(P) Lesson 2: Platelet Function and Primary Hemostasis Flashcards by Shen Gabriel

Forms an initial platelet plug to prevent bleeding.
Is reversible and loose
Requires various factors for successful hemostasis (e.g. blood vessels, platelets, calcium, Von Willebrand factor, Fibrinogen)
Absence of these factors leads to bleeding problems
Assessed via bleeding time (BT)

Primary Hemostasis

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What are the five (5) factors needed for successful hemostasis?

Blood vessels
Platelets
Calcium
Von Willebrand Factor
Fibrinogen

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T or F: Bleeding time does not pinpoint which components are defective.

True

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Stabilizes the plug formed by primary hemostasis into a clot to prevent bleeding.
Involves clotting factors produced by the liver (Factors I-XIII)
Assessed via clotting time (CT)

Secondary

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T or F: An unhealthy liver can result in severe clotting tendencies.

False (bleeding tendencies)

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These are ssessed prior to an operation.
Additional tests may be requested to determine specific bleeding/clotting problems.

BT/CT Assessment

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Main cells involved in hemostasis

Platelets

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What are the four (4) primary stages of development?

Megakaryoblast (MK-I)
Promegakaryocyte (MK-II)
Megakaryocyte (MK-III)
Metamegakaryocyte

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Which stage of development is omitted from some references?

Metamegakaryocyte

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Platelet production in the bone marrow is controlled by what two (2) components?

PF4
Beta-thromboglobulin

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Normal range of platelet count?

150,000 to 400,000 cells/µL

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Increased platelet count can lead to what?

Thrombosis which can lead to infarction and stroke

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Decreased platelet count can result in?

Bleeding problems

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What are the percentages of the produced platelets that enter the blood stream and sequestered in the spleen?

70% enter the bloodstream, 30% sequestered in the spleen

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Enlarged spleen can result in (high/low) platelet counts.

Low

Due to accumulation in spleen

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Splenectomy results in (high/low) platelet count.

High

Absence of storage site

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Match the markers.

Observed in myeloid stem cells (SC).
Precursor cell of blood cells.
Marker specific for platelets.
Marker indicating stem cells.
Together indicate stem cells.

A. CD34
B. Myeloid SC
C. CD41 and CD42
D. CD117
E. CD34, CD41, CD117

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Used to identify abnormal cells in leukemia and myeloproliferative diseases.
Detects specific markers on cell surfaces to differentiate normal and abnormal cells.

Flow Cytometry

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Stress or Normal Platelet?

2.5 um
7 to 10 fL

Normal platelets

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Normal or Stress Platelets?

> 6um
12 to 14 fL

Reticulated/Stress Platelet

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Smaller than RBCs
Anucleated cytoplasmic fragments.
Measure approximately 2 µm in diameter.
Originate from bone marrow megakaryocytes.
Appear as pale blue cells with fine azurophilic granules on Wright’s stain.
Produced from megakaryoblasts in about 1 week.
70% circulate in peripheral blood; 30% are sequestered in the spleen.
Survive for 7 to 10 days in circulation.
Active in hemostasis.

Platelets

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What are the three (3) functions of platelets in hemostasis?

Provide a negatively charged phospholipid surface for factor X and prothrombin activation.
Release substances that mediate vasoconstriction, platelet aggregation, coagulation (thrombin generation), and vascular repair.
Provide surface membrane glycoproteins (GPIIb and GPIIIa) to attach to other platelets via fibrinogen, and GPIb to bind to collagen and subendothelium via vWF.

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What are the four (4) platelet activities?

Shape change
Adhesion
Aggregation
Secretion

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Subdivided into three defined zones, each with unique functional capabilities.
Zones are delineated by the circumferential band of microtubules.

Platelet Structure

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T or F: Impaired function of the platelet membrane, cytoskeleton, granular constituents, and secreted proteins can lead to platelet dysfunction and abnormal hemostasis.

True

* Also called enlarged or giant platelets or stress platelets * Large, almost the same size as RBCs * RBC: 6-8 um * Also has a high volume, correlated with its size * Seen in reactive thrombocytosis which is the normal response of the body for more platelets, causing the BM to release immature platelets * Can be mistaken for as lymphocytes

Reticulated Platelets

What are the four (4) zones in the platelet ultrastructure?

