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Haematology Flashcards

1
Q

What is the site of haematopoeisis?

A

Bone marrow

Liver

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2
Q

Stat the cells of lymphoid lineage.

A

B cell

T cell

NK Cell

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3
Q

Which cells are derived from the myeloid lineage?

A

Megakaryocyte -> Platelets

Erythrocyte -> RBC

Myeloblast -> Basophil; Neutrophil; Eosinophil; Macrophage

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4
Q

Which blood cells are derived from myeloblasts?

A 
Eosinophils
Basophils
Neutrophils 
Mast cells 
Macrophages
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5
Q

Where do B lymphocytes mature?

A

Bone marrow

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6
Q

Where do T lymphocytes mature?

A

Thymus gland

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7
Q

Anisocytosis is a finding in?

A

Variation in size of RBCs is shown in myelodysplasic syndrome and some forms of anaemia

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8
Q

Target cells are seen in?

A

Central area of pigmentation with pale area and ring of thicker cytoplasm

Seen in iron-deficiency anaemia and post-splenectomy

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9
Q

Howell-Jolly bodies are seen in?

A

Post-splenectomy and severe anaemia (regenerating RBCs quickly)

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10
Q

A high amount of reticulocytes are seen in?

A

Haemolytic anaemia or a condition in which there is a high turnover of RBCs

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11
Q

Schistocytes may appear in?

A

Any condition in which they are being damaged by trauma when travelling through the blood vessels

HUS 
DIC
TTP
Metallic heart valves 
Haemolytic anaemia
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12
Q

In which condition are sideroblasts seen in?

A

Immature RBCs containing iron blobs

Occur when BM unable to incorporate iron into Hb molecules thus indicate a myelodysplastic syndrome

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13
Q

In which condition are smudge cells seen in?

A

Chronic lymphocytic leukaemia

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14
Q

Spherocytes are seen in which condition?

A

Autoimmune haemolytic anaemia

Hereditary spherocytosis

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15
Q

What are the criteria for Anaemia?

State this for M, F and pregnant women.

A

M < 130g/L

F < 120g/L

Pregnant < 110g/L

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16
Q

What are the clinical features of anaemia?

A 
Dyspnoea
Fatigue
Headache
Dizziness
Syncope
Confusion
Palpitations
Angina

Bounding pulse
Postural hypotension
Tachycardia
Conjunctival pallor
Shock
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17
Q

How may anaemia be classified?

A

Morphology:

  • Microcytic
  • Normocytic
  • Macrocytic

Aetiology:

  • Reduced RBC production
  • Increased RBC destruction
  • Blood loss
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18
Q

What are the causes of microcytic anaemia? Give 5 examples.

What is the criteria for a microcytic anaemia?

A 
Iron-deficiency anaemia 
Thalassaemia
Sickle cell disease
Sideroblastic anaemia 
Lead poisoning

<82fL

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19
Q

What are the causes of normocytic anaemia? Give 3 examples.

What is the criteria for a normocytic anaemia?

A

Variable stages of either microcytic or macrocytic anaemia

Anaemia of chronic disease
Blood loss
Renal disease
Pregnancy

82-99fL

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20
Q

What are the causes of macrocytic anaemia? Give 3 examples.

What is the criteria for a macrocytic anaemia?

A 
B12 deficiency
Folate deficiency 
Alcoholism 
Liver disease 
Hypothyroidism
Haematological malignancy 
Reticulocytosis
Drugs - Azathioprine
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21
Q

What are the two categories of Haemolytic Anaemia?

Give 3 examples of each.

A

Inherited vs Acquired

Inherited: 
Hereditary Spherocytosis
Hereditary Elliptocytosis
Thalassaemia
Sickle Cell Anaemia
G6PD Deficiency
Acquired: 
Autoimmune haemolytic anaemia
Alloimmune haemolytic anaemia (transfusions reactions and haemolytic disease of newborn)
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Prosthetic valve related haemolysis
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22
Q

What 3 components of a RBC may be affected in inherited haemolytic anaemia?

