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Semester 2 - PathPro > 8. Haemostasis > Flashcards

8. Haemostasis Flashcards

1
Q

Define homeostasis

A

Process of stopping bleeding from an injured blood vessel

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2
Q

What is the function of homeostasis? What can get it along?

A

It’s a rapid process used to prevent blood loss.
It involves blood clotting, vasoconstriction and platelet plug formation.
Haemostasis can also be helped along therapeutically by means such as pressure to a bleeding point, suturing of an injury or application of a topical agent that aids clotting. These interventions slow down blood loss and allow the clotting process to take effect.

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3
Q

What is clotting?

A

Clotting is the process whereby blood becomes a solid mass when it makes contact with connective tissue.

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4
Q

What is clotting controlled by?

A

intricate system involving activation and inhibition of clotting factors

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5
Q

What is the end result of the clotting system?

A

Production of the enzyme thrombin which acts on the circulating plasma protein fibrinogen (soluble) to produce fibrin filaments (insoluble) which are then deposited and trap red blood cells

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6
Q

Which system destroys clots?

A

Fibrinolysis

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7
Q

Which cells cause clotting of blood?

A

All cells except;

- endothelial cells, RBCs, WBCs, unactivated platelets

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8
Q

List and explain the 3 steps of haemostasis

A
  1. The severed artery contracts, not enough to stop the bleeding but enough to decrease the pressure downstream (contraction doesn’t occur in veins but the pressure in them is much lower).
  2. A primary haemostatic plug of activated platelets forms at the hole in the vessel sticking to the injured vessel and the connective tissue outside it. This is fragile but may control the bleeding. It forms in seconds to minutes.
  3. The secondary haemostatic plug forms as fibrin filaments stabilise the platelet plug into a blood clot. This forms in approximately 30 minutes.
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9
Q

What are the 3 main players in haemostasis?

A

Platelets, the process of blood clotting (clotting cascade) and the vascular wall

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10
Q

What are platelets? How are they produced?

A

Platelets are tiny blood cells that help your body form clots to stop bleeding. They’re produced by megakaryocytes in the bone marrow. The platelets will bud from the cytoplasm.

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11
Q

What factors can activate platelets?

A
  • Collagen surfaces (within extravascular areas)
  • ADP (which is released by activated platelets and injured red blood cells and amplifies the platelet response)
  • Thromboxane A2 (a powerful platelet aggregator which is also released by activated platelets)
  • Thrombin (which informs platelets that the clotting sequence is activated).
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12
Q

What is the function of thromboxane A2?

A

Potent vasoconstriction and induces platelet aggregation

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13
Q

How does aspirin work?

A

Irreversibly inactivates cyclooxygenase, one of the enzymes responsible for the production of thromboxane A2. In this way it decreases platelet aggregation

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14
Q

What do platelets do when activated?

A
  1. Stick to the exposed subendothelium specifically to von Willebrand factor which is concentrated on the subendothelial basement membrane.
  2. Aggregate with other platelets. This is how the platelet plug, and then the secondary haemostatic plug, grows. Fibrinogen binds to the platelets and sticks them together.
  3. Swell and change shape into sticky, spiny spheres.
  4. Secrete factors from platelet granules that help the platelet plug to grow and aid clotting, e.g., some fibrinogen, ADP, thromboxane A2,
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15
Q

Describe the process of blood clotting

A

In order for blood to clot fibrin has to be produced and this is the endpoint of the clotting cascade.

The enzyme that cleaves the circulating plasma protein fibrinogen into fibrin is thrombin.
Thrombin can’t circulate in an active state or blood would be solid, therefore thrombin is activated by a group of circulating molecules (clotting factors).

Most of these clotting factors are proenzymes; each proenzyme activates the next in line and amplifies the effect.
Effective clotting also requires the presence of co-factors for the enzymes. Examples are phospholipids and calcium.

The interactions involved in clotting require assembly of the components on a surface.
This surface is provided by the platelet membranes when they swell and change shape during activation.
s that

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16
Q

Which clotting factors are vitamin K dependent?

A

II, VII, IX, X

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17
Q

Which natural anticoagulants are vitamin K dependent?

A

Protein C and protein S

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18
Q

Differentiate between the intrinsic and the extrinsic clotting pathway

A

The intrinsic pathway involves factors, all of which are contained within the blood.
It is triggered by a negatively charged surface (e.g., the collagen subendothelium surface) and no vessel needs to be broken open for it to occur.

The extrinsic pathway requires a tissue factor called thromboplastin to occur, this factor is found outside the blood.
This pathway is triggered by
thromboplastin released from damaged cells adjacent to the area
of haemorrhage.

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19
Q

How is the vascular wall involved in haemostasis?

A

Arterial media contracts and subendothelium traps the platelets

Releases molecules which promote and inhibit clotting.

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20
Q

What molecules does the endothelium release that promote clotting?

A
  • von Willebrand factor

- tissue factor

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21
Q

What molecules does the endothelium release that inhibit clotting?

