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Chapter 17
Blood
Slides by WCR and © Pearson (Marieb &
Hoehn).
Blood Composition
• Blood
– Fluid connective tissue
– Plasma – non-living fluid matrix
– Formed elements – living blood "cells"
suspended in plasma
• Erythrocytes (red blood cells, or RBCs)
• Leukocytes (white blood cells, or WBCs)
• Platelets
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Blood Composition
• Spun tube of blood yields three layers
– Plasma on top (~55%)
– Erythrocytes on bottom (~45%)
– WBCs and platelets in Buffy coat (< 1%)
• Hematocrit
– Percent of blood volume that is RBCs
– 47% ± 5% for males; 42% ± 5% for females
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Figure 17.1 The major components of whole blood.
Slide 1
Formed
elements
1 Withdraw blood
and place in tube.
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2 Centrifuge the
blood sample.
Plasma
• 55% of whole blood
• Least dense component
Buffy coat
• Leukocytes and platelets
• <1% of whole blood
Erythrocytes
• 45% of whole blood
(hematocrit)
• Most dense component
Physical Characteristics and Volume
• Sticky, opaque fluid with metallic taste
• Color varies with O2 content
– High O2 - scarlet; Low O2 - dark red
• pH 7.35–7.45
• ~8% of body weight
• Average volume
– 5–6 L for males; 4–5 L for females
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Functions of Blood
• Functions include
– Distributing substances
– Regulating blood levels of substances
– Protection
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Distribution Functions
• Delivering O2 and nutrients to body cells
• Transporting metabolic wastes to lungs
and kidneys for elimination
• Transporting hormones from endocrine
organs to target organs
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Regulation Functions
• Maintaining body temperature by
absorbing and distributing heat
• Maintaining normal pH using buffers;
alkaline reserve of bicarbonate ions
• Maintaining adequate fluid volume in
circulatory system
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Protection Functions
• Preventing infection
– Antibodies
– Complement proteins
– WBCs
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Blood Plasma
• 90% water
• Over 100 dissolved solutes
– Nutrients, gases, hormones, wastes, proteins,
inorganic ions
– Electrolytes most abundant solutes by
number
– Plasma proteins most abundant solutes by
mass
• Remain in blood; not taken up by cells
• Proteins produced mostly by liver
• 60% albumin; 36% globulins; 4% fibrinogen
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Albumin
• 60% of plasma protein
• Functions
– Substance carrier
– Blood buffer
– Major contributor of plasma osmotic pressure
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Formed Elements
•
•
•
•
Only WBCs are complete cells
RBCs have no nuclei or other organelles
Platelets are cell fragments
Most formed elements survive in
bloodstream only few days
• Most blood cells originate in bone marrow
and do not divide
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Figure 17.2 Photomicrograph of a human blood smear stained with Wright's stain.
Platelets
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Neutrophils
Erythrocytes
Lymphocyte
Monocyte
Erythrocytes
• Biconcave discs, anucleate, essentially no
organelles
• Diameters larger than some capillaries
• Filled with hemoglobin (Hb) for gas
transport
• Contain plasma membrane protein
spectrin and other proteins
– Spectrin provides flexibility to change shape
• Major factor contributing to blood viscosity
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Figure 17.3 Structure of erythrocytes (red blood cells).
2.5 µm
Side view (cut)
7.5 µm
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Top view
Erythrocytes
• Structural characteristics contribute to gas
transport
– Biconcave shape—huge surface area relative
to volume
– >97% hemoglobin (not counting water)
– No mitochondria; ATP production anaerobic;
do not consume O2 they transport
• Superb example of complementarity of
structure and function
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Erythrocyte Function
• RBCs transport O2, CO2: respiratory
gases
• Hemoglobin binds reversibly with
oxygen
• Normal values for hemoglobin protein in
whole blood
– Hgb = 13–18g/dL (males)
– Hgb = 12-16 g/dL (females)
– g/dL = grams / deciliter = grams/100 mL
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Hemoglobin Structure
• Globin composed of 4 polypeptide chains
– Two alpha and two beta chains
• Heme pigment bonded to each globin
chain
– Gives blood red color
• Heme's central iron atom binds one O2
• Each Hb molecule can transport four O2
• Each RBC contains 250 million Hb
molecules
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Figure 17.4 Structure of hemoglobin.
 Globin chains
Heme
group
 Globin chains
Hemoglobin consists of globin (two alpha and two beta
polypeptide chains) and four heme groups.
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Iron-containing heme pigment.
Hematopoiesis
• Blood cell formation in red bone marrow
– Composed of reticular connective tissue and
blood sinusoids
• In adult, found in axial skeleton, girdles,
and proximal epiphyses of humerus and
femur
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Figure 17.5 Erythropoiesis: formation of red
blood cells.
Stem cell
Committed cell
Developmental pathway
Phase 1
Ribosome synthesis
Hematopoietic stem
cell (hemocytoblast)
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Proerythroblast
Basophilic
erythroblast
Phase 2
Hemoglobin accumulation
Polychromatic
erythroblast
Phase 3
Ejection of nucleus
Orthochromatic
erythroblast
Reticulocyte Erythrocyte
Regulation of Erythropoiesis
•
•
•
•
Too few RBCs leads to tissue hypoxia
Too many RBCs increases blood viscosity
> 2 million RBCs made per second
Balance between RBC production and
destruction depends on
– Hormonal controls
– Adequate supplies of iron, amino acids, and B
vitamins
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Hormonal Control of Erythropoiesis
• Hormone Erythropoietin (EPO)
– Direct stimulus for erythropoiesis
– Always small amount in blood to maintain
basal rate
• High RBC or O2 levels depress production
– Released by kidneys (some from liver) in
response to hypoxia
• Dialysis patients have low RBC counts
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Figure 17.6 Erythropoietin mechanism for regulating erythropoiesis.
Slide 1
Homeostasis: Normal blood oxygen levels
1 Stimulus:
Hypoxia
(inadequate O2
delivery) due to
• Decreased
RBC count
• Decreased amount
of hemoglobin
• Decreased
availability of O2
5 O2-carrying
ability of blood
rises.
4 Enhanced
erythropoiesis
increases RBC count.
3 Erythropoietin
stimulates red
bone marrow.
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2 Kidney (and liver to
a smaller extent)
releases
erythropoietin.
Dietary Requirements for Erythropoiesis
• Nutrients—amino acids, lipids, and
carbohydrates
• Iron
– Available from diet
• Vitamin B12 and folic acid necessary for DNA
synthesis for rapidly dividing cells (developing
RBCs)
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Fate and Destruction of Erythrocytes
• Life span: 100–120 days
– No protein synthesis, growth, division
• Old RBCs become fragile; Hb begins to
degenerate
• Get trapped in smaller circulatory channels
especially in spleen
• Macrophages engulf dying RBCs in spleen
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Fate and Destruction of Erythrocytes
• Heme and globin are separated
– Iron salvaged for reuse
– Heme degraded to yellow pigment bilirubin
– Liver secretes bilirubin (in bile) into intestines
– Globin metabolized into amino acids for reuse
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Erythrocyte Disorders
• Anemia
– Blood has abnormally low O2-carrying
capacity
– Sign rather than disease itself
– Blood O2 levels cannot support normal
metabolism
– Accompanied by fatigue, pallor, shortness of
breath, and chills
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Causes of Anemia
• Three groups
– Blood loss
– Low RBC production
– High RBC destruction
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Causes of Anemia: Blood Loss
• Hemorrhagic anemia
– Blood loss rapid (e.g., stab wound)
– Treated by blood replacement
• Chronic hemorrhagic anemia
– Slight but persistent blood loss
• Hemorrhoids, bleeding ulcer
– Primary problem treated
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Causes of Anemia: Low RBC Production
• Iron-deficiency anemia
– Caused by hemorrhagic anemia, low iron
intake, or impaired absorption
– Microcytic, hypochromic RBCs
– Iron supplements to treat
