Thrombosis, ischaemia, embolism and infarction Flashcards

1
Q

What is the definition of thrombosis?

A

A condition in which the blood changes from a liquid to a solid within the CV system and produces a mass of coagulated blood

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2
Q

What is the role of von Willebrand factor in primary haemostasis?

A

Binds to other proteins (particularly factor VIII)
- acts as a carrier, improving the half life
Acts as a bridging molecule for normal platelet adhesion
Promotes platelet aggregation

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3
Q

What is Virchow’s triad?

A

Describes three broad categories of factors that are thought to contribute to thrombosis

  • hypercoagulability
  • haemodynamic changes
  • endothelial injury/dysfunction
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4
Q

What is the difference between arterial and venous thrombosis?

A

Arterial
- ‘white thrombus’
- many platelets with small amounts of fibrin due to high flow
Venous
- ‘red thrombus’
- many fibrin with trapped red cells due to indolent flow

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5
Q

What are the differential diagnoses for a sore leg?

A

Trauma
- fractures, disolcations, muscle strain
Non-traumatic
- MSK causes, oesto, rheumatoid or septic arthritis, gout, Baker’s cyst, bursitis
Skin/soft tissue infections
- cellulitis, erysipelas, abscesses, necrotising fasciitis
Vascular causes
- venous occlusion (DVT, superficial vein thrombosis, venous insufficiency)
- acute ischaemia (cardia thromboembolism, PAD)
- lymphoedema
Bilateral swelling
- systemic oedema (Heart failure, cirrhosos, nephrotic syndrome)

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6
Q

Where is a DVT most likely to occur?

A

The leg

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7
Q

Are you more likely to get a deep vein thrombosis or a superficial vein thrombosis?

A

DVTs make up 2/3rds of all venous thrombosis

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8
Q

What are the risk factors for DVT?

A

Vessel wall
- increasing age, varicose veins, surgery
Blood flow
- obesity, pregnancy, immobilisation, IV catheters, external vein compression
Composition of the blood
- thrombophilias (including family history). inflammatory conditions, oestrogen hormones

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9
Q

How is a DVT diagnosed?

A

Clinical decision
- determination of likelihood (risk factors)
Blood tests
- fibrin D-dimer, a measure of dissolved thrombus
Imaging
- compression ultrasound, venography

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10
Q

Describe the components of the Wells clinical scoring system.

A

All worth one mark
Active cancer
Paralysis or recent plaster immobilisation of lower extremities
Recently bed ridden, or recent surgery (12 weeks)
Entire leg swollen
Calf swollen 3cm or more than the other leg
Pitting oedema
Collateral superficial veins
Previous DVT
Alternative diagnosis more likely than DVT (-2)

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11
Q

What score on the Wells clinical scoring system suggest DVT/PE?

A

2 or more

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12
Q

What are the possible outcomes following a DVT?

A
Painful swollen leg
Pulmonary embolism
- 50% of cases
Recurrent VTE
- 20-30% at 10 years
Venous insufficiency 
- 40-60% have residual thrombus on US at 6-12 months
Post thrombotic syndrome
- 25% at 2 years
- increased risk if DVT is recurrent
- compression stockings reduce risk
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13
Q

What are the possible outcomes following a PE?

A
Dyspnoea, chest pain, haemoptysis
Collapse
Death
- 90% diagnosed PM
- 0.6% risk after DVT
Recurrent VTE
Chronic thromboembolic pulmonary hypertension
- risk increases if PE is recurrent
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14
Q

How is a DVT treated?

A
Prevent thrombus extending or embolising 
- anticoagulant for 3-6 months 
    - heparin (LMWH)
    - warfarin
    - direct oral anti-coagulant (direct Xa or IIa inhibitor) 
Remove risk factors 
Pain relief
Gradual elastic compression stockings
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15
Q

How are VTEs prevented?

