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BRS2 - Cardiovascular & Respiratory Medicine > Disorders of Haemostasis & Thrombosis > Flashcards

Disorders of Haemostasis & Thrombosis Flashcards

1
Q

What is haemostasis?

A

“the cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult”

Physiological response of the vessel to injury in order to limit bleeding

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2
Q

What is the purpose of haemostasis? [3]

A
  1. Prevention of blood loss from intact vessels
  2. Arrest bleeding from injured vessels
  3. Enable tissue repair
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3
Q

Outline the mechanisms of haemostasis.

START: injury to endothelial cell lining.

END: restored vessel integrity.

A
  1. Injury to endothelial cell lining
  2. Vasoconstriction:
    - Vascular smooth muscle cells contract locally
    - Limits blood flow to injured vessel
  3. Primary haemostasis - formation of an unstable platelet plug
    - Platelet adhesion (to vessel wall + each other)
    - Platelet aggregation
    - Limits blood loss and provides surface for coagulation
  4. Secondary haemostasis - stabilisation of the plug with fibrin
    - Blood coagulation
    - Stops blood loss
  5. Fibrinolysis - vessel repair + dissolution of clot
    - Cell migration/proliferation & fibrinolysis
    - Restores vessel integrity
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4
Q

What are the 3 main process that occur in haemostasis?

A
  1. Primary haemostasis
  2. Secondary haemostasis
  3. Fibrinolysis
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5
Q

What is the main purpose of primary haemostasis?

A

Primary haemostasis - formation of an unstable platelet plug

Purpose - limit blood loss and provides surface for coagulation

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6
Q

What is the main purpose of secondary haemostasis?

A

Secondary haemostasis - stabilisation of the plug with fibrin

Purpose - stops blood loss

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7
Q

What is the main purpose of fibrinolysis?

A

Fibrinolysis - vessel repair and dissolution of clot

Purpose - restores vessel integrity

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8
Q

Why do we need to understand haemostatic mechanisms?

A
  1. Diagnose + treat bleeding disorders
  2. Control bleeding in individuals who do not have an underlying bleeding disorder
  3. Identify risk factors for thrombosis
  4. Treat thrombotic disorders
  5. Monitor the drugs that are used to treat bleeding + thrombotic disorders
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9
Q

Normal haemostasis is a delicate balance.

This balance is mediated by a maintained equilibrium between which factors and proteins?

A

Fibrinolytic factors
Anticoagulant proteins

AND

Coagulant factors
Platelets

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10
Q

Normal haemostasis is a delicate balance between fibrinolytic factors/anticoagulants and coagulant factors/platelets.

What could loss of this balance due to a decrease in fibrinolytic factors/anticoagulants or an increase in coagulant factors/platelets cause?

A

Thrombosis

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11
Q

Normal haemostasis is a delicate balance between fibrinolytic factors/anticoagulants and coagulant factors/platelets.

What could loss of this balance due to an increase in fibrinolytic factors/anticoagulants or a decrease in coagulant factors/platelets cause?

A

Bleeding

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12
Q

Normal haemostasis is a delicate balance between fibrinolytic factors/anticoagulants and coagulant factors/platelets.

This balance can be tipped towards bleeding.

How?

A
  1. An increase in fibrinolytic factors or anticoagulant proteins (number/function)
  2. A decrease in coagulant factors or platelets (number/function)
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13
Q

Normal haemostasis is a delicate balance between fibrinolytic factors/anticoagulants and coagulant factors/platelets.

This balance can be tipped towards bleeding.

One of the causes of this would be a lack of a specific coagulant factor or platelets.

How could the potential causes of this be classified?

A
  1. Failure of production
    - Congenital vs Acquired
  2. Increased consumption/clearance
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14
Q

Normal haemostasis is a delicate balance between fibrinolytic factors/anticoagulants and coagulant factors/platelets.

This balance can be tipped towards bleeding.

One of the causes of this would be defective function of specific coagulant factor or platelets.

How could the potential causes of this be classified?

A
  1. Genetic
  2. Acquired: drugs, synthetic defect, inhibition

(Acquired = more common)

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15
Q

Describe the mechanism by which primary haemostasis occurs. [7]

A
  1. Damage to endothelium - exposure of collagen in the vessel wall
  2. Platelet adhesion to wall directly via glycoprotein-1a-R (GPIa-R) or indirectly via glycoprotein Ib-R (GPIb-R) to VWF

Adhesion causes platelet activation + causes them to change shape in a way that encourages platelet-platelet interaction

  1. Platelet release reaction - Adhesion causes release of contents of platelet storage granules (ADP, fibrinogen, VWF)
  2. Thromboxane A2 synthesis:
    - Platelets stimulated to produce this from arachidonic acid
  3. ADP release + thromboxane generation has +ve feedback effect —-> further platelet recruitment, activation + aggregation
  4. Flip-flopping and activation of GPIIb/IIIa receptors on platelets providing fibrinogen binding sites
  5. Fibrinogen binds to GPIIb/IIIa causing ‘outside-in’ signalling leading to further platelet activation
  6. Fibrinogen plays key role in linking platelets —-> formation of platelet plug
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16
Q

Platelet adhesion occurs during primary haemostasis in which platelets bind the injured vessel wall either directly or indirectly.

How do platelets:

a) directly adhere to the wall?
b) indirectly adhere to the wall?

A

Directly to wall via GPIa-R

Indirectly to wall by binding VWF via GPIb receptor

17
Q

Describe the mechanism by which thromboxane A2 synthesis occurs in primary haemostasis.

A

Platelets stimulated to produce the prostaglandin thromboxane A2 from arachidonic acid that is derived from the cell membrane

Arachidonic acid –COX–> cyclic endoperoxides

18
Q

Describe the mechanism by which platelet aggregation occurs in primary haemostasis in order to form the platelet plug.

A
  1. Granular release of ADP + generation of thromboxane A2 from/in platelets
  2. ADP binds P2Y12-R and Thromboxane A2 binds thromboxane A2-R
  3. This has positive feedback effects, resulting in further platelet recruitment activation and aggregation.
  4. Platelet activation also causes a conformational change in the GPIIb/IIIa receptor (known as ‘inside-out’ or ‘flip-flopping’) to provide binding sites for fibrinogen.
  5. Fibrinogen binding to GPIIb/IIIa causes ‘outside-in’ signalling which further activates the platelets.
  6. Fibrinogen has a key role in linking platelets together to form the platelet plug.
19
Q

Describe the mechanism by which thromboxane A2 synthesis occurs in primary haemostasis.

A

Platelets stimulated to produce the prostaglandin thromboxane A2 from arachidonic acid that is derived from the cell membrane

  1. Arachidonic acid –COX–> cyclic endoperoxides
  2. In platelets, thromboxane synthetase converts cyclic endoperoxides into thromboxane A2
20
Q

What are the main functions of thromboxane A2?

A
  1. Promotes platelet aggregation
  2. Vasoconstrictor

(thromboxane A2 is especially important during tissue injury + inflammation)

21
Q

How does platelet activation occur in primary haemostasis?

A
  • Platelet adhesion results in platelet activation
  • Granular release of ADP and generation of thromboxane A2 have positive feedback effects resulting in further platelet recruitment activation and aggregation
22
Q

ADP release + thromboxane generation has +ve feedback effect leading to further platelet recruitment, activation + aggregation.

What receptors do ADP and thromboxane A2 bind to in order for this to occur?

A

ADP binds P2Y12 receptor

Thromboxane A2 binds thromboxane A2 receptor

23
Q

What does platelet activation cause?

A
  • Change in platelet shape from a disc to a more rounded form with spicules to encourage platelet-platelet interaction
  • Activation promotes aggregation
  • Conformational change in the GPIIb/IIIa receptor (known as ‘inside-out’ or ‘flip-flopping’) to provide binding sites for fibrinogen
24
Q

When considering disorders of primary haemostasis, what 3 main components of primary haemostasis do we focus on?

A
  1. Platelets
  2. VWF
  3. Vessel
25
Q

What physiological responses prevent inappropriate platelet aggregation? [2]

A
  1. Active flow of blood
  2. Release of prostacyclin (PGI2) from endothelial cells
    - prostacyclin is a powerful vasodilator and suppresses platelet activation
26
Q

What physiological responses prevent inappropriate platelet aggregation? [2]

A
  1. Active flow of blood
  2. Release of prostacyclin (PGI2) from endothelial cells
    - prostacyclin is a powerful vasodilator and suppresses platelet activation
27
Q

What is prostacyclin (PGI2)?

A

A powerful vasodilator

Suppresses platelet activation

28
Q

What are the main stages of primary haemostasis?

A
  1. Platelet adhesion
  2. Platelet release reaction
  3. Thromboxane A2 synthesis
  4. Platelet aggregation
  5. —-> platelet plug formation
29
Q

What is the term for a low platelet count?

A

Thrombocytopenia

30
Q

What is thrombocytopenia?

A

Condition in which someone has a low platelet count (in their blood)

31
Q

List example causes of thrombocytopenia (at least 3)

A
  • Bone marrow failure, e.g. leukaemia, B12 deficiency, aplastic anaemia
  • Accelerated clearance, e.g. autoimmune (ITP), DIC
  • Alcohol use disorder and alcoholism
  • Cancer treatments, e.g. chemotherapy, radiotherapy

BRS2 - Cardiovascular & Respiratory Medicine (4 decks)

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