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1
Q

4 causes of microcytic anaemia

A 
FAST
• Fe-deficiency anaemia
• Anaemia of chronic disease
• Sideroblastic anaemia
• Thalassaemia
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2
Q

7 causes of normocytic anaemia

A
  • Acute blood loss
  • Anaemia of chronic disease
  • Bone marrow failure
  • Renal failure
  • Hypothyroidism
  • Haemolysis
  • Pregnancy
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3
Q

6 causes of macrocytic anaemia

A
  • Fetus (pregnancy)
  • Antifolates
  • hypoThyroidism
  • Reticulocytosis
  • B12/folate deficiency
  • Cirrhosis

FATRBC

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4
Q

5 signs of iron-deficiency anaemia

A
  • Koilonychia
  • Atrophic glossitis
  • Angular cheilosis
  • Post-cricoid webs
  • Brittle hair and nails
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5
Q

Blood film of iron-deficiency anaemia

A
  • Microcytic
  • Hypochromic
  • Anisocytosis (unequal in size)
  • Poikilocytosis (abnormal shapes)
  • Pencil cells
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6
Q

Causes of iron-deficiency anaemia

A

Bleeding until proven otherwise - menorrhagia in young women

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7
Q

Leading cause of gastrointestinal blood loss in developing countries?

A

Hookworm infestation (ancylostoma duodenale)

Faecally contaminated soil - skin - alveoli - coughed and swallowed - intestine

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8
Q

Why can pregnancy cause iron-deficiency anaemia?

A

Increased utilisation

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9
Q

Why can iron-deficiency anaemia present post gastric surgery?

A
  • Rapid transit

* Less acid which helps Fe absorption

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10
Q

Why can coeliac disease cause iron-deficiency anaemia?

A

Absence of villous surface in duodenum

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11
Q

Investigations of iron-deficiency anaemia if no obvious cause

A
  • OGD + colonoscopy
  • Urine dip
  • Coeliac investigations
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12
Q

Treatment of iron-deficiency anaemia

A
  • Oral iron
  • IV iron if severe - risk of anaphylaxis
  • Blood transfusion if severe infection or sepsis as iron doesn’t absorb well and may fuel sepsis
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13
Q

What happens in ACD and how does it affect iron?

A

Cytokines reduce EPO receptor production by kidneys - reduced response to EPO - reduced red cell production

Cytokines stimulate liver hepcidin production, decreasing iron absorption and causing iron accumulation in macrophages - iron levels are therefore low

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14
Q

Ferritin and transferrin in ACD

A

High ferritin (intracellular protein - macrophages deprive invading bacteria of Fe)

Low transferrin

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15
Q

Management of ACD

A
  1. Treat disease

2. Recombinant EPO

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16
Q

What is sideroblastic anaemia and how is it diagnosed?

A
  • Enough iron but inability to put it into haemoglobin
  • Ineffective erythropoeisis
  • Bone marrow produces ring sideroblasts, which is seen in the marrow but not on film
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17
Q

Sideroblastic anaemia causes and treatment

A
  • Chemotherapy
  • Alcohol excess
  • Lead excess
  • Anti-TB drugs

Remove the cause + pyridoxine (Vit B6 promotes RBC production)

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18
Q 
The following is a sign of what
• Hypersegmented polymorphs
• Leucopenia
• Macrocytosis
• Anaemia
• Thrombocytopaenia
A

Megaloblastic blood film (B12/folate deficiency, cytotoxic drugs)

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19
Q

Source of vitamin B12

A

Meat and dairy

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20
Q
  • Glossitis
  • Angular cheilosis
  • Irriability, depression
  • Paraesthesiae
  • Peripheral neuropathy (loss of vibration and proprioception first, absent ankle reflex, SCDSC)

Features of what condition

A

B12 deficiency

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21
Q

Causes, diagnosis and treatment of pernicious anaemia

A

Autoimmune atrophic gasritis - lack of IF

Parietal cell antibodies, IF antibodies, Schilling test (outdated)

IM hydroxycobalamin (B12)

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22
Q

Source of folate and ‘medical’ causes of folate deficiency

A

Green vegetables, nuts, yeast, liver

Alcohol, methotrexate, phenytoin, trimethoprim

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23
Q

Treatment of folate deficiency

A

Oral folic acid, but treat B12 first if cause of anaemia is not known

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24
Q

Hereditary spherocytosis deficiency, pathogen susceptibility, and diagnosis

A

Spectrin or ankyrin deficiency (membrane protein)

Susceptible to effect of parvovirus B19

Diagnosis
• Spherocytes
• Increased osmotic fragility
• Eosin-5’-maleimide flow cytometry

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25
Cause and blood film in hereditary elliptocytosis
Cause: spectrin mutations Elliptical erythrocytes
26
How can someone with hereditary elliptocytosis present?
Asymptomatic to hydrops fetalis (oedema in at least 2 compartments)
27
Inheritance and benefit of South East Asian Ovalocytosis?
Autosomal recessive Malaria protection
28
Precipitator and blood film of G6PD deficiency
Precipitated by acute stressors, moth balls, broad beans, antimalarials, steroids, certain antibiotics Bite cells, Heinz bodies (blue deposits)
29
Clinical features and treatment of pyruvate kinase deficiency
* Haemolytic anaemia * Severe neonatal jaundice * Splenomegaly Most don't require treatment
30
Which globins make up HbA (95% of normal haemoglobin)?
2 alpha and 2 beta
31
Which globins produce HbA2 and HbF?
HbA2 - 2 alpha and 2 gamma | HbF - 2 alpha and 2 delta
32
How many alpha and beta globin genes do we have?
4 alpha - 2 from each parent (Chr16) 2 beta - 1 from each parents (Chr11)
33
Inheritance of mutation in SCD
Autosomal recessive Single base mutation • Glutamic acid to valine at codon 6 of beta chain • HbA -> HbS
34
Haemoglobin type in: sickle cell anaemia trait
Sickle cell anaemia - HbSS | Sickle cell trait - HbAS (asymptomatic unless stressed)
35
Most common invasive infection in sickle cell disease patients
Strep pneumoniae sepsis
36
What can (non-typhoidal) salmonella infection lead to in sickle cell disease patients?
Osteomyelitis
37
At what age does SCD manifest
3-6 months, coincides with decreasing HbF
38
Blood film findings of SCD
Sickle cells and target cells | Howell-Jolly bodies => hyposplenism
39
Acute and chronic treatment of SCD Treatment in SCD for the following: • Acute painful crises • Acute severe crises * Prophylaxis * Increase HbF * Further chronic treatment * Childhood monitoring
Acute • Opioids for painful crises • Exchange tranfusion in severe crises Chronic • Penicillin V, pneumax, HiB vaccine • Folic acid and hydroxycarbamide increases HbF • Regular exchange transfusions • Carotid doppler monitoring in early childhood
40
``` Patient has the following features • Skull bossing, maxillary hypertrophy, hairs on end skull X-ray* • Hepatosplenomegaly* • Heart failure** • Gonadal failure** ``` What is the condition and the changes in the following in this condition: mutations, Hb changes, EPO, and iron.
``` Beta-thalassaemia • Point mutations - decreased beta-chain synthesis, excess alpha-chains • Increased HbA2 and HbF • Increased EPO* • Iron overload** ```
41
Type of beta-thalassaemia with splenomegaly, bony deformity, gallstones, but no failure to thrive or heart failure.
Intermedia
42
Diagnosis and treatment of beta-thalassaemia
Diagnosis: Hb electrophoresis (Guthrie test at birth) Treatment - blood transfusions with desferrioxamine to stop iron overload, folic acid
43
What does severity of alpha-thalassamia depend on?
Number of the 4 alpha genes deleted * trait - 1-2 deleted, mild anaemia * HbH disease - 3 deleted, splenomegaly, anaemia * Hydrops foetalis - 4 deleted, incompatible with life
44
Name 2 autoimmune acquired haemolytic anaemias
Warm autoimmune haemolytic anaemia (WAIHA) Cold agglutinin disease
45
Ig type and coombs test result in WAIHA and cold agglutinin disease
WAIHA - IgG, +ve Coombs test Cold agglutinin disease - IgM or IgG, +ve Coombs test
46
WAIHA / Cold agglutinin intra or extravascular?
WAIHA - extravascular | Cold agglutinin - intravascular
47
Patient has syphilis and Donath-Landsteiner IgG seen sticking to RBCs. Haemoglobin seen in urine. What is the condition?
Paroxysmal cold haemoglobinuria Donath-Landsteiner IgG seen sticking to RBCs when cold, the complement-mediated haemolysis on rewarming.
48
Name 2 Coombs negative diseases
Paroxysmal nocturnal haemoglobinuria (PNH) Microangiopathic haemolytic anaemia (MAHA)
49
Outline PNH
* Loss of protective surface GPI markers on RBCs * Chronic complement-mediated intravascular haemolysis, especially at night * Morning haemglobinuria, thrombosis, Budd-Chiari syndrome (obstructed hepatic venous outflow)
50
Investigations for PNH
* Altered GPI immunophenotype | * Ham's test (in vitro acid-induced lysis)
51
Outline MAHA and its causes
* RBC destruction after force through fibrin/platelet mesh in damaged vessels * Resultant schistocytes HUS, TTP, pre-eclampsia, adenocarcinoma (release of procoagulant granules)
52
Outline the condition with antibodies against ADAMTS13
TTP • Lead to long strands of vWF • These cut up RBCs
53
Outline HUS and clinical features
E. coli Shiga toxin bind to endothelial cells Clinical features • Diarrhoea • Renal failure • Thrombocytopaenia
54
Why can abx lead to decreased vitamin K?
Vit K activated by bacteria - abx harm gut flora
55
Vitamin K dependent clotting factors
2, 7, 9, 10
56
``` Where do these clotting cascade inhibitors act? • TFPI • Protein C • Protein S • Antithrombin III ```
TFPI - blocks VII to VIIa Protein C - inactivates Va and VIIIa Protein S - co-factor to Protein C Antithrombin - Xa (and IXa/XIIa), thrombin
57
First factor of instrinsic pathway, test used to measure, and what therapy you should monitor with this
Factor XII APTT Heparin therapy
58
First factor of extrinsic pathway, test used to measure, and what therapy you should monitor with this
Factor VII PT Warfarin therapy (INR)
59
First factor of common pathway and test used to measure
Factor V TT (thrombin time)
60
How does clopidogrel work?
* Blocks ADP RECEPTOR | * Decreased platelet activation and fibrin cross-linking
61
Difference between acute and chronic ITP
``` Acute • Children • Preceding infection • Lower plt • Self-limiting ```
62
Haemophilia A factor deficiency, inheritance, presentation, diagnosis, management?
``` Factor VIII deficiency • X-linked recessive • Presents early in life or prolonged bleeding after surgery/trauma (e.g. dental) • High APTT • Factor VIII concentrates ```
63
What should you avoid in haemophilia A (in terms of treatment)?
NSAIDs | IM injections
64
What is haemophilia B, inheritance, presentation, diagnosis, management?
Factor IX deficiency The rest is like haemophilia A
65
What factor does VWD lead to a decrease in?
Factor VIII as vWF carries factor VIII in circulation
66
Clotting, factor change, antigen change, INR, platelets, and management of VWD
* High APTT * Low Factor VIII * Low vWF Ag * Normal INR and platelets Manage with desmopressin (increases VWF and Factor VIII), VWF and Factor VIII concentrates
67
DIC platelets, fibrinogen, D-Dimer, PT, and treatment
* Low platelets * Low fibrinogen * High FDP/D-Dimer * Long PT/INR Treat the cause and give transfusions, heparin
68
Why can warfarin be initially pro-coagulant?
* Warfarin antagonises vit K * Vit K needed for synthesis of protein C/S (as well as the clotting factors) are normally anticoagulant * Therefore warfarin can stop the anticoagulant effect of vitamin K, creating a procoagulant state
69
Most sensitive vitamin K-dependent clotting factor
Factor VII - first deficiency
70
Treatment of vitamin K deficiency (and in acute haemorrhages)
IV vitamin K - FFP for acute haemorrhages | Prothrombin complex concentrate
71
3 inherited causes of venous thrombosis
* Antithrombin deficiency (highest risk) * Protein C deficiency * Protein S deficiency
72
Most thrombogenic acquired condition
Obesity
73
DVT prophylaxis
* Daily subcutaneous LMWH | * TED stockings
74
Initial treatment of DVT/PE
* LMWH (treatment dose), then warfarin or DOAC | * LMWH stopped once INR 2-3 (due to warfarin being initially procoagulant)
75
Long-term treatment time of VTE if: • Known cause • Recurrent VTE
* Known cause - 3 months | * Recurrent VTE - lifelong
76
How does heparin work?
* Potentiates antithrombin III | * This inactivates thrombin, factor IX, X, XI
77
What type of heparin is given in renal impairment?
IV unfractionated heparin
78
Long-term side effect of heparin
