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Haemostasis Flashcards

1
Q

What is haemostasis?

A

specific and regulated cessation of bleeding in response to vascular injury

Stopping blood flow after trauma

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2
Q

Reasons for homeostasis

A

Prevent blood loss
Enable tissue repair

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3
Q

Mechanism of haemostasis

A

Endothelial injury
Vessel constriction - limit blood flow to injured vessels
1º Homeostasis - form platelet plug to limit blood loss
2º Homeostasis - clot stabilisation w/ fibrin
Fibrinolysis - vessel repair/clot destruction

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4
Q

Balance model of haemostasis

A

Bleeding - Fibrinolytics, anticoagulants

Thrombosis - Platelets, coagulants

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5
Q

What can tip the balance towards bleeding

A

Lack of clotting factor - ^consumption/failed production
Clotting actor dysfunction - Genetic/Acq (drugs)

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6
Q

Summarise the mechanism of 1º Haemostasis

A
  1. Adhesion (platelets bind collagen via GP1a/damaged endothelium via VWF/GP1b)
  2. Activation (granule release: ADP/thromboxane A2 -> further activation and aggregation)
  3. Aggregation (GP2b/3a bind fibrinogen to signal formation of platelet plug)
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7
Q

What are the three structures that can be affected in primary haemostasis disorders?

A

Platelets,
VWF,
Vessel Wall

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8
Q

What are the two causes of platelet disorders?

A

Thrombocytopenia (low number),
Impaired Function

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9
Q

What are the two causes of thrombocytopenia, with examples?

A

Bone marrow failure (leukaemia/B12 deficiency)
Accelerated Clearance (ITP, DIC, Splenomegaly)

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9
Q

What is ITP and how does it work?

A

Immune Thrombocytopenic Purpura - autoantibodies bind to platelet and bring to macrophage for removal

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10
Q

What are the two ways of having impaired platelet function?

A

Hereditary (absence of glycoproteins on platelets) - rare
Acquired (NSAIDs, Aspirin, Clopidogrel)

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11
Q

How does aspirin work?

A

Inhibits synthesis of thromboxane A2 from arachidonic acid pathway - cannot form platelet plug

Irreversibly blocks COX

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12
Q

How long do the effects of aspirin last and why?

A

7 days - platelets will be regenerated

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13
Q

How does clopidogrel work?

A

Binds to ADP receptor on platelets preventing activation

Receptor P2Y12

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14
Q

Disorder affecting VWF

A

Von Willebrand disease
Hereditary red./LOF of VWF

can also be acq due to antibodies

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15
Q

2 Functions of VWF in haemostasis

A

Adhesion of platelets via GP1b
Stabilise clotting factor 8

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16
Q

What are the types of Von Willebrand disease?

A

Deficiency (Type 1 & 3), Abnormal function (Type 2)

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17
Q

What are some examples of vessel wall disorders?

A

Inherited - Ehlers Danlos Syndrome / connective tissue disorders
Acquired - Steroid Therapy, Ageing, Scurvy

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18
Q

What are the clinical features of disorders from primary haemostasis?

A

Immediate prolonged bleeding after impact, usually into the skin: nose bleeds (epistaxis), gum bleeds, menstrual heavy bleeds

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19
Q

What are the dermatological features of primary haemostasis disorders and how can you tell them apart?

A

Petechiae, Purpura, Ecchymoses: (bleeding under the skin) purpura is non-blanching with pressure(<3mm, 3-10mm, >10mm)

(pUrpura - Unblanching)

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20
Q

What sign is characteristic of thrombocytopenia

A

Petechiae - small spots caused by subdermal bleeding
<3mm

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21
Q

What are the main tests for primary haemostasis disorders?

