Chapter 17a Circulation Characteristics of Blood RBC and Erythropoiesis

Overview of Vessels Arteries: blood vessels that move AWAY from the heart Veins: vessels that move TOWARD the heart Capillaries: Small vessels created by repeated branching of arteries and veins 1 epithelial cell layer thick allows for gas, waste, and nutrient exchange at the tissue level

Blood Circulation 5. O2 and nutrients diffuse across capillary walls into tissues 6. CO2 and waste move from tissues into vessels 4. Blood leaves left ventricle of the heart via aorta and moves into arteries towards tissues 1. O2 deficient blood moves into veins that enter the right atrium of heart 2. Right ventricle pumps blood through the pulmonary artery, which carries blood to lungs, where it releases CO2 and picks up O2 3. O2 rich blood returns to the heart via pulmonary veins and enters left atrium of heart

Heart Anatomy (pump your blood song) Aortic Valve = L Semi-lunar Valve Pulmonary Valve = R Semi-lunar Valve L Atrioventricular valve = Mitral Valve = Bicuspid Valve R Atrioventricular valve = Tricuspid valve

Heart Valves (Cross Section; Inferior View)

Physical Characteristics of Blood Body’s only fluid tissue Sticky plasma Color: scarlet (O2 rich) to dark red (O2 poor) pH: 7.35–7.45 (slightly basic) Temperature: 38C (100.4F) 8% of total body weight AVG volume: males: 5 - 6 L females: 4 - 5 L

Functions of Blood Distribution: Transportation of Oxygen from lungs to cells Nutrients from intestines to cells Metabolic wastes from cells to lungs and kidneys for elimination Hormones from endocrine glands to target organs

Functions of Blood 2. Regulation: Maintenance of Body temperature pH with buffer proteins and solutes pH imbalances interfere w/ cell activities, causing tissue damage Fluid volume

Functions of Blood 3. Protection: Fights infections Synthesizing and employing antibodies Activating complement proteins Activating WBCs to destroy foreign invaders

Functions of Blood 3. Protection: b. Prevention of blood loss by Activating plasma proteins and platelets Initiating clot formation when a vessel is broken

Composition of Blood Composed of liquid plasma (matrix) and formed elements (cellular)

Composition of Blood Hematocrit = % of RBCs out of total blood volume Males: 47% Females: 45%

Blood Plasma 90% water by volume > 100 solutes, including: 1. Proteins Albumin (liver protein): blood buffer; maintains osmotic pressure Globulins: α, β (liver proteins) : transport lipids, metal ions, fat-soluble vitamins Gamma ɣ: antibodies during immune response Fibrinogen: clotting protein

Blood Plasma 90% water by volume > 100 solutes, including: 2. Lactic acid, urea, creatine 3. Hormones: ex. insulin, erythropoietin, and others 4. Organic nutrients: carbohydrates, amino acids, lipids 5. Electrolytes: Na+, K+, CA2+, Cl-, bicarbonate (HCO3), etc. 6. Respiratory gases: O2 and CO2

Formed Elements Erythrocytes (RBC), leukocytes (WBC), and platelets (for clotting) Only WBCs are complete cells RBCs have no nuclei or organelles platelets are just cell fragments Most survive in the bloodstream for only a few days (RBC: 100 – 120 days) Most are amitotic (do not divide) replaced by stem cells in bone marrow

Components of Formed Blood

Erythrocyte (RBC) Characteristics Biconcave discs  High SA/V ratio (> 30% than spherical) Contributes to blood’s viscosity anucleate (no nucleus), and no organelles, no mitochondria  anaerobic ATP generation; do not use any O2 that they transport Contain spectrin membrane protein on cytoplasmic face  Flexibility Ability to change shape Ease of movement through narrow capillaries

Gas Transport RBCs with > 97% hemoglobin (Hb)  protein used for transport of O2 and CO2 Binding Hb to CO arrests cellular respiration

Hemoglobin (Hb) Structure 4 Globin proteins, each globin bound to a heme group Heme = red pigment w/ an atom of iron (Fe)  binds to O2 and changes to scarlet red Fun Fact: 1 Hb can transport 4 O2 molecules One RBC has 250 million Hb molecules The cell transports 1 billion molecules of O2!

Forms of Hb Oxyhemoglobin – Hb bound to oxygen O2 O2 loading happens in the lungs Deoxyhemoglobin – Hb after O2 diffuses into tissues Carbaminohemoglobin – Hb bound to CO2 CO2 loading happens in the tissues How does loading and unloading of respiratory gasses happen? Watch this video and take notes to find out…

Hematopoiesis Blood Cell Formation Occurs in red bone marrow of: Axial skeleton and girdles Epiphyses of the humerus and femur Hemocytoblasts (adult stem cells of blood): - give rise to all formed elements Erythropoeisis: specific formation of RBC

Erythropoiesis Developmental Pathway Phase 1: Ribosome synthesis for globulin protein formation Phase 2: Hemoglobin accumulates Phase 3: Nucleus and Organelles eject  Reticulocytes: still w/ remnants of RER and ribosomes  Erythrocytes: complete RBC, all ribosomes degraded by enzymes Fun Fact: process takes 15 days; 2 million RBCs made/minute

Dietary Needs 1. Iron (Fe) 2. vitamin B12 and folic acid 65% of Fe in body is in Hb Remainder stored in liver, spleen, marrow as protein-iron complexes: ferritin and hemosiderin free iron ions Fe2+ and Fe3+ are toxic, increasing free radicals, causing cell death 2. vitamin B12 and folic acid For normal DNA synthesis 3. Lipids, CHO, Amino Acids Iron lost daily via waste 0.9 mg/day lost by men 1.7 mg by women (menstrual bleeding)

Control of Erythropoiesis Delicate balance btw RBC formation and destruction Too few RBC hypoxia (lack of O2 in tissues) Too many RBC  blood is too viscous Hormonal Controls Erythropoietin (EPO): hormone made by kidneys directly stimulates RBC formation EPO released in response to: Tissue hypoxia Increased tissue demand for O2

EPO Mechanism Imbalance Start Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Homeostasis: Normal blood oxygen levels Increases O2-carrying ability of blood Imbalance Reduces O2 levels in blood Kidney (and liver to a smaller extent) releases erythropoietin Enhanced erythropoiesis increases RBC count Erythropoietin stimulates red bone marrow

Fate of Erythrocytes RBC w/ no nuclei, no DNA, no new proteins Fragile, lose shape, becomes rigid Hb degenerate RBCs often trapped and fragmented in spleen Dying RBC engulfed and destroyed by macrophages Components of Hb are broken down and some parts recycled for reuse.

Life Cycle of Erythrocytes Low O2 levels in blood stimulate kidneys to produce erythropoietin. Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. New erythrocytes enter bloodstream; function about 120 days. Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. Hemoglobin

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin 2. Globin metabolized into AA and released into blood Amino acids

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin 2. Globin metabolized into AA and released into blood 3. Heme degraded into yellow pigment Bilirubin Bilirubin Iron stored as ferritin, hemosiderin Amino acids

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin 2. Globin metabolized into AA and released into blood 3. Heme degaded into yellow pigment Bilirubin Bilirubin Iron stored as ferritin, hemosiderin Amino acids 4. Iron stored safely as ferritin and hemosiderin in liver

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin 2. Globin metabolized into AA and released into blood 3. Heme degaded into yellow pigment Bilirubin Bilirubin Iron stored as ferritin, hemosiderin Amino acids 4. Iron stored safely as ferritin and hemosiderin in liver 5. Iron is bound to transferrin protein and released into circulation for erythropoiesis

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin 2. Globin metabolized into AA and released into blood 3. Heme degaded into yellow pigment Bilirubin Bilirubin Iron stored as ferritin, hemosiderin Amino acids 4. Iron stored safely as ferritin and hemosiderin in liver 5. Iron is bound to transferrin protein and released into circulation for erythropoiesis 6. The liver secretes bilirubin into intestine with bile from the gall bladder 7. The intestines metabolize it, and it leaves the body in feces as a pigment called stercobilin (brown poop) Bilirubin is metabolized by intestines and excreted in feces

Destruction of Hb 1. Heme and Globin separated Hemoglobin Heme Globin 2. Globin metabolized into AA and released into blood 3. Heme degaded into yellow pigment Bilirubin Bilirubin Iron stored as ferritin, hemosiderin Amino acids 4. Iron stored safely as ferritin and hemosiderin in liver 5. Iron is bound to transferrin protein and released into circulation for erythropoiesis 6. The liver secretes bilirubin into intestine with bile from the gall bladder 7. The intestines metabolize it, and it leaves the body in feces as a pigment called stercobilin (brown poop) Bilirubin is metabolized by intestines and excreted in feces Circulation Food nutrients, including amino acids, Fe, B12, and folic acid are absorbed from intestine and enter blood 8. Raw materials are made available in blood for erythrocyte synthesis.

Erythrocyte Disorders Polycythemia – excess RBCs that increase blood viscosity Causes clotting in small capillaries, leading to Stroke Heart Attack 3 types: Polycythemia vera: bone marrow disease 20 polycythemia: people living at high altitudes. Blood doping : enhancing RBC numbers to increase athletic performance removing blood for a few days, then re-infusing it.

Erythrocyte Disorders 2. Anemia – blood has abnormally low oxygen-carrying capacity Symptom; not a disease Blood oxygen levels cannot support normal metabolism Causes fatigue, paleness, shortness of breath, chills

Anemia: Insufficient Erythrocytes Hemorrhagic anemia: due to acute or chronic loss of blood (ex. stab wounds) Hemolytic anemia: RBCs prematurely destroyed (ex. abnormal proteins of RBCs, abnormal immune system, parasitic) Aplastic anemia: bone marrow failure: does not produce enough RBCs

Anemia: Decreased Hb Content Iron-deficiency anemia results from: hemorrhagic anemia Poor diet: lack of iron-containing foods Impaired iron absorption Pernicious anemia results from: Inability to absorb vitamin B12 Not enough intrinsic factor (protein that aids in B12 absorption)

Anemia: Abnormal Hemoglobin Thalassemias – absent or faulty globin chain in Hb RBCs are thin, delicate, and deficient in Hb Can lead to hemolytic anemia Sickle-cell anemia – from abnormal Hb-S Hb-S due to genetic mutation of a single amino acid (substitution), causing sickle-shape of RBC Both conditions offered some protection from malaria