thrombosis and anticoagulation Flashcards
arterial circulation vs venous circulation
arterial circulation: high pressure: platelet rich
venous circulation: low pressurefibrin rich
where are the main areas of an arterial thrombosis?
Coronary circulation
Cerebral circularion
Peripheral circulation
Other territories
Arterial thrombosis - etiology
Atherosclerosis
Inflammatory
Infective
Trauma
Tumours
Unknown - platelet deriven
Arterial thrombosis - Presentations
coronary artery - IM/ACS - chest pain
cerebral artery - stroke/TIA
Peripheral artery - 6Ps
Others such as renal
Arterial thrombosis: coronary treatment + mnemonic
ALTeR
- Aspirin + antiplatelets
- LMWH / Fondraparinux
- Thrombolytic therapy (dissolves clot)
- Reperfusion (PPI)
how do thrombolytic therapies work and what are the types?
- streptokinase
- tissue plasminogen activator
breaks down clots by generating plasmin which degrades fibrin
Arterial thrombosis: cerebral treatment
aspririn + antiplatelet
thrombolysis
reperfusion
(same as coronary but no heparin because inc risk of hemorrhage)
Arterial thrombosis: treatment - other sites (not coronary and cerebral)
Antiplatelets, statins
Role of anticoagulants evolving
Endovascular vs Surgical
Venous thrombosis common areas
Peripheral:
- Ileofemoral
- femoro-popliteal
Other sites:
– Cerebral, Visceral
Venous thrombosis-diagnosis
- Signs and symptoms-very non-specific
- Blood tests –D-dimer –sensitive but not specific(protein rleased to break down clots) - if high could suggest clot or clotting disorder
- Imaging-usually required eg ultrasound or MRI
what image techniques are usually conducted to diagnose venous thrombosis?
- ultrasound with doppler - detects blood flow and visualises clots
- CT/MRI venography - die injected into veins so they can be visualised using an imaging technique
Venous thrombosis-aetiology
Virchows triad:
blood flow - statuent or slow
endothelium injury - could clot
blood constituents / hypercoagulation - genetic, cancer, hormones
Surgery
Immobilisation
Oestrogens: OC, HRT
Malignancy
Long haul flights
genetic conditions
acquired conditions
Venous thrombosis -genetic (5)
Factor V Leiden (5%)
PT20210A (3%)
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Venous thrombosis-acquired
Anti-phospholipid syndrome:
- autoimmune
- produces antibodies that target proteins that bind to phospholipids - inc risk of clotting
Lupus anticoagulant:
- type of antiphospholipid antibody that interferes with normal clotting cascade
Hyperhomocysteinaemia:
- high levels of homocytesine - risk factor for clotting
Venous thrombosis-treatment
Heparin or LMWH
Warfarin
DOAC - direct oral anticoagulant
Endo-vascular / Surgical procedures eg catheter-directed thrombolysis (CDT), thrombectomy, and stenting
Venous thrombosis-prevention
Mechanical or chemical thromboprophylaxsis
mechanical:
- compression socks
- inflation cuffs that promote blood flow
- LMWH + DOAC
Also early mobilisation and good hydration
Heparin
- Glycoaminoglycan
- Binds to antithrombin and increases its activity
- Indirect thrombin inhibitor
Monitor with APTT, aim ratio 1.8-2.8 (monitors the time taken to clot - assesses heparin effecacy)
Given by continuous infusion in hospital setting
Low molecular weight heparin
- Smaller molecule, less variation in dose and renally excreted
- Once daily, weight-adjusted dose given subcutaneously
- Used for treatment and prophylaxsis (prevention of blood clots)
- longer half life
- can be administered at home and last up to 24hrs
Warfarin
- Orally active
- Prevents synthesis of active factors 2, 7, 9, 10
- Antagonist of vitamin K
- Long half life (36 hours)
- Prolongs the prothrombin time
- Difficult to use,
- Individual variation in dose
- Need to monitor
- Measure INR (international normalised ratio, derived from prothrombin time)(measures how long it takes blood to clot)
- Usual target range 2-3,
- Higher range 3-4.5
Aspirin
Inhibits cyclo-oxygenase irreversibly
Act for lifetime of platelet, 7-10 days
Inhibits thromboxane formation and hence platelet aggregation
Used in arterial thrombosis, 75-300 mg od
Other antiplatelets
Clopidogrel -inhibits ADP induced platelet aggregation by irreversibly binding to the p2y12 receptors
Ticagrelor – p2y12 receptor antagonist
Prasugrel – p2y12 receptor antagonist
magnitude of DVT
25,000 people a year die of DVT and PE a year in UK
50% preventable, premature mortality
More than RTA, AIDS and breast cancer combined
Risk factors for DVT
Surgery, immobility, leg fracture/ POPOC pill, HRT, PregnancyLong haul flights/ travel (rare)Inherited thrombophilia- genetic predisposition; 5% population, familial
Virchows Triad
DVT diagnosis
Symptoms: leg pain, swelling
Signs: tenderness, swelling, warmth, discolouration
Phlegmasia - severe swelling and pain in the leg
PE
DVT investigation
- D-dimer: normal excludes diagnosis
- positive does not confirm diagnosis (non-specific)
- Ultrasound compression - visualise flow and clots
- CT / MR venogram
- catheter venogram - injecting dye to visualise
DVT treatment
LMW Heparin s/c od for min 5 days
Oral warfarin, INR 2-3, (2.5) for 3-6 months
DOAC/NOAC
Compression stockings – symptoms vs PTS
Treat/ seek underlying cause: malignancy, thrombophilia, compression
Spontaneous vs provoked
Re-cannalisation
removing the clot:
Endovenous
Chemical
Mechanical - d
Mechanico-chemical
Stents
Prevention of DVT
Mechanical- hydration and early mobilisation, Compression stockings, Foot pumps
Chemical- LMW Heparin
Thromboprophylaxsis
Low risk: <40 yrs, surgery < 30 mins: early mobilisation and hydration, no chemical, TED if surgical
High risk: hip and knee, pelvis, malignancy, risk factors, prolonged immobilityAll immobile medical, many surgical/ O+G Daltrparin s/c od. No monitoring
Pulmonary Embolism symptoms
breathlessness, pleuritic chest pain, may have signs/ symptoms of DVT, may have risk factors, no other diagnosis more likely
Pulmonary Embolism signs
tachycardia, tachypnoea, pleural rub, those of precipitating cause, none of alternative diagnosis
Pulmonary EmbolismCommon presentation
Differential diagnosis of chest pain and sob
Consider also musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro causes
PE initial investigations
CXR usually normal
ECG sinus tachy, (QI,SI,TIII)
Blood gases: type 1 resp failure, decreased O2 and CO2
Mainly done to exclude alternative causes
PE Further investigations
D-dimer: normal excludes diagnosis
CTPA or spiral CT - visualise segmental thrombi
Ventilation/ Perfusion scan: mismatch defects
Treatment PE
Supportive treatment
LMW Heparin s/c od weight adjusted 5/7
Oral warfarin INR 2-3 (2.5) for 6 months
DOAC
Treat underlying cause
Prevention of PE
Early mobilisation and hydration
Mechanical
Chemical
IVC filters
Pulmonary Embolism -Massive
Hypotension, cyanosis, severe dyspnoea, right heart strain/ failure
Rare
Consider
Catheter mechanico-chemical thrombectomy or surgical thrombo-embolectomy
Haemodynamic instability
Describe the pathophysiology of arterial thrombosis and how it differs from venous thrombosis.
Arterial thrombosis involves clots in arteries caused by plaque rupture, leading to conditions like heart attacks, while venous thrombosis forms clots in veins due to slow blood flow, often resulting in conditions like deep vein thrombosis.
contrast heparin with LMWH
heparin
- larger molecule
- IV or subcutaneous
- lasts 1-2hrs
- required frequent monitoring (aPPT)
LMWH
- smaller molecule
- subcutaneous
- lasts 4-6 hours
- can be done at home
- no monitoring
DVT clinical assessment
Tap test (Schwartz)
Trendelenburgh test
SFJ Incompetence
Tourniquet test
Perforator Incomp
SPJ Incomp
Perthes test
Deep venous Incomp
DVT Investigation
Duplex
Gold standard
MRV
Pelvic
Venography
Pelvic
Treatment – Superficial Venous Disease
Lifestyle
Compression
Sclerotherapy
Endo-venous treatments
Surgical stripping
Treatment – Deep Venous Disease
Lifestyle
Compression
Stents
Valves
