Tissue Ischemia
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Tissue Ischemia
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The essay evaluates the clinical presentation of Maria, a 68-year-old woman who is not just overweight but also leads an inactive lifestyle. Based on symptoms, such as high blood pressure, edema, enlarged heart, and getting tired quacking when cleaning, the essay endeavors to determine why the patient should experience tissue ischemia that may lead to hypoxia. In addition, early mutable changes that transpire in tissue cells during inadequate oxygen supply are highlighted. Moreover, the essay examines detailed cellular alterations resulting from the patient’s heart enlargement.
Tissue Ischemia
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Two reasons Maria would experience tissue ischemia leading to hypoxia
Based on the case-study, the 68-old-year will experience tissue ischemia not just because she has excessive weight but also because she is not engaged in any physical activities; hence sedentary. According to Grossman (2014), ischemia is the inadequate flow of blood hence less oxygenation and other important nutrients needed for healthy functioning of cells. According to Lavie et al. (2016) excessive weight is one of the core problems bedeviling not just public health, but rather public health policy in modern times. Although overweightness can have serious ramifications when it comes to high patient mortality and reduced quality of life (QoL), it may also necessitate negative cardiovascular outcomes. People that are overweight often develop narrow blood vessels that results from the buildup of plague; fats and cholesterol in the walls that interfere with the swift flow of blood and reduced oxygen as is evidenced in Maria’s case with the presence of edema.
Moreover, the limited blood supply is likely to result in hypoxia in Maria’s body organs. In most cases, reduced oxygen culminates to a condition known as hypoxia. The inability of tissues to harvest adequate oxygen makes the oxygen pressure to go down in the tissue; hence reduced mitochondrial cell activity (Grossman, 2014). In most cases, cellular death may be the end result of prolonged hypoxia. The same view is supported by Engelhardt et al., (2015) in alleging that hypoxia occurs when there is low oxygen in the tissue due to the inability of the blood to supply sufficient oxygen to tissues to fulfill bodily needs.
Again, blood pressure is often high as blood flows through thin vessels. Moreover, the sedentary lifestyle is associated with high blood pressure, elevated triglyceride and coronary thrombosis. On the other hand, the heart gets enlarged by trying to pump blood under strenuous conditions. In addition, excessive weight puts Maria at risk for renal disorder, which may alter how the body responds to blood pressure. Nonetheless, due to narrowed vessels, tissue capillaries may experience high pressure, which hampers the production of enough oxygen, an aspect that hinders the cells to create the required energy to eliminate wastes from the body. The inflammation of ankles, feet and legs may be due to a poor circulatory system. In particular, a sedentary lifestyle coupled with the failure of the heart to pump blood effectively around the body owing to increased pressure in the blood vessels and weakening of muscles that forces fluids to seep into the neighboring tissue. In addition, high blood pressure is also responsible for the enlarged left ventricles (Liu et al., 2015).
Two early and reversible changes that occur to tissues cells when hypoxic
According to Menon et al. (2018), during hypoxic cells enlarge or detachment of the ribosomes. In addition, the polysomes separate into monosomes leading to low protein synthesis. Essentially, cell damage is associated with changes in the villous, fats and the diminishing membrane. Therefore, there are revisable changes that take place in the tissue cells when hypoxic. Changes can be reversed to normal cell functioning when there adequate oxygen supply. In this respect, two early signs and rescindable changes that happen in the hypoxic cells include the reduction of the Adenosine triphosphate (ATP) and cellular swelling.
According to Menon et al., (2018), there is low supply of oxygen and aerobic respiration as a result of decreased production of ATP in the event of cell hypoxic. Nonetheless, during glycolysis, the cell aerobic occurs to improve the supply of oxygen. Hence, when these alterations are temporary, the cell can degenerate to its previous state. But this largely relies on the type of organ or tissue. Primarily, brain cells are likely to get long-lasting injury in ten minutes. Consequently, the first line of attack during hypoxic is aerobic respiration. Kumar and Choi (2015) suggest that ATP is important when it comes to tissue activities, including protein synthesis, lipid synthesis and transporting ions. ATP is also vital in the metabolism of phosphor lipid.
Thus, the reduction of ATP is related to inadequate oxygen supply (Grossman, 2014). Again, oxygen as well as other nutrients are absorbed in the cell via the cell membrane. For that reason, hypoxia could happen due to insufficient oxygen supply and nutrients in the cell membrane. On the other hand, the inadequate oxygen supply in the cell primarily depends on the mechanism of anaerobic metabolism. However, there is reduced mitochondria activity as a result of inadequate supply that utilizes the stored ATP. Generally, with inadequate ATP, the cell membrane malfunctions as it is unable to maintain the normal icons. This contributes to significant efflux of potassium ions from the cell and influx of sodium as well as water. In turn, the influx of water and sodium in the cell can result in swelling while distorting the cell because the cytoplasmic membrane becomes permeable. This affects the electronic impulse because it requires an intact membrane, hence hindering the movement of muscles and contraction of cells that can be reversed if there is sufficient supply of oxygen (Grossman, 2014).
Another reversible change is cellular swelling that arises due to the failure of ion pumps reliant on the energy in the plasma membrane. Evidence demonstrates that this mechanism in turn leads to incapacity to maintain not only fluid but also ionic hemostasis (Engelhardt et al., 2014). As a result of decreased aerobic respiration, ATP is produced to improve energy supply. Conversely, it accelerates the accumulation of lactic acid and break down glycogen, which reduce intracellular pH. High accumulation of ions along a reduction of intracellular water so as to maintain isosmotic results in enlargement of cells
Cellular adaptation that has taken place in Maria’s enlarged heart and reasons for arriving at this conclusion?
Some of the cellular changes that have transpired in the patient’s enflamed heart include reversible cell damage that is responsible for the swelling of the mitochondria in an attempt to generate inadequate energy. Alterations in the mitochondria leads to the manufacture of Adenosine triphosphate (ATP) makings the cells to relapse to anaerobic glycolysis leading to a lot of lactic acid, acidity of the cell pH and decreased metabolic activities in the cell (Moreira‐Gonçalves et al., 2015). Owing to increased pressure, the patient’s engorged heart is undergoing a condition known as pathologic hypertrophy, some form of cellular adjustment to pressure.
Pathologic hypertrophy stems from abnormal stressors, such as enlarged heart size as a result of aortic stenosis (Grossman, 2014). With the deposit of plague on the vessel walls, there is not only thinning of the vessels but also changes in the aortic valve that blocks the orifice, which overworks the left ventricle as it pumps blood into the aorta. Pathologic hypertrophy results from reduced heart chambers and the heart incapacity to impel blood to different body parts. Furthermore, the 68-year-old enlarged heart is also a function of continued cell contact to antagonistic stimuli that prompt several adaptive tissue and organ responses. While cells can change to normal when causes are eliminated, failure to return to normalcy can lead to adversarial health outcomes.
Moreover, there is also a condition known as hyperplasia, linked to adaptive cells that cause enflamed organs or tissue. Although the patient’s enlarged heart is trying to adapt to metaplasia, through cellular changes to suit the environment, nonetheless, if unreversed, the process can lead to a severe growth. Owing to the engorged heart, there is atrophy that decreases the cellular dimension, which impact different organs such as the heart, brain and skeletal muscles negatively. Due to atrophy, the cellular activity in the mitochondria may diminish hence negatively impact the vital role associated with muscle contraction. Evidence demonstrates that about five cellular changes happen when the heart is working under extreme pressure among overweight people an issue that lead to a sedentary lifestyle (Moreira‐Gonçalves et al., 2015). By and large, the weakened and enlarged hearts hampers with its ability to pump blood optimally in the chambers hence less oxygen to support cellular activities.
While the patient is the case study is overweight, this alone is not a recipe for heart enlargement since not all obese individuals have engorged hearts. Nevertheless, since she leads a sedentary lifestyle, edema can be seen as emanating from poor circulation, while the enlarged heart could be attributed to pressure on the heart to pump blood. Hence, high blood pressure makes the left ventricle to enlarge while weakening the muscles (Moreira‐Gonçalves et al., 2015). The enlargement of the ventricles, leads to the enlargement of heart as well. Basically, Maria is overweight, which is a risk factor for her high blood pressure and eventually heart enlargement. Even though Lavie et al., (2016) state that while the majority of individuals hardly exhibit symptoms of the inflated heart, the common sign that the patient presents is the build-up of fluids in her ankles and legs that contributes to edema.
Furthermore, since Maria is sedentary, there increased build-up of oily deposits in the cardiovascular system that cause contraction of the artery and supply of oxygen that allow the heart to pump blood. In this case, the heart is functioning under pressure resulting to enlargement as a measure to adapt. Additionally, Maria’s high blood pressure resulting from a sedentary and excessive overweight are causing heart enlargement. In particular, the heart is pumping blood beyond its ability. The patient might also be having idiopathic dilated cardiomyopathy a condition that affects heart muscles and characterized by edema in the ankles.
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References
Grossman, S. C., & Porth, C. M. (2014). Porth\’s pathophysiology: concepts of altered health states (9th ed.). Philadelphia: Wolters Kluwer Health | Lippincott Williams & Wilkins.
Kumar, H., & Choi, D. K. (2015). Hypoxia inducible factor pathway and physiological adaptation:A cell survival pathway?. Mediators of Inflammation, 2015. https://doi.org/10.1155/2015/584758
Lavie, C. J., De Schutter, A., Parto, P., Jahangir, E., Kokkinos, P., Ortega, F. B., … & Milani, R. V. (2016). Obesity and prevalence of cardiovascular diseases and prognosis—the obesity paradox updated. Progress in Cardiovascular Diseases, 58(5), 537-547. https://doi.org/10.1016/j.pcad.2016.01.008
Menon, A., Creo, P., Piccoli, M., Bergante, S., Conforti, E., Banfi, G., … & Anastasia, L. (2018). Chemical activation of the hypoxia-inducible factor reversibly reduces tendon stem cell proliferation, inhibits their differentiation, and maintains cell undifferentiation. Stem Cells International, 2018. https://doi.org/10.1155/2018/9468085
Moreira‐Gonçalves, D., Henriques‐Coelho, T., Fonseca, H., Ferreira, R., Padrão, A. I., Santa, C., … & Duarte, J. A. (2015). Intermittent cardiac overload results in adaptive hypertrophy and provides protection against left ventricular acute pressure overload insult. The Journal of Physiology, 593(17), 3885-3897. https://doi.org/10.1113/JP270685
Polfer, E. M., Sabino, J., Fleming, I., & Means, K. R. (2017). Relative tissue oxygenation changes are more reliable than clinical exam or temperature changes for detecting early tissue ischemia: Level 2 evidence. Journal of Hand Surgery, 42(9), S45. Retrieved from https://meeting.handsurgery.org/files/2018/ePosters/HSEP133.pdf
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