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Fundamentals of Pathology > W10 Haemostasis > Flashcards

W10 Haemostasis Flashcards

1
Q

Haemostasis

A

Protective process evolved in order to maintain a stable physiology

“An explosive reaction designed to curtail blood loss, restore vascular integrity and ultimately preserve life”
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2
Q

DIC

A

disseminated intravascular coagulation

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3
Q

The Horseshoe Crab

A

Limulus Polyphemus

‘A primitive coagulation pathway can be initiated by endotoxin’

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4
Q

The Haemolymph contains amebocytes:

A

Proteins of the coagulation system

Proteins & peptides of the immune system

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5
Q

Life preserving processes designed to maintain blood flow

A

Respond to tissue injury
Curtail blood loss
Restore vascular integrity & promote healing
Limit infection

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6
Q

Four Key Components

A

Endothelium
Coagulation
Platelets
Fibrinolysis

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7
Q

What makes a Blood Clot?

A

Fibrin mesh
Platelets
Red blood cells

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8
Q

Haemostasis simplified steps

A 
Tissue injury
Vasoconstriction
Platelet activation
Haemostatic plug
Coagulation
Stable clot formation
Clot dissolution
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9
Q

Primary haemostasis:

A 
Vasoconstriction (immediate)
Platelet adhesion (within seconds)
Platelet aggregation and contraction (within minutes)
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10
Q

Secondary haemostasis:

A

Activation of coagulation factors (within seconds)

Formation of fibrin (within minutes)

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11
Q

Fibrinolysis:

A

Activation of fibrinolysis (within minutes)

Lysis of the plug (within hours)

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12
Q

The vessel Wall

A 
Normal Endothelium:
	- inhibits coagulation
	- prevents platelet aggregation
Provides a barrier to reactive elements in the subendothelium
	- collagen fibronectin
	- tissue factor
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13
Q

Haemostasis at rest

A

triggers and cofactors separated

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14
Q

Von Willebrand Factor: functions

A

Forms a bridge between damaged vessel wall (collagen) and platelets
(primary haemostasis)

Stabilises and protects Factor VIII from rapid clearance

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15
Q

Loss of VWF function

A

results in a bleeding disorder

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16
Q

VWF synthesis and storage

A

Synthesis
Endothelial cells
Weibel Palade bodies

Megakaryocytes
Platelet a granules

Plasma VWF entirely derived from endothelial cells

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17
Q

Distribution of VWF

A 
Constitutive path (95%)
Regulated path (5%)

Weibel-Palade bodies (storage granules of endothelial cells)

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18
Q

Platelet activation

A

Resting Platelet
Activation
Adhesion + spreading

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19
Q

When a vessel wall is damaged

A

various signalling molecules are expressed / exposed, including tissue factor and collagen

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20
Q

Initiation of coagulation

A

The TF leads to the production of a small local amount of thrombin, which is the initiation step of the coagulation process

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21
Q

Adhesion

A

The exposed signalling molecules attract circulating platelets, which attach themselves to the exposed sub-endothelial tissue

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22
Q

secretion

A

These platelets become activated – principally through the presence of the thrombin – and release further attractant chemicals, which attract more platelets

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23
Q

Aggregation

A

These new platelets bind to the adhered platelets and themselves become activated

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24
Q

contraction

A

Through the conformational changes inherent in activation, the loose platelet plug contracts to form a dense, adherent plug

25
Q

activated platelets also present a substantial area of…

A

of negatively-charged phospholipid membrane at the site of the injury, upon which the subsequent processes of coagulation (secondary haemostasis) can occur, if needed

26
Q

Fibrin mesh

A

Fibrin mesh binds and stabilises platelet plug and other cells

27
Q

Fibrinogen (I)

A

Forms clot (fibrin)

28
Q

Prothrombin (II)

A

Its active form (IIa) activates I, V, VII, XIII, protein C, platelets

29
Q

Tissue factor (III)

A

Co-factor of VIIa

30
Q

Calcium

A

Required for coagulation factors to bind to phospholipid (formerly known as factor IV)

31
Q

V (proaccelerin, labile factor)

A

Co-factor of X with which it forms the prothrombinase complex

32
Q

VI

A

Unassigned - old name of Factor Va

33
Q

VII (stable factor)

A

Activates IX, X

34
Q

VIII (antihaemophilic factor)

A

Co-factor of IX with which it forms the tenase complex

35
Q

IX (Christmas factor)

A

Activates X: forms tenase complex with factor VIII

36
Q

X (Stuart-Prower factor)

A

Activates II: forms prothrombinase complex with factor V

37
Q

XI (plasma thromboplastin antecedent)

A

Activates XII, IX and prekallikrein

38
Q

XII (Hageman factor)

A

Activates prekallikrein and fibrinolysis

39
Q

XIII (fibrin-stabilizing factor)

A

Crosslinks fibrin

40
Q

von Willebrand factor

A

Binds to VIII, mediates platelet adhesion

41
Q

FVII deficiency

A

FVII deficiency causes bleeding

42
Q

FXII deficiency

A

FXII deficiency not associated with bleeding

43
Q

Tissue Factor drives coagulation

A

TF is outside the lumen

Formation of TF-FVIIa complex

Recruitment of FX and formation of thrombin

44
Q

Initiation of coagulation occurs when

A

occurs when sub-endothelial tissue is exposed to the circulation at a site of injury. These tissues express tissue factor at their surface, which binds to endogenous activated FVII

45
Q

This complex binds

A

complex binds small amounts of FX and FV to the exposed endothelial surface, which produce small quantities of thrombin

46
Q

The thrombin activates

A

activates platelets that are attracted to the site by the process, as well as other plasma-borne clotting factors

47
Q

The activated factors (among them FVIII and FIX) enable the binding of ?

A

enable the binding of activated FX and FV to the surface of platelets whose activation has produce conformational changes in their surface membranes to expose the ‘reaction sites’ necessary for continuation of the process

48
Q

the ‘thrombin burst’

A

This leads to the ‘thrombin burst’ that is necessary for the large-scale production of fibrin and so the development of an effective clot

49
Q

coagulation phases

A

These three stages are called the initiation, amplification and propagation phases of coagulation

50
Q

Fibrinolysis

A

Main function
clot limiting mechanism
repair and healing mechanism

Series of tightly regulated enzymatic steps
Feedback potentiation & inhibition

Main Key players
Plasminogen
Tissue plasminogen activator (t-PA) & urokinase (u-PA)
Plasminogen activator inhibitor -1 and -2
α2-plasmin inhibitor

51
Q

Plamin formation

A

Plasminogen to plasmin through tPA (tissue plasminogen activator)

52
Q

D dimers

A

D dimers are generated when cross-linked fibrin is degraded.

53
Q

FDP (Fibrin degradation products)

A

FDP (Fibrin degradation products) are generated if non-cross linked fibrin or fibrinogen is broken down

54
Q

tPA and a bacterial activator used for..

A

tPA and a bacterial activator, streptokinase, are
used in therapeutic thrombolysis for myocardial
infarction (Clot busters) and stroke

55
Q

During thrombosis what increases/decreases

A

Coagulation factors + platelets increase

Fibrinolytic factors, anticoagulant proteins decrease

56
Q

Chronic venous insufficiency

A

Atrophic changes
Hyperpigmentation
Ulceration
Infection

57
Q

During bleeding what increases/decreases

A

Coagulation factors + platelets decrease

Fibrinolytic factors, anticoagulant proteins increase

58
Q

Easy bruising

ecchymosis

A

Virtually all bleeding disorders and often in normals

Fundamentals of Pathology (23 decks)

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