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Human Diseases > Dental and Oral Complications of Bleeding Disorders > Flashcards

Dental and Oral Complications of Bleeding Disorders Flashcards

1
Q

The 4 common mechanisms for bleeding disorders are:

A

Vascular (vessel wall) component problems
Platelet problems
Coagulation factor problems
Fibrin problems

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2
Q

What are the 2 possible types of vascular problems?

A

Congenital eg Ehler’s Danlos (collagen problem leading to hypermobile joints and capillary fragility hence easier bruising)
Acquired eg Scurvy (vitamin c deficiency affecting collagen formation leading to easier bruising)

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3
Q

Platelet disorders can be either disorder of ________ (congenital or acquired) or change in _________ through increased/decreased production/destruction.

A

Function, numbers

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4
Q

What is an example of a congenital functional platelet disorder?

A

Von Willebrand’s disease

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5
Q

What is the spectrum of mild-severe (type I to IV) of the VWD dependent on?

A

Amount of VWF present

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6
Q

Which blood group type has 20% lower VWF than other blood groups?

A

Type O

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7
Q

What does the variation of VWF levels depend on?

A

Age
Blood group type

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8
Q

What are some examples of acquired functional platelet disorders?

A

Aspirin-induced
Renal function induced

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9
Q

What is the platelet disorder with low levels of platelets <150 x 10^9 /L?

A

Thrombocytopenia

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10
Q

What is the platelet disorder with high levels of platelets >400 x 10^9 /L?

A

Thrombocytosis

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11
Q

What can cause thrombocytopenia?

A

Alcoholic liver disease
Malignancy
Drug-induced

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12
Q

Thrombocytopenia results from either ___________ __________ due to abnormal bone marrow or ___________ __________ in normal bone marrow with autoimmune process such as immune cytopenia purpura, splenomegaly, disseminated intravascular coagulation (DIC)

A

Decreased formation, increased destruction

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13
Q

Thrombocytosis generally occurs as a result of one of 3 things:

A

Reactive or secondary thrombocytosis
Familial thrombocytosis
Clonal thrombocytosis including essential thrombocythemia and related myeloproliferative disorders

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14
Q

What are the 2 different types of coagulation disorders?

A

Intrinsic defects - intrinsic pathway affected
Extrinsic defects - extrinsic pathway affected

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15
Q

What can be highlighted in coagulation disorders with intrinsic defects?

A

Prolonged APTT

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16
Q

What can be highlighted in coagulation disorders with intrinsic defects?

A

Prolonged PT

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17
Q

What are some examples of congenital coagulation disorders with intrinsic defects?

A

Haem A & B

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18
Q

What drug can cause acquired coagulation disorder with intrinsic defects?

A

Heparin

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19
Q

Coagulation disorders with extrinsic defects generally tend to be acquired. What are some causes?

A

Liver disease
Warfarin
Vit K deficiency due to malabsorption or obstructive jaundice

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20
Q

Fibrin disorders are usually either the result of __________ __________ eg ___________ or __________ ___________ eg ____________.

A

Thrombolytic therapy, streptokinase, pathological fibrinolysis, tumour

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21
Q

How does vascular wall disorder present clinically?

A

Purpura (superficial bruise at superficial layer)

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22
Q

How does platelet disorder present clinically?

A

Purpura
Epistaxis (nose bleeds), menorrhagia (heavy period bleeds), hematemesis (vomits with blood) or melena (stools with blood)

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23
Q

How does coagulation disorder present clinically?

A

Epistaxis, menorrhagia, hematemesis, melena
Ecchymosis (spreading bruising in deeper layers)

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24
Q

What does the assessment related to bleeding disorders usually entail?

A

History
Examination
Further investigations
Risk assessing patient and procedure(s)

25
Q

What are the systems to look out for in medical history assessment related to bleeding disorders?

A
  1. GIT
  2. Liver disease eg primary biliary cirrhosis, alcoholic-related liver disease
  3. Chronic renal failure -> bone marrow fibrosis -> impaired platelet function (thrombocytopenia)
  4. Other relevant disorders/diseases eg Ehler’s danlos, thrombophilias - factor V Leiden deficiency (more likely to clot therefore have to be on anticoagulant which could cause increased risk of bleeding), antithrombin III deficiency, antiphospholipid syndrome (lupus anticoagulant)
  5. Coagulation system eg haemophilias, disorders of bone marrow including leukaemias and myelodysplasia, platelet disorders including thrombocytopenia and VWD, evidence and probing on bleeding problems eg epistaxis, bruising, family history, previous haemostatic challenges: surgery
  6. Medications eg antiplatelets (aspirin; clopidogrel; prasugrel), anticoagulants (warfarin; heparin including LMWH: tinzaparin and enoxoparin; new direct oral anticoagulants (DOAC) including dabigatran (IIa), rivaroxaban (Xa), apixaban (Xa), edoxaban (Xa)), myelosuppressive (DMARDs including methotrexate; chemotherapy)
26
Q

Worsened outcomes of leukaemia often the genotype in ______ people as opposed to white people

A

Black

27
Q

Myelodysplastic syndrome is more common and the survival is also worst in _______ people than in black or Asian people

A

White

28
Q

Liver has 2 functions:
1. _______ where it creates vitamin K dependent clotting factors 2,7,9,10 and albumin
2. ________ which is it breaks down drugs

A

Synthetic, metabolic

29
Q

During the social history assessment, what should we look out for?

A

Alcohol consumption
- how many units per week
- how long for
* drinking more than 14 units per week on a regular basis increases the risk of damaging the liver

30
Q

If the liver’s damaged and its synthetic function is off, what would be changed? What should we check/measure in a person who drinks too much alcohol?

A

Full blood count - platelet count should be between 150 to 400 x 10^9
Clotting time - PT should be between 13 and 15 seconds; and APTT (less crucial for dental professionals)

31
Q

What are some questions or areas to look out for when assessing dental history related to bleeding disorders?

A

Previous extractions
Spontaneous bleeding gingiva
Previous problems and management required

32
Q

What to look for clinically if we suspect bleeding disorder?

A
  1. Bleeding into skin
    - ecchymosis (is trauma appropriate to extent of bruise?)
    - non-thrombocytopenic or thrombocytopenic purpura
  2. Vascular abnormalities
    - telangiectasia (dilatation of small veins; be aware of spider telangiectasia and hereditary haemorrhagic telangiectasia)
    - haemangioma (abnormality of blood vessels)
  3. Other visual clues of underlying disease
    - alcohol abuse & liver disease
33
Q

What are some possible causes of non-thrombocytopenic purpura?

A

Hereditary haemorrhagic telangiectasia
Ehlers danlos
Infections
Deficiencies
Allergy or connective tissue diseases
Ageing skin “senile purpura” or actinic purpura

34
Q

How to identify thrombocytopenic purpura?

A

Usually comes with petechiae:
1-3mm in diameter
Not disappear on pressure
Disappear after 3-4 days
Signify abnormal capillary fragility, thrombocytopenia, or coagulopathy

35
Q

What are some possible causes of thrombocytopenic purpura?

A

Impaired production of platelets
Excessive platelet destruction
Sequestration of platelets in spleen
Dilutional loss following massive transfusions

36
Q

What could be the cause of thrombocytopenic purpura and impaired production of platelets?

A

Generalised bone marrow failure eg leukaemias, aplastic anaemias, myeloma
Selective reduction in megakaryocytes which produce platelets due to drugs eg co-trimoxazole or alcohol

37
Q

What could be the cause of thrombocytopenic purpura and excessive platelet destruction?

A

Immune problems including autoimmune or triggered by particular viral infections
Coagulation problems eg disseminated intravascular coagulation

38
Q

Telangiectasia normally _______ but can signify underlying disease

A

Benign

39
Q

What subtype of telangiectasia do the following characteristics belong to?
- Radiate from central dot
- Disappear on pressure, refill
- Common in hepatic cirrhosis (yellowish hue in skin from jaundice)

A

Spider telangiectasia

40
Q

What subtype of telangiectasia do the following characteristics belong to?
- Dilated vessels up to 2mm in diameter
- Face, mucous membranes of mouth and nose
- Epistaxis is common and GIT bleeds which may lead to anaemia
- Clinical problem if traumatised but don’t impact on dental therapy because they don’t cause any particular intraoral problems even though they are present in the mouth

A

Hereditary Haemorrhagic Telangiectasia

41
Q

How to identify vascular abnormality of haemangioma?

A

Blanch on pressure when compressed with finger or glass slide
If unsure, ultrasound or fine needle aspirate (FNA)

42
Q

What characteristics of haemangioma should we be concerned about?

A

Traumatised
Involving alveolar mucosa
Extensive (consider bone involvement)

43
Q

What can portal venous hypertension caused by liver disease cause?

A

Splenomegaly
Sequestration of platelets (thrombocytopenia)

44
Q

What can obstruction of bile duct through liver disease cause?

A

Obstructive jaundice
Decreased bile salt excretion (bilirubin)
Decreased fat digestion (steatohorrea)
Decreased absorption of Vit K
Additive effect on inability to synthesis 2,7,9,10

45
Q

What are the visual clues of alcohol-abuse-induced liver disease?

A

Ecchymosis inappropriate to level of trauma
Jaundice
Sialosis
Ascites and fluid retention
Spider telangiectasia aka spider naevi

46
Q

Apart from clinical examination of bleeding into skin, vascular abnormalities and other visual clues, what other further investigations (blood tests) can we do to assess the bleeding disorder?

A

APTT: tests intrinsic pathway of clotting cascade; affected by most factor deficiencies
PT: tests extrinsic and common pathway of clotting cascade; affected by warfarin and alcohol liver disease
FBC: platelet count
Liver function tests: test synthesis and excretion

47
Q

How can liver function tests demonstrate decreased synthesis?

A

Decreased albumin
Decreased coagulation factors
Increased PT

48
Q

How can liver function tests demonstrate decreased excretion (cholestasis)?

A

Increased bilirubin
Increased alkaline phosphatase
Increased GGT (gamma-glutamyl transferase)

49
Q

How can liver function tests demonstrate hepatocyte necrosis?

A

Increased AST (aspartate amino transferase)
Increased ALT (alanine amino transferase)

50
Q

What are some procedures with risk of bleeding?

A

Extractions
Non-surgical and surgical periodontal treatment
Matrix bands
Suction
Block anaesthesia

51
Q

In a series of liver function tests, the following was found:
Decreased albumin
Decreased coagulation factors
Increased PT
What is being demonstrated about the liver?

A

Decreased synthesis

52
Q

In a series of liver function tests, the following was found:
Increased bilirubin
Increased alkaline phosphatase
Increased GGT
What is being demonstrated about the liver?

A

Cholestasis or decreased excretion

53
Q

In a series of liver function tests, the following was found:
Increased AST and ALT
What is being demonstrated about the liver?

A

Hepatocytes necrosis

54
Q

Who to liase with for a patient with bleeding disorder?

A

Haematologist for congenital eg VWD & haemophilia
Oncologist for acquired eg thrombocytopenia due to chemotherapy
Hepatologist if acquired through liver disease

55
Q

What are the local measures for managing bleeding?

A

More pressure (wrap thumb or forefinger in damp gauze and put pressure on the area that’s bleeding)
More LA (make pressure more effective; beware of half-life ~2 hrs)
Suture or ligate
Pack

56
Q

Why do we pack?

A

To temporarily apply pressure (which helps slow the bleeding which helps platelet aggregation and coagulation)
To adjust the coagulation process in a more favourable manner

57
Q

What are the options of packing?

A

Resorpbitive dressing eg oxidised cellulose (Surgicel: synthetic product), gelatin (gelfoam: porcine product), haemostatic collagen (collaplug: bovine product)
Non-resorpbitive dressing (for bone) eg bone wax

58
Q

What are some other local measures for bleeding that are less commonly available in primary care?

A

Fibrin glue: Tisseel (derived from human plasma so small risk of allergy)
Anti-fibrinolytic: Tranexamic acid topical 4.8% mouthwash qds or p.o. tds
Cautery: Chemical or electrical (bipolar or monopolar forceps)

qds = 4x a day; p.o. = oral tablet; tds = 3x a day; cautery = burning

59
Q

Management of coagulopathies:
*always in consultation with haematology
- INR & PT urgent reduction - __________ __ 10mg IV or PO
- INR life threatening - ___________ (Prothrombin complex concentrate from human plasma)
- Thrombocytopenia - depends on cause but platelet transfusion possible
- Factor deficiency - replace factor(s) directly or seek to increase production

A

Vitamin K, Beriplex

Vit K IV allergic reaction risk; Beriplex stimulates extrinsic system

Human Diseases (24 decks)

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