N5315 Advanced Pathophysiology
Hematologic System
Core Concepts and Objectives with Advanced Organizers
Hemostasis
1. Analyze the process of hemostasis:
Hemostasis
Platelet plug: Formed on the damaged endothelium
Coagulation cascade: Fibrin and XIIIa (Two end products of CC) form mesh over platelet plug and
anchor it in place.
a. Analyze the platelet structure and the 4 phases of platelet plug formation:
Platelet structure:
Disc shaped cells
Circulate in the outer portion of the blood vessel.
RBC travel in center of cell -> move platelets to our edge. (Anemic patients have harder time
clotting because platelets can’t reach damage.)
Normal Platelet Lab Level: 150,000-450,000
Platelet Structure Function
Peripheral Zone Made of phospholipids
Outer most portion (Cell membrane) Open canalicular system (OCS): system of
channels that runs from inner most portion
of plt and opens to outside. (Provides
channel for substances produced by plt to
be released.
Thromboxana A2: formed by phospholipid
membrane via arachidonic acid pathway.
Provides site for coagulation proteins and
adhesive proteins to bind
Contains many PTL receptors which are
responsible for ptl adhesion and
aggregation.
Sol-gel zone Provides structure support for the cell
Organelle Zone Contains the organelles
Alpha/dense granules Stores calcium and contains enzymes for
Lysosomes prostaglandin synthesis (inhibits
Mitochondria aggregation of platelets)
Platelet factors Contains ATP, ADP, serotonin, calcium, vWF,
fibronectin, etc.
Contains GF, platelet factor 4, etc.
,Four Phases of Function Anti-platelet How Does It Impair
Platelet Plug Medication Normal Function
Formation
Activation Reorganization of the platelet P2Y12 receptor ADP binds with P2Y12
cytoskeleton with use of Inhibitor – the receptors to stimulate
collagen, leading to dynamic site of inhibition platelet aggregation
changes in platelet shape of the drugs (platelet binding)
from smooth spheres to those clopidogrel and which involves Ca and
with tiny projections and prasugrel TXA2 formation
degranulation – this increases (thromboxane 2)
the platelet’s ability to adhere
to the site of injury These drugs block
ADP from binding
with P2Y12 receptors
thus allowing cAMP to
exert its action (cAMP
prevents platelets from
adhering to one
another), and thus
prevents platelet
aggregation
Adherence Attachment of platelets on a N/A N/A
surface at the site of
endothelial injury; begins
with vWF that binds with
collagen and to GP Ib/IX/V
receptors on platelets which
activates binds with other
receptors and so on causing
anchoring of the platelets into
place
, Aggregation Process by which platelets Glycoprotein Universal inhibition of
interact with one another to IIb/IIIa prostaglandin synthesis
form a hemostatic plug (bind inhibitors by aspirin disrupts
together) by inducing Aspirin platelet function
functional fibrinogen GP IIb/IIIa Receptors:
receptors on the platelet inhibits
GPIIb/IIIa receptors on the Aspirin inhibits the
platelet activate and have a formation of TXA2 by
higher affinity for fibrinogen blocking the COX1
which binds two platelets pathway of the
together arachidonic acid
pathway
Secretion Release of granular contents N/A N/A
and prostaglandin metabolites
from adherent platelets
Activation of ADP, Serotonin,
Fibronectin and
Thrombospondin,
Thromboxane A2, and
Growth Factors
ADP: Enhances adhesion, activates platelets and recruits platelets
Serotonin: Recruits platelets
Fibronectin and Thrombospondin: proteins that stabilize platelets that are adhered to a site of
injury
Thromboxane A2: product of the arachidonic acid pathway that is stored inside the platelet also,
causes vasoconstriction and enhances platelet aggregation
Growth Factors: promotes tissue repair and they have a role in the development of
atherosclerosis
Hematologic System
Core Concepts and Objectives with Advanced Organizers
Hemostasis
1. Analyze the process of hemostasis:
Hemostasis
Platelet plug: Formed on the damaged endothelium
Coagulation cascade: Fibrin and XIIIa (Two end products of CC) form mesh over platelet plug and
anchor it in place.
a. Analyze the platelet structure and the 4 phases of platelet plug formation:
Platelet structure:
Disc shaped cells
Circulate in the outer portion of the blood vessel.
RBC travel in center of cell -> move platelets to our edge. (Anemic patients have harder time
clotting because platelets can’t reach damage.)
Normal Platelet Lab Level: 150,000-450,000
Platelet Structure Function
Peripheral Zone Made of phospholipids
Outer most portion (Cell membrane) Open canalicular system (OCS): system of
channels that runs from inner most portion
of plt and opens to outside. (Provides
channel for substances produced by plt to
be released.
Thromboxana A2: formed by phospholipid
membrane via arachidonic acid pathway.
Provides site for coagulation proteins and
adhesive proteins to bind
Contains many PTL receptors which are
responsible for ptl adhesion and
aggregation.
Sol-gel zone Provides structure support for the cell
Organelle Zone Contains the organelles
Alpha/dense granules Stores calcium and contains enzymes for
Lysosomes prostaglandin synthesis (inhibits
Mitochondria aggregation of platelets)
Platelet factors Contains ATP, ADP, serotonin, calcium, vWF,
fibronectin, etc.
Contains GF, platelet factor 4, etc.
,Four Phases of Function Anti-platelet How Does It Impair
Platelet Plug Medication Normal Function
Formation
Activation Reorganization of the platelet P2Y12 receptor ADP binds with P2Y12
cytoskeleton with use of Inhibitor – the receptors to stimulate
collagen, leading to dynamic site of inhibition platelet aggregation
changes in platelet shape of the drugs (platelet binding)
from smooth spheres to those clopidogrel and which involves Ca and
with tiny projections and prasugrel TXA2 formation
degranulation – this increases (thromboxane 2)
the platelet’s ability to adhere
to the site of injury These drugs block
ADP from binding
with P2Y12 receptors
thus allowing cAMP to
exert its action (cAMP
prevents platelets from
adhering to one
another), and thus
prevents platelet
aggregation
Adherence Attachment of platelets on a N/A N/A
surface at the site of
endothelial injury; begins
with vWF that binds with
collagen and to GP Ib/IX/V
receptors on platelets which
activates binds with other
receptors and so on causing
anchoring of the platelets into
place
, Aggregation Process by which platelets Glycoprotein Universal inhibition of
interact with one another to IIb/IIIa prostaglandin synthesis
form a hemostatic plug (bind inhibitors by aspirin disrupts
together) by inducing Aspirin platelet function
functional fibrinogen GP IIb/IIIa Receptors:
receptors on the platelet inhibits
GPIIb/IIIa receptors on the Aspirin inhibits the
platelet activate and have a formation of TXA2 by
higher affinity for fibrinogen blocking the COX1
which binds two platelets pathway of the
together arachidonic acid
pathway
Secretion Release of granular contents N/A N/A
and prostaglandin metabolites
from adherent platelets
Activation of ADP, Serotonin,
Fibronectin and
Thrombospondin,
Thromboxane A2, and
Growth Factors
ADP: Enhances adhesion, activates platelets and recruits platelets
Serotonin: Recruits platelets
Fibronectin and Thrombospondin: proteins that stabilize platelets that are adhered to a site of
injury
Thromboxane A2: product of the arachidonic acid pathway that is stored inside the platelet also,
causes vasoconstriction and enhances platelet aggregation
Growth Factors: promotes tissue repair and they have a role in the development of
atherosclerosis
