SCIT 1408 Applied Human Anatomy and Physiology II - Blood Ch 17

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Blood

Figure 17.10

The only fluid tissue


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


Components of Whole Blood

Figure 17.1

Plasma expanders restore blood volume, not O2

Packed cells restore O2, maybe not volume


Physical Characteristics and Volume Blood is a sticky, opaque fluid with a metallic taste Color varies from scarlet (> O2) to dark red (<O2) The pH of blood is 7.35–7.45 Temperature is 38C Blood accounts for approximately 8% of body

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

females


Functions of Blood Delivers Oxygen to tissues- from lungs Picks up Carbon dioxide from the tissues- to

lungs

Distribution Regulation Protection


Functions of Blood

1. Distribution of : O2 and nutrients to body cells

Metabolic wastes to the lungs and kidneys for elimination

Hormones from endocrine organs to target organs


Functions of Blood

2. Regulation of Body temperature by absorbing and distributing

heat Normal pH using buffers Adequate fluid volume in the circulatory system


Protection Hemostasis

Activating plasma proteins & platelets Clot formation when a vessel is broken

Immune functions Antibodies- B cells Activating complement proteins Activating WBCs to defend the body against

foreign invaders - Tcells


Blood Plasma Nitrogenous by-products of metabolism—lactic

acid, urea, creatinine Nutrients—glucose, carbohydrates, amino acids

Electrolytes—Na+, K+, Ca2+, Cl–, HCO3–

Respiratory gases—O2 and CO2

Hormones


Blood Plasma 90% water Proteins are mostly produced by the liver

60% albumin 36% globulins 4% fibrinogen


Formed Elements Erythrocytes, leukocytes, and platelets make up the

formed elements WBCs - cells RBCs - no nuclei, few organelles; “a sack of hgb” platelets - cell fragments; “thrombocytes”


Megakaryocyte


Components of Whole Blood

Figure 17.2


Erythrocytes (RBCs)

Figure 17.3

No nucleus


Erythrocytes Structural characteristics contribute to gas transport

Biconcave shape—huge surface area relative to volume

> 97% hemoglobin (not counting water) No mitochondria; ATP production is anaerobic; no

O2 is used in generation of ATP A superb example of complementarity of structure

and function!


Structure of Hemoglobin

Figure 17.4


Hemoglobin (Hb) Oxyhemoglobin – oxygen bound to Hgb (or Hb)

Deoxyhemoglobin - oxygen dissociates from hgb & diffuses into tissues (reduced Hgb)

Carbaminohemoglobin – carbon dioxide bound Hgb

PLAY InterActive Physiology ®: Respiratory System: Gas Transport, pages 3–13


Erythrocyte Function RBCs are dedicated to respiratory gas transport Hemoglobin binds reversibly with oxygen


Hematopoiesis Hematopoiesis

Red bone marrow of the: Axial skeleton (sternum) and girdles (iliac crest) Epiphyses of the humerus and femur

Hemocytoblasts give rise to all formed elements “Pluripotent cell” or stem cell


Production of Erythrocytes: Erythropoiesis

Figure 17.5

Bone marrow

Peripheral Circulation


Regulation of Erythropoiesis

Normal RBC: 4.2-6.1 x 106/ ul whole blood < RBCs = tissue hypoxia > RBCs = > blood viscosity

Erythropoietin (kidneys) – stimulates RBC production RBC production Requires:

iron amino acids B vitamins


Homeostasis: Normal blood oxygen levels

IncreasesO2-carryingability of blood

Erythropoietinstimulates redbone marrow

Reduces O2 levelsin blood

Kidney (and liver to a smallerextent) releases erythropoietin

Enhancederythropoiesisincreases RBC count

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

Start

Imbalance

Imbalance

Erythropoietin Mechanism

Figure 17.6


Hemoglobin

Aminoacids

Globin

Raw materials aremade available inblood for erythrocytesynthesis.

Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis

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

Heme

Circulation

Iron storedas ferritin,hemosiderin

Bilirubin

Bilirubin is picked up fromblood by liver, secreted intointestine in bile, metabolizedto stercobilin by bacteriaand excreted in feces

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.

1

2

3

4

5

6

Figure 17.7

RBC life cycle- (recycle 80-120 days)


Anemias - < RBC (normocytic) Hemorrhagic anemia Hemolytic anemia Aplastic anemia

Signs/symptoms include fatigue, paleness, shortness of breath, and chills

Erythrocyte Disorders – Types of Anemia


Iron-deficiency anemia : (microcytic) (from hemorrhagic anemia) < dietary iron Impaired iron absorption

Pernicious anemia : (macrocytic) Deficiency of vitamin B12

Lack of intrinsic factor needed for absorption of B12

Treatment is intramuscular injection of B12; application of Nascobal

Types of Anemia : Decreased Hemoglobin Content


Types of Anemia: Abnormal Hemoglobin Thalassemias –

defective globin chain gene(s) Many forms Mediterranean decent

Sickle-cell anemia defective globin chain gene with a single aa

substitution This defect causes RBCs to become sickle-shaped

in < oxygen & > oxygen demand situations

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.8

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.


Polycythemia Polycythemia – excess RBCs that increase blood

viscosity Three main polycythemias are:

Polycythemia vera Secondary polycythemia – test pilots Blood doping – atheletes

RX: phlebotomies


Leukocytes (WBCs) Normal WBC: 5-10,000/ ul whole blood

< WBC - leukopenia from bone marrow suppression leads to infection never normal

> WBC – leukocytosis; > 11,000/ul From: infection, exercise, stress, leukemia

Diapedesis- leaks from blood into tissues


Percentages of Leukocytes

Figure 17.9


Granulocytes All have granules, segmented nuclei, and are

phagocytic

Neutrophils – “segs”; first ones to site of inflammation

Eosinophils Basophils

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.10 (a-c)

(a) Neutrophil; multilobed nucleus

(b) Eosinophil; bilobed nucleus, red cytoplasmic granules

(c) Basophil; bilobed nucleus, purplish-black cytoplasmic granules


Neutrophils 50-70% total WBC > Neutrophils – bacterial infections Very active in inflammation

diapedesis


1–4% of WBCs Red-orange granules (acidophilic) > : allergies, parasitic infections

Eosinophils


0.5% of WBCs purplish-black (basophilic) granules;

Histamine

Called mast cells in tissues

Basophils

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.10d, e

(d) Small lymphocyte; large spherical nucleus

(e) Monocyte; kidney-shaped nucleus


25-45% WBCs > in viral infections Large, dark-purple, circular nuclei with a thin rim

of blue cytoplasm Are found mostly enmeshed in lymphoid tissue

(some circulate in the blood) T cells and B cells

T cells function in cell mediated immune response B cells produce antibodies in humoral immune

response

Lymphocytes


4–8% WBC largest leukocytes Macrophages in tissue Phagocytosis, antigen processing or presentation,

inflammation

Monocytes


Leukocytes

Figure 17.10


Leukopoiesis- interleukins & (CSFs) Interleukins are numbered (e.g., IL-1, IL-2),

whereas CSFs are named for the WBCs they stimulate (e.g., granulocyte-CSF stimulates granulocytes)

Macrophages and T cells are the most important sources of cytokines – cytotoxic factors

Many hematopoietic hormones are used clinically to stimulate bone marrow

Production of Leukocytes


(a) (b) (c) (d) (e)

Hemocytoblast

Myeloid stem cell Lymphoid stem cell

Myeloblast MyeloblastMyeloblast Lymphoblast

Stem cells

Committedcells

Promyelocyte PromyelocytePromyelocyte Promonocyte Prolymphocyte

Eosinophilicmyelocyte

Neutrophilicmyelocyte

Basophilicmyelocyte

Eosinophilicband cells

Neutrophilicband cells

Basophilicband cells

Develop-mentalpathway

Eosinophils NeutrophilsBasophils

Granular leukocytes

Plasma cells

Some become

Monocytes Lymphocytes

Macrophages (tissues)

Agranular leukocytesSome become

Figure 17.11


Leukocytes Disorders: Leukemias Leukemias- WBC cancers

Myelocytic leukemia – myeloblasts Lymphocytic leukemia – lymphocytes Acute leukemia- blast-type cells; children Chronic leukemia – more mature cells; adults

Childhood leukemia has high cure rate


Megakaryocyte


Stem cell Developmental pathway

Hemocytoblast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets

Figure 17.12

Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as

shown.

Bone marrow


Hemostasis “blood stop” – 3 Phases Involved

1. Vascular spasms – immediate vasoconstriction in response to injury

2. Platelet plug formation

3. Coagulation – cascade of rxns ending in fibrin clot


Platelet Plug Formation Platelets do not stick to each other or to blood vessels Upon damage to blood vessel endothelium platelets:

With the help of von Willebrand factor (VWF) adhere to collagen

Are stimulated by thromboxane A2 Stick to exposed collagen fibers and form a platelet plug Release serotonin and ADP, which attract still more

platelets The platelet plug is limited to the immediate area of injury

by prostacyclin


A set of reactions in which blood is transformed from a liquid to a gel

Coagulation follows intrinsic and extrinsic pathways The final three steps of this series of reactions are:

Prothrombin activator is formed Prothrombin is converted into thrombin Thrombin catalyzes the joining of fibrinogen

into a fibrin mesh

Coagulation


Coagulation

Figure 17.13a


Detailed Events of Coagulation

Figure 17.13b



Clot Retraction and Repair Clot retracts within 30-60’

Proteins in platelets squeeze serum from clot Repair

Platelet-derived growth factor (PDGF) – repairs vessel wall

Fibroblasts form a connective tissue patch Stimulated by vascular endothelial growth factor

(VEGF), endothelial cells multiply and restore the endothelial lining


Fibrinolysis & Control of Clot Formation

As soon as clot is formed, a fibrinolytic process begins to:

1. inhibit growth of clot

2. to break down the clot (within 2 days)

tPA- tissue plasminogen activator = clot buster Two mechanisms prevent clot growth

Swift removal of clotting factors Inhibition of activated clotting factors

Hemostasis vs Fibrinolysis


Unnecessary clotting is prevented by endothelial lining the blood vessels

Platelet adhesion is prevented by: The smooth endothelial lining of blood vessels- no

plaques, rough spots

Heparin and PGI2 secreted by endothelial cells

Vitamin E quinone, a potent anticoagulant

INFLAMMATION may lead to > clots

Factors Preventing Undesirable Clotting


Hemostasis Disorders:Thromboembolytic Conditions Thrombus – a clot that develops and persists in an

unbroken blood vessel Thrombi can block circulation, resulting in tissue

death Coronary thrombosis – thrombus in blood vessel of

the heart


Hemostasis Disorders:Thromboembolytic Conditions Embolus – a clot on the move (in blood)

Can be fat, cancer cells, etc.

Thromboembolus- blood clot on the move Pulmonary emboli can impair the ability of the

body to obtain oxygen Cerebral emboli can cause strokes


Substances used to prevent undesirable clots: Aspirin – inhibits prostaglandin - thromboxane A2

Heparin – an anticoagulant used clinically for pre- and postoperative cardiac care

Warfarin – used for those prone to atrial fibrillation

Prevention of Undesirable Clots


Disseminated Intravascular Coagulation (DIC): widespread clotting in intact blood vessels

Poor prognosis

Residual blood cannot clot- thrombin tied up in clot Blockage of blood flow and severe bleeding follows Most common in:

Septic shock A complication of pregnancy Incompatible blood transfusions

Hemostasis Disorders


Thrombocytopenia – platelets < 50,000/ul Petechiae Caused by suppression or destruction of bone

marrow (e.g., malignancy, radiation) Treated with whole blood transfusions, plasma

exchanges

Hemostasis Disorders: Bleeding Disorders


Liver disease- Can’t make procoagulants Can’t make vitamin K

Gene defects in genes for clotting factors: Hemophilia A - factor VIII Hemophilia B – factor IX Hemophilia C – factor XI (mild)

Hemostasis Disorders: Bleeding Disorders


Blood Transfusions Whole blood transfusions are used:

When blood loss is substantial In treating thrombocytopenia

Packed red cells (cells with plasma removed) are used to treat anemia


RBC membranes have glycoprotein antigens on their external surfaces

These antigens are: Unique to the individual Recognized as foreign if transfused into another

individual Promoters of agglutination and are referred to as

agglutinogens Presence or absence of these antigens is used to

classify blood groups

Human Blood Groups


Humans have 30 varieties of naturally occurring RBC antigens

ABO and Rh antigens are Landsteiner group Other blood groups (M, N, Dufy, Kell, and Lewis)

Blood Groups


ABO Blood Groups

Table 17.4


There are eight different Rh agglutinogens, three of which (C, D, and E) are common

Presence of the Rh agglutinogens on RBCs is indicated as Rh+

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

However, if an Rh– individual receives Rh+ blood, anti-Rh antibodies form

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

Rh Blood Groups


Hemolytic Disease of the Newborn Erythroblastosis fetalis or HDN: Rh+ antibodies

of a sensitized Rh– mother cross the placenta and attack and destroy the RBCs of an Rh+ baby

Usually first birth ok RhoGAM – blocks antibodies against Rh+ fetus RX- pre-birth transfusions; exchange transfusions

after birth


Life threatening- mismatched blood is infused Antigens (cells) & antibodies (plasma) agglutinate:

Diminished oxygen-carrying capacity Clumped cells that impede blood flow Ruptured RBCs- release hgb Hgb ppts in kidneys- renal failure

Transfusion Reactions


Blood type being tested RBC agglutinogens Serum Reaction

Anti-A Anti-B

AB A and B + +

B B – +

A A + –

O None – –

Blood Typing

Unknown cells Known antisera


SerumAnti-A

RBCs

Anti-BType 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)


Restoring Fluid Volume Hypovolemic shock Restore fluid volume-Plasma, plasma expanders

Dextran, plasminate, human serum albumin

OR the following may be better Normal saline Electrolyte solution – Ringer’s


Diagnostic Blood Tests CBC

# RBCs, WBCs, Hgb, Hct, MCV, MCHC Differential

Microscopic examination reveals variations in size and shape of RBCs, indications of anemias

Hct Serum chemistry analysis can provide a

comprehensive picture of one’s general health status in relation to normal values; i.e. blood glucose


Diagnostic Blood Tests Differential WBC count Prothrombin time and platelet counts assess

hemostasis SMAC, a blood chemistry profile Complete blood count (CBC)


Developmental Aspects- Hematopoiesis Fetal blood cells – formed in yolk sac, liver, spleen By 7th month- in red bone marrow Fetus – HbF; > affinity for oxygen than adult

hemoglobin


Developmental Aspects Age-related blood problems result from disorders

of the heart, blood vessels, and the immune system Increased leukemias are thought to be due to the

waning deficiency of the immune system Abnormal thrombus and embolus formation

reflects the progress of atherosclerosis

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SCIT 1408 Applied Human Anatomy and Physiology II - Blood Ch 17

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