Endocrinology 442/842 Exam II PDF

Name:________________________ Endocrinology 442/842 Exam II October 27, 2015 7-9 pm Instructions: Please Read Carefully! Answer the following questions –...

Name:________________________ Endocrinology 442/842 Exam II October 27, 2015 7-9 pm Instructions: Please Read Carefully! Answer the following questions – T/F, short answer, essay based on the instructions for each question. For the essay questions answer them in as detailed a fashion as space will allow. Material written on the side of the page on which questions are typed will be considered in awarding a score for your answer. Material written on the back of pages will not be considered in grading of answers but you can use it to organize your thoughts. Ten percent of the points awarded will result from organization and legibility of your answer. Organize your thoughts before you start writing the answer. Be convincing in what you write- let your instructor know that you understand what you are putting down on paper. Points for each question are in parentheses A. True or False—If it is False then change the sentence to make it true. ( 2 pts each; 30%) T or F 1.) Leptin stimulates the orexogenic center within the arcuate nucleus of the hypothalamus to decrease appetite. T or F 2.) Ghrelin stimulates the orexogenic center within the arcuate nucleus of the hypothalamus to increase appetite. T or F 3.) Estrogen is protective again bone demineralization due to production of OPG which can bind PTH and inhibit it binding to RANK to cause production of enzymes that induce demineralization. T or F 4.) If there is not adequate amounts of thyroid peroxidase then an individual will develop hyperthyroidism. T or F 5.) GIP inhibits insulin secretion from the beta cells of the pancreas. T or F 6.) NPY decreases appetite through inhibition of the orexogenic center within the arcuate nucleus. T or F 7.) Glut5 transporter is insulin dependent and will through insulin signal transduction be phosphorylated within recycling vesicles to be inserted within the membrane of muscle and fat cells to increase uptake of glucose into storage forms. T or F 8.) Vitamin D is activated independent of PTH at the kidney. T or F 9) Hypothyroidism may occur due to reduced production of thyroglobulin within the follicular cells of the thyroid. T or F 10) A defect in the ability of the Calcium sensing receptors to sense increased Ca will result in decreased secretion of Parathyroid hormone. T or F 11) Hyperthyroidism induction of diarrhea may be through upregulation of endocrine hormones in the GI tract such as motilin. T or F 12) Glucagon acts to increase glucose uptake and storage in cells. T or F 13) Insulin works through a tyrosine kinase receptor which recruits IRS to stimulate multiple signal transduction pathways. T or F 14) The Glut2 transporter allows glucose to come into pancreatic B cells and stimulate metabolism which closes K channels and opens calcium channels to stimulate fusion of insulin within secretory vesicles and thus exocytosis of these vesicles and secretion of Insulin. T or F 15) PTH stimulates osteoclasts to produce RANKL which will bind to RANK on osteoclasts and cause production of enzymes that break down and demineralize bone. B. Short Answer (40%) 1) If Vitamin D acts like a steroid hormone then how does it act on cells and what does it cause to happen? (3) 2) Describe how a meal will affect Gastrin and what immediate actions Gastrin has (what does Gastrin immediately stimulate?). How is Gastrin positively and then negatively regulated? (6) 3) What is different about the signal transduction through CCKR2 when compared to all of the other signal transduction pathways that are initiated similarly that we have discussed? (3) 4) What does somatostatin do in the pancreas? in the stomach? and what hormones does it regulate in each of these locations? (6) 5) Depending on where CART is injected into the brain it might have very different actions. How it is possible that CART has diverse (stimulatory or inhibitory to appetite) `actions within different regions of the brain? (3) 6) Would overproduction of reverse T3 instead of active T3 be a problem and why? What type of disorder would this result in? (4) 7) If the Na/I symporters were mutated and did not allow for Iodine to enter the thyroid follicle cell then what would this effect within the follicle cell of the thyroid (in general where does Iodine end up?) and what type of disorder would occur? (3) 8) Vitamin D does many different things to promote Ca mobilization list three different organs that it affects and what it does? (3) 9) List two different functions of Calcitonin? (3). 10) Problems in Insulin production and signaling result in two different types of Diabetes. Explain the three differences in Type I and Type II diabetes comparing what occurs with each and how that differs in the other disorder (6 pts) C. Essay (30%) Answer 3 of the 4 following questions for 10 pts a piece. 