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Year 1 HLB > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A
  • haemo = blood - stasis = stop - to stop bleeding
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2
Q

What is haemorrhage?

A
  • escape of blood from damaged blood vessels
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3
Q

What is primary haemostasis?

A
  • platelet and endothelial interactions
  • weak platlet blood clot
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4
Q

What is secondary haemostasis?

A
  • coagulation cascade
  • strong fibrin clot
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5
Q

What is thrombopoiesis?

A
  • thrombosis = platlets forming blood clot
  • formation of platelets
  • part of Erythropoiesis but differentiate into platelets earlier
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6
Q

What is a primitive erythroid progenitor?

A
  • early blood cells
  • differentiate into megakaryocytes
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7
Q

What hormone produced in the kidneys and liver is thrombopoiesis (platelet formation) dependent on to differentiate into megakaryocytes?

A
  • thrombopoietin
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8
Q

What is the myeloproliferative leukemia protein (MPL) receptor, also known as the thrombopoietin receptor?

A
  • Cluster of Differentiation 110 (CD110)
  • receptor on megakaryocytes
  • thrombopoeitin binds and activates megakaryocytes
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9
Q

Once thrombopoietin is bound to the MPL receptor on megakaryocytes, what do they produce?

A
  • platelets
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10
Q

What do megakaryocytes create?

A
  • platelets
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11
Q

What is endomitosis in megakaryocytes?

A
  • replication of DNA within cell
  • does not undergo cytokinesis
  • required to create platelets
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12
Q

What is a key component, structurally of the megakaryocytes that helps form platelets on the periphery of megakaryocytes?

A
  • cytoskeleton
  • specifically microtubules
  • platelets then bud off including part of cytoplasm
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13
Q

Do platelets contain a nucleus?

A
  • no
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14
Q

Do platelets contain any organelles?

A
  • only a few
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15
Q

What do platelets contain on their cell surface that is crucial for adhesion to endothelial and to help cells form aggregates when required?

A
  • glycoproteins
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16
Q

What are the most important glycoproteins that platelets possess?

A
  • GP 1b = binds to Von Willdbrand factor
  • GP2b3a = binds with fibrinogen
  • P2Y12 = binds with ADP
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17
Q

What are alpha granules contained with platelets?

A
  • granules involved in platlet blood clot formation
  • granules involves in the coagulation cascade
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18
Q

What are some of the alpha granules?

A
  • fibrinogen
  • von Willebrand factor
  • factor V (5)
  • heparin antagonist
  • platelet derived growth factor (PDGF)
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19
Q

What are dense granules found within platelets?

A
  • further granule category
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20
Q

What are the most common components of dense granules found within platelets?

A
  • nucleotides
  • serotonin
  • ADP and ATP
  • Ca2+
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21
Q

Why do platelets contain dense granules with ATP, ADP and Ca2+ in them?

A
  • important energy and co-factors for coagulation cascade
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22
Q

When endothelium are damaged, what is one of the first things that plasma comes into contact with that initiates platelet clotting?

A
  • collagen fibres
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23
Q

Once injury to endothelial cells has been identified what do the glycoproteins of platelets help with?

A
  • adhesion to endothelial cells
  • adhesion to other platelets
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24
Q

What does the release of platelet derived growth factor (PDGF) initiate?

A
  • signals smooth muscles cells
  • initiate healing process
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25
Q

What are the 3 functions of platelets?

A

1 - adhesion to endothelial cells

2 - aggregation with other cells

3 - activation of alpha granule content

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26
Q

What is the von Willebrand factor?

A
  • a glycoprotein
  • important for binding proteins
  • important for platelet adhesion
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27
Q

Where is von Willebrand factor produced?

A
  • endothelial cells
  • alpha granules of platelets
  • megakaryocytes
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28
Q

Can deficiencies in the von Willebrand factor cause problems?

A
  • yes
  • inability to for blood to clot
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29
Q

What is the coagulation cascade?

A
  • secondary haemostasis
  • process where stable blood clots form
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30
Q

What are the 3 pathways involved in the coagulation cascade?

A

1 - Intrinsic

2 - Extrinsic

3 - Common

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31
Q

Why is the intrinsic pathway of the coagulation pathway called intrinsic?

A
  • all factors required for activation are found within blood
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32
Q

Why is the extrinsic pathway of the coagulation pathway called extrinsic?

A
  • it is activated by tissue factor
  • tissue factor is located extrinsically to blood
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33
Q

How is the extrinsic factor activated?

A
  • damage to the endothelium
  • Tissue factor (factor III) is activated
  • Tissue factor (factor III) activates factor VII
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34
Q

What is tissue factor?

A
  • protein that acts as catalyst to start coagulation cascade
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35
Q

Where can tissue factor be released from, keeping in mind it is external to the blood?

A
  • smooth muscle cells
  • fibroblasts
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36
Q

Where is factor VII produced and found commonly?

A
  • produced by the liver
  • located in plasma in inactive form
  • activated by factor III (tissue factor)
37
Q

When looking at the coagulation flow, do the arrows mean the factors upstream become what is below them or the factors above are the activating the factors below?

A
  • above factors become activated
  • then become catalyst to active factor below
38
Q

What is the pathway of factors in the intrinsic pathway?

A
  • factor XII (12)
  • factor XI (11)
  • factor IX (9)
  • factor VIII (8)
  • factor X (10) (overlap between intrinsic and common pathway)
39
Q

Are the intrinsic factors XII (12), XI (11), IX (9), VIII (8) and X (10) co-factors or enzymes?

A
  • all are enzymes
40
Q

When factor VII (7) is activated by factor III (tissue factor) what factor can it activate in the common pathway?

A
  • factor X (10)
41
Q

Once factor X (10) is activated what does it do downstream?

A
  • it activates factor V (5)
42
Q

Once factor X (10) has activated factor Va (5a) what does it do downstream?

A
  • forms the prothrombinase complex factor II (2)
43
Q

Once prothrombinase complex factor II (2) has become active, what does it do?

A
  • activates thrombin
  • called factor IIa (2a)
44
Q

What is thrombin?

A
  • enzyme that converts factor I (1) called fibrinogen to factor Ia (1a) called fibrin
  • fibrin is like rope holding platelet clot together
45
Q

In addition to converting fibrinogen into fibrin what does thrombin amplify?

A
  • intrinsic pathway (specifically factor 8 (VIII)
  • factor 5 in common pathway converting prothrombin into thrombin
  • positive feedback loop
  • loop stops when no further thrombin produced
46
Q

Specifically what factors is thrombin able to activate that will in turn amplify the intrinsic coagulation cascade? To remember think of odd numbers 5 and above.

A
  • factor XIII (13)
  • factor XI (11)
  • factor VIII (8) (exception to rule)
  • factor VII (7)
  • factor V (5)
47
Q

How is factor XII (12) in the intrinsic pathway activated?

A
  • when comes into contact with negative charged phosphates
  • negaitvely charged phosphates on activcated platelets
  • negaitvely charged phosphates on subendothelial collagen
48
Q

Where can factor XII (12) bind with negatively charged phosphates to become actived?

A
  • activated platelets
  • exposed sub-endothelial collagen
49
Q

What does factor XIII (13) do in the coagulation pathway, and what activates this?

A
  • forms crosslinks between fibrins and gives stability
  • activated by factor IIa (2a) called thrombin
50
Q

In addition to a number of factors in the coagulation cascade, what else is thrombin able to act upon?

A
  • an enzyme called plasmin
  • plasmin is able to degrade fibrin in blood clots
51
Q

What is the main purpose of the intrinsic coagulation pathway?

A
  • amplify signalling pathway cascade
  • increased fibrin production
52
Q

What is the positive feedback loop that thrombin is involved in?

A
  • ⬆️ thrombin = ⬆️ activation of factors VIII (8) and V (5)
  • ⬆️ activation of factors VIII (8) and V (5) = ⬆️ thrombin
53
Q

What common cation (+ charge) does the intrinsic pathway depend on, and what cells provide this?

A
  • Ca2+
  • Ca2+ located in dense granules in platelets
54
Q

What are the 2 key factors that the common pathway heavily relies on?

A
  • factors X (10) and V (5)
55
Q

What is vitamin K?

A
  • fat soluble vitamin - found in green vegetable and synthesised by bacteria
56
Q

Why is vitamin K important in the coagulation cascade?

A
  • required to activate a number of factors
  • factors II (2) (prothrombin), VII (7), IX (9) and X (10)
  • same factors as heparin (2+7=9…10, 11, 12)
57
Q

If a patient has low vitamin K or a genetic deficiency of vitamin K, what could happen to them if they cut themselves?

A
  • unable to effectively clot - bleed to death
58
Q

Warfarin is a drug that thins the blood. How does it act on vitamin K to ensure blood remains thin?

A
  • inhibits vitamin K reductase
  • vitamin K reductase recycles vitamin K
59
Q

How can liver disease affect vitamin K levels?

A
  • reduced absorption
60
Q

What is tissue factor pathway inhibitor (TFPI)?

A
  • single-chain polypeptide
61
Q

What is the role of tissue factor pathway inhibitor (TFPI)?

