Clotting Flashcards

(137 cards)

1
Q

What is haemostasis?

A

the process by which the body stops bleeding

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2
Q

Which components of blood are involved in clotting?

A

platelets and coagulation factors (make up protein component of blood)

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3
Q

What are the 6 stages of clotting?

A

injury, vascular phase, platelet phase, coagulation phase, clot formation and stabilisation, clot dissolution

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4
Q

What is the platelet phase also known as?

A

primary haemostasis

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5
Q

What is the coagulation phase also known as?

A

secondary haemostasis

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6
Q

What happens during the vascular phase?

A

vasoconstriction, collagen fibres in vessel wall exposed, release of factors from vascular wall (ADP, tissue factor, endothelins)

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7
Q

Which substances are released from the injured vessel wall during the vascular phase?

A

ADP (activates platelets), tissue factor (coagulation phase), endothelins (attract platelets)

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8
Q

What happens during the platelet phase?

A

platelets are attracted to the injury, platelets become sticky (adhesion) and clump together (aggregate) to plug the vessel injury

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9
Q

Which factors attract platelets to the injury site during the platelet phase?

A

exposed collagen and ADP and endothelins which are released from the damaged vascular wall

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10
Q

What is meant by platelet adhesion?

A

platelets develop attachment sites which make them stick to each other

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11
Q

What is meant by platelet aggregation?

A

platelets clump together

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12
Q

Which substances are released by the aggregating platelets?

A

ADP and thromboxane A2 which attract more platelets (positive feedback)

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13
Q

What is the outcome of the platelet phase?

A

platelet plug patches over the injured vessel acting as a temporary, weaker repair compared to final fibrin clot

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14
Q

What is the aim of the coagulation phase?

A

create a more permanent, robust clot (from fibrin)

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15
Q

What is the coagulation cascade?

A

a series of proteins that ultimately lead to clot formation

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16
Q

What are the 2 pathways that can lead to the coagulation cascade?

A

intrinsic and extrinsic pathways

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17
Q

What process occurs alongside the coagulation phase all the time to prevent spontaneous clotting in health?

A

fibrinolysis (clot breakdown)

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18
Q

Where does the intrinsic pathway for the coagulation cascade occur?

A

in the bloodstream

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19
Q

Where does the extrinsic pathway for the coagulation phase occur?

A

in the blood vessel wall

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20
Q

What do the intrinsic and extrinsic pathways diverge to?

A

common pathway

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21
Q

What is the end result of the common pathway (coagulation cascade)?

A

stable fibrin clot (stimulates fibroblasts to regenerate tissue)

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22
Q

How can medications affect clotting?

A

by targeting platelets or targeting coagulation factors

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23
Q

Examples of medications affecting platelets (antiplatelet medication)

