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Finals Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

What is anaemia defined as in men and women?

A

Men - Hb <130g/L

Women - Hb <120g/L

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2
Q

What is the underlying cause of a microcytic anaemia?

A

Cytoplasmic problem resulting in a low MCV

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3
Q

`What are causes of a microcytic anaemia?

A

Iron deficiency
Thalassaemia
Sideroblastic

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4
Q

What are causes of a normocytic anaemia?

A

Blood loss
Chronic disease
Renal failure
Pregnancy

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5
Q

What are the two categories of macrocytic anaemia?

A

Megaloblastic and non-megaloblastic

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6
Q

What is the underlying cause of a megaloblastic anaemia?

A

A nuclear (DNA) problem

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7
Q

What are some causes of a megaloblastic anaemia?

A

Vitamin B12 deficiency
Folate deficiency
Drugs
Pernicious anaemia

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8
Q

What are some causes of non-megaloblastic anaemia?

A

Alcohol/liver disease
Hypothyroidism
Marrow failure - myelodysplasia, aplastic anaemia

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9
Q

What are some signs of iron deficient anaemia?

A

Pallor, tiredness, koilonychia, glossitis, angular chelitis

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10
Q

What test should you do to check the bodies iron levels?

A

Serum ferritin

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11
Q

How is iron deficient anaemia treated?

A

Treat the cause first

Ferrous sulphate orally

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12
Q

What is sideroblastic anaemia?

A

X-linked condition of ineffective erythropoeisis. Results in a microcytic anaemia that does not respond to iron

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13
Q

What is the dietary source of vitamin B12?

A

Animal products

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14
Q

What is the dietary source of folate?

A

Green leafy vegetables

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15
Q

How long do body stores of B12 last?

A

2-4 years

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16
Q

How long do body stores of folate last?

A

4 months

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17
Q

Where is vitamin B12 absorbed in the gut?

A

Terminal ileum

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18
Q

Where is folate absorbed in the gut?

A

Jejunum

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19
Q

What are some causes of B12 deficiency?

A

Veganism, decreased stomach acid, pancreatitis, small bowel issues

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20
Q

What are some causes of folate deficiency?

A

Inadequate intake, coeliac, crohns. pregnancy, anti-convulsants

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21
Q

What are some general symptoms of megaloblastic anaemia?

A

Anaemia, weight loss, diarrhoea, beefy tongue

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22
Q

What are some symptoms specific to B12 deficiency?

A

Neurological problems - neuropathy, dementia, subacute combined degeneration of the cord

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23
Q

How is vitamin B12 deficiency treated?

A

initially, 3 IM injections of hydroxycobalamine per week for 2 weeks
If diet related -> biyearly injections
If not diet related -> injection every 3 months for life

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24
Q

How is folate deficiency treated?

A

Folic acid tablets 5mg/day

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25
Q

If a patient has both B12 and folate deficiency which one should be treated first and why?

A

B12 as folate can precipitate subactube combined degeneration of the cord

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26
Q

What is pernicious anaemia?

A

Autoimmune destruction of gastric parietal cells leading to macrocytosis and pancytopenia

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27
Q

What antibodies will be positive in pernicious anaemia?

A

Anti-GPC, Anti-IF

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28
Q

How is pernicious anaemia treated?

A

B12 injections and folate tablets for life

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29
Q

What is a normal haemoglobin molecule made of?

A

Haem & Globin - 2 alpha chains and 2 beta chains

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30
Q

On what chromosome is the gene for alpha globin chains?

A

Chromosome 16

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31
Q

On what chromosome is the gene for beta globin chains?

A

Chromosome 11

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32
Q

How does alpha trait present?

A

Clinically asymptomatic. Microcytic haemochromatic cells. Normal ferritin. No treatment needed.

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33
Q

What is HbH disease?

A

3 faulty alpha chains (–l-a)

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34
Q

What is seen in bloods of HbH disease?

A

Anaemia, very low MCV and MCH

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35
Q

How does HbH present?

A

Variable - spelnomegaly, jaundice, growth retardation, gallstones, iron

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36
Q

What is the inheritance of HbH disease?

