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3rd year > Haematology > Flashcards

Haematology Flashcards

1
Q

Which type of white cell has a segmented nucleus?

A

Neutrophil

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2
Q

Which type of white cell has a bi-lobed nucleus and orange/red granules?

A

Eosinophils

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3
Q

Which type of white cell has large, deep purple granules?

A

Basophils

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4
Q

Which type of white cell has faintly-staining vacuolated granules?

A

Monocytes

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5
Q

Which type of white cell has a condensed nucleus with a small rim of cytoplasm?

A

Mature lymphocyte

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6
Q

Which type of white cell is the circulatory version of mast cells?

A

Basophils

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7
Q

Which types of white cells are involved in hypersensitivity reactions?

A

Eosinophils, basophils

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8
Q

Which type of white cell binds IgE?

A

Basophils

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9
Q

Which type of white cell has histamine-containing granules?

A

Basophil

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10
Q

Which haematological malignancy is associated with alcohol-induced pain?

A

Hodgkin’s lymphoma

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11
Q

Features of Fanconi’s anaemia

A

Short stature, pigment abnormalities, hypogenitalia, endocrinopathies, GI defects, renal defects, haem disorders. High risk of bone marrow failure and leukaemia

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12
Q

Causes of acquired primary bone marrow failure

A

Idiopathic asplatic anaemia, myelodysplastic syndromes, acute leukaemia

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13
Q

What is asplatic anaemia?

A

Autoimmune response against HSCs causing bone marrow failure

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14
Q

Which cancer can arise from myelodysplastic syndromes?

A

AML

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15
Q

Causes of secondary bone marrow failure

A

Iatrogenic
B12/folate
Malignancy
HIV

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16
Q

Arterial supply of the spleen

A

Splenic artery from coeliac trunk

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17
Q

Venous drainage of the spleen

A

Splenic vein, which forms portal vein with SMV

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18
Q

Causes of hypersplenism

A

Portal hypertension, congestive cardiac failure, systemic diseases such as RA, haem diseases such as splenic lymphoma

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19
Q

How does splenic red cell mass change in hypersplenism?

A

Greatly increases

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20
Q

How does red cell transit change in hypersplenism?

A

Slows

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21
Q

How does the splenic platelet pool change in hypersplenism

A

Increases

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22
Q

Main cause of pancytopenia with hypocellular marrow

A

Aplastic anaemia

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23
Q

Supportive treatment of pancytopenia

A

Red cell + platelet transfusions, sometimes neutrophil transfusion, prophylactic antibiotics

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24
Q

Which aspect of the immune system are B cells part of?

A

Adaptive

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25
Q

Actions of B cells

A

Produce antibodies

Act as antigen-presenting cells

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26
Q

What are the two types of immunoglobulin light chains?

A

kappa (κ) or lambda (λ)

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27
Q

Which Ig(s) are monomeric?

A

IgD, IgE, IgG

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28
Q

Which Ig(s) aredimeric?

A

IgA

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29
Q

Which Ig(s) arepentameric?

A

IgM

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30
Q

How are the variable elements of immunoglobulins generated?

A

V-D-J region recombination

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31
Q

What does the nucleus of a plasma cell allegedly look like?

A

Clock face

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32
Q

Plasma cell appearance

A

Eccentric clock face nucleus
Plentiful blue cytoplasm
Pale perinuclear area

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33
Q

What method is used to classify abnormal immunoglobulins?

A

Serum immunofixation

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34
Q

What test is used to detect immunoglobulin light chains?

A

Urine electrophoresis

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35
Q

Which type of Ig light chain is a monomer?

A

Kappa

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36
Q

Which type of Ig light chain is a dimer?

A

Lambda

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37
Q

Most common cause of paraproteinaemia

A

MGUS

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38
Q

Most common Ig paraprotein in myeloma

A

IgG

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39
Q

Appearance of lytic bone disease in myeloma

A

Multiple ‘punched-out’ lesions

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40
Q

How does lytic bone disease occur in myeloma?

A

Myeloma cells produce IL6, which suppresses osteoblastsand activates osteoclasts

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41
Q

Features of hypercalcaemia

A

Stones, bones, abdominal groans, psychiatric moans, thirst, dehydration, renal impairment

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42
Q

Which form of nephropathy is frequently seen in myeloma patients?

A

Cast nephropathy- light chains in loop of Henle

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43
Q

Treatment of myeloma

A

Chemo
Corticosteroids - dexamethasone, prednisolone
Alkylating Agents - cyclophosphamide, melphan
Novel agents - thalidomide, bortezomib, lenalidomide(If fit - high dose chemo and autologous stem cells)

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44
Q

Which monoclonal antibody can be used in myeloma?

A

Daratumumab

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45
Q

What is vertebroplasty?

A

Injection of sterile cement into a fractured bone to stabilise it - sometimes used in vertebral fractures in myeloma

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46
Q

MGUS criteria

A

Paraprotein <30g/l
Bone marrow plasma cells <10%
No evidence of myeloma end organ damage

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47
Q

Pathophysiology AL amyloidosis

A

Mutated light chains precipitate in tissues as insoluble beta sheets, causing organ damage

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48
Q

Treatment of AL amyloidosis

A

Chemo to reduce light chain productions

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49
Q

Stain used in diagnosis of AL amyloidosis

A

Congo red

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50
Q

Which condition is indium-labelled serum amyloid P scintigraphy used to monitor?

A

AL amyloidosis

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51
Q

Which paraprotein is produced in Waldenstrom’s macroglobulinaemia?

A

IgM

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52
Q

Features of hyperviscosity syndrome

A

Fatigue, visual disturbance, confusion, coma, bleeding, cardiac failure

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53
Q

Treatment of Waldenstrom’s macroglobulinaemia

A

Chemotherapy, plasmapheresis

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54
Q

Most common inheritance pattern of hereditary spherocytosis

A

Autosomal dominant

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55
Q

Which test is used to determine dosage of unfractionated heparin?

A

APTT

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56
Q

Which inherited haematological disorder can present with dactylitis?

A

Sickle cell

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57
Q

Which type of cytotoxic drug is relatively tumour specific?

A

Cell cycle specific agents

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58
Q

Mechanisms of cell cycle specific cytotoxic drugs

A

Antimetabolites, mitotic spindle inhibitors

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59
Q

How does vincristine work?

A

Mitotic spindle inhibitor

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60
Q

How does methotrexate work?

A

Dihydrofolate reductase inhibitor

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61
Q

Types of non cell cycle specific cytotoxic drugs

A

Alkylating agentsPlatinum derivativesCytotoxic antibiotics (anthracyclines)

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62
Q

Which antibiotics are used as chemo?

A

Anthracyclines (___rubicin)

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63
Q

Long term effect of anthracycline chemotherapy

A

Cardiomyopathy

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64
Q

Which chemotherapy agent is a CD20 monoclonal antibody used in NHL?

A

Rituximab

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65
Q

Which monoclonal antibody is used as a bridge to allogenic transplant in Hodgkin’s lymphoma?

A

Brentuximab vedotin

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66
Q

Tyrosine kinase inhibitors used in CML

A

Imatinib, nilotinib, dasatinib, ponatinib

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67
Q

Genetic abnormality in CML

A

t(9:22) translocation resulting in BCR-ABL oncogene on shortened chromosome 22 due to reciprocal translocation

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68
Q

Structure of HbA

A

2 alpha, 2 beta chains

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69
Q

Structure of HbF

A

2 alpha, 2 gamma chains

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70
Q

Breakdown products of haem

A

Iron, bilirubin

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71
Q

Factors affecting G6PD production

A

Stress, drugs

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72
Q

Inheritance of G6PD deficiency

A

X-linked

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73
Q

Distribution of CO2 in the body

A

10% dissolved in solution30% bound to Hb60% transported as bicarbonate

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74
Q

Factors shifting oxygen-Hb dissociation curve right

A

Decrease in PH
Increase in temp
Increase in 2,3-BPGCO2

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75
Q

Factors shifting oxygen-Hb dissociation curve left

A

Increased PH
Decreased temp
Decreased 2,3-BPG

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76
Q

Why does anaemia often occur in CKD?

A

Reduced renal production of erythropoeitin

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77
Q

Why are reticulocytes purple/deeper red than mature RBCs?

A

They still have remnants of protein making machinery

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78
Q

How long does it take to upregulate reticulocyte production in response to anaemia?

A

A few days

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79
Q

What type of defect is implied by a low MCV?

A

Issues with haemoglobinisation

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80
Q

What type of defect is implied by a high MCV?

A

Issues with maturation

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81
Q

What form is circulating iron in?

A

Bound to transferrin

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82
Q

In what condition is transferrin saturation increased?

A

Haemochromatosis

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83
Q

How much iron can a single ferritin protein store?

A

4000 ferric ions

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84
Q

Causes of megaloblastic anaemia

A

B12 deficiency
Folate deficiency
Drugs

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85
Q

What part does folate play in nuclear maturation?

A

Nucleoside synthesis

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86
Q

What part does B12 play in nuclear maturation

A

Products S-adenosyl-methionine, a methyl donor which affects DNA and RNA

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87
Q

Absorption of B12

A

In stomach binds to R-protein which is released from the gastric mucosa
Cleaved from R-protein in duodenum by pancreatic secretions
Intrinsic factor from gastric parietal cells binds
Intrinsic factor-B12 complex absorbed in distal small bowel via cubulin receptors

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88
Q

Which GI condition is associated with pernicious anaemia?

A

Atrophic gastritis

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89
Q

How long do body stores of B12 last?

A

2-4 years

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90
Q

How long do body stores of folate last?

A

Around 4 months

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91
Q

Causes of non-megaloblastic macrocytosis

A

Alcohol, liver disease, hypothyroidism, myelodysplasia, myeloma, aplastic anaemia

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92
Q

Causes of false macrocytosis

A

Reticulocytosis

Cold-agglutinins

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93
Q

Minimum weight for blood donors

A

50kg

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94
Q

How long can red cells be stored?

A

35 days

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95
Q

How long can FFP be stored?

A

3 years

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96
Q

How long can platelets be stored?

A

7 days

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97
Q

Which chromosome codes for ABO blood type?

A

9

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98
Q

Most common blood type in UK

A

O+

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99
Q

What is Landsteiner’s law?

A

When an individual lacks A or B antigen, they produce the corresponding antibody

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100
Q

Which chromosome has genes for Hb alpha chains?

A

16 - 2 genes per chromosome

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101
Q

Which chromosome has genes for Hb beta chains?

A

11 - 1 gene per chromosome

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102
Q

Which haemoglobins are found in embryonic circulation?

A

Gower 1, Gower 2, Portland

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103
Q

What are thalassaemias?

A

Inherited conditions affecting globin chain synthesis

104
Q

Which type of anaemia occurs in thalassaemia?

A

Microcytic hypochromic

105
Q

Why does haemolysis occur in thalassaemia?

A

Unbalanced accumulation of globin chains

106
Q

Which forms of Hb are affected in alpha thalassaemia?

A

HbA, HbA2, HbF

107
Q

Different forms of alpha thalassaemia

A

Alpha thal trait - one or two missing genes
HbH disease - three missing genes
Hb Barts hydrops fetalis - all four genes missing

108
Q

Presentation of alpha thalassaemia trait

A

Asymptomatic

109
Q

Presentation of HbH disease

A

Anaemia with very low MCV and MCH. May be transfusion dependent, splenomegaly, jaundice, growth retardation, gallstones, iron overload.
Red cells inclusions of HbH, which is a B4 tetramer from excess B chains

110
Q

Forms of Hb in Barts hydrops fetalis syndrome

A

Hb Barts (γ4) and HbH (b4)

111
Q

Features of Barts hydrops fetalis syndrome

A

Severe anaemia, cardiac failure, growth retardation, severe hepatosplenomegaly, skeletal abnormalities. Usually die in utero.

112
Q

Forms of Hb affected in beta thalassaemia

A

Only HbA

113
Q

Presentation of B thal trait

A

Asymptomatic, no or mild anaemia, raised HbA2

114
Q

Genotype of B thal trait

A

B+/B or B0/B

115
Q

Genotype of B thal intermedia

A

B+/B+ or B0/B+

116
Q

Genotype of B thal major

A

B0/B0

117
Q

Presentation of B thal intermedia

A

Requires occasional transfusion, moderate anaemia

118
Q

Presentation of B thal major

A

Presents at 6-24 months as HbF falls, pallor and failure to thrive. Hepatosplenomegaly, skeletal changes, organ damage.

119
Q

Management of B thal major

A

Regular transfusion

120
Q

Management of iron overload in B thal

A

Iron chelating drugs such as desferrioxamine, defasirox

121
Q

Makeup of HbS

A

a2Bs2

122
Q

Genotype of sickle cell trait

A

B/Bs

123
Q

Presentation of sickle cell trait

A

Asymptomatic, can have some sickling in severe hypoxia

124
Q

Genotype of sickle cell anaemia

A

Bs/Bs

125
Q

Hb found in sickle cell

A

80% HbS, no normal HbA

126
Q

Why does haemolysis occur in sickle cell?

A

Shortened RBC survival

127
Q

Triggers of sickle cell crisis

A

Hypoxia, dehydration, infection, cold exposure, stress, fatigue

128
Q

Management of severe sickle cell crisis

A

Red cell exchange transfusion

129
Q

Management of sickle cell

A

Prophylactic penicillin, folic acid supplementation, hydroxycarbamide to induce HbF production. Regular transfusion in some cases

130
Q

Diagnostic test for sickle cell

A

High performance liquid chromatography

131
Q

Why can’t high performance liquid chromatography be used to diagnose alpha thal trait?

A

All Hb are reduced, so the ratio remains normal. DNA testing is required

132
Q

Hb form ratios in normal patients

A

HbA >80%
HbF <1%
HbA2 1.5-3.5%

133
Q

Side effects of iron supplementation

A

Constipation, N+V, diarrhoea, black stool

134
Q

What level of response is expected in iron supplementation?

A

5-10g increase in Hb per week

135
Q

Consequences of haemolysis

A

Erythroid hyperplasia

Excess red cell breakdown products

136
Q

Effects of intravascular haemolysis

A

haemoglobinaemia, methaemalbuminaemia, haemoglobinuria, haemosiderinuria

137
Q

Causes of intravascular haemolysis

A

ABO incompatibility, G6PD deficiency, blackwater ever, etc.

138
Q

What do Heinz bodies indicate?

A

Oxidative damage

139
Q

Which type of antibody is found in warm autoimmune haemolysis?

A

IgG

140
Q

Which type of antibody is found in cold autoimmune haemolysis?

A

IgM

141
Q

Direct Coombs’ test

A

Patient RBCs coated with IgG, complement, mouse anti-human IgG. Agglutination = haemolysis

142
Q

Causes of mechanical red cell destruction

A

DIC, haemolytic uraemic syndrome (E. coli O157), TTP, leaking heart valve, infection

143
Q

Which cells are seen on blood film in burn-related haemolysis?

A

Microspherocytes

144
Q

What is Zieve’s syndrome?

A

Acquired RBC membrane defect due to liver disease - presents with anaemia, polychromic macrocytes, irregularly contracted cells

145
Q

Which drug causes oxidative damage resulting in irregularly contracted cells?

A

Dapsone

146
Q

Where do iron absorption mainly occur?

A

Duodenum

147
Q

Which substances enhance iron absorption?

A

Ascorbic acid, alcohol

148
Q

Which substances inhibit iron absorption?

A

Tannins (tea), phytates (cereals, bran, nuts, seeds), calcium

149
Q

Which enzyme of the GI tract reduces Fe3+ to Fe2+?

A

Duodenal cytochrome B

150
Q

Which transporter transport iron into duodenal enterocytes?

A

DMT-1

151
Q

Which substance facilitates iron export from duodenal enterocytes?

A

Ferroportin

152
Q

Which substance released by the liver binds to and degrades ferroportin?

A

Hepcidin

153
Q

How is functional iron assessed?

A

Hb concentration

154
Q

How is transport iron assessed?

A

Transferrin saturation

155
Q

How is storage iron assessed?

A

Serum ferritin

156
Q

Two forms of transferrin

A

Holotransferrin - iron bound

Apotransferrin - unbound

157
Q

Which gene accounts for 95% of hereditary haemochromatosis?

A

HFE - mostly C282Y and H63D mutations

158
Q

How does iron overload occur in haemochromatosis?

A

Decreased hepcidin synthesis results in increased iron absorption

159
Q

Treatment of haemochromatosis

A

Weekly venesection of 450-500ml to maintain ferritin <50

160
Q

Most common cause of death from hereditary haemochromatosis

A

Hepatoma

161
Q

Treatment of secondary iron overload

A

Iron chelating agents (desferrioxamine, deferiprone, deferasirox)

162
Q

Which antibodies are responsible for acute haemolytic transfusion reaction?

A

IgM anti-A or anti-B

163
Q

Complications of acute haemolytic transfusion reaction

A

Shock, increased vascular permeability, DIC, renal failure, death

164
Q

Presentation of transfusion associated circulatory overload

A

Respiratory distress within 6 hours of transfusion, raised BP, raised JVP, positive fluid balance

165
Q

Risk factors for transfusion associated circulatory overload

A

Age, cardiac failure, low albumin, renal impairment, fluid overload

166
Q

Which antibodies are responsible for delayed haemolytic transfusion reaction?

A

IgG antibodies against red cell antigen

167
Q

When do delayed haemolytic transfusion reactions occur?

A

5-10 days post transfusion

168
Q

Biochemical changes in delayed haemolytic transfusion reaction

A

Drop in Hb
Rise in bilirubin
Rise in lactate dehydrogenase

169
Q

What is the lifespan of a platelet?

A

7-10 days

170
Q

Which clotting factor is activated by tissue factor?

A

VIIa

171
Q

Which clotting factors stimulate the conversion of prothrombin to thrombin?

A

V, Xa

172
Q

What is the function of thrombin?

A

Conversion of fibrinogen to fibrin, upregulation of factors VII and IXa

173
Q

What does D-dimer measure?

A

Fibrin degradation products

174
Q

Which clotting factors are assessed by prothrombin time?

A

TF, VIIa

175
Q

Which clotting factors are assessed by APTT?

A

VII, IXa

176
Q

Which clotting factors are inhibited by protein C and protein S?

A

V, Xa, VIII, IXa

177
Q

Urine output in shock

A

<0.5ml/kg/hour

178
Q

Causes of obstructive shock

A

Cardiac tamponade, tension pneumothorax, PE

179
Q

Most common type of shock

A

Distributive shock

180
Q

Most common cause of primary haemostatic failure

A

Thrombocytopenia

181
Q

Inheritance of Von Willebrand disease

A

Autosomal dominant

182
Q

Which type of haemostasis is primarily affected in vWD?

A

Primary

183
Q

Which clotting factors require carboxylation by vitamin K?

A

II, VII, IX, X

184
Q

Where is vitamin K absorbed?

A

Upper intestine

185
Q

Which type of haemophilia is more common?

A

Haemophilia A

186
Q

Severity classification of haemophilia

A

Mild: clotting factor >5% normal
Moderate 2-5%
Severe <2%

187
Q

Which coagulation test can be normal in haemophilia?

A

PT

188
Q

How do clopidogrel and prasugrel work?

A

ADP receptor antagonists

189
Q

What kind of drug is dipyrimadole?

A

Phosphodiesterase inhibitor (anti-platelet)

190
Q

What kind of drug is abciximab?

A

Glycoprotein IIb/IIIa inhibitor - inhibits aggregation of platelets

191
Q

Virchow’s triad

A

Stasis, vessel wall/valve damage, hypercoagulability

192
Q

ECG pattern in PE

A

S1Q3T3

S waves lead I, Q-waves lead III, inverted T lead III

193
Q

What is the action of heparin?

A

Potentiates antithrombin

194
Q

Which test is used for monitoring unfractionated heparin?

A

APTT

195
Q

Which drug is used to reverse heparin?

A

Protamine sulphate

196
Q

Why is warfarin initially pro-thrombotic?

A

It decreases protein C levels

197
Q

What is INR?

A

Patient’s PT/mean normal PT

198
Q

How long does it take for INR to return to normal after withdrawal of warfarin?

A

2-3 days

199
Q

How quickly does vitamin K reverse warfarin?

A

6 hours

200
Q

What class is dabigatran?

A

Oral direct thrombin inhibitor

201
Q

What class is rivaroxaban?

A

Xa inhibitor

202
Q

Causes of microangiopathic haemolytic anaemia (MAHA)

A

DIC, foreign bodies, malignancy, TTP, heart valve issues

203
Q

Which type of haemostatic failure causes mucosal bleeding?

A

Primary

204
Q

What type of hypersensitivity reaction occurs in incompatible blood transfusion?

A

Type 2, IgM

205
Q

Definitions of massive haemorrhage

A 
Loss of one blood volume in 24 hours
50% blood loss in 3 hours
150ml loss per minute
Bleeding leading to HR >100 and BP <90
Bleeding which has already required use of emergency O neg
206
Q

What ratio of blood products is used in massive haemorrhage?

A

2 RBC : 1 FFP, or 1:1 in trauma

207
Q

Which white blood cells are able to stick to blood vessel walls (marginate)?

A

Neutrophils

208
Q

Causes of neutrophilia

A

Tissue necrosis, neoplasia, haemorrhage, bacterial infection, inflammation, smoking

209
Q

Causes of eosinophilia

A

Asthma, helminth infection, eczema, allergy, lymphoma

210
Q

Causes of basophilia

A

CML, polycythaemia

211
Q

Which type of hypersensitivity are basophils involved in?

A

Type 1

212
Q

What are the granules in basophils composed of?

