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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 when
blood clots
Hematocrit
Separate formed elements
from plasma
45% formed elements
55% plasma
Erythrocytes majority of
formed elements
Buffy coatthin layer of white
blood cells & platelets
Physical Characteristics
Scarlet to dark red--O
2
content
Denser, more viscous than H
2
O
pH--7.35-7.45
Temperature--38
o
C, 100.4
o
F
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 10
6
/ cu mm
Females--4.5 X 10
6
/ cu mm
Hematopoiesis
Formation of Blood Cells
Bone marrow
Hemocytoblast or
Hemopoietic Stem Cell
Control of Erythropoiesis
Hormonally controllederythropoietin
(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 used
to treat problem
Abused by athletes to enhance
performance
Dangerextra blood cells +
race dehydration = clotting, stoke,
heart failure
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Disorders Involving RBCs
Anemia--reduced oxygen-carrying
ability
RBCs--hemorrhagic, hemolytic,
aplastic
Abnormal hemoglobin
Thalassemias
Sickle cell
Disorders Involving RBCs
Polycythemia-- RBCs-- viscosity
Primarybone marrow cancer
Secondarydecreased oxygen or
increased EPO production
Blood dopingathletes draw off
blood, increase EPO and cell
production, 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 staining
using Wrights stain
Neutrophils Eosinophils Basophils
Agranulocytes
Round nuclei
No granules
Lymphocytes Monocytes
Neutrophils
PMN, poly
70% of WBCs
Phagocytes
30% of WBCs
T-cells--cell
mediated immunity
B-cells--antibody mediatedimmunity
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)
Chronicproliferation of later
stages (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--Platelets
Break 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
Hemostasis
Stoppage of Bleeding
1. Vascular spasm
Immediate response to blood
vessel 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 by
tissue 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 plasminogen
activator
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 into
plasma 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 PGI
2
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 blood
vessel
Embolus--clot or other substance
free floating in blood
Rx--dissolve clot--tPA, streptokinase
Cause--roughened blood vessel
Prevention--aspirin, heparin,
warfarin (Coumadin)
Disseminated Intravascular
Coagulation (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 common
sex-linked
Factor VIII
Hemophilia B--sex-linked
Factor IX
Hemophila C--both sexes--mild
Factor 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 cause
transfusion problems
Over 90 known blood groups
Based on antigens (proteins) on
red 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-sera
to 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 donorgroup O
theoretical
no antigens on cells to react
Universal recepientgroup 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
Hematology
CBC, Differential
Diseases of Aging
Chronic leukemia
Thromboembolytic disease
Typically related to heart, blood
vessel or immune system
problems
Anemias
Diet or gastrointestinal problems