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Haem- oscar > haemostasis > Flashcards

haemostasis Flashcards

1
Q

give an overview of the response to vessel injury

A
  1. vessel constricts
    2.primary haemostasis- formation of an unstable platelet plug (platelet adhesion and aggregation)
    3.secondary haemostasis- formation of a stable plus (stabilisation with fibrin) (blood coagulation)
    4-dissolution of the clot (via fibrinolysis) and vessel repair
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2
Q

describe primary haemostasis

A

Platelet adhesion- von willebrand factor (vWF) binds to the exposed collagen –> Glycoprotein 1-b on platelets bind to vWF

OR

Platelet directly binds to exposed collagen via Glycoprotein 1-a

Platelet aggregation: binding of platelets activates them–> they release ADP and THROMBOXANE—> +ve feedback activates platelets more–> activates glp-IIb/IIIa on platelet surface–> binds to circulating fibrinogen–> forms platelet aggregate

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3
Q

describe secondary haemostasis

A

intrinsic pathway:XII-XIIa–>XI-XIa–>IX-IXa (tissue factor acts here-activates VII-VIIa) +VIIIa—> X-Xa(where the pathways converge)–> prothrombin-thrombin–>fibrinogen-fibrin+XIIIa–>cross linked fibrin

Extrinsic pathway: tissue factor activates VII-VIIa—>X-Xa—>then same as intrinsic pathway

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4
Q

describe fibrinolysis

A

Plasminogen—(tissue plasminogen activator, tPA)—> plasmin—> fibrin degradation

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5
Q

describe prostacyclin synthesis + location + function

A

membrane phospholipid–> Arachidonic acid—COX–> endoperoxides (PGG2, PGH2)—> PGI2 aka prostacyclin

endothelialial cells

potent inhibitor of platelet function

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6
Q

describe thromboxane synthesis + location + function

A

membrane phospholipid–> Arachidonic acid—COX–> endoperoxides (PGG2, PGH2)—> Thromboxane A2

platelet

endoperoxidases and thromboxane are potent inducers of platelet aggregation

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7
Q

what are the main anti platelet therapies

A

COX-1 inhibitor - aspirin (irreversible)
ADP receptor antagonist - prasugrel
Glp-IIb/IIIa antagonist - abciximab

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8
Q

what are the uses of anti-platelet drugs

A

angina, post-myocardial infarction

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9
Q

mechanism of action of heparin + indications for use

A

it accelerates the action of a natural plasma inhibitor, antithrombin (ie inhibits: thrombin (IIa), F10a, F9a, F11a by forming irreversible complexes with them–> inactivation)

indications: used for immediate anticoagulation in venous thrombosis and pulmonary embolism

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10
Q

mechanism of action of warfarin + indication for use

A

WARFARIN antagonises the action of vitamin K, so warfarin blocks the assembly of the coagulation factors on the platelet surface. (as coagulation factors synthesis is vital-K dependant)
enzyme that is inhibited is a complex called vitamin-K epoxide reductase

indications:Venous thrombosis: warfarin treatment for 6 months. Atrial fibrillation: warfarin treatment is life long.

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11
Q

what are the different lab tests for coagulation

A

Activated partial thromboplastin time (APTT): activated coagulation through FXII and therefore detects abnormalities in intrinsic and common pathways

Prothrombin time (PT): initiates coagulation through tissue factor and therefore detects abnormalities in the extrinsic and common pathways.

Thrombin clotting time (TCT): add thrombin- shows abnormalities in conversion of fibrinogen to fibrin.

Factor assays (for Factor VIII etc.)
In haemophilia, the APTT is prolonged because you are not making factor 8 or 9
  • PT will be normal (extrinsic pathway not affected) – TYPICAL CLOTTING SCREEN FOR HAEMOPHILIA
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12
Q

uses of coagulation tests

A
  • APTT and PT are used together for screening for causes of bleeding disorders
  • APTT is used to monitor heparin therapy in thrombosis
  • PT is used for monitoring warfarin treatment in thrombosis
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13
Q

what are the platelet function tests

A

Bleeding time, 2-9 minutes–indicates that the platelets are acting abnormally with the vessel wall
Platelet count, 150-400 x10^9/L
Platelet aggregation—It is used in inherited platelet abnormalities, and von Willebrand Disease

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14
Q

what are the clinical features of people with primary haemostasis

A

problem with platelets- no formation of unstable plug:

  • Immediate
  • Prolonged bleeding from cuts
  • Epistaxes (nose bleed>10 mins)
  • Gum bleeding (areas of high shear without functioning vWF)
  • Menorrhagia (heavy + prolonged menstrual bleeding)
  • Easy bruising
  • Prolonged bleeding after trauma or surgery
  • Thrombocytopenia > petechiae (small dotted bruising)
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15
Q

what are the clinical features of people with secondary haemostasis

A

problem with stabilisation of platelet plug:

  • Spontaneous bleeding is deep, into muscles and joints (HAEMARTHRITIS)
  • Bleeding after trauma may be delayed and is prolonged
  • Superficial cuts do not bleed (platelets)
  • Bruising is common,
  • Nosebleeds are rare
  • Frequently restarts after stopping
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16
Q

causes of primary haemostasis disorders

A

Platelets:
-Thrombocytopenia: eg Bone marrow failure (leukaemia), DIC (disseminated…)
-Von Willebrand Disease (deficient or impaired)
-Impaired function: Acquired due to drugs, eg aspirin, NSAIDs,
The vessel wall: -
hereditary vascular disorders (Hereditary haemorrhagic telangiectasia),
-scurvy,
-steroids,
-age

17
Q

causes of secondary haemostasis disorders

A

hereditary: Haemophilia A (FVIII) & B (FIX) – X linked,
acquired: liver disease (most cf made in liver), dilution, anticoagulation

Disseminated intravascular coagulation (DIC)

18
Q

fibrinolysis defects:

A

Hereditary
Antiplasmin deficiency

Acquired
Drugs that enhance tPA (tissue plasminogen activator)
Disseminated intravascular coagulation

19
Q

treatment of abnormal haemostasis

A

Failure of production/function

   o Replace missing factor/platelets (Prophylactic or               '          Therapeutic) 

    o Stop drugs causing this

     oDDAVP (desmopressin) – release the body’s own          '       stores of VWF and F8
  • Immune destruction (e.g. immune thrombocytopenia)
      o Immunosuppression (e.g. prednisolone)

  o Splenectomy for ITP (Idiopathic thrombocytopenic                                                       '          purpura)
  • Increased consumption
      o Treat the cause of the DIC

   o Replace what is missing as necessary

  oTranexamic acid – anti-fibrinolytic (competitively inhibits binding of tPA to fibrin)
20
Q

name the 3 different treatment you can give to replace factors

A

Replace Factors:
Plasma: 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.

21
Q

what are the major ABO blood groups

A

A, B, AB, O
A adds N-acetyl galactosamine
B adds galactose

22
Q

what antigens/antibodies would people in the ABO blood group types have

A 
A- A antigens and Anti-B antibodies
B- B antigens and Anti-A antibodies
AB- A and B antigens, no antibodies
O- no antigens, Anti-A and Anti-B antibodies
IgM
23
Q

what are the major Rh blood groups

A

RhD positive
RhD negative
IgG

24
Q

what antigens/antibodies would people in the Rh blood group types have

A

RhD+ would have Rhd antigens and no antibodies

RhD- would have no antigens but Anti-RhD antibodies(after previous exposure to RhD+ blood or fetus can make it)

25
Q

indications for RBC donation

A

Low Hb – can raise the Hb by 10g/l

Major blood loss – needs replacing

26
Q

indications for FFP donation

A

Given in those actively bleeding and have abnormal clotting tests
Those receiving anticoagulant therapy and requiring emergency surgery

27
Q

indications for platelet donation

A

Preventative - prophylactic due to thrombocytopenia e.g. chemotherapy, bone marrow transplant
Therapeutic – treatment of bleeding due to thrombocytopenia or platelet dysfunction e.g. aspirin

28
Q

indications for Cryoprecipitate donation

A

Treatment of DIC, together with other blood components

Fibrinogen deficiency

29
Q

indications for Fractioned Pools Indications

donation

A

Albumin – Burns, hypoproteinaemia, extensive surgery
Factor VIII concentrate – Haemophilia A
Factor IX concentrate – Christmas Disease/Haemophilia B
Immunoglobulins – immunodeficiency states

30
Q

explain the clinical importance of the blood groups

A

because of the Anti-A and Anti-B and Anti-RhD antibodies, you must be careful which type of blood you put in someone, as if you give a patient who has Anti- A antibodies a type A blood, they will become very unwell (delayed haemolytic reaction) also there are some groups not routinely checked for (Rh group –C, c, E, e)

Haem- oscar (3 decks)

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