1. Peripheral Zone 2. Sub-membranous Region 3. Sol-gel Zone 4. Organelle Zone

* Additional zone * Extension of the sol-gel zone

Sub-membranous Region

* Zone which has mitochondria and other organelles inside

Organelle Zone

* Involved in the synthesis of TXA₂ via the cyclooxygenase pathway. * Co-factor for vitamin K-dependent clotting factors or the prothrombin group clotting factors or Vitamin K-dependent clotting factors: II, VII, IX, X

Phospholipids

* Vasoconstrictor to reduce bleeding. * Promotes platelet aggregation.

Thromboxane A2

The unique markers of the peripheral zone and are collectively referred to as platelet phospholipids (PL).

Phospathidylserine and phosphatidylinositol

Receptors bound by ligands

Glycoproteins and Proteoglycans

* Absorbs proteins from plasma (e.g., fibrinogen) to incorporate into platelets. * Stores coagulation proteins for clotting

Glycocalyx

What are the four (4) components of the Platelet Plasma Membrane?

1. Glycocalyx 2. Platelet Membrane 3. Open Cananicular System 4. Submembranous Area

* Anchored in the platelet membrane. * Present in the glycocalyx. * Mediate platelet adhesion and aggregation. * Bind to adhesive macromolecules *(e.g., fibronectin, vitronectin, collagen).*

Glycoproteins

* Involves interaction of GPIb receptor and vWF. * Occurs 1 to 2 seconds after vascular injury.

Adhesion

* Requires a conformational change in GPIIb/IIIa receptor. * Fibrinogen binds to different platelets, promoting interaction. * Begins 10 to 20 seconds after vascular injury. * Requires calcium and/or magnesium.

Aggregation

* Release of ADP and ATP causes shape change in adjacent platelets. * Activated platelets secrete substances that activate additional platelets.

Platelet Activation

* Stores hemostatic proteins found in the glycocalyx. * Enhances interaction between internal and external environments of platelets. * Channel for platelet secretion. * Tubular invaginations of the plasma membrane. * Releases substances stored in dense and alpha granules. * Facilitates collection of plasma procoagulants. * Appears to regulate calcium in the platelet

Surface-Connected Cananicular System

Where are the substances released by the SCCS or OCS stored in?

Dense and alpha granules

* Connects SCCS within the platelet. * Found in the organelle zone * "Control center" for platelet stimulation. * Stores Ca2+. * Carries enzymes for synthesis (e.g., phospholipase A2, cyclooxygenase, thromboxane synthase)

Dense Tubular System

This has a vital role in platelet stimulation.

Calcium

For the conversion of phospholipids to Thromboxane A2.

Thromboxane synthase and cyclooxygenase

* Serve as receptors found on platelets' surface (peripheral zone). * are bound by ligands * Known as cell adhesion molecules or seven-transmembrane receptor (STR)

Glycoproteins

Study the Cluster Designation of Platelet's Glycoproteins.

Gaur.

* The first step * Adhere to the surface of the damaged tissue through collagen

Adhesion

What glycoproteins do platelets use in direct adhesion?

GP VI and Integrin α2β1

What glycoproteins do platelets use in indirect adhesion? ## Footnote Clue: Requires vWF to adhere platelets to collagen.

GP Ib-IX-V

Results to poor platelet adhesion (adherence of platelets to collagen) resulting in longer wound healing time

Bernard-Soulier Syndrome

* Platelets, initially adhere to collagen, but they should also clump or aggregate * An integrin used by platelets to aggregate to close wounds and stop the bleeding * Uses fibrinogen to connect platelets to each another

GP IIb/IIIa

Deficiency of GP IIb/IIIa that results in poor platelet aggregation or clumping leading to prolonged bleeding

Glanzmann thrombasthenia

Very important for primary hemostasis to occur so that the aggregation of the platelets will be successful.

Fibrinogen

T or F: Low calcium levels affect platelet aggregation.

What is the ligand for GP IIb/IIIa?

Fibrinogen or Fibrinogen-Calcium Complex

What are the seven (7) transmembrane receptors all found in the peripheral zone?

