BENIGN BREAST DISEASE Flashcards

1
Q

WHAT IS POLYTHELIA?

A
  • accessory nipple (supranumary nipple) along milk line from axilla to groin (most common) or rarely other ectopic sites
  • 6% population, M=F, bilateral in 50%
  • IMF most common site (when there, L>R)
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2
Q

what is differential for polythelia?

A
  • benign skin lesions such as skin tag, compound nevus, FB granuloma, DF, SK
  • malignant skin lesions such as melanoma, BCC
  • other breast pathology such as breast malignancy/breast mass
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3
Q

what are associations w/ polythelia?

A
  • renal - agenesis, cyst, duplication, neoplasm
  • cardiac - congenital heart, arrythmia, htn
  • pyloric stenosis
  • epilepsy
  • ear anomalies
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4
Q
  • treatment of gynecomastia
A
  • work up - consider testicular exam, investigations for associations (not routinely indicated for adult presentation)
  • excision for tissue diagnosis / rule out other pathology
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5
Q

define polymastia, its epidemiology, treatment principles

A
  • Definition: supernumerary breast
  • Epidemiology
    • 1-2% of female population
    • Mainly sporadic (can be syndromic – Fleischer’s (lateral displacement of nipples, renal hypoplasia))
    • Axilla>IMF>other
    • May or may not be associated nipple-areola complex; most commonly nipple and areola absent or rudimentary
  • Management
    • excision of ectopic breast tissue
    • lower chest wall & IMF – approach through IMF incision
    • must be careful not to injure primary developing breast bud in preadolescent or in patient with developing breasts
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6
Q

what is poland syndrome

A
  • congenital abscence of sternocostal head of pec major muscle
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7
Q

list syndromes associated w/ poland syndrome

A
  • o Klippel-Fiel syndrome – congenital fusion any two vertebrae between C2-C7

o Sprengel’s deformity – winging of scapula (deficiency serratus anterior)

o Moebius, scoliosis, dextrocardia, congenital spherocytosis, leukemia

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8
Q

describe etiology of poland syndrome

A
  • controversial / not definitively proven
  • most commonly thought to be associated with vascular interruption during critical developmental period around 6 wks gestation of subclavian artery
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9
Q

describe clinical presentation of poland syndrome

A
  • Muscle
    • Absence sternocostal head pec major (definition)
    • Absence/hypoplasia pec minor
    • Hypoplasia shoulder musculature (incl LD, serratus)
  • Skeletal
    • Absence costal cartilage (±absent ribs)
    • Sternal rotation
  • Arm
    • Brachysyndactyly (~ 15 – 50%) – hypoplasia of the middle phalanges and central skin webbing
    • Shortening/hypoplasia forearm
  • Breast
    • aplasia/hypoplasia or amazia of the breast, and/or NAC complex (athelia)
  • Other
    • Deficiency of subcutaneous fat & axillary/mammary hair, dextrocardia, renal abnormalities
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10
Q

describe management of poland syndrome

A
  • Goals – correct chest wall deformities, address soft tissue deficiency
  • History and physical
  • Work-up – CXR (ribs, clavicle, sternum, scapula), CT/CTA – confirm presence of LD & assess vessels, surgical planning
  • Timing – after breast maturity (consider TE or Becker during puberty)
  • Non-operative – external prosthesis
  • Operative
    • Thoracic remodeling – thoracic consultation (autologous [split rib graft / other free vascularized bone] vs alloplastic [marlex/prolene mesh, custom implant] vs combined)
    • Soft tissue deficiency
      • Alloplastic – Temporary expander to provide symmetry during breast development; exchanged for permanent implant at completion of development
      • AutologousLD + expander/implant/custom implant (best option, if available) – reconstruct infraclavicular hollow and/or anterior axillary fold. Suture LD to IMF & laterally, then position TE on top of chest wall, cover with LD
        • 2nd option or if ipsilateral LD absent: TRAM with cutaneous paddle, or expand breast pocket 1st with TE and bury TRAM vs. contralateral free LD vs. fat injection
      • don’t forget NAC reconstruction
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11
Q

what features characterize (or potentially characterize) the tuberous breast deformity?

