C HAPTER 17 Blood. B LOOD C OMPOSITION Blood: a fluid connective tissue composed of Plasma Formed elements Erythrocytes (red blood cells, or RBCs) Leukocytes.
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CHAPTER 17
Blood
BLOOD COMPOSITIONBlood: a fluid connective tissue
composed ofPlasma Formed elements
Erythrocytes (red blood cells, or RBCs)
Leukocytes (white blood cells, or WBCs)
Platelets
BLOOD COMPOSITIONHematocrit
Percent of blood volume that is RBCs
47% ± 5% for males42% ± 5% for femalesConsider 45 % as an average
Copyright © 2010 Pearson Education, Inc. Figure 17.1
1 Withdrawblood and placein tube.
2 Centrifuge theblood sample.
Plasma• 55% of whole blood• Least dense componentBuffy coat• Leukocytes and platelets• <1% of whole bloodErythrocytes• 45% of whole blood• Most dense component
Formedelements
PHYSICAL CHARACTERISTICS AND
VOLUME
Sticky, opaque fluidColor scarlet to dark redpH 7.35–7.4538C~8% of body weightAverage volume: 5 L
FUNCTIONS OF BLOOD
1. Distribution of O2 and nutrients to body
cells Metabolic wastes to the
lungs and kidneys for elimination
Hormones from endocrine organs to target organs
FUNCTIONS OF BLOOD
2. Regulation of Body temperature by
absorbing and distributing heat
Normal pH using buffers
Adequate fluid volume in the circulatory system
FUNCTIONS OF BLOOD3. Protection against
Blood loss Plasma proteins and platelets
initiate clot formation
Infection Antibodies Complement proteins WBCs defend against foreign
invaders
BLOOD PLASMA90% waterProteins are mostly produced by the liver60% albumin36% globulins 4% fibrinogen
BLOOD PLASMANitrogenous by-products of
metabolism—lactic acid, urea, creatinine
Nutrients—glucose, carbohydrates, amino acids
Electrolytes—Na+, K+, Ca2+, Cl–, HCO3
– Respiratory gases—O2 and CO2
Hormones
FORMED ELEMENTSOnly WBCs are complete cellsRBCs have no nuclei or organellesPlatelets are cell fragmentsMost formed elements survive in
the bloodstream for only a few days
Most blood cells originate in bone marrow and do not divide
Copyright © 2010 Pearson Education, Inc. Figure 17.2
Platelets
Neutrophils Lymphocyte
Erythrocytes Monocyte
ERYTHROCYTESBiconcave discs, anucleate, essentially no organelles
Filled with hemoglobin (Hb) for gas transportProvide flexibility to change shape as necessary
Are the major factor contributing to blood viscosity
Copyright © 2010 Pearson Education, Inc. Figure 17.3
2.5 µm
7.5 µm
Side view (cut)
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 is
anaerobic; no O2 is used in generation of ATP
A superb example of complementarity of structure and function!
ERYTHROCYTE FUNCTION
RBCs are dedicated to respiratory gas transport
Hemoglobin binds reversibly with oxygen
ERYTHROCYTE FUNCTION
Hemoglobin structureProtein globin: two alpha and two
beta chainsHeme pigment bonded to each
globin chain Iron atom in each heme can bind to
one O2 molecule Each Hb molecule can transport four
O2
Copyright © 2010 Pearson Education, Inc. Figure 17.4
Hemegroup
(a) Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups.
(b) Iron-containing heme pigment. Globin chains
Globin chains
HEMOGLOBIN (HB)O2 loading in the lungs
Produces oxyhemoglobin (ruby red)O2 unloading in the tissues
Produces deoxyhemoglobin or reduced hemoglobin (dark red)
CO2 loading in the tissuesProduces carbaminohemoglobin
(carries 20% of CO2 in the blood)
HEMATOPOIESIS
Hematopoiesis (hemopoiesis): blood cell formation Occurs in red bone marrow of
axial skeleton, girdles and proximal epiphyses of humerus and femur
HEMATOPOIESISHemocytoblasts (hematopoietic
stem cells)Give rise to all formed elementsHormones and growth factors
push the cell toward a specific pathway of blood cell development
New blood cells enter blood sinusoids
ERYTHROPOIESIS Erythropoiesis: red blood cell
production A hemocytoblast is
transformed into a proerythroblast
Proerythroblasts develop into early erythroblasts
REGULATION OF ERYTHROPOIESIS
Too few RBCs leads to tissue hypoxia
Too many RBCs increases blood viscosity
Balance between RBC production and destruction depends onHormonal controls Adequate supplies of iron,
amino acids, and B vitamins
HORMONAL CONTROL OF ERYTHROPOIESIS
Erythropoietin (EPO)Direct stimulus for
erythropoiesis Released by the kidneys in
response to hypoxia
HORMONAL CONTROL OF ERYTHROPOIESIS
Causes of hypoxia Hemorrhage or increased RBC
destruction reduces RBC numbers
Insufficient hemoglobin (e.g., iron deficiency)
Reduced availability of O2 (e.g., high altitudes)
HORMONAL CONTROL OF ERYTHROPOIESIS
Effects of EPOMore rapid maturation of
committed bone marrow cellsIncreased circulating
reticulocyte count in 1–2 days
Testosterone also enhances EPO production, resulting in higher RBC counts in males
Copyright © 2010 Pearson Education, Inc. Figure 17.6, step 5
Kidney (and liver toa smaller extent)releaseserythropoietin. Erythropoietin
stimulates redbone marrow.
Enhancederythropoiesisincreases RBCcount.
O2- carryingability of bloodincreases.
Homeostasis: Normal blood oxygen levels
Stimulus:Hypoxia (low bloodO2- carrying ability)
due to• Decreased
RBC count• Decreased amount
of hemoglobin• Decreased
availability of O2
1
2
3
4
5
IMBALANCE
IMBALANCE
DIETARY REQUIREMENTS FOR ERYTHROPOIESIS
Nutrients— amino acids, lipids, and carbohydrates
IronStored in Hb (65%), the liver, spleen, and
bone marrowStored in cells as ferritin and hemosiderinTransported loosely bound to the protein
transferrin Vitamin B12 and folic acid —necessary for
DNA synthesis for cell division
FATE AND DESTRUCTION OF ERYTHROCYTES
Life span: 100–120 days
Old RBCs become fragile, and Hb begins to degenerate
Macrophages engulf dying RBCs in the spleen
FATE AND DESTRUCTION OF ERYTHROCYTES
Heme and globin are separatedIron is salvaged for reuseHeme is degraded to yellow the
pigment bilirubinLiver secretes bilirubin (in bile)) into
the intestines Degraded pigment leaves the body
in feces as stercobilin Globin is metabolized into amino
acids
Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 1
Low O2 levels in blood stimulatekidneys to produce erythropoietin.1
Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 4
Low O2 levels in blood stimulatekidneys to produce erythropoietin.1
Erythropoietin levels risein blood.2
Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.
3
New erythrocytesenter bloodstream;function about 120 days.
4
Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 5
Aged and damaged redblood cells are engulfed bymacrophages of liver,spleen, and bonemarrow; thehemoglobin isbroken down.
5 Hemoglobin
Aminoacids
GlobinHeme
Circulation
Iron storedas ferritin,hemosiderin
Bilirubin
Bilirubin is picked up from bloodby liver, secreted into intestine inbile, metabolized to stercobilin bybacteria, and excreted in feces.
Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 6
Aged and damaged redblood cells are engulfed bymacrophages of liver,spleen, and bonemarrow; thehemoglobin isbroken down.
5
Raw materials aremade available in bloodfor erythrocyte synthesis.
6
Hemoglobin
Aminoacids
Globin
Iron is bound totransferrin and releasedto blood from liver asneeded for erythropoiesis.
Food nutrients,including amino acids,Fe, B12, and folic acid,are absorbed fromintestine and enterblood.
Heme
Circulation
Iron storedas ferritin,hemosiderin
Bilirubin
Bilirubin is picked up from bloodby liver, secreted into intestine inbile, metabolized to stercobilin bybacteria, and excreted in feces.
Copyright © 2010 Pearson Education, Inc. Figure 17.7
Low O2 levels in blood stimulate kidneys to produce erythropoietin.
1
Erythropoietin levels risein blood.2
Erythropoietin and necessaryraw materials in blood promoteerythropoiesis in red bone marrow.
3
Aged and damagedred blood cells areengulfed by macrophagesof liver, spleen, and bonemarrow; the hemoglobinis broken down.
5
New erythrocytesenter bloodstream;function about 120 days.
4
Raw materials aremade available in bloodfor erythrocyte synthesis.
6
Hemoglobin
Aminoacids
Globin
Iron is bound totransferrin and releasedto blood from liver asneeded for erythropoiesis.
Food nutrients,including amino acids,Fe, B12, and folic acid,are absorbed fromintestine and enterblood.
Heme
Circulation
Iron storedas ferritin,hemosiderin
Bilirubin
Bilirubin is picked up from bloodby liver, secreted into intestine inbile, metabolized to stercobilin bybacteria, and excreted in feces.
ERYTHROCYTE DISORDERS
Anemia: blood has abnormally low O2-carrying capacityA sign rather than a disease
itselfBlood O2 levels cannot support
normal metabolismAccompanied by fatigue,
paleness, shortness of breath, and chills
CAUSES OF ANEMIA
1. Insufficient erythrocytes Hemorrhagic anemia: acute
or chronic loss of blood Hemolytic anemia: RBCs
rupture prematurely Aplastic anemia:
destruction or inhibition of red bone marrow
CAUSES OF ANEMIA
2. Low hemoglobin content Iron-deficiency anemia
Secondary result of hemorrhagic anemia or
Inadequate intake of iron-containing foods or
Impaired iron absorption
CAUSES OF ANEMIA
Pernicious anemia ( a hereditory condition)Deficiency of vitamin B12
Lack of intrinsic factor needed for absorption of B12
Treated by intramuscular injection of B12 or application of Nascobal
CAUSES OF ANEMIA
3. Abnormal hemoglobin Thalassemias (a hereditory
condition) Absent or faulty globin
chain RBCs are thin, delicate,
and deficient in hemoglobin
CAUSES OF ANEMIASickle-cell anemia (a hereditory condition)Defective gene codes for abnormal hemoglobin (HbS)
Causes RBCs to become sickle shaped in low-oxygen situations
Copyright © 2010 Pearson Education, Inc. Figure 17.8
1 2 3 4 5 6 7 146
1 2 3 4 5 6 7 146
(a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain.
(b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin.
ERYTHROCYTE DISORDERS
Polycythemia: excess of RBCs that increase blood viscosity
Results from:Polycythemia vera—bone marrow
cancerSecondary polycythemia—when less
O2 is available (high altitude) or when EPO production increases
Blood doping
LEUKOCYTESMake up <1% of total blood volumeCan leave capillaries via diapedesisMove through tissue spaces by
ameboid motion and positive chemotaxis
Leukocytosis: WBC count over 11,000/mm3
Normal response to bacterial or viral invasion
Copyright © 2010 Pearson Education, Inc. Figure 17.9
Formedelements
Platelets
Leukocytes
Erythrocytes
DifferentialWBC count(All total 4800 –10,800/l)
Neutrophils (50 – 70%)
Lymphocytes (25 – 45%)
Eosinophils (2 – 4%)
Basophils (0.5 – 1%)
Monocytes (3 – 8%)
Agranulocytes
Granulocytes
GRANULOCYTESGranulocytes: neutrophils, eosinophils, and basophilsCytoplasmic granules stain
specifically with Wright’s stainLarger and shorter-lived than
RBCsLobed nucleiPhagocytic
NEUTROPHILSMost numerous WBCsPolymorphonuclear leukocytes
(PMNs)Fine granules take up both acidic
and basic dyesGive the cytoplasm a lilac colorGranules contain hydrolytic
enzymes or defensins Very phagocytic—“bacteria
slayers”
EOSINOPHILSRed-staining, bilobed nuclei Red to crimson (acidophilic) coarse, lysosome-like granules
Digest parasitic worms that are too large to be phagocytized
Modulators of the immune response
BASOPHILSRarest WBCsLarge, purplish-black (basophilic)
granules contain histamineHistamine: an inflammatory
chemical that acts as a vasodilator and attracts other WBCs to inflamed sites
Are functionally similar to mast cells
Copyright © 2010 Pearson Education, Inc. Figure 17.10 (a-c)
(a) Neutrophil; multilobed nucleus
(b) Eosinophil; bilobed nucleus, red cytoplasmic granules
(c) Basophil; bilobed nucleus, purplish-black cytoplasmic granules
AGRANULOCYTESAgranulocytes: lymphocytes and monocytesLack visible cytoplasmic granules
Have spherical or kidney-shaped nuclei
LYMPHOCYTES
Large, dark-purple, circular nuclei with a thin rim of blue cytoplasm
Mostly in lymphoid tissue; few circulate in the blood
Crucial to immunity
LYMPHOCYTES
Two types T cells act against virus-infected cells and tumor cells
B cells give rise to plasma cells, which produce antibodies
MONOCYTESThe largest leukocytes
Abundant pale-blue cytoplasm
Dark purple-staining, U- or kidney-shaped nuclei
MONOCYTESLeave circulation, enter tissues,
and differentiate into macrophagesActively phagocytic cells;
crucial against viruses, intracellular bacterial parasites, and chronic infections
Activate lymphocytes to mount an immune response
Copyright © 2010 Pearson Education, Inc. Figure 17.10d, e
(d) Small lymphocyte; large spherical nucleus
(e) Monocyte; kidney-shaped nucleus
Copyright © 2010 Pearson Education, Inc. Table 17.2 (1 of 2)
Copyright © 2010 Pearson Education, Inc. Table 17.2 (2 of 2)
LEUKOPOIESISProduction of WBCs
Stimulated by chemical messengers from bone marrow and mature WBCs All leukocytes originate from
hemocytoblasts
LEUKOCYTE DISORDERS Leukopenia
Abnormally low WBC count—drug induced Leukemias
Cancerous conditions involving WBCsNamed according to the abnormal WBC
clone involved Acute leukemia and primarily affects
children Chronic leukemia is more prevalent in older
people
LEUKEMIA Bone marrow totally occupied with
cancerous leukocytes Immature nonfunctional WBCs in the
bloodstream Death caused by internal hemorrhage
and overwhelming infections Treatments include irradiation,
antileukemic drugs, and stem cell transplants
PLATELETS Small fragments of megakaryocytes
Formation is regulated by thrombopoietin
Blue-staining outer region, purple granules
Granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF)
PLATELETSForm a temporary platelet plug
that helps seal breaks in blood vessels
Circulating platelets are kept inactive and mobile by NO and prostacyclin from endothelial cells of blood vessels
Copyright © 2010 Pearson Education, Inc. Figure 17.12
Stem cell Developmental pathway
Hemocyto-blast Megakaryoblast
PromegakaryocyteMegakaryocyte Platelets
HEMOSTASIS Fast series of reactions for
stoppage of bleeding1. Vascular spasm
2. Platelet plug formation (this is not clotting)
3. Coagulation (blood clotting)
VASCULAR SPASM
Vasoconstriction of damaged blood vessel
TriggersDirect injuryChemicals released by
endothelial cells and platelets Pain reflexes
PLATELET PLUG FORMATION
Positive feedback cycleAt site of blood vessel injury, platelets
Stick to exposed collagen fibers with the help of von Willebrand factor, a plasma protein
Swell, become spiked and sticky, and release chemical messengersADP causes more platelets to stick and release their contents
Serotonin and thromboxane A2 enhance vascular spasm and more platelet aggregation
Copyright © 2010 Pearson Education, Inc. Figure 17.13
Collagenfibers
Platelets
Fibrin
Step Vascular spasm• Smooth muscle contracts, causing vasoconstriction.
Step Platelet plugformation
• Injury to lining of vessel exposes collagen fibers; platelets adhere.
• Platelets release chemicals that make nearby platelets sticky; platelet plug forms.
Step Coagulation• Fibrin forms a mesh that traps red blood cells and platelets, forming the clot.
1
2
3
COAGULATION A set of reactions in which blood
is transformed from a liquid to a gel
Reinforces the platelet plug with fibrin threads
COAGULATION Three phases of coagulation
1. Prothrombin activator is formed (intrinsic and extrinsic pathways)
2. Prothrombin is converted into thrombin
3. Thrombin catalyzes the joining of fibrinogen to form a fibrin mesh
Copyright © 2010 Pearson Education, Inc. Figure 17.14 (1 of 2)
Vessel endothelium ruptures,exposing underlying tissues(e.g., collagen)
PF3
released byaggregated
platelets
XII
XI
IX
XIIa
Ca2+
Ca2+
XIa
IXa
Intrinsic pathwayPhase 1Tissue cell traumaexposes blood to
Platelets cling and theirsurfaces provide sites formobilization of factors
Extrinsic pathway
Tissue factor (TF)
VII
VIIa
VIII
VIIIa
Ca2+
X
Xa
Prothrombinactivator
PF3
TF/VIIa complexIXa/VIIIa complex
V
Va
Copyright © 2010 Pearson Education, Inc. Figure 17.14 (2 of 2)
Ca2+
Phase 2
Phase 3
Prothrombinactivator
Prothrombin (II)
Thrombin (IIa)
Fibrinogen (I)(soluble)
Fibrin(insolublepolymer) XIII
XIIIa
Cross-linkedfibrin mesh
COAGULATION PHASE 1: TWO PATHWAYS TO PROTHROMBIN
ACTIVATOR
Initiated by either the intrinsic or extrinsic pathway (usually both)Triggered by tissue-damaging eventsInvolves a series of procoagulantsEach pathway cascades toward
factor X
Factor X complexes with Ca2+, PF3, and factor V to form prothrombin activator
COAGULATION PHASE 1: TWO PATHWAYS TO PROTHROMBIN
ACTIVATOR
Intrinsic pathway Is triggered by negatively charged
surfaces (activated platelets, collagen, glass)
Uses factors present within the blood (intrinsic)
Extrinsic pathway Is triggered by exposure to tissue factor
(TF) or factor III (an extrinsic factor)Bypasses several steps of the intrinsic
pathway, so is faster
COAGULATION PHASE 2: PATHWAY TO THROMBIN
Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin
COAGULATION PHASE 3: COMMON PATHWAY TO THE
FIBRIN MESH
Thrombin converts soluble fibrinogen into fibrin
Fibrin strands form the structural basis of a clot
Fibrin causes plasma to become a gel-like trap for formed elements
Thrombin (with Ca2+) activates factor XIII which:Cross-links fibrinStrengthens and stabilizes the clot
Copyright © 2010 Pearson Education, Inc. Figure 17.15
FACTORS PREVENTING UNDESIRABLE CLOTTING
Platelet adhesion is prevented bySmooth endothelial lining of blood
vesselsAntithrombic substances nitric oxide
and prostacyclin secreted by endothelial cells
DISORDERS OF HEMOSTASIS
Thromboembolytic disorders: undesirable clot formation
Bleeding disorders: abnormalities that prevent normal clot formation
THROMBOEMBOLYTIC CONDITIONS
Thrombus: clot that develops and persists in an unbroken blood vesselMay block circulation, leading to tissue
death
Embolus: a thrombus freely floating in the blood streamPulmonary emboli impair the ability of the
body to obtain oxygenCerebral emboli can cause strokes
THROMBOEMBOLYTIC CONDITIONS
Prevented byAspirin
Antiprostaglandin that inhibits thromboxane A2
HeparinAnticoagulant used clinically for pre- and postoperative cardiac care
WarfarinUsed for those prone to atrial fibrillation
BLEEDING DISORDERS Thrombocytopenia: deficient number
of circulating plateletsPetechiae appear due to
spontaneous, widespread hemorrhage
Due to suppression or destruction of bone marrow (e.g., malignancy, radiation)
Platelet count <50,000/mm3 is diagnostic
Treated with transfusion of concentrated platelets
BLEEDING DISORDERS Impaired liver function
Inability to synthesize procoagulants Causes include vitamin K deficiency,
hepatitis, and cirrhosisLiver disease can also prevent the
liver from producing bile, impairing fat and vitamin K absorption
BLEEDING DISORDERS Hemophilias include several similar
hereditary bleeding disorders Hemophilia A: most common type (77% of
all cases); due to a deficiency of factor VIIIHemophilia B: deficiency of factor IXHemophilia C: mild type; deficiency of
