Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
 ...
PMID:Idiopathic hypoparathyroidism in five cats. 202 14

Sudden unexplained death may be seen with treatment of craniovertebral anomalies and surgery of the upper cervical spine. Death is due to sleep-induced apnea, premonitored by periods of confusion, lethargy, and asthenia. There may be associated hypotension, bradycardia, hyponatremia, hypothermia, inappropriate antidiuretic hormone secretion, and difficulty in micturition. The potential for respiratory failure may be predicted if a CO2 response test demonstrates an attenuated or abnormal response. Apnea during sleep may be reversed by arousal or may require ventilatory support for a period of time. The condition is self-limiting, but remains the major life-threatening complication. Both apnea and autonomic dysfunction are treatable and curable with appropriate diagnosis and management.
 ...
PMID:Occult respiratory and autonomic dysfunction in craniovertebral anomalies and upper cervical spinal disease. 375 66

The peak time period for the average beef producer to experience the majority of calf losses has consistently been from the time of birth through the first seven days of life. Weakness is a principal clinical sign of diseases or conditions responsible for mortality including birth trauma, prematurity or dysmaturity, congenital malformations, metabolic defects, intrauterine infection, anoxia or hypoxia, hypothermia, starvation, extremes in birth weight, and post-natal infection. This article discusses anoxia/hypoxia and septicemia in greater detail because of their involvement as a common cause of weakness in the newborn calf.
 ...
PMID:Weakness in the newborn calf. 819 20

Sarin (O-isopropylmethylphosphonofluoridate) is a highly toxic nerve agent produced for chemical warfare. Sarin is an extremely potent acetylcholinesterase (AchE) inhibitor with high specificity and affinity for the enzyme. Death by sarin is due to anoxia resulting from airway obstruction, weakness of the muscles of respiration, convulsions and respiratory failure. The main clinical symptoms of acute toxicity of sarin are seizures, tremors and hypothermia. Exposure to sarin during incidents in Japan in 1994, 1995 and 1998, and possible exposure to low levels of sarin during the Gulf War, resulted in the deaths and injury of many people in Japan and caused possible long-term health effects on Gulf War veterans. Symptoms related to sarin poisoning in Japan still exist 1-3 years after the incident and include fatigue, asthenia, shoulder stiffness and blurred vision. Sarin produced seizures in rats and pigs. Recent studies showed that long-term exposure to low levels of sarin caused neurophysiological and behavioral alterations. Toxicity from sarin significantly increased following concurrent exposure to other chemicals such as pyridostigmine bromide. Further research to examine effects of sarin on the cellular and the molecular levels, gene transcription, endocrine system as well as its long-term impact is needed.
 ...
PMID:Sarin: health effects, metabolism, and methods of analysis. 1238 97