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Respiratory > Thomboembolic disease > Flashcards

Thomboembolic disease Flashcards

1
Q

What is a pulmonary emboli

A

Blockage of a pulmonary artery by a blood clot, fat, tumour or air

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2
Q

What is pulmonary infarction

A

If blood flow and oxygen to lungs is compromised, the lung tissue may die

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3
Q

Most likely place for DVT

A

Ileo-femoral, popliteal is most unlikely

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4
Q

Clinical presentation of DVT

A

Whole leg or calf becomes swollen, hot, tender, red

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5
Q

Differential diagnosis of DVT

A

Baker’s cyst - Popliteal synovial rupture
Superficial thrombophlebitis
Calf cellulitis

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6
Q

Investigating DVT

A

Ultrasound doppler leg scan - Not invasive, exclude popliteal cyst and pelvic mass
CT scan

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7
Q

Types of pulmonary emboli and their presentation

A

Large - CV shock, low BP, cyanosis and sudden death
Medium - Pleuritic pain, haemoptysis, dyspnoea
Small - Progressive dyspnoea, pulmonary hypertension, right heart failure

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8
Q

Risk factors for DVT and PE

A

Thrombophilia, contraceptive pills, hormone replacement therapy, pregnancy, pelvic obstruction (uterus, ovary, lymph nodes), trauma, surgery, immobility - bed rest, long flights, pulmonary hypertension, obesity

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9
Q

Presenting complaint about DVT

A

Dyspnoea, pleuritic chest pain, haemoptysis, leg pain/oedema, collapse/sudden death

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10
Q

Investigating PE

A

ECG with acute right heart strain pattern
D-dimers raised - Increased fibrin degradation products indicative of significant blood clot (thrombus) formation and breakdown in the body, doesn’t tell location
Ventilation/Perfusion mismatch - Isotope lung scan

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11
Q

Prevention of DVT

A

Early post-op mobilisation
TED compression stockings
Calf muscle exercise
A subcutaneous low dose of low molecular weight heparin perioperatively - Dalteparin/Fragmin
Novel Oral Anticoagulant (NOAC) medication -
Dabigatran - Direct thrombin inhibitor
Rivaroxaban/Apixaban - Direct inhibitor of activated factor Xa

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12
Q

When should Heparin be stopped for treating PE

A

Oral Warfarin takes 3 days, antagonises vitamin K dependant prothrombin. Continue Warfarin for 3-6 months with INR aim 2.5-3.5
After 3-5 days, stop Heparin when INR > 2. Can use NOAC instead of LMWH.

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13
Q

When is tenecteplase used

A

Large life threatening PE, low BP and severe hypoxaemia. Tenecteplase is an enzyme that helps in thrombolysis - tissue plasminogen activation (tPA)

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14
Q

Duration of treatment for PE

A 
Unprovoked - 6 months
Provoked/temporary risk factor - 3 months
Low risk distal DVT - 3 months
High risk proximal DVT - 6 months
Recurrent DVT - Life long
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15
Q

How can Warfarin be reversed

A

Vitamin K1

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16
Q

How can Heparin be reverese

A

Protamine sulphate

17
Q

Reversal agent for NOAC

A

Non-available

18
Q

Normal mean pulmonary arterial pressure

A

12-20 mmHg

19
Q

How can pulmonary hypertension be measured

A

Right heart catheter

20
Q

What is cor pulmonale

A

Alteration in structure and function of right ventricle caused by a primary disorder of the respiratory system.
Ex: Secondary to COPD

21
Q

Clinical signs of pulmonary hypertension and right heart failure

A

Central cyanosis if hypoxic, dependant oedema, raised JVP with V waves, right ventricular heave at parasternal edge, tricuspid regurgitation murmur, enlarged liver

22
Q

What is dependant oedema

A

Oedema that is influenced by gravity, in an ambulant patient this might be ankles or legs. In bed bound, might be sacral oedema

23
Q

Treatment of pulmonary hypertension

A

Prophylactic Warfarin (anticoagulant)
Oxygen if hypoxic
Primary vasodilators -
Ca2= channel blockers - Oral Nifedipine, Diltiazem

24
Q

What is chronic thromboembolism pulmonary hypertension (CTEPH)

A

Chronic blood clots in the lungs, with mean arterial pressure > 25mmHg

25
Q

Treatment of CTEPH

A

Riociguat - Soluble guanylate cyclase stimulator
Pulmonary endarterectomy - Surgical removal of blood clot
Balloon angioplasty

26
Q

A pattern of disease in pulmonary oedema

A

Restrictive

27
Q

What is acute respiratory distress syndrome (ARDS)

A

Widespread inflammation in the lungs due to sepsis, pneumonia or trauma

28
Q

Pathogenesis of ARDS

A

Injury causes infiltration of inflammatory cells. Cytokines are released causing oxygen free radicles and causing injury to cell membrane

29
Q

Histological feature of ARDS

A

Hyaline membrane - Fibrinous exudate lining alveolar walls

30
Q

Mechanisms of pulmonary hypertension

A

Hypoxia (vascular constriction), increased flow through pulmonary circulation (congenital heart disease), blockage (PE) or loss (emphysema) of pulmonary vascular bed, back pressure from left sided heart failure

31
Q

Common cause of right ventricular hypertrophy

A

Pulmonary hypertension

32
Q

What is plexiform lesion

A

Histopathological hallmark of pulmonary arterial hypertension. Consists of obliterative endothelial cells proliferation and vascular smooth muscle cell hypertrophy

Respiratory (26 decks)

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