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Year 1 > Coagulation Cascade > Flashcards

Coagulation Cascade Flashcards

1
Q

What is haemostasis and why does it occur?

A

Haemostasis is the maintenace of blood flow through a vasculature. This is especially important when the vasculature is damaged and a clot forms to maintain blood flow in the rest of the vessel.

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2
Q

What is thrombosis and why does it occur?

A

Thrombosis is the formation of a blood clot inside a blood vessel from fibrinogen-> fibrin catalysed by thrombin which disrupts haemostasis.

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3
Q

What is embolisation?

A

A molecule blocks a blood vessel. If this emoblus is caused by part of the blood clot breaking off from the molecule, this is a thromboembolis.

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4
Q

How does a thrombus form?

A

A thrombus is a clot formed by the coagulation cascade.

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5
Q

What are the stages of Haemostasis?

A

Vasoconstriction, Primary Haemostasis and Secondary Haemostasis

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6
Q

What is primary haemostais?

A

When a platelet plug forms over the subendothelial layer which is exposed via binding to vWF and collagen.

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7
Q

What is secondary haemostasis?

A

Formation of a blood clot via the coagulation cascade.

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8
Q

What are platelets and their structure?

A

Platelets are fragments of mega-karyocyte cyptoplasm with no nucleus. They have membrane proteins, secretory granules, microtubules and a surface-connected cannalicular system.

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9
Q

What is the function of microtubules?

A

Allows the platelet to change shape.

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10
Q

What is the surface-connected cannalicular system?

A

It is a network of surface-connected membrane channels. It acts as a channel for the release of secretory granules from platelets and the endocytosis of substances.

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11
Q

What are the components of the platelet secretory granules?

A

Alpha granules and dense granules

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12
Q

What are the components of alpha granules?

A

Adhesive Proteins such as vWF, fibrinogen and fibronectin
Platelet specific proteins such as platelet derived growth factor which aids in vasculature repair following injurt. PF4 (Platelet factor 4) is a chemokine which promotes blood coagulation.
P-selectin initiates the attachment of WBC to platelets or endothelial cells at the site of injury and regulates the rolling of RBC on endothelium
Membrane proteins such as GPIIbIIIa which is a receptor for fibrinogen and vWF for clot formation

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13
Q

What is the function of dense granules?

A

Contains the vasoconstrictive agent serotonin for haemostasis, Ca2+ and Mg for maintaining integrin function and the platelet agonists ADP and ATP.

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14
Q

What are platelet agonists?

A

ADP, ATP and collagen for platelet adhesion and aggregation.

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15
Q

What are the platelet membrane proteins?

A

Prefix GP such as GPIIbIIIa which is a receptor for vWF and fibrinogen.
GPIb-IX-5 complex for vWF interaction
GPIa-IIa complex
GPVI complex

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16
Q

Why do platelets have collagen interactions?

A

Collagen is an adhesive surface for platelets and an agonist. It aids in platelet adhesion to the damaged and exposed layers of the endothelium. Allows initiation of platelet aggregation and coagulation.

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17
Q

Why do platelets have vWF and fibrinogen interaction?

A

Von Willebrand factor binds to both platelets and the endothelium. This allows it to aid in platelet-platelet adhesion and platelet adhesion to the damaged endothelium for formation of a platelet plug.
Fibrinogen is a glycoprotein complex produced in the liver which is converted to fibrin for blood clot formation.

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18
Q

Where is Von-Willebrand factor synthesised?

A

From within endothelial cells of the vasculature.

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19
Q

Where is Fibrinogen synthesised?

A

In the liver

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20
Q

Where is Fibrin synthesised?

A

At the wound site/ from the liver-produced precursor fibrinogen by the thrombin enzyme.

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21
Q

Which membrane proteins interact with collagen?

A

GPIa, GPIIa and GPVI

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22
Q

Which platelet membrane proteins are responsible for platelet aggregation?

A

GPIIaGPIIIb, GPIa, GPIIa, GPVI, GPIB-IX-V

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23
Q

Which platelet membrane proteins have vWF interactions?

A

GPIb-IX-V complex and GPIIbIIIa

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24
Q

How are platelets cleared in the body?

A

Kuppfer cells in the liver and Splenic macrophages.

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25
Q

What are the implications of liver disease on platelets?

A

Prevents clot formation because liver both produces TPO and destroys old/damaged platelet. This will cause thrombocytopenia and lead to prolonged bleeding.

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26
Q

What is the process of platelet adhesion?

A

Platelets bind to the exposed collagen on the subendothelial layer. vWF produced by the cells allows for interaction with platelets via GPIb protein. These form more GPIb-vWF interactions which create stronger adhesion for membrane proteins to create attachments to the subendothelium and release of secretory granules. This forms a platelet monolayer over the subendothelium which releases agonists such as thromboxane A2 and fibrinogen to recruit more platelets and changes shape to allow for more platelet-platelet interactions to create the plug.

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27
Q

What is the coagulation cascade?

A

Series of zymogen precursors which become activated via proteolysis to initiate the formation of blood clots

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28
Q

What is the extrinsic pathway?

A

Formation of a blood clot caused by external trauma

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29
Q

What is the intrinsic pathway?

A

Formation of a blood clot caused by internal damage to vasculature such as haemorrhage and atherosclerosis.

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30
Q

What regulates blood clotting?

A

Factor V and Factor VIII

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31
Q

What are tissue factors?

A

Also known as Factor 3, it is a clotting factor which is exposed when vascular endothelium is damaged by external trauma.

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32
Q

What is the most common collagen type found in blood vessels?

A

Type 1, Type 2 and Type 3 collagen

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33
Q

Where is prothrombinase synthesised?

A

In the liver. It is a complex formed of Factor Xa, Factor Va and serine protease in the coaglation cascade.

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34
Q

What is the function of phospholipase A2?

A

Frees stores of arachidonic acid from membrane phospholipids which activates new platelets.

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35
Q

What is thromboxane A2?

A

Lipid produced by activated platelets during haemostasis which activates new platelets and increases platelet aggregation.

36
Q

How is thromboxane A2 produced?

A

Cycloxygenase 1 (COX 1) catalyses the conversion from arachiodonic acid -> prostagalndin.
Prostaglandin -> thromboxane A2 by thromboxane synthase enzyme

37
Q

How is the platelet shape mediated?

A

Platelet cytoskeleton contains microtubules which mediate the platelet shape to polymerise actin and cause phosphorylisation of myosin to reorganise the cytoskeleton. This causes platelets to change from a bioconcave disc to a sphere with membrane projections which enables aggregations.

38
Q

How is GPIIb/IIIa activated?

A

Agonist

39
Q

What is the tissue factor pathway inhibitor?

A

Inhibits the TF-FVIII complex for prothrombinase formation via Factor Xa.

40
Q

What does anti-thrombin target?

A

Factor X, Factor IX and thrombin.

41
Q

What are the tests for platelet disorders?

A

Platelet aggregometry, prothrombin time and partial thromboplastin time.

42
Q

What does prothrombin time measure?

A

Coagulation time specifically in the extrinsic pathway.

43
Q

What does partial thromboplastin time measure?

A

Coagulation time specifically in the intrinsic pathway.

44
Q

What does prolonged prothrombin time indicate?

A

Liver disease, decreased vitamin K or defective Factor VII because it measures the extrinsic pathway

45
Q

What does prolonged partial prothrombinase time indicate?

A

Defective Factor XII, XI, IV or VIII because it measures the intrinsic pathway.

46
Q

What does prolonged prothrombin time and partial prothrombinase time indicate?

A

Liver disease, Defective Factor V or X.

47
Q

What does normal prothrombin and partial prothrombinase time indicate?

A

Decreased platelet function, Weak collagen, vWF disease, thrombocytopenia

48
Q

What is platelet aggregometry?

A

Measures platelet aggregation in platelet rich plasma by adding an agonist and measuring the light transmission. Changes in graph show biphasic platelet aggregation by adhesion to endothelium, secretion of granules and maximum aggregation. This decreases optical density.

49
Q

What is the most potent platelet aggregation?

A

ADP is the greatest platelet agonist for aggregation. Then adrenaline then collagen.

50
Q

What agonists are used in platelet aggregometry?

A

Collagen, ADP and adrenaline

51
Q

What is the coagulation test used for?

A

Measure the time taken for platelets to coagulate to identify specific deficiencies in Factor proteins and the pathway affected

52
Q

What is prothrombin time?

A

Coagulation time for the extrinsic pathway.

53
Q

What is thrombocytopenia?

A

Reduction in the number of platelets

54
Q

What is primary thrombocytopenia?

A

Sudden onset of platelet reduction. Generally caused by autoimmune disease where IgG antibodies attack GPIIBIIIa complex and initiate clearance in the liver or spleen.

55
Q

What is the cause of thrombocytopenia?

A

Autoimmune condition if it is not idiopathic.

56
Q

How are platelets cleared in the body?

A

Kuppfer cells in the liver and Splenic macrophages.

57
Q

Difference between haemorrhage and haemotoma?

A

Haemhorrage is active bleeding which can be internal or external caused by a wound. Haematoma is a collection of blood which has mainly clotted.

58
Q

What is the signs of Immune thrombocytopenia?

A

Patches of Haemorrage as rashes under the skin called petechia.

59
Q

What is Glanzmann’s thrombasthenia?

A

Frequent bleeding because of issues with platelet function such as bleeding gums or severe haemorrage.

60
Q

What is the cause of Glanzmann’s thrombasthenia?

A

Autosomal recessive genetic condition where there is an issue with the megakaryocyte lineage that leads to thrombopoeisis of platelets with a dysfunctional GPIIb and/or GPIIIa integrin.

61
Q

What is haemophilia?

A

Condition where you have a defective clotting factor protein. It is an X-linked disorder which mainly affects males and causes issues with blood clotting.

62
Q

What are the symptoms of haemophilia?

A

Issues with blood clotting so bleeding gums, bleeding in the joints, haematomas and haemorrhage, nosebleeds, vomiting

63
Q

Difference between Haemophilia A and B?

A

Haemophilia A is when you have defective Fsctor VIII which is more common. Haemophilia B is more rare when you have a defective Factor IX.

64
Q

What is the mechanism of action for aspirin?

A

Aspirin inhibits the COX-1 enzyme which converts arachiodonic acid to thromboxane A2 for platelet aggregation and thromboxane A2 conversion to prostaglandin for inflammation via thromboxane synthase. Aspirin also produces antiinflammation by boosting COX-2 enzyme for conversion of arachiodonic acid to Lipo A4 which is an anti-inflammatory.

65
Q

What is the duration of aspirin action?

A

Long acting for 10 hours

66
Q

What is aspirin indicated for?

A

Ischaemia, Prophylaxis and treatment of Myocardial infarction and coronary stenting

67
Q

What are the side effects of aspirin?

A

GI bleeding and Haemmorhagic stroke.

68
Q

What is the low dose for aspirin?

A

81mg which is the dose which prevents platelet aggregation

69
Q

What is the high dose for aspirin?

A

321mg which is a treatment for acute condition such as myocardial infarction.

70
Q

What is a prodrug?

A

A drug which is metabolised after intake into the active form of the drug.

71
Q

What is clopidogrel?

A

Clopidogrel is a treatment to prevent blockage of myocardial stents. It also reduces thrombosis of patients with myocardial infarction, stroke or peripheral arterial disease.

72
Q

Which receptor does clopidogrel target?

A

P2Y12 receptor for ADP. P2Y1 and P2X1 are still available for ADP binding so there is low level platelet aggregation.

73
Q

What is the side effects of clopidogrel?

A

GI bleeding and Haemorragic stroke but this is less common than aspirin. Thrombic thrombocytopenic purpura.

74
Q

What is thrombotic thrombocytopenic purpura?

A

Formation of blood clots in the body, especially to the vital organs. Caused by intake of clopidogrel.

75
Q

What type of drug is clopidogrel?

A

A pro-drug that is metabolised into its active form by hepatic CYP2C19, a form of P450 enzyme.

76
Q

Who cannot take clopidogrel?

A

Patients with mutations in CYP2C19; alternative ADP antagonist is prasugrel and ticagrelor.

77
Q

What is the role of anticoagulants?

A

Reduce formation of fibrin for platelet clot formation

78
Q

How do anticoagulants work?

A

They inhibit the synthesis or activity of clotting factors

79
Q

What are the types of anticoagulants?

A

They target either thrombin for fibrin formation or Factor Xa.

80
Q

What is heparin?

A

An anti-thrombin Polysaccharide in the form of unfractionated heparin isolated from mammalian tissues. It can be further fractionated into low molecular weight heparin.

81
Q

Mechanism of action of unfractionated heparin?

A

It binds to anti-thrombin and causes a conformational change. This increases anti-thrombin affinity for Factor Xa and thrmobin and UF heparin forms a ternary complex with heparin.

82
Q

Mechanism of action of low molecular weight heparin?

A

It can only inactivate Factor Xa. It does not form a ternary complex with anti-thrombin.

83
Q

Difference between mechanism of action for low molecular weight heparin and unfractionated heparin?

A

UP inactivates Factor Xa and thrombin and forms a ternary complex with anti-thrombin. LMW heparin can only inactive Factor Xa and does not form a ternary complex.

84
Q

Indications for heparin use?

A

Angina, atrial fibrillation, anticoagulant for blood transfusion and surgery and thrombolytic therapy.

85
Q

What is warfarin?

A

It is a Vitamin K antagonist that blocks reformation of KO into reduced vitamin KH2. This is important for carboxylation of glutamic residues for of Factor III (3(, VII (7), IX (9) and X (10).

86
Q

What are the consequences of warfarin use?

A

Severe bleeding which can be treated with Vitamin K injection and foetal haemorrhage because it can cross the placenta.

Year 1 (191 decks)

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