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Path Pro 2023 > Haemostasis > Flashcards

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
Q

Natural anticoagulants

A

Protein C
Protein S
Anti thrombin
Tissue factor pathway inhibitor

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26
Q

APTT

A

Activated partial thromboplastin time

Measures Intrinsic pathway

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27
Q

PT

A

Prothrombin time

Measures extrinsic pathway

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28
Q

TT

A

Thrombin time
Measures final step of pathway
Conversion of fibrinogen to fibrin via thrombin

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29
Q

Tests for clotting defects (3)

A

APPT (activated partial thromboplastin time)
PT (prothrombin time)
TT (thrombin time)

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30
Q

What type of blood are clotting tests done on?

A

Centrifuged

Platelet poor plasma (platelets removed)

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31
Q

Tests and what they measure

A 
PT = extrinsic
APPT = intrinsic
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32
Q

If APPT is prolonged…

A

Deficiency in intrinsic pathway

Factor 12, 11, 9, 8

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33
Q

If PT is prolonged…

A

Commonly due to factor 7 deficiency (extrinsic)

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34
Q

If APPT and PT are BOTH prolonged

A

Common pathway problem

Factor 5, 10, thrombin and fibrinogen deficiency

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35
Q

Vessel wall significance clotting cascade

A

Vasoconstriction
Production of vWF (platelet adherance)
Exposure of collagen and tissue factors initiates clotting cascade

36
Q

What is vWF essential for?

A

Platelet adherance and protection of factor 8

37
Q

How is protein C activated

A

when thrombin binds to thrombomodulin (endothelial cell receptor)

38
Q

What does protein C do?

A

Inactivates factors 8a and 5a

39
Q

Co factor for protein C

A

Protein s

40
Q

Antithrombin 3 mechanism

A

Plasma protein inactivates thrombin

Prevents spread of clot by inactivating clotting factors that are carried away from site of clot

41
Q

Antithrombin activated by…

A

Heparin on the surface of endothelial cells

42
Q

What does tissue factor inhibitor do?

A

Acts in initiation phase (secreted by endothelial cells)
Binds to tissue factor-factor 7a complexes
Inhibits production of factor 10a

43
Q

Thrombocytopenia pathology

A

Deficiency of platelets in blood

Bleeding into tissues, bruisng and slow clotting after injury

44
Q

Thrombocytopenia signs/symptoms

A 
Purpura
petechiae
mucosal bleeding
nose bleeds (epistaxis)
mennorrhagia (excessive menstrual bleeding)
45
Q

Why can decreased platelets occur?

A 
Decreased production
Increased consumption (immune or non immune)
46
Q

Reasons for decreased production of platelets

A

Marrow aplasia/infiltration
Megaloblastic anaemia
Sepsis
Systemic viral/bacterial infection

47
Q

Immune reasons for low platelets

A

Immune thrombocytopenic purpura

Thrombotic thrombocytopenic purpura

48
Q

Immune thrombocytopenic purpura

A

Isolated low platelet cound
Normal bone marrow (other cells normal)
Absence of any other cause

49
Q

Thrombotic thrombocytopenic purpura

A

Blood clots forming in small vessels

Consumption of platelets and RBC

50
Q

Non immune reasons for low platelets

A

Haemolytic-uraemic syndrome

Hypersplenism

51
Q

Haemolytic uraemic syndrome

A

Low RBC’s and platelets
Actute kidney injury
Bloody diarrhoea, fever, vomitting, weakness

E-COLI main cause (effects children more)

52
Q

Hyperspenism

A

Enlargement of spleen
Reduction in circulating blood cells (splenic pooling)
BM tries to compensate by proliferative

SPENECTOMY to treat

53
Q

Coagulation factor disorders inherited

A

Haemophilia A/B

Von Williebrands disease

54
Q

Aquired disorders of coagulation

A

Disseminated Intravascular Coagulation (DIC)
Liver disease
Vit K deficiency
Anticoagulants

