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Pathological Processes > Session 5 Haemostasis, Thrombosis And Embolism > Flashcards

Session 5 Haemostasis, Thrombosis And Embolism Flashcards

1
Q

What is haemostasis?

A

Consequence of tightly regulated process that maintain blood in fluid state in normal vessels but permit rapid formation of haemostatic clot at site of vascular injury

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2
Q

What is thrombosis?

A

Blood clot formation in intact vessel

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3
Q

What are 3 components of haemostasis?

A

Vascular wall
Platelets
Coagulation cascade

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4
Q

What are the 3 layers of vessel wall?

A

Tunica intima = endothelium
Tunica media = smooth muscle
Tunica adventitia = fibroblasts + collagen

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5
Q

What are platelets?

A

Disc shaped, anucleate cell fragments

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6
Q

What is a normal life span of platelets?

A

7-10 days

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7
Q

What are the 3 steps when a vessel is injured?

A

Adhesion
Secretion
Aggregation

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8
Q

What happens during secretion stage?

A

Platelets secrete alpha granules and dense granules

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9
Q

What are 4 examples of what alpha granules contain?

A

Fibrinogen
Factors V and VIII
Platelets factor 4
PDGF

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10
Q

What are 4 examples of what dense granules contain?

A

ADP
ATP
Ionized calcium
Histamine

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11
Q

What happens during platelet aggregation?

A

Platelets cross link to form platelet plug and provide stability

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12
Q

What is the role of thrombin?

A

Binds to a protease-activated receptor on platelet membrane and with ADP to cause further platelet aggregation

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13
Q

What are 3 steps of haemostasis?

A
  1. Severed artery contracts, not enough to stop bleeding but can decrease pressure downstream
  2. Primary haemostatic plug of activated platelets forms on injured vessel and connective tissue - fragile but may control bleeding
  3. Secondary haemostatic plug forms as fibrin filaments stabilize friable platelet plug into blood clot
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14
Q

What are the 4 things that can activate platelets?

A

Collagen surfaces
ADP
Thromboxane A2
Thrombin

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15
Q

What are 4 processes that occur after platelet activation?

A

Stick to exposed subendothelium to von Willebrand factor
Aggregate with other platelets - form primary and secondary plug
Swell and change shape into sticky spiny spheres
Secrete factors from granules that help platelet plug grow and clot

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16
Q

What does aspirin do?

A

Irreversibly inactivated cyclooxygenase which is responsible for pducfion of thromboxane A2, so decreases platelet aggregation

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17
Q

What is the endpoint of the clotting cascade?

A

Formation of fibrin

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18
Q

What does thrombin do?

A

Enzyme that cleaves circulating plasma protein fibrinogen into fibrin

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19
Q

What are thrombin activated by?

A

Clotting factors I to XIII

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20
Q

What does some factors and anticoagulants require to synthesize?

A

Vitamin K

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21
Q

What do the clotting factors do?

A

Activate next pro enzyme on line and amplify effect using co-factors

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22
Q

What are the 2 pathways to clotting?

A

Intrinsic and extrinsic

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23
Q

What is the intrinsic pathway to clotting?

A

Involves factors that are contained within blood, triggered by a negatively charged surface and no vessel needs to be broken upon for it to occur

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24
Q

What is the extrinsic pathway to clotting?

A

Needs tissue factor present outside of blood - thromboplastin which is released from damaged cells adjacent to area of haemorrhage

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25
What are 3 factors that oppose clot formation?
Tissue factor pathway inhibitor Thrombin Antithrombin III
26
How does tissue factor pathway inhibitor oppose clot formation?
Acts in the initiation phase of clotting, secreted mainly by endothelial cells, binds to tissue factor-factor VIIa complexes and inhibits their ability to generate factor Xa
27
How does thrombin oppose clot formation?
Thrombin binds to an endothelial cell receptor called thrombomodulin, eliminating thrombin’s clot producing effects and causes bound thrombin to bind Protein C and S and then in activates Factors VIIIa and Va
28
How does antithrombin III oppose clot formation?
It is a plasma protein that inactivates thrombin and other clotting factors, activated by heparin on surface of endothelial cells and prevents the spread of a clot by rapidly inactivating clotting factors that are carried away from intermediate site of the clot by flowing blood
29
What happens during fibrinolysis?
Fibrin has a built in short term obsolescence, recognized by macrophages and broken down, then destroyed by plasmid
30
What is the inactive precursor of plasmin?
Plasminogen
31
What are 3 things plasminogen activated by?
Tissue plasminogen activator (tPA) Urokinase Streptokinase
32
How are plasminogen activator used therapeutically?
They can dissolve fibrin so they can dissolve thrombi and thromboemboli
33
Why is tPA more commonly used than streptokinase?
Streptokinase is antigenic, tPA is not and it has higher affinity for fibrinogen
34
What is haemophilia?
Lacking step 3 of haemostasis, have normal platelets but impaired clotting so cannot produce adequate amount of fibrin
35
What is Haemophilia A?
Deficiency of factor VIII
36
What kind of inheritance is Haemophilia A?
X linked recessive
37
What are 3 symptoms of Haemophilia A?
Easy bruising Masssive haemorrhages after trauma and surgery Spontaneous haemorrhages from minor trauma
38
What is APTT?
Activated partial thromboplastin time
39
What does APTT test?
Function of intrinsic pathway
40
What factors could be deficient if APTT is prolonged?
VIII IX XI XII
41
What is PT?
Prothrombin time
42
What does PT test?
Extrinsic pathway
43
What factor could be deficient if PT long?
VII
44
What 4 things could be deficient if both APTT and PT is prolonged?
V X Thrombiin Fibrinogen
45
What is TCT?
Thrombin clotting time
46
What does TCT show?
Conversion of fibrinogen to fibrin via action of thrombin
47
What does anti coagulation test show for Haemophilia A?
Prolonged PTT and normal PT
48
What is Haemophilia B?
Severe factor IX deficiency
49
What kind of inheritance is Haemophilia B?
X linked recessive
50
What are the anti coagulation test for Haemophilia B?
Prolonged PTT | Normal PT
51
How to treat Haemophilia B?
Infusion of recombinant Factor IX
52
What is thrombocytopenia?
Deficiency of platelets in blood
53
What is Von Willebrand disease?
Deficiency of abnormality in von Willebrand factor
54
What are the 2 functions of von Willebrand factor?
Assist in platelet plug formation by attracting circulating platelets to sites of vessel damage Stabilizes factor VIII protecting it from premature destruction
55
What will anti coagulation test show for Von Willebrand disease?
Raised bleeding time and APTT
56
What are 2 symptoms of Von Willebrand’s disease?
Nosebleeds | Excessive bleeding from wounds
57
What is the inheritance of Von Willebrand’s disease?
Autosomal dominant
58
What types of Von Willebrand disease is associated with reduced quantity of circulating vWF?
1 and 3
59
What type of Von Willebrand Disease is associated with qualitative defects in vWF?
Type 2
60
What will anti coagulation tests show for thrombocytopenia?
Prolonged bleeding time but normal PT and APTT
61
What are 3 symptoms of thrombocytopenia?
Spontaneous bleeding from small vessels in skin, GI tract and GU tract
62
What are 4 causes of thrombocytopenia?
Decreased production of platelets Decreased platelet survival Sequestration Dilutional
63
What is disseminated intramuscular coagulation?
Thrombohaemorrhagic disorder occurring as a secondary complication
64
What happens during disseminated intravascular coagulation?
Excessive activation of coagulation leading to formation of microthrombi in micro vasculature of body, causing tissue hypoxia and infarction consuming platelets, fibrin and factors causes haemorrhage and bleeding catastrophe
65
What is a thrombus?
Solid mass formed from constituents of blood within heart or vessels during life
66
What is thrombosis?
Process of formation of thrombus?
67
What is the Virchow’s triad?
Changes in vascular wall - endothelial damage Changes in blood flow - slow or turbulent Changes in blood - hypercoagulability
68
What does it take to cause thrombosis?
2 out of 3 of Virchow’s triad
69
When does endothelial damage occur?
``` Myocardial infarction Secondary to haemodynamic stress of hypertension Scarred heart valves After trauma Inflammation Atherosclerosis ```
70
How does endothelial damage cause thrombosis?
When there is endothelial damage, platelets adhere to exposed von Willebrand factor and when blood flow is slow or during stasis, it doesn’t wash away platelets, chemical mediators and clotting factors, forming thrombus
71
How does slow or turbulent flow cause thrombosis?
Abnormal blood flow gives platelets better chance to stick to endothelium and clotting factors a chance to accumulate
72
Why is thrombosis more frequent in veins?
Slower flow
73
When does slow or turbulent flow occur?
``` Cardiac failure Immobilized patients due to lack of muscular contraction and hence blood stasis Aneurysms Abnormal heart valves Myocardial infarction ```
74
When does hypercoagulability occur?
``` Pregnancy Surgery Smoking Cancer Contraceptives ```
75
What are 4 features of arterial thrombus?
Pale Granular Lower cell count Lines of Zahn
76
What are 4 features of venous thrombus?
Soft Gelatinous Deep red Higher cell content
77
What are 5 outcomes of thrombosis?
``` Lysis Propagate Organize Recanalise Embolise ```
78
What is lysis?
Thrombus breaks down
79
Why does lysis occur?
Fibrinolytic system is active and blood flow is re established
80
What is propagation?
Progressive spread of thrombosis, distally in arteries and proximally in veins
81
What is organization?
Thrombus undergoes fibrous repair and forms fibrous scar on vessel wall
82
What is recanalisation?
One or more channels form through area of organizing thrombus, re establishing blood flow but usually smaller capacity
83
What is embolisation?
Part of thrombus breaks off and embolises
84
What are 4 effects of venous thrombosis on tissue?
Congestion Oedema Ischaemia Infarction
85
What are 2 effects of arterial thrombosis on tissue?
Ischaemia Infarction Depends on where and collateral circulation
86
What is an embolism?
Blockage of a blood vessel by solid, liquid or gas at a site distant from its origin
87
What happens if thrombosis happens in vein and a small part breaks off?
It will go through the right heart and embolise in the pulmonary arteries
88
What is atheroma?
Gruel like necrotic material in atherosclerotic plaques
89
What are transient ischaemic attacks?
Episodes of neurological dysfunction that appear suddenly, last minutes to hours and then disappear
90
What are transient ischaemic attacks caused by?
Microscopic emboli usually atherosclerotic emboli, to the brain
91
What are 2 causes for fat emboli to occur?
Complication of bone fractures | Liposuction
92
What happens during a fat emboli?
Bone fracture injure bone marrow fat cells, releasing oil droplets which coalesce and are sucked into gaping venules which have been torn by fracture
93
What are 2 symptoms of fat embolism?
Respiratory distress | Neurological symptoms
94
How does air embolism occur?
Negative pressure in veins of chest and head during inspiration in the upright position and can draw in air after trauma of neck and chest, which is transported to right heart where bubbles gather as a frothy mass and stops circulation Labor as air enters uterus and forced into open veins during uterine contraction
95
How does diving cause emboli?
As pressure is higher underwater, more gases are dissolved in blood and body tissues, when diver surfaces too quickly, the sudden depressurization results in dissolved gases coming out of solution and releasing into body as bubbles, which distort the tissues ans act as emboli in blood
96
What is amniotic fluid embolism?
Complication of labor and C section when amniotic fluid enters maternal circulation through a tear in amniotic membranes
97
What are 5 symptoms of amniotic fluid embolism?
``` Sudden respiratory distress Hypotension Seizures Loss of consciousness Disseminated intravascular coagulation ```
98
What are 5 ways to prevent and treat thromboembolic disease?
``` General prophylaxis Aspirin Heparin Warfarin Filters ```
99
How does general prophylaxis prevent thromboembolic disease?
Mobilize early after operation Elevate legs Measures to increase venous return
100
How does aspirin treat thromboembolic disease?
Irreversibly inhibits cyclooxygenase which prevents prostaglandin synthesis so platelets cannot produce thromboxane A2 so platelets cannot aggregate
101
How does heparin treat thromboembolic disease?
Forms irreversible complexes with antithrombin III activating it
102
How does warfarin treat thromboembolic disease?
Interferes with vitamin K metabolism
103
How do filters treat thromboembolic disease?
Umbrella shaped filter in inferior vena cava prevents pulmonary emboli

Pathological Processes (10 decks)

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