietal cells release HCl to kill microorganism entering with food and also to activate proenzyme, and intrinsic factor to bind Vit B12 and absorbed in ileum. Chief cells release pepsinogen which is proenzyme form of pepsin which digests protein (activated in acidic environment). G cells secretes gastrin(hormone) to stimulate parietal cell(paracrine), to increase intestinal motility(endocrine), and to stimulate pancreatic acinar cell to release enzymes 2 (endocrine). D cells release somatostatin whose main function is to inhibit other enzymatic activities. ECL cells(enterochromaffin like cells) release histamine which stimulates parietal cell (paracrine) Cephalic phase of digestion (low pH and paracrine and endocrine relationships between cells) Low pH is induced by secretion of HCl from parietal cell, and this pH change is detected by chemoRc and it sends information to D cell to produce somatostatin (inhibitory). Somatostatin then inhibit G cells from releasing gastrin, and ECL cell from releasing histamine via paracrine. Reduced gastrin level then reduce histamine release from ECL cell and reduce HCl release from parietal cell 8. Diagram the changes in membrane potential that occurs over time during slow wave and spike potentials in smooth muscle of the GIT and describe the channels and ion movement that produce these changes. What effects do stretch, PNS, SNS, gastrin and motilin have on GI smooth muscle motility and describe how do they achieve these effects Answer: Slow wave – no motility generated Open voltage gated Ca2+ channel to allow depolarization (Ca2+ flux in) and the channel undergoes inactivation and then close (no Ca2+ flux). Then Ca2+ dependent K+ channel open to flux K+ out to repolarize the cell, and the channel closes to stop K+ flux Spike potential – motility(force generated) Open voltage gated Ca2+ channel to allow Ca2+ flux in to depolarize the cell during slow wave. When the Vm reaches threshold (-40mV) for voltage gated Ca2+ channel which cause large influx of Ca2+ channel (large depolarization  spike potential). Ca2+ channel then inactivate and close(no more Ca2+ flux in). Then Ca2+ dependent K+ channel and voltage gated K+ channel opens allowing K+ flux in to repolarize the cell and both channels to close (no K+ flux out) Spike potential is different from AP in a way that it lasts longer (20ms>2ms) and it uses voltage gated Ca2+ channel for depolarization and Ca2+ dependent K+ channel for repolarization PNS(Ach), stretch(induced by food content-myogenic response), gastrin(increase intestinal motility in endocrine manner), and motilin(Migrating motor complex during fasting phase) all increase motility by increasing Vm to increase the possibility of spike potential again(increased spike potential frequency  increased force and increased motility). SNS(NorEpi) decreases motility by decreasing Vm to decrease the possibility of spike potential generation (VIP- vasoactive inhibitory peptide also decrease Vm to decrease spike potential frequency  decreased force and decrease motility) 9. Discuss how vitamin D plays a vital role in the regulation of calcium and phosphate (include detail regarding the specific affects on target tissues in your discussion) Answer: Vitamin is often synthesized in the skin or ingested in a form of food. Vitamin D in plasma then converted to 25-OH-D in liver and then converted to 1,25 (OH)2-D (via 1-alpha-hydroxlase) and 24,25(OH)2D in the kidney. 1,25(OH)2D plays a major role in Ca2+ and phosphate regulation but 24,25(OH)2D has no known function. 1,25(OH)2D in plasma works on kidney to increase phosphate excretion (decreased plasma phosphate level) and to decrease Ca2+ excretion (increased plasma Ca2+ level). It works on bone to increase osteoclast activity to increase bone reabsorption (increased plasma Ca2+ and plasma phosphate level). It also works in small intestine. Since it is derivative of vitamin D(fat soluble) it can enter the cell and bind nuclear membrane receptor and induce genetic expression change(increased protein synthesis). It induces production of Ca2+ channel on luminal side to take more Ca2+ from lumen, also increase production of calbindin which binds Ca2+ to prevent it from working as a secondary messenger (change cell function). 1,25(OH)2D also increase H+-Ca2+ pump, Na+-Ca2+ antiporter (protein) and Na+ HPO4- exchanger. Ultimately all these changes result in increased phosphate and Ca2+ absorption which in turn increase plasma Ca2+ level plasma phosphate level. 