| ¿µ¹® | anemia | ÇÑ±Û | ºóÇ÷ |
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| ¼³¸í | Ç÷¾×ÀÌ ¼øÈ¯ÇÏ´Â ¸ñÀû Áß¿¡¼ °¡Àå Áß¿äÇÑ °ÍÀº ¿©·¯ °¡Áö ¿µ¾ç¼Ò¸¦ ¸»ÃÊÀÇ Àå±â·Î º¸±ÞÇÏ°í ¸»ÃÊÀÇ Àå±â¿¡¼ ³ª¿À´Â ¿©·¯ ³ëÆó¹°À» ÄáÆÏÀ̳ª Æó·Î º¸³» ¹è¼³¹°À» ó¸®ÇÏ´Â µ¥ ÀÖ´Ù. ±× Áß¿¡¼ »ê¼ÒÀÇ ¿î¹ÝÀº °¡Àå Áß¿äÇѵ¥ ¹Ù·Î ÀÌ »ê¼ÒÀÇ ¿î¹ÝÀ» ´ã´çÇÏ´Â °ÍÀÌ ÀûÇ÷±¸ÀÌ´Ù. ÀûÇ÷±¸¿¡´Â Ç÷»ö¼Ò¶ó´Â ¹°ÁúÀÌ ÀÖ¾î À̰ÍÀÌ »ê¼Ò¿Í °áÇÕÇÏ¿© »ê¼Ò¸¦ ¸»ÃÊÀÇ Àå±â·Î ¿î¹ÝÇÒ ¼ö°¡ ÀÖ´Ù. ºóÇ÷À̶õ ´ÜÀ§ºÎÇÇÀÇ Ç÷¾×¼Ó¿¡ ÀûÇ÷±¸ÀÇ ¾çÀÌ ÀûÀº °æ¿ì¸¦ ¸»ÇÑ´Ù. ÀûÇ÷±¸ÀÇ ¾çÀ» ³ªÅ¸³»´Â °ÍÀ¸·Î´Â 3°¡Áö ¹æ¹ýÀÌ ÀÖ´Ù. ÀûÇ÷±¸ÀÇ ¼ýÀÚ¸¦ Á÷Á¢ Ç¥ÇöÇÏ´Â ¹æ¹ý°ú, Ç÷»ö¼ÒÀÇ ¾çÀ» Á¤·®ÇÏ¿© ±× ¾çÀ» Ç¥½ÃÇÏ´Â ¹æ¹ý°ú, Ç÷¾×¼Ó¿¡¼ ÀûÇ÷±¸°¡ Â÷ÁöÇÏ´Â ¾ç(ÀûÇ÷±¸µîÀûÀ²)À» ³ªÅ¸³»´Â ¹æ¹ýÀÌ ±×°ÍÀÌ´Ù. ´ë°³ ºóÇ÷À̶ó ÇÔÀº ³²¼º¿¡¼ Ç÷»ö¼Ò < 14g/dl, Ç÷»ö¼Ò < 42%, ÀûÇ÷±¸ÀÇ ¼ö < 4,000,000/mm3ÀÏ °æ¿ìÀ̰í, ¿©¼º¿¡¼± Ç÷»ö¼Ò < 12g/dl, Ç÷»ö¼Ò < 36%, ÀûÇ÷±¸ÀÇ ¼ö < 3,300,000/mm3ÀÏ °æ¿ì¸¦ ÁöĪÇÑ´Ù. |
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| ¿µ¹® | pernicious anemia | ÇÑ±Û | ¾Ç¼ººóÇ÷ |
|---|---|---|---|
| ¼³¸í | ¾Ç¼º(»ý¸íÀ» À§ÇùÇϸç, Ä¡·á¿¡ ÀúÇ×ÇÏ´Â °æ¿ì¿¡ ´ë°³ ¾Ç¼ºÀ̶ó ºÎ¸§. ¿¹¸¦ µé¾î ÁøÇàµÈ ¾ÏÀÇ °æ¿ì)À̶ó À̸§ºÙ¾î ÀÖÁö¸¸, ½ÇÁ¦ÀûÀ¸·Î´Â ¾Ç¼ºÀÌ ¾Æ´Ï´Ù. ºóÇ÷ÀÇ ÀÏÁ¾ÀÌ´Ù. Á¤»óÀûÀ¸·Î ÀûÇ÷±¸´Â ¹ß´Þ°ú ¼º¼÷°úÁ¤¿¡¼ ºñŸ¹Î B12°¡ ÇʼöÀûÀÌ´Ù. ÀÌ ºñŸ¹Î B12ÀÇ Ç÷Áß³óµµ°¨¼Ò¿¡ ÀÇÇØ ÀûÇ÷±¸»ý¼º¿¡ ÁöÀåÀ» °¡Á®¿À°Ô µÇ°í, Ç÷¾×³»¿¡ Ư¡ÀûÀÎ °Å´ëÀû¸ð±¸(megaloblast)ÀÇ Çü¼ºÀÌ ³ªÅ¸³ª´Â Áúº´À» ¸»ÇÑ´Ù. |
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| ¿µ¹® | hemolytic anemia | ÇÑ±Û | ¿ëÇ÷ºóÇ÷ |
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| ¼³¸í | ¿ëÇ÷ºóÇ÷À̶õ ÀûÇ÷±¸ÀÇ °úµµÇÑ ÆÄ±«¿¡ ÀÇÇÑ ºóÇ÷ÀÌ´Ù. ¿ø·¡ 120ÀÏ Á¤µµÀÇ ¼ö¸íÀ» °¡Áö´Â ÀûÇ÷±¸ÀÇ ¼ö¸íÀÌ Âª¾ÆÁö´Â °ÍÀÌ´Ù. ¿©±â¿¡´Â ¿©·¯ °¡Áö ¿øÀÎÀÌ ÀÖÀ» ¼ö°¡ Àִµ¥ ´ëÇ¥ÀûÀÎ ¿øÀÎÀ¸·Î´Â ÀûÇ÷±¸¿¡ ´ëÇÑ Ç×ü°¡ »ý±â´Â °Í(¹ßÀÛ¼º¾ß°£Ç÷»ö¼Ò´¢Áõ)°ú ÀûÇ÷±¸ÀÚüÀÇ ÀÌ»ó(À¯Àü¼ºµÕ±ÙÀûÇ÷±¸Áõ), ±×¸®°í ´Ù¸¥ Áúº´¿¡ ÀÇÇØ¼ 2Â÷ÀûÀ¸·Î »ý±â´Â °ÍÀÌ ÀÖ´Ù. |
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| ¿µ¹® | aplastic anemia | ÇÑ±Û | Àç»ýºÒ·®ºóÇ÷ |
|---|---|---|---|
| ¼³¸í | Àç»ýºÒ·®¼º ºóÇ÷À̶õ °ñ¼öÀÇ ÀÌ»óÀ¸·Î »ý±â´Â ºóÇ÷ÀÌ´Ù. °ñ¼ö¶õ »À¼Ó¿¡ Á¸ÀçÇÏ´Â °ÍÀ¸·Î Ç÷±¸¸¦ »ý¼ºÇÏ´Â ¼¼Æ÷µé°ú ¹Ì¼º¼÷ÇÑ Ç÷±¸µé·Î ÀÌ·ç¾îÁ® ÀÖ´Ù. À̰͵éÀÌ ¿©·¯ °¡Áö ¿øÀο¡ ÀÇÇØ¼ ÆÄ±«µÇ¾úÀ» ¶§ »ý±â´Â ºóÇ÷À» Àç»ýºÒ·®ºóÇ÷À̶ó°í ÇÑ´Ù. ±×·¯¹Ç·Î ÀûÇ÷±¸¸¸ÀÇ °¨¼Ò°¡ ¾Æ´Ï¶ó ¸ðµç Ç÷±¸ ¼¼Æ÷ÀÇ °¨¼Ò¸¦ º¼ ¼ö ÀÖ´Ù. Ä¡·á·Î´Â Ç÷±¸ »ý¼ºÀ» ÀÚ±ØÇϴ ȣ¸£¸óÀ» Åõ¿©ÇÏ´Â °ÍÀÌ ÀÖÁö¸¸ À̰ÍÀ¸·Î´Â ÆÄ±«µÈ Ç÷±¸¸¦ »ý¼ºÇÏ´Â ¼¼Æ÷ÀÇ Àç»ýÀÌ ÀϾÁö ¸øÇϹǷΠ¿ÏÀüÇÑ Ä¡·á¶ó°í´Â º¼ ¼ö°¡ ¾ø´Ù. ¿ÏÀüÇÑ Ä¡·á·Î´Â ³²ÀÇ °ñ¼ö¸¦ äÃëÇØ¼ À̰Ϳ¡¼ºÎÅÍ Ç÷±¸¸¦ »ý¼ºÇÏ´Â ¼¼Æ÷¸¦ ºÐ¸®, ȯÀÚ¿¡°Ô À̽ÄÇÏ´Â °ñ¼öÀ̽ÄÀÌ ÀÖ´Ù. |
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| ¿µ¹® | iron deficiency anemia | ÇÑ±Û | ö°áÇ̺óÇ÷ |
|---|---|---|---|
| ¼³¸í | ÀûÇ÷±¸ÀÇ ±â´ÉÀº »ê¼Ò¸¦ ¿î¹ÝÇϴµ¥ ÀÖ´Ù. ÀûÇ÷±¸ ¼Ó¿¡ »ê¼Ò¿Í °áÇÕÀ» ÇÏ¿© »ê¼Ò¸¦ ¿î¹ÝÇÏ´Â Ç÷»ö¼Ò¶ó´Â ¹°ÁúÀÌ ÀÖ´Ù. öÀº ÀÌ Ç÷»ö¼ÒÀÇ Áß¿äÇÑ ºÎºÐÀ» ÀÌ·ç´Â °ÍÀ¸·Î öÀÌ ¾øÀ¸¸é Ç÷»ö¼Ò°¡ ¸¸µé¾îÁú ¼ö°¡ ¾ø´Ù. Ç÷»ö¼Ò°¡ ¾øÀ¸¸é ¿ª½Ã ÀûÇ÷±¸µµ ¸¸µé¾îÁöÁö ¾ÊÀ¸¹Ç·Î ü³»¿¡ öÀÌ ºÎÁ·ÇÏ¸é ºóÇ÷ÀÌ »ý±ä´Ù. ÀÌ Ã¶°áÇ̼º ºóÇ÷Àº ºóÇ÷ÀÇ ¿øÀÎ Áß¿¡¼ °¡Àå ÈçÇÑ °ÍÀÌ´Ù(¾à 25%¸¦ Â÷ÁöÇÑ´Ù). öÀúÀå·®ÀÇ ÀúÇÏ-°áÇÌ, Ç÷ûö³óµµÀÇ ÀúÇÏ, Æ®¶õ½ºÆä¸°·® »ó½Â, Æ®¶õ½ºÆä¸°Æ÷ȵµÀÇ ÀúÇÏ, Ç÷»ö¼Ò³óµµ ¶Ç´Â Ç츶ÅäÅ©¸®Æ®ÀÇ ÀúÇÏ, Àú»ö¼Ò¼º´ëÀûÇ÷±¸¸¦ Ư¡À¸·Î ÇÏ´Â ºóÇ÷·Î¼, »ýü ³»¿¡¼ öÀÌ Àå±â¿¡ °ÉÃÄ °áÇÌµÇ¸ç ±× ¶§¹®¿¡ Ç÷»ö¼Ò »ý»ê °¨¼Ò¿¡ ÀÇÇØ ÀϾÙ. âÀÚ¿¡¼ÀÇ Ã¶Èí¼ö·® ºÎÁ·, öÀÇ ¼ö¿ä Áõ´ë(À¯¾Æ±â, »çÃá±â, ÀÓ½Å), ö¼Ò½Ç°úÀ×(ÃâÇ÷)¿¡ ÀÇÇØ ÀϾ¸ç, ƯÈ÷ »çÃá±â¿¡¼ Æó°æ±â±îÁöÀÇ ¿©¼º¿¡°Ô ¸¹´Ù. Áõ»óÀ¸·Î¼´Â ¾ó±¼Ã¢¹é, ÇǷΰ¨, ÇǺÎâ¹é, ¼ÕÅé º¯È(½ºÇ¬ ¸ð¾ç) µîÀ» ³ªÅ¸³½´Ù. ±¸° ¿µ¿ª¿¡¼´Â ÇôÀÇ Á¢ÃËÅë, ¹ßÀû, °ÇÁ¶°¨, »ïÅ´°ï¶õÀ» ¼ö¹ÝÇϸé Ç÷¯¸Ó-ºó½¼(Plummer-Vinson)ÁõÈıºÀ̶ó°í ÇÑ´Ù. Ç÷¾× ¼Ò°ßÀº Ç÷ûöÀº ÀúÇÏÇϸç, ö°áÇÕ´É·ÂÀÇ »ó½Â, Àú»ö¼Ò¼º ÀÛÀºÀûÇ÷±¸¼ºÀ» ³ªÅ¸³½´Ù. |
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| micro | microcyte, microcytic; microscopic |
|---|---|
| AHA | acetohydroxamic acid; acquired hemolytic anemia; acute hemolytic anemia; American Heart Association;... |
| FHH | Familial Hypocalciuric Hypercalcemia = Familial Benign Hypercalcemia |
| FAD | familial Alzheimer dementia; familial autonomic dysfunction; fetal activity-acceleration determinati... |
| FAP | familial adenomatous polyposis; familial amyloid polyneuropathy; fatty acid polyunsaturated; fatty a... |
| AISA | Acquired Idiopathic Sideroblastic Anemia |
|---|---|
| ACD | Anemia of chronic disorders |
| AA | Aplastic Anemia |
| CIAV | Chicken infectious anemia virus |
| CDA | Congenital dyserythropoietic anemia |
| familial microcytic anaemia | A rare type of autosomal recessive hypochromic microcytic anaemia associated with a defect of iron metabolism characterised by high serum iron, hepatic iron deposits, and absence of stainable bone marrow iron stores. (05 Mar 2000) |
|---|---|
| anemia | <haematology> Too few red blood cells in the bloodstream, resulting in insufficient oxygen to tissues and organs. Origin: Gr. Haima = blood (16 Dec 1997) |
| microcytic anaemia | Any anaemia in which the average size of circulating erythrocytes is smaller than normal, i.e., the mean corpuscular volume is 80 cu um or less (normal range, 82 to 92 cu um). (05 Mar 2000) |
| hypochromic microcytic anaemia | Anaemia due to iron deficiency or thalassaemia, and characterised by lower than normal mean corpuscular volume, mean corpuscular haemoglobin, and mean corpuscular haemoglobin concentration. (05 Mar 2000) |
| benign familial chorea | A rare, nonprogressive movement disorder characterised by chorea and athetosis appearing in early childhood, most commonly manifested as gait ataxia and upper limb coordination. Intellect is unaffected. Probably autosomal-dominance inheritance with incomplete penetrance. (05 Mar 2000) |
| benign familial chronic pemphigus | Recurrent eruption of vesicles and bullae that become scaling and crusted lesions with vesicular borders, predominantly of the neck, groin, and axillary regions; autosomal dominant inheritance, presenting in late adolescence or early adult life. Synonym: Hailey-Hailey disease. (05 Mar 2000) |
| benign familial icterus | Mild jaundice due to increased amounts of unconjugated bilirubin in the plasma without evidence of liver damage, biliary obstruction, or haemolysis; thought to be due to an inborn error of metabolism in which the excretion of bilirubin by the liver is defective, ascribed to decreased conjugation of bilirubin as a glucuronide or impaired uptake of hepatic bilirubin. Synonym: benign familial icterus, constitutional hepatic dysfunction, Gilbert's disease, Gilbert's syndrome, Hebra's disease. (05 Mar 2000) |
| cancer, breast, familial | A number of factors have been identified that increase the risk of breast cancer. One of the strongest of these risk factors is the history of breast cancer in a relative. About 15-20% of women with breast cancer have such a family history of the disease, clearly reflecting the participation of inherited (genetic) components in the development of some breast cancers. Dominant breast cancer suceptibility genes, including BRCA1 and BRCA2, appear responsible for about 5% of all breast cancer. (12 Dec 1998) |
