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196 Cards in this Set
- Front
- Back
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LFTs - ALP
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Indicates biliary obstruction and hepatic metastasis
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LFTs - AST
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Liver and skeletal muscle pathologies
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LFTs - Albumin
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If low, capillary leak
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LFTs - ALT
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If high, hepatitis
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V. high ALP, high ALT
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Problem in bile duct
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Very high ALT, high ALP
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problem in liver
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Very very high ALT, high AST
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Severe necrosis of liver
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Very high ASP, high ALT
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Alcoholic cirrhosis
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Neutrophilia
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Acute infection, inflammation, acute necrosis
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Neutropenia
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Viral infection, drug reactions
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Causes of microcytic anaemia
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Iron deficiency, thalassaemia (low MCV, raised RBC), sideroblastic anaemia
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Causes of normocytic anaemia
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Blood loss, chronic disease, bone marrow failure/infiltration, renal failure, hypothyroidism, haemolysis, pregnancy
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Causes of macrocytic anaemia
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B12/folate deficiency, alcohol excess, reticulocytosis, myelodysplastic syndrome, marrow infiltration, hypothyroidism
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Cause of anaemia in renal failure
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Erythropoietin deficiency
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What are Howell-Jolly bodies?
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DNA nuclear remnants in RBCs. They are normally removed by the spleen and seen in post splenectomy and hyposplenism (sickle cell, coeliac, UC, Crohn's)
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What are reticulocytes?
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Young (therefore large) RBCs signifying active erythropoiesis. Increased in haemolysis and haemorrhage.
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Lymphocytes are increased in
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Acute viral infections, chronic infections, leukaemias and lymphomas
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Atypical lymphocytes seen in...
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Epstein-Barr virus infection
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Lymphocytes are decreased in...
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Steroid therapy, SLE, Legionnaire's, HIV, post chemo
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Eosinophils are increased in...
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Drug reactions (erythema multiform), allergies, parasitic infection, skin disease (pemphigus, eczema, psoriasis)
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Most common cause of macrocytic anaemia
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Pernicious anaemia, NOT B12 deficiency
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Causes of megaloblastic anaemia
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B12 and folate deficiency
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Cause of sickle cell anaemia
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Autoimmune substitution of Glu for Val at position 6 of the beta chain
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Homo/heterozygote in SCA
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Heterozygote = HbAS = sickle cell trait. Homozygote = HbSS = SCA
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Expected blood results in SCA
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Haemolysis, Hb ~ 6-9, Reticulocytes raised by 10-20%, raised bilirubin
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Triggers of SC crises
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Cold, dehydration, infection, hypoxia
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Complication of SCA
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Splenic infection therefore susceptibility to infection, poor growth, chronic renal failure, gallstones, retinal disease, iron overload, lung damage.
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Management of chronic SCA
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Hydroxycarbimide if crises are frequent, prophylactic antibiotics, bone marrow transplant
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Management of SCA crisis
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Prompt IV opiates, crossmatch, rehydrate, broad spectrum antibiotics, blood transfusion
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Causes of hypocoagulability
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Acquired - Anticoagulation with warfarin, liver failure, vitamin K deficiency, dengue fever, leukaemia.
Autoimmune - antiphospholipid syndrome Genetic - Haemophilia, Von Willebrand's, Bernard-Soulier syndrome |
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Causes of hypercoagulability
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Congenital - Factor V leiden
Acquired - antiphopholipid syndrome, heparin induced thrombocytopenia, paroxysmal nocturnal haemoglobinuria, cancers, nephrotic syndrome, pregnancy, oral contraceptive |
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Symptoms of hypercoagulability
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DVT, PE, SOB, palpitations, collapse, shock, cardiac arrest, miscarriage (multiple = antiphospholipid syndrome), pre-eclampsia
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Symptoms of hypocoagulability
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Petechiae, purpura, melena, haematochezia, bleeding gums
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How does heparin work?
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Inactivates thrombin (IIa) and factor Xa at a slow rate. Heparin AT-III can also inactivate factors IX, XI, XII and plasmin
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How does warfarin work?
