Blood Flashcards
(85 cards)
1
Q
How much of the blood is plasma?
A
55%
2
Q
How much of the blood is RBC?
A
45%
3
Q
How much of the blood is the buffy coat?
A
less than 1%
4
Q
What is the buffy coat made up of?
A
leukocytes and platelets
5
Q
What do macrophages differentiate from?
A
Monocytes
6
Q
What do basophils, eosinophils, neutrophils and monocytes differentiate from?
A
Myeloblasts
7
Q
Where does haematpoeisis occur?
A
Bone marrow
8
Q
Where does haematopoeisis occur in an embryo?
A
Yolk sac then liver and spleen
9
Q
What is the lifespan of RBC?
A
120 days
10
Q
What is the life span of white blood cells?
A
6 hours
11
Q
What is the lifespan of platelets?
A
7-10 days
12
Q
What are old/dying cells removed by?
A
Spleen
13
Q
What stimulates and controls blood cell production?
A
Hormones
Red cells: erythropoietin (EPO)
White cells: granulocyte colony stimulating factor (GCSF)
Platelets: thrombopoietin (TPO)
14
Q
What is erythropoietin?
A
a hormone produced by the kidney that promotes the formation of red blood cells by the bone marrow. The kidney cells that make erythropoietin are sensitive to low oxygen levels in the blood that travels through the kidney
15
Q
What shape is RBC?
A
biconcave disc
16
Q
What does haemoglobin carry?
A
Oxygen
17
Q
How many RBC in blood?
A
4x10^12/L
18
Q
What is a polycythaemia?
A
Increase in red cells:
Raised erythropoietin
Hypoxia
Reduction in plasma volume:
Dehydration
Smokers
19
Q
What are platelets made from?
A
Megakaryocytes in bone marrow
20
Q
What is the normal platelet range?
A
140-400x10^9/L
21
Q
What is the condition called for low platelets?
A
thrombocytopenia
Platelets <80 increased risk of bleeding
Platelets < 20 spontaneous bleeding / bruising
22
Q
What is the condition called for high platelets?
A
thrombocytosis
Increased rates of arterial and venous thrombosis
23
Q
What do neutrophils do?
A
Phagocytose and kill bacteria
Increased in bacterial infections (neutrophilia)
Release cytokines which cause inflammatory response eg temperature
24
Q
What do coagulation factors convert?
A
Convert soluble fibrinogen into insoluble fibrin polymer
25
What are the 2 most important systems of red cell antigens?
ABO and Rhesus
26
What are the Rhesus blood groups?
Complex system of C, D and E antigens
| D is the most important
27
Why is anti-D important?
pregnant women given anti D to prevent sensitisation. The anti-D immunoglobulin neutralises any RhD positive antigens that may have entered the mother's blood during pregnancy. If the antigens have been neutralised, the mother's blood won't produce antibodies.
Rhesus disease can largely be prevented by having an injection of a medication called anti-D immunoglobulin. This can help to avoid a process known as sensitisation, which is when a woman with RhD negative blood is exposed to RhD positive blood and develops an immune response to it.
28
What are the indications of blood transfusion?
Hypovolaemia due to blood loss
Severe anaemia with symptoms due to inadequate tissue oxygenation (transfusion trigger often = 80 g/L)
Anaemia that cannot be corrected by bone marrow function
29
When is blood transfusion not indicated?
Not indicated for iron deficiency or B12/ folate deficiency.
Not indicated for minor blood loss, especially if fit and healthy
Not indicated for asymptomatic anaemia
30
What are the risks of a blood transfusion?
ABO incompatibility reaction – can be rapidly fatal
Delayed transfusion reactions
Fever, hives
Fluid overload, pulmonary oedema
```
Infections:
Bacterial
Viral (HIV, hepatitis B and C)
Malaria
Prions (vCJD)
```
Long term – iron overload: damage to heart, liver
31
What cells does HIV invade?
CD4 cells
32
What is leukaemia?
Malignancy of (white) blood cells
Acute leukaemia: proliferation of immature cells without differentiation
Chronic leukaemias: proliferation with differentiation
33
What are the symptoms of leukaemia?
Anaemia (fatigue, pallor)
Neutropenia (infections)
Thrombocytopenia (bleeding & bruising)
34
Which cells does acute myeloid leukaemia affect?
Myeloblast
35
Which cells does acute lymophoblastic leukaemia affect?
Common lymphoid progenitor
36
Which cells do chronic myeloid leukaemia affect?
```
Megakaryocyte
basophil
neutrophil
eosinophil
monocyte
```
37
Which leukaemia primarily affects children?
Acute lymphoblastic leukaemia - chemo 2-3 years
38
What is the treatment for acute myeloid leukaemia?
High dose chemo, possible bone marrow transplant
39
What causes chronic myeloid leukaemia?
