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BDS2 BAMS > Diseases of the Blood > Flashcards

Diseases of the Blood Flashcards

1
Q

3 functions of the blood

A
  • transport nutrients
  • removal of waste
  • transport of host defences
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2
Q

what are 2 things blood needs to be able to do?

A
  • able to carry nutrients/waste/defences

- able to self repair

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3
Q

why does blood vessels need to be able to self-repair?

A

if vessel gets a hole in it needs to be able to repair itself so has no long lasting effect on platelets and coagulation

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4
Q

5 blood constitiuents

A
  • cell component
  • plasma protein (albumin, globulin)
  • lipids
  • nutrients
  • water

can replicate each individually in a lab, but getting correct balance is hard

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5
Q

FBC

A

full blood count

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6
Q

RCC

A

red blood count

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7
Q

WCC

A

white cell count

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8
Q

PLT

A

platelet count

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9
Q

HCT

A

Haematocrit

  • ratio of the volume of red blood cells to the total volume of blood.
  • proportion that is cellular compared to liquid plasma
  1. 4/0.45
    - low loosing too much or not making enough for requirements;
    - high too viscous blood
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10
Q

MCV

A

mean cell volume

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11
Q

anaemia

A

low Hb

  • Grams of Hb in litre of blood
  • Lots of RBC with low Hb and be anaemic but can equally have few of RBC with lots of Hb and not be
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12
Q

leukopenia

A

low WCC

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13
Q

thrombocytopenia

A

low platelets

Thrombocytes are responsible for platelets - clotting

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14
Q

pancytopenia

A

all blood cells reduced

Bone marrow not working properly - all low
- One cell type - specific deficiency of something (reactive change)

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15
Q

if there is one blood cell deficiency it is a….

A

reactive change

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16
Q

if there is multiple blood cell deficiencies it is due to….

A

bone marrow failure

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17
Q

polycythaemi

A

raised Hb above the reference range

opposite to anaemia

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18
Q

Leucocytosis

A

raised WCC

can occur in infection and leukaemia

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19
Q

Thrombocythemia

A

raised platelet number

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20
Q

if there is one blood cell type increase…

A

reactive or pre-neoplastic

e.g. WBC higher in infection; raised Hb in higher altitude for lower O2 levels

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21
Q

if there is multiple blood cell types increases then….

A

pre-neoplastic (myelodysplasia)

  • more than one raised cell line to get leukaemia
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22
Q

leukaemia

A

neoplastic proliferation of white cells, usually disseminated

  • high WCC
  • no lumps usually - uncommon to have lumps of white cells in circulation
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23
Q

lymphoma

A

neoplastic proliferation of white cells, usually a solid tumour

  • in circulation and then enters organ e.g. spleen, lymph nodes
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24
Q

when would a blood transfusion be used?

A

when one or more components of the blood has to be replaced quickly (blood loss)

  • red cells, platelets
  • clotting factors (fresh frozen plasma)

or when the bone marrow cannot produce cells (production problems)

but generally avoid

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25
Q

why is it dangerous to have a sudden loss in RBC?

A

lowered O2 carrying capacity

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26
Q

what can occur if have low platelet count?

A

excess bleeding

- may transfuse before extraction

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27
Q

why should blood transfusions be avoided generally?

A

can only test for what we know

- many unknown antigens and diseases of blood that could cause a bad reaction/spread when transfused

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28
Q

blood transfusion process

A

sample taken from patient

Tested against known blood types

  • Basic ABO compatibility
  • Rhesus compatibility
  • Does not always detect irregular antibodies (Too rare/unknown so cannot be tested for)

Tested against donated sample
- Take blood from transfusion packet and test
against patient
- See if any reaction occurs

Matched blood given to patient

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29
Q

group A blood has…

A

A antigens

B antibodies

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30
Q

group B blood has…

A

B antigens

A antibodies

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31
Q

group AB blood has…

A

A and B antigens

no antibodies

32
Q

group O blood has…

A

no antigens

A and B antibodies

33
Q

what is cross matching?

