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CVS topics > Thromboembolism > Flashcards

Thromboembolism Flashcards

1
Q

What is a characteristic of platelets

A

Platelets do not have a nucleus. So they cannot regenerate. Hence when you take aspirin. The anti platelet effect is irreversible

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2
Q

What is haemostasis

A

The arrest of blood flow from a damaged vessel

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3
Q

What is vascular spasm?

A

When a vessel wall is damaged , vasoconstriction occurs

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4
Q

What is coagulation

A

Solidification of blood through an amplifying cascade

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5
Q

What is the main event during coagulation

A
  • soluble fibrinogen becomes insoluble fibrin
  • this fibrin mesh work traps blood cells and platelets
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6
Q

What is the extrinsic pathway

A

Activated after tissue trauma
In vivo
Happens very fast

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7
Q

What is the intrinsic pathway

A

Activated upon contact with abnormal surface
In vivo and in vitro
Very slow

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8
Q

What do the intrinsic and extrinsic merge to form?

A

Common pathway

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9
Q

What is the cascade process of the intrinsic pathway?

A

XII—>XIIa
Which triggers:
XI——> XIa
Which triggers
IX——> IXa

Which forms X—->Xa which is the common pathway

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10
Q

What is the cascade process of extrinsic pathway

A

VII—->VIIa

Then activates
X—->Xa

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11
Q

What does the coagulation cascade happen in the presence of ?

A

Calcium ions

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12
Q

What happens after the common pathway? (Clot)

A

X——>Xa
Which triggers
II (prothrombin) —-> IIa (thrombin)

Which causes activation of (XIII—>XIIIa)
Soluble fibrinogen——> fibrin

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13
Q

What is the function of thrombin

A

Activates factor 13
Causes fibrinogen to form fibrin
Causes vasoconstriction
Strengthens the fibrin strands

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14
Q

What is thrombin inhibited by?

A

Antithrombin III

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15
Q

What is thrombosis

A

An inappropriate blood clot

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16
Q

What is a thrombus

A

Fixed clot in a unbroken blood vessel

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17
Q

What is an arterial thrombosis

A

White platelet plug

18
Q

What is venous thrombosis

A

Red coagulation

19
Q

What is an embolus

A

A thrombus that breaks apart and cam cause ischaemia

20
Q

How do you treat someone who has a defect in their clotting factors (genetics)

A

Vitamin K (orally or iv)

21
Q

Types of thromboembolism

A

MI
STROKE
DVT
PE

22
Q

How would you treat arterial (white) disorders

A

Antiplatelet
Antifibrinolyctic

23
Q

How would you treat a venous (red ) thromboembolism disorder?

A

Oral anticoagulant
I.V anti coagulant

24
Q

Risk factors of thromboembolism

A

Contraceptives
Prosthetic device
Atherosclerosis

25
Q

How does heparin work?

A

Inactivates thrombin (IIa) by increasing activation antithrombin III ( has to happen simultaneously)

26
Q

How does LMWH differ to heparin?

A

LMWH has a different structure (fragment of heparin) so cannot bind to thrombin to activate anti thrombin III

27
Q

How does LMWH work?

A

Binds to antithrombin III and It inhibits the action of factor 10 and thrombin

28
Q

What are direct thrombin inhibitors or doacs

A

They do not depend on the activation of antithrombin

29
Q

How does warfarin work

A

It interferes with the post translational carboxylic of glutamic acid residues in clotting factor 2,7,9 and 10 by inhibiting vitamin k reductase . This causes the inhibition of vitamin K epoxied to its original form being vitamin k hydroquinone

30
Q

Factors that potentiate warfarin (make it too potent)

A

Drugs that inhibit platelet function (aspirin)
Drugs that inhibit the reduction of vitamin k (cephalosporins)
Drugs that inhibit hepatic metabolism (most antibiotics)

31
Q

What lessens the effect of warfarin

A

Vitamin K

32
Q

How do platelets form?

A
  1. Trauma/damage
  2. Platelets are activated and arachidonic acid is produced
  3. This produces cyclic endoperoxides
  4. Thromboxane 2 is synthesised
  5. Leads to more GP IIb and IIIa receptors
  6. Platelets will then form a linkage with these receptors and form platelet aggregation
33
Q

What is the Moa of aspirin

A

Inhibits the production of thromboxane 2 (TXA2)

34
Q

What is the mechanism of action of abciximab (antiplatelet)

A

Antagonises the GP IIb/IIIa receptors

35
Q

What is the Moa of clopidogrel, ticagrelor

A

Irreversible inhibition of P2Y receptors

N.B IN THE BNF

36
Q

How do antiplatelets and anticoagulants and fibrolyctics differ

A

Anticoagulants and antiplatelets stop clots from forming in the first place. But fibrinolytic work when the clot is already formed.

37
Q

How do fibronolyctics work

A

They act on the existing clot. Causing it to dissolve by activating plasminogen to turn into plasmin

Plasmin breaks cross links in fibrin causing it to dissolve

38
Q

What are the benefits of heparin (UFH) compared to LMWH

A

UFH is quickly reversible and has a shorter half-life

39
Q

Why are some patients prescribed heparin and warfarin

A

Warfarin takes about 5-7 days to take its effect. So patients need to take both but once the warfarin is on full effect the heparin stops. Known as patient bridging

40
Q

Why is the volume of distribution of warfarin small

A

Binds to plasma albumin so lower volumw

41
Q

What are the benefits of prescribing DOACS instead of warfarin

A

Fixed daily dose
Fewer drug interaction
Fast acting
No need for regular blood tests

42
Q

What is the moa of rivaroxaban

A

Direct factor xa inhibitor. This in turn interrupts the intrinsic and extrinsic pathway

CVS topics (6 decks)

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