Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Conditions + definitions > Haemotology > Flashcards

Haemotology Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are blood donors tested for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the indications for platlets?

A

Massive haemorrhage
Bone marrow failure
Prophylaxis for surgery
Cardiopulmonary bypass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the plasma components?

A

Fresh frozen plasma

Cyroprecipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the coombs test?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the major haemorrhage protocol?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the risks of blood transfusions?

A 
TACO
TRALI
ATR
Febrile, Allergic, 
vCJD risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is TACO?

A

Transfusion associated circulatory overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is TRALI?

A

Transfusion related acute lung injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you stop haemolytic disease of the newborn?

A

Prophylatic Anti-D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

erythropoietin,
G-CSF,
thrombopoietin agon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the pathway for erthroid differentiation?

A

Erythroblast–>
reticulocyte–>
erythrocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is ertyhropoetin?

A

A hormone produced by kidneys made in response to hypoxia

Increases red cell count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is reticylocyte count?

A

A measure of red cell production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are platelets?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is thrombopoetin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are neutrophils?

A

Target pathogens, especially bacteria/fungi
Include inerleukins
Production regulated by granulocyte-colony stimulating factor (G-CSF)
Regulated by immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the stages of neutrophil differentiation?

A 
Blast
Promyelocyte
Myleocyte
Metamyelocyte
Neutrophil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What can cause netrophilia?

A

Infection
>Left shift, toxic granulation
Inflammation
>eg MI, postoperative, rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What can cause neutropenia?

A 
‘Racial’
Decreased production
>Drugs
>Marrow failure
Increased consumption
>Sepsis
>Autoimmune
Altered function
>eg chronic granulomatous disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are monocytes?

A

Macrophages inside blood

phagocytic cells for injestion of pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the other meyloid cells?

A

Eosinophils

Basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are lymphocytes?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What lymphocytes disease?

A

Lymphocytosis
>Infectious mononucleosis
>Pertussis

Lymphopenia
>Usually post-viral
>lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the subtypes of lymphocytes?

A

B cells – make antibodies
T cells – Helper, cytotoxic, regulatory
NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do B cell mature?

A 
Progenitor B cells
Pre B cells
Immature B cells
Naive B cells
Germinal cenre
Controcyte
Then either Memory B cell or plasma B cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is positive/negative selection of B cells?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the types of human leucocyte antigen?

A

Class I: displays internal antigens on all nucleated cells

Class II: displays antigens eaten by professional antigen presenting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is included ina full blood count?

A 
Haemoglobin
RBC
Platlets
WBC
Neutrophils
Lymphocytes
>Monoyctes
>Eosinophils
>Basophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the different diagnostic tools?

A 
FBC
Clotting times
Bleeding times (platelets)
Cehmical assays
>Ferritin
>B12
>Folate
Marrow aspirate
Lymph node biopsy
39
Q

What can cause splenomegaly?

A 
Infectious 
Haematological-malignant
>various leukaemias and lymphomas
>myeloproliferative disorders
Portal hypertension
Haemolytic disorders
Connective tissue disorders
Sarcoid
Malignant
Amyloid
40
Q

What is anaemia?

A

Reduction in red cells of haemoglobin content

41
Q

What are the main substnaces needed for red blood cell production?

A

Iron
B12
Folic acid
Erythropoetin

42
Q

How are red blood cells broken down?

A

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
Q

What can genetic defects in red blood cells affect?

A

The red cell membrane
Metabolic pathways (enzymes)
Haemoglobin

44
Q

What 5 proteins are often affected in hereditary spherocytosis?

A 
Ankyrin
Alpha Spectrin
Beta Spectrin
Band 3
Protein 4.2
45
Q

What is hereditary spherocytosis?

A 
Mostly autosomal dominant disease
Where red blood cells are spherical
Clinical presentation variable 
>Anaemia
>Splenomegaly
>pigment gallstones
46
Q

How do you treat hereditary spherocytosis?

A

Folic acid (increased requirements)
Transfusion
Splenectomy

47
Q

What are the red cell enzymes commonly disrupted?

A

Pryvuate kinase

Glucose-6-phosphate dehydrogenase

48
Q

What is the function of the pentose phosphate shunt?

A

Protects from oxidative damage

49
Q

What is G6PD deficiency?

A

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
Q

What is the presentation of G6PD deficiency?

A 
Get blister/bite cells
Variable clinical presentation
Neonatal jaundice
Splenomegaly
Broad-bean/infection precipitated jaundice/anaemia
51
Q

What is pyruvate kinase deficiency?

A

Reduced ATP
Increased 2,3-DPG
Cells rigid

Variable severity
>Anaemia
>Jaundice
>gallstones

52
Q

What is normal adult haemoglobin?

A

2 alapha chains
2 Beta chains

Feotal and A2 also exist in smaller amounts, being alpha gamma and alpha delta respectively

53
Q

What are the genes for haemoglobin?

A

2x2 alpha genes on chr16
2x: gamma gamma delta beta on chr 11
>Means that if beta is defective, delta still works

54
Q

What are haemoglobinopathies?

A

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
Q

What is the mutation in skicle cell disease?

A

beta chains are slightly defective,

results in cell changing shape permanently after being exposed to hypoxia

56
Q

What are the consequences of sickle cell disease?

A

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
Q

What is the clinical presentation of sickle cell disease?

A 
Increased infection risk
Painful vasoocclusive crisis
Stroke
Chest crisis
Chromic haemolytic anaemia
Sequestation crises
58
Q

How do you treat a painful crisis of sickle cell?

A 
Analgesia within 30 mins (opiates)
Hydration
Oxygen
Consider antibiotics
No routine role for transfusion
59
Q

What is a chest crisis of sickel cell and how do you managE?

A

Chest Pain
Fever
Worsening hypoxia
Infiltrates on CXRay

Manage:
Respiratory Support
Antibiotics
IV Fluids
Analgaesia
Transfusion
60
Q

What is the long term management for sickle cell?

A

Vaccination
Penicillin prophylaxis
Folic acid

Be careful if needing regular transfusions for iron overload

61
Q

What are the different thalassaemias?

A

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
Q

What is beta thalasemia major?

A 
Severe anaemia
Present at 3-6 months of age
Expansion of ineffective bone marrow
Bony deformities
Splenomegaly
Growth retardation
63
Q

How do you treat thalassaemia major?

A

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
Q

How do you stop iron overloadinh?

A

Iron chelation therapy
s/c desferrioxamine infusions (desferal)
Oral deferasirox (exjade)

65
Q

What is sideroblastic anaemia?

A

Defects in mitochondrial steps of haem synthesis
>ALA synthase mutations
>Hereditary (X-Linked)
>Aquired - Myelodysplasia

66
Q

What factors affect the normal range of haemoglobin?

A 
Age
Sex
Ethnic origin
Time of day of sample
Time taken to analyse
67
Q

What are the general features of anaemia?

A 
Tiredness/pallor
Breathlessness
Swelling of ankles
Dizziness
Chest pain
Depend on age and Hb level
Others relating to underlying cause
68
Q

What can cause anaemia?

A

Disruption of bone marrow
Disruption of red cells
Destruction/loss of red blood cells

69
Q

What are red cell indices?

A 
MCV = Mean cell volume  (cell size)
MCH = Mean cell haemoglobin
70
Q

What are the three types of anaemia?

A

Hypochromic microcytic
Normochormic normocytic
Macrocytic

71
Q

How do you investigate the different anaemias?

A

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
Q

What are the causes of Hypochromic microcytic anaemia?

A

Low ferritin - iron deficiency
Normal/high ferritin
>Thalassaemia
>Secondary anaemia

73
Q

How is iron transported?

A

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
Q

What is iron deficiency anaemia?

A

Commonest cause
But description not diagnosis
Look for cause - ie bleeding, diet, requirements, malabsorption?

75
Q

What are the clinical features of iron deficiency anaemia?

A

Angular cheilitis/stomatitis
Atrophic tongue
Koilonychia

76
Q

How do you manage iron deficiency anaemia?

A

Correct deficiency
>Oral sufficienct, IV if oral intolerable

Correct cause
>Diet
>Ulcer therpay
>Gynae interventions
>Surgery
77
Q

What are the causes of normochromic/cytic anaemia anaemia?

A

Increased reticocyte count
>Acute blood loss
>Haemolysis

Normal/low
>Secondary anaemia
Hypoplasia

78
Q

What is haemolytic anaemia?

A

Accelerated red cell destruction (dec Hb)
Compensation by bone marrow ( inc Retics)
Haemolysis either extra (normal) or intravasculae

79
Q

What can cause haemolytic anaemia?

A 
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
Q

How do you tell if a haemolytic disease is immune mediated or not?

A

Do a direct antiglobulin test

If positive it is autoimmune, if negative it is not

81
Q

How do you diagnose haemolysis?

A

FBC, reticulocyte count, blood film
Serum bilirubin (direct/indirect), LDH
Serum haptoglobin

Then check mechanism
>blood film, coombs tess

82
Q

How do you manage haemolytic anaemia?

A 
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
Q

What is secondary anaemia?

A

70% normochromic normocytic
30% hypochromic microcytic

Defective iron utilisation
>Increased hepcidin in inflammation
>Ferritin often elevated

Identifiable underlying disease

84
Q

What are the causes of macrocytic anaemia?

A 
Megoblastic - B12/folate defiency (the definition)
Or non megablastic
>Myelodysplasia
>Marrow infiltration
>Drugs
85
Q

What are the causes of B12 deficiency?

A

Pernicious anaemia

Gastric/ileal disease

86
Q

What are the causes of folate deficiency?

A 
Dietary
 Increased requirements (haemolysis)
 GI pathology (eg.coeliac disease)
87
Q

What is pernicious anaemia?

A 
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
Q

How do you treat megaloblastic anaemia?

A

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
Q

What allows for normal blood flow?

A

Although ability to clot is always present, the endothelium encourages flow with smooth “non stick” surface

90
Q

What factors contribute towards how long you bleed for?

A 
Platelets
Coagulation factors (fibrin clot)

Natural anticoagulants limit clot to that area

91
Q

What is the clotting process when a blood vessel is damaged?

A

Platelets and coagulation factors become sticky in response to tissue factors

92
Q

What can activate platelets/coagulation factors?

A

Abnormal Surface

Physiological activator

93
Q

What are the roles of platelets in haemostasis?

A

Adhering
Activation
Aggregation

Providing surface for Coagulation

Conditions + definitions (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions