Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > Haemostasis and thrombosis > Flashcards

Haemostasis and thrombosis Flashcards

1
Q

What is interim treatment for DVT

A

interim treatment with parenteral anticoagulant (iv/sc Heparin or dalteparin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is given for when DVT has been diagnosd

A

given maintenance treatment with oral anticoagulant (changes from parenteral to oral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline the molecular level of thrombus formation

A
  1. Tissue factor (TF)
    TF bearing cells activate factors X & V, forming prothrombinase complex
  2. Prothrombinase complex
    This activates factor II (prothrombin) creating factor IIa (thrombin)
  3. Antithrombin (AT-III)
    AT-III….. inactivates fIIa & fXa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is dabigatran

A

ORAL: factor IIa inhibitor

OAC/DOAC

(dabigaTran…. T for thrombin, which is factor 2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is rivaroxaban

A

ORAL: factor Xa inhibitor (think of 10 rivers)

Maintenance treatment

Apixaban also factor Xa inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline the 2 categories of heparin and their MAO

Panopto for subcutaneous

A

Heparin (IV, SC) - activates AT-III (reducing fIIa & fXa)

Low-molecular weight heparins (LMWHs, e.g.Dalteparin) - activate AT-III (reducing fXa)…. GIVEN AS INTERIM, PARENTERAL ANTICOAGULATNT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is warfarin and mechanism of action

A

Vitamin K antagonist - vit K required for generation of factors II, VII, IX & X

ORAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is dalteparin

A

Low-molecular weight heparins (LMWHs, e.g.Dalteparin) - activate AT-III (fXa)

NOTE: the difference in MAO between heparin and LMWH is that the LMWH is also thought to directly inhibit factor Xa, not just increase AT-III

These are used for INTERIM, which is PARENTERAL (oral coagulants are used for maintenance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What test might you do if you suspect PE

A

Multiple-detector computed tomographic pulmonary angiography (CTPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between PE and DVT treatment

A

On cofnrimed diagnosis might give heparin as well as dalteparin for PE

but the same for maintenance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline the risk factors affecting DVT and PE

A
  1. Rate of blood flow
    Blood flow is slow/stagnating –> no replenishment of anticoagulant factors & balance adjusted in favour of coagulation
  2. Consistency of blood
    Natural imbalance between procoagulation & anticoagulation factors (not viscosity!)
  3. Blood vessel wall integrity
    Damaged endothelia –> blood exposed to procoagulation factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What would NSTEMI look like for tests

A

No changes on ECG & elevated troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is NSTEMI

A

partially occluded coronary artery leading to ischaemia due to atheroma formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Differentiate thrombotic lesion and an atherosclerotic lesion and where they occur

A

Red thrombus…. in a vein, not associated with atherosclerosis

White thrombis… in an artery with foam cells and macrophages/athersclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What treatment would be offered for NSTEMI

A

Antiplatelet therapy: ASPIRIN & CLOPIDOGREL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Differentiate the cause of NSTEMI and STEMI

A

Non-ST elevated myocardial infarction (MI)
‘White’ thrombus –> partially occluded coronary artery

ST elevated myocardial infarction
‘White’ thrombus –> fully occluded coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Differentiate treatment for NSTEMI and STEMI

A

NSTEMI: antiplatelets

STEMI: antiplatelets & thrombolytics

18
Q

What is NSTEMI/STEMI caused by

A

Damage to endothelium
Atheroma formation
Platelet aggregation

Different to VIRCHOW’S TRIAD (as it’s more to do with lifestyle… virchow’s is more to do with thrombus, whereas STEMI/NSTEMI more to do with atherosclerosis)

19
Q

Outline difference between the thombus formation in vein and atherosclerosis

A

In atherosclerosis the thombosis is within the wall of the artery, in the plaque
In vein the thrombus is within the lumen

20
Q

Outline the amplification stage of thrombosis formation on a cellular level

A
  1. Thrombin
    Factor IIa –> activates platelets
  2. Activated platelet
    Changes shape
    Becomes ‘sticky’ and attaches other platelets
21
Q

