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Haematology Flashcards

1
Q

Where are blood cells made and developed?

A

Bone marrow-> mostly in pelvis, ribs, sternum and vertebrae

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2
Q

What are pluripotent haematopoetic stem cells?

A
  • Undifferentiated cells

- Can transform to myeloid stem cells, lymphoid stem cells and dentritic cells

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3
Q

How are RBCs developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> reticulocytes-> RBCs

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4
Q

How are platelets developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> magakarocytes-> platelets

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5
Q

How are macrophages developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> promyelocytes-> monocytes-> macrophages

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6
Q

How are neutrophils developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> promyelocytes-> neutrophils

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7
Q

How are eosinophils developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> promyelocytes-> Eosinophils

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8
Q

How are basophils developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> promyelocytes-> basophils

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9
Q

How are mast cells developed?

A

Pluripotent haematopoetic stem cells-> myeloid stem cells-> promyelocytes-> mast cells

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10
Q

How are plasma and memory B cells developed?

A

Pluripotent haematopoetic stem cells-> lymphoid stem cells-> lymphocytes-> B cells (mature in bone marrow)-> plasma + memory B cells

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11
Q

How are CD4 (helper), CD8 (cytotoxic) and natural killer T-cells developed?

A

Pluripotent haematopoetic stem cells-> lymphoid stem cells-> lymphocytes-> T cells (mature in thymus)-> CD4 (helper) + CD8 (cytotoxic) + natural killer

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12
Q

What are the different types of B cells?

A
  • Plasma cells

- Memory B cells

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13
Q

What are the different types of T-cells?

A
  • CD4 (helper)
  • CD8 (cytotoxic)
  • Natural killer T cells
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14
Q

What do blood films show?

A

Shape, size and contents of blood cells

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15
Q

What is anisocytosis on a blood film and what might it indicate?

A
  • Variation in RBC size

- Myelodysplastic syndrome + some anaemias

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16
Q

What are target cells on a blood film and what might it indicate?

A
  • Central pigmented RBCs

- Iron deficiency anaemia + post-splenectomy

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17
Q

What are Heinz-bodies on a blood film and what might it indicate?

A
  • Blobs in RBCs due to denatured globin

- G6PD + alpha-thalassaemia

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18
Q

What are Howell-Jolly bodies on a blood film and what might it indicate?

A
  • Blobs of DNA in RBCs

- Post-splenectomy + in severe anaemia

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19
Q

What are reticulocytes on a blood film and what might it indicate?

A
  • Immature + large RBCs containing RNA, look mesh-like
  • > 1% is abnormal
  • Indicates rapid turnover
  • Eg haemolytic anaemia
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20
Q

What are schistocytes on a blood film and what might it indicate?

A
  • Fragments of RBCs from trauma

- Haemolytic uraemic syndrome, DIC, TTP, metallic heart valves, haemolytic anaemia

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21
Q

What are sideroblasts on a blood film and what might it indicate?

A
  • Immature RBCs + iron-> when unable to incorporate iron into Hb
  • Myelodysplastic syndrome
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22
Q

What are smudge cells on a blood film and what might it indicate?

A
  • Ruptured + fragile WBCs

- CLL

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23
Q

What are spherocytes on a blood film and what might it indicate?

A
  • Spherical RBCs

- AI haemolytic anaemia or hereditary spherocytosis

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24
Q

What is the definition of anaemia?

A

Low levels of Hb due to underlying disease

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25
Q

What is the normal range of Hb for women?

A

120-165g/L

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26
Q

What is the normal range of Hb for men?

A

130-180g/L

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27
Q

What is the normal range of MCV?

A

80-100fl

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28
Q

What can cause microcytic anaemia?

A

TAILS-> thalassaemia, anaemia of chronic disease, iron deficiency, lead poisoning, sideroblastic

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29
Q

What can cause normocytic anaemia?

A

3A’s + 2H’s-> acute blood loss, anaemia of chronic disease, aplastic, haemolytic, hypothyroid

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30
Q

What can cause macrocytic megaloblastic anaemia?

A

Impaired DNA synthesis (not divide normally), B12/folate deficiency

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31
Q

What can cause macrocytic normoblastic anaemia?

A

Alcohol, reticulocytosis (haemolytic, blood loss etc), hypothyroid, liver disease, azathioprine

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32
Q

What are the symptoms of anaemia (in general)?

A

Tired, SOB, headaches, dizziness, palpitations, worsening of angina/HF/PVD

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33
Q

What are the symptoms of iron-deficiency anaemia

A

Tired, SOB, headaches, dizziness, palpitations, worsening of angina/HF/PVD, pica, hair loss

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34
Q

What are the signs of anaemia (in general)?

A

Pale, conjunctival pallor, tachycardia, tachypnoea

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35
Q

What are the signs of anaemia (iron deficiency)?

A

Pale, conjunctival pallor, tachycardia, tachypnoea, koilonychia, angular chelitis, atophic glossitis

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36
Q

What are the signs of anaemia (haemolytic)?

A

Pale, conjunctival pallor, tachycardia, tachypnoea, jaundice

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37
Q

What are the signs of anaemia (due to thalassaemia)?

A

Pale, conjunctival pallor, tachycardia, tachypnoea, bone deformity

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38
Q

What are the signs of anaemia (due to CKD)?

A

Pale, conjunctival pallor, tachycardia, tachypnoea, oedema, HTN, excoriations on skin

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39
Q

How migth anaemia be investigated?

A
  • Bloods-> Hb, MCV, B12, folate, ferritin, blood film
  • OGD + colonoscopy-> if unexplained (urgent GI cancer referral)
  • Bone marrow biopsy-> if cause unclear
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40
Q

What are the causes of iron deficiency anaemia?

A
  • Diet-> common in kids
  • Pregnancy-> requirements increased
  • Loss-> bleed eg GI cancer, oesophagitis, menstruation/menorrhagia, gastritis, IBD
  • Inadequate absorption-> inflammatory, coeliac, IBD, PPIs
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41
Q

How is iron absorbed?

A
  • Mainly duodenum and jejunum
  • Stomach acids keeps soluble in form of ferrous Fe2+
  • Stomach acid drops-> insoluble ferric Fe3+
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42
Q

How can PPis affect iron absorption?

A
  • Mainly duodenum and jejunum
  • Stomach acids keeps soluble in form of ferrous Fe2+-> absorbed
  • Stomach acid drops due to PPI-> insoluble ferric Fe3+
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43
Q

What is transferrin?

A

Carrier protein-> carries Fe3+ in blood

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44
Q

What is total iron binding capacity?

A
  • Blood test related to amount of transferrin in blood

- Measures space on transferrin for iron binding

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45
Q

How is transferrin saturation measured?

A
  • Serum iron / total iron binding capacity
  • Good indicator of total iron
  • Less iron = less saturated eg deficiency
  • High-> overload
  • Better after fasting
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46
Q

What is ferritin and what can measuring it help with?

A
  • Protein in the blood that stores iron
  • High-> can indicate inflammation
  • Low-> iron deficiency
  • Normal-> may still have deficiency
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47
Q

When does serum iron normally increase?

A
  • In the morning

- After food

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48
Q

What does a raised total iron binding capacity mean?

A
  • Iron overload
  • iron supplements
  • Acute liver damage
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49
Q

What does a decreased total iron binding capacity mean?

A

Iron deficiency

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50
Q

What is a normal serum ferritin level?

A

41-400ug/L

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51
Q

What is a normal serum iron level?

A

12-30umol/L

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52
Q

What is a normal total iron binding capacity level?

A

45-80umol/L

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53
Q

What is a normal transferrin saturaton?

A

15-50%

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54
Q

How is iron deficiency anaemia managed?

A
  • Investigate when no clear cause-> OGD + colonoscopy
  • Blood transfusion to correct anaemia
  • Iron infusion (eg cosmofer)-> avoid in sepsis as feeds bacteria
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55
Q

What is pernicious anaemia?

A
  • A cause of B12 deficiency anaemia
  • Autoimmune attack of stomach’s parietal cells-> stop production of intrinsic factor protein (used for vitB12 absorption)-> lack of absorption
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56
Q

What are the symptoms of pernicious anaemia?

A

Peripheral neuropathy, loss of vibration/proprioception, vision, mood/cognition problems

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57
Q

What is important to test for in someone presenting with pins + needles?

A

B12 deficiency and pernicious anaemia

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58
Q

What investigations are done for pernicious anaemia?

A
  • Intrinsic factor auto-antibody

- Gastric parietal cell antibody

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59
Q

How is pernicious anaemia managed?

A
  • Cyanocobalamin-> B12 oral replacement
  • Hydroxycobalamin-> IM B12, eg 3x weekly for 2 weeks then every 3 months
  • Should treat B12 deficiency before folate if present-> risk of subacute degeneration of spinal cord
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60
Q

Why is it important to correct B12 deficiency before folate deficiency if both are present?

A

risk of subacute degeneration of spinal cord

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61
Q

What is haemolytic anaemia?

A

Destruction of RBCs (haemolysis) leading to anaemia

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62
Q

What are the inherited causes of haemolytic anaemia?

A

RBCs more fragile + break down faster

  • Hereditary spherocytosis
  • Hereditary eppiltocytosis
  • Thalassaemia
  • Sickle cell
  • G6PD deficiency
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63
Q

What are the acquired causes of haemolytic anaemia?

A

Increased breakdown of RBCs

  • AI haemolytic anaemia
  • Alloimmune-> transfusion, of newborn
  • Paroxysmal nocturnal haemoglobinuria
  • Microangiopathic
  • Prosthetic valve related
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64
Q

What are the features of haemolytic anaemia?

A
  • Splenomegaly-> full of destroyed RBCs

- Jaundice-> bilirubin released when RBCs die

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65
Q

What are the investigations for haemolytic anaemia?

A
  • FBC-> normocytic anaemia
  • Blood film-> schistocytes
  • Direct Coombs test-> +ve in autoimmune
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66
Q

When will a Direct Coomb’s test be positive?

A

Autoimmune haemolytic anaemia

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67
Q

What is hereditary spherocytosis?

A
  • Autosomal dominant

- RBCs spherical + break down easily when pass through spleen

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68
Q

How does hereditary spherocytosis present?

A

Jaundice, gallstones, splenomegaly, aplastic crisis (triggered by parvovirus)

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69
Q

How is hereditary spherocytosis investigated?

A
  • Clinical + family history
  • Blood film-> spherocytes
  • Raised reticulocytes-> rapid turnover
  • High MCHC
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70
Q

How is hereditary spherocytosis managed?

A
  • Folate supplement
  • Splenectomy
  • May need cholecystectomy
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71
Q

What is hereditary elliptocytosis?

A
  • Autosomal dominant

- RBCs elliptical + break down easily when pass through spleen

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72
Q

How does hereditary elliptocytosis present?

A

Jaundice, gallstones, splenomegaly, aplastic crisis (triggered by parvovirus)

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73
Q

How is hereditary elliptocytosis managed?

A
  • Folate supplement
  • Splenectomy
  • May need cholecystectomy
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74
Q

What is G6PD deficiency?

A
  • X-linked recessive condition
  • Defect in enzyme in RBCs
  • More common in Mediterranean and African population
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75
Q

How does G6PD deficiency present?

A
  • Neonatal jaundice
  • Gallstones
  • Anaemia
  • Splenomegaly
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76
Q

How is G6PD deficiency diagnosed?

A
  • Blood film-> Heinz bodies

- G6PD enzyme assay

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77
Q

What might trigger symptoms in G6PD deficiency?

A

Infections, medications, fava/broad beans, primaquine, ciprofloxacin, sulfasalazine, sulphonylureas

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78
Q

What is warm type autoimmune haemolytic anaemia?

A
  • More common type
  • Antibodies against RBCs lead to destruction
  • Haemolysis at normal/high temps
  • Idiopathic
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79
Q

What is cold type autoimmune haemolytic anaemia?

A
  • Antibodies and RBCs attach together (agglutination) in cold temps-> get destroyed in spleen
  • Often secondary to lymphoma, leukaemia, SLE or infection (HIV, EBV, CMV etc)
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80
Q

How is autoimmune haemolytic anaemia managed?

A

Transfusions, prednisolone, rituximab (against B cells), splenectomy

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81
Q

What is alloimmune haemolytic anaemia?

A
  • Foreign RBCs in blood cause immune reaction + destruction

- Or-> foreign antibodies in blood act against own RBCs

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82
Q

What is haemolytic transfusion reaction?

A
  • Antibodies produced to antigens after transfusion

- Type of alloimmune haemolytic anaemia

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83
Q

What is haemolytic disease of the newborn?

A
  • Antibodies from mother to foetus via placenta

- Type of alloimmune haemolytic anaemia

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84
Q

What is paroxysmal nocturnal haemoglobulinaemia?

A
  • Rare genetic mutation that happens during lifetime

- Loss of proteins on RBC-> activates complement cascade against RBCs-> destroyed

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85
Q

How does paroxysmal nocturnal haemoglobulinaemia present?

A
  • Red urine in morning
  • Anaemia
  • Thrombosis (VTE)
  • Smooth muscle dystonia eg erectile dysfunction
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86
Q

How is paroxysmal nocturnal haemoglobulinaemia managed?

A
  • Eculizumab

- Bone marrow transplant

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87
Q

What is microangiopathic haemolytic anaemia (MAHA)?

A

Structural abnormalities of small BVs cause haemolysis of RBCs when pass through

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88
Q

What causes microangiopathic haemolytic anaemia (MAHA)?

A
  • HUS
  • DIC
  • TTP
  • SLE
  • Cancer
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89
Q

What causes prosthetic valve haemolysis?

A

Turbulence around valve + collision of RBCs-> churned up + broken

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90
Q

How is prosthetic valve haemolysis managed?

A

Monitoring, oral iron, transfusion if severe, revision surgery if needed

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91
Q

What is thalassaemia?

A
  • Autosomal recessive
  • Genetic defect in protein chains that make up Hb
  • Can be alpha or beta
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92
Q

What is the pathophysiology of the signs ofthalassaemia?

A
  • Genetic defect in protein chains making up Hb
  • RBCs more fragile + break down-> spleen collects destroyed RBCs-> splenomegaly
  • Bone marrow expands to produce more RBCs-> fractures, pronounced forehead + malar eminences (cheekbones)
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93
Q

What are the signs and symptoms of thalassaemia??

A

Microcytic anaemia, fatigue, pallor, jaundice, gallstones, splenomegaly, poor growth + development, forehead + cheekbone prominence

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94
Q

How is thalassaemia diagnosed?

A
  • FBC-> microcytic anaemia
  • Hb electrophoresis-> globin abnormalities
  • DNA testing
  • Screened for in pregnancy
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95
Q

What causes iron overload in thalassaemia?

A

Faulty RBCs-> recurrent transfusions-> increased absorption in response to anaemia

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96
Q

What are the symptoms of iron overload in thalassaemia?

A

Fatigue, cirrhosis, infertility, impotence, HF, arthritis, DM, osteoporosis

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97
Q

How is iron overload in thalassaemia managed?

A
  • Limit transfusions

- Iron chelation

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98
Q

What causes alpha-thalassaemia?

A
  • Gene on chromosome 16

- Defect in alpha-chains of Hb

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99
Q

How is alpha-thalassaemia managed?

A
  • Monitor FBC + complications
  • transfusions
  • Splenectomy
  • Bone marrow transplant
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100
Q

What is beta-thalassaemia?

A
  • Defect in beta-chains of Hb

- Chromosome 11

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101
Q

What are the types of beta-thalassaemia?

A
  • thalassaemia minor
  • thalassaemia intermedia
  • thalassaemia major
102
Q

What is thalassaemia minor?

A
  • Beta-thalassaemia
  • Carrier-> 1 normal + 1 abnormal gene
  • Mild microcytic anaemia
103
Q

What is thalassaemia intermedia?

A
  • Beta-thalassaemia
  • 2 abnormal genes-> 2 defective or 1 defective + 1 deletion
  • Significant anaemia
  • May need transfusions + iron chelation
104
Q

What is thalassaemia major?

A
  • Beta-thalassaemia

- Homozygous for deletion-> no beta-Hb

105
Q

How does thalassaemia major present?

