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Phase 2a BASICS > Haematology > Flashcards

Haematology Flashcards

1
Q

What is a reticulocyte count?

A

not part of routine FBC, requested specifically

number of ‘young’ red blood cells, measures rate of red blood cell production

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2
Q

Describe the classification of anaemias.

A

MICROCYTIC:
iron deficiency
thalassaemias
chronic disease

NORMOCYTIC:
chronic disease
renal disease
acute bleeding

MACROCYTIC:
folate deficiency
b12 deficiency
haemolytic
bone marrow disorders

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3
Q

Why does folate deficiency cause macrocytic red blood cells?

A

folate is needed for DNA synthesis

if there is a deficiency then the RBC cannot divide and continues to mature and get larger

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4
Q

How much iron should the average person eat in a day?

A

15mg

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5
Q

Where is iron absorbed?

A

duodenum and jejunum

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6
Q

What is the name for the process of blood cell production?

A

haematopoesis

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7
Q

Describe briefly the differentiation tree in haemotopoesis.

A

haematopoietic stem cells differentiates to either a MYELOID PROGENITOR or a LYMPHOID PROGENITOR

Myeloid progenitor can differentiate into:
- megakaryocyte
- erythrocyte
- mast cell
- myeloblast

Lymphoid progenitor can differentiate into a NATURAL KILLER CELL or SMALL LYMPHOCYTE

The small lymphocyte can become a T cell or B cell

B cells can further differentiate into plasma cells

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8
Q

What commonly causes neutrophilia?

A

acute bacterial infections

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9
Q

What commonly causes neutropenia?

A

myeloma, lymphoma

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10
Q

What is a common cause of lymphocytosis?

A

chronic infection (hepatitis, EBV)
malignancy
stress

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11
Q

What commonly causes lymphocytopenia?

A

AIDS/ autoimmune condition
steroids
chemotherapy

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12
Q

What does a raised eoisinophil count suggest?

A

parasitic infection

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13
Q

What does elevated monocytes suggest?

A

myelodysplastic syndrome

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14
Q

What is koilonychia?

A

spoon shaped nails
sign of iron deficiency

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15
Q

What is angular stomatis?

A

irritated, cracked sores at the corners of the mouth

commonly caused by iron or B12 deficiency

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16
Q

What does jaundice imply in a haematological sense?

A

haemolytic anaemia

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17
Q

What is classed as microcytic anaemia?

A

mean corpuscular volume (MCV) < 80

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18
Q

What are the causes of microcytic anaemia?

A

TAILS

T- thalassaemia
A- anaemia of chronic disease
I- iron deficiency
L- lead poisoning
S- sideroblastic anaemia

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19
Q

Why does iron deficiency cause anaemia?

A

iron is required to produce haemoglobin
so an iron deficiency causes a haemoglobin deficiency

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20
Q

What causes iron deficiency anaemia?

A
  • reduced intake (diet)
  • reduced absorption (malabsoption conditions, PPIs/ tetracyclines)
  • increased requirements, e.g. pregnancy
  • blood loss
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21
Q

How does iron deficiency anaemia present (other than the common universal signs of anaemia)?

A

tired, cold, palpitations

koilonychia
brittle hair
tachycardia
angular stomatis

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22
Q

How is iron deficiency anaemia treated?

A

ferrous sulfate

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23
Q

What causes a triad of dysphagia, iron deficiency and oesophageal webs?

A

Plummer vinson syndrome

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24
Q

What does it mean if an elderly person presents with iron deficiency anaemia?

A

it’s a cause for concern as most common cause in the elderly is bleeding due to a colon cancer

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25
Q

What are the causes of anaemia of chronic disease?

A

chronic infection
chronic inflammation
neoplasia

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26
Q

How does anaemia of chronic disease show on a blood test?

A

FBC: low Hb, normal/ low MCV, HIGH ESR
iron studies: normal/ raised ferritin, low serum iron, low transferrin saturation

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27
Q

What is thalassaemia?

A

a mutation in the alpha or beta units of Hb resulting in reduced production of Hb

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28
Q

What is the most common type of thalassaemia?

A

beta thalassaemia

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29
Q

What inheritance pattern does thalassaemia follow?

A

autosomal recessive

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30
Q

How is thalassaemia diagnosed?

A

Hb electrophoresis: will show abnormal Hb
blood film: microcytic, hypochromic cells

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31
Q

How is thalassaemia treated?

A
  • regular blood transfusions
  • venesection
  • splenectomy
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32
Q

Why is splenectomy a treatment for thalassaemia?

A

decreases the consumption of RBCs and reduce transfusion complications

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33
Q

What is the main possible complication of thalassaemia?

A

organ failure

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34
Q

What inheritance pattern does sickle cell anaemia follow?

A

autosomal recessive

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35
Q

What is sideroblastic anaemia?

A

when the iron levels in the body are normal, but the body cannot insert iron into haemoglobin

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36
Q

How does sideroblastic anaemia show up in investigations?

A

increased iron, transferrin, ferritin
ringed ‘sideroblasts’ on blood film

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37
Q

What is the MCV for normocytic anaemia?

A

MCV 80-100

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38
Q

What are the common causes of normocytic anaemia?

A

acute blood loss
haemolysis (leading to haemolytic anaemia)
haematological malignancy
pregnancy
CKD

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39
Q

How does the presentation of haemolytic anaemia differ from other types of anaemia?

A

present with jaundice and dark urine

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40
Q

How will haemolytic anaemia show on investigations?

A

raised reticulocytes (in chronic cases)
raised bilirubin
raised urobilinogen
schistocytes on blood film

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41
Q

What are the causes of haemolytic anaemia?

A

autoimmune destruction
sepsis
sickle cell anaemia
thalassaemia

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42
Q

What is pernicious anaemia?

A

lack of intrinsic factor which is required for B12 absorption in the terminal ileum

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43
Q

What cells produce intrinsic factor?

A

parietal cells

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44
Q

What are the causes of B12 deficiency anaemia?

A

pernicious anaemia
malabsorption
decreased dietary intake
chronic nitrous oxide use

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45
Q

How does B12 deficiency anaemia present and show up on investigations?

A

bloods: raised MCV, low Hb, low B12

‘megaloblastic’ anaemia on blood smear- oval shaped RBCs, hyperhsegmented neutrophils

S+S: general anaemia presentations plus neurological symptoms

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46
Q

What can happen in severe B12 deficiency?

A

demyelination of the spinal cord

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47
Q

What is it called when B12 deficiency anaemia cause neurological symptoms?

A

subacute combined degeneration

48
Q

What are the causes of macrocytic anaemia aside from b12 deficiency?

A
  • diseases of the liver and spleen
  • haem malignancy
  • chronic alcohol consumption
49
Q

How can you tell the difference between macrocytic anaemia caused by disease of the liver/ spleen and alcohol induced anaemia?

A

anaemia caused by liver/ spleen disease will show ‘codocytes’ on the blood film whereas alcohol-induced will not

50
Q

What are the potential causes of thrombocytosis?

A

infection/ inflammation
tissue injury
splenectomy

51
Q

What is leukaemia (most simple definition)?

A

cancer of the bone marrow

52
Q

How is leukaemia categorised?

A

either myeloid or lymphoid

myeloid:
acute myeloid
chronic myeloid

lymphoid:
acute lymphoblastic
chronic lymphoblastic

53
Q

Describe the basic pathophysiology of leukaemia.

A
  • immature blast cells uncontrollably proliferate
  • this takes up space in the bone marrow and infiltrates into tissues
  • lack of space within the bone marrow means fewer healthy cells can mature and be released into the blood
54
Q

What is the most common leukaemia in young children?

A

acute lymphoblastic leukaemia

55
Q

What causes ALL pathophysiologically?

A

proliferation of immature lymphoblasts

56
Q

What is the prognosis for ALL?

A

high cure rates

5 year survival:
90% in children
30-40% in adults

57
Q

What are the risk factors for ALL?

A
  • Down’s syndrome
  • neurofibromatosis
  • radiation
58
Q

What is neurofibromatosis?

A

genetic condition that causes tumours to grow on nerves

59
Q

How does ALL present?

A
  • general anaemia symptoms
  • bleeding/ bruising
  • infections
  • hepatosplenomagaly
  • lymphadenopathy
  • swollen testicles
60
Q

What does headaches suggest in a patient with ALL?

A

that the leukaemia has infiltrated the central nervous system

may go on to develop central nerve palsies

61
Q

How is ALL diagnosed?

A
  • > 20% lymphocytes on blood film
  • FBC: anaemia, thrombocytosis, neutropenia
  • CXR/ CT to investigate lymphadenopathy
62
Q

How is ALL managed?

A
  • blood and platelet transfusions
  • chemotherapy - methotrexate
  • steroids
  • stem cell/ bone marrow transplant \
  • antibiotics
63
Q

What is CLL?

