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2a Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

What is myeloma?

A

Malignancy of plasma cells leading to progressive bone marrow failure. It is associated with production of characteristic paraprotein, bone disease and renal failure.

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2
Q

In order to make a diagnosis of myeloma, there must be evidence of mono-clonality. What is mono-clonality?

A

Abnormal proliferation of a single clone of plasma cell leading to immunoglobulin secretion and causing organ dysfunction especially to the kidney.

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3
Q

What disease often precedes myeloma?

A

Monoclonal gammopathy of undetermined significance (MGUS).

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4
Q

What is MGUS?

A

A common disease with paraprotein present in the serum but no myeloma. Often asymptomatic. <10% plasma cells in the bone marrow.

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5
Q

In approximately 2/3 of people with myeloma, what might their urine contain?

A

Immunoglobulin light chains with kappa or lamda lineage.

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6
Q

Give 3 symptoms of myeloma.

A
  1. Tiredness.
  2. Bone/back pain.
  3. Infections.
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7
Q

Give 4 signs of myeloma.

A

CRAB!

  1. Calcium is elevated.
  2. Renal failure.
  3. Anaemia.
  4. Bone lesions.
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8
Q

Why is calcium elevated in myeloma?

A

There is increased bone resorption and decreased formation meaning there is more calcium in the blood.

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9
Q

Why might someone with myeloma have anaemia?

A

The bone marrow is infiltrated with plasma cells. Consequences of this are anaemia, infections and bleeding.

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10
Q

Why might someone with myeloma have renal failure?

A

Due to light chain deposition.

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11
Q

What investigations might you do in someone who you suspect has myeloma?

A
  1. Blood film.
  2. Bone marrow aspirate and trephine biopsy.
  3. Electrophoresis.
  4. X-ray.
  5. CT scan.
  6. MRI scan.
  7. Chromosomal abnormalities.
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12
Q

What would you expect to see on the blood film taken from someone with myeloma?

A

Rouleaux formation (aggregations of RBC’s).

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13
Q

What are you looking for on a bone marrow biopsy taken from someone with myeloma?

A

Increased plasma cells.

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14
Q

What are you looking for on electrophoresis in a patient with myeloma?

A

Monoclonal protein band.

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15
Q

What are you looking for on an X-ray taken from someone with myeloma?

A

Bone lesions.

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16
Q

What is the treatment for MGUS and asymptomatic myeloma?

A

Watch and wait.

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17
Q

Describe the treatment for symptomatic myeloma.

A

Chemotherapy, analgesia and bisphosphonates.

Radiotherapy and bone marrow transplant can also be done.

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18
Q

What is lymphoma?

A

A malignant growth of WBC’s predominantly in the lymph nodes.

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19
Q

Although predominantly in the lymph nodes, lymphoma is systemic. What other organs might it effect?

A
  1. Blood.
  2. Liver.
  3. Spleen.
  4. Bone marrow.
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20
Q

Give 4 risk factors for lymphoma.

A
  1. Primary immunodeficiency.
  2. Secondary immunodeficiency e.g. HIV.
  3. Infection e.g. EBV, HTLV-1.
  4. Autoimmune disorders e.g. RA.
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21
Q

Describe the pathophysiology of lymphoma.

A

There is impaired immunosurveillance and infected B cells escape regulation and proliferate. (This is just a theory).

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22
Q

Give 4 symptoms of lymphoma.

A
  1. Enlarged lymph nodes in arm/neck.
  2. Symptoms of compression syndromes.
  3. General systemic ‘B’ symptoms e.g. weight loss, night sweats, malaise.
  4. Liver and spleen enlargement.
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23
Q

What investigations might you do in someone who you suspect has lymphoma?

A
  1. Blood film.
  2. Bone marrow biopsy.
  3. Lymph node biopsy.
  4. Immunophenotyping.
  5. Cytogenetics.
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24
Q

What are the two sub-types of lymphoma?

A
  1. Hodgkins lymphoma.

2. Non-hodgkins lymphoma.

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25
Q

What are the symptoms of Hodgkins lymphoma?

A
  1. Painless lymphadenopathy.

2. Presence of ‘B’ symptoms e.g. night sweats, weight loss.

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26
Q

What is needed for diagnosis of Hodgkins lymphoma?

A

Presence of Reed-sternberg cells.

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27
Q

Describe the staging of Hodgkins lymphoma.

A
  1. Stage 1: confined to a single lymph node region.
  2. Stage 2: Involvement of two or more nodal areas on the same side of the diaphragm.
  3. Stage 3: involvement of nodes on both sides of the diaphragm.
  4. Stage 4: Spread beyond the lymph nodes e.g. liver.

Each stage is either ‘A’ - absence of ‘B’ symptoms or ‘B’ - presence of ‘B’ symptoms.

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28
Q

What is the treatment for stage 1 - 2A Hodgkins lymphoma?

A

Short course combination chemotherapy followed by radiotherapy.

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29
Q

What is the treatment for stage 2B - 4 Hodgkins lymphoma?

A

Combination chemotherapy.

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30
Q

What are the possible complications of treatment for Hodgkins lymphoma?

A
  1. Secondary malignancies.
  2. IHD.
  3. Infertility.
  4. Nausea.
  5. Alopecia.
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31
Q

Describe low grade non-hodgkins lymphoma.

A

Slow growing, advanced at presentation, often incurable. Median survival is 10 years.

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32
Q

What is the treatment for low grade non-hodgkins lymphoma?

A

If symptomless - do nothing.

Radiotherapy, combination chemotherapy and mAb may be used if symptomatic.

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33
Q

Describe high grade non-hodgkins lymphoma.

A

Aggressive. Nodal presentation, patient unwell. Often curable.

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34
Q

Describe the treatment for high grade non-hodgkins lymphoma.

A
  • Early: short course chemotherapy and radiotherapy.

- Advanced: combination chemotherapy and mAb.

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35
Q

What is leukaemia?

A

A malignant proliferation of haemopoietic stem cells.

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36
Q

Name 4 sub-types of leukaemia.

A
  1. AML - acute myeloid leukaemia.
  2. CML - chronic myeloid leukaemia.
  3. ALL - acute lymphoblastic leukaemia.
  4. CLL - chronic lymphoblastic leukaemia.
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37
Q

What is acute myeloid leukaemia?

A

Neoplastic proliferation of blast cells.

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38
Q

What can increase the risk of developing AML?

A
  1. Preceding haematological disorders.
  2. Prior chemotherapy.
  3. Exposure to ionising radiation.
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39
Q

Give 5 symptoms of leukaemia.

A
  1. Anaemia.
  2. Infection.
  3. Bleeding.
  4. Hepatomegaly.
  5. Splenomegaly.
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40
Q

Why are anaemia, infection and bleeding symptoms of leukaemia?

A

Because of bone marrow failure.

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41
Q

Why are hepatomegaly and splenomoegaly symptoms of leukaemia?

A

Because of tissue infiltration.

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42
Q

What investigations might you do on someone who you suspect has leukaemia?

A
  1. Blood film.
  2. Bone marrow biopsy.
  3. Lymph node biopsy.
  4. Immunophenotyping.
  5. Cytogenetics.
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43
Q

Describe the treatment for AML.

A
  1. Supportive care.
  2. Chemotherapy: curative v palliative.
  3. Bone marrow transplant.
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44
Q

What is CML?

A

Chronic myeloid leukaemia, there is uncontrolled clonal proliferation of basophils, eosinophils and neutrophils.

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45
Q

What would the FBC from someone with CML look like?

A

High WBC’s.

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46
Q

What chromosome is present in >80% of people with CML?

A

Philadelphia chromosome.

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47
Q

What is the treatment for CML?

A

Tyrasine kinase inhibitors.

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48
Q

What is ALL?

A

Acute lymphoid leukaemia. There is uncontroleld proliferation of immature lymphoblast cells.

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49
Q

What is the treatment for ALL?

A

CNS directed therapy and stem cell transplant.

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50
Q

What is CLL?

A

Chronic lymphoid leukaemia. Proliferation of B lymphocytes leads to the accumulation of mature B cells that have escaped apoptosis.

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51
Q

What is the treatment for CLL?

A
  1. Do nothing.
  2. Chemotherapy.
  3. mAb.
  4. Bone marrow transplant.
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52
Q

Name the 3 broad categories of red cell disorders.

A
  1. Haemoglobinopathies.
  2. Membranopathies.
  3. Enzymopathies.
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53
Q

What is normal adult haemoglobin made of?

