A.Where are glucocorticoids made? (cells, organ) B.What organ/or cells secrete them? (may differ from site of formation) C.What stimulates their secretion? Explain negative feedback control of secretion. D.Where do they work (target) E.What do they regulate: physiological outcome?
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A.Where are glucocorticoids made? (cells, organ)
B.What organ/or cells secrete them? (may differ from site of formation)
C.What stimulates their secretion? Explain negative feedback control of secretion.
D.Where do they work (target)
E.What do they regulate: physiological outcome?
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- A.Where are Epinephrine and Norepinephrine made? (cells, organ) B.What organ/or cells secrete them? (may differ from site of formation) C.What stimulates their secretion? Explain negative feedback control of secretion. D.Where do they work (target) E.What do they regulate: physiological outcome?An elderly gentleman has recently been diagnosed with cirrhosis of the liver. He admits to being a heavy drinker. This man is your patient. Given the damage to his liver, you would have concerns about all of the following except a. regulating his ability to maintain body temperature, because of decreased thyroid hormone levels. b. internal bleeding, because he has impaired ability to synthesize clotting proteins. c. edema, because of impaired synthesis of plasma proteins (e.g., albumin). d. jaundice, because his liver is less efficient at removing bilirubin from the blood.c. Draw a picture comparing and contrasting how each might cause its target cell to do this. Don't look it up! You have all the information you need from the notes to come up with a reasonable, logical hypothesis. d. If somebody develops hyperparathyroidism (the parathyroid glands produce too much PTH), do you expect that person's blood levels of calcium to be too high or too low as a result? Explain. e. If somebody develops hyperparathyroidism, will their bones gain or lose density?
- A. What is the difference between preproinsulin and proinsulin? B. What is cleaved out of proinsulin to allow the mature insulin molecule to be formed? C. What is the C peptide and why is it medically significant? D. What is the purpose of the signal sequence and why isn’t it present in the mature insulin molecule?Define the following terms:a. second messengerb. desensitizationc. target celld. insulin resistancee. adenylate cyclaseFigure 37.11 Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statement about these two conditions is true? A pancreatic tumor and type I diabetes will have the opposite effects on blood sugar levels. A pancreatic tumor and type I diabetes will both cause hyperglycemia. A pancreatic tumor and type I diabetes will both cause hypoglycemia. Both pancreatic tumors and type I diabetes result in the inability of cells to take up glucose.
- Growth hormonea. increases the usage of glucose.b. increases the breakdown of lipids.c. decreases the synthesis of proteins.d. decreases the synthesis of glycogen.e. All of these are correct.Secretory cells of the mucous membrane of the mucosal layer of the gastrointestinal tract (GI tract) are classified as ___ cells if they secrete fluids and enzymes into the lumen and ___ cells if they release hormones into the bloodstream. Group of answer choices exocrine : endocrine endocrine : absorptive endocrine : exocrine exocrine : absorptivee) (i) People living in tropical region usually do not have deficiency in vitamin D even if their diet is low in vitamin D. Briefly explain this. (ii) Briefly describe the activation of vitamin D.
- Which of the following statements about insulin is true? a. Insulin acts as a transport protein, cany in g glucose across the cell membrane. b. Insulin facilitates the movement of inti acellular glucose transporters to the cell membrane. c. Insulin stimulates the breakdown of stored glycogen into glucose. d. Insulin stimulates the kidneys to reabsorb glucose into the bloodstream.a. What hormone is released in response to increased blood glucose? 2. b. The binding of this hormone to its receptor increases the rate of action of a particular transporter. What transporter is this? c. How is the rate increased? d. What enzyme directly involved in glycogen metabolism is activated by this hormone?1. (a)When glucocorticoidis misused, What harm will it cause? (b)Why can't patients who take large amounts of glucocorticoids for a long time suddenly stop taking them?