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"Refractory anaemia with excess of blasts"¿¡ ´ëÇÑ °Ë»ö °á°úÀÔ´Ï´Ù. °Ë»ö °á°ú º¸´Â µµÁß¿¡ Tab ۸¦ ´©¸£½Ã¸é °Ë»ö âÀÌ ¼±Åõ˴ϴÙ.
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  • antibody excess zone
    Ç×ü°úÀ×´ë(ù÷ô÷Φí¥Óá).
  • antibody excess zone
    Ç×ü°úÀ×´ë(ù÷ô÷Φí¥Óá).
  • antigen excess
    Ç׿ø°ú´Ù(ù÷ê«Î¦Òý).
  • antigen excess zone
    Ç׿ø°úÀ×´ë.
  • antigen excess zone
    Ç׿ø°úÀ×´ë.
  • antigen excess zone
    Ç׿ø°úÀ×´ë.
  • base excess
    ¿°±â °úÀ×(Φí¥)
  • base excess =BE
    ¿°±â°úÀ×(ç¤ÐñΦ í¥).
  • base excess/deficit
    ¿°±â°úÀ×/°áÇÌ
  • convergence excess
    ´«¸ðÀ½°ú´Ù, ÆøÁÖ°ú´Ù
  • divergence excess
    ´«¹ú¸²°ú´Ù, °³»ê°ú´Ù
  • divergence excess exotropia
    ´«¹ú¸²°ú´Ù¿Ü»ç½Ã,°³»ê°ú´Ù¿Ü»ç½Ã
  • excess
    °úÀ×(Ë´Ëö), À׿©.
  • excess anesthetic gas
    À׿©¸¶Ãë°¡½º.
  • excess chlorine
    °úÀ׿°¼Ò.
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ECG Electro-Cardio-Graphy(-Gram); ½ÉÀüµµ
   = EKG
  1. Conducting System Structu...
AME amphotericin methyl ester; apparent minerallocorticoid excess; aseptic meningoencephalitis
BE bacillary emulsion; bacterial endocarditis; barium enema; Barrett's esophagus; base excess; below-el...
REMA repetitive excess mixed anhydride
XEF excess ejection fraction
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NHF normal human fibro-blasts
AME Apparent Mineralocorticoid Excess
BE Base Excess
EWL Excess Weight Loss
EPOC Excess post-exercise oxygen consumption
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refractory rickets Rickets that does not respond to treatment with usual doses of vitamin D and adequate dietary calcium and phosphorus. Most often due to inherited renal tubular disorder e.g., Fanconi syndrome.
Renal rickets, a form of rickets occurring in children in association with and apparently caused by renal disease with hyperphosphatemia.
Synonym: pseudorickets, renal fibrocystic osteosis, renal infantilism, renal osteitis fibrosa.
(05 Mar 2000)
refractory state Subnormal excitability immediately following a response to previous excitation; the state is divided into absolute and relative phases.
(05 Mar 2000)
relative refractory period The period between the effective refractory period and the end of the refractory period; fibres then respond only to high intensity stimuli and the impulses conduct more slowly than normally.
(05 Mar 2000)
effective refractory period The period during which impulses may appear but are too weak to be conducted; the longest interval between adequate stimuli, falling just short of the time necessary to allow a propagated response to be evoked in a tissue by the second stimulus; it differs from the functional refractory period in that it is a measure of stimulus interval rather than response interval of time.
(05 Mar 2000)
total refractory period The absolute refractory period plus the relative refractory period.
(05 Mar 2000)
functional refractory period The minimum interval possible between successive responses to stimulation of a tissue.
(05 Mar 2000)
achlorhydric anaemia A form of chronic hypochromic microcytic anaemia associated with achlorhydria or achylia gastrica; observed most frequently in women in the third to fifth decades.
Synonym: Faber's anaemia, Faber's syndrome.
(05 Mar 2000)
achrestic anaemia A form of chronic progressive macrocytic anaemia that can be fatal in which the changes in bone marrow and circulating blood closely resemble those of pernicious anaemia, but in which there is only transient or no response to therapy with vitamin B12; glossitis, gastrointestinal disturbances, central nervous system disease, and pyrexia are not observed, and there is only little bleeding or haemolysis.
Origin: G. A-priv. + chresis, a using
(05 Mar 2000)
acquired haemolytic anaemia Nonhereditary acute or chronic anaemia associated with or caused by extracorpuscular factors, e.g., certain infectious agents, chemicals (including autoantibodies or therapeutic agents), burns, toxic materials from higher plant and animal forms (including snake venoms).
(05 Mar 2000)
addisonian anaemia <haematology> A form of anaemia (low red blood cell counts) that results when the bone marrow fails to produce adequate numbers of red blood cells due to a deficiency in vitamin B12. Intrinsic factor, necessary for normal B12 absorption, may be the underlying cause for B12 deficiency if is not produced in the gastric glands (in the stomach).
Origin: Gr. Haima = blood
(27 Sep 1997)
Addison's anaemia <haematology> A form of anaemia (low red blood cell counts) that results when the bone marrow fails to produce adequate numbers of red blood cells due to a deficiency in vitamin B12. Intrinsic factor, necessary for normal B12 absorption, may be the underlying cause for B12 deficiency if is not produced in the gastric glands (in the stomach).
Origin: Gr. Haima = blood
(27 Sep 1997)
anaemia <haematology> Too few red blood cells in the bloodstream, resulting in insufficient oxygen to tissues and organs.
Origin: Gr. Haima = blood
(16 Dec 1997)
anaemia, aplastic A form of anaemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.
(12 Dec 1998)
anaemia, Cooley's Better known today as thalassaemia (or as beta thalassaemia or thalassaemia major).The clinical picture of this important type of anaemia was first described in 1925 by the paediatrician Thomas Benton Cooley. Another name for the disease is Mediterranean anaemia. The name thalassaemia was coined by the Nobel Prise winning pathologist George Whipple and the professor of paediatrics Wm Bradford at Univ. Of Rochester because thalassa in Greek means the sea (like the Mediterrranean Sea) + -aemia means in the blood so thalassaemia means sea in the blood. Thalassaemia is not just one disease. It is a complex contingent of genetic (inherited) disorders all of which involve underproduction of haemoglobin, the indispensable molecule in red blood cells that carries oxygen. The globin part of normal adult haemoglobin is made up of 2 alpha and 2 beta polypeptide chains. In beta thalassaemia, there is a mutation (change) in both beta globin chains leading to underproduction (or absence) of beta chains, underproduction of haemoglobin, and profound anaemia. The gene for beta thalassaemia is relatively frequent in people of Mediterranean origin (for example, from Italy and Greece). Children with this disease inherit one gene for it from each parent. The parents are carriers (heterozygotes) with just one thalassaemia gene, are said to have thalassaemia minor, and are essentially normal. Their children affected with beta thalassaemia seem entirely normal at birth because at birth we still have predominantly foetal haemoglobin which does not contain beta chains. The anaemia surfaces in the first few months after birth and becomes progressively more severe leading to pallor and easy fatiguability, failure to thrive (grow), bouts of fever (due to infections) and diarrhoea. Treatment based on blood transfusions is helpful but not curative. Gene therapy will, it is hoped, be applicable to this disease.
(12 Dec 1998)
anaemia, dyserythropoietic, congenital A familial disorder characterised by anaemia with multinuclear erythroblasts, karyorrhexis, asynchrony of nuclear and cytoplasmic maturation, and various nuclear abnormalities of bone marrow erythrocyte precursors. Type II is the most common of the 3 types of congenital dyserythropoietic anaemia; it is often referred to as hempas, based on the hereditary erythroblast multinuclearity with positive acidified serum test.
(12 Dec 1998)
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