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Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

types of microcytic anaemia

A

iron deficiency, chronic disease, sideroblastic

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2
Q

most common haem cancer in children

A

acute lymphoblastic leukaemia

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3
Q

what cells are affected in ALL

A

lymphoid cells

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4
Q

what do you see on the blood film in ALL

A

blast cells, more white cells than normal

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5
Q

How do you manage ALL

A

fluid, blood products and chemotherapy

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6
Q

what age group are affected most by myeloma

A

older patients

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7
Q

what cells are affected in myeloma

A

malignant B cell proliferation

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8
Q

what might you see on X-ray in a patient with myeloma

A

osteolytic bone lesions

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9
Q

name protein abnormalities seen in myeloma

A

IgA, IgG abnormalities

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10
Q

What protein can be found in the urine of myeloma patients

A

Bence Jones protein

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11
Q

what are risk factors for Hodgkins

A

EBV, SLE, post-transplant and obesity

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12
Q

what age group get hodgkins

A

young adults or the elderly

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13
Q

what happens in hodgkins

A

malignant proliferation of lymphocytes which get stuck in the nodes

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14
Q

describe the lymphadenopathy seen in hodgkins

A

enlarged, non tender

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15
Q

describe the blood film in hodgkins

A

cells with mirror image nuclei, Reed-Sternberg cells

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16
Q

treatment of hodgkins

A

chemotherapy and radiotherapy

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17
Q

most common acute leukaemia in adults?

A

acute myeloid leukaemia

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18
Q

what is the physiology behind AML

A

neoplastic proliferation of blast cells

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19
Q

what is seen on the blood film in AML

A

Auer rods

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20
Q

treatment of AML

A

allogenic BM transplant

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21
Q

what is the difference between Hodgkins and non-hodgkin

A

Reed-sternberg cells

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22
Q

management of low grade non-hodgkins

A

usually incurable, treat symptoms

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23
Q

management of high grade non-hodgkins

A 
RCHOP 
rituximab 
cyclophosphamide 
h-doxorubicin 
o- vincristine 
prednisolone
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24
Q

what disease is the philadephia chromosome found in

A

chronic myeloid leukaemia

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25
Q

what age range does CML affect

A

40-60

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26
Q

CML may predispose to what conditions

A

AML, ALL

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27
Q

bone marrow appearance in CML

A

hypercellular

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28
Q

management of CML

A

tyrosine kinase inhibitors - Imatinib

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29
Q

what is the science behind CML

A

proliferation of myeloid cells

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30
Q

what is the most common leukaemia worldwide

A

CLL

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31
Q

what is the science behind CLL

A

accumulation of mature B cells that escape apoptosis

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32
Q

describe lymphadenopathy in CLL

A

enlarged rubbery nodes

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33
Q

management for CLL

A

fludarabine and cyclophosphamide

radiotherapy for the nodes

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34
Q

what is the definitive diagnostic test for ALL and AML

A

immunophenotyping

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35
Q

what do you see on blood film in myeloma

A

rouleaux

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36
Q

what does congo red stain show

A

amyloid deposition in myeloma

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37
Q

stage 1 in Hodgkins is

A

single region of nodes affected

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38
Q

stage 2 in Hodgkins is

A

2 sites affected on the same side of the diaphragm

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39
Q

stage 3 in Hodgkins is

A

several sites affected on both sides of the diaphragm

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40
Q

stage 4 in Hodgkins is

A

non-lymphatic spread

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41
Q

does alcohol make Hodgkins worse

A

yes

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42
Q

what cell is the target of Rituximab

A

CD20

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43
Q

what is polycythaemia

A

over production of red cells

44
Q

describe apparent polycythaemia

A

not overly increased. caused by diuretics, obesity and HTN

45
Q

describe primary polycythaemia

A

caused by polycythaemia ruba vera. increased red blood cells, increased wcc, and increased platelets

46
Q

what are the causative factors of secondary polycythaemia

A

hypoxaemia, renal issues and other miscellaneous

47
Q

management of polycythaemia

A

venesection, aspirin and cytotoxic therapy

48
Q

what is essential thrombocytopenia

A

uncontrolled platelet production

49
Q

what do patients with essential thrombocytopenia present with

A

usually a thrombotic event

50
Q

blood film appearance of essential thrombocytopenia

A

increased platelets

51
Q

bone marrow appearance of essential thrombocytopenia

A

increased megakaryocytic

52
Q

management of essential thrombocytopenia

A

aspirin and hydroxyurea

53
Q

wha tis myelofibrosis

A

when the bone marrow is replaced by fibrous tissue, therefore lowered red and white cell production

54
Q

blood film appearance in myelofibrosis

A

leukoerythroblastic, tear drop RBCs

55
Q

bone marrow appearance in myelofibrosis

A

usually a dry aspirate

56
Q

management of myelofibrosis

A

give blood products, Abx, stem cell transplant, JAK2 inhibitors e.g. Ruxolitinib

57
Q

target cells

A

sickle cell, iron, hyposplenism, liver disease

58
Q

tear drop poikilocytes

A

myelofibrosis

59
Q

spherocytes

A

hereditary spherocytosis, haemolytic anaemia

60
Q

basophilic stippling

A

lead, thalassaemia, sideroblastic, myelodysplastic

61
Q

howell-jolly bodies

A

hyposplenism

62
Q

heinz bodies

A

g6PD, alpha-thal

63
Q

schistocytes

A

intravascular haemolysis, DIC

64
Q

pencils

A

iron

65
Q

burr cells

A

uraemia, pyruvate kinase

66
Q

hypersegmented neutrophils

A

megaloblastic anaemia

67
Q

translocation seen in CML

A

t(9:22)

68
Q

translocation seen in Burkitts

A

t(8:14)

69
Q

cells of lymphoid progeny

A

t, NK, B (plasma cells), dendritic

70
Q

bacterial infection results in spike in what type of cell

A

neutrophils

71
Q

action of heparin

A

prevents 2 9 10 11 activation

72
Q

action of warfarin

A

prevents 2 7 9 10 synthesis

73
Q

bleeding results in haemophilia

A

APTT - up
PT - normal
bleeding time - normal

74
Q

bleeding results in vWF

A

APTT - up
PT - normal
bleeding time - up

75
Q

bleeding results vitamin K deficient

A

APTT - up
PT - up
bleeding time - normal

76
Q

what kind of anaemia do people on epileptic drugs get

A

macrocytic, they are on anti-folate drugs

77
Q

name the components of tumour lysis syndrome

A

hyperkalaemia
hyperphosphataemia
hyperuricaemia
hypocalcaemia

78
Q

most common hereditary thrombocytopenia

A

factor V Leiden

79
Q

monitoring unfractionated heparin

A

APTT

80
Q

monitoring LMWH

A

anti-Xa

81
Q

heparin reversal

A

protamine sulphate

82
Q

how long to vitb12 stores last

A

3 years

83
Q

treatment of vitb12 deficiency

A

IM hydrooxycobalamin 3x for 2 weeks then once every 3 months

84
Q

what regulates the process of stem cell development to common progeny cells

A

activation of transcription factors

85
Q

what regulates the process of common progeny cells to precursor cells

A

increased expression of colony stimulating factors (CSF)

86
Q

what regulates process of precursors to end cells

A

transcription and CSF induced maturation

87
Q

what is neutrophil maturation regulated by

A

G-CSF

88
Q

what are megakaryocytic regulated by

A

thrombopoietin

89
Q

name the cell stages of eyrthropoeisis

A

pro –> baso/early norm –> poly/inter norm –> ortho/late normo –> reticulocyte

90
Q 
ferritin is (soluble or insoluble) 
haemsiderin is (soluble or insoluble)
A

ferritin is soluble

haemsosiderin is insoluble

91
Q

what is produced when haemoglobin is degraded

A

LDH, amino acids, iron, unconjugated bilirubin

92
Q

causes of iron deficiency anaemia

A 
blood loss (GI, menstrual, malignancy) 
malabsorption (coeliac), high demand
93
Q

investigate iron deficiency anaemia

A

FBC - microcytic hypochromic
ferritin - low
transferrin/TIBC high

94
Q

manage iron deficiency anaemia

A

ferrous sulphate 200mg BD/TDS

95
Q

counsel a patient about ferrous sulphate

A

causes black stools, reflux, nausea

96
Q

describe sideroblastic anaemia

A

reduced haemoglobin synthesis leading to iron accumulation

97
Q

congenital causes of sideroblastic anaemia

A

x-linked, wolframs syndrome

98
Q

acquired causes of sideroblastic anaemia

A

myelodysplasia, myeloma, polycythaemia, leukaemia, RA, alcohol, preganncy

99
Q

investigate sideroblastic anaemia

A

bone marrow - sideroblastic rings seen

MCV

100
Q

manage sideroblastic anaemia

A

desferrioxamine chelation

congenital = pyridoxine

101
Q

high MCV without anaemia may indicate

A

myeloma, hyperglycaemia

102
Q

what would cause megaloblastic macrocytic anaemia

A

impaired DNA synthesis due to B12 or folate deficiency

103
Q

what does vitamin b12 combine with?

where is this product absorbed

A

gastric intrinsic factor

absorbed in the terminal ileum

104
Q

what is pernicious anaemia?

A

rare, autoimmune chronic tropic gastritis

105
Q

investigate pernicious anaemia

A

anti-IF, FBC, Schilling test

Finals (11 decks)

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