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Phase 2a Annabel > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the 6 main cells to investigate on FBC?

A

RBC
Neutrophils
Lymphocytes
Platelets
Eosinophils
Monocytes

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2
Q

What are RBCs primarily used to diagnose on FBC?

A

Anaemias

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3
Q

What does a neutrophil value of >7.5 x10^4/L indicate?

A

Neutrophilia
Eg. Acute bacterial infection

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4
Q

What does a neutrophil value of <2 x 10^4/L indicate?

A

Neutropenia
Eg. Myeloma or lymphoma

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5
Q

What does a lymphocyte value of >3.5 x 10^4/L indicate?

A

Lymphocytosis
Eg. Chronic infection

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6
Q

What does a lymphocyte value of <1.3 x 10^4/L indicate?

A

Lymphocytopenia

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7
Q

What does a platelet value of >400 x 10^9/L indicate?

A

Thrombocytosis

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8
Q

What does a platelet value of <1.3 x 10^9/L indicate?

A

Thrombocytopenia

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9
Q

When are eosinophils elevated?

A

Parasitic infection

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10
Q

When are monocyte levels elevated?

A

Myelodyplastic syndromes

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11
Q

Define neutrophilia

A

Elevated neutrophil levels

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12
Q

Define neutropenia?

A

Low neutrophil levels

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13
Q

Define lymphocytosis

A

High lymphocyte levels

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14
Q

Define lymphocytopenia

A

Low lymphocyte levels

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15
Q

Define thrombocytosis

A

Elevated platelet levels

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16
Q

Define thrombocytopenia

A

Low platelet levels

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17
Q

What are 3 tests used for a clotting screen?

A

PT/INR (prothrombin time)
APTT (activated partial prothrombin time)
Fibrinogen

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18
Q

What is PT/INR used to investigate?

A

Coagulation speed through extrinsic pathway

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19
Q

How is INR calculated?

A

Patient PT
—————
Reference PT

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20
Q

What is normal INR without anticoagulants?

A

0.8-1.2

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21
Q

What is normal INR on warfarin?

A

2-3

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22
Q

What are 4 factors that may increase INR?

A
  1. Anticoags
  2. Liver disease
  3. Vit K deficiency
  4. DIC (disseminated intravascular coagulation)
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23
Q

What does APTT measure?

A

Coagulation speed through intrinsic pathway

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24
Q

What is the normal PT/INR time?

A

10-13.5s

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25
Q

What is the normal APTT time?

A

35-45s

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26
Q

What are 3 conditions where PT is normal and APTT is prolonged?

A

Haemophilia A
Haemophilia B
VWF disease

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27
Q

What is the normal fibrinogen -> fibrin time?

A

12-14s

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28
Q

Define anaemia

A

Low haemoglobin in the blood below the reference for the patients age and sex

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29
Q

How long does a RBC live?

A

120 days

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30
Q

Is anaemia a disease?

A

No- it is a result of an underlying disease

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31
Q

What is measured after an anaemia diagnosis?

A

Mean corpuscular/cell volume (MCV)

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32
Q

What are the 3 main classifications of anaemia?

A

Microcytic
Normocytic
Macrocytic

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33
Q

When should transfusion be considered for anemia?

A

Hb <70g/L
Or
Hb <80/L and cardiac comorbidity

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34
Q

What are the symptoms of anaemia?

A

Fatigue
Dysponea
Headache
Dizziness
Palpitations

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35
Q

What are 4 signs of anaemia?

A

Pallor
Conjunctival pallor
Tachycardia
Inc. respiratory rate

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36
Q

What level indicate microcytic anaemia?

A

<80

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37
Q

What are 5 causes of microcytic anaemia?

A

TAILS

Thalassaemia
Anaemia of chronic disease (sometimes!)
Iron deficiency (MC)
Lead poisoning
Sideroblastic anaemia

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38
Q

What is the most common cause of anemia worldwide?

A

Iron deficiency

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39
Q

Outline the pathophysiology of iron deficiency anaemia

A

Insufficiency of iron to produce RBCs

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40
Q

What are 4 causes of Fe deficient anaemia?

A

Blood loss- assume until proven otherwise!
Pregnancy
Impaired absorption
Poor diet

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41
Q

What are 3 causes of blood los that may result in Fe deficiency anaemia?

A

Menorrhagia
GI bleeding
Hookworm

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42
Q

What are 2 causes of impaired absorption that can result in Fe deficiency anaemia?

A

Coeliac or Chrons (as iron absorbed in GI tract)
Low stomach acid

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43
Q

When may Fe deficiency occur in infants?

A

Premature
Delayed mixed feeding (breast milk has low iron)

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44
Q

What are the symptoms of Fe deficiency anaemia?

A

General anaemia symptoms
Pruritis (itchy)
Nails changing - koilonychia
Angular stomatitis
Atrophic glossitis

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45
Q

What is koilonychia?

A

Spoon shaped nails

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46
Q

What is angular stomatitis?

A

Ulceration at corners of mouth

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47
Q

What is atrophic glossitis?

A

absence of papillae on tongue- looks smooth

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48
Q

How is Fe deficiency anaemia diagnosed on FBC and film?

A

Microcytic and hypochromic (pale) RBC
Poikilocytosis and anisocytosis
Howell Jolly bodies (nucleated RBC)

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49
Q

What is poikilocytosis?

A

Variation in RBC shape

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50
Q

What is anisocytosis?

A

Variation in RBC size

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51
Q

How is Fe deficiency anemia diagnosis confirmed?

A

Serum ferritin is LOW- reflects low amount of stored iron

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52
Q

What other bloods indicate Fe deficiency anaemia?

A

Low serum Fe
High TIBC (total iron binding capacity)
Low transferrin saturation
Low reticulocytes

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53
Q

What should be investigated when Fe deficiency anaemia occurs in older people?

A

Colonoscopy for GI bleed

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54
Q

How is Fe deficiency anemia treated?

A

Treat underlying cause
Oral Fe eg. Ferrous sulphate or ferrous gluconate
In extreme cases IV iron

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55
Q

What are the side effects of ferrous sulphate?

A

Black/green stools
Nausea
Diarrhoea or constipation

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56
Q

What are the normal percentages of haemoglobin in an adult human?

A

HbA = 97%
HbA2 (delta) = 2%
HbF (foetal) = 1%

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57
Q

What are thalassaemias?

A

Genetic disease of unbalanced Hb synthesis with underproduction of one globin chain

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58
Q

What is the normal structure of a Hb?

A

Haem + 2 alpha + 2 beta

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59
Q

How can thalassaemias lead to haemolysis?

A

Precipitation of imbalanced globin chains in precursors -> cell damage and death of precursors -> precipitation of imbalanced globin chains in mature cells -> haemolysis

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60
Q

Where are thalassaemias common?

A

Areas from Mediterranean to Far East
- in areas with prevalent malaria

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61
Q

Define beta thalassaemia

A

Reduced B chain synthesis
Excess A chain synthesis

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62
Q

Define alpha thalassaemia

A

Reduced A chain synthesis
Excess B chain synthesis

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63
Q

Which thalassaemia is most common?

A

Beta thalassaemia

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64
Q

What types of haemoglobin are increased in beta thalassaemia?

A

HbA2 (delta)
HbF (gamma)

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65
Q

What type of genetic mutation causes beta thalassaemia?

A

Autodom recessive
Often caused when genes MUTATED on chromosome 11

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66
Q

What type of gene mutation causes alpha thalassaemia?

A

Autodom recessive

Often caused by gene DELETIONS on chromosome 16

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67
Q

What are the 3 categories of beta thalassaemia?

A

B- thalassaemia minor
B- thalassaemia intermedia
B- thalassaemia major

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68
Q

What type of B-thalassaemia is a carrier heterozygous state?

A

B-thalassaemia minor

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69
Q

What are the symptoms of B-thalassaemia minor?

A

Asymptomatic
Mild or absent anaemia
Hypochromic (pale) RBC

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70
Q

How is B-thalassaemia minor distinguished from iron deficiency anaemia?

A

Serum ferritin and iron stores are normal
May have slightly raised HbA2 and usually raised HbF

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71
Q

Outline the pathophysiology of B-thalassaemia intermedia

A

reduced + absent beta genes
OR
Reduced + reduced beta genes

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72
Q

What are the symptoms of B-thalassaemia intermedia?

A

Symptomatic with moderate anaemia- doesn’t require regular transfusions
Splenomegaly
Recurrent leg ulcers
Gallstones
Bone deformities

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73
Q

Outline the pathophysiology of B-thalassaemia minor

A

Normal + reduced beta
OR
Normal + absent beta

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74
Q

Outline the pathophysiology of B-thalassaemia major

A

Absent + absent beta genes

FULL autorecessive

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75
Q

When does B-thalassaemia major present?

A

In first year of life

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76
Q

What are the symptoms of B-thalassaemia major?

A

Failure to thrive + bacterial infections
Severe anaemia at 3-6 months old
“Chipmunk” face
- bone expansion especially around cheekbones and
teeth protrude
Extramedullary haematopoesis -> hepatosplenomegaly

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77
Q

How is B-thalassaemia major diagnosed?

A

Microcytic
Large and small pale RBCs
Normal serum ferritin
High reticulocytes

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78
Q

What is the gold standard test for thalassaemia diagnosis?

A

Hb electrophoresis (testing for different types of haemoglobin)

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79
Q

How is B-thalassaemia major treated?

A

Transfusion every 2-4 weeks
Iron chelating agents to prevent iron overload
Large dose of ascorbic acid to inc. iron in wee
Marrow transplant if severe
Folic acid

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80
Q

What are 2 iron chelating agents?

A

Oral deferiprone
SC desderrioxamine

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81
Q

What are the side effects of iron chelating agents?

A

Pain
Deafness
Cataracts
Retinal damage

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82
Q

What are long term complications of transfusion?

A

Progressive increase in body iron load
- deposited in liver and spleen -> cirrhosis
- deposited in endocrine glands and heart -> diabetes, hypocalcaemia, death

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83
Q

What is HBH made from?

A

4 beta chains

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84
Q

What are the symptoms of a single gene A-thalassaemia?

A

Normal bloods- carrier

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85
Q

What are the symptoms of 2 gene A-thalassaemia deletion?

A

Microcytosis with/without mild anaemia

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86
Q

Outline the pathophysiology of 3 gene deletion A-thalassaemia?

A

Severe reduction in alpha chain synthesis -> HbH disease

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87
Q

What are the symptoms of 3 gene deletion A-thalassaemia?

A

Moderate anaemia
Splenomegaly

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88
Q

Outline the pathophysiology of 4 gene deletion A-thalassaemia

A

Deletion of both genes on both chromosomes -> ONLY HbH Bart’s is present

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89
Q

What is the prognosis of 4 gene A-thalassaemia deletion?

A

Incompatible with life
- Babies can die in uterine, stillborn or die very shortly after birth

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90
Q

How does 4 gene deletion A-thalassaemia present?

A

Pale
Oedematous
Hydrous fetalis
- enormous liver and spleen

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91
Q

Define sideroblastic anaemia

A

Defective Hb synthesis within mitochondria causing iron to be stuck in mitochondria

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92
Q

What causes sideroblastic anaemia?

A

X-linked
B6 deficiency
Idiopathic

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93
Q

Outline the pathophysiology of sideroblastic anaemia

A

Ineffective erythropoiesis -> inc. Fe absorption -> deposition in RBC

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94
Q

How would sideroblastic anaemia appear on a blood test?

A

Ringed sideroblastics
High serum ferritin
High serum iron

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95
Q

How is sideroblastic anaemia treated?

A

Hereditary may respond to pyridoxine (B6)

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96
Q

Define anaemia of chronic disease

A

Anaemia secondary to chronic disease

If body is ill, bone marrow will be too -> anaemia

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97
Q

Describe the MCV of anaemia of chronic disease

A

Usually normocytic but can be microcytic

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98
Q

What is the most common type of anaemia in hospital patients?

A

Anaemia of chronic disease

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99
Q

What are 5 conditions associate with anaemia of chronic disease?

A

TB
Chrons
Rheumatoid arthritis
SLE
Malignant disease

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100
Q

Outline the pathophysiology of anaemia of chronic disease

A

Decreased Fe release from marrow -> inadequate erthyropoetin response (drives RBC production) -> decreased RBC survival

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101
Q

What are the symptoms of anaemia of chronic disease?

A

Fatigue, headaches
Dysponea
Angina (CHD)
Anorexia

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102
Q

How is anaemia of chronic disease diagnosed?

A

Low serum Fe
Low TIBC

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103
Q

When may RBCs be microcytic in anaemia of chronic disease?

A

Rheumatoid arthritis
Chrons

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104
Q

How is anaemia of chronic disease treated?

A

Treat underlying cause
Erythropoietin can raise haemoglobin level

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105
Q

What MCV is normocytic?

A

80-95

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106
Q

What are the 2 categories of normocytic anaemia?

A

Haemolytic
Non- Haemolytic

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107
Q

What are 5 types of haemolytic normocytic anaemia?

A

Sickle cell
Hereditary spherocytosis
G6PD deficiency
Malaria
Autoimmune haemolytic

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108
Q

What are 2 types of non-haemolytic normoplastic anaemias?

A

CKD
Aplastic

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109
Q

What is an example of a RBC membrane defect?

A

Hereditary spherocytosis

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110
Q

Define hereditary spherocytosis

A

Autodom condition affecting the RBC membrane via causing a spectrin deficiency

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111
Q

Outline the pathophysiology of hereditary spherocytosis

A

RBC loses part of membrane -> Na+ moves out -> Sa/V ratio decreases -> RBCs become spherocytic -> more rigid -> cant pass through spleen so become trapped and destroyed via haemolysis

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112
Q

What are the symptoms of hereditary spherocytosis?

A

General anaemia
Neonatal jaundice
Splenomegaly
Can have gallstones

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113
Q

How is hereditary spherocytosis diagnosed?

A

Spherocytes and reticulocytes
Raised serum bilirubin and urinary urobilinogen
Negative Coomb’s test (rules out autoimmune)

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114
Q

How is hereditary spherocytosis treated?

A

Folate supplements+ splenectomy

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115
Q

Define G6PD deficiency

A

Deficiency of glucose-6-phosphate dehydrogenase

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116
Q

What causes G6PD deficiency?

A

Heterogenous X linked- affects men primarily but can affect women via lyonisation

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117
Q

What countries are most affected by G6PD deficiency?

A

Africa
Mediterranean
Middle East
SE Asia

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118
Q

Outline the pathophysiology of G6PD deficiency?

A

G6PD is vital for providing NADPH which can protect the RBC from oxidative damage -> reduced = more susceptible to damage -> shorter lifespan

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119
Q

What are the symptoms of G6PD deficiency?

A

Usually asymptomatic
Can cause HAEMOLTIC/OXIDATIVE CRISIS

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120
Q

What can cause oxidative/haemolytic crisis?

A

Aspirin
Antimalarials
Antibacterial
Fava beans can make it worse!

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121
Q

What is oxidative crisis/stress?

A

disturbance in the balance between the production of reactive oxygen species (free radicals) and antioxidant defenses

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122
Q

How is G6PD deficiency diagnosed?

A

Blood count normal between attacks
In attacks:
- Irregularly contracted cells
- Bite cells and Heinz bodies
- Increased reticulocytes
- Low G6PD right after the attack

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123
Q

How is G6PD treated?

A

Stop offending drugs or fava beans
Blood transfusion to save life
Splenectomy isn’t usually helpful

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124
Q

What are the symptoms of an oxidative crisis?

A

Rapid anaemia
Jaundice

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125
Q

What are the 2 types of autoimmune haemolytic anaemia?

A

Cold and warm subtypes

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126
Q

What is the most common subtype of autoimmune haemolytic anaemia?

A

Warm

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127
Q

Outline the pathophysiology of autoimmune haemolytic anaemia

A

Autoantibodies bind to RBCs and cause haemolysis

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128
Q

How is autoimmune haemolytic anaemia diagnosed (dd = hereditary spherocytosis)?

A

Positive direct Coombs test

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129
Q

What are 2 non-haemolytic anaemia?

A

CKD
Aplastic anaemia

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130
Q

Why does anaemia occur in CKD?

A

Fall in erythropoietin

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131
Q

What are the 3 characteristics of CKD anaemia?

A

Normocytic
Chronic
Decreased reticulocytes

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132
Q

How is autoimmune haemolytic anaemia treated?

A

Blood transfusion
Prednisolone
Rituximab (monoclonal Ab against B cell) Splenectomy

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133
Q

Define aplastic anaemia

A

Rare stem cell disorder of pancocytopenia (reduction of blood cells) and aplasia of bone marrow- essentially bone marrow stops making haemopoetic stem cells

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134
Q

What are the causes of aplastic anaemia?

A

Idiopathic
Inherited eg. fanconis anaemia
Benzene and sniffing glue
Chemotherapy
Antibiotics
Infection: EBV, HIV, TB

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135
Q

Outline the pathophysiology of aplastic anaemia

A

Reduction in erythropoetic cells and fault in remaining cells -> bone marrow can not be repopulated -> deficiency in major blood cells

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136
Q

What are the symptoms of aplastic anaemia?

A

Because of RBC, WBC and platelet deficiency

  • Anaemia
  • Increased infection
  • Bleeding
  • Bleeding gums and blood blisters in mouth
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137
Q

How is aplastic anaemia diagnosed?

A

FBC: pancocytopenia and low reticulocytes
Bone marrow: hypocellular marrow and increased fat spaces

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138
Q

How is aplastic anaemia treated?

A

Treat underlying cause
Broad spectrum antibiotics
RBC and platelet transfusion
Bone marrow transplants

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139
Q

When may a patient with aplastic anaemia need immunosuppressive therapy?

A

> 40
<40 with severe disease and no HLA sibling donor
Transfusion dependent

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140
Q

What is used for immunosuppressive treatment in aplastic anaemia?

A

Antithymocyte globulin (ATG)
Ciclosporin

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141
Q

Define sickle cell anemia

A

Autosomal recessive single gene defect in beta chain of haemoglobin

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142
Q

What gene is affected by sickle cell anaemia?

A

HBB

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142
Q

Who is primarily affected by sickle cell anaemia?

A

African
- Also India, Middle East and Southern Europe

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143
Q

What mutation causes sickle cell anaemia?

A

Single base mutation of GAG -> GTG which causes an amino acid substitution from glutamic acid -> valine on chromosome 11

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144
Q

What is sickle cell haemoglobin known as?

A

HbS

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145
Q

What are the characteristics of HbS?

A

Flexibility is reduced and cells become rigid, and eventually they will become irreversibly sickled

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146
Q

What are the affects of sickling on haemoglobin?

A

Shortened RBC survival -> haemolysis
Impaired passage through micro circulation -> obstruction of small vessels and tissue infarction

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147
Q

Why may patients with sickle cell anaemia feel well?

A

The cells release their oxygen more readily than normal RBCs usually!

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148
Q

What are the symptoms of heterozygous sickle cell anaemia?

A

Usually none!
Can experiments hypoxia in unpressurised plane or under anaesthetic

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149
Q

What are the general symptoms of homozygous SS anaemia?

A

Dactylitis(hands and feet swelling episode)
Anaemia
Jaundice
Splenomegaly
Delayed puberty

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150
Q

What are the symptoms of SSA vaso-occlusive crisis?

A

Dactylitis due to vaso-occlusion of small vessels in children
Pain in long bones in adults
CNS infarctions in children -> stroke, seizures

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151
Q

How often does vaso-occlusive crisis occur?

A

Depends on patient- can be every day to once a year

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152
Q

What is acute chest syndrome?

A

Vaso-occlusive crisis of the pulmonary vasculature

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153
Q

What is the most common cause of disease in adults with SSA?

A

Pulmonary hypertension and chronic lung disease

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154
Q

What causes acute chest syndrome?

A

Infection
Fat embolism
Pulmonary infarction (cells get stuck in vessel)

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155
Q

What are 3 symptoms of acute chest syndrome?

A

SOB
CP
Hypoxia

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156
Q

What causes pulmonary hypertension in patients with SSA?

A

Only 10%
Repeated chest crisis and repeated thromboembolism + intravascular haemolysis

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157
Q

What is aplastic crisis?

A

Occurs in SSA
Rapid fall in haemoglobin due to failure of erythopoesis

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158
Q

What causes aplastic crisis?

A

Parvovirus
Erythrovirus B19

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159
Q

What is splenic sequestration?

A

Sickle cells become trapped in spleen

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160
Q

What are the complications of splenic sequestration?

A

Fibrotic spleen
Painful enlargement
In children need URGENT transfusion

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161
Q

How is SSA diagnosed?

A

Heel prick at birth
FBC: 60-80Hb and raised reticulocytes
Positive sickle solubility test

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162
Q

What is the gold standard diagnosis for SSA?

A

Hb electrophoresis
- Shows 80-95% HbS and NO HbA

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163
Q

How is sickle cell anaemia treated?

A

Hydroxycarbamide (raises HbF)
Avoid precipitating factors
Stem cell transplant

164
Q

How are complicated attacks of SSA treated?

A

IV fluids
Analgesia
Oxygen and antibiotics
Transfusion

165
Q

What MCV value indicates macrocytic anaemia?

A

95 <

166
Q

What are the 2 subcategories of macrocytic anaemia?

A

Megaloblastic
Non-megaloblastic

167
Q

What are 2 types of megaloblastic anaemia?

A

B12 deficiency
Folate deficiency

168
Q

What are 3 causes of non-megaloblastic anaemia?

A

Hypothyroidism
Alcohol excess
Liver disease

169
Q

What is the main cause of B12 deficiency anaemia?

A

Pernicious anaemia

170
Q

Where is B12 found?

A

NOT PLANTS

Meat
Fish
Dairy

171
Q

How is B12 absorbed?

A

Binds to transcobalamin-1 in mouth -> binds to intrinsic factor -> absorbed in terminal ileum

172
Q

What produces intrinsic factor?

A

Parietal cells in the stomach

173
Q

Where is B12 absorbed?

A

Terminal ileum

174
Q

Outline the pathophysiology of B12 deficiency anaemia

A

Lack of B12 -> lack of thymidine -> lack of DNA synthesis -> delayed nuclear maturation -> large and decreased RBCs

175
Q

Why does B12 deficiency anaemia take years to manifest?

A

Body’s stores last around 4 years

176
Q

Define pernicious anaemia

A

Autoimmune disorder where the parietal cells are attacked -> atrophic gastritis -> loss of intrinsic factor production -> B12 malabsorption

177
Q

What are 3 causes of B12 anaemia?

A

Diet
Malabsorption
Pernicious anaemia

178
Q

What are the risk factors of B12 anaemia?

A

Elderly
Female
Vegan
Fair hair and blue eyes
Blood group A
Thyroid and Addisons

179
Q

What are the symptoms of B12 deficiency anaemia?

A

General anaemia
Lemon-yellow skin (pallor + jaundice)
Glossitis
Angular stomatitis

180
Q

How is pernicious anaemia (specifically) diagnosed?

A

Parietal cell antibodies
Intrinsic factor antibodies- 50% (GS)

181
Q

When do neurological symptoms appear in pernicious anaemia?

A

VERY low levels of B12

182
Q

What are some neurological symptoms of B12 deficiency anaemia?

A

Symmetrical parasthesia in fingers and toes
Loss of vibration sense and proprioception
Dementia and psychiatric problems

183
Q

How is B12 deficiency anaemia treated?

A

If not pernicious treat cause
Malabsorption = injections
Dietary = oral B12
IM hydrocycolbamin

184
Q

How does B12 deficiency anaemia show up on blood film?

A

Macrocytic
Megaloblasts
Low reticulocytes

185
Q

What are megaloblasts?

A

Hypersegmented nucleated neutrophils (6+) and basophilic

186
Q

What is folate found in?

A

Green veg
- Spinach
- broccoli
- Nuts
- yeast
- Liver

187
Q

Why does folate deficiency manifest much quicker than B12 deficiency anaemia?

A

Body stores only last 4 months

188
Q

Where is folate absorbed?

A

Duodenum and proximal jejunum

189
Q

Outline the pathophysiology of folate deficiency anaemia

A

Needed for DNA synthesis so folate deficiency -> impaired DNA synthesis -> delayed nuclear maturation -> large RBCs and reduced production

190
Q

How can folate deficiency affect foetal development?

A

Can cause neural tube defects eg. Spina bifida

191
Q

What are 4 causes of folate deficiency?

A

MC: poor intake eg. Poverty, alcoholics, elderly
Malabsorption
Increased demand eg. Pregnancy
Anti folate drugs

192
Q

What are 2 drugs that can cause folate deficiency?

A

Methotrexate
Trimethoprim

193
Q

What are the signs of folate deficiency anemia on bloods?

A

Macrocytic cells
Oval macrocytes (large RBCs)
Hypersegmented neutrophil polymorphs
Low serum folate

194
Q

How is folate deficiency anaemia treated?

A

Folic acid tablets daily for 4 months
Give with B12 unless patient is known to have normal B12

195
Q

Why is B12 given alongside folic acid tablets?

A

In low B12 states, folate can precipitate subacute combined degeneration of the spinal cord

196
Q

How can alcohol cause anaemia?

A

Toxic to RBCs
Depletes folate

197
Q

How can hypothyroidism cause anaemia?

A

Interference with erythropoietin

198
Q

How can liver disease cause anaemia?

A

Liver decompensated cirrhosis associated with macrocytic anaemia

199
Q

What are the 2 main types of blood cancer?

A

Leukaemia
Lymphoma

200
Q

What are the 4 main subtypes of leukaemia?

