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02F > Haematology > Flashcards

Haematology Flashcards

1
Q

define anaemia

A

low Hb

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2
Q

TAILS: causes of microcytic anaemia?

A
  • Thalassaemia
  • Anaemia of chronic disease
  • Iron def
  • Lead poisoning
  • Sideroblastic
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3
Q

3As and 2Hs: causes of normocytic anaemia?

A
  • Acute blood loss
  • Anaemia of chronic disease
  • Aplastic anaemia
  • Haemolytic anaemia
  • Hypothyroidism
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4
Q

how can macrocytic anaemia be classified?

A
  • megaloblastic

- normoblastic

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5
Q

causes of megaloblastic anaemia?

A
  • B12 def

- folate def

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6
Q

causes of normoblastic, macrocytic anaemia?

A
  • alcohol
  • reticulocytosis
  • hypothyroidism
  • liver disease
  • azathioprine therapy
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7
Q

symptoms of anaemia?

A
  • tiredness
  • SOB
  • headaches
  • dizziness
  • palpitations
  • worsening of other disease
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8
Q

which conditions may worsen with anaemia?

A
  • angina
  • heart failure
  • PVD
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9
Q

which 3 symptoms of anaemia are specific to iron deficiency anaemia?

A
  • pica
  • hair loss
  • restless leg syndrome
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10
Q

signs O/E of anaemia?

A
  • pale skin
  • conjunctival pallor
  • nail signs
  • tachycardia
  • raised RR
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11
Q

which signs O/E are specific to iron deficiency anaemia?

A
  • koilonychia (spoon nails)
  • angular chelitis
  • atrophic glossitis
  • brittle hair and nails
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12
Q

which type of anaemia is jaundice specific to?

A

haemolytic anaemia

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13
Q

which type of anaemia do bone deformities indicate?

A

thalassaemia

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14
Q

findings O/E of anaemia due to CKD?

A
  • oedema
  • HTN
  • excoriations on the skin
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15
Q

bloods done to investigate for anaemia?

A
  • Hb
  • MCV
  • B12 and folate
  • ferritin
  • blood film
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16
Q

non-blood test investigations done in anaemia?

A
  • oesophageal-gastroduodenoscopy (OGD)

- bone marrow biopsy

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17
Q

causes of iron deficiency?

A
  • insufficient dietary uptake
  • increased requirements (e.g. pregnancy)
  • iron being lost from a slow bleed
  • inadequate absorption (e.g. coeliac)
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18
Q

where in the gut does iron get absorbed? what is the soluble form of iron?

A
  • duodenum and jejunum

- ferrous (Fe 2+)

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19
Q

how is iron converted from the insoluble Fe3+ to the soluble Fe2+?

A

using stomach acid

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20
Q

how can PPIs cause an iron deficiency?

A
  • they reduce gastric acid secretion
  • stops iron being converted to the soluble form of Fe 2+
  • therefore not absorbed
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21
Q

most common cause of iron deficiency in adults not menstruating?

A

blood loss in the GI tract

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22
Q

most common cause of iron deficiency in children?

A

dietary insufficiency

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23
Q

how can transferrin saturation be calculated?

A

serum iron / TIBC

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24
Q

what can cause a raised ferritin?

A

infection

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25
Q

how are TIBC and transferrin affected by iron deficiency?

A

both increase

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26
Q

how are TIBC and transferrin affected by iron overload?

A

both decrease

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27
Q

what could cause iron studies to give an iron overload impression?

A
  • iron supplements

- acute liver damage

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28
Q

3 management options for iron deficiency anaemia?

A
  1. blood transfusion
  2. iron infusion
  3. PO ferrous sulfate
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29
Q

how should Hb rise with oral iron supplements?

A

10g/L per week

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30
Q

what are the 2 causes of B12 deficiency?

A
  • insufficient dietary uptake

- pernicious anaemia

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31
Q

what is needed to absorb B12? where is this secreted?

A
  • intrinsic factor

- parietal cells of the stomach

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32
Q

where in the gut does B12 get absorbed?

A

terminal ileum

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33
Q

neuro signs of B12 deficiency?

A
  • peripheral neuropathy, incl numbness / paraesthesia
  • loss of vibration / proprioception
  • visual changes
  • mood / cognitive changes
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34
Q

pathophysiology of pernicious anaemia?

