This document discusses various benign breast diseases, including their development, classification, presentation, imaging, and management. It begins with breast development during puberty under the influence of hormones like estrogen. It then covers breast physiology such as lobular development and hormonal cycling. Various benign breast conditions are classified as congenital, infectious, traumatic, or pregnancy-related. Common symptoms include lumps, pain, and discharge. Evaluation involves clinical examination, imaging, and pathology. Management depends on the specific condition and may include observation, aspiration, excision, or medications. The goal of treatment is tailored to individual needs based on disease natural history and risk factors for malignancy.
4. Puberty:
The morphological structure of Human
Breast is identical in males and females
until Puberty
The 5-stage Tanner Scale shows the development
stages of Secondary Sex characteristics when the
female sex hormones (principally Estrogen) in
conjunction with growth hormone promote
sprouting, growth and development of breast of
pubescent girls in Thelarche.
Ref:http://en.m.wikipedia.org/wiki.Breast
EMBRYOGENESIS
10. PREGNANCY
11
Progesterone
• Growth and branching of Ductal system
• Fat deposition in stroma
Estrogen
• Growth of Alveolar Lobular System
• Secretory changes in Epithelial Cells
21. MANAGEMENT PROTOCOL
23
Fibroadenoma(Clinical Diag)
Tripple assessment
Multiple Giant/Juvenile
Age>30yrs
Results do not
concur
Age<30yrs
All results concur
Observe Wide local excision Excision of largest
Extra-capsular
Excision
No change in size Increase in size
SBE Excision
35. MANAGEMENT
37
• Assess type of pain
• Assess severity of pain ( Pain diary + Visual analogue scale )
• Evaluation with Triple assessment
• Treatment :
Reassurance is the key to management
Use of supportive undergarments
Low fat, Methyl xanthine restricted diet
Stop Oral contraceptives / HRT etc
Review patient. Sucessful in the majority ( 80 – 85 % ) of patients
Start drugs in those not responding to nonpharmacological
treatment
Review and assess response
44. BREAST ABSCESS
46
1. Lactational infections
Diminishing incidence
Usually caused by S.aureus
Clinical features : Pain, redness,
swelling, tenderness & systemic
symptoms
Treatment :
Antibiotics (E.G. Flucloxacillin,
Coamoxyclav etc) before pus
formation
Abscess : Repeated aspiration / mini
incision with topical anaesthetic
cream ( I& D under GA occasionally)
May continue to breast feed
2. NonLactational infections : Central
Usually due to Periductal mastitis
Affects younger women. Often smokers in the
West
May present as : inflammation +/- mass, abscess,
mammary duct fistula
Aerobic + anaerobic organisms may be involved
Treatment :
Antibiotics (E.G. Co amoxyclav etc) before pus
formation
Abscess : Repeated aspiration / mini incision with
topical anaesthetic cream ( I& D under GA
occasionally)
MDF : Excision fistula + Total duct excision
60. CONCLUSION
62
Benign breast disorders & diseases are common
The aetiopathogenesis is complex and not fully understood
The ANDI classification is a unifying concept
Histological risk factors for future malignancy are relative and not
absolute risk factors
Lump and pain are the most common complaints
Evaluation is done by Triple assessment
Treatment is based on the natural history of clinical problems
Management algorithms are general guidelines
Treatment must be tailored to individual needs
During the second month of gestation, two bands of slightly thickened ectoderm appear on the ventral body wall extending from above the axilla to below the groin. These bands are the milk lines and represent potential mammary gland tissue. In humans, only the pectoral portion of these bands will persist and ultimately develop into adult mammary glands. Occasionally, vestigial, or even functional, breast tissue may arise from other portions of the milk line.
The glandular portion of the breast develops from the ectoderm. It arises from the local thickening of the epidermis (Fig. 3-2A). From this thickening, 16 to 24 buds of ectodermal cells grow into the underlying mesoderm (dermis) during the twelfth week (Fig. 3-2B). These buds, at first solid, will become canalized near term to form the lactiferous ducts (Fig. 3-2C). The tips of the buds will give rise to the secretory acini during lactation. The epidermal surface of the future nipple is at first a shallow pit (Fig. 3-2D). Near term it becomes everted (Fig. 3-2E). The areola is said to be visible from the fifth month onward. Note that an inverted nipple may be a developmental arrest rather than a true pathological condition.
