copyright © 2010 pearson education, inc. blood composition blood: a fluid connective tissue...

Copyright © 2010 Pearson Education, Inc.

Blood Composition

• Blood: a fluid connective tissue composed of

• Plasma

• Formed elements

• Erythrocytes (red blood cells, or RBCs)

• Leukocytes (white blood cells, or WBCs)

• Platelets


Blood Composition

• Hematocrit

• Percent of blood volume that is RBCs

• 47% ± 5% for males

• 42% ± 5% for females

Copyright © 2010 Pearson Education, Inc. Figure 17.1

1 Withdrawblood and placein tube.

2 Centrifuge theblood sample.

Plasma• 55% of whole blood• Least dense componentBuffy coat• Leukocytes and platelets• <1% of whole bloodErythrocytes• 45% of whole blood• Most dense component

Formedelements


Physical Characteristics and Volume

• Sticky, opaque fluid

• Color scarlet to dark red

• pH 7.35–7.45

• 38C

• ~8% of body weight

• Average volume: 5–6 L for males, and 4–5 L for females


Functions of Blood

1. Distribution of ?

3. Protection against

• Blood loss

• Plasma proteins and clot formation

• Infection

• Antibodies

• WBCs defend against foreign invaders


Blood Plasma

• 90% water

• Proteins are mostly produced by the liver

• 60% albumin

• 36% globulins

• 4% fibrinogen


Platelets

Neutrophils Lymphocyte

Erythrocytes Monocyte


2.5 µm

7.5 µm

Side view (cut)

Top view


Erythrocytes

• Structural characteristics contribute to gas transport

• Shape—huge surface area

• >97% hemoglobin

• No mitochondria

• No nucleus


Hemegroup

(a) Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups.

(b) Iron-containing heme pigment.a Globin chains

b Globin chains


Hemoglobin (Hb)

• O2 loading in the lungs

• Produces oxyhemoglobin (ruby red)

• O2 unloading in the tissues

• Produces deoxyhemoglobin or reduced hemoglobin (dark red)

• CO2 loading in the tissues

• Produces carbaminohemoglobin (carries 20% of CO2 in the blood)


Hematopoiesis

• Hematopoiesis; blood cell formation

• Occurs in red bone marrow, girdle and proximal epiphyses of humerus and femur


Stem cell

HemocytoblastProerythro-blast

Earlyerythroblast

Lateerythroblast Normoblast

Phase 1Ribosomesynthesis

Phase 2Hemoglobinaccumulation

Phase 3Ejection ofnucleus

Reticulo-cyte

Erythro-cyte

Committedcell

Developmental pathway

Erythropoiesis:red blood cell production


Regulation of Erythropoiesis

• Too few RBCs leads to tissue hypoxia

• Too many RBCs increases blood viscosity

• Balance depends on

• Hormonal controls

• Adequate supplies of iron, amino acids, and B vitamins


Hormonal Control of Erythropoiesis

• Erythropoietin (EPO)

• Direct stimulus for erythropoiesis

• Released by kidneys in response to hypoxia

• Testosterone also enhances EPO production, resulting in higher RBC counts in males


Hormonal Control of Erythropoiesis

• Causes of hypoxia

• Hemorrhage or increased RBC destruction reduces RBC numbers

• Insufficient hemoglobin (e.g., iron deficiency)

• Reduced availability of O2 (e.g., high altitudes)


Kidney (and liver toa smaller extent)releaseserythropoietin. Erythropoietin

stimulates redbone marrow.

Enhancederythropoiesisincreases RBCcount.

O2- carryingability of bloodincreases.

Homeostasis: Normal blood oxygen levels

Stimulus:Hypoxia (low bloodO2- carrying ability)

due to• Decreased

RBC count• Decreased amount

of hemoglobin• Decreased

availability of O2

1

2

3

4

5

IMBALANCE

IMBALANCE


Fate and Destruction of Erythrocytes

• Life span: 100–120 days

• Macrophages engulf dying RBCs in spleen

• Iron is salvaged for reuse

• Heme is degraded to yellow bilirubin

• Liver secretes bilirubin (in bile)) into the intestines

• Degraded pigment leaves the body in feces as stercobilin


Low O2 levels in blood stimulate kidneys to produce erythropoietin.

1

Erythropoietin levels risein blood.2

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

3

Aged and damagedred blood cells areengulfed by macrophagesof liver, spleen, and bonemarrow; the hemoglobinis broken down.

5

New erythrocytesenter bloodstream;function about 120 days.

4

Raw materials aremade available in bloodfor erythrocyte synthesis.

6

Hemoglobin

Aminoacids

Globin

Iron is bound totransferrin and releasedto blood from liver asneeded for erythropoiesis.

Food nutrients,including amino acids,Fe, B12, and folic acid,are absorbed fromintestine and enterblood.

Heme

Circulation

Iron storedas ferritin,hemosiderin

Bilirubin

Bilirubin is picked up from bloodby liver, secreted into intestine inbile, metabolized to stercobilin bybacteria, and excreted in feces.


Erythrocyte Disorders

• Anemia: abnormally low O2-carrying capacity

• A sign rather than a disease itself

• Blood O2 cannot support normal metabolism

• Accompanied by fatigue, paleness, shortness of breath, and chills


Causes of Anemia

1. Insufficient erythrocytes

• Hemorrhagic anemia: acute or chronic loss of blood

• Hemolytic anemia: RBCs rupture prematurely

• Aplastic anemia: destruction or inhibition of red bone marrow


Causes of Anemia

2. Low hemoglobin content

• Iron-deficiency anemia

• Secondary result of hemorrhagic anemia or

• Inadequate intake of iron-containing foods or

• Impaired iron absorption


Causes of Anemia

• Pernicious anemia

• Deficiency of vitamin B12

• Lack of intrinsic factor needed for absorption of B12

• Treated by intramuscular injection of B12


Causes of Anemia

• Sickle-cell anemia

• Defective gene codes for abnormal hemoglobin (HbS)

• Causes RBCs to become sickle shaped in low-oxygen situations


1 2 3 4 5 6 7 146

1 2 3 4 5 6 7 146

(a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain.

(b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin.


Erythrocyte Disorders

• Polycythemia: excess of RBCs that increase blood viscosity

• Results from:

• Polycythemia—bone marrow cancer

• Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases

• Blood doping


Formedelements

Platelets

Leukocytes

Erythrocytes

DifferentialWBC count(All total 4800 –10,800/l)

Neutrophils (50 – 70%)

Lymphocytes (25 – 45%)

Eosinophils (2 – 4%)

Basophils (0.5 – 1%)

Monocytes (3 – 8%)

Agranulocytes

Granulocytes


Leukopoiesis

• Production of WBCs

• Stimulated by chemical messengers from bone marrow and mature WBCs


Hemocytoblast

Myeloid stem cell Lymphoid stem cell

Myeloblast Myeloblast MonoblastMyeloblast Lymphoblast

Stem cells

Committedcells

Promyelocyte PromyelocytePromyelocyte Promonocyte Prolymphocyte

Eosinophilicmyelocyte

Neutrophilicmyelocyte

Basophilicmyelocyte

Eosinophilicband cells

Neutrophilicband cells

Basophilicband cells

Developmentalpathway

Eosinophils NeutrophilsBasophils

Granular leukocytes

(a) (b) (c) (d) (e)Monocytes Lymphocytes

Agranular leukocytes

Some becomeSomebecome


Leukocyte Disorders

• Leukopenia

• Abnormally low WBC count—drug induced

• Leukemias

• Cancerous conditions involving WBCs

• Named according to the abnormal WBC clone involved

• Myelocytic leukemia involves myeloblasts

• Lymphocytic leukemia involves lymphocytes

• Acute leukemia involves blast-type cells and primarily affects children

• Chronic leukemia is more prevalent in older people


Leukemia

• Bone marrow totally occupied with cancerous leukocytes

• Immature nonfunctional WBCs in the bloodstream

• Death caused by internal hemorrhage and overwhelming infections

• Treatments include irradiation, antileukemic drugs, and stem cell transplants


Platelets

• Form a temporary platelet plug that helps seal breaks in blood vessels

• Circulating platelets are kept inactive and mobile by NO and prostacyclin from endothelial cells of blood vessels


Stem cell Developmental pathway

Hemocyto-blast Megakaryoblast

PromegakaryocyteMegakaryocyte Platelets


Hemostasis

• Fast series of reactions for stoppage of bleeding

1. Vascular spasm

2. Platelet plug formation

3. Coagulation (blood clotting)


Vascular Spasm

• Vasoconstriction of damaged blood vessel

• Triggers

• Direct injury

• Chemicals released by endothelial cells and platelets

• Pain reflexes


Collagenfibers

Platelets

Fibrin

Step Vascular spasm• Smooth muscle contracts, causing vasoconstriction.

Step Platelet plugformation

• Injury to lining of vessel exposes collagen fibers; platelets adhere.

• Platelets release chemicals that make nearby platelets sticky; platelet plug forms.

Step Coagulation• Fibrin forms a mesh that traps red blood cells and platelets, forming the clot.

1

2

3

Copyright © 2010 Pearson Education, Inc. Figure 17.14 (1 of 2)

Vessel endothelium ruptures,exposing underlying tissues(e.g., collagen)

PF3

released byaggregated

platelets

XII

XI

IX

XIIa

Ca2+

Ca2+

XIa

IXa

Intrinsic pathwayPhase 1Tissue cell traumaexposes blood to

Platelets cling and theirsurfaces provide sites formobilization of factors

Extrinsic pathway

Tissue factor (TF)

VII

VIIa

VIII

VIIIa

Ca2+

X

Xa

Prothrombinactivator

PF3

TF/VIIa complexIXa/VIIIa complex

V

Va

Copyright © 2010 Pearson Education, Inc. Figure 17.14 (2 of 2)

Ca2+

Phase 2

Phase 3

Prothrombinactivator

Prothrombin (II)

Thrombin (IIa)

Fibrinogen (I)(soluble)

Fibrin(insolublepolymer) XIII

XIIIa

Cross-linkedfibrin mesh


Thromboembolytic Conditions

• Prevented by

• Aspirin

• Antiprostaglandin that inhibits thromboxane A2

• Heparin

• Anticoagulant used clinically for pre- and postoperative cardiac care

• Warfarin

• Used for those prone to atrial fibrillation


Bleeding Disorders

• Hemophilias include several similar hereditary bleeding disorders

• Hemophilia A: most common type (77% of all cases); due to a deficiency of factor VIII

• Hemophilia B: deficiency of factor IX

• Hemophilia C: mild type; deficiency of factor XI

• Symptoms include prolonged bleeding, especially into joint cavities

• Treated with plasma transfusions and injection of missing factors


ABO Blood Groups

• Types A, B, AB, and O

• Based on the presence or absence of two agglutinogens (A and B) on surface of RBCs

• Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present


Rh Blood Groups

• Anti-Rh antibodies are not spontaneously formed in Rh– individuals

• Anti-Rh antibodies form if an Rh– individual receives Rh+ blood

• A second exposure to Rh+ blood will result in a typical transfusion reaction

• RhoGAM containing anti-Rh can prevent the Rh– mother from becoming sensitized


ABO Blood Typing

Blood Type Being Tested

RBC Agglutinogens

Serum Reaction

Anti-A Anti-B

AB A and B + +

B B – +

A A + –

O None – –


SerumAnti-A

RBCs

Anti-B

Type AB (containsagglutinogens A and B;agglutinates with bothsera)

Blood being tested

Type A (containsagglutinogen A;agglutinates with anti-A)

Type B (containsagglutinogen B;agglutinates with anti-B)

Type O (contains noagglutinogens; does notagglutinate with eitherserum)

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