Neurological, Breast and Haematology Flashcards

1
Q

Vasogenic vs cytotoxic cerebral oedema

A

Vasogenic: from leaky capillaries, EC, spreads through white matter with grey matter sparing, seen around ring-enhancing lesions
Cytotoxic: low-attenuation, affects white and grey matter, appears as loss of grey matter definition, seen around areas of ischaemia in stroke

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2
Q

Cerebral abscess

A

Should be considered in any patient with raised ICP, esp with fever or increased WCC

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3
Q

Cause of cerebral abscess

A

May follow ear, sinus, dental or periodontal infection, skull fracture, congenital heart disease, endocarditis, bronchiectasis

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4
Q

Ix for cerebral abscess

A

Raised WCC
Raised ESR
CT/MRI: ring-enhancing lesion, surrounded by vasogenic oedema

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5
Q

Mx of cerebral abscess

A

Urgent neurosurgical referral

Treat raised ICP

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6
Q

Mnemonic for cerebral ring-enhancing lesions

A
Metastasis
Abscess
Glioblastoma multiforme
Infarct
Contusion

Demyelinating disease
Radiation necrosis or resolving haematoma

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7
Q

Multi-infarct dementia

A

~25% of all dementias
Cumulative effects of many small strokes, thus sudden onset and stepwise deterioration is characteristic (but often hard to recognise)
Look for evidence of vasculopathy

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8
Q

Causes of CNVII palsy

A

Bell’s palsy (most common)
Ramsay Hunt syndrome
Infectious: Lyme, meningitis, TB, viruses (HIV, polio)
Brainstem lesions
Cerebello-pontine angle pathologies: acoustic neuroma, meningioma
Systemic: DM, sarcoidosis, GBS
ENT: parotid tumours, cholesteatoma, trauma

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9
Q

Bell’s palsy

A

Idiopathic facial nerve palsy

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10
Q

Distinguishing features of Bell’s palsy

A

Abrupt onset
Complete unilateral facial weakness at 24-72hr
Ipsilateral numbness or pain around ear
Decreased taste
Hypersensitivity to sounds (from stapedius palsy)

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11
Q

Mx for Bell’s palsy

A

If given within 72 hrs, high dose prednisolone speeds recovery
Eye protection to prevent exposure keratinopathy

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12
Q

Fibroadenoma

A

Benign overgrowth of collagenous mesenchyme of one breast lobule

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13
Q

Presentation of fibroadenoma

A

Firm, smooth, mobile, non-tender

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14
Q

Breast cysts

A

Common >35 years, esp perimenopausal

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15
Q

Infective mastitis/breast abscess

A

Infection of mammary duct often associated with lactation (Staph aureus is usual organism)

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16
Q

Presentation of breast cyst

A

Benign, fluid-filled rounded lump, not fixed to surrounding tissue
Occasionally painful

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17
Q

Presentation of breast abscess

A

Painful hot swelling of breast segment

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18
Q

Mx of infective mastitis/breast abscess

A

Abx

Open incision or percutaneous drainage if abscess

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19
Q

Duct ectasis

A

Ducts become blocked and secretions stagnate

Typically around menopause

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20
Q

Presentation of duct ectasia

A

Nipple discharge (green/brown/bloody) +/- nipple retraction +/- lump

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21
Q

Mx of duct ectasia

A

Usually not required

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22
Q

Fat necrosis

A

Fibrosis and calcification after injury to breast tissue; scarring results in firm lump

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23
Q

Ix of fat necrosis

A

Triple test

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24
Q

Mx of fat necrosis

A

Not needed

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25
Q

Staging of breast cancer

A

1: confined to breast, mobile
2: growth confined to breast, mobile, LNs in ipsilateral axilla involved
3: tumour fixed to muscle but not chest wall, ipsilateral LNs matted and may be fixed, skin involvement larger than tumour
4: complete fixation of tumour to chest wall, distant metastases

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26
Q

Treatment of stage 1-2 breast cancer

A

Surgery: removal by wide local excision or mastectomy +/- reconstruction, + axillary node sampling/surgical clearance or sentinel node biopsy
Radiotherapy: recommended for all patients with invasive cancer following WLE
Chemotherapy: e.g. epirubicin + CMF (cyclophosphamide + methotrexate + 5-FU)
Endocrine agents: tamoxifen (ER blocker), aromatase inhibitors (e.g. anastrozole)
Herceptin if HER2+

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27
Q

Neoadjuvant

A

Given BEFORE main treatment, to shrink tumour

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28
Q

Paget’s disease of breast

A

Intra-epidermal spread of an intraduct cancer, which can look just like eczema
Any red, scaly lesion at the nipple must suggest PDB so do a biopsy!

