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3rd BDS IHD > Haematology > Flashcards

Haematology Flashcards

1
Q

what are the two broad causes of coagulopathies

A

medication
conditions

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2
Q

what are the two main congenital conditions causing coagulopathies

A

Haemophilia (A and B)
von Willebrand’s disease

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3
Q

name 5 congenital conditions that cause coagulopathies

A

Haemophilia A and B
Von Willebrands
Bernard Soulier syndrome
Wiscott Aldrich syndrome
Idiopathic thrombocypenic purpura
Ehlers Danlos syndrome

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4
Q

what is haemophilia a and b

A

A = factor VIII deficency
B = factor IX defiency

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5
Q

what is primary and secondary haemostasis

A

primary hemostasis makes a weak platelet plug at the injury site while secondary hemostasis makes it strong by generating a fibrin mesh on it

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6
Q

how does haemophilia cause coagulopathies

A

X linked rcessive mutation
deficient factor IX or VIII both affecting the extrinisc pathway of fibrin formation for secondary haemostasis
primary haemostasis can occur but secondary cannot
no strengthening of platelet clot = increased bleeding

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7
Q

what are some signs and symptoms of haemophilia

A

Nosebleeds with no cause
Easy bruising - large
Spontaneous gingival bleeding
GI bleeds - blood in urine or stool
Difficult clotting after cuts - very small
Bleeding into joints (haemarthrosis)
Cranial bleeds

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8
Q

what classifications of haemophilia are there and how do we classify(not A and B)

A

severe = clotting factor < 1% spotaenous bleed
moderate = 2 < clotting factor < 5% may bleed
mild = 6 < clotting factor < 40% bleed after trauma/surgery
carrier = factor level may vary

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9
Q

what percentage in the blood would class as ‘normal range’ for clotting factor VIII and IX

A

50-100%

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10
Q

what is the first, second and third line treatment for haemophilia

A

anti-fibrinolytics e.g. tranexamic acid
DDAVP - encourages release of factor VIII and VWBf
Direct factor replacements

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11
Q

why do we try other treatments for haemophilia before using direct factor replacement

A

they are expensive
over time body may build immunity to the factors

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12
Q

how does tranexamic acid work (2)

A

Anti-fibrinolytic agent that inhibits the breakdown of fibrin clots
Blocks the binding of plasminogen and plasmin to fibrin therefore preventing fibrinolysis

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13
Q

can a dentist prescribe tranexamic acid and why

A

no
not in dental BNF

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14
Q

what are the (post) instructions for use of tranexamic acid (5)

A

Use QDS, start 5-10 minutes post extraction
Rinse with 5mls of 5% solution and hold for 2 mins, then spit
Continue for 5 days
Can be used to soak in absorbent gauze, to provide additional pressure to extraction site
avoid drinking for 1 hour after

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15
Q

what is DDAVP and how does it work

A

desmopressin
synthetic vasopressin - hormone that reduces urine output
DDAVP stimulates the release of endogenous FVIII and VWF from stores in patients endothelium of blood vessels with mild Haemophilia A and VWD

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16
Q

how is desmopressin given

A

prescribed by haematologist
nasally, intravenously, or as an oral or sublingual tablet

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17
Q

what are the two functions of VWBf

A

Promotes platelet aggregation (primary haemostasis)
Carrier protein for factor VIII (secondary haemostasis)

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18
Q

what is type I VWBd (3)

A

commonest type 80%
autosomal dominant
quantative deficency

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19
Q

how do we treat the most common type of VWBd

A

80% of people have type I
autosomal dominant
trial of DDAVP desmopressin, if unresponsive then factor substitute

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20
Q

what is type II VWBd

A

autosomal dominant, 15% of people
qualitative deficiency of VWBf

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21
Q

how do we treat type II VWBd

A

factor VIII concentrate

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22
Q

what is type III VWBd

A

severe quantative deficency of VWBf
<1%
autosomal recessive

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23
Q

how dow e treat VWBd type III

A

factor concentrate

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24
Q

compare type I, II and III VWBd (4)