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Vitamin K antagonist therefore inactivates Vit K dependent clotting factors (II, VII, IX, X, protein C, protein S)
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Describe the intrinsic pathway
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Caused by damaged surface.
XII -> XIIa XI -> XIa IX -> IXa X -> Xa Prothrombin (II) -> Thrombin (IIa) V -> Va Fibrinogen -> Fibrin Hence factor V leiden causes hypercoagulability |
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Describe the extrinsic pathway
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Trauma
Tissue factor X -> Xa Prothrombin (II) -> Thrombin (IIa) V -> Va Fibrinogen -> Fibrin Hence factor V leiden causes hypercoagulability |
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How and why do we test prothrombin time?
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Addition of thromboplastin to the plasma to test the extrinsic system. It tests for abnormalities in factors I, II, V, VIII, IX, X, XI, XII
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How and why do we test thrombin time?
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Thrombin added to plasma to convert fibrinogen to fibrin. Prolonged by heparin treatment.
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Normal time to haemostasis in bleeding time test?
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10 mins
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To correct anaemia or blood loss...
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Use packed RBCs
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To correct clotting defects/warfarin overdose...
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Use FFP
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Early transfusion complications
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TRALI, bacterial infection, anaphylaxis, fluid overload, acute haemolytic reactions
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Late transfusion complications
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Viral infection, graft vs host disease, iron overload, post transfusion pupura
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Tumour lysis syndrome
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Caused by a massive destruction of cells leading to increased potassium, urate and renal impairment.
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Signs and symptoms of ALL
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Marrow failure: Anaemia, susceptibility to infection, bleeding, fatigue, dizziness, palpitations, dyspnoea, epistaxis.
Infiltration: Hepato and splenomegaly, lymphadenopathy, orchidomegaly, cranial nerve palsy, papilloedema, unilateral testicle enlargement, renal enlargement. |
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Investigations of ALL
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Blast cells on blood film, mediastinal lymphadenopathy on CXR, anaemia of chronic disease, low reticulocyte count, leukocytosis, raised WBC
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Basic support in ALL
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IV fluids, prophylactic antibiotics, allopurinol (prevent tumour lysis syndrome)
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Chemotherapy in ALL
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Remission induction via vincristine, prednisolone, L-asparaginase + daunorubicin
CNS prophylaxis - intrathecal methotrexate Maintenance - mercaptopurine (daily), methotrexate (weekly), vincristine and prednisolone (monthly) |
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Differentiating symptoms in AML
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Gum hypertrophy, CNS involvement is rare
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Differentiation in CML is via...
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Presence of the Philadelphia chromosome. Features of gout due to purine breakdown. WCC raised across the spectrum.
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The commonest form of leukaemia is...
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CLL
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Rai stages of CLL
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0 = Lymphocytosis alone = 13 yr
1= LCT + lymphadenopathy = 8yr 2- LCT + splen/hepat meg = 5yr 3= LCT + anaemia = 2yr 4 = LCT + platelets < 100 = 1yr |
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Signs of CLL
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Enlarged, rubbery, tender nodes. Hepatosplenomegaly
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Tests for CLL
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High lymphocytes. Low Hb, neutrophils and platelets
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Treatment of CLL
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Fludarabine + cyclophosphamide
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Treatment of CML
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Imatinib
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Characteristic cells of Hodgkin's lymphoma
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Reed-Sternberg cells
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Presentation in Hodgkin's lymphoma
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Enlarged, rubbery PAINLESS cervical nodes (painful in CLL), alcohol induced lymph node pain,
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Staging of Hodgkin's lymphoma
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Is via the Ann Arbor system
1. Confined to single lymph node region 2. Two or more nodal areas on same side of diaphragm 3. Nodes on both sides of diaphragm 4. Spread beyond lymph nodes (liver or bone) |
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Treatment of Hodgkin's lymphoma
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ABVD - Adriamycin, bleomycin, vinblastine, dacarbazine
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Differentiating pathogenesis of non-Hodgkin's lymphoma
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No Reed-Sternberg cells featured
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Clinical features of Non-Hodgkin's lymphoma
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Disease of the oropharyngeal lymphoid tissue (Waldeyer's ring) = difficulty breathing + sore throat.
