CARDIOVASCULAR SYSTEM Blood

Blood – General Characteristics Blood is C.T. Plasma = Liquid Matrix 55% Plasma, 45% Formed Elements (Cellular) Formed via Hematopoiesis (Stem Cells in Bone Marrow give rise to Cell types)

General Characteristics continued Avg. Vol. = 5 liters pH = 7.35 to 7.45 Formed (cellular) Elements: Erythrocytes (RBCs) Leukocytes (WBCs) Thrombocytes (Platelets)

Blood - Functions Transports (Gases, Nutrients, Hormones, Wastes) Regulates pH & Electrolyte Balance in Interstitial Fluid Prevents Fluid Loss from Bleeding Defends against Pathogens & Toxins Aids in Body Temperature Regulation

Components - Plasma Liquid Component of Blood 91% Water 7% Proteins: Albumins (Most Abundant, Osmotic Pressure) Globulins (Antibodies, Transport Proteins, Lipoproteins) Fibrinogen (Clotting) 2% Inorganic Salts, Carbohydrates, Lipids, Hormones, Gases, Wastes, etc. Globulins: Transport of fat-soluble vitamins (B12), steroid hormones (cortisol, thyroid hormones)

Components - Erythrocytes Red Blood Cells (RBCs) Most Abundant Blood Cell Anucleate when mature Biconcave Discs (shaped like “LifeSaver”) Shape increases Surface Area/Volume Ratio Live 120 Days

Erythrocytes - continued Hemoglobin (Hb) Red Pigment Contains 4 Heme Groups (Fe++) Reversibly binds Oxygen In High [O2], Binds O2  OxyHb (Bright Red) In Low [O2 ], Releases O2  DeoxyHb (Darker) Each RBC contains about 280 million hemoglobin molecules.

Erythrocytes - continued Hematocrit = % RBCs in Blood RBC Count = 5 million/mm3 2 million produced/second Humans have over a trillion RBCs Blood is viscous (4X thicker than water) Production  with  O2 or Blood Loss

Fate of Erythrocytes Unable to divide, grow, or synthesize proteins Wear out in 100 to 120 days Removed by phagocytes in the spleen or liver New RBCs made by stem cells in bone marrow

Erythrocyte Disorders Anemia (RBC or Hb Deficiency) Hemorrhagic (Blood Loss) Hemolytic (RBC Destruction) Aplastic ( Bone Marrow Function) Sickle Cell (Inherited Hb Mutation) Polycythemia (Abnormal  in RBCs)  Viscosity & B.P. with  O2 Delivery Cyanosis, Blood Clots Pernicious Anemia – lack intrinsic factor (& poor Vitamin B12 absorption) from stomach mucosa Iron deficiency Anemia – lack of dietary iron, heavy menstrual bleeding, chronic bleeding ulcer

Components - Leukocytes White Blood Cells (WBCs) Defend Against Microbes Use Blood for Transport, But Occur Mostly Outside Circ. System in Tissues Diapedesis – Squeeze through Capillary Walls Ameboid Motion to move once outside bloodstream

Diapedesis of WBCs

Leukocytes - continued Chemotaxis (positive) – Chemicals released from sites of damage or inflammation attract WBCs Phagocytosis – ingestion of bacteria, debris Five Types Based on: Size Nuclear Shape Cytoplasmic Granules Affinity for Stain

Positive Chemotaxis in WBCs

Types of Leukocytes

Leukocyte Types Granulocytes Cytoplasmic Granules Differential Staining of Granules Approx. 2X Size of RBC 3 Types: Neutrophils Eosinophils Basophils

Types of Granulocytes Neutrophils (PMN) 65% of circulating WBCs Nucleus has 2-5 lobes Neutral Rxn to stain (light pink to purple) Phagocytic  in Bacterial Infections

Types of Granulocytes Eosinophils (Acidophils) 2-4% of circulating WBCs Bilobed Nucleus Reddish-to-orange granules Active in Detoxifying Foreign Proteins  in Allergies, Parasitic Infections

Types of Granulocytes Basophils 0.5-1% of circulating WBCs Bilobed Nucleus Blue-violet granules Granules contain histamine & heparin Intensify inflammation

Leukocyte Types Agranulocytes No apparent granules Most variable in size 2 Types: Lymphocytes Monocytes

Types of Agranulocytes Lymphocytes 20-25% of circulating WBCs Smallest WBC Large, spherical nucleus, little cytoplasm Immune response, produce antibodies Include: B-cells, T-cells, & Natural Killer cells

Types of Agranulocytes Monocytes 3-8% of circulating WBCs Kidney-shaped or C-shaped nucleus Abundant cytoplasm Largest leukocyte Differentiate into phagocytic Macrophages

Components - Platelets Cellular fragments of Megakaryocytes (reside in bone marrow) 300,000/mm3 Active in Hemostasis Contain actin & myosin; able to contract Platelets live for 5-9 days. Form from myeloid stem cells + thrombopoietin /hormone produced by liver  megakaryoblasts  megakaryocytes  platelets (2000 – 3000) . Removed by macrophages in spleen & liver.

