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Alterations in Sexual Maturation
P816-819
 Process of sexual maturation (puberty) is marked by development of 2ndary sexual
characteristics, rapid growth and the ability to reproduce. Delayed or early puberty involves
a disrupted onset of sex hormone production by the gonads.
o Delayed puberty
 Thelarche (breast development) should begin at 13 for girls, boys 1st sign
around 14 years old is enlargement of testes/thinning of scrotal skin.
Considered delayed if NO signs of puberty by 13 in girls and 14 in boys.
 95% of cases attributed to physiologic delay (hormonal levels are normal &
HPG (hypotha-pituit-gonad) is intact but maturation is slow)
 tends to be familial and more common in boys than girls
 other causes may be related to consequences of any chronic condition
that delays bone aging (lung disease, renal failure, cystic fibrosis)
 5% of cases caused by disruption of the HPG axis
o Precocious puberty (early onset)
 Sexual maturation before age 6 in black girls or 7 in white girls, and before age
9 in boys
 Rare, 1/10,000 girls and less than 1/50,000 boys (much more common in
girls)
 Causes are either:
 central (GnRH dependent: HPG axis working normally but
prematurely)
 or peripheral (GnRH independent: sex hormones produced by some
mechanism other than stimulation by gonadotropins)
o this may include sex-steroid releasing tumor, testotoxicosis,
hormonal contraceptives
 Forms are:
 Complete: onset/progression of all pubertal features (thelarche,
pubarche & menarch)
 Partial/incomplete: partial development of appropriate 2ndary
characteristics alone or in combination (example: girl undergos
thelarch or pubarche but rarely premature menarche)
 Mixed/heterosexual: virilization of a girl or feminization of a boy
causes child to develop 2ndary characteristics of opposite sex
Hormonal/Menstrual Alterations of Female Reproductive System (FRS)
P819-828
 Primary Dysmenorrhea
o What is it?
 Painful menstruation associated with release of prostaglandins in ovulatory
cycles (NOT associated with pelvic disease)
 Severity related to duration/amount of menstrual flow, between 50-90% of
women aged 15-25 years old are affected
 Secondary dysmenorrhea is related to pelvic pathology, manifests in later
reproductive years & may occur any time in menstrual cycle
o Pathologic mechanism?
 Excessive endometrial prostaglandin production (enhanced by progesterone)
o Symptoms?
Pelvic pain associated with onset of menses, backache, anorexia, vomiting,
diarrhea, headache
o Treatment?
 Hormonal contraceptive, non-steroidal/non-inflammatory meds, regular
exercise, stress reduction, heat, massage
Amenorrhea
o What is it?
 Lack of menstruation
 Primary = failure of menarche/absence of menstruation by age 14 w/out
development of 2ndary sex characteristics of by age 16 regardless of presence
of 2ndary characteristic
 Differs from delayed puberty in that most cases of delayed puberty
require only reassurance
o Mechanism?
 Compartment IV disorders (CNS disorders, in particular the hypothalamus)
 Hypoth-pituit-ovarian axis is dysfunctional. Hypoth doesn’t secrete
GnRH, which doesn’t stimulate pituitary to release LH/FSH, therefore
the ovary doesn’t receive hormonal signals that would initiate
menstruation.
 b/c ovarian hormones are absent, estrogen-dependent sex
characteristics don’t develop
 Compartment III disorders (anterior pituitary problems, including tumors)
 Tumors, lesions, trauma, hydrocephalua, etc. can interfere with
hypothal-pituit unit, which interrupts the secretion of GnRH/LH/FSH.
 These lesions develop between the onset & conclusion o puberty, so
skeletal growth & 2ndary characteristics may develop, but sexual
maturation is interrupted before menarche can begin
 Compartment II disorders (involve the ovary)
 Includes genetic problems such as gonadal dysgenesis (Turner
syndrome), androgen insensitivity syndrome (AIS), poly-X
o Turner syndrome: ovaries lack gametes/ovarian failure is
complete, so follicular development & estrogen secretion can’t
occur
 This leads to lack of 2ndary sex characteristics &
menstruation
o AIS: person is genetically male but has female morphology
o Poly-x: “superfemale syndrome” XXX (extra X chromosome in
female)
 Compartment I disorders (anatomic defects of the outflow tract associated
with primary amenorrhea)
 Includes congenital absence of a vagina & uterus, congenital uterine
hypolplasia (infantile uterus)
 Skeletal growth & 2ndary sex characteristics occur but no menstruation
and uterus doesn’t respond during puberty
o Symptoms?
 Pregnancy (if you don’t have menses, you may be pregnant)
o Treatment?


Correct underlying problems, hormone replacement therapy, surgical
alteration of genitalia
Secondary Amenorrhea
o What is it?
 The absence of menstruation for a time equivalent to 2+ cycles or 6 months in
women who have previously menstruated
 May be associated with dramatic weight loss, disease, and is normal during
early adolescence, pregnancy & lactation
 Most common causes (after pregnancy) are thyroid disorders,
hyperpolactinemia, HPO interruption 2ndary to excessive exercise, stress,
weight loss and polycystic ovary syndrome
o Mechanism?
