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Biomedical Sciences > Haematology > Flashcards

Haematology Flashcards

1
Q

What is aplastic anaemia?

A

Shortage of all three types of blood cells (red blood cells, white blood cells and platelets)

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2
Q

What are the three types of blood cell?

A

Red blood cell
White blood cell
Platelet

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3
Q

What is neutropenia and what causes it?

A

Shortage of neutrophils. Can be transient (e.g. Due to infections like TB) or chronic due to conditions such as aplastic anaemia.

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4
Q

What is the etiology of a disease?

A

The cause

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5
Q

What is the sequelae of a disease?

A

Secondary consequences of a disease

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6
Q

Whole blood

A

Cells and plasma

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7
Q

Packed cells

A

Concentrated rbc

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8
Q

Plasma

A

Fluid separated from unclotted blood

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9
Q

Serum

A

Fluid separated from clotted blood

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10
Q

Intramedullary

A

In the bone marrow

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11
Q

Extramedullary

A

Outside the bone marrow

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12
Q

Erythropoiesis

A

Production of rbc

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13
Q

Myelopoiesisl

A

Production of myeloid cells ie rbc, platelets, wbc apart from lymphocytes

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14
Q

Thrombopoiesis

A

Production of thrombocytes (platelets)

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15
Q

Haematuria

A

Blood in urine

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16
Q

Menorrhagia

A

Heavy periods

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17
Q

Purpura

A

Diffuse bleeding in tissues

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18
Q

Petechia

A

Haemorrhagic rash

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19
Q

Malaena

A

GI bleed via rectum

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20
Q

Occult blood

A

Hidden GI bleed from rectum

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21
Q

Coffee grounds

A

Dark brown blood from old bleed

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22
Q

Haematoma

A

Blood blister

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23
Q

Epistaxis

A

Nose bleed

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24
Q

Haemoptysis

A

Respiratory bleed

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25
Q

Haemoglobinuria

A

Free haemoglobin in the urine

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26
Q

Haemoglobinaemia

A

Free haemoglobin in the blood

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27
Q

Haemosiderinuria

A

Iron within the urine

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28
Q

Bilirubinuria

A

Bilirubin in the urine

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29
Q

Bilirubinaemia

A

Bilirubin in the blood

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30
Q

Haematinics

A

Anaemia treatments

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31
Q

Haemoglobinopathy

A

Genetic disease of haemoglobin

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32
Q

Enzymopathy

A

Genetic disease of enzyme function

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33
Q

Haemangioma

A

Disordered overgrowth of blood vessels

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34
Q

Name 4 anticoagulants

A

EDTA
Citrate
Heparin
Oxalate

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34
Q

What is EDTA used for?

A

Whole blood haematology cell counts

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35
Q

What is citrate used for?

A

Coagulation studies on plasma

WBC transfusions and donations

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36
Q

What is heparin used for?

A

Whole blood immuno typing

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37
Q

What is oxalate used for?

A

Blood sugar tests on plasma

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38
Q

Packed cell volume (erythrocyte mass)

A

Directly measured after high speed centrifugation

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39
Q

Haematocrit (erythrocyte mass)

A

Mean corpuscular volume*rbc/10

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40
Q

MCV

A

Mean (red) cell volume

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41
Q

MCH

A

Mean cell haemoglobin (weight of HB in each cell)

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42
Q

MCHC

A

Mean cell haemoglobin concentration

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43
Q

ESR

A

Erythrocyte sedimentation rate

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44
Q

What is rouleaux and what causes it?

A

Red cells sticking together due to reduced zeta potential

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45
Q

Haematamesis

A

GI bleed via mouth

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46
Q

What colour is oxyhaemoglobin?

A

Bright red

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47
Q

What colour is deoxyhaemoglobin?

A

Dark red

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48
Q

Methaemoglobin

A

Transformation of oxyhaemoglobin. Normal oxyhaemoglobin contains ferrous iron (2+). Methaemoglobin contains ferric iron (3+). Methaemoglobin is useless for respiration

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49
Q

What % of Hb is methaemoglobin?

A

1 - 2%

50
Q

What disease is associated with methaemoglobin?

A

Cyanosis

51
Q

What deficiency is associated with cyanosis?

A

Cytochrome b5 deficiency

52
Q

What is carboxyhemoglobin?

A

Carbon monoxide bound to haemoglobin

53
Q

What is the normal % of carboxyhaemoglobin and what is it for smokers?

A

3% and 15%

54
Q

What causes sulfhaemoglobin?

A

Haemoglobin combining with sulfur containing medicines

55
Q

What is the treatment for sulfhaemoglobin?

A

No treatment - must wait for rbc to die as part of normal life cycle

56
Q

Is sulfhaemoglobin able to transport oxygen?

A

No

57
Q

Why must all haemoglobins be converted to cyanmethaemoglobin to estimate Hb levels?

A

Because all haemoglobins have different wavelengths

58
Q

What is used to convert haemoglobin to cyanmethaemoglobin?

A

Drabkins solution

59
Q

What does drabkins solution do?

A

Lyses rbc and converts all haemoglobin to cyanmethaemoglobin

60
Q

What is the peak absorption wavelength for cyanmethaemoglobin?

A

540nm

61
Q

What is drabkins solution made out of?

A

A surfactant to promote rapid lysis of rbc

Ferricyanide to convert all haemoglobin to methaemoglobin

Cyanide to convert methaemoglobin to cyanmethaemoglobin

62
Q

What is drabkins solution made out of?

A

A surfactant to promote rapid lysis of rbc

Ferricyanide to convert all haemoglobin to methaemoglobin

Cyanide to convert methaemoglobin to cyanmethaemoglobin

63
Q

Anisocytosis

A

Variation in rbc size

64
Q

Anisochromasia

A

Variation in rbc colour

65
Q

Which factors affect ESR?

A 
Red cell size
Red cell content
Red cell number
Red cell shape
Zeta potential

Plasma protein concentration
Plasma lipid concentration

66
Q

What is the difference between haemoglobinopathy and thalassemia?

A

Haemoglobinopathy is a defect in haemoglobin function

Thalassemia is a defect in haemoglobin production

67
Q

What is intravascular haemolysis?

A

Haemolysis in the blood vessels

68
Q

What is extravascular haemolysis?

A

Haemolysis in the liver and spleen

69
Q

Which antibodies are against ABO antigens?

A

IgM (cannot cross placenta)

70
Q

Which antibodies are against Rh antigens?

A

IgG (can cross placenta)

71
Q

What is epigenetic change?

A

Changes in transcription of genes

72
Q

What % of malignancies are haematological?

A

7

73
Q

Which disease is associated with acute leukaemia?

A

Down’s syndrome

74
Q

What are 4 types of chronic lymphoid leukaemia?

A

CLL (b cells)
Hairy cell leukaemia (b cells)
Sezary syndrome (t cells)
Mycosis fungoides (t cells)

75
Q

Philadelphia chromosome

A

T(9,22). BCR-ABL. Tyrosine kinase. Constitutively active. Loss of extrinsic control of haematopoiesis.

76
Q

Which type of leukaemia is the philadelphia chromosome associated with?

A

CML

77
Q

What are the 3 hallmarks of cancer cells?

A

Purposeless proliferation
Immortality
Loss of extrinsic control

78
Q

Who gets CML?

A

Old people. Slightly more common in males.

79
Q

What are the translocations seen in CML?

A

T(9,22) BCR ABL

T(5,12) TEL ABL or TEL PDGFR

80
Q

What are the symptoms of CML?

A 
Fatigue (RBC)
Weight loss (cachexins)
Fever (cytokines)
Easy bruising (platelets)
Retinal haemorrhage due to hyperviscosity of blood
81
Q

What are the lab findings associated with CML?

A 
Splenomegaly
Hepatomegaly
Lymphadenopathy
Leucocytosis
Normochromic normocytic anaemia
Increased M : E ratio in the bone marrow
82
Q

What are the treatments for CML?

A

IHAHA

Imatinib

Hydroxyurea

Alpha interferon

HSCT

Allopurinol

83
Q

How does imatinib work?

A

Kinase inhibitor which prevents ATP binding to BCR ABL

84
Q

How does alpha interferon work?

A

Reduces leucocytosis

85
Q

How does hydroxyurea work?

A

It is an antimetabolite which inhibits ribonucleotide reductase in rapidly dividing cells. Reduces leucocytosis but does not reduce BCR-ABL clonal frequency so does not stop progression of the disease to AML and ALL

86
Q

How does allopurinol work?

A

Reduces risk of gout from high purine turnover. Inhibits xanthine oxidase which breaks down purines to urea

87
Q

How does imatinib resistance develop?

A

Increased drug efflux
BCR-ABL amplification
BCR-ABL mutation

88
Q

What causes tumour lysis syndrome?

A

Chemotherapy

89
Q

What is tumour lysis syndrome?

A

Where there is an increase in potassium, phosphate and uric acid in the blood due to release from dying cells. This can cause neuropathy and death

90
Q

What are 5 common mutations seen in leukaemia?

A 
Ras
Rb
ATM
FLT3
TAL1/SCL
91
Q

Ras mutation

A

Ras is an oncoprotein regulated by GTP. (Active when bound to GTP). Ras mutations uncouple it from GTP regulation and make it constitutively active)

92
Q

FLT3 mutation

A

FLT3 gene encodes a receptor tyrosine kinase which regulates proliferation in haematopoiesis. Mutation = overproliferation

93
Q

ATM mutation

A

ATM arrests the cell cycle if there is DNA damage by activating p53. Mutation in ATM means cell cycle is not arrested following dna damage

94
Q

Which type of leukaemia is ATM associated with?

A

CLL

95
Q

Which type of leukaemia are FLT3 mutations associated with?

A

AML

96
Q

RB mutation

A

Tumour supressor gene. Controls cell cycle

97
Q

TAL1/SCL mutations

A

These are transcription factors that control haematopoietic genes. Mutation = over transcription of haematopoietic genes

98
Q

CLL

A

Monoclonal B cell expansion from memory B cells

99
Q

Which is the only leukaemia which is not associated with radiotherapy?

A

CLL

100
Q

Who gets CLL?

A

Old people

1st degree relative increases risk 30 fold

Common in the west but rare in the far east

101
Q

What causes CLL?

A

Mutations in the ATM gene

Overactive Bcl which inhibits apoptosis

Autorine and paracrine signalling promotes cell survival

102
Q

What are the lab findings associates with CLL?

A

Splenomegaly
Hepatomegaly
Lymphadenopathy
Lymphocytosis
Infiltration of the bone marrow by lymphocytes (nodular or interstitial)
Hypergammaglobulinemia
Immunophenotyping shows lots of cells expressing CD20 which is found on all b cells
Normocytic normochromic anaemia towards the end stages as a result of marrow infiltration
Autoimmune haemolytic anaemia

103
Q

CLL treatment

A 
30% need no treatment
Depends on binet staging
CAIT
Corticosteroids (lymphotoxic)
Alkylating agents
Immunotherapy anti CD20
Thalidomide
104
Q

CLL slide morphology

A

High WBC count

Lymphocytosis

105
Q

Who gets AML?

A

Old people

106
Q

What causes AML?

A 
Benzene
Alkylating agents
Radiotherapy
T(5,12) TEL ABL
T(15,17) PML RAR alpha (blocks differentiation)
T(8,21) ETP AML-1
FLT3 mutation
107
Q

What are the symptoms of AML?

A 
Petechia
Easy bruising
Skin and gum infiltration
Infection
Anaemia
Fatigue
Fever
Weight loss
Bone pain
108
Q

What are the lab finding associated with AML?

A

Large numbers of blast cells in the blood

Cytopenia

DIC

Sudan black staining

Non specific esterase (monoblasts orange, myeloblasts blue)

Auer rods

Immunophenotyping (CD33 and CD117 are indicative of blasts)

109
Q

What is used to treat AML?

A 
FLT3 inhibitors
All trans retinoic acid
Ionising radiation
Alkylating agents
Anthracyclines
110
Q

T(15,17)

A

PML and RAR alpha. RAR alpha is unable to form heterodimers with RXR to trigger transcription and differentiation of promyelocytes.

111
Q

How does all trans retinoic acid treatment work?

A

Marks PML RAR alpha for degradation. Contains retinoic acid to cause RAR alpha to form heterodimers with RXR

112
Q

ALL

A

Clonal proliferation of lymphoblastic cells and accumulation in the bone marrow

113
Q

Who gets ALL?

A

Children (hygiene theory)

Peaks again at old age

114
Q

What causes ALL?

A

Inherited SNPS
Radiation
T(5,12) TEL ABL
T(12,21) TEL AML-1 (requires second genetic hit to cause ALL)

115
Q

T(15,17)

A

PML and RAR alpha. RAR alpha is unable to form heterodimers with RXR to trigger transcription and differentiation of promyelocytes.

116
Q

How does all trans retinoic acid treatment work?

A

Marks PML RAR alpha for degradation. Contains retinoic acid to cause RAR alpha to form heterodimers with RXR

117
Q

ALL

A

Clonal proliferation of lymphoblastic cells and accumulation in the bone marrow

118
Q

Who gets ALL?

A

Children (hygiene theory)

Peaks again at old age

119
Q

What causes ALL?

A

Inherited SNPS
Radiation
T(5,12) TEL ABL
T(12,21) TEL AML-1 (requires second genetic hit to cause ALL)

120
Q

ALL symptoms

A 
Fatigue
Fever
Lymphadenopathy
Splenomegaly
Hepatomegaly
Testicular swelling
Skeletal abnormalities
121
Q

What are the lab findings associated with ALL?

A 
Lymphoblasts in blood
>20% lymphoblasts in bone marrow
Mediastinal masses 
PAS positive blast cells
Leukaemic cells can spread to CSF
122
Q

ALL treatments

A

Corticosteroids
Asparaginase
Imatinab
CNS treatment

Biomedical Sciences (6 decks)

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