| 영문 | congenital rubella syndrome | 한글 | 선천풍진증후군 |
|---|---|---|---|
| 설명 | 임신기간 중에 산모가 풍진에 걸리면 이 풍진 바이러스는 태반을 통해서 태아에게 전달되어서 태아의 풍진감염을 일으킨다. 임신 첫 3개월 동안, 특히 임신 첫달에 태아가 풍진의 감염을 받으면, 신생아에서 선천기형, 즉 눈에서 촛점을 정확히 맞추어주는 렌즈의 역할을 하는 수정체의 혼탁(백내장), 심장기형, 귀머거리 및 심한 지능박약을 동반하는 소두증 등이 발생하는 수가 많다. |
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| 영문 | carpal tunnel syndrome | 한글 | 손목굴증후군 |
|---|---|---|---|
| 설명 | 손목에는 아홉 개의 힘줄과 한 개의 신경이 통과하는 굴이 있는데 이곳을 손목굴이라 하고, 이곳을 지나는 신경이 눌리면 새깨손가락을 제외한 네 손가락이 아프고 저린 증상이다. 이것을 손목굴증후군이라 한다. 검사 방법으로는 근육 검사와 신경전달검사가 있다. 심할 때는 아침이나 저녁에 아파서 잠을 깨고 손목뿐만 아니라 어깨까지 아프다. 손목을 굽히고 있으면 통증이 심하다. 손목을 반복적으로 사용하는 운전자, 가정주부, 악기 연주자, 공장라인의 근로자, 컴퓨터 사용자, 목수가 해당된다. 손바닥뼈가 깨지거나 넘어지면서 손바닥으로 짚었을 때도 발생하며 드물게 진동하는 공구를 사용해도 나타나기도 한다. 임산부, 통풍, 류마티스 관절염, 갑상샘 기능 저하증, 당뇨병 등이 있을 때 이런 증상이 올 수 있다. 여자에게 더 많고 주로 자주 쓰는 손목이 해당된다. 심할 때는 손목에 땅콩만한 크기로 부어오른다. 누르면 안으로 쑥 들어가기도 하고 다시 움직이면 튀어나온다. 손목뼈 여덟 개 중에 반달뼈라 불리는 작은뼈의 인대가 이완되어 생긴다. 통증을 감소하는 치료로 부목, 얼음찜질, 이뇨제, 항생제를 사용하기도 하며 통증이 계속되면 코르티코스테로이드 호르몬을 손목부에 주사하여 통증을 줄인다. 부작용으로는 재발률이 높다. |
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| 영문 | sudden infant death syndrome | 한글 | 영아급사증후군 |
|---|---|---|---|
| 설명 | 한 살 이하의 건강한 아기가 아무런 조짐이나 원인 없이 갑자기 사망했을 경우에 내리는 진단이다. 이 증후군은 생후 1~4개월 사이에 가장 많이 발생하며, 대부분 밤 10시에서 오전 10시 사이에 발생한다. 조산하거나 부모가 흡연자일 경우, 20세 이하 산모의 초산, 임신전 건강관리에 소홀한 산모에게서 태어난 영아에게서 많이 발생한다. 이 증후군으로 사망한 영아의 형제일 경우 일반적인 영아보다 걸릴 확률이 높은 것으로 알려져 있다. |
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| 영문 | severe acute respiratory syndrome(SARS) | 한글 | 중증급성호흡증후군 |
|---|---|---|---|
| 설명 | 중국 광동 지역에서 가장 먼저 발생한 전염성호흡기병으로 세계보건기구(WHO)에서 ‘중증급성호흡증후군(SARS)'으로 명명했다. 섭씨 38도 이상의 고열과 기침, 호흡곤란, 저산소증, X선상의 폐렴증상 중 하나 이상의 증상이 나타나며, 두통, 근육통, 식욕부진, 피로감, 발진, 설사를 동반할 수 있다. 초기 증상은 감기와 비슷하지만 폐렴으로 발전하면 치명적일 수 있다. 현재 밝혀진 감염경로는 환자가 재채기나 기침할 때 내뿜는 침방울이고, 이것이 다른 사람의 호흡기로 들어갈 때 전염된다. 침방울이 전달되는 거리는 보통 1m로 보고 있다. 공기를 통해 전염이 가능하다는 주장이 제기됐지만 아직 확인되지 않았다. 원인균은 변종 코로나바이러스로 밝혀졌다. |
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| 영문 | syndrome | 한글 | 증후군 |
|---|---|---|---|
| 설명 | 증상의 집합. 어떤 질병의 징후의 총합을 말한다. 대개 그 원인은 알 수 없으나, 증상이 복합적으로 나타나고 이에 대한 치료가 일정한 경우 하나의 증후군으로 취급한다. |
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| nem | nutritional milk unit [Ger. Nahrungs Einheit Milch] |
|---|---|
| NIA | National Institute on Aging; nephelometric inhibition assay; niacin; no information available; Nutri... |
| NST | neospinothalamic [tract]; nonshivering thermogenesis; nonstress test; nutritional support team |
| PNI | peripheral nerve injury; postnatal infection; prognostic nutritional index |
| ADS | acute death syndrome; acute diarrheal syndrome; Alcohol Dependence Scale; alternative delivery syste... |
| anaemia, iron deficiency | Deficiency of iron results in anaemia because iron is necessary to make haemoglobin, the key molecule in red blood cells responsible for the transport of oxygen. In iron deficiency anaemia, the red cells are unusally small (microcytic) and pale (hypochromic). Characteristic features of iron deficiency anaemia in children include failure to thrive (grow) and increased infections. The treatment of iron deficiency anaemia, whether it be in children or adults, is with iron and iron-containing foods. Food sources of iron include meat, poultry, eggs, vegetables and cereals (especially those fortified with iron). According to the National Academy of Sciences, the Recommended Dietary Allowances of iron are 15 milligrams per day for women and 10 milligrams per day for men. Anaemia characterised by low or absent iron stores, low serum iron concentration, elevated free erythrocyte porphorin, low transferrin saturation, elevated transferrin, low serum ferritin, low haemoglobin concentration or haematocrit, and hypochromic microcytic red blood cells. Symptoms may include pallor, angular stomatitis and other oral lesions, gastrointestinal complaints, retinal haemorrhages and exudates, and thinning and brittleness of the nails. Among the causes of iron-deficiency anaemia are inadequate iron intake, impaired iron absorption, increased blood loss and increased requirements such as infancy, pregnancy, and lactation. (12 Dec 1998) |
