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Haematology Phase 2a Recap Session: Blood Constituents and Disorders

Refresh your knowledge on blood constituents such as RBCs, WBCs, platelets, and coagulation. Learn about anaemia types and investigation methods.

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Haematology Phase 2a Recap Session: Blood Constituents and Disorders

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  1. 2017/2018

  2. Haematology Phase 2a Recap Session Ella Kulman, Oanh Kieu Vo, Melanie Coulson 01/02/2018 The Peer Teaching Society is not liable for false or misleading information…

  3. Phase 1 Physiology Revision • Constituents of blood. • Bleeding and coagulation. The Peer Teaching Society is not liable for false or misleading information…

  4. Constituents of Blood 44% 1% The Peer Teaching Society is not liable for false or misleading information…

  5. Red Blood Cells (Erythrocytes) Nucleated or Anucleated? What is the lifespan of a RBC? Biconcave and Anucleated 120 days Where does eryptosis occur? Where are RBC’s produced? Old RBC’s are mopped up by the spleen, liver and bone marrow and destroyed In the bone marrow The Peer Teaching Society is not liable for false or misleading information…

  6. White Blood Cells REMEMBER: WBC’s have a major role in the defence against infection! NEUTROPHILS GRANULOCYTES BASOPHILS EOSINOPHILS LYMPHOCYTES MONOCYTES The Peer Teaching Society is not liable for false or misleading information…

  7. Neutrophils They are phagocytic and play a role in inflammation, infection and myeloid leukaemia Multi-lobular nucleus The Peer Teaching Society is not liable for false or misleading information…

  8. Eosinophils Eosinophil numbers are often raised in parasitic infections They show diurnal variation; being more common in the morning Bi-lobular or tri-lobular nuclei The Peer Teaching Society is not liable for false or misleading information…

  9. Basophils They have a similar role to mast cells, when stimulated they secrete histamine Basophils are associated with hypersensitivity reactions The Peer Teaching Society is not liable for false or misleading information…

  10. Lymphocytes B Cells - Mediators in humoral immunity e.g. antibody mediated responses T Cells - Mediators in cellular immunity: Cytotoxic (CD8+) T Helper (CD4+) Lymphocyte numbers decrease in HIV and chemotherapy Lymphocyte numbers increase in viral infection, inflammation and leukaemia The Peer Teaching Society is not liable for false or misleading information…

  11. Monocytes Immature cells that differentiate once they leave the bloodstream Many monocytes form macrophages The Peer Teaching Society is not liable for false or misleading information…

  12. Platelets What are the functions of platelets? What are platelets derived from? Megakaryocytes in the bone marrow They have a major role in clotting: Platelet plug Coagulation cascade The coagulation cascade helps to strengthen the platelet plug. Fibrin is ultimately produced The Peer Teaching Society is not liable for false or misleading information…

  13. Haemostasis Pro-thrombin -> thrombin. Fibrin is an essential component of a blood clot! Converts fibrinogen -> fibrin Thrombin Functions Activates factor XIII into XIIIa Positive feedback effect on further thrombin production The Peer Teaching Society is not liable for false or misleading information…

  14. Haemostasis The Peer Teaching Society is not liable for false or misleading information…

  15. Fibrinolytic System Plasminogen -> plasmin. Plasmin cuts fibrin into fragments. This prevents blood clots from growing and becoming problematic. The Peer Teaching Society is not liable for false or misleading information…

  16. Fibrinolytic System The Peer Teaching Society is not liable for false or misleading information…

  17. Coagulation Factors Why is the liver important in clotting? • The liver synthesises many coagulation factors. • The liver produces bile salts that are needed for vitamin K absorption... Factors 2, 7, 9 and 10 are vitamin K dependent! The Peer Teaching Society is not liable for false or misleading information…

  18. Anaemia A decrease in the amount of haemoglobin in the blood below the reference range. Haemoglobin is composed of 2 alpha and 2 beta chains. Function: carries and delivers oxygen to tissues. The Peer Teaching Society is not liable for false or misleading information…

  19. Anaemia MICROCYTIC MCV <80 NORMOCYTIC MCV 80-100 MACROCYTIC MCV >100 The Peer Teaching Society is not liable for false or misleading information…

  20. Microcytic Anaemia Iron Deficiency Haemoglobinopathies e.g. Thalassaemia AETIOLOGY Anaemia of chronic disease e.g. CKD and so lack of EPO The Peer Teaching Society is not liable for false or misleading information…

