Kidneys and Hypertension
The provided video discusses kidneys. It is mentioned that kidney damage can be caused by hypertension (“Don’t Die Young,” n.d.). In this paper, we would like to describe in more detail the mechanism in which high blood pressure can damage the kidneys.
It is known that in people with hypertension the muscle tissue that is a component of the vessels becomes tense, which results in the narrowing of the vessel’s lumen. It causes the increased pressure of blood on the vessels from the inside, which may lead to artery damage, causing the vessels to further narrow, harden, or become weaker. The lack of blood supply can cause damage to the tissues of the kidney; for instance, capillaries may become unable to provide nephrons with the necessary blood, and they, having not received the required nutrients, cease functioning and may die. As a result, the kidney starts losing its ability to filter blood (Gargiulo, Suhail, & Lerma, 2015).
In addition, kidneys produce renin, a hormone that allows the organism to regulate blood pressure. Therefore, not only hypertension can lead to kidney damage, but the damage, in turn, exacerbates hypertension (Gargiulo et al., 2015). It is also noteworthy that hypertension is dangerous not only due to the possible damage to the kidney but also (and mostly) due to the possibility to cause damage to other organs, such as the heart or brain.
To avoid these adverse effects, it is important to keep the blood pressure at the level of no more than 140/90 mm Hg. Even though for healthy people maintaining levels of blood pressure lower than 140/90 did not have a significant effect on kidneys, individuals who already have kidney disease should strive to keep it lower than 140/90 (Weir, 2014).
To sum up, hypertension leads to a lack of blood supply for kidneys, which impairs the functioning of the kidneys. Because kidneys also produce rennin, damaged kidneys further exacerbate hypertension.
Myocardial Infarction
Normal physiology
- In a normal heart, the blood flow to the heart muscles occurs properly. The heart receives all the blood it needs.
- The heart’s tissues are undamaged, and it normally conducts electricity, which is important for the sinus rhythm.
Pathophysiology
- Due to various factors (most often, because of an occlusion of coronary arteries), blood flow to the myocardium ceases or is disrupted severely.
- If the impaired blood flow lasts long enough, the cells of the cardiac muscle die, mostly due to necrosis.
- The resulting myocardial scarring damages the function of the heart (arrhythmias, impaired electrical conduction, not proper cardiac output and blood pressure).
- These impairments may cause further problems such as the worsening of ischemia, ventricular or atrial fibrillation, sudden cardiac death, etc.
Genetics
- Numerous factors increase the risk of vessel occlusion, cardiovascular disease, and other problems that raise the chance of myocardial infarction (diabetes, obesity, hypertension, etc.).
- There exist genetic causes that increase the risk of development of these factors.
- Nearly 30 loci in the genes were found to be associated with the increased risk of myocardial infarction (O’Donnell & Nabel, 2011).
Cultural influences
- Such factors as smoking, sedentary lifestyle and poor diet may lead to an increased risk of myocardial infarction.
Management options
- Interventions must be provided with utmost urgency.
- Interventions must be aimed at limiting the size of infarction. This is accomplished by preventing irreversible damage to the myocardium tissue; the process must continue until the ischemia is alleviated (Wagner, 2012, pp. 387-388).
- The possible fallout of the infarction, such as hypertension, lower cardiac output, arrhythmias (especially ventricular fibrillation), must also be handled.
Labs
- Cardiac biomarkers (mainly cardiac troponins).
- Imaging (chest radiograph, CT, etc.).
- Electrocardiogram.
Interactions between these components
- Cultural influences, genetic, and many other factors contribute to the development of the impaired functioning of heart (i.e., normal physiological processes are substituted by pathophysiological) and result in ischemia. The presence of symptoms means that laboratory and other tests need to be performed. If they are positive, management options need to be employed.
References
Don’t die young. Episode 1 – Kidneys. (n.d.). Web.
Gargiulo, R., Suhail, F., & Lerma, E. V. (2015). Hypertension and chronic kidney disease. Disease-a-Month, 61(9), 387-395. Web.
O’Donnell, C. J., & Nabel, E. G. (2011). Genomics of cardiovascular disease. The New England Journal of Medicine, 365(22), 2098-2109. Web.
Wagner, G. S. (Ed.). (2012). Myocardial infarction: Measurement and intervention [Google Books version]. Web.
Weir, M. R. (2014). Hypertension and kidney disease. Journal of the American Society of Hypertension, 8(11), 855-857. Web.