A

Avoid risk factors
Risk assess at hospital admission or surgery
Provide thrombo-prophylaxis when appropriate
- anti-embolism stockings
- heparin (LMWH daily sub cut)
Educate patients on risk and avoidance measures
- early mobilisation

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16
Q

List some possible causes of chest pain?

A
MSK
- rib fracture, muscular, chondritis 
Cardiac
- angina, MI
Lung
- pleuritic pain (infection, infraction or malignancy)
Vascular
- PE, aortic dissection 
Oesophageal 
- GORD, hiatus hernia
17
Q

Briefly describe the pathophysiology of coronary artery disease.

A

Atheromatous aterio-vascular disease
Development of atheroma/plaques
Progressive narrowing and stenosis of artery
- plaque rupture
- acute thombus (vascular occlusion, downstream ischaemia and infarction)

18
Q

What is the difference between atheroma and a fibrous plaque?

A

Atheroma is thickening of the wall due to lipid accumualtion
Fibrous palque is due to smooth muscle and collage accumulation within the vascular wall

19
Q

Name the 4 coronary arteries.

A

Right coronary artery
Left anterior descending coronary artery
Circumflex artery
Left main coronary artery

20
Q

What are the risk factors for CV disease?

A
Smoking 
Hypertension
Hyperlipidaemia 
Diabetes
Obesity 
Family history
21
Q

How is an MI or ACS diagnosed?

A
Suggestive history
Clinical evidence of cardiac dysfunction
ECG findings 
Biochemical evidence of myocardial damage (ischaemia)
- elevated troponin
Visualisation of coronary arteries 
- cardiac catheterisation
22
Q

During a STEMI or an NSTEMI, what are the ECG changes?

A
STEMI
- ST elevation
NSTEMI 
- ST depression
- T wave inversion
23
Q

How is ACS treated?

A
Prevent thrombus extension 
- anti-platelet agent (clopidogrel, aspirin)
- anticoagulant (heparin)
Remove the thrombus 
- thrombolysis (alteplase, tenecteplase)
- remove clot via PCI
Widen the stenotic plaque 
- balloon angioplasty, insert coronary artery stent 
Prevent further thrombus
- anti-platelet agent
- statin
24
Q

Describe the histology of a heart that has had a myocardial infarction within the last 12-72 hours.

A

Swelling of mitochondria and endoplasmic reticulum
Relaxation of myofibrils
Infiltration of neutrophils
Progressive coagulative necrosis of mycoyctes
- loss of nuclei

25
Q

Describe the histology of a heart that has had a myocardial infarction within the last 3-7 days.

A

Dead myocytes begin to disintegrate
- removed by macrophages and enzyme proteolysis
Proliferation of fibroblasts with formation of granulation tissue
- replaces necrotic tissue

26
Q

Describe the histology of a heart that has had a myocardial infarction within the last 6 weeks.

A

Healing is complete by fibrosis

  • contraction band necrosis
  • characterised by hypereosinphilic transverse bands of precipitated myofibrils in dead myocytes
27
Q

What are the possible complications following an MI?

A
Death
Arrythmia
Pericarditis 
Myocardial rupture 
Mitral valve prolapse
Left ventricular aneurysm
- with or without thrombus
Heart failure
28
Q

Name some possible causes of limb weakness.

A
MSK
- myopathy
- arthropathy 
Neurological
- peripheral neuropathy 
- spinal lesion
- cerebral lesion (ischemia, inflammation, malignancy)
29
Q

What are the two types of atrial fibrillation?

A

Non-valvular AF

Valvular AF

30
Q

How are strokes/AF treated?

A
Removal of the thrombus
- thrombolysis
- carotid end-arterectomy 
Remove/correct the source of the thrombus 
- anticoagulation (warfarin or DOAC)
- revert to sinus rhythm (cardioversion)
- replace defective heart valve
Address other CVD risk factors
- HBP
- hyperlipidaemia