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Lachie FRACS - Brainscape Not Good > Breast > Flashcards

Breast Flashcards

1
Q

Phyllodes tumour

A

Rare <1%
40-60 years age
Rapid growing
Fibroadenoma but with stromal component increasing with hypertrophy ++ and less epithelial component
Leaf like growth pattern of stroma
Classified WHO as either benign, borderline or malignant based on the border, the cells in the stroma and the mitosis
If 1cm margin recurrence rate:
benign 10%
Borderline 30%
Malignant 35% and 30% will metastasis (they don’t go to lymph nodes, act like a sarcoma haematogenously)
may benefit from radiotherapy
No chemo or hormonal
No axilla treatment

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2
Q

BIRADS

A

BIRADS

0: Incomplete, need repeat or additional
1: negative, normal, reg surveillance
2: Benign, zero percent probability of malignancy
3: Probably benign MMG, <2% probability, shorter f/u i.e. 6 months
4: Suspicious for malignant 2-94% malignant, further investigation
5: Highly suggestive for malignancy, biopsy
6: Known malignant lesion

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3
Q

Axillary artery

A

Arises from subclavian as it crosses the lateral border of the 1st rib behind the midpoint of the clavicle
Nominally becomes brachial artery as it crosses lower border of teres major
3 parts in relation to pectoralis minor (Some times this life seems a pain) – mnemonic)
1st part above
Superior thoracic artery (STA)

2nd part behind
Thoracoacromial (clavicular, deltoid, acromial and pectoral)
Lateral thoracic artery

3rd part below
Subscapular (gives thoracodorsal)
Anterior and posterior circumflex arteries

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4
Q

Draw the Brachial Plexus

A
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5
Q

Describe the long thoracic nerve

A
  • This nerve takes origin from the roots of the brachial plexus (C5, C6, C7)
  • Passes behind the axially artery and vein
  • Descends on the serratus anterior just behind the mid-axillary line deep to the fascia over the muscle
  • Innervates serratus anterior which protracts the scapula, injury leads to winging
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6
Q

Describe the thoracodorsal nerve

A
  • The thoracodorsal nerve arises from the posterior cord of the brachial plexus with fibres from the sixth, seventh and eighth cervical nerves.
  • After branching from the posterior cord between the upper and lower subscapular nerves, the thoracodorsal nerve runs down the posterior axillary wall.
  • At its origin it is posterior to the subscapular (thoracodorsal) artery.
  • However, as it descends along the posterior wall of the axilla it comes to lie anterior to the artery, then called the thoracodorsal artery.
  • The thoracodorsal nerve crosses the lower border of the teres major muscle and enters the deep surface of the latissimus dorsi with terminal branches of the nerve extending to the inferior border of the muscle.
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7
Q

Describe intercostobrachial nerve

A
  • a lateral cutaneous branch of the second intercostal nerve
  • supplies sensation to the skin of the axilla.
  • It leaves the second intercostal space at the midaxillary line and subsequently pierces the serratus anterior muscle to enter the subcutaneous tissues of the axilla.
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8
Q

Congenital abnormalities of the breast

A
  • Amastia
    • 90% of absence of chest wall muscles
    • Poland’s Syndrome; amastia with associated chest wall muscle absence and upper limb deformity, more common in males
  • Polymastia
  • Athelia
  • Polythelia
  • Tubular breast
  • Chest wall abnormalities pectus excavatum, scolios can may breast appear asymmetry
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9
Q

How can you classify benign breast disease? What is in each group?

A

Aberations of normal breast development and involution.

  • Non-proliferative
    • Cyst
    • Mild duct hyperplasia
    • Fibroadenoma
    • PASH (pseudoangiomatous hyperplasia)
    • Simple columnar alteration
  • Proliferative without atypia
    • Florid ductal hyperplasia
    • Complex fibroadenoma
    • Columnar hyperplasia
    • Mammary adenosis
    • Radial scar/complex sclerosing lesion
    • Papilloma
  • Proliferative with atypia
    • Atypical ductal hyperplasia
    • Atypical lobular hyperplasia
    • Lobular carcinoma insitu
    • Flat epithelial atypia
    • Atypical papilloma
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10
Q

Mild duct hyperplasia

A
  • Benign breast disease/normal proliferation and involution of the breast
  • Epithelial cell based lesion
  • Mild hyperplasia of the usual type is an increase in the number of epithelial cells within a duct that is more than two, but not more than four, cells in depth.
  • The epithelial cells do not cross the lumen of the involved space
  • Can be varying cell types including apocrine
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11
Q