A

aspirin, clopidogrel, dipyridamole, ticagrelor

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24
Q

Examples of anticoagulant medications

A

warfarin, edoxaban, rivaroxaban, apixaban, dabigatran

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25
Example of injectable anticoagulant
heparin (LMWH - low molecular weight heparin)
26
Possible reasons for someone being on an antiplatelet medication
coronary disease (to prevent MI or stroke), peripheral arterial disease (narrowed arteries - reduce symptoms)
27
Possible reasons for a patient to be on anticoagulants
prosthetic heart valves (prevent clot), atrial fibrillation, treat/prevent pulmonary embolism/DVT
28
Why may a patient be on a prophylactic LMWH (heparin)?
following surgery or pregnancy in which patient has been immobilised for a long time so blood has tendency to clot, or to treat pulmonary embolism/DVT
29
What is aspirin?
a very common antiplatelet medication
30
What are the 2 doses of aspirin that may be given to a patient?
75mg or 300mg
31
Why may a patient take 75mg of aspirin once a day?
as secondary prevention (prevents reoccurrence) for coronary artery disease and transient ischaemic attack (mini-stroke)
32
When would a patient be given 300mg of aspirin?
acute MI / stroke (basic life support)
33
What is the mechanism of action for aspirin?
inhibits COX1 enzyme (cyclic oxygenase) to reduce thromboxane A2 therefore reduces further platelet aggregation
34
Do you need to stop aspirin for dental treatment?
no - but inform patient what to do if bleeding following surgical procedure
35
How long does aspirin have an effect for once it has been administered?
7-10 days as this is the lifespan of platelets
36
What is warfarin?
anticoagulant medication that is less common nowadays
37
Which family of drugs does Warfarin belong to?
Coumarin
38
What is the main indication for warfarin use nowadays?
prosthetic heart valve (metallic) which leads to stagnation of surrounding blood which creates risk of clotting
39
What is the mechanism of action of warfarin?
inhibits production of active vitamin K which is essential in forming coagulation factors II, VII, IX, X (2,7,9,10) so less fibrin clot is formed
40
Examples of medications and foodstuffs that warfarin interacts with
metronidazole (antibiotic), fluconazole (antifungal), NSAIDs (e.g. ibuprofen), alcohol, grapefruit
41
Why does warfarin require careful monitoring?
patients are on different doses to achieve the desired effect
42
How is warfarin monitored?
International Normalised Ratio (INR)
43
What is the INR?
international normalised ratio - blood test which indicates how long blood takes to clot (how thick or thin)
44
How is the INR value worked out?
patient prothrombin time (PT) / mean normal PT so time taken for patient's blood to clot divided by normal time.
45
What is a normal INR value in theory?
1
46
What does a higher INR value indicate?
patient's blood takes a longer time to clot
47
What INR value is required for dental treatment?
INR < 4
48
Where can an INR test be done?
hospital, GP surgery, home by a nurse, some pharmacies and some dental settings
48
How soon before an invasive procedure should a patient's INR be checked?
no more than 24hrs before (or up to 72hrs if patient is stably anticoagulated)
49
Where is a patient's INR value recorded?
yellow book
50
What is the newer family of anticoagulant medications (to replace warfarin)?
Direct Oral Anticoagulants (DOACs)
51
Which patients use direct oral anticoagulants (DOACs)?
patients with atrial fibrillation or pulmonary embolism / deep vein thrombosis
52
Examples of direct oral anticoagulants (DOACs)
edoxaban, rivaroxaban, apixaban, dabigatran
53
What is the mechanism of action for DOACs?
inhibit coagulation factor Xa (clue: drugs have Xa in name)
54
In addition to inhibiting factor Xa, which other factor does Dabigatran also inhibit?
thrombin
55
Why are DOACs taking over from warfarin?
DOACs are more user friendly, have fewer interactions and do not require monitoring (unlike warfarin which requires INR)
56
How does the onset differ between Warfarin and DOACs?
warfarin onset is slow, DOACs rapid onset
57
How does the dosing differ between Warfarin and DOACs?
Warfarin dosing is variable from patient to patient, DOACs dosing is fixed
58
How do food interactions differ with Warfarin and DOACs?
Warfarin can interact with foods via vitamin K metabolism while DOACs do not
59
What is the difference in the number of drug interactions between Warfarin and DOACs?
Warfarin has many drug interactions while DOACs only have few
60
How does the requirement for monitoring differ between Warfarin and DOACs?
Warfarin requires monitoring via INR whereas DOACs do not
61
How does the offset differ between Warfarin and DOACs?
Warfarin offset is long whereas DOACs offset is shorter
62
What is the advantage of DOACs having a shorter offset compared to Warfarin?
DOACs can be stopped shortly before dental treatment and the anticoagulant effect will be reversed
63
What is the form of injectable anticoagulants?
low molecular weight heparin (LMWH)
64
Examples of low molecular weight heparin / injectable anticoagulants
Dalteparin, Enoxaparin
65
When are injectable anticoagulants most commonly given?
