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Exam I: Take-Home Short Essay Key
For self-grading: I’ve put the answers to each question in italics. Each question has a point
value assigned to it. I have answered the questions in a very complete form with some
extra information for clarity. Be reasonable in your self-assessment- make sure that you
have addressed EXACTLY what the question is asking, don’t worry that your answers
include all of the information that my answers include. But, do be sure that your responses
answer the questions CORRECTLY and COMPLETELY. You can assign partial credit to
yourself.
Remember, this is to benefit your learning, so the more you pay attention to the grading
and the more honest you are with yourself, the more you will get out of it!
Short Essay
1.
a. List 2 hormones that affect the use of energy by cells (glucose &/or fatty acid
use, ATP production, gluconeogenesis, glycogenolysis, glycogenesis, lipolysis or
fat storage) For each, state the class it belongs to, where it’s produced, two effects
that it has, and what stimulates its release. Briefly describe one disorder
associated with one of these hormones.
Hormone:
Many possibilities here:
in the first row I will list
most of the hormones
that would count. In
the next, I will provide
a specific example and
fill out each of the
columns. If you have
questions, ask!
Growth Hormone
Thyroid Hormone
Cortisol
Epinephrine
Glucagon
Insulin
Class
Where
produced
Two effects
What
stimulates
release
Example:
Cortisol
Steroid
Adrenal cortex,
zona fasciculata
Gluconeogenesis, Low circulating
Lipolysis
cortisol 
CRH 
ACTH
Disorder (Name hormone and describe):
Varies, as long as you did this in your own words, give yourself credit!
b. Now do the same for 2 hormones that affect calcium in blood and/or bone, either
directly or indirectly. Do not describe a disorder for one of these.
Hormone
Class
Where produced
Two effects
Peptide
Parathyroid glands Stimulate calcitriol
activation
Stimulate osteoblasts
What stimulates
release
PTH
Calcitonin
Calcitriol
PTH
Low circulating
Calcium
2. a. Describe one hormone (other than any listed from #1) that is ultimately under
the control of the hypothalamus/adenohypophysis. Name the hormone/factor
from the hypothalamus, the hormone from the adenohypophysis, and the final
hormone and where it comes from (kidney, etc). Describe one effect this final
hormone will have on target cells. How do hormones get from the hypothalamus
to the adenohypophysis?
The possible hormones you could use here: thyroid, growth, cortisol, testosterone,
estrogen, progesterone. Make sure that the hormone you chose here is different from #1!
Here is an example of a complete answer:
Progesterone is under the ultimate control of the hypothalamus/adenohypophysis.
Gonadotropin Releasing Hormone (GnRH) from the hypothalamus causes the release of
Leutenizing Hormone from the adenohypophysis. LH from the adenohypophysis causes
the release of progesterone from the ovaries. Progesterone acts on the uterus and causes it
to prepare for a possible pregnancy.
Releasing hormones from the hypothalamus get to the adenohypophysis via the
hypophyseal portal system.
b. A person with symptoms of hypothyroidism (for example, sluggishness and
intolerance to cold) is found to have abnormally low plasma concentrations of
T4, T3, and TSH. After an injection of TRH the plasma concentrations of all
three hormones increase. Where is the site of the defect leading to the
hypothyroidism?
The hypothalamus; Thyroid Releasing Hormone, like all Releasing Hormones, comes
from the hypothalamus. If an injection of TRH leads to normal production of TSH from
the pituitary and T3, T4 from the thyroid, then the hypothalamus is not sending enough
TRH to those organs.
c. Vera is receiving very large doses of a cortisol-like drug to treat her arthritis.
Theoretically, what should happen to her own production/secretion of cortisol (increase or
decrease)? What hormone should a drug mimick if you wanted to increase Vera’s
production of ACTH?
Since the production of Corticotropin Releasing Hormone from the hypothalamus is
determined by circulating blood cortisol, injections of cortisol should change the
hypothalamus’ output of CRH. Specifically, the hypothalamus produces more CRH when
cortisol levels are low and less CRH when cortisol levels are high. Vera is receiving
injections of cortisol; therefore, her circulating cortisol will be high and the hypothalamus
will produce less CRH.
If the hypothalamus produces less CRH, then her natural production ACTH from the
pituitary would decrease; then, her natural production of cortisol will decrease.
If you want Vera to increase her natural production of AdrenoCorticotropic Hormone
(ACTH), you would give her injections of a drug that mimicks CRH.
3. This example has absolutely no basis in reality. If you know how the hormones
can affect their target cells and which use 2nd messengers, you can predict how any
hormone, fake or real, will act. Hormone X is a hormone in the Who species (you
know, the kind that Horton heard and the Grinch wanted to repress). Hormone
X allows the Whos to sing for extended periods of time. It does so by affecting
metabolism in a number of different ways. One of the specific effects Hormone X
has is in muscle cells of the larynx: it stimulates those cells to increase the number
of enzymes involved in ATP production.
a. Let’s say Hormone X is a peptide hormone. Describe how it will affect a
muscle cell of the larynx, starting with its arrival at the target cell and
ending with the production of more active enzyme (be sure to state why
there’s more active enzyme)
X lands on an external receptor on the cell’s membrane. This binding causes the release
of an associated G-protein within the cell. G-protein moves along the membrane in the
interior cell until it bumps/binds an adenylate cyclase enzyme. This activates adenylate
cyclase, and it converts an ATP to cyclic AMP (cAMP). cAMP then activates kinases
within the cell. The kinases then activate cellular proteins by phosphorylating them.
For example, some proteins that might be activated in this cell are glyolytic enzymes; those
involved in making ATP via glycolysis.
b. Now repeat, only this time pretend Hormone X is a steroid hormone.
X as a steroid would diffuse into the cell and bind a receptor on the interior of the
membrane. Together, the hormone/receptor complex would enter the cell nucleus (or,
perhaps, a mitochondrion), and bind a DNA sequence near a specific gene. This binding
will cause gene activation.
For example, genes that might be activated in this cell would code for glycolytic enzymes,
and cause more to be built.
4. You are an employee for a company who just hired a new manager. On his second day,
he came barging into your office telling you that he’s been going through your records and
watching your performance, and if things don’t shape up dramatically and soon, you’re
outta there. You were completely unaware of any problem and have no idea how to
remedy the situation, so everyday for the next month or so you enter the office of eggshells
wondering if today is the day you will be fired. Oh, and you have no savings or prospects
for jobs and for some reason are ineligible for unemployment compensation. Assuming
that you are a reasonably sensitive person (ie, this actually will affect you),
a. Briefly describe your Autonomic Nervous System response when the boss came
in and barked this information at you. Be sure name the dominating division and
to include 4 specific effects of the dominating division.
This event caused a sympathetic response; specifically, as part of the stress
response, this is called the Alarm Phase.
Sympathetic activity dominates your physiological response. Here are some
examples of what might be happening to you (be sure to have four listed for full
credit!)
-increase heart rate, increase respiration, increase blood pressure, dilate pupils,
increase sweating, decrease digestive activity, shunt blood from digestive organs to
muscle and brain, lipolysis, glycogenolysis
b. Describe your endocrine response starting with the first traumatic event and then
the subsequent long-term response (ie, go through the phases of the stress
response). Be sure to name the dominant hormones of each phase, and the effects
each of the hormones will have.
As you went through the alarm phase, hormones were also being released to get
you into the resistance phase, which marks the long-term response. Some
hormones with some specific effects:
-Epinephrine- all effects described above for sympathetic response; also, works
closely with cortisol and glucagon for glycogenolysis, gluconeogenesis, and lipolysis
-Cortisol- the primary hormone of this phase- glycogenolysis, gluconeogenesis,
lipolysis, proteolysis, increase vascular reactivity, suppress immune function
-Glucagon- glycogenolysis
-Growth Hormone- enhance effects of the above
-ADH- retain water
-Aldosterone- retain Na+ and indirectly, water
*you must have at least Epinephrine, cortisol and Aldosterone for full credit. You
must list at least 2 functions of epinephrine and cortisol for full credit.
c. Why are the maintenance of blood glucose and the mobilization of lipids the
major themes of the long-term response?
To keep all cells fed: with fats; and, to make sure that glucose is always available for
the brain. Making sure most cells have access to fats, mobilizing glucose stores, and
breaking down body proteins to make glucose all help to accomplish this goal.
