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Semester 2 disease > Thrombosis, Embolism and Infarction > Flashcards

Thrombosis, Embolism and Infarction Flashcards

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1
Q

What is a thrombus?

A

A solidification of blood contents that forms within the vascular system during life

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2
Q

What is Thrombosis?

A

A pathological process that denotes the formation of a thrombus within the noninterupted vascular system

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3
Q

What is Virchow’s triad?

A
  • Endothelial injury
  • Abnormal blood flow
  • Hypercoagulative injury
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4
Q

Describe the endothelial injury part of Virchow’s triad

A

• Important in the formation of the thrombi in the heart and arteries

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5
Q

Give examples of where thrombi are developed

A
  • Left ventricle at sites of myocardial infarction
  • On ulcerated plaques in advanced atherosclerosis
  • Injured endocardium (cardiac surgery, myocarditis)
  • Valves with inflammatory valve disease and prosthetic valves
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6
Q

What are the potential bases of endothelial injury?

A
  • Radiation
  • Chemical agents:exposure and endogenous
  • Bacterial toxins or endotoxins
  • Immunologic injuries
  • Neoplastic involvement
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7
Q

What is the role of platelets in thrombosis?

A

After injury to a vessel, platelets undergo 3 reactions: (known as platelet activation)
• Adhesion
• Secretion
• Aggregation

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8
Q

What is the Pathogenesis of thrombosis?

A
  1. Vasoconstriction (constrict to protect exposed part)
  2. Platelets adhere to exposed collagen
  3. Platelets change shape and release granules: ADP, TXA2 and will recruit more platelets
  4. Platelets attach to each other via fibrinogen and to the endothelium
  5. Fibrin
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9
Q

What are the 2 types of alteration in normal blood flow and what kind of thrombus do they lead to?

A
  • Turbulence which contributes to the development of arterial and cardiac thrombi
  • Stasis which contributes to venous thrombosis
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10
Q

What are the effects of turbulence and stasis?

A
  • Disrupts laminar flow
  • Prevents the dilution of coagulation factor
  • Retard the infow of inhibitors of clotting factors
  • Promote endothelial cell activation
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11
Q

What are the types of hyper coagulability?

A
  • Primary (genetic)

* Secondary (acquired)

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12
Q

What is hyper coagulability?

A

An alteration of the blood coagulation mechanism that in someway predisposes thrombosis

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13
Q

Describe primary (genetic) hyper coagulability

A
  • Mutation in the factor V gene (Leiden mutation)
  • Antithrombin III deficiency
  • Protein C and S deficiency
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14
Q

Describe secondary (acquired) hyper coagulability

A
  • High risk: bed rest (immobilisation, Myocardial Infarction, Tissue damage, CA prosthetic valves, DIC)
  • Lower risk: AF, cardiomyopathy, nephrotic syndrome, oral contraceptive, sickle cell anaemia, smoking
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15
Q

Mural thrombi

A

In heart or aorta

• Applied to one wall of underlying structure , occur in the capacious lumina of the heart chambers and the aorta

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16
Q

Arterial thrombi

A 
• Usually occlusive
• May be mural
• Frequent in:
- Coronary 
- Cerebral 
- Femoral 
• Grey- white and friable
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17
Q

Describe the histological appearance of a thrombus

A
  • Lines of Zahn
  • white lines of fibrin and platelets
  • Red band of red blood cells
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18
Q

Venous thrombosis

A

• Invariably occlusive and dark red
• Affect the veins of the lower extremities (90%)
- deep calf, femoral, popliteal, iliac veins

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19
Q

What is Thrombophlebitis?

A

Inflammed and thrombosed vein

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20
Q

What are the outcomes for a Thrombus?

A
  • Resolution
  • Emboblization to the lungs
  • Organised and recanalized and then organised into the wall
  • Propagation to the heart
  • Complete occlusion
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21
Q

What are the clinical features of Arterial Thrombosis?

A
  • lord of pulse distal to the thrombus
  • Area becomes Perishing cold, Pale, Painful, Paraesthesia
  • Eventually tissue dies and gangrene results
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22
Q

What are the types of Venous Thrombosis?

A

• Superficial (Saphenous system)
- congestion, swelling, pain, tenderness (rarely embolise)
• Deep
- Foot and ankle oedema, Homans’ sign
- Could be asymptomatic and recognised only when they have embolised

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23
Q

What are Homans’ sign

Study These Flashcards
A

Calf pain at the dorsiflexion of the foot

24
Q

What are the treatments for thrombosis?

