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UB PGY 452 - Endocrinology Previous EXAM Questions

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PGY452/552 Endocrinology previous EXAM questions; Dr. Morales, Spring 2011. 1 These are all my old test questions worth seeing. I have eliminated bad questions, questions that I would not ask again because they don’t reflect current material, and near duplicate questions. The key is at the back, along with the percent correct. The table of abbreviations that will be used on the exam is also in back. Refer to it often, it may help. The first 38 questions came from last year. A word about test taking: Many students do worse on my tests than they otherwise would because of poor test‐taking skills. As you go through the practice exam, please remember • Read the whole question carefully • Read all the answers carefully • If you know the answer, great. If you are not sure, understand that multiple choice tests are about falsification. If you’re stuck, try treating the question as a series of five true‐false questions. • Some questions are hard. Others are pretty easy. Don’t over think because an answer just seems “too easy.” I am not trying to intentionally fool you. • Since I don’t intentionally recycle questions and answers, there are likely to be a couple bad questions or more likely a couple of bad “distracters” (incorrect answers that really could be correct); don’t get cute. Just pick the best answer, and if there is a problem with the test, we’ll figure it out after the analysis comes in. • Some questions might seem obscure and unrelated to material covered in class. These questions always refer to a larger underlying principle that was covered in class. Recognize those principles and apply them to these questions if the answer doesn’t come to you right away. really were covered in class. Instead of assuming that you have forgotten something, look hard for the general principle that is buried in that question 1. Which tissue is the major site for gluconeogenesis? a. Adipose b. Skeletal muscle c. Liver d. Pancreatic α‐cells e. Brain 2. Which hormone binds to a receptor that is autophosphorylated? a. Thyroid hormone b. GLP1 c. IGF1 d. CRH e. Epinephrine 3. Which property is different between neurotransmitters of the central nervous system and hormones from the endocrine system? a. Neurotransmitters from the CNS only influence neurons b. Endocrine hormone signaling is faster than neural signaling c. Neurotransmitters recognize cell surface receptors d. Neurotransmitters are not secreted into the blood e. Hormones come from glands, neurotransmitters from neurons PGY452/552 Endocrinology previous EXAM questions; Dr. Morales, Spring 2011. 2 4. Why are analogs of T4 rather than T3 generally thought to be the most appropriate treatment for hypothyroidism? a. T4 is the only form of thyroid hormone that can be transported into target cells b. The concentration of free T4 is higher than that of T3 c. T4 is not subject to feedback inhibition d. T4 is more potent e. T4 has a slower turnover rate 5. Which property is true of hormones synthesized in the hypothalamus? a. Their levels are higher at night b. They are all releasing hormones c. Their concentration is highest in the anterior pituitary d. They respond to sensory input e. They are subject to feedback control by steroid hormones 6. Many peptide and glycoprotein hormones bind to Gαs‐coupled receptors. Which process is NOT a common mechanism for down regulation of the signal generated by a Gαs‐coupled receptor? a. Hydrolysis of cAMP by phosphodiesterase b. Internalization of the hormone bound receptor c. Down regulation of receptor biosynthesis d. Calcium reuptake into intercellular stores e. Antagonism by Gαi‐coupled signaling 7. To date, 37 common alleles (gene variants) have been discovered that are linked with obesity. The most common are alleles of MCR4, the hy pothalamic receptor for αMSH, which is the primary neurotransmitter secreted from POMC/CART neurons. Why are individuals with these mutations likely to be obese? a. Deficiency in response to GLP1 b. Deficiency in stimulatory signaling to the "decrease energy intake/satiety" pathway c. Deficiency in inhibitory signaling between POMC/CART neurons and NPY/AgRP neurons d. Deficiency in stimulatory signaling to the "increase energy intake/hunger" pathway e. Deficiency in leptin response 8. The half‐life of ACTH is 10 minutes, while the half life of IGF1 is 2 hours. What property accounts for this discrepancy? a. IGF1 is associated with a binding protein b. ACTH is a peptide c. ACTH is subject to negative feedback d. IGF1 is a steroid e. IGF1 is not subject to feedback control PGY452/552 Endocrinology previous EXAM questions; Dr. Morales, Spring 2011. 3 9. Growth hormone has been used as an athletic performance enhancer. However, available evidence suggests that growth hormone does not improve performance in any sport, and abuse can lead to serious medical complications. What would be the effects on hormone levels in an individual who chronically abuses growth hormone? a. Increased leptin levels b. Increased GHRH levels c. Increased insulin levels d. Decreased IGF1 levels e. Decreased epinephrine levels 10. Refer to the Figure 1. Which structure secretes a hormone that directly regulates thirst? a. A b. B c. C d. D e. None of the above 11. Thyroid releasing hormone binds to a Gαq‐coupled receptor. What happens in the targe t cell immediately after TRH binding to its receptor? a. Decreased cytoplasmic calcium con cen tration b. Increased intracellular diacylglycerol c. Receptor autophosphorylation d. Activation of PKA e. Activation of hormone sensitive lipase 12. Which property of thyroid hormone is NOT shared with most steroid hormones? a. Signaling through transcriptional regulation b. Transport through the blood in association with a bin ding protein c. Relatively long serum half lives d. Synthesis from a protein precursor e. Participation of feedback loops with hypothalamic releasing hormones 13. A new class of drug has been developed for patients with type 2 diabetes. They work by inhibiting the DPP4 protease, which normally degrades GLP1, inactivating the hormone. Inhibition of the DPP4 protease increases the half‐life (t½) of GLP1 greatly. Why is this beneficial for many type 2 diabetes patients? a. Increased skeletal muscle insulin sensitivity b. Increased leptin secretion c. Increased insulin secretion d. Increased glucagon


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