A

Autosomal recessive

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37
Q

What is Hb Barts Hydrops Fetalis?

A

Most severe form of alpha thalassamia - –l–

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38
Q

What haemoglobin types are commonly seen in Hb Barts hydrops fetalis?

A

Hb Barts and HbH

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39
Q

Why is Hb Barts so bad?

A

It has a high affinity for oxygen and so does not give it up readily to tissues

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40
Q

How does Hb Barts present?

A

Pallor, oedema, cardiac failure. Most babies die in utero or shortly after birth

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41
Q

What is seen on alpha thalassaemia blood films?

A

Anisopoikilocytosis

Target Cells

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42
Q

What is the inheritance of B-thalassaemia?

A

Autosomal recessive

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43
Q

How will beta-thalassaemia trait present?

A

Asymptomatic. Low MCV/MCH.

Raised HbA2 is diagnostic.

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44
Q

What is beta thalassaemia intermedia?

A

Two defective copies of B gene or one absent B gene and one defective B gene

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45
Q

How is beta thalassaemia intermedia treated?

A

Occasional blood transfusion

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46
Q

What is beta thalassaemia major also known as?

A

Cooley’s anaemia

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47
Q

What is seen in FBC of beta thalassaemia major patients?

A

Moderate to severe anaemia

Very low MCV/MCH

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48
Q

What is seen on blood film in beta thalassaemia major?

A

Reticulocytosis
Anisopoikilocytosis
Target cells

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49
Q

What does liquid chromatography (HPLC) show in beta thalassaemia major?

A

Mainly HbF
Small HbA
Increased HbA2`

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50
Q

When does beta-thalassaemia major present?

A

Aged 6-24 months

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51
Q

How does beta-thalassaemia major present?

A

Failure to thrive, pallor, extramedullary haematopoesis, hepatosplenomegaly, skeletal changes, organ damage

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52
Q

How is beta-thalassaemia major managed?

A

Regular transfusions to maintain Hb 95-105g g/L

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53
Q

What are some complications of beta-thalassaemia major?

A

Viral infections, alloantibodies, iron overload, iron overload, transfusion reactions

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54
Q

What is sickle cell disease?

A

Point mutations change the structure of B globin chains to make HbS

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55
Q

How is sick cell disease inherited?

A

Autosomal recessive

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56
Q

What happens to HbS in periods of low oxygen?

A

Polymerises and damages RBC, leading to sickling where cells are fragile, haemolyse and block small vessels

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57
Q

What is sickle cell trait?

A

One abnormal copy of the gene, asymptomatic carrier state. HbS levels too low to polymerise

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58
Q

What are some precipitants of sickle cell crisis?

A

Hypoxia, dehydration, infection, cold, stress, fatigue

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59
Q

What is the management of sickle cell crisis?

A

Opiate analgesia

Hydration, rest, oxygen, antibiotics if infection

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60
Q

How could a severe sickle cell crisis be managed?

A

Blood transfusion

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61
Q

What causes an aplastic crisis in sickle cell disease?

A

Parvovirus B19

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62
Q

What is a sequestration crisis?

A

Pooling of blood in the spleen - requires an urgent transfusion

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63
Q

What temperature should red blood cells be stored at?

A

4 degrees C - in fridge

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64
Q

What temperature should platelets be stored at?

A

22 degrees C - room temperature

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65
Q

What temperature should FFP be stored at?

A

-30 degrees C - freezer

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66
Q

How long do you have to transfuse red cells and FFP?

A

Must be transfused within 4 hours

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67
Q

How long do you have to transfuse platelets?

A

Must be transfused within 1 hour

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68
Q

On what chromosome is ABO determined?

A

Chromosome 9

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69
Q

On what chromosome is Rhesus status determined?

A

Chromosome 1

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70
Q

What test should you use to screen patients plasma for irregular red cell antibodies?

A

Indirect antiglobulin test

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71
Q

What blood type is the universal donor?

A

O negative

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72
Q

What blood type is the universal acceptor?

A

AB positive

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73
Q

What antibody mediates an immediate transfusion reaction?

A

IgM - attack on RBCs

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74
Q

How does an immediate transfusion reaction present?

A

May occur after only 1ml has been transfused - fever, dizziness, sweating, tachycardia, hypotension, DIC, AKI, shock

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75
Q

How should you manage an immediate transfusion reaction?

A

STOP TRANSFUSION
Start IV fluids to maintain BP and urine output
Check bag of blood to see patient identity
Take bloods (FBC, U&Es, coag, cultures, LDH, blood film)
Contact haematology and return blood to the lab

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76
Q

What antibody mediates a delayed haemolytic transfusion reaction?

A

IgG - attack on antibodies in transferred blood

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77
Q

When does a delayed haemolytic transfusion reaction occur?

A

5 to 10 days following transfusion

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78
Q

How does a delayed haemolytic transfusion reaction present?

A

Jaundice, unexpected fall in Hb, AKI,

Lab results show anaemia, spherocytic red cells, raised bilirubin and raised LDH

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79
Q

How do you manage a delayed haemolytic transfusion reaction?

A

Supportive care for any AKI/clotting issues

Screen for irregular antibodies and give an antibody reference card for future transfusions

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80
Q

What is a febrile non-haemolytic reaction?

A

Reaction to white blood cells within the transfusion

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81
Q

When and how does a febrile non-haemolytic reaction present?

A

About 30 mins into transfusion - fever, rigors etc

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82
Q

How is a febrile non-haemolytic reaction managed?

A

Slow/stop transfusion. Paracetamol. Close monitoring. Next transfusion - give leucodepleted blood products

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83
Q

What mediates an urticarial transfusion reaction?

A

IgE - response to infused plasma proteins

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84
Q

How does an urticarial transfusion reaction present?

A

Rash/wheals within first few minutes

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85
Q

How is an urticarial transfusion reaction managed?

A

Slow/stop transfusion
Supportive care
Antihistamines

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86
Q

What is associated with an anaphylaxis transfusion reaction?

A

IgA deficiency

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87
Q

How does an anaphylactic transfusion reaction present?

A

Hypotension, mucosal swelling, stridor

88
Q

How should an anaphylactic transfusion reaction be treated?

A 
STOP TRANSFUSION
ABCDE and fluid challenge
Adrenaline 0.5ml 1:1000 IM
Hydrocortisone 200mg IV
Chloramphenimine 10mg IV

Give IgA depleted bloods next transfusion

89
Q

What is the commonest childhood cancer?

A

ALL

90
Q

How does ALL present?

A

Anaemia, infection, bleeding, bone pain, hepatosplenomegaly, orchidomegaly, lymphadenopathy

91
Q

What sort of anaemia does ALL cause?

A

Normocytic normochromic anaemia, neutropenia and high WCC

92
Q

How is ALL managed?

A

Multi-agent chemotherapy
Targeted therapies
Allogenic stem cell transplant

93
Q

What is the cure rate of ALL in children?

A

90%

94
Q

What is the cure rate of ALL in adults?

A

30-40%

95
Q

What is AML?

A

Neoplastic proliferation of myeloid cells (e.g. monocytes, macrophages, neutrophils etc)

96
Q

How does AML present?

A

Anaemia, infection, bleeding, hepatosplenomegaly, gym hypertrophy, skin involvment

97
Q

What anaemia does AML show?

A

Normocytic normochromic anaemia

98
Q

What is seen on the blood film and marrow biopsy of AML?

A

Auer Rods

99
Q

How is AML managed?

A

Intensive treatment with chemotherapy

Bone marrow transplants

100
Q

How is AML t(15;17) treated?

A

Can use vitamin A analogues

101
Q

What is the commonest overall leukaemia?

A

CLL

102
Q

What is the main cell origin of CLL?

A

B cells (99%)

103
Q

How does CLL present?

A

Often asymptomatic - often an incidental finding on blood film in elderly
May be anaemia, infection prone, weight loss, enlarged rubbery non tender lymph nodes

104
Q

What anaemia does CLL produce?

A

Normocytic normochromic anaemia

105
Q

What is seen on blood film in CLL?

A

Smudge/Smear cells

106
Q

What is seen on electrophoresis in CLL?

A

Hypogammaglobulinaemia

107
Q

What is Richters transformation of CLL?

A

Transformation into a high grade lymphoma

108
Q

What fraction of patients do not progress in CLL?

A

1/3rd do not progress, 1/3rd progress in time, 1/3rd actively progressing

109
Q

If CLL is actively progressing how is it treated?

A

Chemotherapy +/- stem cell transplant

110
Q

What is the median survival of CLL?

A

6.5-12 years

111
Q

What is CML?

A

Myeloproliferative disorder

112
Q

What is a genetic cause for CML?

A

Philadelphia chromosome t(9;22)

113
Q

How does CML present?

A

Chronic and insidious weight loss, tiredness, fevers, sweats, gout, MASSIVE splenomegaly

114
Q

What anaemia does CML give patients?

A

Normocytic normochromic anaemia

115
Q

How is CML treated?

A

Tyrosine kinase inhibitors - IMANTINIB

116
Q

What is a blast crisis in CML?

A

When maturation fails and blast cells accumulate resulting in AML

117
Q

When are the two peaks of incidence of Hodgkins lymphoma?

A

15-30yrs and >55 years

118
Q

How does Hodgkins lymphoma present?

A

Painless lymphadenopathy, alcohol induced pain, weight loss, fever, night sweats, SVC obstruction, Pel-Ebstein fever (cyclical)

119
Q

What does an excisional lymph node biopsy and immunohistochemistry of Hodgkins lymphoma show?

A

Reed-Sternberg Cells (‘mirror nuclei’)

120
Q

How is Hodgkins lymphoma treated?

A

Chemoradiotherapy

121
Q

What is Non-Hodgkins lymphoma?

A

Any lymphoma except Hodgkins

122
Q

What cell type is more common in Non-Hodgkins lymphoma?

A

B cell (90%) T cell (10%)

123
Q

What is Non-Hodgkins lymphoma associated with?

A

Immunodeficiency

124
Q

How does Non-Hodgins lymphoma present?

A

Enlargement of a group of lymph nodes, night sweats, weight loss, indigestion, raised ICP, cranial nerve palsies, hepatosplenomegaly

125
Q

How is Non-Hodgkins lymphoma treated?

A

Watch & wait in low grade disease
Chemoradiotherapy (dependent on stage)
Monoclonal antibodies - RITUXIMAB

126
Q

What is Burkitts lymphoma?

A

High grade B cell lymphoma of childhood

127
Q

What genetic problem is Burkitts lymphoma associated with?

A

c-myc gene translocation t(8;14)

128
Q

What appearance is seen on microscopy of Burkitts lymphoma?

A

Starry sky appearance

129
Q

What are the 4 stages of normal haemostasis?

A

Vasoconstriction
Primary haemostasis
Secondary haemostasis
Fibrinolysis

130
Q

What is primary haemostasis?

A

Formation of platelet plug

131
Q

What is secondary haemostasis?

A

Formation of fibrin clot

132
Q

What are vascular causes of failure of primary haemostasis?

A

Hereditary haemorrhagic telangastasia

Henoch schonlein purpura

133
Q

What is the inheritance of HHT/OslerWeberRendu?

A

Autosomal dominant

134
Q

What are some platelet causes of failure of primary haemostasis?

A

Decreased production - aplastic anaemia, leukaemia, myeloma

Increased destruction - ITP, SLE, hypersplenism, TTP

135
Q

What is the inheritance of Von Willebrands disease?

A

Autosomal dominant

136
Q

What is the role of Von Willebrand factor?

A

Platelet adhesion

Binds to factor VIII

137
Q

How does Von Willebrands disease present?

A

Bruising, epistaxis, menorrhagia

138
Q

What does a clotting screen show for Von Willebrands disease?

A

Increased APTT
Increased bleeding time
Decreased factor VIII assay

139
Q

How is Von Willebrands managed?

A

Vasopressins for minor bleeds

VWF rich factor VIII concentrate for surgeries

140
Q

What causes a failure of secondary haemostasis?

A

Single or mutliple clotting factor deficiencies

141
Q

What are two causes of multiple clotting factor deficiencies?

A

Liver failure

Vitamin D deficiency

142
Q

What is haemophilia A?

A

Deficiency of factor VIII

143
Q

How is haemophilia inherited?

A

X-linked recessive

144
Q

How does haemophilia present?

A

Abnormally prolonged bleeding, haemoarthosis, haematomas

145
Q

What is haemophilia B?

A

Deficiency of factor IX

146
Q

What is haemophilia B also known as?

A

Christmas disease

147
Q

What does a clotting screen from haemophilia A show?

A

Increased APTT
Normal PT
Normal bleeding time
Decreased factor VIII assay

148
Q

What does a clotting screen for haemophilia B show?

A

Increased APTT
Normal PT
Normal bleeding time
Decreased factor IX assay

149
Q

How is haemophilia A treated?

A

Factor VIII concentrate IV when bleeding. Prophylaxis if severe. Desmopressin prophylaxis if mild

150
Q

How is haemophilia B treated?

A

Factor IX concentrates

151
Q

What is disseminated intravascular coagulation?

A

Excessive and inappropriate activation of the haemostatic system. Initally causes thrombosis of small vessels then a bleeding tendency

152
Q

What are some causes of DIC?

A

Sepsis, obstetric emergencies, drugs, shock

153
Q

How do patients with DIC present?

A

Acutely ill, shocked, bleeding

154
Q

How is DIC treated?

A

Treat underlying cause
Transfuse platelets and plasma
Replace fibrinogen

155
Q

What does the prothrombin time evaluate?

A

Extrinsic pathway (I,II,V,VII,X)

156
Q

What is a normal prothrombin time?

A

12-16 seconds

157
Q

What does the activated partial thromboplastin time evaluate?

A

Intrinsic pathway (I, II, V, VIII, IX, X, XI, XII)

158
Q

What is a normal APTT?

A

26-37 secs

159
Q

What are the natural anticoagulants?

A

Antithrombin
Activated Protein C
Protein S

160
Q

What are the vitamin K dependent factors?

A

II, VII, IX, X, protein C, protein S

161
Q

What is Factor V Leiden?

A

A disease where there is a resistance to activated protein C`

162
Q

How does factor V leiden present?

A

Premature, unusual and recurrent thromboses

163
Q

What is antiphospholipid syndrome?

A

Acquired thrombophilia associated with recurrent thromboses, fetal loss and mild thrombocytopenia

164
Q

How should an initial venous thrombotic event in antiphospholipid syndrome be treated?

A

Warfarin 6 months

INR 2-3

165
Q

How should recurrent venous thrombosis in APLS be treated?

A

Warfarin lifelong

INR 2-3 (or 3-4 if the event occured while on warfarin)

166
Q

How should arterial thrombosis in APLS be treated?

A

Warfarin lifelong

INR 2-3

167
Q

How does heparin work?

A

Potentiates antithrombin

168
Q

How is unfractionated heparin monitored?

A

Check APTT

169
Q

How is LMWH heparin monitored?

A

Anti-Xa assay

170
Q

What is the antidote for heparin?

A

Protamine sulphate

171
Q

How does warfarin work?

A

Blocks ability of vitamin K to carboxylate factors II, VII, IX, X

172
Q

What is INR?

A

International normalised ratio - patients PT time/mean normal PT time

173
Q

What is dabigatran?

A

Direct thrombin inhibitor

174
Q

What are rivaroxiban/apixiban?

A

Direct factor X inhibitors

175
Q

What is aspirin?

A

Platelet agonist - inhibits cyclo-oxygenase

176
Q

What are clopidogrel/prasugrel/ticagrelor?

A

ADP receptor blockers

177
Q

What is dipyridamole?

A

Phosphodiesterase inhibitor

178
Q

What is abciximab?

A

GP IIb/IIa inhibitor that inhibits aggregation

179
Q

What score is used in DVT and PE?

A

Wells Score

180
Q

If a patient has 2 or more in the DVT Wells score what do you do?

A

Refer for proximal leg vein scan within 4 hours

If cannot be done in 4 hours - d-dimer/interum dose of LMWH

181
Q

If a patient had a DVT Wells score of 1 or less what do you do?

A

Do a d-dimer first
If positive -> proximal leg vein scan within 4 hours
If cannot be done within 4 hours - interum dose of LMWH

182
Q

If a patient has a confirmed DVT, what should be done?

A

Start warfarin within 24 hours of diagnosis

Continue LMWH for 5 days or until INR 2 or above for 24 hours

183
Q

How long should a patient with a DVT stay on warfarin and at what target INR?

A

At least 3 months

Target INR - 2.0-3.0

184
Q

If a patient has a PE wells score above 4, what should be done?

A

Hospital admission for immediate CTPA

If there is a delay –> start LMWH

185
Q

If a patient has a PE Wells score of 4 or less, what should be done?

A

Arrange a d-dimer test

If positive do immediate CTPA. If delay –> start LMWH

186
Q

Once a PE is confirmed, what should be done?

A

Give warfarin within 24 hours

Continue LMWH for 5 days or until INR 2 or above

187
Q

How long should warfarin be given following a PE and at what target?

A

At least 3 months

Target INR 2-3

188
Q

What should pregnant women with PE be treated with?

A

LMWH until the end of pregnancy

189
Q

What should patients with unprovoked PE/DVT be investigated for?

A

Thrombophilias

Malignancy

190
Q

How should a patient with a major bleed on warfarin be managed?

A

Stop warfarin

Refer urgently for IV vitamin K and/or prothrombin complex concentrate or FFP

191
Q

How should a patient with an INR above 8 be managed?

A

Stop warfarin
Give 0.5-1mg Vitamin K by IV injection or 5mg orally
Repeat in 24hrs if INR still high
Restart warfarin when INR below 5

192
Q

How should a patient with an INR of 6-8 be managed?

A

Stop warfarin

Restart warfarin when INR below 5

193
Q

How should a patient with an INR below 6 but 0.5 above target be managed?

A

Stop or reduce warfarin

Restart when INR below 5

194
Q

How should a patient with an INR below 5 but is high be treated?

A

Dose reduction and omit a few doses

195
Q

How should a patient with a low INR be managed?

A

Temporarily increase dose and give LWMH boosters

196
Q

What dose change results in a change in INR of 1?

A

a 15% dose change causes INR to change by 1

197
Q

What do Howell-Jolly bodies suggest?

A

Hyposplenism

198
Q

Which type of Hodgkins lymphoma carries the worst prognosis?

A

Lymphocyte depleted

199
Q

What antibody is warm haemolytic anaemia associated with?

A

IgG

200
Q

What antibody is cold haemolytic anaemia associated with?

A

IgM

201
Q

What metabolic complication may a blood transfusion cause?

A

Hyperkalaemia

202
Q

What does a JAK2 mutation indicate?

A

Polycythaemia Rubra Vera

203
Q

Why is polycythaemia rubra vera?

A

Myeloproliferative disorder causing increased red cell volume

204
Q

What are features of polycythaemia rubra vera?

A

Hyperviscosity, itch after hot bath, splenomegaly, plethora, hypertension

205
Q

What is multiple myeloma?

A

Neoplasm of bone marrow cells

206
Q

What are clinical features of multiple myeloma?

A

Bone disease (pain, fractures), lethargy, infection, renal failure, hypercalcaemia

207
Q

What is seen in the urine in myeloma?

A

Bence Jones Proteins

208
Q

What are tear drop cells on blood film associated with?

A

Myelofibrosis

209
Q

What is aplastic anaemia characterised by?

A

Pancytopenia and hypoplastic bone marrow

210
Q

How does hereditary spherocytosis present?

A

Failure to thrive, jaundice, splenomegaly,

211
Q

How is hereditary sphercytosis investigated?

A

Osmotic fragiltity test

212
Q

How is hereditary spherocytosis managed?

A

Splenectomy

Folate replacement

213
Q

What is the commonest Hodgkins lymphoma?

A

Nodular sclerosing

214
Q

What is the Hodgkins lymphoma with the best prognosis?

A

Lymphocyte predominant

215
Q

What factor is the major constituent of cryoprecipitate?

A

Factor VIII

216
Q

‘Rouleaux formation’

A

Myeloma

217
Q

‘IgM paraprotein’

A

Waldenstroms macroglobulinaemia

Finals Revision (22 decks)

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