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Basic Pharmacology > 19. Anticoagulants > Flashcards

19. Anticoagulants Flashcards

1
Q

Why do dentists know about drugs and clotting?

A
  • thrombo-embolic diseases are a major cause of death in developed countries
  • drugs used to affect blood clotting modify blood coagulation or platelet adhesion/activation
  • haemorrhage and bleeding in GIT, mucus membranes, gingiva and urinary tract are side effects
  • since patients take anticoagulants are on the edge of a haemorrhagic state, must take precautions in surgical procedures
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2
Q

Define ‘haemostasis’

A

spontaneous arrest of blood loss from damaged blood vessels
- essential to life

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3
Q

Steps of haemostasis

A
  • vasoconstriction
  • platelet adhesion and aggregation (eicosanoids)
  • fibrin formation (coagulation system vs fibrinolytic system)
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4
Q

Define ‘thrombosis’

A

unwanted formation of haemostatic plug of thrombus within blood vessel or heart

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5
Q

Why can thrombosis occur?

A
  • vascular disease e.g atherosclerosis
  • prosthetic heart valves
  • atrial fibrillation
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6
Q

Consequences of thrombosis

A
  • deep vein thrombosis
  • pulmonary embolism
  • myocardial infarction
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7
Q

How does a thromboembolus can look layered. This is typical of a thrombus where?

A
  • large vein of pelvis
  • lower extremity
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8
Q

Explain role of atheroma and the thrombus in a lumen

A
  • atheroma plaques narrow the lumen significantly
  • then thrombus occludes completely
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9
Q

Difference in a clot vs thrombus

A
  • clot forms in vitro - amorphous
  • thrombus forms in vivo - distinct structure (white head, red tail)
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10
Q

2 types of thrombus

A
  • arterial
  • venous
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11
Q

Features of an arterial thrombus

A
  • atherosclerotic
  • large head
  • platelets
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12
Q

Features of venous thrombus

A
  • normal
  • large tail, small head
  • gives rise to emboli
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13
Q

Define ‘blood clotting’

A
  • complex series of enzymatic activations
  • produces active clotting factors from precursors
  • cascade mechanism which results in production of fibrin
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14
Q

What controls blood clotting?

A
  • enzyme inhibitors
  • fibrinolysis
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15
Q

Role of anticoagulants
Examples

A
  • modify blood clotting mechanisms
  • heparin and oral anticoagulants like warfarin
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16
Q

Intrinsic pathway of clotting

A
  • triggered by exposure of collagen in damaged vessels
  • factor 12 activates 11 activates 9
  • vWF activates 8
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17
Q

How long does blood clotting take?

A

under 5 mins
without any help

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18
Q

Extrinsic pathway of clotting

A
  • triggered by damaged tissue which releases 3
  • which activates 7
  • 3 and 7 together activate 9
19
Q

Explain the common pathway

A
  • factor 9 activates 10
  • 10 causes prothrombin to become thrombin/factor 2 which activates 13
  • thrombin activates fibrinogen to fibrin
20
Q

What positive feedback occurs in clotting cascade?

A
  • thrombin reinforces intrinsic pathway by activating 11
  • activated 10 activates 7 and 3
21
Q

What is heparin?

A
  • a parenteral anticoagulant
  • family of sulphated mucopolysaccharides
  • sulphate groups required for binding to antithrombin
  • fragments or synthetic varieties - low-molecular weight heparins (LMWHs)
22
Q

Where is heparin found?

A

in secretory mast cells

23
Q

How to get heparin?

A

extracted from animal liver

24
Q

Explain the pharmacodynamics of heparin

A
  • requires antithrombin III (a2 globulin) for activity
  • AT III inactivates thrombin, IX, X, XI and XII
  • heparin binds to AT III to accelerate this process
  • LMW heparins more consistent
  • all types have immediate onset of action
25
Q

Explain pharmacokinetics in heparin

A
  • inactive orally - not absorbed through GI tract
  • administered with iv or sc for LMWHs
  • short half life of less than an hour (low doses), 2 hours for higher doses but LMWH have longer duration of action
  • eliminated mainly by renal excretion
26
Q

Side effects of heparin

A
  • hypersensitivity
  • bleeding
27
Q

How to treat heparin overdose?