1) Marissa has gone to the doctor because she has put on an extreme amount of weight. Her endocrinologist immediately took biopsies and conducted Insulin and leptin radioreceptor assays shown in a) and RIA of Insulin and Leptin in blood shown in b) from these assays please determine: A) What does the RRA say about receptors for Marissa? B) What does the hormone amounts of Insulin and Leptin mean and from both of these RIA standard curves with percent bound? -3) What might be two different problems (mechanistically) with what is causing her weight gain? 2) Joe has been experiencing problems. His heart rate is up, he can’t seem to maintain his weight and is constantly having stomach upsets. He went to the endocrinologist and they conducted Thyroid hormone- T3 and T4 assays. It does not appear that he is producing reverse T3. A) What does the RIA for T3 look like below? B) What does this mean Joe has (disorder)? C) Explain three different things (mechanistically that occurs in the follicular thyroid cell) that could be going wrong to cause the disorder that you listed in B. 3. Stephen and Laura have had a little boy who is not developing his bones normally and appears to have some problems with ca remodeling. The geneticist has determined that their little boy Joshua has a Ca sensing receptor that has a mutation where it always thinks Ca is bound. A) how would this affect regulation of PTH knowing what you do about PTH regulation from class and Vit D; B) what type of disorder might this develop in Joshua? C) what might be a way to treat this disorder? 4. We discussed how extreme disorders can tell us a lot about particular hormones and enzymes that may be involved in their actions. In particular we discussed mutation of the prohormone convertase 2 enzyme and how that caused individuals to be extremely obese at the age of 3. Explain how faulty actions of prohormone convertase 2 may cause this extreme obesity by describing A) How Pro-hormone convertase affects production of specific hormones B) How those hormones in particular affect satiety/and or appetite regulation; and C) How difficult would it be to treat this disorder and what might be done.  Name:________________________ Endocrinology 442/842 Exam II October 30, 2017 7-9 pm Instructions: Please Read Carefully! Answer the following questions – T/F, short answer, essay based on the instructions for each question. For the essay questions answer them in as detailed a fashion as space will allow. Material written on the side of the page on which questions are typed will be considered in awarding a score for your answer. Material written on the back of pages will not be considered in grading of answers but you can use it to organize your thoughts. Ten percent of the points awarded will result from organization and legibility of your answer. Organize your thoughts before you start writing the answer. Be convincing in what you write- let your instructor know that you understand what you are putting down on paper. Points for each question are in parentheses. A. True or False—If it is False then change the sentence to make it true. (2 pts each; 30%) T or F 1.) Both POMC and CART utilize Prohormone Convertase (PC1/3) and PC2 to cleave their sequence to make other hormones. T or F 2.) Gastrin and motilin are in the same hormone family. T or F 3.) The pancreatic beta cell synthesizes and secretes glucagon which regulates uptake of glucose into cells. T or F 4.) The parathyroid gland is responsible for secretion of all hormones that are involved in calcium regulation and homeostasis. T or F 5.) When Leptin is secreted it stimulates production of POMC in the anorexogenic center of the arcuate nucleus of the hypothalamus allowing for satiety signals. T or F 6.) Iodine is necessary for insulin production. T or F 7.) NPY stimulates the anorexogenic center of the arcuate nucleus of the hypothalamus to stimulate alpha MSH secretion to cause increased feed intake. T or F 8.) Osteoblasts in response to PTH stimulate the production of RANKL. T or F 9) Thyroid peroxidase is necessary to add Iodines to Tyrosine residues on Thyroglobulin to  produce T3 and T4. T or F 10) RANKL promotes bone demineralization by binding to its receptor RANK to activate osteoclasts. T or F 11.) Insulin acts through the JAK/STAT pathway to elicit its signal transduction events in cells. T or F 12.) Glucagon acts on muscle cells to breakdown glycogen. T or F 13.) The thyroid gland produces calcitonin and PTH which are both responsible for regulation of calcium metabolism. T or F 14.) All GI hormones work through 7 transmembrane G-coupled receptors to elicit their effects. T or F 15.) Vitamin D is activated by PTH in the liver. B. Short Answer (40%) 1. Gastrin stimulates production of gastric acid and initiation of protein digestion. List two other hormones increased through Gastric acid production and protein digestion that are secreted and what their functions are. (4) 2. Name 2 cell types in the pancreas that secrete hormones and what each hormone’s function is in the body. (6) 3. List four symptoms of an individual with overproduction of reverse T3. (4) 4. Describe three ways estrogen prevents bone demineralization.(3) 5. What is the primary function of insulin on the following organs? (6) A- Liver B- Muscle  C- Adipose tissue 6. Answer the following questions about Vit. D: (5) a. What type of hormone is Vit. D? b. How it is degraded and excreted from the body? c. Where is it’s receptor located and how does it act on cells to elicit a response? d. What are the roles of Vitamin D on calcium regulation? 7. List three different cases (steps in production of T3 and T4 or otherwise) which could result in the  disorder hyperthyroidism. (6) 8. Within the GI tract there are several hormones that are in the same family place a family member (another hormone in the same family) next to each hormone listed (6): a. Gastrin b. Pancreatic polypeptide c. Secretin  C. Essay – (Pick three of the following four essay questions to answer for (10 pts each). 1. Scientists have just identified a new growth factor X that they hypothesize if overexpressed will induce differentiation of osteoprogenitor cells into osteoclasts. In order to test their hypothesis, they are going to inject growth factor X into adult mice. A) Explain how this growth factor may affect: parathyroid hormone, calcitonin secretion and Vitamin D (Calcitrol) activation and B) what potential disorder may this lead to and C) how can it be treated? 2. Francesca appears to have type I diabetes. Her doctors ran a test to measure insulin and Francesca had 98% binding (see diagram below). A) What test did the doctors run? And what are the general principles of the test and what does the 98% mean? B) Explain to Francesca how insulin (after it is transcribed and translated) is processed in the cell to be ready to be secreted. C) Give Francesca two potential hypotheses of malfunctions in this system that may result in her disorder and a potential therapy for Francesca? 3. Virginia appears to have a problem with her thyroid follicular cells because they are overproducing a phosphodiesterase that is interfering with thyroid hormone production. Virginia has come to you as a budding endocrinologist to explain to her why overexpression of phosphodiesterase would affect production of T3 and T4 within the thyroid gland. A) Please explain in detail how this would disrupt thyroid hormone production; B) what disorder is this causing to occur; C) how would you treat it? 4. Penelope Plump has a disorder that is caused by a mutation in production of POMC at all organs that POMC is produced. A) Explain how POMC is processed in different organs in the body; B) How might reductions in these hormones alter Penelope’s appearance and what other problems may she have? C) If you were going to determine if POMC was not being made what hormone(s) might you measure? What assay will you use? and if these hormones are reduced what from this assay would tell you whether they are reduced? ----explain  Name: ___________________ Endocrinology ASCI442/842 Exam II October 29, 2019 Instructions: Please Read Carefully! Answer the following questions – T/F, list, short answer and essay questions Material written on the side of the page on which questions are typed will be considered in awarding a score for your answer. Material written on the back of pages will not be considered in grading of answers but you can use it to organize your thoughts, diagram, etc. Points for each question are in parentheses  True or False—If it is False then change the sentence to make it true. (2 pts each; 30%) T or F 1) TSH through its actions at the TSHR elicits activation of protein kinase C to activate thyroid iodinase. T or F 2) Leptin acts at a tyrosine kinase receptor with JAK/STAT as a second messenger. T or F 3) Calcium is released from osteocytes in response to high levels of PTH. T or F 4) Beta cells in the pancreas secrete glucagon. T or F 5) Gastrin inhibits GI growth and increases GI blood flow. T or F 6) The most active form of thyroid hormone is T3. T or F 7) Gastric inhibitory peptide inhibits gastrin and gastric acid secretion. T or F 8) Insulin will stimulate translocation of GLUT4 transporters to the plasma membrane in skeletal muscle, adipose and the liver. T or F 9) Parathyroid hormone is synthesized in a pre-pro form and regulated by calcium levels. T or F 10) The orexigenic center is responsible for satiety signaling and contains neurons producing NPY and AgRP. T or F 11) CCK and Gastrin has similar affinity for the CCK1 receptor. T or F 12) Glucagon is released from the alpha cells of the pancreas in response to low levels of glucose and insulin. T or F 13) Thyroid peroxidase is involved in iodination of tyrosine into DIT or MIT. T or F 14) Ghrelin stimulates the POMC/CART neurons to increase appetite. T or F 15) The kidney is responsible for Vitamin D activation through hydroxylation through PTH’s actions. Short Answer (40%) 1. Explain how estrogen is important in calcium regulation? What does it do specifically? 3pts 2. Answer the following questions about Insulin: 8pts A. Which cell type in the pancreas secretes Insulin? B. What is the receptor type for Insulin? What is the second messenger? C. How is insulin secretion regulated? D. What is the main role of this hormone? 