factor XI Symptoms include prolonged bleeding,
especially into joint cavities Treated with plasma transfusions and
injection of missing factors
TRANSFUSIONS
Whole-blood transfusions are used when blood loss is substantial
Packed red cells (plasma removed) are used to restore oxygen-carrying capacity
Transfusion of incompatible blood can be fatal
HUMAN BLOOD GROUPS
RBC membranes bear 30 types glycoprotein antigens that arePerceived as foreign if transfused
blood is mismatchedUnique to each individual Promoters of agglutination and are
called agglutinogens Presence or absence of each antigen is
used to classify blood cells into different groups
BLOOD GROUPSHumans have 30 varieties of
naturally occurring RBC antigensAntigens of the ABO and Rh blood
groups cause vigorous transfusion reactions
Other blood groups (MNS, Duffy, Kell, and Lewis) are usually weak agglutinogens
ABO BLOOD GROUPSTypes A, B, AB, and O Based on the presence or absence of
two antigens (agglutinins), A and B on the surface of the RBCs
Blood also contain anti-A or anti-B antibodies (agglutinins) in the plasma that act against transfused RBCs with ABO antigens not normally present
Anti-A or anti-B form in the blood at about 2 months of age
Copyright © 2010 Pearson Education, Inc. Table 17.4
RH BLOOD GROUPS
There are 45 different Rh agglutinogens (Rh factors)
C, D, and E are most common
Rh+ indicates presence of D
RH BLOOD GROUPS
Anti-Rh antibodies are not spontaneously formed in Rh– individuals
Anti-Rh antibodies form if an Rh– individual receives Rh+ blood
A second exposure to Rh+ blood will result in a typical transfusion reaction
HOMEOSTATIC IMBALANCE: HEMOLYTIC DISEASE OF THE
NEWBORN
Also called erythroblastosis fetalisRh– mother becomes sensitized
when exposure to Rh+ blood causes her body to synthesize anti-Rh antibodies
Anti-Rh antibodies cross the placenta and destroy the RBCs of an Rh+ baby
HOMEOSTATIC IMBALANCE: HEMOLYTIC DISEASE OF THE
NEWBORN
The baby can be treated with prebirth transfusions and exchange transfusions after birth
RhoGAM serum containing anti-Rh can prevent the Rh– mother from becoming sensitized
TRANSFUSION REACTIONS
Occur if mismatched blood is infused Donor’s cells
Are attacked by the recipient’s plasma agglutinins
Agglutinate and clog small vesselsRupture and release free hemoglobin
into the bloodstream Result in
Diminished oxygen-carrying capacityHemoglobin in kidney tubules and
renal failure
BLOOD TYPINGWhen serum containing anti-A or
anti-B agglutinins is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogens
Positive reactions indicate agglutination
ABO BLOOD TYPING Blood Type Being Tested
RBC Agglutinogens
Serum Reaction
Anti-A Anti-B
AB A and B + +
B B – +
A A + –
O None – –
Copyright © 2010 Pearson Education, Inc. Figure 17.16
SerumAnti-A
RBCs
Anti-B
Type AB (containsagglutinogens A and B;agglutinates with bothsera)
Blood being tested
Type A (containsagglutinogen A;agglutinates with anti-A)
Type B (containsagglutinogen B;agglutinates with anti-B)
Type O (contains noagglutinogens; does notagglutinate with eitherserum)
RESTORING BLOOD VOLUME
Death from shock may result from low blood volume
Volume must be replaced immediately withNormal saline or multiple-electrolyte
solution that mimics plasma electrolyte composition
Plasma expanders (e.g., purified human serum albumin, hetastarch, and dextran) Mimic osmotic properties of albuminMore expensive and may cause significant complications
DIAGNOSTIC BLOOD TESTS
HematocritBlood glucose testsMicroscopic examination reveals variations in size and shape of RBCs, indications of anemias
DIAGNOSTIC BLOOD TESTS
Differential WBC countProthrombin time and platelet counts assess hemostasis
SMAC, a blood chemistry profile
Complete blood count (CBC)
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