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Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

What is anaemia?

A

Defined as low haemoglobin concentration, may be due either to a low red cell mass or increased plasma volume
Low Hb = <135g/L for men, <115g/L for women

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2
Q

What are the symptoms of anaemia?

A

Fatigue, dyspnoea, faintness, palpitations, headache, tinnitus, anorexia

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3
Q

What are the signs of anaemia?

A

Pallor, hyper dynamic circulation e.g. tachycardia

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4
Q

What are the pathological consequences of anaemia?

A

Myocardial fatty change, fatty change in liver, aggravate angina/ claudication, skin and nail atrophic changes

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5
Q

What is the normal mean cell volume?

A

MCV should be 76-96 femtolitres

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6
Q

What are the 4 main types of anaemia?

A

Microcytic - low MCV
Normocytic - normal MCV
Microcytic - high MCV
Haemolytic - can be normocytic/macrocytic

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7
Q

What are the causes of microcytic anaemia?

A 
Iron-deficiency anaemia (most common)
Thalassaemia
Sideroblastic anaemia (rare)
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8
Q

What are some examples of microcytic anaemias?

A

Iron deficiency, anaemia of chronic disease, sideroblastic anaemia, thalassaemia

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9
Q

What are the causes of normocytic anaemia?

A

Acute blood loss, anaemia of chronic disease, renal failure

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10
Q

What are some examples of normocytic anaemia?

A

Aplastic anaemia, haemolytic - sickle cell disease, infections - malaria, haemorrhage

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11
Q

What are the causes of macrocytic anaemia?

A

B12/folate deficiency
Alcohol excess - liver disease
Hypothyroidism
Marrow infiltration

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12
Q

What are some examples of macrocytic anaemia?

A

Megaloblastic
B12/folate deficiency
Pernicious anaemia

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13
Q

How is anaemia diagnosed?

A

FBC + film, reticulocyte count, B12/folate/ferritin
Iron deficiency - ferritin, iron studies
Chronic disease - lab + clinical investigation, renal failure
B12 deficiency - intrinsic factor antibodies, Schilling test, B12 replacement

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14
Q

What is iron-deficiency anaemia and how is it caused?

A

A reduction in Hb concentration due to inadequate iron supply. Microcytic
Causes: blood loss, menorrhagia, malabsorption, poor diet

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15
Q

What are the signs and tests for iron-deficiency anaemia?

A

Tiredness, often asymptomatic
Blood film: microcytic, hypochromic anaemia
Decreased MCV, MCH and MCHC
Low ferritin

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16
Q

How is iron-deficiency anaemia treated?

A

Treat the cause, give oral iron e.g. ferrous sulfate

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17
Q

What is anaemia of chronic disease and what are its causes?

A

Reduced Hb related to chronic inflammatory disorders, chronic infections and malignancy. Microcytic/ normocytic
Causes: chronic infection/inflammation, vasculitis, autoimmune disorders, renal failure, malignancy

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18
Q

What are the tests for anaemia of chronic disease and how is it treated?

A

Ferritin normal, check blood film - B12, folate, TSH and tests for haemolysis
Treat underlying disease, give erythropoietin to raise Hb levels

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19
Q

What is sideroblastic anaemia?

A

A form of anaemia in which the bone marrow produces ringed sideroblasts rather than healthy blood cells.

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20
Q

What is the pathology behind sideroblastic anaemia?

A

Ineffective erythropoiesis, leading to increased iron absorption and iron loading in marrow - body has enough iron but cannot incorporate it into Hb

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21
Q

How is sideroblastic anaemia tested for and treated?

A

Increased ferritin, hypochromic blood film, sideroblasts in the marrow
Remove the cause, repeat transfusion for severe anaemia

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22
Q

What are the causes of folate deficiency?

A

Macrocytic anaemia - poor diet, malabsorption, alcohol, drugs (methotrexate)

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23
Q

How is folate deficiency tested for and treated?

A

Blood film - large oval macrocytes, serum and red cell folate assay
Assess for underlying cause
Treated with folic acid

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24
Q

What is pernicious anaemia?

A

Macrocytic - an autoimmune condition in which atrophic gastritis leads to a lack of IF secretion from the parietal cells of the stomach. Dietary B12 therefore remained unbound and consequently cannot be absorbed by the terminal ileum

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25
Q

How does pernicious anaemia present?

A

Fatigue, dyspnoea, jaundice, irritability, depression

Neurological (B12 causes) - paraesthesia, peripheral neuropathy

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26
Q

How is pernicious anaemia tested for and treated?

A

FBC: decreased Hb, increased MCV
Megaloblasts in the bone marrow, IF antibody test
Treat cause - oral B12

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27
Q

What is haemolytic anaemia?

A

Anaemia due to haemolysis, the abnormal breakdown of red blood cells

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28
Q

What is aplastic anaemia and how is it caused?

A

Anaemia due to bone marrow failure (bone marrow stops making cells)
Causes: autoimmune, drugs, viruses, irradiation, inherited

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29
Q

How does aplastic anaemia present?

A

Symptoms and signs of anaemia, bruising with minimal trauma, blood blisters in mouth

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30
Q

How is aplastic anaemia tested for and treated?

A

Marrow examination needed, pancytopenia, hypo cellular aplastic bone marrow with increased fatty space
Support blood count, bone marrow transplant, immunosuppression

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31
Q

What is polycythaemia vera?

A

A condition marked by an abnormal increase in the number of circulating red blood cells.

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32
Q

How does polycythaemia vera present?

A

May be asymptomatic, headaches, dizziness, visual disturbance, itching after a hot bath, burning sensation in finger and toes, facial plethora, splenomegaly

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33
Q

How is polycythaemia vera diagnosed?

A

FBC: increased RCC, Hb, PCV, WBC and platelets
JAK 2 testing
Marrow shows hyper cellularity with erythroid hyperplasia

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34
Q

How is polycythaemia vera managed?

A

Aim to keep haematocrit <0.45 to reduce risk of thrombosis. Low dose aspirin

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35
Q

What are haemoglobinopathies?

A

Genetic diseases of haemoglobin. Categorised by thalassaemia syndromes and structural haemoglobin variants

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36
Q

Explain the genetic pathology of sickle cell disease

A

Sickle cell anaemia is an inherited autosomal recessive disorder in which the production of abnormal haemoglobin results in vaso-occlusive crises.
HbS is caused by a point mutation in the beta globin gene on chromosome 11. Has polymerises into rod-like aggregates which cause the red cell to adopt a sickle shape

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37
Q

How does sickle cell anaemia present?

A

Asymptomatic, asthenia, jaundice and ulcers around the ankles. Bone deformities and infections

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38
Q

What are the complications of sickle cell anaemia?

A

Acute - painful crisis, sickle chest syndrome, stroke

Chronic - renal impairment, pulmonary hypertension, joint damage

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39
Q

How is sickle cell anaemia diagnosed?

A

Neonatal screening, blood test: increased reticulocytes and bilirubin
Hb electrophoresis - single major HbS band
Film - sickle cells
Sickle solubility test: +ve

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40
Q

How is sickle cell anaemia managed?

A

Disease modifying treatment - transfusion, stem cell transplant, prophylaxis in cases of hyposplenism and immunocompromised
Hydroxycarbamide

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41
Q

What is thalassaemia?

A

A group of inherited red cell disorders caused by the underproduction of alpha/beta globin chains

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42
Q

What is beta thalassaemia major and how does it present?

A

Significant abnormalities in both beta-globin genes, presenting with severe anaemia and failure to thrive.
Failure to feed, lacking energy, crying, pale

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43
Q

How is beta thalassaemia major diagnosed?

A

FBC: MCV and MCH very low
Film: large and small very pale red cells, nucleated RBCs
Hb electrophoresis

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44
Q

How is beta thalassaemia major managed?

A

Regular transfusions, iron chelation, endocrine supplementation, ferritin monitoring

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45
Q

What is iron overload?

A

Thalassaemia major requires lifelong blood transfusions to grow and develop. This consequently increases the body iron load - there is no means for the body to eliminate the excessive iron.
Excess iron is deposited mainly in the liver and spleen - leading to liver fibrosis and cirrhosis.
Deposited in endocrine glands and heart - diabetes, heart failure and premature death

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46
Q

What is alpha thalassaemia?

A

There are two separate alpha-globin genes on each chromosome 16 - four genes termed aa/aa. When one/some of these are deleted, it is termed alpha thalassaemia

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47
Q

What are membranopathies?

A

Autosomal dominant conditions which result in an abnormally shaped red cell. Deficiency of red cell membrane proteins caused by a variety of genetic lesions

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48
Q

What is hereditary spherocytosis?

