| 영문 | Raynaud disease | 한글 | 레이노병 |
|---|---|---|---|
| 설명 | 기능적 혈관 경련을 일으키는 병으로 건강한 젊은 여성의 팔다리 작은 동맥을 침범한다. 프랑스 의사 M.레이노(1834~1881)가 보고한 것으로 이 병은 주로 손가락, 손, 때로는 코끝이나 발등, 몸의 말단부 소동맥을 침범한다. 한냉과 감정자극에 의하며 손가락은 백색으로 다음은 청색으로, 그리고 적색으로 변한다. 여성에게 호발한다. |
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| 영문 | rheumatic heart disease | 한글 | 류마티스심장병 |
|---|---|---|---|
| 설명 | 사슬알균감염 후 생기는 심장판막병이다. 원인은 A군 -용혈사슬알에 의한 인두염후 일종의 면역반응으로 발병한다. 진단은 존의 기준에 의한다. (1) 주요기준은 관절염 심장염(심장비대, 심장잡음, 심장기능상실 등) 무도증: 무당이 춤을 추는 것 같은 행동의 발작증세. 연변홍반: 빨간 테두리를 가진 피부병변은 피하결절(subcutaneous nodule): 피부 밑에 생긴 결절, (2)참고 기준은 열, 관절통, EKG상 PR연장: 심전도 소견 급성기 반응물질(예: ESR, CRP)의 상승, 류마티스열 치료는 페니실린으로 치료하고 심장의 후유증 또한 페니실린으로 예방한다. |
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| 영문 | chronic obstructive pulmonary disease | 한글 | 만성폐쇄폐병 |
|---|---|---|---|
| 설명 | 만성적으로 기도의 폐쇄를 가져오는 병을 이르는 말. 대개 만성기관지염, 기관지 천식, 폐기종의 3가지 병을 말한다. 만성기관지염이란 기관지의 만성염증을 말한다. 기관지의 염증으로 인해서 기관지의 점막에 부종이 생기고 이로 인해서 기관지의 내경이 좁아져서 기도의 폐쇄를 가져온다. 대개 흡연과 밀접한 연관을 가지며, 호흡곤란, 기침, 그리고 가래(대개 색이 푸르고 점도가 높은 가래)가 증상으로 나타난다. 폐기종은 기관지의 벽을 지지하는 조직의 파괴에 의해서 기관지가 제 모양을 갖추지 못하고 무너지게 되어 기도의 폐쇄가 일어나는 병이다. 즉 기관지가 관 모양으로 팽팽하게 펴지는 것을 지지하는 조직의 파괴에 의해서 관모양으로 펴지지 못해 결국은 폐포내에 공기가 차고 폐포벽이 파열되고 기관지가 좁아지게 되는 병을 말한다. 기관지천식이란 여러 가지 자극에 대해서 기관지가 과민한 반응을 보여서 생기는 기관지의 가역적인 폐쇄를 의미한다. 즉 정상인에게서는 기관지의 폐쇄를 보이지 않는 자극에 대해서 기관지의 폐쇄가 생기고 그 자극이 없을 경우에는 기관지의 폐쇄가 없어지는 병을 말한다. |
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| 영문 | Buerger disease | 한글 | 버거병 |
|---|---|---|---|
| 설명 | 말초 동맥과 정맥에 염증을 일으키는 병. 청장년층의 남자에게 잘 걸리는 다리 동맥에 생기는 병으로 동맥이 막히고 통증 때문에 발을 절기도 하는데 원인은 알려져 있지 않다. 병명은 이 병을 최초로 상세하게 보고한 미국의 의사 L. 버거(1879~1943)의 이름에서 연유한다. 동양인에게 많은 병으로, 대부분 젊은 남성, 특히 장년기 남성에게서 나타난다. 원인은 알 수 없으나 흡연이 병의 악화를 초래한다. 사지의 동맥과 정맥에 염증이 일어나 혈전이 생기면 내강을 막아 혈액이 흐르지 못하게 되어 그 앞의 말초조직이 괴사에 빠지거나 손발이 차갑고, 손가락-발가락이 보라색 또는 검은색으로 변한다. 또, 이 증세가 계속되는 동안 손발가락에 통증이 일어나고 궤양이 발생한다. 치료는 증세의 정도와 폐색된 혈관의 부위에 따라 연고를 바르거나 혈관확장제-순환개선제-혈소판응집억제제를 사용하나, 어떤 치료도 효과가 없을 경우 손발가락의 소절단, 드물게는 무릎 이하의 대절단을 해야 한다. 일반적으로 이 병의 예후는 양호하여 혈류가 회복되고 궤양만 치료되면 재발이 적다. |
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| 영문 | Behcet disease | 한글 | 베체트병 |
|---|---|---|---|
| 설명 | 심한 포도막염, 망막혈관염, 시각신경위축, 구강-성기의 아프타성 궤양, 광범위한 혈관염의 징후와 증상을 나타낸다. 원인불명의 희귀한 병으로 젊은 남자에게 잘 발생한다. |
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| AD | accident dispensary; acetate dialysis; active disease; acute dermatomyositis; addict, addiction; ade... |
|---|---|
| PD | Doctor of Pharmacy; Dublin Pharmacopoeia; interpupillary distance; Paget disease; pancreatic duct; p... |
| RD | radial deviation; radiology department; rate difference; Raynaud disease; reaction of degeneration; ... |
| BG | basal ganglion; basic gastrin; Bender Gestalt [test]; beta-galactosidase; beta-glucuronidase; bicolo... |
| GLU | glucose; glucuronidase; glutamate; glutamic acid |
| 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) |
| 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) |
| carbonic anhydrase II deficiency syndrome | <syndrome> An inherited deficiency of carbonic anhydrase II that results in osteopetrosis and metabolic acidosis. Synonym: osteopetrosis with renal tubular acidosis. (05 Mar 2000) |
| 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) |
| vitamin a deficiency | A nutritional condition produced by a deficiency of vitamin a in the diet, characterised by night blindness and other ocular manifestations such as dryness of the conjunctiva and later of the cornea (xerophthalmia). Vitamin a deficiency is a very common problem worldwide, particularly in developing countries as a consequence of famine or shortages of vitamin a-rich foods. In the united states it is found among the urban poor, the elderly, alcoholics, and patients with malabsorption. (12 Dec 1998) |
| vitamin B12 deficiency | A form of anaemia (low red blood cell counts) that results when the bone marrow fails to produce adequate numbers of red blood cells due to a deficiency in vitamin B12. Intrinsic factor, necessary for normal B12 absorption, may be the underlying cause for B12 deficiency if is not produced in the gastric glands (in the stomach). (27 Sep 1997) |