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Y4 Cancer > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the 4 main types of leukaemia ?

A

Acute myeloid leukaemia
Acute lymphoblastic leukaemia
Chronic myeloid leukaemia
Chronic lymphocytic leukaemia

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2
Q

What leukaemia most commonly affects children under 5 ?

A

Acute lymphoblastic leukaemia

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3
Q

How can leukaemia present ?

A

Fatigue
Fever
Pallor
Petechiae
Abnormal bleeding
Hepatosplenomegaly

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4
Q

What are some differentials for a non-blanching rash ?

A

Leukaemia
Meningococcal septicaemia
Vasculitis
Henoch-schonlein purpura
ITP
Non-accidental injury

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5
Q

What is acute lymphoblastic leukaemia associated with ?

A

Down’s syndrome

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6
Q

How does acute lymphoblastic leukaemia cause pancytopenia ?

A

Affects the lymphocyte precursor cells causing acute proliferation of a single type of lymphocyte usually B cells.
Excessive accumulation of these cells replaces the other cell types in the bone marrow leading to pancytopenia.

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7
Q

What occurs in chronic lymphocytic leukaemia ?

A

Slow proliferation of a single type of well-differentiated lymphocyte usually B cells.

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8
Q

How does chronic lymphocytic leukaemia present ?

A

Asymptomatic
Infections
Anaemia
Bleeding
Weight loss

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9
Q

What is Richter’s transformation ?

A

The rare transformation of chronic lymphocytic leukaemia into high grade B cell lymphoma.

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10
Q

What appears on a blood film in chronic lymphocytic leukaemia ?

A

Smear or smudge cells due to ruptured white blood cells that occur while preparing the blood film due to cells being fragile and aged.

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11
Q

What are the 3 phases of chronic myeloid leukaemia ?

A

Chronic phase
Accelerated phase
Blast phase

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12
Q

What happens in the first phase of chronic myeloid leukaemia ?

A

Often asymptomatic and patients are diagnosed after an incidental finding of a raised white cell count.

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13
Q

What happens in the second phase of chronic myeloid leukaemia ?

A

Abnormal blast cells take up a high proportion of the bone marrow and blood cells.
Patients become symptomatic and develop anaemia, thrombocytopenia and immunodeficiency.

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14
Q

What happens in the final phase of chronic myeloid leukaemia ?

A

An even higher proprioception of blast cells in the blood
Severe symptoms and panctyopenia
Often fatal

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15
Q

What can acute myeloid leukaemia be a transformation of ?

A

A myeloproliferative disorder such as polycythaemia ruby vera or myelofibrosis

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16
Q

What is seen on a blood film and biopsy in acute myeloid leukaemia ?

A

High proportion of blast cells
Auer rods in the cytoplasm of blast cells are also characteristic

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17
Q

What is the general management of leukaemia ?

A

Chemotherapy and targeted therapies
Examples of targeted therapy - tyrosine kinase inhibitors and monoclonal antibodies

Radiotherapy
Bone marrow transplant
Surgery

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18
Q

What are some complications of chemotherapy ?

A

Failure to treat the cancer
Stunted growth and development in children
Infections
Neurotoxicity
Infertility
Secondary malignancy
Cardio toxicity
Tumour lysis syndrome

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19
Q

What in tumour lysis syndrome and what does it result in ?

A

Results from chemicals released when cells are destroyed by chemotherapy, resulting in :
- high uric acid
- high potassium
- high phosphate
- low calcium

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20
Q

What complications can occur from tumour lysis syndrome ?

A

AKI - uric acid can form crystals in the interstitial space and tubules of the kidneys
Cardiac arrhythmias - from hyperkalaemia
Systemic inflammation - release of cytokines

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21
Q

What is tumour lysis syndrome managed ?

A

Very good hydration and urine output before chemotherapy is required
Allopurinol or rasburicase may suppress uric acid levels

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22
Q

What are some poor prognostic features of acute myeloid leukaemia ?

A

Over 60 years old
More than 20% blasts after first course of chemo
Deletion of chromosome 5 or 7

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23
Q

What are some features of acute myeloid leukaemia ?

A

Anaemia - pallor, lethargy
Neutropenia
Thrombocytopenia- bleeding
Splenomegaly
Bone pain

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24
Q

What is the Philadelphia chromosome and what is its relevance ?

A

Translocation between the long arm of chromosome 9 and 22. Results in abnormal tyrosine kinase activity.
It is present on more than 95% of patients with chronic myeloid leukaemia.

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25
Q

At what age is chronic myeloid leukaemia most common ?

A

60-70

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26
Q

What are some features of chronic myeloid leukaemia ?

A

Anaemia - lethargy
Weight loss and sweating
Splenomegaly

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27
Q

What is the management for chronic myeloid leukaemia ?