A
  1. constricted skin envelope (horizontal and vertical)
  2. constricted base
  3. breast parenchyma hypoplasia
  4. high IMF
  5. Areolar hypertrophy
  6. Pseudoherniation of gland through areola
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12
Q

what is the classification for tuberous breast?

A
  • von heimberg classification
  • · Hypoplasia of lower medial quadrant

· Type 2 – Hypoplasia of lower medial and lateral quadrants, sufficient skin in subareola

· Type 3 – Hypoplasia of lower medial and lateral quadrants, limited skin in subareola

· Type 4 – Severe breast constriction, minimal breast base

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13
Q

what are goals of treatment for tuberous breast?

A
  • · Overarching aim is to restore normal breast shape
    1. Expand constricted base
    2. Expand skin envelope (lower hemisphere)
    3. Correct hypoplasia / augment breast when necessary
    4. Lower IMF
    5. Reduce herniated tissue
    6. Correct areolar size
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14
Q

what are surgical principles / steps for treatment of tuberous breast ?

A
  • make correct diagnosis
  • decide on 1 vs. 2 stage
    • most get 1 stage; von heimberg 4 +/- some type 3
  • make breast markings
    • current footprint
    • desired footprint including level of IMF and NAC
  • decide if pt better addressed w/ reduction/mastopexy vs. augment
  • make implant selection: usually high profile anatomic gels
  • decide on incision
    • IMF if not areola reduction / herniation correct required, otherwise peri-areolar
  • dissection approach - always prophylactic hemostasis; consider radial scoring or other autoaugmentation/re-orientation approach
  • decide on pocket (DP II/III for most)
  • perform areola reduction / correction of herniation
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15
Q

what are types of fibrocystic breast disease and associated relative risk for invasive cancer?

A
  • non-proliferative (70%)
    • no increased risk alone
    • increased risk when non-proliferative associated with gross cysts (RR 1.5 cyst alone; 3.0 when cyst + FHx)
  • proliferative
    • no atypia 26%
      • RR 1.6; 2.1 when w/ FHx
    • atypica 4%
      • RR 4.4; 8.9 when w/ FHx
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16
Q

how do you manage breast lump in pre-menopausal woman?

A
  • history, physical exam
  • mammogram & ultrasound
  • core biopsy if:
    • clinically concerned (do after imaging)
    • high birads or other concerning features on imaging (decided on by radiology)
    • follow up clinically and radiologically in 6 months
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17
Q

what is prognosis of fibroadenoma?

A

o Fibroadenoma, normal surrounding tissue =>have 0.1-0.3% chance of developing CA in the fibroadenoma

o Proliferative surrounding tissue or complex fibroadenoma => RR 3.1 (+ family history – RR = 3.87)

o 10-15% with CA in fibroadenoma will eventually develop CA in contralateral breast

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18
Q

what is phyllodes tumour? what is the treatment?

A
  • variant of fibroadenoma, a non-epithelial breast tumour having predominantly stromal and also glandular components
  • has benign, intermediate and maligant
  • Treatment – WLE (tumour <5cm –> 2cm margin, >5cm –> 5cm margin, large –> simple mastectomy), re-excision if suspicious elements, nodal dissection not necessary; poor response to chemo/rads/hormonal manipulation. Goal is 1cm clear pathologic margins to minimize risk of recurrence
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19
Q

what is mondor’s disease? what is it’s management?

A
  • Superficial thrombophlebitis of lateral thoracic or superior thoracoepigastric veins
  • Etiology – trauma, infection, breast surgery, excessive physical strain, rheumatoid arthritis, 2-12% associated with CA
  • Presentation – tender subcutaneous cord in the breast +/- dimpling of the skin, no systemic signs of infection
  • Investigations – mammogram if cancer suspected
  • Management – self-limiting, resolving in 2-10 weeks; local application of heat; analgesics;, NSAID’s, if persistent – ligation of vein
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20
Q

what is differential diagnosis of nipple discharge?