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29
Q

Mx of Paget’s disease of breast

A

As for breast cancer

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30
Q

Gynaecomastia

A

Abnormal amount of breast tissue in men; may ocur in normal pubery

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31
Q

Causes of gynaecomastia

A

Hypogonadism
Liver cirrhosis (increased oestrogens)
Hyperthyroidism
Oestrogen-producing tumours (e.g. testicular, adrenal)
Drugs (e.g. oestrogens, spironolactone, digoxin, testosterone, marijuana)

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32
Q

Mx of gynaecomastia in hypogonadism

A

Testosterone +/- anti-oestrogen (e.g. tamoxifen)

33
Q

Nipple adenoma

A

Rare intraductal papilloma

Can be mistaken for adenocarcinoma on biopsy but is benign

34
Q

Presentation with nipple adenoma

A

Lump

May be ulceration, pain, swelling or discharge

35
Q

Mx of nipple adenoma

A

WLE

36
Q

Approach to haemolytic anaemia

A

1) Increased RBC breakdown: normal or increased MCV, increased unconjugated bilirubin, increased urinary urobilinogen, increased LDH
2) Increased RBC production: reticulocytosis, increased MCV, polychromasia
3) Extra- or intra-vascular haemolysis: extravascular leads to splenomegaly, intravascular shows increased free Hb, decreased haptoglobin, haemoglobinuria

37
Q

Acquired causes of haemolytic anaemia

A

Immune-mediated and direct Coombs test +ive: drug-induced (e.g. penicillin, quinine), AIHA (warm or cold), paroxysmal cold Hburia
Direct Coombs -ive AIHA (20% of all AIHA; in AIH, HBV/HCV, post-flu, drugs e.g. piperacillin, rituximab)
Micro-angiopathic haemolytic anaemia (MAHA): due to mechanical disruption, seen in HUS, TTP, DIC, pre-eclampsia and eclampsia, and with mechanical heart valves
Infection: malaria
Paroxysmal nocturnal Hburia

38
Q

Hereditary causes of haemolytic anaemia

A

Enzyme defects: G6PD deficiency, PK deficiency
Membrane defects: hereditary spherocytosis, hereditary elliptocytosis, hereditary ovalocytosis and stomatocytosis
Haemoglobinopathy: sickle cell, thalassaemia

39
Q

Abnormalities on film in G6PD

A

Bite cells
Blister cells
Heinz bodies

40
Q

Schistocytes

A

Cell fragments, sign of microangiopathic anaemia (e.g. in DIC)

41
Q

Fibrin strands on smear

A

HUS, TTP (slice up RBCs leading to microangiopathy)

42
Q

Hypochromic microcytic anaemia

A

IDA

Thalassaemia

43
Q

Sickle cell anaemia

A

AR disorder causing production of abnormal B globin changes

44
Q

Thalassaemia

A

Genetic diseases of unbalanced Hb sythesis (may be B or a)

45
Q

B thalassaemia minor or trait (B/B+; heterozygous)

A

Carrier state, usually asymptomatic
Mild, well-tolerated anaemia which may worsen in pregnancy
Microcytic, often confused with IDA

46
Q

B thalassaemia intermedia

A

Intermediate state with moderate anaemia but not requiring transfusions
Causes: mild homozygous B thalassaemia mutations, or co-inheritance of B thalassaemia trait with another haemoglobinopathy (NOT sickle cell - this produces a picture similar to sickle cell)

47
Q

B thalassaemia major (Cooley’s anaemia): abnormality and features

A

Abnormalities in both B genes
Presents in 1st year with severe anaemia and failure to thrive, oestopaenia, extramedullary haematopoiesis leading to skull bossing and hepatosplenomegaly

48
Q

Mx of B thalassaemia major

A

Regular (~2-4 weekly) life-long transfusions, resulting iron overload/deposition manifests after ~10 years as endocrine failure, liver disease and cardiac toxicity
Iron chelators
Large doses of ascorbic acid to increase urinary excretion of iron
Mx of endocrine complications
Histocompatible marrow transplant may offer change of cure

49
Q

3 groups of bleeding disorders

A

Vascular defects
Platelet disorders
Coagulation disorders

50
Q

Immune thrombocytopaenia purpura (ITP)

A

Antiplatelet autoAbs

51
Q

Presentation of ITP

A

Acute: usually children, 2 weeks after infection, self-limiting
Chronic: mainly women, fluctuating course of bleeding, purpura, epistaxis and menorrhagia

52
Q

Ix for ITP

A

Increased megakaryocytes in marrow

Presence of antiplatelet Abs

53
Q

Mx of ITP

A

None if mild
If symptomatic or platelets 80%, or consider immunosuppressants e.g. azathioprine
Platelet transfusions not helpful!

54
Q

DIC

A

Widespread activation of coagulation, from release of procoagulants into circulation with consumption of clotting factors and platelets
Fibrin strands fill small vessels, haemolysing passing RBCs, fibrinolysis is activated

55
Q

Causes of DIC

A

Malignancy (e.g. leukaemia)
Sepsis
Trauma
Obstetric events

56
Q

Ix for DIC

A
Thrombocytopaenia
Increased PT, APTT
Decreased fibrinogen
D-dimer positive
Schistocytes on film
57
Q

Rx of DIC

A

Treat cause

Replace platelets if

58
Q

Polycythaemia: types and causes

A

Relative (due to decreased plasma volume and normal RBC mass) or absolute (increased RBC mass)
Relative causes: acutely dehydration, chronic associated with obesity/HTN/high alcohol and tobacco intake
Absolute causes: primary (polycythaemia rubra vera, PRV) or secondary to hypoxia or inappropriately elevated EPO secretion (e.g. RCC, HCC)

59
Q

Polycythaemia rubra vera

A

Malignant proliferation of RBCs, WBCs and platelets, leading to hyperviscosity and thrombosis
Mutation in JAK2 present in >90%

60
Q

Characteristic signs of PRV

A

Itch after a hot bath

Erythromelalgia (burning in fingers and toes)

61
Q

Myelofibrosis

A

Hyerplasia of megakaryocytes which produce platelet-derived growth factor, leading to intense marrow fibrosis and myeloid metaplasia

62
Q

Film appearance of myelofibrosis

A
Teardrop cells
Leukoerythroblastic cells (nucleated RBCs)
63
Q

Presentation of myelofibrosis

A

Hypermetabolic state: fever, weight loss
Abdominal discomfort due to splenomegaly
Bone marrow failure

64
Q

Prognosis of myelofibrosis

A

4-5 years from diagnosis

65
Q

Causes of thrombocytosis

A
Essential thrombocythaemia
Platelets >450 may be a reactive phenomenon seen in:
Bleeding
Infection
Chronic inflammation (e.g. collagen disorders)
Malignancy
Trauma
Post-surgery
Iron deficiency
66
Q

Causes of marrow fibrosis on bone marrow trephine

A
Myelofibrosis
Any myeloproliferative disorder
Lymphoma
Secondary carcinoma
TB
Leukaemia
Irradiation
67
Q

Aplastic anaemia

A

Rare stem cell disorder leading to pancytopaenia

68
Q

Presentation in bone marrow failure

A

Anaemia
Infection
Bleeding

69
Q

Causes of aplastic anaemia

A
Mostly AI (triggered by drugs, infection or irradiation)
Inherited (e.g. Fanconi anaemia)
70
Q

Mx of aplastic anaemia

A

Marrow support: red cell transfusion, platelets, neutropenic regimen (full barrier nursing, avoid IM injections, look for infection and take regular swabs, regular bloods)
Allogeneic marrow transplant in young patients (can be curative)
Immunosuppression with ciclosporin and antihymocyte globulin may be effective

71
Q

Causes of leukopenia

A
Steroid therapy
SLE
Uraemia
Legionnaire's disease
HIV
Marrow infiltration
Post-chemotherapy or radiation
72
Q

Causes of leukopenia

A
Steroid therapy
SLE
Uraemia
Legionnaire's disease
HIV
Marrow infiltration
Post-chemotherapy or radiation
73
Q

Causes of lymphadenopathy

A

Reactive: infective, non-infective

Infiltrative

74
Q

Causes of reactive lymphadenopathy

A

Bacterial: pyogenic, TB, brucella, syphilis
Viral: EBV, HIV, CMV, infectious hepatitis
Others: toxoplasmosis, trypanosomiasis
Non-infective: sarcoidosis, amyloidosis, berylliosis, RA, SLE, dermatological, drugs (e.g. phenytoin)

75
Q

Causes of infiltrative lymphadenopathy

A

Malignant: haematological, metastatic carcinoma

Benign histiocytosis

76
Q

Myelodysplastic syndromes

A

Heterogeneous group of disorders that manifest as marrow failure with risk of life-threatening infection and bleeding
Most are primary, but may be secondary to chemotherapy or radiotherapy
30% transform to acute leukaemia
Most pts elderly

77
Q

Mx of myelodysplastic syndromes

A

Multiple transfusions of RBCs or platelets as needed
EPO + G-CSF to lower transfusion requirement
Immunosuppressives e.g. ciclosporin, antithymocyte globulins
Curative allogeneic stem cell transplant
Thalidomide analogues

78
Q

Causes of leukocytosis

A

Infection
Malignancy (leukaemia, lymphoma, disseminated)
Drug reactions

79
Q

Causes of leukocytosis

A

Infection
Malignancy (leukaemia, lymphoma, disseminated)
Drug reactions