Translocation between chromosomes 9 and 22
Forms “Philadelphia” chromosome
40
What is the treatment for chronic myeloid leukaemia?
Targeted therapy (tablets)
Imatinib
Survival – similar to general population
41
What is the treatment for chronic lymphocytic leukaemia?
Gentle, outpatient chemotherapy
More targeted oral treatments becoming available
Survival – several decades
42
What causes chronic lymphocytic leukaemia?
Proliferation of mature lymphocytes (usually B cells)
43
What is lymphocytosis?
a high lymphocyte count, is an increase in white blood cells called lymphocytes.
44
What is lymphoma?
Malignancy of lymphoid cells, predominantly in lymph nodes
45
What are the two types of lymphomas?
Hodgkin’s lymphoma
| Non Hodgkin lymphoma
46
How is high grade lymphoma treated?
Aggressive, acute, treat with chemotherapy / curable
47
How is low grade lymphoma treated?
Chronic, indolent, may not require treatment / incurable
48
What is a Myeloma?
Malignant proliferation of plasma cells
| Produces monoclonal immunoglobulin (paraprotein)
49
What are the clinical features of myeloma?
Calcium (hypercalcaemia – bone pain, constipation)
Renal failure
Anaemia
Bone lesions (lytic lesions, fractures, pain)
50
What is the treatment for myeloma?
Treatment – outpatient, mainly oral chemotherapy
51
What are the two methods of creating an intravascular solid?
Coagulation - protein level
Platelets - cellular level
52
What are the 2 pathways of coagulation?
Intrinsic pathway
Extrinsic pathway
coalesce to form same final common pathway
53
What is the intrinsic pathway triggered by?
Negatively charged molecules from endothelial trauma (phospholipids released into blood) and factor XII (9) - this activates coagulation on the inside of the vessel
54
What is the extrinsic pathway triggered by?
Blood starts leaking out - comes into contact with subendothelial tissue just under endothelial layer, which contains collagen that activates the extrinsic pathway
55
What reaction happens at the end of the coagulation cascade
FIbrongen --> fibrin by an enzyme
56
Which test measures the extrinsic pathway and the final common pathway?
Prothrombin time -PT
| INR - international normalised time
57
Which test measures the intrinsic pathway and the final common pathway?
APTT - activated partial thromboplastin time
58
How is blood stopped from coagulating when taking it to measure it? and how is this reversed in the lab?
Blood collected in CITRATE - lemon juice
this chelates Ca2+ (removes)
Ca2+ is clotting factor IV; required for both intrinsic and extrinsic pathways
In lab, an excess of Ca2+ is added to overcome citrate and then other things are added to activate either extrinsic or intrinsic pathway
tissue factor for extrinsic
phospholipid for intrinsic
59
How is prothombin time measured?
Tissue factor added to blood sample in lab, and time how long to clot
Measure factors I, II, VII and X (1, 2, 7, 10) - 2, 7, 9, 10 - inhibited by warfarin
60
What is INR?
Patient’s PT: normal PT
Under specific laboratory conditions - 25 degree c at sea level etc
Used to assess Warfarin’s effect
INR of 2 - patient's extrinsic pathway of coagulation is twice as long under specific laboratory condition
61
What is APTT?
Activated Partial Thromboplastin Time
Phospholipid, silica & Ca2+ added to sample
Time how long to clot formation
- measure intrinsic and final common pathway
- measures factors I, II, V, VIII, IX, X, XI, XII
2, 9, 10 - warfarin also affects APTT but not measured
VIII (8) and IX deficiency (9) - haemophilia
62
Which factors that are deficient cause haemophilia?
VIII (8) and IX deficiency (9) - haemophilia - prolonged APTT, normal PT
63
What are the causes of haemostatic problems?
Congenital bleeding disorders:
- Haemophilia - A = factor 8 deficiency VII
B - factor 9 deficiency IX
(increased APTT)
- von willebrand's - shortage of VWBF which are important in platelet adhesion - which increases bleeding time (marker of platelet function), VWBF binds to factor 8 and stops it being broken down in the blood which causes increased APTT
Acquired bleeding disorders:
- medical conditions:
Liver:
- cancer. cirrhosis/jaundice, paracetamol overdose (PT is the first marker of the failing liver)
Kidney:
- related to platelet function not number
- prolonged bleeding time
- will be on heparin (blood thinner) during dialysis, if they need a tooth out, schedule for non-heparin day.
Cardiac (due to drugs…)
Cancer (due to drugs or myelosupression - bone marrow suppressed, RBC and platelets production lower)
ITP - immunothromboperpura, ITTP - idiopathic version of the above
- drugs:
- warfarin
-aspirin
-clopidogrel
-heparin
new, more predictable so don't need regular weekly INR tests:
- dabigatran (direct thrombin inhibitor)
- rivaroxaban (directed activated factor X)
64
Where are all vitamin K dependent coagulation factors produced?
In the liver
| liver makes most coagulation factors - all vitamin K but other non vitamin K factors produced here too
65
Where is aspirin first metabolised?
Liver - main therapeutic effect needs to be within hepatic portal vein before reaching liver because liver will take it out
66
What is the reason for efficacy of aspirin?
Reason for efficacy is IRREVERSIBLE INACTIVATION of COX within platelets - platelet function is reduced
Lasts the life of the platelet
Reversal requires 7 days of discontinuation
67
What is the simplified Arachidonic acid pathway?
arachidonic acid is metabolised into other things in inflammation e.g. leukotrienes - attracts wbc
metabolisd into prostaglandins via COX 1, 2, 3- pain and regulated gastric regulation
metabolised into thromboxane A2, TXA2 - platelet aggregating factor attracts other platelets, if blocked irreversibly, then antiplatelet effect
68
What does vitamin K do to factors 2, 7, 9, 10 and Protein C and S?
Activates them when vitamin K changes to vitamin K epoxide
vitamin K is co-factor for this reaction
then vitamin K epoxide turns back to vitamin K via vit K epoxide reductase
warfarin blocks vit K epoxide turning back so factors aren't becoming active - coagulated state
A lot of vitamin K can reverse effects of warfarin to drive reaction forward and produce more active factors
69
What does heparin bind to?
Binds to and activates antithrombin III - this molecules blocks factor 10 and 2
70
What chemical reverses heparin?
protamine sulphate
71
How does clopidogrel work?
Affects platelet function
it's a P2Y 12 inhibitor - important receptor of the platelet
P2Y12 involved in platelet aggregation and linking to the fibrin meshwork
72
How can you avoid haemorrhage in certain patients?
Warfarinised patient
- check INR within 72hrs of procedure
- INR <4 (if greater than 4, don't take tooth out)
- avoid ID blocks where possible
Antiplatelets patient (aspirin, clopidogrel, dipyridamole)
- monotherapy - continue as planned
- if on multiple drugs, no evidence of increases bleeding risk but may consider hospital-based treatment
Haemophilia/VWB
- Liase with haematologist
- give DDAVP - for haemophilia A desmopressin
- Recombinant factor A - VIII/ B - IX
- mild may need no preoperative management
- Tranexamic acid - procoagulant afterwards
NOACS: SDCEP guidelines - exam question
- if 3 more more teeth, or if surgical extraction carry on as normal
- once a day med - stop on morning of surgery, then take 4 hour after extraction
- twice a day med - generally omit morning dose
73
What are the types of haemorrhage
Primary
– as soon as tooth is removed
– will be due to bleeding disorder or local cause
Reactionary
– not immediate, but within 48hrs of extraction
– ETOH, exercise, heat, anaesthetic wearing off
Secondary
- approximately 1 week after surgery, due to infection e.g. ENT
74
What are the standard measures to achieve haemostasis in any tooth?
- firm pressure/ bite on gauze
- compress socket
- post-op instructions (reactionary haemorrhage)
75
What are the 2 potential sources of bleeding after an extraction?
1. Bone - haemostatic pack in socket
2. Gingivae- suture
Do both
76
What can you use to pack the bone?
Surgicel
- resorbable oxidised cellulose
helps clot form
Gelatin sponge
- absorbs up to 45 times own weight in blood
pressure tamponades bleed
77
How does suturing help achieve haemostasis?
Will compress gingival blood supply, stemming soft tissue bleed
Also will act to prevent haemostatic pack from falling out
78
How can you manage an ongoing bleed? (drugs)
Tranexamc acid
May need reversal of anticoagulant if possible
- warfarin - omit/vitamin K given
- Heparing - omit/protamine sulphate given
Need to weigh up against risks of thrombosis, and is actually very rarely done where INR has been correctly checked pre-op
Accept very small amount of oozing for a few days if known bleeding disorder
79
What tests would you do if there was an ongoing bleed of an unknown cause?
- Coagulation screen/ bleeding time
- Full blood count (platelets)
- Factor assay
80
How does aspirin have its effects?
Irreversible inhibits COX, preventing TXA2 formation and therefore platelet aggregation
81
What blood test is INR a ratio of?
PT - prothrombin time
82
Give 4 measure to deal with haemorrhage from a dental socket
```
Pressure/bite on gauze
stitch
pack
Tranexamic acid
Local anaesthetic injection - vasoconstriction adrenaline
```
83
How is the action of warfarin reversed in a severe, life threatening event?
Vitamin K, 2-10mg
84
How does DDAVP react?
Induces release of factor VIII from a vascular endothelia into circulation
85
What other names are there for DDAVP?
Desmopressin
Synthetic vasopressin
Synthetic ADH
