| family practice | A medical specialty concerned with the provision of continuing, comprehensive primary health care for the entire family. (12 Dec 1998) |
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| family practice physician | <specialist> A physician expert in the management of a wide scope of health problems in adults and children. Once referred to as a general practitioner or family physician. (27 Sep 1997) |
| family predisposition | <genetics> A disease or condition that is present in a blood relative (grandparent, parent or sibling). (27 Sep 1997) |
| family relations | Behavioural, psychological, and social relations among various members of the nuclear family and the extended family. (12 Dec 1998) |
| family therapy | A form of group psychotherapy. It involves treatment of more than one member of the family simultaneously in the same session. (12 Dec 1998) |
| abelson leukaemia virus | A defective murine leukaemia virus capable of transforming lymphoid cells and producing a rapidly progressing lymphoid leukaemia after superinfection with friend, moloney, or rauscher virus. (12 Dec 1998) |
| Abelson murine leukaemia virus | A retrovirus belonging to the Type C retrovirus group subfamily (family Oncovirinae) which is associated with leukaemia and produces in vitro transformation of mouse cells. (05 Mar 2000) |
| accelerated phase of leukaemia | Refers to chronic myelogenous leukaemia that is progressing. The number of immature, abnormal white blood cells in the bone marrow and blood is higher than in the chronic phase, but not as high as in the blast phase. (12 Dec 1998) |
| acute granulocytic leukaemia | <haematology> A form of leukaemia which is characterised by the proliferation of immature white blood cells (granulocytes) in the bloodstream. Occurs primarily in adults and in infants under 1 year of age. Complications include abnormal bleeding and susceptibility to infections. Symptoms include fatigue, weight loss, fevers, weakness, pallor, bone pains, bleeding gums, nosebleeds, easy bruising, enlarged lymph nodes and joint pains. Treatment includes chemotherapy and/or bone marrow transplant. Origin: Gr. Haima = blood (27 Sep 1997) |
| acute leukaemia | <haematology> A rapidly progressive cancer of the blood of sudden onset and characterised by the uncontrolled proliferation of immature blood cells which take over the bone marrow and spill into the blood stream. If left untreated is fatal within a few weeks or months. See: acute lymphoblastic leukaemia, acute myeloid leukaemia. Origin: Gr. Haima = blood (11 Nov 1997) |
| acute lymphoblastic leukaemia | <haematology> A rapidly progressing cancer of the blood affecting the type of white blood cell known as lymphocytes. Approximately 650 new cases are diagnosed every year in the UK and it is the most common form of childhood leukaemia. Acronym: ALL Origin: Gr. Haima = blood (11 Nov 1997) |
| acute lymphocytic leukaemia | <radiology> 95% of cases of leukaemia in children, bone changes in 50-70% of kids (vs. 10% in adults); seen as early as 1 month after onset of symptoms, wrists and knees most commonly affected, bony defects: metaphyseal radiolucent bands! (similar findings in scurvy, JRA, syphilis), osteolytic lesions, periosteal reaction, osteosclerosis (12 Dec 1998) |
| acute monocytic leukaemia | <haematology> The most common translocation in this disorder of poorly differentiated monocytic cells involves chromosome region 11q in a large percentage of cases. The translocation involves a cellular oncogene, c-ets which is mapped to the 11q23-24 region. The most common translocations reported are t(6;11), t(9;11), t(11;17) and t(11;19), of which t(9;11) (p21-22;q23) is by far the most frequently detected and implicated in acute myeloid leukaemia. The cells express CD14 surface antigen, which is diagnostic of monocytic cells. Acronym: AML Classification: FAB M5 (07 Apr 1998) |
| acute myeloblastic leukaemia | <haematology> A rapidly progressing cancer of the blood affecting immature cells of the bone marrow, usually of the white cell population. It is much more common in adults than in children. Symptoms include fatigue, weight loss, fevers, weakness, pallor, bone pains, bleeding gums, nosebleeds, easy bruising, enlarged lymph nodes and joint pains. Treatment includes chemotherapy and/or bone marrow transplant. This leukaemia demonstrates granulocyte differentiation, eosinophilia and Auer rods and is associated with a reciprocal translocation between 8 and 21 (q22;q22), which is the most common translocation in acute myeloid leukaemia and is found more often in younger patients than in older patients. The oncogene involved in this translocation is AML1, which can be detected by Southern blot. Numerical abnormalities, particularly monosomy-7, trisomy-4, trisomy-8, trisomy-21, -Y, monosomy-7 and deletions of the long arms of chromosomes 5 and 7 are quite common in all acute myeloid leukaemia and not restricted to any one FAB classification. Many of these abnormalities are observed at diagnosis and at later stage disease, particularly after chemotherapy. Prognosis is generally more favorable than in FAB-M2 patients showing no translocation, because the latter patients show better remission rates for longer periods of time. Immunophenotyping is useful in diagnosis and expression of one or more of the myeloid antigens CD13, CD14 or CD33 must be detected to make a diagnosis of acute myeloid leukaemia. Acronym: AML Incidence: 2,000 new cases per year in the UK. Origin: Gr. Haima = blood (07 Apr 1998) |
| acute myelogenous leukaemia | <haematology> A rapidly progressing cancer of the blood affecting immature cells of the bone marrow, usually of the white cell population. It is much more common in adults than in children. Symptoms include fatigue, weight loss, fevers, weakness, pallor, bone pains, bleeding gums, nosebleeds, easy bruising, enlarged lymph nodes and joint pains. Treatment includes chemotherapy and/or bone marrow transplant. This leukaemia demonstrates granulocyte differentiation, eosinophilia and Auer rods and is associated with a reciprocal translocation between 8 and 21 (q22;q22), which is the most common translocation in acute myeloid leukaemia and is found more often in younger patients than in older patients. The oncogene involved in this translocation is AML1, which can be detected by Southern blot. Numerical abnormalities, particularly monosomy-7, trisomy-4, trisomy-8, trisomy-21, -Y, monosomy-7 and deletions of the long arms of chromosomes 5 and 7 are quite common in all acute myeloid leukaemia and not restricted to any one FAB classification. Many of these abnormalities are observed at diagnosis and at later stage disease, particularly after chemotherapy. Prognosis is generally more favorable than in FAB-M2 patients showing no translocation, because the latter patients show better remission rates for longer periods of time. Immunophenotyping is useful in diagnosis and expression of one or more of the myeloid antigens CD13, CD14 or CD33 must be detected to make a diagnosis of acute myeloid leukaemia. Acronym: AML Incidence: 2,000 new cases per year in the UK. Origin: Gr. Haima = blood (07 Apr 1998) |