Haematology PDF

HAEMATOLOGY  H AEMATOPOLESIS AND HAEMOSTASIS BLOOD Haematology : The study of blood (7 %...

HAEMATOLOGY  H AEMATOPOLESIS AND HAEMOSTASIS BLOOD Haematology : The study of blood (7 % ! Adults 51 of blood of body weight) · have PLASMA CELLULAR IMBALANCES : (55 %) COMPONENTS (55 % ) TYPE DECREASE INCREASE Myeloid Pancytopenia Pancytosis RBC Count Anaemia Erythrocytosis WBC Count Leukopenia Leukocytosis Neutrophil Neutropenia Neutrophilia * study functions N/A Eosinophilia Eosinophil NIE Basophilia Basophil · Haematopoiesis is the process Monocytopenia Monocytosis Monocyte where RBC a re made. I t st ar ts with Lymphocyte Lymphopenia Lymphocytosis Special cells (haematopoietic Stem cells) Platelet Thrombocytopen Thrombocytosis that differentiate to form - different i a · This process first happens in the types of blood cells and liver After yolk s ay then spleen. birth it happens in bone marrow of cells Then in adults it happens in - all. bone marrow of cranium pelvis ribs, vertebra. , , The bone niche is like home · marrow cozy a for stem that helps them ce lls grow. cells that live in niche : 1) Macrophages 2) Fibroblasts (provide mechanical support) 3) Fat cells (store energy) interact with stem factors (chemicals) They by releasing growth · ce lls or direct contact The ECF · supports Stem cells · pluripotent haematopoietic Stem cells (HSCs) are special cells in the bone mar row that can : 1) self-renew (make more stem cells) 2) Differentiate into different blood cells (this depends the factors receive) on growth they G ROWTH FACTORS Colony-stimulating Factors (CSF) Activates intracellular signalling pathways : that causes cells to proliferate and differentiate. Multi-CSF (IL-3) · bone marrow Stem : stimulates cells to differentiate into myeloid cells. · GM-CSF (Granulocyte Macrophage) : Cytokine that promotes myeloid cell development/maturation - EPO(erythropoietin) Signals : for production of more RBC ↑ PO (thrombopoietin) : signals for production of more platelets EXAMINATIONS · BM is from the back hip (posterior mostly taken of the bone iliac crest) using a procedure called BM ASPIRATE process : small amount of BM sucked out stained , and observed · , Mix o f different diff cells at stages · A healthy sample contains of development (more myeloid ce lls - han lymphoid cells) · When liquid bone mar row can't be drawn a BM BlopSY is done. In this a small piece of bone with mar row inside is t ake n (trephine biopsy · - 50 % haematopoietic tissue A healthy sample contains ) 50% ↳ Fat GRANULOPOIESIS (making granulocytes) As blood cells develop they : 1) Shrink 2) The nucleus becomes more compact 3)The nucleus shape changes 8)Granules appear in cytoplasm WBC (known a s band cells) are found blood · Sometimes a few immature in the. These band released cells a re during infection THE OMBOPOLESIS plat-lets thrombocytes) a re · made from giant called cells megakaryocytes STEPS : 1) Megakaryocyte nucleus and cytoplasm grows 2) cytoplasm develops tiny granules 3) cytoplasm splits into thousands of s m a l l pieces (platelets) 1000-5000 platelets 1 Megakaryocyte = To is kidneys blood vessel bM cells · the liver a protein made by , , cells , Low platelets = More TPo available to make more platelets · Platelets made in BM are stored in spleen it When released destroying · they control amount of TPO by destroyed · older platelets a re in the liver and spleen by special immune cells called the mononuclear phagocyte system ERYTHROPOLESIS kidneys is · Epo is Land liver in fetus] When the a hormone made by the body low on oxygen (anaemia high alttiude) It helps body make more RBC by :Stimulating early stages or. of RBC development "Other factors that can help include iron , vit Biz , folic acid 2) working later 3) production · RBC in Encouraging usually leave BM as reticulocytes 24-08 hours of hemoglobin in blood break · Then mature R i s c live for 120 before down these days macrophages them in the spleen/liver/Bm · When they break, iron and amino acids from hemoglobin a re reused. Heme ring is converted to