A

type I = dominant, 80%, quantitive deficiency, treat DDAVP then factor
type II = dominant, 15%, qualitative deficiency, treat concentrate
type III = recessive, severe, <1%, treat concentrate

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25
Q

which is the most severe type of VWBd

A

type 3, <1%

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26
Q

why might a coagulopathy be cause of dental anxiety

A

some pts may not be diagnosed until a large bleed after a dental XLA which would be traumatic and scary for the patient
associate with the dentist

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27
Q

what are barriers to dental care of coagulopathies

A

dental anxiety
tired of treatments
Transfusion infections e.g. hep from the past when no screening occur
Access to dental care
Previous refusal
Lack of knowledge and management
Bad previous experience (including hospital admissions)
Haemarthrosis and mobility

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28
Q

what types of treatment are risk of bleeding and what must we do prior to these treratments with a pt with a bleeding disorder

A

BPE
Local anaesthetic - particularly IANB
Supragingival restorations with use of matrix bands
Scaling or periodontal disease management
Extractions
Biopsies

Any of these - liase with haematoligist

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29
Q

how do we safely manage an examination of a pt with bleeding disorder (4)

A

no BPE
safe, careful soft tissue examination
place intra-oral films carefully with x-rays or use OPT
thourough pt MH with point of contact established

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30
Q

how do we take a bleeding MH (7)

A

history of bleeding
how it is controlled - medications
what happens if they get a cut
wether affects primary or secondary coagulation
have they had injections before
haematologist point of contact
if they live far away and if they live alone

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31
Q

what parts of a dental procedure can cause bleeding with haemophiliacs

A

LA: Dental blocks and lingual infiltrations can cause haematomas that cause airway issues
Matrix bands, cotton wool rolls (can dry, sticky, tear out = bleed) and aspirators
BPE, 6 point chart, USS

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32
Q

which dental injections are likely to cause bleeding and what is the implication of this with haemophiliacs

A

Dental blocks and lingual infiltrations can cause haematomas that cause airway issues

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33
Q

what types of isolation are dangerous for haemophiliacs (2)

A

matrix bands
cotton wool (stick, tear off = bleed)

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34
Q

how can we prevent a bleed in surgery with a bleeding disorder pt

A

refer, very safe low risk examination
have point of contact established and thorough MH
follow local and government guidelines

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35
Q

how do we manage a bleeding emergency

A

call for help
stay calm
Patients generally know how to manage their condition
Local measures – apply pressure
Contact haemophilia centre or point of contact on MH and seek advice over phone

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36
Q

what are some acquired bleeding disorders

A

Chronic kidney disease
Liver disease (alcohol dependence/misuse, HIV, hepatitis)
Chemotherapy
Heart failure
Haematological malignancy
Myeloproliferative disorder

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37
Q

what blood tests should be taken prior to a dental procedure for haemophiliacs

A

Full blood count (which includes platelet levels) - find from haemotologist
Normal platelet levels 140-350 x 109/litre
Thrombocytopenia can aggravate surgical or traumatic bleeding
<20 spontaneous bleeding
>80 haemostatic and safe for surgical procedures
Clotting screen - for XLA but liaise with haemotologist

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38
Q

what is a safe, normal and dangerous level of platelets in the blood

A

Normal platelet levels 140-350 x 109/litre
<20 spontaneous bleeding
>80 haemostatic and safe for surgical procedures

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39
Q

what needs to be included in medication medical history of a bleeding disorder pt (3)

A

What medicines are you taking?
Prescribed and non prescribed (over the counter)
Herbal and complimentary medicines (e.g. St Johns Wort, garlic, Gingko biloba)
How long will you be taking them for? (e.g. LMWH can be a few weeks after large surgery) - Short term or long term

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40
Q

what needs to be included in medication medical history of a bleeding disorder pt (3)

