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

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

1
Q
  • 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)
A

Primary Hemostasis

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2
Q

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

A
  1. Blood vessels
  2. Platelets
  3. Calcium
  4. Von Willebrand Factor
  5. Fibrinogen
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3
Q

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

A

True

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4
Q
  • 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)
A

Secondary

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5
Q

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

A

False (bleeding tendencies)

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6
Q
  • These are ssessed prior to an operation.
    Additional tests may be requested to determine specific bleeding/clotting problems.
A

BT/CT Assessment

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7
Q

Main cells involved in hemostasis

A

Platelets

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8
Q

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

A
  1. Megakaryoblast (MK-I)
  2. Promegakaryocyte (MK-II)
  3. Megakaryocyte (MK-III)
  4. Metamegakaryocyte
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9
Q

Which stage of development is omitted from some references?

A

Metamegakaryocyte

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10
Q

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

A
  1. PF4
  2. Beta-thromboglobulin
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11
Q

Normal range of platelet count?

A

150,000 to 400,000 cells/µL

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12
Q

Increased platelet count can lead to what?

A

Thrombosis which can lead to infarction and stroke

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13
Q

Decreased platelet count can result in?

A

Bleeding problems

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14
Q

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

A

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

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15
Q

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

A

Low

Due to accumulation in spleen

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16
Q

Splenectomy results in (high/low) platelet count.

A

High

Absence of storage site

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17
Q

Match the markers.

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

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

A
  1. A
  2. B
  3. C
  4. D
  5. E
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18
Q
  • Used to identify abnormal cells in leukemia and myeloproliferative diseases.
  • Detects specific markers on cell surfaces to differentiate normal and abnormal cells.
A

Flow Cytometry

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19
Q

Stress or Normal Platelet?

  • 2.5 um
  • 7 to 10 fL
A

Normal platelets

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20
Q

Normal or Stress Platelets?

  • > 6um
  • 12 to 14 fL
A

Reticulated/Stress Platelet

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21
Q
  • 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.
A

Platelets

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22
Q

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

A
  1. Provide a negatively charged phospholipid surface for factor X and prothrombin activation.
  2. Release substances that mediate vasoconstriction, platelet aggregation, coagulation (thrombin generation), and vascular repair.
  3. 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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23
Q

What are the four (4) platelet activities?

A
  1. Shape change
  2. Adhesion
  3. Aggregation
  4. Secretion
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24
Q
  • Subdivided into three defined zones, each with unique functional capabilities.
  • Zones are delineated by the circumferential band of microtubules.
A

Platelet Structure

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25
Q

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

A

True

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26
Q
  • 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
A

Reticulated Platelets

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27
Q

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

A
  1. Peripheral Zone
  2. Sub-membranous Region
  3. Sol-gel Zone
  4. Organelle Zone
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28
Q
  • Additional zone
  • Extension of the sol-gel zone
A

Sub-membranous Region

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29
Q
  • Zone which has mitochondria and other organelles inside
A

Organelle Zone

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30
Q
  • 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
A

Phospholipids

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31
Q
  • Vasoconstrictor to reduce bleeding.
  • Promotes platelet aggregation.
A

Thromboxane A2

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32
Q

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

A

Phospathidylserine and phosphatidylinositol

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33
Q

Receptors bound by ligands

A

Glycoproteins and Proteoglycans

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34
Q
  • Absorbs proteins from plasma (e.g., fibrinogen) to
    incorporate into platelets.
  • Stores coagulation proteins for clotting
A

Glycocalyx

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35
Q

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

A
  1. Glycocalyx
  2. Platelet Membrane
  3. Open Cananicular System
  4. Submembranous Area
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36
Q
  • Anchored in the platelet membrane.
  • Present in the glycocalyx.
  • Mediate platelet adhesion and aggregation.
  • Bind to adhesive macromolecules (e.g., fibronectin, vitronectin, collagen).
A

Glycoproteins

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37
Q
  • Involves interaction of GPIb receptor and vWF.
  • Occurs 1 to 2 seconds after vascular injury.
A

Adhesion

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38
Q
  • 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.
A

Aggregation

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39
Q
  • Release of ADP and ATP causes shape change in adjacent
    platelets.
  • Activated platelets secrete substances that activate additional
    platelets.
A

Platelet Activation

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40
Q
  • 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
A

Surface-Connected Cananicular System

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41
Q

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

A

Dense and alpha granules

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42
Q
  • 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)
A

Dense Tubular System

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43
Q

This has a vital role in platelet stimulation.

