Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Applied pharmacology > Anticoagulant > Flashcards

Anticoagulant Flashcards

1
Q

What is haemostasis?

A

Mechanism designed to prevent the loss of blood after injury to the blood vessel. Controlled by a complex and balanced series of positive and negative feedback systems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the stages of haemostasis?

A
  • Blood vessel contraction - contraction of smoth muscle = constriction = slow rate of blood flow = decrease in pressire and pushes opposing surfaces of vessel together.
  • Platelet plug formation - exposure to collagen allows platlets to adhere by binding to Von Willebrand’s factors. Release ADP, 5-HT and thromboxane A2 causing platelets to aggregate while fibrin acts to bind them together. Release of prostoglandin by intact endothelium inhibits platelet plug & acts to limit the extent of the clot.
  • Clot formation: meshwork of fiBrin and platelets. Prothrombin activator converts prothrombin to thrombin. This thrombin converts fibrinogen into fibrin. Fibrin reinforces the platelets.
  • Fibrinolysis - repair of vessel is underway to dissolve the clot.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is fibrin formed?

A

From fibrinogen from the action of thrombin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What needs to happen to the vessel wall for blood to clot?

A

Roughened surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What factors are associated with the intrinsic prothrombin activator?

A

Factor V, factor VIII -XII and Ca2+ IONS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What factors require vitamin K for synthesis

A

Factor VII, IX and X and prothrobin (II)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the two types of fibrinolysis processes:

A 
Primary = normal body processes of controlling clor
Secondary = Break down of clot due to medicine or medical disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the mechanism of fibrinolysis?

A

The enzyme plasmin cuts the fibrin mech at various places leading to prduction of circulating fragments which are cleared by proteases or kidney/liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can happen when a clot forms in a vein?

A
  • Restrict blood flow whcih can lead to a build up behind the clot leading to pain and swelling i.e. DVT. (venous thrombosis)
  • If the clot breaks off it can cause pulmonary embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does atherosclerosis aid the development of clots in arteries?

A
  • Atherosclerosis is the hardening of arteries where plaque builds up along the vessel walls causing it to narrow
  • This causes increase in pressure that can often tear the vessel walls
  • Stimulating the clotting formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why are pregnant, menopausal, or women taking contraceptive pill more at risk to venous thrombosis?

A

oestrogens increase the activity of the coagulation pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is it important to get the correct dose for patients who need anticoagulant therapy?

A
  • Too high= haemorrhage

- Too low = embolism remains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What conditions/ medical history indicate a person is taking anticoagulants?

A
  • Myocardial infarction
  • Cerebrovascular thrombosis
  • Venous thrombosis
  • Pulmonary embolism
  • Prosthetic heart valve
  • Post-operative prophylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is heparin?

A

Sulphated acidic mucopolysaccharide that is widely distributed in the body.
Unfractional heparin is extracted from pig or ox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the dose of heparin expressed as?

A

Terms of units of biological activity as it is composed of polymers of different molecular weights.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does heparin need to be given via injection?

A

Poorly absorbed by the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When is heparin given?

A

Hospitalised patients as the first anticoagulant.

E.g. myocardial infarction, thrombophlebitis, DVT, pulmonary embolism and post-operative prophylaxis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does heparin act as an anticoagulant?

A

Unfractional heparin does not break down clots that are already formed instead it encourages the body’s naural lysis to work.

  • Heparin binds to enzyme inhibitor antithrombin III = limits blood clot by inactivating thrombin and other proteases, especially factor Xa.
  • It inhibit platelt aggregation
  • rate of inactivation can be increase by up to 100 fold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the advangates of unfractional heparin over the use of low molecular weight heparin?

A

LMWH is eliminated solely by renal excretion so unfractional heparin has superseded it can be given to patients with renal dysfunction and is more predictable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does LMWH work?

A

Inhibit factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the adverse effects of heparin?

A
  • Bleeding
  • Heparin induced thrombocytopenia (platelets -<50,000/microlitre- low platelet count)
  • systemic reaction can occur to intravenous infusion (1/4 patients)
  • skin rash
  • osteoporosis
  • vertebral collapse (rare but found in young people with prolonged use)
  • alopecia
  • hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Can heparin be used by a pregnant women?