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Treatment of Non-Hodgkin's lymphoma
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R-CHOP regimen: Rituximab, Cyclophosphamide, Hydroxydaunorubicin, Oncovin (trade name of vincristine) and Prednisolone
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Classification of the myeloproliferative disorders.
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RBCs = polycythaemia rubra vera
WBCs = chronic myeloid leukaemia Platelets = Essential thrombocytopenia Fibroblasts = Myelofibrosis |
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Signs and symptoms of polycythaemia rubra vera
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headaches, dizziness, tinnitus, itchy after hot bath, burning sensation in peripheries, visual disturbances, gout due to raised urate from RBC turnover
other signs include facial plethora, bleeding, splenomegaly, and bruising. |
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Characteristic investigative result of myeloma is...
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Monoclonal band (2/3 IgG, 1/3 IgA). Urine often contains Bence-Jones protein. Increased blast cells on bone marrow biopsy.
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Symptoms of myeloma
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Osteolytic pain, pathological fractures and hypercalcaemia (increased osteoclasts), anaemia, neutropenia, thrombocytopenia, recurrent bacterial infections, renal failure
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Compatible blood for A+ patient
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A+, A-, O+, O-
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Compatible blood for A- patient
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A-, O-
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Compatible blood for B+ patient
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B+, B-, O+, O-
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Compatible blood for B- patient
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B-, O-
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Compatible blood for AB+ patient
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Anything
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Compatible blood for AB- patient
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Anything negative
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Compatible blood for O+ patient
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O-, O+
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Compatible blood for O- patient
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O-
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Blood results for polycythaemia
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Hb > 18.5 in men, Hb > 16.5 in women
Presence of Jak 2 tyrosine kinase |
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Treatment of polycythaemia
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Daily venesection of 400-500 mL
Chemo with hydroxycarbimide Low dose aspirin If > 70, give radioactive 32P to reduce risk of leukaemia |
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Sickle cell blood smear
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Nucleated red cells, sickle shaped cells, Howell-Jolly bodies
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ALL ages
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Polyphasic. Childhood (3-4), adulthood (30s), old age (80s)
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AML bloods
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Presence of blasts, Auer rods
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Mgmt of AML
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Induction therapy via cytarabin and an anthracycline (daunorubicin). Fluids + rasburicase + hydroxycarbimide.
If there is high risk of treatment failure, consider allogeneic transplantation. |
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CLL
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Commonest form of leukaemia, typically found in the elderly. Incurable.
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CLL bloods
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smudge cells
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Mgmt of CLL
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<3 lymphoid areas enlarged - watch and wait
If > 3 and/or anaemia and/or thrombocytopenia - treat 30% require no treatment FCR therapy - Fludarabine + cyclophosphamide + rituximab |
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Absolute indications for CLL treatment
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Marrow failure
Recurrent infection Massive/progressive splenomegaly and/or lymphadenopathy Doubling of lymphocyte count in 6 months Systemic symptoms |
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CML bloods
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Philadelphia chromosome
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CML treatment
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Imatinib
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Key ivx in myeloma
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Urinary excretion of light chains - (Bence-Jones protein)
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Presentation of myeloma
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Typically an elderly patient with bone destruction, hypercalcaemia, anaemia, neutropenia, thrombocytopenia, and renal impairment. Increased osteoclastic activity. Raised ESR and CRP.
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Treatment of myeloma
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Induction therapy via dexamethasone + thalidomide or vincristine + doxorubicin + dexamethasone.
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Characteristic of Hodgkin's lymphoma
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Presence of Reed-Sternberg cells. Associated with EBV.
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Presentation of H lymphoma
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Painless lymphadenopathy of the cervical or supracervical nodal chain.
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Ivx of H lymphoma
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Low Hb and platelets, raised ESR, mediastinal widening on CXR. Raised LDH indicates poor prognosis. Stage with CT scan and PET.
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Staging of H lymphoma
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Ann arbor system
1. Confined to a single node group (90% 5 year survival) 2. Two or more groups on the same side of the diaphragm 3. Both sides of the diaphragm 4. Extra-lymphatic sites (60% 5 year survival) |
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Mgmt of H lymphoma
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Stage 1 or 2 = radiotherapy
Stage 3 or 4 or symptomatic = chemo via doxyrubicin + bleomycin + vinblastine + decarbazine |
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NH lymphoma bloods
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nucleated RBC with giant platelets
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NH lymphoma mgmt
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RCHOP21 (Rifluximab, cyclophospamide, doxorubicin, vincristine, prednisolone - 3 cycles of 21 days)
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Signs of iron deficient anaemia
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Brittle hair and nails, angular stomatitis, smooth red tongue
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IVx in iron deficient anaemia
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MCV < 80 fL, mean corpuscular haemoglobin <27 pg. Also variation in size and shape. Serum ferritin is low. Total iron binding capacity is high.
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What is pernicious anaemia?
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An autoimmune condition featuring atrophic gastritis, which leads to failure of intrinsic factor production and therefore vitamin B12 malabsorption.
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Which autoimmune diseases is pernicious anaemia associated with?
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Thyroid disease, Addison's, vitiligo.
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Clinical features of pernicious anaemia
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Progressive anaemia. May be jaundice due to excessive haemoglobin breakdown.
Neuro features reflect low B12 levels and include polyneuropathy and subacute combined degeneration of the cord, which presents with weakness, ataxia, and paraplegia if untreated. Dementia and visual disturbances can also occur. |
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Management of pernicious anaemia
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IM hydroxycobalamin or oral B12
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What is aplastic anaemia?
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A pancytopenia with hypocellularity of the bone marrow
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Clinical features of aplastic anaemia
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Reflect losses in cell lines.
i.e. anaemia, bruising/bleeding, increased susceptibility to infection |
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What is neutropenic sepsis?
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Pyrexia, new onset confusion, tachycardia, hypotension, dyspnoea, or hypothermia in a neutropenic patient (neutrophils <1 x 10^9/L)
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Management of neutropenic sepsis
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Contact microbiology for specific advice.
Start empirical antibiotic therapy with taz and gent, add vancomycin if clinical deterioration, fever persists, or suspicion of MRSA. Once apyrexial, swap to oral abx and continue for 10-14 days. |
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Blood film for haemolytic anaemia - abnormal red cells may indicate...
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Thalassaemia, sickle cell
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Blood film for haemolytic anaemia - spherocytes present and DCT negative indicates...
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Hereditary spherocytosis, malaria
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Blood film for haemolytic anaemia - spherocytes present and DCT positive indicates...
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Autoimmune haemolytic anaemia, drugs (methyldopa, quinine, NSAIDs, interferon)
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Blood film for haemolytic anaemia - fragmentation indicates...
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Eclampsia, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, DIC
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Blood film for haemolytic anaemia - other abnormalities (bite cells, Heinz bodies, blister cells) may indicate...
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Enzyme defects (deficiency in G6PD, pyruvate kinase, pyrimidine 5 nucleotidase)
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What is thalassaemia
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Disturbance in the 1:1 balance of alpha to beta chains in Hb.
alpha = reduced alpha chain synthesis beta = reduced beta chain synthesis |
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Clinical features of beta thalassaemia minor
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Asymptomatic carrier state. Anaemia is mild or absent, with a low MCV or MCH. Iron stores are normal.
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Clinical features of beta thalassaemia intermedia
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Moderate anaemia (Hb 7-10). Does not require regular transfusions. Splenomegaly, bone deformities, recurrent leg ulcers and gallstones feature.
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Clinical features of beta thalassaemia major
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Presents in the first year of life with severe anaemia, failure to thrive and severe infections.
