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Pathological Processes > PP 5 Intro To Haemostasis > Flashcards

PP 5 Intro To Haemostasis Flashcards

1
Q

What is haemostasis?

A

Stopping of blood flow

Maintains fluid stasis in vessels whilst permitting rapid clot formation

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2
Q

What are the 3 components of haemostasis?

A

Intact vascular wall
Platelets
Coagulation cascade - (anti)coagulation factors

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3
Q

Aim of haemostasis

A

Stop bleeding after trauma to blood vessel

  1. Make clot
  2. Control clotting
  3. Breakdown clot
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4
Q

Process of haemostasis

A

1- contraction of vessel wall
2- formation of platelet plug at site
3- formation of fibrin clot to stabilise

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5
Q

Vessel wall structure

A

Tunica intima - endothelium
Tunica media - smooth muscles
Tunica adventitia - comprised of fibroblasts + collagen

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6
Q

What happens to the vessel wall in haemostasis

A
  • vasoconstriction- increased blood flow
  • production of vWF
  • exposure of collagen + tissue - initiates activation of clotting factor
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7
Q

What is vWF?

A

Von Willebrand factor

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8
Q

Von Willebran factor function

A

Platelet adherence
Carries + protects factor VIII

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9
Q

What are platelets made from?

A

Cytoplasm of megakaryocyte in bone marrow

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10
Q

Platelet life span

A

7-10 days

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11
Q

Describe platelets

A

Disc shaped
Anucleated

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12
Q

Platelet action at injury

A

Adhesion
Activation/secretion
Aggregation

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13
Q

Describe platelet adhesion

A
  • After vessel wall damage - exposure of underlying tissues
  • Platelets adhere to collagen via vWF
  • vWF acts as a bridge between platelets + collagen
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14
Q

Describe platelet activation/secretion

A
  • Platelets secrete granules containing ADP, thoromboxane etc..
  • Granules get activated + activate other platelets
  • Activation of clotting cascade
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15
Q

Describe platelet aggregation

A
  • Cross linking of platelets to form platelet plug
  • Provides some stability but friable
  • Need to form clot - more stable
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16
Q

List mediating factors of platelet action + their functions

A
  • fibrinogen- links platelets
  • collagen- binds platelets
  • ADP + thromboxane- causes interaction of platelets to make plug
  • thrombin- converts fibrinogen to fibrin
  • von Willebran factor- platelet adherence
  • platelet receptors- glycoproteins complexes e.g. GP1, GPIIa/Ia - binding site for fibrinogen
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17
Q

Fibrinogen function in clotting cascade

A

Links platelets to from platelet plug

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18
Q

Collagen function in clotting cascade

A

Binds platelets

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19
Q

ADP + thromboxane function in clotting cascade

A

Cause interaction of platelets to make plug

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20
Q

Thrombin function in clotting cascade

A

Converts fibrinogen to fibrin

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21
Q

Von Willebrand factor function in clotting cascade

A

Platelet adherence
Carries factor VIII

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22
Q

What are tests for clotting defects performed on?

A

Platelet poor plasma

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23
Q

Test for clotting defects

A

APTT activated partial thromboplastin time
PT prothrombin time
TT thrombin time

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24
Q

What does APTT test?

A

Activated partial thromboplastin time
Intrinsic pathways
Factors VIII, IX, XI, VIII

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25
Q

What does PT test?

A

Prothrombin time
Tests extrinsic pathway
PET

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26
Q

What does TT test?

A

Thrombin time
Tests conversion of fibrinogen to fibrin by thrombin

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27
Q

What converts fibrinogen to fibrin?

A

Thrombin

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28
Q

What factors are in the common pathway?
What do deficiencies in them do?

A

Factors of 10
Factor V
Factor X
Prothrombin II
Fibrinogen I

Prolong APTT + PT

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29
Q

What do deficiencies in factors V, X thrombin + fibrinogen prolong?
Why?

A

APTT and PT
In the common pathway

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30
Q

Functions of natural anticoagulants

A

Stop over clotting
Breakdown clot

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31
Q

Natural anticoagulant examples

A

Antibthromin
Protein C + S

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32
Q

Function of anttithrombin

A

Inhibits action of thrombin

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33
Q

Explain the action of antithromin

A
  • Activated by heparin on surface of endothelial cells
  • Prevent spread of a clot by rapidly inactivating clotting factors - carried away in blood
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34
Q

Explain how protein C is activated

A
  • thrombin binds to thrombomodulin
  • this complex activates protein C
  • activated protein C inactivates factor VIIIa + Va&raquo_space; prevents prothrombin > thrombin
  • protein S is a cofactor for APC
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35
Q

Function of activated protein C

A

Prevents prothrombin > thrombin

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36
Q

Function of tissue factor (extrinsic) pathway inhibitor

A

Opposes clot formation
Inhibits ability to generate Xa

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37
Q

What are the two pathways of the clotting cascade?

A

Contact activation (intrinsic) pathway
Tissue factor (extrinsic) pathway

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38
Q

What converts prothrombin to thrombin?

A

Factor Xa + Va

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39
Q

What is the intrinsic pathway measured by?

A

Activated partial thromboplastin time

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40
Q

What is the extrinsic pathway measured by?

A

Prothrombin time

41
Q

Factors in the intrinsic pathway of the clotting cascade

A

INtrinsic - 12INch sub
XII > XIIa
XI > XIa
IX > IXa
VIII
X > Xa

42
Q

Factors in extrinsic pathway of clotting cascade

A

Extrinsic - sEvEn
VII > VIIa
X > Xa

43
Q

What triggers the intrinsic pathway of the clotting cascade?

A

Exposure of collagen after blood vessel is damaged

44
Q

What triggers the extrinsic pathway of the clotting cascade?

45
Q

Do natural anticoagulants destroy clots?
If not, what do they do?

A

No
They oppose production of fibrin to control clotting cascade

46
Q

When does tissue factor pathway inhibitor act?

A

Initiation phase of clotting

47
Q

What breaks down fibrin ?

48
Q

Function of plasmin

A

Breaks down fibrin
Dissolves thrombus

49
Q

What does fibrin get broken down into?

A

D-dimers
+ other fibrin degradation products

50
Q

What can be tested in the blood for clotting?

51
Q

What converts plasminogen to plasmin?

A

Tissue plasminogen activator (tPA)

52
Q

How can tPA be used therapeutically?

A

Dissolving thrombin and thromboembolisms

53
Q

Side effect of tPA usage therapeutically

A

Undesired bleeding

54
Q

What are bleeding disorders due to?

A

Abnormalities in vessel wall, platelets or coagulation factors

55
Q

What is thrombocytopenia?

A

Deficiency of platelets

56
Q

Presentation of thrombocytopenia

A

Puparia
Petechiae
Mucosal bleeding
Epistaxis
Menorrhagia

57
Q

What is purpura?

A

Red/purple blemishes/bruises

58
Q

What is petechiae?

A

Small round spots on skin from bleeding

59
Q

What is epistaxis?

A

Nose bleeds

60
Q

What is menorrhagia?

A

Heavy periods

61
Q

What is the condition where you have low platelet count with the absence of a cause?

A

Immune thrombocytopenia purpura

62
Q

What is immune thrombocytopenia purpura?

A

Low platelets
With absence of cause

Immune disease

63
Q

What is thrombotic thrombocytopenia purpura?

A
  • Blood clots form in small vessels
  • Increased consumption of platelets + RBCs due to breakdown

Immune disease

64
Q

What is haemolytic uraemic syndrome?

A

Low RBC + platelets
Acute kidney injury
Associated with E. coli
In children more than adults
Non immune

65
Q

Signs + symptoms of haemolytic uraemic syndrome

A

Fever
Vomiting
Weakness
Kidney failure
Low platelts
Bloody diarrhoea

66
Q

What is hypersplenism?

A

Enlargement of spleen
Decreased circulating blood cells
Proliferation response in bone marrow
Non immune disease

67
Q

Treatment of Hypersplenism

A

Splenectomy

68
Q

List congenital coagulation factor disorders

A

Haemophilia A
Haemophilia B
Von Willebrand’s disease

69
Q

List acquired coagulation factor disorders

A

Disseminated Intravascular coagulation
Liver disease
Vitamin K deficiency
Anticoagulants

70
Q

Presentation of haemophilia

A

Muscle haematomas
Joint pain + deformities
Recurrent haemarthroses
Prolonged bleeding post dental extraction
Life threatening post-op + trauma bleeding
Intracerebral haemorrhage
Spontaneous bleeding

71
Q

Where does spontaneous bleeding occur in haemophilia?

A

In sites subject to trauma e.g. joints

72
Q

What causes haemophilia A?

A

Factor VIII deficiency

‘Ate’

73
Q

Treatment of haemophilia A

A

Recombinant factor VIII

74
Q

Clotting test in haemophilia A

A

Factor VIII in intrinsic pathway
Prolonged APTT
Normal PT

75
Q

What type of genetic condition is haemophilia?

A

X linked recessive

76
Q

Who do X linked recessive conditions effect?

A

All males
Homozygous for mutation females

77
Q

What causes haemophilia B?

A

Factor IX deficiency

‘Benign’ - B nine

78
Q

Clotting tests in haemophilia B

A

Factor IX in intrinsic pathway
Prolonged APTT
Normal PT

79
Q

Treatment of haemophilia B

A

Recombinant factor IX

80
Q

Which haemophilia has a increased risk of bruising and mucosal bleeds?

81
Q

What type of genetic condition is Von Willebrand disease?

A

Autosomal dominant

82
Q

Cause of Von Willebrand disease

A

Several genetic defects

83
Q

vWF function and how is it effected in Von Willebrand disease?

A
  • Carries factor VIII - decreased factor VIII + activity
  • Mediates platelet adhesion - abnormal platelet adhesion to vessel
84
Q

Presentation of Von Willebrand disease

A

Epistaxis
Excessive wound bleeding
Menorrhagia
Prolonged bleeding time with normal platelet count

85
Q

Platelets in haemophilia

A

Platelets unaffected
Low clotting factors > less fibrin made

86
Q

What type of anaemia is DIC?
Describe how it causes anaemia

A
  • Microangiopathic haemolytic anaemia
  • Many microthrombi formed in circulation > increased consumption of clotting factors + platelets
87
Q

What is DIC?

A

Disseminated intravascular coagulopathy

88
Q

Clotting tests in DIC

A

Raised PT
Raised APTT
Low fibrinogen
Raised D dimers

89
Q

Causes of DIC

A

must always be a trigger
Malignancy
Massive tissue injury e.g. burns
Infection
Massive haemorrhage
Amniotic fluid embolism
Pre-eclampsia
Placental abruption

90
Q

Complications of anticoagulants and what to do dependent on the drug used

A

Bleeding

  • if warfarin - stop
    - give vitamin K
    - if emergency > prothrombin complex
    concentrate
  • if heparin - stop
    - give protamine sulphate if needed
91
Q

Where is prothrombin made?

92
Q

What is prothrombin?

A

Protein
Clotting factor

93
Q

What are the vitamin K dependent clotting factors?

A

II - prothrombin
VII
IX
X
Anticoagulants - Protein C + S

94
Q

What do DOACs do?

A

Inhibit thrombin + factor Xa

95
Q

Examples of DOACs

A

Dabigatran
Rivaroxaban
Apixaban

96
Q

Causes of thrombophilias

A
  • Congential - deficiency in natural anticoagulants
    - abnormal factor V > factor V Leiden
  • Acquired - antiphospholipid syndrome
97
Q

What are thrombophilias?

A

Abnormality in blood coagulation that increases the risk of thrombosis

98
Q

Presentation of vessel wall abnormalities

A

Bruises easily
Spontaneous bleeding from small vessels
Purpura
Petechiae

Pathological Processes (14 decks)

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