Pubic Hair Scale (both males and females)
Stage 1: No hair
Stage 2: Downy hair
Stage 3: Scant terminal hair
Stage 4: Terminal hair that fills the entire triangle overlying the pubic region
Stage 5: Terminal hair that extends beyond the inguinal crease onto the thigh
Female Breast Development Scale
Stage 1: No glandular breast tissue palpable
Stage 2: Breast bud palpable under areola (1st pubertal sign in females)
Stage 3: Breast tissue palpable outside areola; no areolar development
Stage 4: Areola elevated above contour of the breast, forming “double scoop” appearance
Stage 5: Areolar mound recedes back into single breast contour with areolar hyperpigmentation, papillae development and nipple protrusion
Male External Genitalia Scale
Stage 1: Testicular volume < 4 ml or long axis < 2.5 cm
Stage 2: 4 ml-8 ml (or 2.5-3.3 cm long), 1st pubertal sign in males
Stage 3: 9 ml-12 ml (or 3.4-4.0 cm long)
Stage 4: 15-20 ml (or 4.1-4.5 cm long)
Stage 5: > 20 ml (or > 4.5 cm long)
Before puberty, the breast is composed primarily of dense fibrous stroma and scattered ducts lined with epithelium.
low-amplitude pulses of pituitary gonadotropins, which increase serum estradiol concentrations.
this hormone-dependent matura- tion (thelarche) entails increased deposition of fat, the formation of new ducts by branching and elongation, and the first appearance of lobular units. This process of growth and cell division is under the control of estrogen, progesterone, adrenal hormones, pituitary hormones, and the trophic effects of insulin and thyroid hormone.
The term prepubertal gynecomastia refers to
symmetrical enlargement and projection of the breast bud in a girl before the average age of 12 years, unaccompanied by the other changes of puberty.
The postpubertal mature or resting breast contains fat, stroma, lactiferous ducts, and lobular units. During phases of the men- strual cycle or in response to exogenous hormones, the breast epithelium and lobular stroma undergo cyclic stimulation. The dominant process appears to be hypertrophy and alteration of morphology rather than hyperplasia. In the late luteal (premen- strual) phase, there is an accumulation of fluid and intralobular edema. This edema can produce pain and breast engorgement.
These physiologic changes can lead to increased nodularity and may be mistaken for a malignant tumor. Ill-defined masses in premenopausal women are generally observed through the course of the menstrual cycle before any intervention is undertaken.
With pregnancy, there is diminution of the fibrous stroma and the formation of new acini or lobules, termed adenosis of pregnancy.
After birth, there is a sudden loss of placental hormones, which, combined with continued high levels of prolactin, is the principal trigger for lactation.
The actual expulsion of milk is under hormonal control and is caused by contraction of the myoepithelial cells that surround the breast ducts and terminal ductules. There is no evidence for innervation of these myoepithelial cells; their contraction appears to occur in response to the pituitary-derived peptide oxytocin. Stimulation of the nipple appears to be the physiologic signal for continued pituitary secre- tion of prolactin and acute release of oxytocin. When breastfeed- ing ceases, the prolactin level decreases and there is no stimulus for release of oxytocin. The breast returns to a resting state and to the cyclic changes induced when menstruation resumes.
Menopause is defined by cessation in menstrual flow for at least 1 year; in the United States, it usually occurs between the ages of 40 and 55 years, with a median age of 51 years. Meno- pause may be accompanied by symptoms such as vasomotor dis- turbances (hot flashes), vaginal dryness, urinary tract infections, and cognitive impairment (possibly secondary to interruption of sleep by hot flashes). Menopause results in involution and a general decrease in the epithelial elements of the resting breast.
These changes include increased fat deposition, diminished con- nective tissue, and the disappearance of lobular units. The persis- tence of lobules, hyperplasia of the ductal epithelium, and cyst formation all can occur under the influence of exogenous ovarian hormones,
Estrogen, acting through its ER receptor, promotes duct growth, with other mediators, such as GH and IGF-1.
The GH effects on ductal growth are mediated through stimulation of IGF-1.
GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development
estrogen promotes GH secretion and increases GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.
Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones.
maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL [3.1nmol]), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase (11).
Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone.
Total estrogen excretion increases from 20–20,000 mg per 24 hours between early and late pregnancy.
This greatly stimulate the ductal arborization begun at puberty and the differentiation of epithelial cells into ductal, acinar, and myoepithelial elements.
As the acinar-ductal system expands, it replaces much of the fatty tissue of the breast and is organized into mature, functional, lobular-alveolar-ductal units surrounded by hypertrophied myoepithelial elements .
In addition to its effect on the mammary cells themselves, estrogen stimulates the synthesis and release of prolactin from the pituitary lactotrophs. Rising prolactin levels appear to be necessary for estrogen to exert its biologic effects on the mammary gland.
In addition, prolactin induces the enzymes necessary for the acinar secretory activity seen after delivery. Prolactin levels increase from 20–200 ng/ml during pregnancy.
It is based on the fact that most benign breast disorders are relatively minor aberrations of the normal processes of development, cyclical hormonal response and involution.
The endocrine causes are due to a disturbance of the hypothalamic- pituitary gonadal steroid axis with an increase in circulating hormone levels. The altered prolactine profile is responsible for the production of galactorrhoea in some cases.
Non endocrine causes include uses of methylxanthines, stress, diet rich in saturated fat
(altered essential fatty acid profile causes super sensitivity to normal levels of Estrogen
and Prolactin) and Iodine deficiency
Breast myxoid fibroadenomas (MFAs) are characterized by a distinctive hypocellular myxoid stroma, and occur sporadically or in the context of Carney complex, an inheritable condition caused by PRKAR1A-inactivating germline mutations. Conventional fibroadenomas (FAs) are underpinned by recurrent MED12 mutations in the stromal components of the lesions.
Fibroadenomas showing circumscribed margins, even distribution of epithelial and stromal components and low stromal cellularity - particularly the upper lesion
PAP stained FNA from a fibroadenoma - detail of a large stromal fragment (blue arrow), vessel fragment (red arrow) and small epthelial group (yellow arrow).
Very large dense mass with well-defined margins, posterior and slightly superior to the nipple.
well circumscribed well defined ovoid mass at the 12 o'clock position 2 cm from the nipple. The mass is predominantly solid, contains multiple small cystic spaces and large areas of echogenic material which appeared to stream (consistent with fluid).
Breast Phyllodes tumors account for about 0.5% of all breast neoplasms. A combination of stromal and epithelial cellular elements form the Phyllodes tumor.
Phyllodes breast tumors represent about 2% to 3% of all fibroepithelial breast tumors. it develops in the connective tissue of the breast (the ‘stroma’).
So, a Phyllodes breast tumor does not develop in the epithelial tissues that line the breast ducts and lobules.
Phyllodes breast tumors quite often present as a firm, bumpy, and smooth-sided mass. Furthermore, the breast skin covering the tumor might be warm to the touch and reddish in color.
On breast ultrasound, a phyllodes tumour will usually appear as a well-defined ‘macro-lobulated’ mass with heterogeneous internal echoes. Some phyllodes breast tumors show posterior acoustic enhancement, but not all.an inhomogeneous, solid-appearing mass is the most common manifestation. A solid mass containing single or multiple, round or cleft like cystic spaces and demonstrating posterior acoustic enhancement strongly suggests the diagnosis of phyllodes tumor. Vascularization is usually present in the solid components.
So, if sonography suggests a fluid filling clefts or ‘elongated spaces’ in the mass, this would also point to a diagnosis of Phyllodes tumor.
Mammography
Typically seen as non-specific large rounded oval or lobulated, generally well circumscribed, lesions with smooth margins. A radiolucent halo may be present. Calcification (typically coarse and plaque like) may be seen in a very small proportion.
However, neither mammogram nor breast ultrasound will be able to distinguish convincingly between a Phyllodes breast tumor, or a breast fibroadenoma. So, a biopsy will be necessary.
Primary : WLE 1cm normal tissue
Recurrence: Re excision/mastectomy with or without reconsrtruction.
Primary : WLE 1cm normal tissue
Recurrence: Re excision/mastectomy with or without reconsrtruction.
Cysts within the breast parenchyma are fluid-filled, epithelial- lined cavities that vary in size from microscopic to large palpable masses containing 20 to 30 mL of fluid.
Cysts are derived from the terminal duct lobular unit. In most cysts, the epithelial lining is either flattened or totally absent. In only a small number of cysts,
Cysts are influenced by ovarian hormones, a fact that explains their variation with the menstrual cycle. Most cysts occur in women older than 35 years; the incidence steadily increases until menopause and sharply declines thereafter.