A

Imatinib - first line - inhibitor of tyrosine kinase

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28
Q

What are some complications of chronic lymphocytic leukaemia ?

A

Anaemia
Hypogammaglobulinaemia
Warm autoimmune haemolytic anaemia
Richter’s transformation

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29
Q

What symptoms are present in richters transformation ?

A

Lymph node swelling
Fever without infection
Weight loss
Night sweats
Nausea
Abdominal pain

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30
Q

What are some features of acute lymphoblastic leukaemia ?

A

Anaemia - lethargy and pallor
Neutropenia - severe and recurrent infections
Thrombocytopenia - easy bruising and petechiae
Splenomegaly and hepatomegaly

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31
Q

What are some poor prognostic factors of acute lymphoblastic leukaemia ?

A

Age less than 2 or above 10
WBC more than 20*10^9 at diagnosis
T or B cell surface markers
Non-Caucasian
Male sex

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32
Q

What is lymphoma ?

A

The malignant proliferation of lymphocytes which accumulate in lymph nodes or other organs. Lymphoma may be classified as either Hodgkin’s lymphoma or non-Hodgkin’s

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33
Q

What is Hodgkin’s lymphoma ?

A

A specific type of lymphoma characterised by the presence of reed-sternberg cells

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34
Q

What are some risk factors of non-Hodgkin’s lymphoma ?

A

Elderly
Caucasian
History of viral infection - Epstein Barr virus
Family history
Certain chemical agents
History of chemo or radiotherapy
Immunodeficiency - HIV DM
Autoimmune disease - SLE, sjogrens or coeliac

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35
Q

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

A

Painless lymphadenopathy - non-tender asymmetrical
B symptoms - fever, weight loss, lethargy
Extranodal disease - gastric ( dyspepsia, dysphagia, weight loss ) bone marrow ( pancytopenia, bone pain), lung and skin

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36
Q

How is Hodgkin’s lymphoma differentiated from non-Hodgkin’s lymphoma ?

A

In Hodgkin’s - alcohol induced pain in the nodes
B symptoms occur earlier in Hodgkin’s lymphoma
Extra nodal more common in non-Hodgkin’s

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37
Q

What are some signs of non-Hodgkin’s lymphoma ?

A

Weight loss
Lymphadenopathy
Palpable abdominal mass
Testicular mass
Fever

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38
Q

What is aplastic anaemia ?

A

Characterised by pancytopenia and hypoplastic bone marrow

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39
Q

What features are present in aplastic anaemia ?

A

Nomochromic normocytic anaemia
Leukopenia
Thrombocytopenia

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40
Q

What are some causes of aplastic anaemia ?

A

Idiopathic
Congenital - Franconia anaemia
Drugs - cytotoxics
Toxins
Infections
Radiation

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41
Q

What is autoimmune haemolytic anaemia ?

A

May be divided into warm and cold types according to what temperature the antibodies best cause haemolysis.

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42
Q

What causes autoimmune haemolytic anaemia ?

A

Idiopathic
Secondary to lymphoproliferative disorder, infection or drugs

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43
Q

What investigations are performed for autoimmune haemolytic anaemia ?

A

FBC
Blood film
Coombs’ test

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44
Q

What is warm autoimmune haemolytic anaemia ?

A

Most common type
The antibody causes haemolysis best at body temperature and haemolysis tends to occur in extra vascular sites.

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45
Q

What are some causes of warm autoimmune haemolytic disorder ?

A

Idiopathic
Autoimmune disease
Neoplasia
Drugs

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46
Q

What is the management of warm autoimmune haemolytic anaemia ?

A

Steroids +/- rituximab

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47
Q

What causes cold autoimmune haemolytic anaemia ?

A

Neoplasia - lymphoma
Infections - mycoplasma, EBV

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48
Q

What are some features of beta thalassaemia major ?

A

Presents in the first year of life with failure to thrive and hepatosplenomegaly
Microcytic anaemia
HbA absent

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49
Q

What is the management of beta thalassaemia major ?

A

Repeated transfusion -
Can lead to iron overload - and then organ failure
Iron chelation therapy

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50
Q

What is beta thalassaemia trait ?

A

A group of genetic disorders characterised by a reduced production rate of either alpha or beta chains.
Autosomal recessive

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51
Q

What are some features of beta thalassaemia trait /

A

Mild hypochromic microcytic anaemia
HbA2 raised

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52
Q

What do target cells on a blood film indicate ?

A

Sickle cell
Iron deficiency anaemia
Hyposplenism
Liver disease

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53
Q

What do tear drop poikilocytes on a blood film indicate ?