Fibroadenoma

A
  • Benign breast disease/normal proliferation and involution of the breast
  • Fibroepithelial cell based lesion and is non-proliferative
  • MMG = popcorn
  • USS hypoechoic, can be lobulated, often wide>tall, posterior shadowing sometimes
  • Microscopic pattern pericanalicular or intracanalicular; both have epithelial hyperplasia and myxoid stroma
  • If larger or growing >2-3cm or any complex features then should be excised as can be a pylodes tumour
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12
Q

PASH

A
  • Pseudoangiomatous stromal hyperplasia
  • Fibroepithelial, non proliferative
  • More stromal
  • Dense collagen with slit like spaces resembling blood vessels in the stroma, can be confused for angiosarcoma
  • If suspicious for malignancy dont accept diagnosis of PASH on core biopsy, do excisional biopsy
  • Dont need to excise if asymptomatic and concordant imaging
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13
Q

Simple columnar alteration

A
  • Non proliferative, epithelial
  • Change of cuboid to columnar <2 layers of these cells
  • Elongation of the nuclei
  • No treatment needed
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14
Q
A
  • Florid ductal hyperplasia
  • Prolfierative (without atypia), epithelial
  • >70% of the duct lumen
  • Observation and normal surveillance
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15
Q

Other types of fibroadenoma

A
  • Proliferative, no atypia, fibroepithelial lesion
  • Complex
    • Cysts > 3 mm, sclerosing adenosis, epithelial microcalcifications or papillary apocrine metaplasia
  • Juvenile fibroadenoma
    • Increased stromal cellularity
    • Increased epithelial hyperplasia with gynecomastoid-like micropapillary projections
    • Fascicular stromal arrangement
    • Pericanalicular growth pattern
    • May show rapid growth and large size
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16
Q
A
  • Comlunar hyperplasia
  • Proliferative, metaplasia
  • Change of cuboidal to column >2 layers of cells, crowded
  • 5-15% associated with another pathology and cancer
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17
Q

Mammary adenosis

A
  • [Proliferative]
    • Benign proliferation of the lobular units – more glands than usual
    • Subtype of sclerosing type of mammary adenosis where there is fibrosis of the stroma
    • Observation OK
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18
Q

Complex sclerosing lesion/radial scar

A
  • [Proliferative, sclerosing lesion]
    • Stellate collagen centre with entrapped epithelial elements (these can have adenosis or hyperplasia)
    • If >1cm then complex sclerosing lesion
    • They normally look like cancer on MMG, hard to see on USS, excision to be sure there isn’t a malignancy, 10% chance of DCIS or invasive cancer
    • These can look identical to cancer on many modalities
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19
Q

Papilloma

A
  • [Proliferative]
  • Definition:
    • Proliferation of epithelial and myoepithelial around a fibrovascular stalks – like a polyp
  • Epidemiology
    • Common
  • Pathophysiology
    • Growth within the duct
    • 90% subareolar region, central (more benign) and peripheral (less benign)
  • Macroscopic
    • Most within 2 cm of the nipple
    • Benign can be solitary or multiple
  • Microscopy
    • Intraductal papillomas all contained within the duct
  • Clinical manifestation
    • If grow in a peripheral duct then you can present with bloody nipple discharge from one duct in the nipple
    • Discharge
    • May present as a mass
    • Imaging
  • Management
    • Often excise and need to exclude atypia or papillary DCIS or invasive carcinoma (core biopsy is not representative of the whole lesion – need to get the whole thing out due to the heterogeneity)
    • Multiple papillomas, 3RR for cancer
    • If large or multiple definitely excised
    • Surgical excision with microdochectomy
    • May need to be hookwire guided excision
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20
Q

Atypical ductal hyperplasia

A
  • Atypical ductal hyperplasia [Proliferative with atypia]
    • Increased cells
    • Cells show atypia, ?low grade DCIS
    • Less than 2-3mm in size
    • Shouldn’t fill 2 duct spaces
    • Excision is management, only difference between this and DCIS is the size, 10-20% may be upgraded to cancer
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21
Q

Atypical lobular hyperplasia

A
  • Atypical lobular hyperplasia [Proliferative with atypia]
    • Lose e cadherin
    • Proliferation of monomorphic, discohesive cells within the ducts and lobules
    • Lobular unit <1/2 filled with these cells and no distension
    • Not necessarily going to cause cancer
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22
Q

Lobular carcinoma insitu

A
  • Proliferation of monomorphic, discohesive cells within the ducts and lobules
  • More than ½ the unit filled and distended with these cells
  • Lose e cadherin staining
  • Excise and keep on surveillance
  • Pleomorphic LCIS (high grade nuclei, necrosis, calcification)  warrants excision
  • Classic LCIS maybe just surveillance
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23
Q

Flat epithelial atypia

A
  • Proliferative with atypia
  • Change from cuboidal to columnar but with nuclear atypia
  • RR1.5x
  • On excision 5-15% will be upgraded to DCIS, therefore ok to excise
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24
Q

Atypical papilloma

A
  • [Proliferative lesion with atypia]
    • Nuclear atypia (proliferation of monomorphic cells)
    • Increased malignancy risk
    • 67% are actually malignancy
25
Q

Mammary duct ectasia

A
  • Aberration of normal develop and involution of the breast
  • Post menopause, 60-70 years
  • Ducts dilate and shorten
  • Nipple can invert, slit like symmetrical retraction
  • Palpable mass
  • Cheesy yellow thick discharge

Duct ectasia is most often recognized by the presence of palpable dilated ducts filled with desquamated ductal epithelium and proteinaceous secretions.

Periductal inflammation is a distinguishing histologic characteristic in this condition. The pathogenesis of duct ectasia is obscure but probably periductal mastitis, leading to weakening of the muscular layer of the ducts and secondary dilation, is the primary process.

Surgery is indicated only if the discharge is troublesome. Surgery with the aim of everting the nipple is often unsuccessful in the long term and is not encouraged. Duct ectasia should not be confused with periductal mastitis, which develops in young women, mainly cigarette smokers, and is associated with recurrent subareolar infection

26
Q

Periductal abscess chronic subareolar abscess

A
  • Zuska disease
  • Chronic recurring abscesses under the NAC with a fistula draining into the areolar
    • 20-70 years
    • Nipple discharge or inversion
    • Draining sinus at the edge of the areola
    • USS to rule out underlying malignancy
    • Multifactorial (subareolar duct epithelium changes from cuboidal to squamous, this produces kerretin that can block, that duct ruptures and causes inflammation, this abscess then drains to the edge of the areolar
    • Mixed anerobes and aerobes
    • Smokers
    • Drainage with aspiration or I&D
    • Definitive operation (excision of the fistula tract and the disease duct)
      • Identify the involved duct (lacrimal probe or blue dye down the fistula tract)
  • Periareolar incision
27
Q

Interigo

A
  • Inflammation between skin folds
  • Keep clean and dry
  • Antifungals controversial
  • Use cotton bra or cotton tshirt under bra, hair drier, don’t use powders
  • Additional exacerbating factors for intertrigo include irritant and allergic contact dermatitis. The chronically irritated skin of intertrigo increases susceptibility for these disorders. Common causes of allergic contact dermatitis include fragrances in perfumes, colognes, and moisturizers; preservatives in moisturizers and diaper wipes (eg, methylchloroisothiazolinone [MCI] and methylisothiazolinone [MI]); and topical medications (including topical corticosteroids). Irritant contact dermatitis may result from urine, feces, soaps, detergents, and other irritants that are not thoroughly rinsed from skin in involved areas.
28
Q

Capsular contraction

A

Classification of capsular contraction

Grade I (absent)

The breast is soft with no palpable capsule and looks natural.

Grade II (minimal)

The breast is slightly firm, with a palpable capsule but looks normal.

Grade III (moderate)

The breast is firm with an easily palpable capsule and looks abnormal.

Grade IV (severe)

The breast is hard, cold, painful and distorted.

29
Q

Lymphoedema

A
  • swelling resulting from excessive accumulation of ECF in the interstitium due to defective lymphatic drainage
  • Classification
    • Primary

Secondary (most common) – filarial, obstructive

  • Think congenital TIIN – trauma, infection, inflammatory, neoplasm central obstructing or secondary to radiation or surgery
    • Primary (Confusing classifications in this group!)
      • Familial lymphoedema
      • Congenital primary lymphoedema
        • Incidence 1:33000; M > F
        • lymphatic hypoplasia / aplasia
        • presents within 1 yr of birth; usu bilat
      • Idiopathic
        • Incidence 1:6000, F>M (3:1)
        • Lower limb usu affected
        • Distal obliterative lymphoedema (90%)
          • Affects girls at puberty
          • Due to ↓ed / absent lymphatics
        • Proximal obliterative lymphoedema
          • M>F (2:1); 50% are bilaterally
          • ↓ed / fibrotic inguinal / pelvic LNs
        • Massive localized lymphoedema of thigh
          • Predisposing factors: Obesity, Hypothyroidism, trauma/surgery
        • Megalymphatics – absence of lymphatic valves → reflux +/- fistulation into pleural /peritoneal / uterine cavity
    • Secondary
      • Filarial infection: Wuchereria bancrofti, Brugia malayi / timori
      • Obstruction due to
        • LN surgery (eg groin → up to 50% lymphoedema risk)
        • Malignancy – eg peu d’ orange, Kaposi sarcoma
        • Recurrent vv surgery (risk ≈0.5%)
        • Radiotherapy changes
        • Trauma
        • Infection – eg TB, fungi
        • Phlebolymphodemea = lymphatic dysfx in advanced chronic venous insufficiency
        • Secondary to RA / psoriatic arthritis – mechanism uncertain
  • Pathology
    • Under physiological conditions (Starling’s equilibrium) 10-15% of the capillary ultrafiltrate remains in interstitial tissues and is then drained by the lymphatic system
    • If the amount of water and protein exceeds the transport capacity, oedema will occur
    • Lymphatic failure in lymphoedema may often coexist with venous failure
  • Clinical
    • 2 typical presentations:
      • Birth-2 years age = Milroy Disease
        • Autosomal dominant
        • Entire lower limb
        • Bilateral
        • Associated intestinal lymphangiectasia & cholestasis
        • VEGFR inactivation mutation
      • Puberty – 35 = Miege Disease (praecox)
        • Autosomal dominant
        • Associated vertebral defects, cerebrovascular malformation, hearing loss, double row eyelashes
      • Lymphoedema tarda
        • Age over 35
        • Filiarial infection → elephatitis
        • Late-onset primary lymphoedema usu becomes apparent in early adulthood +/- minor Hx of trauma
        • Distal obliterative lymphoedema: usu bilateral to the knee;
          • Chonically: odedema, hyperkeratotic skin, squashed, squared-off toes,
    • Differential Dx
      • CHF, venous oedema, hereditary angio-oedema, av malformations, Kippel-Trenaunay syndrome (rare congenital vascular disorder port wine stains, limb hypertrophy)
    • Staging: International Society of Lymphology
      • Stage 0. Latent or subclinical condition where swelling is not evident despite impaired lymph transport. It may exist months or years before overt edema occurs (stages I–III).
      • Stage I: Early accumulation of fluid relatively high in protein content (eg, in comparison with “venous” edema)
        • Subsides with limb elevation
        • Pitting may occur
      • Stage II.
        • Limb elevation alone rarely reduces tissue swelling
        • Pitting may or may not occur as tissue fibrosis develops.
      • Stage III. Lymphostatic elephantiasis
        • Where pitting is absent.
        • Trophic skin changes, such as acanthosis, fat deposits, and warty overgrowths, often develop.
    • Positive Stemmer sign = inability to grasp the skin over the dorsum of the 2nd digit of foot lymphoedema
  • Investigations:
    • Diagnosis / assessment of arm lymphoedema (NB definitions vary in the literature)
      • Arm circumference measurements
        • measure at set distances from bony landmarks & in upper + lower arm - ie 10cm above & below the olecranon
        • Eg >2cm difference btwn arms
      • Volume / water displacement = most accurate; but cumbersome & impractical
        • Eg >100mL difference btwn arms
      • Tissue tomography: the amount of compressabilility of tissues correlates with vol. Bioimpedence
    • Duplex USS to rule out venous insufficiency
    • CT / MRI / USS to look for obstructing lesions / abN LN
    • Microscopic detection of filarial larvae (microfilaria) in peripheral bld +/- strongly +ve complement fixation test
    • Radioisotope lymphography
      • Tc-99 labled colloid is injected into a web space of the affected limb
      • Cannot distinguish between primary and secondary pathologies
    • Contrast lymphangiography (under GA):
      • Lymphatics are identified with patent blude die then cannulated
    • MR
      • Thickening of the skin, “honeycombing” of the subcutaneous tissue due to the presence of fibrotic tissue and fluid surrounding adipose accumulation
      • Epifascial fluid lakes
      • Absence of edema within muscular compartments
      • Dermal back filling
  • Management:
    • Non surgical
      • Compression – grade IV
      • +/- intermittent pneumatic compression
      • Massage / manual lymph drainage
      • Exercise
      • Leg / arm elevation
      • Prevention of acute infection – meticulous skin & nail care
      • Medical Rx (nothing really helps)
        • Diuretics – no use long-term
        • ?Benzopyrones (eg coumarin) – controversial… claimed to ↑ proteaolysis by macrophages → ↓ protein content of oedema fluid → ↑s reabsorption… but RCTs are lacking
    • Surgical
      • Indications:
        • Servere deformity
        • Prox obstruction with patent distal lymphatics
        • Lymphocutatnous fistualae and megalyphtics
      • Debulking procedures
      • Homans op: excise subcut tissue but leave skin ≈ intact
      • Charles op: excise skin and subcut tissue then graft
      • Lymphovenous anastomosis or lymphatic bypass
      • Liposuciton
  • Prognosis / Natural Hx:
    • Chromic lymphodedma ↑s the risk for devpt of lymphangiosarcoma
    • In women previously treated for breast CA = Stewart-Treves syndrome
    • Follow-up
30
Q

BRCA recommendations

A
31
Q

BRCA

A
  • Tumour suppressor gene: repair of double stranded DNA breaks. Failure of this gene leads to chromosomal instability
  • Cancers
    • BRCA1 (Breast 70%, epithelial ovarian 40%, prostate 8xRR)
    • BRCA2 (Breast 55%, ovarian 15%, male breast cancer, bile duct, pancreas, prostate 3xRR, stomach, melanoma, B lymphocytes)
  • Targeted therapy
    • PARP inhibitors (Olaparib) - inhibition of PARP leads to double stranded DNA breaks in BRCA def cells which cannot be repaired leading to cell death
32
Q

PTEN

A
  • Tumour suppressor gene
  • MOA; reg cell growth, apoptosis, angiogenesis,adhesion and cell movement
  • Cowden syndrome/multiple Hamartoma syndrome
  • Autosomal dominant
  • Ch 10
  • 30-50% breast cancer risk
  • 5% thyroid cancer (follicular)
  • CNS/cerebellar gangliocytoma
  • Endometrial cancer
  • Benign features
    • See spots!
    • Mucocutaneous papillomatous papules (tongue/mouth)
    • Hamartomatous SB and colonic polyps
    • Adenomas or MN goitre thyroid
    • Fibrocystic change in breast
33
Q

Li Fraumeni

A
  • Tumour suppressor gene
  • Le Fraumeni syndrome and most common sporadic mutation
  • Breast 80% risk (commonly triple negative)
  • Sarcoma
  • Brain tumours
  • Adrenocortical carcinoma
34
Q

ATM

A
  • Tumour suppressor gene
  • Autosomal recessive! (Only one)
  • If two of these genes are inherited child will develop Ataxia Telangectasia
  • If one copy, then higher risk
    • Breast 30%
    • Pancreatic cancer
  • Radiation sensitivity
35
Q

CHECK2

A
  • Cell cycle check point regulator
  • Tumour suppressor
  • 28-37% risk breast cancer
36
Q

Adjuvant radiotherapy in DCIS

A
  • As in the treatment of invasive breast cancer, the standard of care for patients undergoing BCT is to deliver adjuvant
    • Whole-breast radiation therapy (WBRT)
    • Typically within eight weeks of surgery
    • Conventionally dosed WBRT consists of 2 Gy daily fractions over 5 weeks to a total dose of 50 Gy,
    • Often followed by a boost to the surgical bed, 10-16Gy in 2Gy/fraction (an additional ~1-2 weeks
  • High risk
    • No endocrine therapy
    • Close margins
    • 3 or more excisions
    • Young
    • Large area
    • High nuclear grade
    • HER2 + or ER PR negative
    • Molecular gene assay; OncotypeDX breast assay
  • 2009 meta-analysis of RT compared with no further treatment following lumpectomy
    • Reduction in the risk of all ipsilateral breast events (HR 0.49)
    • Number needed to treat of nine women to prevent one ipsilateral breast recurrence
  • May be omitted in small (~<1.5cm), low grade DCIS with clear margins and in elderly patients
  • Doesn’t improve overall survival or prevent metastasis
37
Q

SERM

A
  • Competitively inhibiting binding oestrogen receptor
  • Tamoxefen (20mg daily dose – contraindicated in DVT PE, pregnancy, Stroke) and remaefen
  • Side effects
    • Hot flushes
    • Endometrial cancer
    • DVT PE
    • Stroke
  • 5 years but ATLAS study and ATOM study 10 year treatment good for mortality
38
Q

Aromatase inhibitors

A
  • Anastrozole
  • Stop peripheral enzyme conversion of androgens to oestrogen
  • Post menopausal patients where ovaries aren’t making oestrogen any more
  • Side effects
    • Arthalgia
    • Osteoporosis (DEXA)
    • Cardiovascular disease
    • Fatigue
    • Sexual dysfunction
  • Trials
    • Duration MA17R – 5 vs 10 years, improved DFS and contralateral breast cancer with 10 years
39
Q

DCIS grading

A
  • No universally accepted grading system for DCIS but more recently endorsed classification systems stratify DCIS by nuclear grade (low, intermediate, high) and presence or absence of necrosis
  • Nuclear grade:
    • Low grade:
      • Monotonous, round nuclei with smooth contours, small size nuclei (size of normal ductal epithelial cell or 1 - 1.5 diameter of normal red blood cell)
      • Diffuse fine chromatin, absent or indistinct nucleoli, no or rare mitotic figures, necrosis is uncommon but does not preclude the diagnosis of low grade DCIS
    • Intermediate grade:
      • Moderate pleomorphism, mild to moderate variability in nuclear size
      • Variably coarse chromatin, occasional nucleoli, infrequent mitoses, features in between low and high grade DCIS
      • Loss of monotony can mimic usual ductal hyperplasia
    • High grade:
      • Prominent pleomorphism, large size nuclei (> 2.5 size of normal ductal epithelial cell)
      • Vesicular chromatin with irregular distribution, prominent nucleoli, frequent mitoses, comedo necrosis frequent but not required
  • Necrosis:
    • College of American Pathologists DCIS protocol recommends reporting necrosis as not present or present and if present must be differentiated as focal or comedo
40
Q

Invasive ductal carcinoma grading

A
  • Modified Bloom Richardson index
    • 3 areas
      • Tubule[glands] formation
      • Nuclear pleomorphism
      • Mitotic figures
    • Proportion of cells with normal tubule formation
      • >75% 1 point
      • 10-75% 2 points
      • <10% 3 points
    • Nuclear pleomorphism
      • Small, uniform, similar size, without many nucleoi 1 point
      • Nuclei are enlarged and lots of nucleoli 2 points
      • Pleomorphic large nuclei and many nucleoli
    • Mitotic figures in 10x HPF
      • 1 point, rare 0-9
      • 2 point frequent, 10- 19
      • 3 points many >20 mitosis
    • Total
      • 3-5 low grade, well differentiated
      • 6-7 grade 2
      • 8-9, poorly differentiated grade 3 tumour
  • Ki 67
    • Low <14%
    • High >20%
  • Assessing pathological response to neoadjuvant treatment: Residual Disease Characterisation Working Group of the Breast International Group North American Breast Cancer Group (BIG NABCG)
41
Q

Mammographic density

A
  • Classification for density
    • A: Entirely fibrofatty tissue
    • B: scattered fibroglandular density
    • C :heterogeneously dense with patches of density that may obscure small lesion
    • D: extremely dense breast
  • Difficult to detect, independent risk factor
42
Q

MMG

A
  • MMG
    • Density A_B_C_D
    • Craniocaudal (CC)
      • Upper half is lateral
      • Lower half is medial
    • Mediolateral oblique (MLO)
    • Tips
      • Special views
        • Masses need compression views
        • Calcifications need magnification views
        • Implants need pinch back views
      • Check the MLO - pec major muscle included down to level of nipple?
      • Symmetry
      • Distortion or masses
      • Densities
      • Calcifications (~macro good, micro bad)
      • Nipple retraction and skin involvement
      • Lesions (quadrants or clockface)
      • Compare to old MMG
      • Spiculated, architectural distorsion, microcalcification <0.5mm/pleomorphic/clustered in one area
    • Report BIRADS
      • 0: Incomplete, need repeat or additional
      • 1: negative, normal, reg surveillance
      • 2: Benign, zero percent probability of malignancy
      • 3: Probably benign MMG, <2% probability, shorter f/u i.e. 6 months
      • 4: Suspicious for malignant 2-94% malignant, further investigation
      • 5: Highly suggestive for malignancy, biopsy
      • 6: Known malignant lesion
43
Q