10. Type I diabetes is the result of reduced ability to make insulin. Describe the effects of low insulin levels on skeletal muscle, liver and adipose tissue. How would these effects alter blood glucose levels? How would this level of blood glucose affect alpha cells of the pancreas? Answer: Skeletal muscle – has GLUT 4(insulin sensitive) to transport glucose into the cell. Site of glucose uptake, glycogen synthesis, aa uptake and glycolysis Decreased GLUT4 population on Rm (because insulin induces the increase in GLUT4). Decreased glycogen synthesis (because you have reduced GLUT4) by reducing hexokinase (glucose  G6P), and glycogen synthase (G1P  glycogen) Decreased glycolysis (because of reduced GLUT4, you have less glucose coming in which is a substrate for glycolysis) by reducing phosphofructokinase (F6P F1-6 biphosphate), and pyruvate dehydrogenase(pyruvate acetyl CoA) Decreased amino acid uptake Adipose cells – has GLUT4(insulin sensitive) to transport glucose into the cell. Also it can release glycogen in forms of fatty acid and glycerol(T/G - triacylglycerol) Site of glucose uptake, and T/G synthesis Decreased GLUT4 on Rm Decreased T/G synthesis by decreasing pyruvate dehydrogenase (pyruvate  acetyl CoA), decreasing acetyl CoA carboxylase (Acetyl CoA  malonyl CoA) (decreased lypogenesis) and decreasing FFA synthase (malonyl CoA  FFA) Liver cells- has GLUT2 (insulin insensitive) to transport glucose into the cell and also transport glucose out of the cell 3 Site of glucose uptake, glycogen synthesis, and T/G synthesis Decreased glucose uptake by decreasing glucokinase (glucose  G6P) and increasing G-6Phosphatase (G6P  glucose) Decreased glycogen synthesis(glycogen is synthesized from glucose therefore in response to decreased glucose uptake, it decreases glycogen synthesis) by increasing glycogen phosphorylase (glycogen  G1P) and decreasing glycogen synthase(G1P  Glycogen) Decreased T/G synthesis by decreasing phosphofructokinase (F6P  F1-6 biphosphate), pyruvate dehydrogenase (pyruvate  acetyl CoA), acetyl CoA carboxylase (Acetyl CoA  Malonyl CoA), and FFA synthase (malonyl coA  FFA) Net result is decreased ability to store glucose which leads to an increase in plasma glucose level which would inhibit alpha cell in pancreas (islets of Langerhans) from releasing glucagon 11. Describe the local regulation of pepsinogen in the stomach in the gastric phase of gastric acid secretion. Describe specifically how gastrin and histamine affect parietal cell to alter their acid secretion Answer: Release of pepsinogen by Chief cell is regulated both locally and centrally. Chemo Rc senses decreased pH and this sends information to enteric plexus which stimulate chief cell to produce more pepsinogen which is converted to pepsin in acidic environment. Pepsin digests protein and produce smaller peptides and amino acid. The presence of amino acid then stimulates G cells to produce more gastrin and this stimulates histamine release in ECL cells and HCl release in parietal cells. HCl release lowers pH and this feeds back to enteric plexus to increase pepsinogen release from chief cell. ECL- histamine  increase [cAMP]  increase K+ channel on basolateral side to hyperpolarize the cell and this electrogradient(-ve inside) pulls Cl- out to luminal side, increase Cl- on luminal side (using hyperpolarization from K+ channel  drives Cl- out) and increase H+/K+ ATPase on luminal side(using [K+] gradient established by K+ channel, drive K+ into the cell and H+ out of the cell antiport) * somatostatin and prostaglandins inhibit all these reactions from occurring G cell- gastrin  increase [Ca2+]  increase Cl- on luminal side (using hyperpolarization from K+ channel  drives Cl- out) and increase H+/K+ ATPase on luminal side(using [K+] gradient established by K+ channel, drive K+ into the cell and H+ out of the cell antiport) * Ach (PNS) induces the same reactions 12. Describe the levels of estrogen, follicle stimulating hormone, and luteinizing hormone found in the blood at the end of the follicular phase that are necessary to produce ovulation. Describe the central and local control of estrogen required to achieve these hormonal levels Answer: Cerebral cortex (sexual behavior, or thoughts), and limbic system(emotion) stimulates hypothalamus to produce GnRH(gonadotropin releasing hormone) and GnRH stimulates anterior pituitary (via adrenal hypophysis) to release LH(luteinizing hormone) and FSH(follicular stimulating hormone) to body(gonads). Theca cell releases estrogen, and androgen in response to LH, and granulosa cell releases P450 aromatase (androgen  estrogen). Local control: Estrogen from theca cell and from granulose ce
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