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Y2 MCD > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis

A

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

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2
Q

What is the function of haemostasis

A

to prevent blood loss from intact and injured vessels, enable tissue repair

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3
Q

What are the 4 stages of haemostasis

A
  1. Vessel constriction
  2. Formation of an unstable platelet plug
  3. Stabilisation of the plug with fibrin
  4. Vessel repair and dissolution of clot
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4
Q

Describe the vessel constriction response in haemostasis

A

Mainly important in small blood vessels
Local contractile response to injury
Limits blood flow to the injured vessel

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5
Q

What is involved in unstable platelet plug formation and what is the purpose

A

Platelet adhesion and aggregation

Limits blood loss + provides surface for coagulation

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6
Q

What is involved in stabilisation of a platelet plug and what is the purpose

A

Blood coagulation

Stops blood loss

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7
Q

What does vessel repair involve and what is the function

A

Cell migration/proliferation and fibrinolysis

Restores vessel integrity

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8
Q

Describe the normal vessel wall

A 
Endothelial cell - anticoagulant barrier (TM, EPCR, TFPI, GAG)
Subendothelium - procoagulant
Basement membrane - elastin, collagen
VSMC  - TF
Fibroblasts - TF
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9
Q

Describe platelets (size, organelles, lifespan, count)

A 
Small (2-4µm)
Anuclear
Lifespan - 10 days
Platelet count = 150-350 
10^11 produced every day
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10
Q

What is the role of the platelet cytoskeleton

A

Important for morphology, shape change, pseudopods, contraction and clot retraction

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11
Q

What are the ultrastructural features of the platelet

A 
On membrane:
Alpha granules 
Dense granules 
Thrombin receptor 
Phospholipid membrane
Microtubules and actomyosin
Glycoproteins (GbIb/V/IX)
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12
Q

What is contained in the alpha granules of platelets

A

Growth factors,
Fibrinogen
FV
VWF

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13
Q

What is contained in the dense granules of platelets

A

ADP
ATP
Serotonin
Ca2+

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14
Q

Describe platelets and VWF in a normal blood vessel

A

Platelets circulate in close contact with the endothelial cell lining of the blood vessel wall
VWF circulates in a globular conformation. Binding sites are hidden from GpIb

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15
Q

What is vWF

A

vWF is a blood-borne glycoprotein which also adheres to endothelial collagen, and binds Gp1b especially well under high shear stress.

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16
Q

What occurs in the adhesion stage of platelet plug formation

A
  1. Platelets bind to exposed endothelial collagen with their Gp1a.
  2. Platelets bind to von Willebrand factor (vWF) with their Gp1b.
  3. vWF unravel under high shear stress
  4. Binding of VWF to to platelets recruits other platelets (also Bia GPVI and a2b1 on collagen at low shear)
  5. Activation of platelets
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17
Q

What occurs in the aggregation stage of platelet plug formation

A

Release of ADP and thromboxane by platelets causes them to stick together via fibrinogen using their GpIIb/IIIa. Ca2+ has to be present.

18
Q

What are prostaglandins important metabolites of and which structures are involved in their formation

A

Arachidonic acid

Platelets and endothelial cells

19
Q

What do platelets convert arachidonic acid to

A

Thromboxane A2 via COX-1

Thromboxane A2 is a potent inducer of platelet aggregation.

20
Q

What do endothelial cells covert arachidonic acid to

A

Prostacyclin (PGI2) via cyclooxygenase-2 (COX-2).

Prostacyclin inhibits platelet aggregation.