A

Calcium

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44
Q

For the conversion of phospholipids to Thromboxane A2.

A

Thromboxane synthase and cyclooxygenase

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45
Q
  • Serve as receptors found on platelets’ surface (peripheral
    zone).
  • are bound by ligands
  • Known as cell adhesion molecules or
    seven-transmembrane receptor (STR)
A

Glycoproteins

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46
Q

Study the Cluster Designation of Platelet’s Glycoproteins.

A

Gaur.

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47
Q
  • The first step
  • Adhere to the surface of the damaged tissue through collagen
A

Adhesion

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48
Q

What glycoproteins do platelets use in direct adhesion?

A

GP VI and Integrin α2β1

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49
Q

What glycoproteins do platelets use in indirect adhesion?

Clue: Requires vWF to adhere platelets to collagen.

A

GP Ib-IX-V

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50
Q

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

A

Bernard-Soulier Syndrome

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51
Q
  • 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
A

GP IIb/IIIa

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52
Q

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

A

Glanzmann thrombasthenia

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53
Q

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

A

Fibrinogen

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54
Q

T or F: Low calcium levels affect platelet aggregation.

A

T

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55
Q

What is the ligand for GP IIb/IIIa?

A

Fibrinogen or Fibrinogen-Calcium Complex

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56
Q

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

A
  • 5HT-2: Serotonin
  • TP: TXA2
  • PAR 1: Thrombin
  • PAR 4: Thrombin
  • P2Y1 and P2y12: ADP
  • EP3: Prostaglandin E2
  • α2: Epinephrine

Receptor - Ligand

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57
Q

Study the table for platelet STR-ligand receptor interaction.

A

Gaur.

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58
Q

T or F: Reduction of cAMP decreases ADP.

A

False (increases ADP)

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59
Q

The promoter of platelet aggregation.

A

ADP

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60
Q
  • 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
A

Gq and G12

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61
Q
  • Ligand is prostracyclin
  • Activates Gs
  • Increases cAMP
A

IP

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62
Q

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

A

Hemostasis

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63
Q

Associated with HITTS (Heparin-induced Thrombotic
Thrombocytopenic Syndrome)

A

FcyIIA

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64
Q
  • Administered to individuals with infarctions
  • It is given so that the BVs won’t get completely blocked
  • Too much causes thrombus
A

Heparin

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65
Q
  • Used to describe this zone
  • Preserves the shape of the cell so that it won’t collapse
A

Cytoskeleton

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66
Q
  • 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
A

Microtubules

67
Q

The counterpart of actin-myosin
complexes in skeletal muscles

A

Thrombosthenin

68
Q
  • 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.
A

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

69
Q
  • 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
A

Microfilaments

70
Q

Present within the matrix of the sol-gel zone.

A

Submembranous filaments

71
Q

Responsible for the metabolic activities of the platelet

A

Organelle Zone

72
Q

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

A
  1. 5 to 8 Mitochondria
  2. Cytoplasmic Granules
  3. Anucleated
  4. Golgi Body and RER
73
Q

Released upon contraction of the platelet

A

Platelets Granules

74
Q
  • Most numerous (50-80)
  • Stores various substances important for hemostasis
A

Alpha granules

75
Q
  • Beta-thromboglobulin (B-TG), PF4, PDGF, Thrombospondin
  • Activates fibroblasts and connective tissues for
    vascular repair.
  • Contributes to smooth muscle repair and wound
    healing.
A

Platelet-derived

76
Q
  • vWF, Factor V, Factor VIII, Fibronectin, Albumin,
    HMWK, α-2 Antiplasmin, Plasminogen
  • Activates fibroblasts and connective tissues for
    vascular repair.
A

Platelet-Plasma Derived

77
Q

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

A

Fibrinogen

78
Q
  • Smaller and fewer (2-7)
  • Stores ADP, ATP, ionic calcium, serotonin, and phosphates
A

Dense Granules

79
Q
  • 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
80
Q

Help disrupt subendothelial structure after
vascular injury

81
Q
  • 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
A

Glycogen Granules

82
Q
  • 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.
83
Q
  • Derived from the smooth ER of immature megakaryocytes.
  • Site of prostaglandin and thromboxane synthesis.
  • Sequesters calcium, triggering platelet contraction and
    activation.
A

Dense Tubular System

84
Q

From the plasma absorbed by the platelets

A

Endocytosed

85
Q

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

86
Q

Known as rough surface of the BV wall

A

Atherosclerosis

87
Q

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

A

Vasculature

88
Q

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

A
  1. Tunica Intima (Inner)
  2. Tunica Media
  3. Tunica Adventitia (Outer)
89
Q
  • 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.
A

Endothelial Cells

90
Q
  • Located in the connective tissue layer.
  • Produce collagen, important for maintenance, tissue
    metabolism, and structural framework.
A

Fibroblasts

91
Q
  • Present in the walls of all blood vessels.
  • More numerous in arteries than veins, occasionally in
    capillaries.
  • Promote contraction during injury, initiating primary hemostasis.
A

Smooth Muscle Cells

92
Q
  • 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).
A

Physical Presence of Endothelial Cells

93
Q
  • Carbohydrate layer covering ECs, consisting of
    proteoglycans and glycoproteins.
  • Negative charge repels cellular components, preventing
    binding to adhesion molecules.
A

Glycocalyx

94
Q
  • 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.
A

Prostacyclin

95
Q
  • Induces smooth muscle relaxation and vasodilation.
  • Inhibits platelet activation.
  • Promotes angiogenesis through VEGF and bFGF.
A

Nitric Oxide

96
Q
  • Controls activation of the TF pathway.
  • Limits thrombin generation by inhibiting the TF:VIIa:Xa
    complex.
A

Tissue Factor Pathway Inhibitor

97
Q
  • Anticoagulant from linoleic acid via the lipooxygenase
    pathway.
  • Smooths BVs.
  • Prevents platelet adhesion.
A

13-hydroxyoctadecadienoic acid

98
Q
  • Antigen on endothelial cells.
  • Converts excess ADP to ATP to prevent unwanted
    aggregation.
99
Q

Promotes activation of protein C, leading to
anticoagulation.

A

Thrombomodulin

100
Q
  • 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.
A

Heparan Sulfate

101
Q
  • 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.
A

Vasoconstriction

102
Q
  • 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.
A

Exposure of Collagen

103
Q
  • 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.
A

Secretion of Von Willebrand Factor

104
Q
  • Synthesized in the liver and is labile, requiring
    binding with VWF for stability.
  • Protected by vWF to maintain functionality.
105
Q
  • Macromolecule in the blood.
  • Facilitates platelet adhesion
A

vWF-Factor 8 Complex

106
Q
  • Causes platelets to aggregate in the presence of
    ristocetin
  • Assesses platelet aggregation in vitro.
  • Adheres in vivo.
A

vWF Ristocetin Cofactor

107
Q
  • Converts fibrinogen to fibrin clot.
  • Excessive thrombin can cause clotting elsewhere.
108
Q
  • Endothelial cell receptor regulating excess clotting
    factors.
  • Forms a complex with thrombin to activate Protein C (Pc) bound to Protein S (Ps).
A

Thrombomodulin

109
Q

Prevents further clotting by deactivating
Factors V and VIII.

A

Pc-Ps Complex

110
Q

Cascading activation of clotting factors.

A

Secondary Hemostasis

111
Q
  • 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.
A

Adhesion Molecules

112
Q
  • 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.
A

Exposure of Tissue Factor

113
Q

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

114
Q

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

115
Q

What are the critical components of platelet adhesion?

A
  1. Collagen
  2. vWF
  3. ADAMTS-13
  4. Adhesion Molecules
116
Q

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

117
Q
  • Counterpart of 13-HODE.
  • Promotes platelet adhesion.
  • Source: Platelets.
118
Q

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

A

Anticoagulants

119
Q

GP Ib-IX-V is required by vWF.

A

vWF Receptor

120
Q
  • 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).
121
Q
  • Platelet adheres due to adhesion molecules.
  • Contains collagen and vWF.
A

Cold Platelet

122
Q

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

A
  1. GP IIb/IIIa
  2. Fibrinogen
  3. Calcium
123
Q

Receptors critical for platelet aggregation.

A

GP IIb/IIIa

124
Q

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

A

Fibrinogen

125
Q

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

126
Q

Essential for activating vitamin
K-dependent clotting factors.

A

Phospholipid Exposure

127
Q

Specific phospholipid crucial for
vitamin K-dependent clotting factors.

A

Phosphatidylserine

128
Q

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

129
Q
  • 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.
A

White Clot

130
Q
  • 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
131
Q

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

A

Hypofibrinogenemia

132
Q

Platelet aggregation is also affected.

A

Hypocalcemia

133
Q
  • Essential for vitamin K-dependent clotting factors.
  • Referred to as Clotting Factor K or Platelet Phospholipid in
    exams.
A

Phosphatidylserine

134
Q
  • Release their contents for further platelet activation and
    aggregation.
  • Contain various factors essential for clotting and healing.
A

Alpha granules and dense granules

135
Q
  • Needed for further platelet stimulation.
  • Play roles in signal transduction pathways that activate
    platelets.
A

G1, Gq, and G12 (G-Proteins)

136
Q
  • Endpoint of the cyclooxygenase pathway within
    platelets.
  • Promotes platelet aggregation and vasoconstriction.
A

Thromboxane A2

137
Q
  • Endpoint of the cyclooxygenase pathway in endothelial
    cells.
  • Inhibits platelet activation and promotes vasodilation.
A

Prostacyclin (PGI2)

138
Q

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

A
  1. A, B, C
  2. D, E
  3. F
  4. G
  5. H
  6. I, J
  7. K
139
Q
  • 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.
A

Alpha Granules

140
Q
  • Neutralizes heparin to prevent interference with clot
    formation.
  • Ensures thrombin activity is not inhibited by heparin’s
    antithrombin properties.
141
Q

Involved in fibrinolysis.

A

Plasminogen

142
Q

Occurs when platelets release all their contents.

A

Platelet Release Reaction

143
Q

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

144
Q

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

145
Q

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

146
Q

What two pathways are involved in the synthesis of eicosanoids?

A
  1. Cyclooxygenase Pathway
  2. Lipoxygenase Pathway
147
Q

What is the objective of Eicosanoids Synthesis?

A

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

148
Q
  • 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).
A

Prostaglandin

149
Q
  • A product of the cyclooxygenase pathway.
  • Plays a key role in platelet aggregation and
    vasoconstriction.
A

Thromboxane

150
Q
  • Phospholipase C cleaves PI-4,5-P2 into IP3 and DAG.
  • This triggers actin-microfilament contraction and release of ionic calcium.
A

G protein-dependent Mechanism

151
Q

Activates Phospholipase A2.

152
Q

Activates phosphokinase and pleckstrin

153
Q

What are the stages of hemostasis activity?

A
  1. Adhesion
  2. Aggregation
  3. Release Reaction
  4. Shape Change
154
Q

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

155
Q

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

A

Aggregation

156
Q

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

A

Release Reaction

157
Q

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

A

Shape Change

158
Q

What is the purpose of clot retraction?

A
  • Shrinks the clot to restore blood flow.
  • Prevents obstruction of blood vessels and ensures
    smooth circulation.
159
Q

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

A

Clot Retraction Time

160
Q

What are the consequences of poor clot retraction?

A
  1. Blood Flow Turbulence
  2. Red Cell Damage
  3. Normalization of Blood Flow
161
Q

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

A

Blood Flow Turbulence

162
Q
  • RBCs squeezed through the fibrin clot may fragment into
    schistocytes.
  • Results in hemolysis (destruction of RBCs).
A

Red Cell Damage

163
Q

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

A

Normalization of Blood Flow

164
Q

Congrats pi, good night.

Hematology 2 (9 decks)

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