Bony abnormalities include the thalassaemia facies (enlarged maxilla and prominent frontal and parietal bones). Hepatosplenomegaly. |
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Management of beta thalassaemia major
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Blood transfusions. Iron overload from repeated transfusions may lead to damage of the endocrine glands, liver, pancreas and heart - death in second decade from heart failure. Treat with iron chelating agents (desferrioxamine)
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Investigations of polycythaemia
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RBC >18.5 in men and >16.5 in women
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Management of polycythaemia
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Venesection, chemo via hydroxycarbamide and busulfan to reduce platelet count, allopurinol to decrease uric acid levels
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Which chromosomal abnormality is associated with CML and ALL?
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Philadelphia chromosome t(9:22), (95% of CML cases, less common in ALL although incidence increases with age)
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What is the pathognomonic cell type in AML?
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Auer rods
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ALL management
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Remission induction via vincristine + dexamathasone + asparaginase + daunorubicin
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Clinical course in untreated CML
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Chronic phase for 3-4 years before progression to AML and rapid death. CML may also transform into myelofibrosis leading to death from bone marrow failure.
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CLL management (not curative)
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Oral chlorambucil +/- prednisolone.
Fludarabine + cyclophosphamide +/- rituximab can induce remission. If disease is still progressing, add alemtuzumab. |
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What is lymphoma?
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Neoplastic transformations of normal B or T cells which reside in lymphoid tissues. They are commoner than leukaemias and separated into Hodgkin's and non-Hodgkin's
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Who gets Hodgkin's lymphoma?
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Young adults, typically with previous EBV infection
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Presenting features of Hodgkin's lymphoma
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Painless, rubbery lymph node enlargement. There may be hepatosplenomegaly.
B symptoms include fever, drenching night sweats, and weight loss. Other symptoms include pruritus, fatigue, anorexia and ALCOHOL INDUCED PAIN AT THE SITE OF THE LYMPH NODE!! |
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Clinical features of NH lymphoma
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Similar to Hodgkin's lymphoma but extranodal involvement is more common
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What is myeloma?
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Malignant disease of the plasma cells of bone marrow
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Classic urine excretion in myeloma
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Bence-Jones protein
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Clinical features of myeloma
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Bone pain due to increased osteoclastic activity. Back ache is most common presenting symptom - pathological fractures with spinal cord compression. Hypercalcaemia present.
Can cause AKI via deposition of light chains, hypercalcaemia, hyperuricaemia and amyloid deposition in the kidneys. |
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Diagnostic features of myeloma
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Presence of two of...
1. Paraprotinaemia or Bence-Jones protein of the urine 2. Radiological evidence of lytic bone lesions 3. Increase in bone marrow plasma cells on aspiration |
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Myeloma management
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Slow progression of bone disease with bisphosphonates.
Combination chemo with melphalan, prednisolone and thalidomide. If relapse, use lenalidomide + bortezomib. |
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How are red cells stored and transfused?
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Stored at 4 degrees for maximum of 35 days, must be used within 4 hours of removal from fridge
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When is a red cell transfusion indicated?
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Acute bleeds in combination with a crystalloid or colloid (if blood loss >30%) and correction of anaemia
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How are platelets stored and what are they used for?
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Stored at 20-24 degrees (can't be stored cold due to irreversible aggregation). They are used to treat or prevent bleeding in patients with severe thrombocytopenia.
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When is fresh frozen plasma used?
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Acquired coagulation factor deficiencies
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How is cryoprecipitate obtained?
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Obtained from thawing fresh frozen plasma at 4 degrees. Used in DIC when fibrinogen is low.
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What is the prime function of neutrophils?
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Ingest and kill bacteria, fungi, and damaged cells
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What causes raised neutrophils?
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Bacterial infection, tissue necrosis, inflammation, steroid therapy, haemorrhage, haemolysis, leukaemia
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What causes lowered neutrophils?
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Severe bacterial infection, megaloblastic anaemia, pancytopenia, drugs.
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What causes raised monocytes?
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Chronic bacterial infection (TB), malignancy, myelodysplasia
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What causes raised eosinophils?