A

Shortage of red blood cells, autosomal dominant, less deformable spherical RBCs, so trapped in spleen - extravascular haemolysis

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49
Q

What is hereditary elliptocytosis?

A

Abnormally large number of the erythrocytes are elliptical, autosomal dominant, mostly asymptomatic

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50
Q

What is glucose-6-phosphate dehydrogenase (G6PD) deficiency?

A

X-linked recessive, lack of enzyme that maintains protective protein against oxidant injury. May get oxidative crises due to decreased glutathione production but most are asymptomatic.

51
Q

How is G6PD deficiency tested for and treated?

A

Enzyme assay, film: bite and blister cells

Transfuse if severe

52
Q

What is pyruvate kinase deficiency?

A

Autosomal recessive, decreased ATP production causes decreased RBC survival, may have haemolysis and splenomegaly in later life

53
Q

Where are platelets produced?

A

Bone marrow

54
Q

How does platelet dysfunction present?

A

Mucosal bleeding, easy bruising, petechiae, Purpura, traumatic haematomas

55
Q

Name some conditions that result in low platelets due to decreased marrow production?

A

Aplastic anaemia, megaloblastic anaemia, marrow replacement

56
Q

Name some conditions that result in low platelets due to excess destruction?

A

Immune thrombocytopenia, thrombotic thrombocytopenia

57
Q

How are platelet dysfunctions managed?

A

Immunosuppression, treat underlying cause, clopidogrel and aspirin to inhibit a function of the platelets, splenectomy is last resort

58
Q

Define thrombosis

A

The formation of a blood clot in a blood vessel.

59
Q

Where can abnormal arterial thrombi occur?

A

Coronary circulation - MI
Cerebral circulation - strokes
Peripheral circulation - gangrene/ PVD

60
Q

What are the risk factors for abnormal blood clotting?

A

Smoking, hypertension, diabetes, hyperlipidaemia, obesity/ sedentary lifestyle, stress/ type A personality

61
Q

What drugs can be used to manage abnormal blood clotting?

A

Heparin, LMW heparin, aspirin, warfarin, DOACs

62
Q

How does heparin manage abnormal blood clotting?

A

Binds to antithrombin and increases its activity (indirect thrombin inhibitor)

63
Q

How does aspirin manage abnormal blood clotting?

A

Inhibits cycle-oxygenase irreversibly, and inhibits thromboxane formation and hence platelet aggregation

64
Q

How does warfarin manage abnormal blood clotting?

A

Prevents synthesis of active factors II, VII, IX and X, antagonist of vitamin K - prolongs prothrombin time

65
Q

How do DOACs manage abnormal blood clotting?

A

Directly acting on factor II and X, used for extending thromboprophylaxis

66
Q

What is deep vein thrombosis?

A

A blood clot that develops within a deep vein in the body, usually in the leg

67
Q

What is thromboembolism?

A

The obstruction of a blood vessel by a blood clot that has become dislodged from another site in the circulation

68
Q

What are the causes for DVTs/ Thromboembolisms?

A

Circumstantial - surgery, immobilisation, long haul flights
Genetic - Factor V Leidein, antithrombin deficiency
Acquired - anti-phospholipid syndrome, lupus anticoagulant

69
Q

How can DVTs/ thromboembolisms be prevented?

A

Mechanical - hydration and early mobilisation, compression stockings, foot pumps
Chemical - LMW heparin

70
Q

What is thromboprophylaxis?

A

The prevention of clots forming in the veins

71
Q

How do DVTs/thromboembolisms present?

A

Symptoms and signs are non-specific, clinical diagnosis unreliable.
Pain, swelling, tenderness, warmth, decolorisation

72
Q

How are DVTs/thromboembolisms diagnosed?

A

D-dimer: normal excludes diagnosis
US compression test proximal veins
Venogram for calf

73
Q

How are DVTs/thromboembolisms managed?

A

Oral warfarin, LMWH, DOAC, compression stockings, treat underlying cause

74
Q

What is a pulmonary embolism?

A

A blockage in one of the pulmonary arteries in your lungs, often caused by blood clots that travel to the lungs from the legs (DVTs).

75
Q

How do pulmonary embolisms present?

A

Breathlessness, pleuritic chest pain, cyanosis, tachycardia, no signs of alternative diagnosis (differential diagnosis of chest pain and SOB)

76
Q

How are pulmonary embolisms diagnosed?

A

ECG: sinus tachycardia
Blood gases: type 1 RF, decreased O2 and CO2
D-dimer: normal excludes diagnosis

77
Q

How are pulmonary embolisms managed?

A

IV alteplase to thrombolyse

LMWH, DOAC, warfarin

78
Q

Give some examples of vascular defects

A

Congenital - connective tissue disease

Acquired - Senile Purpura, infection, steroids

79
Q

Give some examples of coagulation disorders

A

Congenital - haemophilia, von Willebrand’s disease

Acquired - anticoagulants, liver disease, vitamin K deficiency

80
Q

What is von Willebrand Disease?

A

An inherited bleeding tendency caused by a quantitative or qualitative deficiency of vWF

81
Q

Describe the pathology of von Willebrand disease

A

vWF acts as an adhesion molecule which allows platelets to bind to sub endothelial tissues and it also acts as a carrier for factor VIII.
Lack of vWF leads to a bleeding tendency due to a combination of failure of platelet adhesion and factor VIII deficiency

82
Q

What is haemophilia A?

A

An inherited disorder of haemostasis characterised by bleeding tendency due to a deficiency of factor VIII

83
Q

What is haemophilia B?

A

An inherited disorder of haemostasis characterised by bleeding tendency due to a deficiency of factor IX

84
Q

How is haemophilia A treated?

A

Avoid NSAIDs and IM injections, desmopressin raises factor VIII levels

85
Q

How is haemophilia B treated?

A

Recombinant factor IX

86
Q

What is acute lymphoblastic leukaemia (ALL)?

A

A malignancy of lymphoid cells (lymphoblasts), affecting B/T lymphocyte cell lineages, arresting maturation and promoting uncontrolled proliferation of immature blast cells, with marrow failure and tissue infiltration

87
Q

How does acute lymphoblastic leukaemia present?

A

Marrow failure - fatigue, SOB
Infection - tonsilitis, fevers
Bleeding - thrombocytopenia
Hepato/splenomegaly

88
Q

How is acute lymphoblastic leukaemia diagnosed?

A

Characteristic blast cells on blood film and bone marrow

89
Q

How is acute lymphoblastic leukaemia treated?

A

Blood/platelet transfusions, IV fluids, Hickman line for IV access
Chemotherapy

90
Q

What is acute myeloid leukaemia?

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements (myeloblasts)

91
Q

How does acute myeloid leukaemia present?

A

Marrow failure - infection, bleeding

Infiltration - hepatosplenomegaly, gum hypertrophy

92
Q

How is acute myeloid leukaemia diagnosed?

A

Bone marrow biopsy - AML differentiated from ALL by Auer rods
WCC is often increased

93
Q

How is acute myeloid leukaemia treated?

A

Chemotherapy, supportive measures - blood transfusion, IV fluids
Bone marrow transplant

94
Q

What is chronic myeloid leukaemia?

A

An uncontrolled clonal proliferation of myeloid (basophils, neutrophils, eosinophils) cells

95
Q

What is the Philadelphia chromosome?

A

A hybrid chromosome comprising reciprocal translocation between the long arms of chromosome 9 and the long arm of chromosome 22 – t(9;22).

96
Q

How does chronic myeloid leukaemia present?

A

Weight loss, tiredness, fever, sweats, bleeding, splenomegaly, hepatomegaly, anaemia, bruising

97
Q

How is chronic myeloid leukaemia diagnosed?

A

WBC - increased neutrophils, monocytes, basophils, eosinophils
Film: left shift + basophilia
Philadelphia chromosome

98
Q

How is chronic myeloid leukaemia treated?

A

Target molecular therapy - Imatinib (Tyrosinase kinase inhibitors)

99
Q

What is chronic lymphocytic leukaemia (CLL)?

A

A progressive accumulation of a malignant clone of functionally incompetent beta cells.

100
Q

How does chronic lymphocytic leukaemia present?

A

Anaemia, infection-prone, weight loss, sweats, enlarged, rubbery, non-tender nodes, splenomegaly

101
Q

How is chronic lymphocytic leukaemia diagnosed?

A

Increased lymphocytes, autoimmune haemolysis, marrow infiltration

102
Q

How is chronic lymphocytic leukaemia treated?

