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HAEMATOLOGY > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

the arrest of bleeding WHILST maintaining vascular patency

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2
Q

What qualities must haemostasis have to be effective?

A
  • ready to act quickly
  • localised response (prevent clots everywhere)
  • must protect against unwanted thrombosis
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3
Q

How are platelets formed and how long do they last in the circulation?

A
  • budding off of megakaryocyte cytoplasm

- anucleate cells => only live for 7-10 days

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4
Q

What is formed during Primary Haemostasis?

A

Platelet plug at injury site

- can stop bleeding in minor injuries, but often overcome in larger wounds

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5
Q

How is the platelet plug formed?

A
  • Endothelial (vessel wall) damage
  • exposes collagen/ releases Von Willebrand Factor (VWF) and other proteins
  • platelets have receptors to these => adhesion at site of injury
  • platelets secrete chemicals to aggregate other platelets at site
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6
Q

WHat is the role of vWF in the platelet plug?

A

Allows platelets to stick to collagen and to each other

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7
Q

How long before a procedure must aspirin be stopped to allow for enough platelet formation to clot the blood?

A

1 week

- gives body time to make platelets but doesn’t overexpose patients to risk of clot

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8
Q

Why may the platelet plug fail to form?

A
  • lack of collagen in vessels (due to increasing age or conditions e.g. scurvy [need Vit C to make collagen])
  • platelet dysfunction (reduced no. [thrombocytopenia] or reduced function [due to drugs e.g. NSAIDs])
  • vWF deficiency disorder (familial disorder)
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9
Q

What are the clinical consequences or symptoms patients will experience if they fail to make a platelet plug?

A
  • spontaneous bruising and purpura (wont blanche)
  • usually in lower limb (Thighs)
  • mucosal bleeding
    => Nose, GI tract, conjunctival, retinal, menorrhagia, blood blisters in mouth

In severe cases:
- intracranial haemorrhage (v. low platelet function)

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10
Q

Why do more female patients present with bleeding disorders than men?

A
  • many female patients present with menorrhagia which warrants referral
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11
Q

WHat screening tests can be used for Primary Haemostasis?

A
  • FBC and make sure to check platelet count
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12
Q

What is formed in secondary haemostasis and where does this take place?

A
  • fibrin clot formation

- occurs on surface of platelet plug

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13
Q

How are various clotting factors attracted to the surface of the platelet plug?

A
  • Platelet plug surface = phospholipid (-ve charge)
  • Ca2+ released and is attracted to -ve surface
  • Ca2+ forms positive layer over platelet plug
    => -ve charged clotting factors are attracted to +ve Ca2+ layer
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14
Q

What clotting factors are involved in the initiation of the clotting cascade?

A 
Tissue Factor(TF) and Factor VII complex
=> TF/VIIa
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15
Q

Describe the activation of each complex in the coagulation cascade

A

EXTRINSIC

  • TF/VIIa activates V/Xa
  • These then cleave Prothrombin (Factor II) to active Thrombin (Factor IIa)
  • active Thrombin (IIa) can then change Fibrinogen to Fibrin (to make clot)

INTRINSIC

  • Thrombin also causes activation of VIII/IXa complex
  • this activates V/Xa again, causing further amplification of the cascade
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16
Q

What clotting factor complex is involved in the amplification of the coagulation cascade?

A

VIII/IXa

17
Q

What stage of the coagulation cascade is known as propagation?

A

Prothrombin -> thrombin

as thrombin is most important to go on and activate fibrinogen and intrinsic pathway

18
Q

What can cause failure of a fibrin clot?

A
  • Single clotting factor deficiency (hereditary)
    eg Haemophilia
  • Multiple clotting factor deficiencies (acquired)
    eg Disseminated Intravascular Coagulation (DIC)
  • Increased fibrinolysis (=> more clot breakdown)
    e. g. in complex coagulopathy
19
Q

What clotting factor can be lost in haemophilia?

A

Problem with VIII/IX complex

=> Haemophilia A = Factor VIII deficiency
=> Haemophilia B = Factor IX deficiency

20
Q

Why does DIC tend to occur?

A

lots of inflammation and tissue damage in body causes high release of Tissue Factor (TF)
=> clots appear throughout the body

21
Q

What is the usual aim of fibrinolysis when the body has had to clot blood?

A

Breaks down the EDGE of the blood clot to allow blood to still flow past it

=> maintains blood vessel patency

22
Q

Describe the fibrinolysis cascade

A

Tissue plasminogen activator (tPA) activates plasminogen -> plasmin

Plasmin changes fibrin (in clots) to fibrin degradation products

23
Q

If patients cant form fibrin clots, how do they clinically present?

A
  • No characteristic clinical picture
  • May be combined primary/secondary haemostatic failure => may have low platelets
  • bleeding into joints (ankles, knees, elbows) and muscle common in haemophilias
  • massive bruising due to internal bleeding
24
Q

What can tPA be used for clinically if it has the ability to breakdown clots?

A
  • Stroke

- PE

25
Q

How can fibrin degradation products be measured to ensure a patient is undergoing fibrinolysis?

A

measured as “D-dimers”

- hence why this may be raised in DVT/PE

26
Q

How do we screen for secondary haemostasis?

A

BLOODS

PURPLE = FBC (tube contains EDTA to prevent blood from clotting)

BLUE = Sodium Citrate Coagulation screen [fill blood up to line so that conc. of anticoag. is correct for vol.]

27
Q

What clotting factor complex is excluded in the measurement of prothrombin time and how is this clinically relevant?

A

PT = measure of extrinsic pathway
=> avoids VIII/IXa complex

=> In haemophilia disorders, prothrombin time will be NORMAL

28
Q

How is Activated Partial Thromboplastin Time (APTT) measured?

A

Contact activator given to activate VIII/IXa pathway to make the blood clot

29
Q

Which of Prothrombin Time (PT) and APTT are abnormal in a multi clotting factor deficiency?

A

Both will be obscured

30
Q

What should you ask about in a bleeding disorder Hx?

A

Hx

  • check for bruising/ bleeding
  • check duration they’ve had symptoms (i.e. since birth?)
  • prolonged bleeding? (in familial diseases they may think prolonged bleeding = normal)

FHx - for signs of familial link

DHx
- do drugs interfere with platelet function? (aspirin, clopidogrel, NSAIDs)

31
Q

What should you look for on examination of a patient with a suspected bleeding disorder?

A 
EYES - fundal haemorrhages
MOUTH - mucosal bleeding
SKIN - purpura
ABDOMEN - splenomegaly
MSK - muscle and joint bleeds
32
Q

What is the body’s naturally occurring anticoagulant called and what is its job?

A

Anti-thrombin

- neutralises thrombin => turns off both coagulation pathways

33
Q

What drug helps anti-thrombin to perform its job?

A

Heparin

34
Q

What other proteins help to switch off coagulation?

A

Protein C - switches off Factor VIII

Protein S - switches off Factor V

35
Q

What does thrombin do when it realises its job is finished and no more clotting is required?

A
  • binds to thrombomodulin

- This signals to protein C and S to switch off their factors

36
Q

Some families may be deficient in anti-thrombin or Protein C/S. What can happen in this case and what is this called?

A
  • increased risk of clotting if you cant turn coagulation cascade off properly
  • especially venous clots => DVT/PE
  • this is called a “Thrombophilia”

HAEMATOLOGY (24 decks)

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