| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
| transcription factor that acts on HSC and multipotent progenitors (MP) to differentiate | SCL |
| cytokine that acts on HSC | SCF |
| stimulates platelet formation, acts on MP, CMP, and megakaryocytes. | TPO (Thrombopoietin) |
| IL-7 | The interleukin that acts on Multipotent Progeniter to make Common Lymphoid Progeniter |
| acts on T cells to make T cell subsets | IL-2 and IL-6 |
| acts on CMP to make Megakaryocyte Erythocyte Progeniter or Granulocyte Macrophage Progeniter. Also acts on GMP to form Granulocytes | IL-3 |
| stimulates RBC production. Acts on MEP to make RBCs. | EPO |
| acts in CMP to make GMP | CM-CSF |
| acts on MP to make CMP | GATA2 |
| acts on CMP to make MEP and MEP to make RBCs targeting haemoglobin genes. | GATA1 |
| acts on CLP to make T cells | IKAROS |
| acts on GMP to make granulocytes | C/EbPa |
| acts on CMP to make GMP | SPI1 |
| acts on CLP to make B cells. | PAX 5 |
| JAK-STAT pathway | JAK is activated when 2 JAK bind to one another. Once paired they become activated and this leads to recruitment and phosphorylation of STATs. JAK activates the STAT pathway. Phosphatised STAS form dimers that then binds to the promoter sequences and regulates genes in multiple key pathways. Must be turned off by negative regulator SOC’s once task is done and can be switched back on by cytokines. |
| half like of 5h-5d. Increase in infection. Receptors are present for chemotactic factors. Multilobed nucleus. Primary responders. 3 granulocyte types. MPO granule converts H2O to other molecules, NE /Cathepsin and G-proteins act on bacteria. Kill by phagocytosis. Lysosome fuses with phagosome to form phagolysosome. Granule contents are detected and are killed and digested by enzymes. Can also form Nets, the nuclear DNA is discharged and entraps microbes. Made from GMP with G-CSF, IL-2 &3 and C/EbPa. | Neutrophils |
| Mostly found in the tissue. Half-life 8-12 d. responds to parasitic infection and allergies. Bi lobes nucleus. Receptors to chemokines antibodies and complement. Attracted to chemokines like CCL11. Kill parasites using granule components like MBP, ECP and EPOx. Helps maintain blood flow. Granule plasminogen used in clot breakdown. Histamine used in inflammation. Made from GMP with G-CSF, IL-2 &3 and C/EbPa. | Eosinophils |
| increase in response to infection and allergies. Bi lobed nucleus. Receptors for antibodies, cytokines, chemokines, and complement. Granules include Histamine, prostaglandin (inflammation) and heparin (clot breakdown) Attracted by IgE. Made from GMP with G-CSF, IL-2 &3 and C/EbPa | Basophils |
| Have mitochondria. Receptors for microbial products, cytokines, chemokines, and lysosomes. Act late in infection. Phagocytose microbes and dying cells. Recruit other WBCs by secreting cytokines and chemokines. Made from a GMP with M-CSF. | Monocytes and Megakaryocytes |
| Small cell fragments of Megakaryocytes. Created from GATA 2 and GATA 1 factors and cytokines TPO, EPO and IL-3. Half life of 7-10d. lack a nucleus. Have mitochondria use glycogen for energy. Membrane bound glycoproteins BP1b and 11b/11a for adhesion and aggregation. At rest are smooth and non-sticky once activated become spiky and stick to injured surfaces. | Platelets |
| Red Cell Development | primitive red cells develop in the blood isles of the yolk sac. First immune cells in AGM. Cells populate the foetal liver and thymus to make first mature RBS. In adults happens in RBM. Spleen removes old RBC. Goes from HSC-MP-CMP-MEP-RBC. Mediated by factors GATA2-GATA1. Cytokines SCF, TPO- IL-3, TPO-EPO. EPO important regulator of RBC production |
| Plasma Proteins | Albumin most common, Globulin’s alpha and beta and gamma. Fibrinogen (clotting). And hormones. |
| Erythropoiesis | RBC production, happens in bone marrow. Will be manufactured until they account for 40% of dry weight of cell. The nucleus of cell is squeezed out. Differentiation driven by GATA1 and EKLF (From a CMP). Use of EPO for final differentiation. |
| Factors that inhibit clotting | produced by endothelial cells, prostacyclin, thrombomodulin, heparin. |
| Factors that activate clotting | produced by endothelial cells. Von Willebrand factor, Tissue factor. |
| Factor that cause clot breakdown | Tissue plasminogen activator, TPA. |
| Clotting - platelet plug formation | most factors made in liver. Is Vitamin K dependant. Forms thrombin and fibrin. Initial adhesion mediated by vWF binding to Gplb this releases granule contents and expression of glycoproteins Gpllb- lla. This binds to fibrinogen and forms platelet plug. |
| Extrinsic clotting | tissue damage pathway. Trauma – cleavage of Factor V11-> FV11a + membrane bound TF. Is rapid. |
| Intrinsic clotting | contact activation pathway. Exposed collagen – Cleavage of Factors X11- X11a – X1-X1a- 1x- 1xa. Is slow. |
| Common pathway | happens after either extrinsic or intrinsic pathways. Cleaves factor X to Xa. Makes thrombin form to prothrombin. Thrombin with calcium leads to thrombolysis. Fibrinogen forms crosslinked net that stabilises clot. Adhesion of clot is mediated by vWF binding to Gplb blocks ADP that enables Gpllb - llla to bind to fibrinogen. |
| Fibrinolysis | breakdown of clot. Endothelial cells release thrombomodulin that inhibits the clotting cascade. T-PA negatively regulates clot by controlling plasminogen conversion to plasmin that is important in clotting. |
