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BBIO 351: Principles of Anatomy & Physiology I
Exam 1 (intro/endo)
Winter 2016
Name: ____Dr. C___________
You will have 2 hours for this exam unless prior arrangements have been made with DRS. You
may use a pre-prepared double-sided 4-inch by 6-inch notecard or piece of paper. If you want
clarification of a question, please ask. Good luck!
Point values were as follows: your name, 1 point; multiple-choice questions, 3 points
apiece; #6A (the 2nd #6, concerning the adrenal gland), 8 points; #7, 4 points; #8, 4 points;
#13, 6 points; all other short-answer questions, 5 points apiece. These add up to a total of
104 possible points. Everyone got credit for #5, which was a bad question, and for #9f,
which was just silly.
1. Based on everything you’ve learned about thyroid hormones (T3 and T4), do you think their
receptors are on the cell surface, inside the cell, both, or neither? Explain your reasoning.
Receptors for thyroid hormone are intracellular. If they were on the cell surface, transporters
across the cell membrane would not be needed, yet mutation of a transporter like MCT8 clearly
causes problems for the animal. (Other answers are possible. 1 point was deducted if you
correctly discussed the hydrophobicity of the thyroid hormones but didn’t discuss the
transporters.)
2. Imagine that a protein called MBATF might be a transcription factor for gene DAG. Briefly
describe a test or experiment by which you could determine whether MBATF really is a
transcription factor for this gene.
Many answers are possible here. For example:
 You could compare the rate of transcription of gene DAG in the absence and presence of
MBATF. If MBATF changes this rate (as determined by the amount/levels of mRNA
produced), there is a good chance it is a transcription factor.
 You could see how well RNA polymerase binds to the DAG gene in the absence and
presence of MBATF. If MBATF changes RNA polymerase’s binding strength, it is
probably a transcription factor.
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BBIO 351: Principles of Anatomy & Physiology I
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3. A sweat gland is shown in the figure at right
(from naturallyhealthyskin.org). Is this an endocrine
gland? Explain why you think it is or isn’t an
endocrine gland, OR why you can’t decide and what
further information you would need.
By definition, endocrine glands release hormones
into the blood. Sweat glands do not produce
hormones and do not release their products into the
blood, so they are exocrine glands, not endocrine
glands. It’s OK if you did not know this but
explained the criteria that must be met for something
to qualify as an endocrine gland.
4. The image at right is a piece of a previously
studied figure (from J. Bernal et al., Nature
Reviews Endocrinology 11: 406-417, 2015)
showing the effects of MCT8 mutations on various
tissues, including Brown Adipose Tissue (BAT).
Predict the effects, if any, of MCT8 mutations on
BAT. (Would the BAT be altered? If so, how?)
BAT normally increases its concentration of
uncoupling proteins (UCPs) in response to thyroid
hormone.
 The mutation in MCT8 might reduce the
amount of T3 and T4 that can get into BAT,
thus reducing UCP production and reducing
BAT’s ability to generate heat.
 Alternatively, as long as T4 is able to enter
BAT cells (perhaps via a different
transporter), BAT can convert T4 to T3 with
its deiodinase (DIO2) and thus get the usual
effects of T3, i.e., heat production.
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BBIO 351: Principles of Anatomy & Physiology I
Winter 2016
5. Our body has deiodinases like
those included in the figure above.
Among the four processes pictured
in the figure at right, deiodinases
DIO1, DIO2, and DIO3 collectively
contribute most directly to
a. Activation and binding
b. Activation and inactivation
c. Binding and Inactivation
d. Secretion and activation
e. Secretion and binding
BAD QUESTION. Ignore!
6. The left figure below (from Edith C. Friesema et al., Lancet 2004) shows the structure of the
MCT8 gene, which has 6 exons (labeled I through VI). Imagine that you were able to study a
large population of people with point mutations (not large deletions) in each of the exons, and
that you collected the data shown on the right. How would you interpret these data?


What you already knew: The patients described in the paper have elevated levels of T3 in
their blood because the MCT8 mutations impair transport of T3 into cells.
New information: You now can see from the graph that point mutations in any of the
exons, except VI, lead to similarly high levels of T3. Patients with point mutations in VI
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have much lower T3 levels, suggesting that T3 uptake is not as impaired in these patients.
Therefore, exon VI may code for a region of the protein that is less critical to T3
transport, or that tolerates amino acid variations better than the regions corresponding to
the other exons.
6A. A patient has above-normal levels of CRH, above-normal levels of ACTH, and belownormal levels of cortisol.
a. What is the clinical name for this disorder? Addison’s disease. (Other terms are also possible,
e.g., adrenal insufficiency, hypocortisolism, hypoadrenalism.)
b. Where in the hypothalamic-pituitary-adrenal axis is the primary defect? The adrenal cortex
itself.
c. List 2 symptoms this person is likely to have. Low blood pressure, immune system
hypersensitivity (e.g., autoimmune attacks), weight loss, poor response to stressors.
7. To what extent do you agree with the following statement? “Beta-adrenergic receptors on
skeletal muscle cells allow vasodilation so that these muscles can get the blood they need during
exercise.” Explain.
The beta-adrenergic receptors are on the SMOOTH muscle cells in the walls of the arterioles that
bring blood to the skeletal muscles. The statement is fine otherwise. Some of you also correctly
pointed out that these receptors are beta-2 receptors, not beta-1 receptors.
8. Consider this scenario: a biology student fasts overnight, then wakes up at time “0,” then eats
lunch 3 hours later (time = 3 hours). Fill in the graph below.
Basically, rate should be high during fasting, then go low after the meal, then start to creep up
again later.
9. Which of the following statements are true of G proteins? Check ALL that are true!
__NO__ They directly bind extracellular signals (“1st messengers”).
__YES_ They often consist of three (3) subunits that split apart upon activation.
__YES_ They are physically linked to GPCRs.
__YES_ They bind guanine nucleotides (GDP and GTP).
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__YES_ They can cause changes in levels of cyclic nucleotides like cAMP by activating
enzymes like adenylate cyclase or phosphodiesterase.
__*___ They are the signal-transduction proteins responsible for laughter (G stands for
“Giggle”).
*Laughter is a complex process. G proteins are certainly involved in many of the neurons,
endocrine cells, and muscle cells that control it. This line was not graded.
10. In the context of negative feedback control of temperature regulation, an “error signal” is
a. the discrepancy between the “cold” receptors and the “hot” receptors
b. the discrepancy between the integrator (hypothalamus) and the effectors (e.g., sweat glands)
c. the discrepancy between normal body temperature and current body temperature – YES
d. the incorrect information provided by some temperature receptors
e. the time lag between sensing that you are cold and launching an effector response to that
11. Neuroendocrine cells are found in the
a. Adrenal cortex
b. Adrenal medulla
c. Posterior pituitary
d. Thyroid gland
e. Both B and C – YES
12. Hypophysis is another word for
a. adrenal gland b. hypothalamus
c. hypothesis
d. pituitary gland-YES
e. thyroid gland
13. For the figure below, clearly list (A) all components that are enzymes and (B) all components
that are protein kinases.
A. Enzymes: glycogen phosphorylase, glycogen synthase, phosphorylase kinase, protein kinase.
1 point off per item that should be there but isn’t, or that is there but shouldn’t be, up to a max of
4 points off.
B. Protein kinases: phosphorylase kinase, protein kinase A; no points off if glycogen
phosphorylase was listed because it is a kinase, but not a protein kinase. 1 point off per item that
should be there but isn’t, or that is there but shouldn’t be, up to a max of 2 points off.
If you got everything right except for not listing the two protein kinases as also being enzymes,
only 1 point was deducted.
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BBIO 351: Principles of Anatomy & Physiology I
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14. A normal, healthy 75-kilogram person has a basal metabolic rate (BMR) of 300 mL O2
consumed per minute. Jo, who weighs 50 kilograms, has a BMR of 200 mL O2 consumed per
minute. These data are consistent with Jo being
a. hyperthyroid
b. hypothyroid
c. iodine-deficient
d. normal – YES
e. chronically overheated
15. The figure at right (from
krauthammerlab.med.yale.edu)
shows 2 pathways that produce
which kind(s) of signaling
molecule?
a. Amino acid derivative – YES
b. Eicosanoid
c. Polypeptide
d. Steroid
e. both A and D
16. The elbow is _____ to the fingers but _____ to the shoulder.
a. Anterior; posterior
b. Caudal; cranial
c. Proximal; distal – YES
d. Superficial; deep
e. Ventral; dorsal
17. Thyroid hormones T3 and T4 have the following effect on Na/K pump expression:
a. T3 and T4 decrease the density of Na/K pumps, decreasing ATP use by the cells
b. T3 and T4 decrease the density of Na/K pumps, increasing ATP use by the cells
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c. T3 and T4 increase the density of Na/K pumps, decreasing ATP use by the cells
d. T3 and T4 increase the density of Na/K pumps, increasing ATP use by the cells – YES
18. Let’s say that you want to develop a drug for eventual use in humans to disrupt a process like
that shown below (Sherwood Figure 3-21). What would be an advantage of designing the drug
to block the function of the cell-surface receptor? What would be an advantage of designing the
drug to disrupt the function of the “phosphorylated (activated) protein” farther downstream?
Multiple answers were possible, but here were the most common ones:
 Advantage of blocking cell-surface receptor: by inhibiting the “top” of the cascade, you
can potentially prevent all of the amplification steps with a relatively small concentration
of the drug. So your drug might be especially potent in this case.
 Advantage of blocking the downstream protein: you can inhibit the specific cellular
process that you want to interrupt, rather than simultaneously perturbing many cAMPdependent processes. So your drug might have fewer side effects in this case.
19. Which organ/tissue is NOT fed by arterioles with large numbers of beta-adrenergic
receptors?
a. Heart
b. Intestines – YES
c. Skeletal muscles
d. Skin
e. none of these
20. In response to insulin secretion, GLUT4
a. Migrates to the cell interior in brain cells
b. Migrates to the cell membrane in skeletal muscle cells – YES
c. Migrates to the Golgi apparatus in the adrenal medulla
d. Migrates to lysosomes in the thyroid gland
e. Migrates to South America in the fall.
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21. Thyroglobulin (Tg)’s functions in the thyroid gland include
a. Binding to thyroid hormones in the blood
b. Binding to TSH from the anterior pituitary
c. Carrying thyroid hormones from the colloid back into follicular cells – YES
d. Catalyzing the oxidation of iodide ions
e. Transporting iodide into follicular cells
22. Cortisol and epinephrine are similar in all of the following ways EXCEPT
a. Both are “stress hormones”
b. Both are produced by the adrenal cortex – YES
c. Both have the effect of raising blood glucose
d. Both are non-polypeptide hormones
e. All of the above are similarities.
23. Which of the following produce tropic hormones such as releasing hormones (as defined in
class and in the textbook, whether or not “releasing hormone” is part of the hormone’s name)?
a. hypothalamus
b. pituitary
c. both the hypothalamus and the pituitary – YES
d. neither the hypothalamus nor the pituitary
24. The physical abnormality of the person at right
(picture: longislandentdoctors.com) could, in principle,
be caused by any of the following except
a. chronically elevated TSH levels
b. excessive iodine intake – YES
c. thyroid gland tumor
d. thyroid-stimulating immunoglobulin (TSI)
e. ANY of the above could cause this problem.
25. Explain how problems with the immune system could lead either to hyperthyroidism or to
hypothyroidism.
 Hyperthyroidism could result from production of Thyroid-Stimulating Immunoglobulin
(TSI), which binds to TSH receptors and stimulates overproduction of thyroid hormone.
Alternatively, immune attacks on the thyroid could cause the thyroid to be inflamed and
“leaky,” so that more thyroid hormone than usual leaks into the blood.
 Hypothyroidism: In Hashimoto’s disease, the thyroid gland is attacked and destroyed by
the immune system, reducing production of thyroid hormone.
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