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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
What is Fibrin broken down into?
* Fibrin depredation products | * Including D dimers which are a good measurement of fibrinolysis
26
What is a therapeutic use for Streptokinase of tPA?
Treatment for clot bursting: Acute myocardial infarction, thrombotic stroke
27
How long does thrombolysis take and why is its timing important?
<3-4 hours | Some risk of bleeding after 4 hours
28
How can coagulation be measured?
``` • Full blood count - platelent size - platelet count - platelet granules • Bleeding time • Prothrombin time ```
29
Explain the ranges of platelet counts in a blood count and what they mean
Reference range: 150-400x109/l • <30-50: easy bruising and purpura • <10: major risk of bleeding
30
Why is the bleeding time test unreliable?
• Lots of poorly controlled variables: - thickness of skin - Warmth of skin - May have punctured a vessel
31
What is Prothrombin time?
* Coagulation test carried out on citrated plasma * At 37 C, thromboplastin and Ca++ is added * The time until a clot forms is measured
32
Which route of clotting does PT test?
Extrinsic
33
What would prolong the time in a PT test and what would this be an indicator of?
• Low levels of factor II • Low levels of factor VII • Low levels of factor X - indicates liver disease, warfarin
34
Which factors does warfarin reduce?
* II * VII * IX * X
35
What is the Activated partial thromboplastin test?
* 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
What is the function of adding phospholipids in Activated partial thromboplastin test?
imitates the activation of the intrinsic system (when the endothelial lining has been damaged and phospholipids are exposed)
37
If a test was prolonged, what else could you do to further test?
* 50:50 mix with normal plasma to see if it is corrected | * Factor assay to look if there is a particular deficiency
38
What is Haemophilia A a result of?
• VIII deficiency on the X chromosome
39
What is Haemophilia B a result of?
• IX deficiency
40
What is mild haemophilia?
Chance finding, may be an issue for surgery
41
What is severe haemophilia?
Frequent bleeds into joints and soft tissues
42
What are the treatments for haemophilia?
* Gene therapy * Transfusions * Recombinant factor replacement
43
What mutation is responsible for haemophilia?
F9 mutation on the X chromosome resulting in a frameshift
44
What is Von Willebrand disease
* Autosomal dominant (usually) * defect in platelet adhesion and binding of VIII * Mild= bruising and heavy periods * Severe = Joint/ soft tissue bleeding
45
What is acquired coagulation disease?
* 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
What is Disseminated intra-vascular coagulation (DIC)?
``` • 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
How is DIC treated?
Treating the underlying cause and replace the clotting factors
48
What could a low platelet be due to?
* Under-production * Increased use * Abnormal distribution (e.g. in the spleen)
49
What are the potential causes of Thrombocytopenia due to under production?
* 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
What are the potential causes of Thrombocytopenia due to increased use?
Immune thrombocytopenia • Autoimmune • May be triggered by infection or drugs • Auto-immunity to platelets
51
How could Thrombocytopenia due to increased rate be treated?
* Watch and wait * Steroids * Immunoglobins * Splenectomy * Drugs to mimic thrombopoietin
52
Describe abnormal distribution, causing thrombocytopenia
* Splenomegally e.g. portal hypertension, leukaemia | * Large haemangloma
53
What is Virchow's triad?
``` 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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