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1. ÁÖÈ¿´É¤ý È¿°ú
°¨±â·Î ÀÎÇÑ ¹ß¿ ¹× µ¿Åë, µÎÅë, Ä¡Åë, ¿ù°æÅë, ½Å°æÅë, ¿äÅë, °üÀýÅë, ±ÙÀ°Åë, ·ù¸¶Æ¼¾ç
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2. ´ÙÀ½ Áúȯ¿¡µµ »ç¿ëÇÒ¼ö ÀÖ´Ù.
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1) ÀÌ ¾à ¶Ç´Â ´Ù¸¥ »ì¸®½Ç»êÁ¦Á¦¿¡ °ú¹ÎÁõÀÇ º´·ÂÀÌ Àִ ȯÀÚ
2) ¼Òȼº±Ë¾ç ȯÀÚ
3) ¾Æ½ºÇǸ°Ãµ½Ä(ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦ µî¿¡ ÀÇÇÑ Ãµ½Ä¹ßÀÛÀÇ À¯¹ß) ¶Ç´Â ±× º´·ÂÀÌ Àִ ȯÀÚ
4) Ç÷¿ìº´ ȯÀÚ
5) ÁßÁõÀÇ °£Àå¾Ö ȯÀÚ
6) ÁßÁõÀÇ ½ÅÀå¾Ö ȯÀÚ
7) ÁßÁõÀÇ ½É±â´ÉºÎÀü ȯÀÚ
8) ÃâÇ÷ °æÇâÀÌ Àִ ȯÀÚ
9) ¸ÞƮƮ·º¼¼ÀÌÆ® 15¹Ð¸®±×¶÷(15mg/ÁÖ) ÀÌ»óÀÇ ¿ë·®À» º´¿ë Åõ¿©Çϴ ȯÀÚ
10) ÀӽŠ3±â¿¡ ÇØ´çÇÏ´Â ÀӺΠ(7. ÀӺΠ¹× ¼öÀ¯ºÎ¿¡ ´ëÇÑ Åõ¿© Ç× Âü°í)
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1) ½ÅÀå¾Ö ȯÀÚ ¶Ç´Â ½ÉÇ÷°ü ¼øÈ¯ ±â´É ÀÌ»ó ȯÀÚ(½ÅÇ÷°ü Áúȯ, ¿ïÇ÷¼º ½ÉºÎÀü, ü¾× °¨¼Ò, Å« ¼ö¼ú, ÆÐÇ÷Áõ ¶Ç´Â ÁÖ¿ä ÃâÇ÷ »ç°í µî)
2) °£Àå¾Ö ¶Ç´Â ±×ÀÇ º´·ÂÀÌ Àִ ȯÀÚ
3) ½É±â´ÉÀÌ»ó ȯÀÚ
4) Ç÷¾× ÀÌ»ó ¶Ç´Â ±× º´·ÂÀÌ Àִ ȯÀÚ
5) ±â°üÁöõ½Ä ȯÀÚ
6) ¼ö¼úÀüÀÇ È¯ÀÚ
7) 3¼¼ ÀÌÇÏÀÇ À¯¾Æ
8) ÁøÅëÁ¦, ¼Ò¿°Á¦, Ç×·ù¸¶Æ¼½ºÁ¦¿¡ ´ëÇÑ °ú¹ÎÁõ ¹× ´Ù¸¥ ¾Ë·¹¸£±â ÁúȯÀÇ º´·ÂÀÌ Àִ ȯÀÚ
9) °í·ÉÀÚ
10) Ç×ÀÀ°íÁ¦¸¦ º´¿ëÅõ¿©Çϴ ȯÀÚ (6. »óÈ£ÀÛ¿ë Ç× Âü°í)
11) ÁßÁõ Æ÷µµ´ç-6-Àλ꿰 Å»¼ö¼ÒÈ¿¼Ò(G6PD) °áÇÌÁõ ȯÀÚ. ÀÌ ¾àÀÌ ¿ëÇ÷ ¹× ¿ëÇ÷¼º ºóÇ÷À» À¯µµÇÒ ¼ö ÀÖ´Ù. ¿ëÇ÷ÀÇ À§ÇèÀ» Áõ°¡½Ãų ¼ö ÀÖ´Â ¿äÀÎÀº °í¿ë·® Åõ¿©, ¿, ±Þ¼º°¨¿°ÀÌ´Ù.
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±âÀçµÈ ÀÌ»ó¾à¹°¹ÝÀÀÀº ¾Æ½ºÇǸ° Á¦Á¦ÀÇ ´Ü±â, Àå±â °æ±¸ Åõ¿©¸¦ Æ÷ÇÔÇÑ ÀÚ¹ßÀû ½ÃÆÇ ÈÄ º¸°í¿¡ ±Ù°Å ÇÏ¿´´Ù.
1) ¼îÅ© : ¼îÅ© ¹× ¾Æ³ªÇʶô½Ã¾ç Áõ»ó(È£Èí°ï¶õ, Àü½ÅÈ«Á¶, Ç÷°üºÎÁ¾, µÎµå·¯±â µî)ÀÌ ³ªÅ¸³ª´Â °æ¿ì°¡ ÀÖÀ¸¹Ç·Î ÃæºÐÈ÷ °üÂûÇÏ¿© ÀÌ»óÀÌ È®À뵃 °æ¿ì¿¡´Â Åõ¿©¸¦ ÁßÁöÇϰí ÀûÀýÇÑ Ã³Ä¡¸¦ ÇÒ °Í. ÀÌ ¾àÀº õ½Ä¹ßÀÛÀ» À¯¹ßÇÒ ¼ö ÀÖ´Ù.
2) °ú¹ÎÁõ : È«¹Ý, °¡·Á¿ò, ÄÚ¸·Èû, ½ÉÀå-È£Èí±â Àå¾Ö, ¶§¶§·Î ¹ßÁø, ºÎÁ¾, µÎµå·¯±â, ºñ¿°¾ç Áõ»ó, °á¸·¿° µîÀÇ °ú¹ÎÁõ»óÀÌ ³ªÅ¸³¯ ¼ö ÀÖÀ¸¹Ç·Î ÀÌ·¯ÇÑ Áõ»óÀÌ ³ªÅ¸³¯ °æ¿ì¿¡´Â Åõ¿©¸¦ ÁßÁöÇÑ´Ù.
3) ÇǺΠ: µå¹°°Ô ¸®¿¤ÁõÈıº(Áßµ¶¼ºÇ¥ÇDZ«»çÁõ), ½ºÆ¼ºì½º-Á¸½¼ÁõÈıº(ÇǺÎÁ¡¸·¾ÈÁõÈıº), ¹ÚÅ»¼º ÇǺο°ÀÌ ³ªÅ¸³¯ ¼ö ÀÖÀ¸¹Ç·Î ÃæºÐÈ÷ °üÂûÇϰí ÀÌ»óÀÌ ÀÖÀ» °æ¿ì¿¡´Â Åõ¿©¸¦ ÁßÁöÇϰí ÀûÀýÇÑ Á¶Ä¡¸¦ ÇÑ´Ù.
4) Ç÷¾× : µå¹°°Ô Àç»ýºÒ·®¼ººóÇ÷, ºóÇ÷, ¹éÇ÷±¸°¨¼Ò, Ç÷¼ÒÆÇ°¨¼Ò, Ç÷¼ÒÆÇ±â´É ÀúÇÏ(ÃâÇ÷½Ã°£ÀÇ Áö¿¬) µîÀÌ ³ªÅ¸³¯ ¼ö ÀÖÀ¸¹Ç·Î ÃæºÐÈ÷ °üÂûÇϰí ÀÌ»óÀÌ ÀÖÀ» °æ¿ì¿¡´Â Åõ¿©¸¦ ÁßÁöÇϰí ÀûÀýÇÑ Á¶Ä¡¸¦ ÇÑ´Ù. ÁßÁõÀÇ Æ÷µµ´ç-6-Àλ꿰 Å»¼ö¼ÒÈ¿¼Ò(G6PD) °áÇÌ ÁßÁõ ȯÀÚ¿¡¼ ¿ëÇ÷ ¹× ¿ëÇ÷¼º ºóÇ÷ÀÌ º¸°íµÇ¾ú´Ù.
5) ¼Òȱâ°è : ½Ä¿åºÎÁø, °¡½¿¾²¸², À§Åë, ±¸¿ª, ±¸Åä µîÀÇ Áõ»óÀÌ ³ªÅ¸³¯ ¼ö ÀÖ°í Àå±âÅõ¿©½Ã À§Àå°ü¿¡ ´ëÇÑ ÀÌ»ó¹ÝÀÀ ƯÈ÷ À§ÀåÃâÇ÷, ¼Òȼº±Ë¾ç ¹× ¶Õ¸²(õ°ø)ÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù.
6) Á¤½Å½Å°æ°è : ±Í¿ï¸², ±Í ¸ÔÀ½, ¾îÁö·¯¿ò, µÎÅë, ÈïºÐ µîÀÇ Áõ»óÀÌ ³ªÅ¸³¯ ¼ö ÀÖÀ¸¹Ç·Î ÀÌ·¯ÇÑ Áõ»óÀÌ ³ªÅ¸³¯ °æ¿ì¿¡´Â ¿ë·®À» ÁÙÀ̰ųª Åõ¿©¸¦ ÁßÁöÇÑ´Ù.
7) °£Àå : µå¹°°Ô °£Àå¾Ö°¡ ³ªÅ¸³¯ ¼ö ÀÖ´Ù. ¸Å¿ì µå¹°°Ô °£ Æ®·£½º¾Æ¹Ì³ªÁ¦ »ó½Â¿¡ µû¸¥ ÀϽÃÀûÀÎ °£¼Õ»óÀÌ º¸°íµÇ¾ú´Ù.
8) ½ÅÀå : ½ÅÀå¾Ö¿Í ±Þ¼º½ÅºÎÀüÀÌ º¸°íµÇ¾ú´Ù.
9) ±âŸ : °úÈ£Èí, ´ë»ç¼º »êÁõ µîÀÌ ³ªÅ¸³¯ °æ¿ì¿¡´Â Ç÷Áß³óµµ°¡ ÇöÀúÇÏ°Ô »ó½ÂµÉ ¼ö ÀÖÀ¸¹Ç·Î ¿ë·®À» ÁÙÀ̰ųª Åõ¿©¸¦ ÁßÁöÇÑ´Ù.
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1) Ç×ÀÀ°íÁ¦, Ç÷Àü¿ëÇØÁ¦/´Ù¸¥ Ç÷¼ÒÆÇÀÀÁý¾ïÁ¦Á¦, ÁöÇ÷Á¦ ¹× ´ç´¢º´Ä¡·áÁ¦(Àν¶¸°Á¦Á¦, ÅçºÎŸ¹Ìµå µî) : ÀÌ ¾àÀÇ È¿°ú°¡ Áõ°¡µÇ¾î ÃâÇ÷¿¡ ´ëÇÑ À§Ç輺ÀÌ Áõ°¡µÉ ¼ö ÀÖÀ¸¹Ç·Î ¿ë·®À» °¨¼Ò½ÃŰ´Â µî ½ÅÁßÈ÷ Åõ¿©ÇÑ´Ù.
2) ¿ä»ê¹è¼³ÃËÁøÁ¦(º¥Áîºê·Î¸¶·Ð, ÇÁ·Îº£³×½Ãµå) : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ¿ä»ê¹è¼³ ÀÛ¿ëÀÌ ¾ïÁ¦µÈ´Ù. Ä¡¾ÆÁþ°è ÀÌ´¢Á¦ÀÇ ÀÛ¿ëÀ» °¨¼Ò½Ãų ¼ö ÀÖ´Ù.
3) ¸ÞÅ䯮·º¼¼ÀÌÆ® : ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦(NSAIDs) ¹× »ì¸®½Ç»ê°úÀÇ º´¿ëÅõ¿©·Î ½Å¼¼´¢°ü¿¡¼ ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ ¹è¼³ÀÌ Áö¿¬µÇ¾î Ä¡¸íÀûÀÎ ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ Ç÷¾×ÇÐÀû µ¶¼ºÀÌ Áõ°¡µÉ ¼ö ÀÖÀ¸¹Ç·Î °í¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®(15mg/ÁÖ ÀÌ»ó)´Â ¾Æ½ºÇǸ°°ú º´¿ëÅõ¿©ÇÏÁö ¾ÊÀ¸¸ç º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â Àú¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®¿Í ½ÅÁßÈ÷ Åõ¿©ÇÏ¿©¾ß ÇÑ´Ù.
4) ¸®Æ¬Á¦Á¦ : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ¸®Æ¬ÀÇ Ç÷Áß³óµµ°¡ »ó½ÂÇÏ¿© ¸®Æ¬Áßµ¶ÀÌ ³ªÅ¸³µ´Ù´Â º¸°í°¡ ÀÖÀ¸¹Ç·Î º´¿ë½Ã¿¡ °üÂûÀ» ÃæºÐÈ÷ ÇÏ°í ½ÅÁßÈ÷ Åõ¿©ÇÑ´Ù.
5) ´Ù¸¥ ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦(NSAIDs) ¹× »ì¸®½Ç»ê Á¦Á¦ : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ÃâÇ÷ÀÌ Áõ°¡µÇ°Å³ª ½Å±â´ÉÀÌ °¨¼ÒµÉ ¼ö ÀÖÀ¸¹Ç·Î º´¿ëÅõ¿©ÇÏÁö ¾Ê´Â´Ù.
6) À̺ÎÇÁ·ÎÆæ : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ¾Æ½ºÇǸ°¿¡ ÀÇÇÑ ºñ°¡¿ªÀû Ç÷¼ÒÆÇ ÀÀÁý¾ïÁ¦ ÀÛ¿ëÀÌ °¨¼ÒµÈ´Ù. ½ÉÇ÷°ü°è Áúȯ¿¡ ´ëÇÑ À§ÇèÀÌ Áõ°¡µÈ ȯÀÚ¿¡°Ô ÀÌ ¾à°ú À̺ÎÇÁ·ÎÆæ º´¿ëÅõ¿©½Ã ¾Æ½ºÇǸ°ÀÇ ½ÉÀå º¸È£ È¿°ú°¡ Á¦ÇÑµÉ ¼ö ÀÖ´Ù.
7) ¼±ÅÃÀû ¼¼Æ÷Åä´Ñ ÀçÈí¼ö ¾ïÁ¦Á¦(SSRIs) : ÀÌ ¾à°ú º´¿ë Åõ¿©½Ã »óºÎ À§Àå°ü ÃâÇ÷ À§Ç輺À» Áõ°¡½Ãų ¼ö ÀÖ´Ù.
8) µð°î½Å : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ½ÅÀå ¹è¼³ÀÌ °¨¼ÒµÇ¾î µð°î½ÅÀÇ Ç÷Àå ³óµµ°¡ Áõ°¡ÇÒ ¼ö ÀÖ´Ù.
9) Àü½Å ÀÛ¿ë ºÎ½ÅÇÇÁúÈ£¸£¸ó Á¦Á¦(¾Öµð½¼º´ ´ëü¿ä¹ý¿ë È÷µå·ÎÄÚÆ¼¼Õ Á¦¿Ü) : ÀÌ ¾à°ú º´¿ë Åõ¿©½Ã »ì¸®½Ç»ê Á¦Á¦ÀÇ Ç÷Áß ³óµµ¸¦ °¨¼Ò½ÃŲ´Ù.
10) ¾ÈÁö¿ÀÅٽŠÀüȯ È¿¼Ò ¾ïÁ¦Á¦(ACE inhibitor) : ÀÌ ¾àÀÇ °í¿ë·®°ú º´¿ë Åõ¿©½Ã Ç÷°üÈ®À强 ÇÁ·Î½ºÅ¸±Û¶õµòÀÇ ¾ïÁ¦·Î ÀÎÇØ »ç±¸Ã¼ ¿©°úÀ²ÀÌ °¨¼ÒÇϰí, Ç÷¾Ð °ÇÏ È¿°ú°¡ °¨¼ÒµÈ´Ù.
11) ¹ßÇÁ·Î»ê : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ´Ü¹é°áÇÕ Ä¡È¯À¸·Î ÀÎÇØ ¹ßÇÁ·Î»êÀÇ µ¶¼ºÀÌ Áõ°¡ÇÑ´Ù.
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Çöóºò½º 1x90, ¾Æ½ºÆ®¸¯½º 100mg 1x90, µôÅ×¶õ180mg 1x90, ¿¤·ÎÅæ 50mg 2x90
¸®ÇÇÅä 10mg 1x90, ÄÚµð¿À¹Ý 12.5mg 1x90
| |
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| 0 Àü³â.12.9 CC : rest½Ã ÈäÅë, È£ÈíÀÌ Èûµé´Ù. BP 145/90mmHg
12.16 CC : Chest pain (recent : ³»¿øÀÏ »õº®, remote : ³»¿ø 20ÀÏÀü)
DX : Unstable angina
PI : 20³âÀü HTN Áø´Ü¹Þ°í medÇÏ´ø Áß ³»¿ø 20ÀÏÀüºÎÅÍ chest painÀ¸·Î º»¿ø OPD¿¡¼ W/U ¿¹Á¤À̾úÀ¸³ª pain aggravation(³»¿øÀÏ »õº®0½Ã, 5½Ã, ¾ÆÄ§8½Ã)µÇ¾î ER ÅëÇØ ³»¿ø
PHx : smoking (+), alcohol(-)
2D-echo : mild LA enlargement, global function 55-60%
=> concentric LVH, mild LA enlargement
12.17 CAG) LAD : atherosclerotic
Ramus : mild diffuse severe
LCX : mid severe subtotal eccentric, distal severe diffuse stenosis,
small calibered
=> Medication Tx À¯ÁöÇϱâ·Î ÇÔ. (Astrix 100mg, Plavix 75mg Åõ¿©)
12.24 Åð¿ø¾à : Astrix 100mg, Plavix 75mg, herben, isomack, tritace, lipitor
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| Àü³â.12/17
| 12/30
| µ¿³â.1/27
| 3/2
| 4/27
| 6/24
| Åõ¾àÀϼö
| Astrix 100mg
| 1x15
| 1x30
| 1x40
| 1x60
| 1x60
| 1x90
| 295ÀÏ
| clopidogrel 75mg
| 1x15
| 1x30
| 1x40
| 1x60
| 1x60
| 1x90
| 295ÀÏ
|
| ¼Ò
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| LCX mid severe sub-total severe stenosis·Î PCI ÇÊ¿äÇϳª ºñ±³Àû small caliberÀ̸ç PCI °ÅºÎÇÏ¿© PLAVIX Åõ¿©°¡ ÇÊ¿äÇÏ´Ù°í »ç·áµÊ.
|
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| ¢º »óº´¸í : ±Þ¼º ½É³»¸·ÇÏ ½É±Ù°æ»öÁõ, ¿ïÇ÷¼º ½ÉÀå±â´É»ó½Ç(½ÉºÎÀü), ´ç´¢º´, ¼ø¼ö °íÄÝ·¹½ºÅ×·ÑÇ÷Áõ, ºÒ¾ÈÁ¤¼º Çù½ÉÁõ, ½É±Ù°æ»öÁõÀ» À¯¹ßÇÏÁö ¾Ê´Â ½ÉÀ嵿¸ÆÇ÷ÀüÁõ
¢º ÁÖ¿äû±¸³»¿ª [ó¹æÀü]
Çöóºò½º 1x90, ¾Æ½ºÆ®¸¯½ºÄ°¼¿100mg 1x90, µð°í½Å 1x90, ·¹´ÏÇÁ¸± 10mg 1x90,
ÄáÄÚ¸£ 50mg 0.5x90, ¾Æ¸¶¸±Á¤ 2mg 2x90, ¶ó½Ä½ºÁ¤ 0.5x90
| Áø
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| 0 2³âÀü.6.7 CC : abd distension, chr cough, dyspnea
PI : local¿¡¼ ½ÃÇàÇÑ Sono»ó ascites ÀÖ¾î evaluationÀ§ÇØ ³»¿ø
constipation(¡¾), epigastric soreness(-)
6.8 AF, RVR·Î ¼øÈ¯±â³»°ú Consult, Sono»ó R/O Rt heart decompensation
PX : depas 0.5g, lasix 4mg, aldactone 25mg
6.10 2D-echo : enlarged LV and LA, RA, mild LVH
valve structure(normal), regional wall motion (diffuse hypokinesia)
global function 10-15%, pericardium (minimal effusion)
=> severe LV dysfunction, moderate pulmonary HTN, mild LVH, LVE, LAE, and RAE,
Hepatic congestion, minimal pericardia effusion
6.12 PX : digoxin 0.25mg, enalapril 5mg, alsactone 12.5mg, lasix 40mg
8.24 BP 140/70mmHg, irregilar heart beat
PX : digoxin 0.25mg, enalapril 5mg, alsactone 12.5mg, lasix 20mg, Astrix
¾È°ú : cataract-¼ö¼ú È¿°ú±â´ë ¸øÇÔ.
10.19 Plan : ¥Â-blocker
12.18 PX : digoxin 0.25mg, enalapril 5mg, alsactone 12.5mg, lasix 20mg, Astrix, Concor
0 Àü³â. 4.12 °¥Áõ, BP : 110/60mmHg
PX : 12/18ÀÏ PX + Plavix
6.2 holter :underlying atrial fibrillation, tachy-brady syndrome was observed
(Max HR 114ȸ/ºÐ, pause 3secs)
tachy-brady syndrome with Af
6.7 FBS 327, PP2h 586
6.11 PX : ¾Æ¸¶¸±, Glucoban
0 µ¿³â.3.22 BP 138/69mmHg, BST 150/180 PX : repeat
¡Ø ¾àÁ¦Ã³¹æ³»¿ª
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| 2³âÀü.8/24 Àü³â.4/12 µ¿³â.6/21
| Astrix 100mg
| <--------------------------------------------------------->
| clopidogrel 75mg
| <------------------------------------->
|
| ¼Ò
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| ÀüÇüÀû ÈäÅëÀ¸·Î ÀÎÇØ CAG ÇÊ¿äÇϳª echo¿¡¼ EF 10%·Î ¸Å¿ì ÀúÇϵǾî ÀÖ°í CAG°ÅºÎÇÑ »óÅ·Î
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| ¢º »óº´¸í : Àν¶¸°ºñÀÇÁ¸¼º ´ç´¢º´, ½ÉºÎÀüÀ» µ¿¹ÝÇÑ °íÇ÷¾Ð¼º½ÉÀåÁúȯ, ºÒ¾ÈÁ¤¼º Çù½ÉÁõ, ³ú°æ»öÁõ, °í±Û¸®¼¼¶óÀ̵åÇ÷Áõ
¢º ÁÖ¿äû±¸³»¿ª [ó¹æÀü±³ºÎ]
Çöóºò½º 1x60, ¾Æ½ºÇǸ°ÇÁ·ÎÅØÆ® 100mg 1x60, ¿¤·ÎÅæ 50mg 1x60, ¹ÌÄ«¸£µð½º40mg 1x60
¾Æ¹Ýµð¾Æ 4mg 1x60, ¾Æ¸¶¸±Á¤ 2mg 2x60
| |
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| 0 Ÿº´¿ø Áø·áÀÇ·Ú¼(2³âÀü.12¿ù)
: HT¿Í DMÀ¸·Î ³»°ú local¿¡¼ Ä¡·á Áß ³»¿ø 10ÀÏÀüºÎÅÍ ¿îµ¿½Ã dyspnea & chest discomfort°¡ develop µÇ¾î further evaluation À§ÇØ Àü¿øÇÔ.
0 Àü³â.6.23 CC : effort½Ã dyspnea -> admission recommend ÇßÀ¸³ª refuse
6.27-7.3 ÀÔ¿ø-DM, Angina
1 CAG : LAD-sever diffuse sclerotic change beaded appearance : 70% stenosis
LCX-chronic total occlusion in prox portion bridge collateral flow(G¥°-¥±)
RCA-severe diffuse sclerotic change beaded appearance
=> Con) OM1 with remodeling process -> Plan) 2nd prevention
7.2 Chest PA : mild cardiomegaly
7.16 FBS 150-230/280-330, 2D-echo : EF 30%, 75.9/59.3, 10.8/7.7, 26.1/56.4
Px : aspirin, plavix, lipitor, tritace, lasix, aldacton, isoket, ¾Æ¸¶¸±4mg
8.27 ½ÄÀü 150-200/165-300 => ¾Æ¸¶¸± 6mg Áõ·®
µ¿³â. 1.28 ½ÄÀü 130-170/180-200, ¾È°úÄ¡·á Áß-retinopathy
3.30 CAG : LAD-diffuse stenosis, LCX-total occlusion
4.12 CAG : LAD-severe diffuse sclerotic change beased appearance
LCX-chronic total occlusion in prox. portion bridge collateral flow(G1-2)
RCA-severe diffuse sclerotic change beaded appearance
=> previous CAG¿Í ºñ±³½Ã no interval change => Plan) medication
¡Ø ¾àÁ¦Ã³¹æ³»¿ª
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| Àü³â.7/16 µ¿³â.6/17
| Aspirin 100mg
| <--------------------------------------------------------->
| clopidogrel 75mg
| <--------------------------------------------------------->
|
| ¼Ò
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| ´ç´¢, Çù½ÉÁõȯÀÚ·Î Coronary angio»ó 3vessel·Î CABG¼ö¼ú ¹Þ¾Æ¾ß Çϳª ¼ö¼ú ºÒ°¡´É »óÅ·Πplavix Åõ¿©°¡ ÇÊ¿äÇÏ´Ù°í »ç·áµÊ.
