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

Thrombosis, Embolism and Infarction Flashcards

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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
Arterial thrombi
Usually occlusive May be mural Frequent in arteries Grey, white and friable
26
State the common places for arterial thrombi (most common last)
Coronary Cerebral Femoral
27
Describe the histological appearance of thrombus
28
Venous thrombosis
Invariably occlusive and dark Affects the veins of the lower extremities (90%)
29
State where venous thrombi form
Deep calf Femoral Popliteal Iliac veins
30
State the fates of the thrombus | 5 Fates
1. Resolution 2. Embolisation to lungs 3. Organised and incorporated into wall 4. Organised and recanalised 5. Propagation towards heart
31
Clinical correlations of thrombi
Cause obstruction of arteries and veins Provide possible sources of emboli
32
5 P's of Arterial Thrombosis
Area becomes : - Perishing cold - Pale - Painful - Paraesthesia - Pulse loss (distal to thrombus)
33
What happens due to arterial thrombosis ?
Eventually tissue dues and gangrene results
34
Symptoms of superficial venous thrombosis
Congestion Swelling Pain Tenderness (rarely embolism)
35
Symptoms of deep venous thrombosis
Foot and ankle oedema Homan's sign
36
Hofman's sign
Discomfort in the calf muscles on forced dorsiflexion of the foot with the knee straight.
37
Treatment for thrombosis
Stockings (prevention) Anticoagulant drugs
38
Function of anticoagulant drugs
Prevent the clot form growing any larger and to prevent/stop an embolism
39
State the 2 main forms of anticoagulant drugs
Heparin Warfarin (oral)
40
What is an embolus ?
A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a distant site from its point of origin.
41
Thromboembolism
99% of all emboli arise in thrombi
42
What do rare forms of emboli include ?
Fragments of : - Bone/marrow - Atheromatous debris - Fat droplets - Bits of tumour - Foreign bodies - Bubbles of air or nitrogen
43
Pulmonary embolism
Occlusion of a large/medium sized pulmonary artery >95% arise in thrombi within large deep veins of lower leg
44
Saddle embolism
Rare type of acute pulmonary embolism (PE) that can lead to sudden hemodynamic collapse and death
45
Lines of Zahn
Thick bands formed by nested platelets wrapped in fibrin. CHARACTERISTIC of thrombus
46
Large PE (pulmonary embolism)
Virtually instantaneous death Pulsless Electrical Activity
47
Smaller PE (pulmonary embolism)
Acute respiratory and cardiac problems
48
How to detect pulmonary embolism ?
Pulmonary Lung Scanning (using RADIO-NUCLEOTIDES) ECG - occlusion puts strain on heart Chest X-ray : wedge shaped infiltrate SPIRAL CT
49
Systemic embolism
Emboli that travel through the arterial circulation 80-85% arise from thrombi within the heart
50
State the major sites of lodgement of systemic embolisms
Lower extremities (70-75%) The brain (10%) Viscera (10%) Upper limbs (7-8%)
51
Air embolism
Presence of bubbles of air or gas within circulation. This obstructs vascular flow and damages tissues.
52
Barotrauma
Air embolism
53
Causes of air embolism
Delivery/abortion Performance of pneumothorax Injury to the lung or chest wall Caisson disease or compression sickness
54
Who does Caisson disease affect ?
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
Acute form of air embolism
The bends/ the chokes
56
Chronic form of air embolism
Caisson disease
57
Treatment of air embolism
Recompression chamber
58
Fat embolism
Minute globules of fat can be demonstrated in circulation following : - Fractures of shafts of long bone - Soft tissue trauma and burns
59
Fat embolism syndrome
1% of individuals with severe skeletal injury
60
Pathogenesis of fat embolism
Mechanical obstruction Chemical injury
61
Fat embolism histology
Rounded holes appearing in vascular spaces
62
Characteristics of fat embolism
Pulmonary insufficiency Neurological symptoms Anaemia and Thrombocytopenia
63
Onset of symptoms of fat embolism
24-72 hour period - tachypnea - dyspnea - tachycardia - irritability - restlessness
64
Amniotic fluid embolism
Rare complication of labour Maternal mortality (86%) Infusion of amniotic fluid into maternal circulation
65
Pulmonary microcirculation contents
Epithelial squames from foetal skin
66
Presentation of amniotic fluid embolism
Respiratory difficulty Convulsions Profound coma
67
Infarction
Area of ischaemic necrosis caused by occlusion of blood supply
68
Main causes infarcts
Thrombosis Embolism
69
Other causes of infarcts
Twisting of vessels Vasospams Traumatic rupture
70
Factors that influence the development of infarct
Nature of vascular supply Rate of development of occlusion Vulnerability to hypoxia Oxygen content of blood
71
State the 3 types of infarct
Red White Septic
72
Red infarct
Haemorrhage - venous occlusions - in loose tissues - in tissues with dual circulation
73
White infarct
Anaemic - arterial occlusions - solid organs
74
State dual supply
Liver Hand Intestines
75
State single supply
Kidneys Spleen
76
Time of Ischaemic coagulative necrosis
Minutes to Days
77
Time of inflammatory response
Hours to 7 days
78
Time of restorative response
1-2 Weeks
79
Time of scarring
2 weeks to 2 months

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

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