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human diseases > 13 Haemostasis and bleeding disorders > Flashcards

13 Haemostasis and bleeding disorders Flashcards

1
Q

In normal haemostasis, how are bleeds arrested?

A
  • Large blood vessels: physical means e.g. pressure, vessel constriction, surgery
  • Microvascular vessels: bleeding arested by blood coagulation through the activity of platelets and clotting factors
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2
Q

What initiates coagulation?

A

Breach in a blood vessel wall

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3
Q

What are primary and secondary haemostasis?

A
  • Primary haemostasis: platelets bind to breach in BV wall and form platelet plug
    Tissue factor activates the coagulation cascade.
  • Secondary haemostasis: strong fibrin clot formation on top of platelet plug
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4
Q

What is the primary cellular initiator of blood coagulation in blood vessels?

A

Tissue factor (TF)
- All BVs are surrounded by a sheath of TF and prothrombotic collagen
- As soon as blood comes into contact with TF and collagen, coagulation is activated
(TF activates clotting factors and clotting cascade)

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5
Q

What is the outcome of platelet adhesion?

A

A weak platelet plug is created.
Provides a surface for coagulation factors to form a stable clot.

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5
Q

What is the role of Von Willebrand factor in blood clotting?

A

VWF is found in blood
- When the BV wall is breached, VWF bound to collagen binds to platelets
- VWF and platelet binding is known as platelet adhesion
- VWF principally acts as a brige connecting collagen and platelets

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6
Q

Which coagulation factors are vitamin K dependent?

A
  • Prothrombin (FII)
  • FVII
  • FIX
  • FX
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7
Q

Describe the action of vitamin K dependent coagulation factors.

A
  • Produced in the liver in non-functional form
  • Converted by vit K into functional form
  • Factors can now bind to the surface of activated platelets
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8
Q

During the process of converting vit K dependent factors from non-functional to functional, how does the vitamin K change?

A

The conversion changes vitamin K to vitamin K epoxide.
Then it is converted back to vitamin K by vitamin K reductase.

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9
Q

What does warfarin inhibit?

A

Warfarin inhibits vitamin K reductase.
Means that vitamin K epoxide cannot be converted back to vitamin K.

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10
Q

What is the action of warfarin on clotting factors?

A
  • Pt on warfarin will produce normal amounts of clotting factors
  • The factors produced won’t work properly because they haven’t been converted into the form with a negatively charged tail
  • No negatively charged tail = no binding of factors to platelets
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11
Q

What is the role of factor IX?

A
  • Activates other clotting factors
  • Causes amplification of factor X and conversion into FXa (active form)
  • FXa activates prothrombin to thrombin
  • Thrombin coagulates the blood
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12
Q

What is the action of thrombin?

A
  • Thrombin cleaves fibrinogen
  • Produces fibrin
  • Fibrin spontaneously polymerises into large fibrin clots, crosslinked by factor XIII to produce large clot
  • Stabilises the platelet plug
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13
Q

Describe fibrinolysis.

A
  • Breaking down clot
  • As the clot forms, an inactivated protein called plasminogen binds to fibrin
  • The plasminogen is converted to an active form called plasmin which breaks down the clot

In the mouth, clots are broken down more rapidly.
If clots are broken down too quickly, the individual will bleed excessively.

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14
Q

Why are coagulation tests performed?

A

Used to assess how well blood coagulates.
Only useful in pts who are currently bleeding or have a history of bleeding.

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15
Q

What coagulation tests can be performed?

A

FBC:
- Check for low platelet levels
- Low Hb

Coagulation screen:
- Prothrombin time (PT)
- Activated partial thromboplastin time (aPTT)
- Thrombin clotting time (TCT)
- Fibrinogen level

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16
Q

How is Warfarin reversed?

A
  • Vit K
  • In an emergency: Octaplex
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17
Q

What does INR stand for?

A

International normalised ratio

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18
Q

How should a socket be managed post XLA for a pt taking Warfarin?

A

Gently pack the socket with abosrbable haemostatic dressing (Surgicel) and suture the socket.

19
Q

Describe the action of rivaroxaban and apixaban.

A

Inhibit factor Xa, reduces thrombin therefore reducing conversion of fibrinogen to fibrin.

20
Q

Describe the main features of DOACs.

A
  • Directly inhibit factor Xa or thrombin (Dabigatran)
  • No need for INR monitoring
  • Dose based on weight
  • Renal excretion
  • No reversal agent
  • Short half life, so can be stopped before procedure if necessary
21
Q

What deficiency do people with Haemophilia A have?

A

Factor VIII deficiency

22
Q

What deficiency do people with Haemophilia B have?

A

Factor IX deficiency

23
Q

Describe the main features of Haemophilia.

A
  • Both A and B present identically in clinical situations
  • X-linked recessive (men more commonly affected)
  • Diagnosis: prolonged aPTT
  • Ranges in severity depending on amount of clotting factor in the body (mild, moderate or severe)
24
Q

What clinical signs/symptoms may a pt with severe haemophilia experience?

