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IMS > Thrombotic disease > Flashcards

Thrombotic disease Flashcards

1
Q

what is thrombosis

A

formation of blood clot inside vessels –> blocking blood circulation

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2
Q

what does thrombosis cause

A
  • ischaemia
  • malfunction
  • pain or swelling
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3
Q

what does arterial thrombosis

A
  • MI
  • AF
  • Peripheral vascular disease (PVD)/ leg
  • stroke
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4
Q

what does venous thrombosis cause

A
  • DVT/arm,leg

- Pulmonary embolism/ lungs

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5
Q

what is Virchow’s traid for causes of thrombsis

A
  • stasis
  • hypercoagulability
  • vessel wall injury
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6
Q

what is atrial thrombosis cause

A
  • atherosclerosis
  • inflammation of vessel wall
  • infiltration of macrophages
  • fat deposits
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7
Q

what are the phases of thrombotic response

A
  • plaque fissure, rupture
  • adhesion & activation of platelets
  • activation of coagulation cascade
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8
Q

what is mural thrombi (arterial thrombosis)

A
  • does not occlude vessel
  • unstable angina
  • transient ischaemia
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9
Q

what is occlusive thrombi (arterial thrombosis)

A
  • occludes vessel
  • MI
  • cerebral infarction
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10
Q

what is thrombi driven by

A

uncontrolled platelet activation

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11
Q

what are the prothrombic stimulatory agonists

A
  • ADP
  • adrenaline
  • colagne
  • fibrinogen
  • thrombin
  • thromboxane A2
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12
Q

what are the antithrombic inhobitory agonists

A
  • adenosine
  • nitric oxide
  • prostacyclin
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13
Q

what is the primary haemostatic response

A 
- Platelets bind to collagen​
​- Adhesion and activation​
- Release of pro-aggregatory substances ADP, TxA2​
- Autocatalytic expansion of thrombus​
- Controlled by endothelial NO and PGI2
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14
Q

what is thrombotic response

A
  • Platelets bind to collagen and exposed to oxidised lipids from plaques​
  • Activation​
  • Release of proaggregatory substances ADP, TxA2​
  • Autocatalytic expansion of thrombus​
  • Reduced bioavailability of endothelial NO and production of PGI2​
  • Occlusive thrombi​
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15
Q

what do platelet derived soluble agonists do

A

drive expansion of the thrombus​

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16
Q

how are ADP, TxA2 & Thrombin derived from platelets

A
  • ADP: Released from platelet dense granules​
  • TxA2: Synthesised and release by platelet from arachidonic acid​
  • thrombin: generated on the platelet surface as the endpoint of the coagulation cascade​
17
Q

what does plaque content (oxidised lipids) do

A
  • promote 2ry agonists

- reduce inhibitors’ actions (NO, PGI2)

18
Q

how is atherothrombosis treated

A

1) Antiplatelets​
- Aspirin (inhibition of COX-1 and thromboxane production)​
- Anti aIIbb3 (receptor for fibrinogen and vWF)​
- Anti P2Y (receptor for ADP induced platelet aggregation)

2) Fibrinolytics (tPA/uPA derivatives)​

19
Q

where is DVT most common

A
  • area with low blood flow

- vulnerable around the valves

20
Q

what is the most dangerous pathology associated with DVT

A
  • pulmonary embolism
21
Q

what are symptoms of DVT

A
  • calf swelling
  • pain
  • lack of venous return
  • associated odema
22
Q

what increase the risk of DVT

A
  • stasis: endothelial dyfunction hyercoaguable state
  • immobilization​
  • surgery ​
  • cancer​
  • pregnancy​
  • oral contraceptives​
  • genetic risk factors:
    1) Deficiencies in coagulation inhibitors​
    2) Factor V Leiden mutation​
23
Q

what are the potential mechanisms for venous thrombosis

A
  • circulatory stasis
  • endothelial injury
  • hypercoaguable state
24
Q

describe circulatory stasis

A
  • loss of laminar flow around valves, gaps between endo cells and minor platelet activation​
25
Q

describe Endothelial dysfunction

A

inflammation leads to activation and exposure of TF​

26
Q

describe Hypercoagulable state

A
  • localised inflammation​
  • loss of inhibitor function – activity of thrombomodulin (TM) and protein C/S system leading to thrombin accumulation
  • lupus anticoagulants (anti-phospholipid antibodies) ​
  • impaired fibrinolysis​
27
Q

what is treatment for venous thrombosis

A

1) Immediate onset of anticoagulant effect:​
- Unfractionated Heparin (intravenous – helps antithrombin to inhibit thrombin and Xa)​
- Low Molecular Weight Heparin (LMWH; subcutaneous)​

2) Slow onset:​
- VKA, monitored by INR​

​3) Direct thrombin inhibitors (Dabigatran) promising in clinical trials​

IMS (18 decks)

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