A

Tip: 3 components of RBC are membrane, Hb and metabolic machinery. Thus, defect to any of these may cause an inherited haemolytic anaemia.

Membrane: Hereditary spherocytosis

Hb-opathies: Sickle cell anaemia; alpha and ß-thalassaemia

Internal machinery: G6PD deficiency

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23
Q

What is the mechanism of immune-mediated destruction causing haemolytic anaemia?

A

Abs against RBC membrane thus fixing of complement and phagocytosis by macrophages - e.g. AIHA

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24
Q

What is the mechanism of non-immune mediated destruction causing haemolytic anaemia?

A

Various mechanisms related to cause.

Prosthetic heart valve
Microangiopathic haemolytic anaemia 
Infection
Hypersplenism
Drugs
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25
What clinical features would a patient with haemolytic anaemia display on top of the usual anaemia features?
Jaundice Abdominal pain Dark urine Neurological signs Splenomegaly
26
How is Haptoglobin changed in Haemolytic anaemia?
Haptoglobin binds Hb then the Haptoglobin-Hb complex is removed by the liver thus decreasing the Haptoglobin level
27
A 10 year old patient presents with a normocytic anaemia and some jaundice. It has been going on for a few months now. What investigations will you conduct?
``` Commence a haemolytic screen: FBC LFTs LDH Blood film Haptoglobin ``` Potentially: DAT; Hb electrophoresis and sickle cell screening
28
How is Hereditary Spherocytosis inherited?
Autosomal dominant
29
What is the management for a patient with hereditary spherocytosis?
Supportive or Surgery: Splenectomy
30
How is Glucose-6-phosphate dehydrogenase deficiency inherited?
X-linked
31
What is the pathophysiology of G6PD deficiency?
Glucose 6 phosphate dehydrogenase aids generation of NADPH which is a reducing agent to scavenge oxidative metabolites which can damage RBCs
32
What is the management of G6PD deficiency?
Supportive: Haematology referral; avoid Fava, avoid Henna and numerous drugs
33
How is Sickle Cell inherited?
Autosomal recessive
34
What are the two types of AIHA? Give examples of each.
1) Warm (>37) whereby Abs react against RBCs at higher temperature leading to agglutination. ``` Idiopathic Infection Chronic inflammation/Inflammatory disorders Malignancy HIV EBV Malignancy e.g. CLL; NHL ``` 2) Cold (<32) whereby Abs react against RBCs at lower temperature leading to agglutination. Idiopathic M pneumoniae EBV Haematological malignancies e.g. Lymphoma
35
Infection of a patient with hereditary spherocytosis with parvovirus can cause?
Aplastic crisis
36
The presence of Heinz bodies on blood film is indicative of which condition?
G6PD deficiency
37
Give 3 medications which can precipitate G6PD deficiency.
Ciprofloxacin Sulfonylureas Sulfasalazine Primaquine (anti-malarial)
38
Give the two causes of Alloimmune Haemolytic Anaemia.
1) In hemolytic transfusion reactions red blood cells are transfused into the patient. The immune system produces antibodies against antigens on those foreign red blood cells. This creates an immune response that leads to the destruction of those red blood cells. 2) In haemolytic disease of the newborn there are antibodies that cross the placenta from the mother to the fetus. These maternal antibodies target antigens on the red blood cells of the fetus. This causes destruction of the red blood cells in the fetus and neonate.
39
A patient presents with red urine in the morning. They have anaemia and have had several episodes of DVT. Additionally, they experience oesophageal spasms, and have done for years. What is your diagnosis? What is the cause of this? What is the management?
