BLOOD PHYSIOLOGY

Jammaella Vernice T. Gomez, PTRP

 FUNCTIONS

Distribution
Regulation
Protection
 DISTRIBUTION

 Delivers oxygen from the lungs and nutrients

from the digestive tract to all body cells
 Transports metabolic waste products from
cells to elimination sites (to the lungs for
elimination of carbon dioxide, and to the
kidneys for disposal of nitrogenous wastes in
urine).
 Transports hormones from the endocrine
organs to their target organs.
 REGULATION

 Maintains appropriate body temperature

 Maintains normal pH in body tissues
 Maintains adequate fluid volume in the
circulatory system
 PROTECTION

 Prevents blood loss

 Prevents infection
 CHARACTERISTICS AND
VOLUME
 Sticky
 Metallic taste
 Color:
 Scarlet (oxygen rich)
 Dark red (oxygen poor)
 5x more viscous than H20
 pH: 7.35 to 7.45
 Temperature: 38°C
 Accounts for 8% of body weight
 Volume:
 Male: 5-6 L
 Female: 4-5 L
BLOOD COMPOSITION
COMPOSITION OF BLOOD
 BLOOD PLASMA

 Water
 Solutes
 WATER

 90% of plasma volume

 Dissolving and suspending medium for solutes of
blood
 Absorbs heat
 SOLUTES

 Plasma proteins
 Nonprotein nitrogenous substances

 Nutrients (organic)

 Electrolytes

 Respiratory gases

 Hormones
 PLASMA PROTEINS

 8% (by weight) of plasma volume

 Maintains water balance in blood by osmotic
pressure
 an important reserve supply of amino acids for cell
nutrition
 ALBUMIN
 the smallest and most abundant; 60% of
plasma protein; Produced by liver
 Main contributor to osmotic pressure

 Reductions - result in a loss of fluid from the

blood and a gain of fluid in the interstitial
space
 plays an important role in plasma transport
of substances (drugs, hormones and fatty
acids)
 GLOBULINS
 36% of plasma proteins
 Three classes:
 Alpha,
 Beta
 Gamma

 The globulins include :

 high density lipoproteins (HDL), an alpha-1 globulin
 low density lipoproteins (LDL), a beta-1 globulin
 ALPHA, BETA

 Produced by liver
 Mostly transport proteins that bind to lipids, metal
ions and fat-soluble vitamins
 GAMMA

 Antibodies released by plasma cells during immune

response
 FIBRINOGEN

 4% of plasma proteins
 Produced by liver

a soluble precursor of a sticky protein

called fibrin, which forms the
framework of blood clot.
 plays a key role in coagulation of
blood
 NONPROTEIN NITROGENOUS
SUBSTANCES
 By products of cellular metabolism
 Urea
 Uric acid
 Creatinine
 Ammonium salts
 NUTRIENTS (ORGANIC)

 Materials absorbed from the digestive tract and

transported for use throughout the body
 Glucose and other simple carbohydrates
 Amino acids
 Fatty acids
 Glycerol and triglycerides (fat products)
 Cholesterol
 Vitamins
 ELECTROLYTES

 Includes:
 Sodium
 Potassium
 Calcium
 Magnesium
 Chloride
 Phosphate
 Sulfate
 Bicarbonate
 RESPIRATORY GASES

 Oxygen
 Carbon dioxide
 HORMONES

 Steroid and thyroid hormones carried by plasma

proteins
 FORMED ELEMENTS

 Erythrocytes

 Leukocytes

 Platelets
ERYTHROCYTES
(RED BLOOD CELLS)
STRUCTURAL CHARACTERISTICS

 Biconcave discs
 Anucleated, no organelles
 Life span: 120 days
 Production:
 Early few week sof embryonic life:
 yolk sac
 Middle trimester of gestation:
 Liver, spleen & lymph node
 Latter part of gestation & After birth
 5 y/o- bone marrow
 >20 y/o- membranous bones
 Normal values:
 Male: 5.2 to 6.4 million/mm3
 Female: 4.8 million/mm3
 FUNCTION

