ENDOCRINOLOGYPotential Final Exam Questions

The final exam will be held on Friday, April 30 at 10:15 a.m. in LSE 204. It will consist of 6 or 7 of the questions listed below, with at least one chosen from each topic. I will also include questions about student seminars. Not all of these have been received or edited; further information will follow. I will be on campus all week prior to the exam, though not always in my office. Feel free to contact me with specific questions or concerns. Good luck on your other final exams!!

PARTURITION

  1. Interestingly, CRH plays an important role in parturition. Describe its site of

synthesis during pregnancy; its effects on the mother and fetus as gestation proceeds; and its receptors (and their regulation) important to parturition. Where is CRH more commonly found in non-pregnant adults?

  1. Describe the oxytocin positive feedback mechanism important to parturition. Through what second messenger system does it induce uterine contraction?

ADRENAL GLAND/ADRENAL MEDULLA

3. The adrenal gland is engineered such that the products of the zona fasciculata influence the adrenal medulla. Why is it advantageous for glucocorticoids to induce PNMT activity in the adrenal medulla?

  1. Describe the synthesis of catecholamines in the adrenal medulla.
  1. Compare and contrast a1, a2 and b catecholamine receptors with respect to their structure and second messenger system(s). What is the overall physiological result of activation of the sympathoadrenal system?

ADRENAL CORTEX AND STEROIDS

  1. What actions are stimulated in renal collecting duct epithelia by aldosterone? Where is its receptor with respect to these cells? What is the outcome in the body when aldosterone is present?
  1. What is renin? Where is it synthesized? What is its function? How is it regulated?

GROWTH

  1. Describe the interrelationship of growth hormone and insulin-like growth factors (IGFs) in cell growth, using bone as an example.
  1. Describe the GH receptor.
  1. When Dr. Houle from UAMS lectured on his work on spinal cord regeneration, I asked him about nerve growth factor (NGF). His colleagues have attempted to use NGF in spinal cord injured mice, and found that they became very aggressive when treated with NGF. These researchers surmised that the NGF caused an increase in pain sensation in these animals. How might that happen? Might there by another (endocrinological) reason for this aggression in these mice?

ENDOCRINE PANCREAS

  1. How does insulin release lead to lowered blood glucose levels? (Be complete.)
  1. Describe the insulin receptor and how it functions.
  1. What is the role of glucagon? That is, when is it released? What are its target organs/tissues? What does it do at its target organs/tissues to accomplish its role?
  1. Why are diabetics at higher risk for arteriosclerosis (so “heart attack” and stroke)? For blindness? For kidney dysfunction?