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CVS II > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

What’s thrombosis?

A

Solid mass of blood formed within the CVS involving interaction of endothelial cells, platelets, coagulation cascade which impedes blood flow

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2
Q

Features of arterial thrombosis?

A

Result from atheroma rupture (MI, stroke)
Platelet-rich “white” thrombosis
Block downstream arteries

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3
Q

Features of venous thrombosis?

A

Result from stasis or hypercoagulant state
Platelet-poor “red” thrombus
May move to lungs

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4
Q

What makes a blood clot?

A

Endothelium
Platelets
Coagulation
Fibrinolysis

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5
Q

What’s normal haemostasis?

A

state of equilibrium

fibrinolytic factors, anticoagulant proteins vs coagulation factors, platelets

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6
Q

Describe process of haemostasis

A
  • response to injury –> vessel constriction
  • formation of unstable platelet plug : platelet adhesion + aggregation
  • fibrin stabilises plug : blood coagulation
  • fibrinolysis : dissolution of clot + vessel repair
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7
Q

What does development of a thrombus depend on?

A

Changes in normal blood flow
Alterations in blood constituents
Damage to endothelial layer

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8
Q

Risk factors of endothelial dysfunction?

A

smoking + hypertension

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9
Q

Risk factors of endothelial damage?

A

surgery, catheter (PICC lines), trauma

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10
Q

eg of hereditary factors of hypercoagulability?

A

factor V Leiden, prothrombin G20210A, protein C + S deficiency

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11
Q

eg of acquired factors of hypercoagulability?

A

cancer, chemo, oral contraceptive/hormone replacement therapy, pregnancy, obesity, HIT

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12
Q

Risk factors of stasis?

A

immobility, stroke, cardiac failure, pelvic obstruction, dehydration, hyperviscosity, polycythemia –> endothelial injury

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13
Q

What’s Virchow’s Triad?

A

endothelial damage
hypercoagulability
stasis

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14
Q

Mechanism when endothelial damage?

A

1º
-collagen + vWF binds, activates platelets
-platelets enlarge + release granule contents
-exposing phospholipid surface + express receptors
-TF + collagen initiate coagulation cascade
2º
-activated platelet + fibrin form mesh

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15
Q

Describe the fibrinolytic system

A
  • endothelial cells release tPA
  • tPA activates plasminogen
  • plasminogen -> plasmin
  • plasmin breaks up clot
  • forming fibrin fragments + D-dimers
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16
Q

What’s PL?

A

charged phospholipids on platelet surface for coagulation

17
Q

Describe the cell based model of coagulation

A
  • damaged tissue releases TF
  • TF activates 7a
  • 7a initiates thrombin required for amplification
  • 8a + 9a on platelet surface activates 10a
  • 10a has cofactor 5a
  • 10a + 5a induces prothrombin
  • prothrombin -> thrombin
  • thrombin induces fibrinogen -> fibrin
18
Q

What’s initiation of cell based model of coagulation?

A

TF released with 7a activating thrombin

19
Q

What’s amplification of cell based model of coagulation?

A

generating more thrombin

9a + 8a on platelet activates 10a

20
Q

What’s propagation of cell based model of coagulation?

A

10a + 5a propagate more induction of thrombin

21
Q

What’s the common pathway of coagulation?

A
  • 10a with cofactors: 5a, PL, Ca2+ on platelet surface
  • 10a activates prothrombin -> thrombin
  • thrombin activates fibrinogen -> fibrin
22
Q

What’s the extrinsic pathway of coagulation?

A
  • tissue damage activates TF

- TF, 7a, Ca2+ activates 10 -> 10a

23
Q

What’s the intrinsic pathway of coagulation?

A
  • 12 -> 12a
  • 12a activates 11 -> 11a
  • 11a activates 9 -> 9a
  • 9a with cofactors: 8a, PL, Ca2+
  • 9a activates 10 -> 10a
  • 10a activates prothrombin -> thrombin
24
Q

How’s 10 activated?

A

EXTRINSIC : TF, 7a, Ca2+ activates 10 -> 10a

INSTRINSIC : 9a with cofactors: 8a, PL, Ca2+ activates 10 -> 10a

25
Q

What’s activated protein C (APC)?

A

formed from protein C + S

inhibits 8a + 5a -less amplification

26
Q

What’s antithrombin III?

A

inhibit 10 + thrombin

27
Q

What are the natural coagulation inhibitors?

A

activated protein C (APC), antithrombin III

28
Q

What’s antithrombin III deficiency?

A

factor 5 Leiden - mutation in 5, which is resistant to APC so induces clotting

29
Q

Why’s there increased risk of stasis at valves?

A

blood eddy around valves

30
Q

Where is the riskier DVT?

A

above knee increases risk of PE

31
Q

What’s the annual incidence DVT?

A

1:1000

32
Q

What’s inherited thrombophilia?

A

8:100

33
Q

Clinical features of DVT?

A

pain, tenderness of veins, limb swelling, superficial venous distension, increased skin temp, discoloration due to obstruction to the venous drainage

34
Q

What are anticoagulants + eg?

A

prevent

warfarin, heparin, direct oral anticoagulants

35
Q

What are ‘clot busters’ + eg?

A

reverse

plasminogen activators, streptokinase

36
Q

What are the bleeding complications from anticoagulants?

A

👁, bruising, intracerebral bleeding

CVS II (19 decks)

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