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Cardiovascular MBCHB2 > Lecture 21: Thrombosis and embolism > Flashcards

Lecture 21: Thrombosis and embolism Flashcards

1
Q

What is heamostasis?

A

The physiological response of a blood vessel to injury

  • It serves to prevent blood loss by plugging leaks in injured vessels.
  • In healthy vessels heamostasis is actively switched off to maintain the blood in a fluid state.
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2
Q

What do healthy vessels do?

A

Endothelial cells inhibit haemostasis

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3
Q

How do endothelial cells inhibit haemostasis?

A
  • Physically insulating tissues from blood
  • Producing enzymatic and chemical inhibitors of platelet activation i.e NO and Prostacyclins
  • Producing antithrombin on their surface which binds and inactivates the coagulation enzyme thrombin
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4
Q

When vessels are injured, heamostasis is accomplished by co-operation between;

A
  • Endothelial cells
  • Platelets
  • The ‘clotting cascade’ = coagulation cascade
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5
Q

How do endothelial cells promote haemostasis?

A

Injured endothelial cells;

Produce:

  • Endothelin -> vasoconstriction
  • von Willebrand factor (super glue) -> promoting platelet adhesion to the ECM proteins exposed by vessel injury.
  • Tissue factor = thromboplastin -> activates the coagulation cascade.
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6
Q

Write some notes on platelets;

A
  • Derived from megakaryocytes
  • 7 day life span in circulation
  • Chocolate chip like structures are alpha and dense granules that contain chemical mediators of haemostasis (spit these granules out and drive things)
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7
Q

How are platelets activated and what do they secrete?

A
  • They become activated by ECM proteins (esp. collagen) that are exposed when the endothelial monolayer is damaged.
  • Secrete chemical signals including Thromoxane A2, Vasoactive amines, and ADP
    = Promote vasoconstriction and platelet aggregation
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8
Q

How is the importance of platelets demonstrated?

A

The importance of platelets is demonstrated by the effects on haemostasis of reduced platelet number or function

  • Purpura (bleeding from skin capillaries)
  • Major spontaneous haemorrhage
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9
Q

Describe the coagulation system:

A
  • The coagulation system is a cascade of proteolytic reactions
  • Inert circulating zymogens (precursors) are sequentially activated
  • The cascade is initiated by several stimuli, esp tissue factor
  • The penultimate step in the cascade is the activation of thrombin
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10
Q

Describe the coagulation cascade from thrombin:

A
  • Thrombin catalyses fibronogen -> fibrin monomers
  • Fibrin monomers then polymerise into fibrin strands
  • Thrombin also activates platelets, and catalyses several earlier steps in the coagulation cascade
  • Fibrin strands form a meshwork with fused platelets to form a stable haemostatic plug
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11
Q

What is thrombosis;

A
  • Thrombosis occurs when the physiological mechanisms of haemostasis are activated inappropriately
  • The formal definition of a thrombus is ‘a mass formed from blood constituents within the circulation during life’

Can break off as embolus and cause obstruction

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12
Q

What are thrombi composed of?

A

Thrombi are composed of:

  • Fibrin and platelets
  • Entrapped red and white blood cells
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13
Q

Is a thrombus a blood clot?

A

Thrombus does not equal blood clot

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14
Q

What is a blood clot?

A

Blood clot is formed in static blood:

  • Involves primarily the coagulation system
  • W/o interaction of platelets with the vessel wall
  • i.e in vitro when blood is placed in a tube test tube or p.m
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15
Q

Describe a clot:

A
  • Soft, jelly-like, and unstructured

- Clot is composed of a random mixture of blood cells suspended in serum proteins.

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16
Q

Describe Virchows triad:

A 
Endothelial injury
\+
Hypercoagulation (The blood constituents)
\+
Abnormal blood flow (The blood flow)

= Thrombosis

17
Q

What can damage the endothelium? (5 things)

A
  • Atherosclerosis
  • Hypoxia i.e heart endothelium
  • Infection/inflammation
  • Physical damage i.e crushing of veins, haemodynamic stress of hypertension
  • Chemical damage
18
Q

What can happen with artificial surfaces?

A

Artificial surfaces can;

  • Activate the intrinsic coagulation cascade
  • Bind pro-inflammatory compliment cascade proteins
  • Bind other proteins that may activate platelets.

I.e can form thrombi, so, anti-coagulants, thus challenge is to create non-thrombogenic

19
Q

What can change blood flow in arteries or the heart

A

In arteries or cardiac chambers, turbulence is a key cause

  • Narrowing (atheroscelrosis)
  • Aneurysms
  • Infarcted MI
  • Abnormal cardiac rhythm or valvular disease
20
Q

What can change blood flow in veins?

A

In veins, stasis is an important cause

  • Failure of the right side of the heart
  • Immobilisation
  • Compressed veins
  • Varicose veins
  • Blood viscosity (i.e sickle cell anemia, dehydration)
21
Q

What do changes in blood flow cause?

A
  • Platelets to come into contact with endothelium
  • Impaired removal of pro-coagulant factors
  • impaired delivery of anti-coagulant factors
  • Directly cause injury or activation of endothelium
  • Atherosclerotic plaques which are pro-coagulant
22
Q

What do changes in blood constituents lead to?

A

Increased tendency to coagulate

23
Q

What can cause changes in blood constituents?

A

Genetic causes

  • Deficiency of anti-thrombin 3
  • Deficiency protein C

Acquired causes

24
Q

What are the acquired causes that lead to changes in blood constituents?

A

Tissue damage i.e trauma, MI

  • Acute phase response from liver
  • Pro-inflam / pro-coagulant / compliment factors
  • Cytokines cause platelet release from bone marrow
Post-operative
Malignancy
Smoking (increased platelet activ)
Elevated blood lipids
Oral contraceptives (increase clotting)
25
Q

What are the physiological mechanisms that limit coagulation?

A
  • Restricted to local site of vascular injury
  • 3 types of natural anti-coagulants
    + Antithrombins
    + Proteins C&S - Vit K dependant
    + Tissue factor pathway inhibitor
  • Fibrin cascade limits the size of final clot through action of plasmin which breaks down fibrin.
26
Q

What is an emboli?

A
  • An embolus is an intravascular mass (Solid, liquid or gas) carried by blood flow from its point or origin to a distant site
27
Q

What are the effects of emboli?

A
  • Stenosis -> Occlusion
  • Pulmonary embolus can lead to;
  • > Pulmonary infarction
  • > Reduced CO
  • > Right heart failure
  • > Death if severe
  • Mural thrombosis from LV or aorta -> enters systemic arterial system and can pass to brain, kidney, spleen etc
28
Q

How does the loss of endothelial cells lead to thrombosis?

A

Loss of endothelial barrier exposes underlying cells which activate;

  • Platelets
  • The coagulation cascade

Cardiovascular MBCHB2 (31 decks)

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