A

Histamine and heparin

213
Q

Causes of monocytosis

A

Chronic bacterial infection, malignancy, connective tissue disease

214
Q

How long do monocytes circulate before entering tissues?

A

1-2 days

215
Q

Appearance of T cells in EBV infection

A

Abundant blue cytoplasm wrapping around neighbouring red cells

216
Q

How long do neutrophils live?

A

7-8 hours

217
Q

Which embryonic tissue do haemopoietic stem cells arise from?

A

Mesoderm

218
Q

Site of erythroid activity before birth

A

Yolk sac up to week 10
Liver starts by week 6
Bone marrow by week 16

219
Q

Where is bone marrow extracted in children?

A

Tibia

220
Q

Normal myeloid:erythroid ratio:

A

1.5:1 - 3.3:1

221
Q

What does granulocyte-colony stimulating factor do?

A

Stimulates neutrophil precursor maturation

222
Q

What is the action of thrombopoietin?

A

Regulates growth and development of megakaryocytes from their precursors

223
Q

Where do B cells mature?

A

Bone marrow

224
Q

Where do T cells mature?

A

Thymus

225
Q

Where does the spleen lie?

A

Level of 9th - 11th ribs

226
Q

Size of spleen

A

1 inch thick, 3 inches wide, 5 inches long

227
Q

Which organs is the visceral surface of the spleen in contact with?

A

Left kidney
Gastric fundus
Tail of pancreas
Splenic flexure

228
Q

What is in the red pulp of the spleen?

A

Sinusoids, cords

229
Q

What is in the white pulp of the spleen?

A

Peri-arteriolar lymphoid sheath

230
Q

How can acute leukaemia be distinguished from chronic myeloproliferative disorders on blood film?

A

In acute leukaemia, there is a block on maturation so cells are homogenous. In chronic disorders, there is proliferation, but no issues with maturation

231
Q

Which test can distinguish ALL and AML?

A

Immunophenotyping

232
Q

How is remission defined in acute leukaemia?

A

<5% marrow blasts

233
Q

Cure rate of childhood ALL

A

85-90%

234
Q

Cure rate of adult ALL

A

30-40%

235
Q

Cure rate of AML in under 60s

A

40-50%

236
Q

Cure rate of AML in over 60s

A

10%

237
Q

T cell enhancer used in leukaemia

A

Blinatumomab

238
Q

Characteristics of lymphadenopathy in lymphoma

A

Non-tender, soft, non-tethered, without skin inflammation

239
Q

What kind of biopsy should be performed in suspected lymphoma?

A

Surgical - fine needle or core often insufficient

240
Q

What are Reed Sternberg cells?

A

Large multinuclear cells found in Hodgkin’s lymphoma, derived from B lymphocytes

241
Q

What is mantle cell lymphoma?

A

A low grade lymphoma which is fast growing

242
Q

Which cell are most NHLs derived from?

A

B cell (90%)

243
Q

Gene in CML

A

BCR-ABL1 due to Philadelphia chromosome

244
Q

Tyrosine kinase inhibitor used in CML

A

Imatinib

245
Q

What is erythromelagia?

A

Vascular disorder where palms and soles become hot and painful, seen in MPDs

246
Q

What mutation is prevalent in polycythaemia rubra vera?

A

JAK2

247
Q

What is the result of JAK2 mutation?

A

Loss of auto-inhibition, causing activation of erythropoiesis in the absence of EPO

248
Q

Mutations found in essential thrombocythaemia

A

JAK2 in 50%
CALR, MPL in some
15% all absent

249
Q

JAK2 inhibitor

A

Ruxolitinib

250
Q

Which GABA receptor is targeted by benzos, barbiturates, and alcohol?

A

GABA-A

251
Q

First line treatment for functional symptoms

A

CBT

252
Q

Life expectancy with Alzheimer’s

A

7 years

253
Q

Lifetime risk of Alzheimer’s

A

10%, or 25% if 1st degree relative affected.

254
Q

Drugs that cause thrombocytopenia

A

quinine
abciximab
NSAIDs
diuretics: furosemide
antibiotics: penicillins, sulphonamides, rifampicin
anticonvulsants: carbamazepine, valproate
heparin

255
Q

Immune thrombocytopenic purpura

A 
Isolated thrombocytopenia
Autoantibodies against platelets - often membrane glycoproteins
Follows viral infection
Presents with purpuric rash and bleeding
Most cases treated with only steroids
256
Q

Test for definitive diagnosis of sickle cell

A

Haemoglobin electrophoresis

3rd year (6 decks)

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