 Respiratory gas (oxygen and carbon dioxide)

transport
 Transports hemoglobin → carries O2 from the lungs to the
tissues
 Contains large quantity of carbonic anhydrase
 Responsible for most of the buffering of the whole blood
 HEMATOPOIESIS (BLOOD
CELL FORMATION)
`

➢OCCURS IN THE RED BONE

MARROW
Within 2 days of release,
reticulocytes become
Proerythroblasts give
PROERYTHROBLAST Asrise
EARLY
They to erythroblast
early
produce NORMOBLAST
huge ERYTHROBLAST
LATE Mature
begins when a ERYTHROBLASTS
number
is transformed
of ribosomes
to TheNucleus
When result isdegenerates
aERYTHROCYTES
normoblast has
HEMOCYTOBLAST is
Hemoglobin
color of the accumulated
synthesis
cell cytoplasm and
andpinched
changes as thealmost all of its
off and
transformed into a hemoglobin, it ejects most of
iron accumulation
blue-staining ribosomes becomeassume
occur biconcave
masked by
its organelles
the pink color of hemoglobinshape
HEMATOPOIESIS – BLOOD CELL FORMATION
REGULATION OF RBC
 Tissue oxygenation – basic regulator of RBC
production
 Any condition that will decrease the qty. of O2
transported to the tissues → inc. rate of RBC production
 Anemia
 Destruction of major portions of bone marrow

 High altitude

 Cardiac failure & lung diseases

 REGULATION OF RBC

 Erythropoietin
 Principal factor that stimulates RBC production
 Areas formed:
 Kidney – 90%
 Liver

 Non-renal sources- epinephrine, noreepinephrine & prostaglandins →

stimulates kidneys
 Main effect:
 Stimulates the formation of proerythroblast from its stem cell
 Speeds up the production/differentiation of new cells from
proerythroblast to different erythrroblastic stage
ERYTHROGENESIS
MATURATION OF RBC

 Folic acid
 Vitamin B12
 HEMOGLOBIN

 under normal conditions, oxygen is carried to the

tissues almost entirely by hemoglobin; Binds with
oxygen
 15 grams of hemoglobin in each 100ml of blood
 Protein that makes red blood cells red
 Made up of globin (4 protein chains) bound to iron-
containing heme
 Carries oxygen (oxyhemoglobin) and carbon
dioxide (carbaminohemoglobin)
 Normal Values:
 Male: 13–18 g/dL
 Female: 12–16 g/dL
FORMATION OF HEMOGLOBIN
DESTRUCTION OF RBC
 Once released from the cell → It will burst & RELEASE
HEMOGLOBIN → hemoglobin will be phagocytized
by macrophages in the liver (kupffer), spleen &
bone marrow
 After a few days → iron from hemoglobin is released
by macrophage→ blood:
 Bone marrow produce new RBC
 Liver or other tissues stores (ferritin) → porphyrin (heme)→
bilirubin → released into the blood → liver →bile →
excreted in the form of urine
DISORDERS OF RBC

the red blood

cells become
rigid and
sticky and are
shaped like
sickles or
crescent
moons
DISORDERS OF RBC
 Anemia  Polycythemia
 Deficiency of RBC
 Too rapid loss of RBC
 Too slow production of

RBC
LEUKOCYTES
 LEUKOCYTES (WBCS)

 Complete cells with nuclei and usual organelles

 <1% of total blood volume
 Produced & stored:
› Bone marrow: granulocytes, monocytes & lymphocytes
› Lymph tissue: lymphocytes & plasma cells
 4800-10,800/mm3
 Help protect the body from diseases by:
› Phagocytosis & immunocytic
LEUKOCYTES (WBCS)

 Life span:
 Granulocytes: blood: 4-8 hours; tissues: 4-5 days
 Monocytes: blood: 10-20 hours; tissue (macrophages)-
months- years
 Lymphocytes: weeks – years depending in the body’s
needs
TYPES OF WBC
 GRANULOCYTES

