Lec 11 - Blood (Anatomy 10B: Introduction to Human Physiology Fall 2024 PDF)

© 2013 Pearson Education, Inc. Anatomy 10B: Introduction to Human Physiology Fall 2024 Mt. San Antonio College Lecture: Blood Anatomy 10B...

© 2013 Pearson Education, Inc. Anatomy 10B: Introduction to Human Physiology Fall 2024 Mt. San Antonio College Lecture: Blood Anatomy 10B: Introduction to Human Physiology Fall 2020 Blood B BLOOD is a connective tissue composed of cells and a liquid part called plasma Total Blood Volume: ~ 7% of total body weight 70-Kg male: 5L 58-Kg female: 4L Blood consists of: Plasma Erythrocytes Leukocytes Thrombocytes One drop of blood (approx. ~) 4-6 million RBCs 4-12 thousand WBCs 250 thousand platelets § Total blood volume: § 70-Kg male: 5L Functions ofBlood Blood Functions of Blood od § Total blood volume: § 70-Kg male: 5L § 58-Kg female: 4L § Total blood volume: § 70-Kg male: 5L § 58-Kg female: 4L § Blood consists of: § Plasma § Erythrocytes § Leukocytes § WHOLE BLO § Blood consists of: Thrombocytes § § WHOLE BLOOD consists of PLA § Plasma § Erythrocytes One drop of blood (approx. ~) § § Leukocytes § WHOLE § 4-6BLOOD consists of million RBCs PLA § Thrombocytes § 5-10 thousand WBCs § 250 thousand platelets § One drop of blood (approx. ~) § 4-6 million RBCs Whole WholeBlood: Plasma Blood: Plasma § PLASMA PLASMA isliquid is the the ECF portion portion of blood of blood -.300 an and contains Osm/300 mOsm osmolarity of ~.300 Osm/300 mOsm § Consists Consists of 90% primarily water(90%) of water and other dissolved and other substances dissolved solutes § Nutrients, Nutrients, metabolicmetabolic wastes, wastes, gasses, gasses, electrolytes electrolytes & plasma proteins and plasma proteins  PlasmaProteins Plasma Proteins PLASMA § PLASMA PROTEINS PROTEINS serve a wide serve array a wide of functions: array transport, of functions blood – transport, clotting blood and and clotting coagulation, immunity, andcoagulation, enzymes immunity, and enzymes Ex: ALBUMIN is a key player in maintaining an osmotic gradient between the tissues and bloodstream (helps maintain fluid in your bloodstream) SERUM: Plasma with fibrinogen and other clotting proteins removed Whole Whole Blood: Blood:Cellular CellularElements Elements § ERYTHROCYTES (RED BLOOD CELLS): Function in gas transport § LEUKOCYTES (WHITE BLOOD CELLS): Function in immunity § PLATELETS (THROMBOCYTES): Function in blood clotting and coagulation Hematopoiesis Hematopoiesis PLURIPOTENT HEMATOPOIETIC STEM PLURIPOTENT HEMATOPOIETIC STEM §CELLS: CELLS: Undifferentiated cell that serves as a Precursor §precursor to to all all blood blood cells cells § Undifferentiated cell § Clinical significance – stem cell PROGENITORresearch CELLS: Cell §with Hard to harvest numerous specific fates - will give rise to specific blood cells § PROGENITOR CELLS: cells leave the bone Mature differentiated Cell with §marrow and numerous specificfunctions provide specific fates – will Ex:give rise blood White to specific blood cells cells ….immunity! § Mature differentiated cells leave the bone barrow with specific function Hematopoiesis § HEMATOPOIESIS Hematopoiesis – synthesis of blood cells; begins in embryonic§ development and throughout HEMATOPOIESIS – synthesis of blood cells; lifetime HEMATOPOIESIS is thebegins synthesis of blood in embryonic cells - begins development during and throughout embryonic § At birth:development and all bones throughout till lifetime about lifetime age till 5 about age 5 At birth: all bones § At birth: all bones have the potential to undergo hematopoiesis § Adults: Pelvis, cranium, till about approx. ~ age § Adults: of 5 ribs and Pelvis, proximal cranium, ribs and ends proximal ends of longPelvis, Adults: bones of long bones cranial bones, ribs, and proximal ends of long bones § Hematopoiesis is controlled by CYTOKINES § Hematopoiesis is controlled byare § Cytokines CYTOKINES signaling molecule peptides § Secreted from endothelial cells and WBCs § Cytokines are signaling molecule factors,peptides Hematopoiesis is controlled by§ Trophic CYTOKINES Growth Factors Secreted § Cytokines arefrom endothelial peptide cells andsecreted chemical messengers WBCs from § Trophic endothelial factors, cells