Blood

Multipotent uncommitted stem cell IL-1, IL-6,IL-3

Hematology

Committed myeloid stem cell

Committed lymphoid stem cell

Erythropoiesis hemocytoblast, todiscs, committed cell: Functions Erythrocytes of Blood (RBCs) Substance Biconcave distribution anucleate, (Blood Erythrocyte Disorders anemia Bd has abnormally Erythropoiesis: Nutrient Requirements proerythroblast, to early erythroblasts in hormones 3 phases: transport essentially O no , nutrients, organelles, metabolic filled with waste, hemoglobin Fate and Destruction of Erythrocytes life span of 2 low O -carrying capacity, it is a symptom rather Blood Anemia: Decreased contains Hemoglobin over 100 solutes, Content including: iron2Plasma Erythropoiesis requires: Phase 1 ribosome synthesis in early erythroblasts, Physical Classification Characteristics of Leukocytes: and Volume Formed Leukocytes Elements: (WBCs) RBC, complete WBC cells: & platelets: less numerous Only ), (Hb): Regulation protein of that Bd functions levels of particular in gas transport, substances RBC is 100–120 days, old RBC rigid and fragile, Erythrocyte Anemia: Abnormal Function Hemoglobin respiratory thalassemias gas transport: Hormonal Control of Erythropoiesis erythropoietin than a 2disease itself, Bd Ofrom: levels cannot support Proteins deficiency (albumin, anemia results globulins, clotting secondary proteins, result ...), of 2 Hemoglobin Polycythemia (Hb) excess oxyhemoglobin RBCs increase Hb Bd bound viscosity, to O , Proteins, lipids, and carbohydrates, iron, vitamin Composition Production of of Blood Blood: Cells the hematopoiesis body’s only fluid Bd tissue, cell Phase Hb accumulation in late erythroblasts & 2 Blood Granulocytes is a sticky, neutrophils, opaque fluid eosinophils, with a metallic & basophils, taste WBCs than RBCs, are complete make up cells, 1% of RBCs the total have blood no nuclei volume or (maintains contain PM appropriate protein spectrin temp. that: by absorbing gives RBC &their their Hb degenerate, engulfed byHb, macrophages, Hb absent reversibly or faulty binds globin with chain O , Hb in is composed RBC thin, of: (EPO) release by kidneys is triggered by: Hypoxia 2 normal metabolism, signs/symptoms: fatigue, nonprotein hemorrhagic nitrogenous anemia, inadequate substances intake (lactic of acid, iron3O main loading polycythemias takes place are: in lungs, deoxyhemoglobin B12, and folic acid composed formation, of occurs liquid in plasma red bone & formed marrow elements, of axial normoblasts, Phase 3 ejection of nucleus from nor2 color contain varies cytoplasmic from scarlet granules (oxygen-rich) that stain to specifically dark red organelles, can leave capillaries platelets are via just diapedesis, cell fragments, move through most distributing flexibility, allows heat, to normal change pH shape in body as necessary, tissues: buffer heme & globin separated, iron is salvaged for reuse protein delicate, globin: and deficient 2 alpha in & Hb, 2 beta sickle-cell chains, anemia each bound due to decreased RBCs, decreased O availability, paleness, shortness of breath & chills 2 urea, containing creatinine), foods, organic impaired nutrients iron absorption, (glucose, carboHb Polycythemia after O diffuses vera into tissues (reduced Hb), The body stores iron in Hb (65%), the liver, spleen, formed skeleton include: & girdles, erythrocytes epiphyses of or humerus red blood & cells femur, moblasts: formation of reticulocytes, then mature 2 (oxygen-poor), (acidic, basic, or pH both) of blood with is Wright’s 7.35–7.45, stain, temp. larger is of formed tissue spaces, elements leukocytosis survive in WBC bloodstream count over for 11,000 only systems, RBC are adequate example of fluid complementarity volume), Body of protection structure Fate of Hemoglobin heme degraded to a yellow to results a heme from group, defective each gene heme coding group for bears an an abnormal atom increased tissue demand for O2 ,iron enhanced Anemia: Insufficient Erythrocytes hemorrhagic hydrates, pernicious amino anemia acids), results electrolytes from: deficiency (sodium, of in Carbaminohemoglobin Secondary polycythemia Hb bound to CO , CO and bone marrow, intracellular is stored (RBCs), hemocytoblasts leukocytes give or rise white to all blood formed cells elements (WBCs) erythrocytes. Circulating RBC number remains 2 2 & 38°C, and usually slightly shorter-lived higher than than “normal” RBCs, body have temp. lobed few per cubic days, most millimeter, blood normal cells do response not divide to but bacterial are (prevents & function: blood biconcave loss: activating shape has plasma huge surface proteins area & pigment bilirubin, liver secretes bilirubin as bile to iron, Hb called which HbS: can has bind single one to aa O substitution molecule, each in beta Hb erythropoiesis increases: RBC count in circulating 2 anemia result of acute or chronic loss of Bd, potassium, vitamin B12, calcium, often caused chloride, by lack bicarbonate), of intrinsic respirafactor loading Blood doping takes place in tissues protein-iron complexes as ferritin & hemosiderin, platelets. Hematocrit is % of RBCs of total Bd vol. constant: balance of production & destruction. it nuclei, is 8% all of phagocytic body weight, cells average vol. of Bd is 5–6 L renewed or viral invasion by cells in bone marrow platelets, to vol. ratio, clot discounting formation, water blood prevents content, RBC infection: are intestines, metabolized into urobilinogen, leaves molecule chain, causes can transport RBCs to become 4 molecules sickle-shaped of O in low blood, Ofor ability of thedioxide) blood increases 2 RBC hemolytic anemia prematurely ruptured 2 carrying tory needed gases (oxygen absorption and of carbon B12 circulating iron is loosely bound to the transport Too few RBC: tissue hypoxia, too many RBC: for males, and 4–5 L for females synthesizing 97% Hb, ATP & is utilizing generated antibodies, anaerobically, activating so RBC combody in situations feces: pigment calledor stercobilin, globin is oxygen Aplastic anemia destruction inhibition of red protein transferrin undesirable viscosity. Erythropoiesis is hormonally plement do not consume proteins, O activating WBC against invader) metabolized into aa & released into circulation 2 bone marrow controlled, depends supplies of iron, aa, B vitamins CSF-GM

CFU-Meg

CFU-E

CFU-GM

Erythropoietin

CSF-G

CSF-M

Myeloblast

Megakaryoblast

Lymphoblast

Proerythroblast

Promyelocyte

Monoblast

Early normpblast

Megakaryocyte

Prolymphocyte

E, N, B, Myelocyte Intermediate normoblast

Promonocyte E, N, B, Metamyelocyte Late normoblast

Reticulocyte

Reticulocyte

Granulocyte E, N, B

Monocyte

Platelets

Lymphocyte

Blood

Erythrocyte

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BASIM ZWAIN Tissue LECTURE Macrophage NOTES

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Pathway Cell Description Hematology Cell Type Type Intrinsic Description

DD and LS Function Cells/L and LS Function Cells/L Intrinsic Pathway Extrinsic Pathway System for naming blood – clotting factors Extrinsic Biconcave 4 – 6 million D: 5 –pathway 7 days catalyzes O2 and CO2 Erythrocytes Inhibition of Clotting Factors Contact Tissue thromboplastin(TPL) Contact Agranulocytes Coagulation Phase 2: Prothr. activator Population S. U. of % Groups, of Blood Factors Names Neutrophils 2Frequency types of granules, take up both acidic Human Blood Groups III Anucleate disc LS: 100 – 120 transport Rh Blood Groups ABO Blood Groups D:Disorders Detailed Reactions of Hemostasis HMW-K Tissue plasminogen Urokinase Hemostasis Disorders: Bleeding Fibrinogen I •Platelets Fibrin acts as an anticoagulant by binding Lymphocytes Spherical nucleus 1500 – 3000 days – weeks Cellular or Production Prevention of of Undesirable Leukocytes Clots Kallikrein transformation of prothr. to active enz. thrombin Hemolytic Transfusion Lymphocytes Disease Reactions have of large, the Newborn dark-purple, circular days & basic dyes, cytoplasm lilac colour, peroxidases, 7-8 m Leukemia Platelet Diagnostic Plug Blood Formation Tests activator (t-PA) •Plasma RBC membranes have glycoprotein antigens on Clot Hemostasis Hemophilias: Retraction Volume Disorders: hereditary Expanders and Repair Bleeding bleeding Disorders disorders There are eight different Rh agglutinogens, three Developmental Aspects Prothrombin II XII XIIa Coagulation Phase 1: Two Pathways to Factors Hemostasis Preventing Disorders: Undesirable Thromboembolytic Clotting Pale blue LS: hoursmismatched –mother years antibody directed •thrombin Thrombocytopenia: condition where the number Blood ABO Blood Transfusions Groups and preventing its: Asian Black White Group Blood Leukopoiesis Fragments Substances of used is megakaryocytes hormonally to prevent undesirable stimulated with a blueby clots: two Leukocytes Formation of Leukocytes Phase 3: Fibrin Mesh •Coagulation nuclei Transfusion Rh+ antibodies with a thin reactions of rim a sensitized of occur blue cytoplasm, when Rh– found cross HMW-K hydrolytic enz.s & defensins (antibiotic-like prns), Tissue thromboplastin Immature Platelets Laboratory not white examination stick blood to each cells of other blood are found or can to endothelial assess in the an III Blood Group RBC Antigen Plasma Antibody Blood that can be received external surfaces, these antigens are: unique caused •their When Clot Inability retraction by shock lack to synthesize is of imminent – clotting stabilization procoagulants factors from of low the blood clot by the by volume, liver Leukocyte Hemostasis Disorders: Leukemias XII XIIa of which (C, D, and E) are common Before birth, blood cell formation takes place in cytoplasm immune response Activator •Prothrombin Thrombus: Unnecessary a clotting clot that is develops prevented and by persist the in an Granulocytes Coagulation of circulating platelets deficient Transfusions The ABO blood are groups necessary: consists of: Developmental Aspects •Blood Positive feedback effects of coagulation Calcium IV families staining Aspirin: of outer an