HEMATLOGY 2 UIC-MLS

Clinical Hematology Chapter 13

Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics

[BOOKS AND TRANS] CHAPTER 13: PLATELET PRODUCTION, STRUCTURE, AND FUNCTION
 Polar phospholipids predominate the inner layer
(phosphatidylinositol, phosphatidylethanolamine and
OUTLINE
1) Platelet UltraStructure phosphatidylserine)
A. Peripheral Zone  Made up of arachidonic acid
B. Structural Zone/ Sol-Gen Zone  Cholesterol- maintains fluidity and passage of
C. Organelle Zone/Centromere
D. Membrane System
transmembranous materials
2) Platelet Function  Phosphatidylserine flips to the outer surface upon
A. Platelet Plasma Membrane Receptors that Provide for activation and is the charged phospholipid surface on
Adhesion which the coagulation enzymes, especially
B. The Seven-Transmembrane Receptors
C. Additional Platelet Membrane Receptors coagulation factor complex VIII and IX and
D. Primary Hemostasis coagulation factor complex X and
3) Platelet Activation Pathway  V, assemble.
A. G protein Pathway
B. Inositol Triphosphate–Diacylglycerol Activation Pathway
 Platelet adhesion is mediated by:
C. Eicosanoid Synthesis o 1) vWF
o 2) GPIb
PLATELET ULTRASTRUCTURE o 3) Collagen
 Platelets, although anucleate, are strikingly complex  Platelet aggregation is mediated by:
and are metabolically active. o 1) Calcium
PERIPHERAL ZONE o 2) Fibrinogen
 Composed of membranes which is rich in platelet o 3) GPIIb-IIIa
receptor and is responsible for platelet adhesion o 4) vWF
(platelet to non-platelet.) and aggregation (plt. to plt.) STRUCTURAL ZONE/ SOL-GEN ZONE
 Maintain surface negative charge  Lies directly beneath the platelets and is composed
 Originates from plasma membrane of the of:
megakaryocytes o Microtubules - Composed of protein tubulin which
maintains the platelet disc shape
GLYCOCALYX  Tubulin- Responsible for shape maintenance
 Adhesive layer o Microfilament - Contains actin and myosin which
 Extreme fluffy mucopolysaccharides upon stimulation of the platelets will interact to
 Made up of glycoprotein form actomyosin (thrombosthenin) for clot
o Glycoproteins react with thrombin, vWF, and retraction
fibrinogen  Actin - For platelet contraction; anchors
o Glycoprotein V- Thrombin substrate glycoprotein and proteoglycans
 Composed of glycoprotein including:  Myosin- For Contraction
o Factor V – Labile Factor; Proaccelarin  Thrombasthenin- Clot Retraction
o Factor VIII – Anti-hemophilic Factor o Intermediate filaments
o Factor I – Fibrinogen; Blood Clot Formation  Desmin and vimentin- Connects actin and
PLASMA MEMBRANE tubules to maintain platelet shape
 Support for Cell structure
 Composed of bilayer phospholipid embedded with
 Mechanism for Cell Contraction
integral for surface receptors
 Phospholipid – maintain the fluidity of plasma  Shape Change and Contractibility
membrane and maintains the structure  Interact with the dense tubular system in
o GPIb – serves as the binding and receptor site sequestering
for vWF (vonWillebrand Factor) necessary for ORGANELLE ZONE / CENTROMERE
platelet adhesion  The part where the secretory products of platelets
o GPIIb-IIIa – Binding site for fibrinogen come from
 calcium dependent membrane protein  Major portion of platelet cytoplasm
complex for fibrinogen receptor necessary for  Function: Allows secretion of cellular contents
platelet aggregation Α-GRANULES
 Provides phospholipids that support platelet  Lack of this results to Gray Plate Syndrome (GPS)
activation internally and plasma coagulation  Platelet Factor 4 – anti-heparin or heparin
externally neutralization
 Phosphatidulcholine and sphingomyelin are  B-thromboglobulin – fibroblast chemotaxis
predominant in plasma layer (neutral phospholipids)  Platelet-derived Growth Factor - mitosis
PADAYHAG, RIGIDOR S. | MLS-3D 1
 HEMATLOGY 2
Clinical Hematology
UIC-MLS
Chapter 13
Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics
 Fibrinogen/ Factor I – blood clot formation, platelet  Mitochondria
aggregation o For ATP synthesis used for platelet metabolism
 Factor V – labile factor or proaccelarin o Principal site for ATP synthesis
 Factor XI- Fibrin formation  Lysosomal Granules
 vonWillebrand Factor – for adhesion o Digest materials that are endocytosed by the
o Binding platelets to collagen platelets
 Thrombospondin – for adhesion o Digest vessel wall matrix component during in
o Stabilization of platelets vivo aggregation
 Fibronectin – for adhesion o Contains arylsulfatase, beta-glucoronidase, acid
 Protein C – for coagulation phosphatase and catalase
o Acid Phosphatase
 Protein S: Regulation of Fibrin via protein C pathway
o Hydrolytic Enzyme
 TFPI- Regulation of fibrin formation by inhibiting
MEMBRANE SYSTEMS
factor Factor VII/Tissue factor complex
 Serves as the canal for secretory products
 PAI-1- Inhibitor of fibrinolysis
SURFACE-CONNECTED CANALICULAR SYSTEM
 A2-Antiplasmin – for fibrinolysis
Table 1: Representative Platelet a-Granule Proteins  The plasma membrane invades the platelet interior,
Coagulation Noncoagulati producing its unique surface-connected canalicular
Proteins on Proteins system
Proteins Present in Platelet Cytoplasm and a-  Acts as a canal for the release of granule constituents
Granules and cytoplasm to the exterior of the platelet
Endocytosed Fibronectin Albumin  Enhances platelet interaction with its environment
Fibrinogen Immunoglobuli  Route for endocytosis and secretion of alpha
ns granules upon activation
Megakaryocyte Factor V  The glycocalyx is less developed in the SCCS and
-synthesized Thrombospondin lacks some of the glycoprotein receptors present on
VWF the platelet surface.
Proteins Present in a-Granules but Not Cytoplasm
DENSE TUBULAR SYSTEM
Megakaryocyte b-thromboglobulin EGF
-Synthesized HMWK Multimerin  Derived from smooth endoplasmic reticulum and
PAI-1 PDC1 sequesters calcium for platelet activation process
Plasminogen PDGF  Condensed remnant of the rough endoplasmic
PF4 TGF-b reticulum
Protein C inhibitor VEGF/VPF  DTS sequesters Ca21 and bears a series of enzymes
Platelet Membrane-Bound Proteins that support platelet activation.
Restricted to a- P-selectin GMP33  Include phospholipase A2, cyclooxygenase, and
granule membrane thromboxane synthetase, which support the
membrane eicosanoid synthesis pathway that produces
Osteonectin thromboxane A2, and phospholipase C, which
In a-granule GP IIb/IIIa cap1 supports production of inositol triphosphate (IP3) and
and plasma membrane diacylglycerol
membrane  “Control center” for platelet activation
GP IV CD9  It is also the site of platelet cyclooxygenase and of
GP Ib/IX/V PECAM-1 prostaglandin synthesis
DENSE-GRANULES o Cyclooxygenase – an enzyme that catalyzes the
conversion of arachidonic acid to prostaglandin
 ADP – for aggregation and activation of platelets o Arachidonic Acid – unsaturated fatty acid;
o Platelet agonist- positive feedback to enhance precursor of prostaglandins
platelet response and recruitment PLATELET FUNCTIONS
 ATP – source of energy  Participates in a sequence of events that leads to the
o Activation of Ca2+ channel, agonist for other cells formation of platelet plug and ultimately to formation
 Calcium and Magnesium – bivalent cations for of stable fibrin clot at the site of vessel interruption
platelet activation o Primary hemostasis by adhesion, secretion, and
o Secondary hemostasis aggregation with the end view of hemostatic plug
 Serotonin – vasoconstrictor that binds endothelial o Blood coagulation by releasing Platelet Factor 3
cells and platelet membranes that plays a big role in forming fibrin clot
 Pyrophosphate o Clot retraction by actomyosin

PADAYHAG, RIGIDOR S. | MLS-3D 2

 HEMATLOGY 2
Clinical Hematology
UIC-MLS
Chapter 13
Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics
o Helps in localization of bacteria and other small THE SEVEN-TRANSMEMBRANE REPEAT
objects and producing aggregates too large to RECEPTORS
pass through capillaries  Thrombin, thrombin receptor activation peptide
Table 2: Platelet Role on Hemostasis (TRAP), adenosine diphosphate (ADP), epinephrine,
Platelet Activity and the eicosanoid synthesis pathway (also called the
Factor prostaglandin or the cyclooxygenase pathway)
PF1 Accelerate the conversion of PT to product thromboxane A2 (TXA2) all function
thrombin individually or together to activate platelets
PF2 Accelerates the clotting of purified  Platelet “agonists” are ligands for the seven
fibrinogen by thrombin transmembrane repeat receptors (STRs)
PF3 Phospholipid needed in the intrinsic  Thrombin cleaves two STRs, protease-activated
coagulation pathway receptor 1 (PAR1) and PAR4
PF4 Antiheparin  Thrombin cleavage of either of these two receptors
PF5 Necessary for normal fibrin formation activates the platelet through G-proteins
PF6 Anti-fibrinolysis o Also interacts with platelets by binding or
digesting two CAMs in the leucine-rich repeat
PF7 Formation of intrinsic thromboplastin
family, GP Iba and GP V, both of which are parts
of the GP Ib/IX/V VWF adhesion receptor
PLATELET PLASMA MEMBRANE RECEPTORS  TPa and TPb bind TXA2
THAT PROVIDE FOR ADHESION o produces more TXA2 from the platelet
 Members of the cell adhesion molecule  Epinephrine binds a2-adrenergic sites that also
o (CAM) integrin family, couple to Gproteins and open up membrane calcium
o CAM leucine-rich repeat family, channels.
o CAM immunoglobulin gene family,
 IP binds prostacyclin (prostaglandin I2, PGI2), a
o CAM selectin family,
prostaglandin produced from endothelial cells.
o Seven-transmembrane receptor (STR) family
 Prostacyclin enters the platelet and raises the internal
 Several integrins bind collagen, enabling the platelet
cyclic adenosine monophosphate (cAMP)
to adhere to the injured blood vessel lining
concentration of the platelet, thus blocking platelet
 Integrins are heterodimeric (composed of two activation.
dissimilar proteins) CAMs that integrate their ligands Table 3: Platelet STR Receptor-Ligand Interaction
o bind on the outside of the cell, with the internal Coupled to Signalling
cytoskeleton, triggering activation
Receptor Ligand G Proteins
 GP Ia/Iia - binds the subendothelial collagen and then
PAR1 Thrombin Coupled to G1 protein
promote adhesion of the platelet to the vessel wall that reduces cAMP;
 a5b1 and a6b1 bind the adhesive endothelial cell coupled to Gq and G12
proteins laminin and fibronectin, which further proteins that increase
promotes platelet adhesion IP3 and DAG
 GP VI- key collagen receptor that also binds the PAR4 Thrombin Coupled to Gq and G12
adhesive protein thrombospondin proteins that increase
 GP Ib/IX/V- leucine-richrepeat family CAM IP3 and DAG
o Arises from the genes GP1BA, GP1BB, GP5, and P2Y1 ADP Coupled to Gq protein
GP9. that increases IP3 and
 The two copies of subunit GP Iba bind VWF and DAG
support platelet tethering (deceleration) P2Y12 ADP Coupled to G1 protein
 The accompanying GP Ibb molecules cross the that reduces cAMP
platelet membrane and interact with actin-binding TPa and TXA2 Coupled to Gq protein
protein to provide “outside-in” signaling TPb that increases IP3 and
 The subunits of the integrin GP IIb/IIIa (aIIbb3), are DAG
separate and inactive (aIIb and b3) a2- Epinephrine Coupled to G1 protein
o Form their active heterodimer, aIIbb3, only when adrenergic that reduces cAMP;
they encounter an “inside-out” signaling potentiates effects of
mechanism triggered by collagen binding to GP ADP, thrombin, and
VI TXA2
 The aIIbb3 integrin also binds VWF, vitronectin, and IP PGI2 Coupled to GS protein
fibronectin, all adhesive proteins that share the target that increases cAMP to
arginine-glycine-aspartate (RGD) amino acid inhibit activation
sequence with fibrinogen.
PADAYHAG, RIGIDOR S. | MLS-3D 3
 HEMATLOGY 2
Clinical Hematology
Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics
ADDITIONAL PLATELET MEMBRANE RECEPTORS
 The CAM immunoglobulin family includes the ICAMs
(CD50, CD54, CD102), which play a role in
inflammation and the immune reaction;
 PECAM (CD31), mediates platelet–to–white blood
cell and platelet–to–endothelial cell adhesion; and
FcgIIA (CD32).
o low-affinity receptor for the immunoglobulin Fc
portion
 P-selectin (CD62) is an integrin that facilitates platelet
binding to endothelial cells, leukocytes, and one
another.
 P-selectin or CD62 quantification by low cytometry is
a successful clinical means for measuring in vivo
platelet activation.
PRIMARY HEMOSTASIS
 Refers to the role of Blood vessels (vascular system
which includes the arteries,veins,and capillaries) and
platelets in the primary formation of platelet plug in
response to vascular injury
 TEST: BLEEDING TIME
ADHESION
 Platelet to non-platelet interaction
 REVERSIBLE: seals endothelial gaps, some
secretion of growth factors, in arterioles vWF is
necessary for adhesion
 Occurs during vascular injury
 Initiated by exposure of subendothelial collagen
 Damaged endothelial cells release vWF
o Most likely occurs in the presence of von
Willebrand Factor (vWF) being deposited on the
injured tissues
o Globular- circulating (inactive)
o Fibrilar- Activated
o Attached to GP IB/IX/V complex
 Dependent on glycoprotein Ib/IX/V (GPIb/IX/V) and
vWF
 Platelet- vWF is regulated by ADAMTS-13
 At high shear rates, platelets bind to collagen via GP
VI (this triggers internal platelet activation pathway-
releasing ADP and TXA2)
o OUTSIDE-IN-REACTION”
 Tpa and TPB for TXA2
 P2YI and P2Y12 for ADP
o Triggers “inside-out” reaction
o Increases affinity of integrin a2B1 for Collage
 Platelet loses its discoid shape and spreads
 TXA2 and ADP is released to activate neighboring
 Platelets
 Activates aIIBB3 for fibrinogen interaction in platelet
aggregation
 Associated disorders:
o Von Willebrand disease
o Bernard Soulier disease 2
PLATELET AGGREGATION
PADAYHAG, RIGIDOR S. | MLS-3D
UIC-MLS
Chapter 13
 Platelet to platelet interaction
 IRREVERSIBLE; platelet plug form platelet contents
are secreted, requires fibrinogen
 Simultaneous with platelet release, platelet
stimulating agents (collagen, ADP, epinephrine,
thrombin) bind to the platelets, causing them to
adhere to one another
 Fibrinogen: necessary cofactor for platelet
aggregation
 Released ADP and TXA2 promoted assembly of
allBB3 enhancing platelet aggregation
 P-selectin- promotes platelet aggregation
 During aggregation, platelet lose its shape and
extend pseudopods
o Other platelets are stimulated by ADP to undergo
shape change, exposing the gpIIbIIIa complex
 Phosphatidylserine is flipped to outer layer
 SUBSTRATE: Fibrinogen
 RECEPTOR: GPIIb-IIIa
 Glanzmann’s thrombasthenia: decrease or absence
of plt membrane glycoprotein IIbIIIa (GPIIb-IIIa)
complex, which acts as fibrinogen binding site on the
platelet surface
 Initial platelet activation leading to platelet adhesion.
The glycoprotein (GP) 1ba portion of the GP Ib/IX/V
von Willebrand factor (VWF) receptor site binds VWF
 GP VI binds collagen .
 The bound GP VI initiates the release of thromboxane
A2 (TXA2) and adenosine diphosphate (ADP)
 Which activate a2b1, an additional collagen receptor
 Stabilizing platelet adhesion, and aIIbb3, the arginine-
glycine-aspartate (RGD) receptor site that binds
fibrinogen and VWF to support platelet aggregation.
PLATELET SECRETION
 Platelet granules move to the center of the platelets
and fuse with the OCS (open canalicular system),
content of the granules are extruded to the outside
 ACTIVATED platelets release Granular contents
 Outside-in activation- binding of integrins, STRs,
GPVI triggers actin microfilament contraction
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 HEMATLOGY 2
Clinical Hematology
UIC-MLS
Chapter 13
Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics
 Alpha granules (coagulant proteins) and lysosomes  Disk-shaped → spherical shape (extrusion of
content exit via SCCS numerous pseudopods)
o Alpha granules IX/VIII (tenase) and factor X/V PLATELET ACTIVATION PATHWAYS
(prothrombinase), both supported by ionic G-PROTEIN PATHWAY
calcium secreted by the dense granules  G-proteins control cellular activation for all cells
o A-granule contents fibrinogen, factors V and VIII,  aBY Heterotrimers that bind guanosine diphosphate
and VWF (which binds and stabilizes factor VIII) (GDP) when inactive
are secreted and increase the localized o The Ga portion of the three-part G molecule
concentrations of these essential coagulation briefly disassociates, exerts enzymatic
proteins. guanosine triphosphatase activity, and
hydrolyzes the bound GTP to GDP, releasing a
 Dense granules (vasoconstrictors) migrates to phosphate radical.
plasma membrane  Hydrolysis step provides necessary phosphorylation
 Cyclooxygenase (from platelets) metabolizes trigger to energize eicosanoid pathway or IP3-DAG
arachidonic acid to form prostaglandin Pathway
endoperoxides, which are converted to Thromboxane
A2 (vasoconstrictor and platelet stimulator, causing
platelet secretion and aggregation)
 Aspirin acetylation permanently inactivate
cyclooxygenase, blocking thromboxane A2
production and causing impairment of platelet
function.
COAT PLATELET
 Collagen and Thrombin Activated Platelet

 (1) A ligand (agonist) binds its corresponding

receptor;
 (2) G-protein swaps GDP for GTP
 (3) GTP donates a high energy phosphate radical to
a zymogen, remains attached to the G-protein as
GDP
 (4) the zymogen is activated. The G-protein returns to
a resting state bound to GDP. GDP, Guanosine
diphosphate
 Further activation yields the “collagen and thrombin Table 4: G Proteins in Platelets and Their Functions
activated (COAT)” platelet (PLT) leading to G Coupled Agonist Action Outcom
aggregation. Pro- to (Ligand) e
 Platelets become activated by agonists—for tein Receptor
example, adenosine diphosphate (ADP), G1 PAR1 Thrombin Decelerates Reduce
thromboxane A2 (TXA2), collagen (Col), or thrombin adenylate cAMP
(Thr). P-selectin (CD 62) moves from the a-granules cyclase concentra
to the platelet membrane to support adhesion. tion
 The inactive aIIb and b3 units assemble to form the P2Y12 ADP
active arginine-glycineaspartate (RGD) receptor a2- Epinephri
aIIbb3, which binds fibrinogen (Fg) and von adrenergic ne
Gq PAR1 Thrombin Activates Increase
Willebrand factor (VWF).
phospholipase C IP3-DAG
PLATELET ACTIVATION
PAR4 Thrombin
 Morphologic and functional change in platelets P2Y1 ADP
 Form discoid to spherical with pseudopod formation TPa and TXA2
(Ca2+,actin and myosin/thrombosthenin) TPb

PADAYHAG, RIGIDOR S. | MLS-3D 5

 HEMATLOGY 2
Clinical Hematology
UIC-MLS
Chapter 13
Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics
G12 PAR1 Thrombin Activates protein Activate  One product is DAG, which directly generates actin
kinase C pleckstrin microfilament contraction. The other product is IP3,
, actin which releases ionic calcium from the DTS.
microfila
 DAG, Diacylglycerol; DTS, dense tubular system;
ments
PAR4 Thrombin IP3, inositol triphosphate; PLC, phospholipase C; R1,
P2Y1 ADP
saturated fatty acid remains attached to carbon 1; R2,
unsaturated fatty acid remains attached to carbon 2
TPa and TXA2
TPb EICOSANOID SYNTHESIS
Gs IP Prostacycl Accelerates Increase  Alternatively called the prostaglandin,
in adenylate cAMP cyclooxygenase, or thromboxane pathway
cyclase concentra  Phospholipase A releases arachidonic acid from
tion membrane phosphatidylinositol
 Arachidonic acid is acted upon by cyclooxygenase,
INOSITOL TRIPHOSPHATE–DIACYLGLYCEROL peroxidase, and thromboxane synthase to produce
ACTIVATION PATHWAY TXA
 Second G protein–dependent platelet activation  TXA binds to Tpa or TBB- decelerates adenylate
pathway cyclase leads to decreased CAMP concentration-
 G protein activates phospholipase C leasd to release of platelets from DTS.
 Phospholipase C cleaves phosphatidyllinositol
 4,5-biphosphate to form inositol triphosphate and REGULATION
diacylglycerl  Prostacyclin synthase promotes increase of
 Inositol triphosphate (IP3)- promotes release of ionic prostacyclin
calcium from DTS (triggers contraction; may activate o Accelerates adenylate cyclase
phospholipase A2 o Increase CAMP, decrease release calcium
 Diacylglycerol (DAG)-activates phosphokinase C- o Platelet inactivation
promotes phosphorylation of pleckstrin
 Plecsktrin- regultes actin microfilament contraction
 Internal platelet activation pathways, like internal
pathways of all metabolically active cells, are often
called second messengers because they are
triggered by a primary ligand-receptor binding event.

 Eicosanoid synthesis. Ligands (agonists) ADP,

thrombin, collagen, or epinephrine bind their
 PLC is activated by the G-protein mechanism and respective membrane receptors. The combination
cleaves the phosphodiester bond from carbon 3 of activates phospholipase A2 through the G-protein
phosphatidylinositol. mechanism.
 Phospholipase A2 releases arachidonic acid from
membrane phosphatidyl inositol. Arachidonic acid is
PADAYHAG, RIGIDOR S. | MLS-3D 6
 HEMATLOGY 2
Clinical Hematology
Prelim Topic 2- Platelet Ultrastructure, Function
and Kinetics
acted upon by cyclooxygenase, peroxidase, and
thromboxane synthase to produce TXA2, which
activates the platelet through adenylate cyclase.
When reagent arachidonic acid is used as an agonist,
it bypasses the membrane and directly enters the
eicosanoid synthesis pathway.
 In the endothelial cell, the eicosanoid pathway is
nearly identical, except that prostacyclin synthase
replaces thromboxane synthase. ADP, Adenosine
diphosphate; PgG2, prostaglandin G2; PgH2,
prostaglandin H2; TXA2, thromboxane A2.
 The second messenger system. In the platelet, TXA2
suppresses adenylate cyclase and reduces cyclic
AMP concentration.
 This allows the release of ionic calcium from the DTS.
Ionic calcium supports the contraction of actin
microfilaments, activating the platelet. In the
endothelial cell, prostacyclin (not pictured) has the
opposite effect upon adenylate cyclase, raising cyclic
AMP and sequestering ionic calcium in the DTS.
 ATP, Adenosine triphosphate; AMP, adenosine
monophosphate; DTS, dense tubular system; TXA2,
thromboxane A2.
PADAYHAG, RIGIDOR S. | MLS-3D
UIC-MLS
Chapter 13
Summary/Additional Notes
 a. Adhesion
o 1) Platelets undergo a shape change and adhere
to vascular surfaces.
o 2) Response to collagen exposure in
subendothelium caused by vascular injury
o 3) Dependent on binding of von Willebrand factor
at the GPIb receptor site
o 4) Can be activated by thrombin
 b. The contents of the platelet storage granules are
released into the open canalicular system in response
to internal, cellular contraction.
 c. Aggregation
o 1) Fibrinogen attaches at the Ilb/IIIa receptor of
adjoining platelets, forming the initial platelet plug.
o 2) Platelets release nonmetabolic ADP (platelet
agonist), serotonin, and PF4.
o 3) During aggregation, PF3 is released to provide
the phospholipid surface needed for binding of
clotting factors in secondary hemostasis.
 d. Clot retraction
o 1) Follows clot formation
o 2) Dependent on thrombasthenin and
glycoprotein receptors Ilb/IIIa
o 3) Restores normal blood flow to the vessel.
 4 unique granules among Platelets not Present in other
cells/tissues
o 1-2. PDGF and BTG- Needed for the repair in
damage vessel (vascular endothelium)
o 3-4. PF4 and Thrombospondin- Important in
clotting
 Substances secreted by platelets according to their
roles in hemostasis
PROMOTE COAGULATION
 HMWK, Fibrinogen Factor V, and Factor VIII: vWF
PROMOTE AGGREGATION
 ADP, Calcium, PF4, and Thrombospondin
PROMOTE VASOCONSTRICTION
 Serotonin and Thromboxane A2 precursors
PROMOTE VASCULAR REPAIR
 Plate derived growth factor, and Beta thromboglobulin
OTHER SYSTEMS AFFECTED
 Plasminogen, Alpha 2-antiplasmin, and C1 esterase
inhibitor
 Inhibitors of Platelet Activity: Prostacyclin and Nitric
oxide, CD 39, and Aspirin and NSAIDS--Prevent
formation of TxA2 by inhibiting cyclooxygenase
REFERENCES
University of the Immaculate Conception Powerpoint Presentation
and Discussion Prepared By Ma’am Ann
Keohane, E. M., Smith, L. J., & Walenga, J. M. (2020). Rodak's
hematology: Clinical principles and applications (5th ed.).
St. Louis, MO: Elsevier.
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