<span>Rhabdomyolysis constitutes a common cause of acute renal failure and presents paramount interest. A large variety of causes with different pathogenetic mechanisms can involve skeletal muscles resulting in rhabdomyolysis with or without acute renal failure. Crush syndrome, one of the most common causes of rhabdomyolysis presents increased clinical interest, particularly in areas often involved by earthquakes, such as Greece and Turkey. Drug abusers are another sensitive group of young patients prone to rhabdomyolysis, which attracts the clinical interest of a variety of medical specialties.
We herein review the evidence extracted from updated literature concerning the data related to pathogenetic mechanisms and pathophysiology as well as the management of this interesting syndrome.
Keywords: Rhabdomyolysis, acute renal failure, myoglobin, crush syndrome
The first case of the crush syndrome, which constitutes one of the main causes of rhabdomyolysis, was reported in Sicily in 1908, after an earthquake1,2. In 1930, in the Baltic area, an epidemic of myoglobinuria was observed due to consumption of contaminated fish. Interest in rhabdomyolysis and crash syndrome was stimulated during the World War II particularly after the bombing in London, where the victims developed acute renal failure and myoglobinuria1.
Rhabdomyolysis is a rupture (lysis) of skeletal muscles due to drugs, toxins, inherited disorders, infections, trauma and compression3. Lysis of muscle cells releases toxic intracellular components in the systemic circulation which leads to electrolyte disturbances, hypovolemia, metabolic acidocis, coagulation defects and acute renal failure due to myoglobin4.
The skeletal muscle consists of cylindrical myofibrils, which contain variant structural and contraction proteins. Actin and myosin, arranged in thin and thick filaments respectively, form the repeated functional units of contraction, the sarcomeres5. The sarcoplasmic reticulum constitutes an important cellular calcium storage. It is structurally connected to the t-tubules, that are formed by invaginations of the muscle cell plasma membrane, the sarcelemma, around every fibril (Figure 1). After the sarcelemma depolarization, the stimulation arrives, through the t-tubules junctions, at the sarcoplasmic reticulum, inducing the calcium ions release and triggering muscle contraction6.</span>
Answer:
The answer is only about 40
Explanation:
Whenever something is consumed, only about 10% of the energy is consumed. So when a primary consumer eats the producer, they will get about 4,000 kcal. Then the secondary consumer will get about 400. Finally, the tertiary consumer will only get about 40. Basically, just multiple the original number by 0.1 for every time it goes through consumption.
Answer:
The given blank can be filled with a venule.
Explanation:
A small blood vessel in the microcirculation, which connects the capillary beds to the veins is known as the venules. Various venules combine to form a vein. The walls of a venule are formed of three layers, that is, the inner endothelium formed of squamous endothelial cells, a middle layer of elastic and muscle tissue, and an external layer formed of fibrous connective tissue.
The size of a venule ranges from 8 to 100 micrometers in diameter and are produced when capillaries come in close association. A venule refers to a small blood vessel that permits the deoxygenated blood high in carbon dioxide and waste products to return from capillary beds to the bigger blood vessels known as veins.
The two alleles for fur color in snurfles are Yellow and Green. These alleles are represented by the letters G and g. Homozygous dominant GG is yellow, as well as heterozygous Gg. But recessive gg is green. These are the two colors that can be seen in the traits of fur colors in snurfles. I hope this helps.
