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haemostasis Flashcards

1
Q

What is haemostasis? What is its purpose?

A

Cellular/biochemical process that enables regulated cessation of bleeding in response to injury.
-Purpose to prevent blood loss from intact vessels, stop bleeding from injured vessels & enable tissue repair

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2
Q

What is the first thing that happens as a response to endothelial cell lining injury?

A

Vasoconstriction - vascular smooth muscle cells contract locally to limit blood flow to injured vessel

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3
Q

What is primary haemostasis?

A

Formation of unstable platelet plug (platelet adhesion + aggregation) to limit blood loss & give surface for coagulation

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4
Q

What is secondary haemostasis?

A

Stabilisation of platelet plug with fibrin to stop blood loss

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5
Q

What is fibrinolysis?

A

Vessel repair & clot dissolution

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6
Q

What factors cause and stop bleeding? What is needed between them?

A

Anti-coagulant factors & fibrinolytic factors cause bleeding.
Coagulant factors/platelets cause potential thrombosis.
Balance is needed between the 2.

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7
Q

Under what conditions can the balance be tipped towards bleeding?

A
  1. lack of specific coagulant factor - failure of production, increased consumption
  2. defective function of factor - genetic, acquired, drug
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8
Q

What is the mechanism of primary haemostasis?

A
  • Damage to endothelium exposes collagen in vessel wall.
  • Platelets directly adhere to wall via glycoprotein 1a (GP1a) or indirectly via VWF via GP1b receptor (platelet adhesion).
  • This binding causes release of granular contents (ADP & thromboxane), flip-flopping & activation of GPIIb/IIIa receptors on platelets causing platelet aggregation
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9
Q

What platelet problems can cause disorders of primary haemostasis?

A
  1. platelets - thrombocytopenia due to bone marrow failure (leukaemia, B12 deficiency) - accelerated clearance of platelets (immune thrombocytopenia ITP, disseminated intravascular coagulation DIC), pooling of platelets in enlarged spleen
  2. impaired function of platelets (absence of glycoproteins or storage granules, acquired drugs - aspirin, NSAIDs, clopidogrel)
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10
Q

What is immune thrombocytopenic purpura (ITP)?

A

Anti-platelet antibodies cause phagocytosis of platelets by macrophages. Causes thrombocytopenia

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11
Q

what are some hereditary platelet defects and what happens in each?

A
  1. glanzmann’s thromboasthenia - absence of GPIIb/IIIa receptor on platelets
  2. bernard soulier syndrome - absence of GPIb receptors
  3. storage pool disease - reduction in granular content of platelets (dense granules)
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12
Q

What is mechanism of aspirin? How long does the effect last?

A

Aspirin irreversibly blocks COX so reduced production of thromboxane A2 from arachidonic acid, reduction in platelet aggregation.

  • Also prostacyclin inhibited by COX but can be generated by endothelial cell.
  • Single dose aspirin lasts 7 days until platelet replaced
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13
Q

What is is mechanism of clopidogrel?

A

Irreversibly blocks ADP receptor (p2y12) on platelet cell membrane so reduced platelet aggregation

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14
Q

What does VWF do?

A

Binds to collagen so that platelets can bind.

Stabilises factor 8 (can be low if VWF very low)

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15
Q

What are disorders of VWF function?

A

Von willebrand disease VWD is hereditary disease autosomal inheritance, deficiency of VWF (type 1 or 3) or abnormal VWF (type 2)

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16
Q

What are disorders of the vessel wall in primary haemostasis?

A
  1. inherited haemorrhagic telangiectasia - due to enhler danlos syndrome (collagen problem) & other connective tissue disorders
  2. acquired - steroid therapy can cause atrophy of collagen fibres
  3. ageing (senile purpura)
  4. scurvy (vitamin C deficiency causes defective collagen synthesis & weakening of capillary walls)
  5. vasculitis
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17
Q

What is difference between purpura and petechiae and echymosis?

A
  • Petechiae is <3mm. Petechiae usually only in thrombocytopenia
  • Purpura is between 3-10mm. Purpura does not blanch when pressure applied.
  • Echymosis is >10mm
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18
Q

What are clinical features of disorders of primary haemostasis?

A
  • bleeding immediate, prolonged bleeding from cuts, nose bleeds prolonged >20minutes, prolonged gum bleeding, menorrhagia, bruising easy + spontaneous, prolonged bleeding after trauma/surgery.
    2. thormbocytopenia (petechiae)
    3. purpura - thrombocytopenic or vascular disorders, wet purpura over mucosa like gums
    4. severe VWD - haemophilia like bleeding due to low F8
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19
Q

What are tests for disorders of primary haemostasis?

A

-Platelet count & morphology, bleeding time (PFA100 in lab), VWF assays, clinical observation, coagulation screen (PT, APTT) which are usually normal unless severe VWD causes low f8

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20
Q

What happens in disorders of primary haemostasis as platelet count gets lower?

A

Bleeding with trauma, spontaneous bleeding, severe spontaneous bleeding

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21
Q

What are treatments of abnormal primary haemostasis?

A
  1. replace missing factors/ platelets eg. VWF containing concentrates prophylactically or therapeutically
  2. if immune destruction immunosuppression (prednisolone) or splenectomy for ITP
  3. increased consumption - treat cause, replace
  4. desmopressin causes release of stored VWF (endogenous) for mild disorders
  5. tranexamic acid - anti-fibrinolytic - for trauma & strokes. 6. fibrin glue/spray for surgery
  6. OCP for mennorhagia
22
Q

What is secondary haemostasis goal?

A

To generate thrombin (IIa) which will convert fibrinogen to fibrin.

23
Q

What are disorders of coagulation?

A
  1. deficiency of coagulation factor (haemophilia) / liver disease, anticoagulant drugs (warfarin, direct oral anticoagulants DOACs)
  2. dilution - blood transfusion (inadequate replacement of blood)
  3. increased consumption - DIC or autoantibodies rarely
24
Q

What is haemophilia A & B? what factors are deficiency? What is the inheritence?

A

Haemophilia A (factor 8 deficiency), haemophilia B (factor 9 deficiency). Both sex linked, x-linked.

25
Q

What are clinical features of haemophilia?

A
  • Cant generate fibrin for platelet plug stability.
  • Haemarthrosis.
  • Fibroid synovial lining bleeding (muscle wasting + deformity), extensive haematoma when IM injections (avoid)
26
Q

What do different coagulation factor deficiencies cause (factor 8, 9, prothrombin -2, 11,12)?

A
  • absence of F8,9 (haemophilia) - severe but compatible with life.
  • Prothrombin deficiency F2 is lethal.
  • Factor 11 deficiency causing bleeding after trauma but not spontaneous.
  • Factor 12 deficiency causes no bleeding at all
27
Q

What are some acquired coagulation disorders?

A
  • Liver failure (most coagulation factors made in liver except factor 5 and VWF).
  • Anticoagulant drugs.
  • Dilution (RBC transfusions).
  • DIC (increased consumption of factors).
28
Q

What is DIC? (disseminated intravascular coagulation)

A
  • Generalised activation of coagulation - TF leads to widespread activation of coagulation triggered by things like sepsis and major tissue damage/inflammation.
  • Consumes and depletes coagulation factors and platelets.
  • Activation of fibinolysis depletes fibrinogen so raised D dimer
  • deposition of fibrin in vessels causes organ failure
29
Q

What are clinical features of coagulation disorders?

A
  • Superficial cuts don’t bleed (primary haemostasis handles it), bruising common, nosebleeds rare.
  • Spontaneous bleeding is deep in muscle & joints.
  • Bleeding after trauma can be delayed and is prolonged/frequently restarts after stopping
30
Q

What is difference between bleeding due to platelet & coagulation disorders?

A

Platelet disorders cause superficial bleeding into skin & mucosal surfaces, straight after injury.
In coagulation disorders bleeding is deep into tissues, muscle, joints, bleeding delayed but severe and prolonged

31
Q

What are tests done for coagulation disorders?

A

Clotting screen, PT, APTT, FBC, coagulation factor assays, tests for inhibitors

32
Q

What does prothrombin time PT measure? What pathway + what factors?

A

Extrinsic pathway. Factors 1,2,5,7,10

33
Q

What does activated partial thromboplastin time APTT measure? What pathway + factors?

A

Intrinsic pathway. Factors 1,2,5,8,9,10,11,12

34
Q

What causes prolonged PT with normal APTT?

A

F7 deficiency

35
Q

What causes both prolonged PT & APTT?

A

Liver disease, anticoagulant drugs, DIC, dilution, factors 1,2,5,10

36
Q

What are options for replacement of missing coagulation factors and what factors do they replace?

A
  1. fresh frozen plasma FFP: all coagulation factors
  2. cryoprecipitate - fibrinogen, F8, VWF, F13.
  3. factor concentrates: available for all except factor V.
  4. prothrombin complex concentrates PCC: F2,7,9,10.
  5. recombinant forms of F8 & 9 for prophylaxis of bleeding or treatment
37
Q

What are novel haemophilia treatments?

A

Gene therapy, bispecific antibodies (haem A- emicizumab mimics function of factor 8, binds to 9a & 10). RNA silencing - targets natural anticoagulant antithrombin

38
Q

What is tPA and what can it cause?

A

Tissue plasminogen activator is thrombolytic that breaks down clots. Used in stroke

39
Q

What does heparin do?

A

Anticoagulant (blood thinner)

40
Q

What is presentation of pulmonary embolism?

A

Shortness of breath, tachycardia, hypoxia, chest pain, haemoptysis, sudden death

41
Q

What is presentation of deep vain thrombosis DVT?

A

Painful leg, swelling, red, warm, may embolise into lungs, post-thrombotic syndrome (long standing damage to leg due to valve damage)

42
Q

Why can thrombosis happen and where?

A

Arteries and veins.
Can embolise to lungs
Intravascular coagulation or inappropriate coagulation

43
Q

What is virchows triad ?

A

Factors that contribute to thrombosis

  1. blood - dominant in venous
  2. vessel wall - dominant in arterial
  3. blood flow - in both
44
Q

What disruption in balance can cause thrombosis?

A

increased coagulant factors/platelets, decreased anti-coagulant proteins/fibrinolytic factors

45
Q

What can cause increased coagulant factors?

A

Genetic, can rise in cases like F8 in cancer, pregnancy. Factor 2, factor 5 leiden (increase activity due to activated protein C resistance)

46
Q

What can cause increase in platelets?

A

Myeloproliferative disorders

47
Q

What are anti-coagulant factors and when can we see reduction?

A

Antithrombin, protein C, protein S. nephrotic syndrome when they leak

48
Q

What do anti-coagulant proteins usually do?

A

Antithrombin inactivates thrombin and 10a.

Protein C and co-factor S inactivate factors

49
Q

Is it more common to have pro-coagulant excess or anti-coagulant reduction for thrombosis?

A

pro-coagulant excess

50
Q

What vessel changes can occur causing thrombosis?

A

Proteins active in coagulation expressed on surface of endothelial cells and expression altered in inflammation (TM, EPCR, TF)

51
Q

What blood flow changes can occur causing thrombosis?

A

Stasis - reduced flow, increases risk - surgery, long flight, pregnancy

52
Q

What is treatment of venous thrombosis?

A

Assess/prevent risks, prophylactic anticoagulant therapy. Reduce risk of recurrence/extension - lower pro-coagulant factors (eg warfarin, DOACs), increase anticoagulant activity (heparin)

BRS (81 decks)

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