A

Yes - neither LMWH and unfractional heparin can cross the placenta barrier thus is the prefered oral anticoagulant for pregnant women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How are patients with n overdose of heparin treated?

A

Slow IV infusion of protamine sulphate (immediately reverses the anticoagulant effects)

  • Must be administered within 3 hours of heparin dose
  • Only partially effective against LMWH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When is warfarin used?

A

Areas of slowly running blood e.g. veins and pooled blood behind artificial and natural valves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is used if someone has a sensitivity to warfarin?

A

Phenindione - rarely used, has severe side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Compare warfarin with heparin:

A

Slower than heparin

  • Administered orally
  • Long 1/2 life (administered once a day)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe and explain the onset and duration of Warfarin:

A

Carries on being effective for several days after the drug has been stopped

  • Takes 48-72 hours for anticoagulant effect
  • Until blood level of warfarin builds up and usual plasma stores of clotting factors are depleted
  • Duration of single dose can last 2-5 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the mode of action of Warfarin?

A

Warfarin is structurally closely related to Vitamin K

  • Acts as vitamin K anti-metabolite thus interferes with the synthesis of factors VII, IX, and X and prothrombin.
  • Has narrow therapeutic index.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the pharmacokinetics of warfarin:

A
  • With oral administration absorption is almost complete and max plasma concentration is reached with 2-8 hrs
  • Approx 97% is bound to plasma protein albumin
  • Gains access to foetus but does not appear in breast milk
  • Metabolised in the liver
  • 1/2 life varies significantly
  • Hepatic metabolism leads to conjugation and excretion into the gut in bile Once here deconjugation and resorption occurs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the onset of warfarin dependent on?

A

Catabolism of preformed factors as warfarin acts by inhibiting synthesis of active vitamin K dependent clotting factors. Thus delay between dosing and effect cannot be shortened.

31
Q

What are the indications for warfarin?

A
  • DVT
  • Pulmonary embolism
  • Atrial fibrillation
  • Prosthetic heart valves
  • Long term treatment of thromboembolic diseases e.g. thrombophlebitis and myocardial infarction
32
Q

What are the adverse effects of warfarin?

A
  • Haemorrhage (in elderly increases risk when on haemodialysis) = look for petechial haemorrhage on hard palate !
  • Mild trauma can create ecchymoses (may be evident in the mouth)
  • Coughing up blood
  • Excessive bruising
  • Bleeding from nose/ gums
  • Blood in urine +/- stools
  • Teratogenesis (malformations on foetus)
  • Rashes
  • Oesteoporosis - contraversial
  • Purple toe syndrome - rare, small deposits of cholesterol break lose and cause embolisms in blood vessels in skin of feet causing blue/purplish colour and painful
  • Warafrin necrosis -rare but serious
33
Q

Why is it important that the dose of warfarin is not too high?

A

High doses do not further prevent clot formation but have a huge impact on adverse effects.

34
Q

Name the drug interactions of warfarin:

A
  • Aspirin - competes for the same protein and displaces it form the protein= increase in free plasma warfarin = increases the effects of warfarin . Aspirin has GI disturbances the gastric bleeds become more extensive. Ibuprofen & naproxen however only have a very minor interaction with warfarin so should be prescribed if NSAID is indicated.
  • Other antiplatelet drugs e.g. Clopidogrel
  • Paracetamol - prolonged use
  • Broad spectrum antibiotics -potentiate the effects of warfarin, reduce the flora in GI tract that normal synthesis vitamin K. Amoxicilin and clindamycin have no effect, doxycycline & tetracycline have little effect, Erythromycin and metronidazole have greatest effect. Metronidazole inhibits enzymes that metabolise and destroy warfarin.
  • Antifungals - fluconazole & miconazole (even administered topically) will increase anticoagulant effect of warfarin.
  • Barbiturates -stimulates metabolism of warfarin especially phenobarbital because it induces the liver microsomal enzymes that would normal destroy the anticoagulant.
  • Alcohol - Chronic ingestion stimulates metabolism of warfarin whilst acute intoxication inhibits metabolism
  • Many more - check BNF
35
Q

What is fluconazole & miconazole? and what is it used to treat?

A

Antifungal - thrush, acute erythematous candidiasis, denture stomatitis, chronic hyperplastic candidiasis and angular chelititis

36
Q

What should have if a patient on warfarin has severe bleeding?

