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Anatomy and physiology

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9 views

Written Assignment

Anatomy and physiology

Uploaded by

zedotel
Copyright
© © All Rights Reserved
Available Formats
Download as PDF, TXT or read online on Scribd
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Written Assignment

Anatomy and Physiology

HS 2211 - AY2021-T2

Shelly Watkins (Instructor)

Nephrolithiasis

University of the People

1
Introduction
Nephrolithiasis or kidney stones is the most common kidney disorder, “after
hypertension” (Worcester & Coe. 2008) and it has been described and registered since
ancient times. Even though this is a preventable disease, it nevertheless causes a great
economic stress and its incidence and prevalence are on the rise over the past 30 years from
3.2% to 5.2%. (Ziemba and Malaga. 2017) Incidence tends to affect increasingly more
women than men and the rate of stone formation is generally affected by genetic, diet and
environmental factors. (Runge & Greganti. 2009)

Discussion.
Stones form in the kidney when minerals in urine are at high concentration. If such
calculi (stone) reach more than 5 millimeters in diameter it can cause a blockage of the ureter
which leads to a symptom such as severe pain in the lower back or abdomen, blood in the
urine, vomiting or nausea, or painful urination. (Worcester & Coe. 2008) As previously
mentioned, kidney stone formation might include a combination of genetic, diet and
environmental factors (Runge & Greganti. 2009)
However, there’s several risk factors that trigger its formation such as high urine calcium
levels, obesity, certain foods, medication, calcium supplements, hyperparathyroidism, gout
and not drinking enough fluids. (Runge & Greganti. 2009) Several types of electrolytes are
at the base of stone formation, such as calcium oxalate, high dietary sodium and a low
magnesium dietary intake may also increase stone formation. (Goldfarb et al. 2005) Diet is
considered a risk factor, either for the consumption of certain foods as well as beverages. On
one hand a healthy diet is inconsistent with either prevention or causing kidney stones.
(Goldfarb et al. 2005) An example for such statement is coffee drinking and even of heavy
coffee drinking linked with a protection of stone formation. This may be explained by
caffeine intake and its probable association with the excretion of calcium via urine. (Goldfarb
et al. 2005) Typical western diets which normally contains large proportions of animal
protein create an “acid load that increases urinary excretion of calcium and uric acid and
reduced citrate” and all contribute to kidney stone formation (Goldfarb et al. 2005)

2
Most of the pain receptors of the upper urinary tract responsible for the perception of renal
colic are located submucosally in the renal pelvis, calices, renal capsule, and upper ureter.
(Worcester & Coe. 2008) Renal pain fibers follow nerves at the spinal cord levels of T11 to
L2. In the low ureter, pain signals are also distributed through genitofemoral and ilioinguinal
nerves. (Worcester & Coe. 2008) The pain generated by renal colic is primarily caused by
the dilation, stretching, and spasm caused by the acute ureteral obstruction. The severity of
the pain depends on the degree and site of the obstruction, not on the size of the stone. A
patient can often point to the site of maximum tenderness, which is likely to be the site of the
ureteral obstruction. (Worcester & Coe. 2008)

Conclusion

Nephrolithiasis occurs in all parts of the world. The incidence of urinary tract stone
disease in developed countries is similar to that in the United States; the annual incidence of
urinary tract stones in the industrialized world is estimated to be 0.2%. Stone disease is rare
in only a few areas, such as Greenland and the coastal areas of Japan. A lifetime risk of 2-5%
has been noted for Asia, 8-15% for the West, and 20% for Saudi Arabia. (Worcester & Coe.
2008)
A patient who tends to develop stones should be counseled to seek immediate medical
attention if he or she experiences flank or abdominal pain or notes visible blood in the urine.

References:

Worcester, E. M., & Coe, F. L. (2008). Nephrolithiasis. Primary care, 35(2), 369–vii.
https://doi.org/10.1016/j.pop.2008.01.005

JB Ziemba, BR Malaga. (2017). Epidemiology and economics of nephrolithiasis. Investing


Clin Urol. Sep. 58 (5): 299-306

3
Marschall S. Runge & M. Andrew Greganti. (2009). Netter’s Internal Medicine. 2nd Edition.
USA

Goldfarb DS, Fischer ME, Keich Y, Goldberg J. (2005). A twin study of genetic and dietary
influences on nephrolithiasis: a report from the Vietnam Era Twin (VET) Registry. Kidney
Int. Mar;67(3):1053-61. doi: 10.1111/j.1523-1755.2005.00170.x. PMID: 15698445.

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