Metabolism muscle weakness

The findings of hypomagnesemia include muscle weakness, cramps, agitation, confusion, tremor, seizures, ECG changes (increased PR interval, prolonged QRS complex, and increased QT interval), findings of hypocalcemia (see above), refractory hypokalemia (see above), metabolic alkalosis, and digoxin toxicity.42,47,48... 

Patients with metabolic alkalosis rarely have symptoms attributable to alkalemia. Rather, complaints are usually related to volume depletion (muscle cramps, positional dizziness, and weakness) or to hypokalemia (muscle weakness, polyuria, and polydipsia). 

Differential diagnoses include diabetes mellitus and metabolic syndrome because patients with these conditions share several similar characteristics with Cushing s syndrome patients (e.g., obesity, hypertension, hyperlipidemia, hyperglycemia, and insulin resistance). In women, the presentations of hirsutism, menstrual abnormalities, and insulin resistance are similar to those of polycystic ovary syndrome. Cushing s syndrome can be differentiated from these conditions by identifying the classic signs and symptoms of truncal obesity, "moon faces" with facial plethora, a "buffalo hump" and supraclavicular fat pads, red-purple skin striae, and proximal muscle weakness. 

In individuals who took thyroid hormones, 80% of the weight lost was lean body mass (muscle and bone) rather than excess fat. People taking these extracts experienced muscle weakness and bone breakdown, which led to a condition called osteoporosis, in which bones are weakened and the risk of bone fractures or breaks is increased. Thyroid hormone extracts also made the heart work harder by increasing metabolism, which led to problems such as increased heart rate, palpitations, and irregular heartbeat. These problems were potentially life threatening When the heart beats abnormally (or not at all), it is unable to pump blood and oxygen to the brain and body. Individuals die suddenly from this condition because the brain can only function for a few minutes without oxygen and nutrients. 

No unique signs or symptoms are associated with mild to moderate metabolic alkalosis. Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use. 

The first defect, described in 1962 is, in fact, one of the rarest (Luft s syndrome). It arises from the uncoupling of mitochondria. The resting metabolic rate is markedly raised, there is profuse sweating, fever and generalised muscle weakness. The mitochondria of these patients have an increased permeability, not so much to protons, as in brown adipose tissue mitochondria, but to cations, such as Ca, the entry of which similarly dissipates the proton motive force. 

Adverse effects are usually due to excessive doses (which may occur if the initial increase in metabolism is too rapid) and correspond to symptoms of hyperthyroidism, but they usually disappear after dose reduction or withdrawal of treatment. The most common adverse effects affect the following system as Heart arrhythmias, anginal pain, Central nervous system headache, hyperactivity, sweating, tremor, heat intolerance, Gastrointestinal tract diarrhoea, excessive weight loss, vomiting, Musculoskeletal system muscle cramps, muscle weakness. 

In adults, the signs and symptoms of hypothyroidism include somnolence, slow mentation, dryness and loss of hair, increased fluid in body cavities (e.g., the pericardial sac), low metabolic rate, tendency to gain weight, hyperlipidemia, subnormal temperature, cold intolerance, bradycardia, reduced systolic and increased diastolic pulse pressure, hoarseness, muscle weakness, slow return of muscle to the neutral position after a tendon jerk, constipation, menstrual abnormalities, infertility, and sometimes myxedema (hard edema of subcutaneous tissue with increased content of proteoglycans in the fluid). A goiter (i.e., enlargement of the thyroid gland) may be present. 

Prolonged use or overdose may result in electrolyte or metabolic disturbances (such as hypokalemia, hypocalcemia, and metabolic acidosis or alkalosis), as well as persistent diarrhea, vomiting, muscle weakness, malabsorption, and weight loss. 

Individuals with chronic liver disease may have disorders of fluid and electrolyte balance, including ascites, edema, and effusions. Alterations of whole body potassium induced by vomiting and diarrhea, as well as severe secondary aldosteronism, may contribute to muscle weakness and can be worsened by diuretic therapy. The metabolic derangements caused by metabolism of large amounts of ethanol can result in hypoglycemia, as a result of impaired hepatic gluconeogenesis, and in ketosis, caused by excessive lipolytic factors, especially increased cortisol and growth hormone. 

Muscles require a significant amount of energy in the form of ATP. When energy levels become too low, muscle weakness and exercise intolerance with muscle pain or cramps may occur. Metabolic muscle diseases that have their onset in infancy tend to be the most severe, and some forms are fatal. Those that begin in childhood or adulthood tend to be less severe, and changes in diet and lifestyle can help most people with the milder forms adjust. The more common metabolic diseases are summarised below. 

By extrapolation from the muscle weakness and fatigue seen in children with genetic defects of carnitine biosynthesis or metabolism, it has been... 

In horses, diazepam is distributed widely to the tissues and metabolized extensively the values quoted for elimination half-life range from 3 to 22 h (Muir et al 1982). High doses of benzodiazepines cause muscle weakness, facial and neck muscle fasciculations, ataxia and recumbency. In neonatal foals, the i.v. administration of benzodiazepines can cause respiratory depression or arrest, through accumulation (Norman et al 1997), so resuscitation equipment should be available and repeated doses should be administered with extreme care. 

Ingestion of high doses can lead to burning of the mouth, vomiting, abdominal pain, and gastrointestinal hemorrhage. Acute exposure may also cause severe metabolic acidosis, myotonia, and muscle weakness, which can persist for a long period of time. 

A 36-year-old patient started taking a combination of herbal products including Echinacea, and 2 weeks later she presented with generalized muscle weakness that limited her ambulation and ability to use her hands. She was found to have distal renal tubular acidosis and was extremely hypokalemic (K+ of 1.3). Over 4 days she received 1200 mEq of sodium bicarbonate and 400 mEq of potassium chloride along with other electrolyte supplements to correct the imbalances. After her serum electrolytes were corrected, her muscle weakness improved rapidly. She was diagnosed and treated for Sjogren s syndrome and her condition rapidly improved. The researchers suggested that her use of the immunostimulant Echinacea could have contributed to the activation of her autoimmune disease, which ultimately caused her severe metabolic disturbances. Because she had remained symptom free for more than 3 years, the authors concluded that, after review, her disease was relatively mild and was exacerbated by Echinacea (34). 

There are two distinct types of GSH-S deficiency, both associated with mild chronic hemolysis in one type, hemolysis is the only clinical manifestation. In the other, the major clinical features are mental retardation, severe generalized muscle weakness, tremors, incoordination, hemolytic anemia, and metabolic acidosis. This second and much more severe type of GSH-S deficiency is also known as 5-oxopro-linurta or pyroglutamic aciduria. The difference in severity of these disorders reflects the fact that in the mild form, GSH-S deficiency is confined to the RBCs because in this disorder the GSH-S is unstable. GSH-S activity is present in adequate quantity in young RBCs, but it rapidly declines as the cells age, because the cells are unable to synthesize new molecules of GHS-S. Other cells of the body that have nuclei and ribosomes can compensate for accelerated denaturation of GSH-S by synthesizing more. On the other hand, in the severe systemic form of GSH-S deficiency, aE cells of the body have low activities of GSH-S because they cannot form this enzyme in adequate amounts. In both types of GSH-S deficiency, RBCs exhibit notable reduction in GSH concentration. 

Distal RTA (Type I). Type 1 dRTA occurs most often in mfants (sometimes transiently) or young children, but it may also be encountered in adults, where it is more common than pRTA. Clinical features generally include a metabolic acidosis, muscle weakness, nephrocalcinosis, and urolithiasis. The defect is an inability to secrete hydrogen ions in the distal tubule in the presence of a systemic acidosis. Several subtypes may be seen urinary pH >5.5 is a common feature. ... 

---