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Y2 Pharmacology and Therapeutics > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

What are the initial stages of thrombosis

A

Small-scale thrombin production

  1. Tissue factor bearing cells activate FX and FV forming a prothombinase complex
  2. Prothrombinase complex activates FII (prothrombin) to FIIa (thrombin)
  3. Antithrombin (AT-III) inactivates VIIa and FXa
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2
Q

What are the mechanisms by which drugs can be used to inhibit the initial stages of thrombosis and give examples of each

A

Inhibit factor IIa e.g. Dabigatran
Inhibit factor Xa e.g. Rivaroxaban
Increase AT-III activity e.g. heparin
Reduce levels of other factors e.g. warfarin

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3
Q

What are the risk factors of Virchow’s triad

A

Rate of blood flow
Consistency of blood
Blood vessel wall integrity

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4
Q

How does rate of blood flow contribute to DVT and pulmonary embolism risk

A

Blood flow is slow/stagnating -> no replenishment of anticoagulant factors + balance adjusted in favour of coagulation

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5
Q

How does consistency of blood contribute to DVT and pulmonary embolism risk

A

Natural imbalance between procoagulation + anticoagulation factors

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6
Q

How does blood vessel wall integrity contribute to DVT and pulmonary embolism risk

A

Damaged endothelia -> blood exposed to procoagulation factors

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7
Q

How does DVT and pulmonary embolism present

A

Swollen leg + pitting oedema

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8
Q

How is DVT investigated

A

2-level Wells score
D-dimer
Ultrasound to confirm

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9
Q

How is DVT treated

A

Positive D-dimer test - given interim treatment with parenteral anticoagulant (dalteparin)

Ultrasound scan confirms DVT - given maintenance treatment with oral anticoagulant (rivaroxaban/warfarin)

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10
Q

How do acute coronary syndromes present

A

History of hypertension + hyperlipidaemia

Shortness of breath, sweating, dizziness + chest pain

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11
Q

What are the investigations done for acute coronary syndromes present

A

ECG (no changes)

Troponin (elevated)

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12
Q

What is the treatment for acute coronary syndrome

A

Antiplatelet therapy -> ASPIRIN + CLOPIDOGREL

Used to stop the thrombus from growing larger

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13
Q

What is a NSTEMI

A

Non-ST elevated myocardial infarction (MI)

‘White’ thrombus -> partially occluded coronary artery

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14
Q

What is the treatment for NSTEMI

A

Antiplatelets

aspirin and clopidogrel as well as heparin to reduce DVT risk

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15
Q

What is a STEMI

A

ST elevated myocardial infarction

‘White’ thrombus -> fully occluded coronary artery

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16
Q

What is the treatment for STEMI

A

antiplatelets + thrombolytics

Aspirin and clopidogrel and thrombolysis (if within 12 hours of onset)

17
Q

What are NSTEMIs and STEMIs caused by

A

Damage to endothelium
Atheroma formation
Platelet aggregation

18
Q

Describe amplification stage of thrombosis

A

Platelet activation + aggregation

  1. Factor IIa (Thrombin) activates platelets
  2. Activated platelet changes shape and becomes ‘sticky’ and attaches other platelets
19
Q

Explain how platelets become activated by thrombin during amplification

A
  1. thrombin binds to protease-activated receptor (PAR) on the platelet surface
  2. PAR activation causes a rise in intracellular calcium
  3. Calcium rises
  4. Exocytosis of ADP from dense granules
  5. ADP activates P2Y12 receptors
  6. platelet activation/ aggregation
  7. PAR activation liberates arachidonic acid (AA)
  8. Cyclo-oxygenase (COX) generates thromboxane A2 (TXA2) from AA
  9. TXA2 activation leads to expression of GPIIb/IIIa integrin receptor on platelet surface (involved in platelet aggregation)
20
Q

What are the ways in which the amplification stage of thrombosis can be inhibited by drugs

A

Prevent platelet activation/aggregation e.g. clopidogrel
Inhibit production of TXA2 e.g. aspirin
Prevent platelet aggregation e.g. abciximab

21
Q

Describe what occurs in the propagation stage of thrombolysis

A

Generation of fibrin strands

  1. Activated platelets cause large-scale thrombin production
  2. Factor IIa (thrombin) binds to fibrinogen and converts to fibrin strands
22
Q

What is the mechanism of action for thrombolytics and give an example

A

Convert plasminogen to plasmin (protease degrades fibrin) e.g. Alteplase (IV) -

23
Q

What are the risk factors for a DVT

A

Surgery
Prolonged immobility
Obesity

24
Q

How are PEs treated

A

Same way as DVTs

25
Q

How are PEs treated when the patient is at a severe risk of a cardiac arrest

A

thromboylysis with a 50mg bolus of a tPA such as alteplase

26
Q

Describe warfarin (class, pharmacokinetics, pharmacodynamics and side effects)

A

Vitamin K epoxide reductase inhibitor
Given orally
Reduces vitamin K epoxide (Needed for the conversion of glutamate to gamma-carboxyglutamate. This conversion normally activates factors 2, 7, 9 and 10)
No side effects

27
Q

Describe Dalteparin (class, pharmacokinetics, pharmacodynamics and side effects)

A

Heparin
IV or subcutaneous
Potentiates activity of antithrombin III
No side effects

28
Q

Describe Dabigatran (class, pharmacokinetics, pharmacodynamics and side effects)

A

Direct oral anticoagulant (DOAC)
Oral admin
Thrombin (IIa) inhibitor
Can cause excessive bleeding

29
Q

Describe Rivaroxaban (class, pharmacokinetics, pharmacodynamics and side effects)

A

DOAC
Oral admin
Factor Xa inhibitor
No side effects

30
Q

What are ischaemic strokes caused by

A

Thrombosis in one of the arteries supplying the brain or embolism from somewhere in the body (e.g. in AF)

31
Q

What is the treatment for ischaemic strokes

A

Thrombolysis with alteplase may be considered if within 4.5 hours of onset

> 4.5 hours of onset ->aspirin and clopidogrel are given as well as heparin if the patient is at a high risk of more emboli

32
Q

Describe aspirin (class, pharmacokinetics, pharmacodynamics and side effects)

A

Antiplatelet/NSAID/COX-1 inhibitor
Oral admin
Covalent binding to COX-1, preventing TXA2 production
Side effects: GI irritation and ulceration, bronchospasm, prolonged bleeding, nephrotoxicity

33
Q

Describe Clopidogrel (class, pharmacokinetics, pharmacodynamics and side effects)

A

Antiplatelet
Oral admin
P2Y12 (ADP receptor) antagonist -> stops platelets activation
No side effects

34
Q

Describe Abciximab (class, pharmacokinetics, pharmacodynamics and side effects)

A

Antiplatelet
IV or SC
Monoclonal antibody against GIpIIIa/IIb
No side effects

35
Q

Describe Alteplase (class, pharmacokinetics, pharmacodynamics and side effects)

A

Recombinant tissue type plasminogen activator (rt-PA)
IV
Converts plasminogen into plasmin (Protease that degrades fibrin)
Excessive bleeding at higher doses

36
Q

How do heparins work and how are they administered and why are they used as interim treatment

A

Activates AT-III (Reduces FIIa and FXa)
IV, SC (parenteral)
Rapid action to prevent immediate issues

Y2 Pharmacology and Therapeutics (34 decks)

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