Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CJ: UoL Medicine Semester Two (ESA2) > Pathology - Haemostasis > Flashcards

Pathology - Haemostasis Flashcards

1
Q

What is the definition of haemostasis?

A

The stoppage of bleeding or haemorrhage. May be via vasoconstriction, an obstruction, coagulation or surgical means.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main functions of haemostasis?

A
  • prevent bleeding
  • prevent unnecessary coagulation, allow blood to flow
  • make clot, control the clotting, break it down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where are platelets produced?

A

In the bone marrow by megakaryocytes. They ‘bud’ from the cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the normal life span of a platelet?

A

7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the normal platelet count?

A

150-400,000 per microlitre of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When does platelet adhesion occur?

A

When there is damage to the vessel wall and exposure of underlying tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do platelets secrete?

A

ADP, thromboxane and other substances to become activated and activate other platelets. This helps initiate the clotting cascade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give some mediating factors of platelet clot formation

A
  • Plt receptors - glycoproteins complexes
  • Von willebrands factor
  • fibrinogen
  • collagen
  • ADP
  • thromboxane/arachidonic acid
  • thrombin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the clotting cascade?

A

Amplification system activation of precursor proteins to generate thrombin. Thrombin converts soluble fibrinogen into insoluble fibrin, which meshes the initial platelet plug to make a stable clot.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where are clotting factors made?

A

In the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give some examples of natural anticoagulants

A

Proteins C and S, antithrombin, tissue factor pathway inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give some examples of coagulation factors made in the liver

A

Fibrinogen, prothrombin, factors 5, 7, 8, 9, 10, 11, 12, 13 and tissue factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the intrinsic pathway activated by?

A

Factors VIII, IX, XI and XII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the extrinsic pathway activated by?

A

Factor VII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the process of clot formation

A

Activation of coagulation leads to thrombin formation. Thrombin converts fibrinogen to fibrin, which forms fibrin polymers and blocks the wound. After 24-48 hours these are changed to fibrin fragments via fibrinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are the different routes of coagulation measured?

A

Intrinsic is measured by APTT and extrinsic is measured by PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a ‘thrombin burst’?

A

When lots of thrombin is produced by positive feedback of clotting factors. It converts fibrinogen to fibrin.

18
Q

What is Von Willebrand factor?

A

It is involved with platelet adhesion to the vessel wall, platelet aggregation and also carries FVIII

19
Q

What is the role of the vessel wall in haemostasis?

A
  • first step is vasoconstriction
  • production of Von Willebrands factor (essential for plt adhesion, carrier and ‘protector’ of factor 8)
  • exposure of collagen and tissue factor which initiates activation of clotting factors
20
Q

What do natural anticoagulants do?

A

These stop further coagulation, ensuring that the clot does not become too big

21
Q

Give some examples of congenital coagulation factor disorders

A
  • haemophilia A (factor 8)

- haemophilia B (factor 9)

22
Q

Give some examples of acquired coagulation disorders

A
  • liver disease
  • vitamin K deficiency
  • anticoagulants including warfarin (inhibits vitamin K)
23
Q

Give some symptoms of coagulation factor disorders

A
  • muscle haematomas
  • recurrent haemarthroses
  • joint pain and deformity
  • prolonged bleeding post-dental extraction
  • life threatening post-op and post-trauma bleeding
  • intracerebral haemorrhage
24
Q

What is haemophilia A and how is it inherited?

A
  • congenital lack of factor VIII (varies in severity)
  • X-linked recessive
  • usually diagnosed in infancy (or soon after birth if family history)
  • bleeding into muscles and joints
25
Q

How is haemophilia treated?

A

Recombinant factor VIII or DDAVP

26
Q

What is haemophilia B?

A

Congenital reduction in factor IX.

27
Q

What is Von Willenbrand’s disease?

A

Abnormal platelet adhesion to the vessel wall due to low amounts of VWF, which carries factor VIII.

28
Q

How is Von Willenbrand’s disease inherited?

A

Autosomal dominant, affects males and females.

29
Q

What are the symptoms of Von Willenbrand’s Disease?

A
  • skin and mucous membrane bleeding
  • epistaxis
  • gum bleeding
  • bruising
  • prolonged bleeding after trauma, post-surgery and post dental extraction
  • heavy periods
30
Q

What are symptoms of vessel wall abnormalities?

A
  • easy bruising
  • spontaneous bleeding from small vessels
  • mainly affects skin but can be mucus membranes
31
Q

Give some examples of congenital problems with blood vessels

A
  • Hereditary Haemorrhagic Telangiectasia

- connective tissue disorders eg. Ehlers-Danlos

32
Q

Give some examples of acquired problems with vessels

A
  • senile purpura
  • steroids
  • infection, eg. measles or meningococcal infection
  • scurvy
33
Q

What is immune thrombocytopenic purpura?

A
  • Most common cause of immune destruction of platelets
  • antibodies are formed against the body’s own platelets
  • can be secondary to autoimmune disorders
  • treated with immunosuppression
  • platelets transfusions do not work as the transfused platelets are destroyed too
34
Q

Give some caused of reduced production of platelets

A
  • B12/folate deficiency (failure of the building blocks)
  • infiltration of bone marrow by cancer cells or fibrosis
  • drugs eg. Chemotherapy, antibiotics
  • viruses eg. HIV, infective hepatitis, EBV, CMV
35
Q

What is thrombocytopenia?

A

Low platelet count

36
Q

Give some consequences of severe thrombocytopenia

A
  • easy bruising
  • petechiae, purpura
  • mucosal bleeding
  • severe bleeding after trauma
  • intracranial haemorrhage
37
Q

Which is more common, hereditary or acquired disorders of platelet function?

A

Acquired is very common while hereditary is extremely rare

38
Q

Give some causes of acquired disorders of platelet function

A
  • aspirin/NSAIDs/clopidogrel
  • uraemia
  • hyper gammaglobulinaemia, eg. myeloma
  • myeloproliferative disorders
39
Q

What is disseminated intravascular coagulopathy?

A
  • type of microangiopathic haemolytic anaemia
  • pathological activation of coagulation leads to formation of numerous microthrombi in the circulation
  • platelets and clotting factors are used up and haemolytic anaemia develops
40
Q

What are the main triggers of disseminated intravascular coagulopathy?

A
  • malignancy
  • massive tissue injury eg burns
  • infections (often gram neg sepsis)
  • massive haemorrhage and transfusion
  • ABO transfusion reaction
  • obstetric causes

CJ: UoL Medicine Semester Two (ESA2) (87 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions