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M103 T2 > M103 T2 L2 > Flashcards

M103 T2 L2 Flashcards

1
Q

How is haemostasis prevented from spontaneously occuring in the body?

A

the endothelium secretes anticoagulants

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2
Q

What happens in the endothelium when it is injured?

A

it stops secreting anticoagulants and instead secretes VWF

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3
Q

What are the three platelet-based pathways to repair blood vessels? (PMV)

A 
PHG, meshwork, vasoconstriction
--
the formation of a primary haemostatic plug 
a meshwork on the clot via coagulation  
vasoconstriction to slow down blood flow
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4
Q

What three activities can platelets use to form a primary haemostatic plug?

A

(3As - dcg)
adhesion to the wall - exposed collagen in the basement membrane
activation - exocytose their dense granules
aggregation - the platelets stick together to start forming a plug

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5
Q

What is a clot made up of?

A

lots of little tiny fibres in every direction with cells stuck between them

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6
Q

What types of substances are released for vasoconstriction to occur?

A

the release of vasoconstrictors and coagulants

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7
Q

How many platelets is produced by one megakaryocyte?

A

on average 4000 platelets

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8
Q

What do platelets do when they’re activated?

A

exocytose - excrete various chemicals and vasoconstrictors
they change shape
increase in the amout of o2 they consume

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9
Q

What two terms are used to describe the two states of platelets?

A

quiescence - inactive / at rest - have smooth surfaces

pseudopodia - irregular shape / activated - have irregular surfaces

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10
Q

What three compounds are contained in the dense granules of platelets?

A

(SAC)
serotonin
ADP
calcium

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11
Q

What is the relationship between ADP and platelets?

A

ADP triggers platelet activation and stimulates aggregation

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12
Q

What are examples of blood thinners?

A

Prasugrel and Ticagrelor (antiplatelet agents)

Aspirin and Clopidogrel (anticoagulants)

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13
Q

What is the role of fibrinogen in clotting?

A

help the platelets bind to eachother and to the collagen

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14
Q

What substances are secreted during platelet activation?

A

ADP (activates the P2Y receptor)

TXA2

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15
Q

How does ADP use positive feedback to trigger platelet activation?

A

the ADP secretion will activate one platelet
when other platelets detect the ATP, they also activate
leads to positive feedback where more and more platelets activate

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16
Q

Are factors activated in the blood?

A

no, they mostly circulate in the form of inactive precursors so that reactions only happen when they need to rather than all the time

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17
Q

What special about factors 5 & 8?

A

they are co-factors not enzymes

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18
Q

How does tissue factor work?

A

when an individual cell is damaged, TF in the basement membrane underneath is exposed
it activates inactive clotting factors in the blood

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19
Q

How can atrial fibrillation cause a stroke?

A

the atrium is unable to pump successfully so blood just sits there
can form a thrombus which can travel to the brain

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20
Q

What two chemicals are added to blood to stop it from clotting in the lab?

A

citrate

heparin

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21
Q

What are the stages involved in coagulation?

A

fibrinogen (+ thrombin) > fibrin + factor 13 + Ca2+
causes cross links in the fibrin
forms a stable clot

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22
Q

Which two coagulation cascades are there?

A

the tissue factor pathway (ex)

the contact activation pathway (in)

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23
Q

What is thrombin activated by and how?

A

Factor Xa and Factor Va as a co-factor

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24
Q

How is Factor X activated?

A

by Xase from either the extrinsic or intrinsic pathway

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25
Q

How does positive feedback occur in coagulation?

A

thrombin activates Factor V & VIII into Factor Va and VIIIa
factor VIII contributes to Intrinsic Xase and factor V contributes to the thrombinase
essentially, it will activate thrombin itself, so thrombin activates upstream cofactors IOT activate itself

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26
Q

Which factors belong to the prothrombin group?

A

factors II, VII, IX and X

279,10

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27
Q

Which factors belong to the thrombin group?

A

Factors I, V and VIII

1, 5, 8

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28
Q

When will the amount of thrombin in circulation increase?

A

inflammation
pregnancy
with oral contraceptives

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29
Q

Where are clotting factors in the body?

A

made in the kidney

secreted into the blood

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30
Q

What is vitamin K’s function?

