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POM > haemostasis > Flashcards

haemostasis Flashcards

1
Q

Where and how are platelets formed?

A

Bone marrow by fragmentation of megakaryocytic cytoplasm from myeloid stem cells

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2
Q

Describe the Vasoconstriction stage of Primary Haemostasis

A

Nitric Oxide and prostacyclin concentrations are less than endothelin concentration

So vasoconstriction occurs reducing the amount of blood being lost

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3
Q

Outline the process of Platelet Adhesion during Primary Haemostasis

A

VWF binds to collagen on the endothelium at site of injury and then GPIb receptor on the platelet binds to VWF.

OR platelets stick to collage via the GPIa receptor.

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4
Q

what do alpha granules contain

what do beta granules contain

A

VWF, fibrinogen

serotonin, Ca2+, ADP

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5
Q

How does the Activation and Degranulation of platelets occur in Primary Haemostasis?

what does ADP do

A

Platelet and GPIb receptor changes shape so that it can bind properly to endothelium

The alpha and dense granules of platelets are released

The ADP in dense granules is what activates the GPIIb/IIIa receptors to bind to the fibrinogen
its also a platelet activator resulting in further platelet recruitment

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6
Q

How is Thromboxane A2 synthesis stimulated?

A

Platelets are stimulated to produce the prostaglandin thromboxane A2 from arachidonic acid that is derived from the cell membrane (also is a vasoconstrictor)

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7
Q

Final step of platelet aggregation?

A

Platelet releases Prostaglandin Thromboxane A2 and ADP

Resulting in Positive feedback for more recruitment activation and aggregation as the platelet changes shape and many will bind to a single fibrinogen

Creating the platelet plug

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8
Q

what three things occur after platelet adhesion

A

Change in shape of platelet, can grab onto more platelets
release of granules
release thromboxane A2

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9
Q

What does Prostacyclin do?

A

vasodilator released from the endothelial cells and suppresses platelet activation, preventing inappropriate platelet aggregation by elevating cyclic-AMP levels

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10
Q

How does Aspirin inhibit the activation of platelets?

How does the anti-platelet drug Clopidogrel work?

A

Inhibits the production of thromboxane A2 by irreversibly blocking the action of cyclo-oxygenase (COX) resulting in a reduction in platelet aggregation

Irreversibly blocking ADP receptor (P2Y12) on the platelet cell membrane

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11
Q

function of fibrin

A

To reinforce the platelet plug at the site of injury and make it stronger

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12
Q
  • Describe what happens during the extrinsic and intrinsic pathways of Secondary Haemostasis

what does Xa lead to the activation of

A

Extrinsic pathway:
TF binds to factor VIIa and calcium to activates factor X to Xa
factor Xa, Va and calcium bind to activate factor II (prothrombin) to IIa (thrombin)

Intrinsic pathway
Factor XII encounter phosphate ions and changes from XII to XIa to XI
XI with calcium activates IX to IXa
IXa binds with VIIIa and calcium to activate X to Xa

prothrombin to thrombin

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13
Q

What three co factors does thrombin activate in Secondary Haemostasis (amplification stage)

A

A small amount of thrombin mediates activation of co-factors V & VII and IX

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14
Q

What is the purpose of thrombin?

what does factor 13 do

A

convert fibrinogen to fibrin
activate factors 5,8 , 9
activate platelet
proteolytically cleave factor 13 to 13a

combines with calcium ion
cross link protein chains together

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15
Q

Outline the Propagation stage of Secondary Haemostasis

A

Factor XI converts more IX to IXa

With factor VIIIa, IXa will amplify conversion of factor X→Xa

Leading to a rapid burst in thrombin generation, which cleaves circulating fibrinogen to form insoluble clot

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16
Q
  • What is the function of Proteins C & S?

what does antithrombin inhibit

A

Protein C is activated when thrombin binds to thrombomodulin on endothelial cell surface
Activated protein C in the presence of protein S will inactivate factors Va and VIIIa

Thrombin and factor 10

17
Q
  • How do Antithrombin and Heparin promote anticoagulation?
A

Thrombin and factor Xa inactivated by circulating inhibitor, antithrombin

Heparin enhances the binding capabilities of antithrombin to Factor II (prothrombin)

Inactivation of thrombin requires larger chains of heparin to wrap around both antithrombin and thrombin
18
Q
  • How does Warfarin work as an anticoagulant?

- How do direct oral coagulants work?

A

It is a Vitamin K antagonist working by interfering with protein carboxylation

Therefore reduces synthesis of functional factors II, VII, IX and X by the liver

Directly inhibit thrombin and factor Xa without involvement of antithrombin

19
Q
  • What is meant by a zymogen?
  • What is the function of the Fibrinolytic system?
  • What is plasminogen?
A

A proenzyme = an enzyme that generates another enzyme

To remove clot after vasculature is repaired

The inactive zymogen form of plasmin
20
Q

What does Plasmin do

Outline briefly the fibrinolytic system?

A

Digests Fibrin into Fibrin Degradation Products - breaks down clot
Digests Fibrinogen into Fibrinogen Degradation Products
Digests V & VII
Digests II & XII to prevent clot formation

t-PA (tissue plasminogen activator) and plasminogen bind to lysine residues on fibrin
activate plasminogen to plasmin
so fibrin is broken down
21
Q

What is plasmin inhibited by

A

antiplasmin

alpha 2 macrogloblin

22
Q
  • How does tranexamic acid work as an antifibrinolytic drug?
A

It is a synthetic derivative of lysine that works by binding to plasminogen

In doing so it prevent plasminogen from binding to the lysine residues of fibrin (competitive inhibition)

Prevents activation of plasminogen to plasmin, which would otherwise result in fibrinolysis
23
Q

What is thrombosis?

What 3 changes in blood could increase a person’s risk of venuous thrombosis?

A

Formation of clot within intact blood vessel which usually obstructs blood flow

Reduced anticoagulant factors

Increased coagulant factors

Reduced fibrinolytic activity
24
Q
  • Which coagulation pathway do the aPTT and PT monitor respectively?
  • What is used as the source of TF and phospholipid in PTs?
  • The reduction in activity of which factors may prolong a PT?
A

aPTT - intrinsic

PT - extrinsic

Recombinant thromboplastin

Factor VII, X, V, II or fibrinogen
25
Q
  • What is Virchow’s Triad?
A

3 contributory factors to a pathological clotting or thrombosis

Blood - dominant in venuous thrombosis

Vessel wall - dominant in arterial thrombosis

Blood flow - complex, contributes to both arterial and venuous thrombosis
26
Q

What two types of thrombolytic therapy are there and what is used in each?

A

encouraging clot lysis
recombinant t-PA- generate plasmin to lyse clots
given to patients presenting with ischaemic stroke or pulmonary emboli

preventing clot lysis
tranexamic acid
binds to plasminogen preventing plasminogen binding to lysine residues of fibrin
treat inherited bleeding disorders and bleeding in trauma

27
Q

How is PT measurement carried out

A

blood collected in bottle containing sodium (chelates calcium so blood doesn’t clot in bottle

sample is spun to get platelet poor plasma

source of TF, Phospholipid and calcium is added

time taken for blood to clot is recorded

28
Q

How is APTT measurement carried out?

A

use contact activation of factor 12 by surface such as glass or using a contact activator such as silica or kaolin

contact activator and phospholipid is added to citrated plasma sample followed by calcium

time taken to clot is recorded

29
Q

What do patients with isolated prolonged APTT ( and normal PT) present with

A 
haemophilia A (factor 8 deficiency)
Haemophilia B (factor 9 deficiency)
factor 11 deficiency
or factor 12 deficiency but this does not present with bleeding
30
Q

why is the balance between coagulant and anticoagulant proteins important

A

allows for simulation of blood clotting
limit the extent of clotting at tissue injury site
starts the process of healing via fibrinolysis

POM (47 decks)

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