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Haematology > Haematopoiesis and the White Cell > Flashcards

Haematopoiesis and the White Cell Flashcards

1
Q

what are the three types of granulocytes?

A

neutrophils
eosinophils
basophils

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2
Q

what granulocyte deals with parasites?

A

eosinophils

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3
Q

what is the function of natural killer cells?

A

anti viral

anti tumour

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4
Q

what is the lifespan of a RBC?

A

120 days

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5
Q

what is the lifespan of a neutrophil?

A

7-8 hours

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6
Q

what is the lifespan of a platelet?

A

7-10 days

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7
Q

what are the five stages of neutrophil maturation from a myeloblast?

A 
myeloblast
promyelocyte
metamyelocyte
myelocyte
neutrophil
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8
Q

what is a ‘blast’?

A

a primitive nucleated cell precursor

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9
Q

what cell is a platelet precursor?

A

megakarocyte

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10
Q

are haemopoietic stem cells derived from the endo, ecto or mesoderm?

A

mesoderm

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11
Q

at what gestation does yolk sac haemopoiesis stop by?

A

week 10

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12
Q

at what gestation does liver haemopoiesis start at?

A

week 6

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13
Q

at what gestation does spleen haemopoiesis start at?

A

week 12

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14
Q

at what gestation does bone marrow haemopoiesis start at?

A

week 16

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15
Q

where do you take a bone marrow sample from in a child?

A

tibia

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16
Q

where do you take a bone marrow sample from an adult?

A

iliac crest

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17
Q

what is the name for the minute projections of bone that are found throughout the metaphysis so that bone marrow is close to the bone surface?

A

trabeculae

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18
Q

what is the name for the interface of bone and bone marrow?

A

endosteum

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19
Q

what cells line the endosteum?

A

osteoblasts, osteoclasts and others

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20
Q

what is the name of specialised venules within the bone that forms a reticular network of blood vessels?

A

sinusoids

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21
Q

compare red marrow to yellow marrow?

A

red marrow: active

yellow marrow: fatty and inactive

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22
Q

how do you calculate the marrow cellularity % of a person?

A

100- age

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23
Q

what happens to the ratio of red to yellow marrow as you age?

A

ratio decreases

increase in yellow marrow

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24
Q

what is the myeloid:erythroid ratio?

A

ratio between neutrophils and neutrophil precursors to nucleated red cell precurosors

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25
Q

what factor regulate neutrophil maturation?

A

G-CSF

granulocyte- colony stimulating factor

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26
Q

what hormone regulates growth and development of megakaryocytes?

A

thrombopoietin

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27
Q

what is the name for the study of antigen expression using specific antibodies?

A

immunophenotyping

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28
Q

what are the primary lymphoid tissues?

A

bone marrow

thymus

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29
Q

what are the 2 main secondary lymphoid tissues?

A

lymph nodes

spleen

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30
Q

arterial and venous vessels serving lymph nodes enter and exit where?

A

at the hilum

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31
Q

where is lymph returned to the venous system?

A

junction of L or R subclavian and jugular veins

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32
Q

what is chylous ascites?

A

accumulateion of lymphatic fluid in the peritoneal cavity

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33
Q

what are the 2 main functions of the lymphatic system?

A
  1. return lymph to circulation

2. filter lymph

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34
Q

what artery supplies the spleen?

A

splenic artery from the coeliac trunk

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35
Q

what vein supplies the spleen?

A

splenic vein

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36
Q

what are the 2 main functions of the spleen?

A
  • detects and eliminates unwanted/damaged material

- facilitates immune response to blood bourne antigens

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37
Q

what are the features of hypersplenism?

A
  1. splenomegaly
  2. fall in one or more cellular components of blood
  3. correction of cytopenias by splenectomy
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38
Q

what are the 3 features of splenic enlargement?

A
  • dragging sensation in LUQ
  • discomfort with eating
  • pain if infarction
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39
Q

what is the most cause of hyposplenism?

A

splenectomy

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40
Q

what is the name for the nuclear remnants that can remain with RBCs due to hyposplenism?

A

howell-jolly bodies

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41
Q

does reduced spleen red pulp or white pulp cause howel-jolly bodies?

A

red pulp

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42
Q

which malignancy has the tendency to involve the CNS- ALL or AML?

A

ALL

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43
Q

what are auer rods?

A

clumps of granulated material which form needles in acute myeloid leukaemic cells

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44
Q

what diagnostic tool is used to differentiate between AML and ALL?

A

immunophenotyping to look for CD proteins

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45
Q

what is the curative treatment of acute leukaemia?

A

multi-agent chemotherapy

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46
Q

what line is chemo usually given through?

A

hickman line

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47
Q

what is the name for a cancer which arises from the bone marrow?

A

leukaemia

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48
Q

what is the name for a cancer which arises from the lymph node?

A

lymphoma

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49
Q

what are the 4 main types of leukaemia?

A
  • acute myeloid leukaemia
  • acute lymphoblastic leukaemia
  • chronic myeloid leukaemia
  • chronic lymphocytic leukaemia
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50
Q

what happens to the proliferation and maturation of blood cell precursors in leukaemia?

A

proliferation increases

maturation failure

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51
Q

why can you get bone pain in ALL?

A

bone marrow has expanded

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52
Q

why can you get symptoms of anaemia, infections and increased bleeding in ALL?

A

bone marrow failure

less RBC, WBC and platelets

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53
Q

compare the age groups of those who typically get AML and ALL?

A

AML - over 60 years old

ALL - children

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54
Q

why can the WBC count be high in patients with acute leukaemia despite having low RBC, platlets and neutrophils?

A

increased abnormal WBCs

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55
Q

what particular bacterial infections are you concerned about in neutropenic patients?

A

gram negative bacteria

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56
Q

what are the 3 biggest problems of marrow suppression?

A
  • anaemia
  • neutropaenia –> infections
  • thrombcytopaenia –> bleeding
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57
Q

what is tumour lysis syndrome?

A

a side effect of chemotherapy where the contents of the tumour are released into the bloodsteam causing metabolic disturbances

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58
Q

why is cardiomyopathy a late effect of anthracylcines?

A

they produce free radicals which damage the cardiac muscle

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59
Q

what is remission classed as?

A

<5% marrow blasts with recovery of normal haemopoiesis

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60
Q

what is the pathologenesis of fanconi’s syndrome?

A

unable to correct inter-strand cross links (DNA damage)

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61
Q

what are the 3 main acquired causes of primary bone marrow failure?

A
  • aplastic anaemia
  • myelodysplastic syndromes
  • acute leukaemia
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62
Q

what is aplastic anaemia?

A

autoimmune attack against the haemopoietic stem cell

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63
Q

what is the main inherited cause of primary bone marrow failure?

A

fanconi’s syndrome

64
Q

what malignancy is there a propensity for myelodysplastic syndrome to evolve into?

A

AML

65
Q

how can acute leukaemia cause pancytopaenia?

A

compromises normal stem cell activity

66
Q

why is there a hypercellular bone marrow in B12/flate deficiency?

A

increased EPO stimulates the primitive precursors

67
Q

compare a normal spleen with hypersplenism in terms of splenic red cell mass, cell transit and platelet pool?

A

splenic red cell mass is increased in hyperplenism
red cell transit speed is decreased in hypersplenism
splenic platelet pool is increased in hypersplenism

68
Q

what is the triad of Felty’s syndrome?

A

rheumatoid arthritis
splenomegaly
neutropaenia

69
Q

what is fanconi’s anaemia?

A

inherited bone marrow failure causing pancytopaenia

70
Q

what 3 cell types are reduced in pancytopaenia?

A

red blood cells (anaemia)
neutrophils (neutropenia)
platelets (thrombocytopenia)

71
Q

how do you test for Fanconi’s syndrome?

A

chromosome fragility testing

72
Q

does aplastic anaemia give you hypo or hypercellular bone marrow?

A

hypocellular

73
Q

do myelodysplastic syndromes give you hypo or hypercellular bone marrow?

A

hypercellular

74
Q

does B12/folate deficiency give you hypo or hypercellular bone marrow?

A

hypercellular

75
Q

does hyperslenism give you hypocellular or hypercellular bone marrow?

A

hypercellular

76
Q

what is the specific treatment for idiopathic aplastic anaemia?

A

immunosuppression

anti-lymphocyte globulin

77
Q

what are the 2 main functions of B cells?

A

antibody production

antigen presenting cells

78
Q

what cells make antibodies?

A

B cells

plasma cells

79
Q

what are antibodies made of?

A

2 heavy chains and 2 light chains

80
Q

describe the structure of IgM, IgA, IgG, IgD and IgE?

A

IgM- pentamer
IgA- dimer
IgG, IgD, IgE- monomer

81
Q

what cells does myeloma arise from?

A

plasma cells

82
Q

describe the appearance of a plasma cell?

A

looks like a fried egg- peripheral nucleus

83
Q

what is a paraprotein?

A

monoclonal immnoglobulin

84
Q

how do you detect paraproteins?

