Name: _________________
Lab Day: ____________
Lab Time: ___________
Instructions
1. It is a practice exam....
2. Some of these questions may show up again. Then again, maybe not.
Regardless, the topics that show up are those that I consider
important and (along with ALL of the learning objectives) are what
you should study.
BIO 392 Final
Name: ______________________
Short Answer:
1. This question has two parts: A) In what form is most Oxygen transported within the blood? B) Other than carbon
monoxide (which is not a standard component of the internal environment), list three variables of the body’s internal
environment whose change influences the dissociation of oxygen at tissues. For each indicate the direction of its
change that favors dissociation of oxygen at an active tissue.
 Most Oxygen is transported bound to hemoglobin.
 Some variables: 1) DPG level; increased DPG favors oxygen dissociation. 2) Temperature; increased
temperature favors oxygen dissociation. 3) pH; decreased pH favors oxygen dissociation. 4) Decreased
pO2.
2. Two subjects have a tidal volume of 450 ml. One of the patients has emphysema; the other has no discernible
pulmonary disorder. Which of the two will have greater dead space volume? Why?
The patient with emphysema will have a greater dead space volume because of collapsed and merged alveolar
walls. Accordingly for a given volume of air there will be less respiratory exchange surface and a greater
distance that needs to be overcome before gas contacts an exchange surface.
3. My friend Eve’s son was born at 26 weeks gestation. Provide an explanation to her of why her baby needed to be
treated with aerosolized surfactant.
Premies often don’t produce surfactant. Without surfactant the compliance of the lungs is relatively low.
Without surfactant ventilation would be difficult for an adult, for a pre-mature infant, it could be impossible,
at least continued ventilation could be impossible without surfactant.
4. Define Cardiac Output
Cardiac output is the amount of blood pumped from a ventricle per minute. Accordingly it can be calculated
as stroke volume times heart rate.
5. What are the two primary variables that contribute to mean arterial pressure?
Cardiac Output and Total Peripheral Resistance.
6. List and define the three processes of urine formation.



Glomerular filtration: the formation of ultrafiltrate by the filtering of fluid out the glomerular blood
(across the glomerular capillaries) and into bowman’s space.
Reabsorption: The transport of substances from the nephron tubules into the interstitial fluid and blood
stream.
Secretion: The transport of substances from the blood/interstitial fluid into the nephron’s tubules
7. Briefly, list and explain two reasons that dehydration would decrease glomerular filtration rate.
a) lower BP period means slower flow into tissue
b) lower BP will cause peripheral vasoconstriction (to increase MAP; via carotid baroreceptors), In so doing,
vasoconstriction will further reduce blood flow to the glomeruli and thus decrease filtration
c) increased viscosity will increase resistance to flow
d) increased osmolarity of the plasma will reduce the net filtration pressure
8. Explain, in terms of the Frank-Starling mechanism what is wrong with the following statement, and provide the
correct version. “Exercise, such as running will increase the venous return of blood to the heart, which will decrease
stroke volume according to the Frank-Starling mechanism.”
The “decrease” is the problem. Everything else is true. With increased venous return, ventricular myocytes
will be stretched more than they would be under resting conditions. The additional stretch will bring them
closer to their optimal length increasing the force and extent of their contraction.
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BIO 392 Final
Name: ______________________
Multiple Choice
1. Of the following, which statement is most true concerning countercurrent exchange in the loop of Henle?
a. Sodium pumped out of the descending limb causes loss of water from fluid in the ascending limb via
osmosis
b. Sodium pumped out of the descending limb causes gain of water in fluid of the ascending limb via
osmosis
c. Sodium pumped out of the ascending limb causes loss of water from fluid in the descending limb via
osmosis
d. Sodium pumped out of the ascending limb causes gain of water in fluid of the descending limb via
osmosis
2. Which area actually secretes renin into the blood?
a. macula densa
loop of henle
b. juxtaglomerular cells cortical nephron
3. Renin acts on _____ to convert it to angiotensin I.
a. angiotensin II
angiotensinogen
b. ACE
aldosterone
4. The targets of angiotensin II are blood vessels and _____.
a. nerves
adrenal cortex
b. adrenal medulla
kidney nephron
5. Most (about 70% of) tubular reabsorption occurs at the _____.
a. loop of Henle
distal convoluted tubule
b. proximal convoluted tubule
glomerulus
6. The action of aldosterone is to increase _____.
a. sodium elimination
sodium reabsorption
b. potassium reabsorption
chloride excretion
7. Where does ADH have its greatest effect?
a. loop of Henle
proximal convoluted tubule
b. distal convoluted tubule
glomerulus
c. HEY THIS WASN’T HERE BEFORE: THE BEST ANSWER WOULD BE COLLECTING DUCT
8. As a result of severe sweating (loss of hyposmotic fluid from the body) which of the following will occur?
a. Only plasma ADH levels will rise
b. Only Plasma aldosterone levels will rise
c. Plasma ADH and aldosterone levels will rise
d. Plasma ADH levels will rise and plasma aldosterone levels will fall
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BIO 392 Final
Name: ______________________
Essay:
1. Explain the mechanisms of lung expansion (inspiration) and expiration. In these terms explain why puncturing the
chest wall abolishes one’s ability to expand a lung (a condition termed pneumothorax).