3. Which form of thyroid hormone is found in higher abundance in plasma? If it has a binding protein what is its binding protein? 2pts 4. What receptor type does Glucagon bind to? What is the second messenger system? 2pts 5. How does Ghrelin affect the anorexigenic or orexigenic centers in the hypothalamus? 2pts 6. Vitamin D is critical for Ca regulation in the body. What is the major role of Vitamin D? 3pts 7. In the GI tract there is a hormone that is secreted upon digesta entering the stomach. What is that hormone and what type of receptor does it bind to? 4pts 8. Which hormone upregulates CART and which hormone downregulates CART? 2pts 9. Name one hormone in the Pancreatic Polypeptide family other than Pancreatic Polypeptide. 2pts 10. Why is iodine critical for Thyroid hormone production? What happens if iodine is missing in the diet? 3pts 11. What could be a major problem for each disorder and which hormones is effected? 8pts A. Rabson Mendenhall Syndrome B. Hypothyroidism C. Zollinger-Ellison Syndrome D. Osteoporosis 12. What hormone causes the GI tract to increase digesta movement through the tract? 1pt C. Essay – 442 students can pick two of the following 4 questions to answer for 15 point each or Pick three of the following four essay questions to answer for (10 pts each). 842 students must answer 3 of the 4 questions. 1. One of the case studies that we had in class discussed a toddler with a Leptin receptor mutation. Explain how this particular mutation would affect the anorexogenic and orexogenic centers within the hypothalamus and how this altered regulation of these two centers may affect other hormones such as CART, POMC, NPY and agouti-related peptide. What phenotype would this individual have and would this be life threatening? 2. Calcemia Smith has been having problems regulating her CA levels in her blood. Her Endocrinologist believes that it might be to a dysfunctional CA sensing receptor. A) Explain to Calcemia how this receptor works to regulate CA levels in the blood; B) What hormones it will affect and if they will increase or decrease or how this might affect them and where they are produced; C) What type of treatment would be the most logical due to this inability of the CA receptor to act. 3. In class one of your case studies was Rabson Mendenhall Syndrome which is due to a mutation in the insulin receptor. You have just found out that your only child has this disorder. Because you read this case study thoroughly and understand much of what we went over in class you take the time to inform your spouse: A) Explain what normally happens if the receptor is function and how this mutation affects this situation and be specific in what major organs that this would affect; B) In our case study two potential treatments were recombinant IGF-1 and Leptin—how would each of these treatments work as therapies for this disorder? 4. Jenny has been diagnosed with Graves Disease which means that she is developing antibodies to the TSH receptor that activates it and causes hyperthyroidism. Because Jenny is a cell biologist you are telling her a little more in detail about her disease and the potential treatment plan. A) Please explain how the TSH receptor normally signals and what events in the cell it elicits; B) Explain how this production of antibodies may affect negative feedback on the hypothalamus and pituitary and C) What type of treatment might be the most appropriate for Jenny.  Name:________________________ Endocrinology 842/442 Exam II October 26, 2022 7-9 pm Instructions: Please Read Carefully! Answer the following questions – T/F, short answer, essay based on the instructions for each question. For the essay questions answer them in as detailed a fashion as space will allow. Material written on the side of the page on which questions are typed will be considered in awarding a score for your answer. Material written on the back of pages will not be considered in grading of answers but you can use it to organize your thoughts. Organize your thoughts before you start writing the answer. Be convincing in what you write- let your instructor know that you understand what you are putting down on paper. Points for each question are in parentheses. A. True or False—If it is False then change the sentence to make it true. (2 pts each; 30%) T or F 1.) Melanocortin 2 receptor will bind with equal affinity to ACTH, and alpha MSH. T or F 2.) POMC is a hormone that is made in the hypothalamus and the thyrotroph cells of the anterior pituitary that can be alternatively cleaved by enzymes produced in these different organs to produce different hormones. T or F 3.) The pancreatic alpha cell synthesizes and secretes insulin which regulates uptake of glucose into cells. T or F 4.) Parathyroid hormone (PTH) is secreted in response to low concentrations of Ca in blood sensed by the calcium sensing receptor. T or F 5.) The anorexogenic center of the arcuate nucleus of the hypothalamus is stimulated by Leptin to send satiety signals to higher centers of the brain. T or F 6.) Thyroid eye disease is often associated with individuals that have autoantibodies to TSH receptor and stimulate that receptor causing hyperthyroidism (Graves Disease). T or F 7.) NPY stimulates the orexogenic center of the arcuate nucleus of the hypothalamus to stimulate alpha MSH secretion to cause an increase in feed intake. T or F 8.) Estrogen is protective of bone by producing OPG which binds to RANK and does not allow for binding of RANK to RANKL to promote bone demineralization. T or F 9) GIP stimulates glucagon secretion promoting uptake of of glucose in cells. T or F 10) Vitamin D is activated (added second OH group) by PTH in the liver to allow for active Vitamin D3 which allows for reabsorption of calcium in many different organs to increase CA in blood. T or F 11.) Obese patients are more likely to respond adversely to COVID-19 due to an increased cytokine storm (increased inflammation) than individuals that are not obese. T or F 12.) Low concentrations of AMH in circulation signify reduced number of follicles in women and may also be indicators of increased bone density. T or F 13.) Calcitonin is produced by the C cells of the parathyroid gland. T or F 14.) All melanocortin receptors are 7 transmembrane G coupled receptors that work through Gs and activate second messenger cAMP. T or F 15.) TSH when bound to its receptor TSHR activates DAG and IP3 as its second messengers to stimulate the thyroid follicular cells to produce thyroid hormone. B. Short Answer (40%) 1. List four different problems (steps in production of T3 and T4 or other things) which could result in the disorder hypothyroidism. (4) 2. Explain how insulin is synthesized and packaged for secretion. (4) 3. Name the two major enzymes that cleave POMC or its derivatives. What are the primary products of each enzyme or combination of enzymes in what organs? (4) 4. Name 3 GI hormones that affect GI motility and state whether it is increase or decrease in motility.(6) 5. What are two major differences in Type I and Type II diabetes? (4) 6. What are the organs in the body that are dependent on insulin to get glucose into their cells? (3)  7. What is the major role of osteoclasts in bone? What 2 hormones regulate osteoclast function in bone and do they inhibit or stimulate? (5) 8. Name two hormones that affect centers in the brain to regulate appetite or satiety and then state what center they affect and what is the result of their stimulation. (6) 9. Explain why patients with obesity could develop more severe cases of COVID-19 than others not obese that could be life threatening? (4) C. Essay – (Pick three of the following four essay questions to answer for (10 pts each). 1. Justine has taken her dog to the vet. The vet has done a thorough workup on her dog and has determined that her dog is hyperthyroid. You are an endocrinologist and Justine has come to you to determine exactly what is wrong with her dog so it can be treated properly. You know the mechanisms involved in synthesis of Thyroid hormone so you know the different steps that may be involved in causing hyperthyroidism. a) Explain at least three ways that hyperthyroidism may occur and how each of these may be treated. b) What other disorders can occur in individuals that develop hyperthyroidism that we had a case study on? Explain how hyperthyroidism or Graves disease may also result in this other disorder. 2. Olga Fragilealice appears to have decreased Anti-Mullerian Hormone (AMH) and her doctor is concerned because this may affect her bone density and lead to osteoporosis. Because you listened to our case study on AMH and osteoporosis and you understand how bone deposition, remodeling and demineralization occurs you can explain to Olga several things. Explain how A) PTH affects bone demineralization; B) how estrogen may affect demineralization; C) how reductions in AMH may act as a marker of bone demineralization and the potential role of FSH in bone demineralization as discussed in class. 3. Lenny is obese and so is most of his family. He has gone to the geneticist to determine if there is a mutation in a gene which may explain his and his families’ obesity. Because you excelled in your endocrinology class you became a specialist understanding metabolic disorders that result in increased weight gain. A) Explain to Lenny what 3 different genes or receptors may be a problem that could be inherited and be a reason for his obesity and include the reason that each of these genes or receptors could be a problem. B) What might be a way to mitigate (treat) each of these reasons that you have described in B. C) What center in the brain might be affected with each gene or receptor problem or would any centers be affected that regulate appetite? 4. We discussed in class treatments of Type II diabetes and discussed Susan’s problems related to that along with some other complications that she has developed. A) First Susan has insulin resistance explain mechanistically what that means using your endocrinology knowledge; B) We discussed several different treatments for Susan so explain 2-3 treatments that may help with her disorder and how they work; C) how could you determine if Susan’s cells within her pancreas are making enough insulin? And is this a concern?