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| antibody deficiency disease | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| antitrypsin deficiency | Deficiency of a1-antitrypsin, a glycoprotein of the postalbumin region of human serum. Many forms are known which may be moderate (40 to 60% of normal activity) or severe (less than 10% of normal), all autosomal dominant; the severe form is often associated with familial emphysema or hepatic cirrhosis. (05 Mar 2000) |
| arch length deficiency | The difference between the available circumference of the dental arch and that required to accommodate the succedaneous teeth in proper alignment. (05 Mar 2000) |
| arginase deficiency | <biochemistry> Arginase is the fifth enzyme of the urea cycle and catalyses the hydrolysis of arginine to ornithine and urea as the final step in the detoxification of ammonia. Deficiency of the enzyme results in hyperargininaemia and episodic hyperammonaemia, leading to moderate to severe mental retardation and spasticity. at least two isozymes of arginase exist in man. AI (the enzyme deficient in the disorder) is cytosolic and found primarily in liver and red blood cells, whereas AII is mitochondrial and found predominantly in kidney but also to a lesser extent in liver, brain, and other tissues. While AII activity appears to be induced in AI deficiency, it is only partially effective in maintaining urea cycle function. The normal in vivo function of AII is unclear. Arginase deficiency is diagnosed by observing high arginine concentrations on either qualitative or quantitative plasma or urine amino acid analysis. The diagnosis is confirmed by finding markedly decreased or absent arginase activity in an isotopic red blood cell enzymatic assay. The AI gene has been cloned, sequenced, and localised to human chromosome band 6q23. (17 Dec 1997) |
| ascorbic acid deficiency | A condition due to a dietary deficiency of ascorbic acid (vitamin c), characterised by malaise, lethargy, and weakness. As the disease progresses, joints, muscles, and subcutaneous tissues may become the sites of haemorrhage. Ascorbic acid deficiency frequently develops into scurvy in young children fed unsupplemented cow's milk exclusively during their first year. It develops also commonly in chronic alcoholism. (cecil textbook of medicine, 19th ed, p1177) (12 Dec 1998) |
| beta-d-glucuronidase deficiency | A rare deficiency of beta-d-glucuronidase; an autosomal recessive disorder with several allelic forms, characterised by abnormal mucopolysaccharide metabolism leading to progressive mental deterioration, splenic and hepatic enlargement, and dysostosis multiplex. Synonym: mucopolysaccharidase. (05 Mar 2000) |
| brancher deficiency glycogenosis | Type of glycogen storage disease, due to deficiency of amylo-1,4-1,6-transglucosidase (brancher enzyme). Synonym: brancher deficiency glycogenosis, debrancher deficiency. (05 Mar 2000) |
| calcium deficiency | A low blood calcium (hypocalcaemia) makes the nervous system highly irritable with tetany (spasms of the hands and feet, muscle cramps, abdominal cramps, overly active reflexes, etc.). Chronic calcium deficiency contributes to poor mineralization of bones, soft bones (osteomalacia) and osteoporosis; and, in children, rickets and impaired growth. Food sources of calcium include dairy foods, some leafy green vegetables such as broccoli and collards, canned salmon, clams, oysters, calcium-fortified foods, and tofu. According to the National Academy of Sciences, adequate intake of calcium is 1 gram daily for both men and women. The upper limit for calcium intake is 2.5 grams daily. (12 Dec 1998) |
