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Human Disease > Haemostasis and Thrombosis and Embolism > Flashcards

Haemostasis and Thrombosis and Embolism Flashcards

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1
Q

What exactly is haemostasis

A

blood stopping process
maintain blood in a fluid state in normal vessels
Balance between:
Clotting (thrombosis) — Bleeding (Haemorrhage)
Prothrombotic——————— Anti-thrombotic

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2
Q

What’s the difference between a thrombus and clot?

A

thrombus formed WITHIN the cardiovascular whereas clot formed OUTSIDE or post mortem

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3
Q

Order of haemostasis process

A

Transient vasoconstriction
Primary haemostasis
Secondary haemostasis
Anti-thrombotic counter-regulation

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4
Q

What happen at step 1, transient vasoconstriction, in haemostasis?

A
  • reflex vasoconstriction by endothelin from endothelial cells
  • temporarily slows bleeding
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5
Q

What happen at step 2, primary haemostasis?

A
  • expose thrombogenic subendothelial ECM
  • platelets adhere, activate and release granules to recruit more platelet => platelet plug

note: involve vWF, ADP and Thromboxane A2

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6
Q

What happen at step 3, secondary haemostasis?

A
  • tissue factor (thromboplastin) released
  • tissue factor + factor VII activate coagulation cascade (extrinsic)
  • generate thrombin
  • thrombin convert fibrinogen to insoluble fibrin => fibrin polymerisation
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7
Q

What happen at step 4, anti-thrombotic mechanism, in haemostasis?

A
  • t-PA = fibrinolysis
  • thrombomodulin = block coagulation cascade

both t-PA and thrombomodulin limit platelet plug.

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8
Q

What are the 3 main ingredients of haemostasis?

A
  1. ENDOTHELIUM (vasoconstriction)
  2. PLATELET (platelet plug)
  3. COAGULATION (fibrin formation)
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9
Q

3 roles of a normal endothelium can do

A
  1. anti-platelet : have prostacyclin, NO and ADPase to prevent adhesion and activation
  2. anti-coagulant : anti-thrombin, thrombomodulin, protein C and S, tissue factor inhibitor
  3. Fibrinolysis: t-PA
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10
Q

What is the normal INTACT endothelium’s behaviour?

A
  • anti-thrombotic
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11
Q

An injured endothelium promotes____?

A

thrombosis

- by trauma, cytokines, infectious agents, haemodynamic F, p/m mediators

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12
Q

What effects does injured endothelium produce?

A
  • platelet : adhesion via vWF
  • pro-coagulant : tissue factor
  • anti-fibrinolytic : plasminogen activator inhibitors
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13
Q

What are some main things that platelets contain?

A 
glycogen
alpha-granules (fibrinogen, vWF)
dense granules (ATP, ADP, serotonin, adrenaline)
dense tubular system
mitochondria
microtubules
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14
Q

What makes platelet adhere to site of injury?

A

glycoprotein von Willebrand factor (vWF)

bind to subendothelial collagen

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15
Q

What does platelet secrete?

A

granules

  • dense granules: ADP and serotonin
  • alpha granules: vWF, FV, PF4, Fibrinogen
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16
Q

What does ACTIVATED platelets secrete more?

A

Thromboxane A2, vWF

=> activate more platelets

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17
Q

What is the aggregation receptor for platelet?

A

Gp IIb/IIIa : binds to fibrinogen

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18
Q

What does Thromboxane A2 (TXA2) do? (4)

A
  • it comes from cyclo-oxygenase pathways
  • amplifies aggregation
  • activates more platelets
  • constricts vessels
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19
Q

What can coagulation cascade do?

A
  • enzyme rx occurs on the surface of activated platelets
  • to stabilize the platelet plug
  • here, RBC, WBC trapped make the plug even bigger
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20
Q

What does EXTRINSIC coagulation pathway require?

A
  • Tissue factor

- Factor VII-a

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21
Q

What does INTRINSIC coagulation pathway require?

A
  • Hageman factor

- Factor VIII, IX, XI, XII (8,9, 11, 12)

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22
Q

What does COMMON coagulation pathway require?

A
  • Factor II (thrombin)

- Factor I (fibrinogen

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23
Q

What does it mean by ‘stable meshwork’ in coagulation?

A

cross-linked fibrin that stabilize the platelet plug

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24
Q

What are ways to investigate coagulation?