Types of breast reconstruction

A
  • Implant based
    • Tissue expander and implant
    • Implant +/- dermal matrix
  • Tissue Transfer
    • Latissimus dorsi flap plus implant
    • TRAM flap (free DIEP, muscle sparing TRAM done free DIEA or pedicled off the superior epigastric artery)
    • Superior Gluteal artery flap
44
Q
  • Modified Bloom Richardson index
A
  • 3 areas
    • Tubule[glands] formation
    • Nuclear pleomorphism
    • Mitotic figures
45
Q

BCS considerations and contraindications

A
  • Consideration
    • Tumour/Breast ratio – upto 50%
    • Location: look out for NAC
    • Patient preference
    • Radiation
  • Contraindications
    • Inflammatory breast cancer
    • Multiple quadrant multifocal cancer
    • T4 (locally advanced)
    • Persistent positive margins
    • High risk of breast cancer (i.e. ?prophylactic mastectomy may be more appropriate)
    • Contraindications to radiation
      • Previous breast cancer with radiation
      • Hodgkins lymphoma
      • Collagen-vascular disease (scleraderma, active SLE, RA)
      • Pregnancy
46
Q

What is safe for breast cancer patients in pregnancy?

A
  • CXR is safe with abdominal shield
  • CT chest abdo pelvis not recommended
  • USS liver
  • MRI non con for the spine
  • PET scan not used
  • Bone scans with low dose can be used but not recommended
  • SLNBx
    • Tc99 safe (low dose, same day)
    • Dye not safe
  • Chemo
    • Safe in second and third trimester
    • Methotrexate not safe, regime might be changed by oncology
    • Trastuzumab not safe (oligohydramnios and death)
    • Cease 3 weeks prior so they aren’t immunosuppressed during delivery
  • Radiation delay till post operatively
  • Endocrine therapy not safe
47
Q

Pagets of the nipple definition and pathophysiology

A
  • Eczematous change in skin of nipple due to Paget’s cells (large cells, pale cytoplasm, prominent nucleoli) in the epidermis
  • 2 Hypothesis:
    • “in situ transformation hypothesis” – transformed malignant keratinocytes “Toker Cells (clear cells of the nipple)
    • “epidermo-tropic hypothesis’ – ductal cells migrate along basement membrane of ducts into epidermis of the nipple
      • (DCIS) arising within the ductal system of the breast can extend up the lactiferous ducts and into the skin of the nipple without crossing the basement membrane. The malignant cells disrupt the normally tight squamous epithelial cell barrier, allowing extracellular fluid to seep out and form an oozing scaly crust
48
Q

AMAROS

A
  • AMRAROS
    • P
      • T1-2 cancers
      • LN clinically negative but positive sentinel node (1-2 nodes)
    • I
      • Axillary radiotherapy, no ALNDx
      • 25Gy all axilla levels and supraclavicular
    • C
      • ALNDx, no axillary RTx
    • O
      • Recurrence and survival no significant difference
      • 23% vs 11% arm lymphoedema
    • Note,
      • Only 33% of positive nodes had additional nodes on subsequent dissection
      • ~40% of positive nodes in each group were micro/its positive only
49
Q

Z11

A
  • T1-2 & <3 nodes positive, no LN ECS
  • BCS only, all patients tangential whole breast RT and systemic treatment
  • Control was as above vs above PLUS ALNDx
  • 10 year local recurrence and overall survival – not inferior
50
Q