A

· Physiologic: neonatal, lactational/perpeural

  • Benign: galactorrhea, galactocele, duct ectasia, infection/periductal mastitis, nipple papillomatosis, intraductal papilloma

· Malignant: breast cancer

· Management: MALIGNANT UPO: imaging (mammo, U/S, ductogram), fluid for cytology, biopsy, referral to General Surgery

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21
Q

name 5 breast lesions associated with increased risk of invasive breast cancer

A
  • Fibrocystic disease – proliferative without atypia
  • Fibrocystic disease – proliferative with atypia
  • Multiple peripheral papillomatosis
  • Intraductal papilloma
  • Juvenile papillomatosis
  • Sclerosing adenosis
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22
Q

what is your differential diagnosis of a breast mass?

A

· Infection – abscess, TB

· Inflammatory - sarcoid

· Trauma – hematoma, fat necrosis, breast infarct (pregnancy)

· Benign tumor: cyst, fibradenoma, adenoma, sclerosing adenosis, papiloma, papillomatosis, granular cell tumour, vascular anomaly, lipoma, inclusion cyst

· Malignant: infiltrating breast cancer, phyllodes tumor, lymphoma, sarcoma, metastasis

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23
Q

How do you classify Benign breast disease?

A
  1. Fibrocystic
  2. Neoplastic (proliferative)
  3. Inflammatory (reactive)
  4. Trauma
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24
Q

What is the blood supply to the breast?

A
  1. Internal mammary artery (via perforators in intercostal spaces 2,3,4)
  2. Lateral thoracic artery (via lateral mammary branches)
  3. Posterior Intercostal arteries 3,4,5 (via lateral mammary branches)
  4. Thoracoacromial artery (via pectoral branches)
  5. Thoracodorsal and subscapular
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25
Q

What is the venous drainage of the breast

A
  1. Internal thoracic vein
  2. Axillary vein branches
  3. Posterior intercostal eveins
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26
Q

Where do the lymphatics of the breast drain to?

A
  1. Axillary Lymph nodes (subclavian trunk)
    1. Apical (subclavicular - posterior and superior to pec minor)
    2. Central (posterior to pec minor within axillary fat)
    3. Pectoral (lower border of pec minor)
    4. Subscapular (lateral scapula border along subscapular vessels)
    5. Lateral (along axillary vein)
    6. Interpectoral (Rotter’s group)
  2. Parasternal (along Internal mammary)
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27
Q

What are the levels of ALND and what LN groups are removed in each?

A

Level 1 - lateral and below pec minor = Lateral, Subscapular, Pectoral

Level 2 - Posterior to pec minor = Central

Level 3 - Medial and superior to pec minor = Apical

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28
Q

What is the innervation to the breast?

A
  1. Intercostal nerves (anterior and lateral branches of IC 2-6)
  2. Supraclavicular nerve (anterior and medial branches from cervical pelxus C3,4)

* nipple main innervation is from lateral branch of 4th IC nerve

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29
Q

Describe the embryology of the breast

A

Develops from ectoderm and mesoderm

Independance of placental hormones:

wk 1-5 : galactic band develops from axilla to groin and in thorax, band enlarges while rest regresses

wk 7-14: invagination of chest wall mesenchyme and thickening of ridge

wk 16-20: budding of epithelium and branching, mesenchyme differentiation into NAC SM cells, development of apocrine glands(montgomery), eccrine, sebaceous, hair follicle

Dependance on placental hormones

wk20-30: Canalization of epithelial buds

wk 30-40: differentiation into lobular alveolar structures, lactiferous ducts

Neonate - colostral milk expressed 4-7days postpartum up to 3wks

Child - Ductal branching and further canalization

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30
Q

What hormones play a role in the development of the breast at puberty

A

age 10-12

Estrogen - stimulates ductal growth, with increased CT and terminal ductules

Progesterone -stimulates acinar growth, limits tubular proliferation

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31
Q

What are the alveolus, lobule, acine, terminal end buds

A

Alveolus = resting secretory unit

Acine = pregnancy and lactating secretory unit

Lobule= composed of alveolar buds clustered and draining in to terminal duct

4 structures – lobules (glands), milk ducts, skin & fat, connective tissue

· Gland (lobule) = 10-100 alveoli (acini) -> collect into 40 lobules (intra-lobular duct -> extra-lobular duct -> terminal duct) -> clustered to form 15-20 lobes, each w lactiferous ducts

o Terminal ductal-lobular unit (TDLU) is the basic secretory/functional structure of breast (where Breast Ca is thought to originate) & consists of lobule (many acini), intra & extra-lobular duct, terminal duct

