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Haematology Flashcards

(123 cards)

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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
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

Biomedical Sciences (6 decks)

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