A

What medicines are you taking?
Prescribed and non prescribed (over the counter)
Herbal and complimentary medicines (e.g. St Johns Wort, garlic, Gingko biloba)
How long will you be taking them for? (e.g. LMWH can be a few weeks after large surgery) - Short term or long term

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41
Q

which drugs affect the bleeding of a patient and how (9)

A

NOACS
antiplatelets
anticoagulants
LMWH
cytotoxic drugs associated with bone marrow suppression
NSAID (impair platelet function)
SSRI anti-depressants e.g Citalopram - platelet aggregation
Immunosuppressants - reduce number of available platelets
Drugs affecting nervous system

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42
Q

how do cytotoxic drugs affect bleeding

A

leflunamide, hydrochloroquine, infliximab, gold
associate with bone marrow suppression = less platelets

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43
Q

how do NSAIDs affect bleeding (4)

A

NSAIS are COXI and COXII inhibitors
prevent formation of thromboxane from arachidonic acid
thromboxane needed for vasoconstriction and platelet aggregation
affects primary coagulation

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44
Q

which anti-depressant causes changes in bleeding and how

A

Citalopram - platelet aggregation

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45
Q

give examples of immunosupressants and how they affect bleeding

A

methotrexate, azathioprine, mycophenolate
reduce number of available platelets

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46
Q

give two exmaples of nervous system drugs that affect bleeding

A

gabapentin may impair platelet function
carbamazepine may cause thrombocytopenia

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47
Q

which drug can cause thrombocytopenia

A

carbamazepine may cause thrombocytopenia

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48
Q

pt is on Dalteparin (Fragmin)
Enoxaparin (Clexane)
Tinzaparin (Innohep)
what are they taking and why

A

types of LMW herparin
anticoagulant
thin blood to prevent blood clots

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49
Q

how do patients administer LMWH

A

Usually administered subcutaneously by injection

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50
Q

what are some advantages of heparin

A

short onset of action
short half life

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51
Q

when would herparin be prescribed

A

Short term prescription for Prevention of VTE in pregnancy
after valve replacement
VTE and cancer
spinal injury

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52
Q

what is a VTE

A

venous thromboembolism

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53
Q

how do antiplatelet drugs work and give 4 examples

A

Impair primary haemostasis by interfering with platelet aggregation, reversibly or irreversibly
Clopidogrel (Plavix)
Aspirin
Dipyradimole (Persantin)
Ticagrelor (Brilique)

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54
Q

compare aspirin and clopidogrel

A

both antiplatelet drugs
aspirin is irreversible inhibiton of COX enzymes, clopidogrel is reversible
clopidogrel is a stronger antiplatelet

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55
Q

what is the bleeding time of dual therapy antiplatelets e.g. aspirin + clopidogrel

A

45-60mins

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56
Q

do antiplatelets/anticoagulants affect primary or secondary haemostasis

A

antiplatelets = primary
anticoagulants = secondary

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57
Q

what is warfarin and how does it work (4)

A

Vitamin K antagonist - anticoagulant
prevents formation of vitamin K dependant coagulation factors 2,7,9,10
affecting intrinsic and extrinsic pathways of the coagulation pathway
DVT, AF, Strokes, Valve replacements

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58
Q

what are the disadvantages of warfarin (3)

A

Multiple drug and dietary interactions - BNF
Variation in patient response to the drug
Needs careful monitoring with regular blood tests for INR (International Normalised ratio) is the time taken for a clot to form in a blood sample relative to a standard of 1

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59
Q

why do we ask how much pt has INR checked (3)

A

indication of how stbale their management of haemostasis is
Stable INR history, can be assessed up to 72 hours before the dental procedure - if checked every few months = stable
Unstable INR must be assessed within 24 hours of the dental procedure - if checked every week = unstable

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60
Q

how do we use INR with our management of pt

A

Dental procedures unlikely to cause bleeding continue without adjusting dose. Apply principles of safe treatment, use local measures routinely

Dental procedures likely to cause bleeding (low or high risk) with stable INR check INR at least 72 hours beforehand. Apply principles of safe treatment, use local measures routinely

Dental procedures likely to cause bleeding (low or high risk) with unstable INR check INR 24 hours beforehand. Apply principles of safe treatment, use local measures routinely

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61
Q

what are the principles of safe treatment of a pt with INR checks

A

Principles of safe treatment. Limit to single extraction, sub-gingival scaling 3 teeth then assess before continuing, staged treatment over separate visits, local measures pack and suture

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62
Q

how do we manage a pt with INR > 4

A

Refer back to medical practitioner for advice before proceeding
Do not stop medication yourself- Patient takes this for a clear medical reason and is likely to be at risk of a blood clot.
If providing urgent care, remember warfarin interacts with many antibiotics and antifungals (erythromycin, fluconazole, metronidazole) which can increase the bleeding risk to the patient, refer to the BNF!

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63
Q

what are some drugs that we cannot prescribe with warfarin (3)

A

‘azole’ antifungals = miconazole, itraconazole, fluconazole (nystatin is okay)
metronidazole
amoxicillin
macrolides (erythromycin ,azithromycin, clarithromycin)

basiclaly things that end in azole, mycin and amoxicillin

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64
Q

what are the four major DOACs

A

Dabigatran (Pradaxa)
Rivaroxaban (Xarelto)
Apixaban (Eliquis)
edoxaban

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65
Q

how do the four major DOACs work (2)

A

Dabigatran is a direct thrombin (factor II) inhibitor acting at the final step of the coagulation process preventing fibrinogen to fibrin

Rivaroxaban and Apixaban and Edoxaban inhibit a different clotting Factor - Xa (Xa in name)

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66
Q

give some advantages and disadvantages of DOACs

A

As effective as warfarin
Fast onset
Fixed doses
No blood tests
Less drug interactions
Lower risk of major bleeds
Increased risk of GI bleeding
BUT no antidote but with warfarin, vitamin K is an antidote

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67
Q

how are the 4 major DOACs administered

A

Dabigatran and Edoxaban once daily, AM or PM
Rivaroxaban and Apixaban twice daily AM and PM

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68
Q

what 2 senarios can we not omit DOAC medication for surgery

A

If the patient has started the medication or had a PE/DVT within 3 months they must be discussed with their haemotologist prior to omitting the DOAC

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69
Q

if pt is taking DOACs in the PM, when must they take their PM dose before, the night before surgery

A

6PM

70
Q

what are the post op instructions/procedures after XLA of a pt who has been taken off DOACs for surgery (5)

A

Pack the socket with haemostatic material and suture to achieve haemostasis
Advise the patient to avoid NSAIDs such as Ibuprofen, Naproxen, Diclofenac and high dose Aspirin
Use Tranexamic acid mouthwash if required
If in doubt, ask a senior member of staff for help
take PM dose as long as no bleeding and 6 hours post op

71
Q

what are the local measures for omitting DOAC before high risk bleed procedures (4)

A

once daily DOACS dabigatran and edoxaban: day before = have morning but omit if PM, day of = omit AM and have PM if 6 hours post op

twice daily DOACs apixaban and Rivaroxiban: day before = take AM and PM (aslong as before 6PM) and day of = omit AM

72
Q

what planning can be done before surgical treatment of pt with high risk bleed (herparin, warfarin, DOACs) (4)

A

laise with GP or haematologist
Plan appointment times= Morning slots, so time to sort out if problems, treat early in the week.
Only proceed if there is adequate access to emergency care, does the patient live in a rural area, do they live alone, are they mobile?
refer treatment = if on short term herparin after operation, maybe refer care until off medication

73
Q

how might we alter technique of treatment if pt with high risk of bleeding

A

Careful technique
Use aspirating syringes, administer LA slowly and atraumatically, avoid use of ID blocks where possible, consider use of articaine for mandibular infiltrations in adults (Never use articaine for ID blocks, care with mental blocks), treat tissues as atraumatically as possible