A
  • Severe anaemia
  • FTT
  • Splenomegaly
  • Bone deformity
106
Q

How is thalassaemia major managed?

A

Transfusions, splenectomy, bone marrow transplant

107
Q

What is sickle cell anaemia?

A

Autosomal recessive genetic condition causing crescent shaped RBCs-> fragile + easy destroyed (haemolytic anaemia)

108
Q

What is the pathophysiology of sickle cell anaemia?

A
  • Abnormal beta-Hb gene on chromosome 11-> HbS
  • 1 copy-> sickle cell trait
  • 2 copies-> sickle cell disease
109
Q

What effect does having sickle cell have on malaria?

A
  • Sickle cell trait (1 HbS)-> reduced severity of malaria
  • More likely to survive and pass on genes-> selective advantage
  • High proportion of areas with malaria have SCD
110
Q

How is sickle cell disease diagnosed?

A
  • During pregnancy when high risk of carrier

- Newborn screening heelprick test

111
Q

What are the complications of sickle cell disease?

A

Anaemia, infection, stroke, avascular necrosis (eg of hip), pulmonary HTN, priapism, CKD, SC crisis, acute chest syndrome

112
Q

How is sickle cell disease generally managed?

A
  • Avoid triggers + dehydration
  • Up to date on vaccines
  • Antibiotic prophylaxis-> penicillin V
  • Hydroxycarbamide-> stimulate HbF production (doesn’t sickle)
  • Transfusion
  • Bone marrow transplant
113
Q

What is sickle cell crisis?

A
  • Spectrum of mild to life-threatening acute crises

- Spontaneous or triggered by infection, stress, cold, dehydration

114
Q

How is sickle cell crisis managed?

A
  • Supportive
  • Low threshold for admission
  • Analgesia-> avoid NSAIDs if renal impairment
  • Fluids
115
Q

What is painful crisis (in sickle cell disease)?

A
  • Vaso-occlusive crisis
  • Sickle cells clog capillaries-> distal ischaemia
  • Associated with dehydration
116
Q

What are the symptoms of painful crisis (in sickle cell disease)?

A

Pain, fever, infection, priapism (may need aspiration)

117
Q

What is splenic sequestration crisis (in sickle cell disease)?

A
  • RBCs block blood flow in spleen-> pools

- Severe anaemia + hypovolaemic shock

118
Q

How is splenic sequestration crisis (in sickle cell disease) managed?

A
  • Supportive
  • Transfusions
  • Splenectomy-> prevention + in recurrent
119
Q

What is aplastic crisis (in sickle cell disease)?

A
  • Temporary loss of new RBC creation

- Usually due to parvovirus B19

120
Q

How is aplastic crisis (sickle cell disease) managed?

A
  • Oftens resolves in a week
  • Supportive
  • Transfusion
121
Q

What is acute chest syndrome (in sickle cell disease)?

A
  • Medical emergency with high mortality

- Causes-> pneumonia, bronchiolitis, pulmonary vaso-occulsion, fat emboli

122
Q

How is acute chest syndrome (in sickle cell disease) managed?

A

Treating underlying cause

  • Antibiotics
  • Antivirals
  • Transfusions
  • Incentive spirometry-> encourage breathing
  • NIV or intubation
123
Q

What are the features of acute chest syndrome (in sickle cell disease)?

A

Fever/respiratory symptoms + new infiltrates on CXR

124
Q

What is leukaemia?

A

Cancer of particular line of stem cells in bone marrow causing unregulated cell production

125
Q

What are the main types of leukaemia?

A
  • Acute myeloid (AML)
  • Acute lymphoblastic (ALL)
  • Chronic myeloid (CML)
  • Chronic lymphocytic (CLL)
126
Q

What is the pathophysiology of leukaemia?

A
  • Genetic mutation in precursor cells in bone marrow
  • Excess production of single type of abnormal WBCs
  • Suppresses all cell lines-> pancytopaenia (anaemia, leukopaenia, thrombocytopaenia)
127
Q

What is a way to remember the ages in which patients get the different types of leukaemia?

A

ALL CeLLmates have CoMmon Ambitions

  • ALL-> <5s and >45
  • CLL-> >55s
  • CML-> >65s
  • AML-> >75s
128
Q

At what age to patients usually get ALL and what might it be associated with?

A
  • <5 or >45

- Common in Down’s sydrome

129
Q

At what age to patients usually get CLL?

130
Q

At what age to patients usually get CML?

131
Q

At what age to patients usually get AML?

132
Q

How does leukaemia typically present?

A

Fatigue, fever, FTT, pallor, petechiae, abnormal bruising + bleeding, lymphadenopathy, hepatosplenomegaly

133
Q

What are the differentials of petechiae?

A

Bleeding under skin due to low platelets

  • Leukaemia
  • Meningococcal septicaemia
  • Vasculitis
  • HSP
  • ITP
  • Non-accidental injury
134
Q

How is leukaemia investigated?

A
  • Bone marrow biopsy-> main investigation, aspiration/trephine etc
  • FBC within 48 hours if suspect
  • Immediate admission-> petechiae or hepatosplenomegaly
  • Blood film-> abnormal cells + inclusions
  • Lactate deydrogenase (LDH)-> raised but not specific
  • CXR-> infection, mediastinal LNopathy
  • LN biopsy-> assess for involvement + lymphoma
  • LP-> CNS involvement
  • CT/MRI/PET-> staging
135
Q

What are the different types of bone marrow biopsy used in leukaemia?

A
  • Aspiration-> liquid sample full of cells
  • Trephine-> solid core sample but takes few days to prep
  • Biopsy-> from iliac crest with local anaesthetic, can examine straight away
136
Q

What is acute lymphoblastic leukaemia?

A
  • Malignant change in one of lymphocyte precursor cells
  • Usually acute proliferation of B-lymphocytes
  • Replaces other cell types in bone marrow
137
Q

What is the most common cancer in children?

A

acute lymphoblastic leukaemia

138
Q

What are the associations with acute lymphoblastic leukaemia?

A
  • Down’s syndrome
  • Children
  • Blast cells on blood film
  • Philadelphia chromosome (more so CML)
139
Q

What is chronic lymphocytic leukaemia?

A
  • Chronic proliferation of B-cells usually

- Ritcher’s transformation risk-> can become high-grade lymphoma

140
Q

What are the symptoms of chronic lymphocytic leukaemia?

A
  • 55+ and asymptomatic
  • Infection, anaemia, bleeding, weight loss
  • May have warm AI haemolytic anaemia
141
Q

What blood film result is characteristic of chronic lymphocytic leukaemia?

A

Smear/smudge cells-> aged/fragile WBCs that rupture

142
Q

What is Ritcher’s transformation?

A

The transformation of chronic lymphocytic leukaemia to high grade lymphoma

143
Q

What is chronic myeloid leukaemia associated with?

A

Philadelphia chromosome-> translocation of t(9:22)

144
Q

What are the three stages of chronic myeloid leukaemia?

A
  • Chronic
  • Accelerated
  • Blast
145
Q

What is the chronic stage of chronic myeloid leukaemia?

A

Lasts 5 years-> asymptomatic + incidental raised WCC

146
Q

What is the accelerated phase in chronic myeloid leukaemia?

A
  • Abnormal blast cells take up high proportion of blood + BM cells
  • More symptoms + immunocompromise
147
Q

What is the blast phase in chronic myeloid leukaemia?

A
  • High proportion of abnormal cells in blood (>30%)
  • Severe
  • Pancytopaenia
  • Often fatal
148
Q

What is acute myeloid leukaemia?

A
  • Lots of different types
  • Most common leukaemia in adults
  • Can be transformation of myeloproliferative disorder (eg polycythaemia rubra vera or myelofibrosis)
149
Q

What blood film result would you expect in acute myeloid leukaemia?

A
  • High blast cells

- Auer rods in cytoplasm

150
Q

How is leukaemia managed?

A
  • MDT
  • Chemotherapy + steroids
  • Radiotherapy
  • BM transplant
  • Surgery
151
Q

What are the complications of chemotherapy?

A

Failure, stunted growth + development, infection, immunodeficiency, neurotoxicity, infertility, secondary malignancy, cardiotoxicity, tumour lysis syndrome

152
Q

What is tumour lysis syndrome?

A
  • Uric acid released from cells destroyed by chemo
  • Forms crystals in interstitial tissue + kidney tubules
  • AKI
153
Q

How is tumour lysis syndrome managed?

A
  • Allopurinol or rasburicase
  • K+ and phosphate monitoring and treatment
  • Monitor calcium-> high phosphate can have effect
154
Q

What is lymphoma?

A

Group of cancers-> cancerous lymphocytes in lymphatic system and nodes causing lymphadenopathy

155
Q

What is Hodgkin’s lymphoma?

A

Cancerous lymphocyte proliferation

156
Q

At what age groups is Hodgkin’s lymphoma most common?

A

Bimodal distribution-> 20 and 75 years peaks

157
Q

What are the risk factors for Hodgkin’s lymphoma?

A

HIV, EBV, AI disease (RA, sarcoidosis), FH

158
Q

How does Hodgkin’s lymphoma present?

A
  • Enlarged lymph node(s) in neck/axilla/groin
  • Rubbery, non-tender, may be painful when drink alcohol
  • B symptoms-> fever, weight loss, night sweats
  • Non-specific-> itching, cough, SOB, abdominal pain, infection
159
Q

How is Hodgkin’s lymphoma investigation?

A
  • Biopsy-> LNs
  • Reed-Sternberg cells-> abnormal large B cells with multiple nuclei + nucleoli inside, owl appearance
  • LDH-> raised (non-specific)
  • Other-> CT, MRI, PET for diagnosis + staging
160
Q

What are Reed Sternberg cells and when might they be found?

A
  • Lymph node biopsy-> abnormal large B cells with multiple nuclei + nucleoli inside, owl appearance
  • Hodgkin’s lymphoma
161
Q

What staging system is used in Hodgkin’s and Non-Hodgkin’s lymphoma?

A

Ann Arbor-> based on diaphragm

  • 1-> 1 region of lymph nodes
  • 2-> more than 1 region but same side of diaphragm (above or below)
  • 3-> LNs above + below diaphragm
  • 4-> widespread (eg lungs + liver)
162
Q

What is Hodgkin’s lymphoma managed?

A
  • Chemotherapy-> risk of leukaemia + infertility
  • Radiotherapy-> risk of cancers, tissue damage, infertility
  • Usually curative
163
Q

What is Non-Hodgkin lymphoma?

A
  • A group of lymphomas-> cancerous lymphocytes in lymphatic system and nodes causing lymphadenopathy
  • Types-> Burkitt’s, MALT, Diffuse large B-cell lymphoma
164
Q

What are the different types of Non-Hodgkin lymphoma?

A

Burkitt’s, MALT, Diffuse large B-cell lymphoma

165
Q

What is Burkitt’s lymphoma?

A
  • Type of Non-Hodgkin lymphoma

- Associated with EBV, malaria + HIV

166
Q

What is MALT?