A

iv protamine
- strongly basic protein

28
Q

Explain pharmacodynamics of warfarin

A
  • inhibits hepatic synthesis of vitamin K1 - dependent clotting factors II, VII and X
  • 1-2 day long period
  • genetically determined resistance, reduced binding to vitamin K reductases
29
Q

Side effects of warfarin

A
  • bleeding
  • skin necrosis
30
Q

How to treat a warfarin overdose

A
  • vitamin K1 (iv or oral)
  • fresh frozen plasma (thawed)
31
Q

How does warfarin work as a mode of action?

A
  • 2, 7, 9 and 10 need to be carboxylated and oxidised with oxygen, carbon dioxide and glutamic acid to delta-carboxyglutamic acid residues
  • this enables vitamin K reduced form (hydroquinone) to vitamin K oxidised form (epoxide)
  • it goes back to quinone then hydroquinone when reduced
  • warfarin targets vitamin K reductase at both stages of this reduction to keep it reduced and all the activation of clotting factors can’t happen
32
Q

Pharmacokinetics of warfarin

A
  • dose is highly variable (1-20mg/day)
  • absorption - rapid, almost total
  • plasma protein binding around 99%
  • metabolism - oxidation and reduction
  • excretion - urinary metabolites
  • half life - 15 to 80 hrs
33
Q

Use of anticoagulants in clinical practice

A
  • starts usually with combination of heparin and oral coag like warfarin
  • heparin rapidly effective - monitored through partial thromboplastin time
  • warfarin takes 1-2 days for full effect - monitored with prothrombin test (in INR)
  • heparin covers lag period and can be then withdrawn
34
Q

How to monitor anticoagulant therapy?

A
  • fasting blood taken to establish PT ratio
  • issue with thromboplastin variability required standardisation - assigned international sensitivity index (ISI)
  • patients PT is expressed as INR - internalised normalised ratio
  • INR is PTpt/PTref to the power of ISI
35
Q

Typical warfarin INR value

A

2-4

36
Q

Why are new anticoags better?

A
  • dont need antithrombin
  • directly act and act quicker therefore
37
Q

Drugs that potentiate effect of oral anticoags

A
  • drugs that decrease platelet aggregation e.g aspirin
  • drugs that inhibit cytochrome P450 e.g co-trimoxazole
  • drugs that inhibit reduction of vitamin K e.g cephalosporin antibiotics
38
Q

Drugs that decrease effect of oral anticoags

A
  • drugs that induce cytochromes P450 e.g rifampicin, many anticonvulsants
  • drugs which reduce absorption e.g sucralfate
39
Q

How is aspirin an antiplatelet drug?

A
  • inhibits eicosanoid production to inhibit platelet aggregation
  • platelet-derived TXA2 promotes aggregation and endothelium derived PGI2 inhibits aggregation
  • aspirin irreversibly inhibits COX-mediated synthesis of both
  • endothelium can synthesise new COX, platelets cannot
  • net effect increases PGI2 and inhibits platelet aggregation
40
Q

When is aspirin beneficial as an anticoag?

A
  • disorders of arterial thrombosis
  • includes acute MI and high risk MI
  • after coronary artery bypass grafting
41
Q

Anticoags in a dental patient - how is this considered?

A
  • every effort made to avoid treatment - use preventative care
  • awareness of those, treatment performed if patient in therapeutic dose range and adequate pre- and post-treatment operative observation and care available
  • use of local haemostatic measures like sutures, pressure packs, haemostatic agents like vitamin K
  • awareness of drug-drug interactions
42
Q

Dental implications for patients medicated with antiplatelet therapies

A
  • NSAID interaction with antiplatelet function of aspirin - delay NSAID for 1-2 hrs
  • increased risk of bleeding following minor dental surgery for low dose aspirin
  • increased risk of mucosal damage and bleeding with combined NSAIDS
43
Q

Dental implications for patients medicated with anticoagulants

A
  • antibiotics enhance anticogaluant activity (esp metrodinazole, tetracycline)
  • NSAIDs contraindicative in postoperative pain and inflammation management - high risk of ulcerative bleeding

Basic Pharmacology (16 decks)

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