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Phase 1b - Cardiovascular & Respiratory Medicine > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Define haemostasis.

A
  • The cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult
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2
Q

What is the function of haemostasis (3)?

A
  • Prevention of blood loss from intact vessels
  • Arrest bleeding from injured vessels
  • Enable tissue repair
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3
Q

Outline the process of haemostasis (4 stages).

A
  • Vessel constriction
  • Primary haemostasis: Formation of an unstable platelet plug
  • Secondary haemostasis: Stabilisation of the plug with fibrin
  • Fibrinolysis: Vessel repair and dissolution of clot
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4
Q

Describe the first step of haemostasis (vessel constriction) (1A / 1E).

A

Action:
* Vascular smooth muscle cells contract locally

Effect:
* Limits blood flow to injured vessel

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5
Q

Describe the second step of haemostasis (primary haemostasis) (2A / 2E).

Primary haemostasis: Formation of an unstable platelet plug

A

Action:
* Platelet adhesion
* Platelet aggregation

Effect:
* Limits blood loss
* Provides surface for coagulation

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6
Q

Describe the third step of haemostasis (secondary haemostasis) (1A / 1E).

Secondary haemostasis: Stabilisation of the plug with fibrin

A

Action:
* Blood coagulation

Effect:
* Stops blood loss

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7
Q

Describe the fourth step of haemostasis (fibrinolysis) (2A / 1E).

Fibrinolysis: Vessel repair and dissolution of clot

A

Action:
* Cell migration / proliferation
* Fibrinolysis

Effect:
* Restores vessel integrity

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8
Q

What are the disorders of primary haemostasis divided into (cause specific) (3)?

A
  • Platelets caused
  • Von Willebrand Factor caused
  • Vessel wall caused
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9
Q

What are the platelet caused disorders of primary haemostasis (2)?

A
  • Thrombocytopenia (low numbers)
  • Impaired platelet function
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10
Q

What are the causes of thrombocytopenia leading to disorders of primary haemostasis (3)?

A
  • Bone marrow failure:
    • e.g. Leukaemia / B12 deficiency
  • Accelerated clearance:
    • Immune Thrombocytopenia (ITP) / Disseminated Intravascular Coagulation (DIC)
  • Pooling and destruction in an enlarged spleen
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11
Q

What are the causes of impaired platelet function leading to disorders of primary haemostasis (2)?

A
  • Hereditary absence of glycoproteins or storage granules
  • Acquired due to drugs:
    • Aspirin / NSAIDs / Clopidogrel (common)
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12
Q

What is the Von Willebrand factor caused disorder of primary haemostasis (1)?

A
  • Von Willebrand disease

VWF has two functions in haemostasis:
* Binding to collagen and capturing platelets
* Stabilising Factor VIII
* Factor VIII may be low if VWF is very low

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13
Q

What are the causes of Von Willebrand disease (2)?

A
  • Hereditary decrease of quantity and / or function (common)
    • Deficiency of VWF (Type 1 or 3)
    • VWF with abnormal function (Type 2)
  • Acquired due to antibody (rare)

VWF has two functions in haemostasis:
* Binding to collagen and capturing platelets
* Stabilising Factor VIII
* Factor VIII may be low if VWF is very low

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14
Q

What are the vessel wall caused disorders of primary haemostasis (2)?

A
  • Inherited connective tissue disorders (rare):
    • Hereditary haemorrhagic telangiectasia / Ehlers-Danlos syndrome
  • Acquired (common):
    • Steroid therapy / Ageing (‘senile’ purpura) / Vasculitis / Scurvy (Vitamin C deficiency)
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15
Q

How would a patient with suspected primary haemostasis disorder present (8)?

A

Typical primary haemostasis bleeding:
* Immediate
* Prolonged bleeding from cuts
* Nose bleeds (epistaxis): prolonged > 20 mins
* Gum bleeding: prolonged
* Heavy menstrual bleeding (menorrhagia)
* Bruising (ecchymosis), may be spontaneous / easy
* Prolonged bleeding after trauma or surgery

Skin signs:
* Petechiae
* Purpura

Petechiae and Purpura are caused by bleeding under the skin Purpura do not blanch when pressure is applied
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16
Q

What investigations are suggested in suspected primary haemostasis disorder (5)?

A
  • Platelet count
  • Platelet morphology
  • Bleeding time (PFA100 in lab)
  • Assays of von Willebrand Factor
  • Clinical observation

N.B. Coagulation screen (PT, APTT) is normal (except more severe VWD cases where FVIII is low)

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17
Q

What are the management principles of primary haemostasis disorder (6)?

A

Failure of production/function:
* Replace missing factor / platelets e.g. VWF containing concentrates
* Prophylactic
* Therapeutic
* Stop drugs e.g. aspirin/NSAIDs

Immune destruction:
* Immunosuppression (e.g. prednisolone)
* Splenectomy for ITP

Increased platelet consumption:
* Treat cause
* Replace as necessary

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18
Q

What haemostatic treatments are used in the management of primary haemostasis disorder (4)?

A
  • Desmopressin (DDAVP)
    • Vasopressin analogue
    • 2-5 fold increase in VWF (and FVIII)
    • Releases endogenous stores (so only useful in mild disorders)
  • Tranexamic acid
    • Antifibrinolytic
  • Fibrin glue / spray
  • Other approaches e.g hormonal (oral contraceptive pill for menorrhagia)
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19
Q

What are the disorders of secondary haemostasis divided into (cause specific) (3)?

A
  • Deficiency of coagulation factor production
  • Dilution of coagulation factor
  • Increased consumption of coagulation factor
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20
Q

What are the deficiency-of-coagulation-factor-production-caused disorders of secondary haemostasis (4)?

A

Hereditary:
* Factor VIII/IX: haemophilia A/B (respectively)

Acquired:
* Liver disease - decreased production
* Most coagulation factors are synthesised in the liver
* Anticoagulant drugs
* Warfarin
* Direct Oral Anticoagulants (DOACs)

Deficiency of coagulation factor:
* Factor VIII and IX (Haemophilia)
* Severe but compatible with life
* Spontaneous joint and muscle bleeding
* Prothrombin (Factor II)
* Lethal
* Factor XI
* Bleed after trauma but not spontaneously
* Factor XII
* No bleeding at all

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21
Q

What is the dilution-of-coagulation-factor-caused disorder of secondary haemostasis (1)?

A

Acquired:
* Blood transfusion
* Red cell transfusions no longer contain plasma
* Major haemorrhage requires transfusion of plasma as well as red cells and platelets

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22
Q

What are the increased-consumption-of-coagulation-factor-caused disorders of secondary haemostasis (2)?

A

Acquired:
* Disseminated intravascular coagulation (DIC) (common)
* Immune – autoantibodies (rare)

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23
Q

How would a patient with suspected secondary haemostasis disorder present (8)?

A
  • Superficial cuts do not bleed (platelets)
  • Bruising is common
  • Nosebleeds are rare
  • Spontaneous bleeding is deep, into muscles and joints -> muscle wasting
  • Bleeding after trauma may be delayed and is prolonged
  • Bleeding frequently restarts after stopping
  • Chronic haemarthrosis: The hallmark of haemophilia.
Haemarthrosis
24
Q

How would one make the clinical distinction between bleeding due to platelet and coagulation defects?

A

Platelet / Vascular:
* Superficial bleeding into skin, mucosal membranes
* Bleeding immediate after injury

Coagulation:
* Bleeding into deep tissues, muscles, joints
* Delayed, but severe bleeding after injury; bleeding often prolonged

25
Q

What investigations are suggested in suspected secondary haemostasis disorder (5)?

A
  • Screening tests (‘clotting screen’)
    • Prothrombin time (PT)
    • Activated partial thromboplastin time (APTT)
  • Full blood count (FBC) (platelets)
  • Coagulation factor assays (for Factor VIII etc)
  • Tests for inhibitors
26
Q
  • PT: 10.6 secs (9.6 - 11.6)
  • APTT: 85 secs (26 - 32)

What could cause these results (4)?

A
  • Haemophilia A
  • Haemophilia B
  • Factor XI deficiency
  • Factor XII deficiency
27
Q
  • PT: 26 secs (9.6 - 11.6)
  • APTT: 29 secs (26 - 32)

What could cause these results (1)?

A
  • Factor VII deficiency
28
Q
  • PT: 26 secs (9.6 - 11.6)
  • APTT: 49 secs (26 - 32)

What could cause these results (4)?

A
  • Liver disease
  • Anticoagulant drugs e.g. warfarin
  • DIC (platelets and D dimer)
  • Dilution following red cell transfusion
29
Q

What are the management principles of secondary haemostasis disorder (3)?

A

Failure of production/function:
* Replace missing factor / platelets e.g. VWF containing concentrates
* Prophylactic
* Therapeutic

Increased platelet consumption:
* Treat cause
* Replace as necessary

30
Q

What treatments are used in the management of secondary haemostasis disorder (4)?

A
  • Plasma (fresh frozen plasma FFP)
    • Contains all coagulation factors
  • Cryoprecipitate
    • Rich in Fibrinogen, FVIII, VWF, Factor XIII
  • Factor concentrates
    • Concentrates available for all factors except factor V
    • Prothrombin complex concentrates (PCCs) - Factors II, VII, IX, X
  • Recombinant forms of FVIII and FIX are available
    • ‘On Demand’ to treat bleeds
    • Prophylaxis to prevent bleeds
31
Q

What haemostatic treatments are used in the management of secondary haemostasis disorder (2)?

A
  • Desmopressin (DDAVP)
    • Vasopressin analogue
    • 2-5 fold increase in VWF (and FVIII)
    • Releases endogenous stores (so only useful in mild disorders)
  • Tranexamic acid
    • Antifibrinolytic
32
Q

Outline the pathophysiology of thrombosis (causes 4 diseases).

A

Can cause to:
* Pulmonary Embolism (PE)
* Deep Vein Thrombosis (DVT)
* Heart Attack
* Stroke

33
Q

How would pulmonary embolism (PE) present (6)?

A
  • Tachycardia
  • Hypoxia
  • Shortness of breath
  • Chest pain
  • Haemopysis
  • Sudden death
34
Q

How would deep vein thrombosis (DVT) present (6)?

A
  • Painful leg
  • Swelling
  • Red
  • Warm
  • May embolise to lungs
  • Post thrombotic syndrome
35
Q

The pathogenesis of venous thrombosis can be broken down to Virchow’s triad. What makes up Virchow’s triad?

Virchow’s triad: the three contributory factors to thrombosis

A
  • Blood: dominant in venous thrombosis
  • Vessel wall: dominant in arterial thrombosis
  • Blood flow: contributes to both arterial and venous thrombosis
36
Q

Describe the pathogenesis of thrombosis that makes up the blood from Virchow’s triad (1).

Dominant in venous thrombosis.

A

Increased coagulant factors platelets:
* Factor VIII
* Factor II
* Factor V Leiden
* (increase activity due to activated protein C resistance)
* Myeloproliferative disorders (plts increase)

37
Q

Describe the pathogenesis of thrombosis that makes up the vessel wall from Virchow’s triad (1).

Dominant in arterial thrombosis.

A
  • Many proteins active in coagulation are expressed on the surface of endothelial cells and their expression altered in inflammation (TM, EPCR, TF)

We know little about the role of the vessel wall in venous thrombosis.

38
Q

Describe the pathogenesis of thrombosis that makes up the blood flow from Virchow’s triad (1).

Contributes to both arterial and venous thrombosis.

A
  • Reduced flow (stasis) increases the risk of thrombosis
    • e.g. surgery, long haul flight, pregnancy
39
Q

What is used in the therapeutic management of venous thrombosis (Initial 4 / Long 2)?

A
  • Initial treatment (surgery / angiograph) to minimise clot extension / embolisation (< 3 months):
    • DOAC or LMWH for first few days followed by DOAC or Warfarin
  • Long term treatment to reduce risk of recurrence
    • DOAC or Warfarin
40
Q

What is used in the therapeutic management of atrial fibrillation (2)?

Why is atrial fibrillation managed?
* To reduce risk of embolic stroke

A

DOAC or Warfarin

41
Q

What is used in the therapeutic management of mechanical prosthetic heart valve (1)?

A

Warfarin (DOACs not effective and should be avoided)

42
Q

What is used in the preventative (thromboprophylaxis) management of venous thrombosis (Surgery 2 / Hospital 1 / Pregnancy 1)?

E.g. following surgery, during hospital admission, during pregnancy

A
  • Following surgery: LMWH or DOAC
  • During hospital admission: LMWH (DOACs not effective for use as medical thromboprophylaxis)
  • During pregnancy: LMWH (DOACs not safe in pregnancy)
43
Q

What are the 2 forms of heparin?

A
  • Unfractionated heparin (UFH)
  • Low molecular weight heparin (LMWH)
44
Q

What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to molecular weight?

A
  • As the name suggests, UFH is unfractionated, meaning it has a variable molecular weight. In contrast, LMWH is a fractionated form of heparin with a lower molecular weight.
45
Q

What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to mechanism of action?

A
  • Both UFH and LMWH inhibit clotting factors by binding to antithrombin III, but the binding is more specific and longer-lasting with LMWH.
46
Q

What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to administration?

A
  • UFH is administered through injection into a vein or under the skin, whereas LMWH can be given subcutaneously.
47
Q

What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to monitoring?

A
  • UFH requires regular monitoring of its effect on blood clotting through aPTT (activated partial thromboplastin time) tests, whereas LMWH typically does not require monitoring.
48
Q

What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to reversal?

A
  • In cases of bleeding or overdose, UFH can be reversed using protamine sulfate, while there is no specific reversal agent for LMWH.
49
Q

What are the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) when it comes to indications?

A
  • UFH is commonly used in the treatment of acute thrombotic events, whereas LMWH is often used for prophylaxis against deep vein thrombosis (DVT) and pulmonary embolism (PE) after surgery.
50
Q

What is the mechanism of action of warfarin [Vitamin K Antagonists (VKA)] (3)?

A
  1. Competes with Vitamin K – complicated metabolism
  2. Reduces production of functional coagulation factors
  3. Induces an anticoagulated state slowly

  • Many dietary, physiological and drug interactions
  • Narrow therapeutic index and requires monitoring
51
Q

What is the mechanism of reversing action of warfarin [Vitamin K Antagonists (VKA)] (Slowly 1 / Rapidly 2)?

A
  • Reversed slowly by Vit K administration – takes several hours to work
  • Reversed rapidly by infusion of coagulation factors:
    • PCC (Prothrombin Complex Concentrate- contains Factors II, VII, IX and X)
    • FFP (Fresh Frozen Plasma)
52
Q

What are the adverse effects of warfarin [Vitamin K Antagonists (VKA)]?

A
  • Bleeding
    • Minor 5% pa
    • Major 0.9 – 3.0% pa
    • Fatal 0.25% pa
  • Skin Necrosis
  • Purple toe syndrome
  • Embryopathy – Chondrodysplasia punctata
53
Q

Warfarin [Vitamin K Antagonists (VKA)] requires monitoring when administer. What equation is used for that?

A

INR (International Normalised Ratio)

  • ISI = International Sensitivity Index
  • Indicates sensitivity of particular thromboplastin for warfarin

Unanticoagulated normal INR = 1.0
Target INR usually 2-3

54
Q

What factors can lead to warfarin [Vitamin K Antagonists (VKA)] resistance (4)?

A
  • Lack of patient compliance
    • Measure warfarin levels
    • Proteins Induced by Vitamin K Absence (PIVKA)
  • Diet, Increased Vit K intake
  • Increased metabolism Cyt P450 (CYP2C9)
  • Reduced binding (VKORC1)
55
Q

What are the differences between warfarin [Vitamin K Antagonists (VKA)] and direct oral anticoagulants (DOACs) when it comes to:
* Onset / Offset
* Dosing
* Food effect
* Interactions
* Monitoring required
* Renal dependence
* Reversibility

A

Phase 1b - Cardiovascular & Respiratory Medicine (21 decks)

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