after birth of a significant surgery / hospital stay where a patient is at increased risk of developing a blood clot. Or patients unable to take DOACs
66
What is the mechanism of action of injectable anticoagulants?
inhibits formation of factor Xa and thrombin (same as Dabigatran)
67
How are injectable anticoagulants administered?
patients inject themselves once a day subcutaneously
68
Do injectable anticoagulants need to be stopped for dental treatment?
generally no need to stop injectable anticoagulants for dental treatment
69
Why do dentists need to be aware of antiplatelet / anticoagulant medications?
dental treatment can cause bleeding which needs to be predicted and controlled
70
Which organisation provides guidelines on dental patients taking antiplatelet or anticoagulant drugs?
Scottish Dental Clinical Effectiveness Programme (SDCEP)
71
Examples of dental procedures that are unlikely to cause bleeding
LA, BPE, impressions, fitting orthodontic appliances, restorations with supragingival margins, supragingival plaque/calculus removal
72
Examples of procedures that are likely to cause bleeding but have a low risk of post-op bleeding complications
simple extractions, incision and drainage of intra-oral swellings, 6 point full perio exam, subgingival debridement, restorations with subgingival margins
73
Examples of procedures that are likely to cause bleeding with a higher risk of post-op bleeding complications
complex extractions, 3+ extractions at once, flap raising procedures (e.g. periodontal surgery, implants), gingival recontouring, biopsies
74
What special considerations need to be made for patients on Warfarin before an invasive procedure?
INR should be checked no more than 24hrs before procedure (or up to 72hr is patient stably anticoagulated), treat is INR<4 without interrupting medication, consider limiting / staging treatment, suture and pack socket
75
What should you do if a Warfarin patient has an INR of 4 or above?
delay invasive treatment or refer if urgent (e.g. life threatening abscess)
76
What is the usual drug schedule for apixaban or dabigatran?
taken twice a day
77
What should Apixaban or Dabigatran patients do about their pre-treatment dose (invasive e.g. xla)?
miss their morning dose
78
What should Apixaban or Dabigatran patients do about their post-treatment dose (following invasive procedure)?
take it in the usual time in the evening
79
What is the usual drug schedule for patients on Rivaroxaban or Edoxaban?
taken once a day either in the morning or evening
80
What should patients on Rivaroxaban or Edoxaban who take their dose in the morning do pre-treatment (invasive)?
delay morning dose to 4hr after haemostasis achieved
81
What should patients on Rivaroxaban or Edoxaban who take their dose in the evening do post-treatment (invasive)?
take their dose at the usual time in the evening
82
What considerations should be made for patients on a prophylactic (low) dose of injectable anticoagulants?
treat without interrupting medication
83
What considerations should be made for patients on a treatment (high) dose of injectable anticoagulants?
consult with prescribing clinician
84
What are the general principles that should be adhered to when carrying out an invasive procedure on a high bleeding risk patient?
consult with GP/senior clinician if unsure, if on course of anticoagulants (e.g. for DVT) delay dental treatment until anticoagulant finishes, plan treatment for early in the week and the day, staging treatment, pack and suture, ensure bleeding has stopped, excellent post-op instructions, advise paracetamol for pain relief rather than NSAIDs
85
Why is paracetamol advised for pain relief rather than NSAIDs for high bleeding risk patients following an invasive procedure?
NSAIDs (e.g. aspirin, ibuprofen, diclofenac, naproxen) have an anti-platelet effect (inhibit COX enzyme to reduce thromboxane A2 production which reduces platelet aggregation)
86
Which elements of clotting can bleeding disorders affect?
platelets, coagulation factors or liver disease
87
Why is liver function important for clotting?
coagulation factors are produced in the liver and the liver produces the hormone which stimulates platelet production
88
How can bleeding disorders be categorised?
acquired or inherited bleeding disorders
89
Examples of acquired bleeding disorders
liver disease, thrombocytopenia
90
Examples of inherited bleeding disorders
Von Willebrand disease, Haemophilia A, Haemophilia B
91
What is the most severe form of liver disease?
cirrhosis (scar tissue replaces healthy hepatocytes)
92
What are the 2 effects liver disease has on clotting?
reduced platelet number and function, and impaired production of coagulation factors
93
Why does liver disease lead to reduced platelet number and function?
reduced thrombopoietin (TPO) production in liver
94
What is the function of thrombopoietin?
stimulates platelet production in bone marrow
95
Which coagulation factors have impaired production due to liver disease?
Coagulation factors I, II, V, VII, IX, X, XI and XIII
96
What does thrombocytopenia mean?
low platelets (thrombo - clot, cyto - cell, penia - low)
97
What are the 2 general reasons for thrombocytopenia?
reduced production or increased destruction of platelets
98
Possible causes for a reduced production of platelets (causing thrombocytopenia)
B12 deficiency, folic acid deficiency, chemotherapy, leukaemia, liver disease
99
Possible causes for an increased destruction of platelets (causing thrombocytopenia)
immune driven (ITP), TTP, Heparin-induced thrombocytopenia
100
What is the most common inherited cause of abnormal and prolonged bleeding?
Von Willebrand disease
101
What is the pattern of inheritance for Von Willebrand disease?
autosomal dominant inheritance
102
What is the cause of Von Willebrand disease?
absence or defective von Willebrand factor
103
What is the von Willebrand factor?
an important compound for clotting - helps platelets aggregate and helps transport factor VIII to the wound
104
What is the effect of von Willebrand disease?
impairs platelet aggregation and impairs transport of factor VIII to wound
105
What are the different types of von Willebrand disease?
Type 1 - partial deficiency of VWF Type 2 - reduced function of VWF Type 3 - complete deficiency of VWF
106
What substance would you give a patient with type 1 von Willebrand disease before a procedure likely to cause bleeding?
DDAVP/desmopressin (synthetic hormone that increases VWF production and factor VIII production)
107
What substance would you give a patient with type 2 or 3 von Willebrand disease?
IV infusion or injection of von Willebrand factor concentrate
108
Do patients with von Willebrand disease require daily treatment?
Not generally required
109
Which substance may be given to a type 1 von Willebrand patient undergoing a low risk procedure?
tranexamic acid oral / mouthwash (inhibits break down if blood clot does form)
110
Where is dental care often provided for patients with von Willebrand disease?
special care dentistry setting
111
Whom would you seek advice from when treating a patient with von Willebrand disease?
haematologist
112
What is the pattern of inheritance for haemophilia?
x-linked recessive (rare and primarily affects males)
113
What causes haemophilia A?
deficiency of factor VIII in the intrinsic pathway
114
What causes haemophilia B?
deficiency of factor IX in the intrinsic pathway
115
What do haemophilia patients suffer from?
spontaneous bleeding (into joints) and significant bleeding following minor trauma
116
How is the haemophilia A/B categorised?
based on a spectrum depending on how much of the coagulation factor is produced. Mild (6-40%), moderate (2-5%), severe (<1%)
117
Which products will be administered to haemophilia A patients prior to a procedure?
DDAVP/desmopressin (mild) or factor VIII concentrate (moderate/severe)
118
Which products will be administered to haemophilia B patients prior to procedure?
factor IX concentrate (DDAVP not effective as it increases von Willebrand factor which only affects factor VIII)
119
How long before a procedure should blood products be administered to haemophilia patients?
within 30 min of treatment
120
Which treatments for a patient with an inherited bleeding disorder can be carried out in primary care (GDP)?
simple, non-invasive treatments e.g. dentures
121
What should you do if you are unsure about treating a patient with an inherited bleeding disorder?
refer or ask advice from haematology team
122
What should you avoid when administering LA to patients with an inherited bleeding disorder?
avoid inferior alveolar nerve block (risk of bleeding from muscle can cause haematoma which may compromise airway).
123
How should you administer LA to a patient with an inherited bleeding disorder?
buccal infiltration, intra-papillary injections, intra-ligamentary injections
124
What are the blood tests related to clotting?
full blood count, liver function test, INR, coagulation screen
125
What does a full blood count reveal?
red cell count, platelets, white cell count
126
What does a liver function test reveal?
acute liver damage
127
What is the usual INR range for patients on Warfarin?
about 2-4
128
What does the coagulation screen reveal?
looks at intrinsic and extrinsic pathways, and gives insight into liver's synthetic function
129
What is thrombophilia?
tendency to clot (thrombo - clot, philia - tendency)
130
What are substances of the coagulation cascade that prevent over-clotting (have an inhibitory effect)?
protein C, protein S, antithrombin
131
Which conditions can lead to thrombophilia?
Factor V Leiden (resistance to protein C), protein C/S deficiency, antithrombin III deficiency
132
Examples of blood clots that are likely to develop due to thrombophilia
pulmonary embolism (PE) or deep vein thrombosis (DVT)
133
What is a pulmonary embolism?
blood clot in lung - can interfere with gas exchange and end up in brain
134
What is a deep vein thrombosis?
blood clot in limbs (often leg e.g. after long period of immobility)
135
What are risk factors for thrombophilia (developing a blood clot)?
previous DVT/PE, prolonged immobility, plaster cast, combined oral contraceptive pill / HRT (oestrogen promotes blood clotting), surgical operation, acutely unwell (sepsis), cancer, dehydration, pregnancy
136
How are patients that have a proven thrombophilia (e.g. recent PE/DVT) managed?
anticoagulant medication (usually apixaban) - therefore becomes a bleeding risk