A
  • Vitamin K administered intravenously, has a delayed effect.
  • Renders patient resistant to re-warfarinisation
  • If bleed is life threatening they must be administered fresh frozen plasma.
37
Q

Would management needs to be implemented to a patent who is taking Warfarin?

A
  • Assess underlying disease / why they are taking warfarin
  • Check prothrombin time / INR / dose on anticoagulant card
  • Recommend paracetamol/opoids for pain relief
38
Q

What does an INR show?

A

function of prothrombin time of the patient against the prothrombin time a control partient & sensitivity index.

39
Q

How do you qwork out someones INR?

A

(Prothrombin time of patient / control) x 15 seconds

40
Q

What is meant by prothrombin time? And how is INR standardised

A

time it takes for plasma to clot after addition of tissue factor
(different factor used by different manufacturers therefore it is compared to the international reference tissue factor to produce a standard set of results)- can be compared to any value in the world

41
Q

What are the procedural guidelines for INR ?

A
  1. An INR result within 24 hours of the procedure is a valid indication of the patient’s bleeding time. Record INR in notes.
  2. If INR needs to be lowered by adjustment of Warfarin, consult the physician.
  3. If Warfarin regime has been adjusted, advise patient to recommence Warfarin immediately after surgery.
  4. Low risk procedures may proceed if INR equal to or less than 4.
  5. Moderate risk procedure: INR equal to or less than 3.5.
  6. Surgery should be as atraumatic as possible. Avoid inferior dental blocks if possible.
  7. Local measures should be used to achieve haemostasis. Applying pressure with damp gauze, suturing of sockets using resorbable sutures and/or the placement of oxidised cellulose gauze, e.g. Surgicel.
  8. Post-operative care: written instructions must be given and patients should be advised to seek advice from the care provider or a local hospital should bleeding recommence after treatment and discharge from the dental surgery.
  9. Patients should not be discharged until haemostasis has been achieved. This may take 15-20 minutes. If haemostasis is not achieved, or if bleeding recommences, the following protocol will be applied:

Tranexamic Acid ProtocolTranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin.

42
Q

A patient has still has bleeding 20 mins after the surgery what should happen?

A

Tranexamic Acid Protocol: tranexamic acid is an antifibronlytic that competitvely inhibits the activation of plasminogen to plasmin.

43
Q

How does asprin work as an antiplatelet?

A
  • Antiplatelet
  • Inhibiting the production of thromboxane A2 (synthesised by activated platelets) acts on receptors of platelets causing further platelet activation = platelets plug = clot on vascular smooth muscle = vasoconstriction.
44
Q

How long does aspirin work for?

A

The life of the platelet (irreversible)

45
Q

When is aspirin used?

A
  • Heart attack
  • Stroke
  • TIA
  • Acute coronary syndrome (minor heart attack/ unstable angina)
  • Atrial fibrillation
  • Coronary bypass op
  • Patient at risk to heart attack/stroke (e.g. high cholesterol, bp, diabetes & smokers, smokers)
46
Q

What is the dose for aspirin?

A

Low dose 75mg daily - efficacy not directly related to dose (low doses cause less adverse side effects)

47
Q

What are the side effects of aspirin?

A

Gastric intolerance and upper GI bleeding due to inhibition of COX-1 leads to a decrease in production of gastroprotective PGE2.

48
Q

Name 4 antiplatelet drugs:

A
  • Aspirin
  • Clopidogrel
  • Epoprostenol
  • Dipyridamole
49
Q

When is clopidogrel indicated?

A

When aspirin is not tolerated or when dual antiplatelet therapy is desirable in combination with aspirin to treat patients with acute coronary syndromes, MI and following precutaneous coronary intervention with stent placement.
-Marginally superior to asprin for primary prevention

50
Q

How does clopidogrel work as an antiplatelet?

A
  • Inactive prodrug
  • Converted in liver =active metabolite
  • binds irreversibly and inhibits platelet ADP receptors
  • Lasts the lifetime of the platelet
51
Q

What are the adverse side effects of clopidogrel?

A
  • Haemorrhage
  • Nausea
  • Vomiting
  • Constipation or diarrhoea
  • Vertigo
  • Rashes
52
Q

What is the mode of action of Epoprostenol?

