Transcript PPT
Adult Medical-Surgical Nursing HAEMATOLOGY MODULE: LEUKAEMIA 2 Leukaemia: Description A group of malignant disorders affecting: White blood cells (lymphocytes or leucocytes) Bone marrow Lymph system Spleen (Introduction in Lecture 1) Leukaemia: Classification Acute Myelogenous Leukaemia (AML) (Lecture 1) Acute Lymphocytic Leukaemia (ALL) Chronic Myelogenous Leukaemia (CML) Chronic Lymphocytic Leukaemia (CLL) Acute Lymphocytic Leukaemia Acute Lymphocytic Leukaemia (ALL) Only 15% of adult leukaemia Most common leukaemia of childhood Acute onset Good remission and cure rate in children but not adults ALL: Pathophysiology Lymphoblasts (immature dysfunctional lymphocytes) proliferate in the blood and bone marrow Lymphoblasts frequently pass to the central nervous system (CNS) across the blood-brain barrier Treatment involves intra-thecal chemotherapy (into the cerebrospinal fluid via lumbar puncture) ALL: Clinical Manifestations Sudden onset High susceptibility to infection: Prone to opportunistic infection (as Candida Albicans) Fatigue Pallor Bleeding tendency Bone pain: damaged overcrowded marrow ALL: Diagnosis CBC Blood film: Extremely increased number of immature white cells (lymphoblasts) ↓ RBC and platelets Bone marrow biopsy: crowding of lymphoblasts Lumbar puncture and CT scan for evidence of leukaemia outside blood or bone marrow ALL: Management Intensive chemotherapy including intrathecal Destroys rapidly dividing blast cells (Chemotherapy included in Leukaemia Lecture 1) ALL: Prognosis ALL is more prevalent in childhood Poor prognosis for adults (<25% achieve 5-year continuous remission) Good cure rate (50-75%) in children Chronic Myelogenous Leukaemia CML: Description A chronic malignancy of granulocytes (mature cells, not blast cells) CML: Pathophysiology Related to radiation A stem cell disorder where there is a translocation of genetic material from C22 the “Philadelphia chromosome”→ C9 Dysfunctional granulocytes of all stages are increased in blood and bone marrow Marked splenomegaly: extramedullary (site other than bone marrow) haematopoiesis/ infiltration CML: Clinical Manifestations Gradual onset Chronic fatigue and weakness Pallor Weight loss Compromised immune response Splenomegaly Anaemia Bleeding tendency CML: Diagnosis Patient history and clinical picture CBC Chromosome studies Bone marrow biopsy Granulocytes of all stages in peripheral blood and bone marrow WCC >100, 000/ cmm3 (ref. 5-10,000) Reduced thrombocyte and red cell count CML: Management Less intensive treatment: (Resistant to intensive chemotherapy which is aimed at dividing cells) Steroids Oral chemotherapy Blood transfusions (Maybe splenectomy) CML: Prognosis Poor prognosis: (more serious than CLL) Death from infection or haemorrhage Often becomes acute as AML Chronic Lymphocytic Leukaemia CLL: Description A gradual accumulation of small dysfunctional lymphocytes in: Blood circulation Bone marrow Lymph nodes Spleen CLL: Pathophysiology Non-functioning leukaemic B-cells accumulate slowly in bone marrow, spleen, liver, lymph nodes Lymphocytosis in circulation Immunoglobulins non-functioning Impaired immune response Anaemia Thrombocytopaenia CLL: “Hairy Cell” Leukaemia “Hairy Cell” Leukaemia: hairy appearance of lymphocytes These are intensively destroyed by the spleen → splenomegaly Pancytopaenia → acute infection risk CLL: Clinical Manifestations Gradual onset Chronic fatigue and weakness Pallor Weight loss Compromised immune response Splenomegaly, lymphadenopathy Anaemia Bleeding tendency CLL: Diagnosis Patient history and clinical picture CBC, bone marrow biopsy Lymphocytosis: WCC >100, 000/ cmm3 (ref. 5-10,000) Dysfunctional lymphocytes of all stages in peripheral blood and marrow Presence of “Hairy Cell” lymphocytes CLL: Management Splenectomy (reduce haemolysis) Steroids Oral chemotherapy (Resistant to intensive chemotherapy which is aimed at dividing cells) Supportive blood transfusions CLL: Prognosis Eventually blast crisis → ALL Infection Haemorrhage Death: (survival approximately 7 years)