Assess bleeding as you go along and stop if unexpected bleeding occurs

Clear written post-operative instructions of who to contact (24 hours) and what to do if there is a problem

74
Q

how do we alter anaesthetic application with pts high risk of bleeding

A

use articaine infiltrations on mandible
avoid ID blocks
administer slowly and atraumatically to prevent pressure bleeds
aspirating needles

75
Q

give some packing materials for XLA post op (2)

A

oxidised cellulose
collagen sponge

76
Q

what are some local measures that we can apply post XLA (3)

A

Horizontal mattress sutures
Use haemostatic packing material e.g. oxidised cellulose, collagen sponge
Warm, wet absorbent gauze to put pressure directly on the site of extraction

77
Q

if a pt is on injectable anticoagulants, what number of units OD counts as high or low dose

A

likely to be LMWH
>5000 units O.D is likely high, treatment dose = liase with haematologist
<5000 units OD is likely low, prophylactic dose = treat as normal with local measures

78
Q

What is the main molecule that causes fibrinolysis

A

Plasmin and plasmologen
Tranexamic acid inhibits this therefore decreasing fibrin breakdown

79
Q

how do we dentally manage patients on antiplateletes (3)

A

do not need to be stopped
but bleeding risk is increased and this needs to be taken into account
may need work in stages and consider suturing/packing, consider travel after procedure

80
Q

why might a patient be on anticoagulants

A

following venous thromboembolic events
atrial fibrillation
metallic heart valves (aspirin)

81
Q

what is the only intravenous anticoagulant

A

Unfractionated heparin

82
Q

what is deltaparin

A

subcut Low molecular weight heparins = anticoagulant

83
Q

where can we get herparin

A

only in hospital
very unlikely to meet patients outside of hospital that are on herparin

84
Q

how do we monitor herparins affects

A

Monitor with the APTT test
Aim for ratio 1.8-2.8

85
Q

how is heparin excreted

A

renally

86
Q

what is a usual dose and timing of LMWH

A

once or twice a day
5000 units

87
Q

how do we dentally manage a patient on LMWH (3)

A

if on >5000 units = last dose needs to be 24 hours before , with good renal function

next dose 4 hours after dental surgery
No interruption needed if receiving a prophylactic dose

88
Q

which 5 factors does warfarin act on

A

II, VII, IX, X and VIII
vitamin K dependnat factors made in liver AND
inhibits protein C and S involved in production of factor VIII

89
Q

if putting a patient on warfarin, what must we do

A

provide another anti-coagulant whilst coming onto warfarin due to its 3–4-day onset time

90
Q

what is the INR target for patients:
Treatment of DVT/PE (3-6 months)
Atrial fibrillation (life-long)

A

2-3

91
Q

what is the INR target for patients:
Recurrent DVT/PE on warfarin (life-long)
Mechanical Heart Valves (life-long)

A

3-4 .5

92
Q

what are the reaosns a patient might have an INR target of 2-3 or 3-4.5

A

2-3 = DVT/PE for 3-6 months or AF
3-4.5 = recurrent DVT/PE on wafarin or mechanical valves

93
Q

what are side effects of warfarin

A

bleeding and easy bruising
skin necrosis (only at start of treatment) - related to protein S and C
Embryopathy (if used in first trimester of pregnancy)

94
Q

how does warfarin interact with pregnancy and what do we do about this

A

warfarin is teratogenic during the first trimester of pregnancy
we must move the patient onto dolaparin (LMWH)

95
Q

what are three reversal techniques of warfarin

A

Stop Warfarin= takes 2-3 days more like 4-6
Vitamin K (iv,(sc),o) with iv preparation 80% correction in 6hrs
Clotting Factor Concentrate such as beriplex
Containing factors II, VII, IX, X
complete correction in 10minutes
Short acting, needs vitamin K also

96
Q

what INR range allows us to safely XLA a patient who is on warfarin

A

<4

97
Q

how do we take warfarin into account during dental management

A

high risk procedure e.g. XLA = INR < 4 in past 24 hours
interactions with e,g, metronidazole due to CYP450 metabolism

98
Q

compare heparin and DOACs (2)

A

herparin = only in hospitals, nweight dependant
DOACs = can get as a prescription, set oral doses

99
Q

what is the half life of DOACs

A

6-15hours

100
Q

give some advantages and disadvantages of DOACs

A

+ low half-life, little interactions, set doses (no weight management), do not need to monitor e.g. INR

  • no antidote (apart from dabigatran)
101
Q

which DOAC has an antidote

A

dabigatran

102
Q

when do patients have DOACs

A

after AF - lifetime
acute thrombosis - high dose initially
after orthopaedic surgery - only 3-month prophylactic

103
Q

how do we manage patients taking DOACs and how does this management change

A

if on a high initial dose then wait till a stable dose
if on prophylactic dose, wait until off
if on stable medication + low risk bleed = no change
if on stable medication = high risk bleed = miss morning dose and wait to have evening dose atleast 4 hours after tx

104
Q

summarise DOAC management of a pt with a high-risk bleed procedure

A

on 1 dose/day = delay morning dose, if evening take as normal
on 2 dose/day = miss morning dose, evening as normal

105
Q

how do we treat type I VWBD

A

quantative defect
DDAVP. Some need vWF concentrate
always tranexemic acid

106
Q

how do we treat type II VWBD

A

qualatative defect
DDAVP or FVIII/vWF concentrate (depends on the subtype)
always tranexemic acid

107
Q

how do we treat type III VWBD

A

no VWBf or factor VIII
always need FVIII + vWF concentrate
always tranexemic acid

108
Q

what is beriplex

A

factor concentrate e.g. factor VIII for type A haemophilia or VWBD-3

109
Q

what are the signs and symptoms of Glanzmanns syndrome

A

heavy menstrual bleeding
heavy gingival bleeding
nose bleeds

110
Q

if going to give tranexamic acid, how do we give this to patients

A

as a mouthwash to swallow 3-4 days before the treatment
give for XLA or PMPR

111
Q

how do we contact before going ahead with any tx with a patient with a bleeding disorder

A

Contact the haemophilia centre at RHH in advance

112
Q

what would we see on a normal blood film

A

red blood cells
trinucleated neutrophils, similar in size
leukocytes, similar in size
plateletes

113
Q

what is leukaemia and what two main types are there

A

cancer of blood cells
myeloid = neutrophils
lymphoid = lymphocytes

114
Q

what is neutropenia

A

reduced neutrophils = infection

115
Q

what is anaemia

A

reduced RBCs = pallor, lethargy

116
Q

what is thrombocytopenia

A

reduced platelets = bleeding

117
Q

what is pancytopenia

A

all three blood deficiencies=
neutropenia, thrombocytopenia and anaemia

118
Q

what is acute leukemia

A

Proliferation of primitive precursor cells usually only found in bone marrow, but now found in blood
Proliferation without differentiation

119
Q

what are the four types of leukemia

A

Acute lymphoblastic leukaemia (ALL)
Acute myeloid leukaemia (AML)
Chronic lymphocytic leukaemia (CLL)
Chronic myeloid leukaemia (CML)

120
Q

what would we see on a blood slide of ALL

A

acute lymphoblastic leukaemia
blast cells = very large nucleated cells with very little cytoplasm
large undifferentiated lymphocytes

121
Q

what is Acute lymphoblastic leukaemia

A

Malignant proliferation of lymphoblasts in bone marrow
causes large blast cells in blood

122
Q

who is likely to get ALL

A

Affects mainly children where it has a good prognosis – approx. 90% cure rate
Poor prognosis in adults

123
Q

how do we treat ALL (4)

A

> 40 won’t be treated without stem cells = low prognosis
Minimum of 2-year course of intensive chemo
high prognosis in youth
Allogenic bone marrow transplant for high risk or relapsed disease
CAR-T cell therapy as salvage therapy for those eligible
Self T cells are modified to attack leukaemia cells

124
Q

what is CAR-T cell therapy and when is it used

A

modifieds T cells to attack and destroy cancerous lymphoblast cells to treat acute lymphoblastic leukaemia

125
Q

what is AML

A

acute myeloid leukaemia
malignant proliferation of myeloblasts in bone marrow

126
Q

what causes AML

A

Occurs after chemotherapy = therapy related AML
Genetics p53 mutations
Radiation exposure - chernobyl

127
Q

what type of leukaemia causes gignival hyperplasia

A

AML
Gum infiltration in acute monocytic subtype (M5) - gingival hyperplasia that reduces after chemo

128
Q

what is allogenic bone marrow

A

bone marrow taken from a healthy patient

129
Q

what is prognosis of AML

A

Affects mostly adults
Poor prognosis 15-50% 5year survival (depends on subtype)
Most patients relapse

130
Q

how do we treat AML

A

Intensive chemotherapy
Allogenic bone marrow transplant
Palliative chemotherapy
Supportive care with blood transfusions

131
Q

compare chronic and acute lymphoid cancer

A

acute = undifferentiated cells
chronnic = differentiated cells

132
Q

what is lymphocytosis

A

high lymphocyte count on blood film

133
Q

how might we diagnose CLL

A

chronic lymphocytic leukaemia
anaemia, infections, lymphadenopathy, splenomegaly, night sweats

134
Q

what is the prognosis of CLL

A

very good
living >10 years is in the norm

135
Q

what is the normal blood film lymphocyet count

A

2

136
Q

at what point would CLL be treated and why

A

not very symptomatic
only treated when symptomatic or when lymphocyte count on blood film is >10

137
Q

what are some signs and symptoms of CML

A

High white cell count & splenomegaly

138
Q

what is the Philadelphia chromosome linked with

A

this is a mutation of a chromosome that causes leukaemia
linked with CML chronic myeloid leukaemia and BCR-ABL tyrosine kinase

139
Q

what is the main cause of CML

A

90% causes by genetics
chromosomal mutation = Philadelphia chromosome
leads to increased BCR-ABL tyrosine kinase

140
Q

how do we treat CML

A

90% caused by genetics and BCR-ABL tyrosine kinase formation
most treatment is BCR-ABL tyrosine kinase inhibitors
allogenic marrow transplant is uncommon

141
Q

what are the three phases of CML

A

Chronic, Accelerated and Blast crisis (AML)

142
Q

what is Myelodysplasia

A

Abnormal production of cells within the bone marrow
Often a disease of the elderly
Can be asymptomatic
May present with anaemia, thrombocytopenia, pancytopenia (when they have red blood cell, platelet and neutrophils reduced)

143
Q

what can myelodysplasia turn into

A

acute myeloid leukaemia

144
Q

what is tx for myelodysplasia

A

Supportive care
Low dose outpatient chemotherapy in some cases
Intensive chemotherapy and bone marrow transplantation in the young

145
Q

what are the two types of lymphoma

A

hodgkin and non-hodgkin

146
Q

what are sings of hodgkins lymphoma

A

Painless lymphadenopathy
B symptoms: Sweats, Weight loss, Fever

147
Q

what are B symptoms

A

B symptoms: Sweats, Weight loss, Fever
symptoms associated with Hodgkin lymphoma and general cancer

148
Q

what are the general age groups and survival rate of Hodgkins Lymphoma

A

Two peaks 15-35yrs and >55
10year survival 90%

149
Q

how do we treat Hodkins Lymphoma

A

Chemotherapy
Radiotherapy
Autologous or allogenic stem cell transplantation

150
Q

name the 4 Myeloproliferative Disorders

A

Essential Thrombocythemia (ET) = platelet proliferation
Polycythaemia Rubra Vera (PRV) = Red cell proliferation
Chronic Myeloid Leukaemia (CML) = White cell proliferation
Myelofibrosis = Marrow stroma proliferation

151
Q

what are the main secondary causes of polycythaemia

A

Hypoxic: High altitude, lung or cyanotic heart disease
Inappropriate erythropoietin secretion: Renal tumour

152
Q

what are the main causes of primary polycythaemia`

A

Thrombosis
Splenomegaly, hepatomegaly

153
Q

why is polycythemia a problem and what are the sings of this

A

Too many RBC = stroke risk
symptoms = redness, pinkness, rosy cheeks,

154
Q

what can polycythaemia cause

A

Myelofibrosis (15-20%), AML (2-10%)

155
Q

what are secondary causes of thrombocythaemia

A

Bleeding, Infection, Inflammation, malignancy

156
Q

what are primary causes of thrombocythaemia

A

Uncontrolled malignant proliferation of megakaryocytes
Platelets persistently elevated
Arterial and venous thrombosis
Bleeding with very high counts eg >1500
Treatment with aspirin, hydroxycarbamide, anagrelide, interferon

157
Q

what is multiple myeloma

A

Malignant proliferation of plasma cells in the bone marrow

Plasma cells are terminally differentiated B lymphocytes that produce immunoglobulin

Myeloma has monoclonal immunoglobulin in blood and urine

158
Q

how do we test for multiple myeloma

A

Myeloma has monoclonal immunoglobulin in blood and urine

159
Q

what are symptoms of myeloma

A

Lytic lesions in bones = pain and pathological fractures
Hypercalcaemia due to bone resorption = thirst, polyurea, confusion, constipation
Hyperviscocity due to immunoglobulin
Renal failure
Anaemia
Infections

160
Q

what are some signs of myeloma

A

Lytic lesions cause resorption of skull bone on radiographs moth eaten skull
Plasma cells should the found in the blood
monoclonal immunoglobulin in blood and urine

161
Q

how do we diagnose myeloma

A

Blood and urine tests
X-rays and CT/MRI
Bone marrow

162
Q

how do we treat myeloma

A

Chemotherapy
Bisphosphonates
Do XLA before
Radiation
Stem cell transplantation

163
Q

what dental respresnetations of bone cancers show dentally

A

Lymphoma eg tonsillar, enlarged any lymphatic tissue
Gum hypertrophy eg Acute monocytic leukaemia
Macroglossia due to amyloid deposition

164
Q

when would we give a packed red cell transfusion and what is this

A

Packed red cells are separated from whole blood by centrifugation which also removes the majority of plasma
Indicated in severe/symptomatic anaemia, major haemorrhage

165
Q

when do we provide a platelet tranfusion

A

Thrombocytopenic patients who are bleeding or need surgery/procedures
Prophylactic to patients with reversible BM failure
Patients with platelet function disorders requiring surgery or who are bleeding

166
Q

how do we alter the way we give platelet transfusions with children and adults

A

children = we try limit number of donors and give 1 donor transfusions

167
Q

why is plasma flash frozen in FFP

A

Plasma is separated from whole blood and rapidly frozen to <-25°C to maintain the coagulation factors

168
Q

what are indications for FFP transfusions

A

Prophylactically pre surgery/procedures
As treatment in patients who are bleeding including major haemorrhage alongside RBC and plateletes
Plasma exchange
Not to be used for warfarin reversal

169
Q

explain what Cryoprecipitate is

A

Is produced by slowly thawing FFP which precipitates out FVIII, vWF, fibronectin and fibrinogen. Frozen once completed.

170
Q

what are implications for cryoprecipitate transfusions

A

Low fibrinogen e.g. DIC (bleeding or high risk), following large volume transfusions

171
Q

what are some risks of transfusion

A

volume of fluid infused – risk of circulatory overload
Allergic reactions
Alloimmunisation
Infections – acute or delayed
Electrolyte abnormalities (K+/Ca2+), hypothermia
Psychological – unable to donate blood in the future, Jehovah’s witnesses
Iron overload with repeated transfusions

3rd BDS IHD (14 decks)

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