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Exam I: Take-Home Short Essay Key For self-grading: I’ve put the answers to each question in italics. Each question has a point value assigned to it. I have answered the questions in a very complete form with some extra information for clarity. Be reasonable in your self-assessment- make sure that you have addressed EXACTLY what the question is asking, don’t worry that your answers include all of the information that my answers include. But, do be sure that your responses answer the questions CORRECTLY and COMPLETELY. You can assign partial credit to yourself. Remember, this is to benefit your learning, so the more you pay attention to the grading and the more honest you are with yourself, the more you will get out of it! Short Essay 1. a. List 2 hormones that affect the use of energy by cells (glucose &/or fatty acid use, ATP production, gluconeogenesis, glycogenolysis, glycogenesis, lipolysis or fat storage) For each, state the class it belongs to, where it’s produced, two effects that it has, and what stimulates its release. Briefly describe one disorder associated with one of these hormones. Hormone: Many possibilities here: in the first row I will list most of the hormones that would count. In the next, I will provide a specific example and fill out each of the columns. If you have questions, ask! Growth Hormone Thyroid Hormone Cortisol Epinephrine Glucagon Insulin Class Where produced Two effects What stimulates release Example: Cortisol Steroid Adrenal cortex, zona fasciculata Gluconeogenesis, Low circulating Lipolysis cortisol CRH ACTH Disorder (Name hormone and describe): Varies, as long as you did this in your own words, give yourself credit! b. Now do the same for 2 hormones that affect calcium in blood and/or bone, either directly or indirectly. Do not describe a disorder for one of these. Hormone Class Where produced Two effects Peptide Parathyroid glands Stimulate calcitriol activation Stimulate osteoblasts What stimulates release PTH Calcitonin Calcitriol PTH Low circulating Calcium 2. a. Describe one hormone (other than any listed from #1) that is ultimately under the control of the hypothalamus/adenohypophysis. Name the hormone/factor from the hypothalamus, the hormone from the adenohypophysis, and the final hormone and where it comes from (kidney, etc). Describe one effect this final hormone will have on target cells. How do hormones get from the hypothalamus to the adenohypophysis? The possible hormones you could use here: thyroid, growth, cortisol, testosterone, estrogen, progesterone. Make sure that the hormone you chose here is different from #1! Here is an example of a complete answer: Progesterone is under the ultimate control of the hypothalamus/adenohypophysis. Gonadotropin Releasing Hormone (GnRH) from the hypothalamus causes the release of Leutenizing Hormone from the adenohypophysis. LH from the adenohypophysis causes the release of progesterone from the ovaries. Progesterone acts on the uterus and causes it to prepare for a possible pregnancy. Releasing hormones from the hypothalamus get to the adenohypophysis via the hypophyseal portal system. b. A person with symptoms of hypothyroidism (for example, sluggishness and intolerance to cold) is found to have abnormally low plasma concentrations of T4, T3, and TSH. After an injection of TRH the plasma concentrations of all three hormones increase. Where is the site of the defect leading to the hypothyroidism? The hypothalamus; Thyroid Releasing Hormone, like all Releasing Hormones, comes from the hypothalamus. If an injection of TRH leads to normal production of TSH from the pituitary and T3, T4 from the thyroid, then the hypothalamus is not sending enough TRH to those organs. c. Vera is receiving very large doses of a cortisol-like drug to treat her arthritis. Theoretically, what should happen to her own production/secretion of cortisol (increase or decrease)? What hormone should a drug mimick if you wanted to increase Vera’s production of ACTH? Since the production of Corticotropin Releasing Hormone from the hypothalamus is determined by circulating blood cortisol, injections of cortisol should change the hypothalamus’ output of CRH. Specifically, the hypothalamus produces more CRH when cortisol levels are low and less CRH when cortisol levels are high. Vera is receiving injections of cortisol; therefore, her circulating cortisol will be high and the hypothalamus will produce less CRH. If the hypothalamus produces less CRH, then her natural production ACTH from the pituitary would decrease; then, her natural production of cortisol will decrease. If you want Vera to increase her natural production of AdrenoCorticotropic Hormone (ACTH), you would