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MD2 Core Conditions > Neurological, Breast and Haematology > Flashcards

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
Staging of breast cancer
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
26
Treatment of stage 1-2 breast cancer
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+
27
Neoadjuvant
Given BEFORE main treatment, to shrink tumour
28
Paget's disease of breast
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!
29
Mx of Paget's disease of breast
As for breast cancer
30
Gynaecomastia
Abnormal amount of breast tissue in men; may ocur in normal pubery
31
Causes of gynaecomastia
Hypogonadism Liver cirrhosis (increased oestrogens) Hyperthyroidism Oestrogen-producing tumours (e.g. testicular, adrenal) Drugs (e.g. oestrogens, spironolactone, digoxin, testosterone, marijuana)
32
Mx of gynaecomastia in hypogonadism
Testosterone +/- anti-oestrogen (e.g. tamoxifen)
33
Nipple adenoma
Rare intraductal papilloma | Can be mistaken for adenocarcinoma on biopsy but is benign
34
Presentation with nipple adenoma
Lump | May be ulceration, pain, swelling or discharge
35
Mx of nipple adenoma
WLE
36
Approach to haemolytic anaemia
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
Acquired causes of haemolytic anaemia
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
Hereditary causes of haemolytic anaemia
Enzyme defects: G6PD deficiency, PK deficiency Membrane defects: hereditary spherocytosis, hereditary elliptocytosis, hereditary ovalocytosis and stomatocytosis Haemoglobinopathy: sickle cell, thalassaemia
39
Abnormalities on film in G6PD
Bite cells Blister cells Heinz bodies
40
Schistocytes
Cell fragments, sign of microangiopathic anaemia (e.g. in DIC)
41
Fibrin strands on smear
HUS, TTP (slice up RBCs leading to microangiopathy)
42
Hypochromic microcytic anaemia
IDA | Thalassaemia
43
Sickle cell anaemia
AR disorder causing production of abnormal B globin changes
44
Thalassaemia
Genetic diseases of unbalanced Hb sythesis (may be B or a)
45
B thalassaemia minor or trait (B/B+; heterozygous)
Carrier state, usually asymptomatic Mild, well-tolerated anaemia which may worsen in pregnancy Microcytic, often confused with IDA
46
B thalassaemia intermedia
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
B thalassaemia major (Cooley's anaemia): abnormality and features
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
Mx of B thalassaemia major
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
3 groups of bleeding disorders
Vascular defects Platelet disorders Coagulation disorders
50
Immune thrombocytopaenia purpura (ITP)
Antiplatelet autoAbs
51
Presentation of ITP
Acute: usually children, 2 weeks after infection, self-limiting Chronic: mainly women, fluctuating course of bleeding, purpura, epistaxis and menorrhagia
52
Ix for ITP
Increased megakaryocytes in marrow | Presence of antiplatelet Abs
53
Mx of ITP
None if mild If symptomatic or platelets 80%, or consider immunosuppressants e.g. azathioprine Platelet transfusions not helpful!
54
DIC
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
Causes of DIC
Malignancy (e.g. leukaemia) Sepsis Trauma Obstetric events
56
Ix for DIC
``` Thrombocytopaenia Increased PT, APTT Decreased fibrinogen D-dimer positive Schistocytes on film ```
57
Rx of DIC
Treat cause | Replace platelets if
58
Polycythaemia: types and causes
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
Polycythaemia rubra vera
Malignant proliferation of RBCs, WBCs and platelets, leading to hyperviscosity and thrombosis Mutation in JAK2 present in >90%
60
Characteristic signs of PRV
Itch after a hot bath | Erythromelalgia (burning in fingers and toes)
61
Myelofibrosis
Hyerplasia of megakaryocytes which produce platelet-derived growth factor, leading to intense marrow fibrosis and myeloid metaplasia
62
Film appearance of myelofibrosis
``` Teardrop cells Leukoerythroblastic cells (nucleated RBCs) ```
63
Presentation of myelofibrosis
Hypermetabolic state: fever, weight loss Abdominal discomfort due to splenomegaly Bone marrow failure
64
Prognosis of myelofibrosis
4-5 years from diagnosis
65
Causes of thrombocytosis
``` 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
Causes of marrow fibrosis on bone marrow trephine
``` Myelofibrosis Any myeloproliferative disorder Lymphoma Secondary carcinoma TB Leukaemia Irradiation ```
67
Aplastic anaemia
Rare stem cell disorder leading to pancytopaenia
68
Presentation in bone marrow failure
Anaemia Infection Bleeding
69
Causes of aplastic anaemia
``` Mostly AI (triggered by drugs, infection or irradiation) Inherited (e.g. Fanconi anaemia) ```
70
Mx of aplastic anaemia
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
Causes of leukopenia
``` Steroid therapy SLE Uraemia Legionnaire's disease HIV Marrow infiltration Post-chemotherapy or radiation ```
72
Causes of leukopenia
``` Steroid therapy SLE Uraemia Legionnaire's disease HIV Marrow infiltration Post-chemotherapy or radiation ```
73
Causes of lymphadenopathy
Reactive: infective, non-infective | Infiltrative
74
Causes of reactive lymphadenopathy
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
Causes of infiltrative lymphadenopathy
Malignant: haematological, metastatic carcinoma | Benign histiocytosis
76
Myelodysplastic syndromes
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
Mx of myelodysplastic syndromes
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
Causes of leukocytosis
Infection Malignancy (leukaemia, lymphoma, disseminated) Drug reactions
79
Causes of leukocytosis
Infection Malignancy (leukaemia, lymphoma, disseminated) Drug reactions

MD2 Core Conditions (12 decks)

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