 Neutrophils, eosinophils and basophils

 Roughly spherical in shape

 Larger than erythrocytes

 Lobed nuclei

 Phagocytic in nature
 NEUTROPHILS
 Polymorphonuclear
neutrophils (PMNs) or
simply polys
 50-70% or 40-75%
 2-5 lobes
 Mature cells can
immediately destroy
bacteria and fungi
 Attracted to
inflammatory sites
NEUTROPHILS
 EOSINOPHILS
 2-4%
 2-3 lobes (bilobed)
 Red/orange granules
 Counterattack
parasitic infections:
› Flat worms
› Round worms
 Lessens severity of
allergies
 BASOPHILS
 0.5-1%
 Purplish-black
histamine-containing
granules
 Histamine is an
inflammatory chemical
that acts as a
vasodilator
 Attracts other white
blood cells to the
inflamed site
 Associated with
immediate immune
response (asthma, hay
fever [allergic rhinitis],
anaphylaxis)
 AGRANULOCYTES

 Lymphocytes and monocytes

 Lack visible cytoplasmic granules

 Nuclei are typically spherical or kidney shaped

 LYMPHOCYTES
 25-45%
 Large nucleus with a small
amount of cytoplasm
 Firmly emeshed in lymphoid
tissues
 Types
› B cells
› Produced in the liver
 Important in humoral immunity
 Become plasma cells that produce
antibodies
› T cells
› Produced in the thymus
 Important in cell-mediated immunity
 MONOCYTES
 3-8%
 U-shaped nucleus
 Capable of leaving
the bloodstream
where they become
phagocytic
macrophages
 Crucial in the body’s
defense against
viruses, certain
intracellular bacterial
parasites, and chronic
infections such as
tuberculosis
FORMATION OF WBC
 PLATELETS
 Disc-shaped
 Anucleate
 Cytoplasmic fragments of
megakaryocytes
 Essential in blood clotting process
 Platelet formation is regulated by a
hormone called thrombopoietin
 Life span: 5-9 days
 Normal value: 150,000-400,000/mm3
BLOOD TYPING AND
TRANSFUSION
IMPORTANCE

 Bloods of different people have different antigenic

& immune properties
 2 major blood groups:
 O-A-B system of antigen
 Rh system
O-A-B BLOOD GROUPS

 Agglutinogens – antigens that occur on the surfaces

of RBC
 Causes blood cell agglutination that cause blood
transfusion reactions
 Agglutinins – gamma globulins;
 Produced by the same cells that produces antibodies
 Produced in people who do not have respective
agglutinogen in their RBC
 ABO BLOOD GROUPS

BLOOD RBC PLASMA BLOOD THAT CAN

GROUP ANTIGEN/AGGLUTINO ANTIBODIES/ BE RECEIVED
GEN AGGLUTININS
AB A None A, B, AB, O
B (Universal
recipient)
B B Anti-A B, O

A A Anti-B A, O

O None Anti-A O (Universal

Anti-B donor)
 BLOOD TYPING

contains agglutinogen A

contains agglutinogen B

contains agglutinogens A and B

contains no agglutinogen
RH SYSTEM

 Major difference from A-O-B system:

 Spontaneous agglutinins never occur
 In A-O-B, the agglutinins responsible for causing
transfusion reactions develop simultaneously
 Can cause Erythroblastosis fetalis if mother is Rh (-) and
father is Rh (+)
 Usually manifests in the second baby
SIGNS AND SYMPTOMS

 Anemia
 Enlarged Liver and Spleen

 Generalized Swelling

 Newborn Jaundice
TREATMENT
 Before birth
 - intrauterine transfusion

 - plasma exchange

 After birth
 - transfusion with compatible packed red blood

 - sodium bicarbonate

 - phototherapy
I. RESISTANCE OF THE BODY TO
INFECTION: LEUKOCYTES, GRANULOCYTES,
MONOCYTE-MACROPHAGE SYSTEM AND
INFLAMMATION.

By: Jammaella Vernice T. Gomez, PTRP

WHITE BLOOD CELLS/LEUCOCYTES

 Mobile units of the body’s protective system

 Work together to prevent diseases by:

 Destroying invading agents by phagocytosis

 Forming antibodies that synthesize lymphocytes
 real value: Specifically transported to areas of
serious infection & inflammation
 Production:

 Bone marrow: granulocytes, monocytes and few

lymphocytes
 Lymphoid tissue: lymphocytes and plasma cells
WHITE BLOOD CELLS/LEUCOCYTES
 Life span:
 Granulocytes: blood: 4-8 hours; tissues 4-5 days
 Monocytes: blood: 10-20 hours; tissue (Macrophages)-
months – years
 Lymphocytes: with continuous circulation: weeks –
years
TYPES OF WBC

 GRANULAR
 Polymorphonuclear neutrophils- 60%
Granulocytes
 Polymorphonuclear eosinophils- 2.3%
or polys
Polymorphonuclear basophils- .4%
 AGRANULAR
 Monocytes
 Lymphocytes

 Plasma cells

 Megakaryocytes → fragments → platelets

RESISTANCE OF THE BODY TO INFECTION
A. Phagocytosis
 Cellular ingestion of the offending agent
 Main function of neutrophils and macrophages

 Main destroyer of invading bacteria, viruses & other

injurious agents
 Neutrophils
 Mature cells; can immediately attack & destroy bacteria & viruses
in the circulating blood.
 Can immediately begin phagocytosis
 Macrophages
 Begin as monocytes (immature cells while still in blood)
 Has little ability to fight infection
 Once they enter the tissues → swelling → w/ large nos. of
lysosomes in the cytoplasm → capable of destroying disease agents
RESISTANCE OF THE BODY TO INFECTION

 Mechanism:
 Margination
 Cells enter the tissue spaces via diapedesis
→ moves through the tissues by amoeboid
motion.
 Chemotaxis – phenomenon wherein
neutrophils & macrophages move towards the
source of the chemical in the tissue.
 Causes:
 Bacterial objects

 degenerative product of inflamed tissue themselves

 reaction products of the complement system

 reaction products caused by plasma clotting in the

inflamed area
MOVEMENT OF WBC TOWARDS THE
FOREIGN SUBSTANCES
RESISTANCE OF THE BODY TO INFECTION

 once phagocytized:
 digested by intracellular enzymes
 phagocytic vesicle → digestive vesicle

 contains proteolytic enzymes → digests bacteria and other

foreign substances
 ex. Lysosomes: contains lipases → found only in

macrophages that digests thick lipid membranes

 contains bactericidal agents- peroxisomes
RESISTANCE OF THE BODY TO INFECTION

 Selective Procedures:
 The surface particle is rough→ induces
phagocytosis
 Most natural substances in the body have
protective protein coats that repel phagocytes
 Dead tissues & foreign particles: no protein coats
 Body has its own specific means of recognizing
certain foreign materials
 Main function of immune system: develop antibodies
 Adhere to bacteria – susceptible to phagocytosis

 Combine w/ C3 product of the complement cascade

“opsonization”
RESISTANCE OF THE BODY TO INFECTION

B. Monocyte – Macrophage System: Reticulo-

endothelial system (RES)
 generalized phagocytic system located in all
tissues, especially in those tissue areas where
large quantities of particles, toxins, and other
unwanted substances must be destroyed.
 RES: combination of monocytes, mobile
macrophages, fixed tissue macrophages & few
specialized endothelial cells.
 Originates from monocyte stem cells: “monocyte-
macrophage system”
TYPES OF MACROPHAGES

 Types:
 Mobile macrophages
 Capable of wandering to the tissues
 Fixed tissue macrophages
 Macrophage that upon entering the tissues become attached
until called on to perform specific protective functions
 Special tissue areas where macrophages are
located:
 Skin & subcutaneous tissue- histiocytes
 Lymph nodes- macrophages line the sinuses
 Lungs-alveolar macrophages
 Liver & sinuses – kupffer cells
 Spleen & bone marrow
 Brain – microglia
RESISTANCE OF THE BODY TO INFECTION

C. Inflammation(Role of Macrophage &

Neutrophil)
 Prevents spread of tissue injury by release of chemical
mediators.
 Process/Response:
 Vasodilation of local blood vessels
 Increase permeability of the capillaries w/ leakage of
large quantities of fluid into the interstitial spaces
 Clotting of fluids in the interstitial spaces – d/t excessive
amount of fibrinogen
 Migration of granulocytes &monocytes in the tissues
 Swelling of the tissue cells
INFLAMMATION RESPONSE

74
INFLAMMATION

 “Walling-off effect”
 First result of inflammation
 Tissue spaces are blocked by fibrinogen clots
→ fluid barely flow through the spaces →
delays the spread of bacteria
 Intensity of inflammatory process –
proportional to the degree of tissue injury
MACROPHAGE & NEUTROPHIL
RESPONSE DURING INFLAMMATION
 Tissue macrophages- 1st line of defense
 Both mobile and fixed tissue macrophage immediately begin
phagocytosis activity w/in minutes after injury
 Neutrophil invasion – 2nd line of defense
 Occur w/in the first hour or so
 Reactions:
 Margination
 Diapedesis

 Chemotaxis

 “neutrophilia” – an increase in the number of neutrophils in

the blood
 Monocyte-macrophage invasion – 3rd line of
defense
 Increase in production of granulocytes &
monocytes by the bone marrow – 4th line of
defense
OTHER TYPES OF WBC
 EOSINOPHILS
 Constitutes about 2%
 Weak phagocytes; exhibits chemotaxis
 Produce in large quantity
 Parasitic infection
 Allergy

 BASOPHILS
 Similar to large mast cells
 Plays an important role in IgE type of allergic
reaction
 Produces “heparin” (anti-coagulant)
 Histamine
DISORDERS OF WBC
 Leukopenia/agranulocytosis
 bone marrow stops producing WBC- body is
unprotected against bacteria
 Leukemia
 uncontrolled production of WBC as a result of
cancerous mutation of myologenous and
lymphogenous cells.
II. RESISTANCE OF THE BODY TO
INFECTION: IMMUNITY AND ALLERGY

 IMMUNITY
 Types:
 Innate immunity
 Acquired immunity

 Humoral immunity

 Cell-mediated immunity
INNATE VS. ACQUIRED IMMUNITY
INNATE ACQUIRED

- Antigen independent - Antigen dependent

- Immediate maximal response - There is a lag time between the

exposure & maximal response

- No immunologic memory - (+) immunologic memory

IMMUNITY
A. Innate Immunity (non-specific)
 Immunity that results from general processes rather
from processes directed at specific disease organism
 Examples:
 Phagocytosis by WBC & Tissue macrophage system
 Digestion by the acid secretions of the stomach &
digestive enzymes
 Resistance of the skin to invasion by organism
IMMUNITY
B. Acquired Immunity
 Ability of the body to develop extremely powerful specific
immunity against individual invading agents
 Affords protection against re-exposure to same pathogen
 2 basic types:
 Humoral immunity or B-cell immunity
 Development of circulating antibodies that are capable of

attacking the invading agents

 Produce by B-lymphocytes

 Cell-mediated immunity or T-cell immunity

 Formation of large numbers of activated T- Lymphocytes that

are specifically designed to destroy the foreign agent

IMMUNITY
 Acquired Immunity
 Product of the body’s Lymphocytes System
 Lymphocytes are located mostly in the lymph nodes
& in special lymphoid tissues (spleen, submucosal
areas of the GIT, bone marrow)
 Distributed advantageously to intercept the invading
organism or toxins before they can spread too widely
 Two Major Populations:
 T-Lymphocytes
 B-Lymphocytes
LYMPHOCYTE ORIGINS

Insert figure 16.16

LYMPHOCYTE ORIGINS
COMPARISON OF T AND B CELLS
ANTIGENS/TOXINS
 Substances proteins or large polysaccharides that
are contains toxins or foreign organisms &
recognized as different from the natural
constituents of the body
 Requirements to be considered as antigenic:
 High molecular weight
 Regularity of the recurring molecular groups,
epitopes on the surface of large molecules
 Hapten - low molecular weight substances
 Combination with an antigenic substances will elicit an
immune response
III. HUMORAL IMMUNITY & THE
ANTIBODIES: ROLE OF B-LYMPHOCYTES:

