Bleeding, leukaemia and Denitstry Flashcards

(50 cards)

1
Q

What is the process of haemostasis?

A
Injury and tissue damage
Vascular response - VASOCONSTRICTION
Platelet adhesion and aggregation -VWF/PLATELET/FIBRI
Unstable platelet clot
Coagulation factor cascade
Fibrin - STABILITY TO THE CLOT
Stable clot
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2
Q

Describe the intrinsic pathway?

A

Via factors 12, 11, 9 and 8 to get to factor 10 (activated partial thromboplastin time (APTT))

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3
Q

Describe the extrinsic pathway?

A

Via factor 7 to get to factor 5 (prothrombin time (PT))

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4
Q

What do the intrinsic and extrinsic pathway lead to?

A

Prothrombin - thrombin - fibrinogen to fibrin

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5
Q

What are the 2 types of coagulation defect?

A

GENETIC - haemophilia A, B, C, VWD
ACQUIRED - liver disease, kidney disease, anti platelet, anticoagulation - heparin, warfarin, enoxaparin, dabigatran, rivaroxiban, antiplatelet, liver disease, Vit K deficiency, blood transfusion

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6
Q

What is haemophilia A?

A

Genetic coagulation defect
Deficient in factor VIII
Can be mild, moderate or severe
Spontaneous bleeding which doesn’t stop.
A loose platelet plug will form but blood oozes around
Dental extractions and surgery are dangerous

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7
Q

How do we treat haemophilia A?

A

Give factor VIII and treat ASAP

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8
Q

What is haemophilia B?

A

Genetic coagulation defect

Deficient factor IX

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9
Q

How do we treat haemophilia B?

A

Give factor IX - can be given daily as factor IX has a long half life

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10
Q

What is haemophilia C?

A

Genetic coagulation defect
Deficient factor XI
Rapid fibrinolysis

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11
Q

How do we treat haemophilia C?

A

Give fresh frozen plasma (FFP), factor XI and transexamic acid (stops fibrin breakdown)

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12
Q

What is transexamic acid?

A

Transexamic acid is an antifibrinolytic drug so stops the break down of fibrin

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13
Q

What is von willebrands disease?

A
Deficiency of von willebrand factor (VWF) - required for platelet adhesion
Type 1(mild), 2, 3 and pseudoVWD
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14
Q

How do we treat VWD?

A

Factor VII infusion for upper major procedures
DDAVP (desmopressin) and oral transexamic acid for minor procedures
Factor VIII supplements given if any chance of oral trauma (prior to procedure)
Regional blocks / injections in the floor of the mouth can cause haemhorrage and potential airway obstruction
Avoid intramuscular injections

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15
Q

Name 3 types of anticoagulants?

A

HEPARIN - usually given for immediate effects in acute thromboembolism
ENOXAPARIN - LMWH, Inhibits factor Xa
WARFARIN

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16
Q

Describe warfarin?

A

Warfarin impairs synthesis of Vit K dependant coagulation factors in the liver (2, 7, 9, 10)
Requires active and regular monitoring via INR value
Usually takes 2 - 4 days to become effective

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17
Q

What are the indications for warfarin?

A
SHORT TERM USE :
prophylaxis to prevent DVT
Established DVT
PE
MI
CABG

LONG TERM USE:
Recurrent VTE
Rheumatic heart disease and atrial fibrillation
prosthetic value replacement

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18
Q

What is INR?

A

Prothrombin time - Dependant on weight, mass, diet
Must be check on day, prior to procedures
Normal = 1
4 = no extractions!

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19
Q

What interferes with warfarin?

A

Antiplatelet drugs
Antibiotics - affects INR
Miconazole oral gel
Aspirin and NSAIDs - increased bleeding, less platelet adhesion and increased gastric ulcers
Metronidazole - avoided
Erythromycin - unpredictable effects
Daktarin (antifungal) - fatal, affects INR

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20
Q

Name 4 antiplatelet medications?

A

Aspirin - thrombotic cardio or cerebrovascular disease
Clopidogrel -IHD
Ticlopidine - IHD
Dipyridamole - adjunct to oral anticoagulants with prosthetic heart valves

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21
Q

What is the action of aspirin, clopidogrel, and ticlopodine?

