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PoM > Haematology > Flashcards

Haematology Flashcards

1
Q

What is haemopoesis?

A

Process by which the body produces blood cells.

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2
Q

Which two types of cells derive from multipotent haemopoietic stem cells?

A

Common myeloid progenitor and common lymphoid progenitor.

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3
Q

Which cells derive from common myeloid progenitor?

A

Megakaryocyte, myeloblast, erythrocyte, mast cell.

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4
Q

Which cells derive from common lymphoid progenitor?

A

Natural killer cell and small lymphocyte.

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5
Q

What cells can myeloblasts become?

A

Basophil, neutrophil, eosinophil and monocyte.

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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)

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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.

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8
Q

What does erythropoiesis require?

A

Erythroprotein

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9
Q

How is erythroprotein made?

A

Synthesised in kidney in response to hypoxia.

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10
Q

Which form of iron ion is best absorbed? (Fe2+ or Fe3+)

A

Fe2+ (haem iron)

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11
Q

Why is Fe3+ not absorbed as well?

A
  • Requires reducing agents

- Sources usually contain phytates which reduce absorption

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12
Q

What regulates absorption of iron in the gut?

A

Hepcidin

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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.

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14
Q

How long do RBCs circulate for?

A

Around 120 days.

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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.
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16
Q

What is anisocytosis?

A

RBCs show more variation in shape than normal.

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17
Q

What terms are used to describe RBC shape?

A

Microcytic, macrocytic and normocytic.

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18
Q

What is hypochromia?

A

Larger area of central pallor than normal.

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19
Q

What is polychromasia?

A

Increased blueish tinge to the cytoplasm of RBC. Suggests the cell is young.

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20
Q

What is poikilocytosis?

A

Increased variation in shape of RBCs

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21
Q

What irregular shapes can RBCs be?

A

Spheroytes, irregularly contracted cells, sickle cell, target cell, elliptocytes and fragments.

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22
Q

What may cause target cells?

A

Hyposplenism, obstructive jaundice, liver disease and haemoglobinopathies.

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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)

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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.

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25
Q

What is a leucocyte?

A

A white blood cell or any blood cell that contains a nucleus.

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26
Q

Which cells are granulocytes and indicate which are also phagocytic?

A
  • Neutrophil (Phagocyte)
  • Eosinophil (Phagocyte)
  • Basophil
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27
Q

What do basophil granules contain?

A

Histamine, heparin and proteolytic enzymes.

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28
Q

What is the function of a monocyte?

A

Phagocytosis, antigen-presentation and the store and release of iron.

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29
Q

What is a macrophage?

A

A monocyte outside of the blood (in tissue)

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30
Q

What are the types of lymphocytes?

A

T and B lymphocytes

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31
Q

What is the function of T and B lymphocytes?

A
  • T-lymphocytes contribute to cell-mediated immunity

- B-lymphocytes produce antibodies

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32
Q

What is the function of natural killer cells?

A

To kill tumour and virus infected cells.

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33
Q

What is leucocytosis? Why?

A

Too many white blood cells

Neutrophilia, lymphocytosis, monocytosis, eosinophilia, basophilia.

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34
Q

What are the causes of neutrophilia?

A

Infection, infarction, inflammation, tissue damage, myeloproliferative neoplasms.

Pregnancy, exercise, corticosteroids.

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35
Q

What are the causes of monocytosis?

A

Infection, inflammation, leukaemia.

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36
Q

What are the causes of eosinophilia?

A

Allergy, parasite.

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37
Q

What are the causes of basophilia?

A

leukaemia

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38
Q

What is the other meaning of basophilia?

A

Cell cytoplasm takes up too much basic dye.

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39
Q

What is leucopenia?

A

Reduction in total number of white cells.

Neutropenia, lymphopenia

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40
Q

What are possible causes of neutropenia?

A

Chemotherapies, radiotherapies, autoimmunity, severe bacterial infection, viral infections and drugs.

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41
Q

What is toxic granulation?

A

Heavy course granulation of neutrophils

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42
Q

What is left shift?

A

Increased number of neutrophils in the blood or increase in non-segmented neutrophils.

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43
Q

What are hyper-segmented neutrophils?

A

Increase in average number of neutrophil nucleus lobes (over 3-5).

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44
Q

What is the cause of hyper-segmented neutrophils?

A

Megablastic anaemia

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45
Q

What is coagulation?

A

Blood changes from the liquid state.

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46
Q

What is thrombosis?

A

Mass of coagulated blood

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47
Q

What is haemostasis?

A

The ‘halting of blood’ following trauma to blood vessels.

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48
Q

What is fibrinolysis?

A

The breakdown of fibrin clots

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49
Q

What is the first step of DIRECT primary haemostasis?

A

Platelet binds to endothelium collagen via GPIa receptor.

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50
Q

What is the first step of INDIRECT primary haemostasis?

