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Cardio/Resp > DVT and Pulmonary Embolism > Flashcards

DVT and Pulmonary Embolism Flashcards

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)

A

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

or very few symps

19
Q

Physiology of PE Symptoms (3)

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)

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)

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)

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)

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)

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
Q

if cardiovascularly stable with acute VTE… (2)

A

Anticoagulate
* Immediate anticoagulant effect

  • Heparin then warfarin/DOAC or immediate DOAC-
    Rivaroxaban or apixaban
26
Q

Circulatory collapse due to PE -Thrombolysis (2)

A

Alteplase (tissue plasminogen activator)
(Streptokinase)

  • Followed by heparin and warfarin/DOAC or other –
    prevent recurrence
27
Q

Investigations pre treatment (3)

A

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
Q

Heparin - 2 types (6)

A
  • 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
Q

Low molecular weight heparin (4)

A

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
Q

Side effects of heparin - 2 main (6)

A
  • 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
Q

Warfarin (7)

A

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
Q

Warfarin MoA (2)

A

antagonist of vitamin K dependent clotting factors

  • multiple sites in cag cas = unpredictable effects
33
Q

Warfarin –side effects

A

skin necrosis: give heparin first for Rx of VTE

otherwise can cause clot because you lose inhib factors before coag

34
Q

How is the INR tested? (2)

A

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
Q

Warfarin – Interactions and Bleeding Risk (5)

A

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
Q

Warfarin reversal

A

vit k admin (every few hrs or days)

or replace complexes

37
Q

warfarin + pregnancy (4)

A

crosses placenta= coumarin
embryopathy
* 6-12 weeks
* doses > 5mg
– increased fetal wastage
* intracerebral haemorrhage
* antepartum haemorrhage

38
Q

warfarin is good but… (7)

A
  • 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
Q

DOAC’s Advantages

A
  • 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
Q

New(ish) anticoagulants (3)

A

> Indirect Xa inhibitors - enhance antithrombin
– Fondaparinux
– Idraparinux

> Direct Xa inhibitors ORAL
– Rivaroxaban
– Apixaban

  • Direct thrombin inhibitors ORAL
41
Q

Rivaroxaban (7)

A

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
Q

Apixaban

A
  • 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
Q

Dabigatran etexilate

A

Cardio/Resp (34 decks)

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