bilirubin (excreted) FULL BLOOD COUNT Thrombocytopenia : · BM isn't making enough platelets Platelets get trapped in an enlarged spleen Platelets are destroyed fa ste r Symptoms : bleeding Longer bleeding) Thrombocytosis: caused by : Iron deficiency · Inflammation · cancer · Infection changes in leukocytes can be a result of infection , trauma, allergy, etc. # aemostasis process that stops bleeding when BV is cut : a How it works : 1) platelets stick together to form a temp plug at injury site 2) Fibrin (protein) fo r m s a mesh around platelets to m a ke it stronger 3) This plug is broken once healed When injury BV constricts · blood is les occurs temporarily so l e ss When is injured , platelets in with the · BV stick to the exposed collagen the vessel wall help of a protein called von Willebrand Factor (VWF) This activates. the platelets , causing them to change shape and release granules (ADP , thromboxane A2) These fibrinogen forming · that granules help attrac t more platelets stick together using , f i rst plug primary haemostatic plug · A coagulation cascade is then activated (involves +issue fa c to r and platelet sur faces) This. protease production Fibrin (protein leads to of formed by thrombin). Fibrin forms a strong mesh around the platelets making the initial plug Stable to fully stop the bleeding - Secondary haemostatic plug · The coagulation cascade activates special proteins called clotting factors that tur n prothrombin - thrombin (active enzyme) It changes fibrinogen into Fibrin (creates mesh) · Many clotting · factors a re made in an inactive for m > activated by being - zymogens They. are cut into smaller pieces 2 PATHWAYS : Intrinsic- with triggered by sur faces · contac t * - Activation of Xa (importanT Extrinsic tissue triggered by fac tor · lab is tested by adding phospholipids calcium In the clotting , , and a trigger. in I n the body , clotting happens 2 steps : 1) An initiator and produces pathway starts the process + hrombin 2) Thrombin boosts clotting in a loop · Thrombin activates factor XIII (makes Fibrin clot Stronger Istable) blood clot has done its job , · After a it is broken down (series of using the fibrinolytic system enzyme reactions) : 1) plasminogen Linactive protein) is turned into plasmin by tissue plasminogen activator (made by the endothelial cells) 2) plasmin breaks down fibrin in the clot into smaller pieces called fibrin degradation products (FDPs) including D-dimer (small protein fragments) REGULATION 1)Healthy BV release prostacyclin and NO (keep platelets from sticking together - unnecessary clotting) 2) making sure clotting happens only at injury s i te Proteins like tissue plasminogen activator (t-PA) and thrombomodulin help this process 3) slowing down clotting - Thrombomodulin binds to thrombin t Activates Protein C Breaks down clotting Factors (va , willa) Antithrombin stops thrombin and factor · Xa · Tissue Fac tor Pathway Inhibitor (TFPI) blocks factor Xa Stopping TF-VIla Complex (Starts clotting)  down too order to stop clots breaking early : · In 1) plasminogen activator inhibitors (PAIs) block tPA (prevents plasmin activation) 2) a-antiplasmin binds down clots plasmin it breaking to t from stops TESTS Bleeding · time D-dimers , etc. , check how well blood clots coagulation tests : 1) Prothombrin (PT) : measures how it takes for clot to using extrinsic long a for m pathway 2) Activated partial thromboplastin time (APTT) : How long it takes to form a clot using intrinsic pathway 3) Thrombin Clotting time (TCT) : How it both long takes using DISORDERS Haemophilia A : Factor Vill K NOW THIS * # Genetic Haemophilia B : Factor XI ↳ von wille brand disease prothrombinia AcquiredOliverdiseasecrease fibrinogen > - Low l eve l s > l ow - p l a te l e t count T hrombosis : Blood clot inside By that blocks blood flow Embolus (condition) caused. in vital by clot lodged organs Disseminated Intravascular causes - coagulation (DIC) : A condition where clotting becomes overactive in response to : · Bacterial infections · severe stress · cancer Pregnancy complications ·