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** Pharmacology - CF > Haemostasis, thrombosis and platelet function > Flashcards

Haemostasis, thrombosis and platelet function Flashcards

1
Q

Which three drug groups decrease clotting?

A
  • Anticoagulants
  • Antiplatelet
  • Thrombolytics
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2
Q

What is thrombosis?

A

unwanted haemostatic plug in a blood vessel or the heart

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3
Q

What causes deep vein thrombosis?

A

poor blood flow

sitting for long periods of time

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4
Q

What are the symptoms of deep vein thrombosis?

A

Swelling and heat in leg

Very painful

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5
Q

What can result from a failure to treat deep vein thrombosis?

A

Loss of a leg

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6
Q

Which two things can increase clotting?

A
  • Replacement factors (VIII & IX)
  • Plasminogen ihibitors
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7
Q

Which enzyme does waraffin inhibit?

A

Vitamin K reductase

(stops carboxylation of glutamic acid residues = cannot bind platelet = no proteolysis = no cascade and no clotting)

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8
Q

Which 3 drugs increase the action of waraffin and how?

A
  • Aspirin = displace it from plasma proteins
  • Sulphonamides = interferes with liver function
  • NSAIDs = interferes with platelet function
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9
Q

Which two patient factors increase the action of waraffin?

A
  • Liver disease (decreases factor production and clearance)
  • Reduced vitamin K availiability
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10
Q

What is the average rate of onset for warrafin use?

A

12-16 hours

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11
Q

How long do the effects of warrafin last once you stop taking it?

A

4-5 days

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12
Q

How do we measure the action of warrafin in a patient?

A

Prothrombin time

(the time a sample takes to clot following addition of a standardised amount of Ca = ratio = compared to healthy subjects)

2-2.5 = prophylaxis of deep vein thrombosis

  1. 5 = treatment of deep vein thrombosis/ pulmonary embolism
  2. 5 = recurremt deep vein thrombosis/pulmonary embolism
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13
Q

After starting a patient on warrafin at which intervals do we measure the action of warrafin?

A

Initially daily

Then at longer intervals

Then every 12 weeks

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14
Q

Which two drugs decrease the action of warrafin and how?

A
  • Barbituates = induce metabolising enzymes
  • Colestipol (athlerosclerosis) = decreases absorption
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15
Q

Which two patient factors decreases the action of warrafin?

A
  • Increased vitamin K = promoted clotting factor synthesis
  • Vomitting
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16
Q

What are the side effects of Warrafin (2)?

A
  • Haemorrhage in bowel or brain (stop administration & give vitamin K & replacement factors)
  • Teratogenic (damages foetus)
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17
Q

Name two injectable anticoagulants:

A

Heparin

Low molecular weight heparin

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18
Q

Which two factors does heparin hit?

A

Factor IIa

Factor Xa

= activates antithrombin III

n.b. Heparin also binds to factor IIa but LMW heparin is too short = only hits factor Xa!!

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19
Q

What is the main clinical use for heparin?

A

Clearing blocked IV catheters

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20
Q

What inhibits heparin?

A

Factor IV (LMW heparin not inhibited)

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21
Q

Can factor Xa bind to factors already bound to fibrin?

A

No

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22
Q

What causes heparin to be badly absorbed in the gut?

A

Its large size and charge

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23
Q

In which 2 ways can heparin be administered?

A

IV

Subcutaneous (LMW heparin only)

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24
Q

Why is there an initial rapid removal of heparin?

A

Binds to plasma proteins (heparin only), endothelial cells and macrophages

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25
Q

How is heparin excreted?

A

Slowly through renal excretion

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26
Q

What are the side effects of heparin (5)?

A
  • haemorrhage (counter with heparin antagonist e.g. protamine sulphate)
  • Thrombosis (rare -> when antibodies against heparin cause endothelial damage)
  • Osteoporosis
  • Hypersensitivity
  • Hypoaldosteronism
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27
Q

Name 4 examples of heparin:

A

heparin

calciparine

minihep

monoparin

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28
Q

Name 3 types of LMW heparin:

A

Certoparin

Dalteparin

Enoxaparin

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29
Q

Name 3 antithrombin independant anticoagulants:

A
  • Hirudin (binds thrombin active site -> leeches)
  • Hirugen
  • Bivalirudin
30
Q

Which patients may antithrombin III independant anticoagulants be useful for?

A

Those who produce heparin antibodies

31
Q

What are the possible uses for antithrombin III independent anticoagulants?

A

Percutaneous coronary intervention (angioplasty) = rapid on/off effects = get patient out of hospital as quickly as possible

32
Q

What are the 3 main uses of anticoagulants?

A
  • prevention of deep vein thrombosis (perioperatively since wound increases the liklihood of clot formation)
  • treatment of deep vein thrombosis
  • prevention of thrombosis on prosthetic heart valves
33
Q

Which enzyme does Aspirin irreversibly activate in platelets?

A

Cyclo-oxygenase

34
Q

How long does it take platelets to replace COX?

A

7-10 days

35
Q

Why is it that platelet cells cannot replace COX immediately but endothelial cells can?

A

Platelets do not have a nucleus!!

36
Q

When are antiplatelet drugs used?

A

In acute MI (myocardial infarction) in combination with fibrolytic drugs

37
Q

Tell me the following about Triclopine:

Is it reversible or irreversible?

What is its onset like?

Which other drug does it have a similar efficacy to in reducing stroke?

A

Irreversible

Slow (3-7 days)

Aspirin

38
Q

What are the 3 main side effects of triclopidine?

A

Rash

Diarrhoea

neutropenia (loss of wbc)

39
Q

Tell me the following about clopidogrel:

Is it reversible or irreversible?

How is it administered?

A

Irreversible

Oral prodrug

40
Q

Which group of individuals does clopidogrel not work in?

A

Those with a cytochrome p450 mutation

41
Q

When is clopidogrel given?

A

Given after heart surgery & after an MI

42
Q

Tell me the following about prasugrel:

Is it reversible or irreversible?

What is its onset like?

What is its metabolism like?

A

Irreversible

Faster onset (hours)

More easily metabolised to its active metabolite

43
Q

Tell me the following about Ticagrelor:

Is it reversible or irreversible?

Which other two antiplatelet drugs does it have a similar efficacy to?

A

Reversible = stays in body for a couple of days only = can release patients faster!

Clopidogrel & prasugrel

44
Q

Why can abciximab only be used once?

A

It is an antibody fragement directed against the receptor, repeated use = provokes immune response

45
Q

After use of abciximab how quickly does platelet function recover?

A

in days

46
Q

When is abciximab used?

A

IV

in high risk coronary angioplasty patient on herparin & aspirin

47
Q

What is tirofiban/eptifibatide?

A

A cyclic peptide that resembles the IIb/IIIc ligands

48
Q

How is tirofiban/eptifibatide administered?

A

IV

n.b. long term oral administration may be harmful

49
Q

How quickly is platelet function regained following use of tirofiban/eptifibatide?

A

hours

50
Q

Why are the prostaglandin agonists (epoprostenol) given intravenously?

A

It is chemicallly unstable

51
Q

When is Epoprostenol and other prostaglandin agonists used?

A

In patients undergoing haemodialysis (cannot use heparin)

52
Q

What is the effect of using the phosphodiesterase inhibitor dipyrimidole?

A

it increases platelet cAMP levels

53
Q

What are the 5 clinical uses of antiplatelet drugs?

A
  • Following acute MI
  • Those at risk of MI
  • Following coronary bypass/angioplasty
  • Unstable coronary syndromes
  • following a cerebral stroke
54
Q

Name 3 plasminogen activators:

A
  • Streptokinase
  • Recombinant tPA
  • Urokinase
55
Q

What do plasminogen activators do?

A

they produce plasmin = degradation of clot

56
Q

After administering streptokinase what must be done to block the function?

A

Give antistreptococcal after 4 days

57
Q

How long must you wait before reuse after giving a streptokinase?

A

1 year

58
Q

Which is the most commonly used plasminogen activator?

A

recombinant tPA

59
Q

What are the 3 types of recombinant tPA:

A

Anteplase/duteplase (short half life = IV infusion)

Reteplase (longer half life = IV bolus)

60
Q

At which sites are recombinant tPA more active?

A

At fibrin bound plasminogen (clot specific!)

61
Q

What are the contraindications of Fibrolytic agents (7)?

A
  • Active/recent internal bleeding
  • Recent cerebrovascular incident
  • Invasive procedures (where haemostasis is important)
  • Pregnancy (can cause loss of child)
  • If had cardipulmonary rescissitatopm for hours before
  • Trauma
  • Bacterial endocarditis
62
Q

What are the side effects of fibrolytic agents (3)?

A
  • GI haemorrhage
  • Allergic reaction (/fever)
  • Hypotension (burst of plasmin by streptokinase)
63
Q

What are the clinical uses of fibrolytic agents (4)?

A
  • Acute MI
  • Acute thrombotic stroke
  • Clear thrombosed shunts/cannulae
  • Acute arterial thromboembolism
64
Q

What are anti-thrombolytic drugs used for?

A

To stabilise a clot

65
Q

Name two antithrombolytic drugs:

A
  • Tranexamic acid
  • Aprotinin
66
Q

How does tranexamic acid work?

A

Inhibits activation of plasminogen (stabilises clot)

67
Q

How is tranexamic acid administered?

A

Oral/IV

68
Q

When is tranexamic acid used clinically?

A

when increased risk of bleeding (e.g. dental extraction, prostoectomy etc)

69
Q

What are the side effects of tranexamic acid?

A

Nausea & vomitting

70
Q

How does aprotinin work?

A

Proteolytic inhibitor of plasmin/kallikrein

71
Q

How is aprotinin administered?

A

slow IV

72
Q

When is aprotinin used clinically?

A

patients of high risk of blood loss (e.g. open heart surgery)

** Pharmacology - CF (4 decks)

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