* 5HT-2: Serotonin * TP: TXA2 * PAR 1: Thrombin * PAR 4: Thrombin * P2Y1 and P2y12: ADP * EP3: Prostaglandin E2 * α2: Epinephrine | Receptor - Ligand

Study the table for platelet STR-ligand receptor interaction.

Gaur.

T or F: Reduction of cAMP decreases ADP.

False (increases ADP)

The promoter of platelet aggregation.

ADP

* Increases IP3 and DAG activity * The calcium stored in the dense tubular system, once released, changes the shape of the platelet from a discoid form to a stellate formation for it to release all of its content into the plasma for a successful primary hemostasis and blood clotting

Gq and G12

* Ligand is prostracyclin * Activates Gs * Increases cAMP

This controls the amount of chemicals released for our blood clotting.

Hemostasis

Associated with HITTS (Heparin-induced Thrombotic Thrombocytopenic Syndrome)

FcyIIA

* Administered to individuals with infarctions * It is given so that the BVs won’t get completely blocked * Too much causes thrombus

Heparin

* Used to describe this zone * Preserves the shape of the cell so that it won't collapse

Cytoskeleton

* Encases the entire platelet, maintaining its discoid shape * Composed of protein subunits called tubulin * In stimulated platelets, contraction of the circumferential * band moves organelles toward the center, aiding in secretion * Disappear from the center after secretion and reappear in the peripheral areas like pseudopods * Monitor internal contraction, regulating platelet response to stimuli

Microtubules

The counterpart of actin-myosin complexes in skeletal muscles

Thrombosthenin

* The thrombosthenin which are contractile proteins within the platelets will now contract, disrupting the microtubules * Also induces contraction of the platelet itself to release its contents needed for hemostasis * Occurs upon Ca 2+ released from the dense tubular system.

Disruption of microtubules will result in a shape change into a stellate formation (star-like)

* Randomly interwoven throughout the cytoplasm * Composed of contractile proteins actin and myosin * Includes thrombosthenin, similar to actomyosin * Can convert from an unorganized state to organized parallel filaments capable of contraction

Microfilaments

Present within the matrix of the sol-gel zone.

Submembranous filaments

Responsible for the metabolic activities of the platelet

Organelle Zone

What are the four (4) organelles of the organelle zone?

1. 5 to 8 Mitochondria 2. Cytoplasmic Granules 3. Anucleated 4. Golgi Body and RER

Released upon contraction of the platelet

Platelets Granules

* Most numerous (50-80) * Stores various substances important for hemostasis

Alpha granules

* Beta-thromboglobulin (B-TG), PF4, PDGF, Thrombospondin * Activates fibroblasts and connective tissues for vascular repair. * Contributes to smooth muscle repair and wound healing.

Platelet-derived

* vWF, Factor V, Factor VIII, Fibronectin, Albumin, HMWK, α-2 Antiplasmin, Plasminogen * Activates fibroblasts and connective tissues for vascular repair.

Platelet-Plasma Derived

By the liver, found in plasma, absorbed by platelets via the glycocalyx

Fibrinogen

* Smaller and fewer (2-7) * Stores ADP, ATP, ionic calcium, serotonin, and phosphates

Dense Granules

* Contain enzymes that digest cellular debris * Protection against infection * Open wound exposed to air allows bacteria to enter, hence the bactericidal enzymes in platelets, along with WBCs * Contains microbicidal enzymes, neutral proteases, and acid hydrolases

Lysosomes

Help disrupt subendothelial structure after vascular injury

Proteases

* Involved in platelet metabolism * Source of energy needed by the platelet to survive for a maximum of 12 days after being released from the BM

Glycogen Granules

* Contents of α and dense granules are released during secretion. * Promotes recruitment of additional platelets to the injury site. * Energy-dependent process relying on mitochondrial function. * ATP production occurs through glycolysis and the Krebs cycle.

Secretion

* Derived from the smooth ER of immature megakaryocytes. * Site of prostaglandin and thromboxane synthesis. * Sequesters calcium, triggering platelet contraction and activation.

Dense Tubular System

From the plasma absorbed by the platelets

Endocytosed

Crucial role as primary actors in the initial phase of the hemostatic response.

Platelets

Known as rough surface of the BV wall

Atherosclerosis

Includes arteries, veins, and capillaries carrying blood throughout the body.

