Brainscape's Knowledge GenomeTM

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


See full index

The Cardiovascular System > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What are the three principles of haemostasis

A
  • Normal number and function of platelets
  • Functional coagulation cascade
  • Normal vascular endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What kind of surface do you need for clotting

A

A phospholipid surface membrane. This usually comes in the form of platelets or monocytes.

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

What prevents the adherence of platelets or monocytes and therefore prevents clotting

A

Intact vascular endothelium

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

What does serotonin do

A

Brings about vasoconstriction

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

Why is calcium important in clotting

A

It helps to activate some of the clotting factors and initiate the clotting cascade.

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

What are the three distinct phases in the formation of a platelet rich thrombus

A
  • Platelet adhesion
  • Platelet activation
  • Platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What stabilises the platelet thrombus

A

The conversion of fibrinogen to fibrin by thrombin and polymerisation of fibrin. This produces a platelet-fibrin (“white”) clot

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

What do platelets recognise and adhere to in damaged endothelium

A

Sub-endothelium. They adhere to underlying collagen by glycoproteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two processes of haemostatic plug formation

A

Primary aggregation and secondary coagulation. These occur simultaneously.

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

What is haemostasis triggered by

A

The release of tissue factor from the sub-endothelial space.

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

What do platelet and vessel wall defects lead to

A

Prolonged bleeding time

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

What is thrombocytopenia

A

A reduced number of platelets

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

What causes thrombocytopenia

A

Bone marrow failure or lymphoma/disease of the bone marrow or peripheral consumption of platelets, e.g. due to inflammation

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

What leads to abnormal platelet function

A

Anti-platelet drugs such as aspirin or clopidogrel. Can also be due to renal failure as uraemia (excess protein in the urine) causes platelet dysfunction.

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

What are examples of abnormal vessel wall defects

A
  • scurvy
  • ehlers-danlos syndrome
  • henoch schonlein purpura
  • hereditary haemorrhagic telangiectasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an example of a defect which causes abnormal interaction between platelets and the vessel wall

A

Von Willebrand’s disease

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

What happens in scurvy to cause abnormal vessel wall

A

There is a lack of vitamin C in the blood which is vital for the creation of collagen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does hereditary haemorrhagic telangiectasia result in

A

Bleeding in mucous membranes. This often means bleeding in the skin, gut and lungs. Anaemia and blood loss can result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some examples of drugs that inhibit platelet function (anti-platelets)

A

Aspirin, NSAIDs, dipyridamole, thienopyridines, integrin GPIIb/IIIa receptor antagonists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does aspirin work as an anti-platelet drug

A

Aspirin is an irreversible COX inhibitor. COX enzymes produce prostaglandins which activate platelets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is an example of a reversible COX inhibitor

A

NSAIDs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an example of a thienopyridine

A

Clopidogrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does clopidogrel work as an anti-platelet drug

A

It inhibits ATP mediated activation of platelets.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are two examples of integrin GPIIb/IIIa receptor antagonists

A

abciximab and tirofaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do GPIIb/IIIa receptor antagonists work

A

By preventing platelet aggregation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the three coagulation pathways

A

Intrinsic pathway, extrinsic pathway and common pathway.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens in the intrinsic pathway

A
  • Damaged surface
  • Factor XII to factor XIIa
  • Factor XI to Factor XIa
  • Factor IX to factor IXa
  • Activation of factor X to create factor Xa
  • Common pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What happens in the extrinsic pathway

A
  • Trauma
  • Factor VII to factor VIIa
  • Activation of factor X to create factor Xa
  • Common pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What initiates the first step of the common pathway

A

Activation of factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Where are clotting factors produced

A

The liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which factor can be produced elsewhere (not in the liver)

A

Factor V

32
Q

Which factors are vitamin K dependent and therefore affected by warfarin

A

Factors 2, 7, 9 and 10

33
Q

What factor is important to trigger the clotting cascade

A

Tissue factor

34
Q

What happens in the common pathway

A
  • Factor X is converted to factor Xa
  • Prothrombin is converted to thrombin
  • Fibrinogen is converted to fibrin
  • A cross linked fibrin clot is produced.
35
Q

What is the difference in the production of thrombin between the intrinsic and extrinsic pathways

A

The extrinsic pathway allows the initial burst of thrombin while the intrinsic pathway involves a slow onset of thrombin.

36
Q

What two factors are a complex to form extrinsic tenase

A

Factor VIIa and tissue factor

37
Q

What two factors are a complex to form intrinsic tenase

A

Factor VIIIa and factor IXa

38
Q

What two factors are a complex to form prothrombinase

A

Factor Xa and factor Va

39
Q

What are the four phases of the cell based model of coagulation

A
  • Initiation
  • Amplification
  • Propagation
  • Termination
40
Q

What are three natural inhibitors of the coagulation cascade

A

Tissue factor pathway inhibitor
Ant thrombin
Protein C pathway

41
Q

What does tissue factor pathway inhibitor inhibit

A

The tissue factor-factor VIIa complex and factor Xa

42
Q

What does antithrombin inhibit

A

Thrombin and factor Xa activity

43
Q

What does the protein C pathway inhibit

A

Factor Va and factor VIIIa

44
Q

What is the haemostatic balance between

A

Bleeding and clotting

45
Q

What are three laboratory measurements for clotting

A

Prothrombin time (PT), Activated partial thromboplastin time (APTT) and fibrinogen.

