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HLB > Haemostasis > Flashcards

Haemostasis Flashcards

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
Q

What are the names of the three paths of the coagulation cascade?

A
  • intrinsic
  • extrinsic
  • common
26
Q

Enzymes that take part in the coagulation cascade: how are they circulated in body and name

A
  • 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
Q

Names of the cofactors that participate in the coagulation cascade and general purpose

A
  • VIIIa (8a), Va (5a)
  • proteins that interact with an
    enzyme for a step to be completed
28
Q

Coagulation Cascade: Extrinsic Pathway:

A
  • 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
Q

Coagulation Cascade: Intrinsic Pathway:

A
  • 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
Q

Coagulation Cascade: Common Pathway:

A
  • 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
Q

Platelets are involved in the extrinsic pathway.

True or False?

A

False
Platelets are involved in the intrinsic pathway

32
Q

Coagulation Factors have a short half life in plasma.

True or False?

A

True
few hours
will degrade when not needed

33
Q

What is the coagulation factor with the longest plasma half life?

A
  • Factor I
  • Fibrinogen
  • 90 hours
34
Q

What is the coagulation factor with the second longest plasma half life?

A
  • factor II
  • prothrombin
  • 65 hours
35
Q

Vitamin K and the coagulation cascade

A
  • 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
Q

Vitamin K deficiency in newborns is due to

A

dietary restrictions

37
Q

Vitamin K deficiency in adults can be duet to:

A
  • dietary restrictions
  • liver disease decreases the
    absorption of vitamin K
38
Q

Warfarin can increase the risk of bleeding out. Why?

A
  • 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
Q

Haemostasis: TFPI:

  • stands for
  • type of molecule and size
  • synthesis
  • location
  • function
A
  • 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
Q

Excessive activity of the coagulation cascade

A
  • excessive blood clot formation
  • obstruction of blood flow in the
    circulatory network
41
Q

Coagulation Inhibition: label and describe:

A
  • 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
Q

Protein C cofactor:

A
  • Protein S assists protein C in
    binding on the surface of platelets - - protein S is vitamin K dependent
43
Q

Protein C activation leads to the destruction of which coagulation factors?

A

5 and 8

44
Q

Where is protein C synthesised?

A

liver

45
Q

Protein S and Protein C are both

A

serine proteases

46
Q

Antithrombin as a coagulation inhibitor:

A
  • antithrombin is a small
    glycoprotein, synthesised by
    endothelial cells and enters
    circulation
  • ANTITHROMBIN INHIBITS SERINE
    PROTEASES: factor IX,X,XI (9,10,11)
47
Q

Heparin is an anti-coagulant, enhances the activity of which anti-coagulation inhibitor

A

antithrombin

48
Q

Antithrombin

A
49
Q

Fibrinolysis:

A
  • 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
Q

fibrinolysis

A
51
Q

Thrombocytopenia is

A

Thrombocytopenia: low platelet number.

52
Q

Clotting disorders can affect (3):

A
  • platelet function
  • the coagulation cascade
  • coagulation inhibition.
53
Q

Thrombocytopenia (low platelet number) is a possible sign of

A

bone marrow failure

54
Q

Thrombocytopenia can be caused by

A
  • bone marrow failure?
  • autoimmune disease of platelets
  • rare herediatry disorders that
    affect platelet function can be
    caused by gene mutations
55
Q

Haemophillia A:

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
Q

Haemophilia B:

A
  • deficiency in Factor IX
  • very similar and can be mistaken
  • has a lower prevalence (1/5
    haemophilia A cases)
57
Q

Von Willebrand disease:

A
  • 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
Q

Ashkenazi Jews coagulation disorder

A

Factor XI deficiency (rare)

59
Q

Thrombosis:

A
  • 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
Q

Hereditary risk factors for thrombosis:

A
  • 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

HLB (49 decks)

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