Vasculature

What are the three (3) layers of blood vessels?

1. Tunica Intima (Inner) 2. Tunica Media 3. Tunica Adventitia (Outer)

* Form a smooth, unbroken surface for nonturbulent blood flow. * Supported by a basement membrane and an elastin-rich internal elastic lamina. * Arteries have an additional elastin-rich external lamina. * Complex and heterogeneous, with unique characteristics based on environment and physiological requirements. * Essential roles in immune response, vascular permeability, proliferation, and hemostasis.

Endothelial Cells

* Located in the connective tissue layer. * Produce collagen, important for maintenance, tissue metabolism, and structural framework.

Fibroblasts

* Present in the walls of all blood vessels. * More numerous in arteries than veins, occasionally in capillaries. * Promote contraction during injury, initiating primary hemostasis.

Smooth Muscle Cells

* Rhomboid and contiguous, providing a smooth inner surface. * Promotes nonturbulent blood flow, preventing platelet and coagulation enzyme activation. * Forms a barrier separating platelets from collagen and procoagulant proteins from tissue factor (TF).

Physical Presence of Endothelial Cells

* Carbohydrate layer covering ECs, consisting of proteoglycans and glycoproteins. * Negative charge repels cellular components, preventing binding to adhesion molecules.

Glycocalyx

* Synthesized through the eicosanoid pathway. * Prevents unnecessary platelet activation by antagonizing thromboxane A2 (TXA2). * Derived from phospholipids via cyclooxygenase and prostacyclin synthase. * Opposes TXA2. * Dilates blood vessels (BVs) to prevent blood stagnation. * Prevents platelet adhesion or stimulation. * Promotes vasodilation and smooth muscle relaxation.

Prostacyclin

* Induces smooth muscle relaxation and vasodilation. * Inhibits platelet activation. * Promotes angiogenesis through VEGF and bFGF.

Nitric Oxide

* Controls activation of the TF pathway. * Limits thrombin generation by inhibiting the TF:VIIa:Xa complex.

Tissue Factor Pathway Inhibitor

* Anticoagulant from linoleic acid via the lipooxygenase pathway. * Smooths BVs. * Prevents platelet adhesion.

13-hydroxyoctadecadienoic acid

* Antigen on endothelial cells. * Converts excess ADP to ATP to prevent unwanted aggregation.

CD39

Promotes activation of protein C, leading to anticoagulation.

Thrombomodulin

* Enhances the activity of antithrombin, a serine protease inhibitor. * Similar in structure and function to pharmaceutical heparin. * Released by endothelial cells. * Natural anticoagulant from the liver and BVs. * Has antithrombin properties.

Heparan Sulfate

* Induced by harmful stimuli (mechanical or chemical). * Smooth muscle cells contract, narrowing the vascular lumen and decreasing blood flow. * In veins and capillaries, blood escapes into surrounding tissues, creating extravascular pressure and minimizing blood loss.

Vasoconstriction

* Subendothelial connective tissues rich in collagen are exposed upon injury. * Collagen binds circulating von Willebrand factor (VWF), leading to platelet binding and activation. * Platelets bind to collagen through GPVI and α2β1 receptors, adhering to the damaged area. * Collagen exposure from tissue damage leads to adhesion and aggregation. * Tissue factors mix with plasma, activating Factor VII and the clotting process.

Exposure of Collagen

* Synthesized in endothelial cells, platelets, megakaryocytes. * Promotes platelet adhesion using GP Ib-IX-V. * Without VWF, Factor 8 activity declines, but VWF remains unaffected. * Binds to Factor 8 for protection. * Deficiency affects Factor 8, leading to poor clotting.

Secretion of Von Willebrand Factor

* Synthesized in the liver and is labile, requiring binding with VWF for stability. * Protected by vWF to maintain functionality.

Factor 8

* Macromolecule in the blood. * Facilitates platelet adhesion

vWF-Factor 8 Complex

* Causes platelets to aggregate in the presence of ristocetin * Assesses platelet aggregation in vitro. * Adheres in vivo.

vWF Ristocetin Cofactor

* Converts fibrinogen to fibrin clot. * Excessive thrombin can cause clotting elsewhere.

Thrombin

* Endothelial cell receptor regulating excess clotting factors. * Forms a complex with thrombin to activate Protein C (Pc) bound to Protein S (Ps).

Thrombomodulin

Prevents further clotting by deactivating Factors V and VIII.

Pc-Ps Complex

Cascading activation of clotting factors.

Secondary Hemostasis

* Activated ECs secrete and coat themselves with P-selectin, promoting platelet and leukocyte binding. * ECs also secrete ICAMs and PECAMs, further promoting platelet and leukocyte binding.

Adhesion Molecules

* Subendothelial smooth muscle cells and fibroblasts support TF. * EC disruption exposes TF to circulating blood, activating the coagulation system through contact with factor VII. * Leads to fibrin formation, securing the platelet plug to the damaged area.

Exposure of Tissue Factor

In arterioles and arteries, high blood flow forms a ____ clot consisting of platelets, fibrin, and VWF.

White

In veins, slower blood flow forms a ____ clot consisting of red blood cells, fibrin, and some platelets.

Bulky red

What are the critical components of platelet adhesion?

1. Collagen 2. vWF 3. ADAMTS-13 4. Adhesion Molecules

# Matching Type 1. Facilitates platelet adhesion. 2. Deficiency results in abnormal platelet adhesion. 3. Includes GP Ib-IX-V (uses vWF), GP IV, and α2β1. 4. Promotes platelet adhesion. 5. Cuts a specific point of vWF, fragmenting it and removing its ability to function. A. Collagen B. vWF C. ADAMTS-13 D. Adhesion Molecules

1. A 2. D 3. D 4. B 5. C

* Counterpart of 13-HODE. * Promotes platelet adhesion. * Source: Platelets.

12-HETE

Blood vessels maintain stronger platelet resistance in the absence of wounds or trauma.

Anticoagulants

GP Ib-IX-V is required by vWF.

vWF Receptor

* Protein that controls vWF, exhibiting anticoagulant properties. * Regulates vWF by cutting it at the site of injury to keep the clot localized. * Deficiency leads to Thrombotic Thrombocytopenic Purpura (TTP).

ADAMTS-13

* Platelet adheres due to adhesion molecules. * Contains collagen and vWF.

Cold Platelet

What are the critical components of platelet aggregation (white clot)?

1. GP IIb/IIIa 2. Fibrinogen 3. Calcium

Receptors critical for platelet aggregation.

GP IIb/IIIa

Ligand for GP IIb/IIIa, essential for platelet-to-platelet interaction.

Fibrinogen

Important for forming fibrinogen-calcium complex, aiding in clotting.

Calcium

Essential for activating vitamin K-dependent clotting factors.

Phospholipid Exposure

Specific phospholipid crucial for vitamin K-dependent clotting factors.

Phosphatidylserine

Formed during secondary hemostasis, involving platelet aggregation and clot formation.

Red Clot

* Activated upon aggregation via GP IIb/IIIa. * Releases contents for further activation and aggregation. * Phospholipids exposed upon activation are utilized by vitamin K-dependent clotting factors, activating the blood clotting process. * Contains fibrinogen complex and vWF.

White Clot

* Formed during secondary hemostasis. * Requires platelet-to-platelet interaction, leading to aggregation. * Stimulated by ATP, Thromboxane A2 (TxA2), serotonin, epinephrine, and prostaglandin. * GP IIb/IIIa, platelets, and receptors are critical for successful aggregation. * Fibrinogen or fibrinogen-calcium complex acts as a bridge for platelet aggregation

Red Clot

Blood doesn't clot properly due to affected platelet-to-platelet interaction.

Hypofibrinogenemia

Platelet aggregation is also affected.

Hypocalcemia

* Essential for vitamin K-dependent clotting factors. * Referred to as Clotting Factor K or Platelet Phospholipid in exams.

Phosphatidylserine

* Release their contents for further platelet activation and aggregation. * Contain various factors essential for clotting and healing.

Alpha granules and dense granules

* Needed for further platelet stimulation. * Play roles in signal transduction pathways that activate platelets.

G1, Gq, and G12 (G-Proteins)

* Endpoint of the cyclooxygenase pathway within platelets. * Promotes platelet aggregation and vasoconstriction.

Thromboxane A2

* Endpoint of the cyclooxygenase pathway in endothelial cells. * Inhibits platelet activation and promotes vasodilation.

