Blood

→ The only fluid tissue in the human body

→ Classified as a connective tissue 
▪ Living cells = formed elements
▪ Non-living matrix = plasma
 Erythrocytes (red blood cells, or RBCs)
 Leukocytes (white blood cells, or WBCs)
 Platelets

Physical Characteristics of Blood

 Color range
▪ Oxygen-rich blood is scarlet red
▪ Oxygen-poor blood is dull red
 pH must remain between 7.35–7.45
 Slightly alkaline
 Blood temperature is slightly higher than
body temperature
 5-6 Liters or about 6 quarts /body
▪ 5–6 L for males; 4–5 L for females
Functions of Blood
 Distributing substances
 Regulating blood levels of substances
 Protection
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
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
Protection Functions
 Preventing blood loss
▪ Plasma proteins and platelets initiate
clot formation
 Preventing infection
▪ Antibodies
▪ Complement proteins
▪ WBCs

1 PILONES,RISHELLE MAE M.

Blood Plasma
 Composed of approximately 90 percent
 Includes many dissolved substances
▪ Nutrients 
▪ Salts (metal ions)
▪ Respiratory gases
▪ Hormones
▪ Proteins
▪ Waste products
Plasma proteins most abundant solutes
▪ Remain in blood; not taken up by cells
▪ Proteins produced mostly by liver
▪ 60% albumin; 36% globulins; 4% fibrinogen
▪ Major contributor of plasma osmotic
pressure
Formed Elements
 Erythrocytes = red blood cells  
 Leukocytes = white blood cells
 Platelets = cell fragments
 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

Plasma Proteins
 Albumin – regulates osmotic pressure
 Clotting proteins – help to stem blood loss
when a blood vessel is injured
 Antibodies – help protect the body from
antigens
Albumin
 60% of plasma protein
 Functions
▪ Substance carrier
▪ Blood buffer
2 PILONES,RISHELLE MAE M.

Erythrocytes (Red Blood Cells)
 The main function is to carry oxygen
 Anatomy of circulating erythrocytes
▪ Biconcave disks
▪ Essentially bags of hemoglobin
▪ Anucleate (no nucleus)
▪ Contain very few organelles
 Outnumber white blood cells 1000:1
 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
 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
3 PILONES,RISHELLE MAE M.
 Superb example of complementarity of
structure and function
Erythrocyte Function
 RBCs dedicated to respiratory gas transport
 Hemoglobin binds reversibly with oxygen
 Normal values
→ Males - 13–18g/100ml; Females - 12–16
g/100ml
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
Causes of Anemia
 Three groups
▪ Blood loss
▪ Low RBC production
▪ High RBC destruction
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
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
 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)
 Renal anemia
▪ Lack of EPO
▪ Often accompanies renal disease
▪ Treated with synthetic EPO
 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
Causes of Anemia: High RBC
Destruction
 Hemolytic anemias
▪ Premature RBC lysis
▪ Caused by
→ Hb abnormalities
→ Incompatible transfusions
→ Infections
▪ Usually genetic basis for abnormal Hb
▪ Globin abnormal
→ Fragile RBCs lyse prematurely
 Thalassemias
▪ Typically Mediterranean ancestry
▪ One globin chain absent or faulty
▪ RBCs thin, delicate, deficient in Hb
▪ Many subtypes
→ Severity from mild to severe
 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
Hemoglobin
 Iron-containing protein
 Binds strongly, but reversibly, to oxygen 
 Each hemoglobin molecule has four oxygen
binding sites
 Each erythrocyte has 250 million
hemoglobin molecules
 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
4 PILONES,RISHELLE MAE M.
• O2 loading in lungs
→ Produces oxyhemoglobin (ruby red)
• O2 unloading in tissues
→ Produces deoxyhemoglobin or reduced
hemoglobin (dark red)
• CO2 loading in tissues
→ 20% of CO2 in blood binds to Hb 
carbaminohemoglobin
Leukocytes (White Blood Cells)
 Crucial in the body’s defense against
disease
 These are complete cells, with a nucleus
and organelles
 Able to move into and out of blood vessels
(diapedesis)
 Can move by ameboid motion
 Can respond to chemicals released by
damaged tissues
 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
Leukocyte Levels in the Blood
 Normal levels =4,000 to 11,000 cells/ml
 Abnormal leukocyte levels
▪ Leukocytosis
→ Above 11,000 leukocytes/ml
→ Generally indicates an infection
 Leukopenia
→ Abnormally low leukocyte level
→ Commonly caused by certain
drugs
Types of Leukocytes
 Granulocytes
→ Granules in their cytoplasm can be stained
→ Include neutrophils, eosinophils, and
basophils
→ Larger and shorter-lived than RBCs
→ Lobed nuclei
→ Cytoplasmic granules stain specifically with
Wright's stain
→ All phagocytic to some degree
 Agranulocytes
→ Lack visible cytoplasmic granules
→ Include lymphocytes and monocytes
Granulocytes
 Neutrophils
→ Multilobed nucleus with fine granules
→ Act as phagocytes at active sites of
infection
→ 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"

