Blood Major Components of Blood

? only fluid tissue in body

(fig 18.1)
Blood
? specialized type of connective tissue
? cellular & liquid components
– living blood cells
Karen Marshall, Associate Professor • AKA formed elements
– suspended in a nonliving fluid matrix
Montgomery College » plasma
Takoma Park Campus

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Formed Elements Buffy Coat Plasma

? 1) erythrocytes ~ RBCs
– transport oxygen ? thin, whitish layer ? non-living fluid component of blood
– constitute 45% of total vol (sample) ? RBC-plasma jnc ? constitutes 55% of whole blood
? 2) leukocytes ~ WBCs ? contains WBCs and platelets ? straw-colored sticky fluid
– defend against ds ? make up less than 1% bv ? 90% water
? 3) platelets ~ cell fragments
– help stop bleeding

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Plasma Plasma Proteins Plasma Proteins

? contains formed elements & over 100 ? constitute 8% of wt of plasm a ? variety of functions
diff dissolved solutes (Table 18.1) – albumin acct for 60% of wt – transport various solutes around the body
• most abundant of plasma solutes
– nutrients – distribute heat throughout the body
– globulins acct for 36%
– gases – maintain water balance
• alpha, beta
– hormones – transport proteins
• between blood & tissues
– wastes (urea, uric acid, lactic acid) • gamma – role in blood clotting
– products of cell activity – antibodies released during immune response – act as metabolic enzymes, hormones
– ions – clotting proteins acct for 4%
• fibrinogen
– proteins
• prothrombin
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 Albumin Physical Characteristics of Blood Physical Characteristics of Blood
? accts for 60% of plasma proteins
? sticky, opaque fluid ? characteristic color
? carrier to shuttle molecules through the
circulation – due to presence of RBCs – dependent on amt of oxygen present
• major factor contributing to viscosity • scarlet red - high oxygen
? important blood buffer – sticky, thick • dark red - poor oxygen
? major blood protein contributing to ? characteristic metallic taste
plasma osmotic pressure (OP)
– P keeps water in the bloodstream

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Physical Characteristics of Blood Functions of Blood Functions of Blood

? slightly alkaline ? 1) distributive ? 3) protective
– pH between 7.35 and 7.45 – oxygen and nutrients delivery to tissues – hemostasis
? accounts for 8% of body wt – metabolic waste removal • bleeding stoppage
? avg vol (healthy adult) – hormone transport – infection prevention

– males - 5-6 L ? 2) regulatory

– females - 4-5 L – body temp maintenance ? *Functions overlap & interact to maintain
– blood pH constancy constancy of our internal environment
– adequate fluid volume
? **See page 652 for a detailed listing of overlapping fncs
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Formed Elements
? cellular portion of blood
– RBCs, WBCs, platelets
? unusual features
– 1) cells
– 2) survival time in bloodstream
• a few days
– 3) most blood cells do not divide
• continously renewed by division of cells
– bone marrow where they originate

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 Cells Erythrocytes (RBCs) Erythrocytes (RBCs)
? RBCs ? small cell
? ~7.5 um (diameter)
? bags of Hb
– have no nuceli or organelles
? biconcave disc shape – 97%
? platelets – flattened w/ depressed – RBC protein fncs in gas transport
– cell fragments ctr
? a miniature donut
? contain add’l proteins
? WBCs – fnc to maintain PM or promote changes in
? mature
– complete cells shape
– PM, lack nucleus &
organelles
? *RBCs vastly outnumber the other types

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Erythrocytes (RBCs) Hematocrit RBC & Hb

? measure of RBCs as a % of total bv
? fnc ? healthy male ? Hb binds easily & reversibly with oxygen
– pick up oxygen in capillary beds of lungs & – single RBC
– 47% +/- 5%
releases it to tissue cells • ~250 trillion Hb molecules
? healthy fem ale • carries ~ 1 billion molecules of oxygen
– transports ~20% carbon dioxide back to
lungs – 42% +/- 5% ? most oxygen carried in blood is bound
? ~ 2.5 trillion RBCs in a healthy adult to Hb

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RBC & Hb Hb Physiological Jaundice

? composed of protein
? normal Hb values – globin ? can occur in normal newborns
• bound to red heme pigment
– infants - 14-20 g/100 ml (blood) ? 3-4 days after birth
• 4 polypeptide chains
– adult male - 13-18 g/100 ml – 2 alpha chains
– 2 beta chains
? fetal RBCs are short lived
– adult female - 12-16 g/100 ml
» each bounded to a ringlike iron containing heme – break down rapidly after birth
group
? each Fe atom ? infant’s liver is unable to process
– combine reversibly w/ 1 molecule of oxygen bilirubin fast enough
? 1 Hb molecule
– transport 4 molecules of oxygen

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 Physiological Jaundice Structural Characteristics of Oxygen Loading
RBCs ? lungs
? bilirubin
– breakdown product of Hb pigment ? Contribute to gas transport fnc
? direction of transport
– accumulates in blood – lungs to tissue cells
? 1) small size & biconcave shape
• oxygen deficient blood moves through the lung
– deposits in body tissues – large surface area (30% more) – oxygen diffuses from lung air sacs to blood to RBC
» binds to Hb
? 2) over 97% Hb
» binds specifically to iron
? 3) lack mitochondria & generate ATP by » oxyhemoglobin (new 3D shape, bright red)
anaerobic m eans
– do not consume oxygen they transport

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Oxygen Unloading Carbon Dioxide Transport Homeostatic Imbalances

? Hypoxia
? reverse process ? 20% combines w/ Hb
– decreased oxygen delivery to body tissues
? tissues – binds to a.a. of globin
• not heme group ? Hypoxemic hypoxia
? oxygen detaches from iron
• formation of carbaminohemoglobin – decreased arterial pressure
– Hb resumes its former shape – occurs more readily when Hb is dissociated from O2
– caused by pulmonary ds
• deoxyhemoglobin
– reduced Hb
? loading occurs in tissues – breathing too little oxygen
– dark red – direction of transport is from tissues to ? CO poisoning
– released oxygen diffuses from blood into lungs
– unique type of hypoxemic hypoxia
tissue fluid and then into tissue cells • where CO2 is eliminated from the body

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CO CO Poisoning Hematopoiesis~Hemopoiesis
? dangerous
? CO ? blood cell formation
? no characteristic signs
– colorless, odorless gas ? occurs in red bone marrow
? cyanosis, respiratory distress
– competes vigorously w/ oxygen for heme- – soft network of reticular connective tissue
binding sites ? confused • immature blood cells
• Hb affinity for CO is 200x’s > O2 ? throbbing headache • macrophages
– highly successful competitor • fat cells
? trt
• reticular cells
– 100% oxygen – (fibroblasts secrete fibers)

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 Hematopoiesis~Hemopoiesis Hematopoiesis~Hemopoiesis Hematopoiesis~Hemopoiesis
? daily
? red marrow ? each type of bc produced
– the marrow turns out an oz of new blood
– chiefly – different quantities
• ~ 100 billion new cells
• bones of axial skeleton • changing body needs
• girdles • different regulatory factors ? formed elements have different fncs
• proximal epiphyses of humerus & femur ? as bc’s mature – important similarities
• arise from same type of stem cell
– migrate through the thin walls of sinusoids – hematopoietic stem cell ~ hematocytoblast
• wide blood capillaries » resides in red bone marrow
– enter the bloodstream

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Hematopoiesis~Hemopoiesis Erythropoiesis Erythropoiesis

? maturation pathways differ ? erythrocyte production ? 1) proerythroblast stage
– cell is “committed” to a specific bc pathway – RBCs begin as hemocytoblasts – commited cell stage
• proceed from
• cell cannot change
– 1) proerythroblast stage
? 2) erythroblast stage
? “commitment” – 2) erythroblast stage
– early stage
– signal • ribosome synthesis
– 3) normoblast stage
• appearance of membrane surface receptors – late stage
– 4) reticulolyte stages
– respond to specific hormones or GF • Hb accumulation (Hb synthesis & iron accumulation)
» ‘push’the cell to specialization – 5) erythrocyte

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Erythropoiesis Erythropoiesis Erythropoiesis

? 3) normoblast stage ? reticulocyte (young RBC)
? normoblast stage
– RBC transformed into a young reticuloctye – contains scant network of clumped
(RBC) – ~34 % Hb accumulation
• ejection of organelles ribosomes & RER
– ejection of the nucleus
• end of nuclear function – filled w/ Hb
? 4) reticulolyte stages (3-5 day process) • nucleus degeneration & pinching off – enters bloodstream to transport oxygen
– hemoctyoblast to reticulocyte formation • cell collapses inward – becomes fully mature RBC w/in 2 days of
– young RBC – assumes biconcave shape
release
? 5) erythrocyte • ribosomes degraded by IC enzymes
– accts for 1-2% of all RBCs in blood (healthy)

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 Reticulocyte Counts Erythropoiesis Regulation
Erythropoiesis (fig 18.5)
? used clinically ? # of circulating RBCs constant
? rough ID of rate of RBC formation – new cells produced at rate of 2 mil/s
– reflects balance between RBC production
? indicate abnormal rates of RBC
and destruction
formation • too few RBCs
– tissue hypoxia
» oxygen deprivation
• too many RBCs
– increased viscosity

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Erythropoiesis Regulation Erythropoiesis Regulation Erythropoiesis Regulation

? stimulus
? hormonally
– blood O 2 ? rate of EPO production
– dependent on adequate supplies
• # of RBCs – dependent on cell’s ability to transport
• Fe, a.a., certain B vitamins – hemorrhage enough O 2 to meet tissue demands
– direct stimulus – excess RBC destruction
• erythropoietin (EPO) • O 2 availability
? bloodborne EPO
– glycoprotein hormone – high altitudes – stimulates red marrow “committed”RBCs
– small amts circulate in blood at all times – pneumonia • mature more rapidly
» sustains RBC production at a basal rate • tissue demands for O2 – 1-2 days after EPO blood levels
– produced by kidneys – aerobic exercise » rate of reticulocyte release
» when cells become hypoxic
– also produced in liver ? inhibition
– RBCs or O2 in bloodstream
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Erythropoiesis Regulation (fig 18.6) Erythropoiesis Regulation Erythropoiesis Regulation

? hypoxia ? other stimulants
– does not activate bone marrow directly – result in bursts of RBC production
– stimulates kidneys • chemicals released by
• release EPO – leukocytes
– EPO stimulates red bone marrow – platelets
• reticular cells
? other stimulants
– testosterone
• enhances EPO production by kidneys
– RBC counts and Hb in males

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 Dietary Requirements for Erythropoiesis Life Cycle of Red Blood Cells
Dietary Requirements for Erythropoiesis
(fig 18.7)
? proteins, lipids, CHO ? two B-complex vitamins
? Fe – vitamin B 12
– for Hb synthesis • liver, meat, poultry, dairy products (except
butter, egg)
– available from diet
– folic acid
– absorption into bloodstream • liver, orange juice, green veggies, beef, eggs,
• controlled by intestinal cells grains
– body’s supply – essential for DNA synthesis
• 65% is in Hb • developing RBCs
• remainder stored
– liver, spleen, bone marrow

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Erythrocyte Disorders Anemia Anemia

? cause ? condition
? most are classified as anemias or • C) hemolytic ds of newborn
– 1) insufficient # of RBCs
polycythemias • blood loss – AKA erythroblastosis fetalis
– baby becomes anemic and hypoxic
? anemia • excessive destruction of RBCs – result of Rh- mother having an Rh + baby
– condition • bone marrow failure » second pregnancy
• blood has low O2 carrying capacity – condition » ABs developed against fetus
– inadequate blood O2 to support normal metabolism » ABs cross placenta & destroy baby’s RBCs
• A) hemorrhagic anemia
– fatigue, paleness, SOB, chills – blood loss
– symptom of disorders • B) hemolytic anemia
– RBCs lyse or rupture prematurely
• not ds
» Hb abnormality, transfusion of mixed blood
» bacterial or parasitic infection
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Anemia Anemia Polycythemia

– condition – condition
• C) aplastic anemia • B) pernicious anemia ? abnormal excess of RBCs
– destruction or inhibition of red marrow – deficiency of vitamin B12
» bacterial toxins, drugs or radiation » deficiency in intrinsic factor needed for B12 – blood viscosity
absorption by the stomach
? cause – sluggish flow of blood
– 2) Hb content
? cause – dizziness
• normal Hb molecules – 3) abnormal Hb – RBC count
• fewer RBCs present • production of abnormal Hb
– usually has a genetic basis
– condition
– condition
• A) nutritional anemia
– iron deficiency anemia (microcyte - small, pale RBC)
• A) sickle cell anemia
» 2o result of hemorrhagic anemia – globin part of Hb is abnormal
– RBCs are fragile, rupture prematurely
» inadequate iron intake
» impaired iron absorption – serious, incurable, sometimes fatal
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 Leukocytes (WBCs) Leukocytes
? grouped into two major categories
? only formed elements that are complete cells
– based on structural and chemical
– nuclei, organelles
characteristics
? protect the body from damage
– A. Granulocytes
– bacteria
• contain specialized membrane bound
– viruses
cytoplasmic granules
– parasites – neutrophil
– toxins – basophil
– tumor cells – eosinophil
– B. Agranulocytes
• lack cytoplasmic granules
– lymphocytes
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Differential WBC Count (fig 18.9) Leukocytosis

? diagnostic tool
? gives a determination of ? condition of normal homeostatic
relative proportion of response
individual WBC types
– bacterial or viral invasion of the body
? order from most to least
abundant ? WBC count of over 11,000 cells mm3
– Never let monkeys eat
bananas ? WBCs become mobilized for action
• neutrophils – production of twice the # can appear w/in
• lymphocytes
• m onocytes
hours
• eosinophils
• basophils

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Histamine Macrophage Movement of Leukocytes

? 1) ameboid
? phagocytic protective cell type – WBCs form flowing cytoplasmic extensions
? inflammatory chemical
– crucial to body’s defense • move them along
? acts as a vasodilator
? found ? 2) positive chemotaxis
? attracts other WBCs to inflammed site
– connective & lymphatic tissues – movement of WBCs toward molecules
? present in basophils – organs that phagocytize released by damaged cells or other WBCs
• cells • move to areas of tissue damage in large
• bacteria numbers
– destroy foreign substances
• other foreign debris
? originally monocytes ? 3) diapedis
– slip out of the capillary blood vessels
– differentiate tissues • part of the inflammatory response
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 Leukocyte Production
(fig 18.11)

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Platelet Production (fig 18.12) Hemostasis Events of Hemostasis

? 1) vessel dam age
? “plug-the-hole” defensive mechanism
? 2) vessel spasm m echanism
– prevention of blood loss
– constriction of blood vessel
? response is fast, localized, carefully • vasoconstriction
controlled – triggered by
? series of rxns • direct injury to smooth muscle
– involve many blood coagulation factors • release of chemicals
• normally present in plasma & other substances • reflexes from pain receptors
– released by platelets & injured tissue cells – most effective in smaller bv
– reduce blood loss fo 20-30 min
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• allows time for blood clotting to occur 78

Events of Hemostasis Events of Hemostasis Blood Clotting Mechanism

? 3) platelet adhesion & agglutination ? 4) fibrin trap
? damage to blood vessel
– platelets undergo changes – thin, long threads
• swell and form spiked processes • form a loose meshwork over the injured site
? release of clotting factors (CFs)
• become sticky and adhere to exposed collagen • “molecular glue” for aggregated platelets – by platelets trapped at site and damaged
• platelets granules break down and release • trap blood cells bv wall
chemicals – blood clot (coagulation) ? chain rxn events
– serotonin
» enhances vascular spasm – initated by CFs
– ADP ? blood clot production
» attracts more platelets to site
– transformation from a liquid to a gel
– positive feedback mechanism
• formation of platelet plug
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– temporarily seals break in vessel wall 79 10-Feb-03 80 10-Feb-03 81

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 Blood Clotting (fig 18.13)
? Three critical phases
? 1) CF + Ca form PA ? both pathways
(prothrombin activator)
? 2) PA + Ca convert
prothrombin (plasma
protein) into thrombin
(enzyme)
? 3) Thrombin + Ca
convert fibrinogen
(soluble plasma protein)
into fibrin (insoluble)
Intrinsic vs Extrinsic Intrinsic vs Extrinsic
Clotting Mechanisms Clotting Mechanisms
? both pathways
– initiate clotting – require Ca
– usually triggered by same tissue damage – involve activation of series of
– many intermediates are activated only by procoagulants
platelet phospholipid (PF 3) • fnc as enzymes to activate the next
• found on external surface of aggregated • result in factor X activation
platelets – combines w/ Ca + thromboplastin (TF) OR P F 3
PA
– result in formation of PA
– go through the same 3 critical phases
• subsequently clot in 10 to 15 sec

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Intrinsic vs Extrinsic Intrinsic vs Extrinsic

Clot Retraction & Repair
Clotting Mechanisms Clotting Mechanisms
? platelet induced process
? intrinsic pathway ? extrinsic pathway
? occurs w/in 30-60’post clot formation
– slower – faster
– 1) platelets contract like muscle cells
– all CFs are present in blood – initiates clotting inside the body
– 2) serum is squeezed out
– initiates clotting outside the body • tissues
– 3) ruptured vessel edges are drawn
• test tube – tissue trauma causes release of TF
together
• from injured cells
– subsequently bypass several steps in intrinsic – 4) vessel healing occurs simultaneously
pathway • vessel repaired
– smooth muscle
– connective tissue
– endothelial cell proliferation and migration
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Heparin Disorders of Hemostasis

? natural anticoagulant
Thromboembolytic Disorders
– granules of basophils and mast cells ? two major disorders
? A) thrombus
– 1) thromboembolytic disorders
? ordinarily secreted in small amts into – clot develops and persists in an unbroken
• undesirable intravascular clotting
plasma – AKA “hemostasis” in the wrong place
vessel
? inhibitor of normal clot growth – 2) bleeding disorders – blockage of circulation to cells
– prevents a clot from becoming too large • if clot too large
– death of tissue
? inhibits thrombin
? used clinically to prevent undesirable
clotting
– patients at risk for heart attack or stroke 88 89 90
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Thromboembolytic Disorders
? B) embolus
– occurs when thrombus breaks away from
bv wall & floats freely in bloodstream
– no problem until it encounters a bv too
narrow
Bleeding Disorders Bleeding Disorders
? A) thrombocytopenia ? C) Hemophilias
– platelet deficiency – several different hereditary bleeding
? B) impaired liver function disorders
– similar signs and symptoms
– inability of liver to synthesize its usual
supply of procoagulants – managed clinically
• abnormal & severe bleeding • transfusions of fresh plasma or
– due to vitamin K deficiency • injections of purified CFs
– due to impaired liver fnc
» (vitamin K is needed for production of CFs)

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Leukocyte Disorders Leukemia Leukemia

? 1) overproduction of abnormal ? group of cancerous conditions ? acute conditions
leukocytes – involve WBCs – quick advancing
? cells – derived from blast cells
– A) leukemia
• lymphoblasts
– B) infectious mononucleosis – unspecialized
– more serious forms
– mitotic
? 2) abnormally low WBC • primarily affect children
– impair bone marrow fnc
– A) leukopenia ? chronic conditions
? named according to abnormal cell type – slow advancing
• usually induced by drugs primarily involved
– glucocorticoids – involves proliferation of later cell stages
– anti-cancer agents • m yelocytes
– occur more in the elderly
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Leukemia Leukemia Infectious Mononucleosis

? immature WBCs flood into the ? trt ? highly contagious viral ds
bloodstream – radiation ? children & young adults
? bone m arrow becomes occupied by – antileukemic drugs ? caused by Epstein-Barr virus
cancerous leukocytes ? fatal ? excessive #s agranulocytes
? symptoms – w/o therapy ? symptoms
– severe anemia – tired
– achy
– bleeding
– chronic sore throat
– fever
– fever
– weight loss – no cure
– bone pain
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• recovery in a few weeks w/ rest 99

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 Human Blood Groups Human Blood Groups Human Blood Groups
? RBC-PM bears highly specific glycoproteins – ABO blood group
on external surfaces » A, B, AB, O
? presence or absence of each antigen allows
– antigens~agglutinogens – O blood group
classification into blood groups
? different blood types » no agglutinogens
– two agglutinogens (antigens) » most common in all races
– one person’s RBC proteins will be recognized as
• type A – AB blood group
foreign
• transfused into someone w/ diff RBC type
• type B » has both agglutinogens
• recipient’s agglutinins (plasma ABs) clump the foreign » least prevalent
antigen – A blood group
» A agglutinogen
– B blood group
» B agglutinogen

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Human Blood Groups Human Blood Groups Human Blood Groups

? preformed antibodies present in the plasma
– agglutinins
• act against RBCs carrying ABO antigens not – O blood type – B blood group
present on a person’s own RBC (fig 18.13) » possess neither A nor B antigen » possess B antigen
» possess anti-A and anti-B antibodies~ » possess anti-A antibodies~
» possess a and b agglutinins » possess a agglutinins
– A blood group – AB blood group
» possess A antigen » possess AB antigen
» possess anti-B antibodies~ » possess neither antibodies
» possess b agglutinins

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Rh Blood Groups Rh Blood Groups

? at least 8 different types of Rh
agglutinogens ? anti-Rh antibodies are not
– only 3 common spontaneously formed in blood of Rh-
– each is Rh factor persons
– most Americans – unlike the ABO
• 85% Rh+
– if an Rh- person receives Rh+ blood
– RBCs carry the Rh antigen
• immune system produces anti-Rh AB against
the foreign antigen

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 Transfusion Reactions Transfusion Reactions Blood Types
? occur when mismatched blood infused
? universal donor
? cause fever, chills, nausea, vomiting – O blood type
? donor’s RBCs are attacked by the recipent’s
agglutinins ? trt • contains neither antigen
– alkaline fluids to dilute and dissolve the Hb – give transfusion to any group
? three problems
and get it out of the body ? universal recipient
– 1) oxygen carrying capacity of transfused blood
cells are disrupted – diuretics – AB blood type
– 2) clumping of RBCs in small vessels hinders • lack both antibodies
blood flow to tissues beyond those points – receive transfusions from any group
– 3) Hb escaping into the blood stream enters the
kidneys in [ ] renal failure

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Complete Blood Count (CBC) Anemias & Aging

? counts of different types of formed ? usually result of preexisting conditions
elements – disorder
• heart
? hematocrit • blood vessels
• immune system
? tests for clotting factors

? *see lab manual for add’l info

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