A
  • antibodies have formed against parietal cells / intrinsic factor
  • stops B12 being absorbed in the terminal ileum
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35
Q

how is pernicious anaemia diagnosed?

A

test for the following antibodies:

  • intrinsic factor antibody (1st line)
  • gastric parietal cell antibody
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36
Q

management of insufficient dietary B12?

A

PO cyanocobalamin supplements

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37
Q

management of pernicious anaemia? hint: can’t be oral because won’t be absorbed

A

IM hydroxycobalamin

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38
Q

why is it important to treat a B12 def before a folate def (in pts with both)?

A

giving folic acid to pt with B12 def can cause subacute combined degeneration of the spinal cord

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39
Q

how can causes of haemolytic anaemia be classified?

A

inherited vs acquired

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40
Q

inherited forms of haemolytic anaemia?

A
  • hereditary spherocytosis
  • thalassaemia
  • sickle cell anaemia
  • G6PD deficiency
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41
Q

acquired forms of haemolytic anaemia?

A
  • autoimmune haemolytic anaemia, incl. haemolytic disease of the newborn
  • paroxysmal nocturnal haemoglobinuria
  • microangiopathic haemolytic anaemia
  • prosthetic valve-related haemolysis
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42
Q

signs O/E of haemolytic anaemia? (hint: all due to RBC destruction)

A
  • anaemia
  • splenomegaly
  • jaundice
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43
Q

investigations for haemolytic anaemia?

A
  • FBC (normocytic)
  • blood film
  • direct Coombs test
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44
Q

what is seen on the blood film in haemolytic anaemia?

A

schistocytes (fragments of RBCs)

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45
Q

when does the direct Coombs test give a positive result?

A

autoimmune haemolytic anaemia

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46
Q

mode of inheritance of hereditary spherocytosis?

A

autosomal dominant

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47
Q

presentation of hereditary spherocytosis?

A
  • jaundice
  • gallstones
  • splenomegaly
  • aplastic crisis
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48
Q

which organism can bring on an aplastic crisis in hereditary spherocytosis patients?

A

parvovirus

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49
Q

how is hereditary spherocytosis diagnosed?

A
  • FHx
  • clinical features
  • blood film
  • FBC
  • reticulocyte count (raised)
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50
Q

findings on blood film in hereditary spherocytosis?

A

spherocytes

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51
Q

finding on FBC in hereditary spherocytosis? hint: it’s a rogue one

A

MCHC is raised

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52
Q

treatment of hereditary spherocytosis?

A
  • folate supplements

- splenectomy

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53
Q

key difference between hereditary spherocytosis and hereditary elliptocytosis?

A
  • in the second one, RBCs are ellipse shaped

- otherwise identical

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54
Q

mode of inheritance for G6PD deficiency?

A
  • X linked recessive
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55
Q

G6PD deficiency is more common in patients of which descent?

A

Mediterranean / African

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56
Q

what can trigger a G6PD deficiency crisis?

A
  • infection
  • drugs
  • fava beans (broad beans)
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57
Q

drugs which cause G6PD deficiency crisis?

A
  • primaquine
  • ciprofloxacin
  • sulfonylurea
  • sulfasalazine
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58
Q

how is G6PD deficiency diagnosed?

A

G6PD enzyme assay

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59
Q

signs O/E of G6PD deficiency crisis?

A
  • jaundice (usually in neonates)
  • gallstones
  • anaemia
  • splenomegaly
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60
Q

what is seen on the blood film of someone in G6PD deficiency crisis?

A

Heinz bodies

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61
Q

how can autoimmune haemolytic anaemia (AIHA) be classified?

A
  • warm type: haemolysis at normal or higher temperatures

- cold type: haemolysis at colder temps

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62
Q

causes of warm AIHA?

A

idiopathic

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63
Q

causes of cold AIHA?

A
  • lymphoma
  • leukaemia (e.g. CLL)
  • SLE
  • infections (EBV, CMV, HIV)
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64
Q

management of AIHA?

A
  • blood transfusions
  • prednisolone
  • rituximab
  • splenectomy
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65
Q

what is alloimmune haemolytic anaemia? give 2 types

A
  • immune reaction destroying foreign RBCs in circulation
  • transfusion reaction
  • haemolytic disease of the newborn
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66
Q

what are the chains making up normal adult Hb?

A

2 alpha + 2 beta globin chains

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67
Q

pathophysiology of thalassaemia?

A
  • genetic defect causing defective alpha / beta globin chain production
  • spleen then recognises RBCs as damaged and breaks them all down
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68
Q

potential signs and symptoms of thalassaemia?

A
  • anaemia (microcytic) and assoc signs (fatigue, pallor)
  • jaundice
  • gallstones
  • splenomegaly
  • poor growth and development
  • pronounced forehead and cheekbones
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69
Q

investigations in thalassaemia?

A
  • FBC (microcytic anaemia)
  • Hb electrophoresis
  • DNA testing
  • screened for in pregnancy booking appt
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70
Q

how can thalassaemia (and treatment) result in iron overload?

A
  • increased Fe absorption in response to anaemia

- recurrent blood transfusion therapy

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71
Q

what needs to be monitored in thalassaemia patients? why?

A
  • serum ferritin

- to check for iron overload

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72
Q

presentation of iron overload in thalassaemia? hint: similar to haemachromatosis

A
  • fatigue
  • liver cirrhosis
  • infertility / impotence
  • heart failure
  • arthritis
  • DM
  • osteoporosis, joint pain
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73
Q

where is the affected gene in alpha thalassaemia?

A

chromosome 16

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74
Q

where is the affected gene in beta thalassaemia?

A

chromosome 11

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75
Q

how is iron overload in thalassaemia managed?

A
  • limit blood transfusions

- iron chelation

76
Q

management of alpha thalassaemia?

A
  • monitor FBC
  • blood transfusions
  • splenectomy
  • BM transplant (sometimes curative)
77
Q

what are the types of beta thalassaemia?

A
  • thalassaemia minor
  • ” “ intermedia
  • ” “ major
78
Q

presentation of thalassaemia minor?

A
  • mild microcytic anaemia

- only monitoring needed, no treatment

79
Q

presentation of thalassaemia minor? management?

A
  • mild microcytic anaemia

- only monitoring needed, no treatment

80
Q

presentation of thalassaemia major?

A
  • severe microcytic anaemia
  • splenomegaly
  • bone deformities
81
Q

pathophysiology of sickle cell anaemia?

A
  • abnormal beta globin chain gene on chromosome 11
  • this causes HbS to form instead of HbA
  • HbS causes RBCs to be sickle-shaped
82
Q

what is the relation between sickle cell trait and malaria?

A

having sickle cell trait reduces the severity of malaria infection

83
Q

how is sickle cell disease tested for in newborns?

A

part of the day 5 heel-prick test (Guthrie)

84
Q

complications of sickle cell anaemia?

A
  • increased risk of infection
  • sickle cell crisis
  • avascular necrosis of large joints (e.g. hip)
  • pulmonary HTN
  • CKD
  • priapism in men
  • acute chest syndrome
85
Q

general management principles of sickle cell anaemia?

A
  • avoid crisis triggers (e.g. stay well hydrated)
  • ABx prophylaxis (penicillin V)
  • hydroxycarbamide to stimulate HbF production
  • blood transfusion for severe anaemia
  • bone marrow transplant can be curative
86
Q

potential triggers of a sickle cell crisis?

A
  • infection
  • cold
  • dehydration
  • significant life events
87
Q

management of a sickle cell crisis?

A

all supportive:

  • low threshold for admission
  • treat underlying cause (e.g. ABx, keep warm, hydrated)
  • paracetamol / ibuprofen
  • penile aspiration if priapism
88
Q

pathophysiology of a vaso-occlusive crisis?

A
  • sickle-shaped RBCs clog up capillaries

- causes distal ischaemia

89
Q

presentation of vaso-occlusive crisis?

A
  • pain
  • fever
  • symptoms of underlying infection
  • dehydration
  • raised haematocrit
  • priapism in men
90
Q

pathophysiology of splenic sequestration crisis? how does it present?

A
  • sickle-shaped RBCs blocking blood flow within the spleen
  • blood pools within the spleen
  • causes severe anaemia, may progress to shock
91
Q

management of splenic sequestration crisis?

A
  • emergency
  • blood transfusions
  • fluid resus
92
Q

what is an aplastic crisis in sickle cell disease?

A

temporary cessation of erythropoiesis

93
Q

typical trigger of an aplastic crisis?

A

parvovirus B19 infection

94
Q

management of aplastic crisis?

A
  • blood transfusions if needed

- otherwise self-resolving within a week

95
Q

how is acute chest syndrome of sickle cell disease diagnosed?

A

both must be present:

  • fever / resp symptoms
  • new infiltrates seen on CXR
96
Q

infective causes of acute chest syndrome?

A
  • bronchiolitis

- pneumonia

97
Q

non-infective causes of acute chest syndrome?

A
  • pulmonary vaso-occlusion

- fat emboli

98
Q

management of acute chest syndrome?

A
  • emergency
  • ABx / antivirals for infections
  • blood transfusions for anaemia
  • incentive spirometry (encourages deep breathing)
  • NIV / intubation are last line
99
Q

age groups typically affected by ALL?

A

<5 years and >45 years

100
Q

age group typically affected by CLL?

A

> 55 years

101
Q

age group typically affected by CML?

A

> 65 years

102
Q

age group typically affected by AML?

A

> 75 years

103
Q

presentation of leukaemia? hint: pancytopenia

A
  • non-specific
  • fatigue
  • fever
  • FTT if child
  • pallor (anaemia)
  • petechiae, abnormal bruising (thrombocytopenia)
  • abnormal bleeding
  • lymphadenopathy
  • hepatosplenomegaly
104
Q

differentials for a non-blanching rash?

A
  • leukaemia
  • meningococcal septicaemia
  • vasculitis
  • HSP (lower limbs, buttocks)
  • ITP
  • NAI (children / vulnerable adults)
105
Q

initial investigation for leukaemia?

A

urgent FBC (<48h) for all with suspected leukaemia

106
Q

investigations for leukaemia?

A
  • FBC
  • blood film
  • lactate dehydrogenase (LDH, raised)
  • bone marrow biopsy
  • CXR
  • lymph node biopsy
  • LP
  • CT, MRI, PET (for staging)
107
Q

what might the blood film show in leukaemia?

A
  • abnormal cells

- inclusions

108
Q

where is a bone marrow biopsy usually taken from?

A

iliac crest

109
Q

which cell type over-proliferates in ALL and CLL?

A

usually B-lymphocytes

110
Q

which genetic condition is ALL associated with?

A

downs syndrome

111
Q

blood film findings in ALL?

A

blast cells

112
Q

characteristic chromosomal change seen in CML in adults?

A

philadelphia chromosome

113
Q

what type of anaemia could CLL give?

A

warm autoimmune haemolytic anaemia

114
Q

which other cancer could CLL transform into?

A
  • high-grade lymphoma

- called richter’s transformation

115
Q

blood films findings in CLL?

A

“smudge” / “smear” cells (WBCs which ruptured in the process of preparing the film)

116
Q

3 phases of CML?

A
  • chronic phase
  • accelerate phase
  • blast phase
117
Q

3 phases of CML?

A
  • chronic phase (asymptomatic, 5 years)
  • accelerate phase
  • blast phase
118
Q

what is seen in the blast cells on a blood film in AML?

A

auer rods

119
Q

which cancer could a myeloproliferative disorder (e.g. PRV) transform into?

A

AML

120
Q

management of leukaemia?

A
  • chemotherapy
  • steroids
  • radiotherapy
  • bone marrow transplant
  • surgery
121
Q

complications of chemotherapy for leukaemia?

A
  • failure
  • stunted growth in children
  • neurotoxicity
  • infertility
  • cardiotoxicity
  • secondary malignancy
  • tumour lysis syndrome
122
Q

pathophysiology of tumour lysis syndrome?

A
  • uric acid released from cells destroyed by chemotherapy
  • form crystals in kidneys
  • causes AKI
123
Q

management of tumour lysis syndrome?

A

allopurinol and rasburicase to reduce uric acid levels

124
Q

how can lymphoma be categorised?

A
  • hodgkin’s

- non-hodgkin’s (all the other types)

125
Q

peak ages affected by hodgkin’s lymphoma? hint: bimodal

A

aged 20 and then aged 75

126
Q

risk factors for hodgkin’s lymphoma?

A
  • HIV
  • EBV
  • autoimmune (RA, sarcoidosis)
  • FHx
127
Q

presentation of hodgkin’s lymphoma?

A
  • lymphadenopathy
  • B symptoms
  • fatigue
  • itching
  • cough
  • SOB
  • abdo pain
  • recurrent infections
128
Q

what are B symptoms? list them

A
  • systemic symptoms of lymphoma
  • fever
  • weight loss
  • night sweats
129
Q

investigations in hodgkin’s lymphoma

A
  • lymph node biopsy is diagnostic
  • LDH (raised)
  • CT, MRI, PET to stage
130
Q

lymph node biopsy findings in hodgkin’s lymphoma?

A

reed-sternberg cells (large B cells with multiple nuclei)

131
Q

what is ann arbor staging used for? what does it take into account?

A
  • scoring system used to stage all types of lymphoma
  • considers whether lymph nodes involved are in same region or not
  • considers whether they are on one side of diaphragm (or on both)
132
Q

management of hodgkin’s lymphoma?

A
  • chemotherapy

- radiotherapy

133
Q

prognosis of hodgkin’s lymphoma?

A
  • chemo and radiotherapy are curative
  • they both carry own risk of secondary malignancy
  • B = BAD (B-symptoms have worse prognosis)
134
Q

types of non-hodgkin’s lymphoma?

A
  • burkitt lymphoma
  • MALT lymphoma
  • diffuse large B cell lymphoma
135
Q

key association with MALT lymphoma?

A

H. pylori infection

136
Q

which other conditions are associated with burkitt lymphoma? hint: all infections

A
  • HIV
  • EBV
  • malaria
137
Q

risk factors for non-hodgkin’s lymphoma?

A
  • HIV
  • EBV
  • H. pylori (MALT)
  • hep B / C
  • exposure to pesticides
  • FHx
138
Q

management of non-hodgkin’s lymphoma?

A
  • watchful waiting
  • chemotherapy
  • rituximab
  • radiotherapy
  • stem cell transplant
139
Q

pathophysiology of myeloma? what is multiple myeloma?

A
  • genetic mutation causes rapid proliferation of plasma cells (B cells which produce antibodies) in bone marrow
  • myeloma affecting multiple parts of the body
140
Q

skin sign of pernicious anaemia?

A

gives “lemon tinged” skin

141
Q

most common immunoglobulin to be raised in myeloma?

A

IgG

142
Q

urinalysis finding in myeloma?

A

bence jones protein

143
Q

which bones are most commonly affected in myeloma?

A
  • skull
  • spine
  • long bones
  • ribs
144
Q

effects of myeloma on bone turnover? result of this?

A
  • increases osteoclast activity (reabsorb bone Ca into blood)
  • pathological fractures
  • hypercalcaemia
145
Q

how does myeloma cause renal impairment? hint: multifactorial

A
  • lots of Igs block tubular flow
  • high Ca
  • dehydration
  • bisphosphonate therapy
    … all cause impairment
146
Q

how is plasma viscosity affected in myeloma?

A
  • increases

- due to increased Igs

147
Q

complications relating to increased plasma viscosity in myeloma?

A
  • easy bruising and bleeding
  • visual loss
  • purple extremities
  • heart failure
148
Q

what type of anaemia arises from myeloma?

A

normocytic, normochromic

149
Q

how does myeloma cause anaemia?

A

bone marrow being resorbed

150
Q

presentation of myeloma?

A
  • high Ca
  • Renal failure
  • Anaemia
  • Bone pain / lesions
  • plus complications of plasma viscosity
151
Q

risk factors for myeloma?

A
  • age >65
  • Black
  • male
  • FHx
  • obesity
152
Q

what must be considered in anyone over 60 with bone pain? which investigation is key?

A
  • myeloma

- urgent FBC required

153
Q

findings on bloods for myeloma?

A
  • pancytopenia
  • high Ca
  • raised ESR
  • raised plasma viscosity
154
Q

BLIPE: initial investigations for multiple myeloma?

A
  • Bence jones protein (urine electrophoresis)

rest are all in blood:

  • Light-chain assay
  • Immunoglobulins
  • Protein Electrophoresis
155
Q

diagnostic investigation for multiple myeloma?

A

bone marrow biopsy

156
Q

pereferred investigation to stage multiple myeloma?

A

whole body MRI

157
Q

signs on X-ray in multiple myeloma?

A
  • punched out lesions
  • lytic lesions
  • “rain-drop skull” appearance
158
Q

management of myeloma?

A
  • bortezomide
  • thalidomide
  • dexamethasone
  • stem cell transplant
  • VTE prophylaxis
159
Q

management of bone disease secondary to myeloma?

A
  • bisphosphonates
  • radiotherapy
  • ortho surgery
  • cement augmentation
160
Q

complications associated with myeloma?

A
  • infection
  • peripheral neuropathy
  • spinal cord compression
161
Q

what are the 3 types of myeloproliferative disorder?

A
  • primary myelofibrosis
  • polycythaemia vera
  • essential thrombocythaemia
162
Q

gene mutations associated with myeloproliferative disorders?

A
  • JAK2
  • MPL
  • CALR
163
Q

presentation of myeloproliferative disorders?

A
  • initially asymptomatic
  • B symptoms
  • anaemia
  • abdo pain (splenomegaly)
  • portal HTN
  • bleeding, petechiae (low platelets)
  • red face (raised RBCs)
  • infections (low WCC)
164
Q

feautres of polycythaemia vera?

A
  • plethoric conjunctiva and face
  • “ruddy” complexion
  • splenomegaly
  • pruritis, worse after hot bath
  • HTN
165
Q

findings on FBC in polycythaemia vera?

A

isolated rise in Hb

166
Q

findings on FBC in essential thrombocythaemia?

A

raised platelets

167
Q

findings on FBC in myelofibrosis?

A

more variable:

  • anaemia (low Hb)
  • high OR low WCC
  • high OR low platelets
168
Q

findings on blood film in myelofibrosis?

A
  • teardrop-shaped RBCs
  • varying in size (poikilocytosis)
  • blast cells
169
Q

diagnostic investigation and finding for myeloproliferative disorders?

A
  • bone marrow biopsy

- comes back “dry”

170
Q

management of myelofibrosis?

A
  • if mild, none needed
  • allogeneic stem cell transplant could be curative
  • chemotherapy
  • supportive (for anaemia / splenomegaly / portal HTN)
171
Q

management of polycythaemia vera?

A
  • venesection
  • aspirin
  • chemotherapy
172
Q

management of essential thrombocythaemia?

A
  • aspirin

- chemotherapy

173
Q

findings on FBC in myelodysplastic syndrome?

A
  • anaemia
  • neutropenia (low neutrophils)
  • thrombocytopenia (low platelets)
174
Q

risk factors for myelodysplastic syndrome?

A
  • age >60
  • chemotherapy
  • radiotherapy
175
Q

which malignancy could myelodysplastic syndrome transform into?

A

AML

176
Q

presentation of myelodysplastic syndrome?

A
  • could be asymptomatic / found incidentally
  • fatigue, pallor SOB
  • recurrent infections
  • purpura, bleeding
177
Q

how can a diagnosis of myelodysplastic syndrome be confirmed?

A

on bone marrow aspiration and biopsy

178
Q

management of myelodysplastic syndrome?

A
  • watchful waiting
  • blood transfusions if severely anaemic
  • chemo
  • stem cell transplant
179
Q

causes of thrombocytopenia relating to reduced platelet production?

A
  • sepsis
  • B12 / folate deficiency
  • liver failure
  • leukaemia
  • myelodysplastic syndrome
180
Q

causes of thrombocytopenia relating to increased platelet destruction?

A
  • drugs
  • alcohol
  • ITP
  • TTP
  • haemolytic uraemic syndrome
181
Q

drugs which can cause thrombocytopenia?

A
  • heparin
  • valproate
  • methotrexate
  • isotretinoin
  • antihistamines
  • PPIs
182
Q

presentation of thrombocytopenia?

A
  • easy bruising
  • prolonged bleeding
  • epistaxis
  • menorrhagia
  • bleeding gums
  • blood in urine / stools
183
Q

differentials for prolonged bleeding?

A
  • thrombocytopenia
  • haemophilia A or B
  • vWD
  • DIC
184
Q

pathophysiology of ITP?

A

antibodies made against platelets

185
Q

management of ITP?

A
  • prednisolone
  • IV Igs
  • rituximab
  • splenectomy
186
Q 
CML 
pathophysiology 
RF 
Features 
Investigation 
Management
A

proliferation of mature myeloid cells in particular granulocytes
Philadelphia chromosome translocation 9:22
Features- fatigue, tiredness, easy bruising, hepatosplenomegaly, epistaxis, bone pain pallor

Investigation- Leucocytosis and granulocytosis, reduced reticulocyte count

Management
Imatinib and hydroxyurea

02F (18 decks)

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