A
  • Take blood sample
  • Antibodies in blood
  • Compare against patient sample
34
Q

what blood type can be given to anyone?

A

O

  • no known (A/B) antigens present so cannot stick to any antibodies
  • no coagulation will occur
35
Q

what blood type can receive any blood?

A

AB

  • no known (A/B) antibodies present so cannot stick to any antigens transfused to them
  • no coagualtion
36
Q

3 transfusion complications

A
  • incompatible blood
  • fluid overload
  • transmission of infection
37
Q

what will happen if a patient is transfused incompatible blood?

A 
RBC lysis (burst)
- fever, jaundice, death
38
Q

what will happen if a patient has a blood fluid overload after transfusion?

A

heart failure

  • If healthy physiology and enough blood volume - when give them extra blood also gives extra fluid
  • If they have heart pump issue - can exacerbate due to extra fluid so lead to heart failure more in elderly
39
Q

what infections can be transferred in a blood transfusion?

A

Blood borne viruses
- CMV, Hepatitis B, Hepatitis C, HIV, TT virus

Prion Disease
- vCJD

Bacterial Infections
- Syphilis

40
Q

is the coagulation cascade off when there is no local damage?

A

no - low level of coagulation turnover all the time

when damaged, get local chemical alterations which makes the process happen more rapidly in the area of need

41
Q

how long can you be ok if stop making clotting factor?

A

1-2 days as there is a level present in the tissue due to the constant low level coagulation system

42
Q

what does the coagulation cascade rate depend on?

A

forward enzymes against inhibitors (protein C and S)

43
Q

fibrinolysis

A

break down of clot

44
Q

3 components of haemostatic disorders

A
  • vascular component
  • cellular component
  • coagulation component
45
Q

what is the vascular component of haemostatic disorders?

A

retraction of the vessel (collagen disorder)

  • hole smaller
  • Inherited disorders of collagen - abnormal collagen, doesn’t behave how they should
46
Q

what is the cellular component of haemostatic disorders?

A

Platelets number and function

  • Plug hole
  • Dynamic quick changes
  • Can form antibodies to platelets take out of circulation for a while
47
Q

what is the coagulation component of haemostatic disorders?

A
  • adequate clotting (fibrin on top to stabilise it)

- adequate clot lysis

48
Q

how can we assess platelet number?

A

FBC

49
Q

how can we asses platelet function?

A

‘bleeding time’

unpleasant test

50
Q

what drugs effect platelet function?

A

Aspirin and NSAIDs

  • permanent effect on platelets
  • 7-10 days to form new platelets
  • Platelet adhesion altered for life span of cell
51
Q

if platelet count is correct then how will they be expected to function?

A

normally

52
Q

if there is a preneoplastic platelet count how will they be expected to function?

A

huge excess of platelets

often not normal function

53
Q

if there is too few platelets how will they be expected to function?

A

work normally but not enough

54
Q

what are the 3 factors for the coagulation component of haemostatic disorders?

A
  • adequate amount of clotting factors
  • adequate range of clotting factors
  • proper balance between thrombotic and thrombolytic/fibrinolytic systems
55
Q

what determines if there is an adequate amount of clotting factors coagulation?

A

synthesis and consumption

  • Balance of make and use
  • Drug can interfere with clotting factor synthesis
  • Whole dynamic system run faster after trauma may run out quicker than anticipated
56
Q

what determines if there is an adequate range of clotting factors for coagulation?

A

hereditary deficiency - VIII, IX 9but also 5 and 110

Replace the one CF and should return to normal

  • Not all or nothing - spectrum of disease depend on proportion that you make, reserve in body
  • e.g. haemophilia more men than women as X chromosome linked clotting factor as one wrong than 50% still made whereas men with abnormal X and Y so can may only have a small level of normal

Level of function of chromosome reflects level made
- Can get mid to severe haemophillicas dependnent on how much is expressed

57
Q

when can you get increased tendencies to form blood clots?

