Haemostasis Flashcards

1
Q

What is haemostasis

A

Process which forms blood clots at endothelial damage and vascular injury sites. Also involves lot removal post-repair

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2
Q

Haemostasis defect result

A

Uncontrolled bleeding

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3
Q

Overactive haemostasis result

A

Abnormal clots (thrombi) can lead to tissue ischaemia and cell death

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4
Q

Intact endothelial fx

A

Repel platelets
Prevent platelet-sub endothelial ECM contact
Synth NO and PGI2

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5
Q

Endothelium activated to be procoagulant by

A

Direct injury
Cytokine heamodynamic forces
Infectious agents
Plasma mediators

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6
Q

What causes the main vascular response of vasoconstriction?

A

Local neural reflexes and vasoactive substances released from endothelium and platelets (eg endothelin)

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7
Q

Describe platelets

A

Small anuclear disc shaped fragments

Produced by megakaryocyte in the bone marrow

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8
Q

VWB factor fx

A

Form bridge between subendo collagen and platelet receptors to allow platelet adhesion

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9
Q

Factors in platelet granules

A
5
Calcium
ADP
P selectin
Fibrinogen
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10
Q

Platelet aggregation stimulated by

A

ADP

thromboxane 2

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11
Q

What is wrong with the primary haemostasis plug

A

Loose, could easily be washed away by blood flow

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12
Q

Factor 12 aka

A

Hageman factor

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13
Q

Trigger of intrinsic system

A

Blood exposed to surfaces other than normal endothelium. Activation of 12 in plasma is what other factors are derived from

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14
Q

Entrinsic system triggered

A

Vascular damage which exposes tissue factor (3)

3 may also be induced by cytokines (TNF, IL1, bact endotoxin)

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15
Q

Faster system

A

Extrinsic

Thrombin produced triggers intrinsic - by passing 12.

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16
Q

Anti-inflamm drugs affect

A

Affect TXA2 and PGI2 conc so alter clot risk (decr TXA2 decr risk, decr PGI2 incr risk)

17
Q

Site of fibrinogen synthesis

A

Liver. Present in normal animal blood

Half life 2-4d

18
Q

States that increase fibrinogen

A

Pregnancy

Disease states

19
Q

Where is 13 released from

A

Entrapped platelets

20
Q

Means of tight regulation of cascade and confinement

A

Endo repel clotting factors and prevent 12 activation
Cascade only occur at site of damage as need exposed phospholipids
Endogenous anti-coags eg anti-thrombin 3

21
Q

Factors req vit K as co factor for synth

22
Q

Warfarin and related anticoag method

A

Antagonise vit K

Red vit K bioavailability

23
Q

How to prevent clotting in blood sample

A

Chelate calcium

24
Q

What is tissue factor

A

A procoagulant glycopro

25
Fibrinolytic cascade trigger
Coag cascade act Urokinases Tissue plasminogen activators Tissue damage
26
Plasminogen to plasmin act
12 dep pathway tPA (and other plasminogen activators) kallikrein
27
Where is tPA made
Endotheliump
28
FDP fx
Weak anticoags | Can be measured to diagnose prothrombotic states
29
Free plasmin inactivation
Alpha 2 plasmin inhibitor
30
Small clot fate
Remodel or dispersed in 1-2wk
31
Larger clot fate
Organisation and recanalization
32
Clot retraction time
30-60min
33
Clot retraction fx
Reduce size of clot Pull wound edges together Allow incr blood flow to healing endo
34
Serum
Plasma minus coag factors
35
Bradykinin
Vasodilator Incr vascular permeability Allow incr leucocyte migration Cause smooth muscle contract and maybe pain
36
Kinin-haemostasis link
Act 12 may act kinin system by convert prekallikrein to kallikrein Kallikrein can act 12 too
37
Complement-haemostasis link
Thrombin can trigger inactive precursors in plasma. | Plasmin can activate C3-C3a