A
  • Synthetic prostacyclin (principal endogenous prostaglandin of the large artery endothelium)
  • Acts on receptors on plasma membranes of platelet and vascular smooth muscle.
53
Q

When is epoprostenol used?

A
  • Used as an adjunct to heparin

- useful in haemoialysis

54
Q

How is epoprostenol administered?

A

Infused intravenously

55
Q

When is Dipyridamole used?

A

Chronically in combination with aspirin for an antiplatelet effect in patients with cerebrovascular disease

56
Q

Name the types of heparind:

A
  • Fondaparinux

- Hirdudin

57
Q

What is the mode of action of fondaparinux?

A

-Selectively binds and inhibits factor Xa.

58
Q

When is fondaparinux used?

A
  • Prevent venous thrombo-embolism in patients undergoing orthopaedic surgery (more effective >LMWH)
  • Patients with established DVT or pulmonary embolism (just was effective as unfraction heparin & LMWH)
59
Q

How is fondaparinux administered?

A

Subcutaneously 1x daily

60
Q

What is the mode of action of Hirdudin?

A
  • Direct inhibitor of thrombin (more specific/predictable than heparin)
  • Inhibits lot associated with thrombin and is not dependent on antithrombin III (unlike heparin)
61
Q

Name enzymes used in fibrinolytic drugs:

A
  • Streptokinase

- Alteplase

62
Q

What is the mode of action of fibrinolytic drugs?

A

Promote the conversion of plasminogen to plasmin (natural clot-resolving enzyme).

63
Q

How are fibrinolytic drugs administered?

A

Direct vessel perfusion to clot site.

64
Q

What are the adverse reactions of fibrinolytic drugs?

A
  • Streptokinase is protein thus allergic reactions can occur

- Haemorrhage (contraindicated for those at risk)

65
Q

Name oral direct thrombin inhibitors:

A
  • Ximelagatron (exanta)

- Dabigatran

66
Q

What is the mode of action of Ximelagatron?

A

Inhibit the activity of thrombin (final step of blood clot formation)

67
Q

Compare the use of Ximelagatron with Warfarin:

A
  • Just as effective in patients with AF in preventing strokes or systemic embolic events.
  • Reduces minor & major haemorrhage
  • Warfarin has narrow theraputic window and requires coagulant monitoring and dose titration. Where as Ximelagatron can be given at a fixed dose.
68
Q

What are the advantages of the use of Dabigatrain?

A
  • Prevent stroke and systemic embolism in patients with AF
  • Absorbed quickly
  • Short half lives (in event of excess anticoaglant activity they can be discontinued quickly)
  • No requirement for INR monitoring
  • Only need local measures for haemostasis in dental treatment
  • Fewer drug interactions than warfarin (although best to only use paracetamol as analgesics as aspirin and NSAIDs have antiplatelet effect.
69
Q

Name a drug that is an inhibitor of glycoprotein IIb/IIIa:

A
  • Abciximab
  • Epifibatide
  • Tirofiban
70
Q

How does abciximab work to have an anticoagulant effect?

A
  • Abciximab is monoclonal antibody to glycoprotein IIb/IIIa

- Used as am adjunct to heparin and aspirin to decrease the risk of occlusion following angioplasty

71
Q

What are the adverse effects of Inhibitors of Glycoprotein IIb/IIIa?

A
  • Cause bleeding (restricted to patients with high risk of acute coronary thrombosis)
  • Hypersensitivity can occur
72
Q

When are Epifibatide and tirofiban used?

A

-Under cardiology supervision in patients with early MI

73
Q

What are the medical factors placing patients at higher risk to post-operative heamorrhage?

A
  • Platelet disorders (thrombocytopaenia)
  • Medications that interfere with platelet function e.g. NSAIDs, aspirin
  • Hepatic disease & alcohol abuse (reduced production of clotting facotrs II, VII, IX & X)
  • Anitbiotics & antifungals may potentiate Warfarin (always consult BNF for other drugs that potentiate Warfarin)
  • Certain antiretroviral drugs used to treat HIV can cause thrombocytopenia
  • HIV itself
  • Frail, elderly people
  • Uncontrolled hypertension
  • History of bruising/ excessive bleeding

Applied pharmacology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions