| ¿µ¹® | fever blister | ÇÑ±Û | ¿¼º¼öÆ÷ |
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| ¼³¸í | 1Çü ´Ü¼ø Ç츣Æä½º ¹ÙÀÌ·¯½º(herpes simplex virus)ÀÇ °¨¿°¿¡ ÀÇÇØ¼ »ý±â´Â ÇǺκ´À¸·Î ÁÖ·ÎÀÔ¼ú¿¡ º´º¯À» °¡Áö´Â º´À» ¸»ÇÑ´Ù. ÀÔ¼úÆ÷Áø(herpes labialis)¿Í µ¿ÀǾî·Î ¾²ÀδÙ. Áï ´Ü¼øÆ÷ÁøÁß ÀÔÁÖÀ§¿¡ »ý±â´Â °ÍÀ» ÁöÁ¤ÇÏ´Â ¸»ÀÌ´Ù. ´Ü¼øÇ츣Æä½º(herpes simplex)¶õ º¸Åë ÀÛÀº ¹°ÁýÀÌ ¿©·¯ °³ ¸ð¿© »ý±â´Â ÇǺκ´À» ¸»ÇÑ´Ù. Àß ¹ß»ýÇÏ´Â °÷Àº ÀÔ¼ú, ¿ÜÀ½ºÎ µîÀ̸ç ÁÖ·Î ÇÇºÎ¿Í Á¡¸·ÀÇ ÀÌÇàºÎ¿¡ ³ªÅ¸³´Ù. ¹°ÁýÀº ½Ò¾Ë¸¸ÇÑ Å©±âÀÇ ÀÛÀº ¹°Áý ¶Ç´Â °í¸§À» Æ÷ÇÔÇÏ´Â ¹°ÁýÀ¸·Î ¸î °³°¡ ¹«¸®¸¦ Áö¾î ³ªÅ¸³ª´Âµ¥, ¸çÄ¥ Áö³ª¸é ¹°ÁýÀÇ ¸·ÀÌ ÅÍÁö°í, ÇǺÎÀÇ Ç¥¸éÀÌ Áø¹«¸£°í Çæ¾î¼ ÀÛÀº »óó¸¦ Çü¼ºÇÏ¿© ³ëÃâµÈ´Ù. ±×¸®°í µüÁö°¡ ¾É¾Æ ±»¾îÁø ´ÙÀ½ 7~10ÀÏ °¡·® Áö³ª¸é ÀúÀý·Î ³´´Â´Ù. ´Ü¼ø¼º Æ÷ÁøÀº ¹ß»ý ºÎÀ§¿¡ µû¶ó¼ ÀÔ¼úÆ÷Áø°ú À½ºÎÆ÷ÁøÀ¸·Î ±¸ºÐµÈ´Ù. ÀÔ¼úÆ÷ÁøÀº ÇÇ·ÎÇϰųª °ñÇÁÀå ¶Ç´Â ÇØ¼ö¿åÀå µîÁö¿¡¼ ÇÞºµ¿¡ ½ÉÇÏ°Ô ³ëÃâµÈ ÈÄ¿¡ À¯¹ßµÇ´Â °æ¿ì°¡ ¸¹´Ù. À½ºÎÆ÷ÁøÀº ¼º±³¿¡ ÀÇÇÏ¿© Àü¿°µÇ´Â °æ¿ìµµ ÀÖÀ¸¸ç, ÁßÁõÀÏ ´ë¿¡´Â °Ý½ÉÇÑ ¾ÆÇÄÀ» ¼ö¹ÝÇϸç ÁÖÀ§ÀÇ ¸²ÇÁÀýÀÇ Á¾´ë¸¦ ÃÊ·¡Çϱ⵵ ÇÑ´Ù. Á÷¾÷»ó Á¢ÃË ±âȸ°¡ ¸¹Àº Àǻ糪 °£È£»çÀÇ °æ¿ì´Â ¼Õ°¡¶ô ³¡¿¡ ¹ß»ýÇÒ ¶§µµ ÀÖ´Ù. À¯¾ÆÀÇ °æ¿ì¿¡´Â °í¿°ú ÀεÎÅë µîÀÇ ½ÉÇÑ Áõ¼¼°¡ ³ªÅ¸³ª±âµµ ÇÏ¿© ¶§·Î´Â ¸ñ¼û±îÁö ÀҴ´Ù. |
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| ¿µ¹® | epidemic hemorrhagic fever | ÇÑ±Û | À¯ÇàÃâÇ÷¿ |
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| ¼³¸í | Çѱ¹ÀüÀï´ç½Ã ±¹³»¿¡¼ ¹ß°ßµÇ¸é¼ ÇѶ§ Çѱ¹Çü ÃâÇ÷¿(Korean hemorrhagic fever)À̶ó°íµµ ºÒ¸®¿ü´ø ÀÌ º´Àº °©Àڱ⠽ÃÀÛÇÏ´Â ¿ÀÇÑ, µÎÅë, ±ÙÀ°ÅëÀ» ³ªÅ¸³»°í ÀÌ¾î¼ 3~5ÀÏ ³»¿¡ Àü½Å ÇǺΠ¹× °ø¸·ÃâÇ÷, Ç÷¼ÒÆÇ°¨¼ÒÁõ, ´Ü¹é´¢ ¹× ½ÅÀå ±â´É»ó½Ç µîÀÌ ¿Â´Ù. ¸»±â¿¡´Â ¼îÅ© ¹× Àúü¿ÂÀÌ µÉ ¼ö ÀÖ´Ù. óÀ½ 7~10ÀÏ °£¿¡ »ì¾Æ³²Àº ȯÀÚµéÀº ¼¼È÷ ȸº¹µÇ³ª ´Ü¹é´¢ÀÇ ÇÌ´¢´Â ¼ö ÁÖ°£ Áö¼ÓµÈ´Ù. Áõ¼¼¿¡ µû¶ó¼ ¹ß¿±â, ÀúÇ÷¾Ð±â, °¨´¢±â, ÀÌ´¢±â, ȸº¹±â·Î ºñ±³Àû ƯÀÌÇÏ°Ô ±¸ºÐµÈ´Ù. Hantaan virus¶ó°í ºÒ¸®´Â ÀÌ º´¿øÃ¼´Â ¼¼Æ÷Áú¿¡¼ ÀÚ¶ó´Â RNA ¹ÙÀÌ·¯½ºÀ̸ç Bunyaviridae°ú¿¡ ¼ÓÇÏ´Â Hanta ¹ÙÀÌ·¯½º¼Ó¿¡ ¼ÓÇÏ´Â Á¾(species)À¸·Î ÇÑź ¹ÙÀÌ·¯½º À̿ܿ¡ Puumula virus, Hill virus°¡ ÀÖ´Ù. ÃÖ±Ù¿¡ ȯÀڷκÎÅÍ ÇÑź¹ÙÀÌ·¯½º¿Í´Â ±¸ºÐµÇ´Â Seoul virus°¡ ºÐ¸®, µ¿Á¤µÊ¿¡ µû¶ó¼ ¾ß¿ÜÇü(Hantaan virus)°ú µµ½ÃÇü(Seoul virus)ÀÌ º´¿øÃ¼°¡ ¼·Î ´Ù¸£´Ù´Â Á¡ÀÌ ¾Ë·ÁÁ³´Ù. Çѱ¹À» ºñ·ÔÇÏ¿© ¸¸ÁÖ, ½Ãº£¸®¾Æ µîÁö¿¡¼ À¯ÇàÇÏ´Â ÁúȯÀ¸·Î ¾Ë·ÁÁ³À¸³ª ÇÑź¹ÙÀÌ·¯½ºÀÇ ¹ß°ßÀ» °è±â·Î Ç÷û°Ë»ç°¡ °¡´ÉÇØÁöÀÚ ÇÑź¹ÙÀÌ·¯½º ³»Áö´Â ÀÌ¿Í Ç׿ø±¸Á¶°¡ À¯»çÇÑ ¹ÙÀÌ·¯½º·Î »ý±â´Â °¨¿°ÁõÀÌ ¼¼°è °¢Ã³¿¡ ºÐÆ÷µÇ¾î ÀÖ´Ù´Â °ÍÀÌ ÆÇ¸íµÇ¾ú´Ù. °èÀýÀûÀÎ ¹ß»ýÀº ƯÀÌÇϸç, ±¹³»¿¡¼´Â º½°ú °¡À»¿¡ µÎ ¹øÀÇ À¯ÇàÀÌ ÀÖ´Ù°í ÇÏÁö¸¸ ÃÖ±Ù¿¡´Â °¡À»ÀÇ À¯ÇàÀÌ Å©´Ù. Ư¡ÀûÀÎ À°¾ÈÀû ¼Ò°ßÀº ÄáÆÏ¼ÓÁúÀÇ ÃâÇ÷, ¿À¸¥½É¹æÃâÇ÷, ³úÇϼöü Àü¿±ÀÇ ±«»çÀ̸ç, À̹ۿ¡ Èĺ¹° ¿¬Á¶Á÷ÀÇ ½ÉÇÑ ºÎÁ¾, ü°³»·Î ´©ÃâµÈ ü¾× Àú·ù, À帷ÀÇ »êÀ缺 ÃâÇ÷, µ¹Ã¢ÀÚÀÇ Á¡¸·ÃâÇ÷, ÆóºÎÁ¾ ³»Áö´Â ÆóÃâÇ÷ µîÀÌ´Ù. Á¶Á÷¼Ò°ßÀÇ Æ¯Â¡Àº ¿©·¯ Àå±âÀÇ ÃâÇ÷°ú ÄáÆÏ¼ÓÁú, ³úÇϼöü, ºÎ½Å µî¿¡ »ý±â´Â ÃÊÁ¡¼º ÀÀ°í¼º ±«»ç¿Í °¢ Àå±âÀÇ ±¤¹ü¼º ´ÜÇÙ¼¼Æ÷ ħÀ±À̸ç, ¼¼Á¤¸ÆÀÌ È®ÀåµÇ°í ¿ïÇ÷ÀÌ »ý±â°í Ç÷Àå°ú ÀûÇ÷±¸°¡ Ç÷°ü¿Ü·Î ´©ÃâµÇ°í ºÎÀ§¿¡ µû¶ó¼´Â ÃÊÁ¡¼º ¸ð¼¼Ç÷°ü ÆÄ¿ÀÌ ³ªÅ¸³ª ÀÖ´Ù. |
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| ¿µ¹® | relapsing fever | ÇÑ±Û | Àç±Í¿ |
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| ¼³¸í | Borrelia ¼ÓÀÇ ½ºÇÇ·ÎÇìŸ °¨¿°¿¡ ÀÇÇØ¼ »ý±ä´Ù. ÀÌ Áøµå±â¿¡ ÀÇÇØ ¸Å°³µÇ°í ¾ÆÇÁ¸®Ä«, ¾Æ½Ã¾Æ, ¹Ì±¹, À¯·´ µî, ¼¼°è °¢Áö¿¡¼ º¼ ¼ö ÀÖ´Ù. Àẹ±â´Â 3~10ÀÏ¿¡ ¿ÀÇÑ, ÀüÀ², µÎÅë, ±¸¿ª µîÀ» ¼ö¹ÝÇÏ´Â ¹ß¿·Î ¹ß»ýÇÑ´Ù. ¹ß¿Àº Á¾Á¾ 40¡É ÀÌ»ó¿¡ ´ÞÇϰí 4~5ÀÏ¿¡ ÀÚ¿¬È÷ ÇØ¿µÈ´Ù. ¾à 1ÁÖÀÏÀÇ ¹«¿±â µÚ, ´Ù½Ã ¶È°°Àº Áõ»óÀ» µÇÇ®ÀÌÇÑ´Ù. ÀÌ¿Í °°Àº ¹ßÀÛÀ» ¼³Ê ¹ø µÇÇ®ÀÌÇÑ´Ù. Ç÷¾×À¸·ÎºÎÅÍÀÇ Borrelia °ËÃâ·Î Áø´ÜÀÌ È®Á¤µÈ´Ù. Åë»ó Ç÷¾×µµ¸» Ç¥º»À» °¨ÀÚ¿°»öÇØ¼ °ËÃâÇÑ´Ù. Ä¡·á¿¡´Â Æä´Ï½Ç¸°, Åׯ®¶ó»çÀÌŬ¸°, Ŭ·Î¶÷Æä´ÏÄÝÀÌ È¿°úÀûÀÌ´Ù. |
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| Q fever | query fever |
|---|---|
| SF | Sabin-Feldman [test]; safety factor; salt-free; scarlet fever; screen film; seminal fluid; serosal f... |
| 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... |
familial leiomyomatosis cutis et uteri (°¡Á·¼º ÇǺΠÀڱà ±ÙÁ¾Áõ
| 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) |
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| 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) |
| hypercholesterolaemia, familial | A familial disorder characterised by increased plasma concentration of cholesterol carried in low density lipoproteins (ldl) and by a deficiency in a cell surface receptor which regulates ldl degradation and cholesterol synthesis. It is frequently associated with arcus senilis and premature atherosclerosis. (12 Dec 1998) |
| hyperlipidemia, familial combined | A disorder genetically distinct from the other inherited hyperlipidemias characterised by the type II or type IV lipoprotein pattern (the pattern may change from time to time and the lipid level may be normal at one time and abnormal at another time). (12 Dec 1998) |
| hypophosphatemia, familial | Familial disorder characterised by hypophosphatemia associated with decreased renal tubular reabsorption of inorganic phosphorus. It is sometimes associated with osteomalacia or rickets which do not respond to the usual doses of vitamin d. (12 Dec 1998) |
| Danubian endemic familial nephropathy | A tubulointerstitial disease of unknown aetiology occurring in a limited geographic area including adjacent regions of romania, bulgaria, and yugoslavia. (12 Dec 1998) |
| diffuse infantile familial sclerosis | <radiology> Dysmyelinating disease, autosomal recessive, usually presents by 1 yr, specific enzyme deficiency identified, rapid spontaneous nystagmus, poikilothermia Synonym: Krabbe leukodystrophy (12 Dec 1998) |
| dysautonomia, familial | An autosomal recessive inherited disorder seen predominantly in jewish infants and children. The peripheral autonomic and sensory neurons are affected. The characteristic distinguishing this disorder from other hereditary sensory and autonomic neuropathies is the predominance of autonomic symptoms such as excessive perspiration, defective lacrimation, and hypertension. Insensitivity to pain and areflexia are also present. (12 Dec 1998) |
| type I familial hyperlipoproteinaemia | Hyperlipoproteinaemia characterised by the presence of large amounts of chylomicrons and triglycerides in the plasma when the patient has a normal diet, and their disappearance on a fat-free diet; low alpha-and beta-lipoproteins on a normal diet, with increase on fat-free diet; decreased plasma postheparin lipolytic activity; and low tissue lipoprotein lipase activity. It is accompanied by bouts of abdominal pain, hepatosplenomegaly, pancreatitis, and eruptive xanthomas; autosomal recessive inheritance. See: familial lipoprotein lipase inhibitor. Synonym: Burger-Grutz syndrome, familial fat-induced hyperlipaemia, familial hyperchylomicronaemia, familial hypertriglyceridemia, idiopathic hyperlipaemia. (05 Mar 2000) |
| type II familial hyperlipoproteinaemia | Hyperlipoproteinaemia characterised by increased plasma levels of beta-lipoproteins, cholesterol, and phospholipids, but normal triglycerides; heterozygotes have mild lipid changes and are susceptible to atherosclerosis in middle age, but homozygotes have severe changes often with generalised xanthomatosis and xanthelasma, and frank clinical atherosclerosis as young adults. The primary defect is a deficiency of apoprotein of VLDL, and the disorder is divided into two classes: 1) type IIA, which has elevated LDL due to a deficiency of the receptor or a modified apolipoprotein B-100; 2) type IIB, which has elevated LDL and triglycerides; autosomal dominant inheritance. Synonym: familial hyperbetalipoproteinaemia, familial hypercholesteraemic xanthomatosis, familial hypercholesterolaemia. (05 Mar 2000) |
| type III familial hyperlipoproteinaemia | Hyperlipoproteinaemia characterised by increased plasma levels of LDL, beta-lipoproteins, pre-beta-lipoproteins, cholesterol, phospholipids, and triglycerides; hypertriglyceridemia induced by a high carbohydrate diet, and glucose tolerance is abnormal; frequent eruptive xanthomas and atheromatosis, particularly coronary artery disease; biochemical defect lies in apolipoproteins; there are many varieties. Synonym: carbohydrate-induced hyperlipaemia, dysbetalipoproteinaemia, familial hyperbetalipoproteinaemia and hyperprebetalipoproteinaemia, familial hypercholesterolaemia with hyperlipaemia. (05 Mar 2000) |
| type IV familial hyperlipoproteinaemia | Plasma levels of VLDL, pre-beta-lipoproteins and triglycerides are increased on a normal diet, but beta-lipoproteins, cholesterol, and phospholipids are normal; hypertriglyceridemia is induced by a high carbohydrate diet; may be accompanied by abnormal glucose tolerance and susceptibility to ischemic heart disease; probably autosomal recessive inheritance. Synonym: carbohydrate-induced hyperlipaemia, familial hyperprebetalipoproteinaemia, familial hypertriglyceridemia. (05 Mar 2000) |
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