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Haematology and Renal Medicine > Week 2: Haemostasis > Flashcards

Week 2: Haemostasis Flashcards

1
Q

Define hemostasis in your own words

A

The process of blood clotting and desolution after tissue repair

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2
Q

Fill the blanks

A
  1. artery 2. vein 3. valve 4. endothelium of tunica intima 5. connective tissue (collagen + elastin) 6. tunica media 7. tunica adventitia
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3
Q

Which are the plasma componenets of hemostasis?

A

-coagulation and fibrinolytic proteins - inhibitors of coagulation and fibrinolytic proteins

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4
Q

Which are the main elements that act in primary hemostasis?

A

Blood vessels and platelets

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5
Q

Briefly describe primary hemostasis

A

Minor injury to blood vessels exposes collagen -> platelets bind to collagen via vWF and release platelet factors -> platelet factors trigger vasoconstriction -> platelets aggregate and attract further platelets to agglutinate and form a plug

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6
Q

Briefly describe secondary hemostasis

A

Platelet factors start the coagulation cascade and fibrinogen is converted to fibrin to form a stabilising ‘bandage’ over the plug

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7
Q

What are the three main stages of hemostasis?

A

1) Vasoconstriction 2) Platelet plug formation 3) Coagulation

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8
Q

Describe some of the elements involved in the vasoconstriction phase

A

Only in small vessels: - reflex reaction from smooth muscle - thromboaxane A2 (TXA2) + serotonin contribute - endothelin (strongest constrictor) released from endothelial cells

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9
Q

What kind of granules contain: fibrinogen, vWF, fibronectin, factors V and VIII, and PDGF?

A

alpha granules

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10
Q

What kind of granules contain: ADP, ATP, Ca2+, histamine, serotonin, epinephrine?

A

delta (dense) granules

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11
Q

Name some platelet factors outside of alpha and delta granules

A

glycoproteins, phospholipids, actin, myosin, thrombasthenin, TXA2

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12
Q

Which platelet factors allow platelet adhesion?

A

vWF

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13
Q

Which platelet factors allow platelet aggregation?

A

ADP, TXA2

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14
Q

Run through the steps of platelet plug formation including some of the platelet factors and how they affect the process

A
  • free vWF from plasma leaks into damaged blood vessel tissue - vWF attaches to collagen and allows binding of platelets - platelets stick to vWF via surface receptor GpIb - adhesion causes conformational change from smooth discs to spike spheres, exposing glycoprotein receptors on platelet surface (GpIIb and GpIIIa) - conformational change causes the release of ADP, TXA2, and serotonin - ADP and TXA2 stimulate aggregation of platelets - platelets adhere to each other via fibrinogen, which is bound to surface receptor complex GpIIb-IIIa on each platelet - platelet plug is formed
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15
Q

How does the endothelial cell stop adhesion of platelets in a healthy blood vessel?

A

Endothelial cells release prostacyclin -> prostacyclin enters thrombocytes and upregulates adenylate cyclase to produce more cAMP from ATP. cAMP lowers intracellular Ca2+ concentration. Ca2+ is important for adhesion and aggregation processes. Therefore: prostacyclin -> ↑cAMP ->↓ Ca2+ -> ↓ adhesion and aggegation

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16
Q

How does the effect of prostacyclin on platelets compare with the effect of thromboaxane A2?

A

They are antagonistic. TXA2 increases cytosolic Ca2+ and promotes adhesion, whereas prostacyclin acts the opposite way

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17
Q

What is the trigger for the intrinsic pathway of blood clotting?

A

Blood coming in contact with a negatively charged surface (collagen, phospholipids from damaged platelets)

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18
Q

What is the trigger for the extrinsic pathway of blood clotting?

A

Tissue factor released from damaged cells

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19
Q

Are these factors intrinsic, extrinsic or both?

A

PK - Int HMWK - Int I - Both II - Both III - Ext IV - Both V - Both VII - Ext VIII - Int IX - Int X - Both XI - Int XII - Int XIII - Both

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20
Q

What are the clotting factors’ non-numerical names?

A

Prekallikrein - Fletcher factor High molecular weight kininogen - contact activation factor I - Fibrinogen II - Prothrombin III - Tissue Factor IV - Calcium V - Proaccelerin, laile factor VII - Proconvertin, serum prothrombin conversion accelerator (SPCA) VIII - Antihemophiliac factor A IX - Christmas factor, antihemophilic factor X - Stuart-Prower factor XI - Plasma thromboplastin antecendent (PTA) XII - Hageman factor XIII - Protransglutaminase, fibrin stabilising factor (FSF), fibrinoligase

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21
Q

Match the regulatory proteins

A
  1. von Willebrand factor (vWF) 2. Protein C 3. Protein S 4. Thrombomodulin 5. Antithrombin III
22
Q

Which are the contact factors and what defines them?

A

XII, XI, Pre-Kallikrein, HMWK. These are stable in blood and don’t require Ca2+

23
Q

Which are the VitK dependent factors and what defines them?

A

II, VII, IX, X. These require vitamin K for synthesis, require Ca2+ for activation and are NOT consumed during coagulation

24
Q

Which are the Fibrinogen group factors and what defines them?

A

I (Fibrinogen), V, VIII, XIII. These react with thrombin, are consumed during coagulation and increase during pregnancy

25
Q

Describe the intrinsic pathway of coagulation

A

-Contact with collagen or phospholipids from damaged blood cells activates XII -> XIIa -XIIa acts on XI in the presence of HMWK to get XIa - XIa acts on IX in the presence of Ca2+ to get IXa - IXa and VIIIa combine with Ca2+ and phospholipids to form tenase - tenase activates X to get Xa - From here the pathways merge

26
Q

Describe the extrinsic pathway of coagulation

A

-tissue trauma causes the release of tissue factor aka tissue thromboplastin aka III - III activates VII to get VIIa - III and VIIa combine with CA2+ to form a trimolecular complex which activates X to get Xa -from here the pathways merge

27
Q

Describe the common coagulation cascade from Xa

A
  • Xa and Va, in the presence of Ca2+, form the prothrombin activator - Prothrombin activator converts prothrombin to thrombin - thrombin converts fibrinogen to fibrin monomers - thrombin together with VIII also activates XIII which stabilises fibrin, in the presence of Ca2+ and aids spontaneous polymerisation of fibrin monomers - fibrin polymers form a mesh and stabilise the clot
28
Q

Aside from converting fibrinogen to fibrin, how else does thrombin feed into the cascade?

A
  • Thrombin increases activation of V to Va - Thrombin increases activation of VIII to VIIIa - Thrombin increases activation of XI to XIa - Thrombin cleaves VIII from vWF (vWF binds VIII in plasma) - Thrombin catalyses formation of further thrombin from prothrombin - Thrombin causes release of nitric oxide, PGI2, ADP, vWF and tissue plasminogen activator from enothelial cells - Thrombin can act as an anticoagulant with protein C and S
29
Q

Which pathway is more essential for coagulation?

A

Extrinsic

30
Q

Aside from fibrin and platelets, what else is in a clot?

A

erythrocytes and leukocytes

31
Q

Describe clot retraction

A
  • 20-60 minutes after formation - squeezing serum from clot - actin and myosin released from platelets pulls edges together
32
Q

How does tissue factor pathway inhibitor (TFPI) work?

A

-TFPI combines with the trimolecular complex of III, VII and Ca2+ and inactivates it - This stops extrinsic activation of X

33
Q

How does thrombomodulin work?

A

Thrombomodulin is a glycosaminoglycan released by endothelial cells. It binds and inactivates thrombin. It can also combine with protein C

34
Q

How does protein C work?

A
  • Protein C is activated by thrombin - protein C combines with thrombomodulin-thrombin complex to inactivate thrombin - Protein C together with cofactor protein S binds Va and VIIIa to inhibit the coagulation cascade
35
Q

Where are protein C and S produced?

A

In the liver and in endothelial cells

36
Q

Which nutritional factor is necessary for Protein C and S formation?

A

VitK

37
Q

How does antithrombin III work?

A
  • ATIII is present in plasma and the endothelium - ATIII inactivates IXa, Xa, XIa, and thrombin - ATIII can bind with heparin which enhances and accelerates its activity -
38
Q

What is the role of plasmin?

A

Plasmin causes degradation of fibrinogen and fibrin

39
Q

Which are the intrinsic plasminogen activators?

A

Kallikrein and XIIa

40
Q

What is the role of plasminogen activators?

A

They convert plasminogen into plasmin

41
Q

Which enzyme catalyses the activity of extrinsic plasminogen activators?

A

streptokinase

42
Q

Which are the sources of extrinsic plasminogen activators?

A

Liver, plasma, endothelium

43
Q

What is a common source of heparin?

A

Mast cells (basophils also contain heparin)

44
Q

What is warfarin and how does it work?

A

It is an anti-oral coagulant which decreases prothrombin and procoagulation facctors - inhibits production of VitK dependent factors

45
Q

How does aspirin work? How long does it work for?

A

-It irreversibly inhibits cyclooxygenase which is necessary to produce downstream aggregation factors such as TXA2 - lasts about a week

46
Q

How are the platelets activated?

A

Once they are bound to the vWF, actin protein activates them by causing a conformational change. This exposes their surface receptors and number of factors are released such as ADP, TXA2, vWF.

47
Q

How would you test a patients intrinsic and common pathway and what is the normal range for this test?

A

Through aPPT (activated partial thromboplastin time), 30-45 seconds

48
Q

How would you test a patients extrinsic pathway and what would the normal time range of this test be?

A

Prothrombin time (PT) - Time taken by plasma to clot after tissue factor and calcium are added - Normally this is 10 - 14 seconds

49
Q

Which pathways would clotting time measure and what the normal time range for clotting?

A

All pathways, 3-10 minutes.

50
Q

How would you test primary haemostasis in a patient and what is the normal time range for this test?

A
  • Tests the primary phase of haemostasis (vasoconstriction and platelet plug) - Normally occurs between 3 - 6 minutes
51
Q

How would you assess a patients secondary haemostasis and what is the normal time range for this test?

A

Clotting time, 3-10 minutes

Haematology and Renal Medicine (11 decks)

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