| 영문 | iron deficiency anemia | 한글 | 철결핍빈혈 |
|---|---|---|---|
| 설명 | 적혈구의 기능은 산소를 운반하는데 있다. 적혈구 속에 산소와 결합을 하여 산소를 운반하는 혈색소라는 물질이 있다. 철은 이 혈색소의 중요한 부분을 이루는 것으로 철이 없으면 혈색소가 만들어질 수가 없다. 혈색소가 없으면 역시 적혈구도 만들어지지 않으므로 체내에 철이 부족하면 빈혈이 생긴다. 이 철결핍성 빈혈은 빈혈의 원인 중에서 가장 흔한 것이다(약 25%를 차지한다). 철저장량의 저하-결핍, 혈청철농도의 저하, 트란스페린량 상승, 트란스페린포화도의 저하, 혈색소농도 또는 헤마토크리트의 저하, 저색소성대적혈구를 특징으로 하는 빈혈로서, 생체 내에서 철이 장기에 걸쳐 결핍되며 그 때문에 혈색소 생산 감소에 의해 일어난다. 창자에서의 철흡수량 부족, 철의 수요 증대(유아기, 사춘기, 임신), 철소실과잉(출혈)에 의해 일어나며, 특히 사춘기에서 폐경기까지의 여성에게 많다. 증상으로서는 얼굴창백, 피로감, 피부창백, 손톱 변화(스푼 모양) 등을 나타낸다. 구강 영역에서는 혀의 접촉통, 발적, 건조감, 삼킴곤란을 수반하면 플러머-빈슨(Plummer-Vinson)증후군이라고 한다. 혈액 소견은 혈청철은 저하하며, 철결합능력의 상승, 저색소성 작은적혈구성을 나타낸다. |
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| 영문 | rheumatoid factor | 한글 | 류마티스 인자 |
|---|---|---|---|
| 설명 | IgG의 Fc부위에 있는 항원결정인자에 대한 항체로서 전형적인 또는 확실한 류마티스관절염(rheumatoid arthritis) 환자의 80%에서 발견된다. 류마티스 인자는 IgM, IgG, IgA중 하나가 될 수 있으나 주로 IgM이다. 소아류마티스관절염(juvenile rheumatoid arthritis: 소아기에 발생하는 류마티스관절염)을 비롯한, 다른 결합조직병이나 감염병에도 나타날 수 있다 |
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| 영문 | growth factor | 한글 | 성장인자 |
|---|---|---|---|
| 설명 | 세포의 분화 및 성장에 관여하는 단백질. 성장인자는 정상 세포주기에 필수적이기 때문에 동물의 생명에 중대한 요소가 된다. 무엇보다도 성장인자는 태아의 발육을 조정하고 조직의 유지 및 보수에 중대한 역할을 하며, 혈구의 생성을 자극한다. 또한 암의 진행과정에도 관여한다. |
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| 영문 | risk factor | 한글 | 위험인자 |
|---|---|---|---|
| 설명 | 국제방사선방호위원회(ICRP)가 1977년 권고에서 방사선방호의 목적으로 채택한 지수로, 단위선량(1 Sv)당 확률적 영향의 발생확률을 추정하여 나타낸 것이다. 생식선 선량에 대한 유전적영향의 발생률(4×10－3/Sv)이나 적색골수선량에 대한 백혈병 발생률(2×10－3/Sv)등 외에 뼈, 허파, 갑상샘, 젖샘, 기타 조직의 위험지수를 측정하여, 확률적 영향의 전신에 있어서 치사위험지수의 합계를 16.5×10－3/Sv로 하였다. 그후 ICRP는 1990년 권고에서 대상이 되는 조직과 장기를 추가하고, 수치 개정을 하면서 명칭도 각목적확률지수라고하였다. 이 권고에 의하면, 치사적 확률적 영향의 확률지수의 합계는, 일반인에 있어 60.0×10－3/Sv이다. |
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| CF | calcaneal fibular [ligament]; calcium leucovorin; calf blood flow; calibration factor; cancer-free; ... |
|---|---|
| MD | Doctor of Medicine [Lat. Medicinae Doctor]; magnesium deficiency; main duct; maintenance dose; major... |
| DF | decapacitation factor; decontamination factor; deferoxamine; deficiency factor; defined flora [anima... |
| EF | ectopic focus; edema factor; ejection fraction; elastic fibril; electric field; elongation factor; e... |
| PF | pair feeding; peak flow; perfusion fluid; pericardial fluid; periosteal fibroblast; peritoneal fluid... |
| ATD | 1-antitrypsin deficiency |
|---|---|
| AMD | Acid maltase deficiency |
| AIDS | Acquire Immune Deficiency Syndrome |
| AIDS | Acquired Immune Deficiency Disease Syndrome |
| alpha1ATD | Alpha-1-antitrypsin deficiency |
IGF-II : insulin like growth factor-II의 약자. 많은 장기와 조직에 작용하여 단백 합성과 DNA, RNA의 합성을 증가시켜 세포의 수와 양을 증가
| hageman factor deficiency | A deficiency of a specific blood clotting factor (XII) that may be genetic or acquired. Administration of heparin or severe liver disease may result in factor XII (Hageman factor) deficiency. There are usually no symptoms associated with this deficiency, but there may be symptoms of mild blood loss in some cases. Treatment is generally unnecessary. Individuals should be cautioned against the use of medications (for example aspirin, warfarin, heparin) with anticoagulant activity, due to risk of exaggerated effects. (27 Sep 1997) |
|---|---|
| extrinsic factor deficiency | <disease> An inherited disorder that causes abnormal blood clotting due to the congenital absence of one of the 20 different plasma proteins involved in the coagulation process. Symptoms include bleeding of the gums, nosebleeds, easy bruising, bleeding in muscles or joints and excessive menstrual bleeding. Treatment includes the administration of plasma concentrates of factor VII (extrinsic factor). (27 Sep 1997) |