 See Figure 23-2 on P821
 If there is normal ovarian hormone secretion, causes could be:
 Pregnancy, uterine dysfunction caused by hysterectomy or endometrial
ablation/adhesions (destroys lining of uterus)
 If there is decreased ovarian hormone secretion w/ high gonadotropin levels,
causes could be:
 Menopause, ovarian failure caused by gonadal dysgenesis, resistance to
gonadotropins, autoimmune disease, chemotherapy, environmental
toxins, and premature ovarian failure
 If there is decreased ovarian hormone secretion w/ low gonadotropin levels,
causes could be:
 Secondary ovarian failure caused by hyperprolactinemia, hypoth-piuit
disorders, function hypothal-anovulation caused by starvation or
psychogenic problems
 If there is an increase in ovarian hormone secretion with low/normal
gonadotropin levels causes could be:
 Excessive testosterone/progesterone, ovarian tumor, adrenal tumors
or congenital adrenal hyperplasia
o Symptoms?
 Absence of menses, infertility, vaginal atrophy, acne, osteopenia, and abnormal
hairiness
o Treatment?
 Oral, vaginal or injectable hormone replacement therapy, surgical removal of
tumors
Abnormal/Dysfunctional Uterine Bleeding (DUB)
o What is it?
 Heavy/irregular bleeding in the absence of organic disease
o Mechanism?
 Most are attributed to:
 anovulatory cycles: most prevalent, associated with PCOS, immaturity
of the HPO axis, obesity, hyper/hypothyroidism, and estrogen-secreting
ovarian neoplasms
 corpus luteum defects or atrophic endometrium: due to progesterone
deficiency or estrogen excess
o Symptoms?



Unpredictable/variable bleeding in terms of amount/duration, excessive
bleeding can cause anemia so fatigue, shortness of breath and iron deficiency
are symptoms
o Treatment?
 Hormone therapy, various meds consistent with cause of bleeding,
hysterectomy, ablation or IUD (by decreasing endometrial proliferation, IUD
helps control blood flow)
Polycystic Ovary Syndrome (PCOS)
o What is it?
 Characterized by excessive production of androgen (causes premature
follicular failure & persistent anovulation) & estrogen
 Has at least 2 of the following symptoms: oligo-ovulation or anovulation,
elevated levels of androgens, clinical signs of hyperandrogenism and
polycystic ovaries
 Polycystic ovaries don’t have to be present to diagnose PCOS and alternatively
their presence alone doesn’t indicated PCOS
o Mechanism?
 Unknown cause, genetic factor is suspected
 High levels of LH increase androgens from adrenal gland and testosterone
from the ovaries. Androgens convert to estrogen. High levels of estrogen
continue to raise LH but lower FSH (so follicular growth is stimulated but
never fully matures). Follicles are “left” in ovary and eventually can turn into
cysts.
o Symptoms?
 Change over time with metabolic syndrome becoming more prominent with
age.
 May be associated with Cushing syndrome, acrogmegaly, premature ovarian
failure, simply obesity, congenital adrenal hyperoplasia, thyroid disease, or
ovarian tumors
 Other symptoms include dysfunctional bleeding, hirsutism (excessive hair in
inappropriate places), acne and infertility
o Treatment?
 Difficult to diagnose since so many symptoms/complications can be involved
 Oral contraceptives (progesterone therapy to over-rule high estrogen levels),
antiandrogens and fertility agents used
 Medicine that decreases insulin levels (which seems to play a role associated
with high androgen levels)
 Lifestyle changes such as diet and exercise
Premenstrual Disorders (PMS & PMDD)
o What is it?
 Cyclic recurrence (in luteal phase) of distressing physical, psychological or
behavioral changes that impair interpersonal relationships or interfere with
usual activities
o Mechanism?
 It may be the result of abnormal tissue response to the normal changes of the
menstrual cycle, perhaps due to fluctuating estrogen/progesterone levels.
 Neurotransmitters (GABA, serotonin, and noradrenaline) may have mediating
roles
 Appears to be genetic



o Symptoms?
 Frequency/severity is most important indicator since over 300 physical,
emotional, & behavioral symptoms have been attributed to this one disorder
 Depression, anger, irritability, fatigue are most prominent complaints
o Treatment?
 Eliminate contributing factors, treat coexisting disorders, offer resources for
emotional support, counseling, meditation, exercise, good sleep, dietary
changes, decreasing caffeine/alcohol & increasing water, anti-depressents,
vitamin supplements, oral contraceptives
Infections/Inflammation of FRS
P828-833
 Results from endogenous (includes infections from microorganisms that are already present
in the vagina, bowel or vulva) or exogenous (usually STDs) causes
 Pelvic Inflammatory Disease (PID)
o What is it?
 Acute inflammatory process caused by infection. May involve any organ (or
combination) of the upper genital tract (uterus, fallopian tubes (salpingitis), &
ovaries (oophoritis)) and in its most severe form, the entire peritoneal cavity
o Mechanism?
 Usually due to a failure of defense mechanisms that usually protect against
PID, most often a polymicrobial infection (including facultative and anaerobic
organisms & genital tract mycoplasmas)
 Occurs when pathogenic microbes ascend from infected cervix to uterus and
further, some organisms change endothelium making it more susceptible to
infection
 The more instances one has to PID, the higher their chances of infertility
o Symptoms?
 Sudden, severe abdominal pain with fever OR no symptoms at all, may have
difficulty urinating or irregular bleeding
 15-25% of women after one episode develop long-term sequelae (a condition
that is consequence of a previous disease/injury): infertility, ectopic
pregnancy, chronic pelvic pain, dyspareunia (painful intercourse), pelvic
adhesions, perihepatitis (inflamm of serous/peritoneal coating of liver), tuboovarian abscess
o Treatment?
 Bed rest, avoidance of intercourse, antibiotic therapy
 Vaginitis
o What is it?
 An infection of the vagina usually caused by sexually transmitted pathogens &
Candida albicans
o Mechanism?