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Allergy, protozoal infection, parasitic infection, skin disorders (pemphigus, eczema), malignancy
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What causes raised lymphycytes?
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Viral infection, CLL, TB, lymphoma
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What causes prolonged PT?
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Abnormalities of factor VII, X, V, II, I, liver disease, warfarin.
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What causes prolonged APTT?
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XII, XI, IX, VIII, X, V or I (not VII), heparin.
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What prolongs thrombin time?
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Fibrinogen deficiency, heparin, DIC
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What causes immune thrombocytopenic purpura?
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Children - viral infection. Tends to be acute and self limiting.
Adults - less acute than in children, typically seen in young women with SLE and/or thyroid disease. |
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In general, what causes thrombocytopenia?
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Impaired production via: Bone marrow failure, megaloblastic anaemia, leukaemia, myeloma, myelodisplasia, tumour infiltration, aplastic anaemia, HIV
or Excessive destruction via: ITP, post-transfusion purpura, DIC, thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome, hypersplenism |
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Management of immune thrombocytopenic purpura
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If platelet count >30 x 10^9, no treatment required unless surgery or extreme haemorrhage.
Steroids are first line, splenectomy is second line |
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What is haemophilia A?
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Propensity to bleed with varying severity due to deficiency of factor VIII. It is X linked recessive.
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Clinical features of haemophilia A
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Factor VIII levels <1 IU/dL = frequent spontaneous bleeding into muscles and joints leading to crippling arthropathy
Levels 1-5 = severe bleeding following injury, occasional spontaneous episodes Levels >5 = mild disease with bleeding only on trauma or surgery |
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IVx of haemophilia A
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Prolonged APTT, reduced levels of factor VIII. PT and von Willebrand's Factor are normal.
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Management of haemophilia A
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IV infusion of factor VIII
If disease is mild, synthetic vasopressin can raised levels of factor VIII |
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What is haemophilia B?
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Deficiency of factor IX
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What is DIC?
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Disseminated intravascular coagulation, leading to some areas of increased clotting and some of increased bleeding.
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Most common causes of DIC
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sepsis, trauma, burns, surgery, cancer, obstetric complications, leukaemia
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Investigation of DIC
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Severe thrombocytopenia + prolonged PT, APTT and TT, decreased fibrinogen, elevated FDPs. Blood film shows fragmented red cells.
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Hyposplenism blood film
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Target cells, Howell-Jolly bodies, Pappenheimer bodies, siderotic granules, acanthocytes
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Iron deficiency blood film
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Target cells, pencil poikilocytes, can get a mixed 'dimorphic' film if combined with B12/folate deficiency
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Myelofibrosis blood film
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'Tear drop' poikilocytes
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Intravascular haemolysis blood film
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Schistocytes
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Megaloblastic anaemia blood film
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Hypersegmented neutrophils
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Four types of crisis in sickle cell
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Thrombotic - painful, vaso-occlusive
Sequestration - sickling in organs causes pooling of blood, typically causes acute chest syndrome (dyspnoea, pain, pulmonary infiltrates, low O2) Aplastic - caused by infection with parvovirus, sudden fall in Hb Haemolytic - rare, fall in Hb due to increased haemolysis |
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Which haematological malignancy is t(15;17) translocation seen in?
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Acute promyelocytic leukaemmia
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Which haematological malignancy is t(8;14) translocation seen in?
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Burkitt's lymphoma
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Which haematological malignancy is t(11;14) translocation seen in?
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Mantle cell lymphoma
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Differences between standard and LMWH (administration, duration of action, mechanism of action, side effects, monitoring, uses)
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Standard
- Admin is IV - Duration is short - MOA is activation of antithrombin III, inhibition of Xa, IXa, XIa and XIIa - Side effects include bleeding and osteoporosis - Monitored with APTT - Used in situations where risk of bleeding is high as anticoagulation can be terminated quickly LMWH - Admin is SC - Duration is long - Activates antithrombin III, inhibits Xa - Side effects same as standard but lower risk of osteoporosis and LMWH - Monitoring is via Anti-Factor Xa (not required) - Used in VTE and ACS |
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What is the Wells score?