A

Bleeding time,
Platelet count,
Clinical obs
Coag screen - PT and APTT will be normal

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22
Q

How to treat failure of prod/function of factors

A

Replace missing factors/platelets (can be prophylactic)
Stop causative drugs e.g. NSAIDs

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23
Q

How to treat immune destruction in abnormal haemostasis

A

Immunosuppression - prednisolone
Splenectomy in ITP

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24
What are some additional general abnormal haemostasis treatment?
Desmopressin (^ VWF/factor 8), Tranexamic Acid - antifibrinolytic Fibrin Glue
25
What is the role of coagulation (2º Haemostasis)
Thrombin (IIa) formation for the conversion of fibrinogen to fibrin
26
Mechanism of 2º Haemostasis
1. Initiation - TF on endothelium exp which activates 2,7,9,10 (rq vit.K). Small amount of thrombin formed from prothrombin 2. Amplification - IIa activates 5,8 which lead to greater prothrombin activation 3. Propagation - Huge burst of thrombin made to stabilise the clot
27
3 causes of Coag disorders
Deficiency of Coagulation Factor (Hereditary/acq) Dilution (blood transfusion) Increased Consumption (DIC/autoimmunity)
28
What are the two types of deficiency of coagulation factor with examples?
Hereditary (haemophilia A/B, factor 8/9 deficiency), Acquired (liver disease, anticoagulants)
29
What is Haemophilia
Failure to generate fibrin for stabilisation of platelet plug
30
What are the two hallmark features of haemophilia?
Haemarthrosis - bleeding into joint Chronic leads to muscle wasting
31
What injections should you avoid in haemophilia?
Intramuscular - due to risk of muscle bleeding which is hard to control
32
Different Coag factor deficiencies
Haemophilia A/B (8/9) - severe but compatible w/ life Prothrombin (2) Lethal Factor 11 - Non-spontaneous bleeding post trauma Factor 12 - No bleeding
33
Why does Liver failure cause disordered coagulation
Decreased production - most synthesised in the liver (XCpt VWF/5)
34
What is an example of increased consumption in coagulation disorders?
Disseminated Intravascular Coagulation (DIC)
35
What is DIC and how does it work?
Disseminated Intravascular Coagulation - overactive Tissue Factor -> rapid coagulation -> depletion of platelets/coagulation factors -> deposition of fibrin in vessels causes organ failure
36
What conditions is DIC associated with?
Sepsis, Major Tissue Damage, Inflammation
37
What is consumed in DIC?
Coagulation Factors, Platelets, Fibrinogen
38
What molecule can you detect in DIC blood tests?
D-dimer (breakdown product of fibrin)
39
What are the clinical features of coagulation disorders?
Superficial cuts do not bleed, more deep bleeding. Delayed but prolonged bleeding after trauma (stop start pattern)
40
What is the clinical distinction between bleeding of primary and secondary haemostasis defects?
Primary - superficial bleeding to skin/mucosal membranes immediately after injury Secondary - deep bleeding into tissue, delayed but prolonged bleeding after trauma
41
Tests for coagulation disorders
Coagulation screen - PT, APTT, FBC Measure Factor 8
42
What is the difference between PT and APTT?
Prothrombin Time measures extrinsic pathway (factor 7) Activated Partial Thromboplastin time measures intrinsic pathway
43
What is measured by the PT/APTT
Time taken for clot formation (fibrin activation)
44
What Factors are in the Intrinsic pathway
9,10,11,12 cofactors 5,8
45
What Factors are in the Extrinsic pathway
1,2,3,7,10 cofactor 5
46
What can a prolonged APTT but normal PT be a result of?
Haemophilia A/B, Factor XI or XII deficiency (intrinsic pathway before factor 10)
47
What can a prolonged PT but normal APTT be a result of?
Factor VII deficiency
48
What can a prolonged PT and APTT be a result of?
DIC, Dilution, Liver Failure, Anticoagulant Drugs
49
What can a normal PT and APTT be a result of?
Healthy Patient, Primary Haemostasis Disorder
50
How can you replace coagulation factors?
Fresh Frozen Plasma FFP(has everything), Cryoprecipitate (fibrinogen, VWF, 8), Concentrates (anything apart from 5), Prothrombin Complex concentrates PCC (2,7,9,10) Recombinant Forms (8/9)
51
What are some novel treatments for haemophilia?
Gene therapy, Bispecific antibodies (mimics function of factor 8), RNA Silencing
52
What are two disorders of venous thrombosis?
Pulmonary Embolism, Deep Vein Thrombosis
53
What are the presentations of PE?
Chest pain, (pleuritic) dyspnoea, tachycardia, hypoxia,
54
What are the presentations of DVT?
Painful leg, swelling, red, post-thrombotic syndrome (permanent damage to legs)
55
What type of thrombosis is seen in each component of Virchow's triad
Abnormal blood - venous Abnormal blood flow - venous/arterial Abnormal vessel wall - arterial
56
What is it called if there is a higher hereditary risk to thrombosis?
Thrombophilia (e.g episode of thrombosis early in life)
57
What is the mechanism of protein C and cofactor S
Inactivate 5a/8a
57
What can tip the balance towards thrombosis
Red. anticoags (Antithrombin, protein C/S) Increased coags/platelets (2/5/8/myeloproliferative disorders)
58
What is the role of antithrombin
Inactivates 2a/10a
59
What are examples of blood flow alterations leading to thrombosis?
Reduced flow - long haul flights, pregnancy (compression by baby), surgery
60
How can you prevent thrombosis?
Prophylactic Anticoagulant Therapy
61
How can you reduce the risk of recurring thrombosis?
Warfarin, Direct Oral Anticoagulants, Heparin (improve anticoagulation)
62
Indications to use anticoagulant therapy for a px?
Venous thrombosis (initial and long-term treatment) Atrial Fibrillation Mechanical Heart Valves Thromboprophylaxis e.g. post surgery (low conc) | 1. DOAC/LMWH 2. DOAC/Warf 3. Warf 4. doac/lmwh
63
Where is heparin found?
Produced by mast cells, naturally occuring glycosaminoglycan chain (GAG Chain)
63
What is the mechanism of action of unfractionated heparin?
Enhances antithrombin Change active site to improve binding to Factor 10a/thrombin Long enough to tightly bind thrombin
64
What are the two types of heparin?
Unfractionated (long chains), LMWH (low molecular weight heparin)
65
How are these heparins administered?
Unfractionated - IV, LMWH - subcutaneous
66
What is the action of LMWH?
Inhibit factor 10 too short to properly inhibit thrombin
67
How can you monitor the effectiveness of unfractionated heparin?
APTT - will increase over time
68
How can you monitor the effectiveness of LMWH and why?
Measure Anti-Xa APTT not useful
69
How does Warfarin work
Vit. K antagonist - blocks its recycling .: no 2,7,9,10, C+S
70
Problems with warfarin
Narrow therapeutic Index - differs btw pxs/lots of interactions Requires constant monitoring Takes a while to work
71
Pros of warfarin
Reversible - Vit.K - slow - FFP/PCC - fast
72
What are the side effects of warfarin?
Bleeding, Skin Necrosis, Purple toe syndrome (plaques bleed in extremities), Chondrodysplasia Punctata (bones in fetus fuse early)
73
How can you monitor warfarin?
International Normalised Ratio - using prothrombin time target is usually 2-3
74
How can a patient build resistance to warfarin?
Lack of compliance, increased vit K intake via diet increased metabolism red. binding
74
What do DOACs target?
10a - Rivaroxaban 2a - Dabigatran
74
Compare DOACs and Warfarin on onset of effect
Rapid DOAC, Slow Warfarin
74
Why are DOACs better than warfarin
faster fixed dose fewer drug interactions No monitoring required lower risk of bleeding
74
What drugs do you use for mechanical heart valves?
Warfarin (avoid DOACs as ineffective)
75
What drugs do you use during pregnancy?
LMWH (DOACs unsafe in pregnancy)

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