Paroxysmal Nocturnal Haemoglobinuria Mutation in HPSCs in BM result in loss of surface RBCs which inhibit the complement cascade which results in activation of the complement cascade Eculizumab (C5 mAb) or Surgery: BM Transplantation
40
What is the cause of Pernicious anaemia?
Autoimmune condition whereby Antibodies form against parietal cells or IF thus reduced B12 absorption in the terminal ileum
41
What are the clinical feature of B12 deficiency?
Anaemia S+Sx Neurological symptoms... Peripheral neuropathy with numbness or paraesthesia (pins and needles) Loss of vibration sense or proprioception Visual changes Mood or cognitive changes
42
What is the management for Pernicious anaemia?
Medical: Cyanocobalamin PO or Medical: Hydroxycobalamin IM Inject 3 times weekly for 2 weeks then every 3 months
43
Why should you treat B12 deficiency before folate deficiency?
Treating patients with folic acid when they have a B12 deficiency can lead to subacute combined degeneration of the cord
44
What are the causes of microcytic anaemia?
``` Iron-deficiency Anaemia of chronic disease (normally normocytic) Alpha thalassaemia Beta thalassaemia Hereditary spherocytosis Sideroblastic anaemia Lead poisoning ```
45
What is the total Iron content of the body?
3-4g
46
What are the causes of iron-deficiency anaemia?
Increased requirements: Pregnancy Increased iron loss: GI bleeding; Menorrhagia Reduced uptake: Malabsorption; Poor diet
47
What investigations would you conduct in a patient with suspected anaemia?
``` FBC TFTs LFTs Blood film Iron Ferritin Transferrin levels ```
48
How do you manage iron-deficiency anaemia?
Supportive: Identify and Tx cause + Medical: Ferrous fumarate PO
49
What is the pathophysiology of anaemia of chronic disease?
Chronic disease has chronic inflammation (increased by IL-6) thus increased hepcidin resulting in reduced iron absorption Reduced RBC survival Reduced EPO Reduced erythropoiesis
50
How is anaemia of chronic disease treated?
Identify cause and Tx cause
51
Which populations is ß-thalassaemia most prevalent in?
Mediterranean African SE Asian
52
What are the clinical features of ß-thalassaemia?
Present within first year of life when HbF changes to normal Hb (includes Beta chains) Extramedullary haematopoeisis: Hepatomegaly Splenomegaly Skeletal abnormalities ``` Iron overload: Growth failure DM Hypothyroidism Hypogonadism ```
53
What is the gold standard investigation for ß-thalassaemia?
Hb electrophoresis
54
How is ß-thalassaemia managed?
Blood transfusions ± Surgery: - Splenectomy - HSCS transplant
55
What is the inheritance of Sideroblastic anaemia?
X-linked or acquired
56
Beta globin gene is present on which chromosome?
11
57
Alpha globin gene is present on which chromosome?
Chromosome 16
58
What are the four potential types of alpha thalassaemia? Give the genotypes.
Chromosome 16 contains two genes for alpha Hb. aa/a- = alpha thalassaemia minima a-/a- or aa/-- = alpha thalassaemia trait a-/-- = HbH disease with tetramers of beta globin chains causing moderate to severe haemolytic anaemia --/-- = Hb Barts syndrome, foetal death
59
What is the most severe form of alpha thalassaemia? How many copies of HbAlpha gene are inherited? How many are functional? What occurs?
Hb Barts Syndrome Inherit 4 copies, 0 are functional Foetal death as four gamma goblin chains which cannot carry oxygen due to having a higher oxygen affinity than tissues thus does not deliver oxygen. Causes extramedullary erythropoiesis leading to severe anaemia, cardiac failure, oedema --> Hydrops foetalis
60
What are the clinical features of HbH syndrome?
Highly variable Pallor Anaemia Jaundice (unconjugated due to chronic haemolytic anaemia) Gallstone disease (chronic haemolysis) Extramedullary haematopoiesis: hepatosplenomegaly, skeletal changes Osteopenia/osteoporosis Aplastic/hypoplastic crisis: sudden reduction in red blood cell counts Leg ulcers
61
What is the diagnostic testing for alpha thalassaemia?
Hb analysis by HPLC or electrophoresis Genetic testing
62
How is HbH disease managed?
Medical: Folic acid; Transfusions ( if <70g/L); Desferrioxamine (if iron overloaded) ± Surgery: Splenectomy
63
The beta globin gene cluster is present on which chromosome?
11
64
What are the types of beta thalassaemia?
Beta thalassaemia trait (b+/b OR b0/b) = one abnormal gene, either reduced production or no production - asymptomatic with mild anaemia Beta thalassaemia intermedia (b+/b+) = two abnormal beta globin genes but both reduced Beta thalassaemia major (b+/b0 or b0/b0) = two abnormal genes with one being no production - require transfusions
65
What are the clinical features of beta thalassaemia?
Anaemia S + Sx ``` Jaundice Gallstones Hypogonadism Growth restriction Cardiac arrhythmia Endocrine disorders Extramedullary haematopoeisis - facial deformity; ``` Short limbs OP Bony pain Pulmonary hypertension Clotting disorders Leg ulcers
66
What test is used to diagnose beta thalassaemia?
Hb electrophoresis or HLPC Genetic testing
67
How is beta thalassaemia managed?
Supportive: Blood transfusions (2-3 wees) + Medical: Desferrioxamine (if iron overloaded) ± Surgery: Splenectomy (if symptomatic splenomegaly)
68
How is sickle cell anaemia inherited?
Autosomal recessive
69
What disease does Sickle Cell disease confer an advantage against and why is this?
Protective against malaria as more likely to survive and pass on genes - thus selective advantage to having sickle cell anaemia in areas endemic of malaria
70
A genotype of HbSS suggests? A. Sickle cell anaemia B. Sickle cell disease C. Sickle cell trait D. Sickle-thalassaemia
A
71
A genotype of HbSC suggests? A. Sickle cell anaemia B. Sickle cell disease C. Sickle cell trait D. Sickle-thalassaemia
B
72
A genotype of HbS suggests? A. Sickle cell anaemia B. Sickle cell disease C. Sickle cell trait D. Sickle-thalassaemia
C
73
A genotype of HbSß0 suggests? A. Sickle cell anaemia B. Sickle cell disease C. Sickle cell trait D. Sickle-thalassaemia
D
74
What type of mutation causes Sickle haemoglobin? A. Point mutation causing glutamic acid to be converted to valine B. Point mutation causing valine to be converted to glutamic acid C. Deletion mutation D. Point mutation causing glutamic acid to be converted to lysine
A
75
What is the pathophysiology of Sickle Cell anaemia?
Sickle Hb polymerises at low oxygen tension thus forms sickle shaped cells which undergo chronic haemolysis and vaso-occlusion of BVs
76
What can increase the risk of a Sickle Cell crisis?
Anything which causes low oxygen levels, replicating low oxygen tension Dehydration Infection Cold exposure Acidosis
77
What may vaso-occlusion as a result of sickle cell crisis cause?
``` Acute painful episodes (i.e. painful crisis) Acute chest syndrome (i.e. chest crisis) Renal infarction Bone infarction or dactylitis (inflammation of a digit) Myocardial infarction Stroke Venous thromboembolism Priapism (persistent, painful erection) ```
78
Give 3 examples which may cause an acute drop in Hb in Sickle Cell Disease.
Splenic sequestration Hyperhaemolysis Aplastic crisis
79
Vaso-occlusive phenomena can lead to which two broad umbrella conditions?
Painful episodes Acute chest syndrome
80
How is Sickle Cell Disease diagnosed?
Hb electrophoresis
81
How do you manage sickle cell anaemia?
Supportive: Fluids; Analgesia; Oxygen; Blood transfusions; Pneumococcal vaccine (every 5 years) + Medical: Hydroxyurea (increases HbF levels) --> >3 painful episodes; Acute chest syndrome requiring transfusion ± Infection Medical: ABX ± Neuro complications Intervention: Exchange transfusion
82
What is the indication for Hydroxyurea in Sickle Cell Disease?
≥3 painful episodes requiring hospital or Acute chest syndrome requiring transfusion
83
How is G6PD deficiency inherited?
X-linked
84
What genetic process means females may display G6PD deficiency?
Lyonisation
85
State 3 precipitants of G6PD deficiency.
Medications: ABX; Antimalarials; Dapsone; Methylene blue; Sulfonylureas; Rasburicase Fava beans Infection
86
What investigation allows diagnosis of G6PD deficiency?
Genotype Assessment of G6PD enzyme activity
87
What is the management of G6PD deficiency?
Avoid precipitants of oxidative injury
88
What type of surgery may precipitate B12 deficiency?
Gastrectomy - parietal cells produce IF Ileal resection - absorbed in terminal ileum
89
What are the clinical features of B12 anaemia?
Normal anaemia S + Sx Neuropsychiatric complications... Peripheral neuropathy Subacute degeneration of the cord Focal demyelination Depression Personality change Memory loss
90
What is the management of B12 deficiency?
Cobalamin PO or Hydroxycobalamin IM
91
What are the clinical features of subacute degeneration of the cord?
B12 deficiency with lateral and posterior columns of spinal cord degenerated AND Numbness Weakness Paraesthesia: loss of vibrational sense; loss of proprioception and ataxia Ataxia Sensory deficit Autonomic dysfunction Loss of vibration and proprioception Hyperreflexia Positive Babinski Sign
92
What is the management of Folate deficiency?
Folic acid PO 5mg for 4/12
93
Give a medication which may cause non-megaloblastic anaemia.
Azathioprine Cyclophosphamide Hydroxyurea
94
How is VWD inherited?
Autosomal dominant
95
How is diagnosis of VWD achieved?
Clinical diagnosis
96
How do you manage VWD?
Desmopressin / VWF + Factor VIII (infuse with VWF) Women (menorrhagia) - TXA - Mefanemic acid - COCP - Coil
97
What is the cause of Haemophilia A?
Mutation of Factor 8
98
What is the cause of Haemophilia B?
Mutation of factor 9
99
How are the Haemophilias inherited?
X-linked recessive
100
What are the clinical features of Haemophilia?
Spontaneous haemorrhages Haematomas Recurrent bleeding Haemarthrosis
101
How is Haemophilia diagnosed?
Bleeding scores Coag factor assays Genetic testing
102
How is Haemophilia managed?
IV infusion factor 8/9 Acute: Desmopressin + Infusion of factors + TXA
103
What age does ALL tend to occur?
0-4 years old
104
Which of the following is the most common gene mutation seen in ALL affecting children? A. t(9;22) B. t(12;21) C. t(4;11) D. Hyperdiploid karyotype
B
105
What are the clinical features of ALL?
Anaemia Neutropenia Thrombocytopenia Tissue infiltration - lymphadenopathy; hepatosplenomegaly; bone pain; mediastinal mass; testicular enlargement Leucostasis (∆ mental state; headache; SOB; visual changes)
106
What is the diagnostic test for ALL?
BM aspirate and biopsy
107
A blood film showing blast cells is suggestive of what cancer?
ALL
108
How is ALL managed?
Specialist referral + MDT decision + Chemotherapy (induction and maintenance therapy)
109
What are the complications of ALL?
Tumour Lysis Syndrome Neutropenic Sepsis SVCO Chemotherapy side effects
110
What is the precursor to CLL?
Monoclonal B cell lymphocytosis
111
What are the clinical features of CLL?
``` Weight loss Night sweats Fevers Lethargy Anorexia ``` **Lymphadenopathy** Hepatomegaly Splenomegaly
112
What is the main difference between CLL and MBL?
Both have raised B lymphocyte count however MBL is asymptomatic
113
How is CLL diagnosed?
Flow cytometry
114
Smudge cells are a feature of which haematological condition?
CLL due to so much production but weaker due to vimentin quality/quantity
115
How may you stage CLL?
Binet Staging - number of lymphoid sites affected Stage A = <3 sites Stage B = >3 sites Stage C = presence of anaemia and/or thrombocytopenia
116
How is CLL managed?
Supportive: Watch and wait (3 month assessment); vaccination; ABX for infection; IvIG (if hypogammaglobulinaemia) ± BM failure; Splenomegaly; Symptomatic; Autoimmune complications - Chemotherapy 2nd line Surgery: AlloSCT
117
The formation of an aggressive lymphoma from a CLL is called?
Richter Transformation
118
What are the RFs for AML?
``` MDS Congenital disorders e.g. Downs Syndrome Radiation exposure Previous chemotherapy Toxins (organochlorine insecticides; benzene) ```
119
What age is AML most prevalent in?
70s
120
The presence of Auer rods are suggestive of what condition?
AML Myelodysplastic syndrome
121
What is the gold-standard for diagnosis of AML?
BM aspirate
122
What is the management of AML?
Supportive: referral; education; support + Chemotherapy ± Surgery: AlloHSC transplant
123
What cytogenic finding is most related to CML?
t(9;22) - Philadelphia chromosome
124
What are the phases of CML?
1) Chronic phase: non-specific symptoms of fatigue, weight loss and night sweats 2) Accelerated phase: blasts in the bone marrow; basophils in blood; persistent thrombocytopenia 3) Blast crisis: Resembles an acute leukaemia with rapid expansion of blasts (>30%) and extramedullary blast proliferation
125
How is CML managed?
``` Supportive: patient education; support + TKIs: Imatinib/Dasatinib + Chemotherapy ``` ± Surgery: AlloSCT (in chronic phase if other Tx fail)
126
Give 5 causes of Polycythaemia Vera
Primary polycythaemia Secondary polycythaemia - Smoking - CLD - Obesity - OSA ``` RCC Wilms' Tumour Adrenal tumours Illicit EPO use Androgen use Uterine fibroids ```
127
What gene mutation causes Polycythaemia Vera?
JAK2 gene
128
What are the clinical features of Polycythaemia Vera?
``` Headache Visual disturbance Tinnitus Itching (especially in a warm bath) Fatigue Vertigo Paresthesia ``` ``` Plethora Bruising Excoriation Conjunctival injection Splenomegaly Erythromelalgia ```
129
How may Masked Polycythaemia Vera occur?
Iron-deficiency anaemia with the background of Primary Polycythaemia Vera
130
How is Polycythaemia Vera managed?
Venesection: 200-500mL per time --> aim for Hct <0.45 + Low-dose aspirin: 75mg PO OD ± High-Risk (>65 years or thrombotic events) Medical: Hydroxycarbamide
131
A triad of hepatomegaly + abdominal pain + ascites is part of?
Budd-Chiari Syndrome
132
How does an IVC filter work?
Inferior vena cava filters are devices inserted into the inferior vena cava, designed to filter the blood and catch any blood clots travelling from the venous system, towards the heart and lungs. They act as a sieve, allowing blood to flow through whilst stopping larger blood clots. They are used in unusual cases of patients with recurrent PEs or those that are unsuitable for anticoagulation.
133
Which cells are seen in Hodgkin Lymphoma?
Reed-Sternberg cells - multinucleate cells
134
What is associated with Hodgkin Lymphoma?
EBV Smoking HIV Immunosuppression
135
What are the clinical features of Hodgkin's Lymphoma?
lymphadenopathy (75%) - painless, non-tender, asymmetrical systemic (25%): weight loss, pruritus, night sweats, fever (Pel-Ebstein) alcohol pain in HL normocytic anaemia, eosinophilia LDH raised
136
What are the types of Hodgkin's Lymphoma?
Nodular sclerosing: F; lacunar cells; 70% Mixed cellularity: large number of Reed-Sternberg cells Lymphocyte predominant = best diagnosis Lymphocyte depleted = worst prognosis
137
How is Hodgkin's Lymphoma staged?
Ann-Arbor staging 1 = single lymph node 2 = >2 LN on same side of diaphragm 3 = nodes both sides of diaphragm 4 = spread beyond lymph nodes A = pruritus B = other B symptoms
138
How is Hodgkin's Lymphoma diagnosed?
Lymph node biopsy (FNA/Core Biopsy)
139
How is Hodgkin's Lymphoma managed?
Mnemonic: ABVD Chemotherapy: Doxorubicin + Bleomycin + Vinblastine + Dacarbazine
140
What is the MOA of Doxorubicin?
Anthracycline inhibiting topoisomerase II resulting in DNA inhibition and RNA synthesis
141
What are the side effects of Doxorubicin?
Cardiomyopathy Myelosuppression Skin reactions
142
What is the MOA of Bleomycin?
Inhibits DNA synthesis
143
What are the side effects of Bleomycin?
Pulmonary fibrosis Severe idiosyncratic reaction (hypotension, confusion, fever, wheeze)
144
What is the MOA of Vinblastine?
Inhibit microtubule formation by binding tubulin
145
What are the side effects of vinblastine?
Peripheral neuropathy Bladder atony
146
What is the MOA of Dacarbazine?
Converted to MTIC which acts on guanine, causing methylation
147
What is the side effects of Dacarbazine?
Bone marrow suppression Hepatic necrosis
148
Which of the following is a side effect of doxorubicin? A. Cardiomyopathy B. Pulmonary fibrosis C. Peripheral neuropathy D. Hepatic necrosis
A
149
Which of the following is a side effect of Bleomycin? A. Cardiomyopathy B. Pulmonary fibrosis C. Peripheral neuropathy D. Hepatic necrosis
B
150
Which of the following is a side effect of Dacarbazine? A. Cardiomyopathy B. Pulmonary fibrosis C. Peripheral neuropathy D. Hepatic necrosis
D
151
Which of the following is a side effect of Vinblastine? A. Cardiomyopathy B. Pulmonary fibrosis C. Peripheral neuropathy D. Hepatic necrosis
C
152
Why should patients with Hodgkin's Lymphoma receive irradiated blood?
reduce the risk of transfusion-associated graft-versus-host disease
153
What are the RFs for Non-Hodgkin's Lymphoma?
Elderly Caucasians History of viral infection (specifically Epstein-Barr virus) Family history Certain chemical agents (pesticides, solvents) History of chemotherapy or radiotherapy Immunodeficiency (transplant, HIV, diabetes mellitus) Autoimmune disease (SLE, Sjogren's, coeliac disease)
154
How is Non-Hodgkin's lymphoma staged?
Ann-Arbor staging 1 = single lymph node 2 = >2 LN on same side of diaphragm 3 = nodes both sides of diaphragm 4 = spread beyond lymph nodes A = pruritus B = other B symptoms
155
How is Non-Hodgkin's Lymphoma managed?
Mnemonic: R-CHOP ``` Rituximab (mAb to CD20) + Cyclophosphamide + Doxorubicin + Vincristine + Prednisolone ```
156
What is the MOA of Rituximab?
mAb against CD20
157
What are the side effects of Rituximab?
Infusion reaction Hepatitis B reactivation Progressive Multifocal Leucoencephalopathy
158
What is the MOA of Cyclophosphamide?
Inhibits cross-linking of DNA thus stops DNA synthesis
159
What are the side effects of Cyclophosphamide?
Nephrotoxic/Bladder toxic
160
What are the side effects of Methotrexate?
Nephrotoxic Myelosuppression Idiopathic Pulmonary Fibrosis
161
What is the side effects of Asparagine?
Neurotoxicity Pancreatitis
162
What are the side effects of Cisplatin?
Ototoxic Nephrotoxic
163
What are the side effects of Vincristine?
Peripheral neuropathy
164
What are the side effects of Bleomycin?
Pulmonary fibrosis
165
What are the complications of Non-Hodgkin's Lymphoma?
``` Bone marrow infiltration SVCO Spinal Cord Compression Metastasis Complications from treatment ```
166
In Primary myelofibrosis, what is the proliferating cell line?
HSCs
167
In Polycythaemia Vera, what is the proliferating cell line?
Erythrocytes
168
In essential Thrombocythaemia what is the proliferating cell line?
Megakaryocytes
169
Which form of cancer may Myeloproliferative Disorders become?
AML
170
What is myelofibrosis?
Myelofibrosis is where the proliferation of the cell line leads to fibrosis of the bone marrow. The bone marrow is replaced by scar tissue. This is in response to cytokines that are released from the proliferating cells. One particular cytokine is fibroblast growth factor. This fibrosis affects the production of blood cells and can lead to anaemia and low white blood cells (leukopenia). The scar tissue inhibits haematopoeisis in the marrow thus extramedullary haematopoiesis leads to HSM which can cause portal hypertension or SCC
171
Tear-drop shaped RBCs are seen in which blood disorder?
Myeloproliferative disorders
172
What is the gold-standard diagnosis for myeloproliferative disorders?
Bone marrow biopsy
173
How is Primary Myelofibrosis managed?
Supportive: treat anaemia; splenomegaly; portal hypertension ± Surgery: AlloHST tranplant ± Chemotherapy
174
How is Polycytheamia Vera managed?
Supportive: Aspirin + Venesection ± Chemotherapy
175
How is Essential Thrombocythaemia managed?
Medical: Aspirin + Chemotherapy
176
What is myelodysplastic syndrome?
myeloid bone marrow cells not maturing properly and therefore not producing healthy blood cells. There are a number of specific types of myelodysplastic syndrome.
177
What are the clinical features of myelodysplastic syndrome?
Anaemia Neutropenia Thrombocytopenia
178
How is Myelodysplastic Syndrome managed?
Bone marrow aspiration and biopsy
179
How is Myelodysplastic Syndrome managed?
``` Supportive: Watchful waiting; Transfusion ± Chemotherapy ± Surgery: HSC transplant ```
180
What is multiple myeloma?
haematological malignancy characterised by plasma cell proliferation
181
What are the clinical features of Multiple Myeloma?
Mnemonic: CRABBI Calcium (hypercalcaemia): bones, groans, psychiatric moans, stones Renal (monoclonal production of Ig): dehydration, thirst, amyloidosis, nephrocalcinosis, nephrolithiasis Anaemia (BM crowding): fatigue and pallor Bleeding (thrombocytopenia): bruising and bleeding Bones (BM infiltration): fragility fractures Infection (reduced normal number of immunoglobulins): Recurrent infections
182
Bence Jones Protein is present in which haematological condition?
Present in Multiple Myeloma
183
What is the management of Multiple Myeloma?
Induction therapy: Bortezomib + Dexamethasone + Surgery: HSC Transplant
184
What are the complications of multiple myeloma?
``` Pain Pathological fractures Infection VTE prophylaxis Fatigue ```
185
What conditions are associated with pernicious anaemia?
Hypothyroidism Vitiligo Addisons Atrophic gastritis
186
What are the indications for Hydroxyurea in the management of a vaso-occlusive crises in Sickle Cell Anaemia?
3 or more admissions Cx syndrome Previous stroke
187
What are the components of a haemolytic screen?
Reticulocytes LDH Haptoglobulin Direct anti-globulin test
188
What are the clinical features of a thrombotic crisis in Sickle Cell Disease?
'Painful crisis' as it is painful thus thrombosis occludes the vessel Can be caused by: infection, dehydration, deoxygenation Clinical DDx
189
What are the clinical features of a sequestration crisis?
Sickling within the organs worsening the anaemia Increased reticulocyte count
190
What are the clinical features of acute chest syndrome in Sickle Cell Disease?
Vaso-occlusion in the pulmonary microvasculature resulting in infarction of the lung parenchyma Cx pain SOB CXR: pulmonary infiltrates
191
What is an aplastic crises in Sickle Cell Disease?
Parvovirus infection resulting in aplastic anaemia - Hb drop ± thrombocytopenia ± neutropenia Reduced reticulocyte count
192
What is the clinical features of a haemolytic crises in Sickle Cell Anaemia?
Features of jaundice Increased rate of haemolysis Schistocytes seen on blood film

Medicine (18 decks)

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