A

Myelofibrosis

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54
Q

What do spherocytes on a blood film indicate ?

A

Hereditary spherocytosis
Autoimmune haemolytic anaemia

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55
Q

What does basophilic stripping on a blood film indicate ?

A

Lead poisoning
Thalassaemia
Sideroblastic anaemia
Myelodysplasia

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56
Q

What do Howell jolly bodies on a blood film indicate ?

A

Hyposplenism

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57
Q

What do heinz bodies on a blood film indicate ?

A

G6PD deficiency
Alpha thalassaemia

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58
Q

What do schistocytes on a blood film indicate ?

A

DIC
Intravascular haemolysis

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59
Q

What is non-haemolytic febrile reaction ?

A

From a blood transfusion
Caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cells during storage.

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60
Q

What are some features of non-haemolytic febrile reaction ?

A

Fever
Chills

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61
Q

What is the management of non-haemolytic febrile reaction ?

A

Slow or stop the transfusion
Paracetamol
Monitor

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62
Q

How can anaphylaxis be caused in patients having a blood transfusion ?

A

Can be caused by patients with IgA deficiency who have anti-IgA antibodies

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63
Q

What is the management of anaphylaxis while having a blood transfusion ?

A

Stop the transfusion
IM adrenaline
ABC support - oxygen and fluids

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64
Q

What can cause transfusion - associated circulatory overload ?

A

Excessive rate of transfusion and a pre-existing heart failure

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65
Q

What is the management of transfusion - associated circulatory overload ?

A

Slow or stop the transfusion
Consider IV loop diuretics ( furosemide )

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66
Q

What is transfusion related acute lung injury ?

A

Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood.

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67
Q

What is the management of transfusion related acute lung injury ?

A

Stop the transfusion
O2 and supportive care

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68
Q

What are packed red cells ?

A

Transfusion in chronic anaemia and cases where infusion of large volumes of fluid may result in cardiovascular compromise.

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69
Q

What is fresh frozen plasma ?

A

Prepared from single units of blood
Contains clotting factors, albumin and immunoglobulin

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70
Q

What is burkitt’s lymphoma ?

A

High grade B cell neoplasm

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71
Q

What is seen on microscopy in burkitt’s lymphoma ?

A

Starry sky appearance : lymphocyte sheets interspersed with macrophages

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72
Q

What is the management of Burkitt’s lymphoma ?

A

Chemotherapy
Rasburicase is given before chemotherapy

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73
Q

What are some complications of tumour lysis syndrome ?

A

Hyperkalaemia
Hyperphosphataemia
Hypocalcaemia
Acute renal failure

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74
Q

What is factor V Leiden ?

A

Most common inherited thrombophilia.
Activated protein C resistance

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75
Q

What does factor V Leiden increase the risk of ?

A

Venous thrombosis

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76
Q

What is G6PD deficiency ?

A

Commonest red blood cell enzyme defect

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77
Q

What is the pathophysiology of G6PD deficiency ?

A

Decreases G6PD = reduced NADPH = reduced glutathione = increased red cell susceptibility to oxidative stress

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78
Q

What are some features of G6PD deficiency ?

A

Neonatal jaundice
Intravascular haemolysis
Gallstones
Splenomegaly
Heinz bodies I

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79
Q

What are some drugs that cause haemolysis ?

A

Primaquine
Ciprofloxacin
Sulphasalazine
Sulfonylurea

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80
Q

What inheritance is G6PD deficiency ?

A

X linked recessive

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81
Q

When does graft versus host disease occur ?

A

When T cells in the donor tissue mount an immune response toward recipient cells.

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82
Q

What features are present in graft versus host disease ?

A

Painful maculopapular rash
Jaundice
Watery or bloody diarrhoea
Persistent nausea and vomiting

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83
Q

What is the management of graft versus host disease ?

A

Immunosuppression and supportive measures
IV steroids
Anti-TNF

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84
Q

What can EBV increase the risk of ?

A

Hodgkin’s lymphoma
Burkitt’s lymphoma
Nasopharyngeal carcinoma

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85
Q

What can H.Pylori increase the risk of ?

A

Gastric lyphoma ( MALT )

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86
Q

What are some hereditary causes of haemolytic anaemia ?

A

Hereditary spherocytosis / elliptocytosis
G6PD deficiency
Sickle cell

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87
Q

What are acquired immune causes of haemolytic anaemia ?

A

Warm / cold antibody type
Transfusion reaction
Haemolytic disease of a newborn

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88
Q

What are acquired non-immune causes of haemolytic anaemia ?

A

Microangiopathic haemolytic anaemia
Prosthetic heart valves

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89
Q

What are some Intravascular causes of haemolytic anaemia ?

A

Mismatched blood
G6PD deficiency
DIC

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90
Q

What are some extra vascular causes of haemolytic anaemia ?

A

Sickle cell
Thalassaemia
Hereditary spherocytosis
Haemolytic disease of a newborn

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91
Q

What is haemophilia ?

A

X linked recessive disorder of coagulation

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92
Q

What factor is deficient in haemophilia A ?

A

Factor 8

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93
Q

What factor is deficient in haemophilia B ?

A

Lack of 10

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94
Q

What are the features of haemophilia ?

A

Haemoarthroses
Haematomas
Prolonged bleeding

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95
Q

What is seen on the blood tests in haemophilia ?

A

Prolonged APTT
Normal bleeding time, thrombin time, prothrombin time

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96
Q

What is hereditary angioedema ?

A

An autosomal dominant condition associated with low plasma levels of the C1 inhibitor protein.

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97
Q

What are some symptoms of hereditary angioedema ?

A

Attacks may be proceeded by painful macular rash
Painless non-pruritic swelling of subcut/submucosal tissues

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98
Q

What is the management of hereditary angioedema ?

A

IV C1-inhibitor concentrate, fresh frozen plasma
Prophylactic anabolic steroid Danazol may help

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99
Q

What is hereditary spherocytosis ?

A

Autosomal dominant defect of the red blood cell cytoskeleton
The biconcave disc shape is replaced by a sphere shaped red blood cell

100
Q

How does hereditary spherocytosis present ?

A

Failure to thrive
Jaundice
Gallstones
Splenomegaly

101
Q

What is the management of hereditary spherocytosis ?

A

Treatment is generally supportive
Transfusion if necessary
Folate replacement and splenectomy

102
Q

What are some factors that indicate a poor prognosis in Hodgkin’s lymphoma ?

A

Having B symptoms
Age over 45
Stage 4 disease
Low Hb
High lymphocyte count
Male

103
Q

What are some risk factors for Hodgkin’s lymphoma ?

A

HIV
EBV

104
Q

What are some features of Hodgkin’s lymphoma ?

A

Lymphadenopathy - painless, non-tender, asymmetrical
B symptoms - weight loss, pruritus, night sweats and fever

105
Q

What are som investigations of Hodgkin’s lymphoma ?

A

FBC
LDH
Lymph node biopsy

106
Q

What is seen on the investigations in Hodgkin’s lymphoma ?

A

Normocytic anaemia
LDH raised
Reed - sternberg cells

107
Q

What are some causes of hyposplenism ?

A

Splenectomy
Sickle cell
Coeliac disease, dermatitis herpetiformis
Graves’ disease
SLE

108
Q

What are some features of hyposplenism ?

A

Howell-jolly bodies
Siderocytes

109
Q

What is ITP ?

A

An immune mediated reduction in the platelet count where antibodies are directed against the glycoprotein IIb/IIIa

110
Q

How does ITP present ?

A

Incident finding
Petechiae and purpura
Bleeding
Catastrophic bleed

111
Q

What investigations should be performed for ITP ?

A

FBC
Blood film

112
Q

What is the management of ITP ?

A

Oral prednisolone
Pooled normal human immunoglobulin

113
Q

What are some causes of iron deficiency anaemia ?

A

Excessive blood loss - Menorrhagia, GI upset
Inadequate dietary intake
Poor intestinal absorption - coeliac
Increased iron requirement - during pregnancy

114
Q

What are some features of iron deficiency anaemia ?

A

Fatigue
Shortness of breath
Palpitations
Pallor
Nail changes
Hair loss
Angular stomatitis

115
Q

What are some investigations for iron deficiency anaemia ?

A

FBC
Serum ferritin
Blood film
Total iron-binding capacity

116
Q

What is the management of iron deficiency anaemia ?

A

Identify and manage underlying causes
Oral ferrous sulfate
Iron rich diet

117
Q

What are some differences between iron deficiency anaemia and anaemia of chronic disease ?

A

Iron levels are higher in chronic disease
Ferritin is higher in chronic disease

118
Q

What is lymphadenopathy ?

A

A condition of enlarged lymph nodes, typically indicating an immune response to an infection or malignancy.

119
Q

What are some infective causes of lymphadenopathy ?

A

Infectious mononucleosis
HIV
Eczema
Rubella
CMV
TB

120
Q

What are some neoplastic causes of lymphadenopathy ?

A

Leukaemia
Lymphoma

121
Q

What are some other causes of lymphadenopathy ?

A

Autoimmune conditions - SLE, RA
Graft versus host disease
Sarcoidosis
Drugs - phenytoin

122
Q

What lymphatics do the ovaries drain into ?

A

Para-aortic lymphatics

123
Q

What are some megaloblastic causes of macrocytic anaemia ?

A

Vitamin B12 deficiency
Folate deficiency
Secondary to methotrexate

124
Q

What are some normoblastic causes of macrocytic anaemia ?

A

Alcohol
Liver disease
Hypothyroidism
Pregnancy

125
Q

What is monoclonal gammopathy of undetermined significance ( MGUS ) ?

A

A common condition that causes a paraproteinanemia and is often mistaken for myeloma.

126
Q

What are some features of MGUS ?

A

Usually asymptomatic
No bone pain
increased risk of infection

127
Q

What are some differentiating features of MGUS to myeloma ?

A

Normal immune function
Normal beta-2 microglobulin levels
Lower level of paraproteinaemia than myeloma

128
Q

What are some causes of microcytic anaemia ?

A

Iron deficiency anaemia
Thalassaemia
Congenital sideroblastic anaemia
Anaemia of chronic disease
Lead poisoning

129
Q

What is myelodysplastic syndrome ?

A

Encompasses a heterogeneous group of clonal haematopoietic stem cell disorders characterised by ineffective haematopoeisis, peripheral blood cytopenias and a risk of progression to AML.

130
Q

What causes myelodysplastic syndromes ?

A

Arises from genetic mutations in haematopoietic stem cells
Primary ( 90%)
Secondary ( 10% ) - chemotherapy and radiotherapy - 5 years post treatment

131
Q

How does myelodysplastic syndrome present?

A

Fatigue
Weakness
Pallor - anaemia
Recurrent infections
Easy bruising and bleeding

132
Q

What are the option choices for myelodysplastic syndrome ?

A

Supportive care
DMARDs
Immunosuppressive therapy
Haematoopoietic stem cell transplantation

133
Q

What are some factors that determine treatment for myelodysplastic syndrome ?

A

Subtype of MDS
Patients age
Overall health
Severity of symptoms

134
Q

What is myelofibrosis ?

A

A myeloproliferative disorder thought to be caused by hyperplasia of abnormal megakaryocytes

135
Q

What are some features of myelofibrosis ?

A

Elderly person with symptoms of anaemia ( fatigue )
Massive splenomegaly
Hypermetabolic symptoms - weight loss, night sweats

136
Q

What are the laboratory findings for myelofibrosis ?

A

Anaemia
High WBC and platelet count
Tear drop poikilocytes on blood film
High urate and LDH

137
Q

What is myeloma ?

A

A haematological malignancy characterised by plasma cell proliferation.
Occurs as B cells differentiate into mature plasma cells

138
Q

What are the features of myeloma ?

A

C - calcium ( Hypercalcaemia )
R - renal ( renal damage )
A - anaemia
B - bleeding
B - bones ( pain and pathological fractures )
I - infection

139
Q

How does myeloma cause hypercalcaemia ?

A

Primarily to increased osteoclastic bone resorption caused by local cytokines released by the myeloma cells

140
Q

How does hypercalcaemia present in myeloma ?

A

Constipation
Nausea
Anorexia
Confusion

141
Q

How does myeloma cause renal abnormalities ?

A

Monoclonal production of immunoglobulins results in light chain deposition within the renal tubules. This causes renal damage which presents as dehydration and increasing thirst.

142
Q

How does myeloma cause anaemia ?

A

Bone marrow crowding suppresses erythropoiesis leading to anaemia which causes fatigue and pallor

143
Q

How does myeloma cause bone abnormalities ?

A

Bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates lytic bone lesions.
Presents as bone pain or increased risk of pathological fractures

144
Q

How does myeloma increase the risk of infection ?

A

A reduction in the production of normal immunoglobulins results in increased susceptibility to infection.

145
Q

What is neutropenia ?

A

Low neutrophil count or < 1.5 *10^9

146
Q

What are some viral causes of neutropenia ?

A

HIV
EBV
Hepatitis

147
Q

What are some drugs that cause neutropenia ?

A

Cytotoxic
Carbimazole
Clozapine

148
Q

Other than viral causes and medications what are some other causes of neutropenia ?

A

Myelodysplastic malignancies
Aplastic anaemia
Rheumatological conditions
SLE
RA
Haemodialysis
Severe sepsis

149
Q

What is a common consequence of chemotherapy ?

A

neutropenic sepsis

150
Q

How is neutropenic sepsis defined ?

A

Neutrophil count lower than 0.5 *10^9 in a patient having anti-cancer treatment and has one of the following :
- temp higher than 38 degrees
- other signs or symptoms consistent with clinically significant sepsis

151
Q

What causes neutropenic sepsis ?

A

Coagulase - negative, gram positive bacteria ( staph epidermidis )
- usually due to indwelling lines in patients with cancer

152
Q

What is the management of neutropenic sepsis ?

A

ABx - do not wait for WBC ( tazocin or piperacillin )
Add vancomycin is central venous access
If not responded in 48 hours change to meropenem

153
Q

Which is the more common lymphoma ?

A

Non-Hodgkin’s

154
Q

What are some risk factors for non-Hodgkin’s lymphoma ?

A

Elderly
Caucasian
History of viral illness
FH
Certain chemical agents - pesticides
History of chemotherapy or radiotherapy

155
Q

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

A

Painless lymphadenopathy
B symptoms - fever, weight loss, night sweats
Gastric upset
Bone pain
Nerve palsies

156
Q

What are some signs of non-Hodgkin’s lymphoma ?

A

Signs of weight loss
Lymphadenopathy
Palpable abdominal mass
Testicular mass
Fever

157
Q

What are some investigations of non-Hodgkin’s lymphoma ?

A

Excision all node biopsy
CT chest abdomen pelvis
HIV test
FBC and blood film
ESR

158
Q

What is stage 1 non-Hodgkin’s lymphoma ?

A

Involvement of a single node legion

159
Q

What is stage 2 non-Hodgkin’s lymphoma ?

A

Involvement of two or more lymph nodes on the same side of the diaphragm

160
Q

What is stage 3 non-Hodgkin’s lymphoma ?

A

Involvement of lymph nodes on both sides of the diaphragm which may have involvement of the spleen or extra-lymphatic organ

161
Q

What is stage 4 non-Hodgkin’s lymphoma ?

A

Diffuse and disseminated involvement of one or more extralymphatic organs with or without lymph node involvement

162
Q

What is the management of non-Hodgkin’s lymphoma ?

A

Watchful waiting
Chemotherapy or radiotherapy

163
Q

What are some complications of non-Hodgkin’s lymphoma ?

A

Bone marrow infiltration causing anaemia, neutropenia or thrombocytopenia
Superior vena cava obstruction
Metastasis
Spinal cord compression
Side effects of chemo

164
Q

What are some causes of normocytic anaemia ?

A

Anaemia of chronic disease
CKD
Aplastic anaemia
Haemolytic anaemia
Acute blood loss

165
Q

What are some causes of polycythaemia ?

A

Polycythaemia rubera vera
COPD
Altitude
Obstructive sleep apnoea
Excessive erythropoietin

166
Q

What is polycythaemia vera ?

A

A myeloproliferative disorder caused by clonal proliferation of a marrow stem cell leading to an increase in red cell volume often by overproduction of neutrophils and platelets.
Mutation in the JAK2

167
Q

What are some features of polycythaemia Vera ?

A

Pruritus
Splenomegaly
HTN
Hyperviscosity
Haemorrhage
Low ESR

168
Q

Following history and examination what tests should be performed when suspecting polycythaemia ?

A

FBC / blood film
JAK2 mutation
Serum ferritin
Renal and liver function tests

169
Q

What criteria is needed to be met for a polycythaemia Vera diagnosis ?

A

High haematocrit or raised red cell mass
Mutation in the JAK2

170
Q

What is the management of polycythaemia Vera ?

A

Aspirin - reduces thrombotic events
Venesection - keep Hb in normal range

171
Q

What can polycythaemia Vera develop into ?

A

Myelofibrosis
Acute leukaemia

172
Q

When does post-thrombotic syndrome develop ?

A

A complication of a DVT

173
Q

How does post-thrombotic syndrome occur ?

A

Post DVT - Venous outflow obstruction and insufficiency resulting in chronic venous hypertension

174
Q

What are some features of post-thrombotic syndrome ?

A

Painful, heavy calves
Pruritus
Swelling
Varicose veins
Venous ulceration

175
Q

What helps reduce the risk of post-thrombotic syndrome as well as its management ?

A

Compression stockings

176
Q

Why can DVT occur in pregnancy ?

A

Pregnancy causes a hypercoagulable state
There is an increase in factors VII,VIII, X and fibrinogen
Uterus presses on IVC causing venous stasis in legs

177
Q

What is the management of a DVT in pregnancy ?

A

S/C low molecular weight heparin preferred to IV heparin
Warfarin contraindicated

178
Q

What is chronic granulomatous disease ?

A

Primary Neutrophil immunodeficiency

179
Q

What is the underlying defect in chronic granulomatous disease ?

A

Lack of NAPDH oxidase reduces the ability of phagocytes to produce reactive oxygen species

180
Q

How does chronic granulomatous disease present ?

A

Recurrent pneumonia and abscesses ( particularly staph aureus and aspergillus )

181
Q

What are some B cell primary immunodeficiency ?

A

Common variable immunodeficiency
Bruton’s agammaglobulinaemia
Selective IgA deficiency

182
Q

What is deficient in common variable immunodeficiency ?

A

Antibodies - IgG, IgM and IgG

183
Q

How does common variable immunodeficiency present ?

A

Recurrent chest infections

184
Q

What is the underlying defect in Bruton’s agammaglobulinaemia ?

A

Defect in Bruton’s tyrosine kinase gene that leads to a severe block in b cell development

185
Q

What pattern of inheritance is Bruton’s agammaglobulinaemia ?

A

X linked recessive

186
Q

How does Bruton’s agammaglobulinaemia present ?

A

Recurrent bacterial infections

187
Q

What is deficient in Bruton’s agammaglobulinaemia ?

A

Absence of b cells with reduced immunoglobulins of all classes

188
Q

What is the underlying defect in selective immunoglobulin A deficiency ?

A

Maturation defect in b cells

189
Q

How does selective immunoglobulin A deficiency present ?

A

Recurrent sinus and respiratory infections

190
Q

What is selective immunoglobulin A deficiency associated with ?

A

Coeliac disease

191
Q

What is DiGeorge syndrome ?

A

T cell primary immunodeficiency disorder

192
Q

What is the underlying defect in DiGeorge syndrome ?

A

22q11.2 deletion
Failure to develop 3rd and 4th pharyngeal pouches

193
Q

What are some common features in DiGeorge syndrome ?

A

Congenital heart disease - tetralogy of fallot
Learning difficulties
Hypocalcaemia
Recurrent viral/fungal diseases
Cleft palate

194
Q

What is a combined b and T cell disorder ?

A

Severe combined immunodeficiency

195
Q

What is the most common underlying defect for severe combined immunodeficiency ?

A

Defect in the common gamma chain, a protein used in receptors for IL-2 and other interleukins

196
Q

How does severe combined immunodeficiency present ?

A

Recurrent infections due to viruses, bacteria and fungi

197
Q

What is sickle cell anaemia ?

A

An autosomal recessive condition that results for synthesis of an abnormal haemoglobin chain termed HbS.

198
Q

What is the pathophysiology of sickle cell anaemia ?

A

Polar amino acid glutamate is substituted by a non-polar valine in each of the 2 beta chains. This decreases water solubility. The cells are fragile and haemolyse which can block blood vessels and cause infarction.

199
Q

What is the definitive investigation for sickle cell anaemia ?

A

Haemoglobin electrophoresis

200
Q

What is the management of a sickle cell crisis ?

A

Analgesia
Rehydrate
Oxygen
ABx if infection
Blood transfusion

201
Q

What is the longer term management of sickle cell anaemia ?

A

Hydroxyurea - increases the HbF levels and is used in prophylactic treatment as well
Pneumococcal vaccine every 5 years

202
Q

What are some types of sickle cell crisis ?

A

Thrombotic - vaso-occlusive - painful crises
Acute chest syndrome
Anaemic
Infection

203
Q

What precipitates a vaso-occlusive crisis in sickle cell anaemia ?

A

Infection
Dehydration
Deoxygenation ( high altitude )

204
Q

What is acute chest syndrome ?

A

Vaso-occlusion within the pulmonary micro vasculature causing an infarction in the lung parenchyma.

205
Q

How does acute chest syndrome present ?

A

Dyspnoea
Chest pain
Pulmonary infiltrates on CXR
Low pO2

206
Q

What is the management of acute chest syndrome ?

A

Pain relief
Respiratory support
ABx
Transfusion

207
Q

What causes an aplastic crises ?

A

Caused by an infection with parvovirus

208
Q

What are some features of an aplastic crisis ?

A

Sudden fall in haemoglobin
Bone marrow suppression causes a reduced reticulocyte count

209
Q

What is a sequestration crises ?

A

Sickling within organs such as the spleen or lungs causes pooling of blood with worsening of the anaemia

210
Q

What is sideroblastic anaemia ?

A

A condition where red cells fail to completely form haem, whose biosynthesis takes place partly in the mitochondria. This leads to deposits of iron in the mitochondria that form a ring around the nucleus called a ring sideroblast.

211
Q

What are some causes of sideroblastic anaemia ?

A

Delta-aminolevulinate synthase-2 deficiency
Myelodysplasia
Alcohol
Lead
Anti-TB medications

212
Q

What investigations are used for sideroblastic anaemia ?

A

FBC
Iron studies
Blood film
Bone marrow

213
Q

What is the management of sideroblastic anaemia ?

A

Supportive
Treat for underlying cause
Pyridoxine

214
Q

What are some causes of splenomegaly ?

A

Myelofibrosis
Chronic myeloid leukaemia
Malaria
Portal hypertension
Haemolytic anaemia
Infection - hepatitis
Infective endocarditis

215
Q

What are some causes of severe thrombocytopenia ?

A

ITP
DIC
Haematological malignancy

216
Q

What are some moderate causes of thrombocytopenia ?

A

Heparin induced thrombocytopenia
Drug induced
Alcohol
Liver disease
Hypersplenism
Viral infection
Vitamin B12 deficiency

217
Q

What are some causes of thrombocytosis ?

A

Reactive - stress = severe infection, surgery and iron deficiency anaemia
Malignancy
Essential thrombocytosis
Hyposplenism

218
Q

What is essential thrombocytosis ?

A

A myeloproliferative disorder which overlaps with chronic myeloid leukaemia, polycythaemia ruba Vera and myelofibrosis.

219
Q

What are some features of essential thrombocytosis ?

A

Platelet count more than 600*10^9
Both thrombosis and haemorrhage can be seen
Burning sensation in the hands
JAK2 mutation is found in around 50%

220
Q

What is the management of essential thrombocytosis ?

A

Hydroxyurea
Interferon-alpha
Low dose aspirin - reduce thrombotic risk

221
Q

What are some inherited causes of thrombophilia ?

A

Factor V Leiden
Antithrombin III deficiency
Protein C and S deficiency

222
Q

What are some acquired causes of thrombophilia ?

A

Antiphospholipid syndrome
Drugs - COCP

223
Q

What is thrombotic thrombocytopenic purpura ?

A

Abnormally large and sticky multimers of von Willebrand’s factor cause platelets to clump within vessels

224
Q

What are some features of thrombotic thrombocytopenic purpura ?

A

Rare
Fever
Fluctuating neuro signs
Thrombocytopenia

225
Q

What are some causes of thrombotic thrombocytopenic purpura ?

A

Post infection
Pregnancy
Drugs
Tumours
SLE
HIV

226
Q

What is a thymoma ?

A

Most common tumour of the anterior mediastinum

227
Q

What is associated with a thymoma ?

A

Myasthenia gravis
Red cell aplasia
Dermatomyositis

228
Q

How is a thymoma lead to death ?

A

Compression of the airway
Cardiac tamponade

229
Q

What is tranexamic acid ?

A

A synthetic derivative of lysine

230
Q

What is the primary mode of action of tranexamic acid ?

A

Antifibrinolytic that reversibly binds to lysine receptor sites on plasminogen and prevents plasmin from binding to and degrading fibrin.

231
Q

When is tranexamic acid given ?

A

Major haemorrhage

232
Q

What is tumour lysis syndrome ?

A

A deadly condition related to the treatment of high grade lymphoma and leukaemia.
Usually triggered by the introduction of combination chemotherapy
Causes high potassium and phosphate levels with low calcium.

233
Q

How to prevent tumour lysis syndrome ?

A

IV fluids
Allopurinol or rasburicase ( not given together )

234
Q

How is clinical tumour lysis syndrome diagnosed ?

A

Laboratory tumour lysis syndrome + one or more of :
- increased serum creatinine
- cardiac arrhythmias or sudden death
- seizure

235
Q

What are some general risk factors for venous thromboembolism ?

A

Age
Obesity
Family history
Pregnancy
Immobility

236
Q

What are some underlying conditions that are risk factors for venous thromboembolism ?

A

Malignancy
Thrombophilia
Heart failure
Antiphospholipid syndrome
Sickle cell anaemia

237
Q

What are some drugs that increase the risk of a VTE ?

A

COCP
HRT
Raloxifene and tamoxifen
Antipsychotics

238
Q

How is vitamin b12 absorbed in the body ?

A

Absorbed after binding to intrinsic factor secreted from parietal cells in the stomach and is activity absorbed in the terminal ileum.

239
Q

What are some causes of vitamin b12 deficiency ?

A

Pernicious anaemia
Post-gastrectomy
Poor diet
Crohn’s

240
Q

What are some features of vitamin b12 deficiency ?

A

Macrocytic anaemia
Sore tongue and mouth
Mood disturbances
Distal paraesthesia

241
Q

What is the management for vitamin b12 deficiency ?

A

If no neurological involvement then 1mg of IM hydroxocobalamin

242
Q

What is von willebrand’s disease ?

A

Most common inherited bleeding disorder
Autosomal dominant

243
Q

What is the role of von willebrand factor ?

A

Large glycoprotein which forms massive multimers
Promotes platelet adhesion to damaged endothelium
Carrier molecule for factor VIII

244
Q

What abnormalities are seen during investigations in von willebrands disease ?

A

Prolonged bleeding time
APTT may be prolonged

245
Q

What is the management of von willebrand disease ?

A

Tranexamic acid
Desmopressin
Factor VIII concentrate

Y4 Cancer (12 decks)

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