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Transcript of Chapter 17 Blood Slides by WCR and © Pearson (Marieb & Hoehn).
Chapter 17Blood
Slides by WCR and © Pearson (Marieb & Hoehn).
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
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
© 2013 Pearson Education, Inc.
Figure 17.1 The major components of whole blood.
Withdraw bloodand place in tube.
Centrifuge theblood sample.
Plasma• 55% of whole blood• Least dense component
Buffy coat• Leukocytes and platelets• <1% of whole bloodErythrocytes
• 45% of whole blood (hematocrit)• Most dense component
Formedelements
Slide 1
21
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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 Erythrocytes Monocyte
Neutrophils Lymphocyte
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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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2.5 µm
7.5 µm
Top view
Side view (cut)
Figure 17.3 Structure of erythrocytes (red blood cells).
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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 dedicated to respiratory gas transport
• Hemoglobin binds reversibly with oxygen
• Normal values – Males - 13–18g/100ml; Females - 12–16
g/100ml
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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
Hemegroup
Globin chains
Hemoglobin consists of globin (two alpha and two betapolypeptide chains) and four heme groups.
Iron-containing heme pigment.
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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 1Ribosome synthesis
Phase 2Hemoglobin accumulation
Phase 3Ejection of nucleus
Hematopoietic stemcell (hemocytoblast) Proerythroblast
Basophilicerythroblast
Polychromaticerythroblast
Orthochromaticerythroblast Reticulocyte Erythrocyte
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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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Stimulus: Hypoxia(inadequate O2
delivery) due to O2-carryingability of bloodrises.
Enhancederythropoiesisincreases RBC count. Kidney (and liver to
a smaller extent)releases erythropoietin. Erythropoietin
stimulates redbone marrow.
Figure 17.6 Erythropoietin mechanism for regulating erythropoiesis.
Homeostasis: Normal blood oxygen levels
IMBALANCE
IMBALANCE• Decreased RBC count• Decreased amount of hemoglobin• Decreased availability of O2
Slide 1
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2
3
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Dietary Requirements for Erythropoiesis
• Nutrients—amino acids, lipids, and carbohydrates
• Iron– Available from diet– 65% in Hb; rest in liver, spleen, and bone marrow– Free iron ions toxic
• Stored in cells as ferritin and hemosiderin• Transported in blood bound to protein transferrin
• 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
• Degraded to pigment urobilinogen• Pigment leaves body in feces as stercobilin
– Globin metabolized into amino acids• Released into circulation
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Raw materials aremade available in bloodfor erythrocyte synthesis.
Aged and damagedred blood cells are engulfedby macrophages of spleen,liver, and bone marrow; thehemoglobin is broken down.
New erythrocytesenter bloodstream;function about 120days.
Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.
Erythropoietin levels rise in blood.
Low O2 levels in blood stimulatekidneys to produce erythropoietin.
Figure 17.7 Life cycle of red blood cells.
Hemoglobin
Heme Globin
Bilirubin ispicked upby the liver.
Iron is storedas ferritin orhemosiderin.
Aminoacids
Iron is bound to transferrinand released to bloodfrom liver as neededfor erythropoiesis.
Bilirubin is secreted intointestine in bile whereit is metabolized tostercobilin by bacteria.
Circulation
Food nutrients(amino acids, Fe,B12, and folic acid)are absorbed fromintestine and enterblood.
Stercobilinis excretedin feces.
Slide 11
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3
4
5
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Figure 17.7 Life cycle of red blood cells.
New erythrocytesenter bloodstream;function about 120days.
Slide 5
Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.
Erythropoietin levels rise in blood.
Low O2 levels in blood stimulatekidneys to produce erythropoietin.1
2
3
4
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Raw materials aremade available in bloodfor erythrocyte synthesis.
Aged and damagedred blood cells are engulfedby macrophages of spleen,liver, and bone marrow; thehemoglobin is broken down.
Figure 17.7 Life cycle of red blood cells.
Hemoglobin
Heme Globin
Bilirubin ispicked upby the liver.
Iron is storedas ferritin orhemosiderin.
Aminoacids
Iron is bound to transferrinand released to bloodfrom liver as neededfor erythropoiesis.
Bilirubin is secreted intointestine in bile whereit is metabolized tostercobilin by bacteria.
Circulation
Food nutrients(amino acids, Fe,B12, and folic acid)are absorbed fromintestine and enterblood.
Stercobilinis excretedin feces.
Slide 75
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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; long-term 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
• One amino acid wrong in a globin beta chain
– RBCs crescent shaped when unload O2 or blood O2 low
– 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 normalhemoglobin 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 asingle amino acid change in thebeta 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: WBC count over 11,000/mm3
– 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
• Decreasing abundance in blood– Never let monkeys eat bananas
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Figure 17.9 Types and relative percentages of leukocytes in normal blood.
Formedelements
(All total 4800–10,800/ µl)
GranulocytesNeutrophils (50–70%)
Eosinophils (2–4%)
Basophils (0.5–1%)
AgranulocytesLymphocytes (25–45%)
Monocytes (3–8%)
Platelets
Leukocytes
Erythrocytes
(not drawnto scale)
DifferentialWBC count
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Granulocytes
• Granulocytes– Larger and shorter-lived than RBCs– Lobed nuclei– Cytoplasmic granules stain specifically with
Wright's stain– 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
Neutrophil: Multilobed nucleus, pale red and blue cytoplasmic granules
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Figure 17.10b Leukocytes.
Granulocytes
Eosinophil: Bilobed nucleus, red cytoplasmic granules
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Figure 17.10c Leukocytes.
Granulocytes
Basophil: Bilobed nucleus, purplish-black cytoplasmic granules
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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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Agranulocytes
Lymphocyte (small):Large sphericalnucleus, thin rim ofpale blue cytoplasm
Figure 17.10d Leukocytes.
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Agranulocytes
Monocyte: Kidney-shaped nucleus, abundant pale blue cytoplasm
Figure 17.10e Leukocytes.
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Leukopoiesis
• Production of WBCs– Stimulated by 2 types of chemical
messengers from red bone marrow and mature WBCs
• Interleukins (e.g., IL-3, IL-5)• Colony-stimulating factors (CSFs) named for WBC
type they stimulate (e.g., granulocyte-CSF stimulates granulocytes)
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Stem cells
Committedcells
Developmentalpathway
Hematopoietic stem cell(hemocytoblast)
Myeloid stem cell Lymphoid stem cell
Myeloblast Myeloblast Myeloblast Monoblast B lymphocyteprecursor
T lymphocyteprecursor
Promyelocyte Promyelocyte Promyelocyte Promonocyte
Eosinophilicmyelocyte
Basophilicmyelocyte
Neutrophilicmyelocyte
Eosinophilicband cells
Basophilicband cells
Neutrophilicband cells
Granularleukocytes
Agranularleukocytes
Eosinophils Basophils Neutrophils Monocytes B lymphocytes T lymphocytes
Macrophages (tissues) Plasma cells Effector T cells
Some become Some become
(a) (b) (c) (d) (e) (f)
Some become
Figure 17.11 Leukocyte formation.
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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.
Stem cell Developmental pathway
Hematopoietic stemcell (hemocytoblast)
Megakaryoblast(stage I megakaryocyte)
Megakaryocyte(stage II/III)
Megakaryocyte(stage IV)
Platelets
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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 steps1. 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 via plasma
protein von Willebrand factor– Swell, become spiked and sticky, and release
chemical messengers• ADP causes more platelets to stick and release
their contents • Serotonin and thromboxane A2 enhance vascular
spasm and platelet aggregation
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Hemostasis: Coagulation
• Reinforces platelet plug with fibrin threads
• Blood transformed from liquid to gel
• Series of reactions using clotting factors (procoagulants)– # I – XIII; most plasma proteins– 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.
Step 2 Platelet plugformation• Injury to lining of vessel exposes collagen fibers; platelets adhere.
• Platelets release chemicals that make nearby platelets sticky; platelet plug forms.
Step 3 Coagulation• Fibrin forms a mesh that traps red blood cells and platelets, forming the clot.
Collagenfibers
Platelets
Fibrin
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Coagulation: Overview
• Three phases of coagulation– Prothrombin activator formed in both
intrinsic and extrinsic pathways– Prothrombin converted to enzyme thrombin– Thrombin catalyzes fibrinogen 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– Involves a series of procoagulants
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Coagulation Phase 1: Two Pathways to Prothrombin Activator
• Intrinsic pathway– Triggered by negatively charged surfaces
(activated platelets, collagen, glass)– Uses factors present within blood (intrinsic)
• Extrinsic pathway– Triggered by exposure to tissue factor (TF) or
factor III (an extrinsic factor)– Bypasses several steps of intrinsic pathway,
so 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: Common Pathway to the Fibrin Mesh
• Thrombin converts soluble fibrinogen to fibrin
• Fibrin strands form structural basis of clot
• Fibrin causes plasma to become a gel-like trap for 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)
Intrinsic pathway Extrinsic pathwayVessel endotheliumruptures, exposingunderlying tissues(e.g., collagen)
Tissue cell traumaexposes blood to
Platelets cling and theirsurfaces provide sites formobilization of factors
Tissue factor (TF)
XII
XIIa
Ca2+
VIIXI
XIa
IX Ca2+
VIIa
IXa
VIII
VIIIa
IXa/VIIIa complex TF/VIIa complex
X
Xa
Ca2+
PF3 Va V
Prothrombinactivator
PF3
released byaggregated
platelets
Phase 1
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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)
Fibrin(insolublepolymer)
Cross-linkedfibrin mesh
XIIIa
XIII
Ca2+
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Figure 17.15 Scanning electron micrograph of erythrocytes trapped in a 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 is a fibrin-digesting enzyme
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Factors Limiting Clot Growth or Formation
• Two mechanisms limit clot size– Swift removal and dilution of clotting factors – Inhibition of activated clotting factors
• Thrombin bound onto fibrin threads
• Antithrombin III inactivates unbound thrombin
• Heparin in basophil and mast cells inhibits thrombin by enhancing antithrombin III
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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
Blood thinners*
Drugs to prevent, reduce, or undo blood clotting
Antiplatelets, anticoagulants, thrombolytics
Antiplatelet drugs block platelet plug formationAspirin, Plavix, etc.
Anticoagulants block fibrin mesh formationCoumadin (warfarin), heparin, hirudin, etc.
Thrombolytic drugs break down existing clotsClot-busters, useful just after MI or strokeMust be given <6 hrs post event, sooner is betterTissue plasminogen activator (tPA), streptokinase, etc.
*Misleading term, since the drugs do not affect viscosity
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Anticoagulant Drugs
• Aspirin– Antiprostaglandin that inhibits thromboxane A2
• Heparin– Anticoagulant used clinically for pre- and
postoperative cardiac care
• Warfarin (Coumadin)– Used for those prone to atrial fibrillation– Interferes with action of vitamin K
• Dabigatran directly inhibits thrombin
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/.
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Bleeding Disorders
• Thrombocytopenia: deficient number of circulating platelets– Petechiae appear due to spontaneous,
widespread hemorrhage – Due to suppression or destruction of red bone
marrow (e.g., malignancy, radiation, drugs)– Platelet count <50,000/μl is diagnostic – Treated with transfusion of concentrated
platelets
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Bleeding Disorders
• Impaired liver function– Inability to synthesize procoagulants – Causes include vitamin K deficiency,
hepatitis, and cirrhosis– Impaired fat absorption and liver disease can
also prevent liver from producing bile, impairing fat and vitamin K absorption
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Bleeding Disorders
• Hemophilia includes several similar hereditary bleeding disorders – Hemophilia A: most common type (77% of all cases);
factor VIII deficiency– Hemophilia B: factor IX deficiency – Hemophilia C: mild type; factor XI deficiency
• Symptoms include prolonged bleeding, especially into joint cavities
• Treated with plasma transfusions and injection of missing factors– Increased hepatitis and HIV risk
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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 oxygen-carrying capacity
• Transfusion of incompatible blood can be fatal
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