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Cardiovascular: pharmacology > Antiplatelet, anticoagulant and thrombolytic drugs and the mechanism of clotting > Flashcards

Antiplatelet, anticoagulant and thrombolytic drugs and the mechanism of clotting Flashcards

1
Q

What is the starting process in almost all clot formations?

A

It begins with a local event that causes damage to the wall

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2
Q

What does the damage to the endothelial wall expose?

A

Tissue factor and collagen

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3
Q

What does the exposed collagen bind to?

A

vWF

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4
Q

What does collagen bound vWF act as ?

A

a cross bridge because it will also allow the platelets to bind to it through the glycoprotein Ib (GP Ib) receptor on the platelet surface.

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5
Q

What is the receptor on the platelet that binds to vWF – collagen complex?

A

Glycoprotein Ib

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6
Q

How is the binding of the platelet to the blood vessel further stabalised ?

A

Interactions are formed by Integrin A2 B1 and glycoprotein VI on the platelet binding to collagen

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7
Q

Which two things initiate platelet activation?

A

Glycoprotein VI anchoring and thrombin

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8
Q

What does the platelet do in response to activation?

A

a. 1.changes shape (extends pseudopodia) which then gives aggregated platelets
b. 2.The platelet also starts to synthesise thromboxane A2 (TA2,)

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9
Q

How is TA2 formed?

A

It is formed from arachidonic acid through the enzyme COX1

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10
Q

TA2 acts in both an —– and ____ manner.

A

TA2 acts in both an autocrine and paracrine manner.

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11
Q

what is the receptor called that TA2 binds to?

A

GPCRTXA2

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12
Q

what does the binding of TA2 to GPCR TXA2 do?

A

causes the release of

i) 5-hydroxytryptamine (aka seratonin) and ADP
ii) vWF and factor V

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13
Q

what do the dense granules release?

A

5- hydroxytryptamine (5-HT) (aka seratonin) and ADP

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14
Q

what do the alpha granules release?

A

vWF and factor V

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15
Q

why do the blood vessels vasoconstrict?

A

because TXA2 acts directly on smooth muscle and also 5-HT binds to receptors on the surface causing vasoconstriction

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16
Q

what does ADP bind to ?

A

platelet GPCR P2Y12 receptors

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17
Q

what does the binding of ADP do? 3 things

A

i) activation of further platelets
ii) Increases the expression of glycoprotein IIb and IIIa receptors
iii) causes exposure of acidic phospholipids on the platelet surface - this facilitates the formation of the clot

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18
Q

what do GP IIb and IIIa do?

A

they are binding points for fibrinogen on the platelet surface

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19
Q

what is the KEY event in the coagulation cascade?

A

the production of protease thrombin (factor IIa) that cleaves fibrinogen to fibrin to form a solid clot

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20
Q

what is coagulation?

A

the conversion of the soft plug to form a solid clot which assists in the healing process.

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21
Q
  1. what does the tissue injury expose ?
A

matrix tissue factor (thromboplastin)

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22
Q

2.which factor binds to TF?

A

VII - this complex TF:VIIa is now active

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23
Q

3.what does the TF:VIIa complex do?

A

activates factor X (x- Xa)

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24
Q
  1. what does the activates Xa bind to ?
A

Va

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25
5. what does the Complex VaXa do?
converts prothrombin to thrombin - this is the key player
26
6. what is the first thing that thrombin does?
activates further platelets - in doing so it causes the release of factor V from alpha granules in the platelet cytoplasm - when these factors reach the surface they become active
27
7. what does thrombin do to TF:VII (8) ?
It liberates factor VIII which then becomes active
28
8.what does thrombin do to XI?
converts it to XIa
29
9.how is IX activated?
by wither TF- VIIa or XIa
30
10. what does IXa do?
binds with VIIIa to convert X to Xa
31
11. what dies the Xa form a complex with in order to bind prothrombinase?
Va
32
12.what does the Xa and Va complex do?
convert II to IIa
33
13.what does thrombin do?
cleaves fibrinogen, forming fragments that spontaneously to form fibrin
34
14. Which factor then cross links the polymer to form a fibrin fibre network and a solid clot ?
VIIIa
35
what are the main components of arterial thrombus?
white thrombus: mainly platelets in a fibrin mesh and relatively few RBCs
36
where do arterial thrombus normally do to cause problems ?
they embolise and if this happens in the carotid arteries , then can get a stroke
37
what are arterial thrombus normally treated using?
antiplatelets
38
what are the main components of venous thrombus?
white head, jelly like tail and fibrin rich red thrombus
39
what normally happens to venous thrombi?
if detaches forms an embolus that usually lodges in the lung (pulmonary embolism) also can get DVT
40
what are venous thrombi treated with?
anticoagulants
41
which clotting factors require post-translational modification for subsequent function of the active factors?
II,VII,IX,X
42
VIIa, IXa, Xa that act as ____- proteases
VIIa, IXa, Xa that act as serine proteases
43
what is the specific reaction happening in post-translaitonal modification?
carboxylation of glutamate residues
44
factor II goes from being _______ to ______ with vitamin K modification. It is still inactive though
factor II goes from being descarboxythrombin to prothrombin with vitamin K modification. It is still inactive though
45
The carboxylase enzyme that mediates ______ ________ requires vitamin __ in its _____ form as an essential _____
The carboxylase enzyme that mediates gamma carboxylation requires vitamin K in its reduced form as an essential cofactor
46
what is the oxidised form of vitamin K called?
epoxide
47
what is the reduced form of vitamin K called?
hydroquinone
48
what is the enzyme that converts vitamin K from oxidised to reduced?
vitamin K reductase
49
what is the role of warfarin?
blocks vitamin K reductase so get get a reduced Gamma carboxylation of 2,7,9,10 and this interrupts the coagulation cascade
50
what are anticoagulants used for ? 4 things?
- deep vein thrombosis (DVT) - prevention of post-operative thrombosis - patients with artificial heart valves - atrial fibrillation
51
what risks do anticoagulants carry?
haemorrhage
52
warfarin Blocks coagulation in ____, not in ___
Blocks coagulation in vivo, not in vitro
53
what is the downside of warfarin?
it has a low therapeutic ratio
54
what has to be checked regularly with warfarin?
INR
55
name 3 ways to potentiate warfarin action?
- liver disease – decreased clotting factors - high metabolic rate – increased clearance of clotting factors - drug interactions
56
name 3 ways to lessen warfarin action?
Physiological state – pregnancy (increased clotting factor synthesis) – hypothyroidism - reduce metabolism (decreased degradation of clotting factors) - Vitamin K consumption - drug interactions
57
how is warfarin overdose treated?
vitamin K administration or concentrate of plasma clotting factors
58
name the important inhibitor of coagulation in the body
antithrombin III
59
what is the action of AT III
it neutralises all serine protease factors by binding to their active sites in a 1 to 1 ratio
60
what is the action of heparin?
it binds to ATIII increasing its affinity for serine protease clotting factors to greatly increase their rat of inactivation
61
what clotting factors is heparin particularly aimed at?
Xa and IIa (thrombin)
62
what must heparin bind to to inhibit IIa?
both IIa and AT III
63
what must heparin bind to to inhibit Xa?
only AT III
64
give 2 examples of LMWH?
enoxaparin and dalteparin
65
when is heparin preferred to LMWH?
in renal failure because heparin is eliminated by routes other than the kidneys
66
which factor do LMWH and fondaparinux inhibit?
Xa
67
give 4 side effects of heparin and LMWH
1. haemorrhage 2. osteoporosis 3. hypoaldosteronism 4. hypersensitivity reactions
68
what substance inactivates heparin and is used in haemorrage?
protamine sulfate
69
name a new orally active agent that is a direct inhibitor of thrombin
dabigatran etexilate
70
name a new orally active agent that is a direct inhibitor of Xa
rivaroxiban
71
what are the advantages of the new orally active anticoagulant agents? 2
convenience of administration predictable degree of anticoagulation, but no specific agent available to reduce haemorrhage in overdose
72
what are dabigatran etexilate and rivaroxiban used in?
to prevent venous thrombosis in patients undergoing hip and knee replacements
73
how does aspirin work on platelets?
it irreversibly blocks COX in platelets preventing TXA2 synthesis
74
how does aspirin work on endothelial cells
blocks COX inhibiting the production of antithrombotic prostaglandin I2
75
what is aspirin mainly used for?
thromboprophylaxis in pateints at high cardiovascular risk
76
what are the main side effects of aspirin?
gastrointestinal bleeding and ulceration
77
how does clopidogrel work?
links to the P2Y12 receptor by a disuphide bond producing irreverible inhibition
78
when is it used?
in patients intolerant to aspirin and alongside aspirin
79
how does tirofiban work?
blocks GPIIb IIIa receptor - preventing fibrin linking
80
what does plasmin do?
breaks fibrin into fibrin fragments to get clot lysis
81
what is the plasmin precursor?
plasminogen
82
what is the enzyme required to form plasmin
endogenous tissue plasminogen activator (tPA)
83
name three drugs that activate plasminogen
streptokinase, alteplase and duteplase
84
what is the role of fibrinolytics?
they are usedto reopen occluded arteries in acute MI or stroke
85
what is a side effect of streptokinase?
allergic reactions - should not be given to patients with recent streptococcal infections
86
alteplase and duteplase and more effective on ___ bound plasminogen than____ plasminogen
alteplase and duteplase and more effective on fibrin bound plasminogen than plasma plasminogen
87
what is used if there is a haemorrhage with fibrinolytics?
tranexamic acid which inhibits plasminogen activation

Cardiovascular: pharmacology (6 decks)

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