Tetany or tetanic seizure is a medical sign consisting of the involuntary contraction of muscles, which may be caused by disorders that increase the action potential frequency of muscle cells or the nerves that innervate them. Muscle cramps caused by the disease tetanus are not classified as tetany; rather, they are due to a lack of inhibition to the neurons that supply muscles. Tetanic contractions (physiologic tetanus) are a broad range of muscle contraction types, of which tetany is only one. Signs and symptoms
Tetany is characterized by contraction of distal muscles of the hands (carpal spasm with extension of interphalangeal joints and adduction and flexion of the metacarpophalangeal joints) and feet (pedal spasm) and is associated with tingling around the mouth and distally in the limbs. Causes
The usual cause of tetany is a deficiency of calcium. An excess of phosphate (high phosphate-to-calcium ratio) can also trigger the spasms. Underfunction of the parathyroid gland can lead to tetany. Low levels of carbon dioxide cause tetany by altering the albumin binding of calcium such that the ionized (physiologically influencing) fraction of calcium is reduced; one common reason for low carbon dioxide levels is hyperventilation. Low levels of magnesium can lead to tetany. Clostridium tetani toxin, via inhibition of glycine-mediated and GABA-ergic neurotransmission, may lead to tetany.An excess of potassium in grass hay or pasture can trigger winter tetany, or grass tetany, in ruminants. Osteomalacia and rickets due to deficiency of vitamin DMetabolic alkalosis with hypokalemia like Gitelman syndrome  and Bartters syndrome can cause tetany.
This inflammatory reaction can be described as chronic rather than acute, with a slow ongoing progression of the immune system attempting to eliminate the foreign fibers. Macrophages phagocytose (ingest) the fibers and stimulate fibroblasts to deposit connective tissue. Due to the asbestos fibers natural resistance to digestion, some macrophages are killed and others release inflammatory chemical signals, attracting further lung macrophages and fibrolastic cells that synthesize fibrous scar tissue, which eventually becomes diffuse and can progress in heavily exposed individuals. This tissue can be seen microscopically soon after exposure in animal models. Some asbestos fibers become layered by an iron-containing proteinaceous material (ferruginous body) in cases of heavy exposure where about 10% of the fibers become coated. Most inhaled asbestos fibers remain uncoated. About 20% of the inhaled fibers are transported by cytoskeletal components of the alveolar epithelium to the interstitial compartment of the lung where they interact with macrophages and mesenchymal cells. The cytokines, transforming growth factor beta and tumor necrosis factor alpha, appear to play major roles in the development of  scarring inasmuch as the process can be blocked in animal models by preventing the expression of the growth factors. The result is fibrosis in the interstitial space, thus asbestosis. This fibrotic scarring causes alveolar walls to thicken, which reduces elasticity and gas diffusion, reducing oxygen transfer to the blood as well as the removal of carbon dioxide. This can result in shortness of breath, a common symptom exhibited by individuals with asbestosis.