A

chronic lymphoblastic leukaemia

proliferation o B lymphocytes + failure of cell apoptosis

64
Q

What age group is mostly affected by CLL?

A

60+

65
Q

What us the most common type of leukaemia in adults?

A

chronic lymphoblastic

66
Q

What is the prognosis for CLL?

A

85% 5-year survival

67
Q

How does CLL present?

A

often asymptomatic !!

  • lymphadenopathy
  • night sweats/ weight loss
  • bone marrow failure
68
Q

How is CLL diagnosed?

A

SMUDGE CELLS ON BLOOD FILM

FBC: anaemia, thrombocytopenia

69
Q

How is CLL managed?

A

watch and wait in early stages

chemotherapy (rituximab)

stem cell/ bone marrow transplant

70
Q

What is a possible complication of CLL?

A

RICHTER TRANSFORMATION

sudden transformation of CLL/ SLL into a significantly more aggressive form of large cell lymphoma

commonly presents as sudden and dramatic increase in size of lymph nodes

71
Q

Which type of leukaemia has the worst prognosis?

A

acute myeloid leukaemia

only 15% 5-year survival

72
Q

What is AML?

A

acute myeloid leukaemia

proliferation of immature myeloblasts

73
Q

What age group is most commonly affected by AML?

A

elderly

74
Q

How does AML present?

A

general anaemia symptoms
bleeding/ bruising
infections
hepatosplenomegaly
GUM HYPERTROPHY

75
Q

How is AML diagnosed?

A

AUER RODS ON BONE MARROW BIOPSY

FBC: anaemia, thrombocytopenia

76
Q

How is AML managed?

A

blood and platelet transfusions
chemotherapy
stem cell/ bone marrow transplant
antibiotics

77
Q

What is CML?

A

chronic myeloid leukaemia

proliferation of myeloid blood cells (overproduction of myeloid progenitor)

78
Q

What age group is most affected by CML?

A

adults over 40

79
Q

What is the genetics of CML?

A

vast majority of cases are associated withe the PHILADELPHIA CHROMOSOME

80
Q

How does CML present?

A

GOUT

general anaemia symptoms
bleeding/ bruising
infections
hepatosplenomegaly
weight loss and night sweats

81
Q

How is CML diagnosed?

A
  • genetic testing for BCR ABL/ Philadelphia chromosome

FBC: anaemia, thrombocytopenia, leukocytosis

82
Q

Describe the association between BCR ABL gene and the ‘Philadelphia chromosome’.

A
  • A piece of chromosome 9 and a piece of chromosome 22 break off and trade places
  • The BCR-ABL gene is formed on chromosome 22 where the piece of chromosome 9 attaches
  • The changed chromosome 22 is called the Philadelphia chromosome.
83
Q

How is CML managed?

A

chemo
stem cell/ bone marrow transplant
tyrosine kinase inhibitors (imatinib)

84
Q

What are the best factors to differentiate between the 4 types of leukaemia?

A

ALL- children < 6 years old, may see swollen testicles and CNS palsies

CLL- smudge cells on blood film

AML- auger rods on bone marrow biopsy, may see gum hypertrophy

CML- Philadelphia chromosome, may see gout

85
Q

Describe the features of Hodgkin’s and Non Hodgkin’s lymphoma.

A

both H and NH includes proliferation of lymphocytes in the lymph nodes and are associated with EBV + immunosuppression

however, Hodgkins has a bimodal incidence distribution (e.g. peaks in early 20s and again in 70s) but non-hodgkins predominantly affects adults over the age of 40

86
Q

Describe the presentation of Hodgkin’s and non Hodgkins lymphoma.

A

Get B symptoms with both (fever, night sweats, weight loss)

lymphadenopathy with both however it’s painless in non-hodgkins and painful upon drinking alcohol in Hodgkins

non-hodgkins may also present with hepatosplenomegaly

87
Q

How is Hodgkin’s lymphoma diagnosed?

A
  • raised ESR
  • CT/CXR for staging
  • lymph node biopsy REED STERNBERG CELLS
88
Q

How is non-hodgkin’s lymphoma diagnosed?

A
  • imaging CXR/ CT for staging
  • NO REED STERNBERG CELLS ON THE LYMPH NODE BIOPSY
89
Q

What is the easiest way to differentiate between Hodgkins and non-hodgkins lymphoma?

A

Reed Sternberg Cells only present on lymph node biopsy in HODGKINS, never in non-hodgkins

90
Q

How is lymphoma managed?

A

H and NH both possibly treated with radiotherapy and chemotherapy

for Hodgkins- chemo is ABVD therapy
non-hodgkins- chemo is RCHOP therapy

Hodgkin’s patients may also take steroids and have a stem cell/ bone marrow transplant

91
Q

What is ABVD chemotherapy?

A

doxorubicin
bleomycin
vinblastine
dacarbazine

92
Q

What is RCHOP chemotherapy?

A

rituximab
cyclophospamide
hydroxy-daunorubicin
vincristine
prednisolone

93
Q

How is lymphoma staged?

A

ANN ARBOR STAGING

stage 1: the disease is in ONE AREA ONLY
stage 2: the disease is in TWO OR MORE areas on the SAME SIDE of the diaphragm
stage 3: the disease is in TWO OR MORE areas on BOTH SIDES of the diaphragm
stage 4: the disease has spread BEYOND the lymph nodes

94
Q

What is the prognosis for multiple myeloma?

A

55% 5-year survival

95
Q

What is multiple myeloma?

A

plasma cell cancer in the bone marrow

96
Q

What condition is linked to myeloma?

A

close link to a condition called monoclonal gammopathy of undetermined significance (MGUS) which is when there is too much of an immunoglobulin released by abnormal plasma cells

1% of cases turn into myeloma

97
Q

How does myeloma present?

A

CRAB

C- hyperCalcaemia
R- renal impairment
A- anaemia (fatigue, dizziness, etc)
B- bone lesions (bone pain)

98
Q

How is multiple myeloma diagnosed?

A
  • FBC: anaemia
  • ESR: raised
  • Blood film: ROULEUX FORMATION
  • Serum and urine electrophoresis: Bence Jones protein in urine
  • bone marrow biopsy
  • x-ray/ CT: bone lesions
99
Q

How is multiple myeloma managed?

A
  • chemo (VCD, VTD, MTP)
  • stem cell transplant
  • analgesics
  • bisphosphonates (zoledronic acid)
  • blood transfusions
100
Q

What is polycythaemia?

A

high concentration on erythrocytes in the blood

101
Q

How is polycythaemia categorised?

A

absolute:
- primary (AKA polycythaemia vera)
- secondary

relative

102
Q

What is relative polycythaemia?

A

when there is a normal number of erythrocytes but a reduction in plasma

103
Q

What causes reactive polycythaemia?

A

obesity
dehydration
excessive alcohol consumption

104
Q

What is polycythaemia vera?

A

primary absolute polycythaemia

myeloproliferative neoplasm

increased number of erythrocytes due to an abnormality in the bone marrow

105
Q

What is secondary polycythaemia?

A

when a disease outside of the bone marrow causes over-stimulation of the bone marrow causing increased number of erythrocytes

106
Q

What causes secondary polycythaemia?

A

COPD
sleep apnoea
PKD
renal artery stenosis
kidney cancer

107
Q

What is the most common cause of polycythaemia vera?

A

JAK2 mutation

108
Q

What occurs in polycythaemia vera other than increased number of erythrocytes?

A

may also produce excessive amounts of platelets and white blood cells

109
Q

How does polycythaemia present?

A

headaches
dizziness
fatigue
blurred vision
red skin (hands, face, feet)
hypertension
itching (after contact with warm water)
hepatosplenomegaly

110
Q

How is polycythaemia vera diagnosed?

A

FBC: raised: Hb, haematocrit, white cell count, platelet count

genetic testing for jak2 mutation

serum erythropoietin decreased

111
Q

How is polycythaemia managed?

A

venesection
daily low dose aspirin
hydroxycarbamide (for those at high risk of thrombus)

112
Q

What is venesection?

A

quickest way to remove RBCs by removing approx. 1 pint of blood at a time

113
Q

What is the most common cause of B12 deficiency?

A

pernicious anaemia

114
Q

When would you see Howell-jolly bodies on a blood film?

A

patient who has had a recent splenectomy or has hyposplenism

115
Q

What are the risks of vitamin B3 deficiency?

A

the 3 d’s

dementia
dermatitis
diarrhoea

116
Q

Where are RBCs broken down?

A

spleen

117
Q

What is the concern when somebody presents with infection symptoms within 14 days of having chemotherapy? What is the treatment?

A

neutropenic sepsis

take blood cultures and administer IV piperacillin with tazobactam while waiting results

Phase 2a BASICS (6 decks)

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