Osteoporosis
79
Why does haemoglobin drop in pregnancy?
Diluation anaemia
80
What is HELLP syndrome and the management?
Haemolysis, elevated liver enzymes, low platelets Supportive management, delivery of foetus
81
Which Ig can cross placenta?
Only IgG
82
In whom and how/when do you prevent anti-D formation?
* RhD negative women * Give mother IM anti-D Ig if high risk of feto-maternal haemorrhage * Routine antenatal prophylaxis at 28 and 34 weeks * If sensitising event occurs e.g. abortion, miscarriage * At delivery if baby is RhD +ve
83
In which leukaemia is testicular and thymic enlargement seen?
acute lymphoblastic leukaemia
84
Which genetic disorder increases risk of acute leukaemia?
Down's syndrome
85
Which marker is seen in acute leukaemia
CD34 - blast cell marker
86
When are auer rods seen?
AML
87
Which marker is seen on flow cytometry in AML but not ALL?
MPO - myeloid cells
88
What is the most common leukaemia in the west?
CLL
89
General difference between CLL and small lymphocytic lymphoma (SLL)
Same disease process but slightly different presentations | CLL - bone marrow, SLL - lymph nodes
90
Leukaemia which is mostly diagnosed on routine bloods, has symmetrical painless lymphadenopathy, and autoimmunity association
CLL
91
What is Richter's transformation
Transformation of CLL or SLL to more aggressive form of large cell LYMPHOMA
92
Leukaemia with Philadelphia chromosome, massive splenomegaly, and high basophils
CML
93
Binet staging for CML
A: < 3 groups of enlarged lymph nodes B: 3+ groups of enlarged lymph nodes C: anaemia or thrombocytopaenia
94
Treatment for CML
Imatinib (BCR-ABL tyrosine kinase inhibitor) or dasatinib/nilotinib for resistance
95
Which sex does Hodgkin's lymphoma affect more and which virus is it associated with?
Males EBV
96
Clinical presentation of H. lymphoma
* Asymmetrical painless lymphadenopathy * Fever >38 * Drenching night sweats * Weight loss >10% in 6 months * Pain after alcohol
97
Diagnosis of H. lymphoma
* CT-PET * LN or BM biopsy - CD15 and CD30 * Reed-Sternberg cell ('owl eyed') surrounded by fibrotic collagen bands
98
Most common subtype of H. lymphoma
Nodular sclerosing
99
Ann-Arbor staging of H. lymphoma
1 - one LN region (includes spleen) 2 - two or more LN regions on same side of diaphragm 3- two or more LN regions on opposite sides of the diaphragm 4 - extranodular sites A - no constitutional symptoms B - constitutional symptoms
100
H. lymphoma combination chemo treatment
ABVD (adriamycin, bleomycin, vinblastine, dacarbazine)
101
What is autologous stem cell transplant?
* Own SCs harvested * High dose treatment to eradicate malignant cells at cost of bone marrow ablation * SCs reintroduced
102
What is the most common lymphoma?
Non-Hodgkin's (80%)
103
How is the presentation of NH lymphoma different to H?
No pain after alcohol
104
Translocation and gene overexpressed in Burkitt's lymphoma (NH, B cell)?
t(8;14) translocation | c-myc oncogene
105
Histology of Burkitt's lymphoma
Starry sky appearance
106
Histology of diffuse large B-cell (NH, B cell)
Sheets of large lymphoid cells
107
Angular nuclei - hearts/crests in cells, are seen in which subtype of NH B cell lymphoma?
Mantle cell
108
Cause of gastric and parotid MALT (NH, B cell) lymphoma
Chronic antigen stimulation • H. pylori => gastric • Sjogren's => parotid lymphoma
109
Treatment for B cell lyphomas
Rituximab (or remove antigenic stimulus in MALT)
110
Alk-1 protein expression is seen in which lymphoma?
Anaplastic large cell lymphoma (T cell)
111
Cause of adult T cell leukaemia/lymphoma and population greatly affected
HTLV-1 infection | Caribbean and Japanese
112
Blood film of adult T cell leukaemia/lymphoma
Flower cells
113
Disease associations with enteropathy-associated T cell lymphoma and cutaenous T cell lymphoma
EATL - coeliac disease | Cutaneous - mycosis fungoides (red rashes)
114
Treatment for T cell lymphomas
Alemtuzumab (anti-CD52)
115
What is multiple myeloma?
Neoplasia of plasma cells of bone marrow - production of monoclonal immunglobulin (IgG most common)
116
Ethinicity with increased incidence of MM
Afro-caribbeans
117
Clinical features of MM
C - high calcium (groans, moans, stones, thirst) R - renal failure A - anaemia B - pain, osteoporosis, osteolytic lesions, hyperviscosity syndrome myeloma cells release osteoclast activating / osteoblast inhibiting factors Fatigue - must be MM over MGUS or smouldering MM
118
MM diagnosis
* Dense narrow band on serum electrophoresis (in gamma region) * Rouleaux on blood film * Bence-Jones protein in urine * High ESR * >10% plasma cells in BM
119
Treatment for MM
Supportive for CRAB symptoms Induce remission for autologous SCT: 1. Bortezomib (proteosome inhibitor), dexamethasone (steroids cytotoxic to lymphoma) 2. auto-SCT or daratumumab
120
Amount of M-spike in MGUS, smouldering myeloma and MM
MGUS + smouldering myeloma <30g/l MM >30g/l
121
Clonal plasma cells in MGUS, smouldering myeloma and MM
MGUS <10% Smouldering myeloma >10% MM - any clonal plasma cell population
122
Is treatment needed in MGUS, smouldering myeloma and MM?
MGUS and smouldering MM: no treatment needed MM: treatment needed
123
In whom does Waldenstrom's macroglobinaemia (lymphoplasmacytoid lymphoma - LPL) more commonly present?
Elderly men
124
What is LPL?
* Low-grade NHL (lymphoplasmacytic) | * Lymphoplasmacytoid cells produce monoclonal serum IgM that infiltrates the LNs/BM
125
Lymphoma with hyperviscosity syndrome (visual problems, confusion etc.) and is treated with chlorambucil?
LPL (Lymphoplasmacytic) - Waldenström’s macroglobulinaemia is the most common one
126
What causes AL amyloidosis and which ratio is abnormal
Mis-folded light chains deposit in tissues | Abnormal kappa:lambda light chain ratio (although increased lambda, and decreased ratio = MM)
127
Diagnosis of AA amyloidosis
* Biopsy of affected organ * Congo-red stain * Apple green birefringence
128
What is myelodysplastic syndrome and how is it different to aplastic anaemia?
Differentiation of abnormally maturing myeloid stem cells (give rise to RBCs, neutrophils, platelets, macrophages, basophils etc.) and ineffective proliferation. Aplastic anaemia is a quantitative deficiency rather than functional. The bone marrow stops producing new cells, rather than producing abnormal cells.
129
What does myelodysplastic syndrome risk transforming into?
Acute myeloid leukaemia (AML)
130
What does the bone marrow look like in myelodysplastic syndrome and describe the RBCs, WBCs and platelets?
Hypercellular BM * RBCs - ring sideroblasts * WBCs - hypogranulation, Pseudo-Pelger-huet anomaly (hyposegmented neutrophil) * Platelets - micromegakaryocytes, hypolobated nuclei
131
What does a ring sideroblasts look like and what causes it?
* Increased ferritin as ineffective erythropoiesis | * Nucleated erythroblast with granules of iron in the mitochondria surrounding the nucleus
132
What are hypomethylating agents useful for treating?
Myelodysplastic syndromes and AML
133
Scoring system for prognosis of myelodysplastic syndrome
International prognostic scoring system • BM blast % • Karyotype - degree of cytopenia
134
What are the classifications of aplastic anaemia?
Primary • Idiopathic (70%) • Inherited (10%) Secondary (10-15%) - malignancy, radiation, drugs (e.g. chloramphenicol), chemo, viruses, autoimmune
135
Which inherited aplastic anaemias are responsible for these presentations? 1. • pancytopaenia • skeletal abnormalities, short stature, cafe-au-lait spots, hypogonadism, microcephaly, developmental delay 2. • Chromosome instability - telomere shortening • Skin pigmentation, nail dystrophy, oral leukoplakia 3. • Primary neutrophilia • Skeletal abnormalities, endocrine and pancreatic dysfunction, hepatic impairment, short stature 4. • Red-cell aplasia • Dysmphorphology
1. Fanconi anaemia 2. Dyskeratosis Congenita 3. Schwachman-Diamond syndrome 4. Diamond-Blackfan syndrome
136
What can myeloproliferative disorders all progress to?
Myelofibrosis
137
Name a philadelphia chromosome positive myeloproliferative disroder
CML
138
Name 3 ph (philadelphia chromosome)-negative myeloproliferative disorders
* Polycythaemia vera * Myelofibrosis * Essential thrombocytosis
139
What mutations are ph -ve mp disorders associated with?
JAK2 mutations
140
What are the primary and secondary causes of polycythaemia?
Primary (abnormality in BM) • Polycythaemia vera • Familial polycythaemia Secondary (EPO) • Diseases states (renal cancer) • High altitude • Chronic hypoxia
141
What is relative (pseudo) polycythaemia and what can cause it?
* Red cell mass normal but plasma volume reduced (normal Hb) | * Dehydration, burns, vomiting, diarrhoea, smoking
142
What causes polycythaemia rubra vera?
* Erythroid precursors dominate the BM | * Point mutation JAK2
143
Clinical features of polycythaemia rubra vera
* Blurred vision * Headache * Plethoric, red nose * Gout * Splenomegaly * Aquagenic pruritis
144
Treatment for polycythaemia rubra vera
* Venesection - younger patients * Hydroxycarbamide - maintenance * Aspirin - decrease thrombosis risk
145
Clinical features of myelofibrosis
* Pancytopaenia-related * Hepatomegaly * Massive splenomegaly * Fever * Budd-Chiari syndrome
146
Patient has dry tap from bone marrow. What would you expect to see on blood film and what mutations would you find?
Blood film - tear-drop poikilocytes (dacrocyte), leukoerythroblasts (primitive cells) JAK2 mutation, MPL mutation (myelofibrosis)
147
Treatment for myelofibrosis
Supportive - blood producs, splenectomy Cytoreductive - ruloxitinib (JAKi) Curative - SCT
148
What are 50% of essential thrombocythaemias associated with?
JAK2 mutations
149
Which cell type dominates the BM in essential thrombocythaemia?
Megakaryocytes
150
Clinical features in thrombocythaemia?
Often incidental finding Venous and arterial thrombosis Erythromelalgia (redness and burning in feet, hands, ears)
151
Investigation findings in essential thrombocythaemia
aka thrombocytosis, so: • Platelet count >600 • Blood film - large platelets and megakaryocyte fragments
152
Treatment for essential thrombocythaemia
* Aspirin * Anagrelide (reduces platelet formation) * Hydroxycarbamide (chemo) * Interferon (<40yo)
153
What is the red cell transfusion threshold if asymptomatic and symptomatic?
Asymptomatic - 70g/l | Symptomatic - 80g/l
154
Do you tranfuse red cells first or treat iron/folate/B12 deficiency?
Treat deficiency first unless active bleeding
155
When should platelets be transfused?
* Consumptive disorders e.g. DIC, TTP | * Only if active bleeding
156
What is the universal blood type when transfusing red cells?
O- (red cells can't be destroyed by anti-A or anti-B antibodies)
157
What is the universal blood type when transfusing FFP?
AB (no anti-A or anti-B antibodies in plasma)
158
How long does FFP need to thaw?
30 mins
159
Which acute (<24 hours) transfusion reactions present with the following: 1. Pulmonary oedema 2. IgM-mediated intravascular haemolysis: restlessness, chest/loin pain, vomiting, collapse
1. Transfusion-related circulatory overload | 2. ABO incompatibility
160
What are potential delayed (>24 hours) reactions to transfusions?
Delayed-haemolytic transfusion reaction • Within 1 week • Extravascular haemolysis - IgG-mediated GVHD • Donor lymphocytes recognise recipient's HLA as foreign • Diarrhoea, liver failure, skin desquamation, BM failure Delayed infections • CMV • Parvovirus • Variant CJD
161
Outline haemolytic disease of the newborn
1) RhD sensitising event 2) Maternal anti-D crosses placenta (IgG) and coats fetal RhD +ve cells • Cells destroyed in fetal spleen and liver
162
How is HDN prevented?
* Anti-D Ig given to mother if she is RhD negative (so has anti-RhD antibodies) and foetus is RhD positive * This destroys the fetal cells in the mother, bypassing the mother's immune response * Given at delivery, foeto-maternal haemorrhage, spontaenous miscarriage, during abdo trauma or ECV
163
Most common cytogenic abnormality in myeloma
Hyperdiploid karyotype

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