A
  • plasminogen activator

- thrombomodulin (activate protein C)

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22
Q

What are 3 things that can oppose clotting?

A

Dilution of clotting factors by

  • blood flow
  • natural anticoagulants

Fibrinolysis - fibrin degradation products

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23
Q

What do natural anticoagulants do and what are the main ones?

A

Oppose formation of fibrin (but don’t destroy it after its been formed)
Main ones are antithrombin III, Protein C and Protein S

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24
Q

Platelets in blood clots eventually die.

What process do these platelets carry out as they die?

A

As platelets die they cling to the fibrin and pull by their actin-myosin filaments in a mechanism which is basically the same as muscle contraction.
This clot retraction helps in pulling together the sides of small wounds and may toughen the clot by squeezing out fluid.

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25
Q

What breaks down blood clots?

A

Once the hole in the vessel has been repaired the blood clot is dissolved by fibrinolysis. Fibrin has a built in short term obsolescence. Macrophages recognise it and break it down and it is destroyed by plasmin, the enzyme responsible for fibrinolysis

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26
Q

What activates plasminogen?

A

Like thrombin, plasmin circulates as an inactive precursor. This is called
plasminogen and it, is
made in the liver. It is activated by tissue plasminogen activator (tPA) which also circulates in the blood

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27
Q

What are 3 types of plasminogen activators?

A
  • tissue plasminogen activator (circulates in the blood)
  • urokinase (found in urine)
  • streptokinase (obtained from streptococci, not usually present in the body)
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28
Q

Why are plasminogen activators used clinically and what are the side effects?

A

used therapeutically as they dissolve fibrin and therefore thrombi and thromboemboli.
Side effect is Bleeding, this commonly occurs from the gums or nose but more seriously can occasionally occur in the brain

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29
Q

Why should therapeutic streptokinase be only given to an individual once as opposed to tissue plasminogen activator (tPA) ?

A

Streptokinase is antigenic and therefore a person should only be given it once. tPA has a higher
affinity for fibrinogen than streptokinase and is not antigenic so it can be given more than once.

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30
Q

What factor causes an increase in tissue plasminogen activator?

A

It is actually the clotting cascade that sets fibrinolysis in motion as fibrin increases the activity of tissue plasminogen activator which produces plasmin which in turn breaks down fibrin to fibrin degradation products

31
Q

In what conditions would there be an increase in FDPs? give examples

A

Increased in conditions where there is thrombosis:

e.g. disseminated intravascular coagulation, deep vein thrombosis and pulmonary embolism

32
Q

What happens to fibrinolytic activity after surgery, how long does this last and what is the implication of this?

A

Fibrinolytic activity drops and remains low for

7-10 days, the time period that coincides with the increased risk of postoperative thrombosis

33
Q

What is a blood clot eventually replaced by?

A

The clot will eventually become organised (undergo fibrous repair) and be replaced initially by granulation tissue and then a tiny scar

34
Q

How can coagulation be measured?

A

In the lab you can look at prothrombin time (PT) which is used to measure how long it takes for the extrinsic pathway to work or you can look at activated partial thromboplastin time (APTT) which is a measure of the speed of the intrinsic pathway.

For example if a patient has an issue with factor 7 it means that they’ll have an increased prothrombin time. This helps to highlight an issue with the extrinsic pathway.

The fibrinogen levels can also be counted using a fibrinogen count.

35
Q

List 3 types of inherited bleeding disorders

A
  1. Haemophilia A
  2. Haemophilia B
  3. Von Willebrand disease
36
Q

What does haemophilia mean for a person?

A

People with haemophilia lack step 3 of the three steps of haemostasis.
This means that they can’t form a secondary platelet plug.

They have normal platelets but impaired clotting so they can’t produce an adequate amount of fibrin.

37
Q

What is haemophila A?

A

Factor VIII deficiency

- (decreased amount or decreased activity)

38
Q

What is haemophila B?

A

Factor IX deficiency

39
Q

What inheritance pattern does haemophilia A and B show and who does it affect more?

A

X linked recessive

- affects males more

40
Q

At what percentage activity of VIII are symptoms seen?

A 
Mild symptoms (5-60%)
Severe symptoms (<1%)
41
Q

What do patients with haemophilia present with?

A
  • easy bruising
  • massive haemorrhage after trauma and surgery. -
  • “Spontaneous” haemorrhages occur in areas subject to minor trauma, e.g., joints
  • recurrent bleeding into joints leads to joint deformities
42
Q

Are petechiae seen in haemophilia?

A

No, they are caused by blood leaking from capillaries, which is typically the result of vasculitis
or abnormalities in the number or function of platelets

43
Q

Which clotting tests are affected in haemophilia?

A

A patient with haemophilia has a normal platelet count, bleeding time (as this is a measure of platelet activity), and PT but prolonged APTT (which measures the intrinsic pathway of which factor VIII is a part). They will
have a low factor VIII assay.

44
Q

How are haemophilia A and B treated?

A

Recombinant factor VIII and IX

45
Q

What is Von Willebrand Disease?