cytokines antiprostaglandin region (hematopoetic and a purple that granular factors) inhibits – center All leukocytes originate from hemocytoblasts Typing Thrombin catalyzes polymerization of fibrinogen placenta, blood mostly is enmeshed infused attack & in destroy lymphoid RBCs tissue of an (some Rh+ in baby Bd), XI XIa lymphocytes VIIa VII Agranulocytes and monocytes: bacterial slayers. Eosinophils 1–4% of WBCs, redbloodstream lining individual’s of Bd state vessels. in all of leukemias health Upon damage to vessel; they: to individual, recognized foreign if transfused to squeezing •results volume Hemophilia in must severe serum be A: replaced bleeding most from common the disorders fibrin type strands (83% of all Cancerous Series of reactions conditions designed involving to stop white bleeding blood cells Neutrophil Multi-lobed 3000 – 7000 D: 6 – 9 days Bacterial Factors Limiting Clot Growth or Formation Presence of the Rh agglutinogens on RBCs is 5 – 17 m the fetal yolk sac, liver, and spleen Proaccelerin V final •unbroken May be initiated by either the intrinsic or structural blood and molecular vessel characteristics of 2+of The thee steps of this series reactions are: 5 4 4 AB Ca Ca Patients show petechiae (small purple blotches on When Two antigens substantial (A and blood B) on loss surface occurs of the RBCs •thromboxane Age-related blood problems result from disorders Ability to speed up the production of prothrombin interleukins Granules contain and A2 colony-stimulating serotonin, Ca , enzymes, factors (CSFs) ADP, Hemocytoblasts to myeloid stem cells and Serum containing anti-A or anti-B agglutinins is AB A and B None A, B, AB, and O into fibrin •another, two Rh– Donor’s types: mother cells T cells become are (function attacked sensitized: in by immune the Rh+ recipient’s blood response) (from & nucleus LS: 6 hours 2 phagocytosis Lack visible cytoplasmic granules, similar TPL staining, bi-lobed nuclei connected via band of Are Bone Microscopic stimulated marrow examination: becomes by thromboxane totally occupied A2 with Proconvertin VII promoters of agglutination: agglutinogens Repair Causes Plasma due can or to plasma range a deficiency from expanders vitamin of factor can K VIII administered: deficiency to Monocytes Kidney shaped 100 – 700 D: 2 – 3 days Phagocytosis According Three phases to abnormal occur in rapid white sequence blood cells involved: •cases) Two homeostatic mechanisms prevent clots from Prekallikrein activcators indicated Rh+ IX as month, IXa red bone marrow is the By the 7th extrinsic pathway •endothelial Can block cells circulation, lining the resulting blood vessels in tissue death Prothrombin activator is formed the skin) due to spontaneous, widespread Two In certain antibodies hemostatis in the disorders plasma (anti-A and anti-B) days of the heart, blood vessels, and the immune system 10 – 14 m via factor V and •activator Interleukins Heparin: platelet-derived an anticoagulant are numbered growth factor used (e.g., clinically IL-1, (PDGF) IL-2), for CSFs preAntihemophilic factor VIII lymphoid stem cells added to blood, agglutination will occur between Insoluble fibrin strands form the structural basis previous plasma B cells(give agglutinins pregnancy rise to plasma causing: of Rh+ cell: baby produce or transfusion) antibodies) structurally, but functionally distinct & unrelated nuclear material, has red to crimson(acidophilic) PL Ca •cancerous Variations Stick to exposed leukocytes in size collagen and shape fi, form of RBCs a platelet – plug nucleus LS: months Develop into Presence/absence of these antigens are used to hepatitis Platelet-derived Hemophilia Plasma and expanders cirrhosis B: results growth have of