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MSRA Content > Level 2 - Haematology COPY > Flashcards

Level 2 - Haematology COPY Flashcards

1
Q

Most common brain tumours? How common?

A
  • Mostly primary and 60% intratentorial (below cerebrum)
  • Most common solid tumour in children
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2
Q

Name the different types of brain tumours?

A

Astrocytoma

Medulloblastoma

Ependymoma

Brainstem glioma

Craniopharyngioma

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3
Q

Most common brain tumour?

A

Astrocytoma

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4
Q

What is astrocytoma?

A

 In cortex

 Varies from benign to malignant (glioblastoma multiforme)

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5
Q

What is medulloblastoma?

A

 Arises in midline of posterior fossa

 May seed through CNS via CSF and often have spinal metastases

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6
Q

What is ependymoma?

A

 Mostly in posterior fossa, behaves like medulloblastoma

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7
Q

What is craniopharyngioma?

A

 Midline

 Arises from squamous remnant of Rathke pouch

 Locally invasive but not malignant

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8
Q

General symptoms of brain tumours?

A
  • Related to raised ICP o Headaches (worse in the morning), vomiting, behaviour changes, visual disturbance, papilloedema o Separation of sutures, increased head circumference
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9
Q

Focal neurological signs in brain tumours?

A

o Supratentorial

 Seizures, hemiplegia, focal signs

o Midline

 Visual field loss, growth failure, diabetes insipidus, weight gain

o Cerebellar

 Truncal ataxia, abnormal eye movements, coordination difficulties

o Brainstem

 CN defects, pyramidal signs

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10
Q

Symptoms in spinal tumours?

A

o Back pain, peripheral weakness of arms and legs, bladder/bowel dysfunction depending on level of lesion

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11
Q

Investigations in brain tumours?

A
  • MRI scan
  • Magnetic Resonance spectroscopy
  • NO LP IF RAISED ICP
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12
Q

Management of brain tumours?

A
  • Urgent referral is unexplained headache and focal symptoms
  • Surgery

o Aimed to treat hydrocephalus, provide tissue diagnosis and resection

  • Radiotherapy and Chemotherapy depending on tumour type and size
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13
Q

Definition of haemophilia? Types?

A
  • X-linked recessive blood disorder
  • Haemophilia A = Factor VIII deficiency (most common)
  • Haemophilia B = Factor IX deficiency
  • Usually carrier females and affected males
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14
Q

Epidemiology of haemophilia?

A
  • Most common inherited coagulation disorder

o Haemophilia A – 1 in 5000 live male births

o Haemophilia B - 1 in 30000 live male births

  • Males affected more common
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15
Q

Presentation of haemophilia?

A
  • Most present towards end of first year of life
  • Can present in neonatal period with intracranial haemorrhage, bleeding post-circumcision, oozing heel prick
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16
Q

Grading of haemophilia?

A
  • Graded:

o Severe: Spontaneous joint/muscle bleeds, arthropathy/arthritis, haematomas

o Moderate: Bleed after minor trauma

o Mild: Bleed after surgery

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17
Q

Investigations of haemophilia?

A
  • Diagnose by increased APTT and decreased FVIII/IX assay
  • Can perform CT head or USS to identify extent of bleeding
  • Prenatal DNA analysis available
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18
Q

Management of haemophilia?

A
  • Minor bleeds

o Pressure and elevation

o Desmopressin raises Factor VIII

  • Major bleeds

o Recombinant Factor VIII/IX concentrate IVI

 Home treatment can be taught

 To 50% of normal (life-threatening bleeds need levels of 100%)

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19
Q

Best management approach and what to avoid?

A
  • MDT approach , specialised physio to strengthen muscles and limit damage, psychosocial support and self-help groups
  • Avoid IM injections, NSAIDs and aspirin
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20
Q

Complications of haemophilia treatment?

A
  • Inhibitors (antibodies to Factor VIII/IX)

o Reduce or inhibit effect of treatment

  • Transfusion transmitted infections
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21
Q

What is HSP?

A

Henoch Schönlein Purpura

  • Acute IgA immune complex mediated vasculitic condition, causing medium sized arteries to become inflamed
  • The IgA and IgG interact to produce complexes that activate complement and are deposited in affected organs leading to inflammatory response – vasculitis
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22
Q

Epidemiology of HSP?

A
  • Occurs between 3-10 years
  • Boys 2:1
  • Peaks during winter
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23
Q

Aetiology of HSP?

A
  • Unknown – potentially genetic disposition and antigen exposure
  • Infections: for example, Group A streptococci, mycoplasma, Epstein-Barr virus
  • Environmental exposures: for example, drug and food allergens, pesticides, cold exposure, insect bites
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24
Q

What precedes HSP in most cases?

A
  • Preceding URTI in 50-90% cases
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25
Q

Symptoms of HSP?

A

Skin rash Arthralgia Colicky abdo pain Renal nephropathy Scrotal oedema

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26
Q

Features of skin rash in HSP?

A

Palpable purpura symmetrically over the lower limbs

Commonly extensor surfaces and buttocks

It may also involve arms, face and ears but usually spares the trunk

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27
Q

Features of arthralgia in HSP?

A

o Knees and ankles mainly o 2/3 of patients and usually resolves

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28
Q

Features of abdo pain in HSP?

A

o Occurs commonly

o Can cause haematemesis, and melaena

o Intussusception (2/3%)

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29
Q

Features of renal nephropathy in HSP?

A

o 80% of cases have micro/macro-scopic haematuria or mild proteinuria

o Complete recovery is normal but if proteinuria is severe, nephritic syndrome may occur - PROTEINURIA, HYPOALBUMINAEMIA, OEDEMA

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30
Q

DDx of HSP?

A
  • Connective tissue diseases
  • eg, systemic lupus erythematosus (SLE).
  • Other causes of purpuric rash
  • eg, thrombocytopenia, leukaemia, ITP
  • Other causes of glomerulonephritis
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31
Q

Investigations of HSP?

A
  • Bedside Tests

o Mid-stream urine dipstick – proteinuria, +/- haematuria

o BP - Blood Tests o FBC (ESR, WCC), U&E, IgA

  • Imaging

o Renal US and Biopsy if renal complications

o Abdominal US if needed

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32
Q

Management of HSP? Complications?

A
  • Most resolve in <2 months
  • Usually self-limiting, regular paracetamol and NSAIDs may help joint pain but caution in renal insufficiency
  • If severe, prednisolone may help resolve abdominal pain
  • May require admission to hospital for monitoring of abdominal and renal complications
  • Chronic renal failure occurs in 5%
33
Q

What is leukaemia?

A
  • Cancer of the white blood cells
  • Arises from malignant proliferation of myeloid, lymphoid, pre-B or T-cell lymphoid precursors
34
Q

What are the types of leukaemia?

A

o Acute lymphoblastic leukaemia (ALL), chronic lymphocytic leukaemia (CLL)

o Acute myeloid leukaemia (AML), chronic myeloid leukaemia (CML)

35
Q

Characteristics of acute leukaemia?

A

o Acute characterised by rapid increase in number of immature blood cells

36
Q

Characteristics of chronic leukaemia?

A

o Chronic characterised by build-up of relatively mature but still abnormal white blood cells

37
Q

What are lymphoblastic cells?

A

o Lymphoblastic/cytic are of lymphocytes, mainly B-cells

38
Q

What are myeloid cells?

A

o Myeloid are marrow cells that go on to form red blood cells, platelets

39
Q

Define acute lymphblastic leukaemia?

A
  • Acute lymphoblastic leukaemia (ALL) defined as rapidly progressing, aggressive which requires immediate treatment
40
Q

What is Burkitt leukaemia?

A
  • Burkitt leukaemia is mature B-cell ALL
41
Q

Epidemiology of leukaemia? Peak age?

A
  • ALL accounts for 80% of leukaemias
  • 25% of all malignancies
  • Peak age 2-6 years
  • Incidence highest in white children
42
Q

Aetiology of leukaemia?

A

o Unknown mostly

o Genetic components

 Down’s syndrome increased risk

 Philidelphia chromosome occurs in 15-30%

  • t(9:22) and is associated with poor prognosis

o Environmental Factors

 Prenatal exposure to x-rays

 In utero infection

43
Q

Symptoms of leukaemia?

A
  • Duration usually 2-4 weeks
  • Symptoms

o Pancytopenia (pallor, infection, bleeding)

o Fatigue

o Anorexia

o Fever

o Bone Pain

o Headaches, vomiting

44
Q

Signs of leukaemia?

A

o Painless lumps in neck, axilla, groin

o Anaemia

o Neutropenia

o Thrombocytopenia

o Hepatosplenomegaly

o Orchidomegaly

45
Q

Investigations of leukaemia?

A
  • Bloods

o FBC (increased WCC, normochromic normocytic anaemia, low platelets)

o Increased urate and LDH

  • Bone Marrow biopsy

o Nucleated cells will be blasts

  • Chest X-ray
  • Cytogenic analysis
46
Q

Risk Classification in leukaemia?

A
  • Risk Classification

o Low, standard, high risk groups

o Depends on clinical signs, biologic features of lymphoblasts and response to induction chemotherapy

47
Q

Management of leukaemia?

A

Induction phase

Consolidation phase

Maintenance phase

48
Q

Management in induction phase?

A

 3-drug induction over 4 weeks

 Intrathecal methotrexate, cytarabine and hydrocortisone

 Remission in >95%

 High-risk patients may need daunorubicin

49
Q

Management in consolidation phase?

A

 Further chemotherapy

 Cranial irradiation if CNS signs

50
Q

Management in maintenance phase?

A

 For 2.5 years daily mercaptopurine, weekly methotrexate + vincristine

51
Q

Complications in leukaemia?

A
  • Neutropenic Sepsis
  • Hyperuricaemia
  • Poor growth
  • Cancer elsewhere
  • Relapses
52
Q

Definiton of lymphoma?

A
  • Malignancy of lymphocytes which can be divided into Hodgkin and non-Hodgkin lymphoma
53
Q

What is Hodgkin’s lymphoma?

A
  • Hodgkin’s lymphoma is a malignant tumour of the lymphatic system that is characterised histologically by the presence of multinucleated giant cells (Reed-Sternberg cells)
54
Q

What is non-Hodgkin lymphoma?

A
  • Non-Hodgkin’s lymphomas (NHLs) are an heterogeneous group of lymphoproliferative malignancies. More likely to disseminate to extranodal sites than in Hodgkin’s lymphoma
55
Q

When is HL and NHL more common?

A
  • NHL more common in childhood
  • Hodgkin lymphoma seen more in adolescents
56
Q

Types of HL?

A

 Classical HL (95%) – nodular sclerosis, mixed cellularity, lymphocyte rich/depleted

 Nodular lymphocyte-predominant Hodgkin’s lymphoma (NLPHL)

57
Q

Risk factors for HL?

A

 EBV, HIV, immunosuppression, cigarette smoking

58
Q

Types of NHL?

A

 Mature (peripheral) B-cell neoplasms

  • Diffuse large B-cell lymphoma (30-60%)
  • Mediastinal large B cell
  • Burkitt’s lymphoma
  • Follicular lymphoma (20-25%)
  • MALT lymphoma

 Precursor T-cell neoplasms

 Mature (peripheral) T-cell neoplasms

  • Enteropathy-type T-cell lymphoma
  • Peripheral T-cell lymphoma
59
Q

Risk factors of NHL?

A

 Chromosomal translocations

 EBV, HepC, Kaposi’s sarcoma

 Pesticides, herbicides, hair dye, chemo

 Hashimoto’s thyroiditis

 H.pylori

60
Q

Symptoms of HL? What are the B symptoms?

A

o Painless, large, firm lymphadenopathy

o May cause airway obstruction, SVC obstruction

o Several months

o Systemic B-symptoms

 Sweating, pruritus, night sweats, weight loss, fever

61
Q

Symptoms of NHL? B symptoms?

A

o Mediastinal mass with bone marrow infiltration

o Superior vena cava obstruction

o Lymphadenopathy

o Abdominal pain

o Systemic B-symptoms

 Sweating, pruritus, night sweats, weight loss, fever

62
Q

Investigations in lymphoma?

A
  • Lymph node biopsy
  • Bloods

o FBC, film, ESR, LFT, LDH, urate, Ca

  • Imaging

o CXR, CT

63
Q

Staging in HL?

A

o Ann Arbor system

 Stage 1: single site

 Stage 2: >1 site and on 1 side

 Stage 3: on both sides of diaphragm

 Stage 4: disseminated disease

64
Q

Staging in NHL?

A

o St. Jude System

 Stage 1: single site or nodal area (not abdomen or mediastinum)

 Stage 2: regional nodes, abdominal

 Stage 3: disease on both sides of diaphragm

 Stage 4: bone marrow or CNS disease

65
Q

Management of HL?

A

o Chemotherapy (ABVD) with radiotherapy (if high risk)

o PET scans monitor disease progression

66
Q

Management of NHL?

A

o Chemotherapy (R-CHOP regimen) with radiotherapy

67
Q

Prognosis of lymphomas?

A
  • 5-year survival rate >90% (NHL 70%)
68
Q

Definition of sickle cell anaemia?

A
  • Inherited (autosomal recessive) blood disorder in which red blood cells develop abnormally
69
Q

Pathology of sickle cell disease?

A
  • Abnormal beta-globin chain that causes it to polymerize when deoxygenated, which distorts the erythrocyte into a sickle shape
  • Deformed erythrocytes form clusters which block blood vessels
70
Q

What benefit does heterozygous form of sickle cell disease have?

A
  • Heterozygous form protects against malaria; is most common in people of black tropical descent
71
Q

Epidemiology of sickle cell disease? Where is highest prevalence?

A
  • Most common haemoglobinopathies
  • 1 in every 2000 live births in England, and it is now the most common genetic condition at birth
  • Highest prevalence of sickle cell disease is among Black African and Black Caribbean people
  • Mortality rate 3% in childhood
72
Q

Aetiology of sickle cell disease?

A
  • Genetic, autosomal recessive – can be carrier or homogenous
73
Q

Symptoms of sickle cell disease?

A

Moderate anaemia usually with jaundice due to chronic haemolysis Increased susceptibility to encapsulated organisms (pneumococci, haemophilus influenzae, OSTEOMYELITIS due to Salmonella ) Vaso-occlusive crises Acute anaemic crises Priapism

  • Needs prompt transfusion Splenomegaly
74
Q

Features of vaso-occlusive crises?

A
  • Precipitated by cold, dehydration, excessive exercise/stress, hypoxia or infection
  • Pain affecting many organs
  • Dactylitis with swelling in hands/feet
  • Commonest in limbs and spine
  • Acute chest syndrome

o Severe hypoxia, need ventilation and transfusion

  • Avascular necrosis
75
Q

Investigations for sickle cell disease? What about in a acute crisis?

A

Newborns screened – Guthrie test

Blood Tests - FBC, reticulocyte count

Blood film Hb electrophoresis (HPLC)= definitive test

Acute crisis investigations: Hb decreased, reticulocytes increased, blood culture, U&E, creatinine, LFT, CRP, CXR

76
Q

Prophylaxis treatment in sickle cell disease?

A
  • Up to date with all immunisations
  • Oral penicillin given to prevent infection
  • Oral folic acid
  • Hydroxycarbamide in patients with severe disease
77
Q

Acute sickle cell crisis treatment? General measures? Drug treatment? When to transfuse?

A
  • Avoid other triggers such as cold weather and excessive physical activity.
  • Use distraction techniques, such as games, computers, and television
  • Increase fluid intake (150% IV or oral)
  • Prescribe paracetamol and/or ibuprofen (avoid ibuprofen if the person has renal impairment or significant proteinuria). Add codeine phosphate if these are not effective
  • Abx given if there is infection
  • Oxygen to improve saturations
  • Transfusion for acute chest syndrome, stroke, priapism
78
Q

Management of sickle cell trait?

A
  • Very rarely have symptoms
  • Avoid high altitudes, such as travelling in an unpressurized aircraft.
  • Inform anaesthetist of sickle cell carriers
79
Q

Complications of sickle cell disease?

A
  • Short stature and delayed puberty
  • Stroke
  • Adenotonsillar hypertrophy
  • Cardiac enlargement and heart failure
  • Renal dysfunction
  • Pigment Gallstones
  • Psychosocial problems

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