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Sem 2 - Pathological Processes > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis for?

A

To prevent bleeding and to prevent unnecessary coagulation, allow blood to flow

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2
Q

Principles of haemostasis

A

Make a clot

Control clotting

Break it down

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3
Q

What is essential for haemostasis?

A

Keep blood moving - heart, venous valves, calf pump

Blood vessels

Platelets

Coagulation factors

Anticoagulant factors

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4
Q

What are platelets?

A

Megakaryocytes produce platelets in the bone marrow

Platelets ‘bud’ from cytoplasm

Normal platelet count is 150-400 109/L

Normal lifespan 7-10day

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5
Q

Platelet adhesion?

A

Damage to vessel wall

Exposure of underlying tissues

Platelets adhere to collagen via vWF / receptor

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6
Q

Platelet activation…

A

Secrete ADP, thromboxane and other substaces to become activated and activated other platelets

Involved in activation of the clotting cascade

Provide some coagulation factors by secretion from internal stores

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7
Q

Platelet aggregation

A

Cross linking of platelets to form a platelet plug

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8
Q

What does the clotting cascade mean?

A

Amplification system activation of precursor proteins to generate thrombin (IIa)

Thrombin converts voluble fibrinogen to insoluble fibrin.

Enmeshes initial platelet plug to make stable clot

…Controlled

Natural anticoagulants to inhibit activation

Cot destroying proteins which are activated by thr clotting cascade (carefully balanced).

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9
Q

Where are coagulation factors made?

A

They are made in the liver

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10
Q

What is the clotting cascade?

A

PT - extrinsic pathway. VII

APTT - Intrinsic. VIII IX XI XII

Commo pathway - V, X, Prothrombin, Fibrinogen

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11
Q

Lab tests?

A

PT - measures extrinsic and common pathway. INR is derived from this and it used to measure warfrin.

APTT measured intrinsic and common pathway

Fibrinogen count measues the amount of fibrinogen

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12
Q

VonWillebrand Factor?

A

Involved in platelet adhesion to the vessel wall, platelet aggregation. And also carries factor VIII

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13
Q

Vessel Wall?

A

Vasoconstriction

Production of Von Willebrands Factor (vWF)

  • -Essential for plt adhesion
  • -Carrier and ‘protector’ of Factor 8 (clotting protein).

Exposure of Collagen and Tissue factor which initiates activation of clotting factors (proteins).

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14
Q

Natural anticoagulants?

A

Stop further coagulation

  • Protein C
  • Protein S
  • Anti-Thrombin
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15
Q

Fibrinolysis?

A

Plasminogen to Plasmin which break down clots. This is activated by plasminogen activator.

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16
Q

D Dimers?

A

D-dimer is a fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis.

17
Q

Clinical relevance of haemostasis

A

Bleeding disorders

Arterial rhomboid disorders

Venous thrombotic disorders

Abnormal blood test results

Drug therapy for pro- or anti- thrombotic purposes

18
Q

Coagulation Factor disorders?

A

Congenital : haemophilia A (F8) Haemophilia B (F9)

Acquired: Liver disease, Vitamin K (F2,7,9,10) Anticoagulants including Warfrin (inhibits Vit K - reduction in 2,7,9,10)

19
Q

Clinical symptoms of coagulation factor disorders?

A

Clinical severity correlates with extent of deficiency

Muscle haematomas

Recurrent haemarthroses

Joint pain and deformity

Prolonged bleeding post dental extraction

Life threatening post op and post traumatic bleeding

Intracerebral haemorrhage

20
Q

Haemophilia A?

A

X-linked recessive

Congenital lack of factor VIII

Mild/moderate/severe depending on amount of factor VIII present

Diagnosed pre-nasally or soon after birth if family history, to usually in infancy if new spontaneous mutations

Bleeding into muscles/and joints and post-operatively

Treated with recombinant factor VIII or DDAVP

21
Q

See in blood results?

A

Prolonged APTT as less factor 8

22
Q

Haemophilia B?

A

Similar presentation to haemophilia A

Congenital reduction in factor IX

23
Q

Von Willebrands Disease?

A

Relatively common

  • Usually autosomal dominant, affects makes and females
  • vWF carried Factor VIII and mediates platelet adhesion tot he endothelium

Abnormal platelet adhesion to vessle wall

Reduced FVIII amount / activity (FVIII can be low in addition to low VWF levels)

Several genetic defects cause this condition

Main type due to a reduction in vWF production ie not enough

(others where activity reduced)

24
Q

Symptoms of vWD?

A

Skin and mucous membrane bleeding

  • Epistaxis
  • Gum bleeding
  • Bruising

Prolonged bleeding

  • Heavy periods
  • Post surgery
  • Post dental extraction
25
Q

Vessel wall abnormalities?

A

Easy bruising

Spontaneous bleeding from small vessels

Skin mainly

Can be mucous membranes

26
Q

Problems with Vessles?

A

Congenital

  • -Hereditary Haemorrhagc Telangiectasia (HHT)
    • -Autosomal Dominant
    • -Dilated microvascular swellings increase with time
    • -GI haemorrhage can lead to iron deficiency anaemia
  • Connective tissue disorders - Ehlers Danlos

Acquired

  • Senile purpura
  • Steroids
  • Infection
  • Scurvy
27
Q

Disseminated Intravascuar Coagulopathy?

A

Type of microangiopathic haemolytic anaemia

Pathological activation of coagulation

Numerous microthrombi are formed in the circulation

This leads to consumption of clotting factors and platelets and a haemolytic anaemia

Clotting tests are affected - usually raised PT / INR, low fibrinogen and raised D dimers / fibrin degradation products

28
Q

Triggers of disseminated intravascular coagulopathy?

A

Malignancy

Massive tissue injury eg burns

Infections - usually gran negative sepsis

Massive haemorrhage and transfusion

ABO transfusion reaction

Obstetric causes - placental abruptly, pre-eclampsia, amniotic fluid embolism.

Only way to treat it is to treat underlying cause

29
Q

Thrombophilias?

A

These are acquired or congenital defects of haemostasis which can increase a patient’s risk of thrombosis

Congenital causes include deficiency on natural anticoagulants (Protein C, Protein S and antithrombin) and an abnormal factor V (factor V Leiden - relatively common)

Acquired causes include antiphospholipid syndrome

These are relatively rare conditions and many patients with them do not develop clots unless they have additional risk factors.

Sem 2 - Pathological Processes (13 decks)

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