Circulatory Disturbances II Flashcards

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1
Q

What is haemostasis?

A

Ceasation of blood loss in vessel wall disruption via localised interaction between endothelium, platlets and coagulation factors

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2
Q

How does primary haemostasis occur?

A
  1. Recruiting of platlets
  2. Platlets adhere
  3. Phospholipid complex expression
  4. Granule release ADP/TXA2
  5. Recruitment
  6. Aggregation of primary heamostatic plug
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3
Q

What is the mediator of the coagulation cascade in haemostasis and where is it produced?

A

Tissue factor produced by damaged endothelium is the major activator of the extrinsic pathway of the coagulation cascade

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4
Q

What are coagulation factors? give examples

A

Plasma proteins produced by the liver (mostly):
- Structurally related/functionally interdependent e.g. factors XI, XII, HMWK
- Vitamin-K dependent e.g. factors II, VII, IX, X
- Highly labile fibrinogen group e.g. factors I, V, VIII, XIII

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5
Q

What is fibrinolysis?

A

Mechanism to breakdown the fibrin/platlet clot restricting haemostasis to the site of injury

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6
Q

What is a haemorrhage and what does it cause? How do haemorrhages occur?

A

Extravasation of erythrocytes into the extravascualr space causing:
Rhexis - physical vessel wall disruption or diapedesis - no wall disruption but less RBCs csn escape
Abnormal function of endothelium/blood vessels, platlets or coagulation factors can be inherited or aquired

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7
Q

What are the different types of endothelial abnormalities relating to haemorrhage?

A
  1. Endothelial injury
  2. Developmental collagen disorders
  3. Collagen defects in guinea pigs and primates with vitamin C deficiency
  4. Thrombocytopaenia - reduced platlet count
  5. Thrombocytopathy - abnormal platlet function
  6. Reduced concentration or function of coagulation factors
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8
Q

How does reduced platlet numbers occur?

A
  1. Reduced platlet production (megakaryocyte damage)
  2. Increased destruction of platlets by immune-mediated disease
  3. Increased use of platlets in diffuse endothelial damage or generalised platlet activation
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9
Q

How does decreased concentration of coagulation factors occur?

A
  1. Inherited deficiencies of CFs
  2. Decreased production of CFs in severe liver disease
  3. Decreased production of vitamin K dependent CFs
  4. Increased use of CFs due to increased consumption associated with DIC
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10
Q

How do we classify haemorrhages based on size? give 3 examples

A

Depending on cause, location and severity:
Petechiae - 1-2mm in skin, mucous membranes or serosal surfaces via diapedesis in minor vascualr damage
Eccymoses - up to 2-3cm in more extensive vascular damage
Suffusive - larger continous areas of haemorrhage

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11
Q

What is the significance of haemorrhages?

A

Most commonly local and stopped via haemostasis or local extravascualr tissue pressure matching the intravascualr pressure to end haemorrhage
Significance depends on Volume, Rate and Site

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12
Q

What is thrombosis?

A

Formation of an excessive or inappropriate clot on the endothelium of a blood or lymphatic vessel or within the heart

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13
Q

What is an infarction?

A

Area of peracute ischemia that undergoes coagulative necrosis as a result of occlusion of blood vessels by emboli, vasospasm, vascular compression, torsion or rupture

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14
Q

What are the 3 major determiannts of thrombosis?

A

Endothelial injury
Abnormal blood flow
Hypercoagulabilty

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15
Q

How does endothelial injury cause thrombosis?

A

Damaged endothelium is prothrombotic meaning that it causes synthesis of tissue factor activating the extrinsic clotting cascade producing vWF which leads to platlets adhering to the exposed subendothelial collagen

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16
Q

How does abnormal blood flow cause thrombosis?

A

Normal blood flow is laminar meaning the platlets flow centrally in the vessel lumen seperated from the endothelium by a slower moving layer of plasma
If laminar flow is disrupted this causes endothelial injury/dysfunction