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MD2002 Arvin > Thrombosis, Embolism, and Infarction > Flashcards

Thrombosis, Embolism, and Infarction Flashcards

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

Is thrombosis a pathological or physiological process ?

A

Pathological

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3
Q

What is Virchow’s Triad ?

A

The three components which contribute to thrombosis.

  1. Endothelial Injury
  2. Abnormal blood flow
  3. Hypercoagulability
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4
Q

Endothelial injury is important in the formation of thrombi where ?

A

In arteries and the heart

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5
Q

What are examples of endothelial injuries which can lead to thrombosis ?

A
  • Ulcerated plaques in advanced atherosclerosis
  • Injured endocardium during cardiac surgery or in myocarditis
  • Myocardial infection in left ventricle
  • Valves with inflammatory valve disease, and prosthetic valves
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6
Q

What are potential bases for endothelial injury ?

A
  • Radiation injury
  • Chemical agents: exogenous (e.g. cigarette smoking) and endogenous (e.g. high cholesterol in blood)
  • 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 platelet activation, which is the sum of three important reactions:

1) Adhesion
2) Secretion (release reaction)
3) Aggregation

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8
Q

Describe the sequence of events following endothelial injury.

A
  1. Vasoconstriction due to release of endothelin
  2. Primary Hemostasis: Platelets adhere to exposed collagen, platelets change shape (brick-like), platelets release granules, granules recruit more platelets, platelets aggregate (cycle repeats)
  3. Secondary Hemostasis: Tissue factor released by endothelial cells, phospholipid complex is expressed, thombin is activated, fibrin is polymerised (from fibrinogen, thanks to thrombin)
  4. Thrombus and Antithrombotic Events: Release of t-PA (for fibrinolysis) and thrombomodulin (blocks coagulation cascade) from endothelial cells.
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9
Q

What are the names of some of the granules released from the platelets ?

A

ADP
Thomboxane A2 (TXA2)
Platelet Factor 4 (Pf4)

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10
Q

What factors must be present for the platelets to be able to adhere to collagen ?

A

Von Willebrand’s factor and Gplb (Glycoprotein lb) complex

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11
Q

What are examples of alterations in normal blood flow ?

A

Turbulence

Stasis

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12
Q

Which kind of thrombi is each of turbulence and stasis responsible for ?

A

Turbulence- contributes to the development of arterial and cardiac thrombi

Stasis- contributes to the development of venous thrombi

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13
Q

How does alteration of normal blood flow lead to thrombosis ?

A

Disrupt laminar flow –> Prevent the dilution of coagulation factors –> Retard the inflow of inhibitors of clotting factors –> Promote endothelial cell activation

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14
Q

What are the main features of primary hypercoagulability ?

A
  • Genetic
  • Mutation in the factor V gene = Leiden mutation »
  • Results in Antithrombin III, Protein C and S deficiency
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15
Q

What are the main features of secondary hypercoagulability ?

A
  • Acquired
  • High Risk factors include bed rest (immobilisation). Myocardial Infarction, Tissue damage, CA, prosthetic valves, DIC (Disseminated intravascular coagulation )
  • Lower risk factors include Atrial Fibrillation, cardiomyopathy, nephrotic syndrome, oral contraceptive, sickle cell anaemia, smoking
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16
Q

What are the main kinds of thrombi, morphology-wise ?

A
  • Mural thrombi
  • Arterial thrombi
  • Venous thrombosis (phlebothrombosis)
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17
Q

What is a mural thrombus ? Where does it occur ?

A
  • Thrombus applied to one wall of underlying structure

- Occurs in the capacious lumina of the heart chambers and aorta

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18
Q

What are the main features of arterial thrombi ?

Where do they frequently occur ?

A
  • Usually occlusive
  • May be mural
  • Grey-white and friable
  • By decreasing frequency, Coronary, Cerebral, and Femoral
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19
Q

What are the main histological features of thrombi ?

A

Lines of Zahn (‘alternating pale pink bands of platelets with fibrin and red bands of RBC’)

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20
Q

What are the main features of Venous thrombi ?

Where do they frequently occur ?

A
  • Invariably occlusive
  • Dark red

-Mainly affect the veins of the lower extremities (90%), including deep calf, femoral, popliteal, iliac veins

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21
Q

What is Thrombophlebitis ?

A

“Inflammatory process that causes a blood clot to form and block one or more veins”

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22
Q

What are the possible fates of the thrombus ?

A
  1. Resolution
  2. Embolisation to lungs
  3. Organised and incorporated into wall
  4. Organised and recanalised (channels through thrombus)
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23
Q

What are clinical correlations of arterial thrombi ?

A
  • Loss of Pulses distal to the thrombus
  • Area becomes cold, pale, painful, paraesthesia
  • Eventually tissue dies + gangrene results
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24
Q

What are clinical correlations of veinous thrombi (superficial and deep) ?

A

SUPERFICIAL:
• Congestion, swelling, pain, tenderness (
• Rarely embolise

DEEP:
• Foot and ankle oedema
• Homans’ sign (=”discomfort behind the knee on forced dorsiflexion of the foot”)
• Possibly asymptomatic and only recognised when embolised

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25
Q

What is possible treatment for thrombosis ?

A
  • Stockings (prevention)
  • Anticoagulant drugs: aim to prevent clot growing larger + prevent or stop an embolism. Two main forms of anticoagulant drugs: heparin and warfarin
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26
Q

How are heparin and warfarin administered respectively ?

A

Heparin: IV or SC
Warfarin: Orally

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27
Q

What is an embolism ?

A

A detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

28
Q

What proportion of embolisms occur in thrombi (thromboembolisms) ?

A

99%

29
Q

Give examples of things other than thrombi from which a fragment can detach resulting in an embolism.

A 
– Bone or bone marrow
– Atheromatous debris
– Droplets of fat
– Bits of tumour
– Foreign bodies (such as bullets) 
– Bubbles of air or nitrogen
30
Q

What are the main classifications of embolisms ?

A
  • Pulmonary embolism
  • Systemic embolism
  • Amniotic fluid embolism
  • Air embolism
  • Fat embolism
31
Q

What is the proportion of pulmonary emboli which arise in thrombi within the large deep veins of the lower leg ?

A

95%

32
Q

What is the assumed origin in the occlusion of a large or medium-sized pulmonary artery, until proven otherwise ?

A

Embolic origin

33
Q

Where may pulmonary emboli lodge ?

A

In the main pulmonary artery or at the bifurcation as a saddle embolus

34
Q

What is the name for a pulmonary embolus which has lodged at a bifurcation ?

A

Saddle embolus

35
Q

What are the main pathophysiologic consequences of emboli ?
Clinically, what is the worst case consequence in a large PE ?
Clinically, what is the worst case consequence in a small PE ?

A

In general:
– Respiratory compromise
– Haemodynamic compromise

LARGE PE:
Instantaneous death, possible through Pulseless Electrical Activity

SMALL PE:
Acute respiratory and cardiac problems, including:
- Chest pain, dyspnoea, shock, increased LDH, haemoptysis.

36
Q

What are some clinical techniques used to detect an embolism ?

A
  1. Chest X-ray: discloses a pulmonary infarct as a wedge-shaped infiltrate.
  2. Pulmonary Lung Scanning with Radionuclides (inject one, inhale the other and scan, match between scans of the two should be identical. if not, suspect pulmonary embolism)
  3. Spiral CT (shows intraluminal filling defect = embolus)
  4. ECG: detects strain on heart (caused by embolism)
37
Q

What is a systematic embolism ?

A

Emboli that travel through the arterial circulation.

38
Q

What proportion of systematic embolisms arise from thrombi within the heart ?

A

80-85%

39
Q

Less common (than the heart) sources of systematic embolisms include thrombi developing in relation to ?

A

– Ulcerated atherosclerotic plaque
– Aortic aneurysms
– Infective endocarditis
– valvular or aortic prostheses

40
Q

True or false: Arterial emboli almost always cause infarction ?

A

True

41
Q

What are major sites of lodgement of all systemic emboli ? State the percentage for each site.

A

– Lower extremities (70-75%)
– The brain (10%)
– Viscera (mesenteric, renal, splenic) (10%)
– Upper limbs (7-8%)

42
Q

What is an air embolism ?

A

The presence of bubbles of air or gas within the circulation obstructing vascular flow and damaging tissues.

43
Q

What is the name for damage caused by air embolisms ?

A

Barotrauma

44
Q

What is the pathophysiology of air embolisms (i.e. how can they arise) ?

A

– Delivery or abortion
– The performance of pneumothorax
– Injury to the lung or the chest wall
– Caisson disease or decompression sickness

45
Q

What is Caisson disease ? What is the difference in the name between its acute, and chronic forms ?