21
Q

What are the ways to monitor platelet function

A

platelet count
Bleeding time (40m pressure + incision, normal = 3-8)
Platelet aggregation （vWF)

22
Q

At what platelet counts will spontaneous bleeding and bleeding occur

A

Severe spontaneous - <10x10^9
spontaneous - <40x10^9
With trauma - 100x10^9
Normal - >150

23
Q

Describe vessels disorders and give examples

A

Bleeding due to impaired interaction of platelets with the compromised vessel
e.g. scurvy, allergic vasculitis

24
Q

Give examples of platelet disorders

A

Low platelet count (thrombocytopenia)

Drug-induced

25
Q

What are the 3 mechanisms from which thrombocytopenia can arise

A

Failure to produce platelets
Shortened platelet half life
Increased pooling of platelets in an enlarged spleen

26
Q

What are the cutaneous features of immune thrombocytopenia

A

Purpura
Multiple bruises
Ecchymoses

27
Q

Where are clotting factors produced

A

Liver - most
Endothelial cells - VWF, TM, TFPI
Megakaryocytes - VWF, FV

28
Q

Describe the coagulation cascade

A
  1. Tissue Factor, exposed by vessel damage, forms a complex with FVII
  2. Formation of an active TF-VII complex
  3. Activation of the extrinsic pathway via FX -> FXa
  4. Activation of the intrinsic pathway via FIX -> FIXa
  5. Xa leads to conversion of prothrombin -> thrombin (IIa)
  6. Activation of FV and FVIII by thrombin and platelets
  7. Enhanced thrombin formation
  8. Thrombin then converts fibrinogen to fibrin, which is cross-linked by the XIIIa
    enzyme (activated by thrombin) to form cross-linked fibrin
29
Q

Where are tissue factors highly expressed

A 
Lungs
Brain
Heart 
Testis
Uterus 
Placenta
30
Q

Draw a diagram that represents the initiation of coagulation

A

-

31
Q

Describe how coagulation is regulated (and which each mechanism inhibits)

A

Antithrombin = FXa, FIXa and thrombin
Tissue factor pathway inhibitor = TF-VIIa + FXa
Protein C + protein S = FVa, FVIIIa

32
Q

Describe the protein C pathway

A
  1. Thrombin binds to TM with high affinity
  2. Serine protease activates protein C
  3. Protein C becomes localised to endothelial surface
  4. Thrombin cleaves protein C -> activation peptide released
  5. Activates protein C zymogen to APC
  6. release of APC so PC can bind to EPCR
  7. APC down-regulates thrombin generation
33
Q

What is warfarin and how does it work

A

Anti-coagulant - long-term anticoagulation after venous thrombosis and for atrial fibrillation patients
Inhibits thrombin production by inhibiting vitamin K epoxide reductase

34
Q

Explain how inhibition of vitamin K epoxide reductase (warfarin) causes an anticoagulant effect

A

Before factors II, VII, IX, and X can bind to platelet membrane phospholipids, their glutamate residue needs to be gamma-carboxylated in the liver, using vitamin K.

35
Q

What is heparin and how does it work

A

an anticoagulant
Accelerates the action of antithrombin
Heparin binds to
antithrombin and makes it easier to bind thrombin/Xa.
Heparin is used for immediate anticoagulation in venous thrombosis or pulmonary embolism.

36
Q

Describe fibrinolysis

A
  1. Plasminogen is converted to plasmin via tissue plasminogen activator (tPa) on the fibrin clot surface
  2. Plasmin breaks down fibrin clot
  3. Fibrin degradation products are produced
37
Q

What are the therapeutic uses of tPA

A

Thrombolysis for:
Myocardial infarction
Ischaemic stroke

38
Q

Give examples of anti platelet agents

A

Aspirin (COX-1)

P2Y12 blockers

39
Q

What are the 3 ways of monitoring blood coagulation

A 
Activated partial thromboplastin time (APTT)
Prothrombin time (PT)
Thrombin time (TT)
40
Q

What is the Activated partial thromboplastin time (APTT)

A

This tests the intrinsic and common pathways. Coagulation is initiated via factor XII and any abnormalities can be detected. Used to monitor heparin treatment.

41
Q

What is prothrombin time

A

This tests the extrinsic and common pathways. Coagulation is initiated via tissue factor and any abnormalities can be detected. Used to monitor warfarin treatment.

42
Q

What is thrombin time

A

This tests the common pathway only. Thrombin is added and the conversion of fibrinogen to fibrin can be checked for abnormalities. Also known as thrombin clotting time (TCT).

Y2 MCD (23 decks)

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