回顧問題不定期更新 Study Questions are Made by Prof. Cruz & Prof. Moore from Oberlin College & Conservatory?

本期回顧問題超級超級魔鬼警告！量力而行即可~（這一期不會的就算了吧，別問UP了，UP對這期的問題也頭疼~）

Lectures 18 – 20: Hormones in Animals & Human Reproduction

1. What are the defining qualities of a hormone? What are the different chemical types of animal hormones, and how do they differ? How is it possible that a few dozen hormones are able to regulate thousands of physiological processes over the lifetime of one organism, which may live for decades?

2. Target cells are those that possess receptors for a certain hormone. Describe the series of events that have to occur for a lipophilic (hydrophobic) hormone (example: testosterone) to exert an effect on its target cell.

3. Explain why the pituitary gland is called the ‘master gland’. What does it control, and how does it exercise this control? What, if anything, controls the pituitary?

4. Explain the terms, “-tropic”, “-releasing”, and “-stimulating” in the following terms: a) adrenocorticotropic hormone, b) gonadotropin-releasing hormone, c) follicle-stimulating hormone.

5. Knowing the functions of insulin and glucagon, identify the organs most likely to have receptors for these hormones. Where specifically in the cells of those organs would you expect to find these hormones’ respective receptors?

6. A person who is insulin-deficient would be expected to have generally high, or low?, blood glucose levels? What predictions might you make regarding such a person’s blood pressure?

7. Diabetes Type I is genetic disease caused by death of pancreatic alpha cells, thus, no insulin is made. Diabetes Type II, on the other hand, is caused by malfunctioning or insufficient GLUT4 levels. Why would such patients be expected to have high blood pressure readings? Why would insulin pills not work for either type of diabetes?

8. A person with low levels of glucagon would be more or less? likely to be overweight? Explain your answer.

9. Why are insulin and glucagon said to play complementary roles in the maintenance of blood glucose levels?

10. A person with higher-than-normal ACTH would be expected to be hyperactive? or hypoactive? Explain.

11. Why might CRF deficiency have the same symptoms as ACTH deficiency?

12. Cortisol receptors abound in the liver, which is stimulated to undertake gluconeogenesis and glycogenolysis when cortisol binds to its receptors. Explain how this is consistent with the central role of cortisol in the fight-or-flight response.

13. Although in modern life it is rare that we encounter such dangers as marauding predators and exploding volcanoes, the fight-or-flight (f-o-f) response is elicited in times of emotional stress, such as economic downturns, tough exams, and broken relationships. How can this be?

14. What would be the adaptive significance of having the f-o-f response in addition to the normal metabolic circuit involving glucagon and insulin? Don’t they affect the same functions in the liver? (gluconeogenesis and glycogenolysis)?

15. The glucagon signaling pathway is shown in the figure below. Locate glucagon and its receptor. At the bottom of the diagram is a list of the chemical processes affected by glucagon signaling. Above this list all the way to just below the cell membrane are the molecules and arrows of the signal cascade occurring inside a cell upon glucagon binding to its receptor. (For this class, we can skip the details of the signal cascade.) The cortisol signaling pathway is also shown below. Locate cortisol and its receptor.

a) Explain how the figure on the left makes it clear that glucagon is not a steroid hormone.

b) Explain the overall END result of glucagon signaling (what do all those words ending in ‘–sis’ mean?).

c) What is the target organ for glucagon? What other functions of this organ have we discussed in class?

d) Compare the location of the glucagon receptor with that of the cortisol receptor.

e) Compare the role(s) of the receptor-hormone complex depicted in the left figure with that in the right figure. How do these roles differ? How are they similar?

16. How does negative feedback differ from positive feedback.

17. The recently controversial EpiPen is a commercial preparation of epinephrine, an amine hormone secreted by the adrenal medulla. Epinephrine is useful in counteracting the potentially deadly effects of a severe allergic reaction that catapults the body into what is called “anaphylactic shock”. Here’s how the Mayo Clinic describes anaphylaxis:

The flood of chemicals released by your immune system during anaphylaxis can cause you to go into shock; your blood pressure drops suddenly and your airways narrow, blocking normal breathing. Signs and symptoms of anaphylaxis include a rapid, weak pulse, a skin rash, and nausea and vomiting. Common triggers of anaphylaxis include certain foods, some medications, insect venom and latex. http://www.mayoclinic.org/diseases- conditions/anaphylaxis/basics/definition/con-20014324

Knowing the effects of epinephrine in “mobilizing” (that’s an understatement) glucose metabolism, explain how EpiPen counteracts anaphylactic shock.

18. What are secondary sex characteristics? Give examples of such characteristics in males and females (humans or other animals will work here).

19. What are the functions of LH and FSH, respectively, in humans? Where do these hormones come from, and what are their respective targets?

20. Describe the changes that occur in the follicle during the follicular stage of the human female reproductive cycle (menstrual cycle). Compare with the changes that occur during the luteal phase. Describe the hormones that cause these changes.

21. Differentiate between Sertoli and Leydig cells. Which of these are directly responsible for secondary sex characteristics in males?

22. Testosterone and estradiol are required for sperm and egg maturation, respectively. Explain how the levels of these hormones are maintained within normal ranges in the bloodstream using negative feedback loops.

23. Sertoli cells secrete the hormone inhibin. How would an inhibin-based chemical contraceptive prevent pregnancy?

24. Why are LH, FSH and CG (luteinizing hormone, follicle-stimulating hormone, chorionic gonadotropin) called gonadotropins?

25. Why is progesterone high during the luteal phase but not the follicular phase? What is the effect of rising progesterone levels on the uterine endometrium?

26. A female whose ovaries have been removed immediately goes into menopause, or cessation of menstruation, in spite of the fact that uterus is not removed. Explain why menstrual cycles fail to occur.

27. Why is progesterone called the hormone of pregnancy? How is its sustained production guaranteed during pregnancy if the endocrine gland that secretes it (what’s that organ?) deteriorates into a corpus albicans long before the pregnancy is over?

28. The contraceptive called the mini-pill consists mostly of estradiol, and is taken in successive days for most of the menstrual cycle. This ensures that the estradiol level stays uniformly high (i.e., no peak occurs) during the menstrual cycle. How does it prevent pregnancy?

29. Progesterone-based contraceptives prevent pregnancy…h(huán)ow? (Hint: Look for feedback loops leading from progesterone).

30. A male patient with a tumor in the pituitary gland (which is not a reproductive gland, as we know) manifests his disease via low sperm count. Can you explain how this came about?

31. How does a pregnancy test kit work?

32. Devise a male contraceptive pill, knowing what you now do about the male reproductive cycle, keeping in mind that such a pill will not sell if it affects secondary sex characteristics in any way.

33. In recent news, a drug that suppresses GnRH production is rumored to be in development as a contraceptive for both male AND female persons. Explain how it is able to achieve that function. What could be undesirable effects of such a drug?

注意本文集的Study Question都是不定期更新且沒有答案喔~ 本期內(nèi)容如果有具體問題的話就別找UP主啦~ 饒了我吧太頭大了哈~

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