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Year 5 Pathology > Venous Thrombosis: Aetiology and Management > Flashcards

Venous Thrombosis: Aetiology and Management Flashcards

1
Q

Thrombophlebitic syndrome: occurs when someone has had a ____

3 features

A

DVT: From disruption to circulation of the veins in the leg

recurrent pain, swelling and ulcers

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2
Q

2 Consequenes of thromboembolism

A

Thrombophlebitis sydnrome

Pulmonary HT –> causes HF and can be fatal

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3
Q

What is Virchow’s Triad?

A

3 contributory factors to thrombosis:

Blood composition:

  • viscosity = hct, protein/paraprotein
  • platelet count
  • coagulation system

Vessel wall

Blood flow (stasis)

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4
Q

Coagulation cascade

A
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5
Q

Procoagulant and anti-coagulant factors

A

Pro-coagulant = XII, XI, IX, VIII, X, V, II

Anti-coagulant = TFPI, Protein C/S, thrombomodulin, EPCR, Antithrombin, fibrinolysis

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6
Q

Coagulation definition = balance of htomrbotic and anti-thrombotic factors

A
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7
Q

Give an example of a condition where someone can be predisposed to thrombosis which can precipitate a thromboembolic event

A

pregnancy

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8
Q

What is thrombophilia?

A

Increased tendency to form blood clots

  • tendency towards procoagulant state (excess coag factors/platelets, or deficiency in anti-coags)
  • 50% of thrombophilic events are precipitate (e.g. pregnancy, surgery)
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9
Q

Is vessel wall pro/antithrombotic

A

Antithrombotic

anticoagulant moleculex expressed:

  • thrombomodulin
  • EPCR
  • TFPI
  • Heparans

it does NOT secrete TF

it secretes anti-platelet factors:

  • prostacyclin
  • NO
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10
Q

What is immunothrombosis?

A

change of vessel well from antithrombotic to prothrombotic during inflammation

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11
Q

Stimuli for vessel wall to be prothrombotic

A

Infection

Malignancy

Vasculitis

Trauma

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12
Q

Effects of prothrombotic vessel wall

A

Anticoagulant molecules downregulated, adhesion molecules upregulated

TF expressed, prostacyclin production decreased

VWF released from endothelial cells (makes endothelial cells sticky)

  • platelets captured on these sticky cells and are activated
  • neutrophils are captured when platelets activated
  • neutrophils then produce NETS (neutrophil extrudes on DNA) aka NETosis
  • DNA is procoagulant
  • neutrophils also release neutrophil elastase - breakdown TFPI
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13
Q

Blood flow and thrombosis

Causes of stasis

A

Stasis -> thrombosis

  • activated factors accumulated -> platelet/leukocyte adhesion and transmigation
  • hypoxia promotion -> inflammatory effects on endothelium

Causes of stasis:

  • Immobility (surgery, travel)
  • Compression (tumour, pregnancy)
  • Viscosity (polycythaemia, paraprotein)
  • Congenital (vascular abnormalities)
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14
Q

OCP + FV Leiden ineratction

A
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15
Q

how do we go about VTE

A
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16
Q

2 types of anticoagulant therapy

A

therapeutic = high dose

prophylactic = low dose

17
Q

Heparin: anti-coagulant immediate

A

Unfractionated (IV infusion: monitored) or LMWH (SC: no monitoring)

  • Pentasaccharide (SC) – the key sugar sequence in heparins that mediate its effects
  • Works by increasing anticoagulant activity (potentiating anti-thrombin)

LT cons: require injections, increased risk of osteoporosis, variable renal dependence

18
Q

DOACs: anti-coagulant immediate

A

Anti-Xa: Rivaroxaban, Apixaban, Edoxaban

Anti-IIa: Dabigatran

Properties = PO, short 1/2 life, no monitoring required (unlike warfarin )

immediate acting (peak in 3-4 hours)

useful LT, but NOT useful for prosthetic heart valve patients

19
Q

LMWH vs unfractioned heparin

A

Low molecular weight heparin

  • Reliable pharmacokinetics (so does NOT usually need monitoring – unless renal concerns)
  • LMWHs are smaller and do not bind to inflammatory molecules – less need for monitoring
  • Anti-Xa assays can be used to monitor renal failure and extremes of weight or risk

