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Cardio > Haemostasis > Flashcards

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
Q

What are some additional general abnormal haemostasis treatment?

A

Desmopressin (^ VWF/factor 8),
Tranexamic Acid - antifibrinolytic
Fibrin Glue

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25
Q

What is the role of coagulation (2º Haemostasis)

A

Thrombin (IIa) formation for the conversion of fibrinogen to fibrin

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26
Q

Mechanism of 2º Haemostasis

A
  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
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27
Q

3 causes of Coag disorders

A

Deficiency of Coagulation Factor (Hereditary/acq)
Dilution (blood transfusion)
Increased Consumption (DIC/autoimmunity)

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28
Q

What are the two types of deficiency of coagulation factor with examples?

A

Hereditary (haemophilia A/B, factor 8/9 deficiency), Acquired (liver disease, anticoagulants)

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29
Q

What is Haemophilia

A

Failure to generate fibrin for stabilisation of platelet plug

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30
Q

What are the two hallmark features of haemophilia?

A

Haemarthrosis - bleeding into joint
Chronic leads to muscle wasting

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31
Q

What injections should you avoid in haemophilia?

A

Intramuscular - due to risk of muscle bleeding which is hard to control

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32
Q

Different Coag factor deficiencies

A

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
Q

Why does Liver failure cause disordered coagulation

A

Decreased production - most synthesised in the liver
(XCpt VWF/5)

34
Q

What is an example of increased consumption in coagulation disorders?

A

Disseminated Intravascular Coagulation (DIC)

35
Q

What is DIC and how does it work?

A

Disseminated Intravascular Coagulation - overactive Tissue Factor -> rapid coagulation -> depletion of platelets/coagulation factors -> deposition of fibrin in vessels causes organ failure

36
Q

What conditions is DIC associated with?

A

Sepsis, Major Tissue Damage, Inflammation

37
Q

What is consumed in DIC?

A

Coagulation Factors, Platelets, Fibrinogen

38
Q

What molecule can you detect in DIC blood tests?

A

D-dimer (breakdown product of fibrin)

39
Q

What are the clinical features of coagulation disorders?

A

Superficial cuts do not bleed, more deep bleeding.
Delayed but prolonged bleeding after trauma (stop start pattern)

40
Q

What is the clinical distinction between bleeding of primary and secondary haemostasis defects?

A

Primary - superficial bleeding to skin/mucosal membranes immediately after injury
Secondary - deep bleeding into tissue, delayed but prolonged bleeding after trauma

41
Q

Tests for coagulation disorders

A

Coagulation screen - PT, APTT, FBC
Measure Factor 8

42
Q

What is the difference between PT and APTT?

A

Prothrombin Time measures extrinsic pathway (factor 7)
Activated Partial Thromboplastin time measures intrinsic pathway

43
Q

What is measured by the PT/APTT

A

Time taken for clot formation (fibrin activation)

44
Q

What Factors are in the Intrinsic pathway

A

9,10,11,12
cofactors 5,8

45
Q

What Factors are in the Extrinsic pathway

A

1,2,3,7,10
cofactor 5

46
Q

What can a prolonged APTT but normal PT be a result of?

A

Haemophilia A/B, Factor XI or XII deficiency (intrinsic pathway before factor 10)

47
Q

What can a prolonged PT but normal APTT be a result of?

A

Factor VII deficiency

48
Q

What can a prolonged PT and APTT be a result of?

A

DIC, Dilution, Liver Failure, Anticoagulant Drugs

49
Q

What can a normal PT and APTT be a result of?

A

Healthy Patient, Primary Haemostasis Disorder

50
Q

How can you replace coagulation factors?

A

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
Q

What are some novel treatments for haemophilia?

A

Gene therapy, Bispecific antibodies (mimics function of factor 8), RNA Silencing

52
Q

What are two disorders of venous thrombosis?

A

Pulmonary Embolism,
Deep Vein Thrombosis

53
Q

What are the presentations of PE?

A

Chest pain, (pleuritic)
dyspnoea,
tachycardia,
hypoxia,

54
Q

What are the presentations of DVT?

A

Painful leg,
swelling,
red,
post-thrombotic syndrome (permanent damage to legs)

55
Q

What type of thrombosis is seen in each component of Virchow’s triad

A

Abnormal blood - venous
Abnormal blood flow - venous/arterial
Abnormal vessel wall - arterial

56
Q

What is it called if there is a higher hereditary risk to thrombosis?

A

Thrombophilia (e.g episode of thrombosis early in life)

57
Q

What is the mechanism of protein C and cofactor S

A

Inactivate 5a/8a

57
Q

What can tip the balance towards thrombosis

A

Red. anticoags (Antithrombin, protein C/S)
Increased coags/platelets (2/5/8/myeloproliferative disorders)

58
Q

What is the role of antithrombin

A

Inactivates 2a/10a

59
Q

What are examples of blood flow alterations leading to thrombosis?

A

Reduced flow - long haul flights, pregnancy (compression by baby), surgery

60
Q

How can you prevent thrombosis?

A

Prophylactic Anticoagulant Therapy

61
Q

How can you reduce the risk of recurring thrombosis?

A

Warfarin,
Direct Oral Anticoagulants,
Heparin (improve anticoagulation)

62
Q

Indications to use anticoagulant therapy for a px?

A

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
Q

Where is heparin found?

A

Produced by mast cells, naturally occuring glycosaminoglycan chain (GAG Chain)

63
Q

What is the mechanism of action of unfractionated heparin?

A

Enhances antithrombin
Change active site to improve binding to Factor 10a/thrombin
Long enough to tightly bind thrombin

64
Q

What are the two types of heparin?

A

Unfractionated (long chains),
LMWH (low molecular weight heparin)

65
Q

How are these heparins administered?

A

Unfractionated - IV,
LMWH - subcutaneous

66
Q

What is the action of LMWH?

A

Inhibit factor 10
too short to properly inhibit thrombin

67
Q

How can you monitor the effectiveness of unfractionated heparin?

A

APTT - will increase over time

68
Q

How can you monitor the effectiveness of LMWH and why?

A

Measure Anti-Xa
APTT not useful

69
Q

How does Warfarin work

A

Vit. K antagonist - blocks its recycling
.: no 2,7,9,10, C+S

70
Q

Problems with warfarin

A

Narrow therapeutic Index - differs btw pxs/lots of interactions
Requires constant monitoring
Takes a while to work

71
Q

Pros of warfarin

A

Reversible
- Vit.K - slow
- FFP/PCC - fast

72
Q

What are the side effects of warfarin?

A

Bleeding,
Skin Necrosis,
Purple toe syndrome (plaques bleed in extremities), Chondrodysplasia Punctata (bones in fetus fuse early)

73
Q

How can you monitor warfarin?

A

International Normalised Ratio - using prothrombin time
target is usually 2-3

74
Q

How can a patient build resistance to warfarin?

A

Lack of compliance,
increased vit K intake via diet
increased metabolism
red. binding

74
Q

What do DOACs target?

A

10a - Rivaroxaban
2a - Dabigatran

74
Q

Compare DOACs and Warfarin on onset of effect

A

Rapid DOAC, Slow Warfarin

74
Q

Why are DOACs better than warfarin

A

faster
fixed dose
fewer drug interactions
No monitoring required
lower risk of bleeding

74
Q

What drugs do you use for mechanical heart valves?

A

Warfarin (avoid DOACs as ineffective)

75
Q

What drugs do you use during pregnancy?

A

LMWH (DOACs unsafe in pregnancy)

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