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BDS2; CHHD > Haemostasis + Haemorrhagic Disorders > Flashcards

Haemostasis + Haemorrhagic Disorders Flashcards

1. Knowledge of disorders associated with haemostasis 2. Categorise bleeding disorders 3. Knowledge of signs and symptoms of bleeding disorders 4. Knowledge of oral anticoagulants 5. Knowledge of dental relevance of common bleeding disorders 6. Interpret basic haematological data

1
Q

Define haemostasis

A

The process causing bleeding to stop and so keeping blood in the damaged vessel

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2
Q

How does haemostasis occur

A

Primary haemostasis = platelet clot formation

Secondary haemostasis = coagulation strengthening clot

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3
Q

Describe primary haemostasis

A
  1. Vasoconstriction occurs due to nerve reflex and endothelin release from vascular endothelium
  2. Reduces blood flow
  3. Platelet plug forms via adhesion of platelets via vWF
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4
Q

Describe secondary haemostasis

A

Coagulation occurs to strengthen clot through formation of a fibrin meshwork

  • all clotting factors made in liver apart from VIII
  • factors are activated upon injury
  • collagen exposure causes intrinsic pathway
  • tissue factor causes extrinsic pathway
  • join to form common pathway to give fibrin
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5
Q

Which clotting factors are produced by endothelial cells

A

VIII and vWF

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6
Q

Which clotting factors are vitamin K dependant

A

II, VII, IX, X

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7
Q

List the primary haemostasis bleeding disorders

A
  1. Vascular disorders
  2. Von Willebrand disease
  3. Palatal disorders
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8
Q

List the secondary haemostasis coagulation disorders

A
  1. Clotting factor disorders
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9
Q

List congenital haemostasis disorders

A
  1. Von Willebrand disease
  2. Haemophilia A
  3. Haemophilia B
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10
Q

List acquired haemostasis disorders

A
  1. Thromboytopenia
  2. Platelet dysfunction due to drugs
  3. Antiplatelet therapy
  4. Anticoagulant therapy
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11
Q

Name a vascular disorder

A

Hereditary haemorrhagic telangiectasia (Osler-Rendu-Weber syndrome)

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12
Q

What are the causes of vascular disorders

A
  • Autosomal dominant

- Associated with IgA and vWF deficiency

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13
Q

Describe the clinical presentation of vascular disorders

A
  • Telangiectasia (spidery veins) on skin and mucosa
  • Rarely causes bleeding
  • Adolescent diagnosis due to epistaxis (nose bleeds)
  • Can result in iron deficiency and anaemia due to intestinal bleeding
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14
Q

How can vascular disorders be tested for

A

CT
MRI
Angiography
Capillary microscopy

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15
Q

How can vascular disorders be treated

A
  • Cyrosurgery

- Argon laser treatment if telangiectasis bleed

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16
Q

What are the dental relevances of vascular disorders

A

Bleeding from oral surgery is troublesome

Regional LA should be avoided and infiltration is better

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17
Q

What are the causes of Von Willebrand Disease

A
  • vWF deficiency which is inherited (not sex linked)
  • this mediates platelet adhesion to damaged endothelium and so prevents aggregation in absence
  • stabalises and transports factor VIII
18
Q

Describe the clinical presentation of Von Willebrand Disease

A
  • bruising and epistaxis
  • prolonged bleeding in oral surgery
  • GI bleeding and menorrhagia (XS menstrual bleeding)
19
Q

How is Von Willebrand Disease tested for

A

Lab results show decreased vWF and VIII and lower aggregation, shows prolonged activated partial thromboplastin time

20
Q

How is mild Von Willebrand Disease treated

A

Desmopressin which increases vWF and VIII production

21
Q

How is severe Von Willebrand Disease treated

A

vWF replacement through rich plasma and through antifibrinolytic drugs which decrease the breakdown of clots

22
Q

What is the dental relevance of Von Willebrand Disease

A
  • prolonged bleeding and oozing post-extraction
  • avoid regional LA
  • avoid aspirin and NSAIDs
23
Q

What is a safer alternative for aspirin and NSAIDs for patients with blood clotting disorders

A

Acetaminophen

Co-codamol

24
Q

What causes platelet deficiency

A
  • Hereditary; Bernard-Soulier syndrome = rare (platelets are enlarged and don’t have platelet membrane so cannot adhere)
  • Megakaryocyte suppression
  • Vitamin B12 and folate deficiency
  • Bone marrow failure
  • Thrombocytopenia
  • Splenomegaly (platelet sequestration)
25
What is the dental relevance of platelet deficiency
A platelet count of thrombocytopenic patients should be taken before treatment - PC < 20,000/mm3 increases the risk of spontaneous bleeding
26
What causes platelet dysfunction
- Antiplatelet drugs; aspirin, NSAIDs, clopidogrel, dipyridamole - all but NSAIDs are irreversible on platelet lifespan - NSAIDs are reversible because the drug clears after 24-48 hours For minor procedures the drug should be continued and local haemorragic agents should be given post operatively
27
What is the clinical presentation of platelet dysfunction
Easily bruising and bleeding - petechiae - purpura - ecchymosis
28
What causes haemophilia
X-linked disorders; VIII and IX deficiency
29
What is the clinical presentation of haemophilia
1. Mild = minimal bleeding 2. Moderate = bleed after minor surgery needs attention 3. Severe = bleeds without provocation Haemorrhage stops immediately after injury but there is intractable oozing which causes bleeding into deep tissues Need to monitor signs of haematoma an give prophylactic VIII replacement
30
Outline treatments for haemophilia
Desmopressin (increase FVIII production) Replacement therapy Antifibrinolytic agents = trxnexamic acid, EACA
31
What are the common indications of anticoagulant therapy
Atrial fibrillation, cardiac valvular disease, mechanical prosthetic valves, ischaemic heart disease, DVT, pulmonary embolism, renal dialysis, TIAs of strokes
32
What are the actions of warfarin and how are they monitored
Inhibits vitamin K dependant factors | Monitored via INR/PT (INR is better because it is standardised)
33
What is the relationship between INR and bleeding risk
Increased causes greater risk INR > 4 the patient should be referred to hospital for dental care
34
What are the actions of heparin and give examples of the different types of heparin
Inhibits factors II and X - it is a short lived anticoagulant monitored via APTT Standard heparin (IV) = immediate management of acute thromboembolic events LMWH (subcutaneous) - non-hospitalised ambulatory patents post discharge
35
Why are NOACS useful
Non-vitamin K oral anticoagulants - more predictable levels of anticoagulation - don't require regular monitoring - wider therapeutic range and easier management - more effective and safer
36
Give examples of NOACS and their actions
1. Dabigtran = inhibits IIa 2. Apixaban = inhibits Xa 3. Rivaroxaban = inhibits Xa 4. Edoxaban = inhibits Xa
37
Dental relevance of haemophilia
1. Minimise surgical intervention (preventative dentistry) 2. Risk of haemorrhage after surgery/LA so don't use regional block 3. Ensure adequate levels of clotting factors (VIII/IX) 4. Monitor for signs of haematoma formation 5. For head+neck trauma give prophylactic factor VIII replacement
38
Dental relevance of warfarin
Measure INR within 24 hours of surgery (INR>4 then refer to hospital for dental care) and be aware of drug interactions Increased INR means increased bleeding risk Bleeding risk is minimised by avoiding concurrent use of medications by giving alternative antifungals = Nystatin and using paracetamol/co-codamol
39
What are the potential drug interactions of warfarin
1. Warfarin + metronidazole (given for dental infections) 2. Warfarin + macrolides (erythromycin) 3. Warfarin + azole antifungals (miconazole) 4. Warfarin + aspirin/NSAIDs (enhance warfarin effects)
40
What are the indications for NOACS
``` Stroke prevention in AF patients Thromboembolic disease (DVT, PE) ```
41
How do non-vitamin K oral anticoagulants work and what are the dental recommendations for their use
They have a rapid onset and short half-lives and modify the patients' coagulation For those at low risk their dental treatment should be carried out without treatment interruption For higher bleeding risk patients, advise them to miss (apixaban/dabigatran) or delay (rivaroxaban) on the day of dental treatment for surgical procedures

BDS2; CHHD (32 decks)

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