 Basophils
→ Have histamine-containing granules
→ Initiate inflammation
→ 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

 Eosinophils
→ Large brick-red cytoplasmic granules
→ Found in repsonse to allergies and parasitic
worms
→ Red-staining granules
→ Bilobed nucleus
→ Granules lysosome-like
▪ Release enzymes to digest parasitic
worms
→ Role in allergies and asthma
→ Role in modulating immune response

5 PILONES,RISHELLE MAE M.
 Agranulocytes
 Lymphocytes
→ Nucleus fills most of the cell
→ Play an important role in the immune
response
→ 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
→ Two types
▪ T lymphocytes (T cells) act against virus-
infected cells and tumor cells
▪ B lymphocytes (B cells) give rise to plasma
cells, which produce antibodies
6 PILONES,RISHELLE MAE M.
 Monocytes
→ Largest of the white blood cells
→ Function as macrophages
→ Important in fighting chronic infection
→ Abundant pale-blue cytoplasm
→ Dark purple-staining, U- or kidney-shaped
nuclei
→ 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

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)
 All leukocytes originate from
hemocytoblasts
 Lymphoid stem cells  lymphocytes
 Myeloid stem cells  all others
 Progression of all granulocytes
→ Myeloblast → promyelocyte→
myelocyte→band→ mature cell
 Granulocytes stored in bone marrow
 3 times more WBCs produced than RBCs
→ Shorter life span; die fighting microbes
 Progression of agranulocytes differs
 Monocytes – live several months
▪ Share common precursor with neutrophils
▪ Monoblast →promonocyte→ monocyte
 Lymphocytes – live few hours to decades
▪ Lymphoid stem cell →T lymphocyte
precursors (travel to thymus) and B
lymphocyte precursors
Leukocyte disorders
• Leukopenia
– Abnormally low WBC count—drug induced
7 PILONES,RISHELLE MAE M.
• Leukemias – all fatal if untreated
– Cancer→ overproduction of abnormal WBCs
– Named according to abnormal WBC clone
involved
– Myeloid leukemia involves myeloblast
descendants
– Lymphocytic leukemia involves lymphocytes
• Acute leukemia derives from stem cells;
primarily affects children
• Chronic leukemia more prevalent in older
people
Leukemia
• Cancerous leukocytes fill red bone marrow
– Other lines crowded out→ anemia; bleeding
• Immature nonfunctional WBCs in
bloodstream
• Death from internal hemorrhage;
overwhelming infections
• Treatments
– Irradiation, antileukemic drugs; stem cell
transplants
Infectious Mononucleosis
• Highly contagious viral disease
– Epstein-Barr virus
• High numbers atypical agranulocytes
• Symptoms
– Tired, achy, chronic sore throat, low fever
• Runs course with rest
Platelets
 Derived from ruptured multinucleate cells
(megakaryocytes)
 Needed for the clotting process
 Normal platelet count = 300,000/mm3
 Granules contain serotonin, Ca2+, enzymes,
ADP, and platelet-derived growth factor
(PDGF)
– Act in clotting process
 • Normal = 150,000 – 400,000 platelets /ml
of blood
 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
 Derive from megakaryoblast
– Mitosis but no cytokinesis →megakaryocyte
- large cell with multilobed nucleus
Hematopoiesis – Blood Cell Formation
 Blood cell formation
 Occurs in red bone marrow
 In adult, found in axial skeleton, girdles,
and proximal epiphyses of humerus and
femur
 All blood cells are derived from a common
stem cell (hemocytoblast)
 Hemocytoblast differentiation
→ Lymphoid stem cell produces
lymphocytes
→ Myeloid stem cell produces other
formed elements
 Hematopoietic stem cells
(Hemocytoblasts)
→ Give rise to all formed elements
→ Hormones and growth factors push cell
toward specific pathway of blood cell
development
→ Committed cells cannot change
• New blood cells enter blood sinusoids
Fate of Erythrocytes
 Unable to divide, grow, or synthesize
proteins
 Wear out in 100 to 120 days
 When worn out, are eliminated by
phagocytes in the spleen or liver
 Lost cells are replaced by division of stem
cells
 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
Erythropoiesis: Red Blood Cell
Production
 Stages
▪ Myeloid stem cell transformed into
proerythroblast
▪ In 15 days proerythroblasts develop into
basophilic, then polychromatic, then
orthochromatic erythroblasts, and then
into reticulocytes
▪ Reticulocytes enter bloodstream; in 2 days
mature RBC
Erythropoiesis
 As myeloid stem cell transforms
1. Ribosomes synthesized
2. Hemoglobin synthesized; iron accumulates
8 PILONES,RISHELLE MAE M.
3. Ejection of nucleus; formation of reticulocyte
(young RBC)
 Reticulocyte ribosomes degraded; Then
become mature erythrocytes
 Reticulocyte count indicates rate of RBC
formation
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
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
 Causes of hypoxia
→ Decreased RBC numbers due to
hemorrhage or increased destruction
→ Insufficient hemoglobin per RBC (e.g., iron
deficiency)
→ Reduced availability of O2 (e.g., high
altitudes)
 Effects of EPO
→ Rapid maturation of committed marrow
cells
→ Increased circulating reticulocyte count in
1–2 days
 Some athletes abuse artificial EPO
→ Dangerous consequences
 Testosterone enhances EPO production,
resulting in higher RBC counts in males
 → ADP causes more platelets to stick and
release their contents
→ Serotonin and thromboxane A2
enhance vascular spasm and platelet
aggregation

Vascular Spasms
 Anchored platelets release serotonin
 Serotonin causes blood vessel muscles to
spasm
 Spasms narrow the blood vessel,
Dietary Requirements for
decreasing blood loss
Erythropoiesis  Vasoconstriction of damaged blood vessel
 Nutrients—amino acids, lipids, and
 Triggers
carbohydrates
▪ Direct injury to vascular smooth
 Iron
muscle
▪ Available from diet
▪ Chemicals released by endothelial
▪ 65% in Hb; rest in liver, spleen, and bone
cells and platelets
marrow
▪ Pain reflexes
▪ Free iron ions toxic
 Most effective in smaller blood vessels
→ Stored in cells as ferritin and
hemosiderin
Coagulation
 Injured tissues release thromboplastin
→ Transported in blood bound to protein
 PF3 (a phospholipid) interacts with
transferrin
thromboplastin, blood protein clotting
 Vitamin B12 and folic acid necessary for
factors, and calcium ions to trigger a
DNA synthesis for rapidly dividing cells
clotting cascade
(developing RBCs)
 Prothrombin activator converts
Hemostasis prothrombin to thrombin (an enzyme)
 Stoppage of blood flow
 Thrombin joins fibrinogen proteins into
 Fast series of reactions for stoppage of
hair-like fibrin
bleeding
 Fibrin forms a meshwork (the basis for a
 Requires clotting factors, and substances
clot)
released by platelets and injured tissues
 Reinforces platelet plug with fibrin threads
 Result of a break in a blood vessel
 Blood transformed from liquid to gel
 Hemostasis involves three phases
 Series of reactions using clotting factors
▪ Platelet plug formation
(procoagulants)
▪ Vascular spasms
▪ # I – XIII; most plasma proteins
▪ Coagulation
▪ Vitamin K needed to synthesize 4 of them
Platelet Plug Formation
 Collagen fibers are exposed by a break in a
Blood Clotting
blood vessel
 Blood usually clots within 3 to 6 minutes
 Platelets become “sticky” and cling to
 The clot remains as endothelium
fibers
regenerates
 Anchored platelets release chemicals to
 The clot is broken down after tissue repair
attract more platelets
 Platelets pile up to form a platelet plug
Undesirable Clotting
 Thrombus
 Positive feedback cycle
▪ A clot in an unbroken blood vessel
 Damaged endothelium exposes collagen
▪ Can be deadly in areas like the heart
fibers
 Embolus
▪ Platelets stick to collagen fibers via plasma
▪ A thrombus that breaks away and floats
protein von Willebrand factor
freely in the bloodstream
▪ Swell, become spiked and sticky, and
release chemical messengers
9 PILONES,RISHELLE MAE M.
▪ Can later clog vessels in critical areas such  Based on the presence or absence of two
as the brain antigens
Bleeding Disorders ▪ Type A
 Thrombocytopenia (caused by viruses, ▪ Type B
medications or post-bone CA trtment)  The lack of these antigens is called
▪ Platelet deficiency type O
▪ Even normal movements can cause  The presence of both A and B is called type
bleeding from small blood vessels that AB
require platelets for clotting  The presence of either A or B is called types
 Hemophilia A and B, respectively
▪ Hereditary bleeding disorder Blood Types Determine Blood
▪ Normal clotting factors are missing Compatibility
▪ 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

Blood Groups and Transfusions

 Large losses of blood have serious
consequences
 Loss of 15 to 30 percent causes weakness
 Loss of over 30 percent causes shock,
which can be fatal
 Transfusions are the only way to replace
blood quickly
 Transfused blood must be of the same
blood group
Human Blood Groups
 There are over 30 common red blood cell
antigens
 The most vigorous transfusion reactions
are caused by ABO and Rh blood group
antigens
 RBC membranes bear 30 types of
glycoprotein antigens
▪ Anything perceived as foreign; generates
an immune response
▪ Promoters of agglutination; called
agglutinogens
 Mismatched transfused blood perceived as
foreign
▪ May be agglutinated and destroyed; can be
fatal
 Presence or absence of each antigen is
used to classify blood cells into different
groups
ABO Blood Groups
10
Rh Blood Groups
 Named because of the presence or absence
of one of eight Rh antigens (agglutinogen
D)
 Most Americans are Rh+
 Problems can occur in mixing Rh+ blood
into a body with Rh– blood
Rh Dangers During Pregnancy
 Danger is only when the mother is Rh– and
the father is Rh+, and the child inherits the
Rh+ factor
 The mismatch of an Rh– mother carrying
an Rh+ baby can cause problems for the
unborn child
▪ The first pregnancy usually proceeds
without problems
▪ The immune system is sensitized after the
first pregnancy
PILONES,RISHELLE MAE M.
▪ In a second pregnancy, the mother’s
immune system produces antibodies to
attack the Rh+ blood (hemolytic disease of
the newborn)
Blood Typing
 Blood samples are mixed with anti-A and
anti-B serum
 Coagulation or no coagulation leads to
determining blood type
 Typing for ABO and Rh factors is done in
the same manner
 Cross matching – testing for agglutination
of donor RBCs by the recipient’s serum, and
vice versa
Developmental Aspects of Blood
 Sites of blood cell formation
▪ The fetal liver and spleen are early sites of
blood cell formation
▪ Bone marrow takes over hematopoiesis by
the seventh month
 Fetal hemoglobin differs from hemoglobin
produced after birth
 Fetal blood cells form in fetal yolk sac, liver,
and spleen
 Red bone marrow is primary hematopoietic
area by seventh month
 Blood cells develop from mesenchymal
cells called blood islands
 The fetus forms Hemoglobin F, which has
higher affinity for O2 than hemoglobin A
formed after birth
 Blood diseases of aging
– Chronic leukemias, anemias, clotting
disorders
– Usually precipitated by disorders of
heart, blood vessels, or immune system
Transfusions
• Type O universal donor
– No A or B antigens
• Type AB universal recipient
– No anti-A or anti-B antibodies
• Misleading - other agglutinogens cause
transfusion reactions
• Autologous transfusions
– Patient predonates
Diagnostic Blood Tests
• Hematocrit – test for anemia
• Blood glucose tests – diabetes
• Microscopic examination reveals variations in
size and shape of RBCs, indications of anemias
11
Diagnostic Blood Tests
• Differential WBC count
• Prothrombin time and platelet counts
assess hemostasis
• SMAC, a blood chemistry profile – liver
and kidney disorders
• Complete blood count (CBC) – checks
formed elements, hematocrit, hemoglobin
Basic tests to determine coagulation
1. Activated Partial Thromboplastin Time (aPTT)
→ A reflection of the intrinsic pathway
▪ Isolated prolongations of APPT should
prompt considerations factor VIII,IX,XI or XII
deficiency.
▪ Factor VIII (Haemophilia C) has a variable
phenotype ranging from asymptomatic to
severe bleeding.
▪ Factor XII deficiency is not associated with
a bleeding disorder.
2. Prothrombin Time (PT)
→ This is a reflection of the extrinsic pathway
and common pathway.
→ Test of choice if a patient is on warfarin
therapy
▪ Isolated prolongations of the PT are most
often due to factor VII deficiency .
▪ Common pathway: deficiencies in factors
V,X , thrombin & fibrinogen prolong both
the APTT & PT ,as they are in the common
pathway.
3. Partial thromboplastin time (PTT)
→ Measures coagulation throughout the
intrinsic pathway & common pathway.
▪ Test of choice to monitor a patient on
unfractionated heparin
▪ Routine PTT surveillance is not necessary
for patients on low-molecular weight
heparin.
4. Thrombin Clotting time (TCT)
→ This is a measure of the final step in the
coagulation pathway (the conversion of
fibrinogen to fibrin via the action of
thrombin)
▪ it is sensitive to deficiencies in fibrinogen
and drugs such as direct and indirect
thrombin inhibitors.
5. Bleeding Time (BT)
→ Is a measure of platelet function (how well
platelets can form a clot)
→ Typically elevated in conditions of platelet
dysfunction
PILONES,RISHELLE MAE M.
Coagulation can be initiated by either of time (PTT)* secs
2 distinct pathways Prothrombin 10-13 secs 2x to 3x the
 Intrinsic Pathway time (PT)* or 11-15 normal for
→ Can be initiated by events that take place secs control value in
within the lumen of blood vessels. secs
→ This pathway responds to spontaneous , APTT 30 - 40 secs 1.5x to 2.5x the
internal damage of the vascular normal or
endothelium which requires only elements control value in
(cloting factors , Ca++ , platelet surface secs
etc.) found within ,or intrinsic to the Bleeding Time* 2-7 mins
vascular system.
 Extrinsic pathway
→ Activated secondary to external trauma. Clotting Factors
→ It requires Factor III (tissue FACTOR I Fibrinogen
thromboplastin),a substance which is FACTOR II prothrombin
“extrinsic to” ,or not normally circulating in FACTOR III Tissue
the vessel . thromboplastin or
→ Factor III is released when the vessel wall is tissue factor
ruptured. FACTOR IV Ionized Ca++
 Both intrinsic and extrinsic pathway meet FACTOR V Labile factor or
at a shared point to continue coagulation. proaccelerin
THE COMMON PATHWAY. FACTOR VI unassigned
Liver’s Participation FACTOR VII Stable factor or
▪ The liver must be able to use Vit,K to proconvertin
produce clotting factors FACTOR VIII Antihemophilic factor
III,XII,XI,X,IX,VIII,V,II and I FACTOR IX Plasma
▪ Clotting factors VIII(antihemophilic factor thromboplastin
component or
A), and III (tissue factor) originate from
christmas factor
endothelial cells.
FACTOR X Stuart-power factor
▪ Clotting factor IV (calcium ion) is freely
FACTOR XI Plasma
available in plasma.
thromboplastin
▪ Considerations: antecedent
▫ Newborns need Vit.K FACTOR XII Hageman factor
▫ When the normal intestinal flora is FACTOR XIII Fibrin stabilizing
disturbed factor
Schema of the coagulation cascade
The average size of an RBC
Formula:
HEMATOCRIT
¿ RBC
RBC COUNT