A

2 alpha and 2 beta chains.

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54
Q

What is foetal haemoglobin made of?

A

2 alpha and 2 gamma chains.

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55
Q

What is haemoglobin S?

A

Haemoglobin S is a variant of Hb arising from a point mutation in the beta globin gene. The mutation leads to a single amino acid change, valine -> glutamine.

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56
Q

What is sickle cell disease?

A

A haemoglobin disorder of quality. HbS polymerises -> sickle shaped RBC.

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57
Q

What is the advantage of being a carrier of sickle cell disease?

A

Carriage offers protection against falciparum malaria.

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58
Q

Describe the inheritance pattern of sickle cell disease.

A

Autosomal recessive. Sickle cell disease is homozygous SS.

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59
Q

If both parents are carriers of the sickle trait. What is the chance that their first child will have sickle cell disease?

A

Their offspring have a 1/4 chance of being affected with a sickle cell disease. (50% chance of being a carrier).

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60
Q

How long do sickle cells last for?

A

5-10 days - this explains why sickle cell disease is described as haemolytic.

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61
Q

Give 4 acute complications of sickle cell disease.

A
  1. Very painful crisis.
  2. Stroke in children.
  3. Cognitive impairment.
  4. Infections.
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62
Q

Give 3 chronic complications of sickle cell disease.

A
  1. Renal impairment.
  2. Pulmonary hypertension.
  3. Joint damage.
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63
Q

Describe the treatment for sickle cell disease.

A
  1. Transfusion.
  2. Hydroxycarbamide.
  3. Stem cell transplant.
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64
Q

What is thalassaemia?

A

A haemoglobin disorder of quantity. There is reduced synthesis of one or more globin chains with leading to a reduction in Hb -> anaemia.

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65
Q

If someone has beta thalassaemia do they have more alpha or beta globin chains?

A

They have very few beta chains, alpha chains are in excess.

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66
Q

What is the clinical classification of beta thalassaemia?

A
  1. Thalassaemia major.
  2. Thalassaemia intermedia.
  3. Thalassaemia carrier/heterozygote.
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67
Q

Which clinical classification of thalassaemia relies on regular transfusions?

A

Thalassaemia major.

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68
Q

Which clinical classification of thalassaemia is often asymptormatic?

A

Thalassaemia carrier/heterozygote.

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69
Q

When do people with beta thalassaemia major usually present and why?

A

These patients usually present very young due to having severe anaemia and so a failure to feed/thrive.

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70
Q

Why is it important to monitor iron levels in someone with beta thalassaemia major?

A

There is a risk of iron overload from the regular trasnfusions. Excess iron will be deposited in various organs e.g. the liver and spleen and cause fibrosis.

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71
Q

What is the significance of parvovirus for someone with sickle cell disease?

A

Parvovirus is a common infection in children. It leads to decreased RBC production and can cause a dramatic drop in Hb in patients who already have a reduced RBC lifespan. This can be dangerous for someone with sickle cell.

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72
Q

Describe the inheritance pattern for membranopathies.

A

Autosomal dominant.

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73
Q

Name 2 common membranopathies.

A
  1. Spherocytosis.

2. Elliptocytosis.

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74
Q

Briefly describe the physiology of membranopathies.

A

Deficiency of red cell membrane proteins caused by genetic lesions

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75
Q

What are enzymopathies?

A

Enzyme deficiencies lead to shortened RBC lifespan.

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76
Q

Name a common enzymopathy.

A

G6PD deficiency.

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77
Q

Give 3 signs of G6PD deficiency.

A

Crises characterised by:

  1. Haemolysis.
  2. Jaundice.
  3. Anaemia.
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78
Q

What is anaemia?

A

A decrease in the amount of Hb in the blood below the reference range.

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79
Q

What is the function of Hb?

A

It carries and delivers oxygen to tissues.

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80
Q

What organs are responsible for removal of RBC’s?

A
  1. Spleen.
  2. Liver.
  3. Bone marrow.
  4. Blood loss.
81
Q

Give 3 causes of microcytic anaemia.

A
  1. Iron deficiency.
  2. Anaemia of chronic disease.
  3. Thalassaemia.
82
Q

Give 3 causes of normocytic anaemia.

A
  1. Acute blood loss.
  2. Anaemia of chronic disease.
  3. Combined hematinic deficiency.
83
Q

Give 3 causes of macrocytic anaemia.

A
  1. B12/folate deficiency.
  2. Alcohol excess/liver disease.
  3. Hypothyroid.
84
Q

Where is B12 absorbed?

A

The terminal ileum.

85
Q

Explain how pernicious anaemia leads to B12 deficiency.

A

Pernicious anaemia leads to a loss of parietal cells -> reduced intrinsic factor production -> vitamin B12 malabsorption.

86
Q

Give 5 causes of iron deficiency.

A
  1. Blood loss.
  2. Poor absorption.
  3. Decreased intake in diet.
  4. Hook worm!
  5. Breastfeeding, low iron in breast milk.
87
Q

Give 3 symptoms of anaemia.

A
  1. Fatigue.
  2. Faintness.
  3. Breathlessness.
  4. Reduced exercise tolerance.
88
Q

What investigations might you do in someone with anaemia?

A
  1. Blood tests: FBC and blood film.
  2. Biopsies.
  3. Reticulocyte count.
  4. B12 levels.
  5. Serum ferritin.
89
Q

What is the treatment for anaemia?

A

Treat the underlying cause e.g. if iron deficient give ferrous sulphate.

90
Q

What is polycythaemia?

A

Too many RBC’s, an increase in Hb.

91
Q

What hormone is responsible for regulating RBC production?

A

Erythropoietin.

92
Q

What stimulates EPO?

A

Tissue hypoxia.

93
Q

Name a primary cause of polycythaemia.

A

Polycythaemia rubra vera - over reactive bone marrow.

94
Q

Give 3 secondary causes of polycythaemia.

A
  1. Heavy smoking.
  2. Lung disease.
  3. Cyanotic heart disease.
  4. High altitude.
95
Q

What is the treatment for polycythaemia?

A
  1. If a secondary cause treat the underlying cause.

2. If a primary cause, treatment aims to maintain a normal blood count and prevent complications e.g. aspirin.

96
Q

What is neutrophilia?

A

Too many neutrophils.

97
Q

Give 3 causes of neutrophilia.

A
  1. Infection.
  2. Inflammation.
  3. CML.
  4. Cancer.
98
Q

What is lymphocytosis?

A

Too many lymphocytes.

99
Q

Give 3 causes of lymphocytosis.

A
  1. Viral infections.
  2. Inflammation.
  3. Malignancy.
  4. CLL.
100
Q

What is thrombocytopenia?

A

Not enough platelets.

101
Q

Give 2 causes of thrombocytopenia.

A
  1. Production failure e.g. marrow suppression, marrow failure.
  2. Increased removal e.g. immune response (ITP), consumption (DIC), splenomegaly.
102
Q

What is thrombocytosis?

A

Too many platelets.

103
Q

What is neutropenia?

A

Not enough neutrophils.

104
Q

What is the major risk associated with being neutropenic?

A

Susceptible to infection.

105
Q

Give 3 causes of neutropenia.

A
  1. Marrow failure.
  2. Marrow infiltration.
  3. Marrow toxicity.
106
Q

Where are platelets produced?

A

In the bone marrow. They are fragments of megakaryocytes.

107
Q

What hormone regulates platelet production?

A

Thrombopoietin - produced mainly in the liver.

108
Q

What is the lifespan of a a platelet?

A

7 - 10 days.

109
Q

What organ is responsible for platelet removal?

A

The spleen.

110
Q

What can cause platelet dysfunction.

A
  1. Reduced platelet number (thrombocyotpenia).

2. Reduced platelet function.

111
Q

Platelet dysfunction: what can cause decreased platelet production?

A
  1. Congenital causes e.g. malfunctioning megakaryocytes.
  2. Infiltration of bone marrow e.g. leukaemia.
  3. Alcohol.
  4. Infection e.g. HIV/TB.
112
Q

Platelet dysfunction: what can cause increased platelet destruction?

A
  1. Autoimmune e.g. ITP.
  2. Hypersplenism.
  3. Drug related e.g. heparin induced.
  4. DIC and TTP -> increased consumption.
113
Q

Platelet dysfunction: what can cause reduced platelet function?

A
  1. Congenital abnormality.
  2. Medication e.g. aspirin.
  3. VWF disease.
  4. Uraemia.
114
Q

Give 3 symptoms of platelet dysfunction.