This response assumes you will be exercising, healing, or fasting and will need
access to stored fuel.
d. Is the long-term endocrine response designed to help you survive this particular
type of crisis? What type/s of crises is it designed to help you survive?
No, the stress response is designed to get you through emergencies that involve
more immediate problems and those that affect your body: running away, running
after something, fighting something or somebody, healing, or fasting because of a
lack of food.
Bonus 1 point: Based on the effects of the hormones involved, why do you think
that overeating and a lack of exercise might actually make this stress response
harmful rather than helpful?
When you experience a stress response, you are mobilizing lots of stored energy
such as glucose and fatty acids. What this means is that you have elevated levels of
glucose and fats in your blood. If you exercise, you can burn these excess fuels off,
but if you don’t exercise, they can remain elevated. If you are also overeating, you
are further elevating blood glucose and fatty acids.
Chronically elevated glucose and fats can greatly increase your risk of developing
chronic diseases such as metabolic syndrome, type 2 diabetes, and heart disease.
Exercise also helps to metabolize the stress hormones and bring them back to
normal; it also causes the release of endorphins and other neurotransmitters that
help to protect brain neurons from harmful changes that neurons make that can
lead to depression.
*any reasonable explanation or approximation of these count; if you have a
question about yours, ask!
5. You’re a reporter at the scene of a disaster. Actually, you’re a really tiny reporter
living inside a biology instructor. The disaster is that one of the instructor’s blood
vessels has just been sliced by a scalpel. You’ve arrived at the scene immediately.
a. List the 3 phases of hemostasis, and state one event which will happen
during EACH phase.
Vascular phase- vascular spasms (smooth muscle surrounding injured vessel
contracts, slowing blood loss); endothelial cells retract, basal lamina is
exposed; damaged endothelial cells release chemicals that promote clotting
and immune response, and will be necessary for coagulation.
Platelet phase- platelets stick to exposed basal lamina; more platelets stick to
the first ones, and so on; stuck platelets secrete their chemicals, which
further support platelet aggregation, vascular spasms and immune response,
and will be necessary for coagulation.
Coagulation Phase- clotting proteins will be activated, leading to the
formation of fibrin. This will form a mesh over the injury, trapping cells
and platelets, and forming a temporary plug.
a. How do the first platelets on the scene get stuck/activated?
They stick to the collagen of the exposed basal lamina
b. Name one factor released by platelets/endothelial cells that will promote the
clotting process.
There are lots, any of these will do: serotonin, ADP, thromboxane A,
clotting factors, platelet-derived growth factor, Ca2+, tissue factor,
endothelins
c. Outline or diagram the biochemical cascade of events that occurs once
Factor X is activated.
Factor X is converted to prothrombinase.
Prothrombinase, an enzyme, then converts the blood protein prothrombin
to thrombin.
Thrombin, an enzyme, then converts the soluble blood protein fibrinogen
to the insoluble fibrin
Fibrin forms a mesh around the injured area, trapping cells and debris, and
temporarily closing off the injury.
d. Briefly describe one thing that will aid in the clean-up or control of a clot.
Lots of answers would work here, including:
-Prostacyclin from intact endothelial cells prevents the clot from moving too
far away from the injury site
-Elevated serotonin inhibits ADP action
-Clot retraction helps localize the clot and make platelets less available for
continued aggregation
-Plasmin is activated shortly after thrombin is formed; plasmin digests the
fibrin mesh
6. Tilly, Ermy, Fanny and Si are donating blood. The following shows the results of their
blood tests. Assume that all Rh- people have received Rh+ blood in the past.
Complete the chart by filling in each of their blood types:
Tilly
Ermy
Fanny
Si
Anti-A
No reaction
Agglutination
No reaction
Agglutination
Anti-B
Agglutination
Agglutination
No reaction
Agglutination
Anti-Rh
No reaction
No reaction
Agglutination
Agglutination
6. From which group member/s can Si receive blood? All
7. To which group member/s can Si give blood? None
8. From which group member/s can Ermy receive blood? Tilly
Type?
BABO+
AB+
9. To which group member/s can Fanny give blood? Si
10. Is anyone in this group unable to receive blood from the others (if so, name/s)?
Tilly, Fanny