glycogen and Hypokalemia

Topics: Animals; Biological Transport, Active; Calcium Metabolism Disorders; Glycogen; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hypokalemia; Hyponatremia; Magnesium; Membrane Potentials; Muscles; Myoglobinuria; Neuromuscular Diseases; Phosphorus Metabolism Disorders; Potassium Deficiency; Water-Electrolyte Imbalance

Topics: Acidosis, Renal Tubular; Adipose Tissue; Alkalosis; Animals; Antihypertensive Agents; Blood Volume; Clinical Trials as Topic; Diuretics; Erythrocytes; Ethacrynic Acid; Furosemide; Glucose; Glycogen; Humans; Hyperkalemia; Hypokalemia; Membrane Potentials; Potassium; Pyrazines; Sodium; Spironolactone; Triamterene

Albuterol overdose can lead to tachycardia, hypotension, tremor, hypokalemia, and hyperglycemia in children. Hypoglycemia had been previously reported in only one child. We describe a 3-year-old boy who ingested high-dose albuterol in this report. On arrival to the emergency department, the child was agitated and had noticeable restlessness, sinus tachycardia, mild hypokalemia (3.2 mEq/L), and hyperglycemia (187 mg/dL). Activated charcoal and intravenous hydration were given, and electrocardiogram monitoring was performed. Sinus tachycardia resolved within 4 to 6 hours. Hypoglycemia (45 mg/dL) was identified 4 hours after admission. The child recovered uneventfully within 24 hours with glucose replacement. This case suggests that hypoglycemia could be a late complication of acute albuterol overdose; thus, the period of observation should be extended in these cases.

Topics: Adrenergic beta-Agonists; Albuterol; Charcoal; Child, Preschool; Diseases in Twins; Drug Overdose; Fluid Therapy; Glucose; Glycogen; Humans; Hyperinsulinism; Hypoglycemia; Hypokalemia; Male; Psychomotor Agitation; Tachycardia, Sinus; Time Factors; Tremor

Diuretic therapy is the most common cause of potassium deficiency. Although the extent of potassium deficiency usually does not exceed 200 or 300 mEq, under appropriate circumstances such modest deficiency may have important consequences. Factors that tend to increase the incidence or severity of potassium deficiency in patients who take diuretics include high salt diets, large urine volumes, metabolic alkalosis, increased aldosterone production, and the simultaneous use of two diuretics that act on different sites in the renal tubule. There are many serious complications of potassium deficiency, including cardiac arrhythmias, muscle weakness, rhabdomyolysis, glucose intolerance, and several complications that result directly from increased ammonia production, such as protein and nitrogen wasting and hepatic coma. Emphasized herein are those conditions that impose potential danger in patients with mild hypokalemia. Important factors that identify specific causes of potassium deficiency and its treatment are discussed briefly.

Topics: Animals; Arrhythmias, Cardiac; Cardiovascular System; Diuretics; Glycogen; Homeostasis; Humans; Hypokalemia; Muscle, Smooth; Muscles; Potassium Deficiency; Proteins

In an experimental study on isolated isovolumetric guinea-pig hearts, a 2.2-fold reduction of the coronary duct combined with metabolic block caused by dinitrophenol (0.05 mM) resulted in an eleven-fold drop in the attained pressure, and a shorter electric systole, a smaller P wave, and an ST displacement on the ECG. Deep suppression of mechanical and electric activity was combined with reduced glycogen content, and greater K+ and Na+ withdrawal from the heart. Quantitatively, the drop in contractility correlated with K+ withdrawal and ST displacement. A sudden increase in coronary perfusion rate was accompanied by a rapid increase in the rate of K+ elimination from the heart which was proportionate to the rate of hyperfusion, with a simultaneous transitory rise in attained pressure, a great increment in diastolic pressure and the emergence of arrhythmia and fibrillation, the severity of the changes correlating with the degree of K+ loss. A moderate increase in K+ concentration of the perfusate prevented the development of fibrillation and drastically reduced the degree of contracture and glycogen drop during hyperfusion. The obtained results suggest that moderate accumulation of extracellular K+ during the early phase of energy generation disorder can be of a protective nature, as it contributes to a sharp reduction in contractility and energy spending to improve cell survivability in critical conditions.

Topics: Animals; Coronary Disease; Energy Metabolism; Extracellular Space; Glycogen; Guinea Pigs; Hypokalemia; Myocardium; Organ Culture Techniques; Perfusion; Potassium

The case history, skeletal muscle and heart muscle biopsy findings from an affected member of a family suffering from hypokalaemic periodic paralysis associated with permanent muscular weakness are reported. The patient, a female aged 35 years, while treated with 750 mg and later 1000 mg of acetazolamide daily, developed typical exercise angina pectoris. The ECG during exercise showed ST-segment depression. A coronary angiography was performed because coronary artery disease was suspected. To exclude cardiac muscle disease a biopsy of the left ventricular wall was taken. The angiography was normal. Ultrastructural analysis of the biopsy specimen showed an unusual amount of intermyofibrillary glycogen resembling, although far less abundant, the increase of glycogen found in the skeletal muscle biopsy specimen obtained from the same patient. The possible implications of these findings are discussed with reference to the normal echocardiographic findings in the family.

Topics: Cardiomyopathies; Female; Glycogen; Histocytochemistry; Humans; Hypokalemia; Muscles; Myocardium; Paralyses, Familial Periodic

Topics: Climate; Glycogen; Heat Exhaustion; Hot Temperature; Humans; Hypokalemia; Muscles; Physical Education and Training; Potassium; Sports Medicine

The author presets some data on histochemical studies of muscle carbohydrate metabolism in patients with hypopotassemic periodic paralysis during the attack and in intermissions. The most constant and considerable changes were revealed during the paralytic attack and they lead to a decrease of phosphorylase activity, an increase of glycogen content and glucose decrease in the muscular fibers. In intermissions these changes were expressed either minimally or were absent altogether. The initial biochemical effect remains unknown. Undoubtedly, the carbohydrate metabolism is significantly damaged in this disease, and there is a definite parallelism between the severity of the clinical course and the degree of the revealed histochemical changes in the muscles.

Topics: Adolescent; Carbohydrate Metabolism; Child; Child, Preschool; Fructose-Bisphosphate Aldolase; Glucosidases; Glycerolphosphate Dehydrogenase; Glycogen; Glycogen Synthase; Histocytochemistry; Humans; Hypokalemia; L-Lactate Dehydrogenase; Muscles; Paralyses, Familial Periodic; Paralysis; Periodicity; Phosphorylases; Succinate Dehydrogenase

Topics: Animals; Aorta; Glucosephosphate Dehydrogenase Deficiency; Glycogen; Glycogen Storage Disease; Histocytochemistry; Histological Techniques; Humans; Hypokalemia; Liver; Liver Glycogen; Mice; Microscopy, Electron; Mitochondria, Liver; Mitochondria, Muscle; Muscles; Myocardium; Myofibrils; Osmium; Pancreas; Salivary Glands

Topics: Child, Preschool; Glycogen; Humans; Hypokalemia; Male; Muscles; Paralyses, Familial Periodic; Potassium; Water-Electrolyte Balance

Topics: Adult; Female; Glycogen; Histocytochemistry; Humans; Hypokalemia; Inclusion Bodies; Microscopy, Electron; Muscles; Myofibrils; Paralyses, Familial Periodic; Sarcoplasmic Reticulum

Topics: Adult; Alcoholism; Aspartate Aminotransferases; Chronic Disease; Creatine Kinase; Fructose-Bisphosphate Aldolase; Glycogen; Humans; Hypokalemia; Male; Middle Aged; Muscles; Muscular Diseases; Necrosis; Potassium; Sodium

Topics: Cell Nucleus; Chronic Disease; Diagnosis, Differential; Glycogen; Histocytochemistry; Humans; Hyperthyroidism; Hypokalemia; Lysosomes; Male; Methods; Microscopy; Microscopy, Electron; Middle Aged; Muscles; Myofibrils; Paralyses, Familial Periodic; Paralysis; Sarcolemma

Topics: Coronary Disease; Diagnosis, Differential; Glycogen; Glycogen Storage Disease; Glycogen Storage Disease Type I; Glycolysis; Heart Failure; Histocytochemistry; Humans; Hypokalemia; Lactates; Myocardium; Potassium; Rheumatic Heart Disease

Topics: Adult; Biopsy; Cell Membrane; Endoplasmic Reticulum; Glycogen; Humans; Hyperthyroidism; Hypokalemia; Male; Microscopy, Electron; Muscles; Paralysis

Topics: Adolescent; Adult; Biopsy; Electromyography; Female; Glycogen; Humans; Hypokalemia; Male; Microscopy, Electron; Muscles; Myofibrils; Paralyses, Familial Periodic

Topics: Alkalosis; Animals; Blood Glucose; Diazoxide; Epinephrine; Glucagon; Glycogen; Heptoses; Hydrocortisone; Hypokalemia; Liver Glycogen; Male; Muscles; Potassium Deficiency; Rats

Topics: Animals; Blood Glucose; Carbohydrate Metabolism; Desoxycorticosterone; Fatty Acids; Fatty Acids, Nonesterified; Glycogen; Hypokalemia; Lipid Metabolism; Male; Rats

Topics: Adenine Nucleotides; Adenosine Triphosphate; Adult; Carbohydrate Metabolism; Creatine Kinase; Glycogen; Humans; Hypokalemia; In Vitro Techniques; Male; Mitochondria; Muscles; Oxidative Phosphorylation; Oxygen Consumption; Paralyses, Familial Periodic

Topics: Glycogen; Humans; Hypokalemia; Muscle Spindles; Muscular Atrophy; Muscular Diseases; Muscular Dystrophies; Myofibrils; Myositis; Paralysis; Polymyalgia Rheumatica

Topics: Biopsy; Carbohydrate Metabolism; Glycogen; Humans; Hypokalemia; In Vitro Techniques; Male; Microscopy; Microscopy, Electron; Middle Aged; Myofibrils; Paralyses, Familial Periodic

Topics: Cachexia; Carbohydrate Metabolism; Electrolytes; Glycogen; Humans; Hypokalemia; Hyponatremia; Liver Cirrhosis; Muscle, Skeletal; Muscles; Proteins; Water-Electrolyte Balance

Topics: Alanine; Animals; Carbohydrates; Glycogen; Glycogenolysis; Hypokalemia; Liver; Liver Glycogen; Potassium; Potassium Deficiency; Rats