Ha - VTE Flashcards

1
Q

2 functions of the endothelium

A
  1. physical barrier between blood and sub endothelium
  2. Synthesis of PGI2, TxA2, vWF, tPA
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2
Q

Life span of a platelet? where do they arise?

A

10 days
Originate in bone marrow. 1 megakaryocyte produces 4000 platelets

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3
Q

Platelet adhesion

A

a) Directly to sub endothelium via G1pIa
b) via vWF

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4
Q

Platelet aggregation

A

Platelets are linked via G1pIIb/IIIa
Fibrinogen
Ca2+

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5
Q

Arachidonic acid metabolism - where? What is the product?

A

Vascular endothelium
PGI2 + TXA2

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6
Q

4 roles of thrombin

A
  1. Fibrinogen -> fibrin
  2. Activates platelets
  3. Activates factors 5 + 8
  4. Activates factors 7 + 11 + 13
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7
Q

wtf is the propagation phase

A

The factor8/9a complex on activated platelets activate factor 10 –> thrombin burst –> fibrinogen converted to fibrin

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8
Q

What is the amplification phase?

A

The Factor 10/5a complex generates a small amount of thrombin. Thrombin then activates platelets and factors 5, 8, 11, 13

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9
Q

Fibrinolysis pathway?

A

Plasminogen is converted to plasmin via tPA and urokinase

Plasmin then breaks fibrin into its degradation products

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10
Q

How do antithrombins work? Most active one? which drug is relevant?

A

Antithrombin binds to and inactivates thrombin to be excreted in the kidney
- Antithrombin III
- Heparin = increases AT function

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11
Q

What is the protein C+S pathway?

A

Activated protein C complex will inactivate factors 5 + 8

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12
Q

When is the protein C/S pathway defective?

A

Factor V leiden - Protein C cannot bind to and inactivate it. Therefore hyper coagulable state

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13
Q

TFPI - what does it stand for? what does it do?

A

Tissue factor pathway inhibitor
binds to and neutralises TF and factor 7a

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14
Q

What is thrombophlebetic syndrome?

A

recurrent pain, swelling, ulcers

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15
Q

outcomes of a VTE?

A

5% fatal
20% recur
23% thrombophlebetic syndrome
4% pulmonary HTN

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16
Q

What is virchows triad?

A

Blood - high viscosity
Vessel wall damage
Static blood flow

17
Q

causes of thrombophilia

A

lack of antithrombin / protein C or S
OR
xs coagulation factors / platelets
COMBINED WITH
stimulating factor eg OCP/preg

18
Q

is the vessel wall pro or antithrombotic? how?

A

anti - secretes antiplatelets and has no TF expressed

19
Q

what makes the BV wall thrombotic?

A

inflammation eg infection/preg/trauma/vasculitis

20
Q

why does stasis increase VTE?

A

accumulation of activated factors in the vessel, increased platelet adhesion and leucocytes
also hypoxia induces inflammation

21
Q

list an immediate and delayed anticoag

A

immediate = heparin / apixaban
delayed = warfarin

22
Q

how are DOACs immediate anti coags

A

anti factor Xa and anti IIa

23
Q

benefits of DOACs over warfarin

A

no monitoring needed for DOACs, warfarin needs INR monitoring

24
Q

how does warfarin act?

A

Decreases factors 2,7,9,10

25
Q

which people are at increased risk of thrombosis?

A

inpatients, cancer / surgical pts, prev VTE, FHx VTE, genetic traits, obsese, elderly

26
Q

List thromboprophylaxis

A

LMWH eg enoxaparin
TED stockings
DOACs

27
Q

How is thrombosis treated

A

preventing embolus / extension

28
Q

is INR used to monitor coagulation risk

A

NO - only for warfarin