A
  • Type of Non-Hodgkin lymphoma
  • Mucosa Associated Lymphoid Tissue
  • Around stomach
  • Associated with H.pylori
167
Q

What is diffuse large B-cell lymphoma?

A
  • Type of Non-Hodgkin lymphoma
  • Rapid-growing painless mass
  • Presents in >65’s
168
Q

What are the risk factors for Non-Hodgkin lymphoma?

A

HIV, EBV, H.pylori, Hepatitis B/C, exposure to pesticides, family history, trichloroethylene chemical

169
Q

How does Non-Hodgkin lymphoma present?

A
  • Enlarged lymph node(s) in neck/axilla/groin
  • Rubbery, non-tender, may be painful when drink alcohol
  • B symptoms-> fever, weight loss, night sweats
  • Non-specific-> itching, cough, SOB, abdominal pain, infection
170
Q

How are Hodgkin lymphoma and non-Hodgkin lymphoma differentiated?

A
  • Biopsy results

- Hodgkin-> Reed Sternberg cells

171
Q

How is non-Hodgkin lymphoma managed?

A
  • Depends on type and staging
  • Watchful waiting
  • Chemo
  • Monoclonal antibodies-> rituximab
  • Radiotherapy
  • Stem cell transplant
172
Q

What is myeloma?

A

Cancer of plasma cells (B-lymphocytes that produce antibodies)-> causes large amount of single antibody type produced

173
Q

What is multiple myeloma?

A

-Myeloma-> cancer of plasma cells (B-lymphocytes that produce antibodies)->
causes large amount of single antibody type produced
-Multiple-> affect many areas of body

174
Q

What is o Monoclonal gammopathy of undetermined significance (MGUS)?

A
  • Excess of one antibody type or components of it without cancer features
  • Often incidental finding
175
Q

What is smouldering myeloma?

A
  • Progression of o Monoclonal gammopathy of undetermined significance (MGUS)
  • Higher levels of antibody/components
  • Premalignant
176
Q

What is the pathophysiology of myeloma?

A
  • Genetic mutation causes rapid multiplication of plasma cells
  • Excess antibodies produced-> 1 of 5 types (GMADE) but usually IgG-> ‘monoclonal paraprotein’
177
Q

What is the normal physiology of antibodies?

A
  • Produced by plasma cells (B-lymphocytes) + found in bone marrow
  • 2 heavy chains + 2 light chains
  • Help immune system fight infection-> target pathogen proteins
178
Q

What are monoclonal paraproteins?

A
  • Single type of antibodies produced by malignant plasma cells in myeloma
  • Ig GMADE
  • Usually IgG
179
Q

What is Bence-Jones protein?

A
  • Subunit of antibodies (light chain)

- In urine of patients with myeloma

180
Q

Why do patients with myeloma get anaemia?

A
  • Cancerous plasma cells invade bone marrow (infiltration)

- Suppress other blood cells from developing-> anaemia, neutropaenia, thrombocytopaenia

181
Q

What is the pathophysiology of myeloma bone disease?

A
  • More bone reabsorbed than constructed as cytokine release from plasma + stromal cells
  • Increased osteoclast and suppressed osteoblast activity
  • Commonly cause patchy (osteolytic) lesions in skull, spine, long bones + ribs
  • Pathological fractures-> vertebral + femur
  • Hypercalcaemia-> increased reabsorption from bone to blood
  • Plasmacytomas-> plasma cell tumours in bone + replace tissue
182
Q

What is the pathophysiology of myeloma renal disease?

A
  • High Ig’s-> block flow through tubules
  • Hypercalcaemia + dehydration-> less function
  • Bisphosphonates for bone disease-> harm kidneys
183
Q

Why do patients’ blood become hyperviscous in myeloma and what problems can this cause?

A
  • More proteins (antibodies, inflammation, fibrinogen)-> more viscous
  • Bruising, bleeding, sight loss, purplish palmar erythema, HF
184
Q

What are the 4 main features of myeloma?

A

CRAB

  • Calcium-> high
  • Renal failure
  • Anaemia-> normocytic normochromic
  • Bone lesions + pain
185
Q

What are the risk factors for developing myeloma?

A

Older, male, black, FH, obesity

186
Q

When should you suspect myeloma?

A

Patient age 60+ with persistent back/bone pain or unexplained fracture

187
Q

What are the investigations for myeloma?

A
  • Initial bloods-> FBC (low WBC), calcium (high), ESR (high), plasma viscosity (high)
  • Serum protein electrophoresis
  • Urine Bence-Jones protein
  • Light chain assay
  • Bone marrow biopsy
  • X-ray-> punched out/lytic lesions, raindrop skull sign
  • Other imaging-> whole body MRI, CT, skeletal survey
188
Q

What is the management of myeloma?

A
  • Usually relapsing remitting course
  • MDT
  • Chemotherapy (+VTE prophylaxis)
  • Stem cell transplant
  • For bones-> bisphosphonates, radiotherapy, surgery (eg fractures), cement augmentation
189
Q

What are the potential complications of myeloma and its treatments?

A

Infection, pain, renal failure, anaemia, hypercalcaemia, peripheral neuropathy, SCC

190
Q

What are myeloprofilerative disorders?

A

Uncontrolled proliferation of single stem cell type + consider as bone marrow cancer

191
Q

What are the three main types of myeloprofilerative disorder?

A
  • Primary myelofibrosis-> haemopoetic stem cells
  • Polycythaemia vera
  • Essential thrombocythaemia-> megakaryocytic cell line
192
Q

What gene mutations cause myeloprofilerative disorders?

A

JAK2, MPL, CALR

193
Q

What can myeloprofilerative disorders progress to?

194
Q

What is the pathophysiology of myelofibrosis?

A
  • Cell line proliferation-> release cytokines especially fibroblast growth factor-> bone fibrosis + replacement with scar tissue-> cell production affected-> anaemia + leucopaenia
  • Haematopoesis in liver + spleen-> extramedullary-> hepatosplenomegaly + portal HTN + SCC
  • Can be due to any of three causes of myeloprofilerative disorders (primary, PRV, essential thrombocythaemia)
195
Q

How do myeloprofilerative disorders present?

A
  • Asymptomatic then systemic-> fatigue, weight loss, night sweats, fever
  • Anaemia, abdominal pain, ascites/varices, bleeding, thrombosis
196
Q

How does polycythaemia vera present?

A
  • Asymptomatic then systemic-> fatigue, weight loss, night sweats, fever
  • Anaemia, abdominal pain, ascites/varices, bleeding, thrombosis
  • Conjunctival plethora (redness), ruddy complextion, splenomegaly
197
Q

How are myeloprofilerative disorders diagnosed?

A
  • -Bone marrow biopsy-> ‘dry’ aspiration, test of choice
  • FBC-> high Hb (PCV), high platelets (thrombocythaemia)
  • Myelofibrosis bloods-> anaemia, high WCCs + platelets (primary), low WCCs + plateleys (secondary)
  • Blood film-> tear-drop RBCs, poikilocytosis (various RBC sizes), blasts (immature RBCs + WBCs)
  • Genetic testing-> JAK2, MPL, CALR
198
Q

What would you expect to see on a blood film for myeloprofilerative disorders?

A
  • Tear-drop RBCs
  • Poikilocytosis (various RBC sizes)
  • Blasts (immature RBCs + WBCs)
199
Q

How is primary myelofibrosis (myeloprofilerative disorder) managed?

A
  • Monitoring (mild)
  • Allogenic stem cell transplant
  • Chemo
  • Supportive
200
Q

How is polycythaemia vera (myeloprofilerative disorder) managed?

A
  • Venesection-> keep Hb in normal range
  • Aspirin-> for thrombus risk
  • Chemo
201
Q

How is essential thrombocythaemia (myeloprofilerative disorder) managed?

A
  • Aspirin for clot reduction

- Chemo

202
Q

What is myelodysplastic syndrome?

A
  • When myeloid bone marrow cells not mature properly-> unhealthy cells made
  • Low cells from myeloid line-> anaemia, neutropaenia, thrombocytopaenia
203
Q

Who is myelodysplastic syndrome common in?

A
  • Patients age 60+

- Chemo/radiotherapy patients

204
Q

What is the major risk with myelodysplastic syndrome?

A

Transformation to AML

205
Q

How does myelodysplastic syndrome present?

A
  • Often asymptomatic + incidental
  • Anaemia-> fatigue, pallor, SOB
  • Neutropaenia-> frequent/severe infections
  • Thrombocytopaenia-> bleeding, bruising
206
Q

How is myelodysplastic syndrome diagnosed?

A
  • FBC
  • Blood film-> blasts
  • Bone marrow aspiration + biopsy
207
Q

How is myelodysplastic syndrome managed?

A
  • Watchful waiting
  • Supportive
  • Transfusion in severe anaemia
  • Chemo
  • Stem cell transplant
208
Q

What is thrombocytopaenia?

A

Low platelets due to problem with production or destruction

209
Q

What are some causes of thrombocytopaenia to do with platelet production?

A

Sepsis, B12/folic acid deficiency, liver failure (reduced thrombopoetin production in liver), leukaemia, myelodysplastic syndrome

210
Q

What are some causes of thrombocytopaenia to do with platelet destruction?

A
  • Alcohol, TTP, heparin-induced thrombocytopaenia, HUS

- Medications-> sodium valproate, MTX, isotretinoin, antihistamines, PPIs

211
Q

How does thrombocytopaenia present?

A
  • Asymptomatic
  • Easy bruising, prolonged bleed time, nosebleeds, blood in urine/stools
  • Severe-> intracranial or GI bleeds
212
Q

What are the differentials for abnormal/prolonged bleeding?

A
  • thrombocytopaenia
  • Haemophilia A+B
  • Von Willebrand disease
  • DIC
213
Q

What is Immune Thrombocytopenic Purpura (ITP)?

A

Antibodies produced against platelets-> destroyed by immune system

214
Q

How is Immune Thrombocytopenic Purpura (ITP) managed?

A
  • Medical-> prednisolone, IV Igs, rituximab
  • Splenectomy
  • Monitoring-> platelet count
  • Safety netting-> headaches + melaena
  • Control BP
  • Suppress periods if have them
215
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • Microangiopathy-> clots through small vessel
  • Due to low platelets-> bleed under skin
  • Can be inherited or autoimmune
216
Q

What is the treatment for Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • Plasma exchange
  • Steroids
  • Rituximab
217
Q

What is the pathophysiology of Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • ADAMTS13 protein-> problem

- VWF overactivity-> clots break up RBCS-> haemolytic anaemia

218
Q

What is heparin-induced thrombocytopenia?

A
  • Antibodies produced against platelets in response to heparin exposure
  • Activates clotting + hypercoagulation-> thrombosis
219
Q

How is heparin-induced thrombocytopenia managed?

A
  • Measure HIT antibodies

- Stop heparin + use alternative anti-coagulation

220
Q

What is Von Willebrand disease?

A
  • Inherited cause of abnormal bleeding
  • Autosomal domnant
  • Malfunctioning/absence of VWF glycoprotein
221
Q

How does Von Willebrand disease present?

A
  • Bleeding gums
  • Bruising
  • Epistaxis
  • Menorrhagia
  • Heavy bleed during operation
  • Family history
222
Q

How is Von Willebrand disease managed?

A
  • In response to bleed/major trauma or beore ops
  • Desmopressin-> stimulates release
  • VWF infusion
  • Factor VIII infusion
  • Periods-> tranexamic acid, mefanamic acid, norethisterone, COCP, Mirena, hysterectomy
223
Q

What is haemophilia?

A
  • Inherited severe bleeding disorder-> X linked recessive
  • haemophilia A-> factor VIII deficiency
  • haemophilia B-> factor IX
224
Q

What is haemophilia A caused by?

A

Factor VIII deficiency

225
Q

What is haemophilia B caused by?

A

Factor IX deficiency

226
Q

What does X-linked recessive inheritance mean?

A
  • All X chromosomes need the abnormal gene
  • Men only need 1 copy-> 1 X-> nearly always men
  • Women can be carriers or affected
227
Q

What are the symptoms and signs of haemophilia?

A
  • Bleed XS in minor trauma
  • Spontaneous haemorrhage risk
  • Neonates-> intracranial haemorrhage, haematoma, cord bleeding
  • Haemoarthrosis + bleed into muscles-> joint deformity
  • GI bleeds, haematuria etc
228
Q

How is haemophilia diagnosed?

A
  • Bleeding scores
  • Coagulation factor assays
  • Genetic tests
229
Q

How is haemophilia managed?

A
  • IV clotting factors-> VIII or IX-> can produce antibodies against
  • Desmopressin-> stimulate VWF
  • Antifibrinolytics-> tranexamic acid
230
Q

What causes VTE?

A
  • Secondary to stagnation + hypercoagulable states

- Thrombus (DVT)-> embolise (PE)

231
Q

Why would someone with atrial septal defect be at higher risk of a stroke?

A

-Clot pass through left side of heart-> systemic circulation-> brain-> stroke

232
Q

What are some risk factors for VTE?

A

Immobility, recent surgery, long haul travel, pregnancy, oestrogen (COCP/HRT), malignancy, polycythaemia, SLE, thrombophilias (eg antiphospholipid syndrome)

233
Q

What is given for VTE prophylaxis?

A
  • LMWH-> enoxaparin etc
  • Apixaban, rivaroxaban etc-> if already taking usually
  • Compression stockings
234
Q

When are anti-embolic compression stockings contraindicated?

A

Peripheral arterial disease

235
Q

How does DVT present?

A
  • Unilateral (usually)
  • Calf/leg swelling
  • Dilated superficial veins
  • Tender calf
  • Oedema
  • Colour change to leg
236
Q

How is DVT assessed?

A
  • Measure for swelling-> 10cm below tibial tuberosity-> >3cm difference in significant
  • Well’s score-> RFs
  • D-dimer-> exclude VTE if negative
  • Doppler US of leg + repeat in 6-8 days if negative but +ve D-dimer and Well’s
237
Q

When might a D-dimer be raised?

A
  • VTE
  • Pneumonia
  • Malignancy
  • Heart failure
  • Surgery
  • Pregnancy
238
Q

When should a Doppler US for DVT be repeated?

A
  • If first scan is negative but D-dimer and Wells are positive
  • Repeat in 6-8 days
239
Q

How is PE diagnosed?

A
  • Well’s score-> RFs
  • D-dimer-> exclude VTE if negative
  • CTPA
  • V/Q perfusion scan-> eg severe kidney impairment or contrast allergy
240
Q

How is DVT/PE managed?

A
  • Apixaban or rivaroxaban immediately when suspected
  • Catheter directed thrombolysis-> symptomatic iliofemoral DVT + symptoms <14 days ie direct to clot
  • IVC filter
241
Q

What is the target INR for warfarin treatment in VTE?

242
Q

When is warfarin used first-line for VTE treatment?

A

Anti-phospholipid syndrome

243
Q

What is the first line anticoagulant in pregnancy?

244
Q

How long should VTE treatment (anticoagulation) be continued for in VTE (with a reversible cause)?

A

3 months then review

245
Q

How long should VTE treatment (anticoagulation) be continued for in VTE (unprovoked/unclear cause, recurrent etc)

A

Usually 6 months then review

246
Q

How long should VTE treatment (anticoagulation) be continued for in VTE (in active cancer)?

A

Usually 6 months

247
Q

What is an IVC filter and when are they used?

A
  • Into IVC-> filter blood + catch clots going towards heart/lungs (sieve)
  • Recurrent PEs or unsuitable for anticoagulation
248
Q

How might unprovoked DVT be investigated?

A
  • Review-> history, bloods, exam for cancer

- Test for-> antiphospholipid syndrome, hereditary thrombophilias (eg when 1st degree relatives)

249
Q

What is Budd-Chiari syndrome?

A
  • Thrombosis develops in hepatic vein + blocks outflow
  • Associated with hypercoagulable states
  • Causes acute hepatitis
250
Q

How does Budd-Chiari syndrome present?

A

Abdominal pain + hepatomegaly + ascites

251
Q

How is Budd-Chiari syndrome managed?

A
  • Anticoagulation
  • Investigate underlying cause
  • Treat hepatitis

Medicine (13 decks)

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