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Haemostasis Flashcards

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1
Q

Haemostasis definition

A

mechanism that ensures blood remains fluid, whilst damaged vessels are equickly fixed to stop excess loss

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2
Q

Problems with haemostasis can lead to (2):

A

either haemorrhage or excessive blood clot formation

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3
Q

Primary Haemostasis

A

interactions between platelets and vascular endothelial cells

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4
Q

Secondary Haemostasis

A

clotting factors - coagulation cascade

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5
Q

Erythropoiesis - Thrombopoiesis

A

key thing to know is haematopoetic progenitor starts both pathways, splits off into a megakaryocyte progenitor and a erythopoeitic progenitor

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6
Q

Megakaryoctyes:

  • location
  • form and key features
A
  • reside in the bone marrow
  • form platelets via endomitosis:
    - DNA replication
    - new organelle formation
    - but no cell division
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7
Q

Endomitosis process

A
  • the megakaryocyte skeleton
    rearranges and pro-platelet
    extensions are formed in the
    periphery of the megakaryocyte
  • microtubules facillitate the
    movement of organelles in the pro-
    platelet extensions, which consist
    of part of the megakaryocyte
    cytoplasm
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8
Q

Platelet Membrane:

A
  • membrane glycoprotein: 1a,1b,2a,2b,3a,6
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9
Q

Glycoprotein 1b on platelet membrane

A
  • initial platelet attachment to Von
    Willebrand Factor and the vascular
    endothelium
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10
Q

Glycoprotein 1a,2a,6 on platelet membrane

A

platelet adhesion to collagen

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11
Q

Glycoprotein 2b,3a on platelet membrane

A

adhesion to fibrinogen and additional adhesion to Von Willebrand Factor, platelet to platelet adhesion

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12
Q

Platelet Granules Contents: Electron Dense Granules:

A
  • nucleotides (ADP)
  • serotonin
  • Ca2+: essential for the coagulation
    cascade
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13
Q

Platelet Granules Content: Alpha Granules:

A
  • Fibrinogen: fibrin precursor
  • Von Willebrands Factor
  • Factor V: coag cascade
  • Heparin antagonist
  • Platelet Derived Growth Factor
    (PDGF): vascular repair
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14
Q

Normal Blood Vessel

A
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15
Q

Blood Vessel after Injury

A
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16
Q

Platelet function:

A
  • adhesion
  • aggregation
  • release of alpha granule content
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17
Q

Von Willebrand Factor:

  • is
  • synthesised by
A
  • large multimeric glycoprotein
  • synthesised by endothelial cells
    and megakaryocytes
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18
Q

Megakaryocyte are dependent on

A

protein called Thrombopoeitin (TPO) dependent
binds to receptor on megakaryocytes called MPL,

hence thrombopoetin is essential for formation of megakaryocytes and platelets

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19
Q

Endomitosis is an incomplete form of mitosis.

True or False?

A

True

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20
Q

Megakaryocytes nuclei contain how many chromosomes

A

contain up to 368 chromosomes

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21
Q

Megakaryocytes are multi-nucleated.

True or False?

A

True due to incomplete mitosis (endomitosis)

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22
Q

Platelets are formed as a response to the activity of

A

thrombopoeitin or TPO from megakaryocytes, and platelets are cytoplasmic fragments of megakaryocytes

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23
Q

Platelets contain many organelles.

True or False?

A

False
limited number of organelles, especially mitochondria

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24
Q

Coagulation Cascade:

A

Extrinsic pathway is triggered, feeds into the common pathway. Tissue factor interacts with Factor VIIa (7a), leads to the activation of factor X, which interacts with factor 5 in order to convert a small amount of prothrombin into thrombin.

Interaction between extrinsic and common pathway produces a small amount of thrombin, which is not sufficient to convert substantial amounts of fibrinogen to fibrin, needed for the sealing of vascular wounds by forming a blood clot.

Therefore the thrombin produced from the interaction between the extrinsic and common pathway, is used to initiate the intrinsic pathway, leading to the conversion of more factor 10 into activated form, conversion of more prothrombin to thrombin, a mroe substantial amount

Tissue factor and factor 7 interact to activate factors specific to the intrinsic pathway (9 and 11), which activate factor ten and hence mroe thrombin activated

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25
What are the names of the three paths of the coagulation cascade?
- intrinsic - extrinsic - common
26
Enzymes that take part in the coagulation cascade: how are they circulated in body and name
- circulate in plasma in an inactive form as pro-enzymes and will participate in pathway once activated - XIIa (12a), XIa (11a), IXa (9a), Xa (10a), VIIa (7a), Prothrombin II
27
Names of the cofactors that participate in the coagulation cascade and general purpose
- VIIIa (8a), Va (5a) - proteins that interact with an enzyme for a step to be completed
28
Coagulation Cascade: Extrinsic Pathway:
- initiation of the coag cascade is EXTRINSIC: - begins with the interaction between tissue Factor and Factor VII (7) - the tissue Factor-Factor VII complex will activate Factor X as well as Factor IX and Factor XI (in the intrinsic) - a small amount of thrombin is formed - not sufficient for the conversion of fibrinogen to fibrin
29
Coagulation Cascade: Intrinsic Pathway:
- AMPLIFICATION of coag cascade: - Thrombin (produced during the extrinsic pathway) activates Factor VIII (8) and Factor V (5) - AN EXAMPLE OF A POSITIVE FEEDBACK LOOP - the intrinsic pathway relies on the presence of Ca2+, platelet dense granules contain Ca2+ - more Factor X activated - INCREASED generation of thrombin produced - increased conversion of fibrinogen to fibrin
30
Coagulation Cascade: Common Pathway:
- stops bleeding and clot formation: - Thrombin hydrolyses fibrinogen and releases fibrin monomers - fibrin monomers form fibrin polymer, which is important for platelet aggregation and the formation of a haemostatic plug - the pathway depends on Factor X and Factor V (intrinsic pathway), both of which circulate in the plasma.
31
Platelets are involved in the extrinsic pathway. True or False?
False Platelets are involved in the intrinsic pathway
32
Coagulation Factors have a short half life in plasma. True or False?
True few hours will degrade when not needed
33
What is the coagulation factor with the longest plasma half life?
- Factor I - Fibrinogen - 90 hours
34
What is the coagulation factor with the second longest plasma half life?
- factor II - prothrombin - 65 hours
35
Vitamin K and the coagulation cascade
- fat soluble vitamin, present in veg and synthesised by gut bacteria - essential for the synthesis of the active forms of Factors: II (prothrombin), VII (7), IX (9) and X
36
Vitamin K deficiency in newborns is due to
dietary restrictions
37
Vitamin K deficiency in adults can be duet to:
- dietary restrictions - liver disease decreases the absorption of vitamin K
38
Warfarin can increase the risk of bleeding out. Why?
- warfarin is a vitamin K inhibitor - stops the activity of vitamin K reductase, which recycles vitamin K - lack of vitamin K means less synthesis of active forms of coagulation factors II (prothrombin), VII, IX,X - less likely to form coagulation plug
39
Haemostasis: TFPI: - stands for - type of molecule and size - synthesis - location - function
- tissue factor pathway inhibitor - small protein - produced by endothelial cells - present in platelets and circulates in plasma - TFPI inhibits Xa, VIIa and tissue factor*** - ensures that coagulation cascade is only activated in sites of vascular injury
40
Excessive activity of the coagulation cascade
- excessive blood clot formation - obstruction of blood flow in the circulatory network
41
Coagulation Inhibition: label and describe:
- endothelial cells contain a receptor called thrombomodulin, which binds to thrombin, when thrombin is not needed - interaction between thrombin and thrombomodulin activates Protein C, which is normally present on endothelial cells bound to the endothelial protein C receptor - activation of protein C will lead to the destruction of coagulation factors 8 and 5 and hence the inhibition of the intrinsic pathway - protein C needs cofactor to function, which is protein S - protein S promotes the destruction
42
Protein C cofactor:
- Protein S assists protein C in binding on the surface of platelets - - protein S is vitamin K dependent
43
Protein C activation leads to the destruction of which coagulation factors?
5 and 8
44
Where is protein C synthesised?
liver
45
Protein S and Protein C are both
serine proteases
46
Antithrombin as a coagulation inhibitor:
- antithrombin is a small glycoprotein, synthesised by endothelial cells and enters circulation - ANTITHROMBIN INHIBITS SERINE PROTEASES: factor IX,X,XI (9,10,11)
47
Heparin is an anti-coagulant, enhances the activity of which anti-coagulation inhibitor
antithrombin
48
Antithrombin
49
Fibrinolysis:
- anti-coagulation mechanism to prevent excessive clot formation - acts in balance with blood coagulation - PLASMINOGEN, an inactivated proenzyme IS CONVERTED TO PLASMIN BY THROMBIN - plasmin is a serine protease - plasmin limits the growth of thrombus by degrading fibrin polymers
50
fibrinolysis
51
Thrombocytopenia is
Thrombocytopenia: low platelet number.
52
Clotting disorders can affect (3):
- platelet function - the coagulation cascade - coagulation inhibition.
53
Thrombocytopenia (low platelet number) is a possible sign of
bone marrow failure
54
Thrombocytopenia can be caused by
- bone marrow failure? - autoimmune disease of platelets - rare herediatry disorders that affect platelet function can be caused by gene mutations
55
Haemophillia A:
- deficiency in Factor VIII - hereditary disease that passes on from mother to son (X linked) - prevalence is 30-100/10^6 - 1/3 cases have no family history
56
Haemophilia B:
- deficiency in Factor IX - very similar and can be mistaken - has a lower prevalence (1/5 haemophilia A cases)
57
Von Willebrand disease:
- various mutations can reduce the function of VWF or limit its synthesis - autosomal dominant inheritance - more prevalent in females - degree of bleeding varies between patients
58
Ashkenazi Jews coagulation disorder
Factor XI deficiency (rare)
59
Thrombosis:
- platelets and fibrin form thrombi (blood clotting cascade) at sites of injury - in thrombosis blood clots can form due to inflammation causing blood flow obstruction - eg arterial and venous thrombosis - thrombosis can cause MI, cerebrovascular disease
60
Hereditary risk factors for thrombosis:
- Factor V Leiden gene mutation: changes arg to glut on Factor V hence protein C does not efficiently bind to Factor V, hence not inactivated - hereditary antithrombin deficiency - protein c or s deficiency - hereditary elevated levels of thrombin - elevated levels of VWF

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