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Haemotology Flashcards

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1
Q

Why do blood groups occur?

A

Antigens expressed on cell surface
Two different types - A and B, can have either, neither or both
A and B are co dominant, O is recessive

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2
Q

Why are blood groups important?

A

Will have antibodies against antigens you do not have as are ubiquitous in organisms, including gut flora

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3
Q

Who are the universal donors/receivers for:
Blood?
Plasma products?

A

Blood - universal receiver AB, donor O

Opposite for plasma - Reciever O, donor AB

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4
Q

Why is anti-RhD (resus) important?

A

Resus negative can make anti RhD if exposed (in transfusion or pregnancy)
Can cause haemolytic crisis in newborns/in transfusions in future

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5
Q

What are blood donors tested for?

A

ABO/Rh blood groups
Hep viruses, HIV, syphilis
Other viruses

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6
Q

What blood products are formed from the components?

A

Buffy coat can be separated
>platelets
>white cells

Plasma can be separated into
>Clotting/coagulation factors
>Albumin
>Antibodies

Red blood cells are not separated

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7
Q

What are the indications for red cell transfusion?

A

To correct severe acute anaemia, which might otherwise cause organ damage
To improve quality of life in patient with otherwise uncorrectable anaemia
To prepare a patient for surgery or speed up recovery
To reverse damage caused by patient’s own red cells

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8
Q

What are the indications for platlets?

A

Massive haemorrhage
Bone marrow failure
Prophylaxis for surgery
Cardiopulmonary bypass

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9
Q

What are the plasma components?

A

Fresh frozen plasma

Cyroprecipitate

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10
Q

What is the coombs test?

A

Antihuman immunoglobulin added to blood, if they bunch up (haemolyse) then it is positive

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11
Q

What bloods do you use for red cell availability in:
Needed in minutes?
Urgently needed?
Non-urgent?

A

Minutes – O RhD Neg red cells (AB plasma)
Urgent – Type specific (ABO/ RhD)
Non-urgent – Full cross match
Select correct ABO/ RhD type
if allo-antibodies choose antigen negative blood

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12
Q

What is the major haemorrhage protocol?

A

call 2222
Major haemorrhage protocol activate + ward/location
Bloods delivered ASAP

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13
Q

What are the risks of blood transfusions?

A 
TACO
TRALI
ATR
Febrile, Allergic, 
vCJD risk
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14
Q

What is TACO?

A

Transfusion associated circulatory overload

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15
Q

What is TRALI?

A

Transfusion related acute lung injury

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16
Q

What steps have been taken to reduce prion disease?

A

Leucodepletion 1998
UK plasma not used for fractionation
Imported FFP for all patients born after 1996

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17
Q

How do you stop haemolytic disease of the newborn?

A

Prophylatic Anti-D

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18
Q

What hormones regluate stem cells (and can be used therapeutically)?

A

erythropoietin,
G-CSF,
thrombopoietin agon

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19
Q

What is the pathway for erthroid differentiation?

A

Erythroblast–>
reticulocyte–>
erythrocyte

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20
Q

What is ertyhropoetin?

A

A hormone produced by kidneys made in response to hypoxia

Increases red cell count

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21
Q

What is reticylocyte count?

A

A measure of red cell production

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22
Q

What are platelets?

A

Cells with immune an haemostastic functions
Production regulated by thrombopoetin
7 days lifespan

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23
Q

What is thrombopoetin?

A

Hromone produced in liver
Regulated by plaelet mass feedback
Agonists can be used therapeutically

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24
Q

What pathology affects platelets?

A

Thrombocytosis
>In Myeloid Malignancies: Dominic Culligan

Thrombocytopenia
>Marrow failure
>Immune destruction: ITP: Henry Watson

Altered function
>aspirin, clopidogrel, abciximab etc

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25
What are neutrophils?
Target pathogens, especially bacteria/fungi Include inerleukins Production regulated by granulocyte-colony stimulating factor (G-CSF) Regulated by immune responses
26
What are the stages of neutrophil differentiation?
``` Blast Promyelocyte Myleocyte Metamyelocyte Neutrophil ```
27
What can cause netrophilia?
Infection >Left shift, toxic granulation Inflammation >eg MI, postoperative, rheumatoid arthritis
28
What can cause neutropenia?
``` ‘Racial’ Decreased production >Drugs >Marrow failure Increased consumption >Sepsis >Autoimmune Altered function >eg chronic granulomatous disease ```
29
What are monocytes?
Macrophages inside blood | phagocytic cells for injestion of pathogens
30
What are the other meyloid cells?
Eosinophils | Basophils
31
What are lymphocytes?
Small white blood cells (include T/B cells) Produced in bone marrow >B cells mature in bone marrow, T cells in thymus Circulate in blood, lymph and lymph nodes Differentiate into effector cells in secondary lymphoid organs (lymph nodes or mucosal associated lymphoid tissue) A part of the adaptive, and immune mediates systems
32
What lymphocytes disease?
Lymphocytosis >Infectious mononucleosis >Pertussis Lymphopenia >Usually post-viral >lymphoma
33
What are the subtypes of lymphocytes?
B cells – make antibodies T cells – Helper, cytotoxic, regulatory NK cells
34
How do B cell mature?
``` Progenitor B cells Pre B cells Immature B cells Naive B cells Germinal cenre Controcyte Then either Memory B cell or plasma B cell ```
35
What is positive/negative selection of B cells?
if gene rearrangement results in a functional receptor the cell is selected to survive – positive selection If the receptor recognises ‘self’ antigens - the cell is triggered to die – negative selection: tolerance B cells that survive this selection are exported to the periphery
36
What are the types of human leucocyte antigen?
Class I: displays internal antigens on all nucleated cells | Class II: displays antigens eaten by professional antigen presenting cells
37
What is included ina full blood count?
``` Haemoglobin RBC Platlets WBC Neutrophils Lymphocytes >Monoyctes >Eosinophils >Basophils ```
38
What are the different diagnostic tools?
``` FBC Clotting times Bleeding times (platelets) Cehmical assays >Ferritin >B12 >Folate Marrow aspirate Lymph node biopsy ```
39
What can cause splenomegaly?
``` Infectious Haematological-malignant >various leukaemias and lymphomas >myeloproliferative disorders Portal hypertension Haemolytic disorders Connective tissue disorders Sarcoid Malignant Amyloid ```
40
What is anaemia?
Reduction in red cells of haemoglobin content
41
What are the main substnaces needed for red blood cell production?
Iron B12 Folic acid Erythropoetin
42
How are red blood cells broken down?
Macrophages in spleen start process (can calso occur in liver lymph nodes etc) Globin is broken into amino acids which is reutilised Haem - the iron is reused, the rest is converted to bilverdin, quickly converted to bilirubin
43
What can genetic defects in red blood cells affect?
The red cell membrane Metabolic pathways (enzymes) Haemoglobin
44
What 5 proteins are often affected in hereditary spherocytosis?
``` Ankyrin Alpha Spectrin Beta Spectrin Band 3 Protein 4.2 ```
45
What is hereditary spherocytosis?
``` Mostly autosomal dominant disease Where red blood cells are spherical Clinical presentation variable >Anaemia >Splenomegaly >pigment gallstones ```
46
How do you treat hereditary spherocytosis?
Folic acid (increased requirements) Transfusion Splenectomy
47
What are the red cell enzymes commonly disrupted?
Pryvuate kinase | Glucose-6-phosphate dehydrogenase
48
What is the function of the pentose phosphate shunt?
Protects from oxidative damage
49
What is G6PD deficiency?
Commonest disease causing enzymopathy in the world Cells vulnerable to oxidative damage Confers protection against malaria >Most common in malarial (or historically) areas X Linked
50
What is the presentation of G6PD deficiency?
``` Get blister/bite cells Variable clinical presentation Neonatal jaundice Splenomegaly Broad-bean/infection precipitated jaundice/anaemia ```
51
What is pyruvate kinase deficiency?
Reduced ATP Increased 2,3-DPG Cells rigid Variable severity >Anaemia >Jaundice >gallstones
52
What is normal adult haemoglobin?
2 alapha chains 2 Beta chains Feotal and A2 also exist in smaller amounts, being alpha gamma and alpha delta respectively
53
What are the genes for haemoglobin?
2x2 alpha genes on chr16 2x: gamma gamma delta beta on chr 11 >Means that if beta is defective, delta still works
54
What are haemoglobinopathies?
Inherited abnormalities of haemoglobin synthesis Reduced or absent globin chain production >Thalassaemia (alpha α, Beta β, delta δ, gamma γ) Mutations leading to structurally abnormal globin chain >eg sickle cell
55
What is the mutation in skicle cell disease?
beta chains are slightly defective, | results in cell changing shape permanently after being exposed to hypoxia
56
What are the consequences of sickle cell disease?
Haemolysis leading to vaso-oclusion This then elads to acute chest syndrome, stroke and pain Redced life expectancy (mainly due to childhood/perinatal mortality)
57
What is the clinical presentation of sickle cell disease?
``` Increased infection risk Painful vasoocclusive crisis Stroke Chest crisis Chromic haemolytic anaemia Sequestation crises ```
58
How do you treat a painful crisis of sickle cell?
``` Analgesia within 30 mins (opiates) Hydration Oxygen Consider antibiotics No routine role for transfusion ```
59
What is a chest crisis of sickel cell and how do you managE?
Chest Pain Fever Worsening hypoxia Infiltrates on CXRay ``` Manage: Respiratory Support Antibiotics IV Fluids Analgaesia Transfusion ```
60
What is the long term management for sickle cell?
Vaccination Penicillin prophylaxis Folic acid Be careful if needing regular transfusions for iron overload
61
What are the different thalassaemias?
Homozygous alpha zero thalassaemia (a0/a0) - incompatable with life Beta thalassaemia mahor >No beta chains >A transfusion dependanet anaemia Non transfusion dependent Thalsaemia minor - traits/carrier states
62
What is beta thalasemia major?
``` Severe anaemia Present at 3-6 months of age Expansion of ineffective bone marrow Bony deformities Splenomegaly Growth retardation ```
63
How do you treat thalassaemia major?
Chronic transfusion support - 4-6 weekly >Normal growth and development >BUT - Iron overloading >Death in 2nd or 3rd decades due to heart/liver/endocrine failure if iron loading untreated
64
How do you stop iron overloadinh?
Iron chelation therapy s/c desferrioxamine infusions (desferal) Oral deferasirox (exjade)
65
What is sideroblastic anaemia?
Defects in mitochondrial steps of haem synthesis >ALA synthase mutations >Hereditary (X-Linked) >Aquired - Myelodysplasia
66
What factors affect the normal range of haemoglobin?
``` Age Sex Ethnic origin Time of day of sample Time taken to analyse ```
67
What are the general features of anaemia?
``` Tiredness/pallor Breathlessness Swelling of ankles Dizziness Chest pain Depend on age and Hb level Others relating to underlying cause ```
68
What can cause anaemia?
Disruption of bone marrow Disruption of red cells Destruction/loss of red blood cells
69
What are red cell indices?
``` MCV = Mean cell volume (cell size) MCH = Mean cell haemoglobin ```
70
What are the three types of anaemia?
Hypochromic microcytic Normochormic normocytic Macrocytic
71
How do you investigate the different anaemias?
Hypochromic microcytic - serum ferritin >Normally caused by low iron Normochormic normcytic - reticulocyte count >Tells if bone marrow working well or not Macrocytic >B12/folate then bone marrow tests >Most common cause B12/folate deficency, underlying bone marrow dysplasia
72
What are the causes of Hypochromic microcytic anaemia?
Low ferritin - iron deficiency Normal/high ferritin >Thalassaemia >Secondary anaemia
73
How is iron transported?
Transported from enterocytes and macrophages by ferroportin Transported in plasma bound to transferrin Stored in cells as ferritin Hepicidin (liver protein during inflammation) blocks ferroportin
74
What is iron deficiency anaemia?
Commonest cause But description not diagnosis Look for cause - ie bleeding, diet, requirements, malabsorption?
75
What are the clinical features of iron deficiency anaemia?
Angular cheilitis/stomatitis Atrophic tongue Koilonychia
76
How do you manage iron deficiency anaemia?
Correct deficiency >Oral sufficienct, IV if oral intolerable ``` Correct cause >Diet >Ulcer therpay >Gynae interventions >Surgery ```
77
What are the causes of normochromic/cytic anaemia anaemia?
Increased reticocyte count >Acute blood loss >Haemolysis Normal/low >Secondary anaemia Hypoplasia
78
What is haemolytic anaemia?
Accelerated red cell destruction (dec Hb) Compensation by bone marrow ( inc Retics) Haemolysis either extra (normal) or intravasculae
79
What can cause haemolytic anaemia?
``` Congenital Hereditary spherocytosis (HS) Enzyme deficiency (G6PD deficiency) ``` Acquired (split into immune/ non immune with immune being extra, non being intra mostly) Auto-immune haemolytic anaemia (Extravascular Severe infection Artifical valve
80
How do you tell if a haemolytic disease is immune mediated or not?
Do a direct antiglobulin test | If positive it is autoimmune, if negative it is not
81
How do you diagnose haemolysis?
FBC, reticulocyte count, blood film Serum bilirubin (direct/indirect), LDH Serum haptoglobin Then check mechanism >blood film, coombs tess
82
How do you manage haemolytic anaemia?
``` Support marrow function Folic acid Correct cause >Immunosuppression if autoimmune Remove site of red cell destruction Treat sepsis, leaky prosthetic valve, malignancy etc. if intravascular ```
83
What is secondary anaemia?
70% normochromic normocytic 30% hypochromic microcytic Defective iron utilisation >Increased hepcidin in inflammation >Ferritin often elevated Identifiable underlying disease
84
What are the causes of macrocytic anaemia?
``` Megoblastic - B12/folate defiency (the definition) Or non megablastic >Myelodysplasia >Marrow infiltration >Drugs ```
85
What are the causes of B12 deficiency?
Pernicious anaemia | Gastric/ileal disease
86
What are the causes of folate deficiency?
``` Dietary Increased requirements (haemolysis) GI pathology (eg.coeliac disease) ```
87
What is pernicious anaemia?
``` Commonest cause of B12 deficiency in western populations Autoimmune disease Antibodies against >intrinsic factor (diagnostic) >gastric parietal cells (less specific) ``` Leads to malabsorption of dietary B12 Symptoms take up to 1-2 years to develop
88
How do you treat megaloblastic anaemia?
Replace vitamin B12 deficiency >B12 intramuscular injection >Loading dose then 3 monthly maintenance Folate deficiency >Oral folate replacement >Ensure B12 normal if neuropathic symptoms
89
What allows for normal blood flow?
Although ability to clot is always present, the endothelium encourages flow with smooth "non stick" surface
90
What factors contribute towards how long you bleed for?
``` Platelets Coagulation factors (fibrin clot) ``` Natural anticoagulants limit clot to that area
91
What is the clotting process when a blood vessel is damaged?
Platelets and coagulation factors become sticky in response to tissue factors
92
What can activate platelets/coagulation factors?
Abnormal Surface | Physiological activator
93
What are the roles of platelets in haemostasis?
Adhering Activation Aggregation Providing surface for Coagulation

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