A

Acute lymphoblastic leukaemia (ALL)
Acute myeloid leukaemia (AML)
Chronic myeloid leukaemia (CML)
Chronic lymphocytic leukaemia (CLL)

201
Q

Define leukaemia broadly

A

Presence of rapidly proliferating immature blast cells in the bone marrow that are non-functional

202
Q

Outline the basic pathophysiology of leukaemia

A
  1. Cells rapidly proliferate but have no function -> energy wasting -> less energy to make useful cell
  2. Rapid replication takes up lots of space in the bone marrow -> no space or nutrients for other cells to grow
  3. Normal cells not made so non functional cells enter bloodstream
203
Q

What cells are proliferated in AML?

A

Myeloblasts

204
Q

What 3 cells do myeloblasts give rise to?

A

Basophils
Neutrophils
Eosinophils

205
Q

What is the prognosis of untreated AML?

A

Death in 2 months

206
Q

What is the most common acute leukaemia in adults?

A

AML

207
Q

What are 4 risk factors of AML?

A

associated with myelodysplastic syndromes
Down’s syndrome
Age
Chemo and radiation

208
Q

What are the clinical presentations of AML?

A

BM failure: anaemia, infections and bleeding
Hepatomegaly and Splenomegaly
Gum hypertrophy
Thrombocytopenia

209
Q

How is AML diagnosed?

A

Bone marrow biopsy to differentiate from ALL ( min 20% blasts)
Auer rods
Leukocytosis
Blood film morphology- min 20% (GS)

210
Q

What is given to people undergoing chemo to prevent tumour lysis syndrome?

A

Allopurinol
Chemo releases uric acid which can accumulate -> malignancy

211
Q

How is AML treated?

A

Chemo (cytarabine and anthracycline)
Blood, platelet and marrow transfusion
ATRA for APL subtype
Fluids

212
Q

What are the complications of AML?

A

Infection
Common organisms present oddly

213
Q

The proliferation of which cell causes ALL?

A

Immature lymphoid (lymphoblasts) cells

214
Q

Which cells do immature lymphoid cells give rise to?

A

B lymphocytes
T lymphocytes

215
Q

What is the most common childhood cancer?

A

ALL

216
Q

Who does ALL most commonly affect?

A

People aged 2-4

217
Q

What are some risk factors for ALL?

A

Down’s syndrome
Ionising radiation and X-rays during pregnancy
Genetics

218
Q

What cells are proliferated in the bone marrow in ALL in adults and children?

A

Adults = all T cells
Children = all B cells

219
Q

What are the symptoms of ALL?

A

BM failure: anaemia, infection, bleeding
Bone pain
Hepatosplenomegaly
Lymphadenopathy
CNS infiltration

220
Q

What is the prognosis of ALL?

A

Good prognosis! :)

221
Q

How is ALL diagnosed?

A

FBC: WCC high, blast cells on film and in BM
TdT
Pancytopoenia
BM biopsy >20 % (GS)
Lumbar puncture for CNS involvement

222
Q

How is ALL treated?

A

Blood, marrow and platelet transfusion
Chemo and allopurinol
Neutropenic prophylaxis when in chemo

223
Q

Define chronic myeloid leukaemia

A

Uncontrolled proliferation of mature myeloid cells

224
Q

Which cells rise from myeloid cells?

A

Myeloblasts (->eosinophils, basophils, neutrophils)
Precursors of:
Platelets
RBCs
Monocytes

225
Q

Outline the epidemiology of CML

A

Almost exclusively adults
Slightly more common in males
More than 80% have Philadelphia chromosome

226
Q

What chromosome is affected by Philadelphia chromosome?

A

22

227
Q

Outline the aetiology of the Philadelphia chromosome

A

Translocation between chromosome 9 and 22
BCR fuses with ABL -> BCR/ABL -> oncogene
Oncogene has tyrosine kinase activity -> stimulates cell division

228
Q

What are the 3 phases of CML?

A
  1. Chronic = little if any symptoms
  2. Accelerated phase = increasing symptoms (Splenomegaly, anaemia, thrombocytopenia)
  3. Blast transformation = acute leukaemia symptoms + death (over 30% blasts in blood)
229
Q

What are the symptoms of CML?

A

MASSIVE Splenomegaly
Symptomatic anaemia
gout
Hyperviscosity (headaches and thrombotic events)

230
Q

How is CML diagnosed?

A

High WBC
Low Hb
Hypercellular BM
Karotyping for Philadelphia chromosome (BCR-ABL) (~80%)

231
Q

How is CML treated?

A

Tyrosine kinase inhibitor
- 1st line = imatinib
Chemo in blast crisis

232
Q

What is a complication of blast crisis?

A

Pancytopenia
- All cells deficient in blood

233
Q

What can CML progress to if untreated?

A

AML

234
Q

Define CLL

A

Chronic proliferation of a single type of well differentiated lymphocyte

235
Q

What cell is most commonly proliferated in CLL?

A

B-lymphocyte

236
Q

What are the risk factors of CLL?

A

Older age
Male
Mutations, trisomies, deletions
Can be triggered by pneumonia

237
Q

Outline the pathophysiology of CLL

A

Failure of cell apoptosis- B cells accumulate

238
Q

What are the symptoms of CLL?

A

Can be asymptomatic (diagnosed on FBC)
Anaemia and prone to infection
Hepatosplenomegaly
Non tender lymphadenopathy

239
Q

How is CLL diagnosed?

A

Normal or low Hb
Raised WBC (especially lymphocytes)
Smudge cells on blood film

240
Q

What do smudge cells indicate?

A

CLL

241
Q

What do Auer rods indicate?

A

AML

242
Q

What is the Rai staging system used for?

A

CLL

243
Q

What does a 0 on the rai staging indicate?

A

Clonal lymphocytosis

244
Q

What does a 1 on Rai staging indicate?

A

Lymphocytosis and lymphadenopathy

245
Q

What does 2 on Rai staging indicate?

A

Lymphocytosis and hepatomegaly

246
Q

What does 3 on Rai staging indicate?

A

Lymphocytosis and anaemia

247
Q

What does 4 on Rai staging indicate?

A

Lymphocytosis and thrombocytopenia

248
Q

How is symptomatic CLL treated?

A

Radiotherapy and chemotherapy
IVIg (IV Ig)

249
Q

What is a major complication of CLL?

A

Richters transformation

250
Q

What is Richter’s transformation?

A

B cells massively accumulates in lymph nodes -> lymphadenopathy -> aggressive non-Hodgkin’s lymphoma

251
Q

What is the prognosis of CLL?

A

1/3 wont progress
1/3 progress slowly
1/3 progress actively

252
Q

What are the 2 types of lymphoma?

A

Hodgkin lymphoma
Non-Hodgkin lymphoma

253
Q

What differentiates Hodgkins lymphoma from Non-Hodgkins?

A

Hodgkins has Reed-Sternberg cells
Non-Hodgkins doesnt

Hodgkins = Neutrophilia
Non-Hodgkins = neutropenia

254
Q

What are Reed-Sternberg cells?

A

“Owl eye” nuclei cells

Abnormally large B cells with multiple nuclei and nucleoli - looks like an owl!

255
Q

Define lymphoma

A

Disorders caused by malignant proliferations of lymphocytes -> accumulate in lymph nodes -> lymphadenopathy -> can enter blood or organ

256
Q

Define lymphadenopathy

A

Enlarged lymph nodes

257
Q

Outline the epidemiology of Hodgkin’s lymphoma

A

Peaks in teens and elderly
Male

258
Q

What are the risk factors of Hodgkin’s lymphoma?

A

EBV infection
Affected siblings
Autoimmune conditions
Post transplant

259
Q

What are the symptoms of Hodgkin’s lymphoma?

A

Enlarged non-tender rubbery superficial lymph nodes
Pain after drinking alcohol
B symptoms

259
Q

What are the 3 “B symptoms”?

A

Fever
Weight loss
Night sweats

259
Q

What is the GS for Hodgkin’s lymphoma diagnosis?

A

Excision lymph node biopsy
- Shows Reed-Sternberg cells

259
Q

What are the 2 types of Hodgkin’s lymphoma?

A

Classical Hodgkin’s lymphoma (cHL)
Nodular lymphocyte predominant Hodgkin’s Lymphoma (NLPHL)

259
Q

What type of cell are visible in cHL?

A

Reed-Sternberg cells with mirror image nuclei

259
Q

How do the cells appear in NLPHL?

A

Reed Sternberg variant: popcorn cell

259
Q

What would a Philadelphia chromosome indicate?

A

CML

260
Q

What are bloods like in Hodgkin’s lymphoma?

A

Increased LDH
Increased ESR
Decreased Hb

261
Q

How is Hodgkin’s lymphoma classified?

A

Ann Arbor classification

262
Q

What does I on Ann Arbor staging indicate?

A

Confined to a single lymph node region

263
Q

What does II on Ann Arbor staging indicate?

A

Involvement of 2 or more nodal areas on the same side of the diaphragm (above or below)

264
Q

What does III on Ann Arbor staging indicate?

A

Involvement of nodes on both sides of the diaphragm

265
Q

What does IV on Ann Arbor staging indicate?

A

Spread beyond the lymph nodes
Eg. Liver or bone marrow

266
Q

What does an A on Ann Arbor staging indicate?

A

No systemic symptoms other than pruritus

267
Q

Define pruritus

A

Severe itching of skin

268
Q

What does a B on Ann Arbor staging indicate?

A

Presence of B symptoms

269
Q

How is Ia and IIa Hodgkin’s lymphoma treated?

A

Radiotherapy and short courses of chemo (ABVD)

270
Q

How is stage IIa to IVb Hodgkin’s lymphoma treated?

A

Combination chemo- ABVD

A- Adriamycin
B- Bleomycin
V- Vinblastine
D- Dacarbazine

271
Q

What are 4 side effects of radiotherapy?

A

Increased risks of secondary malignancies
IHD
Hypothyroidism
Lung fibrosis

272
Q

What are 5 side effects of chemotherapy?

A

Myelosuppression
Nausea
Alopecia
Infection
Infertility

273
Q

When does febrile neutropenia occur?

A

Recent high dose of chemotherapy or on carbimazole

274
Q

What 3 symptoms indicate worse prognosis for Hodgkin’s lymphoma?

A

B symptoms
Low Hb
Raised LDH

275
Q

What are the symptoms of febrile neutropenia?

A

Fever
Tachycardia
Sweats
Tachypnoea

276
Q

How is febrile neutropenia treated?

A

piperacillin and tazobactam

277
Q

What is the most common type of non-Hodgkin’s lymphoma?

A

DLBCL- diffuse large B-cell lymphoma

278
Q

What are 3 types of non-Hodgkin’s lymphoma?

A

DLBCL
Burkitts lymphoma
Follicular

279
Q

Outline the aetiology of non-Hodgkin’s lymphoma

A

Strong link between EBV and Burkitts lymphoma
Inc. risk with family history
Hep C
H. Pylori

280
Q

What are the symptoms of non-Hodgkin’s lymphoma?

A

Superficial symmetrical lymphadenopathy- painless and rubbery
B- symptoms
Extranodal disease

281
Q

How is non-Hodgkin’s lymphoma diagnosed?

A

Lymph node excision or BM biopsy- NO Reed-Sternberg cells
CT/MRI for staging

282
Q

How is Non-Hodgkin’s lymphoma classified?

A

Low grade: slowly growing, advanced at presentation
High grade: nodal presentation

283
Q

What is the prognosis of low grade non-Hodgkin’s lymphoma?

A

Incurable but goodish prognosis - median survival 9-11 years

284
Q

What is an example of low grade non-Hodgkin’s lymphoma?

A

Follicular lymphoma

285
Q

What is an example of high grade non-Hodgkin’s lymphoma?

A

DLBCL

286
Q

What is the prognosis of high grade non-Hodgkin’s lymphoma?

A

Aggressive but often curable

287
Q

How is non-Hodgkin’s lymphoma treated?

A

R-CHOP

R- Rituximab
C- Cyclophosphamide
H- Hydroxy-daunorubicin
O- Oncovin/ Vincristine
P- Prednisolone

288
Q

What is rituximab?

A

Monoclonal antibod targeting CD20 from B cell surface

289
Q

What is the typical sign of Burkitts lymphoma?

A

Jaw lymphadenopathy in children

290
Q

What is the difference between lymphadenopathy in Hodgkin’s and non-Hodgkin’s lymphoma?

A

Hodgkin’s is painful after alcohol, non-Hodgkin’s unaffected

291
Q

Define febrile neutropenia

A

Temperature above 38 degrees in a patient with absolute neutrophil count (<1x10^9/L)

292
Q

Define multiple myeloma

A

Neoplastic monoclonal proliferation of plasma cells

293
Q

What are the 2 most common immunoglobulin excesses in MM?

A

IgG (55%)
IgA (20%)

294
Q

Outline the pathophysiology of MM

A

Excess of one Ig -> other Ig levels low -> accumulation of malignant cells -> BM failure

295
Q

What are 3 complications of MM?

A

Bone disease
Hypercalcaemia
Renal failure

296
Q

Outline the epidemiology of MM?

A

peaks at 70 years old
Afro-carribeans

297
Q

What are the clinical presentations of MM?

A

OLD CRAB

OLD age
Calcium elevated
Renal failure (raised Ig)
Anaemia
Bone lytic lesions (back pain)

298
Q

What does Rouleux formation on blood film indicate?

A

MM

299
Q

What do Bence-jones proteins in urine indicate?

A

MM

300
Q

How does MM show on bloods?

A

Normocytic normochromic anaemia
Raised ESR
Rouleux formation

Electrophoresis shows “M spike” of proliferated Ig

301
Q

How does MM show on U&Es?

A

High Ca
High alkaline phosphotase
Bence jones protein in urine

302
Q

How does MM appear on X-ray?

A

Lytic ‘punched out lesions” - Pepper pot skull
Fractures
Osteoporosis

303
Q

What 4 criteria are required for MM diagnosis?

A

Monoclonal protein band in serum or urine
Inc. plasma cells on BM biopsy
Hypercalcaemia/ renal failure/ anaemia
Bone lesions

304
Q

How is MM treated?

A

Chemo- CTD or VAD
Stem cell transplant
Biphosphonates
Dialysis for real failure

305
Q

What is an example of a Biphosphonate?

A

Zolendronate

306
Q

What is CTD chemo?

A

For less healthy people (MM)

Cyclophosphamide
Thalidomide
Dexamethasone

307
Q

What is VAD chemo?

A

For healthier people (MM)

Vincristine
Adriamycin
Dexamethasone

308
Q

What is the differential diagnosis of MM?

A

MGUS- mammloid gammopathy of undetermined significance

<10% plasma cells
Asymptomatic

309
Q

Define polycythaemia

A

Any increase in RBCs

310
Q

Define erythrocytosis

A

An increase in RBC mass

311
Q

What are 4 causes of polycythaemia?

A

Primary: Polycythaemia Vera
Secondary:
Hypoxia
Increased EPO
Dehydration

312
Q

Define polycythaemia Vera

A

Malignant proliferation of a clone derived from one pluripotent stem cell (especially RBCs)

313
Q

Outline the epidemiology of PV

A

Over 95% have JAK2 mutation
>60

314
Q

What is a JAK2 mutation?

A

Mutation from valine -> phenylalanine on chromosome 9

315
Q

How does JAK2 mutation cause PV?

A

JAK2 is a cytoplasmic tyrosine kinase that transducers signals such as haemopoietic factors (erythropoietin)

316
Q

What are the 2 major complications of PV?

A

Hyperviscosity causes:

Thrombosis
Haemmorage

317
Q

What are the clinical presentations of PV?

A

Severe itching after hot bath or when warm
Visual disturbances and headaches
Erythromelalgia
Plethoric complexion
Hepatosplenomegaly

318
Q

What is erythromelalgia?

A

Burning sensation in fingers and toes

319
Q

How is PV diagnosed?

A

Raised WCC and platelets
Raised Hb
JAK2 mutation on genetic screen

320
Q

How is PV treated?

A

No cure- aim to maintain normal BC

Venesection: removal of 400-500ml of blood a week
Chemo in high risk patients
- Hydroxycaramide
Aspirin

321
Q

What is the function of thrombopoetin?

A

Stimulates production of platelets by megakaryocytes

322
Q

Where is TPO produced?

A

Mainly the liver
- Liver damage = reduced TPO = reduced platelets

323
Q

What is the function of P2Y12?

A

Amplifies platelet activation
Activates glycoprotein IIb/IIia

324
Q

What activates P2Y12?

A

ADP

325
Q

What is the function for Gp IIb/IIIa?

A

Receptor for fibrinogen and vWF
Aids platelet adherence and aggregation

326
Q

What are the 3 functions of vWF?

A

Brings platelets to endothelium
Binds platelets
Binds to factor VIII for protection

327
Q

Define thrombocytopenia

A

Deficiency of platelets in the blood

328
Q

What are 2 types of thrombocytopenia?

A

Immune thrombocytopenia purpura (ITP) - MC
Thrombotic thrombocytopenic purpura (TTP)

329
Q

What causes ITP?

A

Immune destruction of antibody coated platelets by IgG antibodies

330
Q

Who is affected by primary/acute ITP?

A

Children age 2-6

331
Q

What are the causes/risk factors of primary ITP?

A

History of recent viral infection
- chickenpox (varicella zoster) or measles
Can follow immunisation

332
Q

What are the 2 features of primary ITP?

A

Muco-cutaneous bleeding
Sudden self limiting purpura (red or purple spots)

333
Q

Who is affected by secondary/chronic ITP?

A

Women
Autoimmune disease such as SLE, thyroid issues, AHA
CLL
HIV and Hep C

334
Q

What are the clinical presentations of ITP?

A

SYSTEMICALLY WELL
Purpuric rash
Easy bleeding
Splenomegaly RARE

335
Q

How is ITP diagnosed?

A

BM: thrombocytopenia with raised megakaryocytes
Platelet autoantibodies in ~70%

336
Q

How is ITP treated?

A
  1. Prednisolone and IV IgG
  2. Splenectomy or azathioprine
337
Q

What type of drug is azathioprine?

A

Immunosuppressant

338
Q

Outline the pathophysiology of TTP

A

Reduction in ADAMTS-13 -> no vWF degradation -> platelet aggregation and deposition -> microthrombi -> Overconsumption of platelets -> thrombocytopenia

339
Q

What are 3 causes of TTP?

A

Idiopathic
Autoimmune
Cancer
Pregnancy
Drugs (quinine)

340
Q

What are the symptoms of TTP?

A

SYSTEMICALLY UNWELL
Florid purpura
Fever
Fluctuating cerebral dysfunction
Haemolytic anaemia and AKI

341
Q

How is TTP diagnosed?

A

Schistocytes
Decreased ADAMTS-13

342
Q

How is TTP treated?

A

Plasma exchange (remove ADAMTS-13)
IV methyprednisolone
IV rituximab

343
Q

What is the MC inherited bleeding disorder?

A

Von Willebrand disease

344
Q

How is haemophilia inherited?

A

X-linked recessive

345
Q

What does haemophilia A cause?

A

Factor 8 deficiency

346
Q

What does haemophilia B cause?

A

Factor 9 deficiency

347
Q

Is haemophilia A or B more common?

A

A

348
Q

What are the symptoms of haemophilia?

A

Haemarthrosis- bleeding into joints]
Haematoma- bleeding into muscles
Spontaneous bleeding

349
Q

How is haemophilia A diagnosed?

A

Low factor 8 on essay
High APTT
Normal PT

350
Q

How is haemophilia B diagnosed?

A

Factor 9 high on essay
High APTT
Normal PT

351
Q

Which pathway is affected in haemophilia?

A

Intrinsic

352
Q

How is haemophilia A treated?

A

Recombinant factor 8 (major bleed)
Desmopressin (Minor bleed)

353
Q

How is haemophilia B treated?

A

Recombinant factor 9

354
Q

What causes Von willebrands disease?

A

Autosomal dominant mutation of vWF gene on chromosome 12

355
Q

What are the 3 subtypes of Von willebrand disease?

A

1: low vWF
2: abnormal vWF
3: undetectable vWF

356
Q

What are the symptoms of Von willebrand disease?

A

Bruising and easy bleeding
Epistaxis- nose bleeds
Menhorragia

357
Q

How is Von willebrand disease diagnosed?

A

high APTT
normal PT
Factor 8 and 9 normal
Low vWF

358
Q

How is Von willebrand disease treated?

A

Desmopressin
VWF containing concentrate

359
Q

What does DIC stand for?

A

Disseminated intravascular coagulation

360
Q

Does DIC occur in isolation?

A

NO - crisis secondary to clinical disorder or trauma

361
Q

What happens in DIC?

A

inappropriate activation of the clotting cascades, resulting in thrombus formation and depletion of clotting factors and platelets.

362
Q

What are 3 causes of DIC?

A

Sepsis
Major trauma
APL (acute promyelotic leukaemia)
Advanced cancer
Obstetric complications

363
Q

What are the symptoms of DIC?

A

Acute illness and shock
Bleeding from nose, mouth, venupuncture sites
Widespread Bruising

364
Q

How is DIC diagnosed?

A

Severe thrombocytopenia
Decreased fibrinogen
Elevated D-dimer
Prolonged PT, APTT

365
Q

How is DIC treated?

A

Treat underlying condition
Replace platelet
Fresh frozen plasma (FFP)

366
Q

What is tumour lysis syndrome?

A

Occurs when malignant cell break down and release their contents in chemotherapy

367
Q

What patients are at risk of tumour lysis syndrome?

A

High grade disease
Renal impairment
Old age

368
Q

How is tumour lysis syndrome treated?

A

Prevented by allopurinol

Aggressive hydration
May need dialysis

369
Q

What are 2 causes of Hyperviscosity syndrome?

A

High levels of Igs (MM)
High cell numbers eg. Leukaemia

370
Q

What are 2 effects of Hyperviscosity syndrome?

A

Vascular stasis
Hypoperfusion

371
Q

What are 3 symptoms of Hyperviscosity syndrome?

A

Mucosal bleeding
Vision changes
SOB
Neurological disturbances
Gum bleeding

372
Q

How is Hyperviscosity syndrome diagnosed?

A

Plasma viscosity level
CT to exclude other signs
FBC and Ig levels

373
Q

How is Hyperviscosity syndrome treated?

A

Hydrated
Avoid transfusion
Plasmapheresis to remove Igs

374
Q

What causes malaria?

A

Female anopheles mosquito carries:
MC: plasmodium faliparum
Also: p.Ovale, P.vivax

375
Q

Outline the epidemiology of malaria

A

Africa
Very young
Very old
Pregnancy

376
Q

What enters the blood from mosquito saliva that can cause malaria?

A

Sporozoites

377
Q

What do Sporozoites transform into in hepatocytes?

A

Merozoites

378
Q

How do merozoites develop in RBCs?

A

Merozoites -> trophozoites -> schizont -> new Merozoites

379
Q

What are the symptoms of malaria?

A

RECENT TRAVEL

Fever
Black water fever
Hepatosplenomegaly
Convulsions in children

380
Q

How is malaria diagnosed?

A

Thick and thin blood film

381
Q

How is malaria treated?

A

Quinine/chloroquine and doxycycline
Severe = IV artesunate

382
Q

What are 2 other names for EBV?

A

Glandular fever
Infectious mononucleosis

383
Q

How is EBV spread?

A

Saliva or bodily fluids

384
Q

How is EBV diagnosed?

A

Atypical lymphocytes on blood film

385
Q

What are 3 conditions associated with EBV?

A

Hodgkins
Burkitts
Nasopharyngeal carcinoma

386
Q

How is EBV treated?

A

Usually self limiting!

387
Q

How is HIV transmitted?

A

Bodily fluids:
Sexual transmission
Sharing needles

388
Q

What are 2 types of HIV?

A

HIV-1: MC, most virulent
HIV-2: LC, less virulent

389
Q

Outline the 6 stages of HIV entering the body

A
  1. HIV binds to Th
  2. Endocytoses RNA and enzymes
  3. Reverse transcriptase RNA->DNA
  4. Integrase viral DNA integrated into host
  5. Protein synthesis
  6. Viral proteins and RNA exocytose and decrease CD4 and Th cells
390
Q

What are the 4 stages of HIV?

A
  1. Infection: CD4 dip
  2. Clinical latency (years)
  3. Symptoms
  4. AIDS
391
Q

What are the symptoms of HIV?

A

Fever
Diarrhoea
Night sweats
Minor infections

392
Q

What CD4 values indicate AIDS?

A

<200/mm^3

393
Q

What are 3 AIDS defining conditions?

A

CMV - MC
PCP (pneumonia) - MC
Cytosporidium infection
TB
Kaposi sarcoma
Toxoplasmosis
Lymphomas

394
Q

How is HIV diagnosed?

A

History and anti HIV Ig (ELISA)
P24 ab
Monitor HIV RNA copies and CD4

395
Q

How is HIV treated?

A

HAART (highly active antiretroviral therapy)
Reverse transcriptase inhibitors

396
Q

Defibe myelodeplastic syndromes

A

myeloid bone marrow cells fail to mature

397
Q

When are Heinz bodies present?

A

G6PD deficency
Thalassaemia

398
Q

How is symptomatic A-thalassaemia treated?

A

Bone marrow and blood transfusion
Splenectomy

399
Q

What is the difference between acute and chronic leukaemia?

A

Acute: impaired differentiation of precursor
Chronic: excessive proliferation of mature cell

400
Q

What are the symptoms of tumour lysis syndrome?

A

2 days after high dose chemo

Dysuria
Abdo pain
Weakness

401
Q

How is tumour lysis syndrome diagnosed?

A

potassium and phosphate are typically raised
Low calcium
Raised uric acid
Electrolyte abnormalities

402
Q

What is the GS for MM diagnosis?

A

Bone biopsy

Phase 2a Annabel (12 decks)

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