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week 3 > blood clotting > Flashcards

blood clotting Flashcards

1
Q

what is haemostasis

A

to prevent blood loss
by stopping of blood flow

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2
Q

what is clotting (coagulation)

A

the conversion of liquid blood to a solid,

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3
Q

what is an anticoagulant

A

compounds that prevent blood clotting

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4
Q

what are factors in terms of clotting

A

Factors in this specific context, clotting factors are enzymes/proteins required for clot formation. As new ones were discovered they were given numbers

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5
Q

what are platelets

A

small pieces
acellular
, small pieces budded from special cells, found in whole blood which when activated play an important role in clotting

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6
Q

explain proteolysis

A

cleavage of peptide bonds in proteins. In blood clotting, many of the factors are very specific proteases, which cleave only certain peptide bonds in their substrates

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7
Q

define thrombus

A

a blood clot, often used to designate a clot which will cause damage, disease; a clot formed where it is not wanted

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8
Q

define thrombus

A

formation of dangerous clots

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9
Q

define thrombin

A

an enzyme (clotting factor) which forms clots

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10
Q

what happens if coagulation does not occur

A

tissues may not be perfused, and there may be significant blood loss which can lead to haemorrhage, shock and can be life-threatening

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11
Q

list the 3 stages of haemostasis

A

1.Vasoconstriction
2.Formation of a platelet plug
3.Coagulation

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12
Q

briefly explain function of vasoconstriction

A

reduces the blood flow to the injured area

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13
Q

what part of the haemostasis does coagulation fit in

A

formation of the platelet plug

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14
Q

what should coagulation lead to

A

the formation of fibrin and a more stable clot

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15
Q

list the 3 divisions of the coagulation cascade

A

intrinsic
extrinsic
common pathway

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16
Q

how are coagulation factors represented

A

in roman numerals

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17
Q

how is the extrinsic pathway initiated ?

A

by tissue factor which is normally due to damaged tissue

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18
Q

where is tissue factor expressed ?

A

many cells found outside blood vessels but not on the surface of circulating blood cells or the endothelium

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19
Q

when the endothelium is damaged, what occurs ?

A

tissue factor comes into contact with blood

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20
Q

after the tissue factor comes into contact with blood what occurs

A

tissue factor combines with circulating factor VII to form a complex that leads to the activation of factor X

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21
Q

what does factor X to trigger

A

the common pathway

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22
Q

how is the activation of the extrinsic pathway tested

A

in the lab by a test called the prothrombin time, abbreviated to PT

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23
Q

what is the intrinsic pathway activated by ?

A

initiated by activated platelets

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24
Q

how does the extrinsic pathway activate the intrinsic pathway

A

using thrombin from the activation of the extrinsic pathway

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25
Q

what does the series of reactions in the intrinsic pathway lead to ?

A

initiation of the common pathway

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26
Q

what does each coagulation factor lead to ?

A

catalysation and activation of the next coagulation factor in the sequence

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27
Q

what is the term when certain reactions activate other reactions

A

cascade

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28
Q

intrinsic pathway: what does surface contact activate

A

factor XII which is activated into factor XIIa

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29
Q

intrinsic pathway: what does factor XIIa activate

A

Factor XIIa activates factor XI -> factor XIa

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30
Q

intrinsic pathway: what does factor XIA activate ?

A

IX -> IXa

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31
Q

what does factor IXa activate

A

factor X

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32
Q

what does factor IXa combine with to activate the next factor

A

factor VIIIa, platelet membrane phospholipid and Ca2+ ions to activate factor X
factor X -> factor Xa

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33
Q

what does factor Xa activate

A

the common pathway generating more thrombin

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34
Q

what is the common pathway

A

the final stage of the coagulation cascade and leads to the formation of thrombin and fibrin.

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35
Q

in the extrinsic pathway what leads to the production of factor X

A

factor VII to factor VIIa

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36
Q

final common pathway
what does factor Xa combine with to produce thrombin

A

factor V .

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37
Q

what does thrombin convert

A

insoluble fibrin from soluble fibrinogen.

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38
Q

how is thrombin formed

A

active enzyme thrombin is formed from inactive prothrombin in the final common pathway

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39
Q

what does soluble fibrinogen allow

A

allows change from soluble to insoluble which leads to the gel-like consistency of the clot.

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40
Q

what is the role of fibrinogen

A

to produce fibrin

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41
Q

what does fibrin allow to be formed

A

. A lattice of fibrin forms, which traps blood cells and forms a soft clot. Cross-links then form between the fibrin strands which leads to a more stable hard clot.

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42
Q

a soft clot can form what ?

A

a hard clot

43
Q

what is plasmin

A

an enzyme

44
Q

what is the role of plasmin

A

it will slowly lyse the clot once it has formed

45
Q

this continuous cycle of the clotting cascade allows for what

A

vast amounts of thrombin can be generated from a single initial stimulus and a thrombus can be formed quickly after injury to limit blood loss.

46
Q

what is the role of thrombin in the intrinsic pathwayb

A

thrombin generates a positive feedback loop by initiating the intrinsic pathway
production of thrombin leads to the formation of more thrombin

47
Q

how does fibrin turn into cross linkked fibrin

A

through factor XIIIa (8)

48
Q

how is plasmin produced ?

A

from plasminogen

49
Q

without regulatory mechanism in coagulation what can be caused

A

the positive feedback loop triggered by thrombin in the intrinsic pathway would continue indefinitely and cause dangerous levels of clotting in the blood.

50
Q

give brief overview of intrinsic pathway

A
51
Q

give a brief overview of the extrinsic pathway

A
52
Q

what is the enzyme plasmin formed from

A

plasminogen

53
Q

what does fibrin have to combine with to form cross linked fibrin and therefore a hard clot

A

XIIIa

54
Q

both the extrinsic and intrinsic pathways require what

A

clotting factors
calcium ions
surfaces

55
Q

why is sodium citrate added to the plasma

A

.sodium citrate is a chelating agent. Chelates calcium and inhibits clot formation (used in blood donation)

56
Q

. Why is the plasma a mixture of plasmas from a large number of donors?

A

Individual clotting times will vary; by pooling plasma, a reproducible average clotting time can be determined

57
Q

what is Phospholipid/kaolin (K

A

suspension of negatively charged phospholipid adsorbed on particles of kaolin (an aluminium silicate clay), which is required to initiate the cascade.

58
Q

what is phospholipid micmicking ?

A

the negatively charged surface of activated platelets. When activated platelets change shape from spherical to finger-like projections

59
Q

compare cscl2 solution used in the lab to normal plasma calcium levels

A

(25 moles L-1) - very much more concentrated than normal plasma calcium levels.

60
Q

what is the role of EDTA in calcium levels

A

EDTA chelates the calcium (bounds it together)
until the concentration of free Ca++ ions is about 10-5 mmoles L-1

61
Q

why is EDTA an effective chelator

A

the four carboxyl groups and the two nitrogen atoms form bonds with the calcium ion and trap it within a cage formed by the EDTA anion.

62
Q

what does heparin solution contain

A

sulphated polysaccharide heparin.

63
Q

what charges does heparin carry

A

Negative charges

64
Q

what is the role of trypsin

A

highly specific endopeptidase
cleaves polypeptides on the carboxyl side of basic amino acid residues such as arginine and lysine.

65
Q

how does the trypsin bind to the polypeptide

A

it has a pocket with a negative charge that binds the positively charged side chain of the basic amino acid in the polypeptide substrate.

66
Q

explain why these two compounds (benzamidine and -aminocaproic acid) are competitive inhibitors of trypsin?

A

same charge and structure of side chain that will fit into the active pocket for trypsin cleavage.

67
Q

what is trypsin ?

A

a protease

68
Q

what are most clotting factors?

A

proteases

69
Q

how can clotting factor be inhibited

A

if they are proteases, they can be inhibited by compounds that fit into their active site

70
Q

Which basic amino acid side chains do benzamidine and ɛ-aminocaproic acid most closely resemble?

A

lysine and arginine

71
Q

what is the role of plasmin

A

removing clots after they have served their purpose

72
Q

what is Streptococci

A

group of pathogenic bacteria some members of which secrete an enzyme streptokinase

73
Q

explain what streptococci does

A

acts in a similar way to human enzymes, such as urokinase or tissue plasminogen activator, which convert inactive plasminogen to active plasmin

74
Q

what is the role of fibrin in an infection of bacteria such as streptococci

A

the formation of a fibrin clot round the site of infection plays a role in limiting the spread of the bacteria.