Study These Flashcards
A 
Platelet count (~150-400 x 10^9)
Platelet function : PFA, bleeding time
Coagulation studies : APTT, PT/INR
25
What are the 2 main inhibitors of coagulation cascade (physiological)?
- Anti-thrombin : enhance by heparin (endothelium) - protein C and S : stop cascade! (activated by thrombin & thrombomodulin) - tissue factor inhibitor : block binding of factor VII-a in extrinsic pathway
26
What is the main inhibitor of fibrin forming (physiological)?
- t-PA : activate plasminogen to break down fibrin
27
What is the process of fibrinolysis (counter mechanism)?
t-PA (tissue plasminogen activator) - started by the activation of coagulation cascade - plasminogen cleaved to plasmin - plasmin breaks down fibrin : D-dimers
28
What pharmaceutical products block platelet R binding?
- monoclonal aB | - clopidogrel
29
What pharmaceutical product inhibit TXA2 product?
Aspirin
30
What pharmaceutical products 'block' coagulation cascade?
heparin warfarin clexane dabigatran
31
What pharmaceutical products 'block' the cleaving of plasminogen to plasmin?
streptokinase
32
What are the main problems with bleeding disorder?
- fragile endothelium or blood vessels - defective/deficient platelet - defective/deficient coagulation factors
33
Common causes of blood vessel wall abnormalities?
- petechiae < purpura < ecchymoses in skin and mucous membrane
34
What are causes of abnormal blood vessel wall?
``` Infection (DIC) Drug Rx (immune) Vitamin C deficiency ```
35
What is thrombocytopenia?
Bleeding disorder | Deficient platelet = 'Low platelet count'
36
What are the causes of thrombocytopenia? (4)
- Reduced platelet function : bone marrow failure and liver disease (reduce thrombopoietin) - Reduced platelet survivals - Sequestration in hyper-splenism - Dilution
37
What makes platelet function defects?
- inherited defects of adhesion, aggregation or secretion | - acquired cause (uremia, drugs and food)
38
What are the inherited cause of abnormal clotting/coagulation factor? (2)
von Willebrand disease | haemophilia A and B
39
What is von Willebrand disaese
Bleeding disorder that reduce platelet function | familial defective vWF (autosomal dominant)
40
What are the consequences of vWD?
prolonged bleeding time bruising tendency menorrhagia female bias
41
What is haemophilia A and B?
Bleeding disorder at joints and m/s with causative mutation - Haemoph A : factor VIII deficiency - Haemoph B : factor IX deficiency
42
How to treat haemophilia A and B?
IV clotting factor - usually as prophylaxis regularly - before surgery or dental treatment
43
What are the acquired causes of abnormal clotting factors, thus result in bleeding?
- vitamin K deficiency - warfarin/heparin - DIC - Severe liver disease
44
What is Warfarin?
Vitamin K antagonist - inhibit carboxylation of clotting factors II, VII, IX and X - to reduce risk of thrombosis
45
What is vitamin K?
It's a biological redox reagent to regulate coagulation factor
46
What does Vitamin K-deficiency result in?
- decrease carboxylation of Vit.K | - thus coagulation factors (2, 7, 9, 10) is non-functional
47
What can Vit K limited to?
``` new born infants (as no transfer across placenta) intestinal malabsorption (lack of bile salts) ```
48
What is haemorrhage?
leakage of blood from vessels into extravascular space | - result in external bleeding or accumulation of blood within tissue (hematoma)
49
What are 3 ranges of haematoma?
- petechia : dot hemorrhage - purpura : small hemorrhage (2-5mm) - ecchymoses : bruises (1-2cm and larger)
50
What haematoma associated with thrombocytopenia, defective platelet function and increased intravascular pressure?
- petechiae | - purpura (also increase vascular fragility, inflammation and trauma)
51
What is the process of ecchymoses?
RBCs leaked and being phagocytosed by Mø Hb (red-blue) ---> bilirubin (green-yellow) ---> hemosiderin (yellow brown)
52
What is Virchow's triad?
Pathogenesis of Thrombosis - Endothelial injury - Abnormal blood flow - Hyper-coagulability
53
What are the 4 possible outcomes after a thrombus formed
- resolution : fibrinolysis - embolisation to lungs : cause PE - organisation and recanalisation : reestablish blood flow - propagation : thrombus occluded vessels (to heart)
54
What is thromboemolism?
thrombus travel through the blood and lodge in narrow vessels. result in vascular occlusion
55
What is pulmonary embolism (PE)?
Thrombi from deep leg veins (DVT) travel to Right side of heart then block at pulmonary trunk.
56
Where does ARTERIAL thromboemboli originate from?
intracardiac mural thrombi - aortic aneurysms - ulcerated atheroscelrotic plaques - valvular vegetations
57
What does arterial emboli result in?
infarction
58
What is another name of large emboli that occlude in the pulmonary trunk centre?
Saddle embolus in PE
59
What is the 'sad' consequence of PE?
sudden death | - due to obstruction of blood flow to lungs as acute right sided heart failure, called 'acute cor pulmonale'

Human Disease (6 decks)

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