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Used to assess likelihood of DVT
Cancer = 1 Paralysis/immobility = 1 Recently bedridden or major surgery within 12 weeks = 1 Tenderness along distribution of vein = 1 Entire leg swollen = 1 Calf swelling >3cm than asymptomatic side = 1 Pitting oedema = 1 Collateral superficial veins = 1 Previously documented DVT = 1 Alternate diagnosis as likely = -2 DVT is likely if >2 DVT unlikely if 1 or less |
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How to investigate DVT if DVT is likely
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Arrange leg US within 4 hours, if negative do a D-dimer. If US cannot be carried out, do D-dimer and administer LMWH
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How to investigate DVT if DVT is unlikely
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Perform D-dimer test, if it is positive arrange US within 4 hours or give LMWH
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How long to keep DVT patients on warfarin
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DVT provoked? 3 months
DVT unprovoked? 6 months |
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What is PRV?
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A myeloproliferative disorder leading to increased red cell volume accompanied by overproduction of neutrophils and platelets.
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Clinical features of PRV
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Hyperviscosity, pruritus after a hot bath, splenomegaly, plethoric appearance, HTN
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IVx of PRV
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Full blood count/film, JAK2 mutation, serum ferritin
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What is Von Willebrand's disease?
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The most common inherited bleeding disorder, typically autosomal dominant.
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Most common presenting features of vWD
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Epistaxis, menorrhagia
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What is hereditary spherocytosis?
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The most common hereditary haemolytic anaemia in people of northern European descent (think of it as white folk SCA). The normal biconcave RBC is replaced by a sphere shaped RBC. Red blood cell survival is reduced as it is destroyed by the spleen.
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Presentation of hereditary spherocytosis
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Failure to thrive, jaundice, gallstones, splenomegaly, aplastic crisis precipitated by parvovirus infection, MCHC elecated
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G6PD vs hereditary spherocytosis (gender, ethnicity, typical history, blood film, diagnostic test)
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G6PD
- Male (X-linked recessive) - African + Mediterranean descent - Neonatal jaundice + gallstones - Heinz bodies on blood film - G6PD enzyme activity Hereditary spherocytosis - Male + female (autosomal dominant) - Northern European descent - Neonatal jaundice, chronic symptoms with crises precipitated by infection (parvovirus), gallstones, splenomegaly - Spherocytes on blood film - Diagnosed via osmotic fragility test |
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Most common type of Hodgkin's lymphoma? Prognosis?
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Nodular sclerosing (70%). Good prognosis.
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Which type of Hodgkin's lymphoma is associated with a -large number- Reed-Sternberg cells?
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Mixed cellularity
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Which type of Hodgkin's lymphoma has the best prognosis?
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Lymphocyte predominant
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Which type of Hodgkin's lymphoma has the worst prognosis?
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Lymphocyte depleted
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Presentation of CML
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Presentation is typically at 40-50 years with anaemia, weight loss, discomfort, splenomegaly, a spectrum of myeloid cells seen in peripheral blood, decreased leukocyte alkaline phosphatase
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What are target cells associated with?
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Sickle cell, thalassaemia, iron deficiency anaemia, liver disease
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What are 'tear drop' poikilocytes associated with?
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Myelofibrosis
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What are spherocytes associated with?
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Hereditary spherocytosis, autoimmune haemolytic anaemia
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What is basophilic stippling associated with?
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Lead poisoning, thalassaemia
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What are Howell-Jolly bodies associated with?
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Hyposplenism
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What are Heinz bodies associated with?
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G6PD deficiency, alpha thalassaemia
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What are schistocytes (helmet cells) associated with?
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Intravascular haemolysis, mechanical heart valve, DIC
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What are 'Pencil' poikilocytes associated with?
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Iron defiency anaemia
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What are burr cells associated with?
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Uraemia, pyruvate kinase deficiency
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What are acanthocytes associated with?
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Abetalipoporoteinemia
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