| ¿µ¹® | iron deficiency anemia | ÇÑ±Û | ö°áÇ̺óÇ÷ |
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| 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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| ¿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÷ |
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| 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÷ |
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| 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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| FA | false aneurysm; Families Anonymous; Fanconi anemia; far advanced; fatty acid; febrile antigen; femor... |
|---|---|
| PA | panic attack; pantothenic acid; paralysis agitans; paranoia; passive aggressive; pathology; patient'... |
| AHA | acetohydroxamic acid; acquired hemolytic anemia; acute hemolytic anemia; American Heart Association;... |
| FAA | folic acid antagonist; formaldehyde, acetic acid, alcohol |
| SFA | saturated fatty acid; seminal fluid assay; serum folic acid; stimulated fibrinolytic activity; super... |
| FA | Folic Acid |
|---|---|
| IDA | Iron Deficiency Anemia |
| AISA | Acquired Idiopathic Sideroblastic Anemia |
| ACD | Anemia of chronic disorders |
| AA | Aplastic Anemia |
| folic acid deficiency | A nutritional condition produced by a deficiency of folic acid in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anaemia, macrocytic anaemia, and megaloblastic anaemia. It is indistinguishable from vitamin b 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in b 12 deficiency do not occur. (merck manual, 16th ed) (12 Dec 1998) |
|---|---|
| folic acid deficiency anaemia | Anaemia due to deficiency of folic acid, characterised by large-sized red blood cells (macrocytosis) and presence of large nuclei in erythroid precursor cells (megaloblasts) in the bone marrow. (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) |
| folic acid | <biochemistry> Pteridine derivative that is abundant in liver and green plants and is a growth factor for some bacteria. The biochemically active form is tetrahydrofolate (see folate). (12 Nov 1997) |
| folic acid antagonist | <pharmacology> A chemical which inhibits a cells capacity to use folic acid and so prevent cell division, for example methotrexate. See: chemotherapy. (12 Nov 1997) |
| folic acid antagonists | Inhibitors of the enzyme, dihydrofolate reductase (tetrahydrofolate dehydrogenase), which converts dihydrofolate (fh2) to tetrahydrofolate (fh4). They are frequently used in cancer chemotherapy. (12 Dec 1998) |
| folic acid conjugate | A folate with three molecules of glutamic acid (pteropterin) instead of one, or with seven (pteroylheptaglutamic acid or vitamin Bc conjugate). (05 Mar 2000) |
| folic acid deaminase | <enzyme> Chemotaxis regulating enzyme; splits folic acid into 6-hydroxymethylpterin and p-aminobenzoylglutamic acid Registry number: EC 3.5.4.- Synonym: folic acid inactivating enzyme, folic acid c9-n10 cleaving enzyme (26 Jun 1999) |
| folic acid oxidase | <enzyme> Enzyme from human red blood cell membranes; catalyses oxidation of folic acid to pterin-6-aldehyde plus p-aminobenzoylglutamic acid in presence of h2o2; singlet oxygen is involved Registry number: EC 1.11.- (26 Jun 1999) |
| 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) |
| Rambourg's chromic acid-phosphotungstic acid stain | <technique> A stain for glycoproteins, used with an electron microscope, with which ultrathin tissue sections reveal complex carbohydrates in the same locations as shown by Rambourg's periodic acid-chromic methenamine-silver stain. (05 Mar 2000) |
| abdominal muscle deficiency syndrome | <syndrome> Congenital absence (partial or complete) of abdominal muscles, in which the outline of the intestines is visible through the protruding abdominal wall; in males, genitourinary anomalies (urinary tract dilation and cryptorchidism) are also found; genetics unclear. (05 Mar 2000) |
| adult lactase deficiency | Onset of lactase deficiency, with resulting milk intolerance and malabsorption, in adulthood. Inherited forms may not be manifested until adulthood; any process that damages the intestinal lining cells can cause lactase deficiency in adults. (05 Mar 2000) |
| alpha-1 antitrypsin deficiency | <chest medicine> Deficiency of the protease inhibitor alpha-1 antitrypsin, leads primarily to degradation of elastin of the alveolar walls, as well as other structural proteins of a variety of tissues. The lack of this protein leads to damage of various organs, but mainly to the lung and liver. symptoms may become apparent at a very early age or in adulthood, manifesting either as shortness of breath or liver related symptoms (jaundice, fatigue, fluid in the abdomen, mental changes, or gastrointestinal bleeding). There are several options for treatment of the lung disease, including replacement of the missing protein. Treatment of the liver disease is a well-timed liver transplant (12 Dec 1998) |
| alpha-1-proteinase deficiency | Absence of a serum proteinase inhibitor that may cause nodular non-suppurative panniculitis. (05 Mar 2000) |
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