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28 Cards in this Set
- Front
- Back
neutrophil - describe and function
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*have granules containing several enzymes
*phagocytosis of bacteria |
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eosinophils - describe and function
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*bi lobed nucleus and large granules
*defense against parasitic helminths; allergic reactions; found in GIT, vagina, bronchi and uterus |
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lymphocytes - describe and function
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*scant cytoplasm; B and T look similar
*B - produce antibodies; T - cell-mediate immunity and kill virus infected cells |
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monocytes - describe and function
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*agranulocyte with kidney shaped nucleus
*precursor of macrophage (monocyte in blood; macrophage in tissue) |
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monocytes - describe and function
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*agranulocyte with kidney shaped nucleus
*precursor of macrophage (monocyte in blood; macrophage in tissue); kill senescent cells |
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basophils - describe and function
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*multi lobed nucleus with many granules
*supplement fn of mast cells in immediate hypersensitivity reactions |
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definition of leukaemia
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progressive malignancy characterised by disordered development and proliferation of leukocytes and their precusors in bone marrow, leading to abnormal amounts of leukocytes entering peripheral blood stream
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def of acute leukaemia
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genetic abnormality in myeloid or lymphoid cells --> lymphoblast/meyloblast entering peripheral blood
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def of chronic lymphocytic leukaemia
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aberrant apoptotic signally pathway in B lymphocytes, resulting in lymphocyte accumulation in peripheral blood and bone marrow
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def of chronic myeloid leukaemia
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*myeloproliferative disorder
*translocation between 9 and 22 chrosome creating bcr-abl infusion *charac by accumulation of mature and immature myeloid cells in blood stream and bone marrow |
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AML affects mainly ______
ALL affects mainly ______ |
*older
*young children |
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ALL consists of ______ of acute leukaemias in paediatric population
Peak incidence in ______ years old and a second peak at ________ |
*80%
*3-4 years old; 50 years old * |
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RF for ALL
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*age - 3-4 years old
*Genetic disorders e.g. Down Syndrome |
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Median age for AML - ?
RF for AML - ? |
*65 years old
*previous radiation/chemical exposure; myelodysplasia |
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AML vs ALL - symptoms and signs
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Both - symptoms related to pancytopenia (secondary to overcrowding of bone marrow by leukaemia cells)
- neutropenia --> fever and infection - thrombocytopenia --> bleeding - anaemia --> fatigue ALL - sometimes ass. with bone pain (bone marrow expansion + subperiosteum infiltration) - hepatomegaly, splenomegaly, gen lymphadenopathy - meningeal involvement - N+V, dizziness, headaches AML - particularly liver and spleen infiltration - DIC - less CNS involvement |
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diagnosing acute leukaemia
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1. FBC + blood film - pancytopenia and blasts
2. Bone marrow examination - *aspirate *trephine biopsy 3. tests carried on these samples *morphology *molecular charac by flow cytometry *cytogenic analysis e.g. FISH |
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Auer rods are found in ____
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AML
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typical karyotypic abnormality in AML
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translocation of chromosome 8 and 21 into region 22
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prognostic factors for ALL
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*age - adults have poorer prognosis
*T cell/B cell - B cell more common and better prognosis *chromosomal translocations - having certain chromosomal abnormalities e.g. Ph chromo worse prognosis *high WCC at diagnosis |
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AML prognostic factors
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*age > 60 years
*2 or more related co-morbidities *high WCC at diagnosis *karyotypic abnormalities *pre-existing myelodysplasia (arising from B/G of myelodysplasia or following chemotherapy --> worse prognosis) |
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Causes of neutropenia - categories
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Divided into two categories - decreased/ineffective productino of neutrophils AND increased destruction of neutrophils
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Causes of decreased/ineffective production of neutrophils
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*drugs e.g. sulfasalazine (used in IBD), amiodarone, penicillins, cephalosporins, enalapril, clozapine, ibuprofen
*myelodysplasia --> defective precursors *megaloblastic anaemia (2 to B12/folate deficiency) *suppression of myeloid stem cells (e.g. aplastic anaemia or tumours) *rare inherited conditions e.g. Kostmann syndrome --> impaired differentiation |
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causes of increased neutrophil destruction
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*overwhelming infection
*immune-mediate e.g. idiopathic, autoimmune e.g. SLE, drugs *hypersplenism |
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when neutropenia is caused by excessive destruction of neutrophils, the marrow is hypo/hyper-cellular??
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hypercellular, with excessive granulocyte precusors
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when neutropenia is caused by ineffective granulopoesis, the marrow is hypo/hyper celluar
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hypercellular
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when neutropenia is caused by drugs suppressing the granulocyte precursors, the marrow is hyper/hypo cellular
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hypocellular
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what organisms can disseminate quickly to cause death in a patient with neutropenia
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usu. candida, aspergillus
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what sort of infections can a patient with neutropenia get?
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*ulcerating necrotising lesions of the oropharynx
*lesions in skin, vagina, GIT and anus *invasive infection in lungs, urinary tract and kidneys |