osmotic factor deficiency (PDGF) properties of factor stimulates that IX •becoming Vascular Myelocytic spasms leukemia (immediate (involves vasoconstriction myeloblasts) in large Anti-Rh antibodies are not spontaneously formed VIII VIIIa 27 20 11 B primary hematopoietic area Eosinophil Bi-lobed nucleus 100 – 400 D: 6 9 days Kill parasitic Christmas factor Triggered by tissue-damaging events IX B blood •hemorrhage Platelet Coronary adhesion thrombosis: is prevented in Bd vessel by: of heart Prothrombin is converted into thrombin B Anti-A B and O Whole Individual with transfusions ABO Bd may are used: have various types Increased leukemias are thought to be due to the Acceleration of the intrinsic pathway by •are and Platelets named postoperative function for the WBCs cardiac in clotting they care mechanism, stimulate (e.g., forming Myeloid stem cells to myeloblasts or monoblasts agglutinin and corresponding agglutinogens of a clot Gray-blue macrophages causes Monocytes Diminished her body 4–8% oxygen-carrying to of synthesis leukocytes, Rh+ capacity largest antibodies leukocytes, cell types, have spherical (lymphocytes) or kidneylarge, coarse, lysosome-like granules, counterattack •classify predictions White Release blood serotonin of cells anemias produced, & ADP to attract though more numerous, platelets X Xa Stuart – Prower factor Red cytoplasmic LS:to 8 lymphocytes) –by 12 days worms X removal groups rebuilding directly Inability Hemophilia increase to of absorb blood C: mild fluid vessel fat type, volume, can wall caused lead used vitamin when a deficiency plasma K is •in response Lymphocytic to injury) leukemia (involves Swift of clotting factors Rh– individuals Blood cells develop from mesenchymal cells called •waning Involves a series of procoagulants Prekallikrein Kallikrein The Embolus: smooth a thrombus endothelial freely lining floating of blood in vessels Bd stream Thrombin catalyzes the joining of fibrinogen into Caused by suppression or destruction of bone •activating of When antigens blood & spontaneously loss is substantial preformed antibodies deficiency of the immune system platelets cytoplasm Common Pathway granulocyte-CSF temporary Warfarin: plug, used helps for stimulates those seal prone breaks granulocytes) to in atrial blood vessels Lymphoid stem cells become lymphoblasts Plasma thromboplastin antecedent ••are Positive reactions indicate agglutination XI Ca Thrombin granules Destroy antigenFibrin causes plasma to become a gel-like trap has The Clumped abundant drug cells RhoGAM pale-blue that impede can cytoplasms, prevent blood the flow purple Rh– mother staining shaped (monocytes) nuclei against parasitic worm, lessen allergies, phagocyto Type Plug not is and functional limited number to area of WBCs of injury (diagnostic by PGI2 of various 28 27 40 A Humans have 30 varieties of RBC antigens deficiencies of not Fibroblasts factor available, XI as form as it purified is a connective fat-soluble human tissue substance serum patch albumin, and is Acute Platelet leukemia plug formation (involves blast-type cells PL factors Va V blood, of activated clotting •Inhibition However, if an Rh– individual receives Rh+ blood islands A A Anti-B A and O Each pathway cascades toward factor X •amarrow Heparin Pulmonary and emboli PGI2 can secreted impair by the endothelial ability of cells the Hageman factor XII fibrin mesh antibody complexby 10 – malignancy, 14 m (e.g., radiation) Agglutinogens In treating thrombocytopenia and their corresponding antibodies 14 24 •fibrillation Abnormal thrombus and embolus formation Thrombin not absorbed to fibrin is inactivated Genesis Macrophages of Platelets and T cells are the most important Myeloblasts to eosinophils, neutrophils, basophils Fibrin in the presence of calcium ions activates •from U-or Ruptured kidney-shaped becoming RBCs sensitized that nuclei, release leave free circulation, hemoglobin enter into -se immune complexes. Basophils 0.5% of WBCs, Thrombin Prothrombin Coagulation diseases) Death is caused (a set by of internal reactions, hemorrhage Bd transformed and •absorbed Antigens of ABO & Rh Bd groups cause vigorous Fibrin – stabilizing factor XIII plasminate Endothelial Symptoms along and include cells dextran with multiply prolonged fat and bleeding restore the and painful Plasmin Plasminogen primarily Coagulation affects (blood children) clotting) antibodies form Basophilto Lobed nucleus 20 –potent 50 activated, D: 3 –a7 days Mediates •anti-Rh The fetus forms HbF, which has higher affinity Once factor X has been it complexes body Vitamin obtain E quinone, oxygen a anticoagulant Platelet counts less than 50,000/mm3 is diagnostic •antithrombin cannot Packed mixed red cells without (cells serious with plasma hemolytic removed) reactions are reflects the progress of atherosclerosis III sources The Flavonoids: stem of cytokines cell substances for platelets found is the in hemocytoblast tea, red wine, & Monoblasts to monocytes Fibrin Fibrinogen High molecular weight kininogen (Fitzgerald factor) HMW-K factor XIII that: •from the tissue, Treatment bloodstream differentiate of hemolytic into macrophages disease of the newborn 40 49 45 O U-orS-shaped nuclei with 2-3 constrictions, large Blue-purple LS: hours – days inflammation overwhelming Chemical liquid analysis to gel, infections intrinsic can provide & extrinsic a comprehensive pathways O disease None Anti-A and Anti-B O transfusion reactions when improperly transfused endothelial •and Liver Isotonic disabled saline lining joints can can also also prevent be used the to replace liver from lost Chronic leukemia more prevalent in older people A second expose to Rh+ blood will result in a for oxygen than adult hemoglobin Cytoplasmic 250,000 – 500,000 D: 4 – 5 days Blood clotting Platelets calcium ions, PF3, and factor V to form •with Cerebral emboli can cause strokes Prekallikrein (Fletcher factor) Pre-K for this condition used to treat anemia Ca XIIIa XIII ••involves Heparin, another anticoagulant, also inhibits cytoplasmic Heparin grape Many Pathway juice hematopoietic is that hemocytoblast, have natural hormones megakaryoblast, anticoagulant are used clinically activity Lymphoblasts to lymphocytes Cross-links fibrin Macrophages Circulating pre-birth hemoglobin highly transfusions mobile precipitates & actively and exchange in phagocytic, the purplish-black (basophilic) granules: histamine picture Treatments of one’s include general irradiation, health status antileukemic in relation to •producing Other Bd gps (M, N, Dufy, Kell, and Lewis) are blood Treatment volume bile, is with which blood is required transfusions for fat and and the Kallikrein Ka fragments LS: 5 – 10 days Seal blood vessel typical transfusion reaction granules prothrombin activator Cross-linked fibrin •promegakaryocyte, Treated with whole blood transfusions thrombin activity to stimulate bone marrow megakaryocyte, and platelets •normal Strengthens and stabilizes the clot Platelet phospholipid transfusions kidneys activate and lymphocytes causes after birth renal to mount failure immune response PL (inflammatory chemical as VD, attracts WBCs Home Exit drugs, and values bone marrow transplants tears mainly used for legalities 2 – 4 m 10 – 12 m vitamin injection K of absorption missing factors Fibrin BASIMFibrin degradation products (FDP) ZWAIN LECTURE NOTES 2+

2+

2+

2+

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