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Respiratory > Thrombosis, Embolism and Pulmonary Hypertension > Flashcards

Thrombosis, Embolism and Pulmonary Hypertension Flashcards

1
Q

What is the difference between a thrombus and a clot?

A

Thrombus- inside vessel

Clot- outside vessel

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2
Q

Where is thrombosis favoured according to Virchow’s triad?

A

Stasis (turbulent blood flow), endothelial injury and hypercoagulability

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3
Q

What can cause a hypercoagulable state?

A

Malignancy, pregnancy, hormone replacement, bowel disease, sepsis

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4
Q

What can cause endothelial injury?

A

Venous disorders, valve damage, trauma, surgery, catheters

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5
Q

What can cause stasis?

A

LV dysfunction, immobility, venous insufficiency/obstruction, pregnancy, obesity

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6
Q

What two things must happen for a thrombus to form?

A

Platelet activation and fibrin production

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7
Q

What does activating platelets do?

A

Makes them stickier so they aggregate more platelets and fibrin

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8
Q

What is the end point of the coagulation cascade?

A

Aggregation of fibrin

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9
Q

What is the first stage of thrombus formation?

A

Endothelial injury which exposes collagen

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10
Q

What happens in the formation of a thrombus after collagen has been exposed?

A

Collagen and Von Willebrand factor bind to glycoproteins on platelets which increases platelet integrins

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11
Q

What do glycoproteins on platelets bind with?

A

Fibrinogen

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12
Q

Describe the intrinsic coagulation pathway?

A

Hageman factor and Kallikrein through factors XII, IX, VIII

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13
Q

What is the extrinsic coagulation pathway?

A

Tissue factor binding with factor VII

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14
Q

What is the common pathway of coagulation?

A

Activated Factor IIa then through X, V, II

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15
Q

What happens after the common pathway of coagulation?

A

Factors II and XIII activate fibrinogen to fibrin

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16
Q

What type of vitamin is vitamin K and where is it stored?

A

Fat soluble in the liver

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17
Q

What does vitamin K produce?

A

Clotting factors II, VII, IX and X

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18
Q

What competes with vitamin K?

A

Warfarin

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19
Q

What is plasmin?

A

Clot buster

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20
Q

What are anti-clotting factors?

A

Protein S, protein C and antithrombin II

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21
Q

What causes inherited disorders of coagulibility?

A

Protein C/S/antithrombin II deficiency or Factor V Leiden

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22
Q

Why are thrombi less common in arteries?

A

High flow blood moves pro-coagulant material away quickly

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23
Q

When is the only occasion that thrombosis occurs in arteries?

A

Atherosclerosis

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24
Q

Why are sites where vessels branch more common?

A

More turbulent blood flow

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25
Q

Where is stasis common?

A

Depp veins, faulty valves and venous insufficiency

26
Q

Where do the biggest PEs tend to come from?

A

Femur

27
Q

Most emboli are thrombi, what else could they be?

A

Gas, fat, foreign bodies, tumour clumps

28
Q

Pulmonary emboli are an important cause of what?

A

Sudden death and pulmonary hypertension

29
Q

Where is the source of most PEs?

A

Deep vein thrombosis

30
Q

What is ischaemia?

A

Insufficient blood flow

31
Q

What is infarction?

A

Tissue death as a result of ischaemia

32
Q

What do large emboli cause?

A

Death, infarction, severe symptoms

33
Q

What do small emboli cause?

A

Pulmonary hypertension but clinically silent

34
Q

What is pulmonary infarction?

A

Compromised blood and oxygen causes lung tissue to die

35
Q

How does a DVT present?

A

Hot, swollen, red, tender calf or whole leg

36
Q

What is the 1st line scan for DVT?

A

Ultrasound Doppler leg scan

37
Q

What is the 2nd line test for DVT?

A

CT of ileo-femoral vein, IVC and pelvis

38
Q

How will a large PE present?

A

CV shock, low BP, central cyanosis, sudden death

39
Q

How will a medium PE present?

A

Pleuritic pain, haemoptysis, breathless

40
Q

How will a small PE present?

A

Progressive dyspnoea, pulmonary hypertension, right sided heart failure

41
Q

What are risk factors for PE?

A

Thrombophilia, contraceptive pill, pregnancy, pelvic obstruction, trauma, surgery, immobility, malignancy, vasculitis, obesity

42
Q

What are clinical features of PE?

A

Tachycardia, tachypnoea, cyanosis, fever, low BP, crackles, rub, pleural effusion

43
Q

What will ABGs for PE show?

A

Low O2- type 1 respiratory failure

44
Q

What will a CXR of PE show?

A

Normal early on, may show a wedge shaped infarct

45
Q

What is the gold standard test for PE?

A

CTPA

46
Q

What is the 2nd line scan for PE which is good in pregnancy?

A

V/Q scan

47
Q

What is a useful rule out test for PE?

A

D-dimers

48
Q

What are some ways a DVT can be prevented?

A

Compression stockings, early post-op mobilisation calf muscle exercise, anticoagulants

49
Q

What are PEs treated with and for how long?

A

Anticoagulation with LMWH or warfarin for 3 months is provoked and longer if not

50
Q

What is the treatment for large life threatening PEs?

A

Thrombolysis

51
Q

What are interactions of thrombolysis?

A

Alcohol, antibiotics, aspirin, NSAIDs, grapefruit

52
Q

What can post-thrombotic syndrome cause?

A

Pain, oedema, hyperpigmentation, eczema, varicose veins, ulceration

53
Q

What is the relative flow/pressure in the pulmonary circulation?

A

High flow, low pressure

54
Q

What is classed as pulmonary hypertension?

A

> 25mmHg

55
Q

What can cause pulmonary venous hypertension?

A

Ischaemia, stenosis, cardiomyopathy

56
Q

What can cause pulmonary arterial hypertension?

A

Hypoxia, multiple PE, vasculitis, drugs, HIV, left to right shunt

57
Q

What is cor pulmonale?

A

Right sided heart failure secondary to lung disease

58
Q

What are signs of cor pulmonale?

A

Central cyanosis, oedema, raised JVP, right ventricular heave

59
Q

What are probably the most important tests for Cor Pulmonale?

A

ECG, CXR, ABGs, echo

60
Q

How is primary pulmonary hypertension diagnosed?

A

By ruling out other causes

61
Q

What is the typical presentation of pulmonary hypertension?

A

SOB on exertion and signs of right sided failure

62
Q

What is treatment for primary pulmonary hypertension?

A

Pulmonary vasodilators and lung transplant

Respiratory (16 decks)

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