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Haematology > Anaemias > Flashcards

Anaemias Flashcards

1
Q

What is the definition of AML?

A

Presence of at least 20% blasts in the bone marrow or peripheral blood is diagnostic of AML (malignant myeloid progenitor cells)

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2
Q

Patient with nose bleeds, tired. What should be included in your differential?

A

Leukaemia

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3
Q

Which investigations for AML?

A

FBC, Blood film, Coag screem, bone marrow, karyotype, flow cytometry

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4
Q

Define pancytopaenia

A

anaemia, leukopenia, thrombocytopaenia

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5
Q

What are typical features in presentation of leukaemias?

A

fatigue, fever, failure to thrive, pallor, petechiae, abnormal bruising and bleeding, menorrhagia, lymphadenopathy, hepatosplenomegaly

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6
Q

Differential diagnosis for petechiae?

A

A result of low plateletes

  1. Leukaemia
  2. Meningococcal septicaemia/meningitis
  3. Vasculitis
  4. Henoch schonlein purpura HSP
  5. Abuse injury (particularly in children and vulnerable adults)
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7
Q

What are the investigations for pancytopaenia in suspected leukaemia?

A

FBC, blood film, BM biopsy, CXR (lymphadenopathy), lymph node biopsy, lumbar puncture if involvement of CNS

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8
Q

What are the three types of bone marrow biopsy?

A
  1. Bone marrow aspiration (liquid sample)
  2. Bone marrow trephine (core solid sample)
  3. Bone marrow biopsy (taken from iliac crest, sample can be analysed straight away, in contrast to trephine which requires a few days for preparation)
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9
Q

Which cell is most typically affected in ALL?

A

B-lymphocytes (85%)

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10
Q

What is seen on blood film in ALL?

A

Blast cells

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11
Q

Which genetic disorder is associated with ALL?

A

Down’s syndrome

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12
Q

What is the general treatment management for leukaemias?

A

Chemotherapy and supportive management. Targeted therapy depending on mutations. Steroids (and potentially bone marrow transplant)

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13
Q

What are the two approaches with chemotherapy?

A

Induction and consolidation

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14
Q

What are the components of supportive management for leukaemias?

A

antifungal/antimicrobial prophylaxis, blood products, palliative treatment

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15
Q

What are the age peaks for ALL?

A

<5 and >45

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16
Q

Which mutations can be observed in ALL?

A

t(15:17) and t(9:22), 30% in children and 30% in adults respectively. Depending on mutation present, treatment will be modified

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17
Q

What is the time frame of treatment for ALL?

A

2-3 years

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18
Q

How should you manage leukaemia e.g. ALL, that has resulted in CNS relapse?

A

administer drugs intrathecally

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19
Q

Which life threatening conditions are associated with leukaemias?

A

Tumour lysis syndrome, leukostasis (low hypoperfusion, risk of MI etc)

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20
Q

Which FBC results would be synonymous with leukaemia diagnosis?

A

Pancytopaenia with leukocytosis

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21
Q

Which cells are abnormal in CLL?

A

Mature lymphoid lineage- B cells

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22
Q

What is Richter’s transformation and in which leukaemia is it present in?

A

CLL can transform into high-grade lymphoma, very aggressive and specific treatment

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23
Q

Which complication can arise from CLL?

A

warm autoimmune haemolytic anaemia (and immune thrombocytopaenia)

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24
Q

Which cells are seen on blood film in CLL?

A

smear/smudge cells- aged/fragile WBCs rupture and leave smudge on film during preparation

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25
Q

In which leukaemia can flow cytometry of peripheral blood be diagnostic?

A

CLL, no need for bone marrow

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26
Q

Should you treat CLL ASAP?

A

no, treating early can be counterproductive. Wait for cytogenetic analysis to confirm type, review clinical picture and age, they might not develop problematic symptoms if left untreated. E.g. if presence of B symptoms then begin treatment

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27
Q

Which age group are affected in CLL?

A

> 55

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28
Q

What are B symptoms?

A

Fever, night sweats, and weight loss- can be present in all leukaemias

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29
Q

What are the three phases that develop in CML?

A

chronic phase, accelerated phase, blast phase

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30
Q

Which mutation is present in CML?

A

t(9:22) BCR-ABL, philadelphia chromosome

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31
Q

Which targeted therapy treats CML?

A

Imatinib

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32
Q

Which is the most common leukaemia in adults?

A

CLL

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33
Q

High numbers of which cells are present in CML?

A

Always basophilia, often eosinophila

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34
Q

Why can some leukaemias present with leukopenia and others leukocytosis?

A

WCC can populate in bone marrow and not reach systemic system. Once in circulation, they can become ‘sticky’

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35
Q

What are the features of cells on blood film in AML?

A

High % of blast cells with rods= auer rods

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36
Q

In which leukaemia is a coag screen particularly critical?

A

APML= acute promyelocytic anaemia

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37
Q

What is the treatment for APML?

A

FFP, fibrinogen, platelets, vitamin A. Easy to correct coagulopathy, however this must be done immediately due to mortality associated with hemorrhage

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38
Q

What is tumour lysis syndrome?

A

release of uric acid from cells destroyed by chemo, this can form crystals in the interstitial space and tubules of the kidney, causing AKI

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39
Q

Name five complications of chemotherapy?

A

failure, stunted growth and development in children, infections, neurotoxicity, infertility, secondary malignancy, cardiotoxicity, tumour lysis syndrome

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40
Q

Immunocompromised patient with neutropenic sepsis + infection. Which antibiotic regimen?

A

Escalate to IV piperacillin/tazobactam (tazocin) + (genatamicin if NEWS >7/septic shock/stem cell or organ transplant)

41
Q

Which antibiotic is added to piperacillin + tazocin when patient is immunocompromised and is in shock?

A

gentamicin

42
Q

Which type of leukaemia is most classically associated with a coagulopathy?

A

acute promyelocytic leukaemia (APML)

43
Q

What is the management of APML?

A

fresh frozen plasma
platelet transfusions
cryoprecipitate or fibrinogen concentrate

44
Q

Which translocation is involved in APML?

A

15+17 PML-RARA

45
Q

What are the consequences of PML-RARA translocation??

A

protein stops promyelocytes from differentiating and promotes tumour-like behaviour

46
Q

What is the emergency ORAL treatment for suspected APML

A

ATRA

47
Q

What is differentiation syndrome?

A

side effect of ATRA, rapid differentiation of malignant promyelocytes into more mature forms, causing a potentially fatal syndrome of weight gain, fever, hypotension, pulmonary infiltrates and respiratory failure as well as third-space fluid collections such as pleural and pericardial effusions.

48
Q

Which three investigations are required to confirm a diagnosis of APML?

A

peripheral blood flow cytometry
bone marrow biopsy
cytogenetics

49
Q

What are three causes of pancytopaenia?

A 
aplastic anaemia
acute leukaemia 
chronic leukaemia
splenomegaly 
drugs
50
Q

Which is the most common malignancy in childhood?

A

ALL, shows bimodal distribution

51
Q

What are the causes of aplastic anaemia?

A 
idopathic (always use this as answer in exam if unsure!!)
drugs
chemical
radiation exposure
viral illness
52
Q

Which drugs can cause aplastic anaemia?

A

carbamazepine, acetazolamide

53
Q

In which condition are target cells observed?

A

IDA, post-splenectomy

54
Q

In which condition are Heinz bodies observed?

A

denatured globin- G6PD and alpha-thalassaemia

55
Q

In which condition are Howell-Jolly bodies observed?

A

Post-splenectomy, spleen normally removes DNA, sickle cell

56
Q

In which condition is raised reticulocyte count observed?

A

1%= normal, raised in haemolytic anaemia

57
Q

Name two conditions in which shistocytes are observed?

A 
=fragments of RBCs
haemolytic uaraemic syndrome
DIC
thombotic thombocytopenic purpura
metalic heart valves
haemolytic anaemia
58
Q

Normal range for Hb in women?

A

120-165 g/L

59
Q

Normal range for Hb in men?

A

130-180 g/L

60
Q

Three symptoms of anaemia?

A 
Fatigue
Dyspnoea
Palpitations
Headache
Faintness
61
Q

Two signs of anaemia?

A 
pallor
conjunctival pallor
tachy
dyspnoea
cardiac enlargement
koilonichia
angular chelitis
atrophic glossitis
brittle hair and nails
62
Q

Two causes of microcytic anaemia?

A 
TAILS
Thalassaemia
Anaemia of chronic disease
IDA
Lead poisonning
Sideroblastic anaemia
63
Q

Two causes of normocytic anaemia?

A 
3A's 2H's
Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism
(+pregnancy, renal failure)
64
Q

Two causes of macrocytic anaemia?

A

Megaloblastic: Vit B12 or folate deficiency. Anti-folate drugs

Normoblastic: alcohol, hypothyroidism, liver disease, reticulocytosis, drugs

65
Q

Two signs of IDA?

A

Koilonychia
angular chelitis
atrophic glossitis
brittle hair and nails

66
Q

Aside from the initial blood test, name one other investigations for anaemia?

A

OGD
colonoscopy
bone marrow biopsy

67
Q

Name a drug that can interfere with iron absorption?

A

PPIs- lansoprazole or omeprazole

68
Q

Name a condition that can interfere with iron absorption?

A

IBD

69
Q

Three causes of IDA?

A

pregnancy
blood loss- mennorhagia, cancer
iron deficiency- poor diet
poor absorption- coeliac, crohn’s

70
Q

How is IDA determined in the lab?

A

TIBC= transferrin saturation

71
Q

Patient has high value for TBC. What does this indicate?

A

high serum iron levels

72
Q

Name two causes of iron overload

A

excess iron in diet

acute liver damage (liver=storage site for iron)

73
Q

Two methods of improving iron levels of patient?

A

oral iron= ferrous sulphate
iron infusion
blood transfusion

74
Q

What is pernicious anaemia?

A

a cause of B12 deficiency

75
Q

Briefly explain the pathophysiology of pernicious anaemia

A

Parietal cells of stomach produce intrinsic factor, which is required for absorption of B12 in the ileum. Pernicious anaemia is an autoimmune condition where antibodies from against parietal cells or intrinsic factor, therefore impacting the ability to absorb B12

76
Q

Two effects of B12 deficiency?

A 
peripheral neuropathy
paraesthesia
loss of vibration and proprioception
visual changes
mood or cognitive changes
77
Q

Patient with peripheral neuropathy and parasthesia. Which haematological condition should you test them for

A

pernicious anaemia and B12 deficiency

78
Q

Two specific investigations for pernicious anaemia?

A

intrinsic factor antibody

gastric parietal cell antibody

79
Q

How can haemolytic anaemia be divided?

A

inherited

acquired

80
Q

Two examples of inherited haemolytic anaemias?

A

hereditary spherocytosis
thalassaemia
sickle cell anaemia
G6PD deficiency

81
Q

Two examples of acquired haemolytic anaemia?

A

autoimmune haemolytic anaemia
prosthetic valve
alloimmune haemolytic anaemia (tranfusions and haemolytic disease of newborn)

82
Q

Three clinical features that result from the destruction of RBCs?

A

anaemia
jaundice
splenomegaly

83
Q

Three investigations for haemolytic anaemia?

A 
Direct Coombs test
FBC
Blood film- schistocytes
Bilirubin- raised from destruction of RBCs
Reticulocyte count
84
Q

Two features of hereditary spherocytosis presentation?

A

jaundice
gallstones
splenomegaly

85
Q

Treatment of hereditary spherocytosis?

A

folate
splenectomy
cholecystectomy

86
Q

Name two triggers for G6PD?

A

infections
medications
fava beans

87
Q

Two drugs that trigger G6PD?

A

primaquine=antimalarial
sulfasalazine
sulphylureas

88
Q

What are the two types of autoimmune haemolytic anaemia

A

warm

cold

89
Q

One cause of cold and one of warm type haemolytic anaemia?

A

warm- idiopathic

cold- lymphoma, leukaemia, SLE, HIV, EBV, drugs

90
Q

Name one drug that causes haemolytic anaemia?

A

penicillin

91
Q

Briefly explain the pathophysiology of thalassaemia

A

Defects in alpha and beta protein chains of haemoglobin

92
Q

Two investigations for thalassaemia

A

FBC- microcytic anaemia

DNA testing

93
Q

WHat is a common complication of thalassaemia?

A

iron overload- monitor ferritin

94
Q

Two effects of iron overload?

A

similar to what is seen in haemochromatosis

  • fatigue
  • liver cirrhosis
  • heart failure
  • arthritis
  • diabetes
95
Q

Which diet is deficient in B12?

A

vegetarian/vegan

96
Q

Does intravascular haemolysis occur in warm or cold type?

A

cold type

97
Q

Three complications of sickle cell anaemia?

A

anaemia
infection risk
stroke
sickle cell crises

98
Q

57 y/o lady with lemon tinge to skin and impaired vibration sense in her distal legs + fatigued. Which anaemia does she have?

A

pernicious anaemia

99
Q

Patient with hypersegmented neutrophils and macrocytic anaemia. What is the likely diagnosis? Which investigation would confirm diagnosis?

A

Megaloblastic anaemia

Haematinics- B12/folate

Haematology (12 decks)

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