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2TRN Human Disease > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

what does the HEALTH of tissues depend on

A

INTACT circulation to deliver oxygen and remove wastes

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2
Q

what structures are involved in normal haemostasis

A
  1. vessel wall
  2. coagulation system
  3. platelet
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3
Q

characteristics of Normal Haemostasis

A
  • Maintains blood in a fluid state in NORMAL VESSELS
  • Rapid formation of a LOCALISED haemostatic plug at site of VASCULAR INJURY
  • Tightly regulated
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4
Q

Primary Haemostasis (first series of events after vascular injury)

A
  1. Transient Vasoconstriction

2. Formation of Platelet Plug

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5
Q

Secondary Haemostasis

A

3.Formation of Fibrin Meshwork –> activates the Clotting System

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6
Q

PRIMARY HAEMOSTASIS: What causes the initial vasoconstriction

A

Neurogenic REFLEX mechanisms

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7
Q

PRIMARY HAEMOSTASIS: What augments the vasoconstriction

A

Locally released ENDOTHELIN

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8
Q

PRIMARY HAEMOSTASIS: Function of exposed Subendothelial ECM

A

Allows platelets to adhere and become activated

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9
Q

PRIMARY HAEMOSTASIS: Activated platelets do…

A

recruit additional platelets to form a HAEMOSTATIC PLUG

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10
Q

SECONDARY HAEMOSTASIS:

What substance is released at injury site and responsible for activation of Clotting Cascade?

A

Tissue Factor. Activates Clotting Cascade in conjunction w secreted PLATELET FACTORS

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11
Q

SECONDARY HAEMOSTASIS:

Clotting Cascade ultimate goals.

A
  1. Activation of THROMBIN

2. Conversion of FIBRINOGEN to FIBRIN

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12
Q

List of substances involved in Control of Haemostasis

A
  1. tPA (Tissue Plasminogen Activator)
  2. Antithrombin III
  3. Protein C, Protein S and THROMBOMODULIN
  4. Tissue Factor Pathway inhibitor
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13
Q

Role of tPA (Tissue Plasminogen Activator)

A
  1. Converts PLASMINOGEN into Plasmin

2. This degrades fibrin strands (Fibrinolysis)

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14
Q

Role of Antithrombin III

A

Binds & INactivates Thrombin and Other Clotting Factors

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15
Q

Role of Protein C, Protein S and THROMBOMODULIN

A
  1. Binding of Thrombin to Thrombomodulin activates protein C
  2. Protein S augments activity of Protein C
  3. Jointly they INACTIVATE Clotting Factors
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16
Q

Definitions of Thrombosis

A

a. Blood clot* formation in UNINJURED vessels
b. Thrombotic OCCLUSION of vessel following minor injury
* aka Thrombus

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17
Q

Define Virchow’s Triad

A

The predisposing factors to Thrombosis

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18
Q

List Virchow’s Triad

Predisposing Factors for Thrombosis

A
  1. Endothelial injury
  2. Stasis OR Turbulent flow
  3. Hypercoagulability
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19
Q

What properties does normal endothelium have

A

Both:

  • Antithrombotic properties
  • Prothrombotic properties
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20
Q

effect of endothelial damage

A

shifts balance in favour of thrombosis (prothrombotic properties)

21
Q

Normal blood flow is

A

Laminar (platelets do not come in contact w endothelium). Turbulence and Stasis causes these to come in contact –> activate Clotting System

22
Q

define Hypercoagulability

A

alteration in the Coagulation Pathways predisposing to Thrombosis. Can be Primary (genetic) or Secondary (acquired)

23
Q

Primary Hypercoagulable States

A
  1. Mutation Factor V Leiden
  2. Antithrombin III deficiency
  3. Prothrombin gene mutation
  4. Protein C deficiency
  5. Protein S deficiency
  6. Others
24
Q

Secondary Hypercoagulable States (Acquired) - High Risk Acquired Factors for Thrombosis

A
  1. Prolonged bed rest OR immobilization
  2. Myocardial infarction
  3. Atrial fibrillation
  4. Prosthetic cardiac valves
  5. Tissue damage (surgery, fracture, burns)
  6. Cancer
25
Q

