The American journal of medicine
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Prescribed medications, over-the-counter drugs, and nutritional supplements are used by many patients. Although most of these products are well tolerated, drug-induced hyperkalemia may develop in patients with underlying renal impairment or other abnormalities in potassium handling. ⋯ However, disturbed cellular uptake of a potassium load as well as excessive ingestion or infusion of potassium-containing substances may also occur. Physicians must be aware of medications that can precipitate hyperkalemia, how these drugs induce alterations in potassium homeostasis, and the patient characteristics that increase the risk of hyperkalemia.
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Neutrophils and other phagocytes manufacture O(2)(-) (superoxide) by the one-electron reduction of oxygen at the expense of NADPH. Most of the O(2)(-) reacts with itself to form H(2)O(2) (hydrogen peroxide). ⋯ These reactive oxidants are manufactured for the purpose of killing invading microorganisms, but they also inflict damage on nearby tissues, and are thought to be of pathogenic significance in a large number of diseases. Included among these are emphysema, acute respiratory distress syndrome, atherosclerosis, reperfusion injury, malignancy and rheumatoid arthritis.
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The superoxide free radical has come to occupy an amazingly central role in a wide variety of diseases. Our metabolic focus on aerobic energy metabolism in all cell types, coupled with some chemical peculiarities of the oxygen molecule itself, contribute to the phenomenon. ⋯ Rather it appears to be a carefully regulated metabolite capable of signaling and communicating important information to the cell's genetic machinery. Redox regulation of gene expression by superoxide and other related oxidants and antioxidants is beginning to unfold as a vital mechanism in health and disease.
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Each cough involves a complex reflex arc beginning with the stimulation of sensory nerves that function as cough receptors. There is evidence, primarily clinical, that the sensory limb of the reflex exists in and outside of the lower respiratory tract. Although myelinated, rapidly adapting pulmonary stretch receptors (RARs), also known as irritant receptors, are the most likely type of sensory nerve that stimulates the cough center in the brain, afferent C-fibers and slowly adapting pulmonary stretch receptors (SARs) also may modulate cough. ⋯ The predominant role of acid in triggering cough by means of this reflex is unclear because of conflicting results from provocative challenge studies. It is interesting to speculate that a distal esophageal-bronchial reflex evolved as an early warning defense so that coughing could be started, just in case the refluxate were to reach the inlet of the lower respiratory tract. That is, thinking teleologically, it is possible that an esophageal-bronchial reflex evolved as one of several mechanisms designed to protect the lungs from aspiration of gastric contents.
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Review
Hiatus hernia: a review of evidence for its origin in esophageal longitudinal muscle dysfunction.
The axial forces exerted on the esophagus by the swallowing-induced contraction of its two longitudinally oriented muscle layers should, if unopposed, herniate the cardia through the diaphragm. A mathematical model of esophageal contraction shows that the magnitude of such a force becomes maximal just above the cardia, which is consistent with anatomic evidence of the existence of an inhibitory innervation in this same region. We propose that the inhibition exerted by these nerves when they discharge in swallowing prevents the supracardiac esophagus from shortening, allowing it to stretch and dissipating the pulling force of longitudinal muscle contraction above the diaphragm. Thus, hiatal hernia could originate from nerve disease, alteration in the viscoelastic properties of distal esophagus, or increased strength of the longitudinal muscle layers.