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103 theme 2 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

what are endothelial cells

A

layer of cells lining the inner surface of all vessel walls (huge total surface area)

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2
Q

what do endothelial cells do in blood vessels

A

Control blood fluidity and flow (controls size, when intact contributes to preventing clots and when injured promotes local clotting on exposed basement membrane)
Signals inflammatory cells to areas needing defence and repair
Gate keeper between blood and tissues (nutrients, hormones, waste, actively controls extravasation of fluid, cells and molecules)

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3
Q

what is Haemostasis

A

Process that causes bleeding to stop

Opposite is haemorrhage

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4
Q

what is the function of Haemostasis

A

Clotting and stopping blood escaping
Keeps blood in damaged vessels
First stage of healing

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5
Q

what can the endothelium do when injured

A

Endothelium secretes inhibitors of haemostasis (injured, stops secretion, instead secretes von Willebrand factor)

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6
Q

what are 3 platelet based pathways to repair blood vessels

A

form primary haemostatic plug
Coagulation meshwork on clot
vasoconstriction

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7
Q

why do platelets form a primary haemostatic plug

A

vessel wall injury (via platelet adhesion, activation and aggregation)

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8
Q

how does coagulation make a meshwork on a clot

A

(enzyme cascade, part of coagulation requires platelets membrane)

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9
Q

how do platelets cause vasoconstriction

A

platelets release pro thrombotic agents (serotonin, adp and thromboxane a2)

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10
Q

what is Virchow’s triad

A

risk factors for each 3

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11
Q

what are megakaryocytes

A 
Found in bone marrow 
Prod 4000 platelets (20x less than rbcs, platelet size = 3x0.5um)
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12
Q

what are thrombocytes

A 
Thrombocyte = platelet
Thrombocytopaenia = low platelet count
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13
Q

how are platelets activated for Haemostasis

A

exocytose (secrete chemicals) + change shape + increase respiratory rate (O2 consumed)

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14
Q

what activation is required for Haemostasis

A

Activation required for haemostais, aggregation of platelets, some coagulation steps (phosolipids)

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15
Q

how do platelets covers wounds

A

Adhesion (to exposed collagen)
Activation (exocytose dense granules, serotonin, adp, calcium)
Aggregation (stimulated by adp, blocked by prasugrel, via fibrinogen)

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16
Q

how does ADP link to activation

A

Secrete adp > activate P2Y receptor > cation flow
Platelets release thromboxane A2 (TXA2)
ADP > positive feedback on platelets

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17
Q

how are clotting factors found

A

circulate as inactive precursors

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18
Q

how are activated clotting factors represented

A

Factor X is activated to be Factor Xa

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19
Q

what are clotting factors

A

enzymes, cleave other factors to activate them

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20
Q

what clotting factors are not enzymes

A

Factor V AND VIII (necessary co factors allowing enzymes to function, inactive initially)

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21
Q

how does activation only happen when needed

A

Initial activating factor is segregated
Eg tissue factors behind endothelial cells, while clotting factor precursors in blood (hard to get together but need to too work, activated when endothelial cell is damaged)

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22
Q

how does thrombosis occur spontaneously

A

blood flow is slow
Eg atrial fibrillation > thrombosis (can travel via BVs) > to brain, stroke
Blood left standing clots (lab stops this with citrate or heparin)

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23
Q

what is plasma and serum

A

Plasma =fluid portion of blood

Serum =fluid left after clotting

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24
Q

what is thrombosis and embolism

A 
Thrombosis = abnormal function of clot locally 
Embolism = abnormal migration of a clot (or other intravascular object)
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25
Q

what is the goal of Haemostasis

A

activate thrombin (normally inactive, prothrombin)

26
Q

what does thrombin do

A

turns fibrinogen into fibrin (cross linked to form a stable clot by XIII and Ca2+)

27
Q

what are the two coagulation cascades

A

Extrinsic and Intrinsic (contact activation) pathway

All factors/ proenzymes are already in place, amplification of process through positive feedback

28
Q

what is the extrinsic pathway

A

tissue factor pathway

Requires secretion of tissue factor to occur, initiation of coagulation

29
Q

what is the intrinsic pathway

A

contact activation pathway

All factors/ proenzymes are already in place, amplification of process through positive feedback

30
Q

how can thrombin be activated

A

Activated poorly by Factor Xa

Factor Va, cofactor to Xa, together activate well

31
Q

how can factor X be activated to Xa

A

Extrinsic Xase, intrinsic Xase, thrombin also activates it (positive feedback)

32
Q

what is intrinsic and extrinsic Xase

A

Extrinsic Xase = tissue factor (under endothelium) + factor VIIa
Intrinsic Xase = factor Viiia + factor IXa

33
Q

what do the extrinsic and intrinsic pathway lead to

A

combine into common pathway

leads to clotting

34
Q

what are the types of coagulation factors of the common pathway

A

Prothrombin group
Thrombin group
Enzymes

35
Q

what factors are in the prothrombin group

A

factors II, VII, IX, X

36
Q

what factors are in the thrombin group

A

factors I, V, VIII
Thrombin activates them
Cofactors are V and VIII, factor I is fibrinogen, increased in inflammation, pregnancy and oral contraceptives

37
Q

what are needed for enzyme cofactors

A

vitamin K needed for synthesis, require Ca2+ for activation, stable

38
Q

what is coagulation based on

A

positive feedback loop, thrombin activates upstream clotting factors

39
Q

what is vitamin k

A

A class of related fat soluble vitamins
Required to synthesis enzyme coagulation factors (prothrombin (11), VII, IX,X (calcium dependant proteases)
Vitamin K is essential for gamma carboxylation of clotting enzymes

40
Q

what can liver dysfunction lead to

A

Clotting factors made by liver (liver dysfunction cirrhosis or hepatitis) can lead to clotting deficiency

41
Q

what is fibrinolysis and inhibition of coagulation used for

A

To balance with clot formation

Imbalance can lead to BV accumulating damage and haemorrhage or clot obstructing vessel lumen

42
Q

what does plasmin do

A

Lyses fibrin – stops or destroys clots
Starts as inactive plasminogen (plasma protein made by liver)
Requires tissue plasminogen activator (tPA) to mature (tPA is on the surface of endothelial cells)

43
Q

what is protein c

A

a coagulation inhibitor
Inactive enzyme made by liver, activated on surface of endothelial cells
Inactivates factor Va and VIIIa (works with cofactor protein s to inactive Va)

44
Q

what is antithrombin III

A

works with heparin
Peptide in blood made by liver
Blocks activity of thrombin (also of Xa and IXa)

45
Q

is the action of heparin reversible

A

Heparin is reversible by protamine sulfate

46
Q

what happens with an anti thrombotic III deficiency

A

AT III deficiency = risk of thrombotic disease

Recombinant form used medically for thrombotic disorders

47
Q

what happens with a vitamin k deficiency

A

Clotting insufficiency
Rare b/c vitamin K is made by large intestine bacteria (also found in leafy green veg)
Caused by GI disease or no fat absorption (liver disease > no bile salts)
Warfarin prevents recycling of vitamin K

48
Q

what is haemophilia A

A

Clotting disorder
Affects large BVs, affects joints and muscles, wounds bleed for a few days
Due to congenital lack of clotting factor VIII
X linked
Treat with purified factor VIII (expensive and rare)
Christmas disease (defect in factor IX, aka haemophilia B, symptoms as per Haemophilia A)

49
Q

what is haemophilia B

A 
Christmas disease (defect in factor IX
symptoms as per Haemophilia A
50
Q

how does atherosclerosis occur (by inflammation)

A

Monocytes enter lesion, become macrophages (consume cholesterol esters), can become foam cells), can die and release contents (attract more monocytes, cytokines, chemo-attractants)
Inflammation leads to Haemostasis, vice versa (Synergistic)

51
Q

how is atherosclerosis caused by lipids

A

LDL deposits lipids in lesion, cholesterol esters non-aqueous (make them solid or hard), cholesterol esters are oxidised (O2 radicals) making them immunogenic, oxidised lipids are consumed by macrophages (become foam cells, explode and attract more monocytes)

52
Q

how is atherosclerosis caused by the endothelium

A

Expresses chemo attractants (for monocytes to find and enter lesion), endothelium lost so collagen stimulates coagulation (normally covers collagen and basement membrane)
Endothelium lost, vessel cannot control its dilation (normally provides NO)

53
Q

how can pharmacology be used to control blood clotting

A

Anti-platelet agents (block platelet activation, good for treating arterial disease)
Anti-coagulants (block production or activity of clotting factors, used for venous disease)
Fibrinolytics (primarily used to dissolve fibrin in arterial disease)

54
Q

how do anti-platelet agents act

A

Prevent clotting in arteries (have limited effects, used in acute coronary syndrome)

55
Q

what are examples of anti-platelet agents

A

Aspirin (cyclo-oxygenase (COX) inhibitor, blocks formation of thromboxane A2 in platelets, lengthens bleeding time, doesn’t increase coagulation time, prophylaxis for myocardial infarction)
ADP receptor inhibitors (prasugrel/ clopidogrel)

56
Q

what do anti-coagulants do

A

Prevent clotting in veins (in low pressure pulmonary circulation, prophylactic for deep vein thrombosis and pulmonary embolism)

57
Q

what are examples of anti-coagulants

A

Heparins (inhibit coagulation (with AT III) by inhibiting factor Xa, different types)
Novel Oral Anti Coagulants (NOACS) – dabigatran (thrombin inhibitor) and rivaroxaban (factor Xa inhibitor)
Warfarin (vitamin K antagonist, slow onset and requires monitoring)

58
Q

what do fibrinolytics do

A

Clotting in arteries (high pressure) used in acute coronary syndrome eg AMI

59
Q

what are examples of fibrinolytics

A

Tissue plasminogen activator (tPA)
Streptokinase ad urokinase
Aka thrombolytic drugs

60
Q

what does adp, serotonin, thromboxane A2 do when secreted by activated platelets

A

adp activates platelets further
serotonin vasoconstriction
txa2 vasoconstriction and aggregation

103 theme 2 (7 decks)

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