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Yr 2 CHHD > Haematology 1A- Haemostatic and Haemorrhagic Disorders > Flashcards

Haematology 1A- Haemostatic and Haemorrhagic Disorders Flashcards

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1
Q

What are 3 functions of von Willebrand factor

A

mediates platelet adhesion to damaged epithelium (1°)
mediates platelet aggregation (1°)
stabilises + transport factor VIII (2°)

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2
Q

What is von Willebrand disease

A

deficiency in vWF
most common inherited bleeding disorder
different types + severity

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3
Q

what are 3 ways to manage von Willebrand disease

A
  1. (Mild) Desmopressin -drug (DDAVP) - stimulate release vWF from platelets and from cells lining blood vessels+ factor VIII - Rx
  2. (Severe) vWF replacement using human plasma - rich in vWF + factor VIII - Rx
  3. Anti-fibrinolytic drugs - slow/prevent clot breakdown - oral or IV
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4
Q

4 ways in which vWD is related to dentistry

A
  1. prolonged oozing post extraction + bleeding in muscles/joint
  2. haematological cover before invasive procedure in severe cases
  3. Avoid regional LA (infiltration/ intra-ligamentary safer)
  4. Avoid aspirin/NSAIDs (acetaminophen/co-codamol safer)
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5
Q

what is 1° haemostasis and what are the components associated with 1° haemostasis

A

platelet plug formation via vWF
blood vessels
vWF
platelets

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6
Q

what is 2° haemostasis and what are the components associated with 1° haemostasis

A

coagulation - strengthen clot so doesn’t break
aim to form fibrin meshwork
by 3 paths - extrinsic, intrinsic + common

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7
Q

where are clotting factors manufactured

A

liver

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8
Q

what are Factor VIII and vWF produced

A

endothelial cells of blood vessels

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9
Q

which factors are vitamin K dependant

A

factors II, VII, IX and X

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10
Q

how are clotting factors present in body

A

in circulation as inactive form

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11
Q

how is extrinsic pathway in haemostasis activated

A

tissue factor released on injury to blood vessel

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12
Q

how is intrinsic pathway activated

A

exposure to collagen

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13
Q

what are 3 1° primary haemostatic (bleeding) disorders

A

vascular disorders
von Willebrand disease (also 2°)
platelet disorder - platelet deficiency + platelet dysfunction

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14
Q

what are 2 2° secondary haemostatic (blood coagulation) disorders

A

von Willebrand disease (also 1°)

clotting factor disorders

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15
Q

name the 3 haemostatic congenital disorders and say which haemostasis stage they are

A 
von Willebrand disease (1°/2°)
haemophilia A (2°)
haemophilia B (2°)
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16
Q

name the 4 haemostatic acquired disorders and say which haemostasis stage they are

A

thrombocytopenia (1°)
platelet dysfunction associated with drugs (1°)
anti-platelet therapy (1°)
anticoagulant therapy (2°)

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17
Q

what are 2 primary haemostasis disorders that are also vascular disorders

A

Hereditary Haemorrhagic Telangiectasia
(Osler-Weber-Rendu Syndrome)
von Willebrand Disease (vWD)

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18
Q

what type of condition is
Hereditary Haemorrhagic Telangiectasia
(Osler-Weber-Rendu Syndrome)

A

autosomal dominant hereditary condition

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19
Q

what are the clinical features that can be seen of
Hereditary Haemorrhagic Telangiectasia
(Osler-Weber-Rendu Syndrome)

A 
Telangiectasia (small vascular malformations) + arteriovenous malformations in skin, mucosa + viscera
normally not present until adolescent
recurrent epistaxis (bleed from nose) super common
Fe+ deficiency anaemia can occur -> chronic bleeding of intestinal tract
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20
Q

what are dental aspects can be seen from Hereditary Haemorrhagic Telangiectasia
(Osler-Weber-Rendu Syndrome)

A

bleeding from oral surgery
regional LA - best avoided - risk of deep tissue bleeding
if GA - avoid nasal intubation

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21
Q

what are 4 clinical features that can be seen from von Willebrand Disease

A

can be present as 1° or 2° haemostasis or both

  1. bruising, epistaxis
  2. prolonged bleed during surgical/dental procedures
  3. GI bleeding + menorrhagia (long periods) frequent
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22
Q

what type of disorder is Bernard - Soulier disorder

A

1° haemostasis

hereditary platelet disorder - deficiency

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23
Q

What are the main causes of platelet disorders - deficiency

A 
megakaryocyte suppression
bone marrow failure
splenomegaly ( sequestration of platelets)
hereditary 
increased destruction of platelets
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24
Q

how does megakaryocyte suppression cause platelet deficiency causing platelet disorder

A

caused by:
chemotherapeutic agents
viruses - parvovirus infection, mumps, HIV

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25
what can platelet disorders ( deficiency) can bone marrow failure cause
aplastic anaemia leukaemia lymphoma metastases
26
how does increased platelet destruction cause platelet deficiency causing platelet disorder
autoimmune - Idiopathic thrombocytopenic purpura drugs - Cytotoxic drugs diseases - Disseminated intravascular coagulation, SLE (lupus?), Malaria
27
what are main 2 causes of platelet dysfunction
anti-platelet drugs | vWD
28
Name the 4 anti-platelet drugs that cause platelet dysfunction
Aspirin NSAIDs (act on platelet until drug leaves system, 48hrs) Clopidogrel, prasugrel Dipyridamole other drugs act irreversibly + permanent on platelet lifespan (7-10 days)
29
what are 3 main clinical features of platelet dysfunction disorder
easy bleeding + bruising petechiae purpura ecchymosis
30
what are dental aspects can be seen from platelet deficiency disorders
Patients suspected thrombocytopenia - Investigate platelet count (PC) - requesting full blood count (FBC) prior dental treatment • Refer to GP/haematologist for further management • Risk of spontaneous bleeding, PC ˂ 20,000/mm3
31
what are dental aspects can be seen from platelet dysfunction disorders
minor dental procedures - continue medication treat with no interrupting antiplatelet medication no stop medication unless consult with GP limit initial treatment area if there is post extraction bleed - use local homeostatic agents for control
32
what are 2 homeostatic agents used to control post extraction bleeding from platelet dysfunction disorders
compressive packing | sutures, absorbed homeostatic agents (oxidised cellulose)
33
what are 3 2° haemostatic hereditary disorders
haemophilia A haemophilia B vWD
34
how can 2° haemostatic acquired disorders occur
if patient going through anticoagulant therapy
35
what are 3 anticoagulant therapies that can cause acquired disorders to occur
warfarin therapy heparin therapy novel/non-vitamin K oral anticoagulant (NOAC) therapy
36
what are 3 ways which 2° haemostatic disorders can occur
hereditary acquired disease conditions
37
what are 3 disease conditions that can cause 2° haemostatic disorders
``` liver disease (inc obstructive jaundice) disseminated intravascular coagulation malabsorption syndromes ```
38
what is haemophilia A caused by
factor VIII deficiency has a
39
what is haemophilia B caused by
factor IX deficiency
40
who is affected by haemophilia
x linked disorders only males | females carrier
41
what clinical features can be seen from mild haemophilia patients
minimal bleeding usually associated with surgery
42
what clinical features can be seen from moderate haemophilia patients
bleed after minor injury + requires urgent attention
43
what clinical features can be seen from severe haemophilia patients
bleed very often with or without provocation
44
what clinical features can be seen from haemophilia a+b patients
haemorrhage appears stop immediately after injury but intractable oozing follows -> bleeding in deep tissues (joints, muscles)
45
what are 2 main ways to manage haemophilia
diagnosis | treatment
46
what are 3 main ways of diagnosing haemophilia
positive fam history clinical presentation investigation - clotting factor assyas
47
what are 3 main ways of treating haemophilia
1. increase production of factor VIII -> desmopressin 2. replacement therapy for specific clotting factor 3. inhibit fibrinolysis by antifibrinolytic agents
48
what 2 places is replacement therapy for specific clotting factor taken from for treating haemophilia
clotting factor concentrate from plasma | commercial produced recombinant factor
49
what are 2 antifibrinolytic agents used to inhibit fibrinolysis to treat haemophilia
tranexamic acid | EACA ( epsilon amino caproic adic)
50
what are 6 dental aspects to be considered for haemophilic patients
1. preventative dentistry - minimise surgical intervention -> serious bleed 2. close co-op with their haematologist 3. sig risk of haemorrhage after surgery or LA 4. ensure adequate clotting factors (VIII/IX) levels 5. post operative -> look signs haematoma forming (swelling) 6. trauma to head + neck -> prophylactic factor VIII replacing is essential
51
if patient has thrombosis , then they will be on anticoagulant therapy. What are 8 common indications of it
1. atrial fibrillation 2. cardiac valvular disease 3. mech prosthetic heart valves 4. ischaemic heart disease (recent myocardial infarction) 5. deep venous thrombosis 6. pulmonary embolism 7. renal dialysis 8. transient ischaemic attacks or strokes
52
what are examples of anticoagulant medication
warfarin heparin NOACs ( non vitamin K oral anticoags)
53
what does warfarin do and how is it used
inhibits vit K dependant clotting factors II, VII, IX, X oral it has narrow therapeutic range - frequent monitor + dose adjustment sensitive to other drugs INR/prothrombin time
54
what are dental aspects to consider for patients taking warafrin
preventative dentistry - minimal surg intervene | measure INR within 24hrs of surgery
55
what are 4 drugs that warfarin can interact with + should avoid prescribing
metronidazole macrolides azole antifungals aspirin/NSAIDs
56
what are 2 ways to minimise risk of warfarin interacting with other drugs
avoid concurrent use of 2 medications | alternative drugs
57
what does heparin do
``` anti coagulant drug inhibits clotting factors II, X short lived effect 2 types: standard + low mole weight monitored by APTT ```
58
when is IV heparin given + when is LMWH (under skin) heparin given
IV - immediate manage of acute thromboembolic events | LMWH - non-hospital ambulatory patients
59
what are 4 types of NOACs
``` Dabigatran - inhibit factor IIa helps convesion of thrombin-> active thrombin (strengthen clot) apixaban - inhibit factor Xa edoxaban - inhibit factor Xa rivaroxaban - inhibit factor Xa ```
60
What are advs of NOACS
more predicatble lvls of anticoags no routine montoring wide TR + easer to manage effective + safer
61
what are indications of giving NOACs
stroke prevention in AF (atrial fibrillation) patients | Thromboembolic disease
62
what is time of action of NOACS
rapid onset action, 2-4hrs | relatively short half lives (5-13hrs)
63
key homeostatic investigations that help diagnose + treat haemostatic disorder
• Full blood count- platelet count • Bleeding time- platelet defects • Prothrombin time (PT)/ international normalised ratio (INR)- extrinsic pathway and warfarin therapy  PT- (10-12 secs)  INR- universal test (Patient’s PT/Control PT) (0.9-1.2)  INR therapeutic range for patients on warfarin (2-3) • Activated partial thromboplastin time (aPTT)- Intrinsic pathway (30-40secs) and heparin therapy  aPTT therapeutic range for patients on heparin (1.5-2.5)
64
what to remember in patients with bleeding disorders
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

Yr 2 CHHD (4 decks)

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