Thrombosis, Embolism, Infarction and Ischaemia Flashcards

1
Q

What is Virchow’s Triad?

A

3 categories of factors which contribute to formation of thrombosis:
- Vessel wall (Trauma/surgery, atherosclerosis)
- Blood flow (AF, varicose veins),
- Blood composition (changes in malignancy, pregnancy, oestrogen therapy, sepsis)

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2
Q

What is the histopathology of arterial and venous thrombus?

A

Arterial - Many platelets and only small amounts of fibrin (white)
Venous - Many fibrin with trapped red cells (red)

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3
Q

What are the differential diagnosis of a sore leg?

A

Trauma - Freactures, dislocations, muscle strain/rupture
MSK - Arthritis (Osteo, rhumatoid, septic), gout and psudogout, bakers cyst, tenosynovitis, bursitis, myopathies.
Skin/soft tissue infections
Vascular - Venous occlusion (DVT,) arterial occlusion (PAD, cardiac thromboemboli) or lymphoedema.

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4
Q

What are the causes of bilateral leg oedema?

A

Usual systemic oedema caused by heart failure, cirrhosis, nephrotic syndrome, malnutrition or immobility

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5
Q

What are the risks for a DVT

A

Vessel wall - Increasing age, varicose veins or surgery.
Blood flow - Obesity, pregnancy, immobilisation, IV catheters.
Composition of blood - Thrombophilia’s, inflammatory conditions, oestrogen hormones

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6
Q

How is the diagnosis of DVT made?

A
  • Clinical history and examination,
  • Blood tests (D-dimer - not very specific)
  • Image venous system of legs using compression ultrasound (Doppler)
  • Well’s score
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7
Q

What are some of the potential outcomes following a DVT?

A
  • Painful, swollen leg,
  • PE,
  • Recurrent VTE,
  • Venous insufficiency,
  • Post thombotic syndrome which can lead to ulceration
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8
Q

What are some of the potential outcomes following a PE?

A
  • Dyspnoea, chest pain, haemoptysis,
  • Collapse,
  • Death,
  • Recurrent VTE,
  • Chronic thomoembolic pulmonary hypertension
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9
Q

What is the treatment of a DVT

A
  • Prevent thrombus extending or embolising via anticoagulant therapy (Heparin, warfarin or DOAC)
  • Remove risk factors (eg oestrogen)
  • Pain relief
  • Graduated elastic compression stockings
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10
Q

Explain the formation of an atheroma

A
  • Damage in endothelium (due to hypertension, smoking, hyperglycaemia) causes LDL deposition (inflammation) in the tunica intimat. Monocytes migrate into the tunica intima and become macrophages and phagocytose the oxidised LDL. This causes them to become foam cells. Foam cells die locally and produce apoptotic bodies. Atheroma develops
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11
Q

What are the risk factors for atherosclerotic disease?

A

Smoking, hypertension, hyperlipidaemia, diabetes, obesity, family history

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12
Q

What is the treatment of acute coronary syndrome?

A
  • Prevent thrombus extension (Anti-platelet and anticoagulant)
  • Remove thrombus (thrombolysis via alteplase or PCI)
  • Widney the stenotic plaque (balloon angioplasty or insertion of stent)
  • Prevent further thrombus (antiplatelet and statin)
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13
Q

What are the complications following an MI

A
  • Death,
  • Arrhythmia,
  • Pericarditis,
  • Myocardial rupture,
  • Mitral valve prolapse,
  • Left ventricular aneurysm +/- thrombus
  • Heart failure
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14
Q

What are some differentials for limb weakness

A

MSK - Myopathy and arthropathy.
Neuro - Peripheral neuropathy, spinal lesion, cerebral lesion

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15
Q

What is the treatment for stroke in AF?

A
  • Remove thrombus (rare) via thrombolysis or carotid end-arterectomy.
  • Treat AF with anticoagulant, rate or rhythm control and replace any defective heart valve.
  • Treat hypertension/hypercholesterolaemia
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