75
Q

what are the symptoms of streptococci

A

infections that give rise to boils and pimples

76
Q

Why might streptokinase be an advantage to these bacteria?

A

. Strep tend to live on skin, once clot is made, the streptokinase will help to break down the clot (plasmin) and allow access to underlying tissue

77
Q

what should be the time for clot formation

A

1-2 minutes

78
Q

What do you observe after the addition of the plasmin solution?

A

Slower process (15-30 for partial lysis) Probably several hours for complete digestion (similar to what you should expect in body),

79
Q

When clots are formed naturally they are red, why is this so?
A11. Trap RBCs

A

Trapped RBCs

80
Q

. Would a plasma sample from a patient with a lack of Factor VIII give a clotting time shorter or longer than normal ?

A

Longer, factor VIII part of intrinsic so APTT assay delayed

81
Q

. Would a plasma sample from a patient with a lack of Factor VII give a clotting time shorter or longer than the one in experiment

A

no effect because testing intrinsic pathway and factor VII is in the extrinsic pathway

82
Q

Would you expect a plasma sample from a patient with a disease causing the spontaneous formation of thrombi to give a clotting time shorter or longer than the one you obtained?

A

these types of diseases are complex and in reality, APTT may not be shortened.

83
Q

how is heparin used monitored

A

using APTT assay

84
Q

what is the importance of monitoring heparin use and anticoagulant use in general

A

effects can vary widely across individuals – needs to be monitored regularly so that clotting is not too fast and not too slow (danger of cerebral hemorrhage).

85
Q

how is warfarin monitored

A

requires the PT test as it affects vitamin K-dependent clotting factors in extrinsic pathway.

86
Q

how is protein c produced

A

in response to thrombin binding to the receptor thrombomodulin on the vascular endothelium.

87
Q

what does protein c activate

A

protein s

88
Q

what does the activation of protein S do ?

A

breaks down factors Va and VIIIa in a negative feedback loop.

89
Q

what is antithrombin

A

a natural anticoagulant that is produced by the liver and destroys factors XIa, Xa and thrombin.

90
Q

what does heparin do

A

an anticoagulant
. enhance the natural effects of antithrombin in inhibiting thrombin and factor Xa.

91
Q

explain Tissue factor pathway inhibitor

A

a protein that binds to and inactivates factor VIIa and factor Xa.

92
Q

what is warfarin

A

Warfarin is a vitamin K antagonist which prevents the synthesis of vitamin K-dependent clotting factors (II, VII, IX and X).

93
Q

why is heparin prescribed with warfarin

A

vitamin K is also required for the synthesis of the natural anticoagulants protein C and protein S so Warfarin may inhibit their production initially.

94
Q

what do coagulation screening tests involve

A

adding triggers to a sample of reversibly anticoagulated plasma (by citrate) and measuring the time taken for fibrin to form.

95
Q

what does prothrombin time (PT) measures

A

time taken for fibrin to form via the extrinsic pathway.

96
Q

what specific factors are measured in PT

A

factor VII; factor X; factor V; prothrombin and fibrinogen.

97
Q

what are causes of prolonged PT

A

Disseminated intravascular coagulation (DIC)

Vitamin K deficiency
Chronic liver disease

98
Q

what does activated thromboplastin time measure

A

time taken for fibrin to form via the intrinsic pathway.

99
Q

what specific factors are measured in APTT

A

actor XII, factor XI, factor IX, factor VIII, factor X, factor V, prothrombin and fibrinogen.

100
Q

what are causes of prolonged APTT

A

Disseminated intravascular coagulation (DIC)
Clotting factor deficiencies (e.g. haemophilia A or B)
Lupus anticoagulant
Von Willebrand’s disease

101
Q

why may the pt test is not accurate

A

does not account for the fact that in vivo (within circulating blood) large amounts of thrombin are produced via a positive feedback loop through the intrinsic pathway

102
Q

Erythropoietin (Epo) is a peptide growth hormone that stimulates the production of erythrocytes (red blood cells).
in which organ is the majority of this hormone produced?

A

the kidney

103
Q

explain the relevance of sodium citrate in blood donation

A

Sodium citrate added to donated blood allows blood to be stored for some time before being given to patients

week 3 (4 decks)

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