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Haemostasis Flashcards

1
Q

What is haemostasis?

A

Tightly regulated process
Maintains fluid status while permitting rapid formation of haemostatic clot at site of vascular injury

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2
Q

3 components of haemostasis

A

Vascular wall
Platelets
Coagulation cascade (clotting factors and anticoagulant factors)

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3
Q

Aim of haemostasis

A

Stop bleeding following trauma to blood vessel

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4
Q

3 processes involved in haemostasis

A

Contraction of vessel wall
Form platelet plug at site
Form fibrin clot to stabilise (achieved by clotting cascade)

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5
Q

Importance of haemostasis

A

More important the larger the vessel is

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6
Q

Role of vessel wall

A

Damage to vessel exposes tissue factors and collagen (from tunica adventitia) to blood
Initiates clotting cascade

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7
Q

Basic principles platelets

A

Anucleate, disc shaped
Made from budding off of megakaryocytes
Life span 7-10 days

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8
Q

Normal platelet conc

A

150-400 x 10^9/ L

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9
Q

What do platelets do when vessel is damaged? (3)

A

Adhesion
Activation
Aggregation

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10
Q

Describe adhesion

A

Seconds
Damage to vessels means exposure of underlying tissues
Platelets adhere to collagen (vWF)

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11
Q

How do platelets adhere to collagen?

A

VWF (von willebrand receptor on platelets, factor is on collagen)

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12
Q

Describe platelet activation

A

Platelets secrete granules containing ADP, thromboxane and fibrinogen

Activate other platelets and clotting cascade

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13
Q

Describe platelet aggregation

A

Crosslinking of platelets to form platelet plug

Provides stability but still delicate

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14
Q

Mediating factors

A 
Platelet receptors (glycoprotein binding sites for fibrinogen)
Von willebrand receptor (platelets bind)
Fibrinogen (links platelets)
Collagen (binds platelets)
ADP, Thromboxane
Thrombin
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15
Q

Clotting cascade define

A

Steps activated in sequence
Conversion of zymogen to active enzyme
Amplification effects

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16
Q

How is clotting cascade controlled?

A

Natural anticoagulants

Clot destroying proteins activated by clotting cascade

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17
Q

Common pathway of clotting cascade

A

Intrinsic and extrinsic pathway result in:

Production of Factor 10
Prothrombin converted to thrombin
Thrombin converts fibrinogen to fibrin

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18
Q

Intrinsic pathway clotting factors

A 
Contact activator 
12 —> 12a
11–> 11a
9 —> 9a
8a (phospholipid and calcium)

(Then common pathway)

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19
Q

Intrinsic pathway activated by

A

Contact activator

Usually from trauma to internal vessel wall

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20
Q

Extrinsic pathway clotting factors

A

Tissue factor
7 —> 7a
Calcium

Then common pathway

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21
Q

Extrinsic pathway activated by

A

Tissue factor

Endothelial (blood vessel) damage that allows blood to escape circulation

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22
Q

What does APPT test?

A

Intrinsic pathway (and common)

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23
Q

What does PT test?

A

Extrinsic pathway (and common)

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24
Q

What does PT and APPT test?

A

Common pathway, extrinsic pathway and intrinsic pathway

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25
Natural anticoagulants
Protein C Protein S Anti thrombin Tissue factor pathway inhibitor
26
APTT
Activated partial thromboplastin time | Measures Intrinsic pathway
27
PT
Prothrombin time | Measures extrinsic pathway
28
TT
Thrombin time Measures final step of pathway Conversion of fibrinogen to fibrin via thrombin
29
Tests for clotting defects (3)
APPT (activated partial thromboplastin time) PT (prothrombin time) TT (thrombin time)
30
What type of blood are clotting tests done on?
Centrifuged | Platelet poor plasma (platelets removed)
31
Tests and what they measure
``` PT = extrinsic APPT = intrinsic ```
32
If APPT is prolonged…
Deficiency in intrinsic pathway | Factor 12, 11, 9, 8
33
If PT is prolonged…
Commonly due to factor 7 deficiency (extrinsic)
34
If APPT and PT are BOTH prolonged
Common pathway problem | Factor 5, 10, thrombin and fibrinogen deficiency
35
Vessel wall significance clotting cascade
Vasoconstriction Production of vWF (platelet adherance) Exposure of collagen and tissue factors initiates clotting cascade
36
What is vWF essential for?
Platelet adherance and protection of factor 8
37
How is protein C activated
when thrombin binds to thrombomodulin (endothelial cell receptor)
38
What does protein C do?
Inactivates factors 8a and 5a
39
Co factor for protein C
Protein s
40
Antithrombin 3 mechanism
Plasma protein inactivates thrombin Prevents spread of clot by inactivating clotting factors that are carried away from site of clot
41
Antithrombin activated by…
Heparin on the surface of endothelial cells
42
What does tissue factor inhibitor do?
Acts in initiation phase (secreted by endothelial cells) Binds to tissue factor-factor 7a complexes Inhibits production of factor 10a
43
Thrombocytopenia pathology
Deficiency of platelets in blood | Bleeding into tissues, bruisng and slow clotting after injury
44
Thrombocytopenia signs/symptoms
``` Purpura petechiae mucosal bleeding nose bleeds (epistaxis) mennorrhagia (excessive menstrual bleeding) ```
45
Why can decreased platelets occur?
``` Decreased production Increased consumption (immune or non immune) ```
46
Reasons for decreased production of platelets
Marrow aplasia/infiltration Megaloblastic anaemia Sepsis Systemic viral/bacterial infection
47
Immune reasons for low platelets
Immune thrombocytopenic purpura | Thrombotic thrombocytopenic purpura
48
Immune thrombocytopenic purpura
Isolated low platelet cound Normal bone marrow (other cells normal) Absence of any other cause
49
Thrombotic thrombocytopenic purpura
Blood clots forming in small vessels | Consumption of platelets and RBC
50
Non immune reasons for low platelets
Haemolytic-uraemic syndrome | Hypersplenism
51
Haemolytic uraemic syndrome
Low RBC’s and platelets Actute kidney injury Bloody diarrhoea, fever, vomitting, weakness E-COLI main cause (effects children more)
52
Hyperspenism
Enlargement of spleen Reduction in circulating blood cells (splenic pooling) BM tries to compensate by proliferative SPENECTOMY to treat
53
Coagulation factor disorders inherited
Haemophilia A/B | Von Williebrands disease
54
Aquired disorders of coagulation
Disseminated Intravascular Coagulation (DIC) Liver disease Vit K deficiency Anticoagulants
55
Haemophlia signs/symptoms
Muscle haematomas Haemarthroses (bleeding into joints) Joint pain/deformity Excessive Post op/trauma bleeding
56
Haemophilia A reason and test results
X linked recessive Lack of factor 8 Prolonged APTT (normal PT)
57
Treatment Haemophilia A
Recombinant factor 8 | DDAVP (Desmopressin)
58
Haemohphilia B
X linked recessive Reduction of factor 9 Prolonged APTT and normal PT
59
Treatment haemophilia B
Infusions of recombinant factor 9
60
Von willebrand disease
Autosomal dominant Abnormal platelet adhesion to vessel wall Reduced factor 8 amount/activity (Usually carries factor 8 and mediates platelet adhesion)
61
Von willebrand disease signs/symptoms
Unnoticed until additional stress Spontaneous bleeding from mucous membranes (nosebleeds) Excessive bleeding from wounds Mennorhagia (heavy menstrual bleeding)
62
Tests results von willebrand
Prolonged bleeding time with normal platelet count
63
Hereditary haemorrhagic telangiectasia (HHT)
Autosomal dominant Dilated microvascular swellings GI haemmorhage = iron deficiency anaemia
64
Congenital vessel wall abnormalities
HHT | Connective tissue disorders (Ehlers Danlos)
65
Aquired vessel wall abnormalities
Senila purpura (bruising from age) Steroids Infections (measles, meningococcal) Scurvy
66
Vessel wall abnormalities presentation
Rash Easy bruising Spontaneous bleeding from small vessels (mucous membranes/skin)
67
DIC
Disseminated intravascular coagulopathy
68
DIC what is it?
Microangiopathic haemolytic anaemia
69
What causes DIC
Pathological activation of coagulation | Malignancy, massive tissue injury, infections sepsis gram -ve, transfusion, haemorrhage
70
What does DIC lead to?
Microthrombi in circulation Consumption of platelets Haemolytic anaemia
71
Clotting tests DIC
Raised PT/INR, APTT, D dimers/fibrin degradation products Low fibrinogen
72
Congenital thrombophilias
Deficiency in anticoagulants (protein C, S and antithrombin) Abnormal factor 5 (resistance to protein C)
73
Aquired thrombophilias
Antiphospholipid syndrome (antiphospholipid antibodies)
74
Anticoagulant drugs
Vit K inhibitors Oral anticoagulants Low molecular weight Heparin Heparin
75
Vit K inhibitors
Affects Vit K dependent factors (2, 7, 9, 20, protein C and protein S) Monitor internal normalised ratio (PT time against normal)
76
Direct oral anticoagulants example
Dabigatran Rivaroxaban Apixaban
77
DOACS
Inhibit thrombin or factor 10a No monitoring but careful if renal function is bad
78
Low molecular weight heparins
Makes antithrombin stronger | Dose by weight
79
Heparin monitor
APTT
80
Anitplatelet drugs
Asprirn | Clopidogrel/ticagrelor
81
Aspirin
Blocks formation of thromboxane A2 in platelets
82
Clopidogrel/ticagrelor
Block platelets ADP receptor
83
Complications with warfarin
Stop Give Vit K Prothrombin complex concentrate
84
Heparin complications
Stop | Give protamine sulphate IV if needed
85
Complications with anticoagulants =
EXCESSIVE BLEEDING
86
Define haemostats

Path Pro ILO's (8 decks)

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