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Semester 2 Molecular Medicine > Coagulation - normal and abnormal > Flashcards

Coagulation - normal and abnormal Flashcards

1
Q

What are the 5 constituents of blood coagulation?

A
  • Vessel wall lined with endothelium
  • Platelets
  • Coagulation factors in unactivated state
  • Inhibitors of coagulation
  • Fibrinolytic system and inhibitors
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2
Q

What are platelets derived from?

A

Megakaryocytes in the marrow

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3
Q

How are endothelial cells involved in blood coagulation/

A
  • Line blood vessels and form a barrier
  • Produce thrombomodulin and heparin sulphate to inhibit thrombin production
  • Enzymes to degrade platelet granule-derived molecules
  • Prostacyclins and nitric oxide
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4
Q

What effect do prostacyclins and nitric oxide have on blood coagulation?

A

Reduces platelet adhesion

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5
Q

What are megakaryocytes?

A

Cells that have undergone nuclear division but not cellular division
• Have extending pseudopods from which the platelets are budded off
• Stimulated by thrombopoietin

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6
Q

What stimulates platelet production?

A

Thrombopoietin

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7
Q

Where are platelets budded off into?

A

Marrow sinusoids

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8
Q

How long can platelets circulate for?

A

5-10 days

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9
Q

Where are platelets stored?

A

around 30% are stored in the spleen

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10
Q

When do platelets form a plug?

A

When they are attracted by lowered prostacyclin (produced by the endothelium) and collagen exposure

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11
Q

What released by platelets causes vasoconstriction?

A
  • Thromboxane A2

* Serotonin

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12
Q

How do platelets adhere to the vessel wall?

A
  • Von Willibrand’s factor

* Glycoprotein Ib

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13
Q

How do platelets adhere to each other?

A
  • Glycoprotein IIb
  • Glycoprotein IIIa
  • Fibrinogen
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14
Q

Which 2 pathways activate the coagulation cascade?

A
  • Intrinsic

* Extrinsic

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15
Q

What triggers the intrinsic pathway?

A

Trauma causing damaged tissue

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16
Q

What triggers the extrinsic pathway?

A

Damaged surface, leaving the endothelium damaged, collagen exposed and the aggregation of platelets

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17
Q

Describe how fibrinogen becomes a fibrin clot

A

Prothrombin (II) is converted to the active form, Thrombin (IIa) which converts Fibrinogen to Fibrin which is cross linked to a fibrin clot

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18
Q

What inhibits coagulation?

A
  • Protein C
  • Cofactor Factor S
  • Antithrombin
  • Heparin cofactor II
  • Heparin
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19
Q

How does Protein C inhibit coagulation?

A
  • It is activated by thombomodulin

* Binds to the thrombin complex

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20
Q

How does Factor S inhibit coagulation?

A
  • Works with protein C

* Degrades factors Va and VIIIa

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21
Q

How does Antithrombin inhibit coagulation?

A

Inhibits Factors Xa and IIa

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22
Q

How does Heparin cofactor II inhibit coagulation?

A

Inhibits factor IIa

23
Q

How does Heparin inhibit coagulation?

A

Stimulates antithrombin and heparin cofactor II

24
Q

How is plasminogen activated and what is it activated to?

A
  • By tissue plasminogen activator (tPA) from endothelial cells
  • Activated to plasmin
25
Q

What is Fibrin broken down into?

A
  • Fibrin depredation products

* Including D dimers which are a good measurement of fibrinolysis

26
Q

What is a therapeutic use for Streptokinase of tPA?

A

Treatment for clot bursting: Acute myocardial infarction, thrombotic stroke

27
Q

How long does thrombolysis take and why is its timing important?

A

<3-4 hours

Some risk of bleeding after 4 hours

28
Q

How can coagulation be measured?

A 
• Full blood count 
- platelent size
- platelet count
- platelet granules 
• Bleeding time 
• Prothrombin time
29
Q

Explain the ranges of platelet counts in a blood count and what they mean

A

Reference range: 150-400x109/l
• <30-50: easy bruising and purpura
• <10: major risk of bleeding

30
Q

Why is the bleeding time test unreliable?

A

• Lots of poorly controlled variables:

  • thickness of skin
  • Warmth of skin
  • May have punctured a vessel
31
Q

What is Prothrombin time?

