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Blood

General Characteristics of Blood

Connective Tissue

Cells--formed elements

Matrix--plasma

No collagen or elastic fibers

Soluble fibrinogen becomes

insoluble fibrin fibers whenblood clots

Hematocrit

Separate formed elements

from plasma

45% formed elements55% plasma

Erythrocytes majority of formed elements

Buffy coat—thin layer of whiteblood cells & platelets

Physical Characteristics

Scarlet to dark red--O2 content

Denser, more viscous than H2O

pH--7.35-7.45

Temperature--38o C, 100.4oF

Quantity--8% of body weight

Males: 5-6 L Females: 4-5 L

Functions

Distribution

Oxygen, nutrients, wastes,

hormones

Regulation

Temperature, pH, fluid volume

Protection

Fluid loss (clotting), infection

Blood Plasma

Straw-colored

Composition

90% water, 10% solutes

Solutes

8% protein (albumin)

2% nitrogenous wastes,nutrients, electrolytes

respiratory gases

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Formed Elements

Erythrocytes--RBCs, red blood cells

Leukocytes--WBCs, white blood cells

Thrombocytes--platelets

Erythrocytes--RBCs

Contain hemoglobin--Carry oxygen

Major contributor to blood viscosity

Normal values

Males--5 X 106 / cu mm

Females--4.5 X 106 / cu mm

HematopoiesisFormation of Blood Cells

Bone marrow

Hemocytoblast or

Hemopoietic Stem Cell

Control of Erythropoiesis

Hormonally controlled—erythropoietin

(EPO)

Dietary requirements--iron and

B-complex vitamins

Life span--120 days

Liver and spleen remove old cells

from blood stream

Renal dialysis patients produce

too little EPO

Genetically engineered EPO usedto treat problem

Abused by athletes to enhance

performance

Danger—extra blood cells +

race dehydration = clotting, stoke,

heart failure

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Disorders Involving RBCs

Anemia--reduced oxygen-carryingability

↓ RBCs--hemorrhagic, hemolytic,aplastic

Abnormal hemoglobin

Thalassemias

Sickle cell

Disorders Involving RBCs

Polycythemia--↑ RBCs--↑ viscosity

Primary—bone marrow cancer

Secondary—decreased oxygen or

increased EPO production

Blood doping—athletes draw off

blood, increase EPO and cellproduction, then reinject cells

Leukocytes--WBCs

Function: Defense against disease

Normal value: 4,000-11,000 / cu mm

Able to leave circulation--diapedesis

Leukocytosis--WBC ↑ 11,000/cu mm

Usually normal physiological

response

Granulocytes

Lobed nuclei

Granules with distinctive stainingusing Wright’s stain

Neutrophils Eosinophils Basophils

AgranulocytesRound nuclei

No granules

Lymphocytes Monocytes

Neutrophils• PMN, poly

• 70% of WBCs

• Phagocytes

• 30% of WBCs

• T-cells--cell

mediated immunity

• B-cells--antibody mediated immunity

Lymphocytes

Monocytes

• 6% of WBCs

• Tissue

macrophages

• Increase in chronic infection

• Important in activating immune

system

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Eosinophils

• 4% of WBCs

• Granules stain

pink-orange

• Granules contain

antihistamine

• Release digestive enzymes

• Increase in allergy and parasitic

infections

Basophils

• < 1% of WBCs

• Granules stain

dark blue

• Release histamine--initiates

inflammatory reaction

• Similar to mast cells of tissue

Never let monkeys eat bananas.

Life span and Production of WBCs

Life span varies according to cell

Leukopoiesis hormonally controlled

• Cytokines--monocytes, T-cells

• Interleukins

• Granulocyte colony stimulating

factor• Complicated, tied to immune

response

Leukocyte Disorders

Leukemias

Myelocytic leukemia

Lymphocytic leukemia

Acute--immature cells (blasts)

Chronic—proliferation of laterstages (cytes)

Cells nonfunctional--death from

infection

Infectious Mononucleosis

Epstein-Barr virus

B-cells involved

Chronic fatigue, sore throat,

low-grade fever

Leukopenia

↓ WBCs

Usually drug induced

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Thrombocytes--PlateletsBreak off megakaryocytes in

bone marrow (myeloid stem cell)