55
Q

Haemophlia signs/symptoms

A

Muscle haematomas
Haemarthroses (bleeding into joints)
Joint pain/deformity
Excessive Post op/trauma bleeding

56
Q

Haemophilia A reason and test results

A

X linked recessive
Lack of factor 8

Prolonged APTT (normal PT)

57
Q

Treatment Haemophilia A

A

Recombinant factor 8

DDAVP (Desmopressin)

58
Q

Haemohphilia B

A

X linked recessive
Reduction of factor 9

Prolonged APTT and normal PT

59
Q

Treatment haemophilia B

A

Infusions of recombinant factor 9

60
Q

Von willebrand disease

A

Autosomal dominant

Abnormal platelet adhesion to vessel wall
Reduced factor 8 amount/activity
(Usually carries factor 8 and mediates platelet adhesion)

61
Q

Von willebrand disease signs/symptoms

A

Unnoticed until additional stress

Spontaneous bleeding from mucous membranes (nosebleeds)
Excessive bleeding from wounds
Mennorhagia (heavy menstrual bleeding)

62
Q

Tests results von willebrand

A

Prolonged bleeding time with normal platelet count

63
Q

Hereditary haemorrhagic telangiectasia (HHT)

A

Autosomal dominant
Dilated microvascular swellings
GI haemmorhage = iron deficiency anaemia

64
Q

Congenital vessel wall abnormalities

A

HHT

Connective tissue disorders (Ehlers Danlos)

65
Q

Aquired vessel wall abnormalities

A

Senila purpura (bruising from age)
Steroids
Infections (measles, meningococcal)
Scurvy

66
Q

Vessel wall abnormalities presentation

A

Rash
Easy bruising
Spontaneous bleeding from small vessels (mucous membranes/skin)

67
Q

DIC

A

Disseminated intravascular coagulopathy

68
Q

DIC what is it?

A

Microangiopathic haemolytic anaemia

69
Q

What causes DIC

A

Pathological activation of coagulation

Malignancy, massive tissue injury, infections sepsis gram -ve, transfusion, haemorrhage

70
Q

What does DIC lead to?

A

Microthrombi in circulation
Consumption of platelets
Haemolytic anaemia

71
Q

Clotting tests DIC

A

Raised PT/INR, APTT, D dimers/fibrin degradation products

Low fibrinogen

72
Q

Congenital thrombophilias

A

Deficiency in anticoagulants (protein C, S and antithrombin)

Abnormal factor 5 (resistance to protein C)

73
Q

Aquired thrombophilias

A

Antiphospholipid syndrome (antiphospholipid antibodies)

74
Q

Anticoagulant drugs

A

Vit K inhibitors
Oral anticoagulants
Low molecular weight Heparin
Heparin

75
Q

Vit K inhibitors

A

Affects Vit K dependent factors (2, 7, 9, 20, protein C and protein S)

Monitor internal normalised ratio (PT time against normal)

76
Q

Direct oral anticoagulants example

A

Dabigatran
Rivaroxaban
Apixaban

77
Q

DOACS

A

Inhibit thrombin or factor 10a

No monitoring but careful if renal function is bad

78
Q

Low molecular weight heparins

A

Makes antithrombin stronger

Dose by weight

79
Q

Heparin monitor

A

APTT

80
Q

Anitplatelet drugs

A

Asprirn

Clopidogrel/ticagrelor

81
Q

Aspirin

A

Blocks formation of thromboxane A2 in platelets

82
Q

Clopidogrel/ticagrelor

A

Block platelets ADP receptor

83
Q

Complications with warfarin

A

Stop
Give Vit K
Prothrombin complex concentrate

84
Q

Heparin complications

A

Stop

Give protamine sulphate IV if needed

85
Q

Complications with anticoagulants =

A

EXCESSIVE BLEEDING

Path Pro 2023 (21 decks)

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