A

under active systems e.g. on a plane, inactive

  • leg or arm thrombosis
58
Q

what controls blood clot formation and brekdown mainly?

A

blood vessel walls (endothelium)
cascading factors in blood

local chemical mediators make system faster in area
- tissue factors

59
Q

what are visual signs of poor coagulation history? (3)

A
  • purpura
  • ecchymosis
  • petechiae
60
Q

what investigations can be down if a patient has a haemstatic disorder? (history of bleeding)

A

FBC (platelet numbers) sensible

Bleeding time (platelet function) tend not to be done, but can assess function

INR & APPT

LFT (Clotting factor synthesis)

  • Ability of body to make prothrombin (how well can produce a clot)
  • Test how well system works and how well can make clotting factors (liver function is inflammatory enzymes but no use for blood - need to see if liver has made clotting factors)
61
Q

what is haemophilia?

A

inherited deficiency of factor VIII or IX

types A and B

62
Q

what sex is affected more by haemophilia?

A

males

X chromosome associated condition

63
Q

what is Thrombophilia?

A

excessive tendency to clot
- usually DVT (life threatening due to pulmonary embolism - clot block heart, wedge valve, no longer pump)

opposite to haemophilia

64
Q

what can exacerbate Thrombophilia?

A
  • Smoking
  • Immobility – travel
  • Surgery
  • Pregnancy
  • Medicines – oestrogen contraceptive pill

but genetically preconditioned

65
Q

what can be used to reduces risk of unnecessary clot and thrombophilia?

A

anticoagulant medicines

66
Q

what is therapeutic coagulopathy?

A

Where the coagulation system is manipulated by medicine to make clotting less likely.

either
- Reduce platelet adhesion and function (Usually prevent arterial thrombosis)

or

  • Reduce activity in the coagulation cascade (Usually prevent venous thrombosis)
67
Q

when would therapeutic coagulopathy be used?

A

Normal human and make blood clot less
- E.g. artificial heart valve don’t want to clot on this to cause it blocking

Give anticoagulants in people more prone to have clots

68
Q

standard antiplatelet drug examples

A
  • aspirin
  • dipyrimadole
  • clopidogrel
69
Q

new antiplatelet drug examples

A
  • prasugrel

- ticagrelor

70
Q

standard anticoagulant drug example

A

warfarin

71
Q

new anticoagulant drug example

A
  • apixiban
  • dabigatran
  • rivaroxaban
72
Q

what are dental aspects of haemostatic disorders?

A

ALWAYS LOOK for bleeding problems!

  • skin - red spots or purpura
  • mucosa - purpura or blood blisters

If in doubt TEST first
- FBC (Platelets), INR, APTT (activated partial thromboplastin time)

If known haemostatic problem ASK ADVICE from a dental specialist
- Before any treatment

Follow available SDCEP Guidance for dental care delivery

REMEMBER Local haemostatic measures
- make clotting more likely and excessive bleeding less

73
Q

porphyria

A

abnormality of haem metabolism

very serious

most people unaware they have it until have an acute episode

74
Q

2 main groups of porphyria

A

hepatic porphyrias

erythropoietic porphyrias

75
Q

clinical effects of acute porphyria episodes

A

Photosensitive rash (at any time)

Neuropsychiatric disturbance in acute attacks (strange, unpredictable behaviour)

  • Motor & sensory changes, seizures
  • Autonomic disturbances

Hypertension & tachycardia

May be fatal

76
Q

what can trigger acute porphyria episodes?

A

poorly understood

  • many drugs - Including local aesthetic and commonly prescribed
  • Pregnancy
  • acute infections
  • alcohol
  • fasting
77
Q

what are dental consideration in relation to porphyrias?

A

drug administration- Be VERY cautious about this

  • Could be consequence when prescribe anything or give LA - can trigger unknown
  • Read in BNF as soon as they say - as very severe

One possible cause of ‘local anaesthetic allergy’ reported by patients

BDS2 BAMS (54 decks)

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