Transcript Composition of Blood - Health and Science Pipeline Initiative

Composition of Blood
• Consists of formed elements (cells) suspended &
carried in plasma (fluid part)
• Total blood volume is about 5L
• Plasma is straw-colored liquid consisting of H20 &
dissolved solutes
– Includes ions, metabolites, hormones, antibodies
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Plasma Proteins
• Constitute 7-9% of plasma
• Three types of plasma proteins: albumins, globulins, &
fibrinogen
– Albumin accounts for 60-80%
• Creates colloid osmotic pressure that draws H20 from interstitial fluid into
capillaries to maintain blood volume & pressure
• Globulins carry lipids
– Gamma globulins are antibodies
• Fibrinogen serves as clotting factor
– Converted to fibrin
– Serum is fluid left when blood clots
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Formed Elements
• Are erythrocytes (RBCs) &
leukocytes (WBCs)
• RBCs are flattened biconcave discs
Fig 13.3
– Shape provides increased surface area
for diffusion
– Lack nuclei & mitochondria
– Each RBC contains 280 million
hemoglobins
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Leukocytes
• Have nucleus, mitochondria, & amoeboid ability
• Can squeeze through capillary walls (diapedesis)
– Granular leukocytes help detoxify foreign substances &
release heparin
• Include eosinophils, basophils, & neutrophils
Fig 13.3
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Leukocytes continued
• Agranular
leukocytes are
phagocytic &
produce antibodies
Fig 13.3
• Include
lymphocytes &
monocytes
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Platelets (thrombocytes)
• Are smallest of formed elements,
lack nucleus
• Are fragments of megakaryocytes;
amoeboid
• Constitute most of mass of blood
clots
• Release serotonin to vasoconstrict &
reduce blood flow to clot area
• Secrete growth factors to maintain
integrity of blood vessel wall
• Survive 5-9 days
Fig 13.3
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Hematopoiesis
• Is formation of blood cells from stem cells in
marrow (myeloid tissue) & lymphoid tissue
• Erythropoiesis is formation of RBCs
– Stimulated by erythropoietin (EPO) from kidney
• Leukopoiesis is formation of WBCs
– Stimulated by variety of cytokines
• = autocrine regulators secreted by immune system
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Erythropoiesis
• 2.5 million RBCs
are produced/sec
• Lifespan of 120
days
• Old RBCs
removed from
blood by
phagocytic cells in
liver, spleen, &
bone marrow
– Iron recycled back
into hemoglobin
Fig 13.4
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RBC Antigens & Blood Typing
• Antigens present on RBC surface specify blood type
• Major antigen group is ABO system
–
–
–
–
Type A blood has only A antigens
Type B has only B antigens
Type AB has both A & B antigens
Type O has neither A or B antigens
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ABO Blood Types
RealMedia Movie
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Transfusion Reactions
• People with Type A blood make
antibodies to Type B RBCs, but
not to Type A
• Type B blood has antibodies to
Type A RBCs but not to Type B
• Type AB blood doesn’t have
antibodies to A or B
• Type O has antibodies to both
Type A & B
• If different blood types are
mixed, antibodies will cause
mixture to agglutinate
Fig 13.5
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Transfusion Reactions continued
• If blood types don't match,
recipient’s antibodies
agglutinate donor’s RBCs
• Type O is “universal donor”
because lacks A & B antigens
• Insert fig. 13.6
– Recipient’s antibodies won’t
agglutinate donor’s Type O
RBCs
• Type AB is “universal
recipient” because doesn’t
make anti-A or anti-B
antibodies
– Won’t agglutinate donor’s RBCs
Fig 13.6
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Hemostasis
• Is cessation of bleeding
• Promoted by reactions initiated by vessel injury:
– Vasoconstriction restricts blood flow to area
– Platelet plug forms
• Plug & surroundings are infiltrated by web of fibrin, forming
clot
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Role of Platelets
• Platelets don't
stick to intact
endothelium
because of
presence of
prostacyclin
(PGI2--a
prostaglandin) &
NO
– Keep clots from
forming & are
vasodilators
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are needed to see this picture.
Fig 13.7a
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Role of Platelets
• Damage to endothelium
allows platelets to bind
to exposed collagen
– von Willebrand factor
increases bond by binding
to both collagen &
platelets
– Platelets stick to collagen
& release ADP, serotonin,
& thromboxane A2
• = platelet release reaction
Fig 13.7b
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Role of Platelets continued
• Serotonin & thromboxane
A2 stimulate
vasoconstriction,
reducing blood flow to
wound
• ADP & thromboxane A2
cause other platelets to
become sticky & attach &
undergo platelet release
reaction
– This continues until
platelet plug is formed
Fig 13.7c
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Role of Fibrin
• Platelet plug becomes infiltrated by meshwork of fibrin
• Clot now contains platelets, fibrin & trapped RBCs
– Platelet plug undergoes plug contraction to form more compact plug
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Conversion of Fibrinogen to Fibrin
• Can occur via 2 pathways:
– Intrinsic pathway clots damaged vessels & blood left in test tube
• Initiated by exposure of blood to negatively charged surface of glass or blood
vessel collagen
–
–
This activates factor XII (a protease) which initiates a series of clotting factors
Ca2+ & phospholipids convert prothrombin to thrombin
» Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh
– Damage outside blood vessels releases tissue thromboplastin that
triggers a clotting shortcut (= extrinsic pathway)
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Fig 13.9
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Dissolution of Clots
• When damage is repaired, activated factor
XII causes activation of kallikrein
– Kallikrein converts plasminogen to plasmin
• Plasmin digests fibrin, dissolving clot
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Anticoagulants
• Clotting can be prevented by Ca+2 chelators (e.g.
sodium citrate or EDTA)
– or heparin which activates antithrombin III (blocks
thrombin)
• Coumarin blocks clotting by inhibiting activation of
Vit K
– Vit K works indirectly by reducing Ca+2 availability
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Prostaglandins (PGs)
• Are produced in almost every organ
• Belong to eicosanoid family -- all derived from arachidonic acid of
plasma membrane
Fig 11.34
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Prostaglandins (PGs) continued
• Have wide variety of functions
– Different PGs may exert antagonistic effects in tissues
• Some promote smooth muscle contraction & some relaxation
• Some promote clotting; some inhibit
– Promotes inflammatory process of immune system
– Plays role in ovulation
– Inhibits gastric secretion in digestive system
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Prostaglandins (PGs) continued
• Cyclooxygenase (COX) 1 & 2 are involved in PG synthesis
(Fig 11.34)
– Are targets of a number of inhibitory non-steroidal antiinflammatory drugs (NSAIDs)
• Aspirin, indomethacin, ibuprofen inhibit both COX 1 & 2 thereby producing
side effects
• Celebrex & Vioxx only inhibit COX 2 & thus have few side effects
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