Haematology Flashcards
(135 cards)
1
Q
What is haemopoesis?
A
Process by which the body produces blood cells.
2
Q
Which two types of cells derive from multipotent haemopoietic stem cells?
A
Common myeloid progenitor and common lymphoid progenitor.
3
Q
Which cells derive from common myeloid progenitor?
A
Megakaryocyte, myeloblast, erythrocyte, mast cell.
4
Q
Which cells derive from common lymphoid progenitor?
A
Natural killer cell and small lymphocyte.
5
Q
What cells can myeloblasts become?
A
Basophil, neutrophil, eosinophil and monocyte.
6
Q
What is haemoglobin?
A
Tetramer made up of four polypeptide chains (2 alpha and 2 beta), each bound to a haem group (ferrous iron ion held in a prophyrin ring)
7
Q
What is the difference between HbA, HbA2 and HbF?
A
All have alpha chains but other two polypeptides are different in each- A2 has delta and foetal has gamma.
8
Q
What does erythropoiesis require?
A
Erythroprotein
9
Q
How is erythroprotein made?
A
Synthesised in kidney in response to hypoxia.
10
Q
Which form of iron ion is best absorbed? (Fe2+ or Fe3+)
A
Fe2+ (haem iron)
11
Q
Why is Fe3+ not absorbed as well?
A
- Requires reducing agents
- Sources usually contain phytates which reduce absorption
12
Q
What regulates absorption of iron in the gut?
A
Hepcidin
13
Q
How does hepcidin function?
A
When iron storage is high> Increased hepcidin secreted by liver> Binds to ferroportin of the duodenum enterocyte causing it to degrade.
14
Q
How long do RBCs circulate for?
A
Around 120 days.
15
Q
What breaks down RBCs? and where do the breakdown products go?
A
Splenic macrophages
- Haem to liver, excreted as bilirubin
- Globin degrade to amino acids
- Iron recycled to bone marrow by Fe-transferrin in plasma.
16
Q
What is anisocytosis?
A
RBCs show more variation in shape than normal.
17
Q
What terms are used to describe RBC shape?
A
Microcytic, macrocytic and normocytic.
18
Q
What is hypochromia?
A
Larger area of central pallor than normal.
19
Q
What is polychromasia?
A
Increased blueish tinge to the cytoplasm of RBC. Suggests the cell is young.
20
Q
What is poikilocytosis?
A
Increased variation in shape of RBCs
21
Q
What irregular shapes can RBCs be?
A
Spheroytes, irregularly contracted cells, sickle cell, target cell, elliptocytes and fragments.
22
Q
What may cause target cells?
A
Hyposplenism, obstructive jaundice, liver disease and haemoglobinopathies.
23
Q
What are vitamen B12 and folate needed for?
A
dttp synthesis (dttp is in turn needed for synthesis of thymidine and therefore DNA synthesis)
24
Q
How is B12 absorbed?
A
B12 in animal products > combines with intrinsic factor (secreted by gastric parietal cells) > B12-IF binds to receptors in ileum > absorption.
25
What is a leucocyte?
A white blood cell or any blood cell that contains a nucleus.
26
Which cells are granulocytes and indicate which are also phagocytic?
- Neutrophil (Phagocyte)
- Eosinophil (Phagocyte)
- Basophil
27
What do basophil granules contain?
Histamine, heparin and proteolytic enzymes.
28
What is the function of a monocyte?
Phagocytosis, antigen-presentation and the store and release of iron.
29
What is a macrophage?
A monocyte outside of the blood (in tissue)
30
What are the types of lymphocytes?
T and B lymphocytes
31
What is the function of T and B lymphocytes?
- T-lymphocytes contribute to cell-mediated immunity
| - B-lymphocytes produce antibodies
32
What is the function of natural killer cells?
To kill tumour and virus infected cells.
33
What is leucocytosis? Why?
Too many white blood cells
| Neutrophilia, lymphocytosis, monocytosis, eosinophilia, basophilia.
34
What are the causes of neutrophilia?
Infection, infarction, inflammation, tissue damage, myeloproliferative neoplasms.
Pregnancy, exercise, corticosteroids.
35
What are the causes of monocytosis?
Infection, inflammation, leukaemia.
36
What are the causes of eosinophilia?
Allergy, parasite.
37
What are the causes of basophilia?
leukaemia
38
What is the other meaning of basophilia?
Cell cytoplasm takes up too much basic dye.
39
What is leucopenia?
Reduction in total number of white cells.
| Neutropenia, lymphopenia
40
What are possible causes of neutropenia?
Chemotherapies, radiotherapies, autoimmunity, severe bacterial infection, viral infections and drugs.
41
What is toxic granulation?
Heavy course granulation of neutrophils
42
What is left shift?
Increased number of neutrophils in the blood or increase in non-segmented neutrophils.
43
What are hyper-segmented neutrophils?
Increase in average number of neutrophil nucleus lobes (over 3-5).
44
What is the cause of hyper-segmented neutrophils?
Megablastic anaemia
45
What is coagulation?
Blood changes from the liquid state.
46
What is thrombosis?
Mass of coagulated blood
47
What is haemostasis?
The 'halting of blood' following trauma to blood vessels.
48
What is fibrinolysis?
The breakdown of fibrin clots
49
What is the first step of DIRECT primary haemostasis?
Platelet binds to endothelium collagen via GPIa receptor.
50
What is the first step of INDIRECT primary haemostasis?
Platelet binds to damaged endothelium via GPIb receptor and von Willebrand factor.
51
What produces von Willebrand factors?
Endothelial cells and platelets (alpha granules)
52
What happens after platelet adhesion to the damaged endothelium in primary haemostasis?
- Binding causes activation (shape becomes more rounded with spicules)
- Release of contents of dense (serotonin, ADP, Ca2+) and alpha granules (VW factor and fibrinogen).
- Platelets also release thromboxane A2 (platelet recruitment)
- Conformational shape change in GPIIbIIIa receptors to form a binding site for fibrinogen (platelet aggregation)
53
What is secondary haemostasis?
Coagulation cascade where each stage is characterised by an inactive zymogen is converted to an active clotting factor, by splitting peptide bonds or exposing active sites.
54
The intrinsic pathway involves which factors?
XII, XI, VIII, X
55
The extrinsic pathway involves which factors?
VII, X and TF
56
The common pathway involves what?
Prothrombin, fibrinogen and V
57
How is protein c activated?
Reaction with thrombomodulin.
58
APC inhibits VIII and V in the presence of what?
Protein S
59
What does antithrombin inhibit?
Prothrombin and X
60
Where are clotting factors synthesised? Which aren't made here?
- Liver
| - VII and VWF
61
Which factors are dependent on vitamin k and why?
- II, VII, IX, X
| - Carboxylation of their glutamic acid residues
62
How is plasminogen converted to plasmin?
By t-PA
63
What does plasmin bind to?
Lysine residues of fibrin clot.
64
What is thrombolytic therapy?
Recombinant t-PA is administered intravenously to patients presenting with ischeamic stroke or pulmonary emboli.
65
Examples of ANTI-PLATELET drugs and their functions.
- Aspirin (Inhibits production of thromboxane A2 by blocking COX)
- Clopidogrel (blocks ADP receptor)
66
Examples of ANTI-COAGULANT drugs and their functions.
- Heparin (Potentiates action of antithrombin)
- Warfarin (Vitamin K antagonist)
- Direct oral anticoagulants (Inhibits thrombin or factor Xa)
67
Example of ANTI-FIBRINOLYTIC drug and its functions.
-Tranexamic acid (Synthetic derivative of lysine - competitive inhibitor)
68
What is haemophilia A?
Deficiency of factor VIII
69
What is haemophilia B?
Deficiency of factor IX
70
What does PT test measure?
Extrinsic pathway
71
What does APTT test measure?
Intrinsic pathway
72
What is the process of PT test?
- Sample spun with sodium citrate, TF, phospholipids and calcium
- Time for clot to form is measured.
73
What is the process of APTT test?
- Contact activation of factor XII
- Added to citrated plasma sample with phospholipid and calcium
- Time for clot to form is measured.
74
What are the causes of prolong bleeding?
- Increased fibrinolysis
- Reduction in platelet function
- Reduction in coagulation factors
- Reduction in platelet number (Splenic pooling, shortened survival or production failure)
75
What are the three factors in Virchow's triad?
Blood, vessel wall and blood flow
76
What makes up 55% of a given blood volume?
Plasma
77
What are the main fluid compartments in the body?
Intracellular, Interstitial, blood plasma, transcellular
78
What is apheris?
Process where blood from a donor is centrifuged to separate one component and the rest is returned.
79
What makes up the 'buffy coat' of centrifuged blood?
Leukocytes and platelets
80
What is serum?
The fluid that separates from clotted blood that lacks substances used in the coagulation process.
81
How do samples of plasma and serum indicate disease?
Elevated levels of certain plasma proteins.
82
What is the advantage of using plasma samples?
Quicker
83
What is the advantage of using serum samples?
Cleaner sample
84
What percentage of plasma is made up by proteins?
7%
85
What is the function of serum albumin?
- Transport of lipids, hormones and ions
| - Maintains osmotic pressure
86
Give examples of beta globulins
Transferrin, C3 and C4
87
Give examples of gamma globulins
Acute-phase C reactive protein and immunoglobulins
88
Give examples of alpha globulins and their functions
- Alpha-1 antitrypsin (Inhibits proteases)
| - Alpha-2-globulins > Haptoglobin (breakdown erythrocytes) and alpha-2-macroglobin (Inhibits proteases)
89
What is serum electrolyte levels?
Concentration of ions in the circulating blood
90
What ions are involved?
Na+, Ca2+, Mg2+, K+
91
What is anaemia?
Reduction in the amount of haemoglobin in a given volume of bood
92
How is anaemia classified?
Classified by size
93
What are the causes of microcytic anaemia?
Iron deficiency, alpha and beta thalassaemia
94
What are the causes of macrocytic anaemia?
Abnormal haemopoiesis/ megabloblastic erythropoiesis, drugs, liver disease, major blood loss, haemolytic anaemia
95
What are the causes of megaloblastic anaemia?
Deficiency of folate or B12
96
What are the mechanisms of anaemia?
- Loss of blood
- Reduced production of RBCs
- Splenic pooling
- Reduced survival of RBCs
- Increased plasma volume (can't persist)
97
What is polycythaemia?
Condition where there are too many red blood cells in circulation
98
What is the cause of pseudo-polycythaemia?
Reduction in plasma volume
99
What are the causes of true polycythaemia?
```
Blood doping/ overtransfusion
Inappropriate erythropoietin synthesis
Polycythaemia vera (myeloproliferative neoplasm)
```
100
What is leukaemia?
Bone marrow disease that results in a cancer of the blood.
101
What is the process of leukaemia?
Series of mutations in a single myeloid or lymphoid stem cell, so that the progeny of that cell show abnormalities in proliferation, differentiation or survival.
102
What are the causes of leukaemia?
Oncogene influences, loss of function of a tumour suppressor gene, mutations to proto-oncogene, dysregulation of a gene or creation of a novel gene.
103
What is the different between chronic and acute leukaemia?
Chronic acts benign for a long period of time where as acute acts in a malignant manner.
104
Why can't leukaemia be described with the usual concepts of invasion and metastases?
Blood cells move all around the body.
105
What mutation is usually responsible for AML?
Transcription factor
106
What mutation is usually responsible for CML?
Gene encoding a protein in the signalling pathway between a cell surface receptor and nucleus.
107
What is the mechanism of AML?
Cells continues to proliferate but can't mature, leading to a build up of myeloblasts but no functioning end cells.
108
What is the mechanism of CML?
Translocation between chromosome 9 and 22 in a hemopoietic stem cells, produces BCR-ABLI. Cell becomes independent of outside influences so there is less apoptosis.
109
What is usually responsible for ALL?
Formation of fusion gene and dysregulation of proto-oncogene by juxtaposition of it to another gene's promoter region.
110
What is the mechanism of ALL?
Increase in lymphoblasts with failure to develop into mature lymphocytes
111
What is the mechanism of CLL?
Mature but abnormal cells
112
What are the effects of an accumulation of abnormal cells?
Leucocytosis, bone pain, hepatomegaly, splenomegaly, lymphadenopathy, thymic enlargement, skin infiltration.
113
What is the treatment for leukaemia?
Systemic and intrathecal chemotherapy, supported by RBCs, platelets and antibiotics.
114
What are the reasons for disease features?
- Tissue infiltration
- Bone marrow failure
- Metabolic disturbance as a result of rapid cell turnover
115
What antigens/antibodies does someone with A blood type have?
A (N-acetylgalactosamine) antigens and anti-B antibodies
116
What antigens/antibodies does someone with B blood type have?
B (Galactose) antigens and anti-A antibodies
117
What antigens/antibodies does someone with AB blood type have?
Both A and B antigens, neither antibodies
118
What antigens/antibodies does someone with O blood type have?
Neither antigens but both anti-A and anti-B antibodies
119
What are H stems?
Glycoprotein and fructose
120
What happens if incompatible blood is given?
Fatal haemolysis
121
Which is the most important antigen in the Rh system?
D
122
What happens if RhD negative patients are exposed to the antigen?
They develop antibodies.
This compromises future transfusion.
Haemolytic disease of the newborn.
123
How is blood screened for antibodies?
Plasma is incubated with 2 or 3 fully typed screening red cells.
124
What is 1 unit of blood?
450ml of whole blood
125
What infections are tested for in donated blood?
HIV, Hep B, C, E, HTLV, syphilis, CMV, T.cruzii and malaria
126
What indicates blood is not compatible?
Agglutination
127
What is component therapy?
Only the required component of blood is administered , not whole blood.
128
What conditions should red cells be kept in?
4°c for 5 weeks
129
What conditions should platelets be kept in?
22°c for 7 days
130
What conditions should FFP be kept in?
-30°c for 3 years, must thaw for 20-30 minutes and then be used immediately.
131
What is cryoprecipitate?
Thawed FFP contains factor VIII and fibrinogen
132
What three types of plasma are used?
FFP, cryoprecipitate, plasma for fractionation
133
When may a patient require platelets?
Bone marrow disorder, massive bleeding, disseminated intravascular coagulation, low platelet, surgery, cardiac bypass.
134
When may a patient require FFP?
Bleeding, abnormal coagulation tests, reversal of warfarin
135
When may a patient require cryoprecipitate?
Massive bleeding, very low fibrinogen, hypofibrinogenaemia.
