Composition of Blood

1
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
Fig 13.3

• Are erythrocytes (RBCs) leukocytes (WBCs)
• RBCs are flattened biconcave discs
• 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
Fig 13.3

• Agranular leukocytes are phagocytic produce
  antibodies
• 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 production

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

Click here to play 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 doesnt 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, recipients
  antibodies agglutinate donors RBCs
• Type O is universal donor because lacks A B
  antigens
• Recipients antibodies wont agglutinate donors
  Type O RBCs
• Type AB is universal recipient because doesnt
  make anti-A or anti-B antibodies
• Wont agglutinate donors RBCs

• Insert fig. 13.6

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

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 Ca2 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 Ca2
  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 anti-inflammatory 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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