Haematology Flashcards Preview

Biomedical Sciences > Haematology > Flashcards

Flashcards in Haematology Deck (123):
1

What is aplastic anaemia?

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

2

What are the three types of blood cell?

Red blood cell
White blood cell
Platelet

3

What is neutropenia and what causes it?

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

4

What is the etiology of a disease?

The cause

5

What is the sequelae of a disease?

Secondary consequences of a disease

6

Whole blood

Cells and plasma

7

Packed cells

Concentrated rbc

8

Plasma

Fluid separated from unclotted blood

9

Serum

Fluid separated from clotted blood

10

Intramedullary

In the bone marrow

11

Extramedullary

Outside the bone marrow

12

Erythropoiesis

Production of rbc

13

Myelopoiesisl

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

14

Thrombopoiesis

Production of thrombocytes (platelets)

15

Haematuria

Blood in urine

16

Menorrhagia

Heavy periods

17

Purpura

Diffuse bleeding in tissues

18

Petechia

Haemorrhagic rash

19

Malaena

GI bleed via rectum

20

Occult blood

Hidden GI bleed from rectum

21

Coffee grounds

Dark brown blood from old bleed

22

Haematoma

Blood blister

23

Epistaxis

Nose bleed

24

Haemoptysis

Respiratory bleed

25

Haemoglobinuria

Free haemoglobin in the urine

26

Haemoglobinaemia

Free haemoglobin in the blood

27

Haemosiderinuria

Iron within the urine

28

Bilirubinuria

Bilirubin in the urine

29

Bilirubinaemia

Bilirubin in the blood

30

Haematinics

Anaemia treatments

31

Haemoglobinopathy

Genetic disease of haemoglobin

32

Enzymopathy

Genetic disease of enzyme function

33

Haemangioma

Disordered overgrowth of blood vessels

34

Name 4 anticoagulants

EDTA
Citrate
Heparin
Oxalate

34

What is EDTA used for?

Whole blood haematology cell counts

35

What is citrate used for?

Coagulation studies on plasma
WBC transfusions and donations

36

What is heparin used for?

Whole blood immuno typing

37

What is oxalate used for?

Blood sugar tests on plasma

38

Packed cell volume (erythrocyte mass)

Directly measured after high speed centrifugation

39

Haematocrit (erythrocyte mass)

Mean corpuscular volume*rbc/10

40

MCV

Mean (red) cell volume

41

MCH

Mean cell haemoglobin (weight of HB in each cell)

42

MCHC

Mean cell haemoglobin concentration

43

ESR

Erythrocyte sedimentation rate

44

What is rouleaux and what causes it?

Red cells sticking together due to reduced zeta potential

45

Haematamesis

GI bleed via mouth

46

What colour is oxyhaemoglobin?

Bright red

47

What colour is deoxyhaemoglobin?

Dark red

48

Methaemoglobin

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

49

What % of Hb is methaemoglobin?

1 - 2%

50

What disease is associated with methaemoglobin?

Cyanosis

51

What deficiency is associated with cyanosis?

Cytochrome b5 deficiency

52

What is carboxyhemoglobin?

Carbon monoxide bound to haemoglobin

53

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

3% and 15%

54

What causes sulfhaemoglobin?

Haemoglobin combining with sulfur containing medicines

55

What is the treatment for sulfhaemoglobin?

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

56

Is sulfhaemoglobin able to transport oxygen?

No

57

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

Because all haemoglobins have different wavelengths

58

What is used to convert haemoglobin to cyanmethaemoglobin?

Drabkins solution

59

What does drabkins solution do?

Lyses rbc and converts all haemoglobin to cyanmethaemoglobin

60

What is the peak absorption wavelength for cyanmethaemoglobin?

540nm

61

What is drabkins solution made out of?

A surfactant to promote rapid lysis of rbc

Ferricyanide to convert all haemoglobin to methaemoglobin

Cyanide to convert methaemoglobin to cyanmethaemoglobin

62

What is drabkins solution made out of?

A surfactant to promote rapid lysis of rbc

Ferricyanide to convert all haemoglobin to methaemoglobin

Cyanide to convert methaemoglobin to cyanmethaemoglobin

63

Anisocytosis

Variation in rbc size

64

Anisochromasia

Variation in rbc colour

65

Which factors affect ESR?

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

Plasma protein concentration
Plasma lipid concentration

66

What is the difference between haemoglobinopathy and thalassemia?

Haemoglobinopathy is a defect in haemoglobin function

Thalassemia is a defect in haemoglobin production

67

What is intravascular haemolysis?

Haemolysis in the blood vessels

68

What is extravascular haemolysis?

Haemolysis in the liver and spleen

69

Which antibodies are against ABO antigens?

IgM (cannot cross placenta)

70

Which antibodies are against Rh antigens?

IgG (can cross placenta)

71

What is epigenetic change?

Changes in transcription of genes

72

What % of malignancies are haematological?

7

73

Which disease is associated with acute leukaemia?

Down's syndrome

74

What are 4 types of chronic lymphoid leukaemia?

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

75

Philadelphia chromosome

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

76

Which type of leukaemia is the philadelphia chromosome associated with?

CML

77

What are the 3 hallmarks of cancer cells?

Purposeless proliferation
Immortality
Loss of extrinsic control

78

Who gets CML?

Old people. Slightly more common in males.

79

What are the translocations seen in CML?

T(9,22) BCR ABL
T(5,12) TEL ABL or TEL PDGFR

80

What are the symptoms of CML?

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

81

What are the lab findings associated with CML?

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

82

What are the treatments for CML?

IHAHA

Imatinib

Hydroxyurea

Alpha interferon

HSCT

Allopurinol

83

How does imatinib work?

Kinase inhibitor which prevents ATP binding to BCR ABL

84

How does alpha interferon work?

Reduces leucocytosis

85

How does hydroxyurea work?

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

How does allopurinol work?

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

87

How does imatinib resistance develop?

Increased drug efflux
BCR-ABL amplification
BCR-ABL mutation

88

What causes tumour lysis syndrome?

Chemotherapy

89

What is tumour lysis syndrome?

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

What are 5 common mutations seen in leukaemia?

Ras
Rb
ATM
FLT3
TAL1/SCL

91

Ras mutation

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

FLT3 mutation

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

93

ATM mutation

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

Which type of leukaemia is ATM associated with?

CLL

95

Which type of leukaemia are FLT3 mutations associated with?

AML

96

RB mutation

Tumour supressor gene. Controls cell cycle

97

TAL1/SCL mutations

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

98

CLL

Monoclonal B cell expansion from memory B cells

99

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

CLL

100

Who gets CLL?

Old people

1st degree relative increases risk 30 fold

Common in the west but rare in the far east

101

What causes CLL?

Mutations in the ATM gene

Overactive Bcl which inhibits apoptosis

Autorine and paracrine signalling promotes cell survival

102

What are the lab findings associates with CLL?

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

CLL treatment

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

104

CLL slide morphology

High WBC count
Lymphocytosis

105

Who gets AML?

Old people

106

What causes AML?

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

What are the symptoms of AML?

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

108

What are the lab finding associated with AML?

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

What is used to treat AML?

FLT3 inhibitors
All trans retinoic acid
Ionising radiation
Alkylating agents
Anthracyclines

110

T(15,17)

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

111

How does all trans retinoic acid treatment work?

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

112

ALL

Clonal proliferation of lymphoblastic cells and accumulation in the bone marrow

113

Who gets ALL?

Children (hygiene theory)
Peaks again at old age

114

What causes ALL?

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

115

T(15,17)

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

116

How does all trans retinoic acid treatment work?

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

117

ALL

Clonal proliferation of lymphoblastic cells and accumulation in the bone marrow

118

Who gets ALL?

Children (hygiene theory)
Peaks again at old age

119

What causes ALL?

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

120

ALL symptoms

Fatigue
Fever
Lymphadenopathy
Splenomegaly
Hepatomegaly
Testicular swelling
Skeletal abnormalities

121

What are the lab findings associated with ALL?

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

122

ALL treatments

Corticosteroids
Asparaginase
Imatinab
CNS treatment