| factor II deficiency | A congenital or acquired disorder of blood clotting where there is a deficiency of factor II (prothrombin), one of 20 necessary plasma proteins for normal blood coagulation. Acquired factor II deficiency may result from vitamin K deficiency, severe liver disease and anticoagulant drugs. Symptoms include abnormal bleeding, nosebleeds, abnormal menstrual bleeding, easy bruising and umbilical cord bleeding at birth. Treatment involves the infusion of fresh frozen plasma. Vitamin K may be administered in select cases. (27 Sep 1997) |
| factor ix deficiency | A form of haemophilia in males that results from a deficiency of clotting factor IX, transmitted as a X-linked trait. Symptoms include easy bruising, nosebleeds, bleeding gums and bleeding into muscle tissue (haematoma) or a joint space (haemarthrosis). Treatment includes the infusion of factor IX concentrates to normalize blood coagulation. (27 Sep 1997) |
| factor v deficiency | An inherited disorder that results in abnormal blood clotting due to the deficiency of factor V, one of 20 plasma proteins responsible for the maintenance of normal blood clotting. Symptoms include excessive bleeding, bleeding gums, nosebleeds, easy bruising, excessive menstrual bleeding and bleeding into muscle tissue (haematoma) or a joint space (haemarthrosis). Treatment includes the infusion of fresh frozen plasma to restore deficient factor V. (27 Sep 1997) |
| factor vii deficiency | An inherited disorder that causes abnormal blood clotting due to the congenital absence of one of the 20 different plasma proteins involved in the coagulation process. Symptoms include bleeding of the gums, nosebleeds, easy bruising, bleeding in muscles or joints and excessive menstrual bleeding. Treatment includes the administration of plasma concentrates of factor VII (extrinsic factor). (27 Sep 1997) |
| factor viii deficiency | A sex-linked genetic disease affecting males that results from a deficiency of clotting factor VIII, a protein factor that is required for normal blood coagulation. Symptoms include easy bruising, bleeding gums, nosebleeds and bleeding into muscle tissue (haematoma) or a joint space (haemarthrosis). Treatment includes the infusion of factor VIII concentrate intravenously to restore this essential factor and normalize blood coagulation. Inheritance: sex-linked. (27 Sep 1997) |
| factor x deficiency | Blood coagulation disorder usually inherited as an autosomal recessive trait, though it can be acquired. It is characterised by defective activity in both the intrinsic and extrinsic pathways, impaired thromboplastin time, and impaired prothrombin consumption. (12 Dec 1998) |
| factor xi deficiency | A deficiency of blood coagulation factor xi (known as plasma thromboplastin antecedent or pta or antihemophilic factor c) resulting in a systemic blood-clotting defect called haemophilia c or rosenthal's syndrome, that may resemble classical haemophilia. (12 Dec 1998) |
| factor xii deficiency | A deficiency of a specific blood clotting factor (XII) that may be genetic or acquired. Administration of heparin or severe liver disease may result in factor XII (Hageman factor) deficiency. There are usually no symptoms associated with this deficiency, but there may be symptoms of mild blood loss in some cases. Treatment is generally unnecessary. Individuals should be cautioned against the use of medications (for example aspirin, warfarin, heparin) with anticoagulant activity, due to risk of exaggerated effects. (27 Sep 1997) |
| factor xiii deficiency | A deficiency of blood coagulation factor xiii or fibrin stabilizing factor (fsf) which enables fibrin to form a firm blood clot. Deficiency of this factor produces a clinical haemorrhagic diathesis. (12 Dec 1998) |
| 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) |
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|