Urinary System

Q1: Describe the mechanisms for regulating renal blood flow.

The two feedback mechanisms involved in regulating the renal blood flow are the intrinsic and
extrinsic regulatory mechanisms. Intrinsic mechanism directly regulate the glomerular filtration rate
despite moderate changes in the blood pressure (between 80 to 180 mmHg mean arterial pressure)
while extrinsic mechanism indirectly regulate the glomerular filtration rate by maintaining systemic
blood pressure which drives filtration in the kidneys (Biga et al, 2018).
Intrinsic mechanisms (a.k.a the autoregulation mechanism), have two mechanisms involved and
these are the myogenic mechanism and the tubuloglomerular mechanism. In the myogenic
mechanism, if there is an increase in the mean arterial pressure increases, there will also be an
increase in the renal blood flow which causes the stretching of the arterial walls causing
vasoconstriction of the afferent arterioles. While in the tubuloglomerular mechanism, this is directed by
the macula densa cells of the juxtaglomerular apparatus located in the ascending loop of Henle. Thus,
if there is an increase in filtration rate, it prompts the release of vasoconstrictor chemical that causes
constriction in the afferent arteriole which hinders blood flow in the glomerulus.
Extrinsic mechanisms also have 2 mechanisms of regulation which includes the neural
mechanism and the hormonal mechanism. The neural mechanism is regulated by the baroreceptors in
the blood vessels which may prompt sympathetic nervous system activation. This sympathetic nervous
activation will then prompt the hormonal mechanism by the subsequent release of humoral substances
which includes renin, including angiotensin II, ADH, and the endothelins. This will produce
vasoconstriction of renal vessels. As angiotensin II is released, aldosterone levels will increase leading
to increased sodium reabsorption in the kidney tubules which increases blood volume and will also
increase the blood pressure.

Q2: Describe how the kidney produces concentrated or dilute urine.

The concentration and dilution of urine is mainly regulated by the presence of the hormone
ADH (antidiuretic hormone). The kidney produces dilute urine when the osmolarity of the fluid inside
the lumen of the tubule increases as it goes down the descending limb in the loop of Henle because
the water is lost (due to the permeability of the descending loop of Henle). Due to the water loss, more
solutes are now concentrated in the filtrate. However, as the filtrate passes the ascending loop of
Henle, these solutes (K+, Na+, Cl-) are being pumped out in the filtrate by the action of the
transporters. Due to the solute loss, the filtrate becomes dilute. This means that there is decreased
osmolarity in the ascending limb. As the filtrate further goes to the distal convoluted tubule and into the
collecting ducts, the osmolarity further decreases which causes the formation of dilute urine (VanPutte
et. al, 2013).
The kidney produces concentrated urine due to low intake of water or due to high water loss
(like sweating) thus the kidney responds by conserving water while still getting rid of the excess waste
through the action of the antidiuretic hormone (ADH a.k.a. vasopressin) causes the kidneys to produce
a small volume of concentrated urine. It acts on the distal convoluted tubule and collecting duct by
stimulating the insertion of aquaporins. In those areas, it causes the water inside the tubes (filtrate) to
move out of the tubes making the filtrate highly concentrated with solutes. This causes the water to be
reabsorbed back into the blood and leaving an increased osmolarity of the urine (VanPutte et. al,
2013).

Q3: Explain the value of urine-specific gravity, serum creatinine, and blood urea nitrogen levels in
evaluating renal function.
Urine-specific gravity, serum creatinine (normal values for male:0.7-1.3 mg/dL and 0.4-1.1
mg/dL for females), and blood urea nitrogen (normal value:6-25 mg/dL) are tests to evaluate kidney

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 function. They are usually used together to know if the person has some kidney/renal function
problems.
Both urea nitrogen and creatinine are waste products of our body which are usually excreted
through the urine since most waste products and toxins are excreted in the urine. The urea nitrogen is
the waste product of the liver and the creatinine, a waste formed from creatine through muscle
breakdown. Thus, an increased value beyond the normal levels can indicate renal failure and
decreased values may indicate hepatic disease malnutrition. Thus, increased values of urea nitrogen
and creatinine in the blood may indicate renal disease due to decreased renal function because of the
kidneys’ inability to filter these waste products so it remains in the blood (Ansel et al., 2017).
The specific gravity of urine is ideally 1.002 to 1.030 which must be typically more closed to
the specific gravity of water which is 1. This is because a specific gravity value closer to water
indicates that there are minimal or almost no solutes are present in the urine which indicates that the
person is well hydrated or has no kidney problems. Urine-specific gravity of less than 1.01 indicates
that the person is well hydrated, and more than 1.030 indicates serious dehydration (Tanner, et al.,
2013).

Q4: Differentiate the intracellular from the extracellular fluid compartments in terms of distribution
and composition of water, electrolytes, and other osmotically active solutes.
Intracellular fluid compartment, the water distribution is 40% of the person's total body weight
while in the extracellular fluid compartment, the water distribution is 20% of the persons’ total body
weight. The extracellular water is further divided into 3 compartments which are the interstitial
compartment (14% of water), plasma compartment (5% of water), and the transcellular compartment
(1%) of water. Intracellular cations consist mainly of potassium (ave: 150mEq/L) and magnesium of
which potassium is the major cation while, extracellular cations consists mainly of sodium (ave: 150
mEq/L) and calcium of which sodium is the major cation. The extracellular anion comprises mainly
chloride (ave: 115mEq/L) and bicarbonate ions while the intracellular anions are composed mainly of
phosphate ions. Some proteins and organic solutes are also found in the intracellular fluid
compartment (Porth and Grossman, 2014).

Q5: Compare the pathology, manifestations, and treatment of diabetes insipidus and the
syndrome of inappropriate antidiuretic hormone.
Diabetes insipidus is caused by inadequate levels of ADH (antidiuretic hormone a.k.a.
vasopressin), either because there is a lack of ADH release in the posterior pituitary gland (neurogenic
diabetes insipidus) or, the receptors of ADH in the kidneys are insensitive to it (nephrogenic diabetes
insipidus) leading to fluid volume decrease and high urinary output. On the other hand, the syndrome
of inappropriate antidiuretic hormone is caused by an excess/inappropriate ADH secretion even when
the fluid volume is low or there is low serum osmolarity leading to fluid volume increase and low
urinary output. In DI, this is usually manifested by dehydration, polyuria (frequent urination), polydipsia
(excessive thirst), and hypernatremia symptoms such as low urine osmolarity, high urine output, and
hyperosmolarity. In contrast, SIADH is manifested by overhydration and symptoms of hyponatremia
such as high urine osmolarity, low urine output, and hypo-osmolarity. Since there are inadequate ADH
levels in DI, the treatment is to give vasopressin/ADH or desmopressin which is a synthetic analog of
vasopressin. Chlorpropamide may also be used to stimulate the release of ADH in neurogenic DI.
Thiazide diuretics are also used for nephrogenic DI which improves salt and water uptake in the
proximal tubule. For SIADH, which is the opposite of DI, the fluid restriction can be done or by giving
demeclocycline since it induces nephrogenic diabetes insipidus (Harris, 2018).

Q6: Relate the functions of potassium to the manifestations of hypokalemia and hyperkalemia.

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 Potassium is important for the function of excitable cells such as nerves, muscles, and heart. It
helps the nerves to function properly, muscles to contract, and help maintain a regular heartbeat. So
when there is hypokalemia the usual symptoms are mainly due to hyperpolarization of the membranes
which decreases neuromuscular excitability causing symptoms such as muscle weakness and
decreased reflexes. Since it decreases the excitability of cells, it also causes decreased activity in the
cardiac muscle such as delayed ventricular repolarization, bradycardia, and hypotension. Opposite to
this, when hyperkalemia happens there is too much excitability of cells. Thus, manifestations of
hyperkalemia are usually caused by the partial depolarization of plasma membranes such as
increased neuromuscular irritability and restlessness, intense cramping, and diarrhea. The increase of
excitability of the heart muscles causes ventricular fibrillation and cardiac arrhythmias which may lead
to cardiac arrest (VanPutte, 2013).

Q7: Describe the associations among intestinal absorption, renal elimination, bone stores, and the
functions of vitamin D and parathyroid hormone in regulating calcium, phosphorus, and
magnesium levels.
Magnesium assists in the activation of vitamin D, which helps regulate calcium and phosphate
homeostasis to influence the growth and maintenance of bones (Uwitonze et al., 2018). Vitamin D
stimulates calcium and phosphorus intestinal absorption through stimulating bonce calcium
mobilization and through increasing renal absorption of calcium in the distal tubule. These functions in
the bone and possibly in the kidney requires parathyroid hormone as it regulates calcium levels in the
blood. As a result of these functions, serum calcium and phosphorus concentrations are elevated to
supersaturating levels required for the mineralization of bone to prevent rickets, osteomalacia, and
hypocalcemic tetany (DeLuca, 1986). Thus, if there is magnesium rise, there is calcium rise, but will
result in a phosphorus level decrease in the blood.

References:
Ansel, H. C., Stockton, S. J., & Bradley, W. T. (2017). Pharmaceutical calculations (15th ed.).
Philadelphia, Philadelphia: Wolters Kluwer.
Biga, L., Dawson, S., Harwell, A., Hopkins, R., Kaufmann, J., LeMaster, M., . . . Runyeon, J. (2018). 25.4
Physiology of Urine Formation: Glomerular Filtration. Retrieved September 05, 2020, from
https://open.oregonstate.education/aandp/chapter/25-4-physiology-of-urine-formation-glomerular-
filtration/
DeLuca H.F. (1986) The Metabolism and Functions of Vitamin D. In: Chrousos G.P., Loriaux D.L., Lipsett
M.B. (eds) Steroid Hormone Resistance. Advances in Experimental Medicine and Biology, vol 196.
Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5101-6_24
Harris, M., MD. (2018). Diabetes Insipidus vs Syndrome of Inappropriate ADH (SIADH) - Comparison
Table Diabetes Insipidus ... Retrieved September 04, 2020, from
https://www.grepmed.com/images/4182/pathophysiology-endocrinology-comparison-diagnosis-
insipidus-diabetes-symptoms
Porth, C. M., RN, MSN, PhD (Physiology). (2014). Chapter 39: Disorders of Fluid and Electrolyte Balance.
In 916764418 720539311 S. C. Grossman PhD, APRN, FNP-BC, FAAN (Author), Porth's
pathophysiology: Concepts of altered health states (9th ed., pp. 1019-1061). Philadelphia,
Philadelphia: Wolters Kluwer.
Tanner, R. K., & Gore, C. J. (2013). Chapter 9. In Physiological tests for elite athletes (2nd ed., pp. 131-
147). Champaign, IL, Ilinois: Human Kinetics.
Uwitonze, A., & Razzaque, M. (2018, March 01). Role of Magnesium in Vitamin D Activation and
Function. Retrieved September 05, 2020, from https://jaoa.org/article.aspx?articleid=2673882
VanPutte, C. L., Regan, J. L., Russo, A. F., Seeley, R. R., Stephens, T. D., & Tate, P. (2013). Chapter 23:
Urinary System and Body Fluids. In Seeley's anatomy and physiology (pp. 717-764). New York, NY,
New York: McGraw-Hill.

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