  21. Iron Deficiency Bleeding e.g. menorrhagia Malabsorption Poor diet AETIOLOGY Breastfeeding Hookworm The Peer Teaching Society is not liable for false or misleading information…

  22. Investigating Iron Deficiency Measure serum ferritin. BUT ferritin is an acute phase protein and so its concentration will increase in response to inflammation and malignancy -> false results. Endoscopy - is the cause due to a GI bleed? The Peer Teaching Society is not liable for false or misleading information…

  23. Reticulocyte Count A reticulocyte count is a measure of how quickly RBC’s are being made in the bone marrow. Raised count - blood loss or haemolytic anaemia. Low count - production problem, may be seen in iron deficiency anaemia. The Peer Teaching Society is not liable for false or misleading information…

  24. Symptoms of Iron Deficiency Koilonychia Angular Stomatitis Atrophic Glossitis Brittle hair and nails The Peer Teaching Society is not liable for false or misleading information…

  25. Treating Iron Deficiency Ferrous Sulphate - iron tablets. Side effects: • Constipation. • Diarrhoea. • Epigastric pain. • GI irritation. • Nausea. The Peer Teaching Society is not liable for false or misleading information…

  26. Normocytic Anaemia Acute blood loss AETIOLOGY Combined haematinic deficiency Anaemia of chronic disease e.g. CKD and so lack of EPO The Peer Teaching Society is not liable for false or misleading information…

  27. Macrocytic Anaemia B12/Folate deficiency (Megaloblastic) Alcohol excess/liver disease AETIOLOGY Metabolic disease e.g. hypothyroidism The Peer Teaching Society is not liable for false or misleading information…

  28. Folate Deficiency Sources of folate: green vegetables, fruit, offal. Malabsorption Poor diet AETIOLOGY Increased demand e.g. pregnancy The Peer Teaching Society is not liable for false or misleading information…

  29. Pernicious Anaemia Loss of parietal cells (Autoimmune) Reduced intrinsic factor production Vitamin B12 malabsorption B12 binds to intrinsic factor and is absorbed in the terminal ileum B12 is needed to make RBC’s Treatment: Vitamin B12 injections or tablets. The Peer Teaching Society is not liable for false or misleading information…

  30. B12 Deficiency Other causes of B12 Deficiency: Atrophic gastritis Gastrectomy Crohn’s Disease Coeliac Disease The Peer Teaching Society is not liable for false or misleading information…

  31. Anaemia Symptoms Fatigue Faintness SYMPTOMS Breathlessness Reduced exercise tolerance The Peer Teaching Society is not liable for false or misleading information…

  32. Anaemia Pale skin Pale mucous membranes SIGNS Tachycardia The Peer Teaching Society is not liable for false or misleading information…

  33. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) What kind of patients might be over anticoagulated? The Peer Teaching Society is not liable for false or misleading information…

  34. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) What kind of patients might be over anticoagulated? -vit K antagonists e.g. warfarin -NOACs e.g. apixiban The Peer Teaching Society is not liable for false or misleading information…

  35. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) What kind of patients might be over anticoagulated? -vit K antagonists e.g. warfarin -NOACs e.g. apixiban Why might they be over anticoagulated? The Peer Teaching Society is not liable for false or misleading information…

  36. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) What kind of patients might be over anticoagulated? -vit K antagonists e.g. warfarin -NOACs e.g. apixiban Why might they be over anticoagulated? -bad patient compliance -artificial valves -new/interacting drugs The Peer Teaching Society is not liable for false or misleading information…

  37. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) What kind of patients might be over anticoagulated? -vit K antagonists e.g. warfarin -NOACs e.g. apixiban Why might they be over anticoagulated? -bad patient compliance -artificial valves -new/interacting drugs Symptoms of over anticoagulation? The Peer Teaching Society is not liable for false or misleading information…

  38. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) What kind of patients might be over anticoagulated? -vit K antagonists e.g. warfarin -NOACs e.g. apixiban Why might they be over anticoagulated? -bad patient compliance -artificial valves -new/interacting drugs Symptoms of over anticoagulation? -bruising, bleeding, melena, epistaxis, hematemesis, haemoptysis The Peer Teaching Society is not liable for false or misleading information…

