| 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 | infectious disease | 한글 | 감염병 |
|---|---|---|---|
| 설명 | 바이러스로부터 기생충 크기까지의 생물을 원인으로 하는 병. 원인은 접촉전염성이며, 병원에서 감염되는 경우도 있다. 감염을 원인균에 따라 분류하면 바이러스, 세균, 클라미디아, 리켓차, 미코박테리움, 곰팡이, 원충, 윤충, 외부기생충 감염으로 나눌 수 있다. |
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| 영문 | hypertensive heart disease | 한글 | 고혈압심장병 |
|---|---|---|---|
| 설명 | 고혈압에 의해서 생기는 심장병. 고혈압심장병이라는 진단을 붙이기 위해서는 최소한 다음과 같은 조건이 부합되어야 하는데, 첫째 심장혈관계에 심장병을 유발할 수 있을 만한 다른 병변이 없이 좌심실 비대가 있어야 하며, 둘째 고혈압을 앓았다는 병력이 있어야 한다. 주로 고혈압에 의한 심장병은 초기에는 좌심실이 비후라는 것으로 특징되어진다. 즉 혈압이 높으므로 혈액을 순환시키기 위해서는 그만큼 심장의 혈액을 보내는 힘이 좋아야 한다. 그 힘을 얻기위해서는 심근의 비후가 필요로 하여 좌심실 근육의 비후가 생긴다. 그리고 고혈압이 지속이 될 경우에는 결국 심장이 제 구실을 하지 못하고 펌프로서의 기능을 잃어버리게 되어 심장기능상실에 빠지게 된다. |
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| 영문 | pelvic inflammatory disease | 한글 | 골반염질환 |
|---|---|---|---|
| 설명 | 골반주위의 장기에 발생하는 염증을 말함. 주로 여성에서 발생하며 원인은 임균(gonococcus)과 비임균에 의한 감염(non-gonorrheal infection)에 의한다. 증상은 초기에는 질분비물, 하복부동통, 여성의 생식기부위에 발생하는 압통, 월경통, 월경량의 증가 등이다. 일찍 치료해야 하며, 계속적으로 병이 지속시 여성의 불임의 원인이 된다. 후진국에서는 가장 많은 여성불임의 원인이기도 함. 치료는 항생제의 투여이다. |
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| 영문 | Graves' disease | 한글 | 그레이브스병 |
|---|---|---|---|
| 설명 | 갑상샘의 비대와 갑상샘호르몬의 과다분비가 특징인 병이다. 이 병은 주로 25~50세에 호발하고 주로 여자에게서 많이 생긴다. 갑상샘 호르몬은 저장되어 있는 에너지를 소모하여 신체의 대사율을 높이는 호르몬이므로 입맛이 좋은 데도 불구하고 계속적인 체중의 감소, 그리고 축적된 에너지를 소모하여 열생많이 하여서 더위를 참기 힘들어하고 만성 쇠약감이나 근력의 약화를 보일 수가 있다. 그리고 눈에 특징적인 증상이 나타나는데 눈꺼풀이 비정상적으로 위로 올라가 있고, 눈이 아래의 물건을 주시할 경우에 눈꺼풀이 정상적으로는 처져야 하지만 갑상샘 호르몬이 과도하게 나올 경우에는 눈꺼풀이 처지지 않는다. 또 눈알이 앞쪽으로 돌출하는 안구돌출을 볼 수가 있다. 또 피부가 아주 부드럽고 물기가 많아서 축축하다. 그리고 특징적으로 하지의 앞쪽에 피부가 두꺼워져 국소적 융기를 이루는 것이 있는데 이것은 이 병의 특징적인 병터이다. |
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| MD | Doctor of Medicine [Lat. Medicinae Doctor]; magnesium deficiency; main duct; maintenance dose; major... |
|---|---|
| CD | cadaver donor; canine distemper; canine dose; carbohydrate dehydratase; carbon dioxide; cardiac dise... |
| HD | Haab-Dimmer [syndrome]; Hajna-Damon [broth]; Hansen disease; hearing distance; heart disease; helix ... |
| CPS | carbamoylphosphate synthetase; cardioplegic perfusion solution; centipoise; cervical pain syndrome; ... |
| MCD | magnetic circular dichroism; mast-cell degranulation; mean cell diameter; mean of consecutive differ... |
| NO Synthase | nitric oxide synthase |
|---|---|
| AIDS | Acquired Immune Deficiency Disease Syndrome |
| ATD | 1-antitrypsin deficiency |
| AMD | Acid maltase deficiency |
| AIDS | Acquire Immune Deficiency Syndrome |
Kugelberg-Welander disease 근 위축증의 유전성 연소형으로서 보통 상염색체성 열성 형질로 유전된다. 척수 전각의 병변이 그 원인이다.
