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(SG) condensed phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

Define iron-deficiency anaemia

A

Lack of iron.

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2
Q

Define pernicious anaemia ‘B12 deficiency’

A

Not enough RBC due to a lack of B12.

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3
Q

Define folate-deficiency

A

Lack of folate.

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4
Q

Define haemolytic anaemia

A

Due to increased destruction of red blood cells.

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5
Q

How does iron-deficiency anaemia clinically present?

A

Anaemia: Fatigue, lethargy, dyspnoea, faintness, palpitations, headache.

Iron deficiency: brittle hair and nails, atrophic glossitis and angular stomatitis.

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6
Q

How does pernicious anaemia ‘B12 deficiency’ clinically present?

A

Anaemia: Fatigue, lethargy, dyspnoea, faintness, palpitations, headache.

B12 deficiency: neurological problems.

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7
Q

How does folate-deficiency clinically present?

A

Anaemia: Fatigue, lethargy, dyspnoea, faintness, palpitations, headache

Folate deficiency: Develops over 4 months of deficiency (due to bodily reserves).

Possibly depression.

Glossitis.

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8
Q

How does haemolytic anaemia clinically present?

A

Anaemia: Fatigue, lethargy, dyspnoea, faintness, palpitations, headache.

Haemolytic: Jaundice, gall stones, leg ulcers, signs of underlying cause.

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9
Q

Iron-deficiency anaemia - note

A

Microcytica.

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10
Q

Pernicious anaemia ‘B12 deficiency’ - note

A

Macrocytic,

megaloblastic.

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11
Q

Folate-deficiency - note

A

Macrocytic,

megaloblastic.

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12
Q

Haemolytic anaemia - note

A

Normocytic.

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13
Q

Pathophysiology of Iron-deficiency anaemia

A

Iron is necessary for the formation of haem.

Insufficient iron

  • > lack of effective rbc
  • > symptoms of anaemia.
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14
Q

Pathophysiology of Pernicious anaemia ‘B12 deficiency’

A

Absorption of B12 occurs in the terminal ileum and requires Intrinsic Factor (from gastric parietal cells) for transport across intestinal mucosa.

This IF is deficient in pernicious anaemia.

This causes megaloblastic anemia.

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15
Q

Pathophysiology of Folate-deficiency

A

Absorbed in the upper intestine.

Insufficient folate causes megaloblastic anaemia.

This is where erythrocytes are larger and have higher nuclear to cytoplasmic ratios to normal.

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16
Q

Pathophysiology of Haemolytic anaemia

A

RBCs are destroyed before their usual 120 day lifespan.

The bone marrow provides compensatory reticulocytes.

RBC destruction can be extra or intra vascular.

Mostly extravascular, where cells are removed from circulation by macrophages, particularly in the spleen.

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17
Q

Cause of Iron-deficiency anaemia

A

Blood loss (most common),

increased demands (growth and pregnancy),

decreased absorption (small bowel disease), poor intake.

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18
Q

Cause Pernicious anaemia ‘B12 deficiency’

A

Autoimmune destruction of parietal cells/IF.

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19
Q

Cause of Folate-deficiency

A

Main cause is poor intake, due to dietary deficiency.

Also possible is an excessive requirement, impaired uptake or antifolate drugs.

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20
Q

Cause of Haemolytic anaemia

A

Inherited: Red cell membrane defect (sphereocytosis),

Haemoglobin abnormalities, metabolic defects

Acquired: Autoimmune,

Mechnical destruction,

secondary to systemic disease (liver failure),

infections (malaria).

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21
Q

Epidemiology of Iron-deficiency anaemia

A

2-5% of men and post menopausal.

Premenopausal are at higher risk due to menses.

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22
Q

Epidemiology of Pernicious anaemia ‘B12 deficiency’

A

1/10,000 in N Europe.

Peak age of 60.

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23
Q

Epidemiology of Haemolytic anaemia

A

Depends on underlying cause.

Sickle cell mainly African peoples.

Autoimmune slightly more common in females.

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24
Q

Diagnostic tests for Iron-deficiency anaemia

A

FBC: hypochromic microcytic anaemia

Serum ferritin: low.

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25
Q

Diagnostic tests for Pernicious anaemia ‘B12 deficiency’

A

Blood film: Macrocytic rbc

Autoantibody: IF antibodies

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26
Q

Diagnostic tests for Folate-deficiency

A

Blood film: Macrocytic

Erythrocyte folate level: Indicated reduced body stores

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27
Q

Diagnostic tests for Haemolytic anaemia

A

Reduced haemoglobin, spherocytes, increased reticulocytosis, increased MCV

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28
Q

Treatment for Iron-deficiency anaemia

A

Iron salts oral.

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29
Q

Treatment for Pernicious anaemia ‘B12 deficiency’

A

(Vitamin B12) Hydroxocobalamin.

If neuro involvement; refer to haematologist.

Do NOT give folic acid instead of B12, this leads to fulminant neurological deficit.

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30
Q

Treatment for Folate-deficiency

A

Folic acid supplement.

Treat any underlying cause.

Advise regarding folate deficiency in pregnancy.

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31
Q

Treatment for Haemolytic anaemia

A

Folate and iron supplement,

immunosuppressive if autoimmune,

splenectomy if hereditary spherocytosis or other approaches fail.

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32
Q

Complications of Iron-deficiency anaemia

A

Side effects of iron salts: black stool,

constipation/diarrhoea,

nausea.

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33
Q

Complications of Pernicious anaemia ‘B12 deficiency’

A

Heart failure,

angina,

neuropathy.

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34
Q

Complications of Folate-deficiency

A

Folate required for foetus development.

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35
Q

Complications of Haemolytic anaemia

A

Cardiac failure.

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36
Q

Define Bone marrow failure ‘Aplastic’

A

Lack of haemopoiesis as a result of bone marrow failure.

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37
Q

Define Sickle cell anaemia

A

Hereditary deformation of RBC as a result of faulty haemoglobin molecule.

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38
Q

Define Thalassaemia

A

Defective subunit of the haemaglobin complex .

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39
Q

Define Glucose-6-phosphate dehydrogenase deficiency

A

Lack of enzyme that maintains protective protein against oxidant injury.

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40
Q

Types of Thalassaemia

A

Alpha and Beta (for which subunit affected).

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41
Q

How does Bone marrow failure ‘Aplastic’ clinically present?

A

Anaemia: Fatigue, lethargy, dyspnoea, faintness, palpitations, headache.

Bone marrow failure: Increased suspectability to infection and bleeding.

Bruising, bleeding gums and epistaxis.

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42
Q

How does Sickle cell anaemia clinically present?

A

Presents once Hb F has circulated out at about 6 months.

Vaso-occlusion: Early childhood acute pain in the hands and feet due to occlusion of the small vessels and avascular necrosis of the bone marrow.

In adults, this affects the long bones, ribs, spine and pelvis.

Variable frequency.

Avascular necrosis -> shortened bones in children.

Anaemia: Fatigue, lethargy, dyspnoea, faintness, palpitations, headache. (Often symptoms of anaemia do not appear, since Hb S release oxygen easily.

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43
Q

How does Thalassaemia clinically present?

A

Variable.

Alpha tends to present in utero, whilst beta in infancy.

Can be asymptomatic if heterozygote, or severe anaemia in homozygotes, with failure to thrive and bone deformities (due to hypertrophy of ineffective marrow).

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44
Q

How does Glucose-6-phosphate dehydrogenase deficiency clinically present?

A

Neonatal jaundice,

haemolytic anaemia,

and acute haemolysis (precipitated by fava beans).

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45
Q

Thalassaemia - note

A

Microcytic

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46
Q

Pathophysiology of Bone marrow failure ‘Aplastic’

A

Reduction in the number of pluripotential stem cells together with a fault in those remaining or a immune reaction against them, such that they are unable to repopulate.

This can occur in only one cell line, leading to isolated deficiencies.

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47
Q

Pathophysiology of Sickle cell anaemia

A

Changes in a sequence of a haemoglobin subunit causes faulty haemoglobin complex.

This distorts the shape of RBC into sickles when deoxygenated, which are easily destroyed and occlude vessels easily.

This process worsens with repeated oxygenation/deoxygenation

Heterozygotes have minor effect, but protect against malaria.

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48
Q

Pathophysiology of Thalassaemia

A

Defective versions of either alpha or beta subunits of haemoglobin

  • > imbalance of subunits available
  • > precipitation of globin chains within rbc (or precursor)
  • > cell damage,

death of precursor (ineffective haemolysis) and haemolysis.

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49
Q

Pathophysiology of Glucose-6-phosphate dehydrogenase deficiency

A

G6PD is an enzyme in the pentose monophosphate shunt, which maintains glutathione in the reduced state.

This protects against oxidant injury in the RBC.

Therefore lack of G6PD -> increased haemolysis.

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50
Q

Causes of Bone marrow failure ‘Aplastic’

A

Congenital, acquired (mostly),

cytotoxic drugs,

infections etc

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51
Q

Cause of Sickle cell anaemia

A

Autosomal recessive condition affecting haemoglobin B subunits.

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52
Q

Cause of Thalassaemia

A

Genetic.

Homozygotes have severe anaemia,

heterozygotes can vary.

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53
Q

Cause of Glucose-6-phosphate dehydrogenase deficiency

A

X linked recessive

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54
Q

Epidemiology of Bone marrow failure ‘Aplastic’

A

2/1,000,000.

More common in Asia.

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55
Q

Epidemiology of Sickle cell anaemia

A

More common in African populations;

sickle cell trait protects against malaria.

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56
Q

Epidemiology of Thalassaemia

A

1% carriers of beta

and 5% carriers of alpha.

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57
Q

Epidemiology of Glucose-6-phosphate dehydrogenase deficiency

A

Most common metabolic RBC disorder.

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58
Q

Diagnostic test for Bone marrow failure ‘Aplastic’

A

FBC: Pancytopenia with low reticulocytes.

Bone marrow biopsy: hypocellular marrow with increased fat spaces.

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59
Q

Diagnostic test for Sickle cell anaemia

A

Identified in neonatal screening.

Otherwise, blood film: sickled cells.

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60
Q

Diagnostic test for Thalassaemia

A

Either genetic testing

or haemoglobin electrophoresis (after identifying microcytosis).

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61
Q

Diagnostic test for Glucose-6-phosphate dehydrogenase deficiency

A

Direct measurements of enzymes in RBC.

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62
Q

Treatments for Bone marrow failure ‘Aplastic’

A

Removal of causative agent.

Cautious blood and platelet transfusion.

If not spontaneous recovery: BMT or immunosuppressive therapy.

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63
Q

Treatment for Sickle cell anaemia

A

Folic acid.

Pain relief.

BMT in severe disease.

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64
Q

Treatments for Thalassaemia

A

Homozygotes: Blood transfusions to try and avoid complications.

Iron chelating agent for iron overload (desferrioxamine).

Ascorbic acid increases iron excretion in urine, helps offset iron overload.

More severe: BMT

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65
Q

Treatment for Glucose-6-phosphate dehydrogenase deficiency

A

Avoid fava beans.

Transfusion if necessary.

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66
Q

Complications of Bone marrow failure ‘Aplastic’

A

Increased infection and bleeding.

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67
Q

Complications of Sickle cell anaemia

A

Chronic pain.

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68
Q

Complications of Thalassaemia

A

Iron overload,

endocrine dysfunction.

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69
Q

Define Polycythaemia rubra vera

A

Genetic condition

-> proportion of blood volume occupied by RBC increases

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70
Q

Define Deep vein thrombosis

A

Thrombus formed in a deep vein.

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71
Q

How does Polycythaemia rubra vera clinically present?

A

Can be asymptomatic.

Pruritus, particularly after exposure to warm water.

Headaches, dizziness and sweating.

Thrombotic complications: MI, stroke, DVT.

Rare but classic: Erythromelalgia (a sudden, severe burning pain in the hands or feet, with red/blue coloration of the skin).

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72
Q

How does Deep vein thrombosis clinically present?

A

Often progresses to pulmonary embolism before presenting.

Classical features: Limb pain and tenderness along the lines of the deep veins,

swelling of the calf,

increase in skin temperature,

pitting oedema.

Resembles cellulitis.

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73
Q

Polycythaemia rubra vera - note

A

Polycythaemia is also used to refer to the state of increased volume of blood composed of RBC.

74
Q

Pathophysiology of Polycythaemia rubra vera

A

Neoplastic proliferation and maturation of erythroid,

megakaryocytic and granulocytic elements.

75
Q

Pathophysiology of Deep vein thrombosis

A

Formation of the thrombus in the deep vein.

This can embolise and often flows up into the pulmonary circulation as a pulmonary embolism.

76
Q

Cause of Polycythaemia rubra vera

A

Somatic mutation in a single haematopoietic stem cell

77
Q

Cause of Deep vein thrombosis

A

Thrombotic RF: obesity,

FH,

male,

smoking,

age,

cancer.

78
Q

Epidemiology of Polycythaemia rubra vera

A

2/100,000 each year

79
Q

Epidemiology of Deep vein thrombosis

A

1/1000 per year

80
Q

Diagnostic test for Polycythaemia rubra vera

A

Haematocrit: high.

JAK2 testing: can be negative (JAK2 negative prv).

81
Q

Diagnostic test for Deep vein thrombosis

A

Ultrasound,

D-dimers,

contrast venography.

82
Q

Treatment for Polycythaemia rubra vera

A

Seek to prevent thrombosis (low dose aspirin).

Intermittent long term phlebotomy.

Possibly myelosuppression.

83
Q

Treatment for Deep vein thrombosis

A

Low molecular weight heparin,

other anticoagulation therapy possible.

84
Q

Complications of Polycythaemia rubra vera

A

Can transform into acute myeloid leukaemia.

Thrombotic events.

85
Q

Complications of Deep vein thrombosis

A

Pulmonary embolism quite likely.

86
Q

Define Over-anticoagulation

A

Excess use of anticoagulation therapy.

87
Q

Define Disseminated intravascular coagulation

A

Coagulation systems (thrombin) activated inappropriately.

88
Q

Define Platelet disorders

A

Disorder affecting the function of the platelets.

89
Q

How does Over-anticoagulation clinically present?

A

Bleeding.

90
Q

How does Disseminated intravascular coagulation clinically present?

A

Underlying condition.

Bleeding from unrelated sites (ENT, GI, resp, site of venepuncture).

Confusion,

fever.

Skin: Purpura, petechiae, localised infarction.

91
Q

Types of platelet disorders

A

Immune thrombocytopenic purpura.

Thrombotic thrombocytopenic purpura.

92
Q

How does Immune thrombocytopenic purpura (platelet disorder) clinically present?

A

Rapid onset of purpura (usually self limiting in children).

Easy bruising,

epistaxis and

menorrhagia.

Major haemorrhage is rare.

93
Q

How does Thrombotic thrombocytopenic purpura (platelet disorder) clinically present?

A

Florid purpura,

fever,

fluctuating cerebral dysfunction

and haemolytic anaemia.

Often renal failure.

94
Q

Immune thrombocytopenic purpura (platelet disorder) - note

A

Immune destruction of platelet cells.

95
Q

Pathophysiology of Over-anticoagulation

A

Anticoagulation causes the blood to inappropriately avoid clotting

-> Bleeding.

(Warfarin knocks out factors II, VII, IX and X).

96
Q

Pathophysiology of Disseminated intravascular coagulation

A

Clotting occurs inappropriately and diffusely, until clotting factors are exhausted.

At this point uncontrolled bleeding occurs.

97
Q

Pathophysiology of Immune thrombocytopenic purpura (platelet disorder)

A

Formation of antibodies against platelets

  • > autoimmune platelet destruction
  • > thrombocytopenia.

The spleen is the site of autoantibody production and the site of platelet phagocytosis.

Therefore splenectomy has a role as a treatment.

98
Q

Pathophysiology of Thrombotic thrombocytopenic purpura (platelet disorder)

A

Deficiency of ADAMTS 13 (protease which degrades vWF)

  • > Widespread adhesion and aggregation of platelets
  • > microvascular thrombosis
  • > profound thrombocytopenia.
99
Q

Cause of Over-anticoagulation

A

Iatrogenic (inappropriate prescription of warfarin / heparin).

100
Q

Cause of Disseminated intravascular coagulation

A

Secondary to infection,

malignancy,

major trauma.

101
Q

Cause of Immune thrombocytopenic purpura (platelet disorder)

A

In children, a result of viral infection.

In adults, occurs in combination with another autoimmune condition (SLE etc).

102
Q

Cause of Thrombotic thrombocytopenic purpura (platelet disorder)

A

Congenital (genetic absence of ADAMTS 13)

or autoantibody mediated (autoantibody against ADAMTS 13).

103
Q

Epidemiology of Immune thrombocytopenic purpura (platelet disorder)

A

5/100,000 in children,

2/100,000 in adults

104
Q

Diagnostic test for Disseminated intravascular coagulation

A

Prothrombin time elevated,

activated partial thromboplastin time elevated,

platelets low,

fibrinogen low.

105
Q

Diagnostic test for Immune thrombocytopenic purpura (platelet disorder)

A

FBC: Isolated thrombocytopenia.

106
Q

Diagnostic test for Thrombotic thrombocytopenic purpura (platelet disorder)

A

Raised lactate dehydrogenase levels (from ischaemic or necrotic cells).

107
Q

Treatments for Over-anticoagulation

A

Warfarin: Phytomenadione

(Vitamin K)

Heparin: protamine sulfate.

108
Q

Treatment for Disseminated intravascular coagulation

A

Consider transfusion of platelets.

109
Q

Treatments for Immune thrombocytopenic purpura (platelet disorder)

A

Oral corticosteroids (prednisolone).

Second line: splenectomy.

110
Q

Treatments for Thrombotic thrombocytopenic purpura (platelet disorder)

A

Plasma exchange to remove autoantibodies to ADAMTS 13.

Splenectomy as a last resort.

111
Q

Complications of Over-anticoagulation

A

Bleeding out

-> Death

112
Q

Complications of Disseminated intravascular coagulation

A

Organ failure by infarction,

death.

113
Q

Complications of Immune thrombocytopenic purpura (platelet disorder)

A

Bleeding.

114
Q

Define Acute lymphoblastic leukemia (ALL)

A

Acute malignant transformation of a clone of lymphoid progenitor cells.

115
Q

Define Chronic lymphocytic leukemia (CLL)

A

Chronic malignant transformation of a clone of mature lymphoid cells.

116
Q

Define Acute myeloid leukemia (AML)

A

Acute malignant transformation of a clone of myeloid progenitor cells.

117
Q

Define Chronic myeloid leukemia (CML)

A

Chronic malignant transformation of a clone of myeloid cells.

118
Q

How does Acute lymphoblastic leukemia (ALL) clinically present?

A

Fatigue, dizziness and palpitations.

Anaemia, bleeding and infection due to bone marrow failure.

Bone pain.

Hepatosplenomegaly.

119
Q

How does Chronic lymphocytic leukemia (CLL) clinically present?

A

Early: Asymptomatic (indolent), but isolated lymphocytosis is frequent.

When symptomatic: Anaemia, bleeding and infection due to bone marrow failure.

Rubbery lymph nodes.

120
Q

How does Acute myeloid leukemia (AML) clinically present?

A

Fatigue, dizziness and palpitations.

Anaemia, bleeding and infection due to bone marrow failure.

Hepatosplenomegaly.

121
Q

How does Chronic myeloid leukemia (CML) clinically present?

A

Insidious onset, fever, weight loss, sweating, anaemia.

Massive splenomegaly.

Untreated, this lasts 3-4 years, before progressing.

122
Q

Acute lymphoblastic leukemia (ALL) - note

A

Prospensity to involve the CNS.

123
Q

Chronic lymphocytic leukemia (CLL) - note

A

Histology: Smudge (smear?) cells.

124
Q

Acute myeloid leukemia (AML) - note

A

Histology: Auer rods.

125
Q

Pathophysiology of Acute lymphoblastic leukemia (ALL)

A

Uncontrolled proliferation of precursor B or T cells

-> Accumulation of leukaemic cells in bone marrow, peripheral blood and other tissues.

Additionally a reduction in red cells, platelets and neutrophils.

126
Q

Pathophysiology of Chronic lymphocytic leukemia (CLL)

A

Uncontrolled proliferation and accumulation of mature B (or T) cells.

Autoimmune haemolysis can occur

-> anaemia.

127
Q

Pathophysiology of Acute myeloid leukemia (AML)

A

Accumulation of leukaemic cells in bone marrow, peripheral blood and other tissues.

Additionally a reduction in red cells, platelets and neutrophils

128
Q

Pathophysiology of Chronic myeloid leukemia (CML)

A

Insidious onset lasts 3-4 years

  • > Blast formation
  • > Acute myeloid leukaemia
  • > rapid death.
129
Q

Causes of Acute lymphoblastic leukemia (ALL)

A

Genetic: Genetic risk.

Down’s Syndrome -> 20x risk

Environmental: Chemicals (benzene compounds) drugs (alkylating agents)

Radiation exposure.

130
Q

Cause of Chronic lymphocytic leukemia (CLL)

A

Genetic: Mutation (11q or 17p deletions for example).

131
Q

Causes of Acute myeloid leukemia (AML)

A

Can transform from myelodysplasia.

Genetic: Can be due to mutation such as translocations.

