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Human Disease > Haemostasis and Thrombosis and Embolism > Flashcards

Haemostasis and Thrombosis and Embolism Flashcards

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?

A 
Platelet count (~150-400 x 10^9)
Platelet function : PFA, bleeding time
Coagulation studies : APTT, PT/INR
25
Q

What are the 2 main inhibitors of coagulation cascade (physiological)?

A
  • 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
Q

What is the main inhibitor of fibrin forming (physiological)?

A
  • t-PA : activate plasminogen to break down fibrin
27
Q

What is the process of fibrinolysis (counter mechanism)?

A

t-PA (tissue plasminogen activator)

  • started by the activation of coagulation cascade
  • plasminogen cleaved to plasmin
  • plasmin breaks down fibrin : D-dimers
28
Q

What pharmaceutical products block platelet R binding?

A
  • monoclonal aB

- clopidogrel

29
Q

What pharmaceutical product inhibit TXA2 product?

A

Aspirin

30
Q

What pharmaceutical products ‘block’ coagulation cascade?

A

heparin
warfarin
clexane
dabigatran

31
Q

What pharmaceutical products ‘block’ the cleaving of plasminogen to plasmin?

A

streptokinase

32
Q

What are the main problems with bleeding disorder?

A
  • fragile endothelium or blood vessels
  • defective/deficient platelet
  • defective/deficient coagulation factors
33
Q

Common causes of blood vessel wall abnormalities?

A
  • petechiae < purpura < ecchymoses in skin and mucous membrane
34
Q

What are causes of abnormal blood vessel wall?

A 
Infection (DIC)
Drug Rx (immune)
Vitamin C deficiency
35
Q

What is thrombocytopenia?

A

Bleeding disorder

Deficient platelet = ‘Low platelet count’

36
Q

What are the causes of thrombocytopenia? (4)

A
  • Reduced platelet function : bone marrow failure and liver disease (reduce thrombopoietin)
  • Reduced platelet survivals
  • Sequestration in hyper-splenism
  • Dilution
37
Q

What makes platelet function defects?

A
  • inherited defects of adhesion, aggregation or secretion

- acquired cause (uremia, drugs and food)

38
Q

What are the inherited cause of abnormal clotting/coagulation factor? (2)

A

von Willebrand disease

haemophilia A and B

39
Q

What is von Willebrand disaese

A

Bleeding disorder that reduce platelet function

familial defective vWF (autosomal dominant)

40
Q

What are the consequences of vWD?

A

prolonged bleeding time
bruising tendency
menorrhagia
female bias

41
Q

What is haemophilia A and B?

A

Bleeding disorder at joints and m/s with causative mutation

  • Haemoph A : factor VIII deficiency
  • Haemoph B : factor IX deficiency
42
Q

How to treat haemophilia A and B?

A

IV clotting factor

  • usually as prophylaxis regularly
  • before surgery or dental treatment
43
Q

What are the acquired causes of abnormal clotting factors, thus result in bleeding?

A
  • vitamin K deficiency
  • warfarin/heparin
  • DIC
  • Severe liver disease
44
Q

What is Warfarin?

A

Vitamin K antagonist

  • inhibit carboxylation of clotting factors II, VII, IX and X
  • to reduce risk of thrombosis
45
Q

What is vitamin K?

A

It’s a biological redox reagent to regulate coagulation factor

46
Q

What does Vitamin K-deficiency result in?

A
  • decrease carboxylation of Vit.K

- thus coagulation factors (2, 7, 9, 10) is non-functional

47
Q

What can Vit K limited to?

A 
new born infants (as no transfer across placenta)
intestinal malabsorption (lack of bile salts)
48
Q

What is haemorrhage?

A

leakage of blood from vessels into extravascular space

- result in external bleeding or accumulation of blood within tissue (hematoma)

49
Q

What are 3 ranges of haematoma?

A
  • petechia : dot hemorrhage
  • purpura : small hemorrhage (2-5mm)
  • ecchymoses : bruises (1-2cm and larger)
50
Q

What haematoma associated with thrombocytopenia, defective platelet function and increased intravascular pressure?

A
  • petechiae

- purpura (also increase vascular fragility, inflammation and trauma)

51
Q

What is the process of ecchymoses?

A

RBCs leaked and being phagocytosed by Mø

Hb (red-blue) —> bilirubin (green-yellow) —> hemosiderin (yellow brown)

52
Q

What is Virchow’s triad?

A

Pathogenesis of Thrombosis

  • Endothelial injury
  • Abnormal blood flow
  • Hyper-coagulability
53
Q

What are the 4 possible outcomes after a thrombus formed

A
  • resolution : fibrinolysis
  • embolisation to lungs : cause PE
  • organisation and recanalisation : reestablish blood flow
  • propagation : thrombus occluded vessels (to heart)
54
Q

What is thromboemolism?

A

thrombus travel through the blood and lodge in narrow vessels.
result in vascular occlusion

55
Q

What is pulmonary embolism (PE)?

A

Thrombi from deep leg veins (DVT) travel to Right side of heart then block at pulmonary trunk.

56
Q

Where does ARTERIAL thromboemboli originate from?

A

intracardiac mural thrombi

  • aortic aneurysms
  • ulcerated atheroscelrotic plaques
  • valvular vegetations
57
Q

What does arterial emboli result in?

A

infarction

58
Q

What is another name of large emboli that occlude in the pulmonary trunk centre?

A

Saddle embolus in PE

59
Q

What is the ‘sad’ consequence of PE?

A

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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