Brainscape's Knowledge GenomeTM

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


See full index

Atrial Fibrillation > Haemostasis and Coagulation > Flashcards

Haemostasis and Coagulation Flashcards

1
Q

Thrombosis

A

Disorder of clotting
Formation of unwanted clots
Causation : venous - clots form in veins due to stasis of blood, Amy travel to lungs to give pulmonary embolism
atrial fibrillation: risk of Transient Ischaemic Attack or stroke

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

Pathways of clotting mechanisms

A

Intrinsic

Extrinsic

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

Intrinsic pathway

A

exposed collagen from injured blood vessel wall, test tube

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

Extrinsic pathway

A

damaged tissue releases thromboplastin

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

Clotting cascade

A

Thromboplastin and clotting factors cause inactive factor X to become active
This causes prothrombin to become thrombin
Which chops fibrinogen to form fibrin
Fibrin becomes stable due to factor XIII
Forms scaffold and clot

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

Atrial fibrillation

A

Tachycardia
Arrhythmia
SA node not pacemaker, but many sites on atria
Leads to uncoordinated contraction of atria
Heart looks like it’s wriggling

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

What is AF a risk factor for?

A

Cardioembolic stroke/TIA if clots form in left side

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

What is fibrinogen a risk factor for?

A

Cardiovascular disease

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

What are platelets

A

Non-nuclear cellular fragments

Form mechanical plugs during damage to blood vessels

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

Steps of platelet action

A
  1. Adhesion
  2. Aggregation
  3. Platelet mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adhesion

A

Platelets adhere to sub-endothelial surface on damage/disease due to binding to Von Willebrand’s factor
Adhesion causes release reaction

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

Aggregation

A

Release reaction : activated platelets release ADP and thromboxane
Promoting platelet aggregation
Platelets activated by ADP and release glycoprotein IIb-IIIa
This crosslinks platelets with fibrinogen and vWF, therefore sticks and scaffold

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

Platelet mass

A

to plug area of endothelial damage
promotes coagulation reaction: -vely charged phospholipids on activated platelets which have adhered to site of damage localize fibrin formation

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

Lab tests

A

Bleeding time
Prothrombin time
Activated partial thromboplastin time

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

Bleeding time

A

Incision in forearm with venous cuff
Time taken for bleeding to stop
Increased in platelet dysfunction/thrombocytopenia

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

Prothrombin time

A

International normalised ratio (INR)
Time for coagulation following addition of thromboplastin
Prolonged due to liver disease or warfarin

17
Q

Arterial thrombosis

A

Platelet aggregation at atherosclerotic sites, leading to arterial blockage
Heart attack and stroke
Blood doesn’t perfuse down stream leading to myocardial infarction

18
Q

Is venous/arterial thrombosis more of a coagulation/platelet event

A

Venous - coagulation (DVT)

Arterial - platelet (MIs and ischaemic strokes)

19
Q

Haemophilia A

A

Genetic - defect on X chromosome, males affected, females carries
Low/lack factor VIII
Haemorrhage and prolonged bleeding when there is slight tissue trauma

20
Q

How to treat haemophilia a

A
  1. Factor VIII from blood donors or analogue of vasopressin (ADH)
  2. Emicizumab - monoclonal antibody, monthly subcutaneous injections
    Bispecific, binds to activated factor IX and X
21
Q

Haemophilia b

A

Christmas disease
Christmas factor (coagulating) affected
Deficiency of factor IX

22
Q

How to treat haemophilia b?

A

Prophylactic factor IX

23
Q

Von willebrand’s disease

A

Hereditary lack/defect in vWF

increased bruising, nose bleeds, mucosal bleeding

24
Q

How to treat Von Willebrand’s disease?

A

Analogue of ADH , factor VIII or vWF

25
Q

Liver disease

A

Reduced synthesis of clotting factors

Leads to increased bleeding (increased prothrombin time)

26
Q

Thrombocytopenia

A

Reduced platelet number
Spontaneous skin bleeding
Causes: idiopathic, viral, drug-induced, toxins

27
Q

Drug-induced thrombocytopenia

A

Immune mechanisms

Eg. Cytotoxic anti cancer drugs may induce due to bone marrow depression

28
Q

How to treat drug-induced thrombocytopenia

A
  1. Stop drug
  2. Treat with steroids, suppress immune response
  3. Remove spleen
29
Q

DIC

A

Disseminated Intravascular Coagulation

30
Q

What is DIC

A

Large amounts of fibrin generated by procoagulant material like amniotic fluid
Vast consumption of clotting factors and platelets therefore none left
Widespread haemorrhage and may also be thrombosis

31
Q

How to treat DIC

A

Give platelets and fresh frozen plasma

32
Q

What is factor V Leiden mutation?

A

Abnormal factor V
Single nucleotide polymorphism (protein has single different AA)
therefore less susceptible to deactivation

33
Q

What does factor v Leiden mutation cause?

A

Increases risk of venous thrombosis

Atrial Fibrillation (9 decks)

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