| carbamoylphosphate synthetase deficiency | <biochemistry> Carbamoylphosphate synthetase is the initial enzyme of the urea cycle, catalysing the synthesis of carbamoylphosphate from ammonia, bicarbonate and ATP as the first step of ammonia detoxification. The enzyme is an intramitochondrial form called CPS I. A different isozyme found in the cytoplasm, called CPS II, is much less active and apparently not involved in the urea cycle. The deficiency state is autosomal recessive and presents in infancy with massive hyperammonaemia and neurologic deficits in survivors. Diagnosis is suggested by the blood biochemistry and confirmed by specific enzyme assay on liver or rectal biopsy. Prenatal diagnosis by molecular methods has been used successfully in informative families. Inheritance: autosomal recessive. (07 Apr 1998) |
| g-6-p-d deficiency | <biochemistry> An inherited condition that results in a deficiency in glucose-6-phosphate dehydrogenase. Particular drugs (sulphonamides) can exacerbate this problem. The result is haemolytic anaemia. (27 Sep 1997) |
| galactokinase deficiency | An inborn error of metabolism due to congenital deficiency of galactokinase, resulting in increased blood galactose concentration (galactosaemia), cataracts, hepatomegaly, and mental deficiency; autosomal recessive inheritance. Galactose epimerase deficiency and galactose-1-phosphate uridyl transferase deficiency produce much the same clinical picture. (05 Mar 2000) |
| galactokinase deficiency galactosaemia | An autosomal recessive disorder resulting in an accumulation of galactose and galactitol. (05 Mar 2000) |
| magnesium deficiency | Can occur due to inadequate intake or impaired intestinal absorption of magnesium. Low magnesium (hypomagnesaemia) is often associated with low calcium (hypocalcaemia) and low potassium (hypokalaemia). Deficiency of magnesium causes increased irritability of the nervous system with tetany (spasms of the hands and feet, muscular twitching and cramps, spasm of the larynx, etc.). According to the national academy of sciences, the recommended dietary allowances of magnesium are 420 milligrams per day for men and 320 milligrams per day for women. The upper limit of magnesium as supplements is 350 milligrams daily, in addition to the magnesium from food and water. (12 Dec 1998) |
| glucocerebrosidase deficiency | Causes Gaucher's disease (type 1), a progressive genetic disease due to an enzyme defect. The enzyme, glucocerebrosidase, is needed to break down the chemical glucocerebroside. The enzyme defect in persons with Gaucher's disease (GD) leads to the accumulation of glucocerebroside in the spleen, liver, and lymph nodes. The most common early sign is enlargement of the spleen (located in the upper left abdomen). Other signs include low red blood cell counts (anaemia), a decrease in blood clotting cells (platelets), increased pigmentation of the skin, and a yellow fatty spot on the white of the eye (a pinguecula). Severe bone involvement can lead to pain and collapse of the bone of the hips, shoulders, and spine. The GD gene is on chromosome 1. The disease is a recessive trait. Both parents carry a GD gene and transmit it for their child with the disease. The parents' risk of a child with the disease is 1 in 4 with each pregnancy. This type of Gaucher's disease (noncerebral juvenile Gaucher's disease) is most common in Ashkenazi Jews (of European origin) and is the most common genetic disease among Jews in the United States. (12 Dec 1998) |