Weakness, muscle

Other Potassium and Sodium Disorders. Potassium and/or sodium deficiency can lead to muscle weakness and sodium deficiency to nausea. Hyperkalemia resulting in cardiac arrest is possible from 18 g/d of potassium combined with inadequate kidney function. Faulty utilisation of K" and/or Na" can lead to Addison s or Cushing s disease. 

An endocrine disorder first described by the British Physician Thomas Addison in the mid 1800 s. The adrenal glands fail to produce sufficient amounts of glucocorticoid hormones (cortisol) and sometime mineralocorticoid (aldosterone). If left untreated it is life-threatening, the patient will show muscle weakness, hyperpigmentation and even depression. Typical treatment is hydrocortisone replacement therapy. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Central core disease (CCD) is an autosomal dominant, non-progressive myopathy characterized by hypotonia and proximal muscle weakness in infancy. CCD is named after detection of characteristic central cores that lack both mitochondria and oxidative enzyme... 

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. 

Isaacs syndrome (an acquired neuromyotonia) is caused by autoantibodies directed against 4-aminopyr-idine or a-dendrotoxin-sensitive K+ channels (Kvl.l and Kvl.6) in motor and sensory neurons. The syndromes include muscle twitching during rest, cramps during muscle contraction, impaired muscle relaxation, and muscle weakness due to hyperexcitability of peripheral motor nerves. 

Neurotoxicity (damage to the nervous system by a toxic substance) may also be seen with the administration of the aminoglycosides. Signs and symptoms of neurotoxicity include numbness, skin tingling, circum-oral (around the mouth) paresthesia, peripheral paresthesia, tremors, muscle twitching, convulsions, muscle weakness, and neuromuscular blockade (acute muscular paralysis and apnea). 

Frequently seen adverse reactions to dragp with anticholinergic activity include dry mouth, blurred vision, dizziness, mild nausea, and nervousness. These may become less pronounced as therapy progresses. Other adverse reactions may include skin rash, urticaria (hives), urinary retention, dysuria, tachycardia, muscle weakness, disorientation, and confusion. If any of these reactions are severe, the drug may be discontinued for several days and restarted at a lower dosage, or a different antiparkinsonism drag may be prescribed. 

Remember to take lithium with food or immediately after meals to avoid stomach upset. Drink at least 10 large glasses of fluid each day and add extra salt to food. Prolonged exposure to the sun may lead to dehydration. If any of the following occurs, do not take the next dose and immediately notify the primary health care provider diarrhea, vomiting, fever, tremors, drowsiness, lack of muscle coordination, or muscle weakness. 

Muscle weakness, loss of muscle mass, tendon rupture, osteoporosis, aseptic necrosis of femoral and humoral heads, spontaneous fractures... 

Notify die primary health care provider of a marked weight gain, swelling in the extremities, muscle weakness, persistent headache, visual disturbances, or behavior change... 

Inform the primary healdi care provider if the following adverse reactions occur edema, muscle weakness, weight gain, anorexia, swelling of the extremities, dizziness, severe headache, or shortness of breath. 

Anorexia, nausea, vomiting, lethargy, bone tenderness or pain, polyuria, polydipsia, constipation, dehydration, muscle weakness and atrophy, stupor, coma, cardiac arrest... 

Anorexia, nausea, vomiting, mental depression, confusion, delayed or impaired thought processes, drowsiness, abdominal distention, decreased bowel sounds, paralytic ileus, muscle weakness or fatigue, flaccid paralysis, absent or diminished deep tendon reflexes, weak irregular pulse, paresthesias, leg cramps, ECG changes Hyperkalemia... 

Adverse reactions seen with magnesium administration are rare. If they do occur, they are most likely related to overdose and may include flushing, sweating, hypotension, depressed reflexes, muscle weakness, and circulatory collapse (see Display 58-2). 

EDMD is another X-linked muscular dystrophy, clinically and genetically completely distinct from DMD and BMD. Affected boys usually have onset in childhood of contractures (especially involving the Achilles tendons, elbows, and spinal muscles), humeroperoneal muscle weakness, and cardiac conduction defects, which tend to be mostly a problem in adult life and may necessitate insertion of a pacemaker. The gene for EDMD is known to map to Xq28, but this localization is... 

The disease in this group is also of recessive inheritance, and seems to follow a yet milder course again, with onset of muscle weakness in the late teens and usually slow progression. 

Late-onset centronuclear myopathies show a predominance of limb-girdle and truncal muscle weakness with only rare facial or eye involvement. Although this group is classified with the congenital myopathies, weakness only becomes appar-... 

Clinical features include neonatal hypotonia, a tendency toward congenital hip dislocation and diffuse muscle weakness. Later on children are frequently of short stature and low body weight and often have long thin faces and high-arched palates. Respiratory difficulties, where present, occur early on and tend to improve with time. In others a virtually static clinical picture is seen. 

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