A

1st line - chemotherapy (rituximab)

Transfusion, IV human immunoglobulin, stem cell transplantation, radiotherapy,

103
Q

What is a lymphoma?

A

A malignant growth of white blood cells - predominantly the lymph nodes but also found in the blood, bone marrow, liver and spleen

104
Q

What is characteristic about Hodgkin’s lymphoma?

A

Characteristic Reed-Sternberg cells with mirror-image nuclei

105
Q

How does Hodgkin’s lymphoma present?

A

Enlarged, non-tender, rubbery superficial lymph nodes, systemic symptoms, anaemia, hepatomegaly

106
Q

How is Hodgkin’s lymphoma diagnosed?

A

Tissue diagnosis - lymph node biopsy (Reed-Sternberg cells)

Imaging - CXR, CT of thorax, abdo and pelvis

107
Q

What are the stages for Hodgkin’s lymphoma?

A

Ann Arbor system
I - confined to a single lymph node region
II - 2 or more nodal areas on same side of diaphragm
III - nodes on both sides of diaphragm
IV - spread beyond lymph nodes on both sides of diaphragm.
A - asymptomatic, B - presence of B symptoms (weight loss, unexplained fever, night sweats)

108
Q

How is Hodgkin’s lymphoma managed?

A

IA-IIA: radiotherapy and short course chemotherapy
IIA-IVB: longer course chemotherapy
ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine

109
Q

What is characteristic about Non-Hodgkin’s lymphomas?

A

These are all lymphomas without Reed-Sternberg cells

110
Q

What are the causes of Non-Hodgkin’s lymphoma?

A

Immunodeficiency - drugs, HIV

Infection - Helicobacter pylori

111
Q

How does Non-Hodgkin’s lymphoma present?

A

Superficial lymphadenopathy, extra-nodal disease, dyspepsia, weight loss, diarrhoea, fever, night sweats

112
Q

How is Non-Hodgkin’s lymphoma diagnosed?

A

Marrow and node biopsy: classify high/low grade
Staging - CT of chest, abdomen, pelvis
Bloods

113
Q

How are low-grade Non-Hodgkin’s lymphomas managed?

A

Indolent, often incurable and symptomless
Radiotherapy curative in localised diseases
Remission maintained by rituximab

114
Q

How are high-grade Non-Hodgkin’s lymphomas managed?

A

More aggressive, often curable with systemic symptoms

Chemotherapy - rituximab, prednisolone

115
Q

What is a myeloma?

A

A malignant tumour of the bone marrow involving myeloma cells

116
Q

What is multiple myeloma and what is it characterised by?

A

Neoplastic proliferation of bone marrow plasma cells

Monoclonal protein in urine, CRAB end organ damage, excess plasma cells in bone marrow

117
Q

How do myelomas present?

A

Tiredness and malaise, bone pain, fractures, recurrent bacteria infections, anaemia, osteolytic lesions, renal failure

118
Q

How are myelomas diagnosed?

A

Proteins in the blood (monoclonal protein band in serum or urine electrophoresis)
CRAB - calcium, renal, anaemia, bone
Excess of 10% plasma cells in bone marrow on biopsy

119
Q

How are myelomas managed?

A 
Analgesia for bone pain
Bisphosphonate to reduce fracture rates
Local radiotherapy 
Trasnfusions to correct anaemia
Chemotherapy
120
Q

What is malaria?

A

An infectious disease caused by protozoan parasites from the Plasmodium family – transmitted by the bite of the Anopheles mosquito or by a contaminated needle or transfusion. Most commonly P. falciparum

121
Q

Describe the life cycle of the malaria parasite

A

Plasmodium sporozoites are passed on via bite of mosquito.
Travel to liver and infect hepatocytes
Proliferate into merozoites -> infect and multiply in red cells/ mature into gametocytes which infect another mosquito
The rupture of erythrocytic schizonts produces clinical manifestations of malaria

122
Q

What are the clinical manifestations of malaria?

A

Fever, headache, malaise, myalgia, diarrhoea, cough

123
Q

How is malaria diagnosed?

A

Detailed travel history
Microscopy of thick and thin blood smear with giemsa stain
Rapid diagnostic test detection of parasite antigen

124
Q

How is malaria managed?

A

Artemisinin combination therapy (ACT) achieve rapid clearance of parasites by combined action at different stages of the parasite cycle.
Chloroquine phosphate

Phase 2a (16 decks)

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