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Phase 2a Medicine - Riona COPY > Haematology > Flashcards

Haematology Flashcards

1
Q

What is deep vein thrombosis?

A

Formation of a blood clot (thrombus) in a deep vein of the body

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2
Q

What are DVTs caused by?

A

Poor blood flow leading to clot formation

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3
Q

Give 5 risk factors for a DVT

A
  • ) Venous flow stasis (e.g. immobility)
  • ) Trauma/surgery
  • ) Hypercoagulability
  • ) Advanced age
  • ) Sickle cell disease
  • ) Pregnancy
  • ) Taking oestrogen (HRT, pill)
  • ) Cancer
  • ) Obesity
  • ) Thrombophilia
  • ) Increased age
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4
Q

Give the steps of the clotting cascade (6)

A

1) Platelets adhere to endothelium
2) Aggregate forms
3) Clotting factors release
4) Prothrombin to thrombin
5) Thrombin catalyses fibrinogen to fibrin
6) Fibrin reinforces clot

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5
Q

Give 3 symptoms/signs of a DVT

A
  • ) May be asymptomatic
  • ) Calf warmth, tenderness, swelling, redness, pain
  • ) Mild fever
  • ) Pitting oedema
  • ) Usually in just one leg
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6
Q

Give 3 tests for DVT

A
  • ) D dimer
  • ) US compression
  • ) Thrombophilia test before anticoagulation if abnormal presentation
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7
Q

What is D dimer?

A

A fibrin degradation product

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8
Q

What does a normal/positive D dimer result mean?

A

Normal - excludes diagnosis

Positive - doesn’t confirm diagnosis

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9
Q

What do we do if an US compression if negative?

A

Perform again after a week as the clot may have spread up and become detectable

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10
Q

Give 3 parts of treatment of a DVT

A
  • ) LMWH/ warfarin
  • ) DOACs
  • ) Underlying cause
  • ) IVC filter in active bleeding/anticoagulants fail
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11
Q

What does DOACs stand for?

A

Direct oral anticoagulants

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12
Q

Give 2 methods of prevention of DVTs

A
  • ) Stop oral contraceptive pill 4 weeks pre-op
  • ) Mobilise early
  • ) LMWH
  • ) Compression stockings
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13
Q

What is a thrombosis?

A

Inappropriate blood coagulation occurs inside a vessel

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14
Q

What is arterial circulation high in?

A

Platelets

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15
Q

What is venous circulation high in?

A

Fibrin

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16
Q

Name 3 places an arterial thrombosis can occur and what it can cause

A
  • ) Coronary circulation - MI
  • ) Cerebral circulation - CVA/stroke
  • ) Peripheral circulation - peripheral vascular disease
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17
Q

What is the treatment for a stroke?

A

Aspirin/clopidogrel, TPA

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18
Q

What is an embolism?

A

The passage of material through the venous or arterial circulations

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19
Q

What is the most common process of an embolism?

A

Thrombo-emolus from a DVT

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20
Q

Give 3 symptoms for an embolism

A
  • ) Asymptomatic possible
  • ) Transient dyspnoea
  • ) Chest pain
  • ) Haemoptysis
  • ) Secondary effusion
  • ) CV collapse
  • ) Sudden death
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21
Q

What is a paradoxical embolism?

A

An embolus that travels through the venous circuit and then across the heart through a patent foramen ovale

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22
Q

Give 2 causes of a systemic arterial embolism

A
  • ) Atherosclerotic plaques

- ) IE

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23
Q

What does the Virchow triad include?

A
  • ) Stasis of blood flow
  • ) Endothelial injury
  • ) Hypercoagulability
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24
Q

What is a pulmonary embolism?

A

Large embolus that blocks the pulmonary arteries

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25
Q

Give 3 symptoms of a pulmonary embolism

A
  • ) Breathlessness
  • ) Pleuritic chest pain
  • ) May have signs/symptoms of DVT
  • ) Haemoptysis
  • ) Dizziness
  • ) Syncope
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26
Q

Give 4 signs of a pulmonary embolism

A
  • ) Tachycardia
  • ) Tachypnoea
  • ) Pleural rub
  • ) Those of precipitating cause
  • ) Cyanosis
  • ) Purexia
  • ) Hypotension
  • ) Raised JVP
  • ) Pleural effusion
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27
Q

What does a pulmonary embolism lead to? (if it doesn’t kill)

A
  • ) Hypotension
  • ) Cyanosis
  • ) Severe dyspnoea
  • ) Right heart strain/failure
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28
Q

What does a pulmonary embolism usually arise from?

A

A venous thrombosis in the pelvis or legs

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29
Q

What are the risk factors for a pulmonary embolism?

A

Same as for DVT

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30
Q

What investigations do we do for a pulmonary embolism?

A
  • ) CXR
  • ) ECG
  • ) Blood gas
  • ) D-dimer
  • ) CTPA
  • ) Echo
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31
Q

What does a blood gas show for a pulmonary embolism?

A

Type 1 respiratory failure of decreased PaO2 and PaCO2

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32
Q

What is a CTPA?

A

CT pulmonary angiogram

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33
Q

What should you consider in patients with a PE and no provoking risk factors?

A

Malignancy

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34
Q

What is the treatment for a pulmonary embolism?

A

As for DVT

  • ) LMWH/ warfarin
  • ) DOACs
  • ) Treat cause
  • ) IVC filter
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35
Q

What is the Wells score?

A

Pretest clinical probability scoring for DVT

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36
Q

What is anaemia defined as?

A

A low Hb concentration due to a low red cell mass or increased plasma volume

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37
Q

What is a low Hb for men?

A

<135g/L

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38
Q

What is a low Hb for women?

A

<115g/L

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39
Q

Give 3 symptoms of anaemia

A
  • ) Fatigue
  • ) Dyspnoea
  • ) Faintness
  • ) Palpitations
  • ) Headache
  • ) Tinnitus
  • ) Anorexia
  • ) Angina if pre-existing CHD
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40
Q

Give 2 signs of anaemia

A
  • ) May be absent even in severe
  • ) Pallor
  • ) Tachycardia
  • ) Flow murmurs
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41
Q

What is the normal MCV range?

A

76-96 femtolitres

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42
Q

What does MCV stand for?

A

Mean cell volume

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43
Q

Where are RBCs produced, and how long do they live for?

A

Bone marrow, 120 days

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44
Q

What are the 3 types of anaemia?

A

1) Microcytic - small
2) Normocytic - normal
3) Macrocytic - large

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45
Q

Give 3 causes for low MCV/ microcytic anaemia

A
  • ) Iron deficiency anaemia
  • ) Thalassaemia
  • ) Anaemia of chronic disease
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46
Q

Give 3 causes for normal MCV/ normocytic anaemia

A
  • ) Acute blood loss
  • ) Anaemia of chronic disease
  • ) Combined haematinic deficiencies (B12 and folate) (think malabsorption)
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47
Q

Give 3 causes for high MCV/ macrocytic anaemia

A
  • ) B12/folate deficiency
  • ) Alcohol excess/liver disease
  • ) Hypothyroid
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48
Q

Where are RBCs removed? (4)

A
  • ) Spleen
  • ) Liver
  • ) Bone marrow
  • ) Blood loss
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49
Q

Give 3 consequences of anaemia

A
  • ) Reduced O2 transport
  • ) Tissue hypoxia
  • ) Compensatory changes
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50
Q

How do we test for anaemia?

A
  • ) History and exam
  • ) B12, folate, ferritin
  • ) FBC
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51
Q

Give 3 causes of iron deficient anaemia

A
  • ) Blood loss (e.g. menstruation)
  • ) Malabsorption
  • ) Hookworm
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52
Q

Give 3 signs of iron deficient anaemia

A
  • ) Koilonchyia (spoon shaped nails)
  • ) Atrophic glossitis
  • ) Lip ulceration
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53
Q

If there is lots of blood loss/problem with too much removal, what will there be lots of in the blood?

A

Reticulocytes (immature RBCs)

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54
Q

How do we treat iron deficiency anaemia?

A

Oral iron ferrous sulphate tablets

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55
Q

Give 3 causes of anaemia of chronic disease

A
  • ) Chronic infection
  • ) Renal failure
  • ) Malignancies
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56
Q

Give 3 signs of anaemia of chronic disease

A
  • ) Headache
  • ) Pallor
  • ) Tiredness
  • ) Weakness
  • ) SOB
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57
Q

What is the treatment for anaemia of chronic disease? (3)

A
  • ) Treat underlying disease
  • ) EPO
  • ) Parenteral iron
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58
Q

What does EPO stand for?

A

Erythropoietin

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59
Q

What does EPO do, and what is it secreted by?

A

Increases rate of production of RBCs in response to decreased O2 levels in tissues, secreted by kidneys

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60
Q

What is pernicious anaemia?

A

Autoimmune condition in which atrophic gastritis leads to a lack of intrinsic factor secretion from the parietal cells of the stomach

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61
Q

How is B12 usually absorbed in the terminal ileum?

A

Binds to IF

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62
Q

What does B12 deficiency do?

A

B12 helps synthesise thymidine and hence DNA, thus deficiency causes decreased RBC production

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63
Q

What type of anaemia is pernicious?

A

Macrocytic

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64
Q

Give 2 causes of B12 deficiency

A
  • ) Dietary
  • ) Malabsorption
  • ) Crohn’s, tapeworm
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65
Q

Give 2 features of B12 deficiency

A

-) Lemon tinge due to pallor and mild jaundice
Glossitis
-) Neuropsychiatric
-) Neurological

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66
Q

What is the treatment for pernicious anaemia? (2)

A
  • ) Hydroxocobalamin (B12) if malabsorption

- ) Oral B12 if dietary

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67
Q

What type of anaemia is folate deficiency anaemia?