Hematopoiesis (Hemopoiesis) Process of Blood Cell Formation Occurs in Yolk Sac (embryo), Liver & Spleen (fetus); Red Bone Marrow (adult) Involves Stem Cells (Hemocytoblasts) & Series of Steps Erythropoietin = Kidney Hormone,  RBCs Also in thymus & lymph nodes of fetus. Red bone marrow becomes primary site last 3 months before birth.

Leukocyte Disorders Normal WBC Count 5,000 – 10,000/mm3 Leukemia – Uncontrolled Production of WBCs with Immature WBCs in Circulation Myeloid (  Granulocytes from Myeloid Stem Cells) Lymphoid (  Lymphocytes from Lymphoid Stem Cells)

Hemostasis Stoppage of Bleeding Fast & localized Involves many clotting factors 3 Phases: Vascular Spasm Narrows vessel, decreasing flow & loss Caused by damage to vessel or neurotransmitter from platelets Vascular spasm occurs in arteries & arterioles, and is effective for several minutes to several hours. Calcium ions assist in the activation of a variety of clotting factors. K+ not involved in actual clot formation but is required for the synthesis of 4 clotting factors by liver cells. Thrombolytic agents (streptokinase from bacteria & t-PA a synthetic form of plasmin) Platelets release thromboxanes which stimulate vascular spasms; endothelin, a peptide released from endothelium of vessels also stimulates vascular spasms

Steps in Hemostasis

Hemostasis - continued Platelet Plug Platelets Become Sticky & Adhere to Endothelium, Collagen, & to One Another Coagulation (Blood Clotting) Most Effective, But Delayed 1 – platelets adhere to exposed collagen (mediated by a protein) 2 – once adhered/aggregated, platelets release chemicals (thromboxane & ADP) which activate other platelets, which in turn adhere, aggregate & release same chemicals. 3 – activated platelets produce receptors for fibrinogen & fibrinogen binds many platelets together, forming a platelet plug

Steps in Hemostasis

Coagulation Formation of Prothrombin Activator (PA) PA converts Prothrombin into Thrombin Thrombin converts Fibrinogen into Fibrin Fibrin sticks to damaged blood vessel, forms meshwork Platelets, blood cells stick to meshwork, clot forms Clot retracts, pulling damaged edges together Injured tissues release tissue factor (TF). TF interacts with K+, Ca2+, platelets (PF3 a phospholipid) to form prothrombin activator. Retraction pulls damaged edges of blood vessel back together, protects against infection & promotes healing. Serum leaks from clot during retraction; serum is plasma minus platelets & clotting factors.

Steps in Hemostasis

Abnormal Clot Formation Thrombus – Clot Formed in Uninjured Vessel Embolus – Thrombus, Broken Loose & Moved Pulmonary Embolism (Lung Clot, Formed Elsewhere) Coronary Embolism (Clot in Coronary Vessel, Formed Elsewhere) Thrombi usually form in veins & may dissolve spontaneously. Emboli are not limited to dislodged blood clots; air bubbles, fat from broken bone, debris may act as emboli.

Thrombus in Artery

Human Blood Types Inherited Involves Identifying Antigens on cell membrane of RBCs (Agglutinogens) Must Avoid Agglutination (RBC Clumping due to Antigen-Antibody Reaction) ABO and Rh Typing Significant in Transfusions

ABO Typing - continued ABO Typing Based on 2 Agglutinogens: A Antigen & B Antigen 4 Types: Type A A Antigen Only 41% of US Type B B Antigen Only 9% US The A & B antigens are glycolipids.

ABO Typing - continued Type AB Both A & B Antigens 3% US Universal Recipient Type O Neither Antigen 47% US Universal Donor

ABO Typing - continued Antibodies (Agglutinins) In Plasma Appear Spontaneously After Birth Only produced if the antigen is foreign React with antigen if the 2 are mixed 2 Types: Anti-A (in Types B, O) Anti-B (in Types A, O)

ABO Typing - continued Compatibility involves Matching RBCs of Donor (i.e.Antigens) & Immune System (Potential Antibodies) of Recipient Type A can receive: Type A, Type O Type B can receive: Type B, Type O Type AB can receive: Types A, B, AB, O Type O can Receive: Type O

Blood Typing

Human Blood Types - continued Rh Typing Based on surface antigen on RBC (Rh factor or antigen D) If antigen present, Rh+ If antigen absent, Rh- Antibodies appear in Rh- persons only after exposure. Subsequent exposure results in agglutination.

Rh Typing - continued Hemolytic Disease of the Newborn (HDN) A.K.A Erythroblastosis Fetalis Occurs when Rh- Mom Pregnant with Rh+ Fetus Mixing of Maternal & Fetal Blood occurs at Birth Mom then Starts to Produce Anti-Rh With 2nd Rh+ Fetus, Anti-Rh Passes from Mom to Fetus Fetal RBC Destruction Rhogam Prevents Mom from Producing Anti-Rh