A
  1. Mucosal bleeding.
  2. Easy bruising.
  3. Petechiae/purpura.
115
Q

Give 4 causes of bleeding.

A
  1. Trauma.
  2. Platelet deficiency e.g. thrombocytopenia.
  3. Platelet dysfunction e.g. aspirin induced.
  4. Vascular disorders.
116
Q

What is the definition of febrile neutropenia.

A

Temperature >38°C in a patient with neutrophil count <1x10^9/L.

117
Q

Give 4 risk factors for febrile neutropenia.

A
  1. If the patient had chemotherapy <6 weeks ago.
  2. Any patient who has had a stem cell transplant <1 year ago.
  3. Any haematological condition causing neutropenia.
  4. Bone marrow infiltration.
118
Q

What is the presentation of febrile neutropenia?

A
  1. Pyrexia, 38°C.
  2. Generally unwell.
  3. Confusion.
  4. Hypotensive.
  5. Tachycardic.
119
Q

Describe the management of febrile neutropenia.

A
  1. Thorough history and examination.
  2. Bloods.
  3. Antibiotics within 1 hour!
120
Q

Give a risk factor for spinal cord compression.

A

Any malignancy that can cause compression e.g. bone metastasis.

121
Q

Describe the presentation of spinal cord compression.

A
  1. Back pain.
  2. Weakness in legs.
  3. Inability to control bladder.
  4. Spastic paresis.
  5. Sensory level.
122
Q

Describe the management of spinal cord compression.

A
  1. Bed rest.
  2. High dose steroids.
  3. Analgesia.
  4. Urgent MRI of the whole spine.
123
Q

What is tumour lysis syndrome?

A

Break down of malignant cells -> content release -> metabolic disturbances; can cause hyperuricaemia, hyperkalaemia, hypocalcaemia.

124
Q

Give 3 risk factors for tumour lysis syndrome.

A
  1. High tumour burden.
  2. Pre-existing renal failure.
  3. Increasing age.
125
Q

Describe the treatment of tumour lysis syndrome.

A
  1. Aggressive hydration.
  2. Monitor electrolytes.
  3. Drugs to reduce uric acid production e.g. allopurinol.
126
Q

What is hyperviscosity syndrome?

A

Increase in blood viscosity usually due to high levels of immunoglobulins.

127
Q

Give 2 consequences of hyperviscosity syndrome.

A
  1. Vascular stasis.

2. Hypoperfusion.

128
Q

Describe the presentation of hyperviscosity syndrome.

A
  1. Mucosal bleeding.
  2. Visual change.
  3. Neurological disturbances.
  4. Breathlessness.
  5. Fatigue.
129
Q

What investigations might you do in someone who you suspect has hyperviscosity syndrome?

A
  1. FBC and blood film; look for rouleaux formation.
  2. U&E.
  3. Immunoglobulins.
130
Q

What is the treatment for hyperviscosity syndrome?

A
  1. Keep hydrated!
  2. Avoid blood transfusion.
  3. Treat the underlying cause.
131
Q

Give 5 signs/symptoms of hypercalcaemia.

A
  1. Confusion.
  2. Bone pain.
  3. Constipation.
  4. Nausea.
  5. Abdominal pain.
132
Q

What might you see in the ECG taken from someone with hypercalcaemia.

A

Shortened QT interval.

Hypercalcaemia = risk of MI.

133
Q

What is the treatment for hypercalcaemia?

A

IV hydration and bisphosphonates.

134
Q

What does rituximab target?

A

Targets CD20 on the surface of B.

135
Q

What is the characteristic genetic abnormality in chronic myeloid leukaemia?

A

t(9; 22) - philadelphia chromosome.

136
Q

How is myeloma bone disease usually assessed?

A

X-ray.

137
Q

What is the commonest cause of microcytic anaemia?

A

Iron deficiency.

138
Q

What is the affect of sickle cell anaemia on reticulocyte count?

A

Reticulocyte count is raised.

139
Q

Why is reticulocyte count raised in sickle cell anaemia?

A

Sickle cell disease is haemolytic, there is increased degradation of RBC’s. Production therefore increases in order to keep up with degradation and so reticulocyte count is raised.

140
Q

What clotting factors depend on vitamin K?

