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2a > Coagulation, DVT, PE > Flashcards

Coagulation, DVT, PE Flashcards

1
Q

What is a pulmonary embolism?

A

PE blockage of an artery in the lungs by a substance arising from elsewhere, usually a venous thrombosis.

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2
Q

What are risk factors for pulmonary embolism?

A

Same as for DVT - age, recent surgery, thrombophilia, leg fracture, bed rest, malignancy, pregnancy, previous PE, oral contraceptive pill/ HRT; genetics [Lecture 10.1.18]

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3
Q

How are venous thrombi and arterial thrombi different?

A

Venous thrombosis is low-pressure, fibrin-rich and causes PE

Arterial thrombosis is high-pressure, platelet-rich and causes MI.

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4
Q

Why is proximal thrombosis more dangerous than distal thrombosis?

A

There is only one vein below the knee but 6 above the knee. Once they extend above the knee, they can cause PE. lecture 10.1.18

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5
Q

What is a compression test?

A

Can be done on knee, thigh or groin, and tests whether it can be compressed.

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6
Q

What does the D dimer test show?

A

It is an exclusion test - normal D dimer excludes thrombosis. D dimer is broken-down cross-linked fibrin, produced when there are clots. ALSO abnormal if pregnant, inflammation, malignancy, recent surgery.

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7
Q

What is INR?

A

International normalised ratio - a measurement of prothrombin time.

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8
Q

Describe the management of DVT and PE.

A

Distinguish cause - provoked thrombosis? Remove provoking factor. Spontaneous? Recurrence more likely, longer treatment.
LMW heparin
DOACs
Compression stocking for surgical patients

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9
Q

How can DVT and PE be prevented in hospital inpatients?

A

Once daily low dose LMW heparin SC injection - much less than for treatment
Early mobilisation
Elevate leg

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10
Q

What is a massive PE?

A

Blocks left and right pulmonary arteries. Cause of sudden death, often mistaken for an MI as cause of death in hospital.

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11
Q

What are the symptoms of PE?

A

Dyspnoea, pleuritic chest pain

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12
Q

What are the signs of PE?

A

Tachycardia, tachypnoea, pleural rub.

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13
Q

What investigation should you do for a suspected PE and why?

A

Excluding other causes:
D Dimer - normal excludes
ECG to exclude ACS. May see sinus tachycardia
CT pulmonary angiogram - spiral CT to visualise thrombi.
Blood gases show T1 resp failure.

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14
Q

What is thrombosis?

A

Blood coagulation inside an intact vessel of a living being.

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15
Q

How does warfarin work?

A

Prevents synthesis of active factors 2, 7, 9 and 10, and is an antagonist of vitamin K.

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16
Q

What are platelets?

A

Biconcave, anucleate cells formed by fragmentation of megakaryocyte cytosplasm in bone marrow. (lecture 19.1.18)

17
Q

What percentage of the blood is plasma?

A

55%

18
Q

What percentage of the blood are red blood cells?

A

44%

19
Q

What percentage of the blood are WBCs and platelets?

A

1% (pts)

20
Q

What is the lifespan of an RBC?

A

120 days (pts)

21
Q

What is eryptosis and where does it occur?

A

Old RBCs are phagocytosed by splenic macrophages in the spleen, liver and bone marrow.

22
Q

What is the coagulation cascade?

A

Helps to strengthen the platelet plug, resulting in fibrin formation.

23
Q

What does thrombin do?

A
  1. converts fibrinogen to fibrin, a major component of blood clots
  2. activates factor 3 to factor 3a
  3. causes positive feedback so more thrombin is produced.
24
Q

What is the fibrinolytic system?

A

A mechanism to prevent blood clots from growing and becoming symptomatic by converting plasminogen to plasmin which then cuts fibrin into fragments.

25
Q

What type of patients may be over-anticoagulated and why?

A

Patients on vitamin K antagonists such as warfarin or DOACs such as apixiban. They may be non-compliant, have artificial valves, orexperience adverse drug interactions.
(PTS)

26
Q

What are symptoms of overcoagulation?

A

Bruising, bleeding, epistaxis, haematemesis, haemoptysis

27
Q

What are signs of overcoagulation?

A

Haematemesis, haemoptysis, melena (upper GI bleeding causing black faeces)

28
Q

What is DIC?

A

Disseminated intravascular coagulation: A rare but serious disease where blood clots form throughout the body blocking small vessels. (google) There is fibrin generation within blood vessels and consumption of coagulation factors and platelets, causing secondary activation of fibrinolysis. There will be initial thrombosis, followed by bleeding tendency. (pts)

29
Q

What is the lifespan of a platelet?

A

7-10 days

30
Q

How is platelet production controlled?

A

Thrombopoietin (TPO), produced in the liver, stimulates platelet production from megakaryocytes.. It binds to MK receptors to stimulate platelet production. When there are lots of platelets, there less free TPO to bind to MKs, so platelet production decreases.
*?

31
Q

Give 3 differential diagnoses of chest pain.

A 
MI
Cancer - mesothelioma = pleuritic pain
Asthma
COPD
GORD
32
Q

What is the main complication of PE and DVT?

A

Pulmonary infarction leading to death

2a (75 decks)

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