Thrombosis Flashcards

1
Q

What is a Thrombosis?

What does it involve?

What is an Arterial Thrombosis?

What is a Venous Thrombosis?

A
  • Solid mass of blood formed within the CVS
  • The interaction of endothelial cells, platelets, and coagulation cascade.
  • Mostly due to an atheroma rupture. Is PLATELET-RICH (“white” thrombosis), and blocks the downstream arteries (smaller diameter).
  • Due to hyper-coagulant state or stasis. Is PLATELET-POOR (“red” thrombosis), and can move to lungs causing a PE.
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2
Q

What are the 4 components involved in Haemostasis?

What is there balance of in normal haemostasis? What does it prevent?

A
  • Endothelium, Platelets, Coagulation, Fibrinolysis

- Balance between Fibrinolytic and Coagulation factors - prevent thrombi formation.

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3
Q

Outline the process of Primary haemostasis, Secondary haemostasis, and Fibrinolysis

A

In Primary haemostasis:
During tissue damage, platelets adhere, activate, and then aggregate.

In Secondary haemostasis:
Plug stabilised with a fibrin mesh - forms blood clot.

In Fibrinolysis:
tPA converts Plasminogen → Plasmin, which breaks up the blood clot.

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4
Q

What is Virchow’s Triad? Give the elements involved.

A
  • Shows what the formation of a venous thrombus depends on, which are:
    • Endothelial damage
    • Stasis
    • Hyper-coagulability (Coagulation factors > Fibrinolytic factors)
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5
Q

What can cause endothelial damage?

How can endothelial damage lead to thrombus formation?

LOOK AT DIAGRAM!

A
  • Smoking, Hypertension, Surgery, Catheters, Trauma

- vWF and Collagen receptors are exposed. So, the coagulation cascade is quickly activated, leading to a blood clot.

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6
Q

What can cause blood hyper-coagulability?

How can hyper-coagulability lead to thrombus formation?

A
  • Hereditary/Acquired through cancers, Chemotherapy, Obesity, Pregnancy
  • If there’s an ↑Coagulation factors and a ↓Fibrinolytic factors in the blood, more blood clots can form and less will be broken down.
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7
Q

What can cause stasis?

A

Immobility (e.g. long flight), Polycythaemia (greater % of Hb in blood), Stroke, Heart failure, Dehydration - stasis can cause endothelial damage.

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8
Q

DVT:
Where are they commonly found? Why?

Where can a DVT form to increase the risk of a PE?

What are clinical features of a DVT? What do the features reflect/suggest?

A
  • Valves - around valves, blood tends to slow down and flow becomes turbulent, therefore increasing risk of stasis.
  • In calf and above
  • Pain & tenderness of veins, Limb swelling, Dilated superficial veins, ↑Skin temperature, Skin discolouration - reflects an obstruction to venous drainage.
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9
Q

Venous thrombosis can reach the lungs:
Describe what will happen if the thrombosis is SMALL

Describe what will happen if the thrombosis is LARGE

LOOK AT PICTURES!

A
  • Can block one of the pulmonary arteries and cause an infarct zone in the lung - CAN BE ASYMPTOMATIC!
  • Can block the whole pulmonary trunk, causing complete blockage of lung perfusion - CAN CAUSE RAPID DEATH!
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10
Q

What is a Proximal and Distal DVT and what are their risks?

LOOK AT DIAGRAM!

A

Proximal DVT:
Above knee - ↑Risk of PE and Post-thrombotic syndrome e.g. pain, swelling, ulceration.

Distal DVT:
Below knee - ↓Risk of PE and Post-thrombotic syndrome

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11
Q

What can be used to treat thrombosis? How do they work?

What’s a complication that can occur with these anti-coagulants?

A
  • • Anti-coagulants e.g. warfarin, heparin, direct oral anticoagulants - prevent blood clot formation.
    • “Clot busters” e.g. plasminogen activators, streptokinase - reverse the formation of blood clot (↑Fibrinolysis).
  • ↑Fibrinolytic factors and a ↓Coagulation factors can cause excessive bleeding - clots can’t form.

Can cause bleeding complications e.g. haemorrhages in eye, limbs, brain.

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