kukuruku 원인 불명이며, 나이지리아에서 볼 수 있는 질환으로, 열
| carbamoylphosphate synthetase deficiency | <biochemistry> Carbamoylphosphate synthetase is the initial enzyme of the urea cycle, catalysing the synthesis of carbamoylphosphate from ammonia, bicarbonate and ATP as the first step of ammonia detoxification. The enzyme is an intramitochondrial form called CPS I. A different isozyme found in the cytoplasm, called CPS II, is much less active and apparently not involved in the urea cycle. The deficiency state is autosomal recessive and presents in infancy with massive hyperammonaemia and neurologic deficits in survivors. Diagnosis is suggested by the blood biochemistry and confirmed by specific enzyme assay on liver or rectal biopsy. Prenatal diagnosis by molecular methods has been used successfully in informative families. Inheritance: autosomal recessive. (07 Apr 1998) |
|---|---|
| antibody deficiency disease | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| deficiency disease | Any disease resulting from undernutrition or an inadequacy of calories, proteins, essential amino acids, fatty acids, vitamins, or trace minerals. (05 Mar 2000) |
| thrombotic disease due to protein c deficiency | Protein C is a protein in plasma that enters into the cascade of biochemical events leading to the formation of a clot. Deficiency of protein c results in thrombotic (clotting) disease and excess platelets with recurrent thrombophlebitis (inflammation of the vein that occurs when a clot forms). The clot can break loose and travel through the blood stream (thromboembolism) to the lungs causing a pulmonary embolism, brain causing a stroke (cerebrovascular accident), heart causing an early heart attack, skin causing what in the newborn is called neonatal purpura fulminans, the adrenal gland causing haemorrhage with abdominal pain, abnormally low blood pressure (hypotension), and salt loss. Protein c deficiency is due to possession of one gene (heterozygosity) in chromosome band 2q13-14. The possession of two such genes (homozygosity) is usually lethal. (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) |
| alpha-antitrypsin deficiency | <enzyme> A specific enzyme (alpha 1 antitrypsinase) that when absent genetically can result in panacinar emphysema (lung disease) and liver disease. There is no specific treatment for this condition other than supportive care for the liver and lung complications. Medications such as alpha-1proteinase inhibitor is given regularly to these patients. Incidence: approximately 1 in 10,000. (02 Jan 1998) |
| anaemia, iron deficiency | Deficiency of iron results in anaemia because iron is necessary to make haemoglobin, the key molecule in red blood cells responsible for the transport of oxygen. In iron deficiency anaemia, the red cells are unusally small (microcytic) and pale (hypochromic). Characteristic features of iron deficiency anaemia in children include failure to thrive (grow) and increased infections. The treatment of iron deficiency anaemia, whether it be in children or adults, is with iron and iron-containing foods. Food sources of iron include meat, poultry, eggs, vegetables and cereals (especially those fortified with iron). According to the National Academy of Sciences, the Recommended Dietary Allowances of iron are 15 milligrams per day for women and 10 milligrams per day for men. Anaemia characterised by low or absent iron stores, low serum iron concentration, elevated free erythrocyte porphorin, low transferrin saturation, elevated transferrin, low serum ferritin, low haemoglobin concentration or haematocrit, and hypochromic microcytic red blood cells. Symptoms may include pallor, angular stomatitis and other oral lesions, gastrointestinal complaints, retinal haemorrhages and exudates, and thinning and brittleness of the nails. Among the causes of iron-deficiency anaemia are inadequate iron intake, impaired iron absorption, increased blood loss and increased requirements such as infancy, pregnancy, and lactation. (12 Dec 1998) |
| antibody deficiency syndrome | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| antitrypsin deficiency | Deficiency of a1-antitrypsin, a glycoprotein of the postalbumin region of human serum. Many forms are known which may be moderate (40 to 60% of normal activity) or severe (less than 10% of normal), all autosomal dominant; the severe form is often associated with familial emphysema or hepatic cirrhosis. (05 Mar 2000) |
| arch length deficiency | The difference between the available circumference of the dental arch and that required to accommodate the succedaneous teeth in proper alignment. (05 Mar 2000) |
| arginase deficiency | <biochemistry> Arginase is the fifth enzyme of the urea cycle and catalyses the hydrolysis of arginine to ornithine and urea as the final step in the detoxification of ammonia. Deficiency of the enzyme results in hyperargininaemia and episodic hyperammonaemia, leading to moderate to severe mental retardation and spasticity. at least two isozymes of arginase exist in man. AI (the enzyme deficient in the disorder) is cytosolic and found primarily in liver and red blood cells, whereas AII is mitochondrial and found predominantly in kidney but also to a lesser extent in liver, brain, and other tissues. While AII activity appears to be induced in AI deficiency, it is only partially effective in maintaining urea cycle function. The normal in vivo function of AII is unclear. Arginase deficiency is diagnosed by observing high arginine concentrations on either qualitative or quantitative plasma or urine amino acid analysis. The diagnosis is confirmed by finding markedly decreased or absent arginase activity in an isotopic red blood cell enzymatic assay. The AI gene has been cloned, sequenced, and localised to human chromosome band 6q23. (17 Dec 1997) |
| 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) |
Synonyms : Carbamoyl Phosphate Synthase (Ammonia) Deficiency Disease, Carbamoyl-Phosphate Synthetase I Deficiency Disease, Carbamoylphosphate Synthetase I Deficiency Disease, Carbamyl Phosphate Synthetase Deficiency Disease
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
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제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|