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Haemostasis Flashcards

1
Q

Haemostasis is the mechanism that _______________

A

keeps blood in a fluid state

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2
Q

Normal hemostasis is dependent upon the complex interaction of plasma _______ and __________ proteins, ______, and the blood vasculature.

A

coagulation

fibrinolytic

platelets

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3
Q

Normal haemostasis can be div. into:
The 3 categories are:
_________ hemostasis
________ hemostasis
_________ hemostasis

A

Primary

Secondary

Tertiary

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4
Q

Normal haemostasis can be div. into:
The 3 categories are:

 Primary hemostasis: the formation of the ________

 Secondary hemostasis: formation of ________________________

 Tertiary hemostasis: the formation of _____________________

A

platelet plug.

fibrin through the coagulation cascade.

plasmin for breakdown of the clot.

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5
Q

5 major components are involved in haemostasis
◼ Blood ________
◼ Blood ________
◼ Coagulation _______
◼ Coagulation __________
◼ ___________

A

vessels

platelets

factors

inhibitors

Fibrinolysis

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6
Q

Blood platelets

 Are ______ of _______ of ________

 (Nucleated or Non- nucleated?)

 Produced mainly by the ___________

A

fragments; cytoplasm; megakaryocytes

Non- nucleated

bone marrow

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7
Q

Blood platelets

Normal platelet count- ____-____ x 109/l

Life span is about ______ days

A

95-400

7-10

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8
Q

Blood platelets

About ___/3 is trapped in the normal _____

A

1

spleen

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9
Q

Blood platelets

Measures about ____-_____

Volume about ____-____ fl

A

3x0.5μm

7-11

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10
Q

Blood platelets

 Contains 3 types of storage granules ◼__________
◼__________/_________
◼ __________

A

Dense granules

Alpha/specific granules

lysosomes

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11
Q

Dense granules:
____________
 __________
 __________

A

Nucleotides(ADP,ATP,5-HT)

Calcium

Serotonin

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12
Q

Lysosomes contain _________

A

catalase

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13
Q

Factor V

Dense or specific granules?

A

Specific

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14
Q

Platelet-derived growth factor

Dense or specific granules?

A

specific

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15
Q

Fibronectin

Dense or specific granules?

A

specific

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16
Q

Β-thromboglobulin

Dense or specific granules?

A

specific

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17
Q

Heparin antagonist(PF-4)

Dense or specific granules?

A

specific

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18
Q

Thrombospodin

Dense or specific granules?

A

Specific

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19
Q

VWF

Dense or specific granules?

A

Specific

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20
Q

Fibrinogen

Dense or specific granules?

A

Specific

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21
Q

Calcium

Dense or specific granules?

A

Dense

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22
Q

Serotonin

Dense or specific granules?

A

Dense

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23
Q

Nucleotides

Dense or specific granules?

A

Dense

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24
Q

Platelet function

Main function is the formation of __________ in response to vascular injury

A

haemostatic plugs

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25
Q

Lack of platelet may lead to spontaneous leakage of blood through vessel walls

T/F

A

T

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26
Q

Primary haemostasis
 Primary hemostasis is defined as the formation of the __________ and involves platelets, the blood vessel wall and __________

A

primary platelet plug

von Willebrand factor.

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27
Q

Primary haemostasis

Abnormalities result in _________ from mucosal surfaces, ______ or _______ hemorrhages, and prolonged bleeding after venipuncture or wounds

A

hemorrhage

petechial or ecchymotic

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28
Q

The normal endothelium prevents hemostasis by providing a ________ and by secreting products which inhibit platelets, including ____________ and _________

A

physical barrier

nitric oxide and prostaglandin I2 (prostacyclin)

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29
Q

The formation of the primary platelet plug involves platelet ______ followed by platelet _______ then _______ to form a platelet plug.

A

adhesion; activation; aggregation

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30
Q

❖ Platlet-vessel wall interaction ( ______ )
❖ Platelet-platelet interaction ( __________ )
❖ Platelet release reaction

A

Adhesion

Aggregation

31
Q

Platelet adhesion
 The _____ event in hemostasis is the adhesion of platelets to ___________

A

1st

exposed subendothelium.

32
Q

Platelet adhesion

In areas of high shear rate (in the microvasculature), this is mediated ______, which binds to gp ____\ in the platelet membrane.

 In areas of low shear rate (e.g. _______), _______ mediates the binding of platelets to the gp _______).

A

vWf; Ib

Aorta ; fibrinogen

Ia/IIa

33
Q

Platelet activation

The _____ of platelets to the vessel wall activates them,
❖ platelets to __________,
❖ activate the _____ on their surface
❖ undergo the _____ reaction
❖ platelets synthesize and release _________ and ________ which are potent platelet aggregating agonists and vasoconstrictors

A

adhesion

change shape

collagen receptor

release

TXA2 and platelet activating factor (PAF),

34
Q

Collagenous receptor is an
_______ receptor called glycoprotein _____/_____

35
Q

PLATELET AGGREGATION

Platelet aggregation is mediated primarily by __________

______has a secondary role

which binds to glycoprotein ______ on adjacent platelets.

A

fibrinogen

vWf

IIb/IIIa

36
Q

PLATELET AGGREGATION

This aggregation leads to the formation of the ________, which must be stabilized by the formation of ________.

A

primary platelet plug

fibrin

37
Q

Platelet procoagulant activity

❖ Following platelet aggregation and release, the exposed membrane phosplolipid(_____) is then available for the _______ and _______ reactions in secondary haemostasis

A

PF3

tenase and prothrombinase

38
Q

Blood coagulation(20 haemostasis)

It’s a biological amplification system characterized by ________ of a cascade of circulating precursors (__________)
culminating in the generation of _________

A

Sequential activation

coagulation factor enzymes

thrombin

39
Q

Blood coagulation(20 haemostasis)

 This involves
❖ circulating _________, which act as
enzymes [which require _______]
❖ cofactors (_____________),
❖_______ and
❖ platelets (platelets provide a source of _________ and a ___________ upon which the coagulation cascade proceeds)

A

coagulation factors; activation

factors V and VIII

calcium

phospholipid [PF3] and a binding surface

40
Q

Defects in the primary hemostasis manifest as more serious bleeding than coagulation cascade

T/F

A

F

Defects in the coagulation cascade manifest as more serious bleeding than primary hemostasis

41
Q

Defects in Coagulation
 Defects in the coagulation cascade manifest as more serious bleeding than primary hemostasis, including bleeding into ____ (chest, joints) and __________.

A

cavities; subcutaneous hematomas

42
Q

Defects in Coagulation

Petechial hemorrhages
are seen in disorders of secondary hemostasis.

T/F

A

F

Not seen

43
Q

Defects in Coagulation cascade

These disorders do share common bleeding symptoms with defects in primary hemostasis, including _________ and _________________-

A

epistaxis and bleeding after surgery or
wounds

44
Q

___________ and ________

this may be the 1st sign of a hemostatic
defect

A

epistaxis and bleeding after surgery or
wounds

45
Q

Defects in Coagulation cascade va defects in primary haemostasis

it may be impossible to distinguish between defects in these 2 pathways based on clinical signs alone.

T/F

46
Q

Coagulation factors

 Factor 1——— ________
 II————-_________
 III- ___________
 V———–________
 VII——— ________
 VIII—-_________
 IX——- ____________
 X ——-____________
 XI——- ________________
 XII—— __________(______)
 XIII—–___________
HMWK (Fitzgerald factor)

A

fibrinogen

prothrombin

Tissue factor

labile factor

Proconvertin

Antihaemophylic factor

Christmas factor

Stuart power factor

plasma thromboplastin antecedent

Hageman (contact) factor

Fibrin stabilizing factor

47
Q

Coagulation invivo depends on enzyme
complex:
◼__________
◼__________
◼____________
◼__________

A

Protease

Cofactor

Phospholipid

Calcium

48
Q

Coagulation invivo depends on enzyme
complex:

 Extrinsic tenase—-(_____,_____ ____,_______ →Xa

 Intrinsic tenase —-(_____,_____,_____,______ ) →Xa

A

VIIa, TF, PL, Ca2+

IX, VIII, PL, Ca2+

49
Q

Coagulation invivo depends on enzyme
complex

Prothrombinase complex—-(_____,_____,______,_______)

A

Xa

Va

Pl,

Ca2+

50
Q

Physiological limitations of Blood
coagulation

Unchecked blood coagulation could lead to serious ____________(_______)

A

vascular occlusion(thrombosis)

51
Q

Coagulation factors inhibitors

 TFPI (synthesized by _______ cells, its present in ______ and ______ and accumulates at sites of injury caused by local platelet activation)

A

endothelial

plasma & platelets

52
Q

Coagulation factors inhibitors

◼ TFPI inhibits:
_____
______
_____

A

Xa

VIIa

TF

53
Q

Coagulation factor Inhibitors

__________
_________
_____________
________
________

A

Antithrombin III

Heparin cofactor II

C1 esterase inhibitor

Protein C

Protein S

54
Q

Coagulation factor Inhibitors

Antithrombin III: effects is enhanced by ________

55
Q

Protein C inhibits _____________

A

FVa &FVIIIa

56
Q

Thrombin binds to ___________, and this complex activate _______

(________ is a cofactor)

A

thrombomodulin

protein C

protein S

57
Q

Blood flow: activated factors are
rapidly ______ by the blood and
destroyed by the _________
cells

A

diluted

liver parenchymal

58
Q

Tertiary hemostasis

 Tertiary hemostasis is defined as the
formation of _______, which is the
main enzyme responsible for
__________(______________)

A

plasmin

fibrinolysis

breakdown of the clot

59
Q

Fibrinolysis

It’s a normal haemostatic response to injury ensuring the _________ of the _______

A

dissolution of the fibrin clot.

60
Q

Fibrinolysis

___________ (tpA) binds to ________ —ensures that ________________

A

Tissue plasminogen activator

fibrin; fibrin generation is
localized to the fibrin clot

61
Q

Fibrinolysis

APC stimulates fibrinolysis by _____________

A

destroying
plasma inhibitors of tpA

62
Q

Fibrinolysis

Thrombin inhibits fibrinolysis by __________________________

A

activating thrombin-activated fibrinolysis inhibitor(TAFI)

63
Q

 Plasmin is capable of digesting:

◼________
◼ _______
◼_____
◼_____

A

Fibrinogen

Fibrin

FV

FVIII

64
Q

Therapeutic fibrinolytic agents

◼_________________
◼ _________ (initially from human urine)
◼ _________ (from haemolytic
streptococci)

A

Recombinant tPA

Urokinase

Streptokinase

65
Q

Inhibitors of plasmin

◼___________________ (PAI)
◼________________

A

Plasminogen activator inhibitor

Alpha2 antiplasmin

66
Q

Tests of Haemostasis

 Defective haemostasis with abnormal
bleeding may result from:
◼ ________ disorder
◼______________
◼ Defective ___________

A

Vascular

Thrombocytopaenia

blood coagulation

67
Q

Tests of haemostasis

_______
______
________

A

Thrombin time

APTT

PT

68
Q

Tests of haemostasis:Thrombin time

•normal range: ___-____secs.

•Prolongation due to ____________

•FDPs(_______)

◼ Associated disorder:
______
________

A

14-16

dysfibrinogenaemias

Fibrin degradation products

DIC; Heparin RX

69
Q

Tests of haemostasis

APTT(_________________)

•Measures the ______ pathway, its global test of haemostasis

•normal range ___-____ secs

•Prolonged in:_________, _______,_____

A

Activated Partial Thromboplastin Time (aPTT)

intrinsic

30-40

Haemophilia

Von willbrand disease

DIC

70
Q

Thrombin time

It measures the time it takes for _______________________________________________

A

a clot to form after the addition of thrombin, a protein involved in the clotting process.

71
Q

Tests of haemostasis: PT

measures the ______ pathway and the common pathway:

•_____,______,_____,______,______

•Normal range—___-___secs

Prolonged in:
◼_______
◼______ therapy
◼_____

A

extrinsic

FVII, X, V, III & fibrinogen

10-14

Liver disease; Warfarin; DIC

72
Q

Tests of haemostasis

Fibrinogen assay: indication is _______ deficiency,

Fibrinogen is (Increased or Reduced?) in DIC

A

fibrinogen

Reduced

73
Q

Tests for Haemostasis

Bleeding Time: Normal range is _____________

A

3-8 minutes

74
Q

Tests of haemostasis

________ assay

_________ Time

__________ count

A

Fibrinogen

Bleeding

Platelet

House Hemat (29 decks)

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