Growth and white Factors blood cells Erythrocyte Homeostasis Erythrocyte Homeostasis ERYTHROPOIETIN (EPO) is secreted primarily by the kidney (also liver) and is released under hypoxic § Erythropoietin (EPO) is either defined as a conditions cytokine or hormone – secreted primarily by Examples for stimulus for release: the kidney (also liver) – released under Anemia hypoxic conditions at kidneys Stimulus for release: Insufficient§pumping of the heart (heart failure) § Anemia Lung disease § Insufficient pumping of the heart Vigorous exercise § Lung disease Ascending to higher altitudes § Vigorous exercise § Ascending to high altitudes Testosterone also stimulates the release of EPO – this accounts for the higher hematocrit in men compared to women Erythrocyte ErythrocyteCharacterization Cell Structure § RBCs are the most abundant cell type of whole blood – function for gas exchange Mature RBCs lack a nucleus and other organelles (mitochondria, ribosomes, Golgi, ER….etc) and Mature § strictly RBCs undergo lack a nucleus glycolysis and other organelles (mitochondria, Golgi, ER, etc.) for ATP production High Energyrate § turn-over production and thus, by RBCglycolysis synthesis isonly continuous High turn-over § Membrane rate andbythus, shape is stabilized RBCs synthesis cytoskeletal filaments is common and frequent Hemoglobin Protein A single RBC has approx. ~ 280 million Hb molecules – oxygen binding to iron is reversible and follows the law of mass action ~70% of iron in the body is found bound to hemoglobin Hemoglobin also binds to carbon dioxide (transports CO2 to the lungs) and H+ (serves as a buffer) Average concentration of Hemoglobin: ~ 14g/100ml in women ~ 15 – 15.5g/100ml in men Erythrocyte Synthesis: The Role of Iron IRON is a mineral that is needed for the synthesis of Hemoglobin Iron balance includes: Iron loss: Urine, feces, and sweat; Women lose an additional amount via menstrual blood Iron gain: Ingestion of iron-containing foods (meat, liver, poultry, egg yolk, beans, nuts) and Iron dietary supplements IRON DEFICIENCY: Can lead to inadequate hemoglobin production HEMOCHROMATOSIS: Excess amount of iron in the body. Can lead to organ failure and chronic diseases: cirrhosis, diabetes, and heart failure Hemochromatosis HEMOCHROMATOSIS caused by a rare inherited condition that causes more dietary iron than usual to be absorbed by the gut Excess iron can lead to liver damage, weakness, skin pigmentation, and diabetes – bronze diabetes Condition called “bronze diabetes” due to the discoloration of the skin and associated disease of the pancreas Erythrocyte Synthesis: The Role of Folic Acid and B12 FOLIC ACID is a vitamin found in large amounts in leafy plants, beans, peanuts, whole grains, and seafood. Folic acid is required for the synthesis of Thymine (T) of DNA, which is essential for cell division. Needed for cells that continuously proliferate…like progenitor cells that give rise to erythrocytes B12 Vitamin is required for red blood cell synthesis B12 from eating meat, poultry, fish, and dairy products Erythrocyte Erythrocyte Synthesis Erythrocyte & & Degradation Production Synthesis Degradation  Turn To Question – 1 Your Partner…. Create a diagram showing RBC synthesis and breakdown – include the roles of EPO, Hb, and Iron Platelets latelets PLATELETS PLATELETS areare the the smallest blood blood smallest cells – fragments produced produced cells - fragments in the bonein marrow that marrow the bone originate that origina from largeare PLATELETS megakaryocytes the smallest blood cells – fragments produced in the bone marrow that originate megakaryocytes. Platelets function in blood clotting – contain secretory vesicles with platelet factors. Upon from large megakaryocytes – Involved in blood clotting activation, Plateletsplatelets functionundergo in blood clotting - contain DEGRANULATION secretory causing vesicles the release with platelets of platelet factors factors, undergo Platelets contain secretory vesicles with platelet factors – Degranulation – process of release Hemostasis HEMOSTASIS is the process of preventing blood loss within a damaged blood vessel VASOSPASM: Vasoconstriction of vascular smooth muscle to decrease blood flow to injured site PAIN REFLEX: NOREPI Endothelial cells: Endothelin PLALELET PLUG FORMATION: Platelet adhesion causes platelet release reaction which forms platelet plug COAGULATION CASCADE: Formation of a BLOOD CLOT Platelet Platelet Release Release Reaction Reaction Reaction Platelet Platelet Release Release Reaction Reaction § Damaged blood vessels exposed collagen stimulates endothelial cells to secrete paracrine signal von § Damaged blood vessels exposed collagen stimulates endothelial cells to secrete paracrine signal von Damaged Damaged bloodvessels blood vesselsexpose exposecollagen, collagen,this thisstimulates stimulates endothelial endothelial cells to secrete secrete paracrine paracrinesignal signalvon von WilliebrandFactor Williebrand Factor(vWF) (vWF) Williebrand Williebrand Factor § Factor vWF §vWF (vWF)platelets (vWF) activate activate platelets– –PLATELET PLATELET RELEASE RELEASE REACTION REACTION vWFactivates vWF activates platelets § §platelets Platelets inducing Plateletscontain contain inducing PLATELET secretory PLATELET secretory RELEASE vesicles RELEASE vesicles REACTION ––activation activation causes degranulation REACTION causes of: ADP, degranulation of: ADP, Serotonin, Serotonin,and and Platelets Platelets release release Thromboxane Thromboxane factors:ADP, factors: A2 Serotonin, A2 ADP, Serotonin,and andThromboxane Thromboxane A2 A2 Plateletfactors § §Platelet factorscauses: causes:1)1)Enhances Enhancesvasoconstriction vasoconstriction and and 2) 2) activation activation of of other other platelets platelets 1) 1) Enhance Enhance vasoconstriction vasoconstriction § FORMATION OF2)2)Activation Activationof PLATELET ofother PLUG other platelets platelets -- eventually eventually leading leading to to the the formation formationofofaa § FORMATION OF PLATELET PLUG PLATELETPLUG PLATELET PLUG Coagulation Cascade Damaged area exposes COLLAGEN FIBERS & TISSUE FACTORS – take part in a cascade of chemical reactions Inactive clotting factors become activated ….. Both intrinsic and extrinsic pathways lead to the formation of a BLOOD CLOT ulation Cascade Blood cot consists of a thick FIBRIN mesh § FIBRIN is the end product of coagulation cascade – localized damaged area is repaired and fibrin is dissolved FIBRIN is the endbyproduct PLASMINof coagulation cascade – localized damaged area is repaired and fibrin is dissolved by PLASMIN  brinolysisCoagulation Cascade Fibrinolysis Fibrinolysis Fibrinolysis Coagulation Cascade IBRIN is the end product of the COAGULATION CASCADE (formation of fibrin mesh) - localized damaged area IBRIN is §the end product FIBRIN is the endof coagulation product cascade of coagulation (fibrin cascade mesh)damaged – localized – localized area isdamaged area eventually repaired and fibrin is dissolved (FIBRINOLYSIS) by PLASMIN repaired and fibrin is dissolved (FIBRINOLYSIS) by PLASMIN s repaired and fibrin is dissolved (fibrinolysis) by PLASMIN TION FIBRIN FIBRINCASCADE is §the end (formation is the end product product is the endof ofoffibrin of the COAGULATION coagulation mesh) CASCADE cascade -(formation (fibrinlocalized mesh) – damaged of fibrin localized area mesh) - localized isdamaged damaged area area onisiseventually § cascade agulation cascade(fibrin FIBRIN repaired –and and mesh) localized fibrin product is is – localized damaged dissolved FIBRIN coagulation area isdamaged cascade FIBRIN (FIBRINOLYSIS) § by – is the end localized is §the by PLASMIN area product damaged end FIBRIN area of product the is the endof COAGULATION coagulation product c of coagula BRINOLYSIS) by PLASMIN repaired repaired and fibrin isfibrin dissolveddissolved (FIBRINOLYSIS) (fibrinolysis) by PLASMIN PLASMIN Turn Turn To Question Turn to Your Partner.. – 2Partner…. To Your Your Partner… Q: Which Marks an Early Event in Hemostasis? a) Conversion of Fibrinogen to Fibrin b) Release of Serotonin and Thromboxane A2 by activated Platelets c) Platelet adhesion to damaged tissue d) Release of Endothelin by damaged endothelial cells causing vasoconstriction e) Fibrinolysis Create Your Question – 3 Diagram… Create a Clear diagram of Hemostasis - include all three phases and the key players involved Anticoagulants Prevent Coagulation Mechanisms that regulate blood clotting & prevention of the formation of a blood clot (THROMBOSIS) Platelets and Blood Vessel Walls INHIBITION OF PLATELET ADHESION: Prostacyclin and Nitric Oxide Platelets and Blood Vessel Walls INHIBITION OF COAGULATION CASCADE: Heparin, Protein C, and Antithrombin III Work by blocking clotting factors in the coagulation cascade  -Clotting Lipids aling as Agents Key Signaling MoleculesAgents Anti-Clotting Anti-Clotting Agents Lipids as Key Signali Molecules Anti-Clotting Anti-Clotting ious drugs Lipids are used as clinically Agents Key to Agents preventSignaling clotting - Lipids Moleculesas Key Signalin signaling Molecules Various drugs are usedandclinically to of prevent drugs mmonly are used used preventionclinically to prevent treatment myocardial Various clotting arction - drugs commonly Pathways §(heart are for attack) used used prevention clinically eicosanoid and to prevent synthesis clottingby mediated - g – commonly commonly Various activationused drugsof areprevention used clinically Phospholipase A and to of prevent Various treatment Damaged drugsusedare used prevention of myocardial endothelial cells clinically and infarction triggers to (heart treatment clotting 2 prevent myocardial and ment of myocardial clotting infarction clotting –Many - commonly Pathways §(heart commonly infarction for attack) used used prevention eicosanoid (heart synthesis prevention and mediated by and key attack) nterferes with endothelial activation of cells’ pharmaceutical normal Phospholipase agents Aanti-clotting inhibit 2 various k) § treatment Damaged treatment of of myocardial myocardial endothelial infarction Damaged endothelial cells triggers clotting infarction (heart and (heart cells: trigger clotting & unctions steps attack) in pathways maged attack) endothelial interferes interferes with cells: endothelial triggers clotting with endothelial cells’ normal anti-clotting § Many pharmaceutical agents inhibit cells’ normal various key anti- & Damaged functions nterferes Damaged §clotting endothelial steps with endothelial § Anti-Inflammatory endothelial cells: in pathways cells: trigger cells’ Steroids: triggers clotting normal Block clotting PIRIN functions interferes (interferes with Phospholipaseendothelial A with production cells’ normal of anti- ticlotting Inhibits nitric COXfunctions & interferes ASPIRIN oxide) enzyme clotting with& functions endothelial § Anti-Inflammatory 2 therefore (interferes cells’ Steroids: inhibits with normal Block production of Phospholipase A2 anticlotting hromboxane § A2 Inhibits nitric functions Aspirin & NSAIDs: synthesis COX oxide) enzyme Block Cyclooxygenase & therefore inhibits Thromboxane Aspirin § A2 & NSAIDs: Block Cyclooxygenase synthesis ASPIRIN: Inhibits COX enzyme - inhibition of nUMADIN ASPIRIN: Thromboxane A2 Inhibits synthesisCOX enzyme - inhibition of Aspirin COUMADIN hibits COX Inhibits enzyme Thromboxane synthesis A2 –synthesis inhibition of clotting factors of § Inhibits InhibitsCOX enzyme synthesis – inhibition of clotting factors of romboxane COUMADIN: A2 synthesis Inhibits synthesis of clotting Thromboxane COUMADIN: A2 synthesis Inhibits synthesis of clotting factorsfactors din Coumadin hibits synthesis § Inhibits of clotting synthesis factors of clotting factors  Hemophilia Hemophilia Hemophilia Hemophilia emophilia Hemophilia Deep internal bleeding is Deep a cause for concern internal bleeding foris hemophiliacs a cause for concern for hemophiliacs § Hemophilia is a coagulation disorder – genetic condition in which individual cannot synthesize (clotting factor VIII; some cases clotting factor IX) § Hemophilia is a coagulation disorder – genetic condition in which individual cannot synthesize § X-linked recessive disorder – Affects more males than females emophilia (clotting Gene § HEMOPHILIA factor istherapy a coagulation has VIII; been some disorder cases demonstrated clotting –disorder genetic factor in to-condition introduce IX)which individual hemophiliacs cannot synthesize withindividuals engineered genes synthesize that § X-linked is a recessive coagulation disorder – Affects genetic more condition males than in which females cannot key clotting lotting factorsynthesis provide VIII; somefor cases CF IX)clotting factor IX) factors involved in coagulation (primarily clotting factor VIII;individual emophilia § Gene is HEMOPHILIA -linked a coagulation therapy has recessive disorder beendisorder –disorder – demonstrated is a coagulation Affects genetic more to -condition introduce genetic males in which insome hemophiliacs than condition females cases with which clotting cannot engineered individuals factorthat synthesize genes cannot IX) synthesize key clotting clotting factor X-linked provide ene therapy VIII; condition synthesissome - for cases affects clotting more CF IX) malesfactor than IX) females factors has been in involved demonstrated to introduce coagulation (primarily hemophiliacs clotting with some factor VIII; engineered genes that cases clotting factor IX) -linked recessive disorder is aIX) – Affects more males than females ovide HEMOPHILIA X-linked synthesis for CF condition - blood affectsclot genetic more males disorder – hemophiliacs have problems synthesizing key clotting than females ene therapy factors has been in involved demonstrated to introduce coagulation (primarily hemophiliacs clotting with some factor VIII; engineered genes that cases clotting factor IX) rovide synthesis X-linkedfor CF IX) that affects more males than females condition  Severity of condition varies - in severe cases, extensive bleeding can occur with Hematology Hematology minor cuts Bleeding can occur in joints and around muscles Hematology COMPLETE BLOOD COUNT (CBC) is a series of tests used to evaluate health and detect any blood disorders Hematology Ex: Leukemia: Low Functional WBCs; Hematology High non-functional cancerous WBCs Hematology Ex: Anemia: Decrease in RBCs or Hemoglobin content HEMATOLOGY is the study of blood, blood-forming organs, and blood diseases Ex: detect Bacterial Infection: disorders Increase (anemia, in infection, Can HEMATOLOGY is the studyclotting of blood,disorders) blood-forming organs, Neutrophilsbloodand Determine typing blood diseases Analysis of types Can anddetect numbers of RBCs, disorders WBCs, (anemia, and platelets infection, clotting disorders) Abnormal number Determine bloodmedical may indicate typing conditions Analysis of types and numbers of RBCs, WBCs, and platelets Abnormal number may indicate medical conditions Complete Blood Count (CBC) - 1 cubic millimeter (1uL) Complete Blood Count (CBC) - 1 cubic millimeter (1uL) § COMPLETE BLOOD COUNT (CBC) – series of tests used to evaluate health and detect numerous blood  Hematocrit Hematocrit Hematocrit Determination Determination Determination WBCs “Buffy Coat” Sample is subjected to centrifugation § HEMATOCRIT DETERMINATION is a simple techniqu the portion (expressed as a percentage) of RBCs in whol HEMATOCRIT DETERMINATION is a simple quick § technique Too many used tolittle or too measure RBCsthe canportion ofaformed indicate certain diseas elements to whole blood Hematocrit determination is expressed as a percentage: Male: 55%-45% Female: 40%-45% Abnormal hematocrit can demonstrate blood loss or a blood disorder Turn To Turn To Your Your Partner… Partner… Question – 4 Turn To Your Partner…. Q: In Which of the Following Conditions Would You Expect Higher than Normal Hematocrit Values? a) Anemia b) Dehydration c) Lung Disease d) Blood Loss e) Pregnancy  Morphology Morphology of of Red Erythrocytes Blood Erythrocyte Morphology Morphology of Erythrocytes Cells § Morphology (cell shape) of RBCs varies depending on ECF osmolarity or specific § Morphology disease Morphology (cell shape)ofof states (cell shape) RBCs RBCs varies varies – depends on ECF osmolarity or specific disease states Morphology (cell shape) of RBCs varies and– can plasma osmolarity determine or specificits the osmolarity disease placedstates in or a may alterdisease specific size/shape state § MEAN § MEANCORPUSCULAR CORPUSCULAR VOLUME (MCV): VOLUME Average (MCV): volume ofvolume RBCs can be abnormally blood large MEAN MEAN CORPUSCULAR CORPUSCULAR VOLUME VOLUME (MCV): (MCV): Average Average volume of Average volume of RBCs RBCs can be of one abnormally largered (macrocytic)cell or small (macrocytic) or small Macrocytic: can be abnormally (microcytic) Abnormally large(macrocytic) or small (microcytic) large (microcytic) § ANEMIA: Condition Microcytic: in which Abnormally there is a decrease of oxygen transport small § POLYCYTHEMIA VERA: Overproduction of RBCs – hyperactive stem cell proliferation (rare Anemia ANEMIA is defined as a decrease in the ability of the blood to carry oxygen – numerous cases can cause anemia DIETARY ANEMIA Iron deficiency anemia Pernicious anemia: B12 deficiency HEMORRHAGE ANEMIA Massive bleeding (trauma or surgery) may cause a rapid loss of blood leading to acute anemia – may lead to SHOCK (inadequate blood flow to tissue to meet their metabolic needs) Anemia Anemia ANEMIA is defined as a decrease in the oxygen-carrying capacity of blood - numerous cases can cause anemia. HEMOLYTIC ANEMIA Malaria (Acquired): Parasite from mosquito bite infect red blood cells Sickle cell anemia (Inherited): Genetic condition that leads to abnormal red blood cells Both causes red blood cell destruction at faster rates than red blood cell synthesis APLASTIC ANEMIA Damage or defect of the bone marrow may lead to failure in producing inadequate amount of blood cells Damage can occur due to radiation, chemotherapy, infection, and drugs RENAL ANEMIA Kidney damage may lead to a decrease in EPO - this will decrease erythropoiesis  When Mixi Blood Blood Typing Typing – ABO blood type is determined by ! ence or absence of certain Human blood type is determined by the presence or absence § Human blood type is determined by the presence or ENSof certain absenceANTIGENS of certain identifiers – ANTIGENS on the O system and Rh factor surface of RBCs Antigens s help help the the body’s body’s immune system to recognize “self” immune ! from “non-self” § Antigens to recognize itshelp ownthe body’s immune system to blood recognize it’s own RBC type Plasma antibodies recognize foreign antigens § Make Ab for different blood type ntibodies recognize foreign § Blood type ABO System AGGLUTINATION: When antibodies come in contact with antigens….clumping occurs § Rh Factor (+/-) Q Donor and recipient blood types are incompatible TINATION: When antibodies § AGGLUTINATION – When Ab come in contact contact with with their corresponding antigens – clumping of ….clumpingparticles occurs Rhesus Blood Groups Rhesus Blood Groups RH BLOOD GROUPS Based on the presence or absence of Rh surface antigens present on RBCs “Rh” comes from the original discovery in Rhesus monkeys RH POSITIVE (Rh+) indicates the presence of Rh surface antigens RH NEGATIVE (Rh-) lacks Rh surface antigens Included in the full blood type: AB+, O- molytic Disease Hemolytic Hemolytic of of Disease Disease the Newborn ofthe the Newborn Newborn father Rh and Rh - mother + father and Rh - mother of aBirth of a Rh+ Rh+ baby baby produces produces Rh antibodies Rh antibodies in in r mother nd pregnancy Second pregnancy with Rh+with babyRh+ baby - Rh - Rh diesantibodies may crossmay thecross the placenta placenta leading to leading to ERYTHROBLASTOSIS FETALIS HROBLASTOSIS FETALIS RhoGAM RhoGRAM RhoGAM is an injection given to women 28 weeks and within 72hrs of birth (if baby is Rh-positive) - drug prevents the body from producing Rh antibodies od od Cell Cell Blood Blood Cancers Cancers Cell Cancers Cell Cancers Blood Cell Cancers Blood Cell Cancer EMIAS - cancers of blood forming tissues LEUKEMIAS - cancers of blood forming tissues cerous cells migrate from origin in red bone Cancerous cells migrate from origin in red bone rrow marrow Blood sence CellCell Blood Presence Cs inWBCs Cancers of increased Cancersand abnormally of increased circulation largelarge and abnormally in circulation LEUKEMIAS o types: LEUKEMIAS Two types: - cancers of blood - cancers forming of blood tissues forming tissues Myeloid Cancerous Cancerous Myeloid leukemia leukemia cells migrate cells migrate from origin from origin in redin bone red bone marrow ymphoid Lymphoidmarrow leukemia leukemia Presence of increased and abnormally large elevated Presence Both have Both of have increased elevated WBCs and WBCs in circulation abnormally WBCs large WBCs in circulation Two types: Two types: Myeloid leukemia Myeloid Lymphoid leukemia leukemia Lymphoid Both leukemia have elevated WBCs Both have elevated WBCs