 Formation of antibodies

 See Diagram
MEMORY CELLS
 New B-lymphocytes formed from the initial
exposure to a specific antigen= primary response
 Responsible for a much more rapid & more
potent antibody response
 Upon subsequent exposure to the same antigen =
“secondary response”
MEMORY CELLS: PRIMARY VS SECONDARY
RESPONSE
Primary Response Secondary Response

Occurs on first exposure to a Occurs after a second exposure to

specific antigen the same antigen

Delay in appearance Begins rapidly after exposure

Weak potency More potent

Short life Forms antibodies for many

months
 NATURE OF ANTIBODIES
 Gamma globulin called immunoglobulins (Ig)
 Constitute 20% of all plasma proteins

 Composed of combinations of light & heavy polypeptide

chains:
 2 light & 2 heavy chains to as many as 10 light & 10
heavy chains
STRUCTURE OF ANTIBOBIES
CLASSES OF ANTIBODY
MECHANISM OF ACTION OF ANTIBODIES
COMPLEMENT
 collective term that describes a system of about
20 proteins, particularly enzyme precursors
 Principal actors: 11 proteins : C1 through C9, B
&D
 Enzyme precursors are activated in 2 ways:
 Classical pathway
 Alternate pathway
 ACTIVATION OF THE “COMPLEMENT SYSTEM”:
MECHANISM OF ACTION OF ANTIBODIES

A. Classical Pathway
Important effects:
 “Opsonization & phagocytosis”

 “glueing process” → attaches the bacteria to neutrophils &

macrophages
 C3b enzyme

 Chemotaxis

 Agglutination

 Neutralization of viruses

 Lysis

 Formation of lytic complex

 Direct effect: rupturing of the cell membrane of the bacteria
ACTIVATION OF THE “COMPLEMENT
SYSTEM”: MECHANISM OF ACTION OF
ANTIBODIES
B. Alternate Pathway

 Activated in response to a large

polysaccharide molecules in the cell
membranes of invading organisms
 React with complement factors B & D →
form a product that activates C3 level
CELL MEDIATED IMMUNITY: RELEASE OF
ACTIVATED T-LYMPHOCYTES

 Principal difference from B-lymphocytes:

 Whole activated T-lymphocytes are formed &
released in the lymph → circulation
 T-lymphocyte memory cells are formed in the
same manner as that of B-memory cell
 3 Major Types of T-cells:
 Helper T- cells

 Cytotoxic T- cells

 Suppressor T- cells
TYPES OF T-CELLS
 Helper T- cells
 Most numerous
 Help in functions of the immune system –
serve as a major regulator of all immune
system by forming a series of protein
mediator called lymphokines
Absence: remainder of immune system is

almost paralyzed
TYPES OF T-CELLS

 Cytotoxic T-cells
 AKA. Killer cells
 Plays an important role in destroying cancer
cells, heart transplant cells
TYPES OF T-CELLS
 Suppressor T- cells

 AKA. Regulatory cells

 Plays a role in limiting immune tolerance

 Factors
that may interfere with successful
immune response:

 Microorganisms may adapt

 Immune response mas be excessive,
damaging the host
 Immune reaction maybe underactive
ALLERGY & HYPERSENSITIVITY
 Undesirable side effects of immunity
 Types:

 Type I reaction – mediated by IgE

 Type II – mediated by IgM or IgG
 Involves rxn’s against foreign antigen or
against self-antigen
 Type III – mediated by antigen-antibody
complexes
 Type IV- cell-mediated reaction
FIGURE 22.23 AN INTEGRATED SUMMARY OF THE
IMMUNE RESPONSE

Figure 22.23
FIGURE 22.25 THE COURSE OF THE BODY’S RESPONSE
TO BACTERIAL INFECTION

Figure 22.25a,
b
HEMOSTASIS & BLOOD
COAGULATION
By: Jammaella Vernice T. Gomez, PTRP
MECHANISM OF EVENTS
 Vascular spasm
 Formation of platelet plug

