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Y2 - PHARM > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

List some procoagulants

A
  • Prothrombin
  • Factors V, VII-XIII
  • Fibrinogen
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2
Q

List some anticoagulants

A
  • Plasminogen
  • TFPI (tissue factor pathway inhibitor)
  • Proteins C and S
  • Antithrombin
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3
Q

Where do venous thrombi tend to form?

A
  • Within the lumen of the vein
  • Attached to the tunica intima
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4
Q

What are venous thrombi composed of, and why are they called red thrombi?

A
  • Composed of high amount of erythrocytes → hence the name ‘red thrombi’
  • High fibrin content also
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5
Q

What are the components which are high in arterial thromboses, and why are arterial thromboses called ‘white thrombi’?

A
  • High in lipids → hence the name ‘white thrombi’
  • High in platelets
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6
Q

What happens in thrombus formation with atherosclerosis?

A
  • Thrombus forms in between tunica intima and tunica media
  • The thrombus is formed within the atherosclerotic plaque
  • When the atherosclerotic plaque ruptures, the thrombus is released into the lumen, causing ischaemia and potentially embolising and causing stroke, MI
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7
Q

Describe Virchow’s triad and how it describes the likelihood of thrombus formation

A

1. Rate of blood flow

  • If blood flow is slow or stagnates → no replenishment of anticoagulant factors so balance tips in favour of coagulation and thus thrombus formation

2. Consistency of blood

  • Natural imbalance between procoagulants such as clotting factors and anticoagulants

3. Damage to endothelial cells

  • Damaged endothelia causes exposure to procoagulants, thus promoting thrombus formation
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8
Q

Outline the cell-based theory of coagulation and for each step also mention what can act against these effects or steps

A

INITIATION PHASE

  • Small-scale production of thrombin on tissue factor bearing cells
  • Anticoagulants act against this

AMPLIFICATION PHASE

  • Large scale production of thrombin on surface of platelets
  • Antiplatelets act against this

PROPAGATION PHASE

  • Thrombin mediated generation of fibrin strands by conversion of fibrinogen into fibrin
  • Thrombolytics against this
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9
Q

Mention again the initiation phase of the cell-based theory of coagulation is and then outline the 3 parts of it that occur

A
  • Thrombin formation on the surface of tissue factor bearing cells
  1. Prothrombinase complex formation - tissue factor bearing cells activate factors X and V to form the prothrombinase complex
  2. Prothrombinase action - prothrombinase converts prothrombin (FII) into thrombin (FIIa)
  3. Antithrombin (AT-III) action - inactivates FIIa and FXa, thereby both inhibiting thrombin (FIIa) directly and inhibiting the formation of thrombin by inhibiting the prothrombinase complex by inactivating (FXa)
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10
Q

Give 5 anticoagulant drugs that target the initiation phase of the cell-based coagulation theory, start by outlining how they work and then mention their names and expand if necessary

A
  • Inhibit FIIa (thrombin) directly: DABIGATRAN
  • Inhibit FXa and thus prothrombinase and therefore impair thrombin formation: RIVAROXABAN
  • Increase activity of anti-thrombin (AT-III): HEPARIN, LOW MOLECULAR WEIGHT HEPARIN E.G. DALTEPARIN (impairs FXa only via antithrombin, not FIIa)
  • Reduce levels of other factors: WARFARIN - vitamin-K antagonist (vitamin-K needed for clotting factor formation)
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11
Q

Give 3 uses when anti-coagulant use is indicated

A
  1. DVT and PE (pulmonary embolism) - VENOUS THROMBOSIS mainly
  2. Thrombus formation in surgery
  3. Atrial fibrillation - prophylaxis to decrease stroke risk
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12
Q

Mention again briefly what happens in the amplification phase of the cell-based theory of coagulation and then go on to outline the physiological mechanisms behind this phase

A
  • Large scale production of thrombin on the surface of activated platelets, but also more importantly for therapeutics, PLATELET AGGREGATION occurs
  • Thrombin (FIIa) activates platelets by binding PAR receptors and then having the following 3 effects directly / indirectly:
  1. PAR activation → rise in intracellular [Ca2+] → exocytosis of ADP from dense granules → autocrine action, it binds P2Y12 receptors on platelets which stimulate platelet aggregation
  2. PAR activation liberates arichidonic acid (AA) and activates cyclo-oxygenase (COX) which converts arichidonic acid into thromboxane A2 (TXA2)
  3. TXA2 causes expression of GpIIb / GpIIIa integrin receptors on the surface of the platelets. This promotes platelet aggregation
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13
Q

Outline how 3 anti-platelet drugs that target platelet aggregation work and mention their names

A
  1. Clopidogrel - ADP (P2Y12) receptor antagonist
  2. Aspirin - irreversible COX-1 inhibitor - prevents conversion of ararchidonic acid into TXA2 thromboxane
  3. Abciximab - Inhibit GpIIb / GpIIIa
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14
Q

When is antiplatelet use generally indicated, and give 2 particular examples?

A
  • Indicated in arterial thrombosis e.g.
  • MI
  • Prophylaxis against stroke following atrial fibrillation
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15
Q

Mention again briefly what happens in the propagation phase of the cell-based coagulation theory and then mention how thrombolytics that target this work, giving a named example

A
  • Thrombin mediated generation of fibrin strands by conversion of fibrinogen into fibrin
  • Thrombolytics accelerate degradation of the fibrin mesh
  • E.g. Alteplase converts plasminogen into plasmin. It is a rt-Pa (recombinant type plasminogen activator)
  • Plasmin degrades the fibrin mesh
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16
Q

When is thrombolytic use indicated?

A
  • Both arterial and venous thrombosis
  • E.g. stroke and ST-elevated MI
17
Q

What happens in DVT (deep vein thrombosis)?

A
  • Venous thrombus forms in the deep popliteal vein
  • ‘Red thrombus’
  • Occurs due to decreased rate of blood flow and damage to the endothelium
18
Q

What happens in PE (pulmonary embolism)?

A
  • Embolisation of a venous thrombus which is a pulmonary embolus
19
Q

Outline the common pathophysiologies of NSTEMI and STEMI (myocardial infarctions) and then what is different in these pathophysiologies, and then the aim of treating each of these / how to treat

A

NSTEMI = non-ST elevated myocardial infarction

STEMI = ST-elevated myocardial infarction

  • In both, they are caused by endothelial damage, platelet aggregation and atheroma formation
  • In NSTEMI, there is only partial occlusion of the coronary artery
  • In STEMI, there is complete occlusion of the coronary artery

TREATMENT

  • In both we want to reduce lipid aggregation
  • In NSTEMI, we want to reduce platelet aggregation mainly so we use anti-platelets such as clopidogrel and aspirin
  • In STEMI, we want to both reduce platelet aggregation AND MORE importantly, we want to destroy the clot so we use thrombolytics

Y2 - PHARM (27 decks)

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