Week 1 - Additional Simulated clinical dentistry P1 Flashcards

(22 cards)

1
Q

Bleeding disorders occur due to defects in (3)

A
  • platelets
  • Clotting factors
  • Blood vessels
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2
Q

What is thrombocytopenia

A

condition where there’s a reduced circulating levels of platelets

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3
Q

what causes thrombocytopenia

A

Decreased platelet production
- anything that impacts bone marrow (leukemia, aplastic anemia, HIV)

Increased pooling in spleen

Decreased survival

  • immune e.g. immune thrombocytopenia
  • non immune e.g. severe hypertension, mechanical heart valves
  • Drugs

Inherited dirsorder e.g. von willebrand’s disease

Acquired e.g. aspirin and NSAID use

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4
Q

what are some inherited coagulation defects (3)

A
  • Hemophilia A
  • Von willebrand disease (interacts with factor 8
  • Hemophilia B (mutation in factor 9)
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5
Q

What are some acquired coagulation defects

A
  • liver disease (affects most clotting factors)
  • Vitamin K deficiency
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6
Q

What is disseminated intravascular coagulation

A

life threatening condition characterized by widespread activation of the coagulation cascade leading tot eh formation of micro clots throughout the blood vessel. This abnormal clotting consumes platelets and coagulation factors resulting in a paradoxical bleeding tendency

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7
Q

What are vascular disorders

A
  • Blood vessel walls are weak or damaged by inflammatory/immune response
  • Easy to trigger bleeding in small vessels
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8
Q

What is hypercoagulability

A

an increased tendency of the blood to clot. Leads to higher risk of developing abnormal blood clots within blood vessels

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9
Q

what does hypercoagulability cause

A
  • heart attacks
  • strokes
  • pulmonary embolism
  • deep vein thrombosis

(where blood clot forms and moves to block blood flow)

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10
Q

What causes hypercoagulability

A

increased platelet function OR increased activity of the coagulation cascade

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11
Q

managing hypercoagulability in patients

A
  • risk of blood clots is reduced by anti coagulant drugs
  • anti platelet agents
  • Anti coagulants e.g. warfarin, DOACs
  • Many patients will be on anticoagulant therapy and will require careful management in the clinic
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12
Q

What are anti platelet drugs

A

medication that prevents platelets from clumping together to form blood clots

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13
Q

What are examples of anti platelet drugs

A

Aspirin
- blocks COX-1 causing no TXA2
- long term, low risk patients

  • PDE inhibitors - increase cAMP levels
  • Anti-GPIIb/IIa inhibits aggregation

Anti-P2Y12 (clopidogrel) inhibits actions of ADP

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14
Q

How to manage a patient on antiplatelet medication

A
  • As within anticoagulants patients should not stop therapy
  • Use local hemostatic measure to control any prolonged or excessive bleeding
  • Keep up to date with recommendations from ADA
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15
Q

What is the treatment for hypercoagulability

A
  • Vitamin K antagonists (Warfarin)
  • Direct oral anti-coagulants (DOACs)
  • Heparin
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16
Q

How does vitamin K antagonists (warfarin) reduce coagulation

A
  • Vitamin K is a co factor in synthesis of a number of clotting factors (prothrombin and factors 7, 9 and 10)
  • Reduced by epoxide reductase
17
Q

what can easily upset the activity of warfarin

A
  • high vitamin K rich food
  • some antibiotic since vitamin K is produced by bacteria in the gut
18
Q

How to manage patients on warfarin

A
  • primary concern is excessive bleeding
  • Prior recommendation was to cease the anti-coagulant or antiplatelet therapy prior to surgical procedures
  • HOWEVER STOPPING TREATING PRIOR TO DENTAL SURGERY IS NOT RECOMMENDED
  • use local hemostatic measures
19
Q

What are some direct oral anticoagulant drugs

A

TGS approval:
Competitive inhibitors
- Rivaroxaban
- Apixaban

Competitive antagonist
- Dabigatran

20
Q

What is the INR when warfarin is given

21
Q

What is heparin

A
  • interacts with antithrombin 3
  • used where an immediate anticoagulant action is required
  • not commonly used in dental surgery
22
Q

What is dabigatran

A

DOAC used to prevent and treat blood clots
works by inhibiting thrombin cleavage of fibrinogen