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year 5 path haematology > Y2: Haemostasis + Thrombosis > Flashcards

Y2: Haemostasis + Thrombosis Flashcards

1
Q

What is a D-Dimer test?

When is it perfomed?

What are the consequences?

A

Test the break down products of Fibrin –> performed when susprected of thrombosis

•Positive D-dimer test - diagnosis of deep-vein thrombosis (DVT) –> interim treatment with parenteral anticoagulant

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2
Q

What is the Wellls score?

A

A score to determine someones likelyhood of having a thrombosis

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3
Q

What happens in the initiation stage of blood coagulation?

A

Oervall: there is a small scale thrombin production

  • Tissue factor (III + VII) activates FX and FV. Together they form the prothrombinase complex
  • ​Prothrombinase Complex (Xa+Va) activate prothrombin to Thrombin (II –> IIa)

Regulation occurs via Antithrombin

  • inhibits IIa and Xa
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4
Q

What happens in the amplification state of blood coagulation?

A

Platelet activation & aggregation

FIIa activates the Platelets

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5
Q

What happens to the platelets during platelet activation? (overwiew)

A

2.Activated platelet

  • Changes shape
  • Becomes ‘sticky’ and attaches other platelets
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6
Q

Explain the process of platelet activation on a cellular level

A

Everything due to activation of PAR by Thrombin:

  1. ADP release
    • Thrombin binds to protease-activated receptor (PAR) on platelet surface.
    • PAR activation –> rise in intracellular Ca2+
    • Ca2+ rise –> exocytosis of adenosine diphosphate (ADP) from dense granules
  2. ADP activates P2Y12 receptors–> platelet activation/ aggregation
  3. COX-activation
    • PAR activation –> liberates arachidonic acid (AA)
    • Cyclo-oxygenase (COX) generates thromboxane A2 (TXA2) from AA
  4. Glycoprotein IIb/IIIa receptor (GPIIb/IIIa)
    • TXA2 activation –> expression of GPIIb/IIIa integrin receptor on platelet surface
    • GPIIb/IIIa - involved in platelet aggregation
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7
Q

What happens when Thrombin binds to the PAR on platelets?

A

PAR= protease-activated receptor

leading to

  1. intracellular Ca2+ release
    1. triggers release of ADP
  2. Freeing of Arachidonic Acid
    • Production of TxA2 by COX
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8
Q

What is the effect of ADP release from the platelet?

A

ADP activates P2Y12 receptors leading to platelet activation/ aggregation

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9
Q

What is the effects of COX activation in the plateley by thrombin binding to PAR?

A
  1. PAR activation –> liberates arachidonic acid (AA)
  2. Cyclo-oxygenase (COX) generates thromboxane A2 (TXA2) from AA
    1. TXA2 activation –> expression of GPIIb/IIIa integrin receptor on platelet surface
    2. GPIIb/IIIa - involved in platelet aggregation
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10
Q

What is the effect of TXA2 in the platelet?

A
  • TXA2 activation ® expression of GPIIb/IIIa integrin receptor on platelet surface
  • GPIIb/IIIa - involved in platelet aggregation
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11
Q

What are anticoagulants?

A

Drugs that directly target the initiation stage of blood coagulation

(Also used as expression for all anti-thrombosis/haemostasis drugs)

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12
Q

Name some direct-acting anti-coagulants and their MOA

A
  1. Dabigatran (oral)
    • FIIa inhibitor
  2. Rivaroxaban
    • FXa inhibitor
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13
Q

Which Drug inhibits FIIa?

A

Dabigatran

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14
Q

Which drug inhibits coagulation Factor Xa?

A

Rivaroxaban

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15
Q

What is the MOA of Dabigatran?

A

It is a FIIa inhibitor

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16
Q

What is the MOA of Rivaroxaban?

A

FXa inhibitor

17
Q

What is the MOA of Heparin?

What is its ROA?

A

IV, SC

–> enhances the activity of Antithrombin II (indirectly decreases the acitvity of FII+ FX

18
Q

Which drugs increae the activity of Anti-thrombin?

A

Heparin and low-molecular weight heparins (e.g. Dalteparin)

19
Q

What is the MOA of LMWHs?

A

Low molecular weight heparins

  • activate anti-thrombin III –> decrease activity of FX
  • (also have some effect but overall less effect on IIa)
20
Q

What is the MOA of Warfarin?

What is its ROA?

A

Oral administration

It is a Vit K antatgonist

  • Vit K is needed for generation of FII, VII, IX and X
21
Q

How do you treat a DVT?

Why?

A
  1. Immediate treatment with parenternal anticoagulants (e.g. Deltaparin)
  2. Maintainance with oral anticoagulants (Warfarin and Rivaroxaban)

–> Because it is a Red thrombus –> treatments are more effective

22
Q

What is a red thrombus in compariston for a white thrombus?

A

Red thrombus–> mainly venous, coagulatied blood

White thrombus –> mainly arterial and have a high content of foam cells

23
Q

What kind of treatments would you use to treat a reed vein thrombus?

A

Anti-coagulants like

  • Heparin
  • Dabigatran
  • Rivaroxaban
  • warfarin

–> All are prophylactic

24
Q

What kind of drugs would you use to treat a white thrombus?

A

Anti-platelets like

  • Clopidogrel
  • Aspirin
  • Abciximab

–> As prophylaxis!

25
Q

What is the Difference between a STEMI and a NSTEMI?

How would they differn in the treatment?

A

The ST elevation on an ECG but often:

  • STEMI: full occlustion of a Coronary artery
  • NSTEMI: partial occlustion of a coronary artery

STEMI: Anti-platelet and thormbolysis

NSTEMI: Anti-platelet

26
Q

What is the Virchows triad?

A

RISK FACTORS that make you more suspectible to DVT+ PE

  • SLow rate of blood flow
  • Imbalance between pro-coagulation & anticoagulation factors
  • Damage to epithelial wall
27
Q

What is the MAO of clopidogrel?

What is the ROA?

A

ROA: oral

  • it is a ADP receptor (P2Y12) receptor antagonist
  • –> prevents platelet activation + aggregation
28
Q

Which drug is an P2Y12 receptor antagoinst?

A

Clopidogrel

29
Q

What is the MOA and ROA of Aspirin?

A

ROA: oral

Irreversible COX-1 inhibitor –> Inhibit production of TXA2

NB: High doses no more effective BUT more side-effects

30
Q

Which drug is an irreversible COX-1 inhibtor?

A

Aspirin

31
Q

What is the MOA and ROA of Abciximab?

A

ROA: IV, SC

3.Prevent platelet aggregation, GP IIb, IIIa inhibition –> too effective

Limited use AND only by specialists

32
Q

What are the commonly used Anti-platlet drugs?

A
  • Aspirin–> COX-1 inhibitor
  • Clopidogrel –> P2Y12 antagonsit
33
Q

What happens during the Propagation stage of haemostasis?

A

Formation of a Fibrin Mesh

  • IIa –> activates Fibrinogen into Fibrin (I –> Ia)
34
Q

Explain the process of Thrombolysis

A

Thrombolysis can remove a pre-formed cloth:

  • acitvation of plasminogen into plasmin (that degrades fibrin)
35
Q

Explain the MOA and ROA of Alteplase

A

Thrombolytic drug:

IV administration

recombinant tissue type plasminogen activator (rt-PA)

acitivation of plasminogen into plasmin –> fibrin degradation

36
Q

Which drug is a recombinant tissue type plasminogen activator (rt-PA)?

A

Alteplase

year 5 path haematology (18 decks)

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