Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

What is lymphoproliferative disease?

A

neoplastic, clonal proliferation of lymphoid cells

basically cancer of white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 classes go lymphoma?

A

Hodgkin lymphoma
Non-hodgkin lymphoma (2 classes: aggressive and indolent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the classes of non-hodgkin lymphoma other than aggressive and indolent?

A

B cells - 90%
T cells - 10%
NK cells - <1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

At what rate does indolent lymphoma progress?

A

slow growing and advanced at presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Is indolent lymphoma curable?

A

no.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the subtypes of indolent lymphoma?

A

follicular
marginal zone
mantle cell
CLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the survival of indolent lymphoma?

A

median survival of 9-12 years but variable across sub-groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the risk factors of indolent lymphoma?

A

most cases cause is unknown

primary immunodeficiency (e.g. wiscott-aldrich syndrome, common variable immunodeficiency)

secondary immunodeficiency (e.g. HIV, transplant recipients)

infection (e.g. EBV, HTLV-1, Helicobacter pylori)

autoimmune disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do most indolent lymphomas present?

A

painless lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What investigations can confirm a diagnosis of indolent lymphoma?

A

lymph node biopsy- core needle biopsy/ excision node biopsy (not FNA)

bone marrow biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is existent of a breast lump relevant to diagnosing lymphoma?

A

If a patient has breast cancer the tumour may spread to axilla, so it wouldn’t actually be lymphoma but a spread of the breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do we stage indolent lymphoma?

A

Lugano staging classification typical for most indolent lymphomas, requires imaging (CT neck, thorax, abdomen, pelvis, PET-CT)

bloods

bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are B symptoms?

A

fever
night sweats
weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the treatment for indolent lymphoma?

A

incurable

watch and wait/ active surveillance for asymptomatic patients, follow up regularly, does compromise overall survival

radiotherapy for symptomatic patients for palliative reasons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the types of chemoimmunotherapy?

A

alkylating agents (e.g. chlorambucil, bendamustine, cyclophosphamide)
anthracyclines (e.g. doxorubicin)
vina alkaloids (e.g. vincristine)
corticosteroids

mostly use combinations of these

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are myelodysplastic syndromes?

A

abnormal bone marrow syndromes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does ‘myelo’ mean?

A

marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is acute myeloid leukaemia?

A

AML is a heterogenous clonal malignancy characterised by:

  • immature myeloid cell proliferation
  • bone marrow failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the main risk of myelodysplastic syndromes?

A

they can progress to acute myeloid leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do myelodysplastic syndromes cause harm?

A
  • bone marrow cells fail to make enough healthy blood cells (quantity and quality of cells are effected)
  • abnormal cells crowd out remaining normal cells
  • risk of progression to acute myeloid leukaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are cytopenias?

A

low blood cell counts
can be red cells, white cells or platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does low red cell count present?

A

fatigue
shortness of breath
lightheadedness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does low white cell count present?

A

increased risk of frequent and/ or severe infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does low platelet count present?

A

bleeding/ bruising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you diagnose AML?

A

full blood count/ blood film
white cells can be low, normal or high but red cells and platelets will be low

bone marrow aspirate and trephine biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the morphology of myelodysplastic syndrome?

A
  • requirement of 10% dysplasia in any cell line(s)
  • blast % can be anywhere from 0-19%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What do you do if there are blasts on a FBC?

A

refer straight to haematology- there shouldn’t be any blasts on the FBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the morphology of myeloid leukaemia?

A

minimum 20% blasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is paraprotein?

A

abnormal immunoglobulins produced by clonal plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the signs and symptoms of multiple myeloma?

A

CRAB
C- hyperCalcaemia
R- renal impairment, oedema, decreased urine output
A- anemia, neutropenia, thrombocytopenia
B- osteolytic bone lesions: pepper pot skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What other rare syndromes might a patient present with in multiple myeloma?

A

paraethesia
fever (<1%)
splenomegaly (1%)
hepatomegaly (4%)
lymphadenopathy (1%)
neurological syndromes: hyperviscocity syndrome, spinal cord compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What % of patients with multiple myeloma will experience spinal cord compression?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What investigations can confirm a diagnosis of multiple myeloma?

A

bloods
protein electrophoresis and immunofixation
urine protein electrophoresis
serum light free chains
bone marrow aspirate/ biopsy
skeletal survey (x-ray)
CT/MRI
beta-2 microglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How does multiple myeloma show on a blood test?

A

FBC- marrow failure
ESR- raised
blood film- rouleaux formation
U&Es- raised urea and creatinine
Hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does multiple myeloma show on protein electrophoresis and immunofixation tests?

A

increased number of antibodies
monoclonal protein band

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does multiple myeloma show on protein electrophoresis and immunofixation tests?

A

increased number of antibodies
monoclonal protein band

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does multiple myeloma show on urine protein electrophoresis?

A

Bence Jones’ protein- monoclonal light chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does multiple myeloma show on serum free light chains test?

A

ratio of light chains kappa and lambda

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does multiple myeloma show on a bone marrow biopsy?

A

increased plasma cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does multiple myeloma show on an x-ray/ skeletal survey?

A

lytic lesions
pepper pot skull
vertebral collapse
lytic punched out lesions
fracture risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does multiple myeloma show on a CT/MRI?

A

lesions that may not have been identified on x-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the principle behind treatment of multiple myeloma?

A

it is incurable, so treatment aims to increase periods of disease remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is induction therapy in multiple myeloma?

A

initial treatment option
combination of 3 drugs
this treatment is dependent on high-risk features and co-morbidities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give an example of induction therapy for multiple myeloma.

A

VELCADE (bortezomib)- protease inhibitor
REVLIMIN (lenalidomide)- immunomodulatory imide drug
inhibits tumour angiogenesis, tumour-secreted cytokines and tumour proliferation
induces apoptosis
DEXAMETHASONE- steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is ASCT in multiple myeloma?

A

autologous stem cell transplant
best treatment option for long periods of remission
is combined with high dose chemo (e.g. melphalan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What drugs are used to maintain remission for multiple myeloma?

A

bortezomin/ lenalidomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which molecule is a prognostic tool for multiple myeloma?

A

beta2 micro-globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How is multiple myeloma staged?

A

Uses international staging system (ISS) for myeloma which grades based on levels of serum beta-2 micro globulin and albumin levels

stage 1: median survival 62 months
stage 2: median survival 44 months
stage 3: median survival 29 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the three categories of red cell disorders?

A

haemoglobinopathies
membranopathies
enzymopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is a haemoglobinopathy?

A

deficiency related to low quality or quantity of haemoglobin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is membranopathy?

A

deficiency related to red blood cell membrane protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is enzymopathy?

A

deficiency related to RBC enzyme synthesis, leads to shortened lifespan due to oxidative stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the normal range for haemoglobin?

A

120-180g/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the difference between adult and foetal haemoglobin?

A

adult (HbA): 2 alpha and 2 beta chains
foetal (HbF): 2 alpha and 2 gamma chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is haemoglobin S?

A

variant of Hb arising from a point mutation in the beta globin gene, leading to a single amino acid change (valine to glutamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is sickle cell disease?

A

a haemoglobin disorder of quality- polymerisation of HbS results in characteristic sickle shaped RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the lifespan of a sickle cell?

A

5-10 days- described as haemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What factors can precipitate sickling in sickle cell anaemia?

A

trauma
cold
stress
exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Why does sickle cell anaemia not present until after 6 months old?

A

HbF is not affected by sickle cell anaemia as it is made up of 2 alpha and 2 gamma chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does sickle cell anaemia affect reticulocyte count?

A

raised- 2-3% (normally 0.45-1.8%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Why is reticulocyte count raised in sickle cell anaemia?

A

sickle cell disease is haemolytic- increased degradation of RBcs
production is inceased
reticulocyte count is raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Why is reticulocyte count raised in sickle cell anaemia?

A

sickle cell disease is haemolytic- increased degradation of RBcs
production is inceased
reticulocyte count is raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What drug is used to prevent painful crises in people with sickle cell anaemia?

A

hydroxycarbamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the acute complications of sickle cell disease?

A

painful vast-occlusive crisis (sickle chest syndrome)
stroke in children
cognitive impairment
infections

64
Q

What are the chronic complications of sickle cell disease?

A

renal impairment
pulmonary hypertension
joint damage

65
Q

What is the treatment for sickle cell disease?

A

blood transfusion
hydroxycarbamide
stem cell transplant
gene therapy and gene editing

66
Q

How is parvovirus related to sickle cell disease?

A

Common URTI in children, leading to decreased RBC production. In individuals with sickle cell disease it can cause a dramatic drop in Hb due to inherently reduced RBC lifespan

67
Q

What is thalassaemia?

A

A Hb disorder of quantity

globing chain disorder resulting in diminished synthesis of one or more globing chains, leading to a reduction in Hb and inherent anaemia

68
Q

What are the 2 main types of thalassaemia?

A

alpha and beta thalassaemia

69
Q

How is beta thalassaemia classified?

A

THALASSAEMIA MAJOR- transfusion dependent

THALASSAEMIA INTERMEDIA- less severe and individual can survive without regular transfusions

THALASSAEMIA CARRIER/ HETEROZYGOUS- asymptomatic

70
Q

What is the major difference between alpha and beta thalassaemia?

A

alpha thalassaemia is categorised by a deficiency in the alpha chains whereas beta thalassaemia is deficiency of beta chains

71
Q

When does beta thalassaemia tend to present?

A

6-12 months

72
Q

What is the clinical presentations of beta thalassaemia?

A

severe microcytic anaemia resulting in failure to feed/ thrive, pallor, crying

73
Q

What are the blood characteristics of an individual with beta thalassaemia?

A

Hb: 40-70g/L
Very low MCV (RBC size) and MCH (RBC Hb content)
HbF > 90%
blood film- irregularly sized very pale nucleated RBCs

74
Q

What is the risk of regular transfusions in an individual with beta thalassaemia major?

A

risk of iron overload
excess iron is deposited in various organs (liver, spleen, etc) and cause fibrosis

75
Q

What is the treatment for beta thalassaemia major?

A

regular transfusion
iron chelation
endocrine supplementation (fertility)

76
Q

Describe the essential monitoring in individuals with beta thalassaemia major

A

ferritin (monitoring tool for iron overload)

cardiac and liver MRI

endocrine testing (gonadal function, diabetes screening, growth and puberty, vitamin D, calcium, PTH, thyroid)

DEXA scanning for bone health

77
Q

What is the inheritance pattern of membranopathies?

A

autosomal dominant

78
Q

What are the two most common membranopathies?

A

spherocytosis (horizontal)- more severe, presents as neonatal jaundice and haemolysis

elliptocytosis (vertical)

79
Q

What are the two most common membranopathies?

A

spherocytosis (horizontal)- more severe, presents as neonatal jaundice and haemolysis

elliptocytosis (vertical)

80
Q

What is polycythaemia vera?

A

AKA erthyrocytosis, having a high concentration of RBCs
blood neoplasms

81
Q

What is a normal haematocrit?

A

45%

82
Q

What is the synthesis of blood cells called?

A

haematopoiesis

83
Q

Where does haematopoesis happen?

A

bone marrow

84
Q

Where does haematopoesis happen?

A

bone marrow

85
Q

How is haematopoeisis regulated?

A

through action of cytokines

86
Q

Define myeloproliferative neoplasms

A

haematological malignancies
chronic conditions- they present and evolve over many years

87
Q

How do myeloproliferative neoplasms manifest?

A

accumulation of mature blood cells in circulation

88
Q

Where do myeloproliferative neoplasms arise from?

A

haematopoietic stem cells

89
Q

What causes myeloproliferative neoplasms?

A

genetic mutations in haematopoietic stem cells

cells inappropriately and permanently switched on by signalling cytokines that control haemoatopoiesis

90
Q

What causes myeloproliferative neoplasms?

A

genetic mutations in haematopoietic stem cells

cells inappropriately and permanently switched on by signalling cytokines that control haemoatopoiesis

91
Q

What is the prognosis of Polycythaemia vera?

A

13 years

92
Q

How common is Polycythaemia vera?

A

2 cases per 100,000 people per year

92
Q

How common is Polycythaemia vera?

A

2 cases per 100,000 people per year

93
Q

What are the symptoms of Polycythaemia vera?

A

itching
fatigue

94
Q

What are the differential diagnoses for Polycythaemia vera?

A

ELIMINATE SECONDARY CAUSES:
lung disease
alcohol
apparent erythrocytosis
erythropoietin (EPO) secreting tumours

95
Q

What is the management of Polycythaemia vera?

A

venesection (removing blood)
aspirin
hydroxycarbamide
management of cardiovascular risk factors

96
Q

What are the complications of Polycythaemia vera?

A

arterial thrombosis - stroke/ MI
venous thrombosis- DVT, portal vein thrombosis, splanchnic vein thrombosis

97
Q

What is the possible progression of Polycythaemia vera?

A

transform to acute leukaemia and myelofibrosis

98
Q

What is essential thrombocytosis?

A

elevated platelet count

99
Q

What is the prognosis of essential thrombocytosis?

A

normal life expectancy

100
Q

How common is essential thrombocytosis?

A

2 cases per 100,00 per year
RARE

101
Q

What causes essential thrombocytosis?

A

mostly JAK mutation- thrombopoetin (TPO) always switched on

102
Q

What is the differential diagnosis of essential thrombocytosis?

A

ELIMINATE SECONDARY CAUSES:
infection
inflammation (including post-surgical)
solid tumours

102
Q

What is the differential diagnosis of essential thrombocytosis?

A

ELIMINATE SECONDARY CAUSES:
infection
inflammation (including post-surgical)
solid tumours

103
Q

How is essential thrombocytosis managed?

A

assess and manage cardiovascular risk
aspirin
hydroxycarbamide

104
Q

What are the complications of essential thrombocytosis?

A

arterial thrombosis
venous thrombosis
bleeding

105
Q

What is the possible progression of essential thrombocytosis?

A

acute leukaemia
myelofibrosis

106
Q

What is myelofibrosis?

A

bone marrow cancer

107
Q

What is the prognosis of myelofibrosis?

A

5 years

108
Q

How common is myelofibrosis?

A

very rare

1 case per 100,000 per year

109
Q

What are the causes of myelofibrosis?

A

predominantly JAK2 mutation

110
Q

What are the symptoms of myelofibrosis?

A

weight loss
fatigue
features of cytopaenias

111
Q

How is myelofibrosis managed?

A

supportive management:

blood transfusions, EPO, treat infection
hydroxycarbamide
allogenic stem cell transplant (ASCT)
ruxolitinab (JAK1/2 inhibitor)

112
Q

What are the complications of myelofibrosis?

A

bone marrow failure
cytopaenias (low Hb, platelets, neutrophils)
bone marrow filled with reticulin fibrosis
elevated white cell count
blasts in circulation
splenomegaly

113
Q

What is the possible progression of myelofibrosis?

A

acute leukaemia

114
Q

What is chronic myeloid leukaemia?

A

elevated white cell count (granulocytes- neutrophils, basophils)

elevated platelets

splenomegaly

115
Q

How rare is chronic myeloid leukaemia?

A

7 cases per year in UK

116
Q

What causes chronic myeloid leukaemia?

A

almost all patients have a translocation between chromosome 9 and chromosome 22 (‘Philadelphia chromosome’) that creases a ‘fusion gene’ from BCR and ABL kinase

116
Q

What causes chronic myeloid leukaemia?

A

almost all patients have a translocation between chromosome 9 and chromosome 22 (‘Philadelphia chromosome’) that creases a ‘fusion gene’ from BCR and ABL kinase

117
Q

How is chronic myeloid leukaemia managed?

A

inhibitors of ABL kinase, i.e. imatinib

118
Q

What can chronic myeloid leukaemia progress to?

A

‘blast phase’ - acute leukaemia

118
Q

What can chronic myeloid leukaemia progress to?

A

‘blast phase’ - acute leukaemia

119
Q

What is the common clinical presentation of alpha thalassaemia?

A

anaemia
splenomagaly
gallstones
delayed growth

120
Q

What is the treatment for alpha thalassaemia major?

A

blood transfusions
splenectomy
stem cell transplant

121
Q

Describe the pathophysiology of membranopathies

A

deficiency of red cell membrane proteins caused by genetic lesions, haemolytic anaemia

122
Q

What are the common clinical features of membranopathies?

A

jaundice
anaemia
splenomegaly

123
Q

Name a common enzymopathy

A

G6PD deficiency
mostly asymptomatic but can lead to haemolytic anaemia

124
Q

Name a common enzymopathy

A

G6PD deficiency
mostly asymptomatic but can lead to haemolytic anaemia

125
Q

Describe the inheritance pattern for G6PD deficiency

A

X-linked

126
Q

Describe the inheritance pattern for G6PD deficiency

A

X-linked

127
Q

What are the common clinical features of G6PD deficiency?

A

haemolysis
jaundice
anaemia

128
Q

Which drugs can not be given to patients with G6PD deficiency?

A

primaquine
sulphonamides
nitrofurantoin
quinolones
dapsone

129
Q

Describe bilirubin metabolism

A
  • Haem > Biliverdin > Bilirubin
  • Bilirubin binds with albumin = unconjugated bilirubin
  • Unconjugated bilirubin combines with glucuronic acid = conjugated bilirubin (Excretable, example of phase 2 metabolism)
  • Conjugated bilirubin forms bile, which gets pushed into the duodenum
  • Bacteria in the gut breaks down conjugated bilirubin into urobilinogen (AKA faecal stercobilinogen)
  • Urobilinogen can be reabsorbed and excreted via the urine as urobilin (makes urine yellow)
  • Urobilinogen can become stercobilin and excreted in the faeces (makes poo brown)
129
Q

Describe bilirubin metabolism

A
  • Haem > Biliverdin > Bilirubin
  • Bilirubin binds with albumin = unconjugated bilirubin
  • Unconjugated bilirubin combines with glucuronic acid = conjugated bilirubin (Excretable, example of phase 2 metabolism)
  • Conjugated bilirubin forms bile, which gets pushed into the duodenum
  • Bacteria in the gut breaks down conjugated bilirubin into urobilinogen (AKA faecal stercobilinogen)
  • Urobilinogen can be reabsorbed and excreted via the urine as urobilin (makes urine yellow)
  • Urobilinogen can become stercobilin and excreted in the faeces (makes poo brown)
130
Q

What is anaemia?

A

low level of Hb in blood
results of an underlying disease, not a disease itself

131
Q

What Hb level is considered anaemic for men and women at sea level?

A

men: <135 g/L
women: <115 g/L

131
Q

What Hb level is considered anaemic for men and women at sea level?

A

men: <135 g/L
women: <115 g/L

132
Q

What are the 3 main categories of anaemia?

A
  • microcytic anaemia (low MCV indicating small RBCs)
  • normocytic anaemia (normal MCV indicating normal sized RBCs)
  • macrocytic anaemia (large MCV indicating large RBCs)
133
Q

What are the main causes of microcytic anaemia?

A

TAILS

T- thalassaemia
A- anaemia of chronic disease
I- iron deficiency anaemic
L- lead poisoning
S- sideroblastic anaemia (unable to put iron in Hb)

134
Q

What is haemoptysis?

A

coughing up blood

135
Q

What are the main causes of normocytic anaemia?

A

AHAHA!
Acute blood loss
Haemolytic anaemia
Anaemia of chronic disease
Hypothyroidism
Aplastic anaemia

135
Q

What are the main causes of normocytic anaemia?

A

AHAHA!
Acute blood loss
Haemolytic anaemia
Anaemia of chronic disease
Hypothyroidism
Aplastic anaemia

136
Q

What are the main causes of macrocytic anaemia?

A

B12 deficiency
folate deficiency
alcohol
reticulocytosis
hypothyroidism
liver disease
iatrogenic

137
Q

What are the main causes of macrocytic anaemia?

A

B12 deficiency
folate deficiency
alcohol
reticulocytosis
hypothyroidism
liver disease
iatrogenic

138
Q

What are the general signs and symptoms of anaemia?

A

tiredness
shortness of breath
headaches
dizziness
palpitations
pale skin
conjunctival pallor
tachycardia
raised respiratory rate

139
Q

What is anaemia of chronic disease?

A

most common form of anaemia amongst hospital patients and 2nd commonest worldwide

results from poor use of iron during erythropoiesis, cytokine shortening of RBC lifespan, and decreased production or response to EPO

140
Q

What is an autologous stem cell transplant?

A

stem cells are obtained from the patient

the cells are frozen before patient undergoes chemotherapy

used for myeloma and lymphoma

141
Q

What is an allogenic stem cell transplant?

A

stem cells from a suitable donor

used for blood cancers like AML, ALL, MDS that cannot be cured with chemotherapy

142
Q

What is anaemia?

A

lower than normal concentration of Hb or RBCs

143
Q

What is the general presentation of anaemia?

A

symptoms: fatigue, headache, dizziness, dyspnoea (especially on exertion)
signs: tachycardia, skin pallor, conjuctiva pallor, intermittent claudation

144
Q

What is intermittent claudation?

A

muscle pain that happens when you’re active and stops when you rest

145
Q

What are the rarer signs of anaemia and what causes them?

A
  • Koilonychia (spoon-shaped nails)- iron deficiency
  • Angular stomatitis- iron deficiency, B12 deficiency
  • Lemon-yellow skin- B12 deficiency
  • Jaundice/dark urine- haemolytic anaemia
146
Q

What are the main types of anaemia?

A

Microcytic- reduced MCV
Normocytic- normal MCV
Macrocytic- normal MCV

Haemolytic- increased breakdown of RBCs
Aplastic- decreased production of new blood cells incl. RBCs, WBCs and platelets

147
Q

What is sideroblastic anaemia?

A

the body produces enough iron but can’t put it into Hb

148
Q

What is a healthy MCV for men and women?

A

80-100 femtolitres

149
Q

Why might the MCV be in a normal range for microcytic/ macrocytic anaemia?

A

It is a mean volume, so if some cells are too big and some are too small, the mean will be normal

150
Q

What are the main causes of microcytic anaemia?

A

TAILS
Thalassaemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anaemia

151
Q

What is Thalassaemia?

A

Inherited condition where body doesn’t produce enough haemoglobin

Phase 2a (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions