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POM (Principles of Medicine) (RF) > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

Process involving stoppage of blood through blood vessels following trauma

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2
Q

What is primary haemostasis?

A

Formation of unstable platelet plutons at the site of damaged vessel wall

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3
Q

What is secondary haemostasis?

A

Coagulation, formation of stable fibrin clot

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4
Q

What is coagulation?

A

Stimulation of blood clotting process whereby blood transitions from a liquid to semi-solid state, forming a coherent mass

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5
Q

What is thrombosis?

A

Limit the extent of the response to the area to injury to prevent excessive or generalised blood clotting
Thrombosis is localised coagulation

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6
Q

What is fibrinolysis?

A

Initiating the process to enzymatically breakdown the fibrin in blood clots.

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7
Q

What is the structure of platelets?

A

Non-nucleated discoid granule containing cells

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8
Q

What cells do platelets derive from?

A

Megakaryocytic cytoplasmic fragmentation

Myeloid progenitor cells, formed in the bone marrow

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9
Q

What glycoprotein receptor do platelets directly bind onto within the collagen exposed damaged endothelium?

A

Glycoprotein-1a receptor

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10
Q

What receptor do platelets indirectly bind onto?

A

Von willebrand factor

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11
Q

What does Von Willebrand factor bind with?

A

Glycoprotein-1b

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12
Q

What results from platelet adhesion?

A

Structural changes from sacs to rounded discs with interlacing projections

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13
Q

What term describes the interlocking projections on platelets?

A

Spicules and filopodia

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14
Q

What is the function of spicules and filopodia?

A

Encourages platelet-platelet interaction

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15
Q

What proceeds platelet adhesion?

A

Initiates activation and release of clotting factors from storage granules (alpha dense granules), membrane invaginated to form canalicular system through which granules secrete contents, ADP

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16
Q

What platelet system is formed upon platelet adhesion and activation?

A

Canicular system

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17
Q

What storage granules release clotting factors?

A

Alpha and dense granules

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18
Q

What is also released upon platelet activation?

A

ADP

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19
Q

What is produced during platelet activation?

A

Thromboxane A2 (prostaglandin)

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20
Q

What is thromboxane A2?

A

Prostaglandin

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21
Q

What is thromboxane A2 synthesised from?

A

Arachidonic acid

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22
Q

What is the function of thromboxane A2?

A

Stimulates platelet aggregation, and the activation of new platelets (positive feedback lipids mediator)
Vasoconstrictor

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23
Q

How does thromboxane A2 cause platelet aggregation?

A

Binds to thromboxane a2 receptor, finalised by conformational change (ADP induced) in GP2B; gp3A to provide binding sites for fibrinogen.

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24
Q

Which glycoproteins undergo conformational change due to thromboxane A2?

A

GP2B

GP3A

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25
What is fibrinogen?
Soluble blood protein, essential for linking platelets together to form untstable platelet plug
26
What is prostacyclin?
Potent vasodilator, suppresses platelet activation, and prevents inappropriate platelet aggregation. Stabilises clot
27
What is the mechanism of action of aspirin?
Aspirin inhibits the production of thromboxane A2 by irreversibly blocking the action of cycle-oxygenase (COX); thereby reducing platelet aggregation
28
How long does a single dose of aspirin persist?
7 days,
29
What is the mechanism of Acton of clopidrogel?
Irreversibly blocks the ADP receptor P2Y12 on platelet cell membrane; thus ADP induced conformation change cannot occur
30
What is von Willbrand factor?
Multimeric glycoprotein synthesised by endothelial cells and megakaryocytic, mediates the adhesion of platelets binding onto glycoprotein-1b receptor.
31
What is secondary haemostasis?
Secondary haemostasis is responsible for the formation of a stable clot through coagulation mechanisms. The primary platelet plug is insufficient for larger vessel injury (structurally weak)- Fibrin formation stabilises the platelet plug, adding integrity.
32
What is the function of thrombin?
Proteolytic enzyme cleaves fibrinogen to an insoluble protein, fibrin; forms fibrin mesh fibre
33
Where are the majority of clotting factors synthesised in?
Liver
34
Whereis factor V synthesised?
megakaryocytes
35
Where is VWF made?
Megakaryocytes + endothelial cells
36
Which clotting factors are dependent on vitamin K?
Factors II (Prothrombin) VII (7) IX (9) X (10)
37
Why is vitamin K essential for the four clotting factors?
For their glutamic acid resides to be carboxylated into activation
38
What is the term for inactive enzyme (proenzyme)?
Zymogen
39
How are proenzymes activated?
Splitting of peptide bonds.
40
What are cofactors?
V and VIII (5 & 8)
41
What is the function of calcium ion in the clotting cascade?
Essential for binding of activated clotting factors to the phospholipid surfaces of platelets
42
What triggers the coagulation cascade?
Tissue factor
43
Which cells present tissue factor?
Endothelial cells, leukocytes | Exposed at site of injury
44
Which factor does TF bind to?
VIIa activaes factors IX --> IXA | X --> Xa
45
What does Xa and IXa lead to?
Activation of prothrombin (ii) to thrombin (IIa) (Small initial amount)
46
What mediates activation of co-factors V, 8 XI, and platelets?
Thrombin
47
What does factor XI do?
Mediates IX --> IXa, concerted with 8a, amplifies X to Xa | Rapid burst of thrombin generated, converted fibrinogen to fibrin
48
What is the mechanism of action of warfarin and direct oral anticoagulants?
Potentiates antithrombin leading to the inactivation of Xa and IIa (Thrombin)
49
How is Heparin administered?
Intravenously or by subcutaneous injection
50
What is the mechanism of a action of Warfarin?
Vitamin K antagonist, interferes with the carboxylation of glutamic acid residues Thus interrupting II,VII, IX and X
51
How is warfarin prescribed?
Orally
52
What is the purpose of natural anticoagulation pathways?
Confined to site of injury and prevents spontaneous activation
53
Which proteins are important in regulating the coagulation system?
Antithrombin Protein c Protein S
54
What activates Protein C?
Thrombin binds to thrombomodulin on the endothelial cell surface Activated protein c, inactivates Va, and VIIIa in the presence of co factor protein S
55
What is the function of protein S?
Behaves as a cofactor
56
How are thrombin and factor Xa inactivated?
Antithrombin
57
How is antithrombin action potentiated?
By heparin
58
What is fibrinolysis?
Fibrinolysis proceeds after haemostasis to cleave and lyse fibrin clots.
59
Which enzyme is involved in fibrinolysis?
Plasmin
60
What is the inactive form of plasmin?
Plasminogen
61
How is plasminogen activated into plasmin?
Tissue plasminogen-activator (t-PA), following binding to the lysin residues of fibrin
62
What is formed from the degradation of fibrin?
Fibrin degradation products
63
What are the clinical applications of recombinant t-pa?
Increased plasmin activation, thereby this stimulates elevated levels of fibrinolysis; lysising thrombosis
64
What are the risks with thrombolytic therapy?
High risk of associated bleeding
65
What is an example of an antifibronlytic drug?
Transexamic acid, synthetic derivative of lysine
66
How does Transexamic acid work?
Plasminogen binding, behaves as a competitive inhibitor; prevents lysine from binding to lysine residues in fibrin Cannot be activated into plasmin, fibrin is therefore not lysed
67
What disorder will tranexamic acid be used for?
Haemophillia
68
What are the three phases of coagulation?
Initiation, amplification and propagation.
69
What clotting factors are intrinsic?
9, 10, 11, 12 | 8 and 5
70
Which clotting factors are extrinsic?
Tissue factor | 7, 10, 5
71
Name the two types of coagulation tests:
``` Prothrombin time (PT) Activated partial thromboplastin time (APTT) ```
72
Which pathway measures the integrity of the extrinsic?
Prothrombin time
73
How is blood collected for prothrombin time?
Collected with sodium citrate,chelates calcium, prevents blood clotting in bottle, spun to produce platelet poor plasma
74
What is added to prothrombin time blood?
TF & recombinant thromboplastin added to citrated plasma; added with calcium to start reaction
75
What does prothrombin time measure?
The time it takes for the mixture to clot upon calcium addition
76
Why my prothrombin time be prolonged?
Due to the reduction in the activity of , 7, 10, 5, 2 or fibrinogen (prothrombin is a misnomer)
77
How is warfarin measured?
INR ratio, prothrombin time used to measure vitamin K antagonist therapy
78
Which pathway does APTT measure?
The intrinsic pathway
79
Which factor is activated by a contact activator?
XII (12)
80
What are the examples of a contact activator?
Silica or kaolin
81
How is APTT measured?
Contact activator, with phospholipid added to the citrated plasma, sample followed by calcium, time taken to clot is measured
82
What does prolongation of the APTT mean?
Reduction in single or multiple clotting factors
83
What is haemophilia A?
Factor VIII deficiency
84
What is haemophilia B?
Factor 9 deficiency
85
What may cause bleeding?
Reduction in platelet number or function Failure of platelet production caused by bone marrow infiltration, megaloblastic anaemia, drugs, viruses, B12 and folate deficiency Hereditary thrombocytopenia
86
What is disseminated intravascular coagulation?
Formation of miniature clots throughout the blood stream depletes platelet resources
87
What are blood abnormalities divided into?
Congenital and acquired
88
What are the congenital causes?
Reduction in VMF, and inherited bleeding disorder
89
What can be used as treatment for haemophilia?
Recombinant factor concentrates
90
What are some examples of acquired causes of reduced coagulation factors?
Disseminated intravascular coagulation Clotting factors and plasma fibrinogen depleted- impairs haemostatic activity, excessive bleeding, high FDPs Causes: Bacterial sepsis, advanced cancer, obstetric emergencies Liver disease
91
What is thrombosis?
Condition in which blood transforms from a liquid to a solid state within the cardiovascular system- produces mass of coagulated blood (thrombus) within an intact vessel. Thrombosis in an artery obstructs the blood flow to the tissue it supplies.
92
What is an embolism?
Carried blood clot that becomes lodged within the circulatory system
93
What is Virchow's triad?
Blood Blood flow Vessel wall
94
What is dominant in vessel walls?
Arteriole thrombosis
95
What is dominant in blood flow?
Both arterial and venous thrombosis
96
What is venous thrombosis dominant in?
Blood
97
What leads to thrombosis?
Reduced levels of anticoagulant proteins (antithrombin deficiency) thrombopenia Reduced fibrinolytic actibity Increased levels of clotting factors Factor VIII increases during pregnancy

POM (Principles of Medicine) (RF) (34 decks)

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