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Physical & Health Assessment COPY - Grayson > Hemostasis and Coagulation (Exam III) Stephen's Cards > Flashcards

Hemostasis and Coagulation (Exam III) Stephen's Cards Flashcards

1
Q

About how long can clot dissolution occur after it has formed?

A
  • minutes to days later
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2
Q

Coagulation proteins are typically found in what form?

A
  • inactivated form
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3
Q

What are two reasons why clotting factors do not attach to the endothelium of the vessel?

A
  • Endothelium is smooth
  • Undamaged endothelium doesn’t express tissue factor or collagen
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4
Q

If the endothelium becomes damage or is injured what does that cause?

A
  • Tissue Factor and Collagen expression → platelet plug formation and coagulation cascade.
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5
Q

What are the three layer of a blood vessel?

A
  • Intima → endothelial layer
  • Media → subendothelial layer (middle)
  • Adventitia → outer layer
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6
Q

Which clotting mediators/factors belong to the intima (endothelial) layer?

A
  • VWF
  • Tissue factor
  • Prostacyclin
  • Nitric oxide
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7
Q

Which clotting factors belong to the Media (subendothelial) layer?

A
  • Collagen
  • Fibronectin
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8
Q

How do the endothelial cells of the intima modulate hemostasis?

A

Synthesize and secrete:

  • Procoagulants
  • Anticoagulants
  • Fibrinolytics
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9
Q

Which two vascular mediators are released by the Intima endothelial cells?

A
  • Vasoconstrictors
  • Vasodilators
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10
Q

What does vWF do?

A

vWF → help platelets adhere to subendothelial layer

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11
Q

What does Tissue Factor (TF) do?

A
  • TF → activates clotting cascade when vessel is injured
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12
Q

Which mediators that are released by the endothelial cells cause vasoconstriction? Which cause vasodilation?

A
  • Constrict → thromboxane A2 and ADP
  • Dilate → NO and PGI₂
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13
Q

What are the functions of the following Procoagulants:

  • Coagulation factors
  • Collagen
  • vWF
  • Fibronectin
  • Thrombomodulin
A
  • Coagulation factors → coagulation
  • Collagen → tensile strength & plt adhesion
  • vWF → plt adhesion
  • Fibronectin → cell to cell adhesion
  • Thrombomodulin → anticoagulation
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14
Q

What are the functions of the following Anticoagulants:

  • Antithrombin IlI
  • Tissue pathway factor inhibitor (TFPI)
A
  • Antithrombin IlI → Degrades factors XII XI X IX II (2, 9, 10, 11, 12)
  • TFPI → Inhibits TF
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15
Q

What are the functions of the following Fibrinolytics:

  • Plasminogen
  • tPA
  • Urokinase
A
  • Plasminogen →Converts to plasmin
  • tPA → Activates plasmin
  • Urokinase → Activates plasmin
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16
Q

Besides vasodilation what other function does Prostacyclin provide?

A
  • Inhibits aggregation
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17
Q

Which layer of a blood vessel is extremely thrombogenic and very active?

A
  • Media (subendothelial)
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18
Q

Which two substances does the media contain that play important roles in clotting? What does each substance do?

A
  • Collagen → potent stimulus for platelet attachment to vessel wall
  • Fibronectin → Facilitate anchoring of fibrin during hemostatic plug formation
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19
Q

How does the adventitia control blood flow?

A
  • Influences blood flow via vessel contraction using NO and prostacyclin
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20
Q

How does vasodilation of the adventitia limit the activity of procoagulant mediators?

A
  • ↑ BF washes the procoagulants away
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21
Q

Briefly explain how NO enables vasodilation?

A

NOS → L-arginine to NO → NO activates sGC in muscle → sGC activates cGMP → relaxation/dilation

  • Nitro Oxide Synthaze converts L-arginine to NO
  • NO diffuses into VSM and activates soluble guanylate cyclase (sGC)
  • sGC activates cGMP which then causes VSM relaxation
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22
Q

What are Eicosanoids?

A

PGs and other compounds such as:

  • Prostacyclin
  • Leukotriene
  • Thromboxane
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23
Q

What are the 4 phases of Hemostasis and Coagulation?

A
  • Vascular phase (Vascular spasm)
  • Primary hemostasis (Formation of platelet plug)
  • Secondary hemostasis (Coagulation and formation of fibrin)
  • Fibrinolysis (Lysis of clot)
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24
Q

What happens during the Vascular Phase of hemostasis and coagulation?

A
  • Damaged blood vessels cause vascular spasm of smooth muscle in vessel wall
  • Localized to the injured area
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25
Q

What are the primary hormones involved in the Vascular Phase of hemostasis and coagulation? What do they do?

A
  • Endothelins → stimulate VSM and cell division of endothelial smooth muscle and fibroblast cells which help repair damaged site
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26
Q

Vasospasm MAY slow down/stop bleeding depending on what?

A

BP

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27
Q

What phase occurs after vascular contraction causes tamponade?

A
  • Primary hemostasis
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28
Q

What two things occur during Primary Hemostasis?

A
  • Injured blood vessel attracts platelets
  • Initiates the phases of platelet formation
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29
Q

What are the three phases of platelet plug formation?

A
  • Adherence
  • Activation
  • Aggregation
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30
Q

What effect causes the platelet circulating in the blood to be positioned near the vessel wall?

A
  • Platelets are smaller than RBCs/WBCs and get pushed to the sides of the vessel
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31
Q

What shape do platelets have that allow them to circulate freely in the blood?

A

They are round and disk-like

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32
Q

Where are platelets formed?

A

In the bone marrow from megakaryocytes

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33
Q

According to our class what is the normal concentration of platelets in the blood? How long do they live?

A
  • 150000 to 300000 /mm3
  • 1-2 wk lifespan
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34
Q

Which 2 systems clear old platelets from the blood?
How much of the circulating platelets are stored in the spleen?

A
  • Macrophages in the reticuloendothelial system
  • Spleen (holds ⅓ of circulating plts)
35
Q

In general what do the glycoproteins on the external membrane of the platelet do? What about GpIb and GpIIb-IIIa?

A
  • Adheres to injured endothelium collagen and fibrinogen
  • GPIb → attaches platelet to vWF
  • GPIIb-IIIa → links activated platelets together to form plug
36
Q

What do the phospholipids on the surface of the platelet do?

A
  • Substrates to PG synthesis
  • Produce TXA2 which activates platelet
37
Q

Which platelet surface glycoprotein doesn’t have a lot of options to reverse its effects?

A
  • GPIIb-IIIa
38
Q

What are the 5 platelet surface receptors for antiplatelet therapy?

A
  • ADP
  • GP1b
  • GPIIb-IIIa
  • Thrombin
  • TXA2
39
Q

Describe the role of each of the following substances/structures found inside a platelet:

  • Actin and myosin
  • ADP
  • Calcium
  • Fibrin-stabilizing factor
  • Growth factor
  • Serotonin
  • Thrombosthenin
A
  • Actin and myosin → Contraction to form the PLT plug
  • ADP → PLT activation and aggregation
  • Calcium → Plays a role in the coagulation cascade
  • Fibrin-stabilizing factor → Cross links fibrin
  • Growth factor → Repairs damaged vessel walls
  • Serotonin → Activates nearby PLT
  • Thrombosthenin → PLT contraction
40
Q

Explain the process by which platelets adhere to each other?

A
  • vWF released from endothelial cells onto the endothelial lining
  • GPIb receptors emerge from platelet surface
  • GPIb binds to vWF and this process attracts other platelets
41
Q

What change does the presence of TF cause to the platelet?

A
  • Platelet has conformational change and is activated
  • GPIIb-IIIa projects outward from platelets and links them to each other → purpose is to create a platelet plug
  • Seal it and heal it…
42
Q

During aggregation which mediators are released from the platelets themselves (when they are activated)?

A
  • alpha and dense granules
  • contractile granules
  • thrombin
43
Q

During aggregation what is the role of the mediators released from the activated platelets?

A
  • Promote procoagulant activity
  • Form a primary unstable clot
44
Q

What is the difference between a primary clot and a secondary clot?

A
  • Small injury → primary clot (or plug) is enough to provide hemostasis
  • Large injury → clotting cascade must be activated to create/stabilize secondary clot for hemostasis
45
Q

During secondary hemostasis fibrin production requires which clotting factors in order to proceed?

A
  • all of them
46
Q

Which protein is probably the single most important protein in the clotting cascade?

A
  • Fibrin
47
Q

What is a very general explanation of the clotting cascade?

A
  • A series of enzymatic reactions (clotting cascade) that ultimately activate prothrombin to thrombin which then converts soluble fibrinogen to fibrin
48
Q

What are the 2 paths of the clotting cascade? They ultimately join together to form…?

A
  • Intrinsic
  • Extrinsic
  • Common path
49
Q

What are the Vitamin K dependent clotting factors?

A
  • Factors II, VII, IX, X
50
Q

What is the name and source of factor I? Is it Vitamin K dependent?

A
  • Name: Fibrinogen
  • Source: Liver
  • Vit K: no
51
Q

What is the name and source of factor III? Is it Vitamin K dependent?

A
  • Name: Tissue Factor (TF) or Thromboplastin
  • Source: vascular wall/extracellular membrane/released from injured cells
  • Vit K: No
52
Q

What is the name and source of factor II? Is it Vitamin K dependent?

A
  • Name: Prothrombin
  • Source: Liver
  • Vit K: Yes
53
Q

What is the name and source of factor IV? Is it Vitamin K dependent?

A
  • Name: Calcium
  • Source: Diet
  • Vit K: n/a
54
Q

What is the name and source of factor V? Is it Vitamin K dependent?

A
  • Name: Proaccelerin
  • Source: Liver
  • Vit K: No
55
Q

What is the name and source of factor VII? Is it Vitamin K dependent?

A
  • Name: Proconvertin
  • Source: Liver
  • Vit K: Yes
56
Q

What is the name and source of factor VIII:C? Is it Vitamin K dependent?

A
  • Name: Antihemophiliac factor
  • Source: Liver
  • Vit K: No
57
Q

What is the name and source of factor VIII:vWF? Is it Vitamin K dependent?

A
  • Name: vonWillibrand Factor
  • Source: Vascular endothelial cells
  • Vit K: n/a
58
Q

How can we compensate for vWF deficiency?

A
  • DDAVP infusion
59
Q

What is the name and source of factor IX? Is it Vitamin K dependent?

A
  • Name: Christmas Factor
  • Source: Liver and other tissues
  • Vit K: Yes
60
Q

What is the name and source of factor X? Is it Vitamin K dependent?

A
  • Name: Stuart-Prower Factor
  • Source: Liver
  • Vit K: Yes
61
Q

What is the name and source of factor XI? Is it Vitamin K dependent?

A
  • Name: Plasma thromboplastin antecedent
  • Source: Liver
  • Vit K: No
62
Q

What is the name and source of factor XII? Is it Vitamin K dependent?

A
  • Name: Hageman Factor
  • Source: Liver
  • Vit K: No
63
Q

What is the name and source of factor XIII? Is it Vitamin K dependent?

A
  • Name: Fibrin Stabilizing Factor
  • Source: Liver
  • Vit K: No
64
Q

Which clotting factors come from the liver?

A
  • All of them except III IV and vWF (VIII:vWF)
65
Q

Explain how the Extrinsic pathway works up to the common path.

A

For37cents you can purchase theextrinsicpathway
* TF released from subendothelium during injury → TF or factor 7 activates extrinsic path
* TF activates factor 7
* Factor 7 activates factor Xin the presence of factor 4 (Ca++)
* Prothrombin activator and platelet phospholipids activate factor 2 (thrombin) → this leads to common path
* Note: Factor 5 ↑ the production of prothromin activator (+ feedback)

66
Q

If the patient is low on Ca++ how will this effect the extrinisic path of the clotting cascade?

A
  • It won’t work as well
67
Q

How long does it take a clot to form via the extrinsic path?

A
  • 12 to 15 sec
68
Q

Explain how the Intrinsic pathway works up to the common path.

A

If you can’t buy theintrinsicpathway for $12 you can buy it for $11.98.
* Blood trauma or exposure to Collagen → activates factor XII
* Factor XIIa activates factor XI → this step needs HMW kininogen and accelerated by prekalllikrein
* Factor XIa activates factor IX
* Factor IXa and VIII activate factor X
* Prothromin activator and phospholipids activate factor IIa (thrombin) → leads to common path

69
Q

Which pathologies will prevent factor X from being activated in the intrinsic path?

A
  • Hemophilia A → Factor VIII missing
  • Thrombocytopenia → Platelets (phospholipids) missing
70
Q

How long does it take to creat a clot via the intrinsic path?

A
  • 6 minutes
71
Q

Explain how the Common pathway works.

A

The final common pathway can be purchased at the five(V) and dime(X) for 1(I) or 2(II) dollars on the 13th (XIII) of the month
* Prothrombin activator changes prothrombin (II) to thrombin (lla)
* Thrombin changes fibrinogen to fibrin in the presence of Ca++
* Fibrin is added to platelet plug
* Activated fibrin-stabilizing factor (XIlla) cross-links fibrin-fibers to complete the clot

72
Q

When the clotting cascade gets activated what else does the body activate?

A
  • Fibrinolysis
73
Q

What is fibrinolysis?

A
  • Prevents clotting from going out of control (+ feedback loop)
  • Prevents excessive deposition of fibrin
74
Q

What is the primary mechanism that begins Fibrinolysis? What is a secondary activator?

A
  • tPA released by damaged endothelial cells
  • urokinase
75
Q

Where is urokinase produced and what is its purpose?

A
  • Produced by kidneys → helps prevent small clots from clogging up kidneys
76
Q

What are two fibrinogenic factors involved in fibrinolysis? What do they do?

A
  • Kallikrein
  • Neutrophil elastase
  • Convert plasminogen to plasmin → plasmin breaks down fibrin
77
Q

Explain how fibrinolysis works?

A
  • Plasminogen is converted to Plasmin via tPA and UPA
  • Plasmin degrades fibrin into “split” products
78
Q

What is a normal platelet values for our class?

A
  • 150,000 to 300,000/mm3
79
Q

What is a normal bleeding time (BT) for our class?

A
  • BT = 3-10 min
80
Q

What is a normal PT for our class?

A
  • PT = 12-14 sec
81
Q

What is a normal aPTT for our class?

A
  • aPTT = 25-35 sec
82
Q

What is a normal thrombin time (TT) for our class?

A
  • TT = 30 secs
83
Q

What is a normal activated clotting time (ACT) for our class?

A
  • ACT = 80-150 secs
84
Q

What is a normal fibrinogen level for our class?

A
  • Fibrinogen ≥ 150 mg/dL

Physical & Health Assessment COPY - Grayson (24 decks)

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