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76 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)
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Causes of normocytic anaemia
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Blood loss, chronic disease, bone marrow failure, 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.
Infiltration: Hepato and splenomegaly, lymphadenopathy, orchidomegaly, cranial nerve palsy |
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Investigations of ALL
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Blast cells on blood film, mediastinal lymphadenopathy on CXR
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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
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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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