A

Inhibit platelet aggregation to the blood vessel walls

Lasts for the life of the platelets (7 - 10 days)

22
Q

What is the action of dipyridamole?

A

Acts directly on the enzyme in platelets and vessel walls

Reversible

23
Q

Name 2 non steroidal antiplatelet medications?

A

NSAIDs - not used clinically for antiplatelet function

Ibuprofen/ diclofenac - reversible effect once the drug is cleared, platelet function restored

24
Q

What is the normal bleeding time?

A

2 - 10 minutes

25
What is the effect of antiplatelet agents?
Longer bleeding time
26
Name 5 coagulation defects?
``` Liver disease Hepatocellular failure Vitamin K deficiency Increased fibrinolysis Thrombocytopoenia (less platelets) ```
27
What is the treatment for autoimmune causes of coagulation defects?
steroids | splenoctomy
28
What is the treatment for leukaemia, aplastic anaemia causes of coagulation defects?
Platelet transfusion
29
What is leukaemia?
Neoplastic proliferation of white blood cells in the bone marrow
30
What is leukaemia due to?
``` Genetic Ionizing radiation chemicals virus Lymphoblastic and non lymphoblastic causes ```
31
Descirbe acute lymphoblastic leukaemia (ALL)?
peak incidence 2 - 4 yrs B lymphocyte neoplasm blasts > clasts so white cells decrease Pale / anaemic / gingival swelling
32
Describe acute myeloid leukaemia (AML)?
Non lymphoblastic (myeloblastic) Proliferation of myeloblasts in tissues Most common in adults swollen sore bleeding gums, no infection
33
Describe chronic lymphocytic leukaemia (CLL)?
``` Most common type of leukaemia Anaemic proliferation of lymphoytes Older patients M>F thrush, inflitration of gingival tissues Recurrs/ relapses Need chemo ```
34
What is chemotherapy?
Gets rid of malignant and non rapidly dividing cells Cytotoxic agents also affect the bone marrow and reusult in : leukopoenia, neutropoenia, thrombocytopoenia, anaemia
35
What is oral screening?
Intervention to eliminate any likely causes of dental sepsis Needs to be timed during count recovery High dose regimes need extra vigilance as opportunistic infections can prove fatal
36
What do patients experience during chemo?
Sever mucositis oral ulceration superimposed opportunistic infections
37
Name 5 aids to symptomatic treatment?
``` Corsodyl rinse Betnesol mouth rinse Difflam rinse Beclotide spray Bite guards ```
38
What is mucositis?
Breach in oral mucosa Fibrous slough and ulcers Affects QoL - eating and drinking Can become peri oral
39
What is neutropoenic gingivitis?
No neutrophils Ulcers with no neutrophil response, leads to septacaemia Increased perio disease and tooth loss
40
What patients does neutroppoenic gingivitis occur?
Immunocompromised
41
Name 3 opportunisitc infections?
Systemic aspergillosis Herpes Simplex Herpes zoster
42
What is systemic aspergillosis?
An opportunistic infection It invades and kills bone Antifungals reduce the severity but need to remove bone
43
What is herpes simplex virus?
An opportunistic infection Spread by saliva Flu for 1 week, temperature, pan oral ulceration, coldsores Brought on by UV, tiredness, low immune system
44
What is herpes zoster?
Chicken pox virus HIV, older, low immune system Unilateral (never crosses the midline)
45
What is recommended prior to cancer therapy?
supplementation with chlorhexidine Stabilise carious teeth Smooth any sharpness Remove teeth with doubtful prognosis
46
What is recommended during cancer therapy?
``` Chlorhexidine continued Fluoride mouthwash Decrease mucositis alleviate symptoms of xerostaemia avoid dental treatment ```
47
What is recommended is the patient is neutropoenic at the time of treatment?
Likely to induce bacteraemia so give prophylactic antibiotic cover
48
When is platelet cover required for surgeical procedure?
When platelet count
49
When is it best to provide treatment for those on chemo?
Best to treat just before or just after chemo (check platelets and neutrophils)
50
When can dental infections be fatal?
When pt on high dose of chemo | So remove any teeth likely to be pulpally involved or advanced perio disease.