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Haematology > Exam Revision > Flashcards

Exam Revision Flashcards

1
Q

What blood cell attacks parasited

A

eosinophils

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2
Q

what is a circulating macrophage

A

monocyte

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3
Q

what do NK cells do

A

virus and tumour destruction

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4
Q

red cell lifespan

A

120 days

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5
Q

neutrophil lifespan

A

7-8 hours

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6
Q

platelet lifespan

A

7-10 days

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7
Q

what are blasts

A

nucleated precursor cells

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8
Q

what cell are megakaryocytes the precursor of

A

platelets

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9
Q

what cell are reticulocytes the precursor of

A

red cell

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10
Q

what are myelocytes the precursor for

A

neutrophils

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11
Q

where is the first site of haemopoesis in the fetus

A

yolk sac

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12
Q

what other sites of haemopoesis are there in the fetus

A

liver by 6 weeks

then spleen by 12 weeks

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13
Q

where is the site of haemipoesis in the adult

A

bone marrow

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14
Q

what covers the endosteum

A

osteoclast and osteoblasts

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15
Q

what is the endosteum

A

the interface between bone and bone marrow

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16
Q

what type of marrow increases in elderly

A

yellow (fatty) marrow

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17
Q

what happens to the myeloid:erythroid ratio in haemolysis

A

it shows evidence of erytroid hyperplasia so it is reduced

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18
Q

what stimulates the maturation of erythroid precursors to become rbcs

A

erythropoietin

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19
Q

what tests are used to look at immature cells

A

immunophenotyping

cytochemistry

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20
Q

CD20

A

b cells

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21
Q

cells of myeloid lineage

A 
rbcs
platelets
granulocytes 
macrophages
dendritic cells
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22
Q

cells of lymphoid lineage

A

t cells
b cells
nk cells
dendritic cells

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23
Q

what is normal haematocrit

A

50 percent

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24
Q

what is koilonychia a sign of

A

iron deficiency

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25
Q

leg ulcers sign of

A

sickle cell

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26
Q

bone deformities a sign of

A

thalassaemia

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27
Q

glossitis a sign of

A

B12 deficiency

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28
Q

if there is reduced MCV this indicated

A

problem with haemoglobinisation

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29
Q

if there is large MCV indicated

A

problem with maturation

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30
Q

where does haemoglobin synthesis occur

A

cytoplasm

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31
Q

what anaemias result from decreased porphyrin

A

lead poisoning

sideroblastic anaemia

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32
Q

difference between blood components and blood products

A

blood components - one donor - red cells, plasma

blood products- many donors - albumin, Ig, anti d

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33
Q

how much of a therapeutic dose of platelets can you get from one donor

A

one quarter

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34
Q

what anticoagulant is used in donated blood

A

citrate based

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35
Q

how quickly must you obtain a blood donation sample

A

within 15 mins

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36
Q

what temp and for how long are red cells kept at

A

4 degrees

35 days

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37
Q

how long and at what temp are platelets stored at

A

22 degrees

shelf life five days

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38
Q

how long and at what temp is fresh frozen plasma kept at `

A

-30

up to two years

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39
Q

what type of antibodies are ABO

A

IgM

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40
Q

what chormosomes is our blood group on

A

chromosome 9

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41
Q

what type of antibodies are anti d and irregular antibodies

A

IgG

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42
Q

how soon must red cells be transfused once they have left the fridge

A

within 4 hours

after been out for 30 mins must transfuse or disguard

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43
Q

what process means that a therapeutic dose of platelets can be obtained from a single donor

A

apheresis

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44
Q

indications for fresh frozen plasma

A

bleeding
anti coagulant over dose
DIC

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45
Q

what three actions should you take in ABO incompatability reaction

A

Stop transfusion
give IV saline
Obtain bloods!

do not remove cannula

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46
Q

why is direct coombs test usually negative in ABO reactions

A

no intact red cell material

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47
Q

what is a delayed transfusion reaction usually due to

A

irregular antibodies

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48
Q

is direct coombs test positive in delayed transfusion reaction

A

yes

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49
Q

who do febrile no haemolytic transfusion reactions tend to occur in

A

people who are transfused more often

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50
Q

what mediated febrile non haemolytic transfusion reactions

A

HLA exposure in previous transfusion

anti bodies to contaminated white cells

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51
Q

what mediated urticarial reactions

A

IgE

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52
Q

what bacterial infections occur in red cells

A

pseudomonas

yersinella

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53
Q

what bacterial infection occur in platelets

A

staph, strep, salmonella

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54
Q

what virsus cannot be tested for in blood transfusion products

A

JC virus

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55
Q

what is the risk of HIV infection after a transfucsion

A

1 in 7 million

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56
Q

what two things occur in red cell destruction

A

reticulocytes

erytroif hyperplasia

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57
Q

what is the normal level of reticulocytes in blood

A

0.3-3 percent

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58
Q

what products are produced in extravascular haemolysis

A

normal products:
unconjugated bilirubinaemia
urobilinogenaemia

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59
Q

what products are produced in intravascular haemolysis

A

haemoglobinaemia
haemoglobinurea
haemosiderinuria

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60
Q

give examples of intravascular haemolyissi

A 
ABO
G6pD
malaria
pnh
pch
DIC
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61
Q

what is the function of haptoglobin

A

it mops up free Hb in blood

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62
Q

what happens to haptoglobin levels in haemolysis

A

decrease

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63
Q

which type of coombs test is used to test for haemolytic anaemias

A

coombs

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64
Q

how is hereditary spherocytosis inherited

A

autosomal dominant

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65
Q

how is G6PD deficiency inherited

A

x linked

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66
Q

what is the problem in G6PD

A

unable to reduce glutathione which is an antioxidant

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67
Q

what can autoimmune haemolytic anaemia be divided in to

A

warm or cold

68
Q

what antibody mediated warm

69
Q

what antibody mediated cold

70
Q

what condition arises from mechanical damage eg DIC

71
Q

what appears in the blood in burns related haemolysis

A

microspherocytes

72
Q

what is zieves syndrome

A

haemolysis
alcoholic liver disease
hyperlipidaemia

73
Q

pappernheimer bodies

A

b thalassaemia

74
Q

describe the structure of HbH and when is it present

A

haemoglobin with four beta chains

alpha thalassaemia

75
Q

what are Heinz bodies

A

red cell inclusions

G6PD

76
Q

howell joly bodies

A

DNA remnant inclusions

hyposplenism eg sickle cell, post spenectomy

77
Q

morphological features of neutrophil

A

segmented nucleus

78
Q

morphological features of eosinophils

A

bilobed nucleus

orange stain

79
Q

colour of basophils

A

deep purple stain

80
Q

morphological features of monocyted

A

kidney bean shaped nucleus

pale blue cytoplasm

81
Q

most common childhood malignancy

82
Q

things that make you more at risk of leukaemia

A 
benzene 
fanconi anaemia
ataxia telangiectasia
downs syndrome
Philadelphia chromosome
83
Q

what is a common symptoms in ALL

84
Q

where are auer rods seen

A

AML and APML

85
Q

what antibiotics are given for neutropenic sepsis

A

taxobactam

ampercillin

86
Q

what is remission in leukaemua

A

less than 5 percent blasts

return of normal erythropoesis

87
Q

treatment of acute promyelocytic leukaemia

A

vit a analogue and arsenic

88
Q

alcohol induced pain

A

hodgkins lymphoma

89
Q

b cell zone in lymph node

90
Q

t cell zone in lymph node

A

paracortex

91
Q

plasma cell zone in lymph node

92
Q

high grade non hodgkins lymphomas

A

burkits
diffuse large B cell
mantle

93
Q

low grade non hodgkins

A

follicular
small lymphocytic
marginal zone

94
Q

most common hodkins lymphoma

A

nodular sclerosing

95
Q

best prognosis hodkins lymphoma

A

lymphocyte dominant

96
Q

worse prognosis hodgkins lymphoma

A

lymphocyte deplete

97
Q

pathagnomaonic feature of hodgkins

A

reed Steinberg cells

98
Q

what is the philodelphia chromosome

A

translocation between 9 and 22

99
Q

what is imatinib and what does it treat

A

tyrosine kinase inhibitor

CML

100
Q

secondary causes of polycythaemia

A

smoking
chronic hypoxia eg COPD
erythropoeitn secreting tumour

101
Q

causes of pseudopolycythaemia

A

dehydration
diuretics
due to decreases plasma vol not increased red cells

102
Q

what is the mutation on polycythaemia rubra vera

103
Q

what is the erythropoeitn leveln in polycythaemia rubra vera

A

low

high in secondary polycythaemia

104
Q

treatment of polycythaemia rubra vera

A

venesect
aspirin
can use chemo in some cases - hydroxycarbamide

105
Q

side effect of hydroxycarbamide

A

megaloblastic anaemia

106
Q

what is essential thrombocythaemia

A

increased platelets

107
Q

myelofibrosis

A

idiopathic or secondary to polycythaemia rubra vera or ET

108
Q

what is seen in the blood on myelofibrosis

A

marrow failure
leukoerythroblastic blood
tear dropped RBCs
extramedullary haemopoiesis

109
Q

examples of cell cycle specific agents

A

anti metabolites eg methotrexate. hydroxyurea

mitotic spindle eg taxotere, alkaloids

110
Q

what phase of cell cycle do antimetabilites work

111
Q

phase of cell cycle that mitotic spindle effect

112
Q

difference between cell cycle specific and non cell cycle specific in terms of dose and duration

