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Medicine Year 1 - Semester 2 - Part 1 > Thrombosis, Embolism and Infarction > Flashcards

Thrombosis, Embolism and Infarction Flashcards

1
Q

What is thrombosis ?

A

A pathological process.

It denotes the formation of a thrombus within the non-interrupted vascular system.

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2
Q

What is a thrombus ?

A

A thrombus is a solidification of blood contents that forms within the vascular system DURING LIFE.

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3
Q

Pathogenesis of thrombosis

A

Endothelial injury
Alterations in normal blood flow
Hypercoagulability

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4
Q

Give examples of where thrombus develops

A

Left ventricle (at sites of MI)

On ulcerated plaques in advanced atherosclerosis

Injured endocardium (cardiac surgery)

Valves with inflammatory valve disease, and prosthetic valves.

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5
Q

State some causes of endothelial injuries

A

Radiation injury

Chemical agents (exogenous and endogenous)

Bacterial toxins or endotoxins

Immunological injuries

Neoplastic involvement

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6
Q

State the role of platelets in thrombosis

A

After injury to a vessel, platelets undergo 3 important reactions :

  • Adhesion
  • Secretion
  • Aggregation
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7
Q

Describe primary haemostasis

A
  1. Platelet adhesion
  2. Shape change
  3. Granule release
  4. Recruitment
  5. Aggregation
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8
Q

Problem with : von Willebrands factor

A

Causes von willebrands disease

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9
Q

Problem with : GpIb

A

Causes Bernard-Soulier Syndrome

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10
Q

Problem with : GpIIb-IIIa

A

Causes Glanzmann’s Thrombasthenia

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11
Q

Describe secondary haemostasis

A
  1. Tissue Factor
  2. Phospholipid Complex Expression
  3. Thrombin Activation
  4. Fibrin Polymerisation
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12
Q
A
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13
Q

State alterations in blood flow

A

Turbulence

Stasis

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14
Q

Turbulence

A

Contributes to development of arterial and cardiac thrombi

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15
Q

Stasis

A

Contributes to venous thrombosis

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16
Q

What do turbulence and stasis do ?

A

Disrupt laminar flow

Prevent the distribution of coagulation factors

Retard the inflow of inhibitors of clotting factors

Promotes endothelial cell activation

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17
Q

What is hyper-coagulability ?

A

Can be defined as an alteration of the blood coagulation mechanism that in some ways predisposes thrombosis.

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18
Q

Causes of Hyper-coagulability

A

Primary (genetic)
Secondary (acquired)

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19
Q

Describe primary cause of hyper-coagulability

A

Mutation in factor V gene
Anti-thrombin III deficiency
Protein C and S deficiency

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20
Q

Describe the secondary cause of hyper-coagulability

A

2 risk groups

High risk
Low risk

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21
Q

High risk for hyper-coagulability

A

Bed rest (immobilisation)
MI
Tissue damage
Carcinoma
Prosthetic valves
DIC

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22
Q

Low risk for hyper-coagulability

A

AF
Cardiomyopathy
Nephrotic Syndrome
Oral Contraceptive
Sickle cell anaemia
Smoking

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23
Q

Phlebothrombosis

A

Venous thrombosis

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24
Q

Mural Thrombi

A

Solidification of blood contents occurring in the chambers of the heart/aorta

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25
Q

Arterial thrombi

A

Usually occlusive
May be mural

Frequent in arteries

Grey, white and friable

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26
Q

State the common places for arterial thrombi
(most common last)

A

Coronary
Cerebral
Femoral

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27
Q

Describe the histological appearance of thrombus

A
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28
Q

Venous thrombosis

A

Invariably occlusive and dark

Affects the veins of the lower extremities (90%)

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29
Q

State where venous thrombi form

A

Deep calf
Femoral
Popliteal
Iliac veins

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30
Q

State the fates of the thrombus

5 Fates

A
  1. Resolution
  2. Embolisation to lungs
  3. Organised and incorporated into wall
  4. Organised and recanalised
  5. Propagation towards heart
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31
Q

Clinical correlations of thrombi

A

Cause obstruction of arteries and veins

Provide possible sources of emboli

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32
Q

5 P’s of Arterial Thrombosis

A

Area becomes :

  • Perishing cold
  • Pale
  • Painful
  • Paraesthesia
  • Pulse loss (distal to thrombus)
33
Q

What happens due to arterial thrombosis ?

A

Eventually tissue dues and gangrene results

34
Q

Symptoms of superficial venous thrombosis

A

Congestion
Swelling
Pain
Tenderness (rarely embolism)

35
Q

Symptoms of deep venous thrombosis

A

Foot and ankle oedema
Homan’s sign

36
Q

Hofman’s sign

A

Discomfort in the calf muscles on forced dorsiflexion of the foot with the knee straight.

37
Q

Treatment for thrombosis

A

Stockings (prevention)

Anticoagulant drugs

38
Q

Function of anticoagulant drugs

A

Prevent the clot form growing any larger and to prevent/stop an embolism

39
Q

State the 2 main forms of anticoagulant drugs

A

Heparin
Warfarin (oral)

40
Q

What is an embolus ?

A

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

41
Q

Thromboembolism

A

99% of all emboli arise in thrombi

42
Q

What do rare forms of emboli include ?

A

Fragments of :

  • Bone/marrow
  • Atheromatous debris
  • Fat droplets
  • Bits of tumour
  • Foreign bodies
  • Bubbles of air or nitrogen
43
Q

Pulmonary embolism

A

Occlusion of a large/medium sized pulmonary artery

> 95% arise in thrombi within large deep veins of lower leg

44
Q

Saddle embolism

A

Rare type of acute pulmonary embolism (PE) that can lead to sudden hemodynamic collapse and death

45
Q

Lines of Zahn

A

Thick bands formed by nested platelets wrapped in fibrin.

CHARACTERISTIC of thrombus

46
Q

Large PE

(pulmonary embolism)

A

Virtually instantaneous death

Pulsless Electrical Activity

47
Q

Smaller PE

(pulmonary embolism)

A

Acute respiratory and cardiac problems

48
Q

How to detect pulmonary embolism ?

A

Pulmonary Lung Scanning (using RADIO-NUCLEOTIDES)

ECG - occlusion puts strain on heart

Chest X-ray : wedge shaped infiltrate

SPIRAL CT

49
Q

Systemic embolism

A

Emboli that travel through the arterial circulation

80-85% arise from thrombi within the heart

50
Q

State the major sites of lodgement of systemic embolisms

A

Lower extremities (70-75%)

The brain (10%)

Viscera (10%)

Upper limbs (7-8%)

51
Q

Air embolism

A

Presence of bubbles of air or gas within circulation.

This obstructs vascular flow and damages tissues.

52
Q

Barotrauma

A

Air embolism

53
Q

Causes of air embolism

A

Delivery/abortion
Performance of pneumothorax
Injury to the lung or chest wall

Caisson disease or compression sickness

54
Q

Who does Caisson disease affect ?

A

Scuba and deep sea divers
Workers engaged in underwater tunnelling

(if individual decompresses too rapidly, then helium and nitrogen tend to persist to form gaseous emboli)

55
Q

Acute form of air embolism

A

The bends/ the chokes

56
Q

Chronic form of air embolism

A

Caisson disease

57
Q

Treatment of air embolism

A

Recompression chamber

58
Q

Fat embolism

A

Minute globules of fat can be demonstrated in circulation following :

  • Fractures of shafts of long bone
  • Soft tissue trauma and burns
59
Q

Fat embolism syndrome

A

1% of individuals with severe skeletal injury

60
Q

Pathogenesis of fat embolism

A

Mechanical obstruction
Chemical injury

61
Q

Fat embolism histology

A

Rounded holes appearing in vascular spaces

62
Q

Characteristics of fat embolism

A

Pulmonary insufficiency
Neurological symptoms
Anaemia and Thrombocytopenia

63
Q

Onset of symptoms of fat embolism

A

24-72 hour period
- tachypnea
- dyspnea
- tachycardia

  • irritability
  • restlessness
64
Q

Amniotic fluid embolism

A

Rare complication of labour
Maternal mortality (86%)

Infusion of amniotic fluid into maternal circulation

65
Q

Pulmonary microcirculation contents

A

Epithelial squames from foetal skin

66
Q

Presentation of amniotic fluid embolism

A

Respiratory difficulty
Convulsions
Profound coma

67
Q

Infarction

A

Area of ischaemic necrosis caused by occlusion of blood supply

68
Q

Main causes infarcts

A

Thrombosis
Embolism

69
Q

Other causes of infarcts

A

Twisting of vessels
Vasospams
Traumatic rupture

70
Q

Factors that influence the development of infarct

A

Nature of vascular supply
Rate of development of occlusion
Vulnerability to hypoxia
Oxygen content of blood

71
Q

State the 3 types of infarct

A

Red
White
Septic

72
Q

Red infarct

A

Haemorrhage
- venous occlusions
- in loose tissues
- in tissues with dual circulation

73
Q

White infarct

A

Anaemic
- arterial occlusions
- solid organs

74
Q

State dual supply

A

Liver
Hand
Intestines

75
Q

State single supply

A

Kidneys
Spleen

76
Q

Time of Ischaemic coagulative necrosis

A

Minutes to Days

77
Q

Time of inflammatory response

A

Hours to 7 days

78
Q

Time of restorative response

A

1-2 Weeks

79
Q

Time of scarring

A

2 weeks to 2 months

Medicine Year 1 - Semester 2 - Part 1 (51 decks)

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