A

Deficiency or abnormality in von Willebrand factor.

Patients who have this condition can vary from asymptomatic to severe.

46
Q

What are the functions of vWF?

A
  • assists in platelet plug formation by attracting circulating platelets to sites of vessel damage
  • stabilises factor VIII protecting it from premature destruction
47
Q

What clotting tests are affected in von Willebrand disease?

A

Bleeding time and APTT raised

- platelets are normal (instead of being lowered)

48
Q

What is most probably affected in a mucosal bleed (skin, nose gums etc.)?

A

Platelets (platelet type bleed)

49
Q

What is most probably affected in a joint or muscle bleed?

A

Clotting factors (factor type bleed)

50
Q

What is the normal range for platelet count?

A

150-400 x 10^9 /L

51
Q

Below what platelet count is considered thrombocytopenia?

A

< 100 x 10^9/L

52
Q

< 100 x 10^9/L

A

< 20 x 10^9/L

53
Q

What clotting tests are affected in thrombocytopenia?

A

Prolonged bleeding time but normal PT and APTT

54
Q

Where can spontaneous bleeding occur in thrombocytopenia?

A

Small vessels in places such as the skin, GI tract and genitourinary tract.
Occasionally intracerebral bleeding can occur.
The bleeding appears as petechiae

55
Q

which step of homeostsis will be affected in patients with low platelet count?

A

Patients with such a low platelet count
(or non-functional platelets) will lack step 2 of the three steps of
haemostasis

56
Q

What are the causes of thrombocytopenia?

A

The causes of thrombocytopenia can be classified as:
1. Decreased production of platelets - e.g., due to bone marrow
infiltration by malignancy; drugs, e.g., cytotoxic drugs; infections, e.g., measles and HIV; B12 and folate deficiency (which are needed for platelet production)

  1. Decreased platelet survival - e.g., due to immunologic
    destruction,
    e.g., immune thrombocytopenic purpura; non- immunologic destruction, e.g., disseminated intravascular coagulation.
  2. Sequestration - in an enlarged spleen (hypersplenism)
  3. Dilutional - due to massive blood transfusions (blood stored for
    more than 24 hours does not contain platelets).
57
Q

What is DIC?

A

Thrombohaemorrhagic disorder occurring as a secondary complication in a variety of conditions

58
Q

What happens in DIC and what is the implication of this?

A

Activator of clotting gets into the blood and microthrombi are formed throughout the circulation.
This process consumes platelets, fibrin and coagulation factors and activates fibrinolysis
Patient may then experience haemorrhage

59
Q

What can cause DIC?

A
  • sepsis
  • severe trauma
  • extensive burns
  • complications of childbirth (e.g., amniotic fluid embolism, retained dead foetus)
  • malignancy
  • snake bite.
60
Q

Sepsis cuased by which type of bacteria increases risk of DIC and why?

A

Gram negative bacteria produce endotoxin which activates clotting

61
Q

Severe trauma to which organ increases risk of DIC and why?

A

Brain as it contains large amounts of thromboplastin (tissue factor, FIII)

62
Q

What is the primary treatment for DIC?

A

Treat the underlying cause.

63
Q

If bleeding is prominent in DIC, how may it be treated?

A

Transfusions of:

  • platelets
  • fresh frozen plasma (FFP, which contains clotting factors)
  • cryoprecipitates (which contain factor VIII, fibrinogen, von Willebrand factor and factor XIII)
  • and red blood cells may well be needed
64
Q

What are the effects of the microthrombi in DIC?

A

neurological impairment, gangrene of the skin, renal failure, respiratory distress and GI ulceration

65
Q

What are the effects of the haemorrhage in DIC?

A

Intracerebral bleeding, petechiae, haematuria,

epistaxis and gastrointestinal bleeding

66
Q

What FDP is produced in DIC?

A

Large amounts of D-dimer produced

67
Q

How does DIC lead to anaemia and what type of anaemia is it?

A

Red blood cells are often traumatised and fragmented as they squeeze past the microthrombi
- microangiopathic haemolytic anaemia

68
Q

When are protein C and S activated and what do they do?

A

Activated in the presence of thrombin (FIIa)

Block factor V and VIII

69
Q

What does antithrombin III do and which anticoagulant can activate it?

A

Binds to and inhibits thrombin

- can be activated by heparin

70
Q

What are thrombophilias?

A

Inherited or acquired defects of haemostasis resulting in a predisposition to thrombosis

71
Q

What are the main thrombophilias?

A
  • factor V Leiden
  • antithrombin deficiency,
  • protein C or protein S deficiency
  • antiphospholipid syndrome
72
Q

What is factor V Leiden?

A

Abnormal factor V which isn’t deactivated (by protein C or protein S) resulting in thrombosis

73
Q

If a patient is deemed appropriate for thrombolysis, what medication is given?

A

Alteplase - kick starts thrombolysis

74
Q

What are the side effects of alteplase?

A

bleeding from teeth, gums, nose, mucosal membrane (GI, GU)

Semester 2 - PathPro (16 decks)

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