 Related to loss of local defense mechanisms (skin integrity, immune reaction,
and vaginal pH)
 Can be caused by douching, spermicides, hygiene sprays/deodorant sprays,
tampons, diabetes/pregnancy, antibodies
o Symptoms?
 Marked change in color of discharge or discharge becomes copious
(overabundant amount), malodorous (bad smell) or irritating



o Treatment?
 Maintaining an acidic environment, relieving symptoms, administer
antimicrobial/antifungal meds
Cervicitis
o What is it/Mechanism?
 Nonspecific term to describe inflamm of the cervix prior to the identification of
pathogens
 Specific cervicitis includes:
 Mucopurulent cervicitis (MPC) is caused by 1+ more sexually
transmitted pathogens
o Cervix becomes red/edematous, mucus drains from external
cervical os (external orifice of the uterus)
o Symptoms & Treatment?
 pelvic pain, bleeding or dysuria, many times there is bleeding during
intercourse or Pap smears
 antibiotic therapy
Vulvovestibulitis (vulvitis)
o What is it/Mechanism?
 Inflammation of vulva or vestibule of genitalia or both
 May represent several disorders w/out identifiable cause, fairly common
 May be caused by:
 contact dermatitis (soaps, detergents, lotions, sprays, shaving, tampons,
tight fitting clothes)
 abnormalities in vestibular mucosa, pelvic floor musculature, or CNS
pain regulatory pathways
 an autoimmune reaction
 vaginal infections that spread to the labia, where they cause inflamm &
edema
o Symptoms & Treatment?
 Behavioral treatment or vestibulectomy (removing the vulvar vestibule)
 Other paproaches with little research to support them include hydrocortisone
cream, applying a water barrier during a period of healing, lidocain application
Bartholinitis
o What is it/Mechanism?
 Inflammation of 1 or both of the ducts that lead from the introitus (vaginal
opening) to the Bartholin glands
 Caused by microorganisms that infect the lower female reproductive tract
(like streptococci, staphylococci), may be preceded by an infection (such as
cervicitis, vaginitis or urethritis)
 This infection causes inflammatory changes that narrow the distal
portion of the duct, leading to obstruction/stasis (slow/stopping of
bodily fluid) of glandular secretions
 This obstruction (or cyst) redeens and is painful, pus may be visible at
opening of duct
o Symptoms & Treatment?
 Fever, malaise (symptoms of infection), most are asymptomatic and require no
treatment, antibiotics may be given
Pelvic Organ Prolapse (POP)
P833-836
 Anatomy overview:
o The bladder, urethra and rectum are supported by the endopelvic fascia & the
perineal muscles (particularly the levator ani group). This muscular/fascial tissue
loses tone & strength with aging (or pregnancy) & may fail to maintain the pelvic
organs in the proper position. Progressive descent of the pelvic support structures
may cause pelvic floor disorders and pelvic organ prolapse.
 Details:
o Nearly 24% of women experience at least 1 POP
o Caused by trauma (childbirth or pelvic surgery or damage to pelvic innervation),
genetic factors play a role, it is progressive and related to the inherent
strength/weakness of the woman’s musculofascial tissue
o Black & Asian women have lowest risk, Hispanic have highest risk
o Evaluation is graded on a scale of 0 (normal position) to 4 (maximal possible decent
of uterus, meaning it is literally protruding out of the vagina, past the hymen, etc.)
 Uterine Prolapse:
o What is it?
 Decent of the cervix or entire uterus into vaginal canal (most severe case the
uterus protrudes from the introitus)
o Symptoms/Treatment?
 Besides seeing a uterus coming out of your vagina, more subtle symptoms
might be a feeling of fullness or heaviness
 Kegel exercises help, estrogen therapy, maintaining healthy body mass index,
preventing constipation and treating chronic cough may help prevent. May
have a pessary inserted, which is a removable mechanical device that holds
the uterus in position
 Surgical repair is last resort
 Cystocele
o What is it?
 Descent of a portion of the posterior bladder wall & trigone (a smooth
triangular area on the inner surface of the bladder) into the vaginal canal
(usually caused by childbirth)
 In severe cases the bladder wall protrudes outside the introitus
 NOTE: it does NOT cause urinary incontinence
o Symptoms/Treatment?
 Woman may explain discomfort as if she’s “sitting on a ball”, slight vaginal
pressure
 Kegel exercises help, estrogen therapy, pessary inserted, surgical repair is last
resort
 Urethrocele
o What is it?
 Sagging of the urethra, commonly associated with cystocele
 Caused by the shearing effect of the fetal head on the urethra during childbirth
 Cystourethrocele
o What is it?
 herniation of the neck of the female bladder and associated urethra into the
vagina



Occurs in nulliparous women (women who have not experienced childbirth),
caused by congenital weakness/relaxation of the musculature of pelvic floor
Rectocele
o What is it?
 Bulging of the rectum & posterior vaginal wall into the vaginal canal
 Damage may occur during childbirth but symptoms don’t occur until years
after menopause
 Familial/genetic & bowel habits contribute to disorder
o Symptoms/Treatment?
 Usually asymptomatic but severe cases cause vaginal pressur,e rectal fullness
and incomplete bowel evacuation
 Treatment focuses on preventing constipation, if needed use of pessary
Enterocele
o What is it?
 Herniation of rectouterine pouch into the rectovaginal septum (between
rectum & posterior vaginal wall). IN other words, the small bowel descends
into the lower pelvic cavity & pushes at the top part of the vagina, creating a
bulge
 Can be congenital or acquired (if acquired usually associated with other pelvic
prolapse disorders)
o Treatment is surgical
Benign Growths & Proliferative Conditions
P846-848
 Benign Ovarian Cysts
o What is it/Mechanism?
 Produced when a follicle (s) are stimulated but no dominant follicle
develops/completes the maturity process
o Details:
 Occur at any time but more common during reproductive years, chances
increase when hormonal imbalances are rampant (puberty & menopause)
 Quite common
o 2 common types of functional cysts (caused by variations of normal physciologic
events)
 follicular cyst:
 What is it?
o a transient condition in which the dominant follicle fails to
rupture or 1+ of the non-dominant follicles fail to regress
 Mechanism?
o reason not well understand. May be that hypothalamus doesn’t
receive/send a message strong enough to increase FSH (which is
needed to develop/mature a dominant follicle). When FSH is
low, estradiol doesn’t increase enough to stimulate LH
 Symptoms & Treatment?
o include bloating, swollen/tender breasts and heavy/irregular
menses
o usually the cyst is absorbed/regresses on its own
 corpus luteum cyst
 What is it?




o Develops when an imbalance in low LH & progesterone levels
causes an inadequate development of the corpus luteum
o Less common than follicular cyst but can cause more
symptoms/pain
Symptoms & Treatment?
o Dull pelvic pain, delayed menstruation, irregular bleeding,
rupture of cyst can occur & results in massive bleeding with
excruciating pain (immediate surgery required)
o Usually they regress in non pregnant women, oral
contraceptives can be used to prevent future cysts
o Dermoid cyst:
 What is it?
 Ovarian teratomas (a tumor derived from more than one embryonic
layer ) that contain elements of all three germ layers (these are
common ovarian neoplasms (a new growth of tissue serving no
physiological function))
 These are the cysts that can contain teeth, hair, bone, etc. They have
malignant potential so should be removed (usually they’re
asymptomatic)
Endometrial Polyp
o What is it/Mechanism?
 Benign mass of endometrial tissue on the lining of the uterus, covered by a
surface epithelium and contains glands, stoma and blood vessels
 Related to estrogen stimulation, usually develops in women 40-50 years old
(although it can occur at all ages)
o Symptoms & Treatment?
 Irregular bleeding, excessive heavy periods, bleeding after menopause
 Known to spontaneously resolve but polypectomy can be performed through
hysteroscopy (endoscope exam of cervic/uterus) for symptomatic women or
those with malignant risk
Leiomyomas (myomas or uterine fibroids)
o What is it/Mechanism?
 Benign smooth muscle tumors in the myometrium (muscle layer) of the uterus
 Most common benign tumors of the uterus (affects 70-80% of women), slow
growing, black and Asian women are at much higher risk than white women
 Cause unknown but appears to be related to estrogen, progesterone, growth
factors, angiogenesis (the formation and differentiation of blood vessels) &
apoptosis (genetically determined cell self-destruction, “cell suicide”)
o Symptoms & Treatment?
 Most remain small & asymptomatic
 May have abnormal bleeding, pain and pressure, attributed to infertility,
growing pressure by the tumor may disrupt nearby structures (bladder for
instance)
 Try to shrink the tumor with contraceptives, GnRH agonists, antidepressants.
Myomectomy remains the standard cure
Adenomyosis
o What is it/Mechanism?
 Endometrial cells from uterus migrate into the myometrial layer
Estrogen/progesterone likely play a role, different from endometriosis in that
it doesn’t respond to cyclic hormone changes
o Symptoms & Treatment?
 Irregular bleeding, uterine enlargement, uterine tenderness during
menstruation
 Treatment includes non steroidal inflammatory drugs, levonorgestrelcontaining IUDS, maybe surgical treatment if serious
Endometriosis
o What is it/Mechanism?
 Presence of functioning endometrial tissue outside the uterus
 Cause unknown but suspected reasons include:
 May be caused by menstrual fluids that move through the fallopian
tubes & empty into the pelvic cavity (retrograde menstruation). Now
likely it since most women experience this but not all women have
endometriosis.
 Another theory is that women with this condition have impaired
cellular/humoral immunity (T cell and natural killer cell activity has
been found to be depressed). At the same time, macrophages are
stimulating endometrial cell proliferation outside the uterus.
 An autoimmune response is also suspected. Or perhaps endometrial
cells spread through lymphatic or vascular systems and somehow
stimulate epithelial cells covering reproductive organs to develop into
endometrial cells.
 Genetic predisposition.
 NOTE: Important to understand that this tissue responds to hormonal changes
of menstrual cycle. So when uterus sheds lining, the ectopic endometrium also
sheds. This bleeding causes inflammation and pain. It can lead to fibrosis,
scarring and adhesions.
o Symptoms/Treatment?
 Infertility, pelvic pain, irregular menses, pain on defecation (dyschezia), pain
on intercourse (dyspareunia), constipation
 Treatment aimed at preventing/decreasing progesterone, alleviating pain and
restoring fertility


Cancer
P841-848
 Malignant tumors of FRS are common; endometrial carcinoma (5.8% of all cancers in
women), ovarian tumors (3.1% of all cancers) and cervical cancers (1.6% of all cancers).
Malignant neoplasms account for 13.3% diagnosed cancers and 11.3% cancer deaths in
women in the US.
 Cervical Cancer
o What is it?
 Most common cancer in women worldwide, higher risk in black women
 Caused by HPV infection, infection of strands 16 & 18 leads to precancerous
dysplasia of the cervix, which leads to cervical cancer
 Precancerous dysplasia (cervical intraepithelial carcinoma, CIN) or
cervical carcinoma in situ (CIS) occurs more often in younger women.
About 50% of young women acquire HPV and the immune system can
usually flush it out.


o Mechanism?
 Slowly progressive, staged according to histology (changes in cells indicated
what stage/severity the cancer is currently at). Stages from least to most
invasive:
 Cervical intraepithelial neoplasia (dysplasia)
o Replacement of some epithelial cells by atypical, neoplastic cells.
Stages within this stage are shown in Table 23-6 on P842
o Most abnormalities here will regress on their own without
further progression
 Cervical carcinoma in situ
o In the “transformation zone” columnar epithelium is replaced by
squamous epithelium in a process known as metaplasia.
Generally this stage is a precursor of invasive carcinoma of the
cervix (Table 23-6 on P842)
 Invasive carcinoma
o Direct invasion into adjacent tissues/metastasis through the
lymphatics (Table 23-6 on P842)
 Cause not really known but like other cancers, cervical cancer requires the
accumulation of genetic alterations for carcinogenesis to occur
o Symptoms & Treatment?
 Asymptomatic so regular Pap test or HPV screening is recommended, if
symptoms exist may include vaginal bleeding or abnormal discharge, foul odor
may be present
 Biopsy performed to confirm progression, laser treatment may be used for CIS
level, burn off cancer cells using LEEP, conization (remove cone-shaped
section of tissue that includes cancer). For invasive carcinoma, surgical
intervention, radiation therapy. Cure rate is very high if caught early.
Vaginal Cancer
o What is it/Mechanism?
 Rare (1-2% of gynecologic cancers). Most are squamous cell-type cancers
(remaining are adenocarcinomas, sarcomas & melanomas)
 Similar etiology as cervical cancer: both start a intraepithelial lesions, occurs
in sexually active women and are associated with HPV (prior carcinoma of
cervix increases risk of vaginal cancer). In utero exposure to nonsteroidal
estrogens also a risk factor.
 Have same stages as cervical cancer (dysplasia, carcinoma in situ and invasive)
& are staged based on extension into local tissues/metastasis to distant organs
o Symptoms & Treatment?
 Asymptomatic generally, vaginal bleeding my occur & in advanced stages
rectal/bladder symptoms, pain/leg edema can occur
 Excised with upper vaginectomy, laser ablation or LEEP, laser surgery, or
surgery with hysterectomy, radiation & chemo
 Chances of recovery go down the worse the stage becomes
Vulvar Cancer
o What is it/Mechanism?
 Responsible for 5% of all gynecologic cancers, majority are squamous cell
carcinomas with the remaining as melanoma, Bartholin gland carcinoma,
sarcoma and adenosquamous carcinoma
History of HPV, chronic vulvar irritation, squamous dysplasia of the
vagina/cervix, smoking and coffee use are all risk factors
o Symptoms & Treatment?
 May have a hard ulcerated area of the vulva, large cauliflower lesions or
lesions similar to those of chronic dermatitis
 Ablative/excisional surgery, sometimes radiation
Endometrial Cancer
o What is it/Mechanism?
 Most common form of pelvic region cancer (13%), arises within the glandular
epithelium of the uterine lining
 Incidence rate higher in whites but mortality is higher in blacks
 Primary risk factor is unopposed estrogen exposure with resultant
hyperplasia (estrogen therapy, early menarche, late menopause, never having
kids, failure to ovulate, obesity)
o Symptoms/Treatment?
 Abnormal bleeding is usually a sign, pain/weight loss are signs of late disease
progression
 Pregnancy & the use of combined hormonal contraceptives containing
estrogen/progestin have protecting effects, changing diet, exercise, surgical
excision may be necessary if serious
Uterine sarcomas
o What is it?
 Rare neoplasms that arise from myometrial smooth muscle of uterus,
endometrial stroma or connective tissue elements
 Chronic excess estrogen exposure, tamoxifen and black race are risk factors
o Symptoms/Treatment?
 Abnormal bleeding, awareness of a mass, pelvic pressure/pain, vaginal
discharge, GI problems
 Total hysterectomy followed by radiation therapy
Ovarian Cancer
o What is it?
 Accounts for 5% of all female cancer deaths, 5th most frequent cancer in
women
 Associated with early menarche, late menopause, nulliparity, and the use of
fertility drugs, also prior pelvic radiation plays a factor
 Cause is unknown, suggested that repetitive ovulatory tissue repair may
produce mutations
o Mechanism?
 Most malignancies are epithelial ovarian neoplasms (develop from the surface
epithelium of the ovary or that which line cysts immediately beneath the
ovarian surface)
 90% of all ovarian malignancies are classified as ovarian
adenocarcinomas (malignant form of epithelial ovarian neoplasms)
 Germ-cell tumors are derived from the primitive germ cells of the embryonic
gonad and may be malignant of benign (almost always occur in
children/adolescents)
o Symptoms & Treatment?






Range of symptoms depending on type of tumor/level of growth, but may
include pain and abdominal swelling, vomiting, alterations in bowel habits,
abnormal vaginal bleeding
Treatment may include surgery, radiation therapy, chemotherapy
Sexual Dysfunction in Females
P848-849
 Organic & psychosocial disorders are implicated. Chronic illness can affect sexual
functioning (see Table 23-9 on P849)
 Some examples:
o Disorders of desire (inhibited sexual desire, decreased libido): may be biologic
manifestation of depression, alcohol/substance abuse, prolactin secreting pituitary
turmos, or testoerone deficiency
o Vaginismus: involuntary muscle spasm in response to attempted penetration, causes
include prior sexual trauma/fear of sex, may be a physical problem too (such as
vulvovestibulitis)
o Anorgasms (orgasmic dysfunction): inability to achieve orgasm, may be caused by
diabetes, alcoholism, neuralgic disturbances, certain meds, hormonal deficiencies &
pelvic disorders (infections, trauma and surgical scarring)
o Rapid orgasm: rare, once orgasm occurs there’s little interest in further sexual
activity (aka, male sex syndrome… j/k)
o Dyspareunia (painful intercourse): psychosocial (history of sexual trauma,
depression, relationship factors play a role) or organic (inadequate lubrication, drugs
with drying effect, disorders such as diabetes, vaginal infections, estrogen deficiency,
infections around vulva area) causes
Impaired Fertility
P849-850
 Affects 15% of all couples, defined as the inability to conceive after 1 year of unprotected
intercourse
 Male factors include diminished quality/production of sperm, female factors associated with
malfunctions with the fallopian tubes, ovaries or reproductive hormones
Disorders of the Male Reproductive System
P850-869
 Disorders of the Urethra
o Urethritis: inflammation of the urethra w/out bladder infection, usually cased be ST
(sexually transmitted) microorg
 Man may feel tingling, itching, burn during urination, may be a discharge,
treated with antibiotics
o Urethral Stricture: fibrotic narrowing of the urethra caused by scarring, usually due
to trauma/infections from long0term use of indwelling urinary catheters
 Man may experience diminished force/caliber of urinary stream, urinary
frequency/discomfort. Treatment is surgical.
 Disorders of the Penis
o Phimosis/Paraphimosis
 Foreskin is too tight to be move easily over the glans penis
 Phimosis: foreskin can’t be retracted back over the glans
 Paraphimosis: foreskin is retracted & can’t be moved forward to cover the
glans
 Can occur at any age, usually due to poor hygiene and chronic infection
Edema, erythema and tenderness along with discharge my be signs (and the
fact that your foreskin is stuck….. hmm….). Paraphimosis can constrict the
penis so it’s important to get that fixed asap. Surgery is usually the preferred
method.
o Peyronie Disease
 Fibrotic condition resulting in varying degrees of curvature and sexual
dysfunction, “bent nail syndrome”
 Can cause painful erection/intercourse, poor erection
 Spontaneous resolution occurs in ½ the cases
o Priapism
 Uncommon, prolonged penile erection, usually painful & not associated with
arousal
 Idiopathic in 60% cases, 40% are associated with spinal cord trauma, sickle
cell, leukemia, pelvic tumors or infections
 It is an emergency since edema and fibrosis develops quickly leading to
impotence. Needle aspiration of blood, surgical treatment or iced saline
enemas are some treatments
o Balanitis
 Inflammation of glans penis and occurs in conjunction (usually) with posthitis
(inflammation of the prepuce)
 Associated with poor hygiene, poorly controlled diabetes mellitus and
candidiasis
o Penile cancer
 Rare in the US, twice as common in black men, usually affects men older than
50, risk factors include PV, smoking and psoriasis; men circumcised at birth
have less than ½ the chance of getting it than uncircumcised
 Mostly squamous cell carcinoma, which beings as small, fat,
ulcerative/papillary lesions on the glans or foreskin that grow to involve the
entire shaft
 May involve circumcision (in extreme situations, the removal of the penis
altogether). Newer techniques involve surgical steps, radiation or chemo
Disorders of the scrotum/tests/epididymis
o Scrotum
 May have a painful/painless mass that can be serious (cancer or torsion) or
benign (hydrocele or cyst). May require surgical intervention or careful
observation
 Varicocele: abnormal dilation of a vein within spermatic
cord/described as a “bag of worms” (“vein filled sac”)
o Cause: incompetent/congenitally absent valves in spermatic
veins (the valves that prevent backflow are absent/don’t
function, permitting blood to pool in the veins rather than flow
into the venous system)
o Can cause infertility
 Hydrocele: collection of fluid w/in the tunica vaginalis, most common
cause of scrotal swelling (“water filled sac”)
o Cause: In newborns it’s a congenital malformation that usually
resolves within 1 year. IN adults, may be caused by an
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imbalance between the secreting/absorptive capacities of
scrotal tissues. An infection/trauma may also cause.
 Spermatocele: painless cyst located between the head of the
epididymis and the testis that’s filled w/ milk fluid that contains sperm
(“sperm filled sac”)
Cryptochidism
 Testicular maldescent (testis don’t drop)
 Cause: could be physical (spermatic cord too short) or hormonal (maternal
gonadotropins are missing)
 Risk of testicular cancer is 35-50 times greater for men with undescended
testis
Ectopy
 Testis that have “strayed” from the normal pathway of descent
 Cause: may be an abnormal connection at the distal end of the gubernaculum
(a fibrous cord that connects testis with bottom of scrotum) that leads the
gonad to an abnormal position
Torsion of tests
 A rotation of the testis, which twists blood vessels in the spermatic cord, can
be very painful & serious b/c it cuts off blood supply
 If it can’t be fixed manually, surgery is performed within 6 hours after onset of
symptoms
Orchitis
 Inflammation of the testes, uncommon except when infection is present or
there is an extended problem relating to epididymitis
 Sudden onset after a mumps infection can occur
Cancer of the testes
 What is it?
 Among the most curable of cancers (cure rates are more than 95%),
pretty rare occurrence (1%) but most common cancer in men aged 1535, white men are at higher risk than black men, more common on the
right side & 50% arise from treated/untreated cryptorchid testes
 Mechanism?
 Most are germ-cell tumors arising from the male gametes. Can be
classified into two types:
o Seminomas: most common, least aggressive
o Nonseminomas: include embryonal carcinomas, teratomas and
choriocarcinomas (most aggressive but rare)
 Metastasis can occur and does so through lymphatic spread & the lungs
are common sites for the cancer to travel to
 Believed to have genetic predisposition
 Symptoms?
 Painless testicular enlargement (gradual), actuve pain can occur,
lumbar pain may be present, may have a cough/bloody sputum (sign of
spread to the lungs), neck swelling, alterationsin vision/mental status
 Treatment?
 Surgery, radiation & chemo
Epididymitis
 Inflammation of the epididymis, generally in sexually active adult males
Cause is usually STD bacteria that has spread to the epididymis
Complications include abscess formation, infarction of the testis, recurrent
infection and infertility
 Treatment may include elevating testes, bed rest, antibiotics, abscess draining
Disorders of the prostate gland
o Benign prostatic hyperplasia (BPH)
 What is it?
 Enlargement of the prostate gland
 Becomes problematic as the prostatic tissue compresses the urethra
 Prevalence in US men 60+ years old is about 50% (90% of men by age
70 have this issue), so it’s very common
 Mechanism?
 Aging/circulating androgens disrupt the balance of growth factor
signaling pathways creating a growth-promoting/tissue remodeling
microenvironment (leading to increased prostate volume)
 Eventually the bladder will be unable to empty all of the urine &
increased volumes are retained (which is why some old men can take
so long using the bathroom; they feel the urgency to urinate but can’t)
 Symptoms/Treatment?
 Weak urinary stream, abdominal straining, incomplete bladder
emptying, repeated urination, over years the bladder will retain urine
to the point of incontinence, bladder may swell and constrict
surrounding structures
 Smaller glands may be treated with laser therapy/microwave
thermotherapy, larger glands may be removed surgically, hormone
therapy (antiandrogen agents block androgens at prostate and causes it
to shrink)
o Prostatitis
 Inflammation of the prostate, usually limited to a few of the gland’s excretory
ducts
 Characterized as:
 Acute bacterial prostatitis: ascending infection of the urinary tract that
occurs in men between ages 20-50 (also associated with BPH in older
men)
o Infection stimulates inflammatory response in which prostate
becomes enlarged, tender and firm
o Can be serious if infection spreads (septicemia)
 Chronic bacterial prostatitis: recurrent urinary symptoms/persistence
of pathogenic bacteria in urine or prostatic fluid
o Most common recurrent urinary tract infection in men
o Usually caused by prostatic calculi so it’s hard to treat, may have
to surgically remove the calculi stones
 Non bacterial prostatitis: prostatic inflammation without evidence of
bacterial infection
o Most common prostatitis syndrome
o Caused by a reflux of sterile urine into the ejaculatory ducts as a
result of high pressure voiding
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Prostatodynia (pain in the prostate) is sometimes considered a form of
prostatitis
 May be caused by spasms in the genitourinary tract or tension in the
muscles of the pelvic floor rather than a pathologic condition
o Cancer of prostate
 in the US it’s the most common cancer in males, accounts for 15% of all cancer
deaths (only lung cancer accounts for more), 75%+ of all prostate cancer is
diagnosed in men older than 65, black men have highest rates of prostate
cancer in the world
 considered a disease associated with aging, thought to metastasize by local
extension/through lymphatic & blood vessels (often asymptomatic until it’s
too late)
 Dietary/Environmental Factors
 Worldwide distributions points to dietary issues involved
 Risk factors include: high intake of fat, high Ca+ levels, low intake of
dietary fiber & complex carbohydrates, high intake of protein,
consumption of excess calories, low levels of sun exposure
 Smoking, excessive drinking and pesticides (carcinogens) can play a
role as well
 Hormonal Factors
 Higher levels of circulating androgens and estrogens seem to have a
negative affect
 Has not be thoroughly studied yet
 Vasectomy
 It’s unlikely that it plays a causal role but it may contribute to the
condition
 Genetic/Epigenetic Factors
 Strong genetic predisposition present
 This is a complicated condition with lots of factors/inter-workings present.
It’s best to read the section from P865 (pathogenesis) to P869 to fully
understand.
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Sexual Dysfunction in Men
P869-870
 Defined as the impairment of any or all of the sexual response processes: erection, emission
& ejaculation
 In men older than 40 years, organic factors are involved in more than 50% of cases:
o Vascular, endocrine, and neurologic disorders
 Any disruption in vasculature can prevent blood from entering shaft, therefore
preventing erection
 Endocrine problems that reduce testosterone production can affect
libido/sexual function
 Spinal cord injury, tumors, multiple sclerosis, peripheral neuropathies all
affect sympathetic/parasympathetic/CNS mechanisms & can lead to erectile
disorders
o Chronic disease (including renal failure and diabetes mellitus)
o Penile diseases/penile trauma
 Infections that cause fibrous tissue to develop, Peyronie disease, any damage
to the erectile tissue
o Iatrogenic factors (surgery, pharmacologic therapies)
Impairment of Sperm Production & Quality
P870-871
 Spermatogenesis requires adequate secretion of FSH/LH by the pituitary & sufficient
secretion of testosterone by the testes. This process depends not only on the appropriate
stimulation (so the gland will release the hormone) but also on the appropriate response of
target organ.
o Fertility is adversely affected if spermatogenesis is normal but the sperm are
chromosomally/morphologically abnormal or are produced in insufficient quantities
o Sperm motility is also an important variable (motility is affected by sperm’s chemical
environment or semen)
Disorders of the Female (and Male) Breast
P871-909
 Galactorrhea: persistent/excessive secretion of a milky fluid from the breasts of a women
who isn’t pregnant (can occur in men too)
o Most common cause is nonpuerperal hyperprlactinema (excessive amounts of
prolactin in blood). May be caused by
 Drugs (phenothiazine, estrogen, narcotics and tricyclic antidepressants)
 Hypothyroidism (causes hypoth to release TRH that stimulates prolactin
release)
 Pituitary tumors (prolactin secreting tumors, putting pressure on pituitary,
etc.)