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Causes of Anemia: Low RBC Production
• Pernicious anemia
– Autoimmune disease - destroys stomach
mucosa
– Lack of intrinsic factor needed to absorb B12
• Deficiency of vitamin B12
– RBCs cannot divide  macrocytes
– Treated with B12 injections or nasal gel
– Also caused by low dietary B12 (vegetarians)
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Causes of Anemia: Low RBC Production
• Renal anemia
– Lack of EPO
– Often accompanies renal disease
– Treated with synthetic EPO
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Causes of Anemia: Low RBC Production
• Aplastic anemia
– Destruction or inhibition of red marrow by
drugs, chemicals, radiation, viruses
– Usually cause unknown
– All cell lines affected
• Anemia; clotting and immunity defects
– Treated short-term with transfusions; longterm with transplanted stem cells
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Causes of Anemia: High RBC Destruction
• Hemolytic anemias
– Premature RBC lysis
– Caused by
• Hb abnormalities
• Incompatible transfusions
• Infections
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Causes of Anemia: High RBC Destruction
• Sickle-cell anemia
– Hemoglobin S (for sickle)
• One amino acid wrong in the beta chain
– Abnormal Hb S sticks together to make long
intracellular rods, which causes…
– RBCs get crescent-shaped (sickle-shaped)
– RBCs rupture easily and block small vessels
• Poor O2 delivery; pain
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Figure 17.8 Sickle-cell anemia.
Val His Leu Thr Pro Glu Glu …
1
2
3
4
5
6
7
146
Normal erythrocyte has normal
hemoglobin amino acid sequence
in the beta chain.
Val His Leu Thr Pro Val Glu …
1
2
3
4
5
6
7
146
Sickled erythrocyte results from a
single amino acid change in the
beta chain of hemoglobin.
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Leukocytes
• Make up <1% of total blood volume
– 4,800 – 10,800 WBCs/μl blood
• Function in defense against disease
– Can leave capillaries via diapedesis
– Move through tissue spaces by ameboid
motion and positive chemotaxis
• Leukocytosis: Abnormally high number of
leukocytes
– Normal response to infection
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Leukocytes: Two Categories
• Granulocytes – Visible cytoplasmic
granules
– Neutrophils, eosinophils, basophils
• Agranulocytes – No visible cytoplasmic
granules
– Lymphocytes, monocytes
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Figure 17.9 Types and relative percentages of leukocytes in normal blood.
Formed
elements
(not drawn
to scale)
Differential
WBC count
(All total 4800–
10,800/ µl)
Platelets
Granulocytes
Neutrophils (50–70%)
Leukocytes
Eosinophils (2–4%)
Basophils (0.5–1%)
Erythrocytes
Agranulocytes
Lymphocytes (25–45%)
Monocytes (3–8%)
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Granulocytes
• Granulocytes
– Larger and shorter-lived than RBCs
– Lobed nuclei
– All phagocytic to some degree
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Neutrophils
• Most numerous WBCs
• Also called Polymorphonuclear leukocytes
(PMNs or polys)
• Granules stain lilac; contain hydrolytic
enzymes or defensins
• 3-6 lobes in nucleus; twice size of RBCs
• Very phagocytic—"bacteria slayers"
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Eosinophils
• Red-staining granules
• Bilobed nucleus
• Granules lysosome-like
– Release enzymes to digest parasitic worms
• Role in allergies and asthma
• Role in modulating immune response
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Basophils
• Rarest WBCs
• Nucleus deep purple with 1-2 constrictions
• Large, purplish-black (basophilic) granules
contain histamine
– Histamine: inflammatory chemical that acts as
vasodilator to attract WBCs to inflamed sites
• Are functionally similar to mast cells
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Figure 17.10a Leukocytes.
Granulocytes
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Neutrophil:
Multilobed nucleus,
pale red and blue
cytoplasmic granules
Figure 17.10b Leukocytes.
Granulocytes
Eosinophil:
Bilobed nucleus, red
cytoplasmic granules
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Figure 17.10c Leukocytes.
Granulocytes
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Basophil:
Bilobed nucleus,
purplish-black
cytoplasmic granules
Agranulocytes
• Agranulocytes
– Lack visible cytoplasmic granules
– Have spherical or kidney-shaped nuclei
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Lymphocytes
• Second most numerous WBC
• Large, dark-purple, circular nuclei with thin
rim of blue cytoplasm
• Mostly in lymphoid tissue (e.g., lymph
nodes, spleen); few circulate in blood
• Crucial to immunity
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Monocytes
• Largest leukocytes
• Abundant pale-blue cytoplasm
• Dark purple-staining, U- or kidney-shaped
nuclei
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Monocytes
• Leave circulation, enter tissues, and
differentiate into macrophages
– Actively phagocytic cells; crucial against
viruses, intracellular bacterial parasites, and
chronic infections
• Activate lymphocytes to mount an immune
response
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Figure 17.10d Leukocytes.
Agranulocytes
Lymphocyte (small):
Large spherical
nucleus, thin rim of
pale blue cytoplasm
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Figure 17.10e Leukocytes.
Agranulocytes
Monocyte:
Kidney-shaped
nucleus, abundant
pale blue cytoplasm
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Leukopoiesis
• Production of WBCs
– Stimulated by interleukins and colonystimulating factors
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Stem cells
Figure
17.11
Leukocyte
formation.
Stimulated
by
interleukins
& colonystimulating
factors
Hematopoietic stem cell
(hemocytoblast)
Lymphoid stem cell
Myeloid stem cell
Committed
cells
Myeloblast
Developmental
Promyelocyte
pathway
Eosinophilic
myelocyte
Myeloblast
Myeloblast
Monoblast
Promyelocyte
Promyelocyte
Promonocyte
Basophilic
myelocyte
Neutrophilic
myelocyte
Eosinophilic
band cells
Basophilic
band cells
Neutrophilic
band cells
(b)
Basophils
Neutrophils
(c)
Monocytes
(d)
B lymphocytes T lymphocytes
(e)
(f)
Some become
Some become
Macrophages (tissues) Plasma cells
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T lymphocyte
precursor
Agranular
leukocytes
Granular
leukocytes
Eosinophils
(a)
B lymphocyte
precursor
Some become
Effector T cells
Platelets
• Cytoplasmic fragments of
megakaryocytes
• Form temporary platelet plug that helps
seal breaks in blood vessels
• Circulating platelets kept inactive and
mobile by nitric oxide (NO) and
prostacyclin from endothelial cells lining
blood vessels
• Age quickly; degenerate in about 10 days
• Formation regulated by thrombopoietin
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Figure 17.12
Formation of platelets.
Hematopoetic stem cell -> megakaryocyte ->
fragments tear off = platelets.
Stem cell
Hematopoietic stem
cell (hemocytoblast)
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Developmental pathway
Megakaryoblast
(stage I megakaryocyte)
Megakaryocyte
(stage II/III)
Megakaryocyte
(stage IV)
Platelets
Table 17.2 Summary of Formed Elements of the Blood (1 of 2)
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Table 17.2 Summary of Formed Elements of the Blood (2 of 2)
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Hemostasis
• Fast series of reactions for stoppage of
bleeding
• Requires clotting factors, and
substances released by platelets and
injured tissues
• Three steps
1. Vascular spasm
2. Platelet plug formation
3. Coagulation (blood clotting)
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Hemostasis: Vascular Spasm
• Vasoconstriction of damaged blood vessel
• Triggers
– Direct injury to vascular smooth muscle
– Chemicals released by endothelial cells and
platelets
– Pain reflexes
• Most effective in smaller blood vessels
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Hemostasis: Platelet Plug Formation
• Positive feedback cycle
• Damaged endothelium exposes collagen
fibers
– Platelets stick to collagen fibers
– Swell, become spiked and sticky, and release
chemical messengers to attract & activate
more platelets
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Hemostasis: Coagulation
• Reinforces platelet plug with fibrin threads
• Forms a local gel
• Series of reactions using clotting factors:
mostly proteins that circulate in the blood,
inactive most of the time
– Vitamin K needed to synthesize 4 of them
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Figure 17.13 Events of hemostasis.
Slide 5
Step 1 Vascular spasm
• Smooth muscle contracts,
causing vasoconstriction.
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Collagen
fibers
Step 2 Platelet plug
formation
• Injury to lining of vessel
exposes collagen fibers;
platelets adhere.
Platelets
• Platelets release chemicals
that make nearby platelets
sticky; platelet plug forms.
Fibrin
Step 3 Coagulation
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Coagulation: Overview
• Three phases of coagulation
1. Make prothrombin activator by intrinsic
and/or extrinsic pathway
2. Prothrombin activator converts prothrombin
to thrombin
3. Thrombin catalyzes the conversion of
fibrinogen to fibrin
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Coagulation Phase 1: Two Pathways to
Prothrombin Activator
• Initiated by either intrinsic or extrinsic
pathway (usually both)
– Triggered by tissue-damaging events which
release tissue factor (activates extr pathway)
and expose collagen (activates intrinsic
pathway)
– Involves a series of enzymes
– Extrnisic pathway somewhat faster
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Coagulation Phase 2: Pathway to Thrombin
• Prothrombin activator catalyzes
transformation of prothrombin to active
enzyme thrombin
• Once prothrombin activator formed, clot
forms in 10–15 seconds
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Coagulation Phase 3:
Convert Fibrinogen to Fibrin
• Thrombin converts soluble fibrinogen to
fibrin
• Fibrin strands form structural basis of clot
• Fibrin mesh catches formed elements
• Thrombin (with Ca2+) activates factor XIII
which:
– Cross-links fibrin
– Strengthens and stabilizes clot
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Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (1 of 2)
Phase 1
Intrinsic pathway
Extrinsic pathway
Vessel endothelium
ruptures, exposing
underlying tissues
(e.g., collagen)
Tissue cell trauma
exposes blood to
Platelets cling and their
surfaces provide sites for
mobilization of factors
Tissue factor (TF)
XII
Ca2+
XIIa
VII
XI
XIa
VIIa
Ca2+
IX
IXa
PF3
released by
aggregated
platelets
VIII
VIIIa
TF/VIIa complex
IXa/VIIIa complex
X
Xa
Ca2+
PF3
Va
Prothrombin
activator
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V
Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (2 of 2)
Phase 2
Prothrombin (II)
Thrombin (IIa)
Phase 3
Fibrinogen (I)
(soluble)
Ca2+
Fibrin
(insoluble
polymer)
XIII
XIIIa
Cross-linked
fibrin mesh
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Fibrinolysis
• Removes unneeded clots after healing
• Begins within two days; continues for
several
• Plasminogen in clot is converted to
plasmin by tissue plasminogen activator
(tPA), factor XII and thrombin
• Plasmin digests fibrin
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Disorders of Hemostasis
• Thromboembolic disorders: undesirable
clot formation
• Bleeding disorders: abnormalities that
prevent normal clot formation
• Disseminated intravascular coagulation
(DIC)
– Involves both types of disorders
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Thromboembolic Conditions
• Thrombus: clot that develops and persists
in unbroken blood vessel
– May block circulation leading to tissue death
• Embolus: thrombus freely floating in
bloodstream
• Embolism: embolus obstructing a vessel
– E.g., pulmonary and cerebral emboli
• Risk factors – atherosclerosis,
inflammation, slowly flowing blood or blood
stasis from immobility
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“Blood thinners”*
Drugs to prevent, reduce, or undo blood clotting
Antiplatelets, anticoagulants, thrombolytics
Antiplatelet drugs block platelet plug formation
Aspirin, Plavix, etc.
Anticoagulants block fibrin mesh formation
Coumadin (warfarin), heparin, hirudin, etc.
Thrombolytic drugs break down existing clots
Clot-busters, useful just after MI or stroke
Must be given <6 hrs post event, sooner is better
Tissue plasminogen activator (tPA), streptokinase, etc.
*Misleading term, since the drugs do not affect viscosity
Hirudin and dagatriban are anticoagulants based on molecules which leeches
create and use to help them suck blood. Medicinal leeches are still used by
some physicians, for example to promote blood flow around skin grafts and
after reattachment surgery. Buy at http://www.leechesusa.com/.
Bleeding Disorders
• Thrombocytopenia: deficient number of
circulating platelets
– Petechiae (little red spots) appear due to
spontaneous, widespread hemorrhage
– Due to suppression or destruction of red bone
marrow (e.g., malignancy, radiation, drugs)
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Bleeding Disorders
• Impaired liver function
– Inability to synthesize procoagulants
– Causes include vitamin K deficiency,
hepatitis, and cirrhosis
• Hemophilia includes several similar
hereditary bleeding disorders
– Genetic mutation in on e of the enzymes of
the clotting cascade
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Transfusions
• Whole-blood transfusions used when
blood loss rapid and substantial
• Packed red cells (plasma and WBCs
removed) transfused to restore oxygencarrying capacity
• Transfusion of incompatible blood can be
fatal
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Human Blood Groups
• RBCs have glycoproteins in their membranes
• Blood is classified according to what
glycoproteins are present on that person’s RBCs
• These glycoproteins also called antigens
because they can cause immune system to
generate antibodies
• These glycoproteins also called agglutinogens
because they can cause agglutination, or
clumping up, of cells
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Human Blood Groups
• Three most important antigens on RBCs:
A, B, and Rh
• Type A: RBCs have A and not B
• Type B: RBCs have B and not A
• Type AB: RBCs have both A and B
• Type O: RBCs have neither A nor B (think
zero or null)
Human Blood Groups
Principles of blood matching
1.The immune system of the recipient will attack
and destroy RBCs with “foreign” antigens.
2.The immune system will not notice and will not
be bothered by the absence of an antigen.
3.The immune system will not attack “self”
antigens.
Human Blood Groups
Human Blood Groups: Rh
• Dozens of named Rh factors
• Blood called “positive” if RBCs have Rh D
antigen, “negative” if RBCs do not
• Rh- (Rh negative) person does not make
antibodies to Rh factor until exposed to it
(unlike A,B antigens & antibodies)
• Rh- person will have bad reaction to Rh+
blood on second exposure (pregnancy
issue for Rh- mom)
Transfusion Reaction
• Occurs if mismatched blood is transfused
• Donated RBCs
– Are attacked by recipient's antibodies
– Agglutinate (form clumps) and clog small
vessels
– Rupture and release hemoglobin into
bloodstream
• Which results in
– Diminished oxygen-carrying capacity
– Little/no blood flow downstream of blockages
– Hemoglobin in kidney tubules  renal failure
Transfusions
• Type O- person is universal donor
– Their RBCs have neither A nor B nor Rh
antigens, so anyone can take it
• Type AB+ person is universal recipient
– Their immune system is “used to” A and B
and Rh antigens, so they can take anything
• Autologous transfusions
– “self-transfusion”, with blood donated and
stored ahead of time
– Blood is living tissue, has limited shelf life