A

serum electrophoresis

85
Q

during serum electrophoresis, what region do immunoglobulins or paraproteins occur in?

A

gamma region

‘gamma globulins’

86
Q

what test allows you to classify/identify the abnormal paraprotein found on electrophoresis?

A

serum immunofixation

87
Q

how do you detect bence jones proteins?

A

urine electrophoresis

88
Q

what are bence jones proteins made of?

A

precipitates of immunoglobulin light chains

89
Q

why are bence jones proteins found in myeloma?

A

large amounts of light chains being over-produced, this passes into the urines

90
Q

why are light chains found in the urine of a patient with myeloma but immunoglobulins arent?

A

Ig is too big to pass into urine, light chains are small enough
also there is an overproduction of light chains

91
Q

what is the commonest cause of paraproteins in the blood?

A

monoclonal gammopathy of undetermined significance (MGUS)

92
Q

why can you get immune suppression in myeloma?

A

overproduction of useless clonal antibody leads to underproduction of useful antibodies (hypogammaglobulinaemia)

93
Q

why can you get hyperviscosity in myeloma?

A

high levels of paraprotein in the blood

94
Q

what causes renal failure in myeloma?

A

multifactorial

  • tubular cell damage by light chains, cast nephropathy
  • hypercalcaemia with dehydration
  • risk of infections leading to sepsis
  • use of NSAIDs for bone pain
  • hyperuricaemia (high cell turn over)
95
Q

what is the most common type of myeloma?

A

IgG myeloma

usually IgG or IgA

96
Q

what is bence jones myeloma?

A

myeloma where the plasma cells can only produce light chains, not full antibodies

97
Q

why does myeloma cause lytic bone disease?

A

plasma cells produce substances (Eg IL 6) which causes overactivity of osteoclasts and suppression of osteoblasts (net loss of bone)

98
Q

what are the 6 main symptoms of hypercalcaemia?

A 
symptoms of renal stones
bone pain
abdominal groans
psych moans
symptoms of dehydration
symptoms of renal impairment
99
Q

in myeloma, what type of injury happens to the PCT in the kidney?

A

toxic injury

100
Q

in myeloma, what type of injury happens to the thick ascending limb in the kidney?

A

cast injury

101
Q

what marker do you use to monitor response to treatment in myeloma?

A

paraprotein level or bence jones protein

102
Q

what is monoclonal gammopathy of uncertain significance? (MGUS)

A

an isolated finding of paraprotein (less than 30g/l) in someone who is well

103
Q

what is AL amyloidosis?

A

a form of amyloidosis in which faulty light chains are overproduced (these form aggregates)

104
Q

how do you diagnose AL amyloidosis?

A

tissue biopsy (ie bone marrow biospy, fat from abdominal wall, rectal biopsy)

105
Q

does AL amyloidosis cause nephrotic or nephritic syndrome?

A

nephrotic (proteinuria)

106
Q

what is characteristically seen under polarised light of AL amyloidisis?

A

apple-green birefringence

107
Q

what is waldenstroms macroglobulinaemia?

A

a neoplasia of cells inbetween a lymphocyte and a plasma cell

108
Q

what paraprotein is produces in walderstroms macroglobulinaemia?

A

IgM paraprotein

109
Q

what is the treatment of waldenstroms macroglobulinaemia?

A 
chemotherapy
plasmapheresis (to treat hyperviscosity syndrome(
110
Q

what are the 2 subgroups of chemotherapy drugs?

A
  • cell cycle specific agents

- non cell cycle specific agents

111
Q

what are the 2 main classes of cell cycle specific chemo agents?

A

antimetabolites

mitotic spindle inhibitors

112
Q

for cell cycle specific chemo agents what is more important- duration of treatment or cumulative dose?

A

duration of treatment

113
Q

what phase in the cell cycle are antimetabolite chemo drugs particularly effective in?

A

S phase

114
Q

what phase in the cell cycle are mitotic spindle inhibitors particularly effective in?

A

M phase

115
Q

how does methotrexate work?

A

an antimetamolite

interferes with folate metabolism (which is important for DNA synthesis)

116
Q

for non-cell cycle specific chemo agents, what is more important- duration of treatment or cumulative dose?

A

cumulative dose

117
Q

which is more likely to damage normal stem cells- cell cycle specific or non-cell cycle specific chemo agents?

A

non cell cycle specific

118
Q

cytotoxic drugs affect rapidly dividing organs, what are the 3 main side effects because of this?

A

bone marrow suppression
gut mucosal damage
hair loss

119
Q

why do you give chemo in cycles?

A

to let the normal organs recover

120
Q

what is a specific side effect of alkaloids? (cell cycle specific agents)

A

neuropathy

121
Q

what is a specific side effect of anthracyclines? (non cell cycle specific agents)

A

cardiotoxicity

122
Q

what is a specific side effect of cis-platinum? (non cell cycle specific agents)

A

nephrotoxicity

123
Q

what are 2 specific side effects of alkylating agens? (non cell cycle specific agents)

A

infertility

secondary malignancy

124
Q

what pathway needs to be functional for chemotherapy drugs to work?

A

p53 apoptosis pathway

125
Q

what chromosome translocation causes chronic myeloid leukaemia?

A

translocation between 9 and 22 (creates philadelphia chromosome )

126
Q

what are myeloproliferative disorders?

A

clonal haemopoietic stem cell disorders with an increased production on one or more haemopoietic cell type

127
Q

what makes myeloproliferative disorders different from acute leukaemia?

A

maturation is preserved

128
Q

what are the 2 broad classes of myeloproliferative disorders?

A

BCR-ABL 1 positive and BCR-ABL 1 negative

129
Q

what is the 1 BCR-ABL 1 positive myeloproliferative disorder?

A

chronic myeloid leukaemia

130
Q

what are the 3 BCR-ABL 1 negative myeloproliferative disorders?

A

polycythaemia rubra vera (PRV)
idiopathic myelofibrosis
essential thrombocythaemia (ET)

131
Q

what are the 3 phases of chronic myeloid leukaemia?

A
  • chronic phase
  • accelerated phase
  • blast phase
132
Q

what causes the BCR-ABL 1 gene?

A

the philadelphia chromosome 22 (translocation between 9 and 22)
acquired mutation

133
Q

what is the main treatment for the BCR-ABL 1 gene?

A

tyrosine kinase inhibitors (eg imatinib)

134
Q

what is polycythaemia rubra vera characterised by?

A

excess RBCs

135
Q

what is essential thrombocythaemia characterised by?

A

excess platelets

136
Q

what are the 3 main causes of pseudopolycythaemia?

A

dehydration
diuretics
obesity

137
Q

what specific itch do you get with polycythaemia rubra vera?

A

aquagenic pruritus

138
Q

will people with primary or secondary polycythaemia have splenomegaly?

A

primary polycythaemia

139
Q

why should you not correct iron deficiency in someone with polycythaemia?

A

will make it worse

140
Q

what mutation is common in polycythaemia rubra vera?

A

JAK 2

141
Q

what is the treatment for polycythaemia rubra vera?

A
  • venesect to haematocrit less than 45%
  • aspirin
  • if resistant: hydroxycarbamide (PO chemotherapy)
142
Q

in essential thrombocythaemia, the platelets are functionally abnormal- what 2 things can this cause?

A
  • thrombosis

- bleeding

143
Q

why can bleeding occur in essential thrombocythaemia?

A

acquired von willebrand disease

144
Q

what mutations are common in essential thrombocythaemia?

A

JAK 2
CALR
MPL

145
Q

what is the treatment of essential thrombothaemia?

A
  • antiplatelet (eg aspirin)

- cytoreductive therapy (eh hydroxycarbamide)

146
Q

what are the 2 main features seen on blood film of idiopathic myelofibrosis?

A
  • leukoerythroblastic appearance

- tear drop RBCs

147
Q

what mutations are sometimes seen in myelofibrosis?

A

JAK 2

CALR

148
Q

what drugs are used in myelofibrosis?

A

JAK 2 inhibitors

149
Q

what CD number is rituximab specific against?

A

CD 20 (on B cells)

150
Q

how do proteosome inhibitors work?

A

inhibit the proteosomes (which are basically bins for old proteins) leading to accumulation of toxic protein in the cell and therefore apoptosis

151
Q

how do Hodgkins lymphoma cancer cells prevent surrounding T cells from attacking them?

A

immune evasion

-produce chemicals which bind to the T cell PD1 receptor and causes the immune system to be switched off

152
Q

what cells are infected in glandular fever?

A

epithelium of the throat

and B lymphocytes

153
Q

is hodgkins lymphoma or NHL more associated with alcohol induced pain?

A

hodgkins

154
Q

is hodgkins lymphoma or NHL more likely in a younger patient?

A

hodgkins

155
Q

what cells are characteristic of hogkins lymphoma?

A

reed sternberg cells

156
Q

what 3 specific infections should you vaccinate those with splenectomys from?

A
  • meningococcus
  • pneumococcus
  • haemophilus influenzae b

Haematology (3 decks)

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