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+ CAPS 301: Muscle, Bodily Fluid, Cardio > Blood – Platelets > Flashcards

Blood – Platelets Flashcards

1
Q

What is the shape of platelets?

A

disc-shaped

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2
Q

Do platelets have nuclei?

A

no

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3
Q

What allows for platelet shape alteration?

A

pseudopodia

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4
Q

What are the 2 types of granules in platelets?

A
  • alpha granules

- dense granules

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5
Q

What do alpha granules contain?

A
  • coagulation factors
  • procoagulants (ie. factor V, vWF)
  • platelet-derived growth factor
  • adhesion molecules
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6
Q

What do dense granules contain?

A
  • ADP
  • ATP
  • Ca2+
  • serotonin
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7
Q

What is thrombopoietin?

A

liver hormone

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8
Q

What does thrombopoietin do?

A
  • stimulates megakaryocyte (precursors to platelets) production in bone marrow
  • produces clotting factors
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9
Q

What type of replication is thrombopiesis?

A

endomitotic synchronous nuclear replication – replicating DNA without cell division occurring

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10
Q

Thrombopoiesis

When does cytoplasmic granulation occur?

A
  • occurs at any stage during maturation

- the earlier granulation occurs, the fewer amount of platelets will be produced

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11
Q

What is thrombopoiesis?

A

generation of platelets

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12
Q

How does platelet formation (thrombopoiesis) occur?

A
  • endomitotic synchronous nuclear replication – megakaryocyte maturation
  • cytoplasmic granulation
  • cell fragments (platelets) break off from edges of megakaryocytes
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13
Q

Where does platelet formation occur?

A

(after release from cells) occurs in bone marrow or quickly following entry into circulation

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14
Q

What does a normal hemostatic response do?

A

acts to arrest bleeding following injury to vascular tissue

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15
Q

What are the 3 hemostasis responses?

A
  1. reaction of blood vessels (vasoconstriction)
    - immediate response to vascular injury
  2. primary hemostasis (platelet plug)
    - occurs quickly, but not sufficient
  3. secondary hemostasis (clot formation)
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16
Q

What is secondary hemostasis?

A

clot formation – network of stable fibrin that is laid on top of platelet plug

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17
Q

Hemostatic Vasoconstriction

What are the 2 components of the hemostatic vasoconstriction response?

A
  • local contractile response (vasoconstrictionm and increased tissue pressure)
  • release of humoral substances
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18
Q

Hemostatic Vasoconstriction

What does increased tissue pressure do?

A

helps compress vessels and reduce their diameter

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19
Q

Hemostatic Vasoconstriction

What does vasoconstriction do?

A

reduces diameter of vessels – blood less likely to flow there

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20
Q

Hemostatic Vasoconstriction

What is a neurogenic spasm?

A

rapid, but short lasting (~60 seconds) response

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21
Q

Hemostatic Vasoconstriction

What is a myogenic spasm?

A

longer lasting response (20-30 minutes)

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22
Q

Hemostatic Vasoconstriction

What are the 3 humoral substances released?

A
  • serotonin – released from activated platelets
  • endothelins – released from injured endothelium
  • clotting factors – blood coagulation cascade reactions
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23
Q

What does serotonin do?

A

promotes vasoconstriction

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24
Q

What does endothelin do?

A

promotes vasoconstriction

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25
Q

What does exposure due to damaged blood vessel result in?

A

contact between substances that do not normally occur

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26
Q

Platelet Plug Formation

A
  1. Platelets adhere to:
  • von Willebrand factor (vWF), mediated by glycoproteins on platelet surface (GpIb)
  • exposed collagen fibers in vascular wall
  1. Activated platelets undergo conformational change (pseudopodia formation), and release:
  • alpha granules (clotting factor V, fibrinogen, vWF)
  • dense granules (ADP, ATP, serotonin, Ca2+)
  • ADP and fibrinogen are responsible for initiation of platelet aggregation
  1. ADP stimulates release of thromboxane A2 (from activated platelets), which acts as potent vasoconstrictor and potentiates platelet aggregation (positive feedback)
    - more platelets = more release of thromboxane A2
  2. Results in formation of unstable hemostatic (platelet) plug
  • plug may be sufficient to stop bleeding in small vascular injuries
  • plug formation is localized due to ADP-induced prostacyclin and NO release
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27
Q

Role of Prostaglandins

What does prostacyclin (PGI2) do?

A

inhibition of platelet aggregation in intact vessels

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28
Q

Role of Prostaglandins

What does thromboxane A2 (TXA2) do?

A

activation of platelet aggregation in damaged vessels

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29
Q

Role of Prostaglandins

How might aggregation and adhesion be prevented?

A

reduction of free cytosolic Ca2+ due to high cAMP levels

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30
Q

Role of Prostaglandins

What is there an enhanced production of in activated platelets? What does this do?

A

enhanced production of TXA2

  • decreases level of cAMP → impacts Ca2+ in cell
  • helps enhance aggregation of platelets
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31
Q

Role of Prostaglandins

What does the pathway in healthy, intact endothelial cells do?

A

results in production of prostacyclin, which is released from endothelial cells

  • prostacyclin acts on activated platelets to increase amount of cAMP
  • increases Ca2+ levels to help prevent release of TXA2-mediated response
  • results in less vasoconstriction, and less aggregation
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32
Q

Role of Prostaglandins

Where is Cox found?

A

endothelial cells

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33
Q

Role of Prostaglandins

What does release of prostacyclin do?

A

helps stop activated platelets from aggregating in that region

  • if platelets are not activated, loss of prostacyclin does not have as big of an impact
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34
Q

Role of Prostaglandins

What does Cox do?

A

if prone to clotting (aggregation of platelets), reducing activity of Cox in platelet itself will help prevent aggregation (prevent platelet plug formation)

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35
Q

What is baby aspirin (aspirin 81)?

A

Cox (cyclo-oxygenase) inhibitor

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36
Q

What is the goal of the coagulation cascade?

A

create stable fibrin formation (clot) to strengthen platelet plug and complete the seal

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37
Q

What is the main requirement for the coagulation cascade?

A

production of thrombin – acts on fibrinogen (factor I) to promote fibrin clot formation

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38
Q

It’s important that coagulation is…

A

localized

39
Q

How is localization of coagulation achieved?

A

by intricate network of amplification and negative feedback loops

40
Q

What are the 3 enzyme complexes that thrombin production is dependent on?

A
  • extrinsic Xase
  • intrinsic Xase
  • prothrombinase
41
Q

What does extrinsic Xase do?

A

activate clotting factor X

42
Q

What does intrinsic Xase do?

A

activate clotting factor X

43
Q

What does prothrombinase do?

A

activate thrombin, which activate fibrin

44
Q

Blood Coagulation – Extrinsic Pathway

What does the extrinsic pathway do?

A

clots blood that has escaped the vessel into surrounding tissue

initial response to tissue damage

45
Q

Blood Coagulation – Extrinsic Pathway

What is the extrinsic pathway activated by?

A

something outside of blood vessel

46
Q

Blood Coagulation – Extrinsic Pathway

What does the extrinsic pathway produce?

A

quick, produces very small amount of thrombin but is enough to activate other cascade reactions

47
Q

Blood Coagulation – Extrinsic Pathway

Describe the steps of the pathway.

A
  1. tissue factor (TF) is exposed following injury to endothelial cells
  2. plasma factor VII binds to TF and is converted to VIIa
  3. TF-VIIa complex binds Ca2+ and acts to convert X to Xa
  4. TF-VIIa-Ca2+ complex (extrinsic Xase) converts small amount of prothrombin to thrombin – ensures propagation of cascading reactions
48
Q

Blood Coagulation – Intrinsic Pathway

What does the intrinsic pathway do?

A

clots blood within the injured vessel

49
Q

Blood Coagulation – Intrinsic Pathway

Describe the steps of the intrinsic pathway.

A
  1. extrinsic Xase complex (from extrinsic pathway) also activates factor IX and factor XI
  2. the small amount of thrombin activated by extrinsic pathway converts V to Va, and VIII to VIIIa
  • VIII is important for increasing activity of intrinsic Xase
  • V is important for completing complex so prothrombinase can function
  1. intrinsic Xase complex (IXa-VIIIa-Ca2+) acts to convert X to Xa
    - this in combination with Va and Ca2+, leads to activation of prothrombinase (Xa-Va-Ca2+)
  2. prothrombinase complex converts massive amount of prothrombin to thrombin
50
Q

Blood Coagulation – Common Pathway

Describe the steps of the common pathway.

A
  1. fibrinogen is hydrolyzed by thrombin into fibrin monomers
  2. fibrin monomers spontaneously polymerize into fibrin polymers
  3. thrombin converts factor XIII to factor XIIIa
  4. XIIIa catalyzes formation of cross-linked lattice with covalent cross-bridging (stable fibrin)
51
Q

What is fibrinolysis?

A

clot breakdown

52
Q

Why can lots of clot formation throughout body (in response to injury) be dangerous?

A
  • at risk for clots breaking away with increase in blood flow
  • eventually there will be blockages of everything, and it’d be difficult for blood to circulate
53
Q

When do clots need to breakdown?

A

once tissue repair has occurred, and we no longer need them

54
Q

What breaks down clot?

A
  • plasmin is found in clot in inactivated form (plasminogen)

- plasmin acts on stable fibrin to break it down

55
Q

Fibrinolysis Process

A
  1. tissue plasminogen activator (t-PA) is released from endothelial tissues and binds to fibrin
  2. t-PA converts clot-bound plasminogen into plasmin (activates it)
  3. plasmin facilitates breakdown of stable fibrin into soluble fragments
    - occurs slowly because plasminogen is buried within clot – only t-PA can access it by breaking down clot layer by layer
56
Q

What happens if an injured area is not ready to release a clot?

A

things are released to inhibit t-PA activity to keep clot there for as long as needed for repair to occur

57
Q

What is the majority of thrombin activation mediated by?

A

prothrombinase (common pathway)

58
Q

What are minor amounts of thrombin activation mediated by?

A
  • thromboplastin (tissue factor) from exposed subendothelial extravascular tissues and activated platelets
  • extrinsic pathway Xase activation (TF-VIIa-Ca2+ complex)
59
Q

What is the role of thrombin? (5)

A
  • enhancement of platelet aggregation – more important in initial response
  • conversion of fibrinogen to fibrin monomers and polymers
  • activation of XIIIa to stabilize fibrin mesh
  • enhancement of VIIIa activation (intrinsic Xase activation) and Va
  • (prothrombinase activation) – feedback enhancement
60
Q

Why is it important that coagulation is local and not occurring inappropriately on a regular basis?

A
  • can impair blood flow

- non-smooth blood flow can cause blood vessel damage

61
Q

How is coagulation regulated to ensure good flow? (4)

A
  • physical factors
  • vasodilators
  • endogenous anticoagulants
  • exogenous anticoagulants
62
Q

What are physical factors that ensure smooth blood flow?

A

smooth lining and negative charge of intact vessels minimizes platelet adhesion – allows laminar/straight/smooth travel through blood vessels

63
Q

What is turbulent blood flow?

A

bump in flow where aggregation of platelets occur

  • common at bifurcation points in vessels
64
Q

What do vasodilators do?

A

ensures good flow through vessels

65
Q

What do NO vasodilators do?

A
  • increases blood flow (vasodilation)

- prevents platelet activation

66
Q

What do prostacyclin (PGI2) vasodilators do?

A

reduces platelet adhesion and aggregation – especially in intact endothelial region

67
Q

What do endogenous anticoagulants do?

A

helps prevent cascade from continuing

68
Q

What are some endogenous anticoagulants? (6)

A
  • antithrombin III (AT III)
  • heparin/heparan sulfate
  • tissue factor pathway inhibitor (TFPI)
  • thrombomodulin
  • α-protease inhibitor
  • protein C and its cofactor protein S
69
Q

What does protein C and its cofactor protein S do?

A

inhibit Va and VIIIa

70
Q

What does α-protease inhibitor do?

A

inhibits IXa

71
Q

What does thrombomodulin do?

A

inhibits activated thrombin

  • stop positive feedback loop that produces thrombin
  • reduce amount of clot formation
72
Q

What does antithrombin III (AT III) do?

A

inhibits IXa and Xa

73
Q

What happens without Xa?

A

amount of thrombin production is reduced

74
Q

What does heparin/heparan sulfate do?

A

stimulates AT III

  • helps anticoagulation
75
Q

What does tissue factor pathway inhibitor (TFPI) do?

A

inhibits extrinsic Xase

  • shuts down extrinsic pathway activation pretty quickly after initiation
  • but enough activity in extrinsic pathway that can promote intrinsic pathway to ultimately activate common pathway
76
Q

What are examples of exogenous anticoagulants?

A
  • heparin
  • warfarin
  • Ca2+ chelators (EDTA, oxalate, citrate)
77
Q

What do Ca2+ chelators (EDTA, oxalate, citrate) do?

A

clinical use – blood collection

  • hematocrit – before we spin blood down test tubes to conduct studies, it needs to be treated with anticoagulant
78
Q

What does heparin do?

A

clinical use – prevention of further clot coagulation

  • increases AT III
  • reduces action of thrombin
79
Q

How is heparin given?

A

through IV – initially very rapid-acting

80
Q

What does warfarin do?

A

similar action/effect to heparin, but slower – used to treat people long-term

  • works on slightly different pathway
  • inhibits production of vitamin K factors produced in liver
  • lower amount of different coagulation factors in circulation – reduces ability to form clots
81
Q

What are the 3 types of hemostasis disorders?

A
  • platelet abnormalities
  • hyperfibrinolysis
  • coagulation defects
82
Q

What are the 2 types of platelet abnormalities?

A
  • thrombocytopenia

- thrombocytosis

83
Q

What is thrombocytopenia?

A

platelet deficiency

  • less able to activate platelets and form platelet plug
  • impacts ability to start cascades (activating some factors, releasing some factors) without platelets to release signalling molecules
84
Q

What is thrombocytosis?

A

excess platelets

  • recruiting platelets to area → more platelets in that population increases ability to recruit even more platelets → increases risk of parts of platelet plug breaking off from plug due to blood flow in the area → potentially cause clot in different area
85
Q

What is hyperfibrinolysis?

A

increased ability to break clot down inappropriately, sooner than we want to

86
Q

What causes hyperfibrinolysis?

A

PAI-1 (plasmin activator inhibitor) deficiency

  • can’t inhibit activation of plasmin
  • plasmin will act to break down clot when it’s not supposed to

**normally inhibits activation of plasmin from plasminogen when ready to break down clot

87
Q

What are the 3 types of coagulation defects?

A
  • vitamin K deficiency
  • hemophilia
  • von Willebrand Disease
88
Q

What is vitamin K required for?

A

vitamin K is required for synthesis of many clotting factors (ie. prothrombin, VII, IX, and X)

89
Q

What occurs as a result of vitamin K deficiency?

A

inadequate production of clotting factors

  • therefore, difficult to produce stable clots
  • same mechanism as warfarin – warfarin is used clinically to impair synthesis of vitamin K-dependent factor
90
Q

What is hemophilia?

A

inherited deficiency of specific coagulation factors, injury can result in uncontrolled bleeding

91
Q

What is Type A hemophilia?

A

deficiency of factor VIII (most common)

92
Q

What is Type B hemophilia?

A

deficiency of factor IX

93
Q

What is von Willebrand disease

A

inherited deficiency of platelet adhesion/aggregation (deficiency in factor VIII and vWF)

  • vWF found under endothelial cells, when tissue is damaged and exposed, helps platelet bind to site of injury
  • deficiency results in harder time recruiting platelets at site of injury

+ CAPS 301: Muscle, Bodily Fluid, Cardio (13 decks)

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