Indications for adjuvant radiotherapy

A
  • To escape:
    • mastectomy with negative SLNBx with no high risk features OR ALNDx and <3LNs and no high risk features…everyone else gets some sort of radiotherapy
    • They are old >65 with ER +’ve or ECOG 4 or patient refuses
  • BCS
    • Whole breast ?age over 65 PRIME II
  • Boost to tumour bed
    • (young patients, high risk tumour, DCIS, triple negative, large tumours) EORTC Boost
  • Post mastectomy chest wall
    • Positive surgical margins
    • T4, T3N1, N2/3
    • T3N0 or T1-2N+ depending upon presence of additional risk factors*.
    • *Additional risk factors for locoregional recurrence include:
      • LVI
      • High tumour grade
      • Multifocal or multicentric tumours
      • Nodal burden
      • Young age
      • ER negative
  • SCF/IMC/Level 3 axilla
    • Recommended in:
      • T4, T3N1, N2/3
    • Consider for:
      • T3N0 or T1-2N+ depending upon presence of additional risk factors*.
    • *Additional risk factors for locoregional recurrence include:
      • Presence of lymphovascular space invasion (LVI)
      • High tumour grade
      • Multifocal or multicentric tumours
      • Young age
      • ER negative
      • Nodal burden
    • MR20
  • Lower axilla (level 1-2)
    • Depends if ALNDx performed or not
      • Dissected axilla
        • Suspected residual microscopic disease
      • Non dissected axilla
        • Positive SLNBx but don’t meet Z11 criteria for a ALNDx (i.e. +T3, >2 LNs)
        • T1-2 with 2 or less LNs
51
Q

Neoadjuvant in breast cancer indications

A
  • Goal
    • No impact on survival unless pCR
    • Enables downstaging (for BCS, avoid ALNDx)
    • Ability to assess & tailor systemic treatment
  • Con’s
    • May over treat
    • May have disease progression
    • Allow for genetic testing (maybe consider prophylactic mastectomy rather than BCS, reconstruction options)
  • Indications
    • Large or locally advanced tumour
    • Inflammatory Breast Cancer
    • Allow BCS or change locally invasive to operable cancer
    • Triple negative or HER2
      • T2+ preferred (+2cm)
      • T1c+ considered (+1cm)
  • Other tests
    • Nuclear MUGA
    • Breast MRI with contrast for treatment response
    • Consider genetics referral
52
Q

Adjuvant chemotherapy breast cancer indications

A
  • Indications
    • HER2
    • Triple negative
    • Large >5cm
    • Positive SLNBx/axilla nodes
    • >2cm if grade 2 or 3
    • LV or perineural invasion
    • Young patient
    • Histological subtypes
      • Apocrine
      • Medullary
      • Adenocystic
      • Metaplastic
53
Q

Systemic treatments for breast cancer (non hormonal)

A
54
Q

5FU

A
  • Fluorouracil (5 FU)
    • MOA: Anti metabolite, metabolised by the liver and Inhibits DNA replication
    • Side effects:
      • Diarrhoea
      • Mucositis
      • Hand-foot
      • Vasospasm
55
Q

rubicin

A
  • doxorubicin/epirubicin
    • MOA: Athracycline, intercalate within DNA base pairs, causing breakage of DNA strands and inhibition of both DNA and RNA synthesis.
    • Doxorubicin inhibits the enzyme topoisomerase II, causing DNA damage and induction of apoptosis.
    • Side effects
      • Nausea and vomiting
      • Bone marrow suppression
      • Cardiomyopathy
      • Febrile neutropaenia
56
Q

Cyclophosphamide

A
  • MOA: alkylating agent of the nitrogen mustard type. 2 An activated form of cyclophosphamide, phosphoramide mustard, alkylates, or binds, to DNA. Its cytotoxic effect is mainly due to cross-linking of strands of DNA and RNA, and to inhibition of protein synthesis
  • Side effects
    • ?
57
Q

Paclitaxel

A
  • Taxane (paclitaxel/docetaxel)
    • MOA: disruption of microtubule function
    • Myalgia arthralgia
    • Hand and foot syndrome
    • Diarrhoea
    • Alopecia
    • Paresthesia
    • Neuropathy greater with paclitaxel
    • Neutropaenia and sepsis higher with docetaxel
58
Q

Referral to genetics for breast cancer

A

Person history

  • Age <40 years
  • TNBC and <50 years
  • 2x primary breast <60 years
  • Jewish ancestry
  • Male
  • Breast and ovarian (any age)

Family history

  • Known or suspected germline mutation; BRCA, TP53, PTEN, STK11, PALB2, CDH1
  • Two 1st/2nd degree relatives with breast or ovarian plus additional high risk feature
  • high risk features
    • Another member with breast/ovarian
    • Breast cancer <50
    • Multiple primaries
    • Breast/ovarian in same woman
    • Jewish
    • Male breast cancer
    • Pancreatic cancer
    • Prostate cancer Gleason 7+

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