 Chronic stress: inhibits PIF (prolactin inhibiting factor)
 Persistent/repeated sucking/squeezing of nipples on daily basis
o Women may experience irregular period, milky breast secretion, headaches, visual
field disturbances and sleep disturbances
 Benign breast disease (BBD): noncancerous changes in the breast
o Nonproliferative (fibrocystic changes): benign alterations in ducts/lobules occur in
the breast that occur with the menstrual cycle (so a kind of waxing/waning affect
going on)
 Common symptoms reported are pain, palpable mass or nipple discharge,
sometimes there is inflammation from a ruptured cyst (most women have this
and it’s not serious)
o Proliferative breast lesions w/out atypia
 Characterized by proliferation of ductal epithelium and/or stroma w/out
cellular signs of malignancy. Classified in the following ways:
 Epithelial hyperplasia: presence of more than 2 cell layers above
basement membrane, moderate to florid hyperplasia is more than 4 cell
layers above basement membrane
 Sclerosing adenosis: number of acini per terminal duct is greater than
twice the number found in uninvolved lobules, calcification is common
but normal lobular arrangement is maintained
 Radial scar: irregular, radial proliferation of ductlike small tubules
entrapped in a dense fibrosis
 Papillomas: multiple finger-like projections/branching axes lined by
myoepithelial cells and luminal cells
o Proliferative breast lesions w/ atypia: there is abnormal structure present
Atypical hyperplasia (AH): increase in the number of cells w/ some variation
in cellular structure, women with AH have a 4x increased risk in developing
cancer
 Ductal hyperplasia: increase number of cells mostly within the lumen of the
terminal ducts
 Lobular hyperplasia: proliferation of small, uniform cells in the lumen of
lobular units
o Treatment consists of relieving symptoms, changing diet, cysts will usually disappear
w/out treatment
Cancer (really complicated section, might want to review P880-908)
o Breast cancer is the most common cancer in American women, leading cause of death
for ages 40-44, & 2nd most common killer of women (lung cancer is first)
o Risen steadily since 1950 (probably due to more diagnosis these days) and leveling
off at 126 cases per 100,000 women. Lifetime risk is 1 in 8 for white women, lower
for black women
o Breast cancer can spread to almost anywhere in the body, but most likely goes to the
bone, lungs, lymph nodes, brain and liver
 This is why it must be treated as a systemic (rather than localized) disease
o Risk factors include:
 Reproductive: nulliparous women are at greater risk (or women who have
their 1st child past 30), the younger the woman is for her 1st birth the less her
risk
 Stem cells are the origin for breast cancer. It’s believed that early
pregnancy reduces stem cells
 Age and reproduction is also suggested to affect lobular involution
(breast epithelium atrophies/disappears). The more involution/higher
rate a woman experiences involution, the lower her risk of breast
cancer
 Hormonal: oral contraceptive & estrogen replacement therapy may be risks
 The key here is tissue remodeling that applies to pubertal growth,
immediately after pregnancy and during involution
 Also important to note that women with higher mammographic density
(less fat) have a higher risk of breast cancer
 Environmental: environment influence most high during differential stages
(puberty, pregnancy, lactation, involution and menopause)
 Radiation: exposure to ionizing radiation increases risk (especially
during pregnancy/adolescence)
 Diet:
o Small relationship between dietary fat and risk (due to high
concentrations of fat-soluble chemicals found in the breast)
o Obesity reduces risk of premenopausal breast cancer, BUT
increases risk in postmenopausal women
o Alcohol consumption increases risk (b/c it hinders the liver’s
ability to di the body of cancer-causing agents & impairs
immune system)
o Soy consumption may decrease risk
 Chemicals: long standing exposure is the key
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o Includes pollution, pesticides, fuels, plastics, detergents and
drugs
 Lifestyle: regular physical activity may reduce risk
 Familial: history of cancer in 1st degree relatives increases risk 2/3 times
 Genes responsible for inherited cancer syndromes appear to be tumorsuppressor genes
 Black women have 32% higher death rate from breast cancer than
white women
 Breast cancer pts younger than 35 have a worse prognosis than older
pts
Ductal carniomas in situ (DCIS): heterogeneous group of proliferations limited ot the
ducts/lobules
Lobular carcinoma in situ (LCIS): originates from the terminal duct-lobular unit
(unlike DCIS, LCIS has uniform appearance and occur in noncohesive clusters in
lobules)
Inflammatory stroma in breast cancer: early alterations in stroma that occur with
wound healing/inflammation may contribute (in other words, inflammation
stimulates tumor cells)
Invasive breast carcinoma: malignant, invasive epithelial lesion derived from
terminal duct lobular unit
Disorders of the Male Breast
P908
 Gynecomastia: overdevelopment of breast tissue in male , affects 30-40% of male
population
o Results from hormonal alterations (which may be idiopathic or result from systemic
disorders, drugs or neoplasms)
o Usually involves imbalance of estrogen/testosterone ratio
 Cancer: male breast cancer accounts for 1% of all male cancers and less than 1% for all
breast cancers combined