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LSS 1 > Cardiovascular systems 12 - Haemostasis > Flashcards

Cardiovascular systems 12 - Haemostasis Flashcards

1
Q

Describe the composition of the blood and surrounding tissue when haemostasis is at rest.

A
  • Factors and cofactors are all separated
  • The endothelium is intact
  • Collagen and tissue factor contained in the subendothelial tissue.
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2
Q

Describe the structure of Von Willeband factor.

A
  • Usually in a rolled up form
  • When bound to collagen, the force of blood flow unwinds it to become a long thin molecule
  • It has multiple binding sites
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3
Q

Describe the key features of platelet structure.

A
  • ADP receptor
  • Thromboxane receptor
  • GP1b-alpha complex binds to von willeband factor
  • GP1a and GPV1 bind to collagen
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4
Q

Describe the process that occurs in the formation of a platelet plug in primary haemostasis.

A
  • Von Willeband factor binds to collagen exposed by vessel damage, and unwinds due to blood flow
  • Platelets are captured as they go past, as receptors for them are exposed when Von Willeband factor is unwound
  • Platelets are activated to release granules by calcium influx, which contain more Von Willeband factor.
  • Platelets are linked by fibrinogen.
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5
Q

Describe what changes occur in activated platelets.

A
  • They change shape
  • Expose phospholipid
  • Present new activated proteins on their surface, such as GpIIb/IIa.
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6
Q

What do the granules released from platelets contain?

A
  • Dense granules release ADP, which binds to receptors on platelets
  • Alpha granules released von willeband factor
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7
Q

Apart from granule release, what else is released by activated platelets?

A

The platelet uses lipids from the membrane to produce thromboxane, to which they have receptors for. This causes positive feedback.

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8
Q

What vessels is primary haemostasis sufficient for?

A

Small vessels - larger vessels require stabillisation with fibrin

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9
Q

Describe what occurs in coagulation up to thrombin formation.

A
  • There is formation of a fibrin mesh, also known as secondary haemostasis
  • Tissue factor binds to Factor VII
  • This activates conversion of factor ix to its active form, as well as conversion of factor x to its active form.
  • Activated fxa converts factor II to thrombin
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10
Q

What are the sites of synthesis for clotting factors, fibrolytic factors and inhibitors?

A
  • The liver (main site)
  • Endothelial cells
  • Megakaryocytes
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11
Q

Describe the regulatory reactions that occur in coagulation.

A
  • Factor x is converted to inactive forms by TFPI, tissue factor pathway inhibitor
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12
Q

Following initial thrombin production, what are the next stages of coagulation?

A
  • Activates factors V and VIII
  • Factor VIII forms a complex with factor ixa (an enzyme), calcium on the surface phospholipids released from platelets
  • The same occurs with activated factor V, though the enzyme is factor x
  • There is also conversion of fxi to its active form, which makes some more ix
  • This makes more thrombin, which converts soluble fibrinogen to insoluble fibrin which forms a mesh
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13
Q

Describe the pattern of thrombin production following activation

A

There is a lag while factor Va and VIIIa are activated, which causes a rush of thrombin production.

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14
Q

Describe the function of the thrombin burst

A
  • Generates a stronger, denser clot more resistant to fibrinolysis
  • Factor xiii is activated by thrombin, which cross links fibrin to inhibit fibrinolysis
  • Activates TAFI which inhibits fibrinolysis
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15
Q

What are the direct inhibitory mechanisms in anticoagulation?

A
  • Antithrombin is an inhibitor of thrombin and other clotting proteinases
  • TFPI in the initiation phase
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16
Q

What is the indirect inhibitory mechanism of coagulation?

A
  • Inhibition of thrombin generation by the protein C anticoagulant pathway
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17
Q

Describe the function of antithrombin.

A
  • It directly binds to thrombin (factor IIa) and neutralises it
  • Heparin makes the antithrombin more active, and helps binding to thrombin
  • In hibits xa, ixa and xia
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18
Q

Describe the protein C pathway

A
  • Thrombin binds to thrombomodulin and is redirected. It is no longer a procoagulant molecule, instead it activates protein C
  • Activated protein C breaks down factor Va and factor VIIIa, using protein S as a cofactor
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19
Q

Describe the process of fibrolysis

A
  • TIssue plasminogen activator and plasminogen bind together on the fibrin
  • Plasminogen is converted to active plasmin, an enzyme which breaks down fibrin to fibrin degredation product
  • Plasmin is regulated by antiplasmin
20
Q

List the characteristics of abnormal bleeding

A

Bleeding that is:

  • Spontaneous
  • Put of proportion with the injury
  • Unduly prolonged
  • Restarts after appearing to stop
21
Q

What is the deficiency in the defects of primary haemostasis?

A
  • Collagen
  • Von willeband factor
  • Platelets
22
Q

What are the common examples of causes of deficient primary haemostasis?

A
  • Steriod therapy/age (collagen)
  • Von willeband disease
  • Aspirin/thrombocytopenia (platelet)
23
Q

Describe the pattern of bleeding in defects of haemostasis.

A
  • Immediate
  • Easy bruising
  • Frequent nosebleeds over 20 mins
  • Gum bleeding
  • Menorrhagia (anaemia- heavy menstral bleeding)
  • Bleeding after trauma
  • Petechiae
24
Q

What are petechiae?

A
  • Red spots on the skin typical of thrombocytopenia (low levels of platelets)
  • Due to damage to capillaries that is unrepaired
25
Q

What is deficient if a patient has a defect of secondary haemostasis?

A
  • Lack of coaglation factors, poor thrombin burst, and poor fibrin mesh
26
Q

List some examples of defects of secondary haemostasis.

A
  • Haemophilia (factor VIII or factor Ix deficiency)
  • Liver disease
  • Drugs, such as warfarin which inhibits synthesis
  • Dilution due to volume replacement
  • Consumption (DIsseminated intravasculr coagulation)
27
Q

What is disseminated intravascular coagulation?

A
  • Generalised activation of coagulation (tissue factor is inside the vasculature)
  • Associated with sepsis, major tissue damage, inflammation
  • Consumes and depletes coagulation factors and platelets.
  • The activation of fibrinolysis depretes fibrinogen
28
Q

What is the consequence of disseminated intravascular coagulation?

A
  • Widespread bleeding from IV lines (bruising/internal)

- Deposition of fibrin in vessels causes organ failure

29
Q

What is the pattern of bleeding in defects of secondary haemostasis?

A
  • It is delayed due to successful primary haemostasis
  • Deep, in the joints and muscles
  • Not from small cuts
  • Nosebleeds are rare
  • Bleeding after trauma/intramuscular injections
30
Q

What is ecchymosis?

A

Easy bruising

31
Q

What is haemarthrosis?

A

Bleeding into joint spaces, a common feature of haemophilia. It results in swelling of the joint and pain.

32
Q

What causes excess fibrinolysis?

A
  • Excess fibrinolytic (plasmin/tPA)

- Deficient antifibrinolytic (antiplasmin)

33
Q

List causes of excess fibrinolysis

A
  • Therapeutic administration/tumours cause excess fibrinolytic
  • Antiplasmin defiency is genetic
34
Q

What causes anticoagulant excess?

A

Usually therapeutic administration - heparin/thrombin and factor xa inhibitors

35
Q

What is thrombosis?

A
  • Innappropriate coagulation inside a blood vessel
  • Not preceded by bleeding
  • May be venous or arterial
36
Q

What are the effects of thrombosis?

A

Obstructed blood flow

  • Artery - myocardial infarction, stroke, limb ischaemia
  • Vein - pain and swelling

Embolism (migration of thrombus)

  • Venous emboli to the lungs (pulmonary)
  • Arterial emboli from the heart, causing stroke/limb ischaemia
37
Q

What is the prevalence of venous thromboembolism?

A
  • Overall 1 in 1000/1-10000 per annum (age dependent)
  • Indicence doubles each decade
  • Causes 10% of hospital deaths
  • 25k preventable deaths a year
38
Q

List the consequences of thromboembolism?

A
  • Death
  • Recurrance (20% in first 2 years and 4% per year after)
  • Thrombophlebitic syndrome (chronic leg pain)
  • Pulmonary hypertension
39
Q

What risk factors are there for thrombosis?

A
  • Genes
  • Effects of age, illness, previous events/medication
  • Acute stimulus
  • This is a cumulative risk from interaction of these risk factors
40
Q

What is virchows triad?

A

There are three factors contributing to thrombosis, which may be genetic or aquired.

  • Blood (hypercoaguability - dominant in venous thrombosis)
  • Vessel wall (injury - dominant in arterial thrombosis)
  • Flow (stasis/turbulent - contributes to both)
41
Q

What deficiencies/excesses can contribute to increased thrombosis risk?

A
  • Deficiency of anticoagulant proteins (antithrombin, protein C/protein S)
  • Excess of coagulant proteins (factor VIII, factor II, factor V leiden, Thrombocytosis)
  • Factor V leiden is increased activity due to protein C resistance
  • Thrombocyteosis is increased platelets
42
Q

What can cause turbulent flow?

A
  • Surgery
  • Fracture
  • Long haul flight
  • Bed rest
43
Q

What is thrombophilia?

A
  • Increased risk of thrombosis
  • Thrombosis occurs at a young age
  • There are multiple thromboses
  • Thrombosis occurs while anticoagulated
  • There is an identifiable cause of increased risk
44
Q

What conditions alter blood coagulation, vessel wall/flow to increase likelihood of thrombosis?

A
  • Pregnancy
  • Malignancy
  • Surgery
  • Inflammatory response
45
Q

What is the treatment for venous thrombosis?

A
  • Treatment to lyse clot (eg. tissue plsaminogen activator)
  • Increase anticoagulant activity (heparin)
  • Lower procoagulant factors (warfarin)
  • Inhibit procoagulant factors (direct inhibitors)

LSS 1 (35 decks)

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