User:Mellowchillgpt/sandbox
Physiology
[edit]Rhabdomyolsis causes the myosin and actin degenerate into smaller sub units proteins that travel in to the circulatory system. The body reacts by increasing intracellular swelling to the injured tissue to send repair cells to the area. This allows creatine kinase and myoglobin to be flushed from the tissue where it travels in the blood until reaching the kidneys. [1] In addition to the proteins released large quantities of ions such as intracellular potassium, sodium, and chloride find their way into the circulatory system. Intracellular potassium ion has deleterious effects on the hearts ability to generate action potentials leading to cardiac arrhythmia's. [2] Consequently, this can affect peripheral and central perfusion that can affect all major organ systems in the body. When the protein reaches the kidney's it causes a strain on the anatomical structures reducing its effectiveness as a filter for the body. The protein acts like a dam as it form into tight aggregates when it enters the renal tubules. [3] In addition, the increased intracellular calcium has greater time to bind due to the blockage allowing for renal calculi to form. [4] As a result this causes urine output to decreases allowing for the uric acid to build up inside the organ. The increase acid concentration allows the iron from the aggregate protein to be released into the surrounding renal tissue. [5] Iron then strips away molecular bonds of the surrounding tissue which eventually will lead to renal failure if the damage is to great on the tissue.
Mechanical Consideration
[edit]Muscle degeneration from rhabdomyolsis destroys the myosin and actin filaments in the affected tissue. This initiates the bodies natural reaction to increase perfusion to the area allowing for an influx of specialized cells to repair the injury. However, the swelling increases the intracellular pressure beyond normal limits. As the pressure builds in the muscle tissue the surrounding tissue is crushed against underlying tissue and bone. [6] This is known as compartment syndrome which leads to greater death of the surrounding muscle tissue around the injury. [7] As the muscle dies this will causes pain to radiate from the affected area into the compartmentalized tissue. A loss of range of motion from swelling will also be seen in the affected limb. Along with muscle strength weakness associated with the muscles involved from loss of filament interaction.
Dehydration is a common risk factor for exertional rhabdomyolsis because it causes a reduction of plasma volume during exertion. This leads to a reduction of blood flow through the vascular system which inhibits blood vessel constriction. [8] Dehydration ac- companied with prolonged strenuous activity such as eccentric contractions or resistance exercise leads to reduced blood flow to active muscles. [9] Reduction of blood flow to the muscle tissue will cause damage to the affected area and if severe enough even death of the cell. Thermal regulation is negatively affected when water content in the intracellular membrane is reduced. [10] Dehydration impacts the water distribution between the intracellular and extracellular compartments. The loss of water content throughout the body leads to reduced functionality in the muscle tissue.
- ^ Thomas, J. Crowhurst, T. “Exertional Heat Stroke, rhabdomyolsis and susceptibility to malignant hyperthermia.” Internal Medicine Journal 43.9 (2013): 1035-1038. Web. 25 Jan 2014.
- ^ Chatzizisis, Yiannis S. Misirli, Gesthimani. et al. “The Syndrome of Rhabdomyolsis: Complication and Treatment.” European Journal of Medicine 19.8 (2008): 568-574. Web. 25 Jan 2014.
- ^ Chatzizisis, Yiannis S. Misirli, Gesthimani. et al. “The Syndrome of Rhabdomyolsis: Complication and Treatment.” European Journal of Medicine 19.8 (2008): 568-574. Web. 25 Jan 2014.
- ^ Rodriguez, Eva. Solar, Maria J. et al. “Risk Factors for Acute Kidney Injury in Severe Rhabdomyolsis.” PLOSONE 10.1371 (2013). Web. 25 Jan 2014.
- ^ Poortsmans, JR. Vanderstraten, J. “Kidney function during exercise in healthy and diseased human. An Update.” Sports Medicine 18.6 (1994): 419-437. Web. 25 Jan 2014.
- ^ Davis, DE. Raikin, S. et al. “Characteristics of patients with chronic exertional compartment syndrome.” Foot & Ankle International 34.10 (2013): 1349-1354. Web. 25 Jan 2014.
- ^ Davis, DE. Raikin, S. et al. “Characteristics of patients with chronic exertional compartment syndrome.” Foot & Ankle International 34.10 (2013): 1349-1354. Web. 25 Jan 2014.
- ^ Cleary Michelle A, Sitler Michael, Kendrick Zebulon. Dehydration and Symptoms of Delayed-! Onset Muscle Soreness in Normothermic Men National Athletic Trainers’ Association. J Athl Train. 2006; 41(1) 36-45 PMCID:PMC1421497!
- ^ Cleary Michelle A, Sitler Michael, Kendrick Zebulon. Dehydration and Symptoms of Delayed-!Onset Muscle Soreness in Normothermic Men National Athletic Trainers’ Association. J Athl Train. 2006; 41(1) 36-45 PMCID:PMC1421497!
- ^ Cleary Michelle A, Sitler Michael, Kendrick Zebulon. Dehydration and Symptoms of Delayed-!Onset Muscle Soreness in Normothermic Men National Athletic Trainers’ Association. J Athl Train. 2006; 41(1) 36-45 PMCID:PMC1421497!