A

Platelet binds to damaged endothelium via GPIb receptor and von Willebrand factor.

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51
Q

What produces von Willebrand factors?

A

Endothelial cells and platelets (alpha granules)

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52
Q

What happens after platelet adhesion to the damaged endothelium in primary haemostasis?

A
  • 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)
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53
Q

What is secondary haemostasis?

A

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.

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54
Q

The intrinsic pathway involves which factors?

A

XII, XI, VIII, X

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55
Q

The extrinsic pathway involves which factors?

A

VII, X and TF

56
Q

The common pathway involves what?

A

Prothrombin, fibrinogen and V

57
Q

How is protein c activated?

A

Reaction with thrombomodulin.

58
Q

APC inhibits VIII and V in the presence of what?

A

Protein S

59
Q

What does antithrombin inhibit?

A

Prothrombin and X

60
Q

Where are clotting factors synthesised? Which aren’t made here?

A
  • Liver

- VII and VWF

61
Q

Which factors are dependent on vitamin k and why?

A
  • II, VII, IX, X

- Carboxylation of their glutamic acid residues

62
Q

How is plasminogen converted to plasmin?

A

By t-PA

63
Q

What does plasmin bind to?

A

Lysine residues of fibrin clot.

64
Q

What is thrombolytic therapy?

A

Recombinant t-PA is administered intravenously to patients presenting with ischeamic stroke or pulmonary emboli.

65
Q

Examples of ANTI-PLATELET drugs and their functions.

A
  • Aspirin (Inhibits production of thromboxane A2 by blocking COX)
  • Clopidogrel (blocks ADP receptor)
66
Q

Examples of ANTI-COAGULANT drugs and their functions.

A
  • Heparin (Potentiates action of antithrombin)
  • Warfarin (Vitamin K antagonist)
  • Direct oral anticoagulants (Inhibits thrombin or factor Xa)
67
Q

Example of ANTI-FIBRINOLYTIC drug and its functions.

A

-Tranexamic acid (Synthetic derivative of lysine - competitive inhibitor)

68
Q

What is haemophilia A?

A

Deficiency of factor VIII

69
Q

What is haemophilia B?

A

Deficiency of factor IX

70
Q

What does PT test measure?

A

Extrinsic pathway

71
Q

What does APTT test measure?

A

Intrinsic pathway

72
Q

What is the process of PT test?

A
  • Sample spun with sodium citrate, TF, phospholipids and calcium
  • Time for clot to form is measured.
73
Q

What is the process of APTT test?

A
  • Contact activation of factor XII
  • Added to citrated plasma sample with phospholipid and calcium
  • Time for clot to form is measured.
74
Q

What are the causes of prolong bleeding?

A
  • Increased fibrinolysis
  • Reduction in platelet function
  • Reduction in coagulation factors
  • Reduction in platelet number (Splenic pooling, shortened survival or production failure)
75
Q

What are the three factors in Virchow’s triad?

A

Blood, vessel wall and blood flow

76
Q

What makes up 55% of a given blood volume?

A

Plasma

77
Q

What are the main fluid compartments in the body?

A

Intracellular, Interstitial, blood plasma, transcellular

78
Q

What is apheris?

A

Process where blood from a donor is centrifuged to separate one component and the rest is returned.

79
Q

What makes up the ‘buffy coat’ of centrifuged blood?

A

Leukocytes and platelets

80
Q

What is serum?

A

The fluid that separates from clotted blood that lacks substances used in the coagulation process.

81
Q

How do samples of plasma and serum indicate disease?

A

Elevated levels of certain plasma proteins.

82
Q

What is the advantage of using plasma samples?

A

Quicker

83
Q

What is the advantage of using serum samples?

A

Cleaner sample

84
Q

What percentage of plasma is made up by proteins?

A

7%

85
Q

What is the function of serum albumin?

A
  • Transport of lipids, hormones and ions

- Maintains osmotic pressure

86
Q

Give examples of beta globulins

A

Transferrin, C3 and C4

87
Q

Give examples of gamma globulins

A

Acute-phase C reactive protein and immunoglobulins

88
Q

Give examples of alpha globulins and their functions

A
  • Alpha-1 antitrypsin (Inhibits proteases)

- Alpha-2-globulins > Haptoglobin (breakdown erythrocytes) and alpha-2-macroglobin (Inhibits proteases)

89
Q

What is serum electrolyte levels?

A

Concentration of ions in the circulating blood

90
Q

What ions are involved?

A

Na+, Ca2+, Mg2+, K+

91
Q

What is anaemia?

A

Reduction in the amount of haemoglobin in a given volume of bood

92
Q

How is anaemia classified?

A

Classified by size

93
Q

What are the causes of microcytic anaemia?

A

Iron deficiency, alpha and beta thalassaemia

94
Q

What are the causes of macrocytic anaemia?

A

Abnormal haemopoiesis/ megabloblastic erythropoiesis, drugs, liver disease, major blood loss, haemolytic anaemia

95
Q

What are the causes of megaloblastic anaemia?

A

Deficiency of folate or B12

96
Q

What are the mechanisms of anaemia?

A
  • Loss of blood
  • Reduced production of RBCs
  • Splenic pooling
  • Reduced survival of RBCs
  • Increased plasma volume (can’t persist)
97
Q

What is polycythaemia?

A

Condition where there are too many red blood cells in circulation

98
Q

What is the cause of pseudo-polycythaemia?

A

Reduction in plasma volume

99
Q

What are the causes of true polycythaemia?

A 
Blood doping/ overtransfusion
Inappropriate erythropoietin synthesis 
Polycythaemia vera (myeloproliferative neoplasm)
100
Q

What is leukaemia?

A

Bone marrow disease that results in a cancer of the blood.

101
Q

What is the process of leukaemia?

A

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
Q

What are the causes of leukaemia?

A

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
Q

What is the different between chronic and acute leukaemia?

A

Chronic acts benign for a long period of time where as acute acts in a malignant manner.

104
Q

Why can’t leukaemia be described with the usual concepts of invasion and metastases?

A

Blood cells move all around the body.

105
Q

What mutation is usually responsible for AML?

A

Transcription factor

106
Q

What mutation is usually responsible for CML?

A

Gene encoding a protein in the signalling pathway between a cell surface receptor and nucleus.

107
Q

What is the mechanism of AML?

A

Cells continues to proliferate but can’t mature, leading to a build up of myeloblasts but no functioning end cells.

108
Q

What is the mechanism of CML?

A

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
Q

What is usually responsible for ALL?

A

Formation of fusion gene and dysregulation of proto-oncogene by juxtaposition of it to another gene’s promoter region.

110
Q

What is the mechanism of ALL?

A

Increase in lymphoblasts with failure to develop into mature lymphocytes

111
Q

What is the mechanism of CLL?

A

Mature but abnormal cells

112
Q

What are the effects of an accumulation of abnormal cells?

A

Leucocytosis, bone pain, hepatomegaly, splenomegaly, lymphadenopathy, thymic enlargement, skin infiltration.

113
Q

What is the treatment for leukaemia?

A

Systemic and intrathecal chemotherapy, supported by RBCs, platelets and antibiotics.

114
Q

What are the reasons for disease features?

A
  • Tissue infiltration
  • Bone marrow failure
  • Metabolic disturbance as a result of rapid cell turnover
115
Q

What antigens/antibodies does someone with A blood type have?

A

A (N-acetylgalactosamine) antigens and anti-B antibodies

116
Q

What antigens/antibodies does someone with B blood type have?

A

B (Galactose) antigens and anti-A antibodies

117
Q

What antigens/antibodies does someone with AB blood type have?

A

Both A and B antigens, neither antibodies

118
Q

What antigens/antibodies does someone with O blood type have?

A

Neither antigens but both anti-A and anti-B antibodies

119
Q

What are H stems?

A

Glycoprotein and fructose

120
Q

What happens if incompatible blood is given?

A

Fatal haemolysis

121
Q

Which is the most important antigen in the Rh system?

A

D

122
Q

What happens if RhD negative patients are exposed to the antigen?

A

They develop antibodies.
This compromises future transfusion.
Haemolytic disease of the newborn.

123
Q

How is blood screened for antibodies?

A

Plasma is incubated with 2 or 3 fully typed screening red cells.

124
Q

What is 1 unit of blood?

A

450ml of whole blood

125
Q

What infections are tested for in donated blood?

A

HIV, Hep B, C, E, HTLV, syphilis, CMV, T.cruzii and malaria

126
Q

What indicates blood is not compatible?

A

Agglutination

127
Q

What is component therapy?

A

Only the required component of blood is administered , not whole blood.

128
Q

What conditions should red cells be kept in?

A

4°c for 5 weeks

129
Q

What conditions should platelets be kept in?

A

22°c for 7 days

130
Q

What conditions should FFP be kept in?

A

-30°c for 3 years, must thaw for 20-30 minutes and then be used immediately.

131
Q

What is cryoprecipitate?

A

Thawed FFP contains factor VIII and fibrinogen

132
Q

What three types of plasma are used?

A

FFP, cryoprecipitate, plasma for fractionation

133
Q

When may a patient require platelets?

A

Bone marrow disorder, massive bleeding, disseminated intravascular coagulation, low platelet, surgery, cardiac bypass.

134
Q

When may a patient require FFP?

A

Bleeding, abnormal coagulation tests, reversal of warfarin

135
Q

When may a patient require cryoprecipitate?

A

Massive bleeding, very low fibrinogen, hypofibrinogenaemia.

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