Chapter 17aCirculation

Characteristics of BloodRBC and Erythropoiesis

Overview of VesselsArteries: 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

4. Blood leaves left ventricle of the heart via aorta and moves into arteries towards tissues

5. O2 and nutrients diffuse across capillary walls into tissues

6. CO2 and waste move from tissues into vessels

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)

R Atrioventricular valve= Tricuspid valve

L Atrioventricular valve= Mitral Valve = Bicuspid Valve

Pulmonary Valve = R Semi-lunar Valve

Aortic Valve = L Semi-lunar 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: 38C (100.4F)• 8% of total body weight• AVG volume: – males: 5 - 6 L– females: 4 - 5 L

Functions of Blood

1. 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 Blood2. 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: a. Fights infections– Synthesizing and

employing antibodies– Activating complement

proteins– Activating WBCs to

destroy foreign invaders

Functions of Blood3. 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) andformed 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, creatine3. Hormones: ex. insulin, erythropoietin, and others4. Organic nutrients: carbohydrates, amino acids, lipids5. 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 FlexibilityAbility to change shapeEase 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 enzymesFun Fact: process takes 15 days; 2 million RBCs made/minute

Dietary Needs1. Iron (Fe)• 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

Homeostasis: Normal blood oxygen levels

IncreasesO2-carryingability of blood

Erythropoietinstimulates redbone marrow

Reduces O2 levelsin blood

Kidney (and liver to a smallerextent) releases erythropoietinEnhanced

erythropoiesisincreases RBC count

Stimulus: Hypoxia due todecreased RBC count,decreased amount of hemoglobin, or decreased availability of O2

StartImbalance

Imbalance

Fate of Erythrocytes• RBC w/ no nuclei, no DNA, no new proteins

Fragile, lose shape, becomes rigidHb 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.

Hemoglobin

Erythropoietin levelsrise in blood.

Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.

New erythrocytesenter bloodstream;function about120 days.

Low O2 levels in blood stimulatekidneys to produce erythropoietin.

Aged and damaged redblood cells are engulfed bymacrophages of liver, spleen,and bone marrow; the hemoglobinis broken down.

Life Cycle of Erythrocytes

Hemoglobin

GlobinHeme

Destruction of Hb1. Heme and Globin separated

Hemoglobin

Aminoacids

GlobinHeme

Destruction of Hb

2. Globin metabolized into AA and released into blood

1. Heme and Globin separated

Hemoglobin

Aminoacids

GlobinHeme

Iron storedas ferritin,hemosiderin

Bilirubin

Destruction of Hb1. Heme and Globin separated

2. Globin metabolized into AA and released into blood

3. Heme degraded into yellow pigment Bilirubin

Hemoglobin

Aminoacids

GlobinHeme

Iron storedas ferritin,hemosiderin

Bilirubin

4. Iron stored safely as ferritin and hemosiderin in liver

Destruction of Hb1. Heme and Globin separated

3. Heme degaded into yellow pigment Bilirubin

2. Globin metabolized into AA and released into blood

Hemoglobin

Aminoacids

Globin

5. Iron is bound to transferrin protein and released into circulationfor erythropoiesis

Heme

Iron storedas ferritin,hemosiderin

Bilirubin

Destruction of Hb1. Heme and Globin separated

3. Heme degaded into yellow pigment Bilirubin

4. Iron stored safely as ferritin and hemosiderin in liver

2. Globin metabolized into AA and released into blood

Hemoglobin

Aminoacids

Globin

5. Iron is bound to transferrin protein and released into circulationfor erythropoiesis

Heme

Iron storedas ferritin,hemosiderin

Bilirubin

Bilirubin is metabolized by intestines and excreted in feces

Destruction of Hb1. Heme and Globin separated

3. Heme degaded into yellow pigment Bilirubin

4. Iron stored safely as ferritin and hemosiderin in liver

2. Globin metabolized into AA and released into blood

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)

Hemoglobin

Aminoacids

Globin

8. Raw materials are made available inblood for erythrocyte synthesis.

5. Iron is bound to transferrin protein and released into circulationfor erythropoiesis

Food nutrients,including aminoacids, Fe, B12,and folic acidare absorbedfrom intestineand enter blood

Heme

Circulation

Iron storedas ferritin,hemosiderin

Bilirubin

Bilirubin is metabolized by intestines and excreted in feces

3. Heme degaded into yellow pigment Bilirubin

4. Iron stored safely as ferritin and hemosiderin in liver

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)

1. Heme and Globin separated

2. Globin metabolized into AA and released into blood

Destruction of Hb

Erythrocyte Disorders1. 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

• 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: Decreased Hb Content

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