A

helps blot clot

required to synthesise various enzyme coagulation factors, in particular prothrombin

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31
Q

Which prothrombins require vitamin K to be synthesized?

A

2, 4, 5, 7

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32
Q

What happens if anticoagulant factors go into overdrive?

A

the inhibition of coagulation, fibrinolysis, accumulating blood vessel damage and eventual haemorrhaging

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33
Q

Where does plasmin come from and how does it activate?

A

inactive plasminogen, made as a plasma protein by the liver, activated by tPa

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34
Q

Where does protein C come from? and what is its function?

A

starts an inactive enzyme made by the liver

it is activated on surface of endothelial cells

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35
Q

What substance does antithrombin III work with and why?

A

always works with heparin

by itself, is very inactive / with heparin, powerful

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36
Q

What three substances does antithrombin III and heparin block from working?

A

thrombin
Factor Xa
Factor IXa

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37
Q

How can the effects of heparin be reversed in the lab?

A

protamine sulfate

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38
Q

What are the effects of an antithrombin III deficiency?

A

risk of thrombotic disease

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39
Q

What is the recombiant form of antithrombin III used for medically?

A

thrombotic disorders

40
Q

What are the effects of a vitamin K deficiency?

A

reduced coagulation

41
Q

What is a vitamin K deficiency usually caused by and how?

A

liver disease - it affects the production of bile salts so fat absorption can’t occur
AAR vitamin K can’t be produced by bacteria in the LI

42
Q

What is haemophilia A caused by?

A

a congenital lack of factor VIII

43
Q

Is haemophilia A more common in males or females?

A

Males - the condition is X-linked so with the exception of females who are homozygous for the mutated gene, only males show symptoms

44
Q

How is haemophilia A treated?

A

injected forms of purified factor VIII - purified from an animal or blood products
it’s an expensive and rare medication

45
Q

Why are the symptoms for haemophilia B the same as those for A?

A

haemophilia B involves a genetic defect in factor 9

Factors 8 & 9 are both part of the intrinsic pathway and work together to activate factor 10

46
Q

How can purified factor VIII be generated in a cheaper way?

A

genetically modified animals’ milk

47
Q

What is the positive feedback mechanism caused by atherogenesis?

A

monocytes / WBCs become foam cells
they can die and release their contents (cytokines and chemo-attractants - more signalling) which attract more monocytes
positive feedback mechanism

48
Q

How does atherogenesis cause the reactivity of cholesterol esters?

A

lipids are deposited in lesions by LDL
the deposits can be made to be solid or hard by cholesterol esters in the lesion
the deposits can also be oxidized, making oxygen radicals
the cholesterol esters become so reactive that they can destroy any immune cells that try to regulate them

49
Q

What three things is atherogenesis a disease of? (LIE)

A

lipids
inflammation
endothelium

50
Q

What happens during atherogenesis to cause inflammation?

A

the endothelium expresses chemoattractants - they attract WBCs which allow monocytes to find and enter lesion
when the endothelium is lost, exposing the collagen basement layer, it stimulates coagulation
Endothelium normally covers collagen and basement membrane
when the endothelium is lost, the vessel can’t control its dilation - can’t control haemostasis

51
Q

When are anti-platelet agents used instead of anticoagulants?

A

in acute coronary syndromes to prevent clotting in arteries where anticoagulants have limited effects

52
Q

What are the uses of aspirin?

A

they are commonly used to reduce the risk of heart attack

acts as a blood thinner - is an antiplatelet agent

53
Q

What are the medical uses of anti-coagulants?

A

prevent clotting in veins so it is prophylactic for DVT and PE’s

54
Q

What are three examples of thrombolytics?

A

tPA
Streptokinase
Urokinase

55
Q

What are three common anti-coagulants?

A

heparins
NOACs
Warfarin

56
Q

What are the features of prothrombin Factors?

A

enzymes that need vitamin K for their synthesis and calcium for their activation
are stable
they all ultimately contribute to prothrombin synthesis

57
Q

Why is platelet activation required for some coagulation steps of haemostasis?

A

bc the PPLPDs on the membrane are essential for driving some parts of the rest of haemostasis forward

58
Q

How is vitamin K found in the body?

A

vitamin K has to be taken into the diet

59
Q

What are the features of factors in the thrombin group?

A

activated by thrombin
V & VIII are co-factors - 5 works with 10 and 8 works with 9
Factor I is fibrinogen

60
Q

What is the extrinsic pathway activated by?

A

external trauma

61
Q

What is the overall effect of the extrinsic pathway?

A

it causes blood to escape from the vascular system

62
Q

What is the difference between the extrinsic and intrinsic pathways?

A

extrinsic is quicker than intrinsic

intrinsic is more important than extrinsic

63
Q

Why is it called extrinsic pathway?

A

because it is activated by TF, a protein extrinsic to the blood

64
Q

What is the intrinsic pathway activated by?

A

by trauma inside the vascular system

by platelets, exposed endothelium or collagen

65
Q

How does the intrinsic pathway work?

A

it amplifies the coagulation cascade via positive feedback

66
Q

What is Extrinsic Xase a combination of?

A

tissue factor and factor 7a

67
Q

What is Intrinsic Xase a combination of?

A

Factors 8a and 9a

68
Q

Which factor is fibrinogen?

A

Factor I

69
Q

What is the role of plasmin?

A

it dissolves the fibrin of blood clots

70
Q

Where is Antithrombin III made?

A

in the liver

71
Q

What is haemophilia B caused by?

A

a genetic defect in factor 9

causes a factor IX deficiency

72
Q

What are antiplatelets otherwise known as?

A

anti coagulants

73
Q

What is the use of fibrinolytics?

A

they dissolve fibrin in arterial disease - break clots

74
Q

What are Fibrinolytics otherwise known as?

A

clot-busting drugs

thrombolytic agents

75
Q

What key substance is produced by COX catalysation?

A

thromboxane

76
Q

What is the physiological role of aspirin?

A

it blocks the formation of TXA2 in platelets

77
Q

What substance do heparins work in co-operation with?

A

AT III

78
Q

How are heparins administered?

A

injection into a vein or under the skin

79
Q

What is the role of heparins?

A

they inhibit coagulation by inhibiting Factor Xa

80
Q

What does NOAC stand for?

A

Novel Oral Anti-Coagulant

81
Q

What are NOACs alternatives to?

A

warfarin

for high-risk patients who have atrial fibrillation

82
Q

When is rivaroxaban used specifically?

A

DVT
PE
to prevent blood clots in atrial fibrillation
to prevent blood clots following hip or knee surgery

83
Q

What substance does Rivaroxaban inhibit?

A

factor Xa

84
Q

What terms are associated with warfarin?

A

anticoagulant

vitamin K antagonist

85
Q

What is the onset of warfarin?

A

has a slow onset of 2 days and requires monitoring

86
Q

How is warfarin administered?

A

injection
iv
orally - pills

87
Q

What is the role of warfarin?

A

it prevents the recycling of vitamin K

to reduce clotting

88
Q

What three substances are responsible for vasoconstriction?

A

Serotonin, ADP and TXA2

89
Q

What are the two main types of blood thinners and how do they work?

A

anticoagulants - slow down the coagulation process of the body
antiplatelet agents - prevents platelet aggregation so they can’t develop into a clot

90
Q

What is another term for warfarin?

A

Coumadin

91
Q

How does Prasugrel work as an antiplatelet agent?

A

it inhibits ADP receptors

AAR, it inhibits the ADP-mediated platelet activation and aggregation occurs

92
Q

How do Aspirin and Clopidogrel work as anticoagulants?

A

they slow the blood’s clotting action by making platelets less sticky

93
Q

How does Ticagrelor work as an antiplatelet agent?

A

it blocks the P2Y12 receptor responsible for promoting platelets and blood clots

94
Q

What is the function of protein C?

A

it inactivates Factor Va & Factor VIIIa

it works with a co-factor Protein S to inactivate Va

95
Q

Why are vitamin K deficiencies rare?

A

bc vitamin K is made by bacteria in the LI

it’s also found in leafy green vegetables

96
Q

How do WBCs become foam cells?

A

they enter a lesion and consume local cholesterol esters

97
Q

What is nitrogen oxide’s relationship with inflammation?

A

in normal conditions it is anti-inflammatory

in abnormal conditions it is pro-inflammatory

M103 T2 (9 decks)

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