A

2, 7, 9 and 10.

141
Q

Haemophilia A is due to deficiency of what clotting factor?

A

Factor 8 deficiency.

142
Q

Haemophilia B is due to deficiency of what clotting factor?

A

Factor 9 deficiency.

143
Q

Give 4 symptoms of ALL.

A
  1. Bone pain.
  2. Recurrent infections (neutropenia).
  3. Pale and tired (anaemia).
  4. Bruising (low platelets).
144
Q

Is ALL more common in adults or children?

A

ALL is mainly a childhood disease.

145
Q

What kind of anaemia could methotrexate cause?

A

Macrocytic due to folate deficiency.

146
Q

Give 4 causes of folate deficiency.

A
  1. Dietary.
  2. Malabsorption.
  3. Increased requirement e.g. in pregnancy.
  4. Folate antagonists e.g. methotrexate.
147
Q

Give 3 signs of haemolytic anaemia.

A
  1. Pallor.
  2. Jaundice.
  3. Splenomegaly.
148
Q

Give 4 causes of haemolytic anaemia.

A
  1. GP6D deficiency.
  2. Sickle cell anaemia.
  3. Spherocytosis/elliptocytosis (membranopathies).
  4. Autoimmune haemolytic anaemia.
149
Q

Give 3 things that can cause coagulation disorders.

A
  1. Vitamin K deficiency.
  2. Liver disease.
  3. Congenital e.g. haemophilia.
150
Q

How does warfarin work?

A

It antagonises vitamin K and so you get a reduction in clotting factors 2, 7, 9 and 10.

151
Q

How does heparin work?

A

It activates antithrombin which then inhibits thrombin and factor Xa.

152
Q

What is disseminated intravascular coagulation (DIC)?

A

Pathological activation of the coagulation cascade -> fibrin in vessel walls. There is platelet (thrombocytopenia) and coagulation factor consumption.

153
Q

Give 3 causes of disseminated intravascular coagulation (DIC).

A
  1. Sepsis.
  2. Major trauma.
  3. Malignancy.
154
Q

What is the affect on TT, PTT and APTT in someone with disseminated intravascular coagulation (DIC)?

A

All increased.

155
Q

What is the affect on fibrinogen in someone with disseminated intravascular coagulation (DIC)?

A

Decreased.

156
Q

Give 5 risk factors for DVT.

A
  1. Increasing age.
  2. Obesity.
  3. Pregnancy.
  4. OCP (hyper-coagulability).
  5. Major surgery.
  6. Immobility.
  7. Past DVT.
157
Q

Give 3 symptoms of DVT.

A

Unilateral warm, tender, painful, swollen leg.

158
Q

What forms the differential diagnosis for a DVT?

A

Cellulitis.

159
Q

What investigations might you do in someone to see if they have a DVT?

A
  1. D-dimer in those patients with a low clinical probability.
  2. US compression.
160
Q

What is the name of the score used to determine someones probability of having a DVT?

A

The Wells score.

161
Q

The Wells score determines someones clinical probability of having a DVT. Give 3 factors the score takes into account.

A
  1. Active cancer.
  2. Recently bedridden or major surgery.
  3. Tenderness along deep venous system.
  4. Swollen leg/calf.
  5. Unilateral pitting oedema.
162
Q

Describe the management for a DVT.

A

Aim of management is to prevent a PE!

- Anticoagulants e.g. warfarin/heparin.

163
Q

Explain why philadelphia chromosome causes CML.

A

Philadelphia chromosome leads to a fusion gene that has tyrosine kinase activity and enhanced phosphorylating activity -> altered cell growth.

164
Q

Where would you normally take a bone marrow biopsy from?

A

Posterior iliac crest.

165
Q

What is the most important medical treatment for DVT prophylaxis?

A

LMWH.

166
Q

What is the affect of iron deficiency anaemia on iron binding capacity?

A

Iron binding capacity will be raised.

167
Q

Why might measuring serum ferritin be inaccurate for looking at iron levels?

A

Ferritin is an acute phase protein and so its concentration will increase in response to inflammation.

168
Q

Describe the treatment for iron deficiency anaemia.

A

Ferrous sulphate tablets.

169
Q

What is aplastic anaemia?

A

When bone marrow stem cells are damaged -> pancytopenia.

170
Q

Give 3 symptoms of iron-deficiency anaemia.

A
  1. Koilonychia.
  2. Brittle hair and nails.
  3. Atrophic glossitis.
  4. Tiredness, reduced exercise tolerance.
  5. SOB.
171
Q

What is the difference between Raynaud’s disease and Raynaud’s phenomenon?

A

Raynaud’s disease is idiopathic.

Raynaud’s phenomenon can be due to SLE, scleroderma, RA, drugs e.g. beta blockers.

172
Q

Describe the pathophysiological mechanism behind Raynaud’s disease.

A

Peripheral digital ischaemia due to intermittent spasm in arteries that supply the fingers/toes. Precipitated by cold/stress.

173
Q

Describe the colour changes that are seen in Raynaud’s.

A
  • Pale - due to vasoconstriction.
  • Cyanotic - due to deoxygenation.
  • Red - due to hyperaemia.
174
Q

Describe the treatment for Raynaud’s disease.

A
  1. Physical protection.
  2. Vasodilators.
  3. Nifedipine (CCB).
  4. Stop smoking.
175
Q

State two features with regards to red blood cell appearance that would make you think a patient had anaemia due to iron deficiency.

A
  1. Hypochromia (pale).

2. Microcytosis.

176
Q

Suggest 3 ways in which multiple myeloma can lead to AKI.

A
  1. Deposition of light chain.
  2. Hypercalcaemia.
  3. Hyperuricaemia.
177
Q

In extreme cases, patients with myeloma can present with blurred vision, gangrene and bleeding. What is the pathology behind this?

A

Paraproteins form aggregates in the blood and change the viscosity.

178
Q

Why are patients with myeloma susceptible to recurrent infections?

A

There is a reduction in polyclonal immunoglobulin levels.

179
Q

What kind of anaemia is seen in patients with multiple myeloma?

A

Normochromic normocytic.

180
Q

What chemotherapy regime is used in patients with myeloma?

A

VAD or CTD.

181
Q

What combination chemotherapy regime is commonly used in patients with non hodgkin’s lymphoma?

A

RCHOP.

182
Q

Give 3 environmental causes of leukaemia.

A
  1. Radiation exposure.
  2. Chemicals e.g. benzene compounds.
  3. Drugs.
183
Q

Give 3 signs of anaemia.

A
  1. Pale skin and mucous membranes.
  2. Tachycardia.
  3. Bounding pulse.
184
Q

Describe the appearance of RBC’s seen in iron deficiency anaemia.

A

Hypochromic microcytic.

185
Q

What might you see on a blood count taken from someone with beta thalassaemia major?

A
  1. Raised reticulocyte count.

2. Microcytic anaemia.

186
Q

What can precipitate sickling in sickle cell anaemia?

A

Trauma, cold, stress, exercise.

187
Q

Why does sickle cell anaemia not present until after 6 months of age?

A

HbF is not affected by sickle cell anaemia as it is made up of 2 alpha and 2 gamma chains.

188
Q

What drug can be used to prevent painful crises in people with sickle cell anaemia?

A

Hydroxycarbamide.

189
Q

Give 3 clinical features of a patient with a membranopathy.

A
  1. Jaundice.
  2. Anaemia.
  3. Splenomegaly.
190
Q

Why does a deficiency in glucose-6-phosphate dehydrogenase lead to shortened red cell lifespan?

A

G6PD protects cells against oxidative damage.

191
Q

What 3 blood test values would be increased in someone with polycythaemia?

A
  1. Hb.
  2. RCC.
  3. PCV.
192
Q

Give 3 symptoms of polycythaemia.

A
  1. Itching.
  2. Headache.
  3. Dizziness.
  4. Visual disturbance.
193
Q

What can cause ITP?

A
  1. Viral infection.

2. Malignancy.

194
Q

What antibodies are often found in ITP?

A

IgG.

195
Q

Are PTT and APTT increased or decreased in DIC?

A

Increased.

196
Q

Are fibrinogen and platelets increased or decreased in DIC?

A

Decreased.

197
Q

Name 2 things that are increased and 2 that are decreased in DIC.

A

Increased: PTT and APTT.

Decreased: fibrinogen and platelets.

198
Q

How would you treat haemophilia A?

A

IV infusion of factor 8.

2a Medicine (11 decks)

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