Stem Cell
→ An unspecialized cell that can divide
without limit as needed and can , under
specific conditions , differentiate into
Normal values of blood coagulation tests specialized cells.
→ Divided into several categories according to
TEST NORMAL INR( therapeutic
their potential to differentiate
VALUES range)
 Unipotent & Oligopotent stem cell
Partial 25-30 secs
▪ Oligopotent
thromboplastin or 25-40
12 PILONES,RISHELLE MAE M.
→ Limited to becoming one of a few different
cell types
▪ Unipotent
→ Fully specialized and can only reproduce to
generate more of its own specific cell type.
 Pluripotent Cells
→ Embryonic cells that develop from
totipotent stem cells & are precursors to
the fundamental tissue layers of the
embryo.
→ It is a stem cell is one that has the potential
to differentiate into any type of human
tissue but cannot support the full
development of an organism.
→ Become slightly more specialized , and are
referred to as multipotent cells
 Multipotent Cells
→ Is a stem cell has the potential to
differentiate into different types of cells
within a given cell lineage or small number
of lineages,such as a RBC or WBC.
 Totipotent Cells
→ First embryonic cells that arise from the
division of the zygote are the ultimate stem
cells: these stem cells are described as
because they have the potential to
differentiate into any of the cells needed to
enable an organism to grow & develop
ABO Blood Groups
1st Stage: Vasospasm
 Vasospam of the blood vessels occurs first
in response to injury
 Vasoconstriction is the effect og this initial
response whenever there is a vessel injury
2nd stage: Platelet Plug Formation
 Collagen fibers are exposed by a break in a
blood vessel
 Platelets become “sticky” and cling to the
collagen fibers
 Anchored platelets release chemicals to
attract more platelets
13
 Platelets pile up to form a platelet plug
 During primary hemostasis,platelets clump
up together & form a plug around the site
of injury.Then in the second stage, called
secondary hemostasis, the platelet plug is
reinforced by a protein mesh made up of
fibrin.
3rd stage: Activation of Coagulation
Cascade
 The coagulation cascade involves the
activation of a series of clotting
factors,which are proteins that are involved
in blood clotting
 Each clotting factor is a serine protease , an
enzyme that speeds up the breakdown of
another protein. The clotting factors are
initially in an inactive form called zymogens
4th stage: Formation of “fibrin plug”
 Injured tissues release thromboplastin
 PF3( a phospolipid) interacts with
thromboplastin,blood protein clotting
factors, and calcium ions to trigger a
clotting cascade
 Prothrombin activator converts
prothrombin to thrombin(an
enzymme)
 Blood usually clots withing 3-6 mins
 This clot remains as endothelium
regenerates
 This clot is broken down after issue
repair
PILONES,RISHELLE MAE M.
14 PILONES,RISHELLE MAE M.