Lower risk acquired factors for thrombosis

A
  1. Oral contraceptives
  2. Hyperestrogenic states (eg. pregnancy)
  3. Cardiomyopathy
  4. Smoking
  5. Sickle Cell Anaemia
26
Q

Define Vegetations

A

Thrombi occurring on heart VALVES

usually in cases of infective endocarditis/rheumatic carditis

27
Q

Define Mural Thrombi

A

Thrombi occurring in heart CHAMBERS OR aortic LUMEN

28
Q

Fate of the thrombi: a combination of the following 4 events can happen…

A
  1. Propagation - thrombi accumulate platelets + fibrin causing vessel obstruction
  2. Embolisation - thrombi are transported elsewhere in the vasculature
  3. Dissolution - thrombi removed by fibrinolytic activity
  4. Organization and Recanalization
29
Q

Explain 4.Organization and Recanalization

A
  • thrombi induce inflammation AND fibrosis (organization)
  • they can recanalize OR
  • they can be incorporated into a thickened vessel wall
30
Q

Possible complications of Venous Thrombi

A
  • can cause congestion
  • oedema
  • can embolize lungs and cause death if massive
31
Q

Possible complications of Arterial Thrombi

A
  • can embolize and cause Tissue Infarction

- can cause vascular obstruction at CRITICAL sites (cerebral vessels; coronary)

32
Q

Risks of Deep Venous Thrombosis AT/ABOVE KNEE LEVEL

A
  • they can embolize to the lung
  • asymptomatic in 50% cases
  • may cause local PAIN and OEDEMA
33
Q

Which organs are prime targets for embolism and why

A
  1. Brain
  2. Kidneys
  3. Spleen
    * due to large volume of blood flow
34
Q

Embolus

A
  • a DETACHED intravascular solid
  • liquid or gaseous mass
  • carried by the blood
  • to a site DISTANT from its origin
35
Q

Common and uncommon emboli?

A
  • 95% Thromboemboli
  • Rare: large fat droplets, bubbles of air, nitrogen, atherosclerotic debris, tumor fragments, bits of bone marrow, foreign bodies
36
Q

action of emboli

A

lodge in vessels

results in partial OR complete vascular obstruction –> ischaemic necrosis (infarction)

37
Q

what determines whether an embolus will lodge in the Pulmonary or Systemic Circulation

A

its site of origin

38
Q

Causative agent for Pulmonary Thromboembolism

A

95% - Deep Vein Thrombosis originating ABOVE KNEE LEVEL

39
Q

Pathway travelled

A

depends on size;

  • pass through right side of heart
  • enter pulmonary vasculature
  • may obstruct MAIN PULMONARY VEIN
  • may obstruct SMALLER ARTERIOLES
  • may impact across the BIFURCATION
40
Q

Consequences of Pulmonary Thromboembolism

A

-sudden death
-right ventricular failure
-cardiovascular collapse
medium sized vessel obstruction –> PULMONARY HAEMORRHAGE

41
Q

What do multiple small emboli in the lung cause

A

Pulmonary Hypertension

42
Q

Most frequent cause for SYSTEMIC (Arteriolar) Thromboembolism

A

Intracardiac Mural Thrombi (80%)

Remainder: thrombi on atherosclerotic plaques, fragmentation of valvular vegetations etc.

43
Q

Major sites for Arteriolar Thromboembolism

A

-Lower Extremities (75%)
-The Brain (10%)
Intestines, kidneys and spleen affected to a lesser extent.

44
Q

Consequence of Arteriolar Embolisation

A

Infarction of affected tissues

45
Q

Fat Embolism

A

usually after bone trauma (fractures; orthopaedic operations)

46
Q

Air Embolism

A

after instrumentation of neck veins, obstetric procedures or as a consequence of chest wall injury. Also after sudden changes in atmospheric pressure (decompression sickness)

47
Q

Decompression Sickness

A

Gases dissolve in blood at high pressure

  • come out as bubbles during rapid decompression
  • affects muscles, lungs, brain and heart
48
Q

Amniotic Fluid Embolism

A

A complication of labour and the immediate postpartum period

49
Q

Other types of emboli

A

Septic (infective endocarditis)
Tumour
Foreign material
Cholesterol emboli

2TRN Human Disease (4 decks)

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