A&P II
Case Study
Max’s Maximum: A Case Study on the Urinary System
1. What does the color of Max’s urine tell Tracey about how concentrated or dilute it is?
How does Max’s urine color/concentration compare to the urine specific gravity at the
same time?
Answer: According to Marieb & Hoehn (2019) “When we are over hydrated, ADH
production decreases…If aldosterone is present the DCT and colleting ducts cells can
remove Na+ and selected other ions from the filtrate, making the urine that enters the
renal pelvis more dilute” (p.998).
Before exercise his urine is pale yellow i.e., he is overly hydrated.
On the other hand Max’s urine is dark yellow after exercise contrary to the
aforementioned, Max is not keeping well-hydrated during exercise. This is due to
according to Marieb & Hoehn (2019) “When we are dehydrated, the posterior pituitary
releases large amounts of ADH in the solute concentration of urine may rise.... with
maximal ADH secretion, up to 99% of water in the filtrate is reabsorbed and return to
the blood, and only half a liter per day of highly concentrated urine is excreted” (p.998).
Max’s urine color correlates with specific gravity. Marieb & Hoehn (2019) state “The
ratio of the mass of a substance to the mass of an equal volume of distilled water is it
specific gravity. Because urine is water plus solute, a given volume has a greater mass
than the same volume of distilled water” (p. 1002). This means that when urine is darker
it has more solutes thus specific gravity will rise.
2. Based on the urine color and specific gravity, what might Tracey conclude about the
hydration status of Max’s body at the three different times?
Answer: Before exercise max is overly hydrated. Immediately after exercise max is
dehydrated and 6 hours after exercise max is well-hydrated.
3. Antidiuretic hormone (ADH) regulates the formation of concentrated or dilute urine.
In which time period is Max’s body secreting its highest amount of ADH? Explain your
answer.
Answer: Max’s rigorous 2 hour run is when ADH would be at the highest because when
we run we start to sweat/lose water. While running you are not replacing water, ADH
will tell the body to hold onto as much water as possible in order to survive.
4. Tracey knows that proteinuria (protein in the urine) after intense exercise is
physiological (normal). However, protein is typically not present in urine. Why is that?
Answer: Marieb & Hoehn (2019) state “The filtration membrane is a porous membrane
that allows free passage of water and solutes smaller than plasma proteins” (p984).
Essentially, proteins are just too big for the glomerulus to filter.
5. Tracey had been slightly concerned about the trace glucose that was found in Max’s
urine six hours after his exercise until she discovered that he had eaten an entire large
pizza an hour before the urinalysis. Explain why glucose might show up in Max’s urine
after a particularly heavy meal.
Answer: According to Marieb & Hoehn (2019) The PCT is responsible for the
reabsorption of glucose in the body (p.992). If glucose showed up in Max’s urine this
would mean that the glucose in the pizza was not all absorbed, whatever glucose that
did not get reabsorbed was pee’d out.
6.Lactic acid accumulation can be a consequence of intense exercise. Tracey notes that
Max’s kidneys are working to defend his body against acidosis. How can she tell?
Describe this mechanism.
Answer: She can tell in three ways. First his urine goes from dark yellow to yellow after
6 hours after exercise along with a decrease in specific gravity. Finally you can see Max’s
pH begins to rise thereafter from 4.5 to 5.0. The body is attempting to reach
homeostasis.
7. Based on Max’s urinalysis data, should he drink more water prior to exercise to ensure
that he doesn’t dehydrate during intense activity? Explain your answer.
Answer: Before exercise max’s urine color is pale yellow which tells me he is wellenough hydrated. Max needs to drink water during his exercises as his urine is dark
yellow immediately after.
8. Max’s regular exercise regimen has reduced his high blood pressure, allowing him to
achieve normal blood pressure on a single antihypertensive medication. The medication
he takes is called an angiotensin converting enzyme inhibitor, or ACE inhibitor, which
blocks the activation of angiotensin II. Describe at least two mechanisms by which
angiotensin II targets the kidneys to increase extracellular fluid volume and, therefore,
increase blood pressure.
Answer: According to Marieb & Hoehn (2019) Figure 25.14 explains the effect of
aldosterone on the kidney in order to raise blood pressure, “Angiotensin II can trigger
vasoconstriction of the systemic arterioles which increase peripheral resistance and thus
increases BP. Angiotensin II tells the adrenal cortex to release Na+, Na+ is reabsorbed by
the kidney tubules, which water follows this increase BV and BP (p.988).”
Grandma’s Tum-my Trouble Case Study
Part 1- At The Hospital
1. Are any of the lab values in Table 1 out of normal range? Do you see some that are
too high or too low?
Answer:The following lab values are elevated per table 2 Normal Laboratory Values:
Serum Creatine, BUN, Serum Calcium, Potassium, Bicarb , pH. The following lab value
are below the norm: Serum Sodium, Serum Potassium & Urinary Potassium.
2.Which of the lab values gives you information about how Mrs. Burroughs’ kidneys are
functioning?
Answer: According to Silvestri, L. A. (2017) “Creatine is a specific indicator of renal
function. Increase levels of creatine indicates a slowing of the glomerular filtration rate”
(p.118).
According to Silvestri, L. A. (2017) “Urea nitrogen is the nitrogen portion of urea, a
substance formed in the liver through an enzymatic protein breakdown process. Urea is
normally freely filtered through the renal glomeruli, with a small amount reabsorbed in
the tubules and the remainder excreted in the urine. Elevated levels indicate a slowing
of the glomerular filtration rate. (p.118).
3.Does Mrs. Burroughs have acidosis or alkalosis? Why do you think this?
Answer:Mrs. Burrough pH level is 7.67 indicates that she is alkalotic.
4.Why is the physician interested in Mrs. Burroughs’ kidney function?
Answer:The physician is interested in Mrs. Burrough kidney function because we have
learned in chapter 25 that the kidneys are involved in acid base balance in the body.
Mrs. Burrough’s lab values of creatine and BUN are elevated indicating some sort of
renal dysfunction at this time.
5.What else do you think you will need to know about Mrs. Burroughs? How could you
get this information?
Answer:If I was this patient’s nurse I would be asking the following things:
a.
b.
c.
d.
e.
f.
What mediations are you currently taking, OTC as well?
Current sign and symptoms?
Current medical diagnosis
History of surgical intervention
How long have had symptoms?
Drug and alcohol history?
Part II
1.Should you and the family be concerned about anything that Mrs. Burroughs takes
that is not a prescription medicine? Why or why not?
Answer: Yes, because OTC medication as we know can have harmful side
effects/interactions. In this case we have a patient taking an a very high amount of
calcium into her body between the Tums and Milk.
2.Could any of Mrs. Burroughs’ current problems be related to the drugs (over-thecounter or prescription) she has been taking? Describe why you think there is a
relationship.
Answer: Yes, Mrs. Burrough is taking Tums Ultra 1000mg (CaCO3) and Alka-Seltzer
(NaHCO3). Both of these medications are carbonate compounds, meaning that this
patient has a high amount of bi-carb in her system. The patient appears to be going
through metabolic alkalosis which would possibly explain her vomiting episode.
Patient is taking HCTZ which could explain her low potassium level. According to
Marieb & Hoehn (2019) “selected diuretic cause K+ depletion and H2o loss. Low K+
directly stimulates tubule cells to secrete H+” (p.1033).
3.What is parathyroid hormone (PTH)? Where does it come from and what is its
function?
Answer: The hormone comes from the parathyroid gland. The parathyroid hormone
according to Marieb & Hoehn (2019) “…is the single most important hormone
controlling calcium balance in the blood…falling blood Ca2+ levels triggers PTH
release.
4.Why do you think the physician wants to know about the levels of this hormone?
Answer: The patient Ca2+ levels are elevated and the physician is probably trying to
figure out if it due to this particular hormone or possibly something else.
5. What are the normal level for PTH
Answer: PTH “normal values are 10-55 pg/mL” (UCLA Health, 2020).
Part III.
1. What enzyme catalyzes the formation of H2CO3 from CO2 and H2O? (This
enzyme also catalyzes the formation of H2O and CO2 from H2CO3.)
Answer: Carbonic anhydrase
2. The diagram above (Figure 1) outlines the mechanism by which H+ is actively
secreted into the PCT of the kidney nephron. What other substances must be
transported from the tubular fluid into the PCT cell (across the apical or luminal
membrane) or from the PCT cell into the interstitial fluid (across the basolateral
membrane) as part of the transport of the H+ ?
Answer: According to Marieb & Hoehn (2019):
1. At the basolateral membrane Na+ is pumped into the interstitial space bvy the
Na+ -K ATPase. Active Na+ transport creates concentration gradient that drives:
2. “Downhill” Na+ entry at the apical membrane
3. Reabsorption of organic nutrients and certain ions by cotransports the apical
membrane.
4. Reabsorption of water by osmosis through aquaporins. Water reabsorption
increases the concentration...These solutes can then be reabsorbed as they move
down their gradients:
5. Lipid soluble substances diffuse by the transcellular route.
6. Various ions (e.g., CL-, Ca2+, K+) and urea diffuse by paracellular route (p.991).
3 What would happen to the amount of H+ secreted into the renal tubule if the
activity of the Na+/K+ ATPase were increased? Are there diseases or other conditions
that might enhance the activity of this sodium pump
Answer: If the Na+/K+ ATPase were increased it would be logical (knowing how this
mechanism works) that you would have an increase amount of H+ secreted into the
renal tube.
According to Marieb & Hoehn (2019) A condition that would cause the increase of
the the Na+/K+ ATPase would be low blood pressure or low blood volume (p.994).
Part IV
1. Is there a problem with Mrs. Burroughs’ breathing? What kind of change (if any)
do you expect to see in the respirations of a person with metabolic alkalosis?
Answer: There no problems presents with Mrs. Burroughs’ breathing. What I
would expect to see According to Marieb & Hoehn (2019) “…involves slow
shallow breathing, which allow CO2 to accumulate in the blood” (p.1035).
2. Can you draw a diagram that shows how the respiratory system, under the
control of the central nervous system, responds to alkalosis?
Graph information was sourced from Marieb & Hoehn (2019) (p. 1034-1035).
Blood Sample
pH > 7.45
Alkalosis
HCO3 >26 mEq/L
Pco2 <35 mm Hg
Metabolic Alkalosis
Respiratory Alkalosis
Respiratory
Compensation (hypo
ventilation to allows CO2
to accumulate in the
blood)
Renal Compensation
(Kidneys eliminate more
HCO3-)
3. Why do you think the physician suspected PTH levels that are too low?
Answer: Possibly because the calcium levels were high. I also suspect because
PTH would be triggered if calcium levels were low but in this scenario the patient
was taking an overabundance of calcium.
Answer: According to Marieb & Hoehn (2019) “diuretic cause K+ depletion and
H2o loss. Low K+ directly stimulates tubule cells to secrete H+. Reduced blood
volume elicts the renin-angiotensin-aldosterone mechanism, which stimulate
Na+ reabsorption and H+ secretion” (p.1033).
4. Describe how the thiazide diuretics (like the hydrochlorothiazide that Mrs.
Burroughs takes) can produce or contribute to alkalosis and hypercalcemia.
Answer: Thiazide diuretics can contribute to hypercalcemia. According to
Griebeler, M. L., Kearns, (2016) “Hypercalcemia associated with thiazide use is a
well-known clinical entity. Thiazides exert their antihypertensive effect through
an increase in sodium excretion by blocking the thiazide-sensitive NaCl
transporter in the distal convoluted tubule, which is closely linked to calcium
transport. Thiazides have several metabolic effects contributing to higher serum
calcium levels, but increased renal tubular reabsorption of calcium resulting in
reduced urine calcium excretion is the most likely cause” (p.1166–1173).
Answer: It contributes to alkalosis because when you take HCTZ it contributes to
potassium loss. Low levels of potassium tell the tubule cells to secrete more
hydrogen which then tilts the blood to become more basic (Marieb & Hoehn,
2019, p.1033).
Bibliography
1. Marieb, E., & Hoehn, K. (2019). Human Anatomy and Physiology (11th ed.).
Hoboken, NJ: Pearson Education Inc.
2. Silvestri, L. A. (2017). Saunders Comprehensive Review for the NCLEX-RX
Examination (7th ed.). St. Louis: Elseiver.
3. UCLA Endocrine Center (n.d.). In UCLA Health. Retrieved November 15, 2020,
from https://www.uclahealth.org/endocrine-center/parathyroid-hormone-pthtest
4. Griebeler, M. L., Kearns, A. E., Ryu, E., Thapa, P., Hathcock, M. A., Melton, L. J.,
3rd, & Wermers, R. A. (2016). Thiazide-Associated Hypercalcemia: Incidence and
Association With Primary Hyperparathyroidism Over Two Decades. The Journal
of clinical endocrinology and metabolism, 101(3), 1166–1173.
https://doi.org/10.1210/jc.2015-3964