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Applied Sciences > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

How do platelets adhere to a damaged vessel?

A

Via Von Willebrand factor. VWF binds to collagen on injured endothelial walls which causes it to change conformational shape. The VWF then forms a bridge between the platelet and the endothelium

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2
Q

What causes platelet activation?

A

Binding of platelets to collagen causes platelet activation. When bound, platelets release ADP and serotonin which cause changes in the metabolism, shape and surface proteins of platelets leading to platelets activation.

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3
Q

What causes platelet aggregation?

A

The changes that occur in platelet activation can cause new platelets to adhere to old platelets. This positive feedback process is called platelet aggregation where platelets stick to eachother

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4
Q

What chemical is released from platelet cell membranes into the ECF which also increases platelet activation and aggregation?

A

Thromboxane A2

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5
Q

What chemical forms bridges between activated platelets?

A

Fibrinogen- platelet binding sites become exposed during platelet A&A

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6
Q

What causes clot retraction?

A

Actin and myosin contained in the platelets contracting to strengthen and tighten the platelet plug

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7
Q

What causes vasoconstriction in clot formation?

A

Thromboxane A2- reduces blood flow to area

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8
Q

What prevents the platelet plug from spreading?

A

Healthy endothelial cells secrete prostacyclin/prostaglandin I2 from their cell membranes which inhibits platelet A&A. Additionally, nitric oxide is secreted which causes vasodilation in areas of healthy endothelium.

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9
Q

How are prostacyclin and thromboxane A2 similar?

A

Both formed from arachidonic acid

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10
Q

What two ways does nitric oxide prevent the spreading of a platelet plug?

A

1) direct inhibitor of platelets A&A

2) Causes localised vasodilation

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11
Q

What is the function of a clot?

A

Strengthen and support existing platelet plug and to coagulate any blood that remains in the wound channel

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12
Q

What are inactive clotting factors?

A

Plasma proteins

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13
Q

In simple terms, explain how the clotting cascade works

A

Inactive plasma protein is activated by a proteolytic enzyme converting it into its active form. The active plasma protein catalysis the activation of a subsequent plasma protein by exposing the inactive plasma protein’s binding site.

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14
Q

How does thrombin

1) stabilise a clot
2) increase clotting

A

Thrombin increases the clotting process via positive feedback. ts formation results in positive feedback as thrombin activates platelets and clotting factors resulting in more thrombin being generated

Thrombin stabilises clots by catalysing the fibrinogen/fibrin and the factor 13->factor 13a reaction. Factor 13a is crucial because it catalyses the formation of covalent cross links in a fibrin mesh.

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15
Q

What ion is important in the clotting cascade?

A

Ca2+

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16
Q

Where are plasma proteins activated?

A

on the surface of platelets

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17
Q

What is platelet factor?

A

Phospholipid that’s exposed on the cell membranes of aggregating platelets. Acts as a cofactor activating a number of plasma proteins

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18
Q

What activates the intrinsic pathway of the clotting cascade?

A

‘Contact activation’ - Factor 12 becomes converted into factor 12a when it contains collagen (exposed following endothelial damage)

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19
Q

Describe the intrinsic pathway

A 
12->12a
12a catalyses- 11-11a
11a catalyses- 9-9a
9a catalyses- 10-10a
10a catalyses-PROTHROMBIN TO THROMBIN
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20
Q

Which reactions are catalysed by cofactors 8 and 5?

A

Co-factor 8 , with clotting factor 9a catalyses the reaction from 10-10a
Co-factor 5, with clotting factor 10a catalyses the reaction prothrombin->thrombin

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21
Q

In the majority of affected individuals, what clotting factor is deficient in haemophilia?

A

8

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22
Q

What triggers the extrinsic pathway?

A

Vessel damage exposing tissue factor which binds to factor 7.

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23
Q

What is tissue factor

A

Factor 3, found in certain cell membranes. Not a plasma protein

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24
Q

Describe the extrinsic pathway

A

Exposed tissue factor binds to factor 7 converting it into factor 7a. Factors 7a then catalyses factor 10 to factor 10a which catalyses the formation of thrombin.

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25
Q

What plasma protein in the intrinsic pathway does the extrinsic pathway also activate?

A

9->9a

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26
Q

Which clotting factors do thrombin activates ? (part of the positive feedback process)

A

5
8
11

8+5 both cofactors

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27
Q

Does the intrinsic or extrinsic pathway normally initiate clotting?

A

Extrinsic
The amount of thrombin primarily produced by the extrinsic pathway is insufficient to stop bleeding however the volume of thrombin stimulates the intrinsic pathway by activating platelets and activating clotting factors.

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28
Q

Why is the liver important in blood clotting?

A

Synthesises bile salts. Bile salts help the GI tract absorb vitamin K into the blood. Vitamin K is needed to produce prothrombin needed for thrombin generation.

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29
Q

Briefly state the three factors that oppose clot formation

A

1) Tissue factor pathway inhibitor
2) Thrombin, thrombomodulin and protein C
3) Antithrombin 3

30
Q

How does tissue factor pathway inhibitor oppose clot formation?

A

Stops the complex formed by tissue factor and factor 7a from catalysing the reaction 10-10a

31
Q

Why does the extrinsic pathway only capable of generating small amounts of thrombin?

A

Tissue factor pathway inhibitor - opposes clot formation

32
Q

How does thrombin indirectly oppose clot formation?

A

Binds to thrombomodulin
Thrombin-thrombomodulin complex then binds to protein C
Activated protein C inactivates Co-factors 5a and 8a which limits the intrinsic pathway.

33
Q

How does antithrombin 3 oppose clot formation? What enhances its activity?

A

Inactivates clotting factor that flow away from the site of damaged endothelium. Enhanced by heparin.

34
Q

Describe the fibrinolytic system

A

Plasminogen is converted into plasmin by various plasminogen activators. Plasmin dissolves fibrin resulting in dissolution of clots

35
Q

Give an example of a plasminogen activator

A

t-PA , tissue plasminogen activator

36
Q

What secretes t-PA?

A

Endothelial cells

37
Q

Why is fibrin important in the fibrinolytic system?

A

t-PA binds to fibrin which increase t-PAs catalytic activity.

38
Q

What is the lethal triad?

A

Dilutional acidosis, hypothermia and metabolic acidosis

39
Q

What is Acute Traumatic Coagulopathy (ATC)?

A

ATC describes an endogenous coagulation abnormality that is triggered by direct trauma to the body or by traumatic shock .
ATC is often referred to as the first stage of trama induced coagulopathy.

40
Q

What is the pathophysiology of ATC?

A

Trauma-> haemostasis and wound healing-> consumption coagulopathy->hypocoagulable state-> INCREASED FIBRINOLYSIS .
The most important feature of ATC is hyperfibrinolysis

41
Q

What is traumatic shock?

A

Generalised tissue hypoperfusion induced by trauma

42
Q

What is the suggested mechanism of ATC hyperfibrinolysis? What is this mechanism called?

A

Elevated protein C and elevated thrombomodulin results in thrombin indirectly having a fibrinolytic function. This hypothetical mechanism is called Acute Coagulopathy of Trauma-Shock (ACOTS)

43
Q

What is the definition of Disseminated Intravascular Coagulation (DIC)?

A

Intravascular activation of coagulation with loss of localisation resulting in damage to the microvascular endothelium resulting in multiple organ dysfunction

44
Q

Which pathway does DIC act on?

A

Extrinsic- tissue factor dependent pathway

45
Q

What is resuscitation associated coagulopathy?

A

Second stage of Trauma-induced coagulopathy that is the result of resuscitative interventions such as giving packed red blood cells that result in endogenous secondary pathologies making patients at risk of the lethal triad.

46
Q

Why is tranexamic acid given pre-hospitally to trauma patients?

A

stabilises clot formations in the hyperfibrinolytic patients

47
Q

If a patient is on oral anticoagulation what drug should be given in hospital? Why?

A

Prothrombin complex concentrate.Warfarin is a vitamin K antagonist which is need to form prothrombin.

48
Q

What systolic blood pressure is desired in permissive hypotension? When is permissive hypotension contraindicated in trauma?

A

80-90mmHg

Traumatic brain injury

49
Q

What is damage control resuscitation?

A

Stems from increased knowledge about ATC patients:
CABC
Permissive hypotension
Restrict fluid resuscitation but give blood products instead. A higher ratio of plasma:RBCs has been associated with improved survival ( 1:1:1, plasma, platelets and RBC PROPPR study)
Give TXA
DCS

50
Q

Who receives damage control surgery?

A

Non-definitive surgery performed on patients who are at high risk of the lethal triad and are actively bleeding (ATC patients).

51
Q

After damage control surgery, where does the patient go?

A

ICU to restore physiology

52
Q

What is the aim of damage control surgery?

A

1) Stop bleeding- maintain hemostatic competence
2) Prevent contamination and hence sepsis

-Maintains homostasis, protects cells and organs and maintains endothelium.

More likely to survive definitive treatment

53
Q

What is a code red trauma? When is a code red declared?

A

Systolic BP<90
Active haemorrhage
Poor response to initial fluid resuscitation.

Means that red blood cells are ready for transfusion and in resus fridge

54
Q

What two factors associated with the MOI determine a trauma patient’s observations?

A

1) Injury load- causes sympathetic readings

2) Extent of bleeding

55
Q

Describe what observations you would expect to see in a patient who is profusely bleeding

A

Heart rate- initially tachycardic, then suddenly bradycardic
Tachypnoeic
Blood pressure- initially hypertensive then hypotensive
Reduced GCS

Will interact with injury load

56
Q

What is the vascular response to trauma?

A

Capillaries become more permeable resulting in fluid shifting from the extravascular space into the intravascular space increasing central venous volume and cardiac output.

57
Q

How is haemorrhagic shock classified?

A 
Classes 1-4 (4 being the worst)
Classification system based on observations and % blood lost. 
Class 1- up to 15 % (500-750 mL)
Class 2- 15-30% (750-1500 mL)
Class 3- 30-40% (1500-2000 mL)
Class 4-40%+ (2000mL +)
58
Q

What happens to a persons pulse pressure in severe haemorrhagic shock?

A

Decreases

59
Q

Following haemorrhagic shock, what type of injury is most likely to cause a biphasic heart response (tachycardia followed by bradycardia) ?

A

Penetrating trauma without extensive tissue damage. Bleeding (bradycardia) overrides tissue damage (tachycardia)

60
Q

Name the three reflexes involved in haemorrhage

A

1) Arterial baroreceptor reflex
2) Cardiac vagal C fibres
3) Arterial chemoreceptor

61
Q

What type of receptor are baroreceptors? Where are they located?

A

Stretch receptors- located in carotid sinus and aortic arch

62
Q

What effect does the arterial baroreceptor provide?

A

Systemic vasoconstriction increasing total peripheral resistanceand fluid to shift from the ICF to the ECF

63
Q

What reflex occurs when approximately more than 15% of blood has been lost?

A

Cardiac vagal C fibre reflex

64
Q

Where are the cardiac C fibres located? What do they detect?

A

Left ventricular myocardium

Changes in circulating chemicals and mechanical changes of an underfilled heart

65
Q

Name an advantage and a disadvantage of the cardiac vagal c fibres

A

Advantage- protect the heart from over activity

Disadvantage- vital organ hypopefusion

66
Q

What prevents the cardiac vagal c fibre reflex?

A

Replacement of blood volume

67
Q

Where are the arterial chemoreceptors located? What do they respond to? What do they cause?

A

Aortic and carotid bodies
Respond to changes in oxygen and carbon dioxide
Cause tachypnoea

68
Q

How is the heart rate affected if a trauma patient has consumed alcohol?

A

Moderately increased blood alcohol levels further reduces baroreceptors sensitivity to blood loss therefore a tachycardia is likely to predominate in contrast to a sober patient where the initial increased in heart rate might suppress the baroreceptor response and lead to a bradycardia

69
Q

What is a shock index? What does a higher shock index indicate?

A

Heart rate divided by systolic blood pressure. There is a direct relationship between shock index and magnitude of blood lost.
A higher shock index equates to more blood lost. Used because may be more sensitive than using HR or BP.

70
Q

What is the likely clinical picture for a patient:

a) bleeding from penetrating trauma
b) blunt trauma with severe injury load

A

a) tachycardia followed by bradycardia and hypotension

b) Tachycardia and systemic peripheral vasoconstriction

Applied Sciences (14 decks)

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