132
Q

Cause of Chronic myeloid leukemia (CML)

A

Genetic: 95% of cases:

Philadelphia chromosome: reciprocal translocation (t(9;22)),

creating fusion gene (BCR-ABL) with tyrosine kinase activity which alters cell growth.

133
Q

Epidemiology of Acute lymphoblastic leukemia (ALL)

A

Most common cancer in children.

134
Q

Epidemiology of Chronic lymphocytic leukemia (CLL)

A

Most common leukaemia in the western world.

Usually of older people.

135
Q

Epidemiology of Acute myeloid leukemia (AML)

A

Most common in older adults and elderly.

136
Q

Epidemiology of Chronic myeloid leukemia (CML)

A

Most common in elderly.

137
Q

Diagnostic tests for Acute lymphoblastic leukemia (ALL)

A

Peripheral blood film: anaemia and thrombocytopenia

Bone marrow aspirate: Leukaemic blast cells.

138
Q

Diagnostic tests for Chronic lymphocytic leukemia (CLL)

A

FBC: Anaemia, raised white cell

Blood film: Smudge cells.

139
Q

Diagnostic tests for Acute myeloid leukemia (AML)

A

Peripheral blood film: anaemia, thrombocytopenia, auer rods

Bone marrow aspirate: Leukaemic blast cells.

140
Q

Diagnostic tests for Chronic myeloid leukemia (CML)

A

FBC: Anaemia, raised white cells.

Cytogenetics: Philadelphia chromosome.

141
Q

Treatment for Acute lymphoblastic leukemia (ALL)

A

Chemotherapy with vincristine, dexamethasone, asparaginase and daunorubicin.

Intrathecal: methotrexate.

Follow up maintenance.

142
Q

Treatment for Chronic lymphocytic leukemia (CLL)

A

Incurable.

Chlorambucil (with or without prednisolone)

  • > Decreases blood count
  • > Decreases lymphadenopathy and splenomegaly.
143
Q

Treatment for Acute myeloid leukemia (AML)

A

Low risk of treatment failure: Chemotherapy, in intervals to allow marrow recovery.

Intermediate: Chemotherapy followed by allogenic bone marrow transplant.

High risk: Only curable with allogenic transplantation.

144
Q

Treatment for Chronic myeloid leukemia (CML)

A

Imatinib (tyrosine kinase inhibitor).

If in acute stage: Chemotherapy.

145
Q

Complications of Acute lymphoblastic leukemia (ALL)

A

Children: excellent prognosis (1/5 die).

Adults: Poorer prognosis, only 30% cured.

146
Q

Complications of Chronic lymphocytic leukemia (CLL)

A

Death

147
Q

Complications of Acute myeloid leukemia (AML)

A

Death

148
Q

Complications of Chronic myeloid leukemia (CML)

A

Death

149
Q

Sequelae of Acute lymphoblastic leukemia (ALL)

A

Recurrence (if in remission).

Secondary cancer.

150
Q

Sequelae of Chronic myeloid leukemia (CML)

A

Acute myeloid leukemia.

Myelofibrosis.

151
Q

Define lymphoma

A

Malignant tumour of the lymphatic system

152
Q

Types of lymphoma

A

Hodgkin’s

Non-Hodgkin’s

153
Q

How does Hodgkin’s lymphoma clinically present?

A

Painless rubbery lymph node enlargement,

hepatosplenomegaly,

Systemic ‘B symptoms’: (fever, drenching night sweats, weight loss).

Pruritus, fatigue, anorexia,

and alcohol-induced pain in affected nodes.

Extranodal involvement is possible.

154
Q

How does Non-Hodgkin’s lymphoma clinically present?

A

As Hodgkin’s.

Can be indolent or aggressive (depending on origin cell).

Extranodal involvement more common than in Hodgkin’s.

155
Q

Pathophysiology of Hodgkin’s lymphoma

A

Malignant transformation of normal T or B cell in lymph nodes.

Reed-Sternberg cells seen on histology.

Staging: 1: Single lymph node or site

2: Two or more nodes/sites, same side of the diaphragm
3: Lymph nodes either side of the diaphragm
4: Diffuse or disseminated of one or more extralymphatic tissue

156
Q

Pathophysiology of Non-Hodgkin’s lymphoma

A

70% B cell, 30% T cell by origin.

Clonal expansion of lymphocytes.

Mature lymphocyte transformation: Indolent course.

Proliferating cell: Aggressive.

157
Q

Cause of Hodgkin’s lymphoma

A

Previous Epstein-Barr virus in some cases.

158
Q

Cause of Non-Hodgkin’s lymphoma

A

Usually unknown. H. pylori infection in MALT lymphoma.

EBV infection in Burkitt’s lymphoma.

159
Q

Epidemiology of Hodgkin’s lymphoma

A

More common in young adults.

160
Q

Epidemiology of Non-Hodgkin’s lymphoma

A

Rare before 40.

Specific varieties more common in children.

161
Q

Diagnostic tests for Hodgkin’s lymphoma

A

Lymph node biopsy: showing Reed-Sternberg cells.

CT: Staging.

ESR: raised.

162
Q

Diagnostic tests for Non-Hodgkin’s lymphoma

A

FBC: Possible anaemia

Lymph node biopsy: Needed for diagnosis.

CT: staging.

163
Q

Treatment for Hodgkin’s lymphoma

A

Early stage disease: Brief chemo (ABVD) and irradiation

Advanced: Cyclical chemo (ABVD) and irradiation.

164
Q

Treatment for Non-Hodgkin’s lymphoma

A

Diffuse large b cell lymphoma: Cyclical combination chemo and field irradiation.

Primary gastric lymphoma: H. pylori eradication

Burkitt’s: Cyclical combo chemo.

165
Q

Complications of Hodgkin’s lymphoma

A

Death.

Worse prognosis with B symptoms.

166
Q

Complications of Non-Hodgkin’s lymphoma

A

Death.

167
Q

Define Multiple Myeloma

A

Malignant disease of bone marrow plasma cells.

168
Q

Define Malaria

A

Infection by Plasmodium transmitted by mosquito.

169
Q

How does multiple myeloma clinically present?

A

Bone destruction: Back pain, pathological fractures

Bone marrow infiltration: Anaemia, infections and bleeding

Paraprotein aggregates: Blurred vision, gangrene and bleeding.

170
Q

How does malaria clinically present?

A

Most with falciparum present in the first month, others can incubate for months.

No specific symptoms; take effective history.

Fever, chills, rigors, cough, myalgia, splenomegaly, hepatomegaly

Severe: Impaired consciousness, shortness of breath, bleeding, fits, hypovolaemia.

171
Q

Pathophysiology of multiple myeloma

A

Clonal proliferation of bone marrow cells, usually capable of monoclonal antibodies (usually IgA or IgG).

Can be associated with the excretion of light chains in the urine (Bence Jones protein).

Bone destruction: increased osteoclastic activity

-> bone pain and osteolytic lesions

Infiltration of bone marrow -> reduced function

AKI: due to light chain and amyloid deposition, hypercalcaemia and hyperuricaemia.

Paraproteins: Can aggregate in the blood to greatly increase viscosity

172
Q

Pathophysiology of malaria

A

Bite by infected mosquito

  • > sporozoites in the saliva travel to the liver to mature
  • > rupture to release merozoites into the blood
  • > invade RBC and undergo asexual reproduction to create sporozoites a mosquito can pick up (hence cycle)
173
Q

Cause of multiple myeloma

A

Mutation.

About half of cases; translocation placing oncogene into immunoglobulin heavy chain gene on chromosome 14.

174
Q

Cause of malaria

A

Infection by Plasmodium (usually falciparum).

175
Q

Epidemiology of multiple myeloma

A

Peak presentation at 60 years.

176
Q

Epidemiology of malaria

A

Poor, young, pregnant, elderly all more at risk.

Consider if recently travelled abroad.

177
Q

Diagnostic tests for multiple myeloma

A

Paraproteinaemia,

Bence Jones protein in urine,

CT,

Bone marrow aspirate.

178
Q

Diagnostic test for malaria

A

Blood smear with giemsa stain.

179
Q

Treatments for multiple myeloma

A

Chemotherapy with autologous stem cell transplant.

Paraprotein: plasmapheresis.

Blood transfusion, for anaemia.

Treatment of infection.

AKI can be treated by hydration.

180
Q

Treatments for malaria

A

Non-falciparum: Chloroquine

Falciparum: Quinine sulfate, atovaquone-proguanil and artemether with lumefantrine.

Severe Falciparum: IV quinine dihydrochloride.

181
Q

Complications of multiple myeloma

A

Terminal.

With treatment, median survival is 5 years.

182
Q

Complications of malaria

A

Multiple organ failure and death.

(SG) condensed phase 2a (9 decks)

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