| ¿µ¹® | infectious disease | ÇÑ±Û | °¨¿°º´ |
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| ¿µ¹® | hypertensive heart disease | ÇÑ±Û | °íÇ÷¾Ð½ÉÀ庴 |
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| ¼³¸í | °íÇ÷¾Ð¿¡ ÀÇÇØ¼ »ý±â´Â ½ÉÀ庴. °íÇ÷¾Ð½ÉÀ庴À̶ó´Â Áø´ÜÀ» ºÙÀ̱â À§Çؼ´Â ÃÖ¼ÒÇÑ ´ÙÀ½°ú °°Àº Á¶°ÇÀÌ ºÎÇյǾî¾ß Çϴµ¥, ù° ½ÉÀåÇ÷°ü°è¿¡ ½ÉÀ庴À» À¯¹ßÇÒ ¼ö ÀÖÀ» ¸¸ÇÑ ´Ù¸¥ º´º¯ÀÌ ¾øÀÌ ÁÂ½É½Ç ºñ´ë°¡ ÀÖ¾î¾ß Çϸç, µÑ° °íÇ÷¾ÐÀ» ¾Î¾Ò´Ù´Â º´·ÂÀÌ ÀÖ¾î¾ß ÇÑ´Ù. ÁÖ·Î °íÇ÷¾Ð¿¡ ÀÇÇÑ ½ÉÀ庴Àº Ãʱ⿡´Â Á½ɽÇÀÌ ºñÈĶó´Â °ÍÀ¸·Î Ư¡µÇ¾îÁø´Ù. Áï Ç÷¾ÐÀÌ ³ôÀ¸¹Ç·Î Ç÷¾×À» ¼øÈ¯½Ã۱â À§Çؼ´Â ±×¸¸Å ½ÉÀåÀÇ Ç÷¾×À» º¸³»´Â ÈûÀÌ ÁÁ¾Æ¾ß ÇÑ´Ù. ±× ÈûÀ» ¾ò±âÀ§Çؼ´Â ½É±ÙÀÇ ºñÈİ¡ ÇÊ¿ä·Î ÇÏ¿© ÁÂ½É½Ç ±ÙÀ°ÀÇ ºñÈİ¡ »ý±ä´Ù. ±×¸®°í °íÇ÷¾ÐÀÌ Áö¼ÓÀÌ µÉ °æ¿ì¿¡´Â °á±¹ ½ÉÀåÀÌ Á¦ ±¸½ÇÀ» ÇÏÁö ¸øÇÏ°í ÆßÇÁ·Î¼ÀÇ ±â´ÉÀ» ÀÒ¾î¹ö¸®°Ô µÇ¾î ½ÉÀå±â´É»ó½Ç¿¡ ºüÁö°Ô µÈ´Ù. |
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| ¿µ¹® | pelvic inflammatory disease | ÇÑ±Û | °ñ¹Ý¿°Áúȯ |
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| ¼³¸í | °ñ¹ÝÁÖÀ§ÀÇ Àå±â¿¡ ¹ß»ýÇÏ´Â ¿°ÁõÀ» ¸»ÇÔ. ÁÖ·Î ¿©¼º¿¡¼ ¹ß»ýÇÏ¸ç ¿øÀÎÀº ÀÓ±Õ(gonococcus)°ú ºñÀÓ±Õ¿¡ ÀÇÇÑ °¨¿°(non-gonorrheal infection)¿¡ ÀÇÇÑ´Ù. Áõ»óÀº Ãʱ⿡´Â ÁúºÐºñ¹°, ÇϺ¹ºÎµ¿Åë, ¿©¼ºÀÇ »ý½Ä±âºÎÀ§¿¡ ¹ß»ýÇÏ´Â ¾ÐÅë, ¿ù°æÅë, ¿ù°æ·®ÀÇ Áõ°¡ µîÀÌ´Ù. ÀÏÂï Ä¡·áÇØ¾ß Çϸç, °è¼ÓÀûÀ¸·Î º´ÀÌ Áö¼Ó½Ã ¿©¼ºÀÇ ºÒÀÓÀÇ ¿øÀÎÀÌ µÈ´Ù. ÈÄÁø±¹¿¡¼´Â °¡Àå ¸¹Àº ¿©¼ººÒÀÓÀÇ ¿øÀÎÀ̱⵵ ÇÔ. Ä¡·á´Â Ç×»ýÁ¦ÀÇ Åõ¿©ÀÌ´Ù. |
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| ¿µ¹® | Graves' disease | ÇÑ±Û | ±×·¹À̺꽺º´ |
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| ¼³¸í | °©»ó»ùÀÇ ºñ´ë¿Í °©»ó»ùÈ£¸£¸óÀÇ °ú´ÙºÐºñ°¡ Ư¡ÀÎ º´ÀÌ´Ù. ÀÌ º´Àº ÁÖ·Î 25~50¼¼¿¡ È£¹ßÇϰí ÁÖ·Î ¿©ÀÚ¿¡°Ô¼ ¸¹ÀÌ »ý±ä´Ù. °©»ó»ù È£¸£¸óÀº ÀúÀåµÇ¾î ÀÖ´Â ¿¡³ÊÁö¸¦ ¼Ò¸ðÇÏ¿© ½ÅüÀÇ ´ë»çÀ²À» ³ôÀ̴ ȣ¸£¸óÀ̹ǷΠÀÔ¸ÀÀÌ ÁÁÀº µ¥µµ ºÒ±¸ÇÏ°í °è¼ÓÀûÀΠüÁßÀÇ °¨¼Ò, ±×¸®°í ÃàÀûµÈ ¿¡³ÊÁö¸¦ ¼Ò¸ðÇÏ¿© ¿»ý¸¹ÀÌ ÇÏ¿©¼ ´õÀ§¸¦ Âü±â Èûµé¾îÇÏ°í ¸¸¼º ¼è¾à°¨À̳ª ±Ù·ÂÀÇ ¾àȸ¦ º¸ÀÏ ¼ö°¡ ÀÖ´Ù. ±×¸®°í ´«¿¡ Ư¡ÀûÀÎ Áõ»óÀÌ ³ªÅ¸³ª´Âµ¥ ´«²¨Ç®ÀÌ ºñÁ¤»óÀûÀ¸·Î À§·Î ¿Ã¶ó°¡ ÀÖ°í, ´«ÀÌ ¾Æ·¡ÀÇ ¹°°ÇÀ» ÁÖ½ÃÇÒ °æ¿ì¿¡ ´«²¨Ç®ÀÌ Á¤»óÀûÀ¸·Î´Â óÁ®¾ß ÇÏÁö¸¸ °©»ó»ù È£¸£¸óÀÌ °úµµÇÏ°Ô ³ª¿Ã °æ¿ì¿¡´Â ´«²¨Ç®ÀÌ Ã³ÁöÁö ¾Ê´Â´Ù. ¶Ç ´«¾ËÀÌ ¾ÕÂÊÀ¸·Î µ¹ÃâÇÏ´Â ¾È±¸µ¹ÃâÀ» º¼ ¼ö°¡ ÀÖ´Ù. ¶Ç ÇǺΰ¡ ¾ÆÁÖ ºÎµå·´°í ¹°±â°¡ ¸¹¾Æ¼ ÃàÃàÇÏ´Ù. ±×¸®°í Ư¡ÀûÀ¸·Î ÇÏÁöÀÇ ¾ÕÂÊ¿¡ ÇǺΰ¡ µÎ²¨¿öÁ® ±¹¼ÒÀû À¶±â¸¦ ÀÌ·ç´Â °ÍÀÌ Àִµ¥ À̰ÍÀº ÀÌ º´ÀÇ Æ¯Â¡ÀûÀÎ º´ÅÍÀÌ´Ù. |
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| ¿µ¹® | Raynaud disease | ÇÑ±Û | ·¹À̳뺴 |
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| ¼³¸í | ±â´ÉÀû Ç÷°ü °æ·ÃÀ» ÀÏÀ¸Å°´Â º´À¸·Î °Ç°ÇÑ ÀþÀº ¿©¼ºÀÇ ÆÈ´Ù¸® ÀÛÀº µ¿¸ÆÀ» ħ¹üÇÑ´Ù. ÇÁ¶û½º ÀÇ»ç M.·¹À̳ë(1834~1881)°¡ º¸°íÇÑ °ÍÀ¸·Î ÀÌ º´Àº ÁÖ·Î ¼Õ°¡¶ô, ¼Õ, ¶§·Î´Â ÄÚ³¡À̳ª ¹ßµî, ¸öÀÇ ¸»´ÜºÎ ¼Òµ¿¸ÆÀ» ħ¹üÇÑ´Ù. Çѳðú °¨Á¤Àڱؿ¡ ÀÇÇÏ¸ç ¼Õ°¡¶ôÀº ¹é»öÀ¸·Î ´ÙÀ½Àº û»öÀ¸·Î, ±×¸®°í Àû»öÀ¸·Î º¯ÇÑ´Ù. ¿©¼º¿¡°Ô È£¹ßÇÑ´Ù. |
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| ECG | Electro-Cardio-Graphy(-Gram); ½ÉÀüµµ = EKG 1. Conducting System Structu... |
|---|---|
| PMD | Progressive Muscular Dystrophy; ÁøÇ༺ ±ÙÀÌ¿µ¾çÁõ Types of PMD(Progressive Muscular Dystroph... |
| AR | 1) Aortic Regurgitation = AI Echo¼Ò°ß &... |
| GD | gastroduodenal; Gaucher disease; general diagnostics; general dispensary; gestational day; Gianotti ... |
| TAPVR | Total Anomalous Pulmonary Venous Return = TAPVC 4 Types of TAPVR &... |
| GD | Gaucher disease |
|---|---|
| HSV-2 | Herpes Simplex Virus type I and type 2 |
| HIV-2 | Human Immunodeficiency Virus type 1 and type 2 |
| HSV 2 | herpes simplex virus type 1 or type 2 |
| Type 1 | type |
Kugelberg-Welander disease ±Ù À§ÃàÁõÀÇ À¯Àü¼º ¿¬¼ÒÇüÀ¸·Î¼ º¸Åë »ó¿°»öü¼º ¿¼º ÇüÁú·Î À¯ÀüµÈ´Ù. ô¼ö Àü°¢ÀÇ º´º¯ÀÌ ±× ¿øÀÎÀÌ´Ù.
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| gaucher's disease, type 1 | A progressive genetic disease caused by a defect in an enzyme. The enzyme, called 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) |
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| disease, gaucher's type 1 | A progressive genetic disease caused by a defect in an enzyme. The enzyme, called 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) |
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| gaucher disease | <radiology> Cerebroside lipidosis, autosomal recessive, abnormal accumulation of glucocerebroside, RE system: liver, spleen, lymph nodes, CNS neurons, skeletal disorders, avascular necrosis, Erlenmeyer flask deformity, resorption of trabeculae, lytic/sclerotic changes, hepatosplenomegaly Cf: Niemann-Pick disease (12 Dec 1998) |
| Gaucher's disease | <disease> A chronic congenital disease of lipid metabolism caused by a deficiency of the beta-glucocerebrosidase enzyme. The defect is most common in Ashkenazi Jews. Clinical features are hepatosplenomegaly (enlargement of liver and spleen) and in severe early onset forms of the disease, with neurological dysfunction. Inheritance: autosomal recessive. (27 Sep 1997) |
| Gaucher cells | Large, finely and uniformly vacuolated cell's derived from the reticuloendothelial system, and found especially in the spleen, lymph nodes, liver, and bone marrow of patients with Gaucher's disease; Gaucher cell's contain kerasin (a cerebroside), which accumulates as a result of a genetically determined absence of the enzyme glucosylceramidase. (05 Mar 2000) |
| Gaucher disorder | <disease> A chronic congenital disease of lipid metabolism caused by a deficiency of the beta-glucocerebrosidase enzyme. The defect is most common in Ashkenazi Jews. Clinical features are hepatosplenomegaly (enlargement of liver and spleen) and in severe early onset forms of the disease, with neurological dysfunction. Inheritance: autosomal recessive. (27 Sep 1997) |
| Gaucher, Philippe | <person> French physician, 1854-1918. See: Gaucher cells, Gaucher's disease, pseudo-Gaucher cell. (05 Mar 2000) |
| pseudo-Gaucher cell | A plasma cell, microscopically resembling a Gaucher cell, found in the bone marrow in some cases of multiple myeloma. (05 Mar 2000) |
| Recklinghausen's disease type I | type 2 neurofibromatosis |
| central Recklinghausen's disease type II | type 1 neurofibromatosis |
| glycogen storage disease type I | <disease> An autosomal recessive disease in which gene expression of glucose-6-phosphatase is absent, resulting in hypoglycaemia due to lack of glucose production. Accumulation of glycogen in liver and kidney leads to organomegaly, particularly massive hepatomegaly. Increased concentrations of lactic acid and hyperlipidemia appear in the plasma. Clinical gout often appears in early childhood. Inheritance: autosomal recessive. (12 Dec 1998) |
| glycogen storage disease type II | <disease> Glycogenosis due to alpha-1,4-glucosidase (acid maltase) deficiency. It affects muscle, heart, and other organs. (12 Dec 1998) |
| glycogen storage disease type III | <disease> An autosomal recessive metabolic disorder due to deficient expression of amylo-1,6-glucosidase (one part of the glycogen debranching enzyme system). The clinical course of the disease is similar to that of glycogen storage disease type I, but milder. Massive hepatomegaly, which is present in young children, diminishes and occasionally disappears with age. Levels of glycogen with short outer branches are elevated in muscle, liver, and erythrocytes. Six subgroups have been identified, with subgroups type IIIa and type IIIb being the most prevalent. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type IV | <disease> An autosomal recessive metabolic disorder due to a deficiency in expression of branching enzyme (alpha-1,4-glucan-6-alpha-glucosyltransferase), resulting in an accumulation of abnormal glycogen with long outer branches. Clinical features are muscle hypotonia and cirrhosis. Death from liver disease usually occurs before age 2. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type V | <disease> Glycogenosis due to muscle phosphorylase deficiency. Characterised by painful cramps following sustained exercise. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type VI | <disease> A hepatic glycogen storage disease in which there is an apparent deficiency of hepatic phosphorylase activity. However, studies have not been able to distinguish between phosphorylase deficiency and phosphorylase kinase deficiency in patients with hepatic glycogenosis. (12 Dec 1998) |
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