|
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| ¢º »óº´¸í : ºÒ¾ÈÁ¤¼º Çù½ÉÁõ, ¼ø¼ö°íÄÝ·¹½ºÅ×·ÑÇ÷Áõ, ´ë³ú°æ»öÁõÀÇ ÈÄÀ¯Áõ, ±Þ¼º½É±Ù°æ»ö¿¡ ÀÇÇÑ ÇÕº´ÁõÀ¸·Î¼ ½É¹æ, ½ÉÀÌ ¶Ç´Â ½É½ÇÀÇ Ç÷ÀüÁõ
¢º ÁÖ¿äû±¸³»¿ª [ó¹æÀü±³ºÎ]
Çöóºò½º 1x90, ¾Æ½ºÆ®¸¯½º100mg 1x90, Ç츣º¥Á¤ 4x90, ´ÏÆ®·Î±Û¸®¼¼¸° 0.6mg 1x60,
À̼ÒÄϼ¹æÁ¤ 40mg 0.5x90, ¼¿º¤½º 2x90
| |
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| 0 µ¿³â.2.23(ÀÔ¿ø) CC : chest pain
DX : unstable angina, HTN
PI : 2³âÀüºÎÅÍ HTNÀ¸·Î medication ÁßÀ¸·Î 3³âÀüºÎÅÍ »õº®À̳ª »¡¸® °ÉÀ»¶§ chest pain ÀÖ¾î Ÿº´¿ø¿¡¼ herben medication Áß ÃÖ±Ù Áõ»ó aggravation µÊ. ³»¿øÀÏ »õº® 1½Ã°£°¡·® pain Áö¼ÓµÇ¾î ³»¿ø
Medication : astrix, plavix, lipitor, isoket, herben, tylenol, curon
2.24 CAG : LAD : diffuse sclerosis-esp. diffuse narrowing from mid segment
D1 OS-concentric mild stenosis(50%)
LCX : mild diffuse sclerosis, dominent vessel
RCA : OS-concentric mild to moderate stenosis(70%)
-> IC-NTG & sublingual : no response
¡æ Dx : R/O angina pectoris(mixed angina)
2.25 RCA OS¿¡ stenosis °üÂû -> º¸È£ÀÚ¿¡ PTCA or OP or medical Tx Çʿ信 ´ëÇØ ¼³¸í
2.26 ȯÀÚ ¹× º¸È£ÀÚ medication Çϱâ·Î °áÁ¤ -> Medication¸¸ À¯Áö½Ã problem¿¡ ´ëÇØ ¼³¸í
2.28 chest discomfort-mild, intermittent
3.3 Åð¿ø¾à : Astrix 100mg, Plavix 75mg, isoket 40mg, herben, tylenol, lipitor
¡Ø ¾àÁ¦Ã³¹æ³»¿ª
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| µ¿³â.2/23 µ¿³â.6/8
| Astrix 100mg
| <------------------------------------------------->
| clopidogrel 75mg
| <------------------------------------------------->
|
| ¼Ò
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| Right coronary artery OS significant stenosis·Î PCI ÇÊ¿äÇÑ »óÅÂÀ̳ª PCI °ÅºÎ·Î Plavix Åõ¿©°¡ ÇÊ¿äÇÏ´Ù°í »ç·áµÊ.
|
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| ¢º »óº´¸í : º»Å¼º °íÇ÷¾Ð, Çù½ÉÁõ, ¼ø¼ö °í±Û¸®¼¼¶óÀ̵åÇ÷Áõ, ±âŸ ³ú°æ»öÁõ
¢º ÁÖ¿äû±¸³»¿ª [ó¹æÀü±³ºÎ]
Çöóºò½º 1x60, ¾Æ½ºÆ®¸¯½º100mg 1x60, Æ®¸®ÆÄ¸ôÁ¤ 1x60, µô¶óÆ®·»Á¤ 12.5mg 1x60, ¾ÆÇÁ·Îº§Á¤150mg 1x60, ¸®ÇÇÅä 10mg 1x60
| |
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| 0 Áø·áÀÇ·Ú¼(Àü³â.3.8) : ÃÖ±Ù °ÉÀ» ¶§ chest pain È£¼ÒÇÏ¸ç ¾ÈÁ¤Çϸé Áõ¼¼°¡ »ç¶óÁ® further evaluationÀ§ÇØ Àü¿øÇÔ
0 Àü³â.3.10 Dx : unstable angina
underlying Hypertension, ÃÖ±Ù effort½Ã ¹ß»ýÇÏ´Â ÈäÅë¾ÇÈ
treadmil test½Ã ÈäÅë ÀÖ¾ú°í nitrate ¼³ÇÏ Åõ¿©·Î È£Àü
3.12 2D-echo : normal systolic LV function, hypokinetic wall motionÀÌ basel inferior wall¿¡¼ °üÂû, LVID 43.3/23.1, septum/PW 10.7/10.7, Aorta/LA 33.8/38.0
Astrix, Plavix, Herben
3.13 CAG : critical stenosis°¡ Lt main distal/LAD .Os/LCX.Os¿¡¼ °üÂû
plaque rupture°¡ Lt main distal¿¡¼ ÀǽɵÊ.
Emergency OP : CABG
3.19 2D-echo : ef 45-50%, normal regional wall motion
3.21 CAG : LITA to D1-patent, LITA to OM1-patent, RGEA to LAD distal -None
4.18 Åð¿ø¾à : plavix 75mg, allfgra 180mg, tritace 5mg, aminophylline 100mg, spara 100mg
¡Ø ¾àÁ¦Ã³¹æ³»¿ª
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| Àü³â.3.12 µ¿³â.6/26
| Astrix 100mg
| <----------------------------------------------------------------->
| clopidogrel 75mg
| <----------------------------------------------------------------->
|
| ¼Ò
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| CAG»ó Lt main and LAD OSÀÇ critical stenosis·Î CABG ½ÃÇà¹ÞÀº ȯÀÚ·Î º´º¯ÀÇ ½É°¢¼ºÀ» °¨¾È½Ã Plavix Åõ¿©°¡ ºÒ°¡ÇÇÇÏ´Ù°í »ç·áµÊ.
|
¡á Âü°í»çÇ×
¡Û CECILTextbook of Meicine, goldman/ausiello, 22nd Edition p396, 406-407, 418, 1423
¡Û PDR,2004, p.3032-3036
¡Û The TaskForce on the Management of Acute Coronary Syndromes of theESC(European Society of Cardiology): European heart journal( 2002) 23,1809-1840
¡Û ACC/AHA 2002 Guideline Update for theManagement of Patients With Unstable Angina and Non-ST-Segment ElevationMyocardial InfarctionSummary Article. A Report of theAmerican College of Cardiology/American Heart Association Task Force onPractice Guidelines (Committee on the Management of Patients With UnstableAngina), circulation 2002;106:1893.µî.
¡á ½ÉÀdz»¿ë
- Çöóºò½ºÁ¤(¼ººÐ¸í : Clopidogrel)Àº ¡°³úÁ¹Áß, ½É±Ù°æ»ö ¶Ç´Â¸»Ãʵ¿¸Æ¼ºÁúȯÀÌ Àִ ȯÀÚ³ª ±Þ¼º°ü»óµ¿¸ÆÁõÈıºÀÌ Àִ ȯÀÚ¿¡¼ Á׻󵿸ưæÈ¼º Áõ»óÀÇ °³¼±¡±¿¡ Åõ¿©Åä·Ï Çã°¡¹ÞÀº ¾àÁ¦·Î ½Ä¾àû Çã°¡»çÇ׿¡ ¾Æ½ºÇǸ°ÀÇÈ¿°ú¸¦ »ó½Â½ÃÄ×°í ¾Æ½ºÇǸ°°ú 1³â±îÁö º´¿ëÅõ¿© ÇÏ¿´´Ù.¡°°í¸í½ÃµÇ¾î ÀÖÀ½.
¶ÇÇÑ, ACS(Acute Coronary Syndrome)ȯÀÚÀÇ °æ¿ì¿¡ Çöóºò½ºÁ¤Àº ESC(europeansociety of cardiology) guideline(2002)¿¡¼´Â ÃÖ¼Ò 9-12°³¿ù±îÁö, ACC/AHA(american college of cardiology/american heart association)guidelines(2002)¿¡¼´Â 9°³¿ù±îÁö Åõ¿©±â°£À» ¾ð±ÞÇϰí ÀÖ´Â Á¡ µîÀ» ÂüÁ¶ÇÏ¿©Çöóºò½ºÁ¤°ú ¾Æ½ºÇǸ°À» º´¿ëÅõ¿© ½Ã 12°³¿ù ¹üÀ§ ³»¿¡¼ »ç·Êº°·Î ÀÎÁ¤Åä·Ï ÇÔ.
- ºÒ¾ÈÁ¤¼º Çù½ÉÁõ »óº´¿¡ Coronary stent ½Ã¼úÇÏÁö ¾ÊÀº »óÅ·Π¾à 3°³¿ù¿¡¼ 15°³¿ù Á¤µµ ¾Æ½ºÇǸ°°ú
Çöóºò½ºÁ¤ º´¿ë Åõ¿©ÇÑ µ¿ °Ç(»ç·Ê1-5)Àº 12°³¿ùÁ¤µµ Çöóºò½ºÁ¤ Åõ¿©¸¦ ÀÎÁ¤ÇÔ.
[2005.3.4 Áø·á½É»çÆò°¡À§¿øÈ¸]
°ü»óµ¿¸Æ ½ºÅÙÆ® »ðÀÔ¼ú ÈÄ Ç÷ÀüÁõ°ú Àç ÇùÂø ¹æÁö¸¦ ¸ñÀûÀ¸·Î Åõ¿©ÇÏ´Â Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ý(aspirin, clopidogrel, cilostazol)ÀÇ ÀÎÁ¤¹üÀ§
¡á û±¸ ¹× Áø·á³»¿ª
¡Û û±¸³»¿ª(¿Ü·¡)
-»óº´¸í : ºÒ¾ÈÁ¤¼ºÇù½ÉÁõ, º»Å¼º°íÇ÷¾Ð, ¼ø¼ö°íÄÝ·¹½ºÅ×·ÑÇ÷Áõ
-¿ø¿Ü󹿳»¿ª(¡®06.8.18) : Ç츣º¥¼¹æÁ¤90mg 1T ---------
¾Æ½ºÇǸ°ÇÁ·ÎÅØÆ®Á¤100mg 2T l
Çöóºò½ºÁ¤ 1T l x 60ÀÏ
ÇÁ·¹Å»Á¤100mg 2T ----------
¡Û Áø·á³»¿ª(ÀÔ¿ø)
- ¡¯05.2.17: chest painÀ» ÁÖ È£¼Ò·Î ³»¿ø (¡®05.1.31 ÀÌÈÄ 3Â÷·Ê)
nature:squeezing, duration: 5min, agg. factor: µî»ê, °è´Ü ¿À¸¦ ¶§
relieving:resting, radiating pain(+): Lt arm, resting pain(-)
-¡®05.2.18: CAG & PCI(TherapeuticIntervention)
Lt - Lt main(body) : Discrete eccentric stenosis 80%
LCXand LAD : relatively good patency
Rt- No significant luminal stenosis
Balloon angioplasty with Aqua 3.5x15mm 8atm 10" after then suboptimalresult with RS 50%. Stent insertion with Driver 4.0x15mm 14atm 10"
Åð¿ø ¾à(7ÀÏ): Herben 90mg 2T,
¾Æ½ºÇǸ°ÇÁ·ÎÅØÆ®Á¤100mg 2T, Çöóºò½ºÁ¤ 2T, ÇÁ·¹Å»Á¤100mg 2T
¢Ñ Åð¿ø ÈÄ Çö Áø·áºÐ±îÁö 1³â6°³¿ù°£ 3Á¦¿ä¹ý ó¹æÁßÀÓ.
¡Û û±¸³»¿ª(¿Ü·¡)
-»óº´¸í : ±âŸ ÇüÅÂÀÇ Çù½ÉÁõ, º»Å¼º°íÇ÷¾Ð, Àν¶¸°ºñÀÇÁ¸¼º ´ç´¢º´
-¿ø¿Ü󹿳»¿ª(¡®06.8.7) : Æ®¸®Å×À̽ºÁ¤ 5mg 1T --------
¾Æ¸¶¸±Á¤ 2mg 1T l
º£À̽¼Á¤ 0.3mg 3T l
ÀÚÀÌ·»Á¤0.25mg 2T l x 60ÀÏ
ÄáÄÚ¸£Á¤2.5mg 0.5T l
¾Æ½ºÇǸ°ÇÁ·ÎÅØÆ®Á¤100mg 2T l
Çöóºò½ºÁ¤ 1T l
ÇÁ·¹Å»Á¤100mg 2T ---------
¡Û Áø·á³»¿ª(ÀÔ¿ø)
- ¡¯06.3.30: ³»¿ø 20ÀÏÀü resting½Ã 1½Ã°£ °¡·®ÀÇ chest pain ÀÖ¾úÀ¸¸ç ³»¿ø 1ÁÖÀÏ Àü chest painÀÌ ¼öÂ÷·Ê ÀÖ¾úÀ¸³ª NTG¿¡ response¸¦ º¸¿´°í ³»¿ø ´çÀÏ »õº® ÀÚ´Ù°¡ chest pain ÀÖ¾îÀÔ¿øÇÔ.
°ú°Å·Â) ´ç´¢: À̹ø¿¡ óÀ½À¸·Î Áø´Ü¹ÞÀ½ (¾Æ¸¶¸±Á¤ 2§·*1, º£À̽¼Á¤ 0.3§·*3)
°¡Á··Â) ¾Æ¹öÁö: AMI(+), ¾î¸Ó´Ï CABG Hx(+)
- ¡¯06.3.31: CAG & PCI(TherapeuticIntervention)
CAG>Lt- pLAD, mLCX : minimal stenosis, mLAD : diffuse irregular stenosis 30-75%
pLCX: tubular eccentric stenosis 30%, dLCX :tubular eccentric stenosis 40%
Rt-No luminal stenosis
Balloon angioplasty with Aqua 2.5x20mm 4atm 4atm 6atm 10" Stent implantationwith Cypher 2.75x33mm 8atm 14atm 10" (stent indication : suboptimal resultwith RS 60%)
Åð¿ø ¾à(7ÀÏ): Æ®¸®Å×À̽ºÁ¤5mg 1T, ¾Æ¸¶¸±Á¤2mg 1T, º£À̽¼Á¤0.3mg 3T
Ç㺥Á¤ 90mg 2T, º£½ºÆ¼µòÁ¤20mg 2T,
¾Æ½ºÇǸ°ÇÁ·ÎÅØÆ®Á¤100mg 2T, Çöóºò½ºÁ¤ 1T, ÇÁ·¹Å»Á¤100mg 2T
¢Ñ Åð¿ø ÈÄ Çö Áø·áºÐ±îÁö 5°³¿ù°£ 3Á¦¿ä¹ý ó¹æÁßÀÓ.
¡á Âü°í
¡Û EBH Æò°¡º¸°í¼(2008.12.4)
¡Û ´ëÇѽÉÀåÇÐȸ Àǰß
¡Û Comparison of TripleVersus Dual Antiplatelet Therapy After Drug-Eluting Stent Implantation (fromthe DECLARE-Long trial) Lee SW, Am J Cardiol. 2007 Oct 1;100(7):1103-8
¡Û Reduced 6-monthresource use and costs associated with cilostazol in patients after successfulcoronary stent implantation: Results from the Cilostazol for RESTenosis (CREST)trial Zefeng Zhang, Am Heart J 2006;152:770-6
¡Û Triple Versus Dual Antiplatelet Therapy after Coronary Stenting-Impact on stent Thrombosis
Seung-Whab Lee, J Am CollCardiol 2005;46:1833-7
¡Û Coronary stentrestenosis in patients treated with cilostazol. Douglas JS Jr, Circulation. 2005; 112:2826-2832.
¡á ½ÉÀdz»¿ë
- °ü»óµ¿¸Æ½ºÅÙÆ®»ðÀÔ¼ú ÈÄ ½ºÅÙÆ®Ç÷ÀüÁõ ¹× Àç ÇùÂø ¹æÁö¸¦ ¸ñÀûÀ¸·Î ½ÃÇàÇÏ´Â Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ý(aspirin, clopidogrel, cilostazol)ÀÇÀû¿ë´ë»ó ¹× Åõ¿©±â°£¿¡ ´ëÇÏ¿© ³íÀÇÇÑ °á°ú, Àӻ󿬱¸¹®Çå ¹× °ü·ÃÇÐȸ ÀÇ°ß µî¿¡¼ ½ºÅÙÆ®»ðÀÔ¼ú °ü·ÃÇÑÀç ÇùÂø ¹ß»ý µîÀÌ ³ôÀº °í À§Ç豺Àº ¡®´ç´¢, Long stenting, small lesion,multi-stenting¡¯µîÀ¸·Î º¸°í ÀÖÀ¸¸ç, EBH Æò°¡º¸°í¼¿¡¼ ¡°°ü»óµ¿¸Æ½ºÅÙÆ® ½Ã¼úÈÄ »ç¿ëÇÑ ½Ç·Î½ºÅ¸Á¹À» Æ÷ÇÔÇÑ Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ýÀº ÀÓ»óÀû À¯¿ë¼º Ãø¸é¿¡¼ ±âÁ¸ÀÇ 2Á¦¿ä¹ý°ú ºñ±³ÇÒ ¶§ ÁÖ¿ä½ÉÀå»ç°Ç(MACE) ¹× Ç¥Àûº´º¯Àç½Ã¼ú, Ç¥ÀûÇ÷°üÀç½Ã¼ú, Àç ÇùÂø·ü, Èıâ¼Õ½ÇÀÇ À§ÇèÀ» ÁÙÀ̴µ¥ ´õ ¿ì¿ùÇÑ °á°ú¡±¸¦ º¸¿´´Ù°í ÇÔ.
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[2009.3.2 Áø·á½É»çÆò°¡À§¿øÈ¸]
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| DUR °ü·Ã °í½Ã |
[º´¿ë¿¬·É±Ý±â ÀǾàǰ / ÀӺαݱâ ÀǾàǰ / ºñ¿ëÈ¿°úÀû ÇÔ·® ÀǾàǰ / ¾ÈÀü¼º °ü·Ã ±Þ¿©ÁßÁö ÀǾàǰ]
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 | ÇмúÁ¤º¸ |
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| Ç׸ñ |
³»¿ë |
| DUR (ÀǾàǰ»ç¿ëÆò°¡) |
º´¿ë±Ý±â :
°í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[»óÈ£ÀÛ¿ë/º´¿ë±Ý±â°Ë»ö]
¿¬·É´ë±Ý±â :
°í½ÃµÈ ¿¬·É±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[¿¬·É´ë±Ý±â»ó¼¼°Ë»ö]
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| Mechanism of Action |
Aspirin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ The analgesic, antipyretic, and anti-inflammatory effects of aspirin are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Aspirin directly and irreversibly inhibits the activity of both types of cyclo-oxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes aspirin different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Aspirin's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation–inhibiting effect of aspirin specifically involves the compound's ability to act as an acetyl donor to the platelet membrane; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Aspirin affects platelet function by inhibiting the enzyme prostaglandin cyclooxygenase in platelets, thereby preventing the formation of the aggregating agent thromboxane A2. This action is irreversible; the effects persist for the life of the platelets exposed. Aspirin may also inhibit formation of the platelet aggregation inhibitor prostacyclin (prostaglandin I2) in blood vessels; however, this action is reversible.
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| Pharmacology |
Aspirin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Aspirin (acetylsalicylic acid) is an analgesic, antipyretic, antirheumatic, and anti-inflammatory agent. Aspirin's mode of action as an antiinflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. Aspirin appears to produce analgesia by virtue of both a peripheral and CNS effect. Peripherally, Aspirin acts by inhibiting the synthesis and release of prostaglandins. Acting centrally, it would appear to produce analgesia at a hypothalamic site in the brain, although the mode of action is not known. Aspirin also acts on the hypothalamus to produce antipyresis; heat dissipation is increased as a result of vasodilation and increased peripheral blood flow. Aspirin's antipyretic activity may also be related to inhibition of synthesis and release of prostaglandins.
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| Protein Binding |
Aspirin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ High (99.5%) to albumin. Decreases as plasma salicylate concentration increases, with reduced plasma albumin concentration or renal dysfunction, and during pregnancy.
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| Half-life |
Aspirin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ The plasma half-life is approximately 15 minutes; that for salicylate lengthens as the dose increases: doses of 300 to 650 mg have a half-life of 3.1 to 3.2 hours; with doses of 1 gram, the half-life is increased to 5 hours and with 2 grams it is increased to about 9 hours.
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| Absorption |
Aspirin¿¡ ´ëÇÑ Absorption Á¤º¸ Absorption is generally rapid and complete following oral administration but may vary according to specific salicylate used, dosage form, and other factors such as tablet dissolution rate and gastric or intraluminal pH.
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| Pharmacokinetics |
Aspirin encapsulatedÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Ç÷ÁßÃÖ°í³óµµ µµ´Þ½Ã°£ : ¾à 1-2 ½Ã°£
- Èí¼ö : À§, ¼ÒÀåÀ¸·ÎºÎÅÍ Èí¼öµÊ.
- ºÐÆ÷ : ´ëºÎºÐÀÇ Ã¼¾× ¹× Á¶Á÷À¸·Î ºÐÆ÷µÊ.
- ´ë»ç : À§Àå°ü Á¡¸·, ÀûÇ÷±¸, Ȱ¾×, Ç÷¾× µî¿¡ Á¸ÀçÇÏ´Â esterases¿¡ ÀÇÇØ Ȱ¼ºÇüÀÎ salicylate·Î °¡¼öºÐÇØµÈ´Ù. Salicylate´Â ÁÖ·Î °£ÀÇ microsome È¿¼Ò¿¡ ÀÇÇØ ´ë»çµÇ¸ç ´ë»ç¿¡ Æ÷Ȱ¡ ³ªÅ¸³´Ù.
- ¹Ý°¨±â
- Aspirin : 15-20ºÐ
- Salicylates : ¿ë·®ÀÇÁ¸Àû. Àú¿ë·® (300-600 mg)¿¡¼ 3½Ã°£, °í¿ë·® (1g)¿¡¼ 5-6 ½Ã°£, ´õ °í¿ë·®¿¡¼´Â 10½Ã°£
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| Biotransformation |
Aspirin¿¡ ´ëÇÑ Biotransformation Á¤º¸ Aspirin is rapidly hydrolyzed primarily in the liver to salicylic acid, which is conjugated with glycine (forming salicyluric acid) and glucuronic acid and excreted largely in the urine.
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| Toxicity |
Aspirin¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral, mouse: LD50 = 250 mg/kg; Oral, rabbit: LD50 = 1010 mg/kg; Oral, rat: LD50 = 200 mg/kg. Effects of overdose include: tinnitus, abdominal pain, hypokalemia, hypoglycemia, pyrexia, hyperventilation, dysrhythmia, hypotension, hallucination, renal failure, confusion, seizure, coma, and death.
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| Drug Interactions |
Aspirin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Acetazolamide The salicylate at high dose increases the effect of the carbonic anyhydraseAcetohexamide The salicylate increases the effect of sulfonylureaMethotrexate The salicylate increases the effect and toxicity of methotrexateAnisindione The salicylate increases effect of anticoagulantBetamethasone The corticosteroid decreases the effect of salicylatesChlorpropamide The salicylate increases the effect of sulfonylureaDexamethasone The corticosteroid decreases the effect of salicylatesDichlorphenamide The salicylate at high dose increases the effect of the carbonic anyhydrase inhibitorsDicumarol The salicylate increases effect of anticoagulantValproic Acid The salicylate increases the effect of valproic acidFludrocortisone The corticosteroid decreases the effect of salicylatesGliclazide The salicylate increases the effect of sulfonylureaGlipizide The salicylate increases the effect of sulfonylureaGlisoxepide The salicylate increases the effect of sulfonylureaGlibenclamide The salicylate increases the effect of sulfonylureaTolazamide The salicylate increases the effect of sulfonylureaTolbutamide The salicylate increases the effect of sulfonylureaGriseofulvin Anticipate decrease of ASA efficiency in presence of griseofulvinHeparin Association of ASA/heparin increases risk of bleedingHydrocortisone The corticosteroid decreases the effect of salicylatesPrednisolone The corticosteroid decreases the effect of salicylatesPrednisone The corticosteroid decreases the effect of salicylatesTriamcinolone The corticosteroid decreases the effect of salicylatesWarfarin The salicylate increases the effect of anticoagulantAcenocoumarol The salicylate increases the effect of anticoagulantMethylprednisolone The corticosteroid decreases the effect of salicylatesIbuprofen Ibuprofen reduces ASA cardioprotective effectsInsulin-aspart The salicylate increases the effect of insulinInsulin-detemir The salicylate increases the effect of insulinInsulin-glargine The salicylate increases the effect of insulinInsulin-glulisine The salicylate increases the effect of insulinInsulin-lispro The salicylate increases the effect of insulinKetorolac ASA increases toxicity of ketorolacMethazolamide The salicylate at high dose increases the effect of the carbonic anhydrase inhibitorsProbenecid The salicylate decreases the uricosuric effect of probenecidSulfinpyrazone The salicylate antagonizes the uricosuric effect of sulfinpyrazoneTiclopidine Increased effect of ticlopidineCortisone acetate The corticosteroid decreases the effect of salicylatesGinkgo biloba Association of ASA/ginkgo increases risk of bleedingGlycodiazine The salicylate increases the effect of sulfonylureaInsulin The salicylate increases the effect of insulinParamethasone The corticosteroid decreases the effect of salicylates
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Aspirin¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid drastic changes in dietary habit.Consult your doctor before taking large amounts of Vitamin K (Green leafy vegetables).Avoid alcohol, alcohol appears to cause a 50 to 100% increases in ASA serum levels.Take with food to reduce irritation.Take with a full glass of water.
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| Drug Target |
[Drug Target]
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| SNP Á¤º¸ |
Name:Aspirin (DB00945)
Interacting Gene/Enzyme:Leukotriene C4 Synthase (Gene symbol = LTC4S) Swissprot Q16873
SNP(s):rs730012 (C allele)
Effect:Aspirin-induced urticaria
Reference(s):Mastalerz L, Setkowicz M, Sanak M, Rybarczyk H, Szczeklik A: Familial aggregation of aspirin-induced urticaria and leukotriene C synthase allelic variant. Br J Dermatol. 2006 Feb;154(2):256-60. [PubMed]
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| Description |
Aspirin¿¡ ´ëÇÑ Description Á¤º¸ The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
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| Drug Category |
Aspirin¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Inflammatory Agents, Non-SteroidalAnticoagulantsCyclooxygenase InhibitorsFibrinolytic AgentsPlatelet Aggregation InhibitorsSalicylates
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| Smiles String Canonical |
Aspirin¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(=O)OC1=CC=CC=C1C(O)=O
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| Smiles String Isomeric |
Aspirin¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CC(=O)OC1=CC=CC=C1C(O)=O
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| InChI Identifier |
Aspirin¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C9H8O4/c1-6(10)13-8-5-3-2-4-7(8)9(11)12/h2-5H,1H3,(H,11,12)/f/h11H
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| Chemical IUPAC Name |
Aspirin¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-acetyloxybenzoic acid
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| Drug-Induced Toxicity Related Proteins |
ASPIRIN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Vimentin Drug:aspirin Toxicity:aspirin-induced gastric mucosal microvessels injury . [¹Ù·Î°¡±â] Replated Protein:Angiopoietin-related protein Drug:aspirin Toxicity:damage to microvessels. rupture of capillary walls. necrosis of endothelial cells. damage to endothelial organelles. deposition of fibrin. adherence of platelets to damaged endothelium. [¹Ù·Î°¡±â] Replated Protein:Myeloperoxidase Drug:aspirin Toxicity:haemorrhagic erosions. [¹Ù·Î°¡±â] Replated Protein:Thromboxane A2 receptor Drug:aspirin Toxicity:thrombotic complications. [¹Ù·Î°¡±â] Replated Protein:Integrin beta-3 Drug:Aspirin Toxicity:Antiplatelet effect. [¹Ù·Î°¡±â] Replated Protein:Integrin alpha-Iib Drug:Aspirin Toxicity:Antiplatelet effect. [¹Ù·Î°¡±â] Replated Protein:Nuclear factor NF-kappa-B p105 subunit Drug:aspirin Toxicity:apoptosis in human colon cancer cells. [¹Ù·Î°¡±â]
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The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. ASPIRIN[GGT Increase][Composite Activity](Score) NA(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[SGOT Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[SGPT Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[LDH Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[GGT Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA
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