46
Q

What does abnormal prothrombin time reflect

A

Abnormality in the extrinsic or common pathway

47
Q

What does an abnormal APTT reflect

A

Abnormality in the intrinsic or common pathway

48
Q

What does abnormal APTT and PT indicate

A

Abnormality in the common pathway

49
Q

What are the three most common disorders in the coagulation cascade seen in clinical practice

A

Factor IX deficiency, factor VII deficiency and Von Willebrand disease

50
Q

Which hereditary coagulation factor deficiency does not cause bleeding

A

Factor XII

51
Q

What is the clinical condition brought about by factor XI deficiency

A

Haemophilia B

52
Q

What is the clinical condition brought about by factor VIII deficiency

A

Haemophilia A

53
Q

What is the role of von willbrand factor

A

It is involved in binding factor VIII, platelets and constituents of connective tissue to allow the formation of a thrombus.

54
Q

What is Haemophilia A

A

An x-linked recessive disorder which is a deficiency or dysfunction of factor VIII.

55
Q

What are the differences between severe, moderate and mild haemophilia

A

In severe haemophilia the person will have spontaneous bleeding which may be into the joints. This is when there is less than 1% factor VIII. In moderate haemophilia, there will be bleeding after minor trauma and in mild haemophilia bleeding will occur after major trauma or surgery.

56
Q

What is haemoarthrosis

A

Bleeding into the joints. This can occur in people with severe haemophilia.

57
Q

What is used in the management of haemophilia

A

Supportive measures, replacement of missing clotting protein and antifibrinolytic agents

58
Q

What supportive measures are used in the management of haemophilia

A

Ice or immoblilisation

59
Q

How is missing clotting protein replaced in haemophilia

A

Using coagulation factor concentrates or desmopressin.

60
Q

What is the name of an antifibrinolytic agent used in the management of haemophilia

A

Tranexamic acid

61
Q

What are the signs of congenital haemophilia

A

Haemoarthrosis, muscle bleeds and soft tissue bleeds

62
Q

How is acquired haemophilia different from congenital haemophilia

A

In acquired haemophilia, antibodies to factors VIII and IX are developed. This can happen spontaneously or be due to malignancy

63
Q

What are the bleeding patterns in acquired haemophilia

A

There is often blood in the urine, large haemotomas, cebrebral haemorrhages and compartment syndromes.

64
Q

What are the roles of Von Willebrand factor

A

To promote platelet adhesion to the subendothelium at high shear rates. It is also a carrier molecule for factor VIII.

65
Q

What is the most common heritable bleeding disorder

A

Von Willebrand disease

66
Q

What are the three different types of Von Willebrand disease

A

Type 1 - Reduction in Von Willebrand Factor
Type 2 - abnormal Von Willebrand factor
Type 3 - no Von Willebrand factor

67
Q

What is used to manage Von Willebrand disease

A

Antifibrinolytics (tranexamic acid), DDAVP, Factor concentrated containing von willebrand factor (vaccination against hep A and B), contraceptive pill for menorrhagia.

68
Q

What may lead to the underproduction of coagulation factors

A

Liver failure or vitamin K deficiency.

69
Q

What is disseminated intravascular coagulation (DIC)

A

An acquired syndrome of systemic intravascular activation of coagulation - “thrombin explosion”. There is out of control systemic activation of the coagulation cascade.

70
Q

What can be the result of DIC

A

Widespread deposition of fibrin in the circulation causing ischaemia and multi-organ failure.

71
Q

How can DIC cause excessive clotting and bleeding

A

The excessive thrombus formation in DIC uses up the available platelets and coagulation factors to generate the thrombin. This means there are not enough platelets and coagulation factors left, and this can lead to severe bleeding.

72
Q

What can cause DIC

A
  • Sepsis
  • Trauma
  • Pancreatitis
  • Obstetric
  • Transfusion of ABO incompatible cells
73
Q

What may an examination of the peripheral blood film of someone with DIC show

A

Red cell fragments

74
Q

What tests can be used to investigate DIC

A
  • Prothrombin time - will be prolonged
  • Activated partial thromboplastin time - will be prolonged
  • Fibrinogen - will be low
  • D-dimers - will be high
75
Q

What do raised D dimers indicate

A

D dimers are fibrin degradation products. D-dimers in the circulation means increased breakdown of fibrin.

The Cardiovascular System (15 decks)

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