A
  • Affects scuba divers/workers engaged in underwater tunnelling
  • If the individual decompresses too rapidly, helium and nitrogen tend to persist to form gaseous emboli within blood vessels and tissues.
  • Acute form = the bends or the chokes
  • Chronic form = Caisson disease
46
Q

What is the treatment for Caisson disease ?

A

Recompression chamber

47
Q

What is a fat embolism ?

A

Minute globules of fat blocking the circulation

48
Q

How may fat embolisms arise ?

A

May occur following:
– Fractures of the shafts of long bones
– And rarely, with soft tissue trauma and burns

49
Q

What percentage of individuals with severe skeletal injury manifest clinical signs known as fat embolism syndrome ?

A

1%

50
Q

What are the main consequences (pathogenesis) of fat embolism syndrome ?

A
  1. Mechanical obstruction
    – microagregates of neutral fat cause occlusion
  2. Chemical injury
    – free fatty acids released from fat globules result in
    toxic injury to the vascular endothelium
51
Q

How may one determine the presence of fat globules ?

A

Through special techniques using frozen sections and fat stains.

52
Q

What are the clinical characteristics of fat emboli ?

A

– Pulmonary insufficiency (including tachypnoea, dyspnoea)
– Tachycardia
– Neurologic symptoms (including irritability and restlessness which progress to delirium and coma)
– Anaemia and thrombocytopenia

53
Q

When is the onset of the clinical symptoms of fat emboli ?

A

The symptoms appear after latent 24-72h period, sudden onset of tachypnoea, dyspnoea and tachycardia

54
Q

What proportion of amniotic fluid emboli is fatal ?

A

86%

55
Q

What is the cause of amniotic fluid emboli ?

A

The cause is the infusion of amniotic fluid into the maternal circulation.

56
Q

True or False: Amniotic fluid emboli are a rare complication of labour and one of cause of maternal mortality.

A

True

57
Q

What does the victim’s pulmonary microcirculation contain at post- mortem examination ?

A

Epithelial squames from foetal skin, lanugo hair, fat from vernix caseosa, mucin from foetal respiratory or GI tract.

58
Q

What is the clinical presentation of an amniotic fluid embolism ?

A

– Profound respiratory difficulty
• With deep cyanosis and cardiovascular shock
– Followed by convulsions and
– Profound coma

59
Q

What is an infarct ?

A

Area of ischaemic necrosis caused by occlusion of arterial supply or venous drainage in a particular tissue.

60
Q

What is necrosis ?

A

Refers to a spectrum of morphological changes that follow cell death in living tissue, largely resulting from the progressive action of enzymes on the lethally injured cells.

61
Q

What are the causes of 99% of infarcts ? What are other possible causes of infarcts ?

A

Thrombi and embolisms

  • Vasospasm
  • Expansion of atheroma
  • Compression of a vessel
  • Twisting of the vessels
  • Traumatic rupture
62
Q

What are factors that influence the development of an infarct ?

A

1) Nature of the vascular supply
• Liver, hand, intestines = dual blood supply
• Kidneys and spleen = single

2) Rate of development of occlusion
• E.g. Heart v quickly

3) Vulnerability to hypoxia
• Neurons 3-4min, Myocardial cells 20-30min, Fibroblasts many hours

4) Oxygen content of blood
• Anaemic or cyanotic patients

63
Q

What are the main types of infarcts ? State the main features of each.

A

1) Red (haemorrhagic):
• Venous occlusions
• In loose tissues
• In tissues with dual circulation

2) White (anaemic):
• Arterial occlusions
• Solid organs

3) Septic or bland

64
Q

What are some specific examples of haemorrhagic infarcts ? Describe the main features of each, including morphology.

A

OVARIAN Infarcts

  • Venous occlusion
  • Dark blue

LUNG Infarct

  • In loose tissue
  • Wedge-shaped
  • Red

SMALL INTESTINE Infarct

  • Dual circulation
  • Red
65
Q

What are some specific examples of anaemic infarcts ? Describe the main features of each, including morphology.

A

SPLEEN Infarct
– Wedge-shaped
– White

KIDNEY Infarct
– Wedge-shaped
– White
– Rim of hyperemia

66
Q

Histologically, what are the next steps following an infarction ? What is the time frame of each step ?

A
  1. Ischaemic coagulative necrosis (min - days) (Liquefactive necrosis in the CNS)
  2. Inflammatory response (hours - 7 days)
  3. Reparative response (1 - 2 weeks)
  4. Scaring (2 weeks - 2 months)

MD2002 Arvin (110 decks)

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