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Pathological Processes > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Process of clot formation

A

I dunno look it up

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2
Q

Where are platelets produced and by what?

A

Megakaryocytes produce platelets in the bone marrow

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3
Q

Normal platelet count

A

150-400 x10^9/L

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4
Q

Normal lifespan of platelets

A

7-10 days

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5
Q

What do platelets adhere to collagen via?

A

von Willebrand factor receptor

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6
Q

Platelet activation

A
  • Secrete ADP, thromboxane and other substances to become activated and activate other platelets
  • Involved in activation of the clotting cascade
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7
Q

What is the function of thromboxane?

A
  • Vasoconstrictor
  • Hypertensive agent
  • Facilitates platelet aggregation
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8
Q

Clotting cascade mediating factors

A
  • Glycoprotein complexes on platelets e.g. GPIIb-IIIa
  • Von Willebrands factor (binds to factor VIII)
  • Fibrinogen (forms bridges between platelets by binding to their GPIIb-IIIa receptors)
  • Collagen
  • ADP
  • Thromboxane/arachidonic acid
  • Thrombin
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9
Q

Initiation and activation of the clotting cascade

A
  • Tissue factor exposure activates FVII
  • Prothrombin –> Thrombin
  • Clotting factors activated
  • Thrombin IIa positive feedback??
  • Fibrinogen –> Fibrin clot (cleaved by thrombin)
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10
Q

Fibrinolysis

A
  • Plasminogen –> Plasmin

- Breaks up fibrin clot

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11
Q

Natural anticoagulants

A
  • Protein C
  • Protein S
  • Anti thrombin
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12
Q

What can bleeding disorders be due to?

A

Abnormalities in the vessel wall, platelets or coagulation factors

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13
Q

Congenital coagulation factor disorders

A
  • Haemophilia A (factor 8)

- Haemophilia B (factor 9, rarer)

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14
Q

Acquired coagulation factor disorders

A
  • Liver disease (produce coagulation factors)
  • Vitamin K deficiency
  • Anticoagulants including warfarin
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15
Q

Haemophilia A

A
  • X linked recessive
  • Bleeding into muscles and joints
  • Treated with recombinant factor VIII or desmopressin
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16
Q

Von Willebrand’s disease

A
  • Autosomal dominant
  • Abnormal platelet adhesion to vessel wall
  • Reduced FVIII amount/activity
  • Either not enough vWF produced or reduced activity
17
Q

Clinical presentation of vWD

A
  • Skin and mucous membrane bleeding (epistaxis, bruising)
  • Prolonged bleeding from trauma (heavy periods, post surgery)
  • Spontaneous joint or muscle bleeds are rare
18
Q

Vessel wall abnormalities presentation

A
  • Easy bruising
  • Spontaneous bleeding from small vessels
  • Skin mainly
  • Can be mucous membranes
19
Q

Congenital problems with vessels

A
  • Hereditary Haemorrhagic Telangiectasia (HHT)

- Connective tissues disorders e.g. Ehlers Danlos

20
Q

Hereditary Haemorrhagic Telangiectasia (HHT)

A
  • Autosomal dominant
  • Dilated microvascular swellings increase with time
  • GI haemorrhage can lead to iron deficiency anaemia
21
Q

Acquired problems with vessels

A
  • Senile purpura (vessel walls become thin)
  • Steroids
  • Infection e.g. measles, meningoccocal infection
  • Scurvy (vit C def causing defective collagen production)
22
Q

Immune destruction of platelets

A
  • Immune thromocytopenic purpura (autoantibodies against GP IIb/IIIa and GPIb/IX)
  • Can be secondary to autoimmune disease
  • Treated with immunosupression (cordicosteroids or IVIg first line)
  • Platelet transfusions do not work (why? Haemostasis slide 39)
23
Q

Reduced production of platelets

A
  • B12/folate deficiency
  • Infiltration of bone marrow by cancer cells or fibrosis
  • Drugs e.g. chloramphenicol and co-trimaxazole
  • Vituses e.g. HIV, EBV
24
Q

When do patients become symptomatic in severe thrombocytopenia?

A

When the platelet count is less than 30

25
Q

Hereditary disorder of platelet function

A

Bernard Soulier - associated with impaired platelet granule content release

26
Q

Acquired disorders of platelet function

A
  • Aspirin, NSAIDS, clopidogrel
  • Uraemia
  • Myeloproliferative disorders
27
Q

Disseminated intravascular coagulopathy

A
  • Type of microangiopathic hemolytic anaemia
  • Pathalogical activation of coagulation
  • Numerous microthrombi are formed
  • Leads to consumption of clotting factors and platelets, and a haemolytic anaemia
  • Usually raised PT/INR, raised APTT, low finbrinogen, raised D dimers/fibrin degradation products
28
Q

Triggers for DIC

A
  • Massive tissue injury e.g. burns
  • Infections (usually gram negative sepsis)
  • Massive haemorrhage and transfusion
  • ABO transfusion reaction
  • Obstetric cause (placental abruption, pre-eclampsia, amniotic fluid embolism)

Pathological Processes (6 decks)

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