· Each lactiferous duct dilates as approaches NAC & coalesces -> forms lactiferous sinus/central collecting duct (milk storage)

o Cells: Glands – columnar cells; Lactiferous ducts – cuboidal cells; Sinus – squamous epithelium

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32
Q

What are the Tnner stages of breast development?

A

Tanner stage 1 - at puberty = no glandular tissue, no pigmentation

Tanner stage 2 - age 11+/- 1 = subareolar gland tissue, areola widens

Tanner stage 3 - age 12 +/-1 = increase gland tissue, pigment NAC, contour develops in same plane as NAC

Tanner stage 4 - age 13 +/- 1= NAC forms 2nd mound on breast

Tanner stage 5 - age 15+/-2 = Final adult size, areola returns to contour of breast

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33
Q

What occurs during menstrual cycle in breast tissue

A

Follicular phase = epithelial cells proliferate

Luteal phase = Ducts dilate, alveolar cells proliferate/differentiate to secretory cells, interlobular edema

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34
Q

What occurs to the breast in pregnancy

A

Growth of alveolar, lobular and ductule tissue, increased pigmentation, vascularity

Caused by hormones (placental lactogen, HcG, prolactin, estrogen/progesterone)

Second 1/2 of pregnancy - growth of myoepithelial cells and dilatation of alveoli with colostrum

35
Q

How does lactation occur

A

Lactation: triggered by

  • loss of placenta hormones
  • continued prolactin production

NAC sensory nerves stimulate milk ejection by prolactin release from anterior pituary and oxytocin release from posterior pituary

Prolactin converts epithelial tissue from presecretory state–>secretory state

Oxytocin stimulates myoepithelial cells in alveoli to release secretions into lactiferous ducts

36
Q

What occurs to the breast during menopause

A

regression of epithelial structures and lobules collapse

Fat deposition increased

37
Q

How do you classify congenital breast anomalies?

A
  • Hyperplastic
    • Polythelia
    • polymastia
    • gynecomastia
  • Hypoplastic
    • BIlateral absence associated with ectodermal defect
    • Polands’ syndrome
    • Bilateral absence
38
Q

What is polythelia and your management ?

A

Supernumerary nipple along mammary ridge (90% infra mammary region)

Simple excision

39
Q

What is associated with polythelia

A

“Keep the nipple” going to the heart

K - Kidney cyst, neoplasm, ageneis, duplication

E - Epilepsy

E - Ear anomalies

P - Pyloric stenosis

Heart - arrhtyhmia, HTN

40
Q

What is polymastia and management

A

Supernumerary breast (along mammary ridge - most common AXILLA then inframammary)

May present in pregnancy

Management: excision of ectopic breast tissue

41
Q

What syndrome is associated with polymastia?

A

Fleishner syndrome (polymastia, renal hypoplasia, lateralized nipples)

Fleishner -> big breasts, small kidneys

42
Q

What is congenital ectodermal defects are associated with bilateral amastia?

A

Dysmorphic nails, skin, teeth

CL/P

Microphthalmia, corneal dysplasia

43
Q

What are the clinical features of Polands syndrome

A
  • Unilateral absence/hypoplasia of
    • ribs 2-4 with chest wall depression
    • pectoralis major
    • latissiumus dorsi
    • breast and NAC
  • Upper extremity hypoplasia
    • Brachysyndactyly (short webbed fingers)
    • Shortened forearm bones
    • Absence of axillary hair
  • Scoliosis
  • Dextrocardia
  • Blood dyscrasias
    • leukemia
    • spherocytosis

“thin chest curves towards the short arm, closer to the heart and blood”

44
Q

What is the epidemiology of polands syndrome

A

Right handed boy sporadically named poland with 30Gs

R>L

M>F 3:1

Most sporadic but Familial is AD

1 in 30 000 births

45
Q

What are treatment options for patient with polands requesting breast reconstruction

A
  • Autologous
    • pedicled lat dorsi * if present
    • TRAM, DIEP
  • Alloplastic
    • expander during development, exchange to implant once development complete (age 15 +/- 2yrs - Tanner stage 5)
46
Q

What is the difference between amazia and amastia

A

Amastia - absence of gland and NAC

Amazia - absence of gland, Normal NAC

47
Q

What is associated with bilateral amastia (absence of breast and NAC)?

A

EEC - ectrodactyly - ectodermal - dysplasia cleft syndrome

AD

  • CP
  • high arched palate
  • claw hand deformity
  • skin appendage abnormalities
  • ocualr abnormalities
48
Q

What is your differential diagnosis for acquried amastia/breast dysmorphology in a young female

A
  • biopsy in developing breast (removal of buds)
  • prepubertal radiation
  • burn contracture
49
Q

What is a tuberous breast deformity?

A

Deformity/pathology of the breast base affecting unilat or bilat breasts

Etiology theories

1- thickened superficial fascia causes constricted ring around developing breast

2- adherence between dermis and muscle not divided by developing breast

50
Q

What are the clinical features of a tuberous breast

A
  1. Contracted skin envelope vertically and horizontally
  2. Hypoplasia of breast parenchyma
  3. Constricted base
  4. Elevated IMF
  5. Pseudoherniation of parenchyma into areola
  6. Areola hypertrophy
51
Q

Classify Tuberous breast deformity.

A

Von Heimburg

Type 1 - hypoplasia of lower inner quadrant

Type 2 - hypoplasia of lower inner/outer quadrants and sufficient skin subareolar

Type 3 - hypoplasia of lower inner/outer quadrants but insufficient skin subareolar

Type 4 - Severe contriction, minimal breast base

52
Q

Describe your surgical plan for management of a tuberous breast deformity

A

1- Correct areola size (mark 4cm new areola and de-epitheliaze excess)

2- Increase skin envelope (use TE or release inferior parenchyma from skin envelope)

3- Increase breast parenchyma/improve parenchyma shape (use implant or secure inferior chest wall parenchymal flap and allow superior parenchyma and medial/lateral tissue to reshape around flap

4- Increase base width - radial scoring

5- Correct pseudoherniation - use periareolar incision through inferior NAC and gland

6- Lower IMF -

53
Q

What is fibrocystic breast disease

A

3 groups of FCD based on relative risk of subsequent breast cancer development

  • Non proliferative lesions (Non- P)
  • Proliferative lesions without atypia (P typical)
  • Proliferative lesions with atypia (P atypical = Atypical hyperplasia)
54
Q

What are signs and symptoms fo fibrocystic disease

A
  • bilateral diffuse breast pain for months to years
  • fluctuation with menstrual cycle
  • nipple discharge
  • palpable solid masses/irregularities
55
Q

Name 4 types of non-proliferative fibrocystic breast disease

A
  1. Epithelial calcification
  2. Papillary apocrine change
  3. Cyst
  4. Fibroadenoma
  5. Mild hyperplasia of usual type
56
Q

name 3 types of FCD that is proliferative without atypia

A

1- Intraductal papilloma

2- Moderate hyperplasia of the usual type

3- Sclerosing adenosis

57
Q

Name 2 types of FCD proliferative with atypia

A

* have some but not features of CIS

  1. ALH = atypical lobular hyperplasia
  2. ADH = atypical ductal hyperplasia
58
Q

What is your management of patient presenting with breast mass

A
  • History
  • P/E
  • Mammogram (FCD show cystic change, calcification)
  • U/S distinguish between solid/cystic
  • Needle aspirate - most effective therapy
    • if resolves completely, diagnosis is non-proliferative FCD (cyst)
  • Biopsy if
    • aspirate bloody
    • cyst recurs
    • doesnt completely resolve
  • Adjuntive treatment (FCD)
    • warm compress, anlagesics
    • avoid coffee, chocolate
    • low fat, high fiber diet
    • antigonadatrophin (danazol)
    • prolactin inhibitor (bromocriptine)
59
Q

What is the prognosis/relative risk of developing breast Ca with FCD

A
  • Non-proliferative FCD: no increased risk unless gross cyst + FHx
  • Proliferative no atypia FCD: mild increased risk (RR1.6)
  • Proliferative with atypia: significantly increase risk (RR4.4) + FMHx (8.9)
60
Q

Name 9 benign breast neoplasms or proliferaitve lesions

A
  1. Fibroadenoma (and variants)
  2. Fibromatosis
  3. Adenoma
  4. Papilloma
  5. Phyllodes
  6. Granular cell tumors
  7. Radial Sclerosing lesions
  8. Infarct
  9. Microglandular adenosis

FFAPPGRIM

61
Q

Describe fibroadenoma epidemiology, pathology, clinical presentation, management, prognosis

A
  • Epidemiology
    • most common etiology of benign mass
    • young W aged 20-30
  • Pathology
    • hyperplasia of lobules (single terminal ductal lobular unit)
    • enlarges in response to estrogen
  • Clinical presentation
    • round discrete rubbery
    • non tender mass
    • no skin changes
    • no change in growth with OCP, reduces in size in menopause
  • Investigation
    • Mammogram or U/S
    • FNA
  • Treatment
    • W<25 with typical 2cm fibroadenoma - FNA with regular follow-up
    • W>35, excision to exclude carcinoma with oncoplastic principles
  • Prognosis
    • Ca within fibroadenoma <0.3%, most commonly LCIS
    • if surrounding tissue normal, no increased risk of Ca
    • Increased risk of Ca
      • if surrounding tissue abnormal (comflex fibroadenoma w nonproliferative changes ie. cystic, slcerosing adenosis, epithelial calcification, papillary apocrine changes)
      • +FmHx
62
Q

List 2 fibroadenoma variants

A
  1. Giant Fibroadenoma (>5cm, usually in pregnant/lactating ->excise after pregnancy)
  2. Juvenile fibroadenoma (rapidly enlarging in young W around puberty,associated prominent veins)
    1. DDX: phyllodes, periductal fibrosarcoma, unilateral virgil hypertrophy)
63
Q

Describe Phyllodes tumor epidemiology, pathology, clinical presentation, management, prognosis

A
  • Epidemiology
    • rare
    • 4th decade
  • Pathology
    • fibroepithelial tumor with stromal tissue determining the classification as malingnat or benign
    • may be benign, intermediate, malignant
  • Clinical presentation
    • smooth multinodular, may be 1-40cm in size
    • non-tender
    • may rapidly grow leading to skin ulceration, vein varicosity, erythema
    • effaced nipple
  • Investigations
    • Mammogram/U/S/FNA - all may be unreliable to distinguish fibroadenoma/phyllodes benign ->malignant
    • Need core Bx, incisional or excisional bx
  • Treatment
    • WLE 2-4 cm margins depending on size
    • no ALND recommended
    • If malignant or large, Mx
  • Prognosis
    • 20% local recurrence rate, 5% metastasis (lung, liver, bone)
64
Q

What is an adenoma?

A

Tumor of benign epithelial elements

65
Q

Describe Papilloma epidemiology, pathology, clinical presentation, management, prognosis

A

Solid Intraductal Papilloma

  • Epidemiology
    • 30-50yo
  • Pathology
    • tumor of major lactiferous ducts
  • Clinical presentation
    • bloody discharge (75%)
    • +/- mass near areola
  • Investigation
    • Mammogram
    • Ductogram (can identify duct invovled
  • Management
    • Excision of duct
  • Prognosis
    • slight increased risk of ca compared to gneral RR3.3
66
Q

How does Multiple Peripheral papillomas differ from Solitary intraductal papilloma

A
  • TDLUs are affected in groups of peripheral ducts
  • ADH may be found in association**
  • High risk of ipsilat breast ca (30%)
67
Q

How does Papillomatosis differ from solitary intraductal papilloma

A

Associated with benign epithelial hyperplasia

68
Q

How does Juvenile papillomatosis differ from solitary intralobular papilloma

A

Occurs in young W 20-30

no discharge, mobile mass (similar ot fibroadenoma)

69
Q

What is critical to do if diagnosed with papilloma of nipple?

A

Associated with ipsilateral breast ca - search to identify and treat

Mass beneath nipple with ulceration

70
Q

Describe Microglandular adenosis epidemiology, pathology, clinical presentation, management, prognosis

A
  • >40yo
  • rubbery mass
  • gland hyperplasia
  • Tx with local excision
  • no increased Ca risk
71
Q

Describe Radial Sclerosing lesions

A

Fibroelastic core with duct elements radiating with epithelial hypoerplasia and papillomatosis

Tx - local excision

Prognosis - small increased Ca risk

72
Q

Describe Granular cell epidemiology, pathology, clinical presentation, management, prognosis

A
  • Epidemiology
    • more frequent in blacks, puberty to menopause
  • Pathology
    • granularity of cytoplasm of proliferating cells
  • Clinical presentation
    • palpable mass in inner upper quadrant of breast
  • Tx
    • WLE
73
Q

Describe Fibromatosis pathology, clinical presentation, management, prognosis

A
  • locally invasive proliferation of fibroblasts
  • may be fixed to skin or underlyig muscle
  • Mammogram - indistinguishable from Ca
  • Tx: WLE
74
Q

Describe 5 types of Inflammatory/reactive benign breast disease

A
  1. Ductal Ectasia
  2. Abscess, nonpuerperal
  3. Abscess, puerperal w mastitis
  4. Fistula
  5. FB reaction
75
Q

WHat is Duct Ectasia and how is it managed

A

= periductal mastitis

  • terminal subareolar ductules are blocked/filled with secretions which cause inflaamtory reaction chronically
  • present with nipple inversion, discahrge (green/cream), tenderness, subareolar mass
  • Biopsy and broad spec antibiotics
76
Q

What is nonpuerperal abscess and how is it managed

A
  • subareolar (most commonlly) abscess
  • caused by anaerobes (bacteroides, peptostreptococcus) and aerobes (staph, CNS)
  • Tx:
    • broad spe Abx
    • biopsy of wall
    • excision of ducts beneath areola after inflammation resovled
77
Q

What is a mammary fistula and how is it managed?

A
  • complication of duct ectasia, biopsy, abscess
  • Treated with marsupilization
78
Q

What is puerperal abscess and how is it managed?

A

= cellulitis of lactating breast, risk leading to abscess

  • presents with wedge shaped area of erythema, cracked nipple, systemically unwell
  • Caused by staph aureus

Tx: continue pumping breast milk, antibiotics, manual compession, warmth. If abscess forms, I&D, biipsy wall of abscess

79
Q

What are causes of fat necrosis and how is it managed

A
  • Trauma
  • Iatrogenic
  • Infection
  • Duct ectasia
  • autologous transplantation

Management

  • massage
  • in absence of trauma, biopsy to establish diagnosis
80
Q

What is the appearnace of fat necrosis on imaging

A

MRI

  • central enhancnig on T1, rim enhancing, oil cyst
81
Q

What is mondor disease

A

Superficial thromboplebitis of laterla thoracic vein or superior thorcoepigastric veins

Caused by

  • infection
  • breast surgery
  • trauma
  • associated with Ca 5-10%
  • rheuatoid arthritis

Managed with

  • NSAIDs, heat
82
Q

What is the etiology of Tuberous breast?

A
  • remains controversial
  • thought to be due to thickened & constricted superficial breast fascia that prevents peripheral expansion during pubertal breast growth, leading to a constricted breast base (where the fascia is most tight) and forward growth of breast tissue through the areola, where the fascia forms a ring and is deficient centrally
83
Q

what hormones cause ductular, lobular and alveolar growth during pregnancy?

A
  • estrogen
  • progesterone
  • placental lactogen
  • human chorionic gonadotropic
  • prolactin