A

Macrocytic

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68
Q

What is folate deficiency anaemia caused by?

A

Poor diet and increased demand (pregnancy)

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69
Q

How do we treat folate deficiency?

A

Treat cause and give folic acid

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70
Q

What is haemolytic anaemia?

A

Premature breakdown of RBCs in circulation or reticuloendothelial system

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71
Q

Give 2 causes of haemolytic anaemia

A
  • ) Inherited

- ) Acquired (drugs etc)

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72
Q

Give 2 signs for haemolytic anaemia

A
  • ) Jaundice
  • ) Hepatosplenomegaly
  • ) Gallstones
  • ) Leg ulcers
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73
Q

What type of anaemia is haemolytic?

A

Normocytic or macrocytic

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74
Q

What is aplastic anaemia?

A

Caused by rare stem cell disorder leading to panytopaenia and bone marrow failure

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75
Q

What is panytopaenia?

A

Deficiency of all blood cells

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76
Q

What are most causes of aplastic anaemia?

A

Autoimmune, triggered by drugs/radiation/infection

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77
Q

What is sickle cell anaemia?

A

An autosomal recessive disorder in which production of abnormal Hb results in vaso-occlusive crises

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78
Q

What are the 3 problems in anaemia of chronic disease?

A

1) Poor use of iron in erythropoiesis
2) RBC decreased survival
3) Decreased EPO production and response

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79
Q

What is the genetic problem behind sickle cell anaemia?

A

Amino acid substitution in the gene coding for the beta chain, which leads to the production of HbS rather than HbA

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80
Q

What is the difference between homozygotes (HbSS) and heterozygotes (HbAS) in sickle cell anaemia?

A

HbSS - sickle cell anaemia

HbAS - sickle cell trait

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81
Q

What does sickle cell trait protect the carrier from?

A

Falciparum malaria

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82
Q

What occurs to HbS when it is deoxygenated?

A

It polymerises, causing RBCs to deform, producing sickle cells which are fragile and haemolyse, blocking small vessels

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83
Q

In who is sickle cell anaemia more common?

A

African origin

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84
Q

Give 3 symptoms of sickle cell anaemia

A
  • ) Vaso-occlusive painful crisis
  • ) Aplastic crisis
  • ) Sequestration crisis (children)
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85
Q

What is a vaso-occlusive crisis due to?

A

The occlusion of microvascular

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86
Q

Give 3 triggers for a painful vaso-occlusive crisis

A
  • ) Cold
  • ) Dehydration
  • ) Infection
  • ) Hypoxia
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87
Q

Give 3 other symptoms of sickle cell anaemia

A
  • ) Dactylitis (<3)
  • ) Stroke, seizures, cognitive defects
  • ) Avascular necrosis
  • ) Leg ulcers
  • ) Low-flow priapism
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88
Q

What does the blood film look like in sickle cell anaemia?

A

Sickle and target cells seen

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89
Q

What confirms the diagnosis of sickle cell anaemia after a sickle solubility test?

A

Hb electrophoresis, can also distinguish between AS and SS

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90
Q

How do we treat sickle cell anaemia?

A
  • ) Hydroxycarbamide - if frequent crises
  • ) Prophylaxis (immunisation and antibiotics) - for splenic infarction
  • ) Septicaemia risk
  • ) Bone marrow transplant
  • ) Genetic counselling
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91
Q

What is thalassaemia?

A

A genetic disease of unbalanced Hb synthesis with underproduction of one globin chain

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92
Q

What do unmatched globins do?

A

Precipitate and damage RBC membranes, causing their haemolysis whilst still in the marrow

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93
Q

What are the 3 main types of thalassaemia?

A
  • ) Beta thalassaemia minor
  • ) Beta thalassaemia intermedia
  • ) Beta thalassaemia major
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94
Q

What are beta thalassaemias usually caused by genetically?

A

Point mutations in beta-globin chains on chromosome 11

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95
Q

What state is beta thalassaemia minor and what are its symptoms? (3)

A

Carrier state, usually asymptomatic, possible mild anaemia

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96
Q

What are the symptoms of beta thalassaemia intermedia? (3)

A

Moderate anaemia, not requiring transfusions, maybe splenomegaly

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97
Q

What is beta thalassaemia major?

A

Significant abnormalities in both beta-globin chains

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98
Q

How does beta thalassaemia major present?

A

In 1st year with severe anaemia and a failure to thrive

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99
Q

In beta thalassaemia major, what occurs in response to anaemia?

A
  • ) Extra-medullary haematopoiesis (RBCs made outside of marrow)
  • ) Skull bossing
  • ) Hepatosplenomegaly
  • ) Osteopenia
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100
Q

What do life long blood transfusions in beta thalassaemia major cause?

A

Iron overload/deposition seen after 10 years as endocrine failure

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101
Q

What does the blood film show for beta thalassaemia major?

A

Very hypochromic, microcytic cells, target cells, nucleated RBCs

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102
Q

What is the general treatment for beta thalassaemia? (6)

A
  • ) Fitness and healthy diet
  • ) Folate supplements
  • ) Regular life-long transfusions
  • ) Splenectomy if hypersplenism persists
  • ) Hormonal replacement for endocrine complications
  • ) Marrow transplant
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103
Q

What can we give to mitigate iron overload?

A

Iron-chelators (deferiprone PO and desferrioxamine)

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104
Q

What is it more common to be a carrier of alpha rather than beta thalassaemia?

A

Alpha has 4 genes coding for it rather than 2

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105
Q

What are the alpha thalassaemias mainly caused by?

A

Gene deletions

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106
Q

What does each number of mutations in alpha thalassaemia cause? (4)

A

4 - death in utero
3 - haemoglobin H disease
2 - asymptomatic carrier state
1 - clinically normal

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107
Q

What is relative polycythaemia?

A

Decreased plasma volume, normal RBC mass

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108
Q

What is absolute polycythaemia?

A

Increased RBC mass

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109
Q

What sort of disorder is polycythaemia?

A

Myeloproliferative - overactive bone marrow

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110
Q

What is polycythaemia?

A

The malignant proliferation of a clone derived from one pluripotent stem cell

111
Q

Give 2 causes of absolute polycythaemia

A
  • ) Primary (polycythaemia vera)

- ) Secondary (hypoxia or increased EPO secretion)

112
Q

What is the genetic mutation in in polycythaemia vera?

A

JAK2

113
Q

What is there an excess proliferation of in polycythaemia vera? (3)

A
  • ) RBCs
  • ) WBCs
  • ) Platelets
114
Q

Give 2 causes of relative polycythaemia

A

Acute - dehydration

Chronic - obesity, HTN, high alcohol and tobacco

115
Q

Give 3 signs of polycythaemia vera due to hyperviscosity

A
  • ) Headaches
  • ) Dizziness
  • ) Tinnitus
  • ) Visual disturbance
116
Q

Give 2 signs of polycythaemia vera due to increased urate from high RBC turnover

A
  • ) Itching after a hot bath

- ) Erythromelalgia (burning sensation in fingers and toes)

117
Q

Give 2 signs of polycythaemia vera

A
  • ) Facial plethora
  • ) Splenomegaly
  • ) Features of arterial/venous thrombosis
118
Q

What does the bone marrow show in polycythaemia vera?

A

Hypercellularity with erythroid hyperplasia

119
Q

What is the treatment for polycythaemia vera in younger patients?

A

Venesection (blood removal) & daily aspirin

120
Q

What is the treatment for polycythaemia vera in elderly patients/previous thombosis?

A

Hydroxycarbamide & aspirin

121
Q

Transition to what occurs in polycythaemia vera patients?

A

30% - myelofibrosis (scarring of bone marrow)

5% - acute myeloid leukaemia

122
Q

Give 3 bleeding disorders

A
  • ) Over-anticoagulation
  • ) Haemophilia
  • ) Disseminated intravascular coagulation
  • ) Platelet disorders (ITP and TTP)
123
Q

What drug can cause over-anticoagulation?

A

Warfarin

124
Q

Give 3 risk factors for over-anticoagulation

A
  • ) Age
  • ) Co-morbidities
  • ) Polypharmacy
  • ) Previous bleeding
  • ) High BP
125
Q

What should we give if a bleed occurs due to over-anticoagulation? (3)

A
  • ) Withhold warfarin
  • ) Vitamin K 5mg IV
  • ) Prothrombin complex concentrate/fresh frozen plasma
126
Q

What is haemophilia?

A

An inherited condition that affects the blood’s ability to clot

127
Q

What is the cause of haemophilia A?

A

Factor VIII deficiency, inherited in an X-linked recessive patterns in males

128
Q

What is the presentation of haemophilia A?

A
  • ) Early in life or after surgery/trauma
  • ) Bleeds into joints - crippling arthropathy
  • ) Bleeds into muscles - haematomas
  • ) High pressure - nerve palsies and compartment syndrome
129
Q

What are the 2 things we diagnose haemophilia A by?

A
  • ) Increased APTT

- ) Decreased factor VIII assay

130
Q

What is the management for haemophilia A? (4)

A
  • ) Avoid NSAIDs and IM
  • ) Pressure and elevation for minor bleeding
  • ) Desmopressin raises factor VIII levels
  • ) Recombinant factor VIII for major bleeds (50% of normal)
  • ) Life-theratening bleeds (100% of normal)
131
Q

What is haemophilia B?

A

Factor IX deficiency, inherited in an X-linked recessive pattern

132
Q

How do we treat haemophilia B?

A

Recombinant factor IX

133
Q

What is acquired haemophilia?

A

A bleeding diathesis causing big mucosal bleeds in M+F

134
Q

What is acquired haemophilia caused by?

A

Suddenly appearing autoantibodies that interfere with factor VIII

135
Q

What do the tests for acquired haemophilia show? (2)

A
  • ) Increased APPT
  • ) Increased VIII autoantibody
  • ) Decreased factor VIII activity
136
Q

How do we treat acquired haemophilia?

A

Steroids

137
Q

What is disseminated intravascular coagulation? (DIC)

A

Widespread activation of coagulation from the release of procoagulants into the circulation, with the consumption of clotting factors and platelets leading to an increased risk of bleeding

138
Q

What do fibrin strands do in DIC?

A

Fill small vessels, haemolysing passing RBCs

139
Q

Give 3 causes of DIC

A
  • ) Malignancy
  • ) Sepsis
  • ) Trauma
  • ) Obstetric events
140
Q

Give 2 signs of DIC

A
  • ) Bruising
  • ) Bleeding anywhere
  • ) Renal failure
  • ) Confusion, fever
141
Q

What 5 things do we find on investigation of DIC?

A
  • ) Decreased platelets
  • ) Increased PT
  • ) Increased APTT
  • ) Decreased fibrinogen
  • ) Increased fibrin degradation products (D-dimers)
142
Q

What are seen on blood films in DIC?

A

Broken RBCs

143
Q

How do we treat DIC?

A
  • ) Treat cause
  • ) Replace platelets
  • ) Cryoprecipitate to replace fibrinogen
  • ) FFP to replace coagulation factors
144
Q

What does APTT stand for?

A

Activated partial thromboplastin time

145
Q

What does PT stand for?

A

Prothrombin time

146
Q

What is immune thrombocytopaenia caused by? (ITP)

A

Antiplatelet autoantibodies that reduce the function of platelets

147
Q

What are purpura?

A

Red/purple discoloured spots on the skin that do not blanch on applying pressure

148
Q

What are the pathogenic steps of ITP? (3)

A

1) Abnormal autoantibody with specificity for platelet membrane glycoproteins binds to circulating platelets
2) Autoantibody coated platelets induce phagocytosis by macrophages primarily in the spleen
3) Platelet numbers decrease

149
Q

Where is acute ITP found?

A

In children 2 weeks after infection

150
Q

How does acute ITP present?

A

Sudden self-limiting purpura

151
Q

Where is chronic ITP usually found?

A

Women

152
Q

Give 3 signs of chronic ITP

A
  • ) Bleeding
  • ) Purpura
  • ) Epistaxis
  • ) Menorrhagia
153
Q

What do we see in the marrow in ITP?

A

Increased megakaryocytes

154
Q

What do we give as treatment in symptomatic ITP?

A
  • ) Prednisolone - FIRST LINE
  • ) IV immunoglobulin (temporary)
  • ) Splenectomy
  • ) B cell depletion with rituximab
155
Q

What is thrombotic thrombocytopenia purpura? (TTP)

A

Decrease in circulating platelets due to small blood clots forming suddenly throughout the body

156
Q

What is TTP caused by?

A

Genetic/acquired deficiency of a protease that cleaves vWf

157
Q

What does less inhibition of vWf mean in TTP?

A

More platelet aggregation and fibrin deposition in small vessels, leading to multi system thrombotic microangiopathy

158
Q

Give 4 signs of TTP

A
  • ) Bleeding
  • ) Bruising
  • ) Purpura
  • ) Confusion
  • ) Headache
  • ) Palsies, seizure, confusion, coma
  • ) Fever
  • ) Pallor
  • ) Jaundice
  • ) Proteinuria
159
Q

What is the protease that usually cleaves vWf?

A

ADAMTS13

160
Q

How do we treat TTP?

A
  • ) Plasma infusion/exchnange
  • ) Corticosteroids (prenisolone)
  • ) Rituximab for non-responders/relapse
161
Q

What is rituximab?

A

Monoclonal antibody

162
Q

What is leukaemia?

A

Malignant proliferation of white blood cell precursors

163
Q

What are the 4 types of leukaemia?

A

ALL - acute lymphoblastic leukaemia
CLL - chronic lymphocytic leukaemia
AML - acute myeloid leukaemia
CML - chronic myeloid leukaemia

164
Q

What is the commonest acute leukaemia in adults?

A

AML

165
Q

What is the commonest cancer in children?

A

ALL

166
Q

Which leukaemia is most common in the elderly?

A

CLL

167
Q

What chromosome is present in >80% of CML sufferers?

A

Philadephia chromosome

168
Q

What syndrome is leukaemia associated with?

A

Down’s syndrome

169
Q

Give 4 risk factors for leukaemia

A
  • ) Irradiation (radiotherapy)
  • ) Some drugs (e.g. chemo)
  • ) Some chemicals
  • ) Human T lymphotropic virus
  • ) Family history
170
Q

What cells does ALL affect?

A

Lymphocytes (B/T)

171
Q

What cells does CLL affect?

A

B lymphocytes

172
Q

What cells does AML affect?

A

Myeloblasts

173
Q

What cells does CML affect?

A

Mature myeloblasts (basophils, neutrophils, eosinophils)

174
Q

What cells do acute leukaemias affect?

A

Immature cells

175
Q

How does acute leukaemia progress, and how curable is it?

A

Progresses rapidly, is curable if treated quickly

176
Q

How does chronic leukaemia progress, and how curable is it?

A

Progresses slowly, harder to cure

177
Q

What cells do chronic leukaemias affect?

A

Mature cells

178
Q

What are the signs and symptoms of ALL?

A
  • ) Anaemia
  • ) Infection
  • ) Bleeding
  • ) Hepato/splenomegaly
  • ) Lymphadenopathy
  • ) CNS involvement
179
Q

Give 2 common infections in ALL

A
  • ) Bacterial septicaemia
  • ) Zoster
  • ) CMV
  • ) Measles
180
Q

What are the signs and symptoms of AML?

A
  • ) Anaemia
  • ) Infection
  • ) Bleeding
  • ) Hepato/splenomegaly
  • ) Gum hypertrophy
  • ) Skin involvement
181
Q

What are the signs and symptoms of CLL

A
  • ) Nodal often
  • ) May present as surprise from FBC
  • ) Anaemic
  • ) Infection prone
  • ) Weight loss and sweats if severe
182
Q

What are the signs and symptoms of CML?

A
  • ) Weight loss
  • ) Tiredness
  • ) Fever
  • ) Sweats
  • ) Gout
  • ) Bleeding
  • ) Splenomegaly
  • ) Anaemia
  • ) Bruising
183
Q

Give 4 tests we do in leukaemia

A
  • ) Bone marrow biopsy
  • ) CXR and CT
  • ) Lumbar puncture
  • ) Immunophenotyping/genetics
  • ) Blood film
184
Q

What is seen on a blood film in ALL?

A

Characteristic blast cells

185
Q

Why do we do a lumbar puncture in ALL?

A

CNS involvement

186
Q

How do we differentiate AML from ALL?

A

Microscopy

187
Q

What is the treatment for ALL?

A
  • ) Blood/platelet transfusion
  • ) IV fluids
  • ) Allopurinol
  • ) IV antibiotics for infection
  • ) Chemotherapy
  • ) Allogenic marrow transplant
188
Q

What is the treatment for AML?

A
  • ) Blood transfusions
  • ) IV antibiotics for infection
  • ) Intensive chemo
  • ) Allogenic marrow transplant
  • ) Allopurinol
189
Q

What is the treatment for CLL?

A
  • ) 30% never need treatment
  • ) Chemo
  • ) First line is fludarabine + rituximab +/- cyclophosphamide
  • ) Steroids
  • ) Radio
  • ) Blood transfusions
  • ) IV immunoglobulin if infections
190
Q

What is the treatment for CML?

A
  • ) Targeted therapies

- ) Chemo and stem cell transplant if unsuccessful

191
Q

Give 2 targeted therapies for CML

A
  • ) Imatinib

- ) Tyrosine kinase inhibitor

192
Q

What does haematological remission mean?

A

No evidence of leukaemia in the blood

193
Q

Give 2 common infections of AML

A
  • ) Candida

- ) Aspergillus

194
Q

Which leukaemia is a myeoproliferative disorder?

A

CML

195
Q

Between what ages does CML usually occur?

A

40-60

196
Q

What is a lymphoma?

A

Disorder caused by malignant proliferations of lymphocytes

197
Q

Where do the lymphocytes usually accumulate in a lymphoma?

A

Lymph notes, lymphadenopathy

198
Q

What are the characteristic cells found in Hodgkin’s lymphoma? (HL)

A

Reed-Sternberg cells

199
Q

What are the 2 peaks of incidence of Hodgkin’s lymphoma?

A

Young adults and elderly

200
Q

Give 3 risk factors for Hodgkin’s lymphoma

A
  • ) Epstein Barr virus infection
  • ) Family history
  • ) Immunosuppression
  • ) Obesity
201
Q

What are the 4 HL subtypes?

A
  • ) Nodular sclerosing
  • ) Mixed cellularity
  • ) Lymphocyte rich
  • ) Lymphocyte depleted
202
Q

Where is the mutation in HL?

A

DNA of a B lymphocyte

203
Q

Give 3 symptoms of HL

A
  • ) Enlarged, non-tender, rubbery superficial lymph nodes
  • ) Fever, weight loss, night sweats, pruritus, lethargy (25%)
  • ) Mass effect from mediastinal lymph nodes
  • ) Painful lymph when drinking
204
Q

Give 2 signs of HL

A
  • ) Lymphadenopathy
  • ) Cachexia
  • ) Anaemia
  • ) Spleno/hepatomegaly
205
Q

What is a paraneoplastic complication?

A

Immune system attacks its own platelet cells rather than infections (ITP)

206
Q

What main tests do we do for HL?

A

Lymph node biopsy and blood film

207
Q

What are the 4 stages of lymphomas?

A

I - involvement of single lymph node region
II - involvement of 2 or more on same side
III - involvement of both sides
IV - involvement of extra nodal tissues, spread beyond lymph nodes

208
Q

Each stage of lymphoma is either A or B - what does this mean?

A

A - no B symptoms

B - B symptoms present

209
Q

What are B symptoms?

A

Systemic - weight loss, fever, night sweats

210
Q

What is the treatment for HL?

A
  • ) Radiotherapy and chemotherapy
  • ) ABVD chemo 2-4 cycles or 6-8 cycles
  • ) Possible autologous stem cell transplantation
211
Q

What are the drugs for ABVD chemotherapy in HL?

A

A - adriamycin/doxorubicin
B - bleomycin
V - vinblastine
D - dacarbazine

212
Q

What is Non-Hodgkin’s lymphoma? (NHL)

A

All lymphomas without Reed-Sternberg cells

213
Q

What is the most common NHL?

A

Diffuse large B-cell lymphoma

214
Q

Give 3 risk factors for NHL

A
  • ) Family history
  • ) Ataxia telangiectasia
  • ) H. pylori infection
  • ) EBV, HIV
  • ) Immunosuppression
215
Q

Where is the mutation for NHL?

A

20% - T lymphocytes

80% - B lymphocytes

216
Q

What are the clinical features of NHL?

A
  • ) 75% have superficial lymphadenopathy
  • ) 50% have extra nodal disease - depends on type
  • ) Small bowel lymphomas - diarrhoea, vomiting, abdominal pain, weight loss
  • ) Waldeyer’s ring lymphoma - sore throat, obstructed breathing
  • ) Systemic features less common than in HL
  • ) Pancytopenia
217
Q

What does an increase in lactate dehydrogenase mean?

A

Increased cell turnover, worse prognosis

218
Q

What are the 2 main grades of NHL?

A
  • ) Low grade - indolent, often incurable

- ) High grade - more aggressive, often curable (diffuse B cell)

219
Q

How do we treat low grade NHLs?

A
  • ) Radiotherapy
  • ) Chlorambucil in diffuse
  • ) Interferon alfa/rituximab in remission
220
Q

How do we treat high grade NHLs?

A 
R-CHOP
R - rituximab
C - cyclophosphamide
H - hydroxydaunorubicin
O - oncovin/vincristine
P - prenisolone
221
Q

How does rituximab work?

A

Kills cells by antibody directed cytotoxicity and apoptosis induction, sensitises them to CHOP

222
Q

What type of cell is involved in myelomas?

A

Plasma cell

223
Q

What is the pathophysiology of a myeloma?

A

The abnormal proliferation of a single clone of plasma cell leads to secretion of Ig (IgG/A) or Ig fragment, causing the dysfunction of many organs

224
Q

Give 4 risk factors for myeloma

A
  • ) Increasing age
  • ) Male
  • ) Afro-Caribbean
  • ) Obesity
  • ) Radiation exposure
  • ) Family history
  • ) Immunosuppression
225
Q

Why is there no production of new bone in myelomas? (5)

A

1) Adhesion of stromal cells to myeloma cells
2) Production of RANK-L stimulated
3) RANK-L increases osteoclast formation
4) Increased bone reabsorption
5) Osteoblast activity inhibited by DKK1 produced by myeloma cells

226
Q

What end organ damage can myeloma cause?

A 
CRAB
Calcium (high)
Renal impairment
Anaemia
Bone disease
227
Q

What is the preceding phase of a myeloma?

A

MGUS - monoclonal gammopathy of undetermined significance

228
Q

Give 3 symptoms of myeloma

A
  • ) Backache
  • ) Pathological fractures
  • ) Vertebral collapse
  • ) Hypercalcaemia (confusion)
  • ) Anaemia (tiredness)
  • ) Infection
  • ) Bleeding
229
Q

What is a pathological fracture?

A

Fracture without significant trauma

230
Q

What do we see on an XR in myeloma?

A
  • ) Lytic ‘punched out’ lesions

- ) Pepper-pot skull

231
Q

What are the diagnostic criteria for myeloma? (4)

A

High index of suspicion with bone/back pain

1) Monoclonal protein band in serum/urine electrophoresis
2) Increased plasma cells on marrow biopsy
3) Evidence of end-organ damage (CRAB)
4) Bone lesions

232
Q

What is the supportive treatment for myeloma?

A
  • ) Analgesia (avoid NSAIDs)
  • ) Bisphosphonate
  • ) Local radiotherapy
  • ) Orthopaedic procedures
  • ) Blood transfusions/EPO
  • ) Rehydration
  • ) Antibiotics for infection
233
Q

What is the chemotherapy treatment for myeloma?

A
  • ) Induction therapy (e.g. CTD)

- ) Autologous stem cell transplantation

234
Q

What is CTD chemotherapy?

A

Cyclophosphamide
Thalidomide
Dexamethasone

235
Q

Give 3 other chemotherapy drugs used in the treatment of myeloma (not CTD)

A
  • ) Lenalidomide
  • ) Bortezomib
  • ) Dexamethasone
236
Q

What are the 4 signs of systemic inflammatory response syndrome? (SIRS)

A
  • ) Temperature >38 or <36
  • ) Tachycardia >90bpm
  • ) Respiratory rate >20breathspm
  • ) Very high/low WBC
237
Q

What is sepsis?

A

SIRS with an infection

238
Q

What is septic shock?

A

Severe sepsis with hypotension

239
Q

What is the treatment for SIRS?

A

Cultures and bloods before antibiotics, IV fluids, O2, vasopressors

240
Q

What is neutrophilia?

A

Too many neutrophils

241
Q

Give 3 causes of neutrophilia

A 
Reactive:
-) Infection
-) Inflammation
-) Malignancy
Primary:
-) CML
242
Q

What is neutropaenia?

A

Not enough neutrophils

243
Q

Give 4 causes of neutropaenia

A 
Underproduction:
-) Marrow failure
-) Marrow infiltration
-) Marrow toxicity
Increased removal:
-) Autoimmune
-) Felty's syndrome
-) Cyclical
244
Q

What is lymphocytosis?

A

Too many lymphocytes

245
Q

Give 3 causes of lymphocytosis

A 
Reactive:
-) Infection
-) Inflammation
-) Malignancy
Primary:
-) CLL
246
Q

What is lymphocytopaenia?

A

Too few lymphocytes

247
Q

What is thrombocytopenia?

A

Too few platelets

248
Q

What is thrombocytosis?

A

Too many platelets

249
Q

Give 3 causes of thrombocytosis

A 
Reactive:
-) Infection
-) Inflammation
-) Malignancy
Primary:
-) Essential thrombocythaemia
250
Q

Where are platelets produced?

A

Bone marrow

251
Q

Platelets are fragments of what?

A

Megakaryocytes

252
Q

What is the production of platelets regulated by?

A

Thrombopoietin (TPO)

253
Q

What is the normal lifespan of a platelet?

A

7-10 days

254
Q

What do platelets do?

A

Adhere and aggregate to form platelet plug, primary haemostasis

255
Q

How do platelets adhere to collagen?

A

Via GP1a

256
Q

How do platelets adhere to vWF?

A

Via GP1a and IIb/IIIa

257
Q

What is on the surface of platelets?

A

Glycoproteins

258
Q

Give 3 main causes of low platelets

A
  • ) Production failure (congenital, acquired by drugs etc)
  • ) Increased removal (immune, consumption, splenomegaly)
  • ) Artefactual (EDTA induced clumping)
259
Q

Give 2 causes of impaired platelet function

A
  • ) Congenital (platelet disorders vW disease)

- ) Acuquired (uraemia, drugs)

260
Q

Give 3 clinical features of platelet dysfunction

A
  • ) Mucosal bleeding
  • ) Easy bruising
  • ) Petechiae, purpura
  • ) Traumatic haematomas
261
Q

What are the 2 main causes of thrombocytopenia?

A
  • ) Decreased production

- ) Increased destruction

262
Q

Give 4 causes of decreased production in thrombocytopenia

A
  • ) Congenital
  • ) Infiltration of bone marrow (leukaemia)
  • ) Reduced platelet production by bone marrow (B12/folate/TPO/chemo)
  • ) Dysfunctional production of platelets in BM
263
Q

Give 4 causes of increased destruction in thrombocytopenia

A
  • ) Autoimmune (ITP)
  • ) Hypersplenism
  • ) Drug related immune destruction
  • ) Consumption of platelets (DIC, TTP)
264
Q

What are haemoglobinopathies? (2)

A
  • ) Disorders of quality

- ) Disorders of quantity

265
Q

Give an example of a disorder of quality haemoglobinopathy

A

Sickle cell disease

266
Q

Give an example of a disorder of quantity haemoglobinopathy

A

Alpha/beta thalassaemia

267
Q

What are membranopathies?

A

Deficiency of red cell membrane proteins caused by a variety of genetic lesions

268
Q

What type of genetic conditions are membranopathies?

A

Autosomal dominant

269
Q

What are the 2 most common membranopathies?

A

Spherocytosis and elliptocytosis

270
Q

Give 2 presentations of membranopathies

A
  • ) Neonatal jaundice
  • ) Anaemia
  • ) Gallstones
271
Q

What is the treatment for membranopathies?

A
  • ) Folic acid

- ) Splenectomy

272
Q

What is glucose 6 phosphate dehydrogenase deficiency? (G6PD)

A

X-linked RBC enzyme defect

273
Q

What is the non-asymptomatic presentation of G6PD?

A

Oxidative crises (rapid jaundice and anaemia) due to some drugs (aspirin)/illness/broad beans/henna

274
Q

What do blood films show in G6PD?

A

Bite and blister cells and Heinz bodies

Phase 2a Medicine - Riona COPY (17 decks)

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