A
  • inhibits tissue factor and VIIa (7a) in the extrinsic pathway
  • inhibits factors Xa (10a) in the common pathway
62
Q

Which cells produce tissue factor pathway inhibitor (TFPI)?

A
  • endothelial cells - platelets - present in plasma
63
Q

Once tissue factor, and factors VIIa (7a) and X (10) have been activated by the extrinsic pathway, even though they produce some thrombin, why is this not able to then produce fibrin?

A
  • endothelium injury causes tissue factor (TF) to be released
  • tissue factor pathway inhibitor (TFPI) also activated
  • TFPI inhibits further expression of TF (safety mechanism)
  • reason that intrinsic pathway needs amplifying
64
Q

What is thrombomodulin?

A
  • integral membrane protein
  • expressed on the surface of endothelial cells
65
Q

How does thrombomodulin slow down coagulation?

A
  • thrombomodulin present on healthy epithelial cells
  • excess thrombin binds to thrombomodulin
  • creates thrombin/thrombomodulin complex
  • ⬇️ thrombin in positive feedback loop
66
Q

In addition to reduce in thrombin in the coagulation cascade 2 other proteins are able to bind with the thrombomodulin/thrombin complex, what are they?

A
  • proteins S and C
67
Q

Once proteins S and C are bound to the thrombomodulin/thrombin complex how are they able to inhibit the coagulation cascade further?

A
  • inhibit factors thrombin accentuates, specifically 5 and 8
  • inhibit cofactor V (5) in common pathway
  • inhibit cofactor VIII (8) in intrinsic pathway
  • significant reduction in coagulation cascade
68
Q

What protein is the activation of protein C dependent on?

A
  • protein S
69
Q

What fat soluble vitamin is key for the activity of protein S?

A
  • vitamin K
70
Q

What is antithrombin III?

A
  • small glycoprotein produced by liver
  • synthesised in endothelial cells
  • found in circulating plasma
71
Q

What 2 factors in the common pathway is antithrombin III able to bind with and inhibit?

A
  • factor X (10)
  • thrombin (factor II (2))
  • inhibits factors 2, 7, 9, 10, 11, 12
72
Q

What 3 factors in the intrinsic pathway is antithrombin able to bind with and inhibit?

A
  • factors IX (9) XI (11) and XII (12)
  • lower affinity than common pathway
73
Q

What medication can enhance the affinity of antithrombin III and in doing so inhibit factors VII (7), IX (9) XI (11) and XII (12)?

A
  • heparin
74
Q

What is fibrinolysis?

A
  • gradual degradation of fibrin mesh
75
Q

What plasminogen and where is it created?

A
  • protein produced by liver
  • released into blood stream
76
Q

How does plasminogen degrade fibrin formed blood clots?

A
  • tissue plasminogen activator released by endothelial cells - activated by thrombin and tissue plasminogen activator into plasmin
77
Q

In coagulation disorders what can be affected in primary and secondary haemostasis?

A
  • ⬇️ platelet function - ⬇️ coagulation cascade - ⬇️ coagulation inhibition
78
Q

What is thrombocytopenia?

A
  • thrombo = platelets - penia = lack of - low platelet count
79
Q

What 3 disorders can be causing thrombocytopenia?

A
  • bone marrow failure - autoimmune disease - hereditary disease
80
Q

What is Haemophilia A?

A
  • hereditary disease
  • deficient in factor VIII (8)
  • causes reduced amplification of intrinsic pathway
81
Q

What is Haemophilia B?

A
  • hereditary disease
  • deficient in factor IX (9)
  • causes reduced amplification of intrinsic pathway
82
Q

Is it easy to determine between Haemophilia A and B?

A
  • no - need genetic testing
83
Q

What is the von Willebrand disease?

A
  • autosomal dominant inheritance (only need 1 gene)
  • deficiency in von Willebrand production
  • reduced initial blood clotting
84
Q

What is Ashkenazi Jewish deficiency, also commonly referred to as Haemophilia B?

A
  • deficiency in factor XI (11) in intrinsic pathway
85
Q

What is thrombosis?

A
  • formation of a blood clot
86
Q

If blood clots are not degraded, thrombosis can occur, why is this dangerous?

A
  • they can block circulation
  • myocardial infarctions and cerebrovascular disease
87
Q

What is an embolus?

A
  • thrombosis (blood clot) that has broken free into circulation
88
Q

What is the factor V (5) Leiden gene mutation?

A
  • arginine switched with glutamine
  • protein C cannot effectively inhibit factor V (5)
  • coagulation cannot be inhibited effectively

Year 1 HLB (25 decks)

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