A

cell cycle specific - duration more important than dose

non specific - dose more important than duration

113
Q

examples of non cell cycle specific agents

A

alkylating agents - melphalon, platinum
anthracyclins
chlorambucil

114
Q

primary haemostasis

A

platelet plug formation

115
Q

causes of impaired primary haemostasis

A 
ehloer danlos
henoch schlon pupura
scurvy
aplastic anaemia
DIC, ITP
von willebrand deficiency
116
Q

how is vonwillebrand deficiency inherited

A

autosomal dominant

117
Q

infectins which can cause a failure of platelet production

A

EBV, CMV, varicella

118
Q

treatment of TTp

A

plasmapheresis

119
Q

what can cause multiple clotting factor deficincies

A

liver disease
warfarin therapy or vit k deficiency
dic

120
Q

what clotting factor is particularly low in liver disease

121
Q

why is vit K sometimes reuced in coeliac and crohns

A

it is a fat soluble vitamin absorbed in upper GI tract

122
Q

what is Christmas disease

A

haemophilia B

123
Q

which type of haemophilia is more common

124
Q

what gene is haemophilia carried on

125
Q

what is deficient in haemophilia a

126
Q

deficient in haemophilia b

127
Q

what is prolonged in haemophilia

A

APPT

PT normal

128
Q

what is the clot rich in arterial thrombosis

129
Q

what is the clot rich in in venous thrombosis

130
Q

how would you monitor low molecular weight heparin

A

anti factor 10a assay

131
Q

how would you monitor unfractionated heparin

132
Q

what is Virchow triad

A

hypercoagulability
stasis
vessel wall damage

133
Q

what is factor 5 leidan

A

resistance to activated protein

134
Q

name an acquired cause of thrombophilia

A

antiphospholipid syndrome

135
Q

how is antiphospholipid syndrome treated

A

aspirin and warfarin

because it is both a problem with primary and secondary haemostasis

136
Q

when do you treat factor five leidan with anticoagulation

A

only if recurrent VTEs

can give prophylaxis in periods on known risk eg pregnancy or surgery

137
Q

indications for lifelong coagulation

A

recurrent venous thrombosis
rheumatic mitral valve disease
atrial fibrillation
prosthetic heart valves

138
Q

mode of action of low molecular weight heparin

A

potentiated anti thrombin III and results in inactivation of factor 10a

139
Q

mode of action unfractionated heparin

A

inactivates factor 2a (thombin)

140
Q

side effects of heparin

A

thrombocytopenia

osteoporosis if used long term

141
Q

how is heparin overdose treated

A

stop heparin - short half life

in severe bleeds give protamine sulphate

142
Q

what is used if patient is resistant to warfarin

A

phenindone

143
Q

mode of action of warfarin

A

inhibits vitamin K

144
Q

What clotting factors need vit K to be carboxylated

A

2, 7, 9, 10

also protein c and s

145
Q

where is vit k synthesised

146
Q

what is used to monitor warfarin

147
Q

how is warfarin overdose treated

A

stop warfarin
give vit K
give clotting factors (FFP)

148
Q

how long does vit K take to take effect

149
Q

mode of action dabigatran

A

direct thrombin inhibitor

150
Q

mode of action of ribaroxaban/apixaban

A

direct factor Xa inhibitors

151
Q

when are new anticoagulants used

A

all are used in elective HIP and KNEE surgery for DVT
can be used for AF
can be used for DVT/PE treatment

152
Q

mode of action of aspirin

A

inhibits COX

153
Q

mode of action of clopidogrel

A

ADP receptor antagonist

154
Q

moe of action of dypyramidole

A

phosphodieterase inhibitor

155
Q

mode of action of abciximab

A

GP IIb/IIIb inhibitor

156
Q

how long should antiplatelets be stopped prior to surgery

157
Q

what antiplatelet prevents aggregation of platlets

158
Q

what tissue factors does protein c inactivate

A

Va and VIIIa

159
Q

what stimulates protein c and s

A

thrombin production

160
Q

what breaks down the fibrin clot

161
Q

why can CLL be more difficult to treat with chemotherapy and radiotherapy

A

mutations of p53 can occur - cell does not apoptose in response to damage

162
Q

why are high grade/acute cancers of the blood more responsive to chemo

A

chemo targets rapidly dividing cells - cells are divinding rapidly in acute leukaemias/high grade

163
Q

why are deaths due to fungal infection decreasing in chemotherapy patients

A

all who are high risk are given prophylactic antifungals eg itraconozole

164
Q

what scan is used in hodgkins lymphoma to better target radio/chemo

165
Q

name a monoclonal antibody

166
Q

what does rituximab bind to

A

CD20 on malignant b cells

167
Q

when is rituximab used

A

b cell NHL

Haematology (21 decks)

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