BREAST

PHYSIOLOGY
 Mammary development and function are
initiated by a variety of hormonal stimuli,
including estrogen and progesterone, prolactin,
oxytocin, thyroid hormone, cortisol, and growth
hormone.

Estrogen, progesterone, and prolactin have

profound trophic effects that are essential to
normal breast development and function.

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 Estrogen initiates ductal development
Progesterone primarily responsible for differentiation
of epithelial cells and lobular development
may reduce estrogen binding in mammary
epithelium and limit tubular system proliferation
Prolactin primary hormonal stimulus for lactogenesis
in late pregnancy and in the postpartum period
increases the number of estrogen receptors
and stimulates epithelial cells to act synergistically with
ductular and lobuloalveolar development.

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 HYPOTHALAMUS

GnRH

ANTERIOR PITUITARY

FSH and LH

OVARY

estrogen and progesterone

***Secretion of LH, FSH, and GnRH is regulated by positive and

negative feedback effects of circulating levels of estrogen and
progesterone.

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 The secretion of these mammogenic hormones
throughout the life of the normal female is responsible
for alterations in the hormonal milieu and for
development, function, and maintenance of
lobuloalveolar tissues.

human female neonate plasma estrogen and

progesterone levels decrease after birth

throughout childhood levels remain low as a

result of the regulatory sensitivity of the hypothalamic-
pituitary axis to the negative feedback effects of sex
steroids

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 onset of puberty an increase in the central drive
of the hypothalamus occurs, with a concurrent decrease
in sensitivity to negative feedback by estrogen and
progesterone.
Thereafter, an increase in sensitivity to positive feedback by
estrogen is evident.
These physiologic events thereby initiate an increase in GnRH
secretion, an increase in FSH and LH secretion, and ultimately an
increase in ovarian estrogen and progesterone secretion.

***With the development of positive feedback by estrogen,

the menses are initiated.

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 Cyclic Changes During
the Menstrual Cycle
There are great variations in breast volume
during the menstrual cycle.
Volume is greatest in the second half of the
cycle, after a premenstrual increase in size,
nodularity, density, and sensitivity.
Progesterone may stimulate glandular growth
in the luteal phase.
Changes in the mitotic rate of glandular
components are greater in the luteal phase
than in the follicular phase.

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 Pregnancy
A dramatic increase in secretion and release of
circulating ovarian and placental estrogens and
progestins is evident with pregnancy.

The gland enlarges, the areolar skin darkens,

and the areolar glands become prominent as
ducts and lobules proliferate. In the first
trimester, lobuloalveolar formation is initiated
as ducts branch to form multiple alveoli.

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 With increases in lobular size, proliferating glandular
epithelium replaces connective tissue and the
components of adipose tissue.

second trimester proliferation of ductular

elements increases after stimulation by estrogens and
progestins secreted by the placenta.

These sex steroids cause arborization of glandular

structures to further develop alveoli.
As this glandular system enlarges, the secretory
capacity of the epithelium increases, as is evident by the
accumulation of colloid in the alveoli.

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 third trimester fat droplets accumulate in the
alveolar cells and colostrum fills the alveolar and
ductular spaces
Mammary blood flow increases and myoepithelial cells
hypertrophy.

Late pregnancy limited synthesis of milk fats and

proteins is initiated
This process is stimulated by the lactogenic effects of
prolactin on breast lobular tissue; other pituitary
lactogenic hormones may also have trophic effects

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 Postpartum Lactation
After delivery of the placenta, progesterone
and estrogen levels diminish.

These quantitative decreases in the plasma

estradiol and progesterone levels allow full
expression of the lactogenic action of prolactin.

Maintenance of lactation requires regular

removal of milk and stimulation (milk letdown)
of the neural reflexes to prolactin secretion.

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 Oxytocin initiates contraction
of smooth muscle
components of myoepithelial
cells that surround the
alveoli; compression of the
alveoli occurs, and expulsion
of milk under pressure into
the lactiferous sinuses is
evident.

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 After the weaning of the infant
gland returns to an inactive, nonsecretory
state

Prolactin and oxytocin release subside

The secretory activity of the lactogenic epithelium
decreases, and unremoved dormant milk increases
pressure within the ductular and alveolar structures.
The lobular structure thereafter atrophies and the
secretory cells degenerate

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 Postmenopausal Breast
1. After menopause and the concomitant decrease in
ovarian secretion of estrogen and progesterone, there
is a progressive involution of ductular and glandular
components.
2. A decrease in the number and size of glandular
elements is evident; the epithelium of the lobules and
ducts becomes atrophic or hypoplastic.
3. Surrounding fibrous tissue increases in density, and the
parenchyma is replaced with adipose and stromal
tissue rather than supporting glandular structure.
4. With aging there is loss of fat content and the
supporting stroma, thereby initiating loss of lobular
structure, density, form, and contour

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 Gynecomastia
Gynecomastia implies the presence of a female-type
mammary gland in the male.
Most examples of gynecomastia should not be
considered a disease, because enlargement of the male
breast is common.
Physiologic gynecomastia occurs mostly during three
phases of life:
(1) neonatal period
(2) adolescence
(3) senescence
Common to each is an excess of estrogens in relation to
circulating testosterone.

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 Neonatal physiologic gynecomastia is
caused by the action of placental estrogens on
neonatal breast parenchyma.

In adolescence there is an excess of estradiol

relative to testosterone.

With aging, the plasma testosterone level falls,

and senescent gynecomastia is caused by a
relative hyperestrinism.

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