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1st Year Medicine > PE > Flashcards

PE Flashcards

1
Q

What are symptoms of PTE?

A

SOB, collapse, pleuritic chest pain, heamoptysis and sudden death.

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2
Q

What are the signs of PE?

A

Tachypnoea, wheeze, pleural rub and signs of pleural effusion
hypotension, tachycardia, arrest and fourth heart sound,
Oligemia (water mark) on CXR.

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3
Q

What investigations do we do for PE?

A

ABG’s and D dimers.
CXR, VQ scan and CTPA (CT pulmonary angiogram).
echo, angiography and ECG.

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4
Q

What is the time frame for doing a VQ scan in PE?

What is a con of the test?

A

Within 48 hours of event.

It is poor at discriminating between PE and background lung disease

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5
Q

What is a CTPA? How is it done and what are the disadvantages?

A

CT pulmonary angiogram.
Inject IV contrast and get to hold breath.
It is poor for peripheral lesions.

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6
Q

What are we looking for in an echo for PE?

A

Right sided heart strain and pressures.

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7
Q

What are the objectives of PE treatment?

A

Prevent death.
Prevent post thrombotic syndrome.
Prevent recurrent venous thromboembolism.
Minimise side effects and inconvenience.

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8
Q

What is the recommended treatment for a massive PE?

A

Thrombolysis or surgery.

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9
Q

What is the recommended treatment for a minor PE with RV dysfunction?

A

Anticoagulants and thrombolysis.

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10
Q

What is the recommended treatment for a major PE without RV dysfunction?

A

Anticoagulants.

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11
Q

What is the recommended treatment for a minor PE?

A

Anticoagulants.

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12
Q

What anticoagulants do we give for PE?

A

LMWH and warfarin.
Initial treatment with LMWH.
Induction period with LMWH of 5 days is associated with a lower rate of recurrent PE.
Stop heparin when INT is greater than 2.
Optimal range of warfarin therapy is still to be established. Should continue for at least 3 months.

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13
Q

What thrombolytic therapy do we use for PE?

A

TPA.

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14
Q

What are the effects of TPA on PE?

A

Accelerates resolution but has no effect on the extent of resolution. No effect on frequency of recurrence and may reduce subsequent pulmonary HT.

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15
Q

What are the indications for an IVC filter?

A

Recurrent PE despite anti coagulation.
PE When anti coagulation cannot be used
High risk thrombolysis of DVT e.g. Plegmasia dolens.

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16
Q

What surgery do they do for PE?

A

Endartectomy for chronic thromboembolic pulmonary hypertension.
Pulmonary embolectomy.

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17
Q

What vitamin K antagonists do we use for PE?

A

Warfarin and phenindone

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18
Q

What are new oral anti thrombin agents we can use for PE?

A

Dabigatran and anti XA e.g. Apixaban and rivaroxaban.

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19
Q

What is UFH?

A

Unfractioned heparin.

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20
Q

What are two heparin analogues?

A

Hirudins and danaparoid.

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21
Q

What are the mechanisms of action of anticoagulants?

A

Prevent clot formation and extension.

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22
Q

What are the mechanisms of action of anti platelet drugs?

A

Interfere with platelet activity.

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23
Q

What are the mechanisms of action of thrombolytic agents?

A

Dissolve existing thrombi.

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24
Q

What are the indications for warfarin?

A

Post MI, recurrent MI, stroke or systemic embolisation.
Prevention and treatment of cardiac embolism.
Prophylaxis and/or treatment of:
Venous thrombosis and its extension.
Pulmonary embolism.
Thrombolytic complications associated with AF and cardiac valve replacement.

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25
Q

How do we calculate INR?

A

Patients PT in seconds divided by mean normal PT in seconds.

Multiply this answer by the international sensitivity index.

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26
Q

What are contradictions to warfarin therapy?

A

Pregnancy.
Risk of haemorrhage greater than benefit of treatment.
Uncontrolled alcohol/drug abuse.
Unsupervised dementia/psychosis.

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27
Q

What patient education should we give about anticoagulation?

A

Teach safety, discuss regular INR, counsel on other medications, alcohol and diet. Discover strategies for improving compliance.

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28
Q

How does heparin work?

A

Heparin binds to thrombin inactivating it - inefficiently.
Also activates anti thrombin which in turn inactivates thrombin efficiently.
Also inactivates factors XA, iXa and XIa.

29
Q

How do we monitor heparin?

A

Activated partial thromboplastin time. APTT.

30
Q

What does UFH do?

A

Large molecule, cross links thrombin with antithrombin.
Thrombin inhibition 4 fold compared to action on factor Xa.

It is unpredictable and must be monitored.

31
Q

How does LMWH work?

A

Small molecule, no cross links.
Thrombin inhibition 1 to 1 with action on Xa

Predictable by weight and doesn’t need monitoring.

32
Q

How do we dose LMWH? What is this effective in?

A

Once daily subcut.
Effective in DVT.
Treatment of PE effective and safe.

33
Q

Compare LMWH and UFH?

A

LM has less osteopenia and HIT then UFH.

Outpatient treatment safe and effective.

34
Q

What increases the risk of bleeding with anticoag therapy?

A

Aged over 65 years, past GI bleeding, MI, anaemia, renal failure and DM.

35
Q

What are potential indicators for indefinite anticoag therapy?

A 
Inherited thrombophilia.
Antiphospholipid syndrome.
Recurrent idiopathic VTE.
Malignancy.
Thrombolembolic pulmonary hypertension.
36
Q

What do we need to monitor when we give factor Xa inhibitors?

A

FXa.

37
Q

What do we need to monitor when we give anti-thrombin drugs?

A

APTT.

38
Q

What is the reversibility of dabigatran?

A

Elimination half life 12-17 hours.

Drug cessation usually sufficient.

39
Q

What do we use if we must reverse dabigatran?

A

Recombinant factor VIIa.
FFP
Dialysis

All remove 60% within 3 hours.

40
Q

What is the reversibility of FXa inhibitors?

A

Drug cessation usually sufficient.

Elimination half life 5-9 hours.

41
Q

What do we do if we must reverse FXa inhibitors?

A

Prothrombin complex concentrate. Reliably and completely reverses FXa.

42
Q

What are the classifications of acute PE (thrombo)? What do they present with?

A

Massive - shock or syncope.
Major with right ventricular dysfunction.
Major with normal right ventricular function.
Minor.

43
Q

What is an embolus?

A

Detached intra vascular mass carried to a site in the body distant from its origin.

44
Q

What two important things can PE’s cause?

A

Sudden death and pulmonary hypertension.

45
Q

What type of emboli are most common?

A

Thromboemboli.

46
Q

What is the most common source of pulmonary emboli?

A

DVTs of lower limb.

47
Q

What are the three parts of virchows triad?

A

Stasis, vessel wall damage and hypercoagulability.

48
Q

What are two typical patient populations that suffer from hypercoagulability?

A

MI and cancer patients.

49
Q

What are the risk factors for PE?

A 
Thrombophilia
Family history
Contraceptive pill and HRT
Pregnancy
Pelvic obstruction
Trauma
Surgery
Immobility
Malignancy
MI
Pulmonary hypertension and vasculitis.
50
Q

What are the most and least likely lower limb DVTs to embolise?

A

Most likely are proximal e.g. Ileofemoral. Least likely are distal e.g. Popliteal.

51
Q

What factor does the clinical presentation of PE depend on?

A

The size of the emboli.

52
Q

How does a large PE present?

A

Cardiovascular shock.
Low BP
Central cyanosis
Sudden death

53
Q

How do medium size PEs present?

A

Pleuritic pain, hameoptysis and breathlessness.

54
Q

How do small recurrent PE’s present?

A

Progressive dyspnoea, pulmonary hypertension and right sided heart failure.

55
Q

What will we see in ABG results for PE?

A

PaO2 decreased and decreased sats.

E.g. Type 1 respiratory failure PaCO2 normal or low.

56
Q

What can we expect to see in a CXR for PE?

A

Can be normal early on before infarction.

After infarction we can see basal actelectasis, consolidation and pleural effusion.

57
Q

Why do we do an echo for PE?

A

To measure the pulmonary artery pressure and look for hypertrophy.

58
Q

What will we see on a VQ scan before and after infarction?

A

Before infarction there will be a perfusion defect.

After there will be a perfusion Dan ventilation matched defect.

59
Q

If we cannot find an obvious cause for PE what should we think about?

A

Underlying cancers.

60
Q

How can we prevent DVT?

A 
Early mobilisation after surgeries.
TED stockings.
Calf muscle exercises.
Subcut low dose molecular heparin.
Dabigatran.
61
Q

What will we see on a VQ scan for recurrent PEs?

A

Multiple filling defects which are mismatched to ventilation.

62
Q

What might we see on an angiogram for massive PE?

A

Occluded right main pulmonary artery and filling defect in the left pulmonary artery.

63
Q

What should we expect to see on an ECG for PE?

A

Signs of acute right heart strain e.g. Inverted T waves in V1-3.

64
Q

Does aspirin have a role in the treatment of PE? Why?

A

No as it is an anti platelet drug.

65
Q

What kind of half lives do both warfarin and LMWH have?

A

Long.

66
Q

If we over anticoagulate someone how do we treat them?

A

Address underlying cause.
Maybe cover with FFP or other blood factors.
Reverse anticoags.

67
Q

How do we reverse warfarin?

A

With vitamin K1.

68
Q

How do we reverse heparin?

A

Protamine.

69
Q

What is HIT?

A

Heparin induced thrombocytopaenia

1st Year Medicine (64 decks)

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