Brainscape's Knowledge GenomeTM

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


See full index

CHHD > Haemostasis and bleeding disorders > Flashcards

Haemostasis and bleeding disorders Flashcards

1
Q

What are the mechanisms of haemostasis called

A

Primary and Secondary acting simultaneously

Third stage of fibrinolysis also called tertiary haemostasis

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

What components interact in haemostasis

A

Complex interaction of blood vessels, platelets, Von Willebrand factor (vWF) and clotting factors

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

What are the 2 main responses to vessel injury in primary haemostasis

A

Vascular response = reflex vasoconstriction

Platelet plug formation via vWF

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

What components are associated with primary haemostasis

A

Blood vessels
Platelets
Von Willebrand Factor (vWF)

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

Where are most clotting factors manufactured

A

Liver

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

What clotting factors are produced by the endothelial cells of the blood vessels

A

Factor VIII

vWF

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

What clotting factors are vitamin K dependent factors

A

Factor II
Factor VII
Factor IX
Factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AY BAWS CAN I HABE DE NOTE PLZ

A

Clotting factors are present in the circulation in the inactive form

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

When is tissue factor released and what does it do

A

Tissue factor released on injury to blood vessel activates the extrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What activates the intrinsic pathway of secondary haemostasis

A

Exposure to collagen activates the intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What types of haemostatic disorders can you develop from primary haemostasis

A

Vascular disorders
Von Willebrand disease
Platelet Disorders

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

What types of haemostatic disorders can you develop from secondary haemostasis

A

Clotting factor disorders

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

What congenital haemostatic disorders can you get

A
  • Von willebrand disease (1/2)
  • Haemophilia A (2)
  • Haemophilia B (2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What acquired haemostatic disorders can you get

A
  • Thrombocytopenia (1)
  • Platelet dysfunction associated with drugs (1)
  • Antiplatelet therapy (1)
  • Anticoagulant therapy (2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does von willebrand factor do

A
  • Mediates platelet adhesion to damaged endothelium

- Mediates platelet aggregation (sticking together) - Stabilises and transport factor VIII

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

What is vWF disease caused by

A

vWF deficiency

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

What are the clinical features of vWF disease

A
  • Can present as problems of either 1 or 2 haemostasis or both
  • Bruising, epistaxis
  • Prolonged bleeding during surgical and dental procedures common
  • GI bleeding and menorrhagia also frequent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What can be done to manage vWF disease

A
  • Desmopressin (DDAAVP) - stimulates release of vWF and factor VIII - Rx of mild form
  • vWF replacement using human plasma, rich in vWF and factor VIII- Rx of severe form
  • Anti-fibrinolytic drugs to help slow/prevent clot breakdown- given oral or inject
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the dental relevance of vWF disease

A
  • Prolonged oozing post extraction and bleeding into muscles/joints
  • Haematological cover before any invasive procedure in severe cases
  • Avoid regional LA (Infiltration or intra-ligamentary safer)
  • Avoid aspirin/NSAIDs (acetaminophen or co-codamol safer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What should be used instead of regional LA for patients with vWF disease

A

Infiltration or intra-ligamentary LA

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

What should be used instead of aspirin/NSAIDs for patients with vWF disease

A

Acetaminophen or co-codamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name a hereditary platelet deficiency disorder

A

Bernard-Soulier syndrome

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

What mechanisms can cause platelet deficiency disorders

A

Megakarocyte suppression
Bone marrow failure
Splenomegaly
Increased destruction of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What can cause megakarocyte suppression

A
  • Chemotherapeutic agent

- Viruses - parvovirus infection, mumps, HIV

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

What can cause bone marrow failure

A
  • Aplastic anaemia
  • Leukaemia
  • Lymphoma
  • Metastases
26
Q

How can splenomegaly cause platelet deficiency

A

Causes sequestration of platelets

27
Q

What can cause the increased destruction of platelets

A
  • Autoimmune - idiopathic thrombocytopenic purpura
  • Drugs - cytotoxic drugs
  • Diseases - disseminated intravascular coagulation (DIC), SLE, Malaria
28
Q

What can cause platelet dysfunction disorders

A

Antiplatelet drugs -

  • Aspirin
  • NSAIDs
  • Clopidogrel, Prasugrel
  • Dipyridamole
  • vWF disease
29
Q

Which of the anti platelet drugs has a reversible effect

A

NSAIDs only

30
Q

What are the clinical features of platelet disorders

A

Easy bruising and bleeding

  • Petechiae
  • Purpura
  • Ecchymosis
31
Q

What is the dental relevancy of platelet deficiency

A
  • Patients with suspected thrombocytopenia - Investigate platelet count (PC) by requesting full blood count (FBC) prior to dental treatment
  • Refer to GP/haematologist for further management
  • Risk of spontaneous bleeding, PC ˂ 20,000/mm3
32
Q

What is the dental relevancy of platelet dysfunction

A
  • Minor dental procedures- continue medications
    • Treat without interrupting antiplatelet medication
    • Never stop medications without consulting their GP
    • Limit initial treatment area e.g. single extraction at a time
33
Q

What hereditary 2 haemostatic disorders are there

A
  • Haemophilia A and B

- vWF

34
Q

What acquired causes can cause 2 haemostatic disorders

A

Anticoagulant therapy -

  • Warfarin therapy
  • Heparin therapy
  • Novel/Non-vitamin K oral anticoagulant therapy
35
Q

What diseases can cause 2 haemostatic disorders

A
  • Liver disease, including obstructive jaundice
  • DIC
  • Malabsorption syndromes
36
Q

What causes haemophilia A and B and what chromosome is it found in

A
  • Deficiency factor VIII and IX respectively
  • X-linked disorders- affecting ~ 1 in 5000 males
  • Females are carriers
37
Q

How is haemophilia A and B categorised

A

Based on Factor VIII or IX levels

  • Very mild > 25%
  • Mild - 5-25% of normal
  • Moderate - 1-5% of normal
  • Severe - <1%
38
Q

How can haemophilia be treated

A
  • Desmopressin = increased production of factor VIII
  • Replacement therapy for specific clotting factors
  • Inhibit fibrinolysis- antifibrinolytic agents
39
Q

Name some replacement therapies for specific clotting factors

A
  • Clotting factor concentrate from plasma

- Commercially produced recombinant factor

40
Q

Name some antifibrinolytic agents

A

Tranexamic acid

Epsilon amino caproic acid

41
Q

What are the dental aspects of haemophilia

A
  • All preventative - minimise surgical intervention
  • Close cooperation with haematologist/specialist dentist
  • Big risk of haemorrhage after surgery or injection
  • Post operative - watch for hematoma formation
  • Trauma to head and neck - prophylactic factor VIII replacement is essential
42
Q

What are the common indications of thrombosis or risk of thrombosis

A
  • Atrial Fibrillation
  • Cardiac Valvular disease
  • Mechanical prosthetic heart valves
  • Ischaemic heart disease - recent MI
  • DVT
  • Pulmonary embolism
  • Renal dialysis
43
Q

How is warfarin taken and what does it inhibit

A

Orally

Inhibits vitamin K dependent factors - II, VII, IX, X

44
Q

How is warfarin effect reversed and monitored

A

Monitored = INR/prothrombin time

Reversed with parenteral fresh frozen plasma/vitamin K

45
Q

AY BAWS CAN I HABE DE NOTE PLZ

A

Warfarin has narrow therapeutic range & frequent monitoring and dose
adjustment.
Also sensitive to drug interactions.

46
Q

What dental aspects are present with a patient on warfarin

A
  • Preventive dentistry-minimise surgical intervention
  • Dental care - close cooperation with specialist/physician
  • Measure INR within 24 hours of surgery
  • INR>4 refer for hospital for dental care
47
Q

What are some of the potential drug interactions that warfarin may have

A
  • Warfarin + metronidazole
  • Warfarin + macrolides (erythromycin)
  • Warfarin + azole antifungals (miconazole)
  • Warfarin + Aspirin/NSAIDs
48
Q

What are the effects of warfarin interacting with other drugs and how can you minimise the risk of these interactions

A
  • Increased risk of significant bleeding (increases INR)
  • Avoid concurrent use of both medications
  • Alternative antifungals (Nystatin)
49
Q

What does heparin inhibit and how long does it last

A

Clotting factors II and X

Short lived anticoagulant effect

50
Q

What is used to monitor heparin effect

A

Activated partial thromboplastin time

51
Q

What makes heparins good for immediate management of acute thromboembolic events

A

Short lifespan and rapid onset

52
Q

What are low molecular weight heparins used for

A

non-hospitalised ambulatory patients

53
Q

Name some non vitamin K oral anticoagulants and what factors they inhibit

A
  • Dabigatran- inhibits factor IIa
  • Apixaban – inhibits factor Xa
  • Edoxaban - inhibits factor Xa
  • Rivaroxaban- inhibits factor Xa
54
Q

What are the advantages of using non vitamin K oral anticoagulants (i think compared to heparins)

A
  • More predictable levels of anticoagulation
  • Do not require routine monitoring
  • Wider therapeutic range & easier to manage
  • More effective and safer
55
Q

Describe the onset and short life of non vitamin K oral anticoagulants

A

Rapid onset of action and relatively short half lives allows for rapid modification of patients coagulation

56
Q

How should you handle a patients NOACS medication if they have a low and high risk of bleeding

A

Low risk = treat without interrupting
High risk =
Rivaroxaban - if morning dose, delay and take 4 hrs after haemostasis, if evening dose take as normal
Apixaban, dabigatran - miss morning dose, take evening dose as normal

57
Q

What are the key haemostatic investigations and what each tests for

A
  • Full blood count - platelet count
  • Bleeding time - platelet defects
  • Prothrombin time (PT)/ international normalised ratio (INR) - extrinsic pathway and warfarin therapy
  • Activated partial thromboplastin time (aPTT) - Intrinsic pathway (30-40secs) and heparin therapy
58
Q

What is the ideal INR and PR

A
  • PT- (10-12 secs)

- INR- universal test (Patient’s PT/Control PT) (0.9-1.2)

59
Q

What is the expected INR for patients on warfarin

A
  • INR therapeutic range for patients on warfarin (2-3)
60
Q

What is the expected aPTT for patients on heparin

A
  • aPTT therapeutic range for patients on heparin (1.5-2.5)
61
Q

What steps should be taken when dealing with patients with bleeding disorders

A
  • Obtains a comprehensive medical history
  • Perform a thorough clinical examination
  • Request appropriate special investigations
  • Consult with haematologist and/or physician
  • Refer where necessary to hospital for dental care

CHHD (27 decks)

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