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671A - Anesthesia I > Week 9 - Clotting and Coagulation Cascade > Flashcards

Week 9 - Clotting and Coagulation Cascade Flashcards

1
Q

What is hemostasis?

A

The process by which the body maintains the delicate balance between bleeding and clotting

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2
Q

What are the three layers of the blood vessel?

A

Intimia –> Inner most
Media –> Thickest in arteries (smooth muscle)
Adventitia –> Thickest in veins (outer most layer)

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3
Q

What is the intimia layer composed of primarily?

A

Endothelial cells

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4
Q

What is the importance of the endothelial cells in blood vessels?

A

Synthesize and secrete many mediators in the clotting cascade –> Procoagulants (initiate clots), anticoagulants (inhibit coagulation), fibrinolytics (break down clots)

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5
Q

What mediator secreted and synthesized by the endothelial cells allows platelets to begin sticking to each other?

A

von Willebrand factor

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6
Q

What does Tissue factor do in regards to the clotting cascade?

A

Extrinsic –> Tissue factor (3) activates factor 7 –> this 7a can now activate factor X in the common pathway

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7
Q

When vessel injury occurs, what is the first step that takes place?

A

Endothelial cells secrete Thromboxane A2 and ADP to cause vasoconstriction at the injured site.

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8
Q

What mediators can cause vasodilation of the blood vessel?

A

Nitric oxide (NO) and prostacyclin

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9
Q

Although the endothelial cells within the intimia secrete many mediators contributing to the clotting cascade, what is another important job this tissue does?

A

Prevents the fluid contents of the blood from interacting with the sub endothelial space (media) –> This is where highly thrombogenic material is stored, collagen and procoagulants like fibronectin

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10
Q

Where do platelets tend to flow within the blood vessel?

A

Along the vessel surface –> The endothelial muscle physically repels bigger blood components away (RBCs and WBCs) while smaller components like Platelets get placed conveniently near their site of action

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11
Q

Why is the media layer of the vessel important to coagulation?

A

Sub endothelial layer –> Secretes collagen and fibronectin which aid in platelet plug formation

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12
Q

What layer of the blood vessel is responsible for the degree of contraction or dilation?

A

Adventitia –> Outer most layer, thickest in veins

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13
Q

What mediators act of the adventitia vessel layer?

A

Nitric oxide and prostacyclin –> Dilation
Thromboxane A2 and ADP –> Contraction

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14
Q

Where is nitric oxide and prostacyclin produced?

A

Endothelial cells

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15
Q

What is the purpose of nitric oxide and prostacyclin in regard to coagulation?

A

These mediators dilate the vessel, washing away procoagulants and prevents the formation of a clot

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16
Q

Where are platelets formed?

A

In the bone marrow from megakaryocytes –> They are round and disk like

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17
Q

Normal platelet count and average life span

A

150 - 300 K, 8 - 12 days

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18
Q

How can platelets participate in anaerobic and aerobic metabolism?

A

Contains a mitochondria –> Aerobic
Contains glycogen stores –> Anaerobic

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19
Q

What blood cell stores various contractile proteins, enzymes, and large amounts of calcium?

A

Platelets

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20
Q

Many granules stored within platelets synthesize prostaglandins which _______________

A

platelets to promote vascular and local tissue reactions

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21
Q

What blood cells can produce thrombin?

A

Platelets –> Thrombin’s role includes activating coagulation factors as well as recruiting more platelets to the site of injury

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22
Q

Do platelets contain DNA, RNA, or a nucleus?

A

NO –> So they don’t reproduce

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23
Q

Do platelets float around active?

A

NO –> Largely inactive until activated by vascular trauma

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24
Q

Do platelets work independent relying only on themselves for formation of a platelet plug?

A

NO –> They work in conjunction with plasma proteins and the coagulation cascade

25
Q

What are some procoagulant mediators?

A
26
Q

What are some fibrinolytic mediators?

A
27
Q

What occurs downstream of a blood vessel that just constricted in response to a vascular injury?

A

The area adjacent to this vessel dilates to distribute blood to the surrounding organs and tissue

28
Q

What three things occur AFTER constriction of a blood vessel due to vascular injury?

A

Formation of the platelet plug –>
1. Adhesion
2. Activation
3. Aggregation

29
Q

What happens during the adhesion stage of platelet plug formation?

A

von Willebrand factor emerges from the endothelial cells and attaches to the wall of the damaged vessel –> vWF then attaches to platelets via the GP1b receptor site on the platelet
This activates platelets causing them to become “sticky” and adhere to the site of injury

30
Q

What mediator activates platelets causing a conformational transformation?

A

Tissue factor (factor 3) –> The platelet swells and becomes irregularly shaped

31
Q

What occurs during the aggregation stage of platelet plug formation?

A

Platelets express GP2b/GP3a –> Fibrinogen connects platelets together via these receptor sites. This forms the primary “unstable” plug

32
Q

After platelet plug formation, why would the clotting cascade be initiated?

A

If the injury is large –> This secures this unstable plug into a more stable plug.
If the injury in small and minute, the primary unstable plug is enough to maintain hemostasis and the clotting cascade won’t be needed

33
Q

Do coagulation factors circulate the blood in an active or inactive state?

A

Inactive state

34
Q

What are the two clotting pathways that lead to the common pathway?

A

Intrinsic –> Damage WITHIN the vessel
Extrinsic –> Damage OUTSIDE the vessel

35
Q

Describe the extrinsic pathway

A

Factor 3 (tissue factor) activates this pathway by activating factor 7 (proconvertin) –> 7a now goes and activates the common pathway, starting with factor 10 (Stuart-Prower)

36
Q

Describe the common pathway

A

The intrinsic or extrinsic pathway can activate this…
Factor X is activated via 7a (extrinsic) or 8 (intrinsic) and turns in Xa –> Xa, Factor 5 (proaccelerin), and calcium activate factor 2 (prothrombin) and turn it into factor 2a (thrombin) –> Factor 2a (thrombin) now activates Factor 1 (fibrinogen) and turns in into 1a (fibrin)
Factor 1a and Factor 13 (fibrin stabilizing factor) secure the primary unstable clot.

37
Q

What initiates the intrinsic pathway?

A

Prekallikrein

38
Q

What clotting factors are dependent on vitamin K?

A

2, 7, 9, and 10

39
Q

What factors are synthesized in the liver?

A

All but 3 (tissue factor), 4 (calcium), and 6 which non existent

40
Q

Which factors are part of the common pathway?

A

10, 5, 2, and 1

41
Q

What is the name of factor 12?

A
42
Q

What is the name of factor 8?

A
43
Q

Describe the intrinsic pathway

A

Prekallikren activates factor 12 (hageman) –> Factor 12 (hageman) with factor 4 (calcium) cause a domino effect and activates Factor 11 (plasma thromboplasmin antecedent) which activates Factor 9 (christmas) which activates Factor 8 (anti-hemophiliac) –> This now activates the common pathway, Factor 10 (Stuart-Prower)

44
Q

Platelets can release thrombin, or it can be activated via the common pathway (factor 2a). What other factors can this thrombin now activate?

A

It activates factors 5, 8, 1, and 13. It also recruits more platelets to the site of injury

45
Q

What happens in the extrinsic pathway immediately after factor 3 (tissue factor) activates factor 7 (proconvertin)?

A

TF pathway inhibitor prevents more factor 7 from being activated so only a preset limit remains activated.

46
Q

Factor 2a (thrombin) acts as both a __________ and ___________

A

coagulant, anticoagulant

47
Q

When thrombin is acting as an anticoagulant, what three things does it cause?

A
  1. Releases tPA from endothelial cells –> prevents “run away” clots
  2. Stimulates proteins C and S –> inhibits clotting
  3. Forms a relationship with anti thrombin III –> Anti-thrombin III inhibits thrombin activity by inhibiting factors 12, 11, 10, and 9
48
Q

Heparin only works in the presence of ____________

A

Anti thrombin III

49
Q

Someone has heparin resistance, what do you suspect is the likely cause

A

Anti thrombin III deficiency

50
Q

What factors are ultimately responsible for turning a primary unstable clot into a stable clot during a large injury?

A

Factors 13 (fibrin stabilizing factor) and Factor 1a (fibrin)

51
Q

After a clot is made, it retracts. What does this do to the vessel.

A

Eliminates it serum –> Retracting causes weaving of the edges of the vessel together, healing the site of injury.

52
Q

What are the three steps of coagulation within the cell based theory model?

A
  1. Initiation
  2. Amplification
  3. Propagation
53
Q

What is the purpose of the fibrinolytic system?

A

Degrade fibrin –> Breaks down the clot

54
Q

What initially occurs during activation of the fibrinolytic system?

A

Endothelial cells secrete nitric oxide and prostacyclin to cause dilation of the vessel to wash away procoagulant mediators such as ADP and thromboxane A2.

55
Q

After dilation of the vessel, what occurs next in the fibrinolytic system?

A

THROMBIN changes roles into an anticoagulant now –> This ONLY stops further production of the clot, not breakdown
1. TFPI inhibits TF
2. Proteins C and S inhibit factors 3, 5, and 8
3. Anti Thrombin III inhibits 12, 11, 10, and 9

56
Q

What is the purpose of plasminogen in a clot and where does it come from?

A

This is inactivated plasmin, synthesized by the liver –> It incorporates itself into the clot. Once activated however, it can now break the clot from within by degrading fibrin

57
Q

How does the incorporated plasminogen in the clot become activated thus enabling it to begin breaking down fibrin holding the clot together?

A

Endogenous urokinase and tPA

58
Q

After the clot has been completely dissolved, what mediators shut off the fibrinolytic system?

A

alpha antiplasmin and tissue plasminogen activator inhibitor

59
Q

What factor is used specifically to position the other factors in correct orientation on the surface of the platelet?

A

Factor 4 (calcium)

671A - Anesthesia I (22 decks)

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