 To inspire, the diaphragm contracts, external intercostals elevate and expand rib cage;
 These actions make the pressure on the intrapleural fluid more negative than between breaths and more
negative than the combination of the combination of alveolar elastic recoil and alveolar air pressure.
 As a result, the alveoli expand. According to Boyle’s law, this expansion will decrease the pressure on the
gas contained in the alveoli. When the alveolar pressure falls below atmospheric, an inflow of air results.
 Expiration results when the rib cage lowers and the diaphragm relaxes compressing the thoracic cavity,
and putting positive pressure on the intrapleural fluid and thus on the alveolar gas.
 As soon as the pressure on the alveolar gas exceeds atmospheric pressure, gas is expelled from the lungs.

Puncturing the thoracic wall prevents the eliminates the pressure differential between the intrapleural fluid
and the atmosphere. Attempts to inhale suck gas into the thoracic cavity, rather than into the lung. The
loss of negative pressure in the intrapleural fluid allows the lung to collapse.
2. What renal processes will act to conserve water when one is dehydrated? (what happens to GFR? why? what
happens to the permeability of the collecting ducts to water? Why?, What happens to the reabsorption of Na+? Why?
How?, In what manner does the reabsorption of Na+ affect the retention/loss of water, etc.)
In part, see answer to # 7.
Also, increased sympathetic nerve activity will decrease GFR (via vasoconstriction) and trigger the release of
rennin.
AND:
1. Decreased renal BP AND decreased Na flowing past the macula densa trigger the release of Renin from JG
cells.
2. Renin converts circulating agiotensinogen to angiotensin I;
3. At the lungs Angiotensin I is converted to Angiotensin II by Angiotensin converting enzyme (ACE)
4. Angiotensin II acts as a vasoconstrictor (not needed) and stimulates the secretion of aldosterone from the
adrenal cortex
5. aldosterone stimulates the reabsorption of Na from the distal convoluted tubule;
6. Of course, increased Na reabsorption is osmotically linked to water reabsorption so you will conserve water
too.
AND:
Dehydration will osmoticallly draw water out of hypothalamic neurons causing them to shrink. This triggers
them to generate action potentials that travel to their terminals in the posterior pituitary where they evoke
exocytosis of ADH (Vasopressin). ADH, at the collecting ducts increases water permeability, which allows
more water to be osmotically reabsorbed from the forming urine as it drains from the cortical portion of the
collecting duct to the renal medulla.
3. Compare and contrast excitation contraction coupling in cardiomyocytes with that in skeletal muscle.
Both: action potential kicks things off. However, source is different. In cardiomyocytes it arrives via gap
junctions, and in skeletal muscle it is evoked at the neuromuscular junction.
Both: AP travels down t- tubules. Skeletal AP evokes Ca release via DHP / RYanodine; Cardiac instead evokes
an influx of Ca++ from the ECF that evokes Ca release from the SR. Both: Ca++ binds troponin, which shifts
tropomyosin off of the myosin binding sites on actin. For both: once binding sites are revealed, energized
myosin head (with ADP & Pi) binds to actin  undergoes power stroke, thus pulling z-line toward
center of sarcomere  ADP & Pi are released  ATP binds to head causing its release  hydrolysis
of ATP energizes myosin head (conformational change); ADP & Pi remain bound, and cycle may
repeat.
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BIO 392 Final
Name: ______________________
4. A suspect is running from police. Does MAP change tremendously? Explain in terms of cardiac output and TPR, as
well as the factors that go into these variables. The police shoot the suspect, rupture her brachial artery and she begins
to hemorrhage. As her blood volume drops, her MAP begins to fall. Outline the responses
MAP shouldn’t change dramatically. As a homeostatically controlled variable the notion is that it is kept
relatively constant. Large deviations can be damaging.
Why not? Well, if MAP is the result of CO times TPR, and we know that CO is going up, then TPR must be
dropping (and it does). Why does TPR go down? sympathetic activity causing vasoconstriction to most tissues
(other than those needed in the most acute sense).
Why does CO go up? sympathetic nerve activity and related endocrine activity to the heart increasing SV and
HR. Additionally, increased venous return causing increased SV (see # 8 above in the short answers). Much of
remainder of SV increase: due to beta adrenergic receptor activation on ventricular myocytes  prolonged Ca
elevation, altered affinity of troponin for Ca, decreased Ca ATPase activity. HR increase: decreased
parasympathetic activity (decreased muscarinic ACh receptor activation) increases HR by about 33 % and
increased circulating epinephrine increases it even more by activating beta adrenergic receptors. The
combination of decreased muscarinic activation and increased beta-adrenergic activation combine to increase
the influx of sodium via the funny current (IH) and to increase the influx of Ca through t-type Ca+ channels.
The net effect is that the slope of the SA node pacemaker potential increases and these cells fire at a higher
frequency.
Hemorrhage: blood loss  decreased blood volume  decreased MAP  arterial baroreceptors  CNS 
increase sympathetic outflow and increase release of epinephrine from adrenal medulla  increase HR, SV,
TPR  = attempt to restore, or at least preserve some of, MAP
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