  39. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) DICRARE BUT LIFE THREATENING DISEASE This is when there is generation of fibrin within the blood vessels and also consumption of platelets/coagulation factors causing secondary activation of fibrinolysis. i.e. there will be initial thrombosis followed by bleeding tendency Causes of this; Malignancy, septicaemia, obstetric causes, trauma, infections, haemolytic transfusion reactions, liver disease etc Tx; Treat underlying cause. Maintain blood volume and tissue perfusion. May need transfusions Activated protein C The Peer Teaching Society is not liable for false or misleading information…

  40. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) Thrombocytopenia (this came up in our OSCE!) Causes; • Reduced platelet production in bone marrow • Excessive peripheral destruction of platelets • Problems of in enlarged spleen ITP is more common than TTP The Peer Teaching Society is not liable for false or misleading information…

  41. Bleeding (over anticoagulation, DIC, platelets disorders e.g. ITP, TTP) Thrombocytopenia - Immune thrombocytopenic purpura (ITP) Physiology; Due to immature destruction of platelets. The antibodies coat the platelets which are then removed by binding to Fc receptors on macrophages. Is autoimmune so may be associated with other autoimmune diseases. Clinical features; o Easy bruising o Purpura o Epistaxis o Menorrhagia Investigation; Would have reduced platelets, normal/increased megakaryocytes and may have detection of platelet autoantibodies Treatment; -Corticosteroids i.e. prednisolone -Splenectomy -IV IG -Anti D  The Peer Teaching Society is not liable for false or misleading information…

  42. DVT (and thromboembolism) Causes; Think about Virchow's triad! The Peer Teaching Society is not liable for false or misleading information…

  43. DVT (and thromboembolism) What else could cause a DVT/embolism? The Peer Teaching Society is not liable for false or misleading information…

  44. DVT (and thromboembolism) What else could cause/RFs a DVT/embolism? • Age • Obesity • Varicose veins • Long haul travelling • Immobility and bed rest • plasminogen deficiency • Thrombophilia • Pregnancy • OCP etc The Peer Teaching Society is not liable for false or misleading information…

  45. DVT (and thromboembolism) Symptoms; -calf pain and swelling -calf warmth -ankle oedema -pitting oedema -(complete occlusion can cause cyanotic discolouration and rarely gangrene) Investigations; -D Dimer (for exclusion only! Is not diagnostic!) -Coagulation Screen -FBC including platelets -US Doppler -USE THE WELLS SCORE! Treatment; -LMW Heparin (inactivates factor Xa) -Warfarin (antagonises vit K dependant clotting factors – 2,7,9,10) -NOACS Prevention; -Stockings -Early mobilisations -Leg elevation The Peer Teaching Society is not liable for false or misleading information…

  46. Polycythaemia Polycythaemia – defined as an increase in haemoglobin, PCV (packed cell volume) and RBCS Primary Causes; • Polycythaemia vera- there is a genetic mutation in the JAK2 gene- increases sensitivity of bone marrow cells to Epo=increased RBC production • Primary familial and congenital polycythaemia- mutation in EPOR gene=increased production of RBCs in response to Epo Secondary Causes; • When there are more RBCs due to more circulating Epo e.g. due to; chronic hypoxia, poor oxygen delivery (e.g. high altitude), abnormal RBC structure and tumours which release high levels of EPO The Peer Teaching Society is not liable for false or misleading information…

  47. Polycythaemia Symptoms; -May present with no symptoms -May have; easy bleeding/bruising, fatigue, dizziness, headaches etc. Investigations; -FBC -Bone marrow biopsy -Genetic testing for JAK2 gene Treatment; -Polycythaemia vera- blood letting, aspirin -Secondary- treat the cause! The Peer Teaching Society is not liable for false or misleading information…

  48. Tired A 59 year old woman complains of tiredness, fatigue and weight loss. Blood tests reveal an elevated WCC and, on examination, splenomegaly is palpated. Cytogenics are positive for Philadelphia Chromosome. What is the Diagnosis? What is Philadelphia Chromosome? The Peer Teaching Society is not liable for false or misleading information…

  49. Chronic Myeloid Leukaemia Philadelphia Chromosome • Present in >80% of CML • T(9;22) • Forms fusion gene BCR/ABL on chromosome 22. • BCR/ABL has tyrosine kinase activity • Worse prognosis if absent The Peer Teaching Society is not liable for false or misleading information…

  50. What is Leukaemia?

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