Complex (or complicated or atypical) cyst is a sonographic diagnosis that is characterized by internal echoes or thin septations, thickened and/or irregular wall, and absent posterior enhancement [54]. They are reported in approximately 5%–5.5% of all breast ultrasound examinations. The malignancy rate of complex cysts, which is 0.3%
According to size, the cysts are divided into two categories:
macrocysts: ranging from 1-6 cm in diameter that could be simple cysts or lobulated multilocular lesions
microcysts: <3 mm in diameter
Cysts can be:
solitary lesions
multiple lesions
Sonographic features of a simple cyst include:
anechoic signal (no internal echoes)
smooth walls
well-circumscribed shape
enhanced through transmission: posterior acoustic enhancement
sharp anterior and posterior borders
reverberation artifact
They may display calcifications in their periphery. They should not increase in size in post-menopausal women.
Cyclical mastalgia:
Cyclical pain is related to the menstrual cycle (Fig.1) and is regulated by the hormones involved in this cycle. The characteristic features are:
It is commonly seen 1-2 weeks prior to menstrual bleeding in women and subsides with onset of menstrual bleeding. This pain arises due to proliferation of normal breast glandular tissue which is regulated by ovulatory hormones during late luteal phase.6
It is seen in women between 30-40 years of age.
Pain is usually bilateral and diffuse. It may be more severe in one breast, usually in upper outer quadrant. The pain may radiate to the upper limbs.
Usually, there are no masses palpable.
Nodularity or ‘lumpiness’ of breast tissue is often present and does not necessarily indicate an underlying pathology. This may be a normal variant and is often seen prior to periods as a physiological response to estrogen and progesterone levels.
Non-cyclical mastalgia:
Non- cyclical breast pain is not regulated by menstrual hormones. It is usually unilateral and focal, localized to a quadrant of the breast. The pain may be continuous or intermittent and may be present throughout the menstrual cycle. There are usually no findings on physical examination. The presence of a mass may warrant further investigation. Non-cyclical mastalgia may result from various causes, some of which are listed
The appearance of discharge from the nipple of a nonlactating woman is a common condition and is rarely associ- ated with an underlying carcinoma.
It is important to establish whether the discharge comes from one breast or from both breasts, whether it comes from multiple duct orifices or from just one, and whether the discharge is grossly bloody or contains blood.
The most common cause of spontaneous nipple discharge from a single duct is a solitary intraductal papilloma in one of the large subareolar ducts under the nipple. Subareolar duct ectasia producing inflammation and dilation of large collecting ducts under the nipple is common and usually involves discharge from multiple ducts.
Cancer is a very unusual cause of discharge in the absence of other signs.
Nipple discharge that is bilateral and comes from multiple ducts is not usually a cause for surgery. Bloody discharge from a single duct often requires surgical excision to establish a diagnosis and control the discharge.
A diagnosis of intraductal papilloma is found in most of these cases.
Two types of intraductal papillomas are generally distinguished. The central type develops near the nipple. They are usually solitary and often arise in the period nearing menopause. On the other hand, the peripheral type are often multiple papillomas arising at the peripheral breasts, and are usually found in younger women. The peripheral type are associated with a higher risk of malignancy.
They are the most common cause of bloody nipple discharge in women age 20-40 and generally do not show up on mammography due to their small size. They may be detectable on ultrasound. A galactogram is the most definitive test but is somewhat invasive.
Papillomatosis refers to epithelial hyperplasia, which commonly occurs in younger women or is associated with fibrocystic change. Papillomatosis is not composed of true papillomas but rather consists of hyperplastic epithelium that may fill individual ducts similar to a true polyp but has no stalk of fibrovascular tissue.
Color Doppler sonogram reveals a well-circumscribed, round cystic structure with homogeneous internal echogenicity, posterior acoustic enhancement, and flow to the cyst wall only. (b) True lateral mammogram of another patient shows the fat-fluid level (arrowhead ), which is a specific finding for galactocele.
saponification of local fat. It is a benign inflammatory process and is becoming increasingly common with the greater use of breast conserving surgery and mammoplasty procedures.
At a microscopic level, the initial change is disruption of fat cells where vacuoles with the remnants of necrotic fat cells are formed. They then become surrounded by lipid-laden macrophages, multinucleated giant cells, and acute inflammatory cells. Fibrosis develops during the reparative phase peripherally enclosing an area of necrotic fat and cellular debris. Eventually, fibrosis may replace the area of degenerated fat with a scar, or loculated and degenerated fat may persist for years within a fibrotic scar.