Prolonged bleeding Flashcards

1
Q

What are the two classification of bleeding problems

A

Congenital causes and acquired causes

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2
Q

What congenital causes would cause bleeding problems

A

haemophiliacs and hereditary coagulation problems

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3
Q

what acquired causes lead to bleeding problems

A

Antiplatelet medication

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4
Q

What is the purpose of haemostasis

A

to prevent blood loss

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5
Q

When does the process of haemostasis start

A

As soon as a vessel is ruptured, damaged or severed

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6
Q

Describe the mechanism for haemostasis

A

vascular spasm
leads to platelet activation
leads to platelet aggregation and formation of plug as well as blood coagulation through the intrinsic and extrinsic cascade
this leads to production of fibrin plug
The fibrin plug is then surrounded by many fibroblast cells, monocytes, WBCs which turn the blood clot into fibrous scar -permanent scar to seal the

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7
Q

describe the intrinsic pathway

A

Exposed collagen leads to platelet activation
factor XII activates XI which activated Ix which activated VIII which converts X into Xa
Xa coverts prothrombin to thrombin
thrombin converts fibrinogen to fibrin

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8
Q

describe the extrinsic pathway

A

Tissue damage leads to activation of factor VII
this converts X to Xa
Xa coverts prothrombin to thrombin
thrombin converts fibrinogen to fibrin

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9
Q

What factors does warfarin act on

A

IX, VII, X and prothrombin to thrombin

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10
Q

what is warfarin and how does it work

A

warfarin is an anticoagulant medcation
it works by interfering with vitamin K production
Vitamin K is responsible for factors ii, Vii, iX and X
so warfarin reduces the production of factors ii, Vii, iX and X
so warfarin acts on both intrinsic and extrinsic pathway

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11
Q

how do new oral anticoagulants differ from warfarin

A

These act on specific points in the pathway by mostly preventing activation of factor X to factor Xa

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12
Q

give three examples of new anticoagulants that work by preventing the activation of factor x to factor Xa

A

Apixaban
Rivaroxaban
edoxaban

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13
Q

How does the new anti coagulant dabigatran work

A

acts specifically on the conversion of prothrombin to thrombin

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14
Q

why are the new anti-coagulants beneficial

A

they target specific points in the pathway so the effects are less variable and we have reliable predictable action and also quick onset

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15
Q

what are the disadvantages of warfarin

A

takes a long time to start acting and long time to wear off
can be affected by drug interations
can be affected by some foods we eat

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16
Q

what is the purpose of the endothelial layer of the vessel

A

it prevents the activation of platelet so prevents clotting factors

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17
Q

how does clotting start

A

vessel wall is broken
collagen fibres are exposed
endothelial walls disappear
this will activate the platelets via the intrinsic and extrinsic mechanism

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18
Q

why is it important to have a pathway that breaksdown clots alongside the pathway that forms a clot

A

all haemostatic mechanisms need to be balanced so if the body is creating a blood clot we need a pathway to stop clotting from going uncontrolled and getting bigger and travelling around the body causing damage

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19
Q

describe the cloth breakdown pathway

A

as the clot forms we have prothrombin converting to thrombin
thrombin catalyses plasminogen to plasmin
plasmin breakdown fibrous clots

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20
Q

if a patient attends for an extraction but is on warfarin do we tel the patient to stop their warfarin

A

No, there is evidence that if you stop warfarin there is a greater risk of causing more harm than good

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21
Q

what dos sdcep guidance say about warfarin and extractions

A

Do not stop warfarin for extractions

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22
Q

how would we manage the patient who is on warfarin and is scheduled for an extraction

A

Check INR in his book
if it is stable then check within 72 hours of the extraction
if INR is unstable you check within 24 hours of the extraction

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23
Q

what is abnormal bleeding usually caused by

A

iatrogenic i.e. caused by medication

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24
Q

what medication causes abnormal bleeding

A

anti-platelet or anti-coagulant drugs

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25
Q

give 4 examples of anti platelet drugs

A

aspirin
dipyridamole
clopidogrel
ticlopidine

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26
Q

give 4 examples of anti coagulant drugs

A

warfarin
dabigatran
apixaban
rivaroxaban

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27
Q

what is the common suffix of anticoagulant s

A

an

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28
Q

how does aspirin work

A

aspirin irreversibly inhibits COX1 which is an enzyme that signal platelet aggregation
Cox is required for thromboxane aggregation which is involved in the inflammatory pathway but it is also involved in the platelet pathway

29
Q

How does clopidogrel work

A

this binds irreversibly to P2Y12 receptor

30
Q

why does aspirin and clopidrogel take longer for it’s effect to wear off

A

irreversibly binds to platelet so we need to wait for all the platelets that aspirin has binded to to die for the effect to wear off

31
Q

how long do platelet take to renew

A

10 days

32
Q

Why is ibuprofen a better pain killer

A

binds reversibly so the effects wont last for long as they would with aspirin

33
Q

which patients are likely to be taking aspirin or clopidogrel

A

vascular disease - Ischaemic heart disease
thromboembolic disease e.g. DVT
stroke
peripheral vascular disease
patients who are likely to form platelet aggregation within vascular system

34
Q

what are the three causes for thrombocytopenia:

A

hereditary
caused by illness
caused by a medical procedure

35
Q

what is the normal platelet count

A

150,000-450,000 per microlitre

36
Q

what can reduce the number of platelets in the blood

A

medication (anti convulsants and sulfa-antibiotics)
some anaemia
leukaemia
pregnancy
hereditary

37
Q

What is the disease called in which low platelet count is hereditary

A

Idiopathic thrombocytopaenic purpura (ITP)

38
Q

what are the symptoms of patients with idiopathic thrombocytopaenic purpua

A

bruise easily as not enough platelets to stop small haemorrhages

39
Q

what is the safe platelet count for an extraction

A

80,000 some haematologist allow 50,000

40
Q

What can haematologist do for patient who has come for extraction but their platelet count is low

A

platelet transfusion or steroid for ITP

41
Q

warfarin is prescribed for which types of diseases

A

atrial fibrillation
pulmonary embolism
DVT
prosthetic heart valves

42
Q

how does warfarin act

A

blocks one of the enzymes that uses vitamin K to produce clotting factors
this disrupts the clotting process and takes longer for blood to clot

43
Q

what is the equation for INR

A

Prothrombin time of patient / mean prothrombin of a group of healthy people

44
Q

Patients who are on anticoagulants should carry a yellow book, what is in this book

A

reason for anticoagulation
target INR
contact details of coagulation clinic
dose of warfarin taken
record of recent INR’s

45
Q

What is INR for healthy individual with no warfarin

A

1.0

46
Q

What is the therapeutic warfarin range for INR

A

2.0 - 4.0

47
Q

what is the half-life of warfarin and how would that effect changes in warfarin dose to iNR readings

A

half life is 48 hours so it would take roughly 2 days for change in dose of warfarin to affect INR

48
Q

what is a risk for taking warfarin

A

more likely to bleed

49
Q

what is the benefit of talking warfarin

A

less likely to clot

50
Q

what do we do when managing a patient who is on warfarin but needs dental procedure

A

we do not stop warfarin
we manage to INR instead
we can liase with clinic to adjust INR so if we want INR less than 4 we can ask them to do this for the day of extraction

51
Q

why is it important to have a patient who is taking warfarin to have INR in the therapeutic range for an extraction

A

there is no significant risk of prolonged bleeding

52
Q

what are the drug interaction between anti-fungal steroids and warfarin

A

antifungal agents can affect INR reading if taken with warfarin it can cause spontaneous haemorrhage, rash on palate

53
Q

what drugs increase INR

A

Micanazole
fluconozole
metrondidazole
erythromycin

54
Q

what drugs decrease INR

A

carbamazepine

55
Q

what is the risk associated with increased INR

A

increased risk of bleeding

56
Q

what is the risk associated with decreased INR

A

increased risk of thrombosis

57
Q

what food and drinks can influence warfarin metabolism

A

green tea which is rich in vitamin K may decrease INR
any variations in dietary intake of vitamin K - liver, broccoli, brussels sprouts, green leafy vegetables

58
Q

How do you manage patients with prolonged bleeding in dental surgery

A
  1. surgicel and suture
  2. tranexamic acid - used in hospitals - less in primary dental care - prevents blood clot breaking down
59
Q

if patient is still bleeding after surgicel and suture how can we manage this

A

Get the pt to rinse with tranexamic acid or soaking a gauze in this acid is a good way of getting the blood clot to better establish

60
Q

What post op advice is given following SDCEP guidance

A
  • Take care with drug prescriptions i.e. for pain
  • Avoid drugs that prolong bleeding directly like:
  • NSAIDs
  • COX-2 inhibitors
  • Take care with drugs that might interact adversely with warfarin e.g. antibiotics such as
  • Erythromycin
  • Metronidazole
61
Q

what is the cause for haemophiliacs and clotting disorders

A

inherited deficiency of clotting factors VII, X etc

62
Q

how would you manage a patient who is haemophiliac or has clotting disorders

A

check with patient’s haematologist for instructions

63
Q

which types of patients is antiplatelet drugs prescribed to

A

risk of or following a stroke
risk of or following MI
angina

64
Q

what is the primary anti-platelet drug

A

aspirin

65
Q

how does aspirin affect bleeding time

A

it increases it

66
Q

what is the minimum age to prescribe aspirin

A

16 - cannot prescribe to a child

67
Q

what is the risk of taking anti-platelet drug

A

risk of increased bleeding

68
Q

what is the benefit of anti-platelet drug

A

reducing clot formation

69
Q

what is the guidance for anti-platelet drug and dental surgical procedures

A

does not need to be stopped