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Human Disease > Bleeding, leukaemia and Denitstry > Flashcards

Bleeding, leukaemia and Denitstry Flashcards

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
Q

What is the effect of antiplatelet agents?

A

Longer bleeding time

26
Q

Name 5 coagulation defects?

A 
Liver disease
Hepatocellular failure
Vitamin K deficiency
Increased fibrinolysis
Thrombocytopoenia (less platelets)
27
Q

What is the treatment for autoimmune causes of coagulation defects?

A

steroids

splenoctomy

28
Q

What is the treatment for leukaemia, aplastic anaemia causes of coagulation defects?

A

Platelet transfusion

29
Q

What is leukaemia?

A

Neoplastic proliferation of white blood cells in the bone marrow

30
Q

What is leukaemia due to?

A 
Genetic
Ionizing radiation
chemicals
virus
Lymphoblastic and non lymphoblastic causes
31
Q

Descirbe acute lymphoblastic leukaemia (ALL)?

A

peak incidence 2 - 4 yrs
B lymphocyte neoplasm
blasts > clasts so white cells decrease
Pale / anaemic / gingival swelling

32
Q

Describe acute myeloid leukaemia (AML)?

A

Non lymphoblastic (myeloblastic)
Proliferation of myeloblasts in tissues
Most common in adults
swollen sore bleeding gums, no infection

33
Q

Describe chronic lymphocytic leukaemia (CLL)?

A 
Most common type of leukaemia
Anaemic proliferation of lymphoytes
Older patients
M>F
thrush, inflitration of gingival tissues
Recurrs/ relapses
Need chemo
34
Q

What is chemotherapy?

A

Gets rid of malignant and non rapidly dividing cells
Cytotoxic agents also affect the bone marrow and reusult in :
leukopoenia, neutropoenia, thrombocytopoenia, anaemia

35
Q

What is oral screening?

A

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
Q

What do patients experience during chemo?

A

Sever mucositis
oral ulceration
superimposed opportunistic infections

37
Q

Name 5 aids to symptomatic treatment?

A 
Corsodyl rinse
Betnesol mouth rinse
Difflam rinse
Beclotide spray
Bite guards
38
Q

What is mucositis?

A

Breach in oral mucosa
Fibrous slough and ulcers
Affects QoL - eating and drinking
Can become peri oral

39
Q

What is neutropoenic gingivitis?

A

No neutrophils
Ulcers with no neutrophil response, leads to septacaemia
Increased perio disease and tooth loss

40
Q

What patients does neutroppoenic gingivitis occur?

A

Immunocompromised

41
Q

Name 3 opportunisitc infections?

A

Systemic aspergillosis
Herpes Simplex
Herpes zoster

42
Q

What is systemic aspergillosis?

A

An opportunistic infection
It invades and kills bone
Antifungals reduce the severity but need to remove bone

43
Q

What is herpes simplex virus?

A

An opportunistic infection
Spread by saliva
Flu for 1 week, temperature, pan oral ulceration, coldsores
Brought on by UV, tiredness, low immune system

44
Q

What is herpes zoster?

A

Chicken pox virus
HIV, older, low immune system
Unilateral (never crosses the midline)

45
Q

What is recommended prior to cancer therapy?

A

supplementation with chlorhexidine
Stabilise carious teeth
Smooth any sharpness
Remove teeth with doubtful prognosis

46
Q

What is recommended during cancer therapy?

A 
Chlorhexidine continued
Fluoride mouthwash
Decrease mucositis
alleviate symptoms of xerostaemia
avoid dental treatment
47
Q

What is recommended is the patient is neutropoenic at the time of treatment?

A

Likely to induce bacteraemia so give prophylactic antibiotic cover

48
Q

When is platelet cover required for surgeical procedure?

A

When platelet count

49
Q

When is it best to provide treatment for those on chemo?

A

Best to treat just before or just after chemo (check platelets and neutrophils)

50
Q

When can dental infections be fatal?

A

When pt on high dose of chemo

So remove any teeth likely to be pulpally involved or advanced perio disease.

Human Disease (54 decks)

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