Prostacyclin (PGI2)

# Matching Type 1. Promote smooth muscle and vascular repair 2. Adhesion molecule 3. Neutralizes Heparin 4. Stimulate vascular fibroblast 5. For fibrinolysis 6. Fibrinolysis control 7. Coagulation control A. PDGF B. EGF C. Transforming Growth Factor-Beta D. Fibronectin E. Thrombospondin F. PF4 G. B-thromboglobulin H. Plasminogen I. Plasminogen Activator Inhibitor-1 J. A2-Anti-Plasmin K. Protein C Inhibitor

1. A, B, C 2. D, E 3. F 4. G 5. H 6. I, J 7. K

* Released with the aid of calcium from the G pathways, specifically IP3 and DAG activities. * Contain factors essential for clotting and healing. * Present in plasma and absorbed by platelets.

Alpha Granules

* Neutralizes heparin to prevent interference with clot formation. * Ensures thrombin activity is not inhibited by heparin's antithrombin properties.

PF4

Involved in fibrinolysis.

Plasminogen

Occurs when platelets release all their contents.

Platelet Release Reaction

# Matching Type 1. Activated by thrombin, ADP, epinephrine. 2. Activated by thrombin, ADP, TXA2. 3. Activated by prostacyclin. A. G1 B. Gq C. G12 D. Gs

1. A 2. B, C 3. D

# Matching Type 1. Inhibit adenylate cyclase 2. Activates phospholipases 3. Activates protein kinase C 4. Promotes adenylate cyclase A. G1 B. Gq C. G12 D. Gs

1. A 2. B 3. C 4. D

# Matching Type 1. Activate pleckstrin, actin microfilaments 2. Increase IP3-DAG 3. Increase cAMP concentration 4. Reduce cAMP A. G1 B. Gq C. G12 D. Gs

1. C 2. B 3. D 4. A

What two pathways are involved in the synthesis of eicosanoids?

1. Cyclooxygenase Pathway 2. Lipoxygenase Pathway

What is the objective of Eicosanoids Synthesis?

Stimulate calcium binding to thrombostenin, leading to platelet content release.

* Synthesized in platelets. * Acts as a "pain chemical" to identify areas of pain. * Counteracted by NSAIDs, which inhibit cyclooxygenase, thereby also affecting TXA2 (important for platelet aggregation).

Prostaglandin

* A product of the cyclooxygenase pathway. * Plays a key role in platelet aggregation and vasoconstriction.

Thromboxane

* Phospholipase C cleaves PI-4,5-P2 into IP3 and DAG. * This triggers actin-microfilament contraction and release of ionic calcium.

G protein-dependent Mechanism

Activates Phospholipase A2.

IP3

Activates phosphokinase and pleckstrin

DAG

What are the stages of hemostasis activity?

1. Adhesion 2. Aggregation 3. Release Reaction 4. Shape Change

Platelets adhere to the site of vascular injury, binding to exposed subendothelial structures such as collagen via von Willebrand factor.

Adhesion

Platelets clump together, forming a platelet plug to temporarily seal the site of injury.

Aggregation

Platelets release granule contents (e.g., ADP, serotonin, thromboxane A2) to recruit and activate more platelets.

Release Reaction

Platelets change shape from a discoid to a star-like form, increasing surface area for interactions and promoting clot stability.

Shape Change

What is the purpose of clot retraction?

* Shrinks the clot to restore blood flow. * Prevents obstruction of blood vessels and ensures smooth circulation.

In vivo, the clot must retract adequately to prevent complications.

Clot Retraction Time

What are the consequences of poor clot retraction?

1. Blood Flow Turbulence 2. Red Cell Damage 3. Normalization of Blood Flow

Leads to mechanical stress on red blood cells (RBCs).

Blood Flow Turbulence

* RBCs squeezed through the fibrin clot may fragment into schistocytes. * Results in hemolysis (destruction of RBCs).

Red Cell Damage

Retraction is essential to shrink the clot and prevent further damage to RBCs, ensuring smooth blood flow.

Normalization of Blood Flow

Congrats pi, good night.

Mwa. <3

(P) Lesson 2: Platelet Function and Primary Hemostasis Flashcards

(164 cards)