What is PAR

A

Protease activated receptor

22
Q

Outline the ampification stage of thrombosis on a molecular level

A
  1. Thrombin (IIa)- binds to protease-activated receptor (PAR) on platelet surface.
  2. PAR activation –> rise in intracellular Ca2+, and also liberates AA
  3. Ca2+ rise –> exocytosis of adenosine diphosphate (ADP) from dense granules (not the alpha granules, which contain growth factors)
23
Q

What is the consequence of ADP exocytosis, PAR receptor activation and TXA2 activtation

A
  1. ADP receptors
    ADP activates P2Y12 receptors –> platelet activation/ aggregation
  2. PAR activation liberates arachidonic acid, COX generates TXA2 from the AA
  3. TXA2 activation leads to expression of GPIIbIIIa integrin receptor on platelet surface…. this is involved in platelet aggreation
24
Q

State types of antiplatelet therapy

A

Clopidogrel (oral) - ADP (P2Y12) receptor antagonist

Aspirin (oral) - irreversible COX-1 Inhibitor (inhibits TXA2)

Abciximab (IV, SC)… inhibits GPIIbIIIa receptor (3rd line)

25
Q

What would be use in stroke

A

Thrombolytic therapy–> ALTEPLASE (tPA)

26
Q

Why is CT scan important in stroke

A

To determine whether stroke is iscahemic of haemorrhagic (if you give wrong drug it will kill them here)

27
Q

How does stroke occur compared to DVT/athersclerosis

A

Thrombus forming within the atria of the heart and then embolosing!!!! This may occur due to atria flutter or atrial fibrillation. Lodges in lumen of cerebral artery

due to reduced rate of blood flow

28
Q

What happens to a clot in the propogration stage

A

Generation of fibrin strands

  1. Activated platelets…
    Large-scale thrombin production
  2. Thrombin
    Factor IIa–> binds to fibrinogen and converts to fibrin strands
29
Q

Why is anticoagulants and antiplatelets not used in stroke

A

DO NOT remove pre-formed clots

30
Q

What is the mechanism of action of thrombolytics

A

Convert plasminogen…. plasmin

Plasmin - protease degrades fibrin

31
Q

How does alteplase work

A

Alteplase (IV) - recombinant tissue type plasminogen activator (rt-PA)

32
Q

Why aren’t thrombolytics used in PE/DVT etc?

A

Because they are very dangerous drugs, not used unless very serious

33
Q

What are clot busters

A

Fibrinolytics/thrombolytics

34
Q

Overall, explain the process of coagulation, platelet ativation and actions of fibrin

A

Initial - tissue Factor presentation –> Prothrombinase-mediated formation of factor IIa (thrombin)

Amplification - thrombin (fIIa)-mediated platelet activation –> ADP activates P2Y12 receptor –> COX & GPIIb/IIa

Propagation - thrombin-mediated conversion of fibrinogen  fibrin strands

35
Q

Why is antiplatelet used in athersclerosis

A

Antiplatelets used for prophylaxis, not specifically treatment of atherosclerosis

36
Q

Why is dabigatran not used as a maintenance treatment following DVT

What might be used instead

A

It is a DOAC but it has high side effect profile

Rivoroxaban or warfarin (which isn’t a DOAC, but can be used…. problems with getting the exact correct dose though, and also has lots of drug drug interaction)

37
Q

Downside of rivoroxaban

A

You cannot reverse it if it causes too much bleeding

Rivaroxaban cannot Reverse

38
Q

Which diagnostic tests could be used for DVT

A

D dimer and ultrasound

39
Q

How is dalteparin administered

A

Subcutaneously….

40
Q

How is heparin usually given (not LWMH)

A

Usually intravenously during emergencies, but can be given subcutaneously too

41
Q

What is the prothrombinase complex

A

The prothrombinase complex consists of the serine protein, Factor Xa, and the protein cofactor, Factor Va. The complex assembles on negatively charged phospholipid membranes in the presence of calcium ions

Remember from haemostasis that FVa is the cofactor for FXa

Pharm (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions