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Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What are the steps involved in platelet plug formation?

A
  • Vessel constriction occurs as a first-response to vessel injury
  • Formation of the unstable platelet plug, which involves the processes of platelet adhesion, and platelet aggregation
  • Stabilisation of the plug with fibrin, which involves the blood coagulation system
  • Dissolution of the clot and vessel repair, which involves fibrinolysis
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2
Q

What happens if the platelet plug is not completely stabilised?

A

platelet masses embolises as the fibrin didn’t spread all the way through

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3
Q

What do endothelial cells stop from coming into contact?

A

collagen and tissue factor

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4
Q

Where is tissue factor found and what does it do?

A

expressed on the surface of a number of cells, and triggers coagulation

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5
Q

What are the functions of endothelium?

A
  • Maintain barrier between blood and procoagulant subendothelial structures
  • It is anticoagulant so allows smooth blood flow
  • Synthesis of PGI2, thrombomodulin, vWF, plasminogen activators
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6
Q

What happens when the endothelial lining is damaged?

A
  • The basement membrane is exposed
  • Von Willebrand Factor binds to this collagen that is exposed
  • Glycoprotein-1-b receptors on platelets can bind to vWF, to form a bridge between exposed collagen in the vessel and the platelet indirectly
  • Alternatively, glycoprotein-1-a receptors on platelets bind directly to exposed collagen
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7
Q

What happens when the platelet binds?

A

It becomes activated leading to the release of ADP and thromboxane. This further activates the platelets.
Glycoprotein IIb/IIIa activates and binds to circulating fibrinogen to form a platelet aggregate.

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8
Q

What is the main outcome of the clotting cascade?

A

Fibrinogen is ultimately converted to fibrin, to fully stabilise the clot.

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9
Q

What can thrombin do?

A

Thrombin can also activate platelets, and activate the IIb/IIIa complex

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10
Q

What must happen in order for thromboxane to be generated within the platelet?

A
  • Phospholipases are activated during the platelet activation
  • Phospholipases act on membrane phospholipids to generate arachidonic acid
  • Cyclo-oxygenase then converts arachidonic acid to endoperoxides, which then generate thromboxane A2 (via thromboxane synthetase)
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11
Q

What is the importance of thromboxane?

A

Thromboxane is a potent activator of platelets.

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12
Q

What do anti-platelet drugs like aspirin target?

A

Cyclo-oxygenase to irreversibly inactivate the enzyme

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13
Q

Give examples of anti-thrombotic drugs and what they do and what they act on

A
  1. COX 1 antagonists (aspirin)
  2. ADP receptor antagonists – stop activation (clopidogrel, prasugrel)
  3. Gp IIb/IIIa – stop aggregation (abciximab, tirofiban, eptifibatide)
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14
Q

Name some tests that can be done to monitor platelets and their functions

A
  1. Platelet count to monitor thrombocytopenia
  2. Bleeding time
  3. Platelet aggregation
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15
Q

Go over coagulation cascade

A

during revision

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16
Q

What is the importance of doing a platelet count?

A
  • If the platelet count is progressively reduced, vascular accidents can progressively increase
  • If it drops below 100 109/l, there is no spontaneous bleeding, but bleeding occurs with trauma
  • As the platelet count is progressively reduced, we see more and more spontaneous bleeding
17
Q

What happens in autoimmune thrombocytopenia?

A

Extensive bruising of the limbs. This is caused by autoantibodies against the GpIIb/IIIa complex -> lowers platelet count

18
Q

What is a bleeding time test and why is it done?

A
  • Standard incision is made
  • Cuff with 40mm pressure on arm above cut
  • Done when platelet count is normal but bleeding is still occurring
  • Tests the platelet and vessel wall interaction
  • The time for the bleeding to stop is monitored
  • If the time is prolonged, it indicates that the platelets are acting abnormally with the vessel wall
  • E.g. in renal disease
19
Q

How are platelets formed?

A

stem cell precursors -> megakaryocytes -> megakaryocytes mature and granulate -> megakaryocytes produce ~4000platelets from finger-like structures

20
Q

What is the lifespan of a platelet and where are the majority of them stored?

A

10 days

1/3 stored in the spleen

21
Q

What is the definition of hameostasis?

A

The cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult.

22
Q

What is haemostasis for?

A

To stop blood loss from intact and injured vessels and enable tissue repair

23
Q

What does haemostasis maintain a balance between?

A

bleeding and thrombosis - many regulators are involved in this

24
Q

What can tip the haemostatic balance towards bleeding?

A
  • high number of fibrinolytic factors or anticoagulant proteins
  • low number of coagulants or platelets
25
Q

What can tip the haemostatic balance towards thrombosis?

A
  • low number of fibrinolytic factors or anticoagulants

- high number of coagulants and platelets

26
Q

Why is studying haemostasis important?

A
  • bleeding disorders
  • thrombotic disorders
  • most people die with a haemostatic end point
27
Q

What is the size of a platelets and does it have a nucleus?

A
  • 2-4 micrometeres

- no

28
Q

What is normal platelets count?

A

150 – 400 x 109/l

29
Q

FDFD

A

Platelets – highly coordinated, no nucleus, many receptors on the surface which can interact to help dictate platelet function
Granules in the platelets with growth factors for example
Phospholipid membrane – on a activated platelet it turns inside out, becomes negatively charged which allows it to attract the coagulation factors
Actin and myosin – part of the cytoskeleton allowing shape change

30
Q

What is the importance of the platelet cytoskeleton?

A
  • important for platelet morphology

- needed for changing shape and blocking the bleeding effectively

31
Q

What are the multiple roles of platelets?

A
  • important in cancer metastasis
  • haemostasis and thrombosis
  • atherosclerosis
  • infection
  • inflammation
32
Q

FDF

A

Under normal physiological conditions, platelets circulate in close contact to the endothelial cell lining of the blood vessel wall & VWF circulate in a globular conformation with its plt binding site cryptic.

VWF circulating in the plasma – molecular ball of string which hides platelet binding sites normally in its ball. (golubular) When the vessel is damaged for example, collagen, fibronectin and laminin for example gets exposed and can bind to collagen in the subendothelial layer, it changes and become linear polypeptide due to dhear forces of blood and platelet binding sites are exposed. Platelets can bind to it
VWF can bind to collagen via its A3 domain
Platelet binds via the platelet’s GP1ba to VWF

33
Q

DFD

A

Interaction of platelets with collagen activates the platelets, causes shape change, granules to be releasd e.g. ADP,thrombanxe membrane to change. Released like a cloud so nearby platelets are primed too
Platelets will bind to each other via fibrinogen on activated aIIbb3 integrin. Platelet aggregation

34
Q

What is the importance of integrins on the platelets?

A

When activated can bind to fibrinogen and also bind platelets and cross link them - integrin aIIbb3

35
Q

How does the shape of the platelet change once it activates and why is this important?

A

Change in the platelet shape – philipodia stick out making platelets sticky. They bind to the vessel wall and flatten out and spread to effectively prevent blood loss

36
Q

Where are coagulation factors made?

A
  1. The liver – most plasma haemostatic proteins
  2. Endothelial cells – VWF, TM, TFPI
  3. Megakaryocytes – VWF, FV
37
Q

What are clotting factors?

A

All of them in the plasma are serine protein zymogens

38
Q

DED

A

MK looses its ability to divide, however continue to replicate its DNA becomes polyploid, cytoplasm enlarge. MK matures, becomes granular and form platelets that will be released in the circulation.
model MK migrate from endosteal niche to the vascular niche where they do not pass the EC of sinusoidal blood vessels and remain in vascular niche. They form pseudopodia-like extensions (proplatelets) that extend in the lumen plt are released from tip of these long extensions by shear forces.

Other model is following migration from endosteal niche to vascular niche matuer MK pass the ec barrier and enter the circulation. Due to large size of MK they get trapped in the microvasculature of lungs mechanical force induce fragmentation of MK

Haematology (11 decks)

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