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Cardio/Resp > DVT and Pulmonary Embolism > Flashcards

DVT and Pulmonary Embolism Flashcards

(43 cards)

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1
Q

DVT and PE background (5)

A

blood clot/thrombus forming in the leg

dangerous when above the knee - 50% embolise

common : 1/1000

8/100 have it due to inherited thrombophilia

Multifactorial risk

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2
Q

process (4)

A

thrombus: deep vein or valves

multiple triggers: becomes unbalanced system

above knee - break off and lodge in pulmonary circ (smallest place) : Pulmonary embolus -fragmentation of proximal clot which travels in venous system until it
lodges in the pulmonary circulation

Consequences locally in source limb and/or in
heart or lungs after embolisation

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3
Q

Virchow’s triad – contributing factors to
thrombosis (3)

A
  • endothelial injury
    -stasis (sticky)
  • blood components (clot): Platelets, Coagulation factors, Coagulation inhibitors, Fibrinolytic factors
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4
Q

Thrombosis is multi-factorial genetic and acquired risk factors (3)

A

either end up above threshold naturally (genetics + aging) or via acquired risk

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5
Q

clot formation process (6)

A

1) vessel injury
2) platelets released
3) vasocon + coag cascade
4) platelet aggregation
5) platelet fusion
6) stable haemostatic plug

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6
Q

blood coag cascade (3)

A

intrinsic
extrinsic = most common

haemostatic balance

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7
Q

summarised clot from (4)

A

Response to injury
Vessel constriction

Formation of unstable platelet plug
- platelet adhesion
- platelet aggregation

Fibrin stabilisation of the plug with fibrin
- blood coagulation

Dissolution of clot and vessel repair
- fibrinolysis

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8
Q

Fibrinolysis

A

Plasminogen > plasmin by t-PA

plasmin: breaks fibrin > D-dimer

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9
Q

Clotting factors, fibrinolytic factors and inhibitors and monitoring (5)

A
  • Synthesised in
    – liver
    – endothelium
    – megakaryocytes
    (platelets)

Measurements:
* Prothrombin time –
PT = PTR
* Partial thromboplastin
time – APTT =APTTR
* Thrombin time - TT

wrong = clot or bleed

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10
Q

Venous thrombosis
Risk factors (10)

A
  • stasis
    -coag abnormalties
    -Age
  • Past history or family of VTE
  • Obesity
    -Sepsis
  • Nephrotic syndrome
    -Paroxysmal nocturnal
    haemoglobinuria
    -Behçet’s disease
    -COVID-19
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11
Q

stasis causes (8)

A
  • Prolonged immobility eg surgery, travel
  • Stroke
  • Cardiac failure
  • Pelvic obstruction
  • Dehydration (more sticky)
  • Hyperviscosity
  • Polycythaemia

-flying to holidays

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12
Q

coag abnormality (8)

A
  • Surgery or major trauma
  • Pregnancy and puerperium
  • Oestrogen medication
  • Malignancy
  • Antiphospholipid antibodies (more platelets)
  • Hereditary or acquired
    thrombophilia
    -Thrombocytosis
  • Heparin induced
    thrombocytopenia
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13
Q

Clinical Features of DVT (7)

A
  • Pain, tenderness of veins
  • Limb swelling
  • Superficial venous distension
    -Increased skin temperature
  • Skin discoloration
  • All reflect obstruction to the venous drainage
  • There are multiple differential diagnoses for
    these presenting features
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14
Q

DVT diagnosis (5)

A

Risk assessment
 Evidence based pre test probability score
 D dimer for exclusion
 Diagnostic tests
 Compression ultrasonography
 Venography

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15
Q

DVT risk assessment

A

Clinical risk
score – determines role
for diagnostic imaging vs use of blood test for exclusion

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16
Q

DVT + PE (2)

A
  • > 50% above knee DVT embolise
  • Hospital acquired
    thrombosis 25000pa
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17
Q

PE symptoms (5)

A

 Dyspnoea
 Pleuritic chest pain
 Cough and haemoptysis
 Dizziness
 Syncope

  • patient either very unwell or very well
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18
Q

PE signs (6)

Study These Flashcards
A

 Tachypnoea, tachycardia
 Hypoxia
 Pyrexia
 Elevated jugular venous
pressure
 Hypotension
 ECG changes

or very few symps

19
Q

Physiology of PE Symptoms (3)

Study These Flashcards
A

 Symptoms and signs determined by thrombus size and burden

 Multiple small peripheral thrombi produce a different clinical picture to large proximal thrombus

 Pulmonary infarction is not common – remember the bronchial circulation

20
Q

PE diagnosis (8)

Study These Flashcards
A

 Risk assessment and diagnostic algorithm

 D – dimer for exclusion in low risk cases only

 Mortality stratification - PESI score

 Assessment of compromise - Pa02 + D dimer + ECG + troponin and BNP

 Consider echo

 Diagnostic tests

 CT pulmonary arteries – CTPA

 Ventilation Perfusion Scan

21
Q

VTE Long term consequences (4)

Study These Flashcards
A

10% of all hospital
deaths

30% recurrence at 10years

30% post phlebitic3
syndrome at 10 years

Chronic
thromboembolic pulmonary
hypertension (CTPHE)

22
Q

hospital acquired thrombosis (4)

Study These Flashcards
A

-top prority for NHS since 2010

  • assessing the risks of VTE + bleeding
  • reducing the risk of VTE

-patient information + planning for discharge - extended prophylaxis

23
Q

prevention + Treatment of VTE (8)

Study These Flashcards
A

best care is prevention

  • risk assessemnt
  • prophylatic dose anti-coag
    -intermittend compression devices
    -compression hosiery

treatment:
-anticoag
-thrombolysis
-surgery
-prevention + antic

24
Q

Why and how do we treat? (4)

Study These Flashcards
A
  • correct if there is no bleed risk = dissolves all clots everywhere

Most treatment aims to prevent thrombus propagation and
formation of new thrombus
while allowing the body to
concentrate lysis in the place where it is required

  • Risks are short term impact of thrombus burden and damage to vessels while thrombus
    remains
  • Newer approach – catheter directed thrombolys
25
if cardiovascularly stable with acute VTE... (2)
Anticoagulate * Immediate anticoagulant effect * Heparin then warfarin/DOAC or immediate DOAC- Rivaroxaban or apixaban
26
Circulatory collapse due to PE -Thrombolysis (2)
Alteplase (tissue plasminogen activator) (Streptokinase) * Followed by heparin and warfarin/DOAC or other – prevent recurrence
27
Investigations pre treatment (3)
clotting screen – Prothrombin time (INR) – Partial thromboplastin time – Thrombin time * Full blood count * Urea and electrolytes – usually part of routine screen – to know creatinine clearance * Liver function tests – If clinical suspicion of liver disease
28
Heparin - 2 types (6)
* from dog liver *Glycosaminoglycan * Irreversible * Immediate action * Parenteral administration, iv or sc * Renal excretio unfractionated (UFH): t ½ 1-2 hours * accelerates inhibition of thrombin (IIa) and Xa * Effect easy to measure with standard clotting screen Lower molecular weight: t ½ 4-12 hours * accelerates inhibition of Xa > thrombin (IIa) * Measurement of effect requires Xa level assay
29
Low molecular weight heparin (4)
Renally cleared * Half life 12 hours, peak activity 3-4hours * No monitoring required -Predictability means this is not routine * No reversal agent * Anti Xa monitoring performed under certain circumstances - preg - renal failure - obesity - peak 4 hours post injection
30
Side effects of heparin - 2 main (6)
* Bleeding – LMWH vs UFH less major bleeding (more even control) – stop heparin – give protamine sulphate – LMWH is harder to reverse * Heparin induced thrombocytopenia (HIT) – minor platelet drop at 5 days * transient – HIT with thrombosis syndrome (HITTS): * Thrombocytopenia -IgG antibody to heparin + platelet factor 4 complexes * Thrombosis - venous and arterial and gangrene * Timing - 4-5 days after starting heparin * other cause for thrombocytopenia not found
31
Warfarin (7)
Wisconsin Alumni Research Foundation - decaying sweet clover - 1940s used as rodenticide haemorrhagic death - 1950 and 60s used to treat thromboembolic disease in Presidents Eisenhower & Nixon Rapidly absorbed t½ 36 - 42 hours * 97% albumin bound in plasma – pharmacological effect due to unbound fraction * Eliminated by liver * Interindividual dose variation – genetic factors * CYP2C9 – ↑ sensitivity * VKORC1 – principal genetic modulator * Intraindividual dose variation – compliance / comprehension – diet – co-morbid conditions eg right heart failure – numerous drug interaction book for dosing = prevent interruptions in treatments with no knowledge
32
Warfarin MoA (2)
antagonist of vitamin K dependent clotting factors - multiple sites in cag cas = unpredictable effects
33
Warfarin –side effects
skin necrosis: give heparin first for Rx of VTE otherwise can cause clot because you lose inhib factors before coag
34
How is the INR tested? (2)
venous sample: - labour intensive – accurate – cheap Near patient testing (NPT0 finger prick: -capillary whole blood – quick – patients prefer – immediate advice – 0.5 variation in INR – expensive
35
Warfarin – Interactions and Bleeding Risk (5)
drugs: -increased vit K absorpt -compete for plasma protein binding sites -hepatotoxic -induce hepatic enzymes -have antiplatelet activity = increasing bleeding = fatal , life threatening or minor
36
Warfarin reversal
vit k admin (every few hrs or days) or replace complexes
37
warfarin + pregnancy (4)
crosses placenta= coumarin embryopathy * 6-12 weeks * doses > 5mg – increased fetal wastage * intracerebral haemorrhage * antepartum haemorrhage
38
warfarin is good but... (7)
* Narrow therapeutic window * Frequent monitoring (not always available) * Risk of bleeding (especially intracranial haemorrhage) * Many contraindications and food and drug interactions * Lifestyle restrictions * Poor compliance and persistence * Consequence: many patients are not sufficiently anticoagulatant
39
DOAC's Advantages
- Oral anticoagulant * Rapid onset/offset of action * No need for bridging * Short half life * Easy to control anticoagulant effect * Little or no food-drug interactions * Limited drug-drug interactions * Predictable anticoagulant effect * No need routine monitoring
40
New(ish) anticoagulants (3)
> Indirect Xa inhibitors - enhance antithrombin – Fondaparinux – Idraparinux > Direct Xa inhibitors ORAL – Rivaroxaban – Apixaban * Direct thrombin inhibitors ORAL
41
Rivaroxaban (7)
Direct inhibitor of Xa * Oral agent ,once daily dosing * Rapid onset of action and half life 4-9 hours * Monitoring not usually necessary * Renal excretion * Few food or drug interactions * GI side effects
42
Apixaban
* Direct inhibitor of Xa * Oral agent * Twice daily dosing * Rapid onset of action * Half life 9-14hours * Monitoring not usually necessary * Biliary and renal excretion * Few food or drug interactions * GI side effect
43
Dabigatran etexilate

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