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Pass Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

What do Howell-Jolly bodies suggest?

A

Hyposplenism/non-functioning spleen

Can occur in sickle cell disease due to splenic infarctions

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2
Q

What causes sickle-cell anaemia?

A

Autosomal recessive condition

Synthesis of an abnormal haemoglobin chain termed HbS

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3
Q

How can we diagnose sickle cell anaemia?

A

Haemoglobin electrophoresis

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4
Q

Is sickle cell normocytic, microcytic or macrocytic?

A

Normocytic

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5
Q

What does antiphospholipid syndrome cause?

A

Prolonged APTT and normal PT

Thrombocytopenia

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6
Q

How do we manage antiphospholipid syndrome?

A

Warfarin

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7
Q

What are the features of antiphospholipiid syndrome?

A

Venous/arterial thrombosis
Recurrent fetal loss
Thrombocytopenia
Prolonged APTT

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8
Q

What is antiphospholipid syndrome associated with?

A

SLE
Other autoimmune diisorders
Lymphoproliferative disorders

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9
Q

Does unfractionated heparin require monitoring?

A

Yes - APTT

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10
Q

Does LMWH require monitoring?

A

No

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11
Q

Clinical features of anaemia

A

SOB on exertion
Headaches
Tiredness

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12
Q

What can develop in the elderly if they have anaemia?

A

Congestive heart failure

Angina

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13
Q

Signs and anaemia

A

Koilonychia - Iron deficiency

Jaundice - haemolytic anaemia/megaloblastic anaemia

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14
Q

Investigations in anaemia

A

FBC
Stained blood film
Haematinics

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15
Q

Classification of anaemia by red cell size

A

Macrocytic >98
Normocytic 78-98
Microcytic <78

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16
Q

Macrocytic causes of anaemia

A

Megaloblastic

B12/folate deficiency

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17
Q

Normocytic causes of anaemia

A 
Haemolytic anaemias (mostly)
Anaemia of chronic disease
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18
Q

Microcytic causes of anaemia

A 
Iron deficiency
Thalassemias
Other haemoglobin defects
Congenital sideroblastic anaemia
Some anaemias of chronic disease
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19
Q

What is anaemia of chronic disease?

A

A common, normocytic anaemia that occurs in patients with inflammatory or malignant disease

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20
Q

What might you see in haematinics in anaemia of chronic disease?

A

Reduced serum iron/total iron-binding capacity (transferrin)
Normal/raised ferritin

ESR/CRP usually raised

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21
Q

Pathophysiology of anaemia of chronic disease

A

Hepcidin is release by the liver in response to inflammatory cytokines
Hepcidin reduces iron absorption in gut and reduces release by macrophages into the plasma

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22
Q

How do we treat anaemia of chronic disease?

A 
Treat the chronic disease
Recombinant EPO (if patient has RA, malignancy)
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23
Q

Which protein controls serum iron levels?

A

Hepcidin

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24
Q

Causes of iron deficiency?

A

Blood loss
Increased demand (growth, pregnancy, prematurity)
Malabsorption (rarely main cause)
Poor dietary intake (usually not the main cause)

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25
Q

Signs of iron deficiency?

A

Koilonychia
Angular cheilitis
Glossitis

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26
Q

Laboratory findings in iron deficiency?

A

Hypochromic microcytic anaemia

Raised platelet count

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27
Q

Haematinics in iron deficiency?

A

Serum iron low
Raised transferrin
Iron binding capacity lowered

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28
Q

Transferrin and ferritin

A

Ferritin is a protein that stores iron and so is a measure of your body’s stored iron
Transferrin is the main transporter of iron in the blood

When ferritin is low your body produces more transferrin (TIBC) to allow for more iron transportion

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29
Q

How do we treat iron deficient anaemia?

A

Ferrous sulfate (iron) before meals 3 times a day

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30
Q

Side effects of ferrous sulfate

A

Abdominal pain, diarrhoea, constipation

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31
Q

What is iron overload?

A

This is a pathological state in which the body releases its stores of iron
It is often associated with organ dysfunction as a result of iron deposition

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32
Q

What causes iron overload?

A

Haemochromatosis (genetic) - excessive iron absorption
Excess dietary iron
Repeated blood transfusions in patients with severe refractory anaemia

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33
Q

Clinical features of iron overload?

A

Cardiomyopathy (dysrhythmias, cong. heart failure)
Growth/sexual development reduction: delayed puberty, DM, hypothyroidism
Haemosiderosis or cirrhosis (liver)
Excessive melanin pigmentation
Excessive infections
Arthropathy

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34
Q

Haemochromatosis

A

Autosomal recessive condition
Results in excessive iron absorption
Usually due to a mutation in the HFE gene
Genes coding for hepcidin affected, low production of hepcidin (protein that regulates iron absorption)

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35
Q

Haematinics in haemochromatosis

A

Raised serum iron
Raised transferrin
Raised serum ferritin

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36
Q

Treatment of haemochromatosis

A

Regular venesctions to reduce iron level to normal

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37
Q

What is sideroblastic anaemia?

A

Anaemia in which the body is unable to use iron to make RBCs (haem specifically)
Iron is instead seen in granules around the nucleus in developing erythroblasts (ringed sideroblasts)

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38
Q

What might you see on blood film in sideroblastic anaemia?

A

Hypochromic microcytic red cells

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39
Q

Treatment of sideroblastic anaemia

A

Symptomatic

Regular blood transfusion

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40
Q

Causes of B12 deficiency

A

Inadequate diet (e.g. vegans)
Malabsorption - pernicious anaemia mainly
Gastrectomy etc

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41
Q

What is pernicious anaemia

A

An autoimminune gastritis with reduced secretion of intrinsic factor and acid
Intrinsic factor is required for B12 absorption, so its reduction results in lowered B12 levels

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42
Q

Folate deficiency

A 
Poor dietary intake
Increased utilisation (pregnancy, severe chronic inflammatory and malignant disease)
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43
Q

Clinical features of B12 deficiency

A 
Gradual onset of anaemia features
Mild jaundice - caused by ineffective erythropoiesis
Glossitis
Angular stomatitis
Peripheral symmetrical neuropathy
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44
Q

Laboratory findings in B12 deficiency

A 
Macrocytic anaemia (oval macrocytes, hypersegmental neutrophils - 5+ nuclear lobes)
Reduction in leucocyte and platelet count
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45
Q

Treatment for B12 deficiency

A

Hydroxycobalamin 1mg intramuscularly 2-3 daily till 6 injections given
Then hydroxycobalamin 3 monthly

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46
Q

How do we investigate B12 deficiency?

A

History
IF tests
Parietal cell antibodies (present in 90% of PA)
Serum gastrin level (raised in PA)

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47
Q

Clinical features of folate deficiency

A

Same as B12 except NO peripheral neuropathy

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48
Q

Treatment for folic acid deficiency

A

5mg folic acid daily for 4 months

Either continue weekly or daily at different doses

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49
Q

Other causes of macrocytosis?

A

Alcohol is the most common cause of large RBCs

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50
Q

Clinical features of haemolytic anaemias

A

Anaemia
Jaundice
Splenomegaly

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51
Q

Hereditary causes of haemolytic anaemia

A

Spherocytosis - red cell membrane abnormality

G6PD deficiency - enzyme abnormality

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52
Q

Hereditary spherocytosis

A

Commoner in white people
Blood film shows microspherocytes and polychromasia
Reduction in life span (this can be treated with splenectomy though)
Give prophylactic folic acid

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53
Q

What are pigmented gallstones associated with?

A

Haemolytic anaemias

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54
Q

G6PD deficiency

A

X-linked (males typically affected)
Deficiency results in rbc’s becoming particularly sensitive to oxidative stress (e.g. from infection, drugs)
More common in black, mediterranean and middle-eastern populations

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55
Q

G6PD deficiency blood film

A

Normal inbetween episodes

During crises: red cells with absent haemoglobin, polychromasia

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56
Q

How do we screen for G6PD deficiency

A

NADPH

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57
Q

Management of G6PD deficiency

A

Stop offending drugs
Treat infection
Transfuse rbc’s if needed
Splenectomy

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58
Q

What do thalassemias cause?

A

Haemolytic and microcytic anaemias

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59
Q

Thalassemia

A

Autosomal recessive conditions in which there is a reduced synthesis of alpha or beta globins

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60
Q

How do we treat thalassemia

A

Transfusions of rbc’s

Iron chelation therapy with subcut. desferrioxamine

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61
Q

Laboratory findings in thalassemia

A

Severe anaemia with reduced mcv

Hypochromic, microcytic cells, target cells, erythroblasts

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62
Q

What is thalassemia trait

A

Mild hypochromic, microcytic anaemia

Iron stores are normal

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63
Q

Sickle cell disease

A

A chronic haemolytic anaemia caused by a point mutation in beta globin gene causing glutamic acid to substitute for valine

This causes insolubility of Hb S causing sickling and vascular occlusion

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64
Q

Sickle cell disease features

A

Vaso-occlusive crisis - sickling with blockage of small vessels. Common precipitants are infection, dehydration, acidosis and deoxygenation
Visceral sequestration crisis - sickling with pooling of red cells in liver, spleen and lungs
Aplastic crisis - following infection by B19 parvovirus, causes temporary arrest of erythropoiesis
Resistance to malaria
Increased susceptibility to infection
Pigment gallstones and cholecystitis

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65
Q

What regular testing do you have in sickle cell?

A

Retinal - due to predisposition to stroke/TIAs

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66
Q

Laboratory features of sickle cell

A

Haemoglobin level 70-90
Sickle cells
Large target cells
Splenic atrophy

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67
Q

O2 dissociation curve in sickle cell?

A

Shifted to the right

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68
Q

Which white cells are granulocytes?

A

Eosinophils
Basophils
Neutrophils

69
Q

Which cells are myeloid?

A

Red cells
Platelets
Granulocytes

70
Q

Which cells are lymphoid?

A

B cells
T cells
NK cells

71
Q

Causes of reactive neutrophilia

A 
Bacterial infection
Inflammation
Tauma
Tissue necrosis
DKA
Haemorrhage
72
Q

Causes of malignant neutrophilia

A

Myeloproliferative disorders

Myeloid leukaemias

73
Q

Which drugs cause neutrophilia

A

Steroids

Granulocyte colony-stimulating factor

74
Q

Causes of neutropenia

A 
Decreased production:
Bone marrow failure
Drugs: sulfonamides, chlorpromazine, clozapine, diuretics, deferipone, carbimazole, gold
Viral infection
Kostmann syndrome

Increased destruction:
Hypersplenism
Autoimmune (RA - Felty syndrome, connective tissue disorder)

75
Q

Causes of eosinophilia

A

Allergic diseases - asthma, hay fever, eczema, pulmonary hypersensitivity reaction
Skin diseases
Connective tissue disease

76
Q

Causes of basophilia

A

Myeloproliferative disorders

77
Q

When do you get lymphocytosis

A

Viral infections
Lymphoid neoplasia
Some bacterial infections (e.g. petussis)

78
Q

Hyposplenism

A

Reduces the body’s ability to make antibodies, clearance of intracellular organisms and impairs defence against toxins/organisms in the portal circulation

79
Q

Causes of hyposplenism

A

Recurrent thrombosis affecting the arterial systemic blood flow to the spleen (e.g. sickle cell)
Infiltration of the spleen (e.g. by amyloid)
Autoimmune disease with high levels of antibody-antigen complexes (that I assume can be deposited there?)

80
Q

Splenomegaly

A

Can cause pancytopenia

Can cause anaemia (due to dilution with increased plasma volume)

81
Q

Causes of splenomegaly

A

Haemolytic anaemia: hereditary spherocytosis, thallasemia major, sickle cell disease

Haem malignancies (can cause MASSIVE splenomegaly)

Storage disease - Gaucher, amyloid

Liver disease
Portal HTN
Cong. HF

Infection: malaria, bact. endocarditis, infectious mononucleosis

82
Q

Infectious mononucleosis

A

Caused by EBV of B lymphocytes
Fever, sore throat, lymphadenopathy
Rash if treated with amoxicillin
Jaundice, hepatomegaly and splenomegaly occasionally

83
Q

What does the spleen do?

A

Primarily concerned with filtering the blood (gets rid of old red cells) and also produces antibodies
Also contains half the body’s monocytes

84
Q

When is splenectomy beneficial

A

Haem conditions in which the spleen is the site of excessive destruction of cells

e.g. some haemolytic anaemias

85
Q

What do patients who’ve undergone splenectomy have to take?

A

Prophylactic abx for life - penicillin V or erythromycin

86
Q

Two types of acute leukaemia

A

Lymphoblastic

Myeloblastic

87
Q

AML

A

More common in adults than ALL

May occur as a primary disease, or secondary following a myeloproliferative disorder

88
Q

Features of AML

A 
Anaemia
Neutropenia (WCC will be high, but functioning neutrophils will be low)
Thrombocytopenia
Splenomegaly
Bone pain
89
Q

What classification for AML

A

FAB

90
Q

Features of acute promyeclotic leukaemia (M3)

A

DIC or thrombocytopenia at presentation

91
Q

Laboratory findings in AML but NOT in ALL

A

Auer rods

92
Q

When is ALL most common?

A

Most common malignancy of childhood

93
Q

Features of ALL

A

Anaemia
Neutropenia
Thrombocytopenia

Bone pain
Splenomegaly
Hepatomegaly

94
Q

How to treat acute leukaemia?

A

High dose chemotherapy to induce remission

4-6 weeks per course

95
Q

Remission regime in AML

A 
Anthracycline (daunorubicin)
Cytosine arabinoside (ara-C)
96
Q

Remission regime in ALL

A

Vincristine
Dexamethasone
L-asparaginase

Often with:
Daunorubicin
Cyclophosphamide

97
Q

What can we give in ALL to reduce CNS involvement?

A

Intrathecal injections of methotrexate

98
Q

Who has CML?

A

Marshall

99
Q

What is the Philadelphia chromosome?

A

An abnormal chromosome 22 caused by translocation of part of its arm to chromosome 9

Found in CML patients

100
Q

What is the fusion gene found in CML?

A

BCR-ABL1

101
Q

Peak age for CML?

A

25-45

102
Q

Symptoms of CML

A 
Weight loss
Night sweats
Itching
Left hypochondrial pain
Gout

Caused by viscosity of the blood:
Priapism
Visual disturbances
Headaches

103
Q

How common is splenomegaly in CML?

A

> 90% of cases have massive splenomegaly

104
Q

Laboratory findings in CML?

A 
Raised WCC (mainly neutrophils/myelocytes)
Raised basophils
Platelet count raised
Philadelphia chromosome
BCR:ABL1 gene
105
Q

What is the main cause of death in CML

A

Progression to AML/ALL

106
Q

Chronic phase of CML

A

Blood and bone marrow contain less than 10% blasts

Treat with imatinib (tyrosine kinase inhibitor)

107
Q

Accelerated phase of CML

A

10-19% blasts

Treat with tyrosine kinase inhibitor still but maybe also chemo

108
Q

CLL

A

Most common leukaemia seen in adults

Almost always monoclonal proliferation of well-differentiated B cells

109
Q

Features of CLL

A 
Often asymptomatic
Anorexia, weight loss
Bleeding
Infections
Lymphadenopathy
110
Q

Complications of CLL

A

Anaemia
Hypogammaglobulinaemia
Warm autoimmune haemolytic anaemia
Transformation to high grade lymphoma (Richter’s transformation)

111
Q

What might you see on blood film in CLL?

A

Smudge cells

Smear cells

112
Q

Treatment for CLL

A

Observation

Chemotherapy (cyclophosphamide, rituximab)

113
Q

Features of CLL

A 
Often asymptomatic
Lymphadenopathy**
Anorexia, weight loss
Bleeding
Infections
114
Q

Complications of CLL

A

Anaemia
Hypogammaglobulinaemia
Warm autoimmune haemolytic anaemia
Transformation to high grade lymphoma (Richter’s transformation)

115
Q

What might you see on blood film in CLL?

A

Smudge cells

Smear cells

116
Q

Treatment for CLL

A

Chemotherapy

117
Q

What two staging systems can we use in CLL

A

Rai staging (0-IV)

Binet staging (ABC)

118
Q

Rai staging

A 
0 - Lymphocytosis
I - Lymphocytosis with lymphadenopathy
II - Lymphocytosis with spleno/hepatomegaly
III - Lymphocytosis with anaemia
IV - Lymphocytosis with platelets <100
119
Q

Differentiating symptoms between ALL and AML

A

ALL: Meninges, testes involvement
AML: Skin, bones, gums

120
Q

What is polycythaemia

A

High level of red cells in blood

121
Q

Causes of polycythaemia

A

Can be true (an actual increase in erythrocytes):
Primary: Polycythaemia rubra vera (PRV)
Secondary: High altitude, cyanotic cong. heart disease, chronic lung disease, renal disease

Can be pseudo (relative - e.g. lower blood volume so higher conc.):
Dehydration
Diuretic therapy

122
Q

What causes PRV

A

A change in the JAK2 gene causing the bone marrow to produce too many red cells

This is NOT an inherited condition

123
Q

Symptoms of polycythaemia

A 
Headaches
Blurred vision
Red skin
Tiredness
Dizziness
Bleeding problems
Itchiness

(Blood becomes more viscous)

124
Q

What serious conditions can polycythaemia cause?

A

PE
DVT
MI
Stroke

125
Q

How do we treat polycythaemia?

A

Regular venesection

Hydroxycarbamide - lowers red cells numbers (it’s a chemo)
PPI for GI bleeds

Aspirin - lower risk of complications

126
Q

Treatment for thrombocytosis

A

Anti-platelet agents (e.g. aspirin)

127
Q

Laboratory findings in PRV

A

Raised haematocrit
Raised haemoglobin
Raised red cell amount

Low erythropoetin

128
Q

What is essential thrombocythameia?

A

Increased bone marrow production of thrombocytes

129
Q

What are the clinical features of thrombocythaemia

A

Thrombosis
Headaches
Visual disturbances

130
Q

How do we treat essential thrombocythaemia?

A

Anti-platelet agents (aspirin)

Hydroxycarbamide

131
Q

What is primary myelofibrosis?

A

Collagen fibrosis replacing bone marrow

132
Q

Clinical features of myelofibrosis

A

Massive splenomegaly causing left hypochondrion pain
Fever
Weight loss
Pruritis

133
Q

Laboratory features of myelofibrosis

A

Normochromic normocytic anaemia
Leucocytosis (early, later leucopenia)
Thrombocytosis (early, later thrombocytopenia)
JAK2 mutation

134
Q

Treatment of primary myelofibrosis

A

Chemotherapy (hydroxycarbamide)
JAK2 inhibitors
Thalidomide
Splenectomy

135
Q

What should we be giving in most myelo conditions because of urea?

A

Allopurinol

136
Q

Myelodysplasia

A

A clonal haemopoietic stem cell disorder characterised by cytopenias affecting one or more lineages

137
Q

Primary vs secondary myelodysplasia

A

Secondary is a consequence of chemo/radiotherapy

138
Q

What is the hallmark of myelodysplasia?

A

Involvement of more than one (usually all 3) lineages

139
Q

Treatment of myelodysplasia

A

Supportive care
Transfusions of red cells, platelets
Chemo - low dose ara-C, etoposide, hydroxycarbamide, 6-mercaptopurine)

140
Q

What is multiple myeloma

A

A malignant disorder of plasma cells characterised by:
- A monoclonal paraprotein in serum/urine
Bone changes - leading to pain/pathological fractures
- Excess plasma cells in marrow

141
Q

Features of multiple myeloma

A 
Bone pain (esp. low back)
Pathological fractures
Bone marrow failure due to infiltration
Infection (due to lack of neutrophils)
Renal failure (hypercalcaemia causes it)
Amyloidosis
142
Q

Laboratory features of multiple myeloma

A

Anaemia, neutropenia, thrombocytopenia
Blood film - rouleaux with blueish background staining
Paraprotein is usually IgG

143
Q

X-ray features of multiple myeloma

A

Lytic lesions typically in the skull (tear drop skull)

144
Q

Treatment of multiple myeloma

A 
Chemotherapy if CRAB is present:
C - HyperCalcaemia
R - Renal failure
A - Anaemia
B - Bone lesions
145
Q

How can we treat hereditary haemorrhagic telangiectasia?

A

Autosomal dominant condition with multiple microvascular swellings, typically in the oropharynx

Tranexamic acid

146
Q

Autoimmune thrombocytopenia treatment

A 
Prednisolone
IV immunoglobulins (to temporarily increase thrombocytes)
147
Q

When do we get autoimmune thrombocytopenia?

A

Often after viral infections

148
Q

What is haemophilia A?

A

Factor VIII deficiency - an X linked disorder

149
Q

Investigations in haemophilia A

A

Prolonged APTT
Normal PT
vWF is normal

150
Q

Treatment for haemophilia A

A

Infusions of factor VIII

Desmopressin (raises endogenous factor VIII)

151
Q

What is haemophilia B

A

Factor IX deficiency (Christmas disease) - X linked condition

152
Q

Which is more common: haemophilia A or B?

A

A is 4 times more common than B

153
Q

Treatment for haemophilia B

A

Factor IX infusions

154
Q

What is von Willebrand disease?

A

An autosomal dominant condition in which vWF (a large protein) is affected

155
Q

Function of vWF

A

Carries factor VIII in plasma and mediates platelet adhesion to endothelium

156
Q

Features of vWD

A

Bleeding

157
Q

Ix in vWD

A

APTT prolonged
PT normal
vWF levels reduced

158
Q

Treatment of vWD

A

Factor VIII concentrate

Desmopressin can be helpful

159
Q

In which demographic is factor XI deficiency more common

A

Ashkenazi jews

160
Q

What is DIC

A

This is where procoagulant material stimulates the release of all coagulation and fibrinolytic pathways
This results in thrombocytopenia

161
Q

Features of DIC

A

Bleeding
Thrombosis
Purpura
Renal function impairment

162
Q

Lab. features of DIC

A

Thrombocytopenia
All coagulation and fibrinolysis factors are abnormally low
Haemolytic anaemia

163
Q

Treatment of DIC

A

Treat the cause (e.g. give abx)

Supportive - FFP, platelets, cryoprecipitate

164
Q

PT

A

Extrinsic system

II, V, VII, X

165
Q

APTT

A

Intrinsic system

VIII, IX, XI* and XII*

166
Q

Warfarin

A

Affects the extrinsic pathway by blocking vitamin K, which is required to activate factors II, VII, IX and X

It therefore affects the PT time, not aPTT

167
Q

What does rivaroxaban affect?

A

Dirext Xa inhibitor

168
Q

What does dabigatran affect?

A

Direct factor II inhibitor

169
Q

What does heparin affect?

A

Xa, IXa, XIa

Pass Medicine (24 decks)

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