Study These Flashcards
A
  • Stockings (prevention)

* Anticoagulant drugs- prevent clot growing and prevent/stop an embolism

25
What are the two main forms of anticoagulant drugs?
* Heparin | * Warfarin
26
What is an embolism?
Detached intravascular solid, liquid or gases mass that is carried by the blood to a site distant from its point of origin
27
Where do the majority of emboli arise?
In thrombi
28
What are the classifications
* Pulmonary embolism * Systemic embolism * Amniotic fluid embolism * Air embolism * Fat embolism
29
Pulmonary embolism
* Occlusion of a large or medium sized pulmonary artery is embolic in origin until proved otherwise * More than 95% arise in thrombi within the large deep veins of the lower leg
30
What are the 2 main pathophysiologic consequences of a pulmonary embolism?
* Respiratory compromise | * Haemodynamic compromise
31
What are eh symptoms/causes of a smaller pulmonary emboli?
``` Acute respiratory and cardiac problems: • Chest pain • Dyspnoea • Shock • Increased LDH • Haemoptysis ```
32
How can pulmonary thrombi be detected?
* Chest X ray may disclose a pulmonary infant as a wedge shaped infiltrate * Pulmonary lung scanning using radionuclides * Occlusion puts some strain on the heart which is evident on the ECG * P/Q scan * Spiral CT
33
What is a systemic embolism?
* Emboli that travel through the arterial circulation | * Mainly arise from thrombi within the heart
34
What are the less common sources of systemic embolism?
* Ulcerated atherosclerotic plaque * Aortic aneurysms * Infective endocarditis * Valvular or aortic prostheses
35
What do systemic embolisms almost always cause?
Infarction
36
Where are the major sites of lodgement of systemic emboli?
* Lower extremities (70-75%) * The brain (10%) * Viscera (10%) * Upper limbs (7-8%)
37
What is an air embolism?
The presence of bubbles of air or gas within the circulation obstruct vascular flow and damage tissues just as thrombotic masses • Barotrauma
38
What is the pathophysiology of an air embolism?
* Delivery or abortion * The performance of the pneumothorax * Injury to the lung or the chest wall * Caisson disease or decompression sickness
39
Who would be likely to get Caisson disease?
• Scuba and deep sea divers • Workers engaged in underwater tunnelling (If the individual decompresses too rapidly)
40
What is the treatment for an air embolism?
Recompression chamber
41
What injuries can be followed by a fat embolism?
* Fractures of the shafts of long bones | * Rarely, soft tissue trauma and burns
42
What is the pathogenesis of a fat embolism?
* Mechanical obstruction: microagregates of neutral fat case occlusion * Chemical injury- Free fatty acids released from fat globules result in toxic injury to the vascular endothelium
43
Clinically, what are fat embolisms characterised by?
* Pulmonary insufficiency * Neurologic symptoms ( Irritability and restlessness which progress to delirium and coma) * Anaemia and thrombocytopenia
44
What is an amniotic fluid embolism?
* Rare complication of labour | * Caused by the infusion of amniotic fluid into the lateral circulation
45
What is the morphology of an amniotic fluid embolism?
``` • Pulmonary microcirculation contains: - Epithelial squames from foetal skin - Lanugo hair - Fat from vernix caseosa • Mucin from foetal respiratory or GI tract ```
46
What is the clinical presentation of an amniotic fluid embolism?
• Profound respiratory difficulty - deep cyanosis and cardiovascular shock • Followed by convulsions • Profound coma
47
What is an infarct?
An area of ischaemic necrosis caused by an occlusion of arterial supply or venous drainage in a particular tissue
48
What are the causes of infarcts?
``` 99%: • Thrombosis • Embolism other: • Vasospasm • Expansion of atheroma • Compression of a vessel • Twisting of the vessels • Traumatic rupture ```
49
What are the factors that influence the development of an Infarct?
* Nature of the vascular supply * Rate of the development of occlusion * Vulnerability to hypoxia * Oxygen content of blood
50
What are the types of infarct?
``` • Red (Haemorrhagic) - Venous occlusions - In loose tissues - In tissues with dual circulation (Liver, hand, intestines) • White (anaemic) - arterial occlusions - solid organs • Septic or bland ```
51
Haemorrhagic Ovarian infarct morphology
* Venous occlusion | * Dark blue and haemorrhage
52
Haemorrhagic Lung infarct morphology
* In loose tissue * Wedge shaped * Red and Haemorrhagic
53
Haemorrhagic Small intestine infarct
* Dual circulation | * Red and Haemorrhagic
54
Anaemic spleen infarct
* Wedge shaped | * White
55
Anaemic kidney infarct
* Wedge shaped * White * Rim of hyperaemia
56
Describe the timeline of the histology of an infarction
* Mins-days: Ischaemic coagulative necrosis (liquefactive necrosis in the CNS) * Hours- 7 days: Inflammatory response * 1-2 weeks: Reparative response * 2 weeks- 2 months: Scaring

Semester 2 disease (2 decks)

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