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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
Signs of iron deficiency?
Koilonychia Angular cheilitis Glossitis
26
Laboratory findings in iron deficiency?
Hypochromic microcytic anaemia | Raised platelet count
27
Haematinics in iron deficiency?
Serum iron low Raised transferrin Iron binding capacity lowered
28
Transferrin and ferritin
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
29
How do we treat iron deficient anaemia?
Ferrous sulfate (iron) before meals 3 times a day
30
Side effects of ferrous sulfate
Abdominal pain, diarrhoea, constipation
31
What is iron overload?
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
32
What causes iron overload?
Haemochromatosis (genetic) - excessive iron absorption Excess dietary iron Repeated blood transfusions in patients with severe refractory anaemia
33
Clinical features of iron overload?
Cardiomyopathy (dysrhythmias, cong. heart failure) Growth/sexual development reduction: delayed puberty, DM, hypothyroidism Haemosiderosis or cirrhosis (liver) Excessive melanin pigmentation Excessive infections Arthropathy
34
Haemochromatosis
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)
35
Haematinics in haemochromatosis
Raised serum iron Raised transferrin Raised serum ferritin
36
Treatment of haemochromatosis
Regular venesctions to reduce iron level to normal
37
What is sideroblastic anaemia?
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)
38
What might you see on blood film in sideroblastic anaemia?
Hypochromic microcytic red cells
39
Treatment of sideroblastic anaemia
Symptomatic | Regular blood transfusion
40
Causes of B12 deficiency
Inadequate diet (e.g. vegans) Malabsorption - pernicious anaemia mainly Gastrectomy etc
41
What is pernicious anaemia
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
42
Folate deficiency
``` Poor dietary intake Increased utilisation (pregnancy, severe chronic inflammatory and malignant disease) ```
43
Clinical features of B12 deficiency
``` Gradual onset of anaemia features Mild jaundice - caused by ineffective erythropoiesis Glossitis Angular stomatitis Peripheral symmetrical neuropathy ```
44
Laboratory findings in B12 deficiency
``` Macrocytic anaemia (oval macrocytes, hypersegmental neutrophils - 5+ nuclear lobes) Reduction in leucocyte and platelet count ```
45
Treatment for B12 deficiency
Hydroxycobalamin 1mg intramuscularly 2-3 daily till 6 injections given Then hydroxycobalamin 3 monthly
46
How do we investigate B12 deficiency?
History IF tests Parietal cell antibodies (present in 90% of PA) Serum gastrin level (raised in PA)
47
Clinical features of folate deficiency
Same as B12 except NO peripheral neuropathy
48
Treatment for folic acid deficiency
5mg folic acid daily for 4 months | Either continue weekly or daily at different doses
49
Other causes of macrocytosis?
Alcohol is the most common cause of large RBCs
50
Clinical features of haemolytic anaemias
Anaemia Jaundice Splenomegaly
51
Hereditary causes of haemolytic anaemia
Spherocytosis - red cell membrane abnormality | G6PD deficiency - enzyme abnormality
52
Hereditary spherocytosis
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
53
What are pigmented gallstones associated with?
Haemolytic anaemias
54
G6PD deficiency
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
55
G6PD deficiency blood film
Normal inbetween episodes | During crises: red cells with absent haemoglobin, polychromasia
56
How do we screen for G6PD deficiency
NADPH
57
Management of G6PD deficiency
Stop offending drugs Treat infection Transfuse rbc's if needed Splenectomy
58
What do thalassemias cause?
Haemolytic and microcytic anaemias
59
Thalassemia
Autosomal recessive conditions in which there is a reduced synthesis of alpha or beta globins
60
How do we treat thalassemia
Transfusions of rbc's | Iron chelation therapy with subcut. desferrioxamine
61
Laboratory findings in thalassemia
Severe anaemia with reduced mcv | Hypochromic, microcytic cells, target cells, erythroblasts
62
What is thalassemia trait
Mild hypochromic, microcytic anaemia | Iron stores are normal
63
Sickle cell disease
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
64
Sickle cell disease features
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
65
What regular testing do you have in sickle cell?
Retinal - due to predisposition to stroke/TIAs
66
Laboratory features of sickle cell
Haemoglobin level 70-90 Sickle cells Large target cells Splenic atrophy
67
O2 dissociation curve in sickle cell?
Shifted to the right
68
Which white cells are granulocytes?
Eosinophils Basophils Neutrophils
69
Which cells are myeloid?
Red cells Platelets Granulocytes
70
Which cells are lymphoid?
B cells T cells NK cells
71
Causes of reactive neutrophilia
``` Bacterial infection Inflammation Tauma Tissue necrosis DKA Haemorrhage ```
72
Causes of malignant neutrophilia
Myeloproliferative disorders | Myeloid leukaemias
73
Which drugs cause neutrophilia
Steroids | Granulocyte colony-stimulating factor
74
Causes of neutropenia
``` 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
Causes of eosinophilia
Allergic diseases - asthma, hay fever, eczema, pulmonary hypersensitivity reaction Skin diseases Connective tissue disease
76
Causes of basophilia
Myeloproliferative disorders
77
When do you get lymphocytosis
Viral infections Lymphoid neoplasia Some bacterial infections (e.g. petussis)
78
Hyposplenism
Reduces the body's ability to make antibodies, clearance of intracellular organisms and impairs defence against toxins/organisms in the portal circulation
79
Causes of hyposplenism
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
Splenomegaly
Can cause pancytopenia | Can cause anaemia (due to dilution with increased plasma volume)
81
Causes of splenomegaly
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
Infectious mononucleosis
Caused by EBV of B lymphocytes Fever, sore throat, lymphadenopathy Rash if treated with amoxicillin Jaundice, hepatomegaly and splenomegaly occasionally
83
What does the spleen do?
Primarily concerned with filtering the blood (gets rid of old red cells) and also produces antibodies Also contains half the body's monocytes
84
When is splenectomy beneficial
Haem conditions in which the spleen is the site of excessive destruction of cells e.g. some haemolytic anaemias
85
What do patients who've undergone splenectomy have to take?
Prophylactic abx for life - penicillin V or erythromycin
86
Two types of acute leukaemia
Lymphoblastic | Myeloblastic
87
AML
More common in adults than ALL | May occur as a primary disease, or secondary following a myeloproliferative disorder
88
Features of AML
``` Anaemia Neutropenia (WCC will be high, but functioning neutrophils will be low) Thrombocytopenia Splenomegaly Bone pain ```
89
What classification for AML
FAB
90
Features of acute promyeclotic leukaemia (M3)
DIC or thrombocytopenia at presentation
91
Laboratory findings in AML but NOT in ALL
Auer rods
92
When is ALL most common?
Most common malignancy of childhood
93
Features of ALL
Anaemia Neutropenia Thrombocytopenia Bone pain Splenomegaly Hepatomegaly
94
How to treat acute leukaemia?
High dose chemotherapy to induce remission 4-6 weeks per course
95
Remission regime in AML
``` Anthracycline (daunorubicin) Cytosine arabinoside (ara-C) ```
96
Remission regime in ALL
Vincristine Dexamethasone L-asparaginase Often with: Daunorubicin Cyclophosphamide
97
What can we give in ALL to reduce CNS involvement?
Intrathecal injections of methotrexate
98
Who has CML?
Marshall
99
What is the Philadelphia chromosome?
An abnormal chromosome 22 caused by translocation of part of its arm to chromosome 9 Found in CML patients
100
What is the fusion gene found in CML?
BCR-ABL1
101
Peak age for CML?
25-45
102
Symptoms of CML
``` Weight loss Night sweats Itching Left hypochondrial pain Gout ``` Caused by viscosity of the blood: Priapism Visual disturbances Headaches
103
How common is splenomegaly in CML?
>90% of cases have massive splenomegaly
104
Laboratory findings in CML?
``` Raised WCC (mainly neutrophils/myelocytes) Raised basophils Platelet count raised Philadelphia chromosome BCR:ABL1 gene ```
105
What is the main cause of death in CML
Progression to AML/ALL
106
Chronic phase of CML
Blood and bone marrow contain less than 10% blasts Treat with imatinib (tyrosine kinase inhibitor)
107
Accelerated phase of CML
10-19% blasts Treat with tyrosine kinase inhibitor still but maybe also chemo
108
CLL
Most common leukaemia seen in adults | Almost always monoclonal proliferation of well-differentiated B cells
109
Features of CLL
``` Often asymptomatic Anorexia, weight loss Bleeding Infections Lymphadenopathy ```
110
Complications of CLL
Anaemia Hypogammaglobulinaemia Warm autoimmune haemolytic anaemia Transformation to high grade lymphoma (Richter's transformation)
111
What might you see on blood film in CLL?
Smudge cells | Smear cells
112
Treatment for CLL
Observation | Chemotherapy (cyclophosphamide, rituximab)
113
Features of CLL
``` Often asymptomatic Lymphadenopathy** Anorexia, weight loss Bleeding Infections ```
114
Complications of CLL
Anaemia Hypogammaglobulinaemia Warm autoimmune haemolytic anaemia Transformation to high grade lymphoma (Richter's transformation)
115
What might you see on blood film in CLL?
Smudge cells | Smear cells
116
Treatment for CLL
Chemotherapy
117
What two staging systems can we use in CLL
Rai staging (0-IV) Binet staging (ABC)
118
Rai staging
``` 0 - Lymphocytosis I - Lymphocytosis with lymphadenopathy II - Lymphocytosis with spleno/hepatomegaly III - Lymphocytosis with anaemia IV - Lymphocytosis with platelets <100 ```
119
Differentiating symptoms between ALL and AML
ALL: Meninges, testes involvement AML: Skin, bones, gums
120
What is polycythaemia
High level of red cells in blood
121
Causes of polycythaemia
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
What causes PRV
A change in the JAK2 gene causing the bone marrow to produce too many red cells This is NOT an inherited condition
123
Symptoms of polycythaemia
``` Headaches Blurred vision Red skin Tiredness Dizziness Bleeding problems Itchiness ``` (Blood becomes more viscous)
124
What serious conditions can polycythaemia cause?
PE DVT MI Stroke
125
How do we treat polycythaemia?
Regular venesection Hydroxycarbamide - lowers red cells numbers (it's a chemo) PPI for GI bleeds Aspirin - lower risk of complications
126
Treatment for thrombocytosis
Anti-platelet agents (e.g. aspirin)
127
Laboratory findings in PRV
Raised haematocrit Raised haemoglobin Raised red cell amount Low erythropoetin
128
What is essential thrombocythameia?
Increased bone marrow production of thrombocytes
129
What are the clinical features of thrombocythaemia
Thrombosis Headaches Visual disturbances
130
How do we treat essential thrombocythaemia?
Anti-platelet agents (aspirin) | Hydroxycarbamide
131
What is primary myelofibrosis?
Collagen fibrosis replacing bone marrow
132
Clinical features of myelofibrosis
Massive splenomegaly causing left hypochondrion pain Fever Weight loss Pruritis
133
Laboratory features of myelofibrosis
Normochromic normocytic anaemia Leucocytosis (early, later leucopenia) Thrombocytosis (early, later thrombocytopenia) JAK2 mutation
134
Treatment of primary myelofibrosis
Chemotherapy (hydroxycarbamide) JAK2 inhibitors Thalidomide Splenectomy
135
What should we be giving in most myelo conditions because of urea?
Allopurinol
136
Myelodysplasia
A clonal haemopoietic stem cell disorder characterised by cytopenias affecting one or more lineages
137
Primary vs secondary myelodysplasia
Secondary is a consequence of chemo/radiotherapy
138
What is the hallmark of myelodysplasia?
Involvement of more than one (usually all 3) lineages
139
Treatment of myelodysplasia
Supportive care Transfusions of red cells, platelets Chemo - low dose ara-C, etoposide, hydroxycarbamide, 6-mercaptopurine)
140
What is multiple myeloma
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
Features of multiple myeloma
``` 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
Laboratory features of multiple myeloma
Anaemia, neutropenia, thrombocytopenia Blood film - rouleaux with blueish background staining Paraprotein is usually IgG
143
X-ray features of multiple myeloma
Lytic lesions typically in the skull (tear drop skull)
144
Treatment of multiple myeloma
``` Chemotherapy if CRAB is present: C - HyperCalcaemia R - Renal failure A - Anaemia B - Bone lesions ```
145
How can we treat hereditary haemorrhagic telangiectasia?
Autosomal dominant condition with multiple microvascular swellings, typically in the oropharynx Tranexamic acid
146
Autoimmune thrombocytopenia treatment
``` Prednisolone IV immunoglobulins (to temporarily increase thrombocytes) ```
147
When do we get autoimmune thrombocytopenia?
Often after viral infections
148
What is haemophilia A?
Factor VIII deficiency - an X linked disorder
149
Investigations in haemophilia A
Prolonged APTT Normal PT vWF is normal
150
Treatment for haemophilia A
Infusions of factor VIII | Desmopressin (raises endogenous factor VIII)
151
What is haemophilia B
Factor IX deficiency (Christmas disease) - X linked condition
152
Which is more common: haemophilia A or B?
A is 4 times more common than B
153
Treatment for haemophilia B
Factor IX infusions
154
What is von Willebrand disease?
An autosomal dominant condition in which vWF (a large protein) is affected
155
Function of vWF
Carries factor VIII in plasma and mediates platelet adhesion to endothelium
156
Features of vWD
Bleeding
157
Ix in vWD
APTT prolonged PT normal vWF levels reduced
158
Treatment of vWD
Factor VIII concentrate | Desmopressin can be helpful
159
In which demographic is factor XI deficiency more common
Ashkenazi jews
160
What is DIC
This is where procoagulant material stimulates the release of all coagulation and fibrinolytic pathways This results in thrombocytopenia
161
Features of DIC
Bleeding Thrombosis Purpura Renal function impairment
162
Lab. features of DIC
Thrombocytopenia All coagulation and fibrinolysis factors are abnormally low Haemolytic anaemia
163
Treatment of DIC
Treat the cause (e.g. give abx) | Supportive - FFP, platelets, cryoprecipitate
164
PT
Extrinsic system | II*, V*, VII*, X*
165
APTT
Intrinsic system | VIII*, IX*, XI* and XII*
166
Warfarin
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
What does rivaroxaban affect?
Dirext Xa inhibitor
168
What does dabigatran affect?
Direct factor II inhibitor
169
What does heparin affect?
Xa, IXa, XIa

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