A
  • Coagulation test carried out on citrated plasma
  • At 37 C, thromboplastin and Ca++ is added
  • The time until a clot forms is measured
32
Q

Which route of clotting does PT test?

A

Extrinsic

33
Q

What would prolong the time in a PT test and what would this be an indicator of?

A

• Low levels of factor II
• Low levels of factor VII
• Low levels of factor X
- indicates liver disease, warfarin

34
Q

Which factors does warfarin reduce?

A
  • II
  • VII
  • IX
  • X
35
Q

What is the Activated partial thromboplastin test?

A
  • Ca++, kaolin and phospholipids are added to citrated plasma
  • It is a measure of the intrinsic and common pathway
  • Prolonged by haemophilia and heparin
36
Q

What is the function of adding phospholipids in Activated partial thromboplastin test?

A

imitates the activation of the intrinsic system (when the endothelial lining has been damaged and phospholipids are exposed)

37
Q

If a test was prolonged, what else could you do to further test?

A
  • 50:50 mix with normal plasma to see if it is corrected

* Factor assay to look if there is a particular deficiency

38
Q

What is Haemophilia A a result of?

A

• VIII deficiency on the X chromosome

39
Q

What is Haemophilia B a result of?

A

• IX deficiency

40
Q

What is mild haemophilia?

A

Chance finding, may be an issue for surgery

41
Q

What is severe haemophilia?

A

Frequent bleeds into joints and soft tissues

42
Q

What are the treatments for haemophilia?

A
  • Gene therapy
  • Transfusions
  • Recombinant factor replacement
43
Q

What mutation is responsible for haemophilia?

A

F9 mutation on the X chromosome resulting in a frameshift

44
Q

What is Von Willebrand disease

A
  • Autosomal dominant (usually)
  • defect in platelet adhesion and binding of VIII
  • Mild= bruising and heavy periods
  • Severe = Joint/ soft tissue bleeding
45
Q

What is acquired coagulation disease?

A
  • Caused by liver disease: alcohol/autoimmune disease/hepatitis
  • Affects all coagulation factors in the liver
  • Abnormal PT and fibrinogen, later produces abnormal APPT
  • Bleeding due to abnormal clotting, low platelets (due to lack of thrombopoietin)
  • Portal hypertension causing oesophageal varies and upper GI bleeding
46
Q

What is Disseminated intra-vascular coagulation (DIC)?

A 
• Activation of clotting cascade due to:
- Trauma
- Malignancy e.g. prostate cancer
- Sepsis
- Amniotic fluid embolism 
• Causes depletion of clotting factors and damage due to the clot
47
Q

How is DIC treated?

A

Treating the underlying cause and replace the clotting factors

48
Q

What could a low platelet be due to?

A
  • Under-production
  • Increased use
  • Abnormal distribution (e.g. in the spleen)
49
Q

What are the potential causes of Thrombocytopenia due to under production?

A
  • Abnormal marrow function: acute leukaemia, metastatic tumour, aplastic anaemia
  • Expected side effect of cytotoxic chemotherapy
  • Idiosyncratic and unexpected drug adverse side effects e.g. co-trimoxaxole, anti-inflammatories
50
Q

What are the potential causes of Thrombocytopenia due to increased use?

A

Immune thrombocytopenia
• Autoimmune
• May be triggered by infection or drugs
• Auto-immunity to platelets

51
Q

How could Thrombocytopenia due to increased rate be treated?

A
  • Watch and wait
  • Steroids
  • Immunoglobins
  • Splenectomy
  • Drugs to mimic thrombopoietin
52
Q

Describe abnormal distribution, causing thrombocytopenia

A
  • Splenomegally e.g. portal hypertension, leukaemia

* Large haemangloma

53
Q

What is Virchow’s triad?

A 
Abnormal vessel wall:
• Atheroma and plaque
• Varicose veins
• Aneurysm 
Abnormal flow:
• Atrial fibrillation 
• Immobilised e.g. long distance flight, plaster cast
• Varicose veins 
Abnormal blood component 
• increased haemoglobin/red cell count- polycythaemia
• Increased WBC count- stasis and increased clotting\
• Increased viscosity of plasma
• Reduced coagulation inhibitors

Semester 2 Molecular Medicine (27 decks)

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