Describe The Causes Of Rhabdomyolysis

If the calcium and sodium channels remain open, it would cause a uncontrolled muscle twitch.

- Endurance athletes are particularly vulnerable because over the extended period of time they are not taking in salt, only water. This creates the hypotonic environment outside the cells because of the salt concentration differential.

Electrolytes have are nutrients or chemicals that have many different funtions, from regulation your heartbeat to allowing your muscles to contract. (Dr.Axe, 2015). Electrolytes also help maintain hydration levels which is an extremely inporntant aspect for all athletes. Some examples of electrolytes are potassium, sodium, magnesium, and calcium. A lack of electrolytes can lead to various symptoms that include depression, confusion, muscle cramps, muscle spasms, muscle weakness, and in extreme cases unconsciousness and coma. (Aubri John,

Periodic Paralysis Syndrome is a blanket term for a couple of inherited muscular disorders. The most common types are hypokalemic periodic paralysis and hyperkalemic periodic paralysis. Both of these are inherited and generally present from childhood, tho it is possible for symptoms to start showing later in adolescence. In hyperkalemic periodic paralysis, high levels of potassium in the blood interact with genetically caused abnormalities in sodium channels (pores that allow the passage of sodium molecules) in muscle cells, resulting in temporary muscle weakness and, when severe, in temporary paralysis. This disease may be caused by genetic defects in either the calcium channel or the sodium channel. Hypokalemic disease may be caused by genetic defects in either the calcium channel or the sodium channel (Medline Plus).

It is found in skeletal muscles. Creatine phosphate can house high-energy phosphate bonds. There is an abundance of ATP while the muscle cell is at rest. The creatine kinase transfers the high-energy phosphate bonds of the ATP to the high-energy phosphate bonds of the creatine phosphate. Once the cell is ready to contract, creatine kinase removes the phosphate groups from creatine phosphate and transfers them to ADP to create ATP. ATP is used to drive the contraction since it is a quick energy source. A large amount of creatine kinase should not be present in the bloodstream unless there is a large-scale destruction of muscle cells. The Duchenne muscular dystrophy causes this phenomenon to occur where muscle cell membranes are destroyed spilling out the creatine kinase into the bloodstream.

Muscle atrophy is the loss of skeletal muscle mass and function that occurs when there is a long period of inactivity of the muscles or defects in motor neuron's (Reilly, Beau 2015). Defects in the motor neurons that stimulate the muscle cause the muscle mass to decrease as proteins that initiate contractions of muscle dissipate. Stimulus is not transferred to the weakened muscle fibers effectively, reducing the contractile force possible for generation from the stimulus. Muscle mass increases upon recovery, as restimulation of the muscle enlarges fiber size, thus a greater contractile force can be generated from the stimulus.

Our cardiac muscle remains unaffected in those with Malignant Hyperthermia because this condition is within the skeletal muscles. Here, the brain sends electrical signals that eventually reach the calcium pump and cause a domino effect. There are minimal proven theories about Malignant Hyperthermia’s effect on the cardiac muscle by professionals; however, what is known, is that during a Malignant Hyperthermia crisis, there are increased abnormal heart rhythms frequent in this disorder. These arrhythmias are often attributed to the damage made directly to the cardiac muscle.

As previously stated Rhabdomyolysis can be caused from numerous injuries but it is ultimately the breakdown of muscle tissue that leads to life threatening conditions such as Acute Renal Failure. The process of muscle breakdown leads to depletion of Adenosine Triphosphate, which is where muscles receive their energy, and increased levels of potassium, creatine kinase, urate and myoglobin (Sauret, 2002). In addition to electrolyte disturbances causing toxicity leading to the breakdown of muscle tissue, the increase number of neutrophils from the inflammatory process amplifies muscle damage (Muscal, 2013). Acute Kidney Failure occurs because the increased levels of myoglobin, a large protein, that precipitates in the kidney tubules leading to obstruction that eventually leads to necrosis (Sauret, 2002).

An example of one such category of muscular dystrophy is distal muscular dystrophy. distal muscular dystrophy causes atrophied muscles due to a damaged DYSF or ANO5 gene. The DYSF gene aids in the creation of dysferlin. Dysferlin is found in the thin sarcolemma of the muscle tissue which is thought to aid the sarcolemma in repairing muscles. Since the production of dysferlin is inhibited by this form of muscular dystrophy, the muscles are not able to be repaired, leading them to become progressively more damaged and ineffective over time. Abnormalities in the other ANO5 gene, which produces anoctamin-5 affect muscles by reducing if not eliminating said protein. ANO5 is thought to provide transport for chlorine ions to the muscle cells of a muscle. These two genetic disorders are usually closely linked and it is common for the abnormality of one gene

Chemically what is occurring is the digestive system is producing toxic substances that destroy red blood cells and eventually lead to the symptoms that were mentioned previously and the overall ending (if not treated) of kidney failure, among other possible health issues.

The new information provided in the research articles clarify the exact mechanisms by which diabetes may influence dilation of smooth muscle, and therefore slightly alter our perception of the problem, however the broad concepts featured in both of our hypotheses were confirmed in the information. Specifically, the articles do confirm our initial understanding of how the drugs (specifically isoproterenol and forskolin) create dilation in both groups, as they activate Beta-receptors which in turn activated Adenylyl cyclase, causing an increase in cAMP concentration which ultimately leads to dilation. However, in the second document provided, they state that the impairment in the dilation process due to high glucose levels in the blood took place downstream of cAMP production, at the K+-channel step, immediately before dilation occurs. In our first hypothesis, we focused on a potential impairment in the steps preceding cAMP production. We hypothesized that glucose was not able to be converted into ATP in the cells since insulin prohibits its uptake into cells, leading to the inability for cAMP production from ATP. While this may not be the case, we were on the right path in indicating that there was in

Rhabdomyolysis or myoglobinuria, is the breakdown of muscle tissue that leads to the release of muscle fiber contents into the blood. These substances are harmful to the kidney and often cause kidney damage. When muscle is damaged, a protein called myoglobin is released into the bloodstream. It is then filtered out of the body by the kidneys. Myoglobin breaks down into substances that can damage kidney cells( Medline, 2015). Serum Creatine Kinase (CK) is most useful in the measurement in the condition. CK levels greater than 1000 units/L are indicative of the condition, levels that exceed 5000 unit/L indicate acute renal failure. Rhabdomyolyis, is most frequently seen in traumas that involve crush injuries, immobilization for long periods, and drug and alcohol overdoses. Although the condition is rare, serious complications including hyperkalemia, metabolic acidosis, acute renal failure and DIC (McCance..).

It can cause stiffening of muscle tissue as well, leading to cramps and spasms. Just like calcification leads hardening of the arteries.

twitch muscles. Fast twitch muscles have a fast form of myosin ATP and are very

Muscle Fibre Tear- When the muscles contract they create micro tears within the muscle and require protein in order to mend the muscles. These tears are repaired into stronger and denser fibres. For example if an individual went on the treadmill for 10 minutes, the hamstrings,