| paralysis, familial periodic | An autosomal dominant trait marked by recurring attacks of rapidly progressive flaccid paralysis. There are three types: I, associated with a fall in serum potassium levels (hypokalaemic periodic paralysis); II, associated with a rise therein (hyperkalaemic periodic paralysis, called also adynamia episodica hereditaria); and III, with normal levels (normokalaemic periodic paralysis). (12 Dec 1998) |
| pemphigus, benign familial | Rare hereditary disease characterised by recurrent eruptions of vesicles and bullae mainly on the neck, axillae, and groin. It exhibits autosomal dominant inheritance and is unrelated to pemphigus vulgaris though it closely resembles that disease. (12 Dec 1998) |
| chronic familial icterus | <haematology> A hereditary disorder that leads to a chronic haemolytic anaemia due to an abnormality in the red blood cell membrane. This disorder is caused by a defective gene. Red cells are resistant to stress and rupture easily. Infants may appear jaundiced and pale. Fatigue, weakness and shortness of breath are other symptoms that may be seen in older patients. The spleen may also be enlarged. Treatment includes splenectomy (removal of the spleen). After this is accomplished the life-span of the red blood cells returns to normal. (27 Sep 1997) |
| chronic familial jaundice | <haematology> A hereditary disorder that leads to a chronic haemolytic anaemia due to an abnormality in the red blood cell membrane. This disorder is caused by a defective gene. Red cells are resistant to stress and rupture easily. Infants may appear jaundiced and pale. Fatigue, weakness and shortness of breath are other symptoms that may be seen in older patients. The spleen may also be enlarged. Treatment includes splenectomy (removal of the spleen). After this is accomplished the life-span of the red blood cells returns to normal. (27 Sep 1997) |
| chronic familial polyneuritis | Inflammation of nerves related to infiltration by amyloid. (05 Mar 2000) |
| mixed hyperlipoproteinaemia familial | Type 5 hyperlipidemia, elevations of VLDL and chylomicrons found in plasma. Synonym: mixed hyperlipidemia. (05 Mar 2000) |
| progressive familial scleroderma | A syndrome characterised by calcinosis cutis, Raynaud's phenomenon, sclerodactyly, and telangiectasia; usually due to scleroderma; autosomal dominant form of progressive systemic sclerosis. (05 Mar 2000) |
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