Production hormonally controlled--

thrombopoietin

Life span--10 days

Normal: 250,000-500,000 / cu mm

Release chemicals that act in the

clotting process

HemostasisStoppage of Bleeding

1. Vascular spasm

Immediate response to bloodvessel injury

2. Platelet plug formation

Temporary

Must be reinforced with fibrin

3. Coagulation--blood clotting

Three stage process--gels blood

Coagulation factors activated

Vitamin K and calcium required

Cascade of reactions

Coagulation

Phase I

Intrinsic pathway activated by

exposed collagen

Extrinsic pathway activated bytissue thromboplastin

Common pathway yields

prothrombin activator

Phase II

Prothrombin converted to

thrombin

Phase III

Thrombin converts fibrinogen to

fibrin

Fibrin forms stable clot--retracts

for wound closure

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Fibrinolysis

Removal of clot after healing

Plasminogen incorporated into

clot--activated to plasmin

by tissue plasminogenactivator

tPA released by endothelial cells,

activated factor XII, thrombin

Clotting control

Coagulation positive feedback

Clotting factors quickly removed or inactivated

Flowing blood keeps clotting

factors diluted

Thrombin adsorbed to clot

Thrombin that escapes from clot

quickly inactivated

Heparin released by basophils, mast

cells, endothelial cells secreted intoplasma in small amounts

Thrombin not bound to clot inactivated

by antithrombin III and protein C

All work together to prevent clot from

growing too large

Factors Preventing Undesirable Clotting

Smooth endothelium

Heparin and PGI2 from endothelial

cells prevent platelet adhesion

Vitamin E quinone (E + oxygen)

Disorders of Hemostasis

Thrombolytic

Inappropriate clotting

Bleeding disorders

Platelets

Liver disorders

Coagulation factors

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Thrombolytic Disorders

Thrombus--clot in unbroken bloodvessel

Embolus--clot or other substance

free floating in blood

Rx--dissolve clot--tPA, streptokinase

Cause--roughened blood vessel

Prevention--aspirin, heparin, warfarin (Coumadin)

Disseminated IntravascularCoagulation (DIC)

Widespread clotting in intact

blood vessels

Coagulation factors consumed—blood can not clot appropriately

Pregnancy, septicemia,

incompatible blood transfusion

Bleeding Disorders

Thrombocytopenia

< 50,000 / cu mm

Spontaneous bleeding

Bone marrow depression,

viral infection, certain drugs

Liver dysfunction

Lack of vitamin K or more

serious liver problems

Hemophilias

Hereditary bleeding disorders

Hemophilia A--most commonsex-linked

Factor VIII

Hemophilia B--sex-linked

Factor IX

Hemophila C--both sexes--mildFactor XI

Transfusion and Blood Replacement

Whole blood--substantial loss

thrombocytopenia

Packed Red Cells--anemia

Blood Expanders--replace fluid

Human blood groups genetically

determined

ABO and Rh most commonly causetransfusion problems

Over 90 known blood groups

Based on antigens (proteins) onred blood cell surface

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ABO System

Two antigens--A and B

Body naturally produces antibodies (Ab) to missing

antigen (Ag)

Group A A Ag B Ab

Group B B Ag A Ab

Group AB A & B Ag No Ab

Group O No Ag A & B Ab

Blood cells

mixed with

anti-serato determine

antigens on

cells

Rh Blood Type

C, D, and E antigens--D most

antigenic

Rh + have D antigens

Rh - do not have D antigens

Antibodies to D form only if

individual is exposed to

antigen

ABO antibodies cause agglutination

of red cells

D antibodies cause hemolysis

Erythroblastosis fetalis--HDN

Transfusion Reactions

Universal donor—group O

• theoretical

• no antigens on cells to react

Universal recepient—group AB

• theoretical

• no anitbodies to react with cells

Autologous transfusions

Plasma and Blood Volume Expanders

Used in emergencies

Cross-matching not possible

Plasma--no need to cross-match

Antibodies diluted

Plasma expanders

Serum albumin, plasminate,

dextran, isotonic salt solutions

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Blood Tests

Chemistry--serum

Glucose

lipids

SMAC or SMA 12-60

Coagulation

Protime, platelet count

HematologyCBC, Differential

Diseases of Aging

Chronic leukemia

Thromboembolytic disease

Typically related to heart, blood

vessel or immune system problems

Anemias

Diet or gastrointestinal problems