Unfractionated Heparin

  • Variable kinetics
  • Variable dose-response
20
Q

How do we monitor anticoagulants

A

ALWAYS monitor therapeutic levels with APTT or anti-Xa

Amount of anticoagulant effect you get from unfractionated heparin can be unpredictable, so monitoring is important here

21
Q

Warfarin: anti-coagulant delayed

mechanism for action and on which factors

favoured drug for what condition

how do we reverse its effects

A

Vitamin K antagonist

Reduces 2, 7, 9 and 10 + Protein C/S indirectly by antagonising vitamin K -> delayted onset of action

reverse effects:

  • Immediate reverse: give factors 2, 7, 9 and 10
  • Reverse in 12 hours: give vitamin K
22
Q

Monitoring warfarin therapy

contraindications

A

Measure INR (drived from PT)

Difficult because there are lots of variables at play:

  • Dietary vitamin K intake
  • Variable absorption
  • Interactions with other drugs
  • Teratogenic – warfarin is very rarely given to women who are pregnant

Warfarin is teratogenic:

  • Major teratogenic effects occur in the first trimester (on bone, heart)
  • Warfarin also causes problems in the second trimester (neurological)
  • The key organs that warfarin affects don’t develop for the first 6 weeks
  • If a woman detects her pregnancy within these 6 weeks, warfarin can be stopped
23
Q

Heparin, DOAC and warfarin summary

A
24
Q

INR diagram

A
25
Q

Patients who are at increased risk of thrombosis

what do we call intervening with anticoag therapies to reduce risk of a thromboembolic event

A

Medical inpatients (infection/inflammation, age, immobility)

Patients with cancer (procoagulant molecules, inflammation, flow obstruction)

Surgical patients (immobility, trauma, inflammation)

Previous VTE, family history, genetic traits

Obese patients

Elderly patients

Term is = preventative intervention thromboprophylaxis

26
Q

features of thromboprophylaxis (4)

A

Low molecular weight heparin (LMWH)

  • E.g. Tinzaparin 4500 u/Enoxaparin 40 mg OD
  • Not monitored

TED stockings (for surgery, or if heparin is contraindicated)

Intermittent pneumatic compression (increases flow – reduces stasis)

Sometimes DOAC +/- aspirin (orthopaedics)

27
Q

NICE guidelines thromboprophylaxis

A

all admissions to hospital should be assessed for thrombotic risk and, unless contraindication exists, receive heparin prophylaxis (2010).

28
Q

Risk assessment for VTE

A
29
Q

Risk assessment for bleeding

A
30
Q

Treating thrombosis

A

Thrombolysis ONLY in life-threating PE or limb threatening DVT

  • as thrombi associated with increased risk of intracranial haemorrhage
  • reduces subsequent post-phlebitic syndrome

Thrombosis

  • higher doses of same drugs used in prophylaxis
  • need immediate results (so heparin over warfarin)
  • start on LMWH (e.g. tinzaparin) AND warfarin, as well as starting a DOAC
  • stop LMWH when INR >2 for 2 days
31
Q

Preventing recurrence

A

High risk pts may require LT anticoag

Does the risk of thrombosis if untreated outweigh the risk of bleeding if treated?

Asses recurrence risk (morb and mort of recurrence)

  • depends on factors that triggered initial episode
  • if after surgery = low risk of recurrence -> NO NEED for LT anti-coag
  • idiopathic = high risk of recurrence

Assess risk of therapy (morb and mort of bleeding)

  • variation of risks with different therapies
  • men have a higher risk of recurrence than women
  • proximal thrombosis (popliteal and above) higher recurrence rate than distal
  • PEs have a similar recurrence rate to proximal thrombosis
32
Q

what increases with age

A

fatal bleeding (nearly always intracerebral bleeding)

major bleeding

recurrence rate

33
Q

DOACs > warfarin

A

immediate effects

half the risk of intracranial bleeding

much lower fatality

34
Q

When to LT coag?

A

Idiopathic precipitant

minor precipitant (3 months coag)

  • COCP, trauma, flights
  • longer duration if presence of other thrombotic/haemorrhagic risk factors
35
Q

SBAs part 1

A

SBAs part 2

36
Q
A

Year 5 Pathology (27 decks)

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