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Semester 2 Pathological Processes > L9: Haemostasis > Flashcards

L9: Haemostasis Flashcards

1
Q

What is haemostasis?

A

Process of stopping the flow of blood
Prevent bleeding
Prevent unnecessary coagulation, allow blood to flow

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2
Q

What are the basic steps involved?

A

Make a clot
Control clotting–> liquid to semisolid state
Break it down–> fibrinolysis

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3
Q

What is clotting?

A

The process whereby blood (normally a liquid) becomes a solid mass when it makes contact with connective tissue

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4
Q

What are the three steps of haemostasis?

A

1- Severed artery contracts, decrease pressure down stream
2- Primary haemostatic plug of activated platelets forms at hole in the vessel, sticks to injured tissue and CT outside, seconds to minutes
3- Secondary haemostatic plug forms, fibrin filaments stabilise the fragile platelet plug into a blood clot, 30 mins

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5
Q

What is essential for haemostasis?

A

Blood flow–> needs to keep moving, heart, valves, calf muscles have role
Blood vessels are important–> vasoconstriction ensures reduced blood flow
Platelets
Coagulation factors
Anticoagulation factors

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6
Q

What are the three main players in haemostasis?

A

Platelets
Process of blood clotting
Vascular wall

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7
Q

What are platelets?

A

Produced by megakaryocytes in bone marrow
Bud from cytoplasm
Normal platelet count is 150-400 x10^9/ L
Normal life span 7-10days

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8
Q

What activates platelets?

A
  • Collagen cell surface
  • ADP (released by activated platelets and injured RBC and amplifies there response)
  • Thromboxane A2–> platelet aggregator
  • Thrombin–> informs platelets that clotting sequence is activated
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9
Q

What do platelets do once they are activated?

A
  1. Stick to subendothelium (BM or collagen) specifically to Von Willebrand factor–> concentrated on surface
  2. Aggregate with other platelets
  3. Swell and change shape into sticky tiny spheres –> allow clotting components to assemble on surface
  4. Secrete factors that help form the platelet plug and aid clotting
    (Adhere, activate, aggregation)
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10
Q

What factors mediate the platelet adhesion, activation and aggragation?

A 
Plt receptors (glycoprotein complexes)
Von Willebrand factors
Fibrinogen 
Collagen
ADP
Thromboxane/arachidonic acid
Thrombin
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11
Q

What is the process of blood clotting?

A 
Fibrin needs activating
-Intrinsic pathway--> Factors involved contained within the blood, triggered by negatively charged surface, no vessels need to be open for it to occur
--> Factors, XII, XI, IX, VIII
-Extrinsic pathway--> Needs tissue factor present outside the blood, triggered by thromboplastin released from damaged cells adjacent to area of haemorrhage
--> Factor VII
Converge on factor X--> Xa 
Prothrombin--> thrombin
Thrombin activates fibrinogen --> fibrin
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12
Q

What role does the vascular wall pay in the clotting cascade?

A

Aterial media contracts–> subendothelium traps the platelets
Endothelium- balancing act between opposing and favouring clotting
- Plasminogen activator, von Willebrand factor and tissue factor–> activate
- Thrombomodulin –> Protein C opposes clotting

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13
Q

What laboratory tests are carried out to determine the effects of blood clotting?

A

Measure

  • -> PT (Prothrombin time)–> extended problem with Extrinsic pathway or common pathway
  • -> APTT (Activated partial thromboplastin time)–> extended problem with intrinsic pathway or common pathway
  • -> Measure fibrinogen count–> measure amount of fibrinogen, problem with V or X
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14
Q

What is Von Willebrand Factor involved in?

A

Platelet adhesion to vessel wall
Platelet aggregation
Carries factor VIII

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15
Q

What factors oppose clotting?

A

Dilution of clotting factors
Anticoagulants–> oppose formation of fibrin
–> Protein C, Protein S and anti-thrombin
Fibrin degradation products also inhibit clotting

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16
Q

How does the clot evolve over time?

A

Platelets in clot die
Cling to fibrin, pull by actin-myosin (within platelets) contraction (clot retraction) to pull edges of wound together
Toughen the clot by squeezing out fluid

17
Q

What is fibrinolysis?

A 
Blood clot dissolved
Hole in vessel repaired 
Macrophages recognise and break it down and it is destroyed by plasmin 
Fibrin--> fibrin degradation products 
Macrophages clear
18
Q

How is plasmin produced?

A

Produced from inactive precursor plasminogen
Requires tissue plasminogen activator (tPA)
Urokinase (plasminogen activator) in urine
Streptokinase (plasminogen activator)–> not usually in body from streptococci–> antigenic so only used once

19
Q

Why is the blood clotting cascade clinically relevant?

A

Problems with haemostasis:

  • Bleeding disorders
  • Arterial thrombotic disorders
  • Venous thrombotic disorders
  • Abnormal blood test results
  • Drug therapy for pro- and anti- thrombotic purpose
20
Q

Why do bleeding disorders occur?

A

Abnormality in vessel wall, platelets or coagulation factors

Inherited (haemophilia A or B) or acquired (liver disease, Vit K deficiency, Anticogaulants, Warfarin (inhibits vit K))

21
Q

What are the signs and symptoms associated with coagulation factor disease?

A

Muscle haemotomas
Reccurrent haemotomas
Joint pain and deformity
Prolonged bleeding post dental extraction
Life threatening post op and post traumatic bleed
Intracerebral haemorrhage

22
Q

What is haemophilia A?

A

X linked recessive
Lack of VIII
Mild/moderate/severe forms
Diagnose pre-natally or post birth if family history, presents in infancy if new mutation
Bleeding into muscle and joints and post-operatively
Treatment: Recombinant factor VIII or DDAVP
Normal bleeding time, platelet count, PT but prolonged ATTP

23
Q

What is haemophilia B?

A 
X linked recessive
Factor IX deficiency 
Similar presentation to Haemophilia A 
Prolonges APTT
Treatment: recombinant factor IX
aka Christmas Disease (after person who first had it)
24
Q

What is Von Willebrand disease?

A

Most common inherited bleeding disorder
Autosomal dominant
Carries factor VIII and mediates platelet adhesion to endothelium
Therefore prolonged bleeding time and ATTP time
Several genetic defects mild–> severe
Main due to reduction in vWB factor (other reduced activity)

25
Q

What is the clinical presentation of Von Willebrand factor disease?

A

Skin and mucous membrane bleeding
Prolonged bleeding after trauma
Spontaneous joint or muscle bleeds are rare

26
Q

What are the signs of vessel wall abnormalities?

A

Easy bruising
Spontaneous bleeding
In skin mainly but can be in mucous membrane

27
Q

What are some of the abnormalities that can occur in blood vessels?

A

Congenital

  • -> Hereditary Haemorrhagic Telangiectasia (HHT)
  • Autosomal dominant
  • Dilated microvascular swelling increase with time
  • GI haemorrhage can lead to iron deficiency
  • -> CT dissorders - Ehlers Danlos

Acquired

  • -> Senile purpura
  • -> Steriods
  • -> Infection (measles, meningococcal infection)
  • -> Scurvy, Vit C deficiency causing defective collagen production
28
Q

What is disseminated intravascular coagulopathy?

A

DIC
Microangiopathic haemolytic anaemia
Pathological activation of coagulation
Microthrombi formed
Consumption of clotting factors, platelets, fibrin and activated fibrinolysis
Haemolytic anaemia–> RBC damaged as they squeeze past microthrombi
Measured–> clotting test affected, usually raised PT/INR, raised APTT, low fibrinogen and raised D dimer/fibrin degradation products

29
Q

How does DIC develop?

A

Always triggered by something else–> secondary effect

  • Malignancy
  • Massive tissue injury- burns
  • Infections
  • Massive haemorrhage and transfusion
  • ABO transfusion reaction
  • Obstetric causes - Placental abruption, pre-eclampsia, amniotic fluid embolism
30
Q

What are thrombophilias?

A 
Inherited or acquire congenital defects
Increase risk of thrombosis
Congenital causes--> deficiency in anticoagulants (protein C, S and antithrombin), abnormal factor V
Acquired--> Antiphospholipid syndrome
Relatively rare conditions
31
Q

What are thrombocytopenia?

A

Deficiency in platelets <100x10^9 /L
Prolonged bleeding time
Normal PT and APTT
Spontaneous bleeding in small vessel in skin, GI tract and genitourinary tract, occasional intracranial bleeding
Appears as petechiae (small red dots on skin)
Causes:
- Decreased production of platelets
- Decrease platelet survival
- Sequestration —> hypersplenism
- Dilutional–> massive blood transfusion (blood stored for >24 hrs no platelets)

Semester 2 Pathological Processes (16 decks)

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