give her injections of a drug that mimicks CRH. 3. This example has absolutely no basis in reality. If you know how the hormones can affect their target cells and which use 2nd messengers, you can predict how any hormone, fake or real, will act. Hormone X is a hormone in the Who species (you know, the kind that Horton heard and the Grinch wanted to repress). Hormone X allows the Whos to sing for extended periods of time. It does so by affecting metabolism in a number of different ways. One of the specific effects Hormone X has is in muscle cells of the larynx: it stimulates those cells to increase the number of enzymes involved in ATP production. a. Let’s say Hormone X is a peptide hormone. Describe how it will affect a muscle cell of the larynx, starting with its arrival at the target cell and ending with the production of more active enzyme (be sure to state why there’s more active enzyme) X lands on an external receptor on the cell’s membrane. This binding causes the release of an associated G-protein within the cell. G-protein moves along the membrane in the interior cell until it bumps/binds an adenylate cyclase enzyme. This activates adenylate cyclase, and it converts an ATP to cyclic AMP (cAMP). cAMP then activates kinases within the cell. The kinases then activate cellular proteins by phosphorylating them. For example, some proteins that might be activated in this cell are glyolytic enzymes; those involved in making ATP via glycolysis. b. Now repeat, only this time pretend Hormone X is a steroid hormone. X as a steroid would diffuse into the cell and bind a receptor on the interior of the membrane. Together, the hormone/receptor complex would enter the cell nucleus (or, perhaps, a mitochondrion), and bind a DNA sequence near a specific gene. This binding will cause gene activation. For example, genes that might be activated in this cell would code for glycolytic enzymes, and cause more to be built. 4. You are an employee for a company who just hired a new manager. On his second day, he came barging into your office telling you that he’s been going through your records and watching your performance, and if things don’t shape up dramatically and soon, you’re outta there. You were completely unaware of any problem and have no idea how to remedy the situation, so everyday for the next month or so you enter the office of eggshells wondering if today is the day you will be fired. Oh, and you have no savings or prospects for jobs and for some reason are ineligible for unemployment compensation. Assuming that you are a reasonably sensitive person (ie, this actually will affect you), a. Briefly describe your Autonomic Nervous System response when the boss came in and barked this information at you. Be sure name the dominating division and to include 4 specific effects of the dominating division. This event caused a sympathetic response; specifically, as part of the stress response, this is called the Alarm Phase. Sympathetic activity dominates your physiological response. Here are some examples of what might be happening to you (be sure to have four listed for full credit!) -increase heart rate, increase respiration, increase blood pressure, dilate pupils, increase sweating, decrease digestive activity, shunt blood from digestive organs to muscle and brain, lipolysis, glycogenolysis b. Describe your endocrine response starting with the first traumatic event and then the subsequent long-term response (ie, go through the phases of the stress response). Be sure to name the dominant hormones of each phase, and the effects each of the hormones will have. As you went through the alarm phase, hormones were also being released to get you into the resistance phase, which marks the long-term response. Some hormones with some specific effects: -Epinephrine- all effects described above for sympathetic response; also, works closely with cortisol and glucagon for glycogenolysis, gluconeogenesis, and lipolysis -Cortisol- the primary hormone of this phase- glycogenolysis, gluconeogenesis, lipolysis, proteolysis, increase vascular reactivity, suppress immune function -Glucagon- glycogenolysis -Growth Hormone- enhance effects of the above -ADH- retain water -Aldosterone- retain Na+ and indirectly, water *you must have at least Epinephrine, cortisol and Aldosterone for full credit. You must list at least 2 functions of epinephrine and cortisol for full credit. c. Why are the maintenance of blood glucose and the mobilization of lipids the major themes of the long-term response? To keep all cells fed: with fats; and, to make sure that glucose is always available for the brain. Making sure most cells have access to fats, mobilizing glucose stores, and breaking down body proteins to make glucose all help to accomplish this goal. This response assumes you will be exercising, healing, or fasting and will need access to stored fuel. d. Is the long-term endocrine response designed to help you survive this particular type of crisis? What type/s of crises is it designed to help you survive? No, the stress response is designed to get you through emergencies that involve more immediate problems and those that affect your body: running away, running after something, fighting something or somebody, healing, or fasting because of a lack of food. Bonus 1 point: Based on the effects of the hormones involved, why do you think that overeating and a lack of exercise might actually make this stress response harmful rather than helpful? When you experience a stress response, you are mobilizing lots of stored energy such as glucose and fatty acids. What this means is that you have elevated levels of glucose and fats in your blood. If you exercise, you can burn these excess fuels off, but if you don’t exercise, they can remain elevated. If you are also overeating, you are further elevating blood glucose and fatty acids. Chronically elevated glucose and fats can greatly increase your risk of developing chronic diseases such as metabolic syndrome, type 2 diabetes, and heart disease. Exercise also helps to metabolize the stress hormones and bring them back to normal; it also causes the release of endorphins and other neurotransmitters that help to protect brain neurons from harmful changes that neurons make that can lead to depression. *any reasonable explanation or approximation of these count; if you have a question about yours, ask! 5. You’re a reporter at the scene of a disaster. Actually, you’re a really tiny reporter living inside a biology instructor. The disaster is that one of the instructor’s blood vessels has just been sliced by a scalpel. You’ve arrived at the scene immediately. a. List the 3 phases of hemostasis, and state one event which will happen during EACH phase. Vascular phase- vascular spasms (smooth muscle surrounding injured vessel contracts, slowing blood loss); endothelial cells retract, basal lamina is exposed; damaged endothelial cells release chemicals that promote clotting and immune response, and will be necessary for coagulation. Platelet phase- platelets stick to exposed basal lamina; more platelets stick to the first ones, and so on; stuck platelets secrete their chemicals, which further support platelet aggregation, vascular spasms and immune response, and will be necessary for coagulation. Coagulation Phase- clotting proteins will be activated, leading to the formation of fibrin. This will form a mesh over the injury, trapping cells and platelets, and forming a temporary plug. a. How do the first platelets on the scene get stuck/activated? They stick to the collagen of the exposed basal lamina b. Name one factor released by platelets/endothelial cells that will promote the clotting process. There are lots, any of these will do: serotonin, ADP, thromboxane A, clotting factors, platelet-derived growth factor, Ca2+, tissue factor, endothelins c. Outline or diagram the biochemical cascade of events that occurs once Factor X is activated. Factor X is converted to prothrombinase. Prothrombinase, an enzyme, then converts the blood protein prothrombin to thrombin. Thrombin, an enzyme, then converts the soluble blood protein fibrinogen to the insoluble fibrin Fibrin forms a mesh around the injured area, trapping cells and debris, and temporarily closing off the injury. d. Briefly describe one thing that will aid in the clean-up or control of a clot. Lots of answers would work here, including: -Prostacyclin from intact endothelial cells prevents the clot from moving too far away from the injury site -Elevated serotonin inhibits ADP action -Clot retraction helps localize the clot and make platelets less available for continued aggregation -Plasmin is activated shortly after thrombin is formed; plasmin digests the fibrin mesh 6. Tilly, Ermy, Fanny and Si are donating blood. The following shows the results of their blood tests. Assume that all Rh- people have received Rh+ blood in the past. Complete the chart by filling in each of their blood types: Tilly Ermy Fanny Si Anti-A No reaction Agglutination No reaction Agglutination Anti-B Agglutination Agglutination No reaction Agglutination Anti-Rh No reaction No reaction Agglutination Agglutination 6. From which group member/s can Si receive blood? All 7. To which group member/s can Si give blood? None 8. From which group member/s can Ermy receive blood? Tilly Type? BABO+ AB+ 9. To which group member/s can Fanny give blood? Si 10. Is anyone in this group unable to receive blood from the others (if so, name/s)? Tilly, Fanny