 Formation of blood clot= blood coagulation

 Eventual growth of fibrous tissue into the blood

to close the hole in the vessel permanently
VASCULAR SPASM
 Results from:
 Nervous reflexes
 Initiated by pain or other impulses that originate from the
traumatized vessel or from nearby tissues
 Local myogenic spasm
 Initiated by direct damages to the vascular wall
 Can last for many minutes or even hours → ensuing process

of platelet plugging & blood coagulation can take place

 Local humoral factors from traumatized tissues &
blood platelets
FORMATION OF PLATELET PLUG
 Effective if the rent of the blood vessel is very
small
 Platelets: minute round or oval discs: 2-4 um in
diameter
 Formed in the bone marrow of megakaryocytes
 Annucleated & cannot reproduce but w/ functional
characteristics similar to whole cell:
FORMATION OF PLATELET PLUG
 Functional characteristics:
 In cytoplasm of the platelets- active factors
causes platelet plug:
 Actin & myosin w/ thrombosthenin → cause platelets
to contract
 Residuals of both ER & golgi apparatus that
synthesize various enzymes & stores large quantities
of Ca ions
 Mitochondria & enzyme sys. Forms ATP & ADP
 Prostaglandins
 Fibrin
 Growth factor
FORMATION OF PLATELET PLUG
 Functional characteristics:
 Cell membrane
 Surface is coated w/ glycoprotein
 To avoid adherence to normal endothelium
 Phospholipids
 Plays a role in blood clotting
MECHANISM OF PLATELET PLUG
 Damaged vascular tissue → Platelets change
their characteristics
 Swell
 Assume irregular forms w/ numerous irradiating
pseudopods protruding from their surfaces
 Contractile proteins contract forcefully & release
granules containing multiple active factors
 ADP, Thromboxane A2
 Stick to collagen fibers
 Vicious circle of activation of successively increasing
nos. of platelets → attracts more platelets→ platelet
plug
BLOOD COAGULATION: FORMATION OF
BLOOD CLOT
 Clot begins to develop – if severe trauma: 15-20
secs. If minor: 1-2 minutes
 Activator substances from both the traumatized
vascular wall →initiate the clotting process
 Two causes of blood clot:
 Invaded by fibroblasts→ forms connective tissue all
through the clot
 It dissolves
 Mechanism:
 Depends on 2 factors:
 Procoagulants

 anticoagulants
ESSENTIAL STEPS IN FORMATION OF
BLOOD CLOT
 1. Formation of prothrombin activator
 A. intrinsic Pathway – begin w/ trauma to the
vascular wall & surrounding
 B. Extrinsic Pathway – begins in blood ( Tissue
Factor)
 2. Conversion of prothrombin to thrombin
 3. conversion of fibrinogen into fibrin

 4. Fibrin → clot → seal the injured vessel

PREVENTION OF BLOOD CLOTTING IN
NORMAL VASCULAR SYSTEM

 Intravascular Anticoagulants
 1. endothelial surface factor
 Most important factor for preventing clotting in normal
vascular system
 A. Smoothness of the endothelium- prevents contact
activator of the intrinsic clotting system
 B. Glycocalyx- repels the clotting factors & platelets

 Prevents activation of clotting system

 C. Thrombomodulin- a protein bound w/ endothelial

membrane w/c binds prothrombin

INTRAVASCULAR COMPONENTS

 2. Antithrombin action of fibrin & antithrombin

III
 Most important anticoagulants in the blood that
remove thrombin from the blood
 A. fibrin fiber – formed during the process of clotting
 B. Antithrombin III or anti-thrombin-heparin factor

 3. heparin
 4. alpha-macroglobulin
 Acts as a binding agent for several of the coagulation
factor & prevent proteolytic action
LYSIS OF BLOOD CLOTS: ROLE OF
PLASMIN
 Plasmin
 Most important proteolytic digestive enzyme of
pancreatic secretion
 Resembles trypsin
 Digests the fibrin fiber & other clotting factors in the
blood
 Formed as a result of activation of plasminogen or
profibronolysin
HEMOSTASIS & THROMBOSIS
 Fibrinolytic Cascade
HEMOSTASIS & THROMBOSIS
 Thrombus formation (Virchow's triad)
READING ASSIGNMENTS:

 Embolism
 Pathogenesis of different types
 Infarction
 Morphology
 Shock
 Three major types, related pathogenesis & associated
conditions
 Stages
 Morphology
 Clinical consequences
END OF LECTURE!!!
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