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Year 2 Pharmacology > Anti-thrombotic > Flashcards

Anti-thrombotic Flashcards

1
Q

What is the most important function of the haemostat system?

A

To maintain the integrity of the vascular endothelium and blood fluidity

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2
Q

What are the three stages to haemostasis and briefly describe what happens?

A

Vasoconstriction- reduces size of site of injury
Primary haemostasis- platelet adhesions, shape change, granule release, more recruitment, aggregation
Secondary haemostasis- Tissue factor, phospholipid complex expression, thrombin activation, fibrin polymerisation

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3
Q

What follows haemostasis?

A

Thrombolysis- once the epithelium heals

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4
Q

What is the haemostat system a balance of?

A

Maintenance and balance of avoiding blood loss (haemorrhage) and preventing the formation of clots within blood vessels (thrombosis)- Blood fluidity and endothelium integrity

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5
Q

What three things make up a thrombus?

A

Platelets
Fibrin
Trapped blood cells

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6
Q

What is a partial/total obstruction of a vessel by a thrombus?

A

Primary thrombosis

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7
Q

What is an embolism?

A

Migration of a primary thrombus of the cloys to a distant site

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8
Q

What causes a thrombo-emboilism?

A

Abnormalities of blood flow
Endothelial damage
Hyper coagulability

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9
Q

What can cause endothelial damage?

A 
Trauma
Catherisation 
Neoplasia
Parasites
Atheroclerosis
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10
Q

What can cause abnormalities of blood flow?

A

Hypoperfusion, hypervolaemia, heart failure
Compression on blood vessels
Hyperviscocity- dehydration, hyperglobulinaemia
RBCs redcues elasticity

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11
Q

What causes hyper coagulability?

A

Platelets are hyperaggregatable
Reduces anti-coagulate factors
Hypofibrinolysis

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12
Q

What are the differences between arterial and venous thrombosis?

A

Arterial- Platlets predominant, therapy against PLT aggregation
Venous- Fibrin and RBCs predominant, therapy against secondary haemostasis

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13
Q

What is used for therapy against platelet aggegation and secondary haemostasis (artery/venous thrombosis)?

A

Therapy against platelets (artery)- aspirin, clopidogrel

Therapy against secondary (venous)- heparin

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14
Q

How is thrombosis treated?

A

Dissolution of existing thrombi- surgical extraction, streptokinase, rt-PA, urokinase

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15
Q

How is thrombosis prevented?

A

Anti-PLT drugs
Heparins
Vitamin K antagonists

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16
Q

rt-PA (recombinant tissue plasminogen activators) what is their action, what are some examples, what is the risk?

A

Action- enhance the transformation of plasminogen to plasmin
Examples- alteplase, reteplase, tenecteplase
Risk of spontaneous bleeding

17
Q

What is streptokinase produced by, what is its action and what are its problems?

A

Produced by B-haemolytic streptococci
Enhances plasmin formation
Can cause a systemic lytic state and production of anti-streptokinase antibodies may be present from streptococci infections

18
Q

What is the mode of action of urokinase?

A

Proteasis produced by renal cells and normally present in urine
Activates the plasminogen

19
Q

How can anti-platlet drugs work?

A

Cox- inhibitors
ADP-receptro antagonists
Gp IIb/IIa receptor antagonists

20
Q

What is the mode of action of aspirin, how long do the effects last?

A

Acts by irreversible acetylation of COX receptor
Causes a reduction in synthesis of thromboxane A2
Effects are permanent and last for the entire platelets life

21
Q

What is the action of clopidogrel?

A

Irrevervisle block of the link between ADP and platelet receptor P2Y12
Abnormal activation of receptor GPIIb/IIa

22
Q

What is the action of unfractionated heparin?

A

unfractionated heparin binds to Anti-thrombin III and thrombin IIa
and prevents coagulation factors- IXa, Xa, XIa, XIIa
Blocks fibrin formation and platelet activation

23
Q

What are the pros and cons of unfractionated heparin?

A

Pros- cheap and widely available

Cons- animals with low anti-thrombin III, pharmacokinetics unpredictable

24
Q

What is the half life of unfractionated heparin dependent on?

A

Binds to plasmatic proteins, endothelial cells, macrophages and PLTs so dependent on the half lives of those cells

25
Q

What is the alternative to unfractionated heparin?

A

Low molecular weight heparins

26
Q

What is the action of LMWH?

A

Binds to anti-thrombin III to inhibit Xa

27
Q

What is the down side of LMWH?

A

Expensive

28
Q

What is an example of a vitamin K antagonists, what is their action?

A

Warfarin
Block hepatic carboxylation of factors II,VII, IX, X
Activity monitored by PT
High risk of spontaneous bleeding

Year 2 Pharmacology (11 decks)

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