Anatomy<unk>  results from damage to the intercellular proteins inside the sarcolemma. Myosin and actin break down in the sarcomeres when ATP is no longer available due to injury to the sarcoplasmic reticulum. Damage to the sarcolemma and sarcoplasmic reticulum from direct trauma or high force production causes a high influx of calcium into the muscle fibers increasing calcium permeability. Calcium ions build up in the mitochondria, impairing cellular respiration. The mitochondria are unable to produce enough ATP to power the cell properly. Reduction in ATP production impairs the cells' ability to extract calcium from the muscle cell. Motor endplate of a person with<unk>  The ion imbalance causes calcium-dependent enzymes to activate which break down muscle proteins even further. A high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax. Actin, and myosin The increase of sustained muscle contraction leads to oxygen and ATP depletion with prolonged exposure to calcium. The muscle cell membrane pump may become damaged allowing free form myoglobin to leak into the bloodstream. Physiology<unk>  causes the myosin and actin to degenerate into smaller proteins that travel into 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. 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 heart's ability to generate action potentials leading to cardiac arrhythmias. Consequently, this can affect peripheral and central perfusion which in turn can affect all major organ systems in the body. When the protein reaches the kidneys it causes a strain on the anatomical structures reducing its effectiveness as a filter for the body. The protein acts as a dam as it forms into tight aggregates when it enters the renal tubules. In addition, the increased intracellular calcium has greater time to bind due to the blockage allowing for renal calculi to form. As a result this causes urine output to decrease allowing for the uric acid to build up inside the organ. The increased acid concentration allows the iron from the aggregate protein to be released into the surrounding renal tissue. Iron then strips away molecular bonds of the surrounding tissue which eventually will lead to kidney failure if the tissue damage is too great. Renal tubules of<unk>  Mechanical consideration Muscle degeneration from<unk>  destroys the myosin and actin filaments in the affected tissue. This initiates the body's natural reaction to increasing 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 the underlying tissue and bone. This is known as compartment syndrome which leads to greater death of the surrounding muscle tissue around the injury. As the muscle dies this will cause 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. Compartment syndrome in muscle Dehydration is a common risk factor for<unk>  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.
Exertional rhabdomyolysis
Diabetic myonecrosis
Rhabdomyolysis
Postanesthetic shivering
Sympathicolysis
Thyrotoxic myopathy
Proteus-like syndrome
Rumination syndrome