A
  • Spontaneous or trauma induced joint bleeding
  • Significant bruising
  • Muscle bleeds
  • Urinary tract bleeding
  • Bleeding into the brain (major cause of death), - Oropharyngeal bleeding
  • Delayed prolonged oozing post-surgery
  • Chronic joint damage due to recurrent joint bleeding
25
Q

How are haemophiliacs treated?

A
  • Factor VIII/IX concentrate to replace missing factor
  • For mild cases, desmopressin (DDAVP) may be used, releases stored factor VIII and VWF
  • Tranexamic acid: inhibits fibrinolysis and helps stronger clot to form
26
Q

What is Von Willebrand disease?

A
  • Inherited disease
  • Relatively common (1:100/500)
  • Low levels of VWF
  • Leads to decreased platelet adhesion to vessel wall, decreased platelet aggregation, decreased factor VIII
27
Q

What are the symptoms of Von Willebrand disease?

A
  • Bruising
  • Mucosal bleeding
  • Menorrhagia (heavy periods)
  • Epistaxis (nose bleeds)
  • Prolonged and immediate bleeding from cuts
  • Post-surgical bleeding
28
Q

How is Von Willebrand disease diagnosed?

A
  • VWF levels and FVIII levels measured
  • Both low
29
Q

What considerations should be made by dentists when treating a pt with Von Willebrand disease?

A
  • Higher bleeding risk for extractions
    Prior to dental procedure
  • Correct factor deficiency with Desmopressin (DDAVP), delivered subcutaneously, intranasally or IV
  • Tranexamic acid may be indicated, started 24 hours in advance of treatment, mouthwash used 4-6 times per day
30
Q

Name 5 acquired bleeding disorders.

A
  • Thrombocytopenia
  • Vitamin K deficiency
  • Disseminated intravascular coagulation (DIC)
  • Liver disease
  • Dilutional coagulopathy
31
Q

Are acquired bleeding disorders more rare than inherited bleeding disordes?

A

No, acquired bleeding disorders are relatively more common.

32
Q

What is thrombocytopenia?

A
  • Low platelet count
    Various causes:
  • Bone marrow not producing enough platelets (primary bone marrow disease)
  • Platelets being destroyed by body too quickly (immune mediated, hypersplenism, drugs e.g. quinine, microangiopathic haemolysis)
  • Can be drug induced: aspitin, NSAIDs, antiplatelet drugs e.g. clopidogrel
33
Q

What platelet counts can cause surgical bleeding and what count can cause spontaneous bleeding?

A

Surgical: less than 50
Spontaneous: 10-20

x10^9/L

34
Q

Describe vitamin K deficiency.

A
  • Causes low levels of factor II, VII, X and IX
  • Causes increased PT, aPTT but normal TT
  • All new-borns are given vitamin K at birth due to low levels
    Causes:
  • Malabsorption
  • Obstructive jaundice
35
Q

What is disseminated intravascular coagulation (DIC)?

A

A severe acquired disease which causes inappropriate and uncontrolled activation of coagulation and fibrinolysis in intact BVs.
Causes microvascular thrombi in organs, can cause end organ failure.
Consumption of platelets and clotting factors creates high bleeding risk.

36
Q

What are the causes of DIC?

A
  • Infection e.g. meningococcus
  • Malignancy e.g. prostate
  • Obstetric: placental abruption, eclampsia, amniotic fluid embolism
  • Shock
  • ABO mismatched blood
  • Snake or spider venom
37
Q

How is DIC diagnosed?

A
38
Q

How is DIC treated?

A
39
Q

How does liver disease affect clotting factors?

A
  • Causes low amounts of all factors as they’re all synthesised in the liver
  • Also causes low platelets and low fibinogen
  • Becoming increasingly common
40
Q

What is dilutional coagulopathy?

A

Loss, consumption, or dilution of coagulation factors.

For patients undergoing major haemorrhage, delivered new RBCs and saline, but no clotting factors or platelets meaning you have diluted factors and platelets.
More likely to bleed.

41
Q

How is dilutional coagulopathy managed?

A

Treated quickly with FFP (fresh frozen plasma) and platelets.

42
Q

What pathology does this image show?

A

Recurrent aphthous stomatitis.

43
Q

Briefly describe recurrent aphthous stomatitis.

A
  • Affects 10 - 15% of UK population
  • Most frequent oral mucosal disorder
  • Associated with iron, vitamin B12 or folic acid
    deficiency
44
Q

What haematinic screen is ran for recurrent aphthous stomatitis?

A
  • FBC (Hb)
  • Ferritin
  • Vit B12
  • Folic acid
  • tTG-IgA (coeliac)
45
Q

Why do patients have haematinic deficiencies?

A
  • Inadequate intake (poor diet, vegan etc)
  • Poor absorption (e.g. pernicious anaemia)
  • Loss from GI tract (tumour, haemorrhoids)

human diseases (47 decks)

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