Tetany
Plant Poisoning
Hypocalcemia
Magnesium Deficiency
Renal Tubular Transport, Inborn Errors
Magnesium Oxide
Hypoparathyroidism
Ruminants
Muscle Cramp
Action Potentials
International Classification of Diseases
Postoperative tetany in Graves disease: important role of vitamin D metabolites. (1/99)
OBJECTIVE: To test the authors' hypothesis of the causal mechanism(s) of postoperative tetany in patients with Graves disease. SUMMARY BACKGROUND DATA: Previous studies by the authors suggested that postoperative tetany in patients with Graves disease occurs during the period of bone restoration and resulted from continuation of a calcium flux into bone concomitant with transient hypoparathyroidism induced by surgery. PATIENTS AND METHODS: A prospective study was carried out to investigate sequential changes in serum levels of intact parathyroid hormone (iPTH), calcium and other electrolytes, 25-hydroxyvitamin D (25OHD), 1,25-dihydroxyvitamin D (1,25(OH)2D), and bone metabolic markers in 109 consecutive patients with Graves disease who underwent subtotal thyroidectomy. RESULTS: Preoperative serum iPTH levels negatively correlated with ionized calcium levels and positively correlated with 1,25(OH)2D or 1,25(OH)2D/25OHD. After the operation, there was a significant decline in levels of ionized calcium, magnesium, and iPTH. Serum iPTH was not detected in 15 patients after surgery. Four of these 15 patients, and 1 patient whose iPTH level was below normal, developed tetany. Preoperative serum ionized calcium levels were significantly lower, and iPTH levels were higher, in the 5 patients with tetany than in the 11 patients who did not develop tetany despite undetectable iPTH levels. The tetany group had significantly lower serum 25OHD levels and higher 1,25(OH)2D levels, and had increased 1,25(OH)2D/25OHD as an index of the renal 25OHD-1-hydroxylase activity than those in the nontetany group. These results suggest that patients with a high serum level of iPTH as a result of low serum calcium levels (secondary hyperparathyroidism) are susceptible to tetany under conditions of hypoparathyroid function after surgery. CONCLUSIONS: Postoperative tetany occurs in patients with secondary hyperparathyroidism caused by a relative deficiency in calcium and vitamin D because of their increased demand for bone restoration after preoperative medical therapy concomitant with transient hypoparathyroidism after surgery. Calcium and vitamin D supplements may be recommended before and/or after surgery for patients in whom postoperative tetany is expected to develop. (+info)Role of presynaptic L-type Ca2+ channels in GABAergic synaptic transmission in cultured hippocampal neurons. (2/99)
Using dual whole cell patch-clamp recordings of monosynaptic GABAergic inhibitory postsynaptic currents (IPSCs) in cultured rat hippocampal neurons, we have previously demonstrated posttetanic potentiation (PTP) of IPSCs. Tetanic stimulation of the GABAergic neuron leads to accumulation of Ca2+ in the presynaptic terminals. This enhances the probability of GABA-vesicle release for up to 1 min, which underlies PTP. In the present study, we have examined the effect of altering the probability of release on PTP of IPSCs. Baclofen (10 microM), which depresses presynaptic Ca2+ entry through N- and P/Q-type voltage-dependent Ca2+ channels (VDCCs), caused a threefold greater enhancement of PTP than did reducing [Ca2+]o to 1.2 mM, which causes a nonspecific reduction in Ca2+ entry. This finding prompted us to investigate whether presynaptic L-type VDCCs contribute to the Ca2+ accumulation in the boutons during spike activity. The L-type VDCC antagonist, nifedipine (10 microM), had no effect on single IPSCs evoked at 0.2 Hz but reduced the PTP evoked by a train of 40 Hz for 2 s by 60%. Another L-type VDCC antagonist, isradipine (5 microM), similarly inhibited PTP by 65%. Both L-type VDCC blockers also depressed IPSCs during the stimulation (i.e., they increased tetanic depression). The L-type VDCC "agonist" (-)BayK 8644 (4 microM) had no effect on PTP evoked by a train of 40 Hz for 2 s, which probably saturated the PTP process, but enhanced PTP evoked by a train of 1 s by 91%. In conclusion, the results indicate that L-type VDCCs do not participate in low-frequency synchronous transmitter release, but contribute to presynaptic Ca2+ accumulation during high-frequency activity. This helps maintain vesicle release during tetanic stimulation and also enhances the probability of transmitter release during the posttetanic period, which is manifest as PTP. Involvement of L-type channels in these processes represents a novel presynaptic regulatory mechanism at fast CNS synapses. (+info)Effect of hypertonicity on augmentation and potentiation and on corresponding quantal parameters of transmitter release. (3/99)
Augmentation and (posttetanic) potentiation are two of the four components comprising the enhanced release of transmitter following repetitive nerve stimulation. To examine the quantal basis of these components under isotonic and hypertonic conditions, we recorded miniature endplate potentials (MEPPs) from isolated frog (Rana pipiens) cutaneous pectoris muscles, before and after repetitive nerve stimulation (40 s at 80 Hz). Continuous recordings were made in low Ca2+ high Mg2+ isotonic Ringer solution, in Ringer that was made hypertonic with 100 mM sucrose, and in wash solution. Estimates were obtained of m (no. of quanta released), n (no. of functional release sites), p (mean probability of release), and vars p (spatial variance in p), using a method that employed MEPP counts. Hypertonicity abolished augmentation without affecting potentiation. There were prolonged poststimulation increases in m, n, and p and a marked but transient increase in vars p in the hypertonic solution. All effects were completely reversed with wash. The time constants of decay for potentiation and for vars p were virtually identical. The results are consistent with the notion that augmentation is caused by Ca2+ influx through voltage-gated calcium channels and that potentiation is due to Na+-induced Ca2+ release from mitochondria. The results also demonstrate the utility of this approach for analyzing the dynamics of quantal transmitter release. (+info)A critical role of the nitric oxide/cGMP pathway in corticostriatal long-term depression. (4/99)
High-frequency stimulation (HFS) of corticostriatal glutamatergic fibers induces long-term depression (LTD) of excitatory synaptic potentials recorded from striatal spiny neurons. This form of LTD can be mimicked by zaprinast, a selective inhibitor of cGMP phosphodiesterases (PDEs). Biochemical analysis shows that most of the striatal cGMP PDE activity is calmodulin-dependent and inhibited by zaprinast. The zaprinast-induced LTD occludes further depression by tetanic stimulation and vice versa. Both forms of synaptic plasticity are blocked by intracellular 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ), a selective inhibitor of soluble guanylyl cyclase, indicating that an increased cGMP production in the spiny neuron is a key step. Accordingly, intracellular cGMP, activating protein kinase G (PKG), also induces LTD. Nitric oxide synthase (NOS) inhibitors N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) and 7-nitroindazole monosodium salt (7-NINA) block LTD induced by either HFS or zaprinast, but not that induced by cGMP. LTD is also induced by the NO donors S-nitroso-N-acetylpenicillamine (SNAP) and hydroxylamine. SNAP-induced LTD occludes further depression by HFS or zaprinast, and it is blocked by intracellular ODQ but not by L-NAME. Intracellular application of PKG inhibitors blocks LTD induced by HFS, zaprinast, and SNAP. Electron microscopy immunocytochemistry shows the presence of NOS-positive terminals of striatal interneurons forming synaptic contacts with dendrites of spiny neurons. These findings represent the first demonstration that the NO/cGMP pathway exerts a feed-forward control on the corticostriatal synaptic plasticity. (+info)On the respective roles of nitric oxide and carbon monoxide in long-term potentiation in the hippocampus. (5/99)
Perfusion of hippocampal slices with an inhibitor nitric oxide (NO) synthase blocked induction of long-term potentiation (LTP) produced by a one-train tetanus and significantly reduced LTP by a two-train tetanus, but only slightly reduced LTP by a four-train tetanus. Inhibitors of heme oxygenase, the synthetic enzyme for carbon monoxide (CO), significantly reduced LTP by either a two-train or four-train tetanus. These results suggest that NO and CO are both involved in LTP but may play somewhat different roles. One possibility is that NO serves a phasic, signaling role, whereas CO provides tonic, background stimulation. Another possibility is that NO and CO are phasically activated under somewhat different circumstances, perhaps involving different receptors and second messengers. Because NO is known to be activated by stimulation of NMDA receptors during tetanus, we investigated the possibility that CO might be activated by stimulation of metabotropic glutamate receptors (mGluRs). Consistent with this idea, long-lasting potentiation by the mGluR agonist tACPD was blocked by inhibitors of heme oxygenase but not NO synthase. Potentiation by tACPD was also blocked by inhibitors of soluble guanylyl cyclase (a target of both NO and CO) or cGMP-dependent protein kinase, and guanylyl cyclase was activated by tACPD in hippocampal slices. However, biochemical assays indicate that whereas heme oxygenase is constitutively active in hippocampus, it does not appear to be stimulated by either tetanus or tACPD. These results are most consistent with the possibility that constitutive (tonic) rather than stimulated (phasic) heme oxygenase activity is necessary for potentiation by tetanus or tACPD, and suggest that mGluR activation stimulates guanylyl cyclase phasically through some other pathway. (+info)Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation. (6/99)
To monitor changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor distribution in living neurons, the AMPA receptor subunit GluR1 was tagged with green fluorescent protein (GFP). This protein (GluR1-GFP) was functional and was transiently expressed in hippocampal CA1 neurons. In dendrites visualized with two-photon laser scanning microscopy or electron microscopy, most of the GluR1-GFP was intracellular, mimicking endogenous GluR1 distribution. Tetanic synaptic stimulation induced a rapid delivery of tagged receptors into dendritic spines as well as clusters in dendrites. These postsynaptic trafficking events required synaptic N-methyl-D-aspartate (NMDA) receptor activation and may contribute to the enhanced AMPA receptor-mediatedtransmission observed during long-term potentiation and activity-dependent synaptic maturation. (+info)Direct evidence for biphasic cAMP responsive element-binding protein phosphorylation during long-term potentiation in the rat dentate gyrus in vivo. (7/99)
Phosphorylation of the transcription factor cAMP responsive element-binding protein (CREB) is thought to play a key role in synaptic plasticity and long-term memory. However, direct evidence for CREB phosphorylation during hippocampal long-term potentiation (LTP) in vivo is sparse. Here, we show that, in the intact animal, CREB is rapidly phosphorylated in response to high-frequency stimulation but not low-frequency stimulation of the perforant pathway. CREB phosphorylation occurred in a biphasic manner, with a first peak at 30 min and a second long-lasting peak beginning 2 hr after tetanic stimulation and lasting for at least 24 hr. Only stimuli that generated nondecremental LTP promoted a sustained hyperphosphorylation of CREB but not stimuli that produced decremental LTP. CREB phosphorylation was specifically triggered in the dentate gyrus, as well as the CA1, but not the CA3, hippocampal region. Pretreatment with the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate completely prevented activation of CREB. Together, we have resolved the spatial and temporal dynamics of CREB phosphorylation during hippocampal LTP, showing that the transcription factor CREB is specifically recruited at two distinct time points in some forms of hippocampal synaptic plasticity in vivo. (+info)Mechanism of cannabinoid effects on long-term potentiation and depression in hippocampal CA1 neurons. (8/99)
Cannabinoids, the active constituents of marijuana, are known to impair learning and memory. Receptors for cannabinoids are highly expressed in the hippocampus, a brain region that is believed to play an important role in certain forms of learning and memory. To investigate the possible contribution of cannabinoid receptor-mediated deficits in hippocampal function to the learning and memory impairments produced by marijuana, we studied the effects of cannabinoid receptor activation on two models of learning and memory, long-term potentiation (LTP) and long-term depression (LTD), in hippocampal slices. Although LTP and LTD of CA1 field potentials were blocked by cannabinoid receptor activation in the presence of Mg(2+), they could be induced after Mg(2+) was removed. Similarly, LTP and LTD of whole-cell EPSCs were unimpaired in the presence of cannabinoid receptor agonist when the postsynaptic membrane was depolarized during the LTP or LTD induction protocol. Cannabinoid receptor activation also reduced EPSCs and enhanced paired-pulse facilitation, while having no effect on the amplitude of spontaneous miniature EPSCs. Finally, as with cannabinoid receptor activation, inhibition of LTP by adenosine receptor activation could be overcome by removal of Mg(2+) or depolarization of the postsynaptic membrane during tetanus. Our results indicate that cannabinoid receptor activation does not directly inhibit the molecular mechanisms responsible for long-term synaptic plasticity but instead impairs LTP and LTD by reducing presynaptic neurotransmitter release to a level below that required to depolarize the postsynaptic membrane to relieve Mg(2+) blockade of NMDA receptors. (+info)Tetany is a medical condition characterized by involuntary muscle spasms and cramps, often starting in the hands and feet and can spread to other parts of the body. It is typically caused by an imbalance of minerals such as calcium and magnesium in the blood, which can be due to various underlying medical conditions such as hypoparathyroidism, hypocalcemia, or alkalosis. Tetany can also occur after surgical removal of the parathyroid glands (a procedure called parathyroidectomy). In some cases, tetany can be a symptom of other neuromuscular disorders.
The muscle spasms associated with tetany can be painful and can interfere with normal functioning. They are often triggered by sensory stimuli such as touch, sound, or temperature changes. Tetany can also cause numbness, tingling, or a crawling sensation in the skin (paresthesia). In severe cases, it can lead to seizures, difficulty breathing, and cardiac arrhythmias.
Treatment of tetany typically involves addressing the underlying medical condition causing the imbalance of minerals in the blood. This may involve supplementation with calcium or magnesium, medication to regulate parathyroid hormone levels, or other treatments depending on the specific cause.
Plant poisoning is a form of poisoning that occurs when someone ingests, inhales, or comes into contact with any part of a plant that contains toxic substances. These toxins can cause a range of symptoms, depending on the type and amount of plant consumed or exposed to, as well as the individual's age, health status, and sensitivity to the toxin.
Symptoms of plant poisoning may include nausea, vomiting, diarrhea, abdominal pain, difficulty breathing, skin rashes, seizures, or in severe cases, even death. Some common plants that can cause poisoning include poison ivy, poison oak, foxglove, oleander, and hemlock, among many others.
If you suspect plant poisoning, it is important to seek medical attention immediately and bring a sample of the plant or information about its identity if possible. This will help healthcare providers diagnose and treat the poisoning more effectively.
Hypocalcemia is a medical condition characterized by an abnormally low level of calcium in the blood. Calcium is a vital mineral that plays a crucial role in various bodily functions, including muscle contraction, nerve impulse transmission, and bone formation. Normal calcium levels in the blood usually range from 8.5 to 10.2 milligrams per deciliter (mg/dL). Hypocalcemia is typically defined as a serum calcium level below 8.5 mg/dL or, when adjusted for albumin (a protein that binds to calcium), below 8.4 mg/dL (ionized calcium).
Hypocalcemia can result from several factors, such as vitamin D deficiency, hypoparathyroidism (underactive parathyroid glands), kidney dysfunction, certain medications, and severe magnesium deficiency. Symptoms of hypocalcemia may include numbness or tingling in the fingers, toes, or lips; muscle cramps or spasms; seizures; and, in severe cases, cognitive impairment or cardiac arrhythmias. Treatment typically involves correcting the underlying cause and administering calcium and vitamin D supplements to restore normal calcium levels in the blood.
Magnesium deficiency, also known as hypomagnesemia, is a condition characterized by low levels of magnesium in the blood. Magnesium is an essential mineral that plays a crucial role in many bodily functions, including muscle and nerve function, heart rhythm, bone strength, and immune system regulation.
Hypomagnesemia can occur due to various factors, such as poor dietary intake, malabsorption syndromes, chronic alcoholism, diabetes, certain medications (such as diuretics), and excessive sweating or urination. Symptoms of magnesium deficiency may include muscle cramps, tremors, weakness, heart rhythm abnormalities, seizures, and mental status changes.
It is important to note that mild magnesium deficiency may not cause any symptoms, and the diagnosis typically requires blood tests to measure magnesium levels. Treatment for hypomagnesemia usually involves oral or intravenous magnesium supplementation, along with addressing the underlying causes of the deficiency.
Inborn errors of renal tubular transport refer to genetic disorders that affect the normal functioning of the kidney tubules. The kidney tubules are responsible for the reabsorption and secretion of various substances, including electrolytes and nutrients, as urine is formed. Inherited defects in the proteins that mediate these transport processes can lead to abnormal levels of these substances in the body and may result in a variety of clinical symptoms.
These disorders can affect different parts of the renal tubule, including the proximal tubule, loop of Henle, distal tubule, and collecting duct. Depending on the specific transporter affected, inborn errors of renal tubular transport can present with a range of clinical manifestations, such as electrolyte imbalances, acid-base disorders, growth retardation, kidney stones, nephrocalcinosis, or even kidney failure.
Examples of inborn errors of renal tubular transport include:
1. Distal renal tubular acidosis (dRTA): A genetic disorder that affects the ability of the distal tubule to acidify urine, leading to metabolic acidosis, hypokalemia, and nephrocalcinosis.
2. Bartter syndrome: A group of autosomal recessive disorders characterized by impaired sodium reabsorption in the loop of Henle, resulting in hypokalemia, metabolic alkalosis, and hyperreninemic hyperaldosteronism.
3. Gitelman syndrome: An autosomal recessive disorder caused by a defect in the thiazide-sensitive sodium chloride cotransporter in the distal tubule, leading to hypokalemia, metabolic alkalosis, and hypocalciuria.
4. Liddle syndrome: An autosomal dominant disorder characterized by increased sodium reabsorption in the collecting duct due to a gain-of-function mutation in the epithelial sodium channel (ENaC), resulting in hypertension, hypokalemia, and metabolic alkalosis.
5. Dent disease: An X-linked recessive disorder caused by mutations in the CLCN5 gene, which encodes a chloride channel in the proximal tubule, leading to low molecular weight proteinuria, hypercalciuria, and nephrolithiasis.
6. Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC): An autosomal recessive disorder caused by mutations in the CLCN5 or CLDN16 genes, which encode chloride channels in the thick ascending limb of Henle's loop, resulting in hypomagnesemia, hypercalciuria, and nephrocalcinosis.
Magnesium oxide is an inorganic compound with the chemical formula MgO. It is a white, odorless solid that is highly basic and stable. Medically, magnesium oxide is used as a dietary supplement to prevent or treat low amounts of magnesium in the blood. It is also used as a antacid to neutralize stomach acid and as a laxative to relieve constipation.
Hypoparathyroidism is a medical condition characterized by decreased levels or insufficient function of parathyroid hormone (PTH), which is produced and released by the parathyroid glands. These glands are located in the neck, near the thyroid gland, and play a crucial role in regulating calcium and phosphorus levels in the body.
In hypoparathyroidism, low PTH levels result in decreased absorption of calcium from the gut, increased excretion of calcium through the kidneys, and impaired regulation of bone metabolism. This leads to low serum calcium levels (hypocalcemia) and high serum phosphorus levels (hyperphosphatemia).
Symptoms of hypoparathyroidism can include muscle cramps, spasms, or tetany (involuntary muscle contractions), numbness or tingling sensations in the fingers, toes, and around the mouth, fatigue, weakness, anxiety, cognitive impairment, and in severe cases, seizures. Hypoparathyroidism can be caused by various factors, including surgical removal or damage to the parathyroid glands, autoimmune disorders, radiation therapy, genetic defects, or low magnesium levels. Treatment typically involves calcium and vitamin D supplementation to maintain normal serum calcium levels and alleviate symptoms. In some cases, recombinant PTH (Natpara) may be prescribed as well.
Ruminants are a category of hooved mammals that are known for their unique digestive system, which involves a process called rumination. This group includes animals such as cattle, deer, sheep, goats, and giraffes, among others. The digestive system of ruminants consists of a specialized stomach with multiple compartments (the rumen, reticulum, omasum, and abomasum).
Ruminants primarily consume plant-based diets, which are high in cellulose, a complex carbohydrate that is difficult for many animals to digest. In the rumen, microbes break down the cellulose into simpler compounds, producing volatile fatty acids (VFAs) that serve as a major energy source for ruminants. The animal then regurgitates the partially digested plant material (known as cud), chews it further to mix it with saliva and additional microbes, and swallows it again for further digestion in the rumen. This process of rumination allows ruminants to efficiently extract nutrients from their fibrous diets.
A muscle cramp is an involuntary and forcibly contracted muscle that does not relax. It can involve partial or complete muscle groups, often occurring in the legs and feet (hamstrings, quadriceps, calves, and foot intrinsic muscles) during or after exercise, at night, or while resting. The exact cause of muscle cramps is unclear, but they can be associated with muscle fatigue, heavy exercising, dehydration, electrolyte imbalances, or underlying medical conditions (e.g., nerve compression or disorders, hormonal imbalances). The primary symptom is a sudden, sharp pain in the affected muscle, which may be visibly tightened and hard to touch. Most muscle cramps resolve on their own within a few minutes, but gentle stretching, massage, or applying heat/cold can help alleviate discomfort.
An action potential is a brief electrical signal that travels along the membrane of a nerve cell (neuron) or muscle cell. It is initiated by a rapid, localized change in the permeability of the cell membrane to specific ions, such as sodium and potassium, resulting in a rapid influx of sodium ions and a subsequent efflux of potassium ions. This ion movement causes a brief reversal of the electrical potential across the membrane, which is known as depolarization. The action potential then propagates along the cell membrane as a wave, allowing the electrical signal to be transmitted over long distances within the body. Action potentials play a crucial role in the communication and functioning of the nervous system and muscle tissue.
The International Classification of Diseases (ICD) is a standardized system for classifying and coding mortality and morbidity data, established by the World Health Organization (WHO). It provides a common language and framework for health professionals, researchers, and policymakers to share and compare health-related information across countries and regions.
The ICD codes are used to identify diseases, injuries, causes of death, and other health conditions. The classification includes categories for various body systems, mental disorders, external causes of injury and poisoning, and factors influencing health status. It also includes a section for symptoms, signs, and abnormal clinical and laboratory findings.
The ICD is regularly updated to incorporate new scientific knowledge and changing health needs. The most recent version, ICD-11, was adopted by the World Health Assembly in May 2019 and will come into effect on January 1, 2022. It includes significant revisions and expansions in several areas, such as mental, behavioral, neurological disorders, and conditions related to sexual health.
In summary, the International Classification of Diseases (ICD) is a globally recognized system for classifying and coding diseases, injuries, causes of death, and other health-related information, enabling standardized data collection, comparison, and analysis across countries and regions.
Tetany
Transport tetany
Grass tetany
Trousseau sign of latent tetany
Sophia Getzowa
Chronaxie
Cardiac conduction system
Leonard Findlay
Magnesium in biology
Kenny-Caffey syndrome
Photosensitivity
Parathyroid hormone
Chvostek sign
Alkalosis
Anxiety
Lester Dragstedt
Acid-base homeostasis
Extracellular fluid
Medical Apartheid
Electrolyte imbalance
Nephrotic syndrome
Hypomagnesemia with secondary hypocalcemia
John Howland (doctor)
Ann Stone Minot
Andrew Almon Fletcher
Suxamethonium chloride
Myopathy
List of mass hysteria cases
Francisco Xavier de Mendonça Furtado
Mass psychogenic illness
Tetany - Wikipedia
Anterior tibial compartment syndrome following prolonged tetany | Journal of Neurology, Neurosurgery & Psychiatry
a 16 months old child present with tetany with carpopedal | Pediatric Oncall
Grass tetany in cattle
"Grass Tetany in Cattle" by Cooperative Extension South Dakota State University
tetany | Lifezen Healthcare
Grass Tetany in Livestock
Grass Tetany - 2021 - AcresTV
tetany | Taber's Medical Dictionary
Preventing Grass Tetany - AgSolutions
ICD-10-CM Code R29.0 - Tetany
Puerperal tetany | The Encyclopedia of World Problems
Study Review Helps
Hypomagnesemia with secondary hypocalcemia: MedlinePlus Genetics
Radiology In Ped Emerg Med, Vol 7, Case 7
tetan- | Encyclopedia.com
Eclampsia in Small Animals - Metabolic Disorders - Merck Veterinary Manual
Nutrition and Growth: Domestic Guidance | CDC
Potassium Phosphate/Sodium Phosphate: Uses, Side Effects
Hypocalcemic generalised seizures as a manifestation of iatrogenic hypoparathyroidism months to years after thyroid surgery
Electrical Injuries in Emergency Medicine: Background, Pathophysiology, Etiology
Calcium Chloride (CaCl, CaC12): Side Effects, Dosages, Treatment, Interactions, Warnings
livestock nutrition Archives | Midwestern BioAg
Clinical Assessment-History and Physical Examination
It's That Time of Year - Managing to Prevent Grass Tetany - Southwest New York Dairy, Livestock & Field Crops Program - Cornell...
Isavuconazonium (Oral Route) Description and Brand Names - Mayo Clinic
DailyMed - SUMATRIPTAN SUCCINATE tablet
Free Nursing Flashcards about Endocrine lpn chatt
Preventing Grass Tetany1
- Extension specialists share techniques for preventing grass tetany and controlling weeds in warm-season grass pastures, plus a review on pasture rental rates in 2021. (unl.edu)
Grass staggers3
- No matter whether it is called wheat pasture poisoning, grass staggers, or hypomagnesia, grass tetany in livestock can be a devastating condition. (laysfeedandpetsupply.com)
- Grass tetany is correctly known as Hypomagnesaemia but you may know of it being called something else like magnesium tetany, oat tetany, lactation tetany, grass staggers, magnesium deficiency and pasture flush staggers. (agsolutions.com.au)
- A nutritional disorder known as Grass Tetany, Grass Staggers or Hypomagnesaemia. (wardlab.com)
Parathyroid1
- Underfunction of the parathyroid gland can lead to tetany. (wikipedia.org)
Cattle6
- South Dakota State University, Cooperative Extension, "Grass Tetany in Cattle" (1972). (sdstate.edu)
- Ruminants are susceptible to grass tetany, including cattle, sheep, and goats, and the disease is most common in spring and fall when pasture may not have as much new growth rich in magnesium. (laysfeedandpetsupply.com)
- Deaths from grass tetany could pose quite a significant risk this season especially for cattle under stress from lactation, mustering or first oestrous following rain and the onset of cold conditions immediately after warm weather. (agsolutions.com.au)
- Cool-season grasses tend to be low in magnesium and when cattle become deficient in magnesium, we start to see signs of grass tetany. (midwesternbioag.com)
- The classical "grass" or "spring" tetany occurs in the spring when cattle are turned out to graze lush small grains or pasture grasses. (cornell.edu)
- Cattle that develop tetany are more prone to do so again. (cornell.edu)
Seizures1
- Shortages of magnesium and calcium can cause neurological problems that begin in infancy, including painful muscle spasms (tetany) and seizures. (medlineplus.gov)
Hypocalcemic3
- Calcium Chloride is a mineral indicated in the immediate treatment of hypocalcemic tetany (abnormally low levels of calcium in the body that cause muscle spasm ). (rxlist.com)
- Pieringer H, Hatzl-Griesenhofer M, Shebl O, Wiesinger-Eidenberger G, Maschek W, Biesenbach G. Hypocalcemic tetany in the newborn as a manifestation of unrecognized maternal primary hyperparathyroidism. (medscape.com)
- A few patients present with persistent viral or fungal infections, or with hypocalcemic tetany. (lu.se)
Puerperal Tetany1
- Milk fever, also known as eclampsia or puerperal tetany, occurs when blood calcium is low after giving birth. (lortsmith.com)
20211
- 2021. https://nursing.unboundmedicine.com/nursingcentral/view/Tabers-Dictionary/745913/all/tetany. (unboundmedicine.com)
Pasture5
- verification needed] An excess of potassium in grass hay or pasture can trigger winter tetany, or grass tetany, in ruminants. (wikipedia.org)
- Regardless of the choice, a veterinarian should be contacted right away for this type of health emergency, and if one animal shows symptoms of grass tetany, all animals in the same herd or pasture should be closely monitored to catch additional cases right away. (laysfeedandpetsupply.com)
- Avoid nitrogen fertilizers on pasture grasses, particularly in spring when livestock is most susceptible to grass tetany. (laysfeedandpetsupply.com)
- For example, the greatest risk for grass tetany is when pasture soils are low in available magnesium and calcium, high in available potassium and high in nitrogen. (cornell.edu)
- With the exception of the mixed mostly legume pasture, all of the forages had a minimum Mg concentration that was considered to be in the moderate to high tetany risk. (cornell.edu)
Pastures3
- Grass tetany is usually confined to medium and high-rainfall regions most often where improved pastures have been established. (agsolutions.com.au)
- Consumption of forages such as lush grass pastures or green cereal crops (cover crops) in which magnesium is low can reduce blood magnesium and precipitate the highly fatal crisis called tetany. (cornell.edu)
- Baby calves are hitting the ground, and lush, green pastures ready for grazing, and grass tetany potentially. (wardlab.com)
Occurs7
- It can be difficult to diagnose grass tetany in livestock because symptoms are generally mild until the animal is so badly affected that death occurs. (laysfeedandpetsupply.com)
- Grass tetany is a nervous disorder and occurs when the magnesium (Mg) concentration in the cerebrospinal fluid (CSF - fluid surrounding the brain & spinal cord) falls below a critical level and this is preceded by a decrease in blood magnesium. (agsolutions.com.au)
- Animals showing clinical signs require treatment immediately by a Veterinarian but prevention is preferable to treatment as grass tetany often occurs without warning. (agsolutions.com.au)
- Skeletal muscle tetany occurs at 16-20 mA. (medscape.com)
- Tetany usually occurs near parturition and/or until approximately 2 months postpartum, and the frequency usually increases with older cows. (cornell.edu)
- Transitional" tetany occurs in early spring when grasses are first beginning to "green up. (cornell.edu)
- Though rare, "Autumn" tetany occurs similarly to "spring" tetany on lush grass of fall regrowth. (cornell.edu)
Deficiency of magnesium2
- Most veterinary texts define 'grass tetany' as a deficiency of magnesium (Mg). Though grass tetany is expressed as a magnesium deficiency, the reasons for this expression are complex and varied. (nsw.gov.au)
- Grass Tetany is a deficiency of magnesium that causes them to stagger, look alert and become. (wardlab.com)
Hypocalcemia2
- citation needed] Hypocalcemia is the primary cause of tetany. (wikipedia.org)
- Hypocalcemia is not a term for tetany but is rather a cause of tetany. (wikipedia.org)
Carpopedal spasm2
- a 16 months old child present with tetany with carpopedal spasm.he had similar episode 2 months back,his s.calcium is 9mg percent salk phosphatase is 572.waht could be the cause,her weight is 7 kg. (pediatriconcall.com)
- Carpopedal spasm and tetany are typical manifestations and usually occur within weeks after surgery. (nih.gov)
Hyperventilation2
- Vomiting induced alkalosis and hyperventilation induced respiratory alkalosis also cause tetany because of neuronal irritability. (wikipedia.org)
- Heat tetany (hyperventilation and heat stress). (wellspan.org)
Cows4
- Grass tetany, recognized as a complicated magnesium deficiency, usually makes its appearance when cows are changed from the normal winter feeds to a new growth of grass in the early spring. (sdstate.edu)
- The incidence of grass tetany varies between seasons and locations, with the majority of clinically affected cows dying. (agsolutions.com.au)
- In addition, cows often do not develop signs of tetany until blood calcium concentrations drop below 0.8 mg/dL. (cornell.edu)
- Usually, affected cows will be mature and at the peak of lactation, although tetany may occur before calving or later in lactation. (cornell.edu)
Symptoms3
- An infected animal can die within hours of symptoms first appearing, making it vital that grass tetany be treated immediately. (laysfeedandpetsupply.com)
- Because symptoms may not be noticed right away once an animal begins to exhibit signs of grass tetany, treatment can be difficult. (laysfeedandpetsupply.com)
- Because grass tetany can strike so quickly and fatality can be high, it is better to take preventative steps to protect vulnerable livestock rather than rely on noticing symptoms and administering treatments case-by-case. (laysfeedandpetsupply.com)
Prevent grass2
- Understanding and recognizing the condition, however, can help you keep your animals healthy and prevent grass tetany from taking a toll on your livestock. (laysfeedandpetsupply.com)
- Providing adequate levels of magnesium in the diet cannot be stressed enough to help prevent grass tetany. (agsolutions.com.au)
Seizure1
- 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. (wikipedia.org)
Tetanus1
- Tetanic contractions (physiologic tetanus) are a broad range of muscle contraction types, of which tetany is only one. (wikipedia.org)
Contraction2
- 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. (wikipedia.org)
- This patient presented with facial tetany, involving contraction of the masseter and his neck muscles. (cdc.gov)
Susceptible1
- Any diet low in magnesium can lead to the condition, and high levels of milk production also make an animal more susceptible to grass tetany. (laysfeedandpetsupply.com)
Citation2
- citation needed] The usual cause of tetany is a deficiency of calcium. (wikipedia.org)
- citation needed] EMG studies reveal single or often grouped motor unit discharges at low discharge frequency during tetany episodes. (wikipedia.org)
Highly fatal1
- Grass tetany is a highly fatal disease associated with low levels of magnesium in the blood. (wa.gov.au)
Livestock1
- Grass tetany can be a serious and even fatal problem for different types of livestock. (laysfeedandpetsupply.com)
Disorder1
- Grass tetany is a nutritional or metabolic disorder characterized by low blood magnesium. (midwesternbioag.com)
Prevention1
- The key to successful tetany prevention is an assured daily intake of the required amount of Mg supplement. (cornell.edu)
Calcium level1
- Prolongation of the isoelectric phase of the S-T segment of the electrocardiogram may be present with tetany that is caused by a low serum calcium level. (unboundmedicine.com)
Nitrogen2
- Forages that contain more than 3 percent potassium and more than 4 percent nitrogen (25 percent crude protein) are likely candidates to create grass tetany problems. (cornell.edu)
- High rates of nitrogen and potassium fertilizer are sometimes associated with increased tetany problems. (cornell.edu)
Syndrome1
- verification needed] Osteomalacia and rickets due to deficiency of vitamin D[verification needed] Metabolic alkalosis with hypokalemia like Gitelman syndrome and Bartter's syndrome can cause tetany. (wikipedia.org)
Crops2
- With the increased interest in planting and grazing annual cover crops, producers need to be aware that doing so increases the risk of tetany because the mineral content is different than in perennial forages (Table 1). (cornell.edu)
- Note that of the cover crops, wheat has the greatest potential to cause tetany because of its low Mg and Ca levels, whereas Rye would pose the least risk. (cornell.edu)
Blood1
- Grass tetany is a magnesium deficiency in an animal's blood and is often more common in lactating females or older animals that have more difficulty absorbing magnesium. (laysfeedandpetsupply.com)
High1
- those with Mg levels between 0.1% and 0.2% are considered a low to moderate tetany risk, while values below 0.1% indicate a high tetany risk. (cornell.edu)
Anterior1
- Also, tetany can be demonstrated by tapping anterior to the ear, at the emergence of the facial nerve. (wikipedia.org)
Diagnosis1
- R29.0 is a billable ICD code used to specify a diagnosis of tetany. (icd.codes)
Levels1
- Low levels of magnesium can lead to tetany. (wikipedia.org)