HEMATOLOGY(LEC)

HEMOSTASIS PREPARED OVERVIEW OF HEMOSTASIS

HEMOSTASIS 1. Primary hemostasis

 Vasoconstriction
 Hemostasis involves the interaction of
 Platelet adhesion
vasoconstriction. platelet adhesion and
 Platelet aggregation
aggregation. and coagulation enzyme
2. Secondary hemostasis
activation to stop bleeding.
 Interaction of coagulation factors to
 There are two types of Hemostasis
produce fibrin
 Primary hemostasis. refers to the role of
 Fibrin stabilization by factor XIII
blood vessels and platelets in response to a
3. Fibrinolysis
vascular Injury. or to the commonplace
 Release if tissue plasminogen activator
desquamation of dying or damaged
 Conversion of plasminogen to plasmin
endothelial cells. Blood vessels contract to
 Conversion of fibrin-to-fibrin
seal the wound or reduce the blood flow
degradation products
(vasoconstriction).
 Secondary hemostasis, describes the PLATELETS
activation of a series of coagulation proteins
Platelets are produced from the cytoplasm of
in the plasma, mostly serine proteases, to
bone marrow megakaryocytes. Although
form a fibrin clot.
platelets are only 2 to 3 mm in diameter on a
The four mechanisms of Hemostasis fixed. stained peripheral blood film. they are
complex. metabolically active cells that interact
 VASCULATURE
with their environment and initiate and control
 PLATELETS
hemostasis. At the time of an injury. platelets
 CLOT FORMATION
adhere. aggregate. and secrete the contents of
 FIBRINOLYTIC
their granules.
HEMOSTASIS
INTRODUCTION TO PRIMARY HEMOSTASIS
A system in dynamic balance that when tipped
During Primary Hemostasis platelets become
by deficiencies either congenital or acquired of
activated. adhere to the site of injury. secrete
the procoagulant portion or excesses of the
the contents of their granules, and aggregate
fibrinolytic portion. results in uncontrolled
with other platelets to form a platelet plug.
bleeding (hemorrhage) otherwise it can result in
Vasoconstriction and platelet plug formation
excessive clot formation or persistence of clot
comprise the initial rapid. short-lived response
(thrombosisis)
to vessel damage, but to control major bleeding
STEPS IN HEMOSTATIC RESPONSE in the long term. the plug must be reinforced by
fibrin. Defects in primary hemostasis such as
1. Injury to endothelium collagen abnormalities. thrombocytopenia.
2. Primary Hemostasis through formation of qualitative platelet disorders. or von Willebrand
primary hemostatic plug wherein disease can cause debilitating sometimes fatal
PLATELETS have the main role chronic hemorrhage.
3. Secondary Hemostasis through formation of
fibrin clot, wherein COAGULATION
PROTEINS are the major contributor.
4. Fibrinolysis (removal of clot)
 HEMATOLOGY(LEC)

PRIMARY HEMOSTASIS  Platelet granules move to the center of

the platelets and fuse with the open
2 COMPONENTS OF PRIMARY HEMOSTASIS
canalicular system connected to the
1. VASCULAR SYSTEM outside of the platelet: in this way the
2. PLATELETS content of the granules is extruded to the
outside.
FUNCTIONS OF PLATELETS DURING PRIMARY
HEMOSTASIS
Two Major types of granules
1. PLATELET ADHESION
 When vascular injury occurs, platelets 1. Alpha granules, the most numerous which
come in contact with the nonplatelet includes Platelet factor 4. B-
surfaces such as collagen or fibronectin thromboglobulin. platelet-derived growth
and adhere to portion of it. factor. vWF. fibrinogen. fibronectin and
 Most likely platelet adhesion occurs in the factor V.
presence of the VON WILLEBRAND 2. Dense granules. which includes ADP. ATP.
FACTOR being deposited on the injured calcium, serotonin, and pyrophosphate
tissues  RELEASE DISORDERS (STORAGE POOL
a) Von Willebrand Disease is DEFECTS)
characeterized by an absent or
ALPHA GRANULES DEFICIENCY - GRAY
abnormal form of vWF results in
PLATELET SUNDROME
impaire platelet adhesion
b) Bernard-Soulier Syndrome is DENSE GRANULES DEFICIENCY - HERMANSKY
characterized when platelets lack PUDLAK SYNDROME. CHEDIAK HIGASHI
glycoprotein IB. which functions as SYNDROME AND WISKOTT ALDRICH SYNDROME
a receptor for the vWR
4. PLATELET AGGREGATION
2. PLATELET ACTIVATION
 Morphologic and functional change in  Simultaneously with platelet release.
platelets platelets stimulating agents such as
 Cyclooxygenase (from the plateletsé collagen. ADP. epinephrine and thrombin
metabolizes arachidonic acid to form bind to the platelets, causing them to
prostaglandin enoperoxides which are adhere to one another
converted to thromboxane A2 (a  Fibrinogen is necessary as cofactor for
vasoconstrictor and a platelet stimulator, platelet aggregation
causing platelet secretion and a) Glanzmann thrombasthenia is a syndrome
aggregation) characterized by the decrease or absence of
 Aspirin inactivates the enzyme platelet membrane glycoprotein lib and IIIa
cyclooxygenase complex. which acts as a fibrinogen binding
3. PLATELET SECRETION site on the platelet surface Summary of
 Following activation, the platelet most important substances secreted by
undergoes a shape change most probably platelets and their role in Hemostasis.
caused by contraction of microtubules
 Platelet changes from originally disk
shaped to spherical shape with the
extrusion of numerous pseudopods
 HEMATOLOGY(LEC)

Summary of most important

substances secreted by platelets and
 PROMOTE VASCULAR REPAIR
their role in Hemostasis
 PROMOTION OF SUBSTANCE SOURCE
PRINCIPLE
COAGULATION FUNCTION
SUBSTANCE SOURCE PRINCIPLE PLT DERIVED Alpha PROMOTES
FUNCTION GROWTH FACTOR granules SMOOTH
HMWK Alpha Contact activation MUSCLE
granules of intrinsic GROWTH FOR
coagulation VESSEL REFAIR
pathway BETA Alpha CHEMOTACTIC
FIBRINOGEN Alpha Converted to THROMBOGLOBULI granules FOR
granules fibrin clot N FIBROBLASTS
formation TO HELP IN
FACTOR V Alpha Cofactor in fibrin VESSEL REFAIR
granules clot formation  OTHER SYSTEM AFFECTED
FACTOR VIII; Alpha Assists platelet
SUBSTANCE SOURCE PRINCIPLE
vWF granules adhesion to
FUNCTION
subendothelium
PLASMINOGEN Alpha PRECURSOR TO
to provide platelet
granules PLASMIN,
aggregation
WHICH
 PROMOTE AGGREGATION
INCLUDE CLOT
SUBSTANCE SOURCE
PRINCIPLE LYSIS
FUNCTION ALPHA 2 Alpha PLASMIN
ADP Dense PROMOTES PLT ANTIPLASMIN granules INHIBITOR
granules AGGREGATION C1 ESTERA Alpha COMPLEMENT
CALCIUM Dense SAME INHIBITOR granules SYSTEM
granules INHIBITOR
PLT FACTOR 4 Alpha SAME
granules
BASIC TERMINOLOGIES FOR CLINICAL FINDINGS
THROMBOSPONDI Alpha SAME
IN BLEEDING DISORDERS
N granules
 PROMOTE 1. PETECHIAE - characterized by purplish red
VASOCONSTRICTION pinpoint hemorrhagic spots in the skin
SUBSTANCE SOURCE PRINCIPLE caused by loss of capillary ability to
FUNCTION withstand normal blood pressure and
SEROTONIN Dense PROMOTES trauma
Bodies VASOCONSTRIC 2. Purpura - characterized by hemorrhage of
TION AT INJURY blood into small areas of skin. mucous
SITE membranes, and other tissues
THROMBOXANE Membr SAME 3. Ecchymosis form of purpura in which blood
ane escapes into large areas of skin and mucous
Phosph membranes but not into deep tissues.
olipids corresponds with the lay term bruise.
4. Epistaxis-nosebleeding
 HEMATOLOGY(LEC)

5. Hemarthrosis - leakage of blood into joint

cavities
6. Hematemesis - vomiting of blood
7. Hematoma - swelling or tumor in tissues or
a body cavity that contains clotted blood
8